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    Accsap 9

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    Adeel Lakhiar
    This patient presented with pneumonia and was found to have atrial fibrillation. Warfarin is recommended for anticoagulation due to her high risk score and interactions between her medications for HIV and other anticoagulants like dabigatran or rivaroxaban. A postpartum woman presented with shortness of breath and palpitations. Her EKG shows ventricular tachycardia which should be treated with intravenous lidocaine. A young woman with known pre-excitation presented with respiratory distress and palpitations. Her EKG shows supraventricular tachycardia which should be treated with intravenous verapamil.

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    Accsap 9

    Uploaded by

    Adeel Lakhiar
    3K views936 pages
    This patient presented with pneumonia and was found to have atrial fibrillation. Warfarin is recommended for anticoagulation due to her high risk score and interactions between her medications for HIV and other anticoagulants like dabigatran or rivaroxaban. A postpartum woman presented with shortness of breath and palpitations. Her EKG shows ventricular tachycardia which should be treated with intravenous lidocaine. A young woman with known pre-excitation presented with respiratory distress and palpitations. Her EKG shows supraventricular tachycardia which should be treated with intravenous verapamil.

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    ACCSAP 9

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    This patient presented with pneumonia and was found to have atrial fibrillation. Warfarin is recommended for anticoagulation due to her high risk score and interactions between her medications for HIV and other anticoagulants like dabigatran or rivaroxaban. A postpartum woman presented with shortness of breath and palpitations. Her EKG shows ventricular tachycardia which should be treated with intravenous lidocaine. A young woman with known pre-excitation presented with respiratory distress and palpitations. Her EKG shows supraventricular tachycardia which should be treated with intravenous verapamil.

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    3K views936 pages

    Accsap 9

    Uploaded by

    Adeel Lakhiar
    This patient presented with pneumonia and was found to have atrial fibrillation. Warfarin is recommended for anticoagulation due to her high risk score and interactions between her medications for HIV and other anticoagulants like dabigatran or rivaroxaban. A postpartum woman presented with shortness of breath and palpitations. Her EKG shows ventricular tachycardia which should be treated with intravenous lidocaine. A young woman with known pre-excitation presented with respiratory distress and palpitations. Her EKG shows supraventricular tachycardia which should be treated with intravenous verapamil.

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    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
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    of 936

    Ar

    ryt
    hmi
    as

    1.A67- year-oldwomanwhowasadmi tt
    edf orpneumoni awasincidental
    lyfoundt o
    have par oxysmalat rialfi
    bri
    ll
    ati
    on.She has a hi st
    ory oft ype 2 di abetes,
    hypertension,andhumani mmunodef i
    ciencyvirus.Shetakessubcutaneousi nsul
    in,
    carvedil
    ol,darunavi
    r,andri
    tonavi
    r,andiscompl iantwit
    hhermedi cati
    ons.Whi chof
    thefoll
    owingwoul dbet hepref
    err
    edanticoagulant?

    a. Dabi
    gat r
    an.
    b. Ri
    varoxaban.
    c. Warf
    ar i
    n.
    d. Aspi
    rin.
    e. Cl
    opidogrel
    .

    Answer

    C.War
    far
    in

    This pat i
    enthas a CHA2DS2- VASc score ofatl east4 and meet s cri
    teri
    af or
    anticoagulation.Nei t
    heraspi ri
    n norcl opi
    dogrelal one arer ecommended f or
    prevention ofst roke i
    nt he set t
    ing ofa high CHA2DS2- VASc scor e without
    cont rai
    ndications to ant
    icoagulati
    on.Because ofherpr otease inhi
    bit
    or -
    based
    antiretr
    oviralt her
    apy,sheisnotagoodcandi dat
    ef ordabigatranorr i
    varoxaban
    becauseherhumani mmunodef i
    ciencyvi
    rusmedicat i
    onsarest ronginhibit
    orsof
    cytochromeP4503A4andP- glycoprot
    eindrugeff
    lux.Thisinhibit
    ionresultsinan
    i
    ncr ease int hese drugs'effects.Theref
    ore,war f
    ar i
    nist he bestchoi ce for
    anticoagulation.

    2.A 39- year


    -ol
    d woman 2 weeks post partum i s admi
    tted t
    ot he hospi
    talwit
    h
    shortnessofbreat
    handpalpi
    tat
    ions.Shet akesnomedi cati
    ons.Herexaminat
    ioni
    s
    notableforaheartrat
    eof110bpm,bl oodpr essureof92/60mm Hg,andoxygen
    saturati
    onof98%.Therear
    ebibasil
    arralesandanS3  gal
    lopand2+pitti
    ngedemaof
    herlowerextr
    emiti
    es.Herelectr
    ocar
    diogram i
    sshowni nFi
    gur
    e1.Whi
    choft
    he
    fol
    lowi
    ngint
    ravenousmedicat
    ionsshouldbeadmini
    ster
    ed?

    a. Verapami l.
    b. Ivabradine.
    c. Adenosi ne.
    d. Lidocaine.
    e. Magnesi um.

    Answer

    D.Li
    docai
    ne

    The electr
    ocar diogram demonst rat
    es vent ri
    culart achycardia( VT)wi t
    h a wi de
    regularQRSr hyt hm,ext r
    emer ightaxisdevi at
    ion,QRSdur ati
    onofanat ypicalri
    ght
    bundlemor phol ogywi t
    ht heRwave>t her 'wave.TheQRSdur ati
    oni s>140msec,
    alsofavori
    ngVTi nar i
    ghtbundl emor phologyt achycardia.Ther eisalsoanSwave
    >Rwavei nleadV6  f
    urtherfavori
    ngVT.Oft hechoi cesgiven,lidocaineist hemost
    appropriat
    echoi cef orthetreatmentofVT.Adenosi neisusef ulforthetreatmentof
    supraventr
    iculart achycardi
    a( SVT) .Verapami lisusef ulfort het r
    eatmentofSVT
    andsomeVTs, wi t
    hamor etypicalri
    ghtbundl ebr anchblockmor phology,al ef
    taxis
    deviati
    oninapat i
    entwi t
    hanor malhear t
    .Ivabr adineisusefulf orthetreatmentof
    i
    nappr opri
    atesinust achycardiaandt otreatsinust achycardiai npatient
    swi thheart
    f
    ail
    ure.Magnesi
    um canbeusef
    ulfort
    hetr
    eatmentoft
    orsadesdepoi
    ntes,notas
    f
    ir
    st-l
    inet
    reat
    mentf
    orpati
    ent
    swithmonomorphi
    cVT.

    3.A19- year -oldgi rlwithknownvent ri


    cularpre-exci
    tati
    ononherel ectr
    ocardiogram,
    butnopr iorhi storyofpal pit
    ati
    onsorsyncope,i sseeni nt heemer gencyroom i n
    acuter espiratorydi stressduet obronchospasm.Shei streat edwi t
    hanal buterol
    nebulizer,intravenous ( I
    V)solumedr ol
    ,and I V diphenhydr amine.I nt
    ubat i
    on i s
    avoided, andshei smar kedl
    yimprovedandr eadyfordischar gewhenshesuddenl y
    experiencespal pitati
    onsandchestdi scomfort.Herheartr atei s170bpm,bl ood
    pressure90/ 64,l ungshaveaf ew scatter
    edwheezesandcar diacexami nati
    oni s
    benignexceptf ort achycardi
    a.Anel ect
    rocardi
    ogram isobt ainedandi sshowni n
    Figure1.Car otidsi nusmassageandVal salvamaneuver sarei nef
    fecti
    ve.
    I
    Vadmi ni
    str
    ati
    onofwhi
    choft
    hef
    oll
    owi
    ngi
    sthenextmostappr
    opr
    iat
    est
    epi
    nher
    management?

    a. Metoprolol.
    b. Verapami l
    .
    c. Pr
    ocainami de.
    d. Adenosine.
    e. Cal
    cium gluconat
    e.

    Answer

    B.Ver
    apami
    l

    The pat i
    ent has supr avent r
    icular t achycardia, most l ikely or t
    hodromi c
    atri
    ovent ri
    cul
    ar(AV)r eci
    procatingt achycar dia.Al
    thoughadenosi neisusuallyfi
    rst-
    l
    inetr eatment,t
    hispat i
    entjustrecover edf rom anacut easthmat icexacerbati
    onand
    shouldnotr eceiveadenosi neormet opr olol.Therefore,IV ver apamilshouldbe
    admi nister
    ed.Pr ocainamide is usef ulf ort he treatmentofpr e-
    excited at
    rial
    fi
    bril
    lationandi snotf i
    rst
    - l
    inetreat mentf orAV r e-ent r
    antt achycardia.Calci
    um
    gluconat eisnotusefultotreatAVr e- entrantt achycardia.

    4.A19- year-ol
    dst udentlacr
    ossepl ayercomplainsoff ourepisodesofpalpit
    ati
    ons
    occurri
    ngi nt
    hepast3mont hs.Theepisodesoccurabr uptl
    yandar eaccompani ed
    withmildchestpai n.Theepisodeshavel ast
    ed10- 15mi nut
    esi ndur
    ati
    on.Shehad
    l
    earnedt odoaVal salvamaneuvert obreaktheepisodes.Shetakesnomedi cati
    ons,
    and has no f amily hi
    stor
    y ofcar diac di
    sease orsudden deat h.Herphysi cal
    examinationi
    snor mal ,
    andherelectrocardi
    ogram i
    sshowni nFigure1.
    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    est
    epi
    nhermanagement
    ?

    a.Rest r
    ictionfrom compet i
    ti
    vesports.
    b.Electrophysiol ogystudyandcat heterablat
    ion.
    c.Implant ablecar diovert
    er-def
    ibr
    il
    lator(I
    CD)implant
    ati
    on.
    d.Ami odar onet herapy.
    e.Met oprol olt
    wi cedaily.

    Answer

    B.Electr
    ophysiologystudyandcat heterablation.
    Thepat ienthassympt omaticWol f
    f-Par ki
    nson-Whi t
    e( WPW)syndr ome.Cat heter
    ablati
    oni saCl assIi ndicati
    onduet osympt omsandi ncreasedr i
    skofsudden
    cardiacdeath.Restri
    cti
    onf r
    om compet i
    ti
    vespor tsi
    snotr ecommendedf orpatients
    withWPW,ast heepisodescanoccuratanyt ime,andsuddendeat hcanoccur
    regardl
    essofexer ci
    sebehavi or.I
    CDi mpl antati
    onisaCl assI I
    Irecommendationt o
    preventsuddendeat hi napat i
    entwhohasanar rhythmiacur abl
    ewi t
    hablat i
    on.
    Met opr
    ololandami odar onearenotr ecommendedf orpatientswithWPW.I tmay
    decreasethefrequencyofsupr aventr
    iculartachycardi
    a,butitdoesnotdecreaset he
    r
    iskofsuddencar
    diacdeat
    h.

    5.A 23- year-ol


    d graduate studentcomes t ot he emergency depar
    tmentwi t
    h
    l
    ightheadedness,palpit
    ati
    ons,andshor t
    nessofbreath.Shehasnopr i
    ormedi cal
    hist
    oryand t akes no medicat i
    ons.On physicalexaminati
    on,herhear trat
    ei s
    i
    rregular,appr
    oaching220bpm.Herbl oodpressureis82/56mm Hg.Shei salert
    butanxious.Hercardiacexami nationi
    ssigni
    fi
    cantforanirr
    egul
    artachycar
    dicrate,
    butotherwiseisnormal.Herelectrocar
    diogr
    am isshowninFigure1.

    Basedonherel
    ect
    rocar
    diogr
    am,
    whi
    choft
    hef
    oll
    owi
    ngi
    str
    ue?

    a.Sheisati ncreasedriskforsuddendeat h.
    b.Metoprololwi l
    lter
    mi nat
    ethet achycar
    dia.
    c.Impl
    antat i
    on of an i mplantable cardi
    over
    ter
    -def
    ibr
    il
    lat
    or (
    ICD) i
    s
    appropri
    at e.
    d.Hyperkalemiai spresent.
    e.Adenosinewi llter
    minatethetachycardia.
    Answer

    A.Shei
    satr
    iskedf
    orsuddendeat
    h.

    Thepat i
    enthaspr e- exci
    tedatri
    alfi
    bril
    lation(AF)( AFconduct ingt othevent ricles
    downanaccessor ypat hway).Theel ectrocardiogram demonst ratesani r
    regul ar
    widecompl extachycar di
    aataver yfastr ate.Thef astratesoft het achycar dia,at
    ti
    meswi thR- Ri ntervalsof<250msec,ar ear iskf actorforsuddencar diacdeat h.
    Becauset hemor phol ogyoftheQRScompl exesi ssi mil
    ar,shel ikelyhasasi ngle
    accessor ypat hway.Herpot assium l
    eveli sli
    kelyt obenor mal.Theacut et reatment ,
    becauseshei shemodynami callyst
    abl e,isint
    r avenouspr ocai
    nami de.I funst abl e,
    electr
    icalcar dioversioni sappropri
    ate.I CD impl antati
    oni saCl assIII-indicat ed
    procedur ei n a pat i
    entwho hasan ar rhythmi a amenabl eto cat heterabl ation.
    Met oprolol,adenosine,andot heratr
    iovent ri
    cul
    arnodalbl ocki
    ngagent smayr esul t
    i
    nsel ectiveuseoft heaccessorypathwayandi ncreaseconduct iont othevent ricles
    throught hepat hway.

    6.Unli
    kemostot heror
    alant
    iar
    rhyt
    hmicdrugs,amiodaroneisoftenini
    ti
    atedwi t
    ha
    l
    oad( ahigherdoseforsever
    aldaysorweeks)beforedecreasingtomaintenance
    dosi
    ng.Whichoft hef
    oll
    owi
    ngpharmacol
    ogicproper
    tiesbestexplai
    nst
    her easonto
    l
    oadami odarone?

    a.Multi
    pleantiarrhyt
    hmi cclassef
    fect
    .
    b.Longhal f
    -li
    fe.
    c.Largevolumeofdi st
    ri
    but i
    on.
    d.Fi
    rst-passeffectintheliver.
    e.Highiodineconcent r
    ation.

    Answer

    C.Lar
    gevol
    umeofdi
    str
    ibut
    ion

    Drugssuchasami odarone,whi
    chhaveal ar
    gevolumeofdist
    ri
    but
    ion,areoft
    en
    l
    oadedwi thagr eaterdosageadmini
    ster
    edearl
    yon.Alt
    houghamiodaronedoes
    haveal onghalf
    -li
    fe,incr
    easi
    ngthedoseofthedrugear
    lyondoesnotal l
    ow t
    he
    achievementofasteadystat
    eanyfast
    er.
     

    7.A72- year- ol
    dwomanpr esentswit
    hcompl aintsofweaknessandf at
    igue.Shehasa
    pasthi storysignif
    icantforatri
    alfibri
    ll
    ati
    onmanagedwi t
    hr atecontrolstr
    ategy,
    peri
    pher alvasculardisease,andhyper t
    ension.Sher ecent
    lywasdi schargedfrom
    thehospi talf
    oll
    owingar ecurr
    entepisodeofatrialf
    ibr
    il
    lat
    ionrequi
    ri
    ngcar di
    oversi
    on.
    Shei
    sunclearwhatherhomemedi
    cat
    ionsar
    e,butknowsshewast
    aki
    ngsever
    al
    newmedi
    cationsf
    orherhear
    t.
     

    Uponphysi calexaminati
    on,sheisconfusedandlethar
    gic.Herbloodpressurei
    s
    91/54mm Hgandpul seis103bpm.Physi calexaminati
    onisremarkablefora
    tachycardi
    cr hyt
    hm and no mur murs.She compl ai
    ns ofblurred vi
    sion.An
    elect
    rocardi
    ogram (
    ECG)obt ai
    nedint
    heemer gencydepartmenti
    sshowni nFigur
    e
    1.

    Therecentaddi
    tionofwhichofthefoll
    owingmedi cati
    onstothi
    spat
    ient
    'smedi
    cat
    ion
    regi
    meismostlikel
    yresponsi
    bleforhercl
    ini
    calf
    indingsandECGchanges?

    a.Dronedarone.
    b.Ami l
    odipi
    ne.
    c.Nadolol.
    d.Apixaban.
    e.Labetal
    ol.
    Answer

    A.Dr
    onedar
    one

    Dronedarone i s a pot ent i nhi


    bit
    or of P- glycoprotei
    n. When admi ni
    ster
    ed
    concomitantlywithdigoxin,itmayleadt osubstantiali
    ncreasesindi goxinsteady-
    statelevels.Co- administrati
    on ofdigoxin and dr onedarone r equires a dose
    reduct
    ionindi goxin(asisal sothecasewi thami odaroneco- admi nistrati
    on).The
    ECG demonst rat
    es bidi
    rect i
    onalventr
    icul
    art achycardia,a classi calf indi
    ng in
    digoxi
    nt oxici
    ty.Thepat ientisdigoxintoxi
    candshoul dbet reatedwi t
    hdi goxi
    n
    i
    mmuneFab( ovine).Theot heragentsar enoti nhibit
    orsofP- glycopr otei
    nand
    wouldnotbeexpect edtoresultint
    heclini
    calconditi
    ondescr i
    bed. 

    8.A 67- year


    -ol
    d man pr esent
    st o youroffi
    ce wit
    h complai
    nts ofdizzi
    ness and
    l
    ightheadedness.About3 mont hs ago,he underwenti
    mplantat
    ion ofa dual-
    chamberpacemakerf orsympt omaticcomplet
    ehear tbl
    ock.Hisl ef
    tventr
    icul
    ar
    eject
    ion fr
    acti
    on atthe time was normal.His otherhi
    stor
    yi sremarkablefor
    rheumat oi
    dart
    hri
    ti
    sandhyper tensi
    on. 

    About10daysago,hewasadmi t
    tedtothehospi
    talfol
    lowinganepisodeofatr
    ial
    fi
    bri
    ll
    ati
    onandj oi
    ntpai
    n.Hewascar di
    over
    tedatt hatti
    me.Hewasdi schar
    ged
    homewi thsever
    alnew medi
    cati
    onsthathedoesnotr ecallthenamesof,buthe
    stat
    esthathehasbeencompl
    iantwit
    hthem. 

    Atthet i
    meofyourexami nati
    on,thepati
    ent'
    sbloodpressur
    emeasur ed92/47mm
    Hgint heri
    ghtarm and97/ 52mm Hgi ntheleftarm.Hispul
    semeasur ed39bpm.
    Uponauscul t
    ati
    on,nomur murswereappr eci
    ated.CannonA waveswer enot
    ed
    uponneckexami nation.Labor
    atorystudi
    esincludenormalrenalf
    unctionandan
    i
    nternati
    onalnor
    malizedrati
    oof1.1.

    Therecentaddi
    tionofwhi
    chofthefol
    lowi
    ngmedi
    cat
    ionsi
    smostl
    ikel
    yresponsi
    ble
    fort
    hecli
    nicalf
    indi
    ngsint
    hispat
    ient
    ?

    a.Dof
    eti
    li
    de.
    b.Ver
    apamil
    .
    c.Amiodarone.
    d.Pr
    ednisone.
    e.Fl
    ecaini
    de.

    Answer

    E.Fl
    ecai
    nide

    This pat ientpr esentsf oll


    owi ng a r ecentboutofat ri
    alf ibril
    lati
    on wi th cli
    ni cal
    evidenceofcompl etehear tbl ock.Hi spul seisbr adycar di
    c,andhedemonst rat es
    cannonA waves.Hei spr esumabl ydevi ce-dependentwi thacl inicalhi storyof
    compl etehear tbl ock.Fl ecai nidei sknownt oi ncreasepaci ngt hreshol ds.Att he
    ti
    me of i niti
    at i
    on of cl ass I c agent s, pacer -dependent pat i
    ent s r equi re
    reprogr ammi ngoft heirdevi ceswi t
    hi ncreasedleadout putst oensur emyocar dial
    capt ure.Thi spat ient'
    scl i
    ni calpr esentationi sclassi calf oradevi ce- dependent
    patientwhoi si niti
    atedonacl assI cagentwi t
    hnor epr ogr ammi ngofdevi ceout put s.
    Followi nganadequat eamountofdr ugl oad,pacingt hr esholdr iseandmyocar dial
    capt uremaybel ost,r
    esul t
    ingi nl ossofcapt ureandar esultantescaper hythm.The
    otheragent sl i
    steddonotr aisepaci ngt hresholds(steroidsact uallylowert hem and
    arei ncorpor atedi ntol eadt ipst oreducet hresholdsatt het imeofl eadi mpl ant).I n
    thi
    si nstance,f lecainideshoul dbedi scont i
    nuedandpaci ngout putsi ncreasedt o
    ensur emyocar dialcapt ure.

    9.A 24- year-


    old compet i
    ti
    ve runner present
    s f or evaluati
    on of t achycardic
    palpit
    ati
    ons.Shedescri
    best hem assuddeninonsetandt erminati
    on.Theybegan
    when shewasabout11 year sold.Overt heyears,shehasnot ed thatt hese
    episodesareprogressivel
    ywor seni
    ng infrequencyand sympt oms.Herf ami l
    y
    histor
    yi sr
    emarkabl
    ef oranuncl ewhodi edofamassi vehear tatt
    ackatage51
    years. 

    Baseli
    neelectrocar diogr
    am ( ECG)isnor malasisherphysi calexaminati
    on.Event
    monitori
    ng discloses evi dence ofsust ai
    ned narr
    ow compl ex t
    achycardi
    a.The
    pat
    ientisr ef
    erredf orelectrophysiol
    ogictest
    ingandpossi blecathet
    erabl at
    ion.
    Duri
    ngt hecourseofel ect
    rophysiologytest
    ing,
    thetachycardiashowni nFigure1i s
    i
    nduced.Dur ing t achycardia,a dr ug i
    s administ
    ered,resulti
    ng inthe findi
    ngs
    di
    splayedinFigur e2.
    Fi
    gur
    e1.

    Fi
    gur
    e2.
    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    ymechani
    sm oft
    achycar
    dia?

    a.Orthodromi creciprocati
    ng t
    achycardi
    a uti
    li
    zing a l
    eftl
    ater
    alaccessor
    y
    pathway.
    b.AtypicalAVNRT.
    c.Ventricul
    artachycardia(VT).
    d.Leftatri
    altachycardia.
    e.Typicalatr
    ioventri
    cularnodalre-
    entr
    anttachycar
    dia(AVNRT).

    Answer

    E.Typi
    calat
    ri
    ovent
    ri
    cul
    arnodalr
    e-ent
    rantt
    achycar
    dia(
    AVNRT)
    .

    Figure1demonst ratesi nit


    iationoft achycar dia.Theel ectrogramsar earranged
    from topt obot tom asf ol
    lows:sur f
    aceECG,hi ghr ightatrialrecording,Hisbundl e
    recording,cor onary si nus r ecor ding ( proximalt o distal)
    ,and r i
    ghtvent ri
    cular
    recording.Dur ing t achycar dia,t her ei sat ypicalcol umnarappear ance ofal l
    electr
    icalact i
    vity,wi thaver yshor tvent ri
    culoatr i
    al(VA)t i
    me.Ear l
    iestatri
    alacti
    vi t
    y
    i
    snot edatt heHi sbundl er ecor ding.Thi sshor tVA t imeexcl udest achycardia
    util
    izi
    nganaccessor ypat hwayaspar toft het achycar diccircuit,soor t
    hodromi c
    reciprocatingt achycar diai snotcor rect.Leftat ri
    altachycar diawoul dbeexpect ed
    todemonst r
    ateear liestat r
    ialact ivit
    yatt hedist alcoronar ysinusel ectr
    ograms( CS
    1,2).Thisiscl ear l
    ynott hecaseher e.VTi snott ypical
    lyanar r
    owcompl exinnat ure
    and of ten exhi bit
    sVA di ssoci ation.I nt hisi nstance,t heV and t heA ar e1: 1
    associ atedwi t
    haver yshor tVAi nterval.Thisessent i
    all
    yexcl udesVT.  

    Thedi ff
    erencebet weent ypicalandat ypicalAVNRTi sr elatedt ot heVAi nter
    val
    dur i
    ngt achycar dia, asthi
    sr efl
    ectst hedi recti
    onalityoft here- ent
    rantci rcuit. Typi
    cal
    AVNRTi schar act erizedbyant erogr adeconduct iondownsl ow f i
    ber soft heAVN
    compl ex,wi tht he r etr
    ograde l imb occur ri
    ng overf asterconduct i
    ng fiber s.In
    atypicalAVNRT,t heopposi tei sessent i
    allythecase.Hence,i nat ypicalAVNRT,t he
    VAi nt ervaltypicallyi sprolonged( >70msec) ,andt hi
    smani f
    estsasal ongerRP
    intervalon sur f
    ace ECG.I nt his case,dur i
    ng t achycar dia,t he sur face ECG
    lead V1 doesshowsomeevi denceofshor tRPi nterval(pseudo- R'),reflecti
    veoft he
    veryshor tVAi nter valseenont hei nt r
    acar di
    acel ectrograms.Consequent ly,inthis
    case,t hecor r
    ectansweri st ypicalAVNRT.Thedr ugadmi nisteredi nFi gur e2was
    adenosi ne, result
    ingi nt
    ermi nati
    onoft achycar diawi t
    hbl ocki nthesl owpat hwayof
    theAVnodeandsubsequentcompl eteAVbl ock( notet heat ri
    alel ectrogramswi th
    noassoci atedHi sel ectr
    ogramsorvent r
    icularactivit
    yt other i
    ghtoft het r
    aci ng).

    10.
    An84- year-
    oldfemalewit
    hapastmedi calhist
    orynot
    abl
    ef orat
    ri
    alfi
    bri
    ll
    ationand
    hyper
    tension,present
    stothehospi
    talaft
    erasyncopalepisodewithoutprodrome
    whil
    eeat i
    ngdinner.Sher
    egai
    nedconsciousnessaft
    er20seconds,andotherthana
    contusiononhercheekf rom wher eherf acehi thersoupbowl ,shewasunhar med.
    Therewasno i ncont i
    nenceorgener ali
    zed t onicclonicact i
    vit
    y.Herexam was
    notablef orasyst olicejectionmur mur ,butther ewer enoot hersi
    gni f
    icantf
    indings.
    Anel ectrocardi
    ogr am ( ECG)wasobt ainedthatdemonst r
    atedar i
    ghtbundl ebranch
    block( RBBB)andl eftanter i
    orfasci
    cul arbl
    ock.Anechocar diogram demonst rated
    normalbi vent
    ri
    cularf unctionandaor t
    icscler osis.Myocar di
    alperfusi
    onst r
    esst est
    revealednoevi denceofi schemi a.Att heel ectrophysiol
    ogy( EP)study,therewas
    not evi dence of i nducible vent r
    icular tachycar dia (VT),and t he foll
    owing
    elect
    rogr am wasr ecor ded( Figur
    e1).

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    einhercar
    e?

    a.Single-
    chamberpacemaker .
    b.Dual-chamberpacemaker .
    c.Eventmoni t
    or.
    d.Implantabl
    elooprecorder
    .
    e.Cardiacresynchr
    onizat
    ionther
    apypacemaker
    .
    Answer

    B.Dual
    -chamberpacemaker
    .

    Thepat ientdevel oped syncopei nt heset ti


    ng ofbi fasci
    cularblock.Diagnost i
    c
    testi
    ngr evealsapr ol
    ongedHV i nterval(nor mali s35- 55msec).Int hissetti
    ng,
    permanentpaci ngisindicated.I
    nt hispatientwi thnor malejecti
    onfract
    ion,cardiac
    resynchronizati
    ont herapyisnotindicated.Ani mplant ablecardi
    overt
    er-defi
    bri
    ll
    ator
    i
    snoti ndicated, asherEPst udyshowednoi nducibleVTandherej ecti
    onf r
    acti
    oni s
    >35%.Cur rentgui del
    inesgi veaCl assIi ndi cati
    ont opermanentpaci ngi nt he
    setti
    ngofpr olongedHV i nter
    val,andaCl assI Iai ndicati
    ont oimplantati
    onf or
    unexplai
    nedsyncopei nt hesetti
    ngofbi fascicularblock.

    11.
    A59-year-
    oldmanpr esent
    swithr
    ecur
    rentunexpl
    ainedsyncope,
    wit
    houtpr
    odr
    ome.
    Hispastmedicalhi
    storyisnot
    abl
    eforacoronaryarter
    ybypass10yearsagoand
    hyper
    tensi
    on. 

    Physicalexami nati
    onr evealsahear trateof80bpm,bl oodpr essureof120/ 74mm
    Hg,andj ugularvenouspr essureof8cm.Car di
    ovascul arexami nationisr egul
    ar
    withoutmur mur .Anel ectr
    ocardiogram demonst ratednor malsi nusr hythm with
    QRSdur ati
    onof119msec.Echocar diogram showsi nferol
    ateralakinesi
    sandl ef
    t
    ventri
    cularejecti
    onf r
    act i
    onof45%.Si ngle-photonemi ssioncomput edtomogr aphy
    myocar dialper f
    usion i maging shows i nferol
    ateralscar wi thoutevi dence of
    ischemia.

    Whi
    choft
    hef
    oll
    owi
    ngi
    smostappr
    opr
    iat
    eint
    hecar
    eoft
    hispat
    ient
    ?

    a.Si
    ngl e-
    chamberimpl antablecar
    dioverter
    -def
    ibr
    il
    lat
    or(
    ICD)i
    mpl
    ant
    ati
    on.
    b.Diagnosti
    celectr
    ophysiology(EP)study.
    c.Cardiacmagneticresonancei maging.
    d.Coronaryangiography.
    e.I
    mpl antat
    ionofani mplantabl
    eloopr ecor
    der.

    Answer

    B.Di
    agnost
    icel
    ect
    rophysi
    ology(
    EP)st
    udy.

    The pati
    enthas syncope,str
    uct
    uralhear
    tdisease,and evidence ofscaron
    echocar
    diogr
    am andmyocar di
    alperf
    usi
    onimaging.Ther
    efore,revascul
    ari
    zat
    ion
    andi magingwithanaddi t
    ionalmodali
    ty,suchasmagnet i
    cr esonanceimagi ng,ar
    e
    notindicated.Thenextmostappr opriatestepist oriskstrati
    fyhimf orinducibl
    e
    ventri
    culararr
    hythmiaswithanEPst udy.Onlyifinduci
    blevent r
    icul
    art
    achycar diai
    s
    foundshoul danI CDbeimpl ant
    ed.Apost i
    nfar
    ctionpat i
    entwi t
    hsyncopewar rant
    s
    EPt esti
    ngt oexcludeinducibl
    eventri
    culararrhythmiaspriort oimplant
    ationofa
    looprecorder.

    12.
    A19- year-oldfemalepresentstot heemer gencydepartmentwit
    h6hour shistor
    yof
    recurrentpalpit
    ati
    ons.Anel ect
    rocardiogram isobtained(Fi
    gure1),andadenosine
    is given,t erminat
    ing the rhythm.Att he time ofel ect
    rophysi
    ology test
    ing,
    atri
    oventri
    cular(AV)nodalre-entranttachycardi
    aisinduced.

    Lowerr i
    skofper
    manentcompl
    etehear
    tbl
    ock;hi
    gherl
    ong-
    ter
    m ar
    rhyt
    hmi
    a-f
    ree
    sur
    vival
    .

    a.Samer i
    skofpermanentcomplet
    eheartblock;samel ong-ter
    m arrhyt
    hmia-f
    ree
    survi
    val
    .
    b.Higherriskofpermanentcompl
    eteheartblock;higherlong-ter
    m arrhyt
    hmia-
    fr
    eesurvival
    .
    c.Lowerriskofpermanentcompl
    etehear
    tblock;lowerlong-ter
    m arrhyt
    hmia-f
    ree
    survi
    val
    .
    d.Higherr
    iskofper
    manentcompl
    etehear
    tbl
    ock;l
    owerl
    ong-
    ter
    m ar
    rhyt
    hmi
    a-f
    ree
    survi
    val
    .

    Answer

    B.Higherr
    iskofper
    manentcompl
    etehear
    tbl
    ock:hi
    gherl
    ong-
    ter
    m ar
    rhyt
    hmi
    a-f
    ree
    sur
    vival
    .

    Radiofrequencyablat
    ionprovidesamor edurabl
    elesiont
    hancryoablat
    ion.However,
    the risk of inadvertent permanent i
    njuryt ot he AV node is hi gher wi
    th
    radiof
    requencyablati
    on.Successr atesforsl
    owpat hwaymodifi
    cat
    ionf orAVnodal
    re-ent
    ranttachycardi
    aar e90-95%wi thradi
    ofr
    equencyener
    gy,andar eroughl
    y80%
    withcryoablati
    on.

    13.
    A71- year-ol
    dmanwi thahi st
    oryofatri
    alfibr
    il
    lat
    ionpresentswi t
    hconf usi
    on1
    monthaf t
    erfal
    li
    ngandstr
    iki
    nghisheadwhileonapixaban.Duetot heconfusi
    on,he
    hasnottakenanyofhismedicati
    onsin4days.Physicalexaminati
    ondemonst rat
    es
    abloodpr essur
    eof124/72mm Hg,cl earlungsounds,andar egularr
    hythm.An
    elect
    rocardi
    ogram isobtainedandshowslackofadisti
    nctPwaveandahear trate
    of64 bpm ( Fi
    gure1) .A comput ed t
    omographyscan demonstr
    atesa chronic
    subduralhemat oma.Bef oretaki
    nghimt otheoperat
    ingroom,theneur
    osurgeon
    requestsacar diol
    ogyconsul ttoclari
    fytherhyt
    hm andwhetheranyaddi t
    ional
    i
    nt er
    venti
    onisrequired.

    Whi
    choft
    hef
    oll
    owi
    ngdoyout
    ellt
    hecar
    diol
    ogi
    st?

    a.Thepati
    entisinatri
    alfibri
    ll
    ati
    onandshoul dbest ar
    tedondi goxinanda
    bet
    a-bl
    ocker.
    b.Thepati
    entisin4:
    1r at
    e- contr
    oll
    edatri
    alf
    lutt
    er.Noadditi
    onalint
    erventi
    on
    i
    srequi
    red.
    c.Thepat
    ienti
    sinnormalsi nusrhythm.Nointer
    venti
    onisrequi
    red.
    d.Thepati
    entisi
    n4:1at r
    ialtachycardi
    aandshouldbest ar
    tedonadi lt
    iazem
    dri
    ptocontr
    olther
    ate.
    e.Thepat
    ienti
    sinatr
    ialfl
    utterwithvari
    abl
    eblock.Abeta-bl
    ockerisindi
    cated.

    Answer

    B.Thepat i
    enti
    sin4:
    1rat
    e-cont
    rol
    ledat
    ri
    alf
    lut
    ter
    .Noaddi
    ti
    onali
    nter
    vent
    ioni
    s
    requi
    red.

    The pat i
    enti si nr ate-cont r
    oll
    ed at r
    ialf l
    ut t
    er.Typi cal( type I)at rialfl
    utteri s
    char act eri
    zedbya" sawt oot h"patt
    er ninthei nferior(I
    I,I
    II
    , aVF)leads.Usual ly,at
    rial
    fl
    ut terpr esentsin2: 1conduct i
    onbl ockwher et herearet wof lutt
    erwavesf orever y
    conduct edQRScompl ex.Int heabsenceofat r
    ioventri
    cularnodalbl ockingagent s,
    ratios>2: 1( e.
    g.,3:1,4:1)suggestunder lyingconduct i
    onsyst em di sease.Inthi s
    situation, thepatientwasr atecontroll
    edwi t
    houtt heneedf orratecont roll
    ingagent s
    suchasbet a-bl
    ocker sorcal cium channelbl ockers.Noi nterventi
    oni sneededpr i
    or
    to sur ger y.Af t
    err ecover i
    ng f r
    om sur gery,he was subsequent l
    yt aken tot he
    elect r
    ophysi ologylabor atorywher ethedi agnosi soft ypi
    cal ,cavo-tr
    icuspi dist
    hmus
    atrialflutterwasconf irmed.Heunder wentsuccessf ulradiofrequencyabl ati
    on.

    14.
    A 32-year-ol
    dwomanwi t
    hal onghistoryofr arepal pi
    tat
    ionspresentst oyour
    cardi
    ologycli
    nicwi t
    hincreasingl
    yfr
    equentepi sodes.Sheis10weekspr egnantand
    isotherwiseheal t
    hy.Sher eportsthatdur i
    ngherpr egnancy,herepisodeshave
    become increasinglyfrequent,and int he pastweek,t he episodes have been
    occurr
    ing multipletimes a day lasting severalmi nutes ata t i
    me.She can
    sometimesstopt heepisodeswi t
    hcoughi ngorsquatti
    ng.Herpul seisusuall
    yinthe
    140
    -
    150
    bpm

    rangeduringtheepisodes.Shei soccasi onal


    lydizzywi t
    htheepi sodes,buthasnot
    passedout .Herbaselineel ect
    rocardi
    ogr am (
    ECG)i snormal,butwhi l
    einyourof fi
    ce
    shehasanepi sode,andherECGdur i
    ngt heepisodei sshowni nFigure1.Herbl ood
    pressurewas95/ 60mm Hgdur i
    ngt achycardia.Vagalmaneuver sint heof fi
    ce
    fai
    ledtoterminatetheepi sode,butitstoppedspont aneousl
    yaf t
    er5mi nutes.Aft
    er
    theepisodeterminated, hercardiacexami nat
    ionwasnor mal
    , wit
    hahear tr
    ateof84
    bpm andbl oodpressur eof105/ 60mm Hg.

    Whi
    choft
    hef
    oll
    owi
    ngi
    stheappr
    opr
    iat
    enextt
    her
    apy?

    a.At
    enol
    ol25mgdai
    ly.
    b.Di
    goxi
    n0.125mgdai
    ly.
    c.Adenosine6mgonce.
    d.Cathet
    erablat
    ion.
    e.Amiodarone200mgdail
    y.

    Answer

    1.B.Di
    goxi
    n0.
    125mgdai
    ly

    TheECGi sconsi stentwi t


    hat r
    ioventricularnodalr e-ent ranttachycar di a.Themaj or
    concerndur ingt reat mentofsupr avent r
    iculartachycar dia(SVT)dur ingpr egnancyi s
    thepot entialf oradver seef fectsont hef etus,asal lcommonl yusedant i
    arrhyt
    hmi c
    drugscr osst hepl acent albar riertosomeext ent.Al t
    hought hef ir
    st8weeksaf ter
    concept i
    oni st heper iodassoci at edwitht hegr eatestt er at
    ogeni crisk,ot heradver se
    eff
    ectsmayoccurwi t
    hdr ugexposur el ateri npr egnancy.Themaj orconcer nwi th
    antiarr
    hythmi cdr ugst akendur ingthesecondandt hirdt ri
    mest ersi st headver se
    eff
    ectonf etalgr owt handdevel opmentaswel last her iskofpr oarrhyt hmi a.Aswi th
    manyot herdr ugsusedi npr egnancy, useofcer tai
    nant iarr
    hyt hmicagent shascr ept
    i
    nt ocommonpr acticebecauseofanabsenceofr epor tedilleffects,rathert hanasa
    resultofcont roll
    ed st udi es.Al lant i
    ar r
    hythmi c drugs shoul d be r egarded as
    potentiall
    yt oxi ctot hef etusandshoul dbeavoi dedi fpossi ble,especi allydur i
    ngt he
    fi
    rsttri
    mest er.Al lcurrent l
    yavai lableant iarrhythmi cdr ugst hatar eusedf orSVTar e
    categor i
    zedasCl assCdr ugs( usingt heUSFoodandDr ugAdmi nistration(FDA)
    drugcl assificat i
    onsyst em) ,exceptf orsot al
    ol( aCl assBagent )andat enololand
    ami odarone( ClassDagent s). 

    Inpat ientswi thmi l


    dsympt omsandst ructurallynor malhear ts,not r
    eatmentot her
    thanr eassur anceshoul dbepr ovi ded.Ant i
    arrhythmi cdr ugt herapyshoul dbeused
    onlyi fsympt oms ar ei ntol erable ori ft he t achycar dia causes hemodynami c
    compr omi se.Ifprophyl acticdr ugt her apyi sneeded, thendi goxinorabet a-blocki ng
    agent( i.
    e.,propranol olormet opr olol)ist hef irst-li
    neagent .Theexper iencewi th
    digoxini sext ensive,andi tisconsi der edoneoft hesaf estant i
    arr
    hythmi cdrugst o
    takedur i
    ngpr egnancy;however ,
    itsef fi
    cacyf orar rhythmi at r
    eatmentorpr ophyl axis
    hasneverbeendemonst r
    ated.Pr opranol olandmet opr ololar egenerallyconsider ed
    tobesaf e,butar ebestavoi dedi nt hef irsttri
    mest er.Thepot enti
    alforintrauterine
    growt hr etardationhasbeenr epor tedwi thpr opr anololandhasr aisedconcer ns,
    especi all
    ywheni ti st akeni nt hef irstt ri
    mest er.Lat erst udiesr eport
    edgr owt h
    retardat i
    oni nbabi esr eceivingat enol olint hefirsttrimest erandahi gherpr evalence
    ofpr eterm del i
    very.At enololi s,ther efore,classifiedasacl assDagentbyt heFDA.
    Inviewoft heser esults, beta- bl
    ocker sshoul dbeavoi deddur ingthef i
    rstt
    rimest er,i
    f
    possi ble.Ifthepr eviouslyment ioneddr ugsf ail
    ,t hensot alolmaybeconsi dered.
    Althoughsot alolhasbeenusedsuccessf ullydur i
    ngpr egnancyf orotherindications,
    theexper i
    encei slimit
    ed,socaut i
    onisst il
    ladvised.Catheterablati
    onr equi
    res
    fl
    uoroscopyandshoul dthereforebeavoi dedexceptinr ef
    ract
    orycases.Itmaybe
    appropri
    atef ordr ug-r
    efract
    or y,poorlyt ol
    erated SVT.Ifneeded,i tshoul d be
    perf
    ormedi nt hesecondt ri
    mest er.Adenosinecanbeusedi npr egnancyforacute
    ter
    minationofSVT.However , i
    nthispati
    entwi thfr
    equentparoxysmalepisodesand
    onethathasal readyter
    minat ed,therei
    snoi ndicat
    ionforuseacutely.
     

    15.
    A22- year-oldmanwi t
    hahi st
    oryofsur gical
    lyr epairedtetralogyofFal l
    otpr esents
    toyourcl inicf oreval uationofepisodesofpal pit
    ations.Hehasgener all
    ybeendoi ng
    wel l
    ,butaf ew mont hsagobeganhavi ngepi sodesofpal pi
    tat
    ionswi thel evated
    hear tratesof120- 130bpm,whi chhavebeenl asti
    ngaf ew hoursatat ime.He
    thinkst hatover allhi sexer ci
    secapaci tyhasbeenal i
    ttl
    ewor sef orthepast6
    mont hs as wel l
    .He wor eat r
    anstelephonic moni torpr iortot his vi
    sit,whi ch
    demonst rateda2- hourepi sodeofat rialfl
    utterwi t
    hvar i
    abl eatri
    oventri
    cul ar(AV)
    conduct ion, correlatingwi t
    hhissympt oms.Hi scar diacexami nat
    iont odayr evealsa
    regularr ateandr hythm,nor malS1/ S2 wit
    houtgal l
    op,andagr ade2/ 6syst oli
    c
    ejectionmur mur( unchangedf rom pr i
    or).Electrocar di
    ogram demonst ratessi nus
    rhythm wi t
    haf irst-degr eeAVdel ayandr i
    ghtbundl ebr anchbl ockwi thQRS140
    msec.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    enextst
    epi
    nmanagement
    ?

    a.Transthoracicechocardiogram.
    b.Metopr ol
    ol25mgt wicedaily.
    c.Radiofrequencycat het
    erablati
    on.
    d.Sotalol120mgt wicedaily.
    e.Diagnosticcardiaccatheteri
    zati
    on.

    Answer

    A.Tr
    anst
    hor
    aci
    cEchocar
    diogr
    am

    Whi l
    et reatmentwithmedicati
    onsorabl ationmayevent ual
    lybeappr opriateint his
    patient,t he mostimpor t
    antf i
    rstst ep herei st or eassess hi s structuraland
    hemodynami cstat
    us.Thedevel opmentofat ri
    altachycardia,atrialfl
    utter,orat ri
    al
    fi
    br i
    ll
    ati
    on i n adul
    tcongenitalhear tdi sease patientsis often associ ated wi t
    h
    progressive hemodynami c det eri
    orati
    on of t he under l
    ying di sease.Sur gical
    treatmentoft hehemodynami cpr oblemsdoesnotel i
    minateatrialarrhythmi as,and
    ablationofat ri
    alarr
    hythmiasalonecoul dal l
    owsi gnifi
    canthemodynami cissuest o
    progressandpot enti
    all
    ydeteri
    orate.Successfultreatmenti nvolvesassessi ngbot h
    thear rhythmiaandt hecont r
    ibuti
    nghemodynami cchangesandaddr essingbot h
    whenindicatedandfeasibl
    e.Cardiaccathet
    eri
    zat
    ionmaybeappr opri
    atet
    operform
    mor edetai
    ledhemodynami cassessment,butinl i
    ghtofhisunchangedphysical
    examinati
    on,echocardi
    ographywi l
    lprovi
    deimportanti
    nfor
    mati
    onwi t
    houttheneed
    foraninvasivepr
    ocedure. 

    Early exper i
    ence in adul ts wi th unoper ated at rialsept aldef ects and at r
    ial
    arrhythmiasdemonst ratedt hei mpor tanceofani ntegratedappr oachf orarr
    hyt hmi a
    andhemodynami cpr oblems;si mi larpr i
    ncipl esappl yt opat i
    ent swi thtetr
    alogyof
    Fallot
    ,Ebst ein’
    sanomal y,andsi ngle-ventriclephysi ology;t hesepat i
    entsar eat
    highest r i
    sk of ar rhythmi a devel opment , wi th concur rent hemodynami c
    abnor malit
    ies.Beta-blocker s maydecr ease cat echolami ne- r
    elated tri
    ggers and
    provideAVnodalbl ockadedur ingr ecur r
    entat ri
    alar r
    hythmi as.Onest udyofadul ts
    withtransposi t
    ionofthegr eatar teri
    esandpr ioratrialswitchr epairswi t
    himpl anted
    defibri
    ll
    ators demonst rated supr aventricular t achycardia pr eceding vent ricular
    tachycardiain50%ofpat ients;useofbet a-bl ockermedi cat i
    onsi nt hispopulat i
    on
    wasassoci atedwi t
    hdecr easedi ncidenceofappr opriatedefibril
    latorshocks. 

    Observationalstudiesont heuseofsot alolinACHDpat ientsreportfreedom from


    recur
    rentat ri
    altachycardi
    ai n41- 46%ofpat ient sduri
    ngshor t
    -ter
    mf ollow-up.Use
    ofeithermedi cati
    on int he set t
    ing ofsi gnifi
    cantsi nus node dysf unction may
    exacerbatebr adycardi
    aandr equirescarefulmoni tor
    ing.I ni
    ti
    ati
    onofsot al
    olinthis
    populati
    oni srecommendeddur i
    ngi npatientmoni t
    ori
    ngf orproarrhyt
    hmi afor48- 72
    hours.Mul tipl
    eobser vati
    onalandmul ticenterst udieshavedemonst ratedacut e
    successr atesof65- 100%f ortreatmentofsupr avent
    riculartachycar
    diaassoci ated
    with ACHD.Acut esuccessr atesvar ybyt achycardia mechani sm and t ypeof
    congenitalheartdiseaseandr epair.

    16.
    A30- year-oldmanwhoi sapr ofessi onalsoccerpl ayerisadmi t
    tedt hroughthe
    emer gencydepar t
    mentt ot hecar diologyt elemet ryunitaf t
    errecur rentepisodesof
    syncope.Hehasahi st
    oryofpr emat urevent ri
    cularcont r
    actionandunder went
    premat ureventricularcont r
    actionabl ati
    onf rom t her i
    ghtvent ricular(RV)out f
    low
    tract3year sago.Hi scardiacexami nat ionr evealsar egularrat eandr hythm with
    nor malS1/ S2 
    and no mur murs orgal l
    ops,and t he remainderofhi s physical
    exami nationisnormal .His12- l
    eadel ectrocar diogram (
    ECG)i sshowni nFigure1.A
    car diacmagnet icr esonancei magi ngi sper formed,whi chr eveal samoder ately
    dilated RV wi t
    h moder atelyreduced f unction ( RV ejecti
    on f racti
    on 38%)and
    hypoki nesisofthebasalRVf r
    eewal lwher edel ayedenhancementi salsoseen.An
    electrophysi ol
    ogyst udyisper formed,whi chi nducesvent ri
    culart achycar di
    a(VT)
    (Figur e2) .Heunder goesi mplantationofani mpl ant
    ablecar diover t
    er-defi
    bri
    ll
    ator
    (ICD) .
    Fi
    gur
    e1.

    Fi
    gur
    e2.
    Basedonrecentguidel
    ines,whichofthefol
    lowi
    ngwoul
    dyour
    ecommendt
    othi
    s
    pat
    ientt
    ominimizehisprogressi
    onofdi
    sease?

    a.Ami odaronetherapy.
    b.Calcium channelblockerther
    apy.
    c.Cardiacresynchronizati
    ontherapy.
    d.Beta-blockertherapy.
    e.Cessationofcompet i
    ti
    veathl
    etics.

    Answer

    E.Cessat
    ionofcompet
    it
    iveat
    hlet
    ics.

    Thispati
    enthasarrhythmogenicRVcar diomyopathy(ARVC).Hehasseveralmajor
    ARVCt askfor
    cecriter
    ia,i
    ncludi
    ngepsi l
    onwaves,leftbundlesuperi
    oraxi
    sVT,and
    magneticresonance imaging wi t
    hf ocalRV dysfuncti
    on and reduced ej
    ect
    ion
    fr
    acti
    on.T-wavei nversi
    onst hroughV4inthepr esenceofar i
    ghtbundlebranch
    blockarealsoami norelectr
    ocardiogr
    am cri
    teri
    on.Whi l
    er andomizedcont
    roll
    ed
    dataf ort hemanagementofARVCpat ientsar esomewhatl imited,obser vational
    studiesandwor kext rapol atingthemanagementofvent ricularar r
    hythmi ashave
    beenusedt oder ivet hecur rentgui delinesf orthemanagementofpat i
    ent swi th
    ARVC.Fewsyst emat i
    cdat aar eavail
    abl eont heefficacyofant iar
    rhyt hmicdr ugsi n
    ARVC, andt hei mpactofmedi caltherapyonmor t
    alityi sunknown.Basedl argelyon
    serialel ect r
    ophysi ologyt est i
    ng,beta- blockersar econvent i
    onal l
    yr ecommendedas
    thef irst-li
    neappr oachi npat ient
    swi thf requentvent ricularect opyornonsust ai
    ned
    VT.I nvasi veel ectrophysi ologicaltest i
    ngwi t
    hvol t
    agemappi ngcanbeusedt o
    identifyr egi ons off ibro- fattyreplacementand t o gui de cat heterabl ati
    on of
    ventr i
    cul arar rhythmi as.As nei t
    herant i
    arrhythmi c dr ugs norcat heterabl ation
    providessuf fi
    cientpr otectionagai nstsuddencar di acdeat h,abl ationshoul dbe
    used t or educe t he f r
    equencyofar r
    hythmi a epi sodes r athert han t oi mpr ove
    prognosi s.Endur ancet raining ata compet i
    ti
    vel evelpr obabl yexacer batest he
    phenot ypeofARVC,andmostgui deli
    nest hereforer ecommendavoi danceofhi gh-
    levelexer cise.Ar ecentpr ospect i
    veobser vationst udyofARVCpat i
    entsfoundt hat
    high- levelcompet i
    ti
    veat hleteswhor educet heiract ivitylevelt oeithernoexer cise
    oronl yr ecr eationalact i
    vityhadar educt ioni nvent ricularar rhythmi asorsudden
    deat h.

    17.
    A67- year-ol
    dmani sadmi t
    tedtothecar diacintensi
    vecareuni tafterpresenting
    withpr esyncopeatwor k.Emergencymedi caltechnici
    ansfoundhim wi thasyst oli
    c
    bloodpr essureof70andat hreadypulse.Anext er
    naldefi
    bri
    ll
    atordemonst rateda
    widecompl ext achycardiaat185bpm,andhewassuccessf ull
    ycar diovert
    edwi th
    returnofcirculation.Hewashemodynami callystabl
    eintheemer gencydepar tment ,
    andeval uat i
    onf oracutecoronarysyndromewasnegat i
    ve.Hehasapastmedi cal
    historyofischemi ccar
    diomyopathywithpr i
    orinferi
    ormyocardiali
    nfarction6year s
    pr
    ior
    . 

    His electrocar
    diogram showed i nf
    er iorQ waves and no i schemi c changes.
    Transthoracicechocar diogram r
    eveal ed i
    nfer
    iorakinesi
    sand thinning,withleft
    ventri
    cular(LV)ejecti
    onf racti
    on(
    EF)of35%, sl
    ightl
    yreducedf
    rom hisEFof40%on
    hislastechocardiogram 1yearpr ior.Hi smedicati
    onsathomei ncludeaspi r
    in81
    mgdai l
    y,met oprolol50mgdai ly,andsi mvastat
    in20mgdai ly.Heunder goes
    implantati
    onofasi ngle-chamberimpl antabl
    ecardiover
    ter-
    def
    ibr
    il
    lator(I
    CD).

    Whi
    choft
    hef
    oll
    owi
    ngt
    reat
    ment
    swi
    llr
    educehi
    sri
    skofI
    CDshocks?
    a.Digoxi
    n0. 125mgoncedail
    y.
    b.Li
    sinopri
    l20mgoncedaily.
    c.Sotal
    ol120mgt wi
    cedail
    y.
    d.Fl
    ecaini
    de100mgt wicedail
    y.
    e.Dronedarone400mgtwicedail
    y.

    Answer

    C.Sot
    alol120mg.t
    wicedai
    ly

    Inpat ientswi thst ructuralhear tdi sease,r educedEF,andsecondar yprevention


    ICDs( f
    orhi storyofvent ri
    culararr hythmiasorsyncopewi thinducibleventri
    cular
    arr
    hyt hmi as),bothsot alolandami odar onehavebeendemonst ratedtobothreduce
    ther iskofI CD shocksand r educemor tali
    ty( OPTIC[ OptimalPhar macological
    Ther apy i n CardioverterDef i
    bril
    latorPat ients]st udy,Sot al
    olI CD [Sotal
    olas
    Adjunct ive Therapy t oI mplantabl e Car diovert
    er-Def i
    bril
    lator
    si n Hear
    tFai lure
    Patients]st udy).Empi rictreatmentwi ththesemedi cati
    onsmaybeappr opri
    atei n
    pati
    ent s wi th a historyofvent riculart achycar di
    a( VT)and I CD.However ,t he
    potent i
    alf orsi de ef fects,effects on def i
    bril
    lat
    ion t hreshold,and al t
    ernative
    str
    at egiessuchasVTabl ationshoul dbegi vencar efulconsi derati
    oninthiscli
    nical
    scenar io. 

    TheclassI cant i
    ar r
    hyt hmicmedi cati
    ons(flecaini
    de,propafenone)havebeenshown
    toincreaset heriskofar rhythmi cdeat hinpost myocardiali
    nfarcti
    onpati
    ent
    s( CAST
    [Cardi
    acAr rhythmi aSuppr essionTr i
    al]t
    rial)
    ,andt herefore,shouldbeavoidedi n
    thi
    spat ient.Lisinoprilislikelyindicatedfort hispati
    entwi threducedLVfunction,
    buthas notbeen shown t o have an ef f
    ecton t he incidence ofventri
    cular
    arrhyt
    hmi as.Di goxinhasal sonotbeenshownt or educet her i
    skofVTorI CD
    shocks.Dr onedar onei scont rai
    ndi cat
    edi npat i
    entswithcongest i
    veheartf
    ail
    ureor
    reducedLVsyst olicfunction.

    18.
    A52- year
    -oldmanwi thahi storyofparoxysmalat ri
    alfibril
    lati
    onpr esentst othe
    emer gencydepar t
    mentaf teranepisodeofsyncopewhi l
    ehewascooki ngdi nnerin
    hiskitchen.Her eportshef el
    tli
    ghtheadedf orasecondbef orecollapsi ng;hiswife
    witnessedt heepi sode,andhewokeupandf eltfi
    ne10secondsl ater.Int he
    emer gencydepar t
    ment ,hi
    shear trat
    eis80bpm,hi sbloodpr essurei s140/ 76mm
    Hg,andheappear swel l
    .Homemedi cati
    onsi ncl
    udeflecainide100mgt wicedai l
    y
    andmet oprolol50mgt wicedaily.Hi
    sel ectr
    ocardi
    ogram ( ECG)i nt heemer gency
    depar tment(Figure1)iscompar edwi t
    hhispr i
    orECGf r
    om l astyear( Figure2) .
    Fi
    gur
    e1.

    Fi
    gur
    e2.
    Whi
    choft
    hef
    oll
    owi
    ngmostl
    ikel
    yexpl
    ainshi
    scur
    rentECGf
    indi
    ngsandsyncope?

    a.Increasedvagaltone.
    b.Excessivebeta-bl
    ockade.
    c.Brugadasyndr ome.
    d.Ischemia.
    e.Torsadesdepoi ntes.

    Answer

    C.Br
    ugadaSyndr
    ome

    Thispat ient'sECGdemonst ratest ype1Br ugadapat t


    er n.Sodium channelbl ocker
    s
    (fl
    ecaini de,pr opafenone)canexacer batethetransientECGabnor mal iti
    esthatoccur
    inpat ient swi thBr ugadasyndr omewhocommonl yhavenor malECGs.Ser ialECG
    testi
    ngmaydemonst ratethei ntermi t
    tentchanges,anduseofcl ass1cagent s
    duringel ectrophysi ol
    ogict esti
    ngcanbeusedt ounmaskBr ugadapat t
    ern.This
    patient'sECGandhi storyaremostconcer ni
    ngf orBr ugada- i
    nducedpol ymor phi
    c
    ventricul artachycar dia/ventr
    icul arf ibr
    il
    lati
    on.Excessi vebeta- blockadeandvagal
    tonemayr esultinsyncope,par ticularlyintheset ti
    ngofaconver sionpausef rom
    atri
    alf ibrill
    ation,butt hesewoul dnotexpl ai
    nt heECGchanges.Ther earenoECG
    fi
    ndingsofi schemi a,andt heQTi ntervalisnormal.Tor sadesdepoi nteswoul dbea
    concer ni ft
    hepat i
    entwer eonacl assI I
    Iant i
    arr
    hythmi cdr ug(sotalol
    , dofet
    il
    ide)and
    hisQTwaspr olonged.

    19.
    A68- year
    -ol
    dwomanisadmitt
    edwit
    hdyspneaandwei ghtgai
    nforthepastmonth.
    Shehasnochestpainorsyncope.Shehasahi stor
    yofhyper t
    ensionandbreast
    cancer,buthadbeenprevi
    ousl
    ywell.Onexam,shei scomfortable,wi
    thbl
    ood
    pressureof138/
    80mm Hgandani rregul
    arhear
    trateof138bpm.Hervenous
    pressur eis16cm H2O,car oti
    dsar ebr i
    sk,andl ungexami nati
    onisnot ablefor
    dullnessoverr i
    ghtlungbase.Hear tsoundsar ei r
    regular,withaf ai
    ntrespi
    rophasi c
    systolicmur murovertheleftlowersternalborder;ani ntermitt
    entgall
    opispr esent.
    Theabdomeni sobese,wi t
    hapal pableliveredge.Theext remit
    iesarewar m with
    traceedema.Herel ectr
    ocardiogram showsat ri
    alfibril
    lati
    on( AF)wit
    hal eftbundl e
    branchbl ock.Anechocar di
    ogr am showsanej ecti
    onf racti
    onof35%,wi t
    hanend-
    diastoli
    c di mension of 6 cm,moder atet ri
    cuspid r egurgit
    ati
    on,and mi tral
    regurgitat
    ionwi t
    hl ef
    tatri
    alenl ar
    gement.Thyr oidst i
    mul at
    inghor monei snormal .
    Hergl omer ul
    arfi
    lt
    rati
    onrateis30cc/ min.Acar dioversionisplanned.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    edr
    ugt
    omai
    ntai
    nsi
    nusr
    hyt
    hm?

    a.Amiodar one.
    b.Dofet
    il
    ide.
    c.Sotal
    ol.
    d.Dronedar one.
    e.Fl
    ecainide.

    Answer

    A.Ami
    odar
    one

    Thi spat i
    enti spresent ingwi thacut edecompensat edhear tfailure(HF) ,compl i
    cated
    byr api dAFandr enalf ail
    ure.AftertreatmentofherHF, i
    twoul dber easonabl etore-
    establ i
    sh si nus r hythm because i tmay be pl ayi ng a r olei n hernew- onset
    car diomyopat hy( e.g.,tachycar di
    a- i
    nduced) .Herr enalf ail
    ur emakessot al
    oland
    dof etil
    idepoorchoi cesbecauset heyar ebot hr enallyexcr eted.Fl ecainideandot her
    class I c agent s ar e cont raindicated i n HF. Dr onedar one has si mil
    ar
    electrophysi ologicpr oper t
    iestoami odar one,butl ackst heiodi nemoi ety.Basedon
    theANDROMEDA( IncreasedMor tali
    tyaf terDr onedar oneTher apyf orSever eHeart
    Failure)andPALLASPALLAS( Per manentAt r
    ialfi
    br iLLAti
    onOut comeSt udyUsi ng
    Dronedar oneonTopofSt andar dTher apy)t ri
    als,iti scont raindicatedi npat i
    ents
    withNew Yor kHear tAssoci ationcl assI VHForcl assI IorI I
    IHFwi thar ecent
    decompensat ion r equi r
    ing hospi t
    alization.Ami odar one isar easonabl e choi
    ce,
    althought herear enol ar
    ge-scal er andomi zedt r
    ialsi nacut eHF.I nt heAF- CHF
    (AtrialFibr i
    llationandCongest i
    veHear tFailure)tri
    al ,therewasnomor talit
    ybenef i
    t
    tot hest r ategyofr hythm ver susr atecont rol
    ,al t
    hought hiswasnotat r
    ialofAF
    versussi nusr hythm.  

    20.
    A45-
    year
    -ol
    dmanwi
    thpar
    oxysmalat
    ri
    alf
    ibr
    il
    lat
    ionpr
    esent
    stot
    heemer
    gency
    depart
    mentwi t
    h palpitat
    ions and pr
    esyncope.Hi
    s home medi cati
    ons include
    fl
    ecai
    nide100mgt wi
    cedai l
    yandmet opr
    ololXL25mgdai l
    y.Hisheartrat
    ei s190
    bpm,hisbloodpr essureis82/40mm Hg,andheappear spaleanduncomf ortable.
    Hisiniti
    alelectr
    ocardiogram (ECG)is shown in Fi
    gure 1.Before he can be
    cardi
    overt
    ed,hishear trat
    eabr upt
    lysl
    owst o105bpm.Ar epeatECGi sshowni n
    Figur
    e2.

    Fi
    gur
    e1.
    Fi
    gur
    e2

    Whichoft hef
    oll
    owi
    ngmechani
    smsexpl
    ainswhyhi
    sQRSwaswi
    derathi
    gher
    heartr
    ates?

    a.Funny-cur
    renti
    nhi
    bit
    ion.
    b.Anti
    arr
    hythmiccl
    assIcinducedventri
    culart
    achycar
    dia(
    VT)
    .
    c.Anti
    arr
    hythmiccl
    assIIadrenergi
    cblockade.
    d.Anti
    arr
    hythmiccl
    assIIIr
    everse-usedependency.
    e.Anti
    arr
    hythmiccl
    assIcusedependency.

    Answer

    E.Ant
    iar
    rhyt
    hmi
    ccl
    assI
    cusedependency.

    ClassIcantiarr
    hyt
    hmi cdrugs( fl
    ecai
    nideandpr opafenone)haveuse- dependent
    sodium channelblocking ef
    fectsbecauset hechanneli spreferent
    ial
    lyblocked
    wheni ntheopenst ate.Athigherhear tr
    ates,thesodi um channelisopenf ora
    l
    argerproporti
    onofthecar di
    accycle,r
    esulti
    ngini ncreasedblockade.Thisresult
    s
    i
    nQRSwi dening.Thiscasei l
    lust
    rat
    esaf requentpr esentat
    ionofpatient
    streated
    withclassIcagentsforatr
    ialf
    ibri
    ll
    ati
    on.Themedi cati
    oncansl ow/organi
    zeatri
    al
    fi
    bri
    ll
    ationintofl
    utt
    erandall
    owf or1:1atr
    iovent
    ri
    cularconducti
    on,whichathigher
    heartr
    at esresul
    tsi
    nwidecomplextachycardi
    athatmaybemi st
    akenforVT. 

    Useofbet a-blockersi srecommendedwhenusi ngclassI cagent stor educet her isk


    ofthi shappeni ng.Thi spat ientwasappr opr i
    atel
    yonbet a-blockers,althought his
    does notal ways pr event1: 1 conduct i
    on off l
    utterf rom occur ri
    ng.Cl ass I II
    antiarrhythmi cdr ugs( sotalol,dofeti
    li
    de)blockpot assium channel spreferentiall
    yi n
    thei nactivest ateand,t herefore,haver everseuse- dependentef fects,resultingi n
    greateref fectatsl owerhear trates.Thisexplainswhyr iskoft orsadesdepoi ntesi s
    higheratsl owerhear trates.ClassI Ianti
    arrhythmicdr ugs( beta-blockers)decr ease
    hear trate,butdonotsl ow intramyocardialconduct i
    onsi gnif
    icantlyand,t herefor e,
    donotwi dent heQRS.Funny- currenti
    nhibitors(i
    vabradi ne)actsol el
    yont hesi nus
    node,r esul ti
    ngi nsl owerhear tratesviadecr easedaut omat icit
    y,anddonotaf fect
    QRSdur at ion.Whi leclassI cagent scanhavevent ri
    cul arproar r
    hythmi ceffects,t he
    i
    niti
    alECGi snotconsi stentwi t
    hVT.

    21.
    A60- year-oldwomanhasahi st
    oryofparoxysmalatri
    alfi
    bril
    lat
    ion(AF)t hathas
    beensympt omati
    cenought owar r
    anttr
    eatment.Shewasstartedonsot alol80mg
    bid,whichwast it
    ratedupt o120mgbi dbecauseofongoingrecurrences.Shewas
    start
    edonhydr ochl
    or ot
    hiazi
    de25mgqd1weekagof orhypertensi
    on.Shewas
    brought by ambul ance to t he emergency room for mul ti
    ple episodes of
    li
    ghtheadednessanddi zziness.Herbloodpr essur
    eis120/ 76mm Hg,andher
    serum potassium i
    s3.2mEq/ L.Herel
    ectr
    ocardi
    ogram i
    sshowni nFigure1.
    Fi
    gur
    e1.

    Whi
    choft
    hef
    oll
    owi
    ngshoul
    dbet
    henextst
    epi
    nhermanagement
    ?

    a.Elect
    ri
    calcar diover
    sion.
    b.Tempor arytransvenouspacing.
    c.IVmet oprolol
    .
    d.Intr
    avenous( IV)potassi
    um andmagnesi
    um.
    e.IVami odarone.

    Answer

    D.I
    ntr
    avenousPot
    assi
    um andMagnesi
    um.

    Sot
    alolisaclassI
    IIanti
    arr
    hyt
    hmi cagentusedpri
    maril
    yfort
    het
    reat
    mentofAF.It
    bl
    ockstheinwardrecti
    fyi
    ngpotassi
    um channel
    ,resul
    ti
    nginapr
    olongat
    ionoft
    he
    QTinter
    val
    . 
    Figure1showsnonsust ainedepisodesoft or
    sadesdepointes(TdP),
    account i
    ngf or
    thepatient
    ’scomplaint
    sofpalpitati
    onsanddi zzi
    ness.HerQTcis570msec( QT400
    msec/ squarerootoftheRRi ntervalof600msec) .Ther i
    skofTdPwi thsotalolis
    <2%,buti s hi
    gheri nthe setti
    ng ofbr adycardi
    a,female sex,pre-exi
    sti
    ng QT
    prolongati
    on,hist
    oryofheartfailure,hi
    storyofventri
    cul
    artachycar
    dia/ventr
    icular
    fi
    bril
    lat
    ion,orhypokal
    emia. 

    Thetr
    eatmentofsust ainedTdPinahemodynami call
    yunstablepatientisprompt
    el
    ect
    ricaldef
    ibr
    il
    lat
    ion.I nastabl
    epati
    ent,IVmagnesium iseffect
    iveinbot hthe
    tr
    eat
    mentandpr eventionofTdP.Temporarytr
    ansvenousoverdri
    vepaci ngtotr
    eat
    TdPusuall
    yisreser
    vedf orpat
    ient
    snotr
    espondingtoIVmagnesium. 

    ClassI I
    Iantiarrhyt
    hmi cdrugssuchassot alolhaver everse-usedependence,such
    thattheQTl engthensast heheartrat
    e( HR)sl ows,andt heQTshor t
    ensast heHR
    i
    ncr eases.Thi shelpsexplai
    nwhyt empor arypaci ngandI Visoproter
    enolhelpt r
    eat
    TdPbyi ncreasingt heHRanddecr easi
    ngt heQTi nterval
    ,wher easslowingt heHR
    withbet a-blockerswouldbecont rai
    ndicat ed.I Vami odar one,whichalsopr olongs
    theQT i nt
    erval,woul dbecont r
    aindi
    cat ed.Ther efore,themostappr opriat
    ef ir
    st
    steps int reating thi
    s pati
    entwoul d be t reat
    ing herhypokal emia,infusing IV
    magnesi um andpot assi
    um, anddi
    scontinui nghersot al
    ol.

    22.
    An 81- year-old woman wi th hypertension,noni schemi c car diomyopat hy and
    congest ivehear tfai
    lure, andpermanentat rialfi
    br i
    ll
    ati
    onpr esent st ot heemer gency
    depar tmentwi th alt
    ered ment alst atus and f evers.Home medi cat ions include
    met oprolol,li
    sinopril
    ,di goxi
    n,andf urosemi de.Onexami nation,shei sdi soriented,
    hert emper atureis38° C, herhear
    tratei s140bpm, herbloodpr essur ei s95/ 60mm
    Hg, andshei ssat ur
    ati
    ng93%onr oom ai r
    .Shei stachycardic, wit
    hnor malS1  andS2,
    +S3,and no mur murs.Lung exam r eveal s bibasil
    arr ales,herj ugularvenous
    pressur ei s12cm H2O,andshehas2+bi l
    ateralper i
    pher aledema.Labor at
    or y
    evaluationi snot abl
    ef orawhi tebloodcel lcountof15, 000,cr eatininei s2.5mg/ dl
    ,
    potassium i s5. 6mEq/ L,andur i
    nalysisisconsi st
    entwi t
    haur i
    nar yt ractinfecti
    on.
    Herel ectrocardiogram isshowni nFi gure1.
    Fi
    gur
    e1.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    etr
    eat
    mentf
    orhert
    achycar
    dia?

    a.I
    ntr
    avenous( I
    V)beta-
    blockers.
    b.I
    Vflui
    ds.
    c.I
    Vcalcium channelbl
    ockers.
    d.Di
    goxinimmuneFab.
    e.Amiodarone.

    Answer

    D.Di
    goxi
    nimmunef
    ab.

    Thispat ient'
    sel
    ectrocardi
    ogram demonst r
    atesbidi
    recti
    onalvent r
    iculart
    achycardia
    (VT),whi chismostcommonl yseenint hesett
    ingofdigoxintoxicit
    y.Digoxi
    nblocks
    thesodi um- pot
    assi
    um adenosinet r
    iphosphatase,l
    eadingt oincreasedintr
    acell
    ular
    calcif
    icationandincreasedvagaltone.Toxi ci
    tycanresultinpr oarrhyt
    hmiceffects
    (at
    rialt achycardi
    a wi t
    h block,bidirecti
    onalVT) .Di goxini s excreted by P-
    glycopr oteintranspor t,and t hus,t oxici
    tyr isk i
    si ncreased int he pr esence of
    ami odarone,dronedar one,andver apami l.Di goxinisr enall
    ycl ear ed,andi nt hi
    s
    pat ient,herdecreasedr enalfunct
    ioni sthel ikelyexpl
    anat i
    onf orherdi goxintoxici
    ty.
    Tr eatmentofdi goxint oxicit
    yi ncludes cor rect
    ion ofpot assium/ magnesi um,
    atr opineorpaci ngf orbr adycardi
    a,lidocai nef orVT/ventricul
    arf i
    br i
    llati
    on( VF),and
    Fab ant ibody admi nistrati
    on forr efractory VT/ VF and hyper kalemi a.However ,
    treat mentwi thl i
    docai neorami odar oneal onemayt erminatet heVT,butt hese
    pat ientsmayhaveunder lyi
    ngcompl etehear tblockaswel lbecauseoft hedigoxin
    toxi ci
    ty,andt herefore,i tismor eappr opriatet oreverset het oxicitywi thdigoxin
    i
    mmuneFab.

    23.
    A72- year-ol
    dmanwi t
    hat r
    ialfibr
    il
    lat
    ion,forwhichheisonwar f
    ari
    n,cal
    lsyour
    off
    ice because hi
    si nt
    ernat
    ionalnor mali
    zed rati
    o(INR)was 10.5.He has no
    complaintsanddeniesanyevidenceofbleeding.

    I
    n addi
    ti
    on to hol
    ding warf
    arin,which oft
    hef
    oll
    owi
    ng do you r
    ecommend f
    or
    managementofhisanti
    coagulati
    on?

    a.Monit
    or i
    ngonly.
    b.Pr
    othrombincompl exconcent
    rat
    e.
    c.Or
    alvitaminK.
    d.Fr
    eshfrozenplasma.
    e.Pl
    atel
    ettransf
    usion.

    Answer

    C.Or
    alVi
    tami
    nK

    War f
    arincanber eversedwitheit
    hervi
    taminKorf reshf r
    ozenpl asmat onor malize
    theI NR.Whent heINRis4-10wi t
    houtevi
    denceofbl eedi
    ng, holdingwar far
    infor1- 2
    dosesandf requentINRmoni t
    ori
    ngisgener al
    lyal lthatisr ecommended;asmal l
    or aldoseofvi taminKmaybeconsi der
    edifpatientsar eatel evatedriskofbleeding.
    Forpat i
    ents wi t
    hI NR >10 even withoutbleedi ng,or alvi tamin K shoul d be
    admi ni
    steredandwar f
    ari
    nheldfor1-2doses.Pr othrombi ncompl exconcent r
    at e,
    freshf rozenplasma,andpl at
    elet
    sareallintr
    avenoust herapiest hatwouldr equire
    hospi tali
    zati
    onandar eonlyappropri
    ateforemer gencybl eedingduet other i
    skof
    thr ombot i
    ccompl i
    cat
    ionsandtransf
    usionreacti
    ons. 

    24.
    A45- year
    -oldwomanwit
    hnonvalvul
    arat
    ri
    alf
    ibr
    il
    lat
    ionpr
    esent
    saf
    teramechani
    cal
    fal
    l.Shesli
    ppedandhi
    therheadonthecurbandhaschangesi
    nherment
    alstat
    us.
    Comput
    edt omogr
    aphyoft heheadr eveal
    sasmal lsubdur
    albl
    eed.Hercur
    rent
    medi
    cat
    ionsaremetopr
    ololsucci
    nat
    eanddabigat
    ran.

    Whichofthefol
    lowi
    ngbestdescr
    ibest
    hemechani
    sm bywhi
    chdabi
    gat
    rancauses
    ant
    icoagul
    ati
    on?

    a.Vit
    ami nKantagoni sm.
    b.Anti
    thrombinIIIi
    nhi bi
    ti
    on.
    c.Adenosinediphosphat e(ADP)r
    ecept
    orant
    agoni
    sm.
    d.Dir
    ectthrombininhi bi
    ti
    on.
    e.FactorXainhibit
    ion.

    Answer

    D.Di
    rectt
    hrombi
    ninhi
    bit
    ion.

    Dabigatr
    anisadi rectthrombininhibi
    tor.Warfar
    inisavi t
    aminKant agoni
    st.Low
    molecularweightheparin,aswel lasri
    voroxaban,edoxaban,andapixabaninhi
    bit
    f
    actorXa.Cl opidogrelinhibi
    ts ADP receptor
    s on the plat
    eletsur
    face.Hepari
    n
    i
    nhibit
    santit
    hrombinI I
    I.
     

    25.
    Whichofthefol
    lowi
    ngbestdescr
    ibest
    hemechani
    sm bywhi
    chedoxabanexer
    tsi
    ts
    ant
    icoagul
    antef
    fect
    ?

    a. I
    nhibi
    tionoffactorXa.
    b. I
    ncreasedfi
    brinolysi
    s.
    c. I
    nibi
    ti
    onoft hrombin.
    d. I
    nhibi
    tionofti
    ssuef act
    or.
    e. I
    nhibi
    tionoffactorVII
    .

    Answer

    A.I
    nhi
    bit
    ionoff
    act
    orXa.

    War far
    ini san anticoagul
    antthatwor ksbyi nhibit
    ing thevit
    amin K-dependent
    clotti
    ng factor
    s( II
    ,VI I
    ,IX,and X).Ri var
    oxaban,api xaban,and edoxaban ar e
    anticoagulantsthatwor kt hr
    ough factorXa inhibiti
    on.Dabigatr
    an is a direct
    thrombini nhi
    bit
    or.Alloft
    heseagent
    smaybeusedf ornonvalvul
    aratr
    ialf
    ibr
    il
    lat
    ion. 

    26.
    Concerns r
    egarding dr
    ug int
    eract
    ions have i
    ncr
    eased wi
    tht
    he use ofnewer
    medicati
    onsforcardi
    ovascul
    arther
    apy.
    Whichoft
    hefoll
    owingmedicat
    ionsmayi
    ncr
    easet
    heser
    um l
    evel
    sofdabi
    gat
    rani
    n
    vi
    voviaP-
    glycopr
    otei
    nint
    eract
    ions?

    a.Car bamazepine.
    b.Ami odar one.
    c.Ri
    f ampi n.
    d.Phenyt oin.
    e.St.John' sWor t
    .

    Answer

    B.Ami
    odar
    one

    Thecorrectansweri sami
    odaronebecauseiti
    san inhi
    bit
    orofP- gl
    ycopr
    otein.
    Hence,
    co- admini
    str
    ati
    onof
     ami
    odaronewit
    hdabi
    gat
    ranmayi ncr
    easeser
    um levels
    ofdabi
    gatran.
     

    Theot hermedicat
    ionsareP-glycoprot
    eini
    nducers,therebyexer
    tingt
    heopposi
    te
    ef
    fect.Prescr
    iber
    sshouldbecogni zantofthepot enti
    alforincr
    easedef
    fi
    cacyof
    dabigatr
    anwhencoadmi ni
    ster
    ingP- gl
    ycopr
    otei
    ninhibi
    tors.

    27.
    A 68- year-ol
    dmani sr ef
    erredt oyourcl i
    nicf orevaluati
    onofnew- onsetatr
    ial
    fi
    brill
    ation(AF).Physi calexami nati
    oni sremarkableonlyforani rr
    egularpul
    se.An
    electrocardi
    ogram demonst ratesAFwi thavent ri
    cularresponseofappr oxi
    mately
    90bpm.I naddi t
    iont oor deringanechocar diogram anddi scussingrate-ver
    sus
    rhythm- contr
    olst rategies,you r ecommend ant i
    coagulat
    ion withthe noveloral
    anticoagulantrivaroxaban.Heexpr essesconcer naboutant i
    coagulati
    onbecause
    hisspouseuseswar f ari
    nandhashadt omakedi etaryandmedi cati
    onchangesto
    avoi
    dint
    eract
    ionst
    hatl
    edt
    oexcessbl
    eedi
    ngr
    isk.

    Whi
    chofthefoll
    owi
    ngdr
    ugswoul
    dbemostl
    ikel
    ytocausebl
    eedi
    ngi
    fcombi
    ned
    wi
    thri
    var
    oxaban?

    a. At
    or vastat
    in.
    b. Sotalol
    .
    c. Tr
    imet hoprim-sul
    famet
    hoxazol
    e.
    d. Cl
    ar i
    thromycin.
    e. Phenytoin.
    Answer

    D.Cl
    ari
    thr
    omyci
    n

    Rivaroxabanisanovelor alanticoagul
    antwithasi mil
    areffi
    cacyt owar f
    ari
    nf or
    preventi
    ngstrokeinnonval vul
    arAFandi sassoci
    atedwi thasimi l
    arbleedi
    ngr i
    sk,
    alt
    houghwi thfewerdrug-druganddi et
    aryint
    eract
    ionsthanwar f
    arin.However,asa
    substrateoft
    hecytochromeP450( CYP3A4)andP- glycoprot
    einsystemsi nt
    heliver
    ,
    therearecli
    nical
    lyr
    elevantdrug-drugint
    eract
    ionsthatcanaffectthesafeuseoft he
    drug. 

    Strongi nhi
    bit
    orsofCYP3A4cani ncreaser ivaroxabanl evels,
    leadingt obl eeding:1)
    azole-antimycoti
    cs,i ncluding ketoconazol e,itraconazole,and vor iconazol e;2)
    human i mmunodef ici
    ency vi r
    us pr otease i nhibit
    ors,such as r itonavir;and 3)
    clari
    thromycin.Mostant ibioti
    csincreasewar f
    arinact i
    vit
    ybychangi nggutf l
    oraand
    product i
    onofvitami nK.Sul f
    amet hoxazol eisalsoaCYP2C9i nhibitort hatincreases
    war f
    ari
    nl evel
    s,butdoesnoti ncreaser ivaroxabanl evels.Phenytoini sani nducerof
    CYP3A4andsowoul dbeexpect edt odecr easer ivaroxabanlevel s,andal t
    hough
    thismaybecl inicall
    ysignifi
    cant( decreasedant icoagulati
    onef f
    icacy) ,therewoul d
    notbei ncreasedbl eedi
    ngr isk.Sotalolandat orvastati
    ndonothaveanysi gnificant
    i
    nt er
    actionwithrivaroxaban.

    28.
    A 76- year-old man wi t
    h a hi storyofnoni schemic cardiomyopat hyand mi tral
    regurgitati
    ont reat edwi thami tralvalver epai rwithamechani calvalveisadmi t
    ted
    wi t
    hr ecurrentat rialfibri
    ll
    ation.Hehaspr eviouslybeent reat edwi thdofetil
    ide,but
    hashadt wobr eakt hroughsont histher apy.Onadmi ssi
    on,hishear tr
    ateis125bpm,
    buthei sot herwi sehemodynami call
    yst able.Hehasbeenonwar f
    arinat7. 5mg
    dailyforhismechani calvalveandhi si nternat i
    onalnormalizedr at
    io(INR)hasbeen
    therapeutic f or t he past 3 mont hs. Whi le in hospi tal, he under goes a
    transesophagealechocar di
    ogr am andcar dioversion,andisl oadedonami odarone.
    Ondi schar ge,hecont inuesonmet opr olol12. 5mgor all
    yt wi cedaily,l
    isinopri
    l10
    mgdai l
    y,aldact one25mgdai l
    y,andami odarone200mgdai ly.Whi choft he
    foll
    owi ngistheappr opriat
    eant icoagul ati
    onr egimenondi schar ge?

    a.Api
    xaban5mgor all
    ytwicedail
    y.
    b.Warf
    arin5mgor all
    yeverynightatbedti
    me.
    c.Warf
    arin7.5mgor al
    lyeveryni
    ghtatbedtime.
    d.Ri
    varaoxaban15mgor al
    lydai
    ly.
    e.Warf
    arin10mgor all
    yeverynightatbedti
    me.
    Answer

    B.War
    far
    in5mgor
    all
    yever
    yni
    ghtatbedt
    ime.

    Ami odar onei nhibitsCYP2C9,whi chisi mpor t


    anti nt hemet abol ism ofwar f
    arin.
    Ther efore, ami odar one can i ncr ease t he l evel of war farin and l ead t o
    supr atherapeut i
    cI NRs.Thedoseofwar f
    arinshoul dbeadj ustedt oaccountf orthe
    inter acti
    onwi thami odar one,andt hesuggest edr educt i
    oni s25- 33%.I NRsmustbe
    closel ymoni t
    oredunt ilt hepat i
    enti sonast ablewar f
    arindosei ntheset ti
    ngof
    ami odar one.Leavi ngt hedoseofwar f
    ari
    nt hesame, orincreasingt hewar far
    indose,
    woul d notbeappr opr iatebecausebot h mi ghtl ead to asupr atherapeuti
    cI NR.
    Because t he pat i
    ent has a mechani calmi t
    ralval ve,nei ther api xaban nor
    rivar oxabanar eanappr ovedant icoagulationr egimen.TheRE- ALI GN( Dabigatran
    ver susWar fari
    ni nPat ientswi thMechani calHear tVal ves)st udy,whi chtreated
    pat ients wi th mechani calval ves wi th dabi gatran,showed i ncr eased rates of
    thromboembol ic as wel las bl eeding compl icat i
    ons compar ed wi th war f
    arin.
    Ther efore,thenovelor alant i
    coagul antshavenotbeenappr ovedbyt heFoodand
    Dr ugAdmi nistr
    ationf orusei nt heset ti
    ngofmechani calvalves.

    29.
    A56- year-ol
    dmanwi thahi stor
    yofhypertension,diabet
    es,andparoxysmalatri
    al
    fibr
    il
    lation(AF)wasiniti
    all
    yseeni nyourcli
    nic1yearagof ormanagementofhi sAF.
    Hehadj ustbeendi schargedf r
    om thehospi talforhisAF.Wor kupatt hatti
    me
    incl
    uded a nor malD- di
    mer ,a nor malt hryoi
    d-sti
    mulati
    ng hormone,and an
    echocar diogr
    am demonst rati
    nganej ect
    ionfracti
    onof55%,al ef
    tatri
    aldiameterof
    4.5cm, andventr
    icul
    arwal lthi
    cknessof1.1cm.  

    Hewasst art
    edonapi xabanandmet oprol
    olandwasdi scharged.Att hatti
    meyou
    discussedopt i
    ons,i
    ncludingarat
    e-contr
    olstrategy,anantiar
    rhythmicdrug-based
    rhythm-controlst
    rat
    egy, andacat
    heterablat
    ion-basedrhythm- cont
    rolstrat
    egy.He
    electedtotr
    yanant i
    arrhythmi
    cdrugandwasst art
    edondr onedarone. 

    Her et
    urnstoyourof
    fi
    ce6mont hslat
    erforf
    oll
    ow-upandi
    sfoundtobebacki
    nAF.
    Inthei nt
    eri
    m,her eport
    st hathewasadmi ttedt
    oal ocalhospi
    talwi
    thl
    ower
    extr
    emityedemaandwast reatedforcongeti
    vehear
    tfai
    lur
    e.Hewast ol
    datthat
    ti
    met hathi
    sheartwas"outofrhythm."
    Whi
    choft
    hef
    oll
    owi
    ngi
    sthebestnextst
    ep?

    a.Disconti
    nuemet oprol
    ol.
    b.Disconti
    nuedr onedar
    one.
    c.Addf l
    ecaini
    de.
    d.Addr anol
    azine.
    e.Adddi l
    ti
    azem.

    Answer

    B.Di
    scont
    inuedr
    onedar
    one.

    Based on t he PALLAS ( PermanentAt r


    ialfi
    briLLAti
    on Outcome St udy Using
    Dronedar oneonTopofSt andar dTher
    apy)andATHENA( TheEff
    ectofDronedarone
    on Car diovascular Events i n Atri
    al Fibri
    ll
    ati
    on) st udi
    es, dronedarone is
    contraindicatedinpat i
    entswi t
    hNew Yor kHear tAssociati
    on( NYHA)classIII-
    IV
    sympt oms,wi t
    hcl assIIsympt omsifther
    ei sar ecentdecompensation,orthose
    whohaveper sist
    entAF.Ther efor
    e,t
    hebestopt i
    oni nthi
    spat i
    entistodiscont
    inue
    dronedar one. 

    Stoppingmet opr
    ololmightleadt or ecur
    r entrapidventr i
    cul
    arresponseandwor sen
    bloodpr essurecontrol
    .Whilehemayneedf urtherrat
    e- cont
    rolagentsl
    ikedil
    ti
    azem,
    thebestopt ionhereistodiscontinuet hedr onedaroneandavoi dadverseoutcomes.
    Whi l
    et hecombi nat
    ionofr anolazineanddr onedaronehavel ookedpromisingin
    cli
    nicaltri
    als,thecombinationremai nsinvestigati
    onal.Theaddi t
    ionoffl
    ecai
    nideis
    l
    ikelytobepr oar
    rhyt
    hmic,andt herefore,isnotr ecommended.

    30.
    A 62- year-oldwomanwi t
    hhyper t
    ensionandmi ldobesitypresent
    st ocl i
    nicfor
    evaluationofsever almont hshist
    oryofi nt
    ermit
    tentepisodesofirregul
    arr apid
    heartbeat.Epi sodesaretri
    ggeredbyal coholandexer ci
    se,butareshort-l
    ivedand
    notassoci atedwi t
    hnear-syncopeorsyncope.
    Whichoft hef oll
    owingfactorsincr
    easest heriskthatthesesymptomsar eduet o
    atr
    ialfibri
    ll
    ation(AF)?

    a.Lowbi rthweight.
    b.Blackr ace.
    c.Femal esex.
    d.Increasedhei ght
    .

    Answer
    D.I
    ncr
    easedHei
    ght

    Ar ecentlydevelopedr i
    skscoref orAFi nt heFr amingham Hear tStudyi dent i
    fi
    edt he
    clinicalf
    actorsofage, malesex, elevatedbodymassi ndex,systoli
    cbl oodpr essur e,
    treatmentf orhyper tensi
    on,pr olonged PR i nter
    val,cli
    nicall
    ysi gnifi
    cantcar diac
    mur mur,and hear tfail
    ureto beassoci ated withincidentAF.I nterestingl
    y,t he
    epi demiologyofAFi snotal waysconsi stentwi thothercar diovasculardi seases;
    despi teani ncr
    easedbur denofr iskf actors,blacksareatl essr i
    skt hanwhi tesfor
    devel opi
    ngAF.Par adoxicall
    y,lowbi rthwei ghtandshor tstature,knownr iskfactors
    forcar di
    ovasculardiseaseandmor t
    alit
    y,areinverselyassociatedwi t
    hl aterlif
    eAF.

    31.
    Inpati
    ent
    swithreducedl
    eftvent
    ri
    cul
    arej
    ect
    ionfr
    acti
    ons(LVEF)<40%,
    whichoft
    he
    fol
    lowi
    ngbestdescri
    bescl
    ini
    calout
    comesassoci
    atedwi
    ththeuseofsotal
    ol?

    a.Adecreasedriskofmor t
    ali
    ty.
    b.Anincreasedriskofmor tal
    ity.
    c.Nochangei nmor t al
    it
    y.
    d.Superi
    ort o ami odar one forsuppr ession ofventr
    icul
    artachycar
    diai
    n
    pat
    ient
    swi thimpl antablecar di
    over
    ter-defi
    bri
    ll
    ator
    s(I
    CDs).

    Answer

    A.Adecr
    easedr
    iskofmor
    tal
    it
    y

    Sotalolwasassoci atedwi thincreasedmor talit


    yintheSWORD( Survivalwi t
    hOr alD
    -Sotalol)trial
    .The t ri
    alwas st opped owi ng to excess mor tal
    ityi nt he group
    randomi zedt osotal oltherapy.Thi strialonl yincl
    udedpat ientswi thr educedEFs.
    TheOPTI C( Opti
    malPhar macol ogicalTher apyi nCardi
    overt
    er -Def i
    bril
    latorPatient s)
    tri
    aldemonst r
    atedt hesuper ior
    ityofami odaroneplusbet a-
    bl ockersoversot alolf or
    thesuppr essionofI CD shocksi npat ientswi thICDs.Tobeenr oll
    edi nOPTI C,
    patientshadt odemonst rat
    eanLVEF<40% aswel l
    .Consequent l
    y,t hecor r ect
    answeri st hatsotalolisassoci atedwi thani ncreasedriskofmor tali
    tyinpat ient s
    withdi minishedLVEFwi thoutdef ibr
    il
    lators,andi slesseffectivet hanami odar one
    plusbet a-blockersf orthesuppr essi
    onofappr opri
    ateICDshocksi npat i
    entswi th
    reducedLVEF.

    32.
    A 71-
    year
    -ol
    d woman wi
    th an i
    schemi
    ccar
    diomyopat
    hyand per
    manentat
    ri
    al
    fi
    bri
    llati
    on( AF)underwentbivent
    ri
    culari
    mpl
    antablecardiover
    ter
    -defi
    bri
    ll
    ator(I
    CD)
    i
    mpl antati
    on 6 mont hs pri
    or.She has New York Hear tAssociat
    ion class I
    II
    sympt omsandcont i
    nuest ocomplai
    nofveryli
    mi t
    edf uncti
    onalcapaci
    ty,withno
    changesi nceresynchroni
    zati
    onther
    apywasini
    ti
    ated. 

    Shei scur r
    entl
    ytakingcarvedi
    lol25mgbi d,li
    sinopr
    il10mgqd,f ur
    osemide40mg
    bid,atorvastat
    in40mgqd,aspi r
    in81mgqd,andwar f
    ari
    n5mgqd.Hervi talsi
    gns
    i
    nt heof f
    icetodayarebloodpressure90/60mm Hg, heartrat
    e111bpm, respir
    ati
    on
    rate20,andoxygensat urati
    on94% r oom air
    .Shei safebri
    le.Herexami nati
    onis
    signi
    ficantforbibasil
    arral
    es,irr
    egularheart
    beat,and1+bi l
    aterallowerextremit
    y
    edema.  

    Int
    err
    ogati
    onofherbi vent
    ri
    cul
    arICDrevealsgoodpacingandsensi
    ngthreshol
    ds.
    The bat
    terystatus and l
    ead i
    mpedances are adequat
    e.Ther
    e have been t
    wo
    epi
    sodesofnonsust ai
    nedventr
    icul
    artachycar
    dia,upto15beats,butnoshocks
    havebeenrequi
    red.Sheis25%pacedoverthepast3mont hs.

    I
    nadditiont
    ot r
    eat
    mentofherhear
    tfai
    lur
    e,whi
    choft
    hef
    oll
    owi
    ngshoul
    dbet
    he
    nextst
    epinhermanagement
    ?

    a.I
    ncreasecar vedi
    loldose.
    b.Addsotalol.
    c.Atr
    iovent
    ricularnodalablat
    ion.
    d.Refer
    ralf
    orhear ttranspl
    anteval
    uat
    ion.

    Answer

    C.At
    ri
    ovent
    ri
    cul
    arnodalabl
    ati
    on

    The benef i
    t of cardiac resynchr onizat
    ion t herapy is hi ghest wi t
    h maximal
    biventricul
    arpacing.Thispat i
    entispacedonl y25%oft het i
    meduet oAFwi thrapi
    d
    vent r
    icularresponse.Restorati
    onofsi nusr hythm isunlikel
    yt obesuccessf ulina
    patientwi t
    hper manentAF.Sot al
    oliscont raindicat
    edi npat i
    entswi t
    hhear tf
    ail
    ure.
    Herbl oodpr essureist
    enuous, soincr easi
    ngherbet a-blockerisnotr ecommended.
    Transpl antevaluati
    onpriort outil
    izingavai lableguideli
    ne-directedtherapyisnot
    indicated.

    33.
    A25-year-
    oldwomanpr esent
    stot
    heemergencydepart
    mentaft
    erafai
    nti
    ngspel
    l
    wit
    nessedbyaf r
    iend.Shewasseentosuddenl
    ycollapseandappear
    edtostop
    breat
    hingforabout30seconds, af
    terwhi chshestart
    edt
    oregainconsciousness.A
    si
    mi l
    areventoccurred2mont hsagoaf tersheracedupthreefli
    ght
    sofst air
    s.She
    hasnosi gnif
    icantpastmedicalhi stor
    yandheronl ymedicati
    onisazithromycin,
    whichwasst arted3daysagof oracutebr onchi
    ti
    s.Atpr
    esent,shefeel
    st i
    red,wit
    h
    someshor t
    nessofbr eat
    h.Intheemer gencydepar t
    ment
    ,shelosesconsciousness
    andar hyt
    hm stripi
    srecor
    ded( Figure1).

    Fi
    gur
    e1.

    Whichofthef
    oll
    owi
    ngbestexpl
    ainst
    hemechani
    sm f
    ort
    hei
    nit
    iat
    ionoft
    his
    heartr
    hyt
    hm?

    a.Tri
    ggeredact
    ivi
    tyduetoearlyafter
    depol
    arizat
    ions.
    b.Re-ent
    ryduet oenhancedpot assi
    um eff
    luxdur i
    ngphaseII
    Ioftheact
    ion
    potent
    ial
    .
    c.Re-ent
    ryduetolossoftheepicardi
    alact
    ion-potent
    ialdomei
    nphaseI
    I.
    d.Re-ent
    ryduetomyocardialscarandunidir
    ecti
    onalblock.

    Answer

    A.Tr
    igger
    edact
    ivi
    tyduet
    oaf
    ter
    depol
    ari
    zat
    ions.
    Thispat i
    enthasapr olongedQTi nter valwi t
    hpol ymorphicventriculartachycar dia
    (torsades de poi ntes) qui ckl
    y degener ati
    ng i nt
    o ventri
    cular f i
    bril
    lati
    on.The
    prolongedQTi ntervalt riggersear l
    yaf terdepolar
    izati
    ons.Azit
    hromyci nisknownt o
    i
    ncr easetheQTi ntervalandmaypr edi sposeapat ientwithlongQTsyndr omet o
    thisevent.Ayoungwomanwi t
    houtevi denceofapr i
    ormyocar dialinfarcti
    onisnot
    l
    ikelyt o have scar -
    r elated ventricul ar tachycardia. Catecholami ne-sensitive
    rhythmsar emedi atedt hroughdel ayedaf t
    erdepolari
    zati
    onsi not herwi seheal thy
    ti
    ssueandt ypical
    lyar er elatedt oexer cisewi t
    houtabnor mali
    ti
    esoft heQTi nterval.

    34.
    Whichofthefoll
    owingbestdescri
    besoutcomesassociatedwit
    hami odar
    oneuse
    comparedwithli
    docai
    neusedur i
    ngout-
    of-hospi
    talar
    restexhi
    bit
    ingcardi
    over
    sion
    ref
    ract
    oryvent
    ri
    cularf
    ibr
    il
    lat
    ion(
    VF)?

    a.Sur
    vivalt
    ohospi
    taldi
    schargewashi
    gherinthel
    idocaine-tr
    eatedgr oup.
    b.Sur
    vivalt
    ohospi
    taladmissi
    onwashigheri
    ntheami odarone-tr
    eatedgr oup.
    c.Sur
    vivalt
    ohospi
    taladmissi
    onwashigheri
    ntheli
    docaine-treatedgroup.
    d.Sur
    vivalt
    ohospi
    taldi
    schargewashi
    gherintheamiodarone- t
    reatedgroup.

    Answer

    B.Sur
    vivalt
    ohospi
    taladmi
    ssi
    onwashi
    gheri
    ntheami
    odar
    one-
    treat
    edgr
    oup.

    TheALI VE (Ami odar oneversusLi docai


    nei n PrehospitalVent ri
    cularFi bril
    lati
    on
    Evaluation)t
    rialcompar edtheuseofami odaronever suslidocaineforthet reatment
    ofcar di
    oversionr efr
    act or
    yVFi nthefiel
    d.Ast at
    ist
    icallysignifi
    cantimpr ovementi n
    survivaltohospi taladmi ssi
    onwasobser vedi nt heami odarone-treatedgr oup.
    Therewasnodi ffer
    ence,however ,insurvivaltohospi taldischargebet weent he
    amiodar one-and l idocaine-
    treat
    ed groups int hose pat ients who sur vived t o
    hospi t
    aladmission.

    35.
    A 50- year-oldmanwi t
    hahi storyofpar oxysmalat ri
    alfibril
    lat
    ionandcor onar y
    arterydiseaseisini
    ti
    atedondof eti
    li
    de.Hismedi cat
    ionsi ncludeaspiri
    n81mgdai ly,
    li
    sinopril10mgdai l
    y,simvastatin40mgdai ly,andmet opr ol
    ol50mgt wicedaily.
    Hishear trateis55bpm, bloodpr essureis123/ 75mm Hg, andt heremainderofthe
    exami nation is unremar kable. Hi s electrocardiogram ( ECG) shows si nus
    bradycar diaat54bpm wi t
    hanonspeci f
    icint r
    aventricularconductiondelay,QRS
    dur at
    ionof105msec, andQTi nt er
    valof430msec.Labor at
    or ypanelshowsnor mal
    renalfunct i
    on,andserum potassium levelof5.6mEq/ L.
    Whichofthefol
    lowingef
    fect
    sofdof
    eti
    li
    demayi
    ncr
    easet
    her
    iskf
    ort
    orsadesde
    poi
    ntesi
    nthi
    spat i
    ent?

    a.Decreaseddrugmet aboli
    sm inthepresenceofsimvast atin.
    b.Decreasedpotassium ef
    fluxexacerbatedbyhyper kalemi a.
    c.I
    ncreasedpotassium eff
    luxexacerbatedbyhyper kalemi a.
    d.Usedependencet hatisexacerbatedbybr adycar
    di a.
    e.Reverse-usedependencet hati
    sexacer batedbybr adycar di
    a.

    Answer

    E.Rever
    se-
    usedependencet
    hati
    sexacer
    bat
    edbybr
    adycar
    dia.

    Dofetil
    ideexhi bi
    tsreverse-
    usedependence,wit
    hani ncreasedef fectatsl
    ow heart
    rat
    es.Br adycardi
    ai nt hi
    spatientmayexacerbatet heQT- prol
    ongingeff
    ectsof
    dofeti
    li
    de.Dof etil
    idedoesnothaveadr ugint
    eract
    ionwi thsi mvastati
    n.Dof
    eti
    li
    de
    has many dr ug inter
    acti
    ons,especi
    allythose thatpr olong t he QTc,cause
    hypokal emia, or cause hypomagnesemi a. Verapami l also al t
    ers dof
    eti
    li
    de
    met abolism andincreasestoxi
    cit
    y. 

    36.
    A 64- year-ol
    d man i sreferred tot he cl
    ini
    cf orevaluation ofan abnormal
    elect
    rocardiogram (ECG)( Figure1) .Hispastmedi calhistoryissignif
    icantf
    or
    hypertension f or which he i s tr
    eated with li
    sinopri
    l. He denies cardi
    ac
    sympt omat ol
    ogy.Hisexami nationi
    sunr emarkabl
    e.Hei sacti
    ve,worksful
    l-t
    imeas
    acarsal esman, andplaysgolfregularl
    y.
    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epf
    ort
    hispat
    ient
    ?

    a.Cardi
    acmagnet i
    cresonancei
    magi
    ng.
    b.Echocar
    diogram.
    c.Carot
    idsi
    nusmassage.
    d.Bloodcul
    tures.
    e.Pacemaker.

    Answer

    C.Car
    oti
    dsi
    nusmassage.

    TheECGi sconsi stentwi thsi nusr hythm wi th2: 1atriovent ri


    cular( AV)block.The
    diff
    erent
    iali sMobi t
    zt ype1( Wenckebach)second- degr eeAVbl ockver susMobi t
    z
    type2second- degreeAVbl ock.Noni nvasi vevagalandsympat het i
    cmaneuver scan
    helpt odistinguishonef rom t heot herbecauseMobi t
    zt ype1bl ocki susual lyAV
    nodal,andMobi tztype2bl ocki susual l
    yi nt heHi s-Pur kinjesyst em.I napat i
    ent
    withAVnodalbl ock,car otidsi nusmassagewi llslowthesi nusr ateandwor senAV
    conduction,whi ch wi l
    lwor sen t he AV bl ock.The sl owi ng ofsi nus rate and
    depressi
    onofAVconduct ionwi l
    lhaveapr otectiveeffectont hedi stalconduct ion
    system,soconduct ioni nt heHi s- Purkinjemayi mpr ove.Exer ci
    se( sympat het i
    c
    stimulat
    ion)wi l
    limpr oveAVnodalconduct i
    onandwor senHi s- Purkinjeconduct i
    on.
    HisECG( Figure1)i ssuggest iveofMobi tzt ype1second- degreebl ockbasedont he
    l
    ongPRi nter valandnar rowQRSi nterval.Al thought hedet ectionofst ruct
    ur alhear t
    diseasemayhel pgui depat ientt herapy,iti snott henextbestdi agnost icmaneuver
    to assesst hedegr eeand l evelofAV bl ock.Ther ei sno cl inicalevi denceof
    endocardi t
    is.Ifthesi teofbl ocki swi thi
    nt heAVnodei nanasympt omat i
    cpat ient,a
    pacemakeri snoti ndicated.Car di
    acmagnet i
    cr esonancei magi ngi snoti ndicated.

    37.
    A56- year-oldmal ecomest oseeyouf orevaluat i
    onofpal pi
    tati
    ons,whi chhave
    beenbot hersomenow f oratl east2mont hs.Pr evi
    ousl y,hewasdi agnosedwi t
    h
    severemi t
    ralvalver egurgi
    tat
    ion.Atsur gery,hismi tralvalvewasnott houghtt
    obe
    repai
    rabl e,andt herefor
    e,heunder wentmi t
    ralvalver eplacementwi t
    hamechani cal
    prosthesisanddi dwel lunti
    lr ecent
    ly.Ot hersympt omsi ncludedecr easedeffort
    tol
    erance, shortnessofbr eathwi t
    hexertion,andoccasi onallightheadedness. 
    Exami nationreveal
    sawel l
    -nouri
    shedmaleinnoacutedistress.Hisbloodpressur e
    i
    s110/ 68mm Hg,hear trateis140bpm,andj ugularvenouspr essureisvisible.
    Hear tsoundsar enormal,wit
    hsoftsyst
    oli
    cmur murheardbestatt heapexwi thout
    radiation and no diast
    oli
    c murmur.Lungs have bibasi
    lari nspirat
    ory cr
    ackl es.
    Abdomen i s softand nontender.Thereis no organomegal y.You obt ain an
    electrocardi
    ogram (Fi
    gure1).

    Fi
    gur
    e1.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    ydi
    agnosi
    s?
    a.At
    ri
    ovent
    ri
    cul
    ar(
    AV)nodalr
    e-ent
    rantt
    achycar
    dia.

    b.Si
    nust
    achycar
    dia.

    c.At
    ypi
    calf
    lut
    ter
    .

    d.AVr
    eci
    procat
    ingt
    achycar
    dia.

    Answer

    C.At
    ypi
    calf
    lut
    ter

    Thet r
    acingdemonst ratesatri
    alflutt
    erwi t
    h2: 1conduct i
    on.Thecircuitshowni s
    mostlikel
    yt hel
    eftatr
    ium, aresul
    tofthemi tralval
    vesurgerywit
    hleftatri
    alscar
    ring
    thatprovi
    desasubst rat
    ef orr
    e-entrywit
    hinthel ef
    tat
    rium.Themor phologyoftheP
    wave i s nottypicalofsi nus tachycardi
    a.The 2: 1 conducti
    on r ul
    es outAV
    reci
    procating t
    achycardia,and makes AV nodalr e-entr
    anttachycardia hi
    ghly
    unli
    kely.

    38.
    A35- year -oldother
    wisehealt
    hymanpr esent
    st otheemer gencydepartmentat5: 00
    a.m.af t
    erawakeni ng 2 hoursago wi t
    h a sensation ofa rapid heartrate.An
    electrocar diogram (
    ECG)hasbeenper formedshowi ngat r
    ialf
    ibr
    il
    lat
    ion(AF)atar ate
    of94bpm.Hehasnopastmedi calhistoryanddoesnotconsumeal cohol.Thereis
    nof amilyhi st
    oryofatrialf
    ibri
    ll
    ati
    onexcepti nr elati
    vesovert heageof75.He
    typicall
    yr uns5- 10mi l
    esaday.Onexami nati
    on,hi sheartrat
    ei s96bpm wi tha
    blood pr essure of110/ 60 mm Hg,and t he remai nderoft he examination is
    unremar kabl e.

    Whichofthefol
    lowi
    ngel
    ect
    rophysi
    ologi
    cmechani
    smsbestexpl
    ainst
    hispat
    ient
    's
    i
    nit
    iat
    ionofAF?

    a.Sympatheti
    cactivati
    onoft heI
    KATPchannel.
    b.Phosphoryl
    ati
    onoft heICachannelatslowhear
    trat
    es.
    c.Parasympathet
    icactivat
    ionoftheIKACHchannel
    .
    d.Parasympathet
    icactivat
    ionoftheIfchannel
    .
    e.EnhancedITOact i
    vit
    ydur i
    ngsleep.

    Answer

    C.Par
    asympat
    het
    icact
    ivat
    ionoft
    heI
    KACHchannel
    .
    AFi n young highlyconditi
    oned indivi
    dualswi t
    h ventr
    icularr ates<100 bpm i s
    consistent wit
    h par asympatheti
    call
    y medi ated AF. Par asympathetic (vagal)
    sti
    mul ati
    onacti
    vatesmuscar i
    nicreceptor
    s, whicharecoupl edt otheIKACHchannel
    byaGpr otei
    n.Activat
    ionoftheIKACHchannell eadstosl owi ngofthesinusr at
    e, a
    decreasei natr
    ioventr
    icul
    arnodalconduct i
    on,andi mpor tant l
    y,adecreasei nt he
    durati
    onoft heactionpotenti
    alintheat ri
    um.Thi slastef f
    ecti sthoughttoexpl ain
    theincreasedincidenceofAFi nt heset t
    ingofahei ghtenedvagalt one,suchas
    duri
    ngsl eep.

    39.
    An18- year
    -ol
    dmanpr esentsf
    oraspor
    tspar
    ti
    cipat
    ionphysicalpr
    iort
    ostarti
    ng
    col
    legeasami ddl
    e-di
    stancer
    unner
    .Heisascholarshi
    pathlet
    eataDi vi
    sionI
    schoolandhasnevernot i
    cedanyexerci
    sel i
    mit
    ations.Her eport
    spalpi
    tati
    onsover
    thepastsever alyearsthatoccurevery1- 2mont hs,lastfrom 10secondst o5
    minutes,andspont aneousl
    yremit
    .Thepal pi
    tat
    ionsar eassociatedwit
    hdi zzi
    ness,
    buthehasnothadsyncope.Onexami nation,agrade2/ 6systoli
    cmur murisheard
    atthel ef
    tlowersternalborder
    .At r
    ansthoraci
    cechocar diogram isobtai
    nedand
    showni nVideos

    2.(ht
    tp:
    //medi
    a.mycr
    owdwisdom.com.s3.
    amazonaws.
    com/acc/
    quest
    ions/
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    /cd8293f
    8-2a8f
    -47f
    8-bc05-
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    mp4)and

    3.(ht
    tp:
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    mycrowdwisdom.com.s3.
    amazonaws.com/
    acc/
    quest
    ions/
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    4429-b825-8d95e9ceee66.
    mp4).

    Basedontheechocar
    diogram f
    indi
    ngs,whi
    choft
    hef
    oll
    owi
    ngar
    rhyt
    hmi
    asi
    sthemost
    l
    ikel
    ycauseofhi
    ssympt oms?

    a.At
    ri
    alf
    ibr
    il
    lat
    ion.

    b.Si
    nust
    achycar
    dia.

    c.Vent
    ri
    cul
    art
    achycar
    dia.

    d.Mul
    ti
    focalat
    ri
    alt
    achycar
    dia.

    e.At
    ri
    ovent
    ri
    cul
    arr
    e-ent
    ryt
    achycar
    dia(
    AVRT)
    .

    Answer

    E.At
    ri
    ovent
    ri
    cul
    arr
    e-ent
    ryt
    achycar
    dia(
    AVRT)
    .
    Inapat i
    entwi thEbst ein'sanomal yandpal pitati
    onsconsistentwi that achycar dia,
    themostl ikelycausei sanAVRTr elatedt oabypasst r
    actthatof tenmani f
    est sas
    pre-excitationonar estingelectr
    ocar diogram.Al thoughat r
    ialarrhythmiassuchas
    atri
    alflut
    terorat r i
    alfi
    bril
    lat
    ionoccur ,thoser hythmst endtobeseeni npat i
    ent swi t
    h
    mor esever edi seaseandhear tfail
    ure.Sever ediseasewoul dnotbeexpect edi na
    pati
    entwi t
    hsuf fi
    cientcar di
    opulmonar yf it
    nesst obeaschol arshiptrackat hlete,and
    the echocar diogram shows r elati
    vel y mi l
    d di sease.The epi sodi
    c nat urei s
    i
    nconsi stentwi thsinust achycar
    dia.Mul ti
    focalatri
    altachycardiaismor eof tenseen
    i
    npat ientswi t
    hunder l
    yinglungdi sease.Thought heotherf i
    ndingsar ecommonl y
    foundi npat i
    entswi thEbstein'
    sanomal y,nonewoul dbeexpect edt ober elatedto
    sympt omat icpal pit
    ati
    ons.

    40.
    A70- year-
    oldmanpr esent
    swi thchronicweakness,exer ci
    seintolerance,fat
    igue,
    andnearsyncope.Her eportsthatasayoungmanhef aintedeasilyduringblood
    drawsandmedi calprocedures,butthatheseemedt ogrowoutofi t.Overt hepast5
    or6year s,however,hehasi ncreasingl
    yfel
    tli
    ght headedandmi ldlydiaphoretic
    occasional
    lydur
    ingor di
    naryactivi
    ti
    esandof t
    enfeelsast houghhei sgoingt opass
    outunlesshesitsdown.Hi ssympt omsseem wor sedur inghotweat herandaf ter
    eati
    ng. 

    Hisphysi
    calexaminati
    onisunremarkableexceptthathi
    sbloodpressureis150/85
    mm Hgwhi l
    esupine,130/80mm Hgwhi lesi
    t t
    ing,
    and70/40mm Hgwhi l
    estandi
    ng,
    atwhichti
    mehebecomesl ight
    headedandnearsyncopal.Hisheartrat
    eis80bpm
    supi
    ne,90bpm sitti
    ng,and100bpm st anding.Hehasar esti
    ngtremorand" cog-
    wheel
    ing.
    " 

    Elect
    rocardi
    ogram,echocar
    diogram,and st
    resst
    estresul
    tsarenor
    mal
    ,asar
    e
    resul
    tsfrom t
    hyroi
    dandadrenalstudi
    esandacompl
    etebl
    oodcount
    .

    I
    nadditi
    ont oavoidanceandeducationaboutcount
    erpressuremaneuver
    s,whi
    ch
    ofthefol
    lowingist hemostappropriat
    etherapytoreducethefr
    equencyofthi
    s
    pat
    ient
    ’sl
    ightheadednessandnearsyncope?

    a.Droxidopa.
    b.Cl
    oni di
    ne.
    c.Met oprolol.
    d.Disopyrami de.
    e.Salttablets.
    Answer

    A.Dr
    oxi
    dopa

    Thi
    spati
    enthaswhatsoundslikeahi st
    oryofneur
    ocar
    diogeni
    csyncope,whi
    ch
    maybeassoci
    atedwi
    thor
    thost
    aticst
    ress.

    However,now t hesymptomshavechangedandhehasaphysi calexaminati


    on
    consist
    entwithneurogeni
    corthost
    ati
    chypotension,andthi
    sisalsoconsi
    stentwit
    h
    thefactthathehasevi dencepotenti
    all
    yforPar ki
    nson'sdi
    seasewhichcan,and
    oft
    endoes, occurwi
    thneurogenicor
    thostat
    ichypotensi
    on.

    Thepr oblem canbecompl extomanage.Ther easoni smanysuchpat ientshave


    supine hyper tensi on and or t
    hostatic sympt omat i
    c hypot ension.Tr eati
    ng the
    ort
    hostat i
    chypot ensionmayexacer batet hehyper tension.Onedr ugthatmaybe
    usefulisdr oxidopa.Thi sdr ugisi
    ndi catedf orneurogenicor t
    hostatichypotensi
    on.
    Otheropt i
    onsi ncludepyridosti
    gmine,mi dodri
    ne,andf ludrocort
    isone.Thesedr ugs
    mayexacer batehyper t
    ension.I
    tisal sowor thwhil
    et ohavehi m puttheheadofhi s
    bedupabout30°t oof f
    setthesupineandeveni nghyper t
    ensionwhent her ei
    soften
    fl
    uidr etention.The pat i
    entshoul d al so specifi
    cally avoid eating very sweet
    carbohydrat e-l
    adenf oodsi nthemor ning.

    When symptoms int


    erfere wit
    h qual
    it
    y oflif
    e despi
    te adequat
    e hydrat
    ion and
    i
    sometri
    cexerci
    sesatthet imeofimpendingsyncopetodel ayormiti
    gatelossof
    consci
    ousness,
    medicaltherapymaybeconsidered.
     

    Mi dodri
    nehasbeenshownt oreducesympt omsi nsmallstudi
    es,par
    ti
    cularl
    yin
    pat i
    entswit
    hpredomi nant
    lyhypotensivesymptoms,al t
    houghconfir
    matorystudi
    es
    arel acki
    ng.Therei s some evidence thatclonidine can hel
    p,butitcan also
    exacerbatetheproblem ofhypotension.Andanel der
    lymanshoul dnotbet aki
    ng
    disopyramidebecauseitmayexacer bateuri
    naryretent
    ion.

    41.
    A 56-year-old woman i sr ef
    err
    ed f oreval
    uation ofi nt
    ermit
    tentdi
    zziness wit
    h
    occasi
    onalnear -syncope.Episodesoccur1- 2t i
    mesamont h,donothaveany
    speci
    fi
    ct ri
    ggers,andl ast<1mi nute.Shehasnothadasyncopalevent ,buthas
    comecl ose.Shehasnoot hercardiacsympt omatologyandi sother
    wisehealthy.
    Herfami l
    yhistoryispositi
    vef orhypertensi
    onandat r
    ialfi
    bri
    ll
    ati
    oninhermot her,
    andhergr andmotherhadapacemaker .

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestdi
    agnost
    ict
    estf
    ort
    hispat
    ient
    ?
    a.Tiltt
    ablet est.
    b.Pat i
    ent-activatedeventmoni t
    or.
    c.Electrophysiologi cst
    udy(EPS).
    d.A24- hourcont inuousel
    ectrocar
    diogr
    am (
    ECG)(
    Hol
    ter
    ).
    e.Implant edloopr ecor
    der
    .

    Answer

    B.Pat
    ientact
    ivat
    edmoni
    tor
    .

    Apat i
    ent -
    activatedeventmoni torcanr ecordECGt r
    aci ngsimmedi atelypr iortoand
    duri
    ng sympt oms,al l
    owi ng ident i
    fi
    cat i
    on ofpossi ble arrhyt
    hmi as.A 24- hour
    conti
    nuousECG( Holt
    er)isnotcor r
    ect:Epi sodesarelikel ytobet ooinfrequentt obe
    capturedona24- hourHol t
    er.Ani mplant edloopr ecor dermaybeconsi deredwhen
    noninvasivedi agnostict esti
    ngi sunr eveal i
    ng,ifsympt om frequencyi st ool ow to
    captureoneventmoni tor,ori fthepat i
    ent’ssympt om i ssyncope.Al thoughEPS
    all
    owsdi rectassessmentoft hecar diacconduct i
    on syst em,i tdoesnotal l
    ow
    corr
    elationofsympt omswi t
    hanar r hythmi a.Til
    tt ablet esti
    ngcaneval uatefor
    ort
    host ati
    csympt omsorpost uralor thostatictachycar diasyndr ome,buti snot
    appropr i
    ateforidentif
    yingot herarrhythmi as.

    42.
    A 45-year-ol
    d man sees you i
    n consul
    tati
    on int
    he of
    fi
    ce r
    egarding f
    requent
    pal
    pit
    ations.Hedescr
    ibespoundi
    ngheartbeats,
    1or2perhourt
    hroughouttheday,
    whi chincreaseduringtimesofst r
    ess.Anechocardiogram wasnormal.Anexercise
    stresstesthadt obest oppedduet oincr
    easingventri
    cul
    arectopy,i
    ncludi
    ngaf ive
    beatr unofvent ri
    culart achycardiathatterminat
    edassoonasexer cisestopped;
    therewer enoot herelectrocardi
    ographic(ECG)changesdur i
    ngthest
    resstest.A12
    -leadECGi sshowni nFigur e1.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    yor
    igi
    noft
    hepr
    emat
    urevent
    ri
    cul
    arcont
    ract
    ions
    (
    PVCs)
    .

    a.RVapi calmorphol
    ogy.
    b.Bodyoft heLV.
    c.Rightventri
    cul
    aroutfl
    owtr
    act(
    RVOT)or
    igi
    n.
    d.Leftventr
    icul
    arout
    flowtr
    act(
    LVOT)
    .

    Answer

    D.Lef
    tvent
    ri
    cul
    arout
    fl
    owt
    ract(
    LVOT)
    .

    Thispat i
    ent'spal pitati
    onsar eduet oi di
    opathicvent ri
    cularout flow t ractPVCs.
    These ar e commonl y associated with nonsust ai
    ned and sust ained vent r
    icular
    arrhythmi asdur ing st ressordur ing 24-hourECG ( Holter
    )moni toring.Possi ble
    originsoft hisarrhythmi aar ei
    nt heRVOT( morecommon)orLVOT( l
    esscommon) .
    ThePVCsi ntheECG exampl ehaveal eftbundle,inferi
    or-axismor phol ogy.The
    precor di
    alR- wavet ransi ti
    on(total
    lyposi t
    iveQRScompl exesi nleadV3)i sear l
    ier
    than i stypicall
    yseen i n RVOT vent r
    iculartachycardia.The LVOT ( sinuses of
    Valsal va specif
    ically)i spost eri
    ort ot heRVOT,whi ch resultsi n mor eposi tive
    voltageandear li
    ert ransi ti
    onint heprecordialleads.Wheni diopathicout f
    lowt ract
    PVCsar emor efrequentt han10%oft otalheartbeats,theymaybeassoci atedwi th
    devel opmentofcar diomyopat hy.Bet a-blockers ornondi hydropyridine cal ci
    um
    channelbl ockersar eof teneffecti
    ve,wi t
    habl ati
    onr eservedf orpat ientswhoar e
    refractoryt o medi calt her apyorwi t
    h car di
    omyopat hyduet ot hehi gh- density
    arrhythmi a. 

    43.
    A55- year-oldmanwi th3- yearhi
    storyofparoxysmalatrialf
    ibril
    lat
    ion( AF)presents
    to cli
    nicf or evaluati
    on.He has weekl y episodes ofAF t hat pr oduce an
    uncomf ort
    ablesensat ionofhear traci
    ngandshor t
    nessofbr eath.Hispastmedi cal
    histor
    yi ncludes cor onary arter
    y disease,hyper t
    ension,t ype 2 di abetes,and
    hyperli
    pidemia.Hi scur r
    entmedi cati
    onsar ewar f
    ari
    n5mg/ day,met oprolol50mg
    twicedai l
    y,hydr ochlorothiazi
    de25 mg/ day,r amipri
    l5 mg/ day,si mvastati
    n 20
    mg/day,andglybur
    ide5mg/ day.Hisel ectr
    ocardiogr
    am showssi nusrhythm ata
    rat
    eof55bpm wi t
    hacor rect
    edQTi nter
    valof440msec.Hi slabor
    atorypanel
    showsnor malel
    ect
    rolyt
    esandr enalfunct i
    onandani nt
    ernat
    ionalnor
    malizedrati
    o
    of2.5.Youdeci
    detoinit
    iat
    edofeti
    li
    det ocont r
    olhisAF.

    Whi
    choft
    hef
    oll
    owi
    ngmedi
    cat
    ionchangesi
    srequi
    redwhenst
    art
    ingdof
    eti
    li
    de?

    a.Di
    sconti
    nuehydrochlor
    othi
    azi
    de.
    b.Decr
    easewarfari
    ndose.
    c.Di
    sconti
    nuemet opr
    olol
    .
    d.Di
    sconti
    nueglyburi
    de.
    e.Decr
    easesimvastat
    indose.

    Answer

    A.Di
    scont
    inuehydr
    ochl
    orot
    hiazi
    de.

    Several dr ugs ar e contrai


    ndicated wi t
    h t he use of dof eti
    li
    de, includi
    ng
    hydrochlorothi
    azide,tr
    imethopri
    m,ver apamil,ketoconazol
    e,pr ochlorper
    azine,and
    megestrol.Dof et
    il
    ideisnotcontraindicat
    edint hepresenceofcor onarydiseaseor
    i
    schemi a,nori nheartfai
    lure.Itdoesnothaveani nt
    eracti
    onwi t
    hwar f
    arinor
    si
    mvast ati
    n.Dof eti
    li
    dedoesnoti nteractwit
    hgl yburi
    de.Dofetil
    idedoesnoti nteract
    wit
    hmet opr ol
    ol,andindeed,beta- bl
    ockersshoul dbecont inuedi npat i
    entswi th
    coronaryar t
    erydisease.

    44.
    A50-
    year
    -ol
    dmanunder
    goesr
    out
    ineappendect
    omy.Shor
    tl
    yfol
    lowi
    ngext
    ubat
    ion
    i
    nt her ecoveryroom,heisbrief
    lyunresponsi ve,andt hetr
    acingshowni nFi
    gure1i s
    retr
    ievedf rom themonitor.Hepr esent
    lyissl eepybutr esponsi
    ve,acknowledging
    abdomi nalpain.Review ofpr eoperati
    ve eval uat
    ion shows a nor malst ress
    electr
    ocar diogr
    am 6mont hsagoandnopr iorhi stor
    yofhear tdi
    sease.Hereceived
    adoseoff entanyl30minutesago.Thel astser um potassium was3.6mEq/dl.
    Whi
    choft
    hef
    oll
    owi
    ngshoul
    dbedonepr
    iorhospi
    taldi
    schar
    ge?

    a.I
    mplantablecardioverter
    - defi
    bri
    ll
    atorpl
    acement
    .
    b.Noadditi
    onaleval uat
    ioni srequi
    red.
    c.Chr
    onicami odaronether apy.
    d.Cat
    heterablati
    on.
    e.Cor
    onaryangi ography.

    Answer

    E.Cor
    onar
    yangi
    ogr
    aphy.

    Thet
    raci
    ngshowssi
    nusr
    hyt
    hm f
    orf
    ivebeat
    s,f
    oll
    owedbyapr
    emat
    urevent
    ri
    cul
    ar
    contr acti
    ont hatinitiatespol ymor phi cvent ri
    culartachycar dia(VT)degener atingto
    ventricularf i
    bril
    lation( VF)( Figure1) .Mar chingt heQRScompl exesf orwar di ntothe
    arrhyt hmiadoesnotsuggestar tifact ,andt hepat ientwasbr ieflyunr esponsi ve,
    consi stentwi t
    hanepi sodeofhypot ension,wi t
    hspont aneoust erminationoft he
    arrhyt hmia, whichcanoccurwi thpol ymor phicVTandevenVF.Pol ymorphi cVTdue
    to QT pr olongat ion i s a consi der ation,butt he QT i ntervali s notpr olonged.
    Further mor e,theepi sodei snotpr ecededbyapauseort ransientsl owingofhear t
    rate,asi susual lyseenwi thacqui redl ongQTsyndr ome.Themostl i
    kelycausei s
    myocar dialischemi a,whi chmaybet ransientandneedst obeeval uat ed.Thus,
    optionAi scor rectandshoul dbei mmedi atelyconsidered, taki
    ngi ntoconsi der at
    ion
    ri
    sksi mposedbyt her ecentsur ger yandanyaddi tionalevi dencesuggest ingan
    acutecor onar ysyndr ome.VFduet oanacut eischemi csyndr omeusual lydoesnot
    war rantpl acementofani mpl antabl ecar dioverter
    -defibril
    lator
    .Cat heterabl ationi s
    rarelyper formedf orpol ymor phicVT,andt henonl yf orr ecurrentepi sodeswi t
    h
    premat urevent ricul arcont ract
    ion t ri
    gger sthatar enotduet o acut ei schemi a.
    Althoughacut eint ravenousami odar onet herapycoul dbeconsi der ed,chr onicor al
    therapyshoul dnotbei ni t
    iatedatt hist i
    me.

    45.
    A 52- year-ol
    d woman wi th hypertension and paroxysmalat r
    ialfibr
    ill
    ati
    on (AF)
    presents t o the emergency depar t
    ment wi t
    h acut e onset of pal pit
    ati
    ons,
    li
    ghtheadedness,and dyspnea t hatst ar
    ted approximatel
    y 16 hour s ago.An
    echocar di
    ogram 6 mont hs priorshowed nor mall eftventr
    icularstructur
    e and
    functi
    on.Hercur r
    entmedicati
    onsar eli
    sinopri
    l10mg/ dayandaspi ri
    n81mg/ day.
    Uponpr esent
    ation,sheappearsdyspnei c.Herbloodpr essureis155/ 90mm Hg,
    heartr ateis125bpm andi rregular,andwei ghtis70kg.Ther emainderoft he
    physicalexami nati
    onisnormal .Herel ectr
    ocardi
    ogram showsAFatar ateof118
    bpm withouti
    schemicchanges.Labor
    atorypanelshowsnor malel
    ect
    rol
    ytesand
    renalandhepati
    cfunct
    ion.Dil
    ti
    azem 10mgi ntravenoushasbeenadminist
    ered,
    resul
    ti
    nginaheartr
    ateof80bpm withabloodpressureof135/
    85mm Hg.

    Whichofthefol
    lowingist
    henextbestst
    epi
    nmanagementt
    ophar
    macol
    ogi
    cal
    lyr
    e
    -est
    abl
    ishsinusrhythm?

    a.Pr
    opaf enone150mgbymout honce.
    b.Amiodar one400mgbymout hnowandr epeatin8hours.
    c.Di
    goxin0. 25mgint
    ravenousandrepeataf
    ter6hours.
    d.Di
    lt
    iazem 90mgbymout handrepeatin6hours.
    e.Fl
    ecainide300mgbymout honce.
    Answer

    E.Fl
    ecai
    nide300mgbymout
    honce.

    Cardi oversionofr ecent-onsetAFwi thoralmedi cationissomet imesreferredt oas


    the" pill-
    in-the-pocket "appr oach.Initi
    alrat
    e- contr
    olmedi cationshoul dbepr ovided
    (suchasabet a-blockerorcal ci
    um bl ocker)t opr eventrapidconduct ionofat r
    ial
    fl
    utter/ AF,andshoul dbef oll
    owedbyadmi nistr
    ationofasi ngl ebolusdoseofa
    classIant iarrhythmi cdrug( f
    lecainide200- 300mgorpr opafenone450- 600mg) .
    Not et hatclassIant i
    arrhyt
    hmi cdrugsar econt rai
    ndi cat
    edinpat ientswithstr uctural
    hear tdi sease orconduct i
    on syst em di sease ( bundle branch bl ock).Pat i
    ent s
    receivingt hist herapyshoul dbemoni t
    oredthef ir
    stt imeitisused,assi deef f
    ect s
    i
    ncl udi ng hypot ension can occur .Ami odaronecan beconsi dered,butt ypically
    takesmuchl ongert oachi eveconver si
    oncompar edwi t
    hacl assIcagent .Di goxin
    anddi lti
    azem ar erate-controlagent s,butwillnotcausecar di
    over si
    on.

    46.
    A46- year-oldwomani sr ef
    erredt oyourcli
    nicforrecurrentsyncopalepisodes.The
    episodesar espor adic,buthavei ncreasedinfrequencyi nthepast3mont hs.Most
    occurwhi leshei sst anding,butcanoccurwi t
    hl i
    ttl
    ewar ning.Shehassecondsof
    dizzi
    nesspr i
    ort othef all,buthasnoot hersympt oms.Shei sotherwisei ngood
    healthandi stakingnomedi cati
    ons.Herbl oodpr essureint hecli
    nicis125/ 85mm
    Hg,and hear tr atei s 80 bpm i n si
    nus rhythm.The car di
    ac and r espir
    ator
    y
    exami nat
    ion isunr emar kable.Herechocar di
    ogram showed no st ructuralheart
    disease.A24- hourHol termoni torshowednosi gnif
    icantar r
    hythmias,butshewas
    asympt omat i
    c dur ing t he moni tori
    ng. A tilttablet est was ar r
    anged and
    demonst r
    at edther esult
    sshowni nFigure1.
    Accordi
    ngtother
    esul
    tsoft
    hist
    est
    ,whi
    choft
    hef
    oll
    owi
    ngmanagementst
    epswoul
    d
    yourecommend.

    a.Diagnost
    icelect
    rophysiol
    ogyst udy.
    b.Implant
    ablelooprecorderi
    nsertion.
    c.Permanentpacemakeri mplantation.
    d.Ini
    ti
    atebeta-
    blocker.
    e.Emphasizesaltandfluidi
    ntake.

    Answer

    E.Emphasi
    zesal
    tandf
    lui
    dint
    ake.

    Thet il
    tt abl
    est udyshowsa mi xed vasodepressorand cardio-i
    nhibit
    oryvagal
    response.Thedi agnosi
    si sclear
    ,so adi agnosticelect
    rophysiol
    ogyst udyand
    i
    mpl antable loop recorder are not indi
    cated. Pacemaker i nser
    tion is not
    recommended.Bet a-
    channelantagoni
    stshavenotbeenshownt obeef
    ficaci
    ousf
    or
    vasovagalsyncope.Pat
    ientreassur
    anceandeducation,emphasizi
    ngf
    luidandsal
    t
    intake,
    arerecommended.

    47.
    A57-year
    - oldmanpr esent
    stoyourcli
    nicwit
    hcompl ai
    ntsofshor t
    nessofbr eath
    whil
    ewalkingl esst hanabl ock.Hehasapastmedi calhistorysignif
    icantfor
    cor
    onaryarterydisease,wit
    hananteri
    orSTelevati
    onmyocar dialinf
    arcti
    ont r
    eated
    wit
    hdrug-eluti
    ngstent6mont hsago,
    hypert
    ension,andhypercholester
    olemia. 

    Onphysi calexaminati
    on,bloodpressureis118/72mm Hgandhear trat
    eis38bpm.
    Recentst udies inthe past6 mont hs incl
    ude an echocardiogr
    am wi t
    hal eft
    ventri
    culareject
    ionfracti
    onof50%,andHol t
    ermonit
    or i
    ngwi thsinusbradycardi
    a
    withanaver ageheartrateof40bpm andmi ni
    mum heartr ateof30bpm whi l
    e
    sleeping.Hismedi cati
    onsi ncl
    udeaspi r
    in81mgdai ly,clopidogr
    el75mgdai l
    y,
    met oprol
    ol25mgt wi
    cedai l
    y,at
    orvastat
    in40mgdai l
    y,andlisinopri
    l10mgdai l
    y.

    Whichofthef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    erecommendat
    ionf
    ort
    hepat
    ient
    ’s
    symptoms?

    a.Perform anexer ci
    setreadmi l
    ltest
    .
    b.I
    mpl antadual -chamberpacemaker .
    c.Perform el
    ect
    r ophysiologicstudy.
    d.Disconti
    nuemet oprolol.
    e.Continuecurrentmedi cat
    ions.

    Answer

    B.I
    mpl
    antadual
    -chamberpacemaker
    .

    Basedoncur rentgui del


    ines,thispat ientmeet saCl assIi ndi
    cationforper manent
    pacemaker .Per manentpacemakeri mpl antati
    oni sindicatedf orsympt omat icsi
    nus
    bradycar di
    at hatr esultsfrom r equireddr ugt herapyf ormedi calcondi t
    ions.This
    patientispresent i
    ngwi thsympt omat i
    csi nusbr adycardi athatisli
    mi t
    inghisact i
    vit
    y.
    Althoughmet opr ol
    olcoul dbet hepot entialcausef orhi ssympt omsduet othe
    historyofanant eri
    ormyocar dialinfarctionandhyper tension,thismedi cationisan
    essentialcomponentofhi st r
    eat ment .Becauset hepat i
    entisexper iencingsinus
    bradycar di
    a,treatmenti nterventionisr equired,andnotdoi nganyt hi
    ngisi ncorr
    ect.
    Nof urtherstudiesar enecessar yt oeval uat
    et hepat i
    ent’scondi t
    ion. 
    48.
    A 45-year-
    oldmanpr esentsf oreval uati
    onofpal pi
    tati
    ons.Hehasf el
    tar apid
    heart
    beatfort hepastsever alweeks.Hi sexerci
    set ol
    erancehasdecl inedaswel l
    duri
    ngt hi
    st ime.Hispasthi stor
    yi ncludeshypertension,whichwasdi agnosed5
    yearsagoandt r
    eatedwithmet oprolol50mgt wicedaily.Onexami nat
    ion,hisheart
    rat
    eis85bpm andbl oodpr essur eis145/ 90mm Hg.Hi slungsoundsar eclear.On
    auscult
    ati
    on,t he hear
    tr atei si r
    regular
    .The r emainderoft he exami nati
    on is
    unremarkable.Anelect
    rocardi ogram (ECG)isobtained(Figure1)
    .

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextst
    epi
    nthemanagement
    ?

    a.OrderaHol t
    ermonitor.
    b.I
    ncreasemet oprol
    olto100mgt wi
    cedai
    ly.
    c.Referforcat
    heterablat
    ion.
    d.I
    niti
    atedigoxi
    nat0.25mgdai l
    y.
    e.I
    mpl antadual-chamberpacemaker.

    Answer

    C.Ref
    ert
    ocat
    het
    erabl
    ati
    on.

    ThisECG demonstratesanect
    opi
    catrialr
    hythm atabout100bpm,withsecond
    degreeat
    riovent
    ri
    cularblock(
    Wenckebach)
    .Ther hyt
    hm isnotsinus,astheP
    wavesar enegativeinl eadI I.Thi
    srhythm persist
    sdespitetheadmi
    nist
    rati
    onof
    beta-
    blockade,andher emai nssymptomat i
    c.Thenextst epistoproceedwi t
    h
    el
    ectrophysi
    ologi
    cst udyt omapandabl atetheatrialf
    ocus.Apacemakerisnot
    needed ast helevelofbl ocki sunli
    kelyt o besubnodal.Holt
    ermonitori
    ng i
    s
    unnecessaryatthispointast hediagnosisisclearfr
    om theECG,andt
    hehi st
    oryi
    s
    consi
    stentwithsympt omsr elatedt
    othisrhythm.

    49.
    A75- year-ol
    dmancomest ocl inicf orf oll
    ow- up.Hehasf eltwellunt i
    labout3
    mont hsagoandnowi sshor tofbr eathwhenhewal ks>100yar dsandi sbot hered
    bypul sati
    onsi nhi sneck.Hispasthi storyincludesdyslipidemi a,hyper t
    ension,and
    type2di abetes.Fiveyear sago,heunder wenti mplantationofasi ngle-chamber
    pacemakerf orsyncope,wi tha5- secondpauseseenonaneventmoni tor.He
    previouslyunder wentanucl earst ressi magi ngstudy6mont hsagof orevaluat i
    on
    ofchestdi scomf ort
    ,showi ngnor mall eftvent ri
    cul
    arf unct ionandnoi schemi a.
    Currentmedi cati
    onsar emet opr olol25mgt wi cedail
    y,li
    sinopr il10mgdai l
    y, aspiri
    n
    325mgdai l
    y,andsi mvast atin20mgdai ly.Onphysi calexami nati
    on,hi sbl ood
    pressurei s120/ 70mm Hgandhear trateis60bpm.Thepacemakersi tei swel l
    healedi nt heleftchest.Uponauscul t
    ati
    on,t hehear trhyt hm i sregularand  S2 is
    paradoxicallyspli
    t.Uponi nt
    er rogationofhi spacemaker ,ther eisnoi ntri
    nsicactivity
    atsingle-chambervent ricul
    arpaci ng( VVI)40bpm.Hi sel ectrocar di
    ogram isshown
    inFigure1.
    Whi
    choft
    hef
    oll
    owi
    ngwoul
    dbet
    henextst
    epi
    nmanagement
    ?

    a.Enablerate-
    responsivepacing.
    b.Upgradetodual -chamberpacemaker.
    c.Disconti
    nuemet oprolol.
    d.Raisethepacingr at
    et o80bpm.
    e.Upgradetoabi ventri
    cularpacemaker
    .

    Answer

    B.Upgr
    adet
    odual
    -chamberpacemaker
    .

    Thisel ect rocardiogr am showsr egularvent r


    icularpacingatar ateof60bpm, wi thP
    wavesseenj ustf ollowi ngeachpacedQRScompl exduet oretrogradeconduct i
    on
    throught heat riovent r
    icular(AV)node.Wi thnoi ntri
    nsicact ivit
    yatVVI40bpm, there
    i
    sei thercompl etehear tblockpresentor ,lesslikel
    y,atrialstandst i
    ll(i
    .e.,nointri
    nsic
    sinusact ivit
    y).Hi ssympt omsofexer ciseintoleranceandneckpul sationsar elikel
    y
    tor efl
    ectpacemakersyndr ome.Upgr ade oft he devi ce t o a dual -chamber
    pacemakerwi llr estore AV synchr ony and i mprove sympt oms.Di scontinuing
    met opr ololwi l
    lnotr eversecompl et
    ehear tblockorat r
    ialstandst i
    llifpresentandso
    willnotchanget hepat i
    ent'ssympt oms.I ncreasingt hepaci ngratewi llnotaddr ess
    thel ackofAVsynchr ony.Si milarl
    y,rate-responsivepaci ngmodes( i
    .e.,VVI),will
    notr estoreAV synchr ony.Bi ventri
    cularpaci ng,at reatmentf orhear tfail
    urei n
    patientswi thawi deQRS, alsodoesnotaddr essAVsynchr ony.
    50.
    A35- year-oldwomanpr esentsforeval
    uat i
    onofepi sodesofr api
    dheartbeating,
    whereshef eelsshei saboutt ofai
    nt.Overall
    ,shehasspel l
    saboutonceamont h,
    whichusual lyr esolveontheirowni nabout5- 10mi nutes,butont wooccasions
    haver equi
    redt herapyintheemer gencydepar t
    ment .Witht hi
    spastepisode,she
    wastol dherdi agnosiswassupr avent
    ri
    culartachycardi
    a( SVT)andthatsheshould
    consultwithacar diol
    ogi
    st.Shebr i
    ngswi t
    hhert odayt heelectr
    ocar
    diogr
    am (ECG)
    thatwasobt ained on t
    hel astepisode( Fi
    gure1) .Shedoesnotwantt otake
    medicationandwant st
    oknow mor eaboutcat het
    erabl ati
    on,butisconcerned

    abouti
    tspot
    ent
    ialr
    isks.

    Whichofthefol
    lowi
    ngmajorcompl
    icat
    ionsshoul
    dshebeadvi
    sedofbasedont
    he
    l
    ikel
    yet
    iol
    ogyofSVTrepr
    esent
    edi
    ntheECGshowni nFi
    gur
    e1?

    a.3%r
    iskofstr
    oke.
    b.3%r
    iskoftamponade.
    c.3%r
    iskofpulmonaryvei
    nst
    enosi
    s.
    d.1%r
    iskofphreni
    cnervei
    njur
    y.
    e.1%r
    iskofheartbl
    ock.

    Answer

    E.1%r
    iskofhear
    tbl
    ock.

    ThisECGshowsSVTwi thanar rowPwavei nscr i


    bedatt heendpor tionoft heQRS
    compl ex( bestseenasanegat i
    vedef l
    ectioni nthei nfer
    iorl i
    mbl eadsandaposi tive
    deflect
    ioni nl eadV1)f orwhi cht hemostl ikelydiagnosi sist ypi calat ri
    oventri
    cul ar
    (AV)noder e- entry.Cat heterabl at
    ioni sper f
    ormedi nt hesl ow pat hwayr egi on,
    whichi st reatedbyabl atingj ustant er
    iortot heosoft hecor onar ysinus.Ther iskof
    compl etehear tblocki sl ow,about1%.ForSVTduet oAVr e- entrantt achycar dia
    usinganaccessor ybypasst ract,ifablationi sr equir
    edf rom t hel efthear t
    ,t hen
    anticoagul ationi sadmi nisteredt opr eventst r
    oke,andt her iskofst rokeint his
    sit
    uat i
    oni sest i
    mat edat1%.Phr enicner vei njuryisapot ent i
    alr iskf orablation
    performedneart hehi ghcr istat erminali
    s,whi chi sapot entialconcer ni nablati
    onof
    atri
    alt achycar diamappedt ot hisregion.Pul monar yvei nst enosi si sapot ent i
    al
    concer nf orabl ationint hel eftat r
    ium fortreatmentofat rialfibril
    lation( orfocalatr i
    al
    tachycar diar elatedt oapul monar yvein).

    51.
    An18- year-oldmanpr esentstotheclinicrefer
    redbyhispri
    mar ycarephysi
    cian.He
    denies any past car diac issues and has no hi stor
    y of syncope. Hi s
    electr
    ocardiogram (ECG)showsapat t
    er nofpseudor i
    ghtbundlebranchblockwith
    STel evat
    ionandT- wavei nver
    sioninl eads V1andV2.Youinterpr
    etthisECGasa
    typeIpatternofBr ugadasyndr ome.Hi soldestbrot
    herdiedsuddenlywhenhewas
    25year sold,andnoECGsofhi sbrotherareavai l
    abl
    e.
    Whi chofthefollowingist hemostappr opri
    atenextstep?

    a.Advisetoavoidst r
    enuousact i
    vit
    y.
    b.I
    mpl antimplantabl
    ecar di
    overt
    er-def
    ibr
    il
    lat
    or(I
    CD).
    c.Continuedcli
    nicalfol
    low-up.
    d.Provocativet
    estingwithsodium channelbl
    ockade.
    e.I
    mpl antlooprecorder.

    Answer

    C.Cont
    inuedf
    oll
    ow-
    up.

    Thepati
    enthasat
    ype1Br ugadasyndromeECGpat t
    ern.Anolderbr
    otherwhodied
    suddenl
    ydoesnotincr
    easehisri
    skf orsuddendeath,andbecausethepati
    entis
    asympt omat i
    c,he does notmeetcr i
    ter
    iaforI CD implantati
    on.The ut il
    it
    y of
    electrophysi
    ologicstudyfortr
    eat mentdecisi
    onr emai
    nscont roversi
    al.Provocati
    ve
    testingwithsodium channelblockersisnotindi
    catedinat ype1ECGpat t
    ern.There
    i
    snoneedf orthispati
    enttorefrainfr
    om physicalact
    ivi
    ty.Atthispoint,t
    hepat i
    ent
    needst obef ol
    lowedandadvi sedt oavoiddrugswi thsodium channelbl ocking
    activit
    y(seewww. br
    ugadadrugs.org)
    .

    52.
    A45- year-oldwomanpr esentst oyourcl ini
    cforeval uati
    on.Sher eportshaving
    episodesofr apidheartbeatingfort hepast10year s.Theepi sodesoccur2t o3
    ti
    mesayearwi t
    hsympt omsofchestpai nandl i
    ghtheadedness.Mostepi sodes
    stopspont aneouslywithi
    naf ewmi nutes,butlastmont hsher equiredtreatmentin
    theemer gencydepar t
    mentwi thi ntravenousadenosi ne.Shehasnoot herpast
    medi calhistoryandhast akendi l
    tiazem 180mgdai l
    yaspr escr ibedbyherpr imary
    physician.Revi ew ofherel ectr
    ocar diogram duringanepi sodeshowsanar row
    compl ex tachycar di
    a,shows a hear trate of165 bpm,and i s suggesti
    ve of
    atri
    oventricular(AV)nodalre-entrantt achycardi
    a.Anechocar diogram donedur ing
    heremer gencydepar t
    mentvisitshowednor malfindings.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextmostappr
    opr
    iat
    est
    epi
    nmanagement
    ?

    a. I
    nit
    iateami odarone.
    b. Catheterablati
    on.
    c. I
    nit
    iateflecaini
    de.
    d. Continuedclini
    calfol
    low-
    up.
    e. I
    nit
    iatemet oprolol
    .

    Answer

    B.Cat
    het
    erAbl
    ati
    on

    Thi s pati
    enti s a young woman wi t
    h sympt omati
    c and r ecur
    rentepi sodes of
    supr avent
    riculartachycardiawhocont inuest ohavesympt omsdespi t
    eAVnodal
    blockingagent s.Catheterablat
    ionisaCl assIopt i
    onf ormanagement .Fur ther
    adjustmentofAV nodalbl ocki
    ng agents( eit
    herbyi ncreasing thedi l
    tiazem or
    addi ngmet oprolol)canbeconsideredifdesiredbyt hepat ient.Si
    mi l
    arl
    y,flecainide
    also maysuppr essevent sofsupr aventri
    culartachycardi a.However ,themost
    effecti
    veopt ionf ormanagementi nt hispat i
    entwhohasal r
    eadyf ai
    ledmedi cal
    therapyi scat heterablati
    on,wit
    ha>95% successr at
    e.Inayoungsympt omat i
    c
    pat i
    ent,amiodar onewoul dnotbeagoodl ong- t
    erm choice.
    53.
    A70-year-
    oldmanpr esent
    stot
    heemergencyroom wi
    thseverel
    ight
    headedness,
    shor
    tnessof 
    breat
    h,andchestti
    ght
    nessthatstar
    tedabr
    uptly1hourago.Past
    hist
    oryi ncl
    udes  t
    ype 2 di abetes for t he past 10 year s,hypertension,and
    hyperli
    pidemi a.Heal sohasahi storyofsmoki ng,which hestopped5year sago.
    Currentmedi cat i
    onsar easpi
    rin81mg,met oprolol25mgbi d,li
    sinopril20mg,
    metformin500mgbi d,andatorvastati
    n80mg.Onphysi calexamination,heispale
    anddi aphoret i
    c.Vitalsignsarebl oodpr essure70/ 40mm Hgandhear tr at
    e170
    bpm.Hehascl earl ung f
    iel
    ds,S1- S2 
    distant
    ,t achycar
    dic,and no mur mur .His
    el
    ectrocar di
    ogram (ECG)i sshowni nFigure1.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextst
    epi
    nmanagement
    ?

    a.Over-
    drivepaci
    ng.
    b.Li
    docaine.
    c.Adenosine.
    d.Amiodarone.
    e.Cardi
    oversi
    on.
    Answer

    E.Car
    diover
    sion

    TheECGshowsvent riculart
    achycardi
    a,andthepasthi
    storyi
    shighl
    ysuggest
    iveof
    cor
    onaryarter
    ydisease.Hei shypotensi
    veanduncomfortabl
    e,andt
    hebestcourse
    ofact
    ionistorestor
    esi nusrhythm prompt
    ly.Whil
    eamiodaroneandli
    docai
    necan
    beconsi
    dered,gi
    venthehypot ensi
    on,iti
    sbestnott
    owait.

    54.
    A 75-year-oldmanpr esentst otheemer gencyr oom ( ER)wi t
    hcompl aintsofa
    raci
    nghear tbeat,severelightheadedness,andmoder atechestt i
    ghtness.Hebr ief
    ly
    passedoutwheni tfi
    rststarted.IntheER,hehasawi decompl extachycardiaata
    rateof170bpm,abl oodpr essureof75/ 40mm Hg,andanel ectr
    ocardiogram
    confi
    rmingvent ricul
    art achycar di
    a( VT).Cardiover
    sioni sper f
    ormedi ntheERt o
    rest
    oresinusr hythm.Subsequenteval uati
    oni nthehospi talshowsapeakt roponi
    n
    of1.0ng/ dl.Cardiaccat heterizat
    ionreveal
    st hree-vesselcoronarydiseasewi tha
    lef
    tventri
    cular(LV)ej ecti
    onf ractionof35-40%,conf irmedbyechocar di
    ogram.He
    undergoescor onaryar t
    erybypassgr af
    tsurgeryduringhishospi t
    ali
    zati
    on.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    ep?

    a.I
    nit
    iateami odaroneandr eassessLVf uncti
    onin90days.
    b.Wear ablecardi
    overter-
    defi
    bri
    llatorfor45days.
    c.I
    mpl antICDi fi
    sVTi nducedinel ectr
    ophysiologicst
    udy.
    d.Per
    for m cathet
    erablati
    on.
    e.I
    mpl ant i mplantable cardioverter-
    defibr
    il
    lator (I
    CD) bef
    ore hospi
    tal
    di
    schar ge.

    Answer

    E.I
    mpl
    anti
    mpl
    ant
    abl
    ecar
    diover
    ter
    -def
    ibr
    il
    lat
    or(
    ICD)bef
    orehospi
    taldi
    schar
    ge.

    This patientmeets secondary prevention cri


    ter
    iaf orimplantofan I CD,and
    implantati
    onshouldnotbedel ayedf or90days.TheAVI D(Anti
    arrhythmicsVersus
    Implantable Def
    ibr
    il
    lat
    ors)studyenr ol
    led pati
    ents who werer esuscitated f
    rom
    vent
    r i
    cularfi
    bri
    ll
    ati
    on,wit
    hsustainedVTwi t
    hsyncope,orwithsustainedVTwi than
    LVej ect
    ionfract
    ion<40%associ at
    edwi thseveresympt oms( heartfail
    ure,angi
    na),
    showi ngthesuperiori
    tyofanI CDf orsur vi
    valoveranti
    arrhyt
    hmict her
    apy.About
    10%oft heAVIDpopulati
    onunder wentr evascularization,andthebenefi
    tofanI CD
    was i ndependent of revascular
    izati
    on. Ther efore,t he Ameri
    can College of
    Cardiol
    ogyFoundation/Amer i
    canHear tAssociation/ EuropeanSoci
    etyofCardiology
    gui
    del i
    nesregardtheimpl antofanI CDasaCl assIr ecommendationforpatients
    wit
    hsust ai
    nedVTwi t
    hst ruct
    uralheartdi sease,r egardlessofwhetherstableor
    unstable.

    55.
    A 30- year-ol
    dwomanhasasuddenonsetofpal pi
    tati
    onsandl ightheadedness
    whi leplayi
    ngwi t
    hherchildreninthepark.Af
    teranhour,
    withnorel
    ief,shepresents
    tot heemer gencyroom.Hervi talsi
    gnsarebloodpr
    essure120/70mm Hgandheat
    rate180bpm.Shei sthengi venadenosine6and12mgbutwi thoutef f
    ect.Her
    electrocardi
    ogram (ECG)i sshowni nFigur
    e1.Shei sof f
    eredcardioversi
    onbut
    refuses.

    Whi
    choft
    hef
    oll
    owi
    ngmedi
    cat
    ionsi
    smostl
    ikel
    ytochemi
    cal
    lycar
    diover
    tthi
    srhyt
    hm?
    a.Ibutil
    ide.
    b.Adenosi ne( hi
    ghdose)
    .
    c.Met oprolol.
    d.Verapami l
    .
    e.Lidocaine.

    Answer

    D.Ver
    apami
    l

    Int his young patientwi t


    houtst ructur
    alhear tdi sease,one mustf ir
    stassess
    hemodynami cstabili
    ty.Becauseshehasnochestpai n,dyspnea,orhypot ension,
    emer genttherapyisnotnecessar y.ThisECGshowsat achycardiawithjustami l
    dly
    wideQRScompl ex.Thereisar i
    ghtbundl ebranchbl ock( RBBB) -l
    ikemorphol ogy.In
    a young per son who i s otherwise healthy,this ECG i s mostconsi stentwi th
    i
    diopat hi
    cl ef
    tventricl
    e( f
    ascicul
    ar)vent r
    iculartachycar dia,whichi sar e-entrant
    tachycardiainvolvi
    ngmostcommonl ythel eftposteriorfascicl
    e,givinganRBBB-
    l
    ikeappear anceandasuper ioraxis.Thisrhythm ishi ghlysensiti
    vet overapami l
    .It
    i
    sal ow- r
    isktachycardia,andcat heterablati
    onoft hef ascicl
    einvolvedisusual ly
    curative.

    56.
    Thepat i
    enti sa67- year-oldmanwi thhistoryofcor onaryarter
    ydiseaseforwhich
    he under went cor onar y ar t
    ery bypass gr aft surgery 5 years ago.Recent
    echocardi
    ogr am showed a mi l
    dlyenlar
    ged l ef
    tvent ri
    clewi t
    hal ef
    tventr
    icul
    ar
    eject
    ionfractionof25%.Hei sablet
    oexer cise4t i
    mesaweekf or1hourandal so
    hikesforacoupl eofhour severyweekend.Hei sonopt imalmedicalther
    apywith
    carvedi
    lol
    ,lisinopri
    l,aspirin,andatorvast
    atin.Hiselectrocar
    diogram showsnormal
    sinusrhythm wi thar ightbundl ebranchbl ockpat t
    ernandQRSdur ati
    onof138
    msec.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    erecommendat
    ionf
    ort
    hispat
    ient
    ?

    a.I
    mpl antabivent
    ricul
    arICD.
    b.I
    nit
    iatesotal
    oltherapy.
    c.I
    mpl antabivent
    ricul
    arpacemaker .
    d.Continuecurr
    entmedi calt
    herapy.
    e.I
    mpl antanimplantablecar
    diovert
    er-def
    ibr
    il
    lat
    or(
    ICD)
    .

    Answer

    E.I
    mpl
    antani
    mpl
    ant
    abl
    ecar
    diover
    ter
    -def
    ibr
    il
    lat
    or(
    ICD)
    .
    The pat ientmeet s cr i
    teri
    af ora pr imar y pr evention ICD based on MADI T-II
    (Multi
    cent erAut omatic Def i
    bril
    latorI mpl antation Tr i
    alI I
    )cl inicaltrialr esults.
    Continuingcur rentmedi caltherapyandi niti
    atingsot aloltherapyar eincor r
    ect ,as
    thepatientdoesmeetcr it
    eri
    af ordevi cei mpl antandant iarr
    hythmi cther apyisnot
    demonst ratedt oimprovesur vival.Impl antingabi ventr
    icularICDandi mpl antinga
    biventr
    icularpacemakerar eal soi ncor rect,ast henew devi cet herapygui delines
    from 2012 st ateitis a Cl ass I I
    Ii ndication forbi vent r
    icularpaci ng car diac
    resynchronizationtherapyinpat ientswi t hNewYor kHear tAssoci ati
    oncl assIorI I
    andanon- l
    eftbundlebranchbl ockpat ter nwithQRSdur ati
    on<150msec.

    57.
    A63- year
    -ol
    dmancomestoseeyouinyourcl
    ini
    c.Thepati
    enthasapastmedical
    hist
    oryofcoronar
    yar
    ter
    ydi
    seaseforwhi
    chheunder wentper
    cutaneouscor
    onary
    interventi
    ont ot hemi dleftant eri
    ordescendingandmi dr i
    ghtcoronaryar tery3
    year sago.Hi sr ecentechocar diogram showedadi l
    atedlef
    tventr
    iclewi thal eft
    vent r
    icleej
    ectionfracti
    onof26%.Hei sabletoperform moderatephysicalactivi
    ty3
    timesaweekandf eelsmildlimi t
    ati
    onwhenheexer cisesf
    oroveranhour .Hehas
    nosympt omsorcompl ai
    ntsatt hepr esentti
    me.Hei sonopt i
    malmedi caltherapy,
    including carvedil
    oland l i
    sinopr i
    l.Hi s el
    ect
    rocardiogram shows nor malsi nus
    rhythm andl eftbundlebranchbl ockwi t
    haQRSwi dthof160msec.

    Att
    hispoi
    nt,
    whi
    choft
    hef
    oll
    owi
    ngi
    showt
    hispat
    ientshoul
    dbeadvi
    sed?

    a.I
    mplantadual-chamberI CD.
    b.I
    mplantabiventr
    icul
    arimpl antabl
    ecar
    diover
    ter
    -def
    ibr
    il
    lat
    or(
    ICD)
    .
    c.Cont
    inuecurr
    entmedi caltherapy.
    d.I
    mplantasingle-
    chamberI CD.

    Answer

    B.I
    mpl
    antabi
    vent
    ri
    cul
    ari
    mpl
    ant
    abl
    ecar
    diover
    ter
    -def
    ibr
    il
    lat
    or(
    ICD)
    .

    Therightansweri st oimplantabi ventri


    cul
    arI CDt odecreaset heriskofdeat hor
    heartfailurehospi tali
    zationbasedont her esult
    sf rom MADI T-CRT ( Mul t
    icenter
    Automat i
    cDef i
    bril
    latorImplantati
    onTr i
    alWi t
    hCar diacResynchr oni
    zat i
    onTher apy)
    and RAFT ( Resynchr onizati
    on/Defi
    bril
    lat
    ion forAmbul at
    ory HeartFai lure Tr i
    al)
    ,
    whichdemonst rat
    edt hatabi ventri
    cularICD i napat i
    entwithNew Yor kHear t
    Associati
    oncl assI Ireducedt hecomposi teofdeat handhear tfail
    ureevent s.Int he
    RAFT t ri
    al,t he secondar y endpointofmor tal
    it
    y also was achi eved wi tha
    bi
    ventricularICDcompar edwi thICDal one.Cont i
    nuingcurrentmedi calt herapyi s
    i
    ncorrect,ast hepat ientmeet scri
    teri
    aatt hi
    st i
    mef oradevi ceimplant .I
    nt he2012
    updatet ot he2008Amer i
    canCol l
    egeofCar diol
    ogyFoundat ion/Amer icanHear t
    Associat
    ion/HeartRhyt
    hm Soci
    etydevicegui
    deli
    nes,i
    tisnowaCl assIindicati
    onto
    i
    mpl antabiventr
    icul
    arICDinapatientwit
    hal ef
    tventr
    icleeject
    ionfracti
    onof35%,
    i
    nsi nusrhythm,inNew YorkHeartAssociat
    ionclassII,II
    I,orambul at
    oryI V,wi
    th
    l
    eftbundlebranchblockandQRSdur ati
    on>150msec.

    58.A64- year-
    oldmanwi thahi st
    oryofsinusnodedysfuncti
    onandcompl et
    eheart
    blockwhounder wentdual-chamberpermanentpacemaker2year sagocomest o
    yourof fi
    cecompl ai
    ning ofintermi
    tt
    entpalpi
    tati
    ons.Dur i
    ng perf
    ormanceofhi s
    elect
    rocardiogr
    am bythenur se,hef
    eelstheonsetofpal
    pitati
    ons,whichconti
    nued
    forami nuteaft
    ertheelect
    rocardi
    ogr
    am wascompl et
    ed(Figure1).

    Which oft hef


    oll
    owi
    ng i
    nter
    vent
    ionsi
    smostl
    ikel
    yto decr
    easehi
    ssympt
    omsof
    pal
    pit
    ations?

    a.Vent
    ri
    cul
    arl
    eadr
    evi
    sion.
    b.Shorteni
    nghispost vent
    ricul
    aratri
    alr
    efr
    act
    oryper
    iod.
    c.I
    ncreasinghislowerr at
    et o80bpm.
    d.Metoprolol25mgbi d.
    e.Decreasinghisatr
    ioventri
    culardel
    ay.

    Answer

    D.Met
    ropol
    ol25mg.bi
    d.

    Thebeat sareventricul
    arectopicsand ar enotr el
    ated t
    o pacing.Thereisno
    evidenceofpacemakerl ead malf
    unction,asthereisappr opri
    atesensing and
    ventri
    cularcaptur
    e.At ri
    alofanant i
    arrhythmi
    c,suchasabet ablocker,shoul
    dbe
    attempted.Ifunsuccessfulandher emai nshi
    ghl
    ysympt omatic,t
    henavent ri
    cul
    ar
    tachycardi
    aablati
    oncoul dbeconsidered.

    59.
    A24- year-oldmanwi t
    hapastmedi calhistoryofbi
    cuspidaorti
    cvalvestat
    uspost
    aor t
    ic valve repl
    acementi s admitt
    ed over ni
    ghtaft
    eror thopedi
    c surger
    yf ora
    fracturesust ai
    nedwhi l
    eski i
    ng.Hisor i
    ginalcardi
    acsurgeryseveralyear
    sagowas
    compl i
    catedbysi nusnodedysf unct
    ion,andheunder wentpacemakerpl acement.
    Whi l
    eont elemetr
    y, t
    hefindi
    ngshowni nFigure1wasnot ed.Thepatientwasasleep
    dur i
    ngt hetimeoft heepisode.
    Thef
    indi
    ngsont
    elemet
    ryr
    epr
    esentwhi
    choft
    hef
    oll
    owi
    ngexpl
    anat
    ions?

    a.Undersensing.
    b.Fai
    luretocapt ur
    e.
    c.Normalf unct
    ion.
    d.Rate-dropresponse.
    e.Oversensing.

    Answer

    C.Nor
    malf
    unct
    ion.

    Specif
    icall
    y,whatisdemonstrat
    edismanagedventri
    cul
    arpaci
    ng.Al
    thoughthi
    s
    part
    icularal
    gori
    thm i
    sspeci
    fi
    ctoonecar
    diacdevi
    cecompany,
    mostmanufact
    urer
    s
    now havespeci ali
    zedalgorit
    hmsavai labl etomi nimi zet heamountofvent ri
    cular
    pacing.Theseal gori
    thmsar ei ncr easingl ypopularpr ogr ammi ngchoicesduet o
    findings ofwor sened cardiac funct ion wi t
    h ventr
    icul arpaci ng in heartf ail
    ure
    pat i
    entsandar educedriskofat r
    ialf i
    brillati
    oni npatientswi thsi nusnodedi sease.
    Thepat i
    entisasleep,young,andat hletic.Hehasnohi storyofat ri
    ovent
    ricul
    ar( AV)
    conduct iondiseaseandi sexhi bit
    ingWenckebachphenomenon( Mobit
    zt ypeIAV
    block),whi chisnor mal.Despi teat ri
    alpaci ng,thevent ricleisnotpacedast he
    algor i
    thm isdesignedtoal l
    ow foral ossofAVconduct ionf oronecycl e.Thenext
    ventr i
    cularimpulseisapacedbeat ,andwi t
    hashor tenedpacedAVdel ay,whi chis
    also acl uetot hispacing algorithm.Thi si snotover sensing ori nappropr i
    ate
    inhibiti
    on of paci ng. Undersensi ng i s usual l
    yr ecogni zed by i nappropr i
    ate
    pacemakerar ti
    factdespiteelectricalact ivi
    ty,whichi snotseenher e.Rat e-drop
    responsei sanalgori
    thm thatforcesdual -chamberpaci ngi nr esponset oadr opi n
    nat i
    veat r
    ialr
    ateand i snotdemonst r ated on thi
    st r
    aci ng.Lackofcapt ur eis
    diagnosedwhenapacemakerar tif
    acti snotf oll
    owedbyaPwaveorQRScompl ex.

    60.
    An18-year-ol
    dwomanwi t
    hnosignif
    icantpastmedi calhist
    oryisbei
    ngevaluat
    ed
    atacoll
    egesport
    sphysical
    .Herphysi
    cialexaminati
    oni snormal.Al
    thoughshehas
    swum befor
    e,att
    hesecondmeetoftheyear ,sheexperiencesanepi
    sodeofsudden
    car
    diacdeathwhi
    leswimmi ng.

    Which ofthefol
    lowi
    ng mechani
    smsexpl
    ainst
    hel
    ikel
    ypat
    hophysi
    ologyoft
    he
    suddendeath?

    a.Gainoff
    unct
    ioni
    nthesodium channel
    .
    b.Lossoff
    unct
    ioni
    nthesodium channel
    .
    c.Gainoff
    unct
    ioni
    nthepotassi
    um channel
    .
    d.Lossoff
    unct
    ioni
    nthepotassi
    um channel
    .
    e.Gainoff
    unct
    ioni
    nthecal
    cium channel
    .

    Answer

    D.Lossoff
    unct
    ioni
    nthepot
    assi
    um channel
    .

    A young adul
    twi t
    h sudden cardiac deat
    h shouldr ai
    se the suspici
    on ofan
    under
    lyi
    ngprimaryelect
    ri
    caldisorderorhypertr
    ophiccardi
    omyopat hy.Thereare
    cer
    tai
    nsetti
    ngsthatareregar
    dedascl assicforcer
    tainsyndr
    omes.Oft hese,l
    ong
    QTsyndrometype1,withamut at
    ionintheIKspotassi
    um channelleadingtoaloss
    offuncti
    onandthusadel
    ayi
    nmembr
    aner
    epol
    ari
    zat
    ion,hasacl
    assi
    cpr
    edi
    lect
    ion
    forevent
    swithswimmi
    ng.

    61.
    A 30- year -oldwomanpr esent sf oreval uationofepi sodesof  
    recur rentsyncope.
    Overt hepast20year sshehasf aint ed10t i
    mes,buti nt hepast6mont hsshehas
    hadt hreeepi sodes.Typi calspel l
    soccurwhenshesi ngsi nthechur chchoi randar e
    precededbyabout30secondsofnauseaandsweat ing.Shehasnoti njuredher self
    ,
    butisembar rassed,ast hel asttimeshef ai
    nt edt hepar amedicswer ecal led.She
    has no ot herpastmedi calhi story and t akes no medi cations.On physi cal
    exami nat i
    on,herbl oodpr essur e( BP)i s110/ 60mm Hgandhear tratei s90bpm.
    Herj ugularvenous pul se i s 
    5 cm.Ther ei s a si ngle S1 and physi ologi cally
    split
     S2 withoutmur mur.Ther emai nderofherexami nat i
    oni sunr emar kabl e.An
    electrocardiogr am i ntheof ficeshowsnor malsi nusr hythm atar at eof93bpm.The
    foll
    owi ngday,sheunder goesat il
    tt ablestudyshowi ngasupi neBPof120/ 70mm
    Hgandahear trat
    eof80bpm.Wi thpassi vet i
    lt,theBPovert hef irst5mi nut esi s
    110- 120/ 55- 65mm Hgandhear trat esare80- 100bpm.At8mi nut esint ot het i
    lt
    ,
    shecompl ainsofnauseaj ustl i
    keshef eelsbef oreherusualf ai nts,andt hen30
    secondsaf tert hatshel osesconsci ousness.HerBPr eadingobt ainedabout20
    secondsbef oref ainti
    ngi s65/ 40mm Hgandhear tratei s40bpm.Att hemoment
    whenshef aint s,herhear tr atei s30bpm.Shei simmedi at
    elyl aidsupi ne,wi t
    h
    promptr eturnofherBPandhear trat etobasel inel evel
    s.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nhermanagement
    ?

    a.I
    niti
    atemetoprolol
    .
    b.Avoidtri
    gger
    sforsyncope.
    c.I
    niti
    atemidodri
    ne.
    d.I
    mpl antadual-chamberpacemaker
    .

    Answer

    B.Avoidtriggersf
    orsyncope
    Thispatienthasvasovagalsyncopewi thawel l
    -def
    inedt rigger:st
    andingi nthe
    choiratchur ch.Hert il
    tt abl
    e study suggests a mi xed vasodepr essorand
    cardi
    oinhibit
    oryresponse,and i treproduced hersympt oms.Whi l
    e a cl ini
    cal
    syncopalspel lmay show a di f
    fer
    entphysi ol
    ogicr esponse,t he fi
    rstst ep in
    managementshoul dbeconser vati
    ve,str
    essinghydration,sal t,andavoi danceof
    tr
    igger
    s.Whi l
    eotherdiagnosti
    ctestssuchasechocar diogr am andst resstesti
    ng
    arecommonl yused,thedi agnosisinthispat i
    entiscl ear,wi thouttheneedf or
    furt
    herdiagnosti
    ct esting.Li kewise,electr
    ophysiol
    ogicstudycan beusef ulfor
    pati
    entswithsyncopesuspect edtobeduet oavent r
    icul
    ararrhyt
    hmi a,butdoesnot
    playarol
    ef ortheworkupofvasovagalsyncope.I fconser
    vati
    vemeasur esfai
    l,then
    ani mpl
    antableloopr ecor dercanbeconsi der
    edt odetermineifclinicalepisodes
    showamar kedcardio-inhi bi
    toryresponse(despitetheti
    ltt
    ablefindings),asthere
    canbear oleforpaci
    ngf orpatient
    swi thprol
    ongedper i
    odsofasystole. 

    62.
    A 45- year -
    old man i s sentt o you f orpr eoperati
    ve clear ance because ofan
    abnor malel ect
    rocardiogram ( ECG) .Hehasnopr iormedi calhi storyasidef r
    om a
    ri
    ghti nguinalherni
    af orwhi chhei sscheduledt ounder gosur gicalr epai
    rnextweek.
    Hewasseenbyt heanest hesiologistyesterdayforapr eoperativeassessmentand
    bringst heECGt hatwasper for medatt hattime.Hef eelswel lasidef r
    om discomf ort
    relatedtohi sherni
    aanddeni esanyshor t
    nessofbr eat
    h, chestpai n, pal
    pitat
    ions, or
    dizziness.Heusual l
    ypl aysr acquet bal
    l3t i
    mesaweek, whi chhehasdonesi ncehi s
    collegedays.Het akesnomedi cati
    ons.Hi sphysicalexami nati
    oni sunremar kable,
    withabl oodpressureof115/ 70mm Hgandhear trateof60bpm.Hebr ingsi nthe
    ECGf rom yester
    day’sappoi ntmentwi t
    ht heanest hesiologist(panelA) ,whi chyou
    compar ewiththeECGobt ainedt oday(panelB) ,
    asshowni nFi gur e1.

    Whi
    ch of t
    he
    foll
    owi
    ngis the next
    step in

    management
    ?

    a.Proceedwi
    thherni
    arepai
    r.
    b.Obtainast
    ressECG.
    c.Ordera24-hourHol
    termoni
    tor
    .
    d.Referf
    orel
    ect
    rophysi
    ologi
    cst
    udy.
    e.Orderatr
    anst
    horaci
    cechocar
    diogr
    am.

    Answer
    A.Pr oceedwithherniar epai
    r.
    TheECGi npanelAshowspr e-excit
    ation,indi
    catingabypasst racti
    nt hi
    spat i
    ent,
    butwhi chisnotpresenti ntheECGper f
    ormedt oday(panelB).Hei sasymptomat i
    c
    withregardtothisfinding,andf urt
    hermor e,hehasexcellentexerci
    setoler
    anceby
    histor
    y.Hei sthereforeatver yl ow r
    iskf ornoncardiacsurgeryandcanpr oceed
    withoutf ur
    thertesting.El ect
    rophysiologic study isindicat
    ed ifhe devel ops
    sympt omssuggestiveofsupr aventri
    culartachycardi
    a.

    63.
    A35- year -oldmancomest oyourcl inicforhissympt omsofpal pi
    tati
    ons.Fort he
    past5year shehasf eltani r
    regul arbeatwi t
    hfrequent” skips.”Hesayst hatinthe
    past6mont hshisr unningcapaci tyhasdecl i
    nedaswel l,andi ttakeslongerf orhim
    tocompl etehi susual5- miledailyr un.Hedeni esanysyncopeorchestpai n.Hehas
    nopastmedi calhistory.Fami l
    yhi storyi snotableforanacut emyocar dialinfar
    cti
    on
    in hi
    sf at heratage 50 year s.He t akes no regularmedi cati
    ons.On physi cal
    examination,hi sbl oodpr essurei s108/ 60mm Hgwi thapul seof70bpm.He
    weighs170pounds( bodymassi ndexi s25.8)
    .Thej ugul arvenouspul seisseenat
    6cm,andcar oti
    dupst rokesar enor malandwi t
    houtbr uit.Lungsoundsar eclear,
    andcar diacauscul tationshowsasi ngleS1,physiologicallyspl i
    tS2,andagr ade1/6
    shortsyst olic mur mur .An ect opic beataboutever yt hree beat si s heard on
    auscult
    ation.Anel ectrocardiogram ( ECG)i sobtained.
    Whi
    choft
    hef
    oll
    owi
    ngbestexpl
    ainst
    hef
    indi
    ngsont
    heECG(
    Figur
    e1)
    ?

    a.Automat i
    city.
    b.Micro–re-entryaroundaf i
    xedscar.
    c.Earl
    yaf t
    erdepolari
    zations.
    d.Delayedafterdepolari
    zati
    ons.
    e.Macr o–re-entr
    yar oundthepulmonaryval
    ve.

    Answer

    D.Del
    ayedaf
    ter
    depol
    ari
    zat
    ions

    This ECG shows pr ematur e ventricul


    arcontracti
    ons (PVCs)wi thl eftbundl e
    mor phologyandinfer
    ioraxis,suggest i
    veofafocusatt her i
    ghtvent r
    icularoutfl
    ow
    tract
    .In a young adultwi thoutst ruct
    uralheartdisease,t he PVCs ar ise f
    rom
    tri
    ggeredacti
    vit
    yduet ocatecholami ne-i
    nduceddelayedafterdepolari
    zations.Beta-
    blockersandcalci
    um channelbl ockersmaybeef fect
    ive,
    butcat heterablati
    onoft he
    focusisusuall
    ycurati
    ve.
    64.
    A70- year -
    oldmanpr esentstot heemer gencydepar t
    mentaf teranearsyncopal
    epi
    sodet oday.Her eportsthathewasathomeandhadbeenwal kingtothekit
    chen
    whenhesuddenl yfeltveryf ai
    ntandsliddownt hewalltot hefloor,wherehever y
    nearl
    yl ostcompl eteconsci ousness.Hedi dnotinjur
    ehimsel f
    .Hehashadper iods
    ofbri
    efl ightheadedness,suddeni nonset,lasti
    ngaf ew secondsovert hepast2
    months,whi chpr ompt edhispr i
    mar ycarephysiciantoorderaneventmoni tor.His
    pasthistoryincludeshyper t
    ension,whichistreat
    edwi t
    hl i
    sinopr
    il10mgdai l
    y. 

    Anechocar
    diogr
    am perf
    ormed6mont hsagoshowednormalventri
    cul
    arfunct
    ion
    andval
    ves,
    withamil
    dlydil
    atedl
    eftat
    ri
    um andaneject
    ionf
    ract
    ionof60%.
     

    Hisvi t
    alsignsareabl oodpressureof120/ 70mm Hg,hear trat
    eof70bpm,and
    respir
    ationsof10/minute.Thecardiacexami nat
    ionshowsar egul
    arr hyt
    hm anda
    paradoxicall
    yspl
    itS2 
    withoutmurmur .Aneventmonitorstr
    ipi
    savail
    abletoyouthat
    correspondstothetimeoft hepat
    ient’snearsyncopaleventt
    oday,showni nFi
    gure
    1.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nmanagement
    ?
    a.Referforti
    lttablestudy.
    b.Referforel
    ect rophysi
    ologicstudy.
    c.Referforpacemakeri mpl ant
    .
    d.I
    niti
    atewar farin.
    e.Disconti
    nuel isinopr
    il
    .

    Answer

    C.Ref
    erf
    orpacemakeri
    mpl
    ant
    .

    Thiseventmonitorstr
    ipshowsaper i
    odofasystolewithcompl eteheartblock.
    Therear ebri
    efperi
    odsshownwher econductionresumeswi thapr olongedPR
    i
    ntervalandawideQRScompl ex(which,gi
    venthefi
    ndingsonphysicalexaminati
    on,
    would suggestaleftbundlebranch block)
    .Thisi sasi tuat
    ion wheretherei s
    advancedconducti
    ondiseaseandi nter
    mitt
    entcompleteheartblockast hecause
    forsyncope,
    andapacemakerneedst obeimplantedurgent
    ly.

    65.
    A50- year
    -oldwomanwi thapasthistor
    yofanoni schemi ccardi
    omyopathy,witha
    lef
    tventri
    cularej
    ecti
    onf r
    acti
    onof35%pr esent
    stot hepacemakercli
    nicforrouti
    ne
    fol
    low-upf orherimplantabl
    ecardiover
    ter-def
    ibr
    il
    lator(I
    CD).Adual-chamberI CD
    wasi mplanted6mont hsagoforpr i
    marypr event
    ionf orsuddendeath.Shef eel
    s
    well,
    buthasnot i
    cedbriefpal
    pit
    ati
    onsper cei
    vedasar api
    dheartr
    atef
    oryears. 

    Hercurr
    entmedi
    cati
    onsincl
    udecarvedi
    lol12.
    5mgbid,l
    isi
    nopr
    il10mgdail
    y,and
    aspi
    ri
    n81mgdaily.Herbl
    oodpressur
    eis110/60mm Hgandheartr
    atei
    s65bpm. 

    TheICDiswel lhealedinthelef
    tchest
    .Inter
    rogationofherICDt odayshows15
    epi
    sodesoftachycardi
    ainthepast3mont hs,allofwhicharesuccessful
    lyt
    reat
    ed
    wit
    hantit
    achycardi
    apacing(noshocksneeded).Arepresent
    ati
    veepisodeisshown
    i
    nFigure1.
    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nmanagement
    ?

    a.Ref
    erforablation.
    b.I
    nit
    iatedigoxin0.125mgdail
    y.
    c.Conti
    nuecur rentmanagement.
    d.I
    ncreasecarvedilolt
    o25mgt wicedai
    ly.
    e.I
    nit
    iatesotalol80mgt wi
    cedail
    y.

    Answer

    A.Ref
    erf
    orabl
    ati
    on

    TheICDinter
    rogat i
    onshowst achycardi
    aatar at
    eofabout200bpm,wi t
    htheatri
    al
    si
    gnal consistentl
    yf oll
    owing the vent r
    icular si
    gnal about 30 msec l at
    er.
    Ant
    it
    achycardiapaci ngt henter
    minatesthet achycardi
    a.Thispat
    ter
    ni ssuggest
    ive
    ofsupravent
    riculart achycardi
    a,specif
    icall
    yat ri
    oventr
    icul
    arnoder e-ent
    ry.Ina
    patientwit
    hal ong-standinghi
    stor
    yofpalpit
    ati
    ons,andwi t
    htheconcernthatt
    his
    tachycardi
    amayi ncreaseherri
    skforaninappropr
    iateshock,i
    tisadvi
    sabl
    eforher
    toundergoelectr
    ophysiologi
    cstudyandcathet
    erablat
    ion.

    66.
    An85- year-
    oldmani sseenint hepacemakercl i
    nicforusualdevi
    cefollow- up.He
    feel
    swel loveral
    lwith no specificcomplai
    nts.Hi spasthi st
    oryincludesat r
    ial
    fi
    bril
    lation (
    AF),si
    ck sinus syndrome,hypertension,and moder at
    e Al zheimer’s
    dement i
    a.His AF had been par oxysmaluntil6 mont hs ago when itbecame
    persi
    st entandnow isregardedasper manent.Hei ssedentaryandliveswi t
    hhi s
    caregiverswhoaccompanyhi mt ohisappoi
    ntmentint hepacemakercli
    nic. 

    Curr
    entmedi
    cationsarer
    ivar
    oxaban20mgdai
    ly,
    met
    opr
    olol25mgt
    wicedai
    ly,
    and
    hydr
    ochl
    orot
    hiazide25mgdaily.
     

    Hi
    sbl oodpressuretodayis135/
    80mm Hgwi
    thahear
    trat
    eof70bpm.Hi
    s
    el
    ect
    rocar
    diogram showsAF.
     

    Hehasadual -chamberpacemakert hatwasi mplanted7year sagoandsett oa


    modeofdual -chamber,r
    ate-responsi
    vewi t
    hal owr at
    eof60bpm.Theat r
    ialout
    put
    issetat5V at1msec,andvent ri
    cularoutputissetat2V at0. 5msec.The
    ventri
    cul
    arleadhasexcel lentsensingandpaci ngthresholds.Theatrialleadis
    sensingpoorl
    y;inappr
    opriateatri
    alpacingisnotedondevi ceinter
    rogat
    ion.Batt
    ery
    longevi
    tyi
    sest i
    matedat18mont hsbasedoncur rentset
    tings.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextst
    epi
    nmanagement
    ?

    a.Disconti
    nuet hemet oprolol
    .
    b.Perform acardioversi
    on.
    c.I
    ncr easethesensiti
    vit
    yoft heatri
    all
    ead.
    d.I
    mpl antanewat ri
    alpacinglead.
    e.Repr ogr
    am thepacemakert osingl
    e-chambervent
    ri
    cul
    arpaci
    ng(
    VVI
    ).

    Answer

    E.Repr
    ogr
    am t
    hepacemakert
    osi
    ngl
    e-chambervent
    ri
    cul
    arpaci
    ng(
    VVI
    ).

    Thispat
    ientisi nper manentAFand,t heref
    ore,doesnotr equi
    redual
    -chamber
    paci
    ng,whi ch is contr
    aindi
    cat
    ed int he set
    ting ofpermanentAF.The atri
    al
    under
    sensing and high paci
    ng thr
    esholdsaredr aini
    ng t
    hebatter
    yaswel l
    .By
    reprogr ammi ngthedevi cet oVVI ,t
    hepat i
    entmaywel lavoi
    daf utur
    egener ator
    change by ext ending the batter
    yl ongevity signi
    ficantl
    y.Whilei ncreasing the
    sensitivityoftheat ri
    alleadmayi mprovetheunder sensingproblem,itwoul dnot
    eli
    mi nat ethepossibil
    ityofinappropri
    ateatrialsensi
    ngandf ai
    lur
    et omodeswi tch;
    therefore,programmi ngt oVVIist hebestopt ion.Ast hepacingleadsar echronic,
    dislodgementi shi ghlyunli
    kely.Cardiover
    siont osinusr hythm i
    sal soinadvisabl e
    givent hatAFi sr egardedasper manent .Givent hepat i
    ent’
    scomor bidi
    ties,arat e-
    cont r
    olst rat
    egyismostappr opr
    iate.

    67.
    A 62-year
    -ol
    dmancomest otheemer gencydepar t
    mentwithpalpi
    tat
    ionst
    hat
    star
    ted3hourspri
    or.Hehashadfivepri
    orepisodesoverthepast2weeks,each
    last
    ingupto1minut
    e.Hehashyper
    tensi
    on,butisotherwi
    seheal
    thy.
     

    He takes aspir
    in 81 mg and ramipri
    l5 mg dai ly.Hi
    s blood pr
    essureint he
    emergencyr oom is130/70mm Hgandhear trat
    ei s95bpm.Thel ungsareclear
    wit
    hnoper ipheraledema.Hear
    tsoundsar enormal,andthereisnoj
    ugularvenous
    di
    stenti
    on.Thepr esent
    ingel
    ect
    rocar
    diogram i
    sshowni nFigure1.
    Whi
    choft
    hef
    oll
    owi
    ngi
    sthebestmanagement
    ?

    a.Atr
    opine0. 5mgIV.
    b.Consult
    at i
    onforpermanentpacemakeri
    nser
    ti
    on.
    c.I
    nserti
    onoft emporarypacemakerwir
    e.
    d.Metoprolol5mgi nt
    ravenous(I
    V).
    e.Adenosine6mgI Vpush.

    Answer

    D.Met
    ropol
    ol5mgi
    ntr
    avenous(
    IV)
    .

    Theelectr
    ocardiogram showsat ri
    altachycardi
    aat160bpm,wi t
    h3:2Wenckebach
    conducti
    onandr ightbundl ebranchbl ock.TheWenckebachi sphysi
    ologicdueto
    thehighatri
    alrate,andt heref
    ore,thereisnoindicat
    ionforper
    manentort empor
    ary
    paci
    ngorat ropine.Atrialtachycardiadoesnott ypi
    call
    yrespondtoadenosine,so
    metoprol
    olisthebestr esponse.

    68.
    Theper
    sonwi
    tht
    heel
    ect
    rocar
    diogr
    am showni
    nFi
    gur
    e1haswhi
    choft
    hef
    oll
    owi
    ng?

    a.

    si
    ngl
    e-chamberI
    CDt
    hati
    sunder
    sensi
    ngvent
    ri
    cul
    art
    achycar
    dia.
    b.Adual-chamberICDoperati
    ngintheVATmode.
    c.An i mplant
    able cardi
    overt
    er-
    defi
    bri
    llat
    or (I
    CD) with a pacing rate
    progr
    ammedsi ngle-
    chamberventri
    cularpaci
    ng40bpm.
    d.A dual-chamberpacemakerprogrammeddual -
    chamber
    ,rat
    e-r
    esponsive
    60-120bpm.
    e.AnAAI Rpacemakerprogrammedwi t
    hal owerrat
    eof40bpm.

    Answer

    C.
    Animplant
    ablecardi
    overter
    -defi
    bri
    ll
    ator(
    ICD)wi
    thapaci
    ngr
    atepr
    ogr
    ammed
    si
    ngl
    e-chambervent
    ri
    cularpacing40bpm.

    Thet r
    acingshowsasel f-terminati
    ngr unofventr
    icul
    artachycardi
    a,pr
    obablynot
    treatedbyt heICD duet oi tsrel
    ativelyslow r
    ateofself-termi
    nati
    ngnatur
    e.Itis
    unlikelytobeunder sensingt hisrhyt hm.Thet hi
    rdt olastbeatispacedint he
    vent r
    icl
    eduringthePwave, consist
    entwi thaventr
    icul
    ar-onlypaci
    ngdevi
    ce,wit
    ha
    lowerr ateofapproxi
    mat ely40bpm.I tisnotanat ri
    alpacemaker,asthepacing
    spikecapt ur
    estheventr
    iclewhenpaci ng.

    69.
    A60- year-ol
    dmanpr esentstot heemergencydepar tmentf orincr
    easedswel l
    ing
    aroundhi spacemakersi te.Hehasahi storyofsi
    cksi nussyndr ome,hypertensi
    on,
    andpar oxysmalat rialfi
    bri
    ll
    ation.Adual-chamberpacemakerwasi mplanted10
    yearsago,andt hepacemakergener atorwasr eplaced4mont hsago.Hi slast
    pacemakercheckwas3mont hsagowhenhewast oldeverythi
    ngwaswor king
    normally.Hismedi cati
    onsincludewarfar
    in,metoprolol,andli
    sinopri
    l.Lastweekhe
    noti
    cedsomet endernessar oundhispacemaker ,wi t
    hr ednessdevelopingatt he
    loweredgeoft hepocket2daysago.Hedeni esanyf eversorchill
    s. 

    Onexami nati
    onofthepacemakersi t
    e,thereisasmal lt
    omoder at
    eamountof
    swell
    ingandanar eaofer
    ythemawi t
    hindurati
    ont hati
    sabout2cm insizeatt he
    i
    nferi
    or/l
    ater
    alaspectoft he pacemakersi t
    e.The r emai
    nderofhi s physi
    cal
    examinati
    onisnormal,wi
    thnor malvi
    talsigns.Anechocardiogr
    am isperfor
    med
    withnormalfi
    ndi
    ngs.Bl
    oodcult
    ureshavebeenor dered.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextst
    epi
    nmanagement
    ?

    a.Ini
    ti
    atecephal
    exin,500mgqi d,andr eassessin7days.
    b.Ini
    ti
    atevancomycin,1gintravenousq12hr ,andreassessi
    n3days.
    c.Perf
    orm needl
    easpi r
    ati
    onoft hepacemakerpocket .
    d.Revisepacemakerpocketandr eplacegenerator
    .
    e.Extr
    actpacemakergeneratorandl eads.
    Answer

    E.Ext
    ractpacemakergener
    atorandl
    eads.

    Thispat i
    enthasapacemakerpocketinf
    ecti
    onwi thevi
    denceofabscessf ormation.
    Wi t
    hi nf
    ecti
    oninthepocket
    ,boththegenerat
    orandpaci ngleadsareinvolved,and
    extracti
    onoftheenti
    resyst
    em i
    sneededt oeradicat
    etheinf
    ection(
    ClassI )
    .Ast his
    patientisotherwi
    seingoodheal t
    h,thi
    sist hebestcourseofact i
    on.Ant ibi
    otics
    alonewi llnoteradi
    catetheinfect
    ion.Aspirat
    ion ofthepocketshoul d notbe
    performed(ClassI
    II
    ).

    70.
    A 60- year -
    old woman i s admi tted to t he hospi tal f or palpitati
    ons and
    li
    ght headednessandi sr eferr
    edt oyouf orconsul t
    ati
    on.Fort hepast3mont hs,she
    hashadspel l
    saboutonceaweekwher eshesuddenl yfeelsver yl ightheaded,
    foll
    owedbyasensat ionofbr eathlessnessandanxi ety.Twicei nthepastmont hshe
    hasf ai
    ntedcompl et
    ely,oneofwhi chwaswi t
    nessedbyherson.Herpasthi story
    includesobesi tyandf ibr
    omyal gia.Hermedi cati
    onsar ecitalopram 20mgdai l
    yand
    pregabal in50mg3t imesdai ly.Onphysi calexami nation,herbl oodpr essur ei s
    130/ 80mm Hg,hear tratei s70bpm,andwei ghtis180pounds( bodymassi ndex
    32).Car diovascularexami nation r eveal
    s an i rr
    egularr hythm wi t
    houtmur mur.
    Abdomeni sobese,butt her emai nderoft heexami nati
    oni sunr emar kable.An
    electrocardiogram showssi nusr hythm at80bpm,wi thabor derl
    inePRi ntervalof
    200msec.An echocar diogram wasper f
    or med yesterdaywi th normalf i
    ndi ngs.
    Labor atorystudiesarenor malexceptf orpotassium of3.5mEq/ dl.Ont elemet ry,the
    stri
    psshowni nFigure1wer erecor deddur ingyourphysi calexami nat i
    on.
    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextst
    epi
    nmanagement
    ?

    a. Pacemakeri
    mpl ant
    .
    b. Corr
    ectpot
    assium.
    c. Conti
    nuedobservat
    ion.
    d. Di
    sconti
    nuecit
    alopram.
    e. Di
    sconti
    nuepregabali
    n.

    Answer

    A.PacemakerI
    mpl
    ant

    Thesestri
    psshow second-
    degreeat r
    iovent
    ricular(
    AV)blockwithperi
    odsofbot h
    2:1AVblockandMobi t
    ztype2bl ock.ThefindingofMobi t
    ztype2blockindi
    cates
    thatthesit
    eofblockisbelow theAVnode( attheleveloftheHisbundle)
    ,and
    ther
    efor
    e,i
    smorelikel
    ytoprogr
    esst ocompl eteheartbl
    ock.Shether
    efor
    equalif
    ies
    forapacemaker .Premat ur
    eect opi
    c(narr
    ow)beat sal soar eseen(
    thesedonot
    aff
    ectthesinusrate,whichi sabout75bpm) .Herepi sodesofsyncopear el
    ikel
    y
    rel
    atedtoherconduct i
    ondi sease.Di
    sconti
    nuingmedi cat
    ionsorsupplementi
    ng
    potassi
    um wil
    lnottreathersubnodalconduct
    iondisease.

    71.
    An18- year- ol
    dwomani sref
    err
    edf orevaluati
    onf oraf amilyhistoryofl ongQT
    syndrome( LQTS) .Shef eel
    swellanddeni esanyhi stor
    yoff aint
    ing,al t
    houghshe
    doesnot ethatherhear tpoundswithexerci
    se.Shehasnopastmedi calhistoryand
    doesnotsmokeordr i
    nkalcohol
    .Heruncl ewasr esusci
    tatedfrom acar diacar rest
    and subsequent ly diagnosed wi th LQTS based on hi s postcardiac ar rest
    elect
    rocardiogram ( ECG).Onphysi calexaminati
    on,herbl oodpr essurei s110/ 60
    mm Hgwi thahear trat
    eof70bpm, andtheremainderofherexami nati
    oni snor mal.
    Shebr i
    ngsi nacopyofanECGdonebyherf amilyphysician2weeksago,whi ch
    showssi nusr hythm at75bpm wi thaQTcof460msec.AnECGi nyourof ficetoday
    hassimilarfindings, wi
    thaQTcof450msec.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextst
    epi
    nmanagement
    ?

    a.Implantablecar
    diovert
    er-
    def
    ibr
    il
    lat
    or(
    ICD)i
    mpl
    ant
    .
    b.Electr
    ophysiol
    ogicstudy.
    c.Stresstest.
    d.RepeatECGst anding.
    e.Genetictesti
    ng.

    Answer

    E. Gener
    ict
    est
    ing

    Thispat i
    enthasaf amil
    yhistoryofpr obableLQTSi nheruncl
    e.HerECGshows
    bor derl
    ineQTpr olongat
    ion.Genet i
    ct esti
    ng,starti
    ngwi t
    hheruncl e,shoul
    dbe
    performed.I ni
    ti
    ationofbeta-blockadewoul dber easonabl
    eifadiagnosi
    sofLQTS
    canbemadei nt he18-year-oldpatient.Therei snor ol
    eforelect
    rophysi
    ologi
    c
    testing,andI CD implantcar r
    iesaCl assI Ibindicati
    ononlyint hepresenceof
    strong r i
    sk factorsf orsudden car diac death,whi ch thi
    s patienthas not
    demonst rat
    ed.

    72.
    A69- year-
    oldmalepr esent
    st oyourcli
    nic.Hehasbeenbotheredbyshor t
    nessof
    breaththathasdevelopedovert hepast10mont hswhenwal ki
    ng.Hehasapast
    hist
    oryofcompl etehear tblockforwhi chheunderwentpermanentpacemaker
    implant3 years ago.He al so has a histor
    y ofcor
    onary art
    ery di
    sease and
    underwentpercut
    aneouscor onaryint
    erventi
    ontotheri
    ghtcor
    onaryar t
    ery7years
    ago.Hei spaced100%oft hetime, andhi spacemakeri ssett odual -chamber ,r at
    e-
    responsi vewi thanat ri
    oventri
    culardel ayof180msec.Hi slastpacemakercheck
    was1 mont h ago,and hewast old ever yt
    hing wasf uncti
    oning nor mal l
    y.Hi s
    under l
    yingr hythm issinusr hythm wi thcompl et
    ehear tblockandavent ri
    cular
    escape of45 bpm.Hi s 12- l
    ead el ect
    rocardiogram shows si nus r hythm wi th
    ventri
    cularpaci ngwi t
    hal ef
    tbundl ebr anchbl ock( LBBB)mor phology.TheQRS
    widthis210msec.Anechocar diogr am per for
    medear l
    ierthismont hshowedal ef
    t
    ventri
    cularej ectionfr
    acti
    onof30%.Hi scur rentmedi cat
    ionsincludel i
    sinopr i
    l10mg
    dail
    y,f ur osemi de 20 mg dai l
    y,car vedilol25 mg bi d,spironolactone 25 mg,
    atorvastat i
    n80mg,andaspi ri
    n81mgdai ly.Onphysi calexaminat i
    on,hi sbl ood
    pressurei s108/ 67mm Hgandhear trateis65bpm.Thej ugularvenouspul seis
    seenat6cm H2O.Lungsoundsar ecl ear,andoncar di
    acauscul tat
    ion,ther hythm is
    regularwi th a par adoxi
    call
    y spl itS2.The r emai nderoft he exami nati
    on i s
    unremar kabl e.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    erecommendat
    ion?

    a.Upgradetoabiventr
    icul
    ari
    mpl antablecardi
    over
    ter
    -def
    ibr
    il
    lat
    or(I
    CD).
    b.Conti
    nuecurrentmanagementandr outi
    nepacemakerf
    oll
    ow- up.
    c.Reprogr
    am thepacemakertosi ngle-chambervent
    ri
    cul
    arpacingwit
    halow
    rat
    eof40bpm.
    d.Upgradetoadual-chamberICD.
    e.Upgradetoabiventr
    icul
    arpacemaker .

    Answer

    A.Upgr
    adet
    oabi
    vent
    ri
    cul
    ari
    mpl
    ant
    abl
    ecar
    diover
    ter
    -def
    ibr
    il
    lat
    or(
    ICD)
    .

    Thispat ient '


    sNew Yor kHear tAssoci ati
    on( NYHA)st atusisdet eriorati
    ngdespi t
    e
    guideli
    ne- directed medi cal t herapy of bet a-blocker s, angiotensin- convert
    ing
    enzyme i nhi bi
    tors,and spi r
    onolactone.He has a wi de QRS wi th an LBBB
    mor phologyandi spaced100%oft het i
    me.Het her eforemeet scriteri
    af orupgr ade
    to a cardi
    ac resynchr onization therapy device. The RAFT
    (Resynchr oni zati
    on–Def i
    bril
    lati
    onf orAmbul atoryHear tFail
    ureTr ial)studyi n2010
    showedt hebenef itofabi ventri
    cularI CDf orpatient sinaNYHAcl assI IorI I
    Iwi t
    h
    reducedr at esofdeat horhospi tali
    zationf r
    om hear tf ail
    ure.I
    nclusioncr i
    teri
    afort hi
    s
    studywer eal eftventr
    icularejectionf ract
    ionof30%,QRS>120msec,orapaced
    QRSdur at ionof>200msec.

    73.
    A52- year-
    oldmancomestotheemergencydepart
    mentformil
    dpal
    pit
    ati
    onsthat
    star
    ted thepri
    oreveni
    ng.Pal
    pit
    ati
    onspersi
    sted when heawokethefoll
    owing
    mor ning,andt herefore,hedr ovehimsel ft othehospi t
    al.Hehashadt hreepr i
    or
    episodesovert hepast2mont hs,eachl asti
    ngonl y5-10mi nutes.Hehashada
    priormyocar diali
    nfarctionwithasingleangi oplastyandst enttot heleftci
    rcumf l
    ex
    arteryandanover allleftventri
    cul
    arejectionfracti
    onof45%.Het akesaspirin81mg,
    clopidogrel75mg, rami pri
    l5mgdai ly,bisoprolol5mg, andat orvastati
    n40mgdai l
    y.
    Hei ssomewhatanxi ousappear i
    ng,althoughnoti ndistress.Hi sbloodpr essurein
    theemer gencydepar tmenti s90/65mm Hgandhear tratei s135bpm.Thel ungs
    arecl earwi thnoper ipheraledema.Thepr esenti
    ngel ectrocardiogram (ECG)i s
    showni nFigure1.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nmanagement
    ?

    a.Per
    form car
    oti
    dsinusmassage.
    b.Admini
    steri
    ntr
    avenousadenosi
    ne.
    c.Per
    form synchroni
    zedcar
    dioversion.
    d.Admini
    sterint
    ravenousi
    buti
    li
    de.
    e.Admini
    sterint
    ravenousmetoprolol.

    Answer

    C.Per
    for
    m synchr
    oni
    zedcar
    diover
    sion.

    The ECG shows wi de compl ex tachycardia wi th atrioventri


    culardi ssoci
    ation
    diagnost i
    cofvent r
    iculartachycardia(VT) .Thepat i
    entishemodynami callystable,
    althoughsomewhathypot ensiveandanxi ous.Thepr iorinfarctandVTmor phology
    i
    ssuggest iveofascar -
    basedVT.Car dioversioni sthebestopt i
    onf orthispat i
    ent
    (althoughami odaroneorpr ocai
    nami demaybeconsi deredaswel l)
    .I buti
    li
    dei s
    appr opri
    atef orat r
    ialfibri
    ll
    ationorat rialfl
    utter,whi l
    ecar oti
    dsi nusmassageor
    adenosi newoul dbeappr opriat
    eforsupr avent r
    iculartachycar di
    a.Met oprololalso
    woul dbei neffect
    iveandpot enti
    all
    yhar mfulgivent hepat i
    ent’shypot ensivestate.

    A 44- year-old woman i sreferr


    ed to yourcli
    nicforr ecurrentpal pi
    tat
    ions.The
    episodesar esporadic,buthaveincreasedinfr
    equencyint hepast12mont hs.Most
    aresel f-l
    imit
    ing,butt helastepisodelastedhoursandr esolvedonl yafterbeing
    given 6 mg ofi ntr
    avenous adenosine inthe emer gency depar tment.She i s
    otherwisei ngoodheal thandi staki
    ngnomedi cat
    ions.Herbl oodpr essur
    ei nclini
    c
    i
    s110/ 70mm Hgandhear tratei
    s60bpm.Thecar di
    acandr espirat
    oryexami nat
    ion
    i
    sunr emar kable.Herechocar di
    ogram showednost r
    ucturalhear tdi
    sease.Thel ead
    IIrhythm st ri
    psf rom theemer gencydepart
    mentpr e-and post -adenosinear e
    showni nFigure1.
    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    ydi
    agnosi
    s?

    a.At
    rialtachycar di
    a.
    b.At
    rioventricularnodalre-ent
    ranttachycar
    dia(
    AVNRT)
    .
    c.Ort
    hodr omi cAVr e-entr
    anttachycardi
    a.
    d.At
    rialfl
    utter.
    e.I
    nappr opri
    at esinustachycardi
    a.

    Answer

    B.At
    ri
    ovent
    ri
    cul
    arnodalr
    e-ent
    rantt
    achycar
    dia(
    AVNRT)
    .

    The rhythm str


    ip shows a supraventri
    cul
    art achycardi
    a.Compar ing t
    he QRS
    morphologyduri
    ngt achycar
    diawiththatinsinusr hyt
    hm,t henegati
    vePwaveat
    theterminalpor
    tionoftheQRScanbeeasi lyseen.Asuper i
    orl
    ydirect
    edP-wave
    vect
    orrulesoutinappr
    opriat
    esinustachycar
    dia.Thepr oxi
    mityofthePwavetothe
    QRS( shor
    tRPtachycar
    dia)excl
    udesort
    hodromicAVr e-ent
    ranttachycar
    dia.The
    t
    erminati
    onofthetachycardi
    awi t
    hadenosinedecreasesthelikel
    ihoodofatrial
    t
    achycardi
    aorat
    ri
    alfl
    utt
    er.Themostli
    kel
    ydiagnosi
    sisAVNRT.

    75.A 32- year-oldwomani sat18weeksgest ationofhersecondpr egnancyand


    present stot heemer gencydepar tmentwi t
    h an epi sodeofpal pit
    ati
    ons.Shehad
    mul tipl
    eepisodesdur i
    ngherf i
    rstpregnancy,buttheywer eshor t
    -li
    vedandshedi dnot
    seekmedi calattentionfort hem att hetime.Sheisot herwiseingoodheal thandisonl
    y
    takingpr enatalvitami nsuppl ement s.Herbloodpr essurei s100/60mm Hgandhear t
    ratei s140bpm.Ot herthant het achycardia,
    thecardi acandrespiratoryexaminat
    ioni
    s
    unremar kable.Herel ectr
    ocar diogram isshowni nFigur e1.Shei sgivenadenosine12
    mgi ntr
    avenous, andt her hythm termi nat
    es.

    Which oft
    hef
    oll
    owi
    ng i
    sthebestwayt
    o pr
    eventf
    utur
    erecur
    rencesdur
    ing her
    pr
    egnancy?
    a.Atenol
    ol.
    b.Dil
    ti
    azem.
    c.Amiodarone.
    d.Metoprol
    ol.
    e.Verapamil
    .

    Answer

    C.Met
    ropol
    ol

    The electrocardiogram shows a supr aventriculartachycardia.Forpr ophylacti


    c
    therapy,fi
    rst-
    li
    net herapiesincl udemet opr ol
    olandpr opranolol
    .Digoxinisregarded
    assaf etotakei npregnancy, althoughi tsef f
    icacyhasnotbeendemonst rat
    edi nthe
    prophylaxisofsupr aventr
    iculart achycardia.Ami odaronei sacat egoryD dr ugin
    pregnancyandshoul dbeavoi ded.At enololisal soregardedasacat egoryDdr ug.
    Verapami lcarri
    esacl assIIbi ndicati
    onf orpr ophylaxis.Flecai
    nideandsot alolcan
    beusedsaf el
    yinpr egnancy( classI I
    a).

    76.Thepat ientisa65- year-ol


    dmal ewhopr esent st otheemer gencydepar tmentfor
    evaluation ofsyncope.Thepat i
    entwaswal king i
    n hisnei ghbor hood when he
    suddenl y became di zzy and di aphor
    eti
    c and passed out . He r egai
    ned
    consciousnessspont aneouslywithin30seconds.Uponpr esent ati
    on,hehadno
    compl aints.Fouryear sago,hesuf feredaninferiormyocar di
    alinfarct i
    on.Anuclear
    myocar dialperfusionscan1mont hagoshowedal eftventr
    icularej ecti
    onfr
    action
    (EF)of40%,anonr eversi
    bledefectoftheinferiorwall,andnoi schemi a.Hisother
    pasthi storyincludeshyper tensi
    on.Pr i
    ortot hesyncopalevent ,hehasnotnot ed
    anychangei nhisexer cisetoler
    anceandwasf reeofangi na.

    Onexami nat i
    on, hi
    shear tr
    ateis65bpm, hisbloodpr essureis112/ 74mm Hg, and
    heisaf ebr i
    le.Hisj ugularvenouspr essur eis7cm,l ungsar ecl
    eart oauscul tation,
    and car diac exami nation revealsar egularr hythm and nor malS1- S2 
    without
    mur mur s.Hi selectrocar di
    ogram showssi nusr hythm at70bpm,wi t
    hnor malPR,
    QRS,andQTdur ation,andQwavesseeni nleadsI ,I
    I,andaVF.Hi smedi cations
    consistofaspi r
    in81mgperday, atorvastatin20mgperday, carvedilol12.5mgbi d,
    andl i
    sinopr il10mgperday.Hi sbl oodwor kshowsnor malval uesf orcompl et
    e
    blood count ,electrol
    ytes,and r enalf unct i
    on.Car diacbi omarkerswer enor mal .
    Echocar diogram i nt heemer gencydepar tmentshowednochangei nEFandno
    si
    gnificantval vulardisease.Over ni
    ghtt elemet r
    yr evealsnormalsinusr hythm.
    Which oft
    hef
    oll
    owi
    ng i
    sthemostappr
    opr
    iat
    est
    ep t
    o eval
    uat
    ethi
    spat
    ient
    's
    syncope?

    a.A48- hourHoltermoni tor.


    b.Tiltt
    abletesti
    ng.
    c.Elect
    rophysiologicstudy(EPS)
    .
    d.Exercisestr
    esst esti
    ng.
    e.Implantedloopr ecorder.

    Answer

    C.El
    ect
    rophysi
    ologyst
    udy(
    EPS)
    .

    Thispat ienthassi gnifi


    cantst r
    ucturalheartdiseasewi t
    hpr i
    ormyocar dialinfarction
    andr educedl eftventricularfuncti
    on.Afteranegat i
    veischemi aeval uation,apat ient
    withcor onar
    yar t
    erydi sease( CAD)andsyncopeshoul dunder goEPS.EPSt est
    sinusnodef unctionandat ri
    oventri
    cularconduct i
    onar eal soexcel lentt estst o
    i
    dent i
    fyvent ri
    culart achyar r
    hythmiasandr i
    skofdeat hinpat ientswi thCAD and
    syncope.Pat ientswi thCAD,syncope,andi nduciblevent r
    iculart achycardiaonEPS
    should be t reated wi thi mplantable cardioverter
    -defibr
    ill
    ator.A Hol terorl oop
    moni torcanbeusedi fanEPSi snegat i
    veandadef i
    nit
    ivedi agnosisi sr equired.
    Thispat ienthadaver yr ecentassessmentofi schemiaandEFbynucl earst udy.Ti l
    t
    tablet esti
    ngi snoti ndicatedi nthissettingast hispat i
    enthasst ructuralhear t
    disease, andtherei snoevi denceforvasovagalsympt oms. 

    77.A 28- year -oldmanwi t


    hhyper tr
    ophiccar diomyopat hy (HCM)pr esentstocl i
    nic
    aft
    ermovi ngt othearea.Hewasdi agnosedatage19duet odyspneaonexer t
    ion.
    Hedeni eschestpai n,palpit
    ations,near-syncope,orsyncope.Hi sf amil
    yhi storyis
    negativef orsuddendeat horHCM.Hei sanact ivef at
    heroft wo,butdoesnot
    exerci
    se r out i
    nely.He has been managed wi t
    h met oprololXL 25 mg/ day.
    Examinat ionshowsawel l
    -appear i
    ngman,bl oodpr essur e(BP)124/ 70mm Hg,
    heartr ate72bpm,andnor malj ugularvenouspr essure.Hear trhythm isr egular
    ,
    withanor malS1  andS2,anS4,andasof tgrade2/ 6hol osystolicmur muratt he
    lowerl eftst ernalborder;extremiti
    esar ewi t
    houtedema.Hi sechocar diogr
    am l ast
    yearwasst ablefrom 3year spr i
    orandshowedanej ectionf r
    act i
    onof82%, maximal
    septalwal lt hicknessof26mm,l eftvent
    ricular(LV)out fl
    owgr adientof20mm Hg,
    andmoder at emi t
    ralregurgit
    ation.AHol termoni t
    orwasper formed3mont hsago
    withnoar rhythmi asseen.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestmanagementst
    epf
    orhi
    scar
    e?
    a.Exercisestr
    esst esti
    ng.
    b.Endomyocar dialbiopsy.
    c.Incr
    easemet opr olol
    .
    d.Cardiaccomput edt omographyscan.
    e.Genetictest
    ing.

    Answer

    A.Exer
    cisest
    resst
    est
    ing

    Riskst ratif
    icat
    ionforsuddencar diacdeat h( SCD)i sessent i
    alint hemanagementof
    HCM,andi mplantabledefibril
    latort herapyhasbeenshownt obeef fect
    ivei nt his
    popul ation.Inpat ient
    swhohavenotexper iencedapr iorvent ri
    cularar rhythmi c
    event,t herear efi
    vemaj orr iskf act orsforHCM- associatedSCD:f ami l
    yhi storyof
    SCD ( parti
    cularl
    yi fmul t
    ipl
    e event s)
    ,massi ve LV hyper tr
    ophy ( >30 mm wal l
    thickness) ,syncope,nonsust ainedvent riculart achycar dia,andanabnor malBP
    responset oexercisewi t
    hf ai
    lur et oaugmentBP.Thi spat i
    enthasnof amilyhi story
    ofSCD,LVhyper t
    rophywi th<30mm wal lt hickness,ar ecentnegat i
    veHol ter,and
    nohi stor yofsyncope.Ther eisaCl assI I
    ai ndi cationforexer cisestresst esting to
    assess f or an abnor mal BP r esponse. Wi t
    h t he except ion of vent r
    icular
    tachycar dia/fi
    bri
    ll
    ationandcar diacar r
    est,eachi ndivi
    dualmaj orr i
    skfactorf orSCD
    hasal ow positi
    vepr edict
    iveval ue.Ther i
    sksofmul ti
    plemar kersar enotcl early
    addi t
    ive. 

    Int hei nter


    nationalHCM- i
    mpl ant
    abl ecar diovert
    er -def
    ibri
    ll
    at or(ICD)r egi st
    ry,the
    numberofr iskfactorsdidnotcor r
    elatewitht herat eofappr opr i
    ateICDshocks.The
    dat asuggestt hatthepr esenceofasi ngler i
    skfact ormaybesuf f
    icienttoconsi der
    i
    mpl ant
    ationofanI CD, butt hedecisionshoul dbei ndivi
    dualizedwi threspectt oage
    oft hepatientandst r
    engt hoft heriskfactor.Sever alotherlesswel l-establishedr i
    sk
    factorsar eofincreasingi nterestandhavebeenassoci atedwi t
    hani ncreasedr i
    sk
    ofSCDi nHCM.Thi sincludesl ategadolinium enhancementonmagnet icresonance
    i
    magi ng and sever albet a-myosi n heavy chai n and t r oponin T mut ati
    ons.
    Endomyocar dialbiopsydoesnotpl ayar oleint hemanagementordi agnosi sof
    pat i
    ents with HCM.Car diac comput ed t omogr aphy wi llnotpr ovide addi ti
    onal
    i
    nf ormation.Thi s pati
    enti s asympt omat ic,so t herei s no need f orincr eased
    met oprolol.

    78.A75-year-
    oldmani sseenint heemergencyr oom complai
    ningofpal
    pitat
    ions.He
    hasahistor
    yofhypertensi
    onandcompl et
    ehear tblockforwhi
    chheunder wentdual-
    chamberpacemakerimplantat
    ion2year sago.Hi spacemakerhasbeenpr ogrammed
    totheDDDmode50- 120bpm.Fi gure1istheelectrocar
    diogr
    am (ECG)obt
    ained. 

    Anint
    ervent
    ionisper
    formed,wit
    hresol
    uti
    onoft hepati
    ent
    ’ssympt
    oms.Thesecond
    ECGshowninFigur
    e2i sobt
    ainedaf
    tert
    heint
    ervent
    ion.
    Based on t
    he ECG shown in Fi
    gur
    e 2,whi ch oft
    he f
    oll
    owi
    ng i
    nter
    vent
    ions was
    per
    for
    medi nor
    dertoall
    evi
    atethepat
    ient
    ’ssymptoms?

    Fi
    gur
    e1.

    Fi
    gur
    e2.

    a.Admi
    nist
    eri
    ngadenosi
    ne.
    b.I
    ncreasi
    ngt
    heatr
    ialsensitivi
    ty.
    c.I
    ncreasi
    ngt
    heventr
    icularpaci ngout
    put
    .
    d.Pr
    ogrammingt
    othesi ngle-chambervent
    ri
    cul
    arpaci
    ngVVImode.
    e.Pr
    ogrammingt
    ohyst eresisoff.

    Answer

    D.Pr
    ogr
    ammi
    ngt
    othesi
    ngl
    e-chambervent
    ri
    cul
    arpaci
    ngVVImode.

    Thef irstt r
    aci ng demonst ratesvent ri
    cularpacing at110 bpm,consi stentwi th
    tracking of ei ther a supr aventri
    cular tachycardia or pacemaker -medi ated
    tachycar dia.I nt hesecondt racing,theratehasbeendecr easedt o50bpm wi than
    under lyingat rialtachycar di
    aat110bpm.Ther eisnor elati
    onbet weent hePwaves
    andpacedQRSmor phol
    ogy, consistentwithreprogrammi ngt hedevi cet oasi ngle-
    chambervent ri
    cul arpacingmode.Adenosi necausest ransientat r
    ioventri
    cul ar( AV)
    block,whi chwi l
    lnotaf f
    ectpacemakerf unct
    ion,andt herefore,wi l
    lnotr esol vet he
    rhythm.I ncr easi ng the vent ri
    cularpacerout putis noti ndicated because t he
    pacemakerhasadequat event ri
    cularcapt ur
    e.Increasingt heat rialsensi t
    ivitywi l
    l
    notr esol vet her hythm becauset herei sno evi denceoff ailuret ot rackat rial
    rhythms.Hyst eresis promot es intri
    nsic acti
    vit
    yl owert han t he nor malr ate by
    allowing sl ow but appr opriate intr
    insic rhythms. Changi ng t he hyst eresi s
    par amet er swi llnothel presolvet hetachycardia.

    79.An81- year-oldmani sseenintheemer gencyr oom forinter


    mi t
    tentpal pi
    tat
    ions.He
    al
    sonot esoccasi onalperi
    odsofdizzinessandpr esyncopeimmedi atelyaf t
    eraper i
    od
    ofpalpit
    ati
    ons.Hehasnochr onicmedi calil
    lnessesandt akesonlyamul t
    ivit
    amindaily.
    Onphysi calexami nati
    on,hi
    sbloodpr essurei s160/ 80mm Hgandpul sei s130bpm.
    Hisrhythm isirregular
    ,wit
    hapar adoxicall
    yspl i
    tS2.Ther emainderoft heexami nati
    on
    i
    sunr emarkable.Hi sadmissi
    onel ectrocardiogram dur ingpalpit
    ationsi sshowni n
    Fi
    gure1.  

    Af
    ter10mi nut
    es,thepalpi
    tat
    ionssubside,buthebecomesl ightheadedandnear
    ly
    l
    osesconsci
    ousness.Fi
    gure2isthesecondelect
    rocar
    diogr
    am obtained.

    Fi
    gur
    e1.
    Fi
    gur
    e2.
    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextst
    epi
    nmanagementt
    orel
    ievehi
    ssympt
    oms?

    a.I
    nit
    iati
    onofmet opr
    olol.
    b.I
    nit
    iati
    onofsotalol
    .
    c.Permanentpacemakerimpl ant
    ati
    on.
    d.I
    nit
    iati
    onofmet opr
    ololaft
    erpermanentpacemakeri
    mplant
    ati
    on
    e.Atr
    iovent
    ri
    cul
    arnodeabl ati
    onafterper
    manentpacemakeri
    mplant
    ati
    on.

    Answer

    D.I
    nit
    iat
    ionofmet
    ropol
    olaf
    terper
    manentpacemakeri
    mpl
    ant
    ati
    on.

    Thepat ienthasparoxysmalatr
    ialfi
    bril
    lat
    ion(AF)witharapidventr
    icularresponse
    andsi nusnodedysf unct
    ion(t
    achybr adysyndrome).Thebesttreat
    menti sabet a-
    bl
    ockert ocontroltherat
    eduringAFandapacemakert opreventsignifi
    cantsinus
    bradycardia, which may wor sen af t
    er admi ni
    str
    ati
    on of a bet a-blocker.
    Anticoagulat
    ionalsoshouldbeiniti
    atedtopreventstr
    oke.Administ
    rati
    onofsot alol
    andmet oprol
    olmaydecr easehisepisodesofAFandpal pit
    ati
    ons,butwil
    lli
    kel
    y
    worsenhissinusnodedysf uncti
    on.Paci
    ngwi l
    lunli
    kel
    ysigni
    fi
    cantl
    yaff
    ecthisAF
    burden.Atri
    alofpharmacologi
    ctherapytocont
    rolhear
    trateshoul
    dbeconsider
    ed
    pri
    ortoatri
    ovent
    ri
    cularnodeablati
    on.

    80.A 65- year-oldmanwi thasi ngle-chamberi mplantablecar dioverter-def


    ibril
    lat
    or
    (I
    CD)i mplantedf orpri
    mar ypr event i
    onofsuddendeat h6mont hsagocomest othe
    emer gencydepar t
    menttodayaf terhavingashockf r
    om hi sdevice.Hehadbeenf eeli
    ng
    palpitati
    onsal lduri
    ngtheday, andt henwhenhebr i
    sklywal kedupt wof l
    ightsofst airs
    hef elttheshock.Hedeni esanyshor tnessofbr eathorchestdi scomf or t
    ,norsyncope.
    Hehasahi storyofsystolichear tfail
    ur eresulti
    ngf r
    om anant er
    iorwal lmyocar dial
    i
    nfar cti
    on5year sago,withal eftvent r
    icular(LV)ejecti
    onf racti
    onof25%, andisabl eto
    domostact i
    viti
    esofdailyli
    vingconsi stentwi t
    haNewYor kHear tAssoci ati
    onclassI I.
    Hisot hermedi calpr
    oblemsi ncl udepar oxysmalat ri
    alfibri
    ll
    ati
    on( AF) ,hyperli
    pidemi a,
    andhyper tension.Hismedi cationsar easpi r
    in81mgdai ly,dabigatran150mgt wice
    dail
    y, carvedil
    ol25mgt wi cedai l
    y, l
    isi
    nopr il20mgdai ly,andat orvastatin40mgdai l
    y. 

    Uponpr esent
    ati
    on,hi
    sweightis70kg,hi
    sbloodpr essureis105/60mm Hgwi t
    ha
    heartrat
    eof70bpm, andhi
    sICDsit
    eiswel
    lhealedinthelef
    tchest
    .Hi sj
    ugul
    arvenous
    pressureisat6cm H2O,l ungsoundsareclear,andheartexami nat
    ioni
    snor mal
    withoutmurmur.
     

    His electrocardi
    ogram shows si nus rhyt
    hm at 70 bpm, wi th a nonspeci fi
    c
    int
    raventri
    cularconducti
    ondelayandQRSdur at
    ionof135msec.Inter
    rogationofhis
    ICDisper formed.HisICDi sprogrammedwi t
    htwozones:aVTzonest ar
    tingat170
    bpm treatedwi t
    hful
    lenergyshocks, andaVFzonestart
    ingat200bpm t
    reatedwithfull
    energy shocks.The I CD shock del i
    ver
    ed t
    oday was fora rhyt
    hm ofAF,wi tha
    ventri
    cularrateof173bpm.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextst
    epi
    nmanagement
    ?

    a.Upgradet oadual -
    chamberICD.
    b.Addantitachycar
    diapacingtotheVTzone.
    c.Adddilt
    iazem 120mgdai ly.
    d.Incr
    easecar vedi
    lolto50mgt wicedai
    ly.
    e.Eli
    minatetheVTzoneonhi sICD.
    Answer

    E.El
    imi
    nat
    etheVTzoneonhi
    sICD.

    Thispat ienthadani nappr opr i


    ateshockf orAF,occur r
    ingdur ingexer ci
    se.The
    MADI T-RI T (Multicenter Aut omat i
    c Def ibril
    lat
    or Impl
    antat i
    on Tr i
    al- Reduce
    Inappr opriateTher apy)t rialinvest i
    gatedast rategyofasi nglezoneat200bpm
    compar edwi t
    hconvent ionalpr ogrammi ng( VTzoneof170bpm andVFzoneat200
    bpm) .(Thet ri
    alalsoincl udedadel ayed- t
    her apyarmthatincludedaVTzonewi tha
    60- seconddel ayeddet ection).MADI T-RITshowedt hatthesi ngle-zoneprogram
    strategyr esul
    tedi nar educt i
    oni ninappropr i
    atether
    api
    esandi mpr ovedsurvi
    val.
    Based on hi swei ght,hei satt hemaxi maldosef orcar vedi
    lol.Given hi
    sLV
    dysf unction,hei sapoorcandi dat
    ef ordi lti
    azem.Anti
    tachycardiapaci ngwould
    havenoi mpactonAFwi thar apidr at
    e,andupgr adeofhisdevi ceisnotneeded.
    Upgr adet oadual -chamberdevi cehasnotbeenshownt odecr easet henumberof
    i
    nappr opriateshocks.

    81.A76- year-ol
    dmani sseeninclinictodayt odi
    scusshisupcomi ngneedt oundergo
    replacementofhi spacemakergener ator.Hehasadual -
    chamberpacemakert hat
    wasi mpl anted8year sagoforcompl eteheartblock,andt hegener at
    orhasj ust
    reachedi tsalertforrepl
    acementl astweek.Hef eel
    swel landhasnocompl ai
    nts.
    Hispastmedi calhi
    storyalsoincludeshyper t
    ension,type2di abetes,par
    oxysmal
    atri
    alfibri
    ll
    ati
    on, andapriorst
    roke2mont hsagowi t
    hfullrecovery.Hismedicati
    ons
    i
    ncludel isi
    nopr i
    l,metf
    ormin,met opr
    ol ol,andwarfari
    n.Hi sinter
    nat i
    onalnormali
    zed
    rati
    ousual l
    yr unsintherangeof2. 2-2.8.

    Whichoft
    hefol
    lowi
    ngishowanticoagul
    ati
    oni
    nthi
    spat
    ientshoul
    dbemanagedf
    or
    hi
    supcomingpacemakerpr
    ocedure?

    a.Continuewar f
    ari
    nthroughouttheper i
    procedureper i
    od.
    b.Holdwar far
    in5dayspr i
    orandr esumeaf tertheprocedur e.
    c.Replace warfari
    n with aspir
    in( 325 mg dai ly)starti
    ng 5 days pri
    orto
    procedure.
    d.Holdwar far
    in5dayspr iortoprocedureandbr idgewi thenoxapari
    nunti
    l
    i
    nternati
    onalnormali
    zedr ati
    ois>2postpr ocedure.
    e.Replacewar f
    arinwit
    hdabi gatr
    an( 150mgt wicedaily)start
    ing5dayspri
    or
    toprocedure.
    Answer

    A.Cont
    inuewar
    far
    int
    hroughoutt
    heper
    ipr
    ocedur
    eper
    iod.

    Inpat i
    entsundergoingdevi cepr ocedureswi thant i
    coagul ation,thereist heconcer n
    fori ncreased r
    isk ofbl eedi ng.However ,cont i
    nuing war f
    ari
    nt hroughoutt he
    periprocedureperiodcarri
    esal owerr iskforbl eedingcompar edwi t
    hast r ategyof
    withholding ant
    icoagulati
    on and br i
    dging wi th enoxapar in.BRUI SE CONTROL
    (Bri
    dgeorCont inueCoumadi nf orDevi ceSur geryRandomi zedCont rol
    ledTr ial
    )
    randomi zedpati
    ent stobot hstrategies,butwasst oppedear l
    yfort hefindingoft he
    super i
    orit
    yofmai ntai
    ningwar farin.Mai nt
    ainingant icoagulat i
    onovert hepr ocedure
    periodi spref
    err
    edgi vent hispat ient
    ’shighr iskforst roke( CHA2DS2- VASc) .Whi l
    e
    ther ecentBRIDGE( Eff
    ectivenessofBr i
    dgingAnt icoagul ationf orSur gery)st udy
    showed no benef i
    tt o br i
    dging over wi thholding ant icoagul ants dur ing the
    perioperati
    veperiod,pati
    ent swithahi storyofst r
    okewi t
    hint hepr ior12weekswer e
    excluded.

    82.A65- year-ol
    dwomanpr esent sforf ol
    low- upintheheartfai
    lur
    ecl inic.Shei sabl e
    todoherusualact ivit
    ies, butislimitedwhent r
    yingtowalkupstairs.Shedeni esany
    chestpai n.Herpastmedi calhistor
    yi ncl
    udessyst ol
    icheartfai
    lure( l
    ef tvent
    ricular
    ejecti
    onf ract
    ion30%)f ort hepast3year s,coronaryarter
    ydiseasewi thanant erior
    wallmyocar dialinfarction 5 year s ago,t ype 2 diabet
    es,hyper l
    ipidemia,and
    hypertension.Hermedi cat ionsincludel i
    sinopri
    l20mgdai l
    y,carvedilol25mgbi d,
    atorvastatin40mgdai ly,aspi ri
    n81mgdai l
    y,andmet for
    mi n850mgbi d.On
    exami nati
    on,herbl ood pr essureis100/ 70mm Hg and pul sei s70bpm.Her
    exami nati
    on is otherwi se unr emar kable and euvolemic.Herel ectrocardi
    ogr am
    showssi nusr hyt
    hm at70bpm,wi thal eftbundlebranchblock( LBBB)andQRS
    durationof145msec.

    I
    naddi ti
    ontor
    efer
    ri
    nghertocardi
    acr
    ehabi
    li
    tat
    ion,whi
    choft
    hef
    oll
    owi
    ngi
    sthe
    nextbestst
    epi
    nthi
    spat
    ient
    'scar
    e?

    a.Destinati
    onl eftventri
    cul
    arassi
    stdevi
    ce.
    b.Referforcardiact ranspl
    ant
    ati
    on.
    c.Bi
    vent ri
    cularpaci ng.
    d.Continuecur renttherapy
    Answer

    C.Bi
    vent
    ri
    cul
    arpaci
    ng.

    Theupdatedgui deli
    nesf orbivent
    ri
    cularpaci
    ngspecifythetypeofQRScompl ex,
    QRSdur at
    ion,andNew Yor kHeartAssociat
    ion(NYHA)f unct
    ionalcl
    ass.ClassI
    i
    ndicat
    ionforbiventri
    cularpacingisforaQRSofatl east150msecandanLBBB
    andaNYHAcl assofI I
    ,III,orambulat
    oryIV.Thispat
    ienthasacl assI
    Iaindi
    cati
    on
    wit
    hclass2hear tfai
    lur
    e, LBBB,andQRSdur ati
    onof120-149.

    83.A74- year-
    oldwomanwi thhyper tensionpresentstoclini
    cf orevaluati
    onofnew
    sympt omsofpal pi
    tat
    ions.Shedescr ibesthissensati
    onasaf eel
    ingofherhear t
    skipping a beatand occasi onall
    yr aci
    ng.She does nothave chestpai n or
    discomfort,
    butdoeshavedyspneawi thmorepr ol
    ongedepisodes.Episodesar enot
    tri
    ggeredbyact ivi
    tyorexerciseandmostof tenoccurafterdinner.Shehasnothad
    syncope.Epi sodesoccursever alt i
    mesamont handl astf oraf ew mi nut
    est o
    severalhours.Herbl oodpr essurei smanagedwi t
    hlow- doseat enol
    ol.Shehasa
    familyhist
    oryofst r
    oke.Herelectrocardiogr
    am isshowni nFigure1.
    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nhermanagement
    ?

    a.Stresstest
    .
    b.Eventmoni t
    or.
    c.Increaseat
    enolol
    .
    d.Reassurance.
    e.Holtermonitor
    .

    Answer

    B.Eventmoni
    tor

    When eval uati


    ng palpit
    ati
    ons,the historyi sfundamentalbecause i tenables
    assessmentofbot hthediff
    erenti
    aldiagnosisofsympt omsandt hepossi bil
    it
    yof
    struct
    uralheartdiseasethatputthepatientatarrhythmicr
    isk.Palpit
    at i
    onscanbe
    ofcardiacorigi
    n(supraventr
    icul
    arorventri
    cularectopyorar
    rhythmia, valvul
    arheart
    diseaseorcar diomyopathy),psychosomat i
    c( anxiet
    yordepr ession),neurologic
    (autonomi cner voussyst em dysf unction/neur ocardi
    ogenic),dr ug-i
    nduced,ordue
    toot herpat hology( thyroiddi sorderoranemi a).Evaluati
    onofsympt omatology
    requiresassessmentoft heimpactofsympt omson t hepat i
    ent
    ’slif
    eand t he
    potentialofriskduet ost ructur
    alhear tdiseaseorar r
    hythmi a.Inthiscase,because
    thepat ienthasr iskf actorsforhear tdi sease,correl
    ation ofsympt omswi tha
    potentialarrhythmi aiscr iti
    cal
    ,andr eassur ancewi t
    houtf urtherevaluati
    onwoul d
    notbeopt i
    mal .Increasingat enololwoul dbedi ff
    icul
    tduet obasel i
    nebradycardia.
    Whendeci dingbet weenusi nga24- hourHol terandaneventmoni tortocorrelate
    sympt omswi thapot entialarrhythmi a,thef requencyofsympt omsi simportant.
    Over al
    l,ambul atoryeventmoni t
    oringof2- 4weeksdur ati
    onhasbeenshownt o
    provideahi gheryieldofdi agnosist hanHol t
    er.
     

    84.An82- year -
    oldwomanwi t
    hahi st
    orynoni schemiccar diomyopat hyandNew Yor k
    HeartAssoci ati
    oncl assI Ihear tfai
    lur
    eisseeni nyourof fi
    cef orinter
    mi tt
    entepisodesof
    malaiseandaf ull
    nessi nherneck.Shehadapr imarypr eventi
    onsi ngle-chamber
    i
    mplantabl ecadi overter-defi
    br i
    ll
    ator(
    ICD)impl anted2year sago, whi chisprogrammed
    atVVI40wi t
    hasi nglet achyar r
    hythmiazoneat200bpm t r
    eat edwi thshocks.Device
    i
    nterr
    ogat i
    ondemonst rat
    esnor maldevicefunct i
    onwi t
    hnoar r
    hythmi asrecorded.Her
    medicationsi ncludel i
    sinopril40mgdai l
    y, f
    urosemide40mgdai l
    y,andspi ronolact
    one
    25mgdai ly.Shehaddi scontinuedmet oprolol1yearagoduet oincreasingfati
    gue.Her
    examinationi sunr emar kableexceptf ortr
    acepi tt
    ingedema.Aneventr ecor
    dingdur i
    ng
    anepisodewhi lewal kingtot hebat hr
    oom isshowni nFigure1.
    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextmostappr
    opr
    iat
    est
    epi
    nhermanagement
    ?

    a.Upgradetodual-chamberI CD.
    b.Addcarvedi
    lol6.
    25mgdai ly.
    c.Upgradetocardi
    acr esynchroni
    zationtherapydefi
    bri
    ll
    ator(
    CRT-
    D)syst
    em.
    d.I
    ncreasefur
    osemi deto80mgdai ly.
    e.Cat
    heterabl
    ationofpr ematureventri
    cularcont
    racti
    ons.

    Answer

    A.Upgr
    adet
    odual
    -chamberI
    CD.

    Thispatientcomplai
    nsofmal aiseandneckf ull
    nessdueinpar ttothelossofat r
    ial
    synchronywhenvent r
    icularpacingisat40bpm.Themostappr opri
    ateint
    erventi
    on
    i
    supgr adingherdevi
    cet oadual -chambermodet oall
    owat r
    ioventr
    icul
    arsynchrony.
    Beta-bl
    ockademayal sobei nit
    iatedaf teranatr
    iall
    eadisinsertedfori
    tsbenefit
    sin
    pati
    entswi thhear
    tfail
    ure,buti finit
    iatedbeforeatri
    all
    eadi nsert
    ion,wouldlikely
    worsensympt omsduet ogreaterpaci ng.Shedoesnothavesi gnsofheartfail
    ure,
    soincreasi
    ngdiuret
    icsatt
    histimewoul
    dnotbeappr
    opr
    iat
    e.Shedoesnotmeet
    cr
    it
    eriaforCRTgivenQRSdurat
    ion.

    85.A22- year-oldmanwi tharrhythmogeni crightvent r


    icularcardi
    omyopat hypresentsto
    cli
    nictoestabli
    shcare.Hisdiagnosiswasmadebasedont hefindi
    ngsofsympt omatic
    nonsustainedventr
    icul
    artachycardia,anel ectrocardiogram withT-wavei nver
    sionsin
    leads V1-V3,and a cardiac magnet icr esonance i maging with an el
    evated ri
    ght
    ventri
    cularend-di
    astol
    icvolumeandr egionalhypoki nesis.Hesubsequentlyunderwent
    implantati
    on of an i mplantabl
    e car di
    overter-defibri
    ll
    ator
    . Dur i
    ng discussion of
    managementofhi sconditi
    on, heasksf oradvicer egar di
    nglif
    est
    yleinter
    venti
    ons.

    Whi
    choft
    hef
    oll
    owi
    ngl
    if
    est
    ylemodi
    fi
    cat
    ionsdoyousuggest
    ?

    a.Li
    mitcaffei
    ne.
    b.Li
    mitcompet i
    ti
    vesport
    spar
    ti
    cipat
    ion.
    c.Avoi
    dai rtr
    avel
    .
    d.Li
    mitalcohol.
    e.Rest
    ri
    ctf l
    uidi
    ntake.

    Answer

    B.Li
    mitcompet
    it
    ivespor
    tspar
    ti
    cipat
    ion

    Arr
    hyt hmogeni c car diomyopat hyi s a pr ogressive,herit
    able disease ofcar diac
    muscl er esultingi nahi ghriskofvent riculararrhythmiasandsuddendeat h,even
    when car diacst ructuralchangesar emi nimal.Based on t hei ncr eased riskof
    cardi
    acar restandsuddendeat hinat hl
    eteswi t
    har rhyt
    hmogeni ccar diomyopat hy,
    pati
    ent sar eadvi sedt oavoidcompet iti
    vespor tsandendur ancet raining.Physi cal
    acti
    vitymayaccel eratestructuralpr ogressi onofar rhyt
    hmogeni ccar diomyopat hy;
    i
    n a st udy ofhet erozyogous pl akoglobi n- defici
    entmi ce,endur ance training
    accel
    er ated t he devel opmentofar rhythmi as and r i
    ghtvent r
    icul ardysf unct i
    on.
    Alt
    houghcaf feine,alcohol,dehydr ation,andmi ldhypoxiamayt r
    iggerar rhyt
    hmi ain
    i
    ndividual s,therear enoknownspeci fi
    clinkst oarrhythmogeniccar diomyopat hy.

    86.A40- year-ol
    dwomani sreferredforeval uat
    ionofpal pit
    ations.Shehasf eltski
    pped
    andirr
    egularbeat sforthepast20year s,butint hepast6mont hs,sheisfindingthat
    herexerci
    setolerancei sdecr eased.Shedeni esanychestpai norsyncope.Shehasa
    pastmedicalhistoryofobesi ty.Shesawacar diologi
    st1yearagof orthi
    sproblem and
    remembersget ti
    ngast r
    essechocar diogram,butshewast ol dthepicturesont hetest
    wereunclear;acar di
    accat heteri
    zationwasr ecommended,butshedecl i
    ned.Fami ly
    hist
    oryisnotablef oranuncl ewhodi edofar hythm problem thatoccur r
    eddur inga
    hospi
    tal
    izat
    ion20year
    sagof
    orast
    aphyl
    ococcusi
    nfect
    ion.
     

    Onphysicalexaminati
    on,herbl oodpr essur
    eis123/
    70mm Hg,pul seis60bpm,and
    weighti
    s170pounds( bodymassi ndex30).Thej
    ugularvenouspul
    seisat6cm,wit
    h
    occasi
    onalcannonAwavespr esent.Lungsoundsar eclear
    .Auscul
    tat
    ionshowsa
    si
    ngleS1,si
    ngleS2,andfrequentectopicbeats.
     

    Ther emai
    nderoftheexaminat
    ioni
    snor
    mal
    .Her12-
    leadel
    ect
    rocar
    diogr
    am (
    ECG)
    rhyt
    hm str
    ipi
    sshowninFigur
    e1.
    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nmanagement
    ?

    a.Str
    essnucl earperfusi
    onstudy.
    b.Loopr ecor
    deri mplant.
    c.Cardiacmagnet icresonancei
    magi
    ng(
    MRI
    ).
    d.Cardiaccatheteri
    zati
    on.
    e.Thir
    ty-dayeventmoni t
    ori
    ng.

    Answer

    C.Car
    diacmagnet
    icr
    esonancei
    magi
    ng(
    MRI
    ).

    This ECG shows pr emature vent ricular cont racti


    ons ( PVCs) of mul ti
    ple
    mor phologies.PVCsshow ar i
    ghtbundl emor phol ogy(namel yposit
    iveinV1) ,but
    wi t
    hdi ff
    erentampl i
    tudesint hel atepr ecordi
    all eads.ThePVCsar el i
    kelyar i
    sing
    from theleftvent ri
    cle,butfr
    om di ff
    erentlocations.I nawomanwi thnor iskf actors
    forcor onarydi seaseandal ong- standinghi storyofsympt omsl i
    kelyr elatedt o
    thesePVCs,oneshoul dfi
    rstconsi deracar diomyopat hy.Asanechocar diogram
    waspr evi
    ousl yr egardedassubopt imal,thebestnexti magingst udyisacar diac
    MRI .Thispat ient’scardiacMRIr evealedl ef
    tvent ri
    cularnoncompact i
    on.Anevent
    moni t
    orori mpl antableloopr ecorderi snothel pfulinthi
    scase,ast hef r
    equent
    PVCsar ealreadyevi dentonherof fi
    ceeval uati
    on.

    87.A 55- year -old woman pr esent st ot he emer gency r oom wi th 3 mont hs of
    progr essiveshor t
    nessofbr eathandbi l
    aterallowerext r
    emi tyswel l
    ing.Shehasa
    pastmedi calhi storyofhyper tensi onandat ri
    alfi
    brill
    ation.Hermedi cationsi nclude
    carvedi l
    ol6. 25mgt wi cedai ly,lisinopri
    l10mgdai ly,andhydr ochlorothiazi de12. 5
    mgdai ly.Anucl earmyocar dialper f
    usionscanper for med6mont hsagoshoweda
    normall eftvent ricul
    arej ectionf ractionwi thoutper fusiondef ects.Onexami nation,
    herbl oodpr essur eis105/ 70mm Hg, herhear trateis135bpm, andshei saf ebril
    e.
    Herj ugul arvenouspr essurei s11cm H20;cr acklesar eaudi bleoverbot hl owerl ung
    fi
    elds,andcar diacauscul t
    at i
    onr evealsat achycardi candi rregularhear tr hythm.
    Herl owerext r
    emi ti
    eshave2+ pi t
    ti
    ng edemabi lateral
    ly.Herel ectrocar diogr am
    showsat ri
    alf i
    br i
    ll
    ationat120bpm andl eftbundl ebr anchbl ock.Shei sadmi ttedto
    thehospi tal,andanechocar diogr am revealsagl obal lydilat
    edl eftventriclewi than
    estimat edej ecti
    onf ractionof15%.Ther ei snoevi denceofl eftatr
    ialthr ombuson
    transesophagealechocar diogr aphy.Shei sst art
    edonahepar indrip,lasix40mg
    dai
    ly,andami odar
    one200mgthr
    eeti
    mesdail
    y,whi
    lecar
    vedi
    loli
    sti
    tr
    atedt
    o12.
    5
    mgt wicedail
    y.Sheconver
    tst
    osinusrhyt
    hm wi
    tharateof65bpm onday2of
    hospit
    ali
    zat
    ion.

    Whichoft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    enextst
    epi
    nthemanagementoft
    his
    pat
    ient
    ?

    a.Echocardi
    ogram in3mont hs.
    b.Multi
    gatedacquisi
    tionscan.
    c.El
    ectrophysi
    ologystudy.
    d.24-hourHolt
    ermoni tor
    ing.
    e.Cardi
    acmagnet icresonancei
    magi
    ng.

    Answer

    A.Echocar
    diogr
    am i
    n3mont
    hs.

    Thispati
    enthasat achycardi
    a-inducedcardiomyopat hyduetoatri
    alfi
    br i
    ll
    ationwith
    fastventr
    icul
    arrat es.Controlofat ri
    alfibri
    ll
    ati
    on ( orfastventr
    icularr ates)is
    expect
    edt oresul
    ti nnormalizati
    onofl eftventr
    icularfuncti
    on.Theot herchoi ces
    wouldnotchangemanagement .Alt
    houghaneval uati
    onisnotunreasonabl e,itcan
    bedeferr
    eduntilt
    heef f
    ectsofrestori
    ngsinusrhythm havebeenr eassessed.

    88.A55- year-ol
    dmanisrefer
    redforcar
    diacmagnet
    icresonancei
    magi
    ng(MRI)because
    ofrecurrentri
    ghtbundl
    ebr anchmorphol
    ogicnonsustai
    nedvent
    ri
    cul
    artachycar
    dia
    (Fi
    gure1).

    Fi
    gur
    e 1.
    I
    magesseenoncar
    diacMRIar
    emostconsi
    stentwi
    thwhi
    choft
    hef
    oll
    owi
    ng?

    a.Myocarditi
    s.
    b.Pri
    ormyocar di
    alinfar
    cti
    on.
    c.Hemochr omatosi
    s.
    d.Nonischemiccardiomyopat
    hy.

    Answer

    B.Pr
    iormyocar
    diali
    nfar
    cti
    on

    Car diacMRIi sausef ulmodal ityt o assessf orpossi blecausesofvent ri


    cular
    arrhyt hmia,gi veni t
    sabi li
    tytodemonst ratevariousmyocar dialdi
    seasest hatform
    thesubst ratef orarrhythmia.Thecl assicinfarctscarinvol vesthesubendocar dium
    andmaybenont ransmur al,asshowni nthispat ientwit
    hevi denceofpr i
    ori nf
    erior
    wal lmyocar dialinfarctionbyl atepost -gadolinium enhancementi maging.Unl ike
    i
    nf arctscar ,thef i
    brosisofnoni schemi ccardiomyopat hyismor eli
    kelytoappearas
    mi dmyocar dialhyper enhancement ,andmyocar di
    ti
    smayappearasmi dwal lor
    mor ecommonl yepicardialhyperenhancement .Hemochr omat osi
    sisdet ectednot
    by l at e gadol ini
    um enhancement ,butwi t
    h a di f
    fer
    entnoncont rasti magi ng
    techni quet hatt akesadvant ageoft heef f
    ectofi rononT2* ,amagnet icrelaxation
    par amet erthatshor tenswi thincreasedt i
    ssueirondeposi tion.

    89.A70- year-ol
    dwhi temanpr esentstot heemer gencydepar tmentwi tha1- week
    historyofprogressiveshor tnessofbr eath.Hedeni esanyf ever,sputum product i
    on,
    chestpai n,hemopt ysis,legedema,orpal pit
    ations.Hehasahi st
    oryofi schemi c
    cardiomyopathyf ollowingt wopr iormyocar dialinfar
    cti
    ons5year sago.Hi sleft
    ventri
    cularejection f r
    action is 20%,and he has an i mpl antable cardiovert
    er-
    defibri
    ll
    ator(I
    CD).Duet or ecurrentventriculartachycardiaandI CDshocks,hewas
    placedonami odarone2year sago, af
    terwhi chhehadnof urtherICDshocks.Thr ee
    mont hsago,hewasadmi ttedtot hehospi talfordecompensat edheartf ai
    lure(HF).
    Hiscur rentmedicalr egimeni ncludesmet oprololsuccinate100mgdai ly,enalapri
    l
    10mgbi d,f
    urosemi de40mgbi d,ami odarone200mgdai ly,andmet f
    ormi n1000
    mgdai l
    y. 

    Onphysi
    calexami
    nat
    ion,
    heisi
    nmoder
    ater
    espi
    ratorydist
    ress.Hi
    sbl
    oodpressur
    e
    i
    s110/80mm Hg,hi spulsei
    s110bpm andr egular
    ,andhei safebr
    il
    e.Lung
    examinationreveal
    sdi f
    fusebil
    ateralr
    ales.Hisjugul
    arvenouspr essur
    eis8cm and
    thereisno hepat ojugularref
    lux.Car di
    acexami nati
    on r eveal
    sa nor malS1 and
    S2 wit
    hnoS3  ormur mur.Hisabdomeni sbenign,andhi slowerextremiti
    esar e
    war m andfreeofedema.Labor atorytestsshowacr eatinineof1mg/ dl,N-t
    erminal
    pro–B- t
    ypenat r
    iur
    eticpepti
    de(NT- pr
    oBNP)of300pg/ ml ,andhemogl obin13g/dl.
    ChestX- rayreveal
    sdi f
    fusebil
    aterali
    nfil
    tr
    ates.Theelectrocardi
    ogram showssinus
    tachycardiaandisotherwiseunchangedf rom hi
    sbaseline.

    Whi
    choft
    hef
    oll
    owi
    ngi
    shi
    smostl
    ikel
    ydi
    agnosi
    s?

    a.Pulmonaryemboli
    sm.
    b.AcutedecompensatedHF.
    c.Pneumonia.
    d.Pulmonaryhemorrhage.
    e.Pulmonaryfi
    brosi
    s.

    Answer

    E.Pul
    monar
    yfi
    brosi
    s.

    Thepat ientpr esentswi t


    hacl inicalpi
    ctur econsi stentwithami odaronepul monar y
    toxici
    ty.Physi ciansneedt omai nt
    ainahei ghtenedawar enessoft hispot ential
    ly
    fatalcompl i
    cat i
    on.Ot hertoxicitiesofami odarone,i ncl
    udinghepat icinjur
    y,t hyroi
    d
    distur
    bances,phot osensit
    ivit
    y,ski n di scolorati
    on,per i
    pheralneur opat hy,and
    cornealdeposi t
    s,shoul dber emember edaswel l.Inthecur rentclini
    calscenar i
    o,
    decompensat edHFi slesslikel ygivent heabsenceofj ugularvenousdi stentionor
    hepatojugularr efl
    ux and t he NT- proBNP l evel.Ther e wer e no const it
    utional
    sympt omsorsput um productiont osuggestpneumoni a,norwast herehemopt ysis
    oranemi atosuggestpul monar yhemor rhage.Apul monar yembol uswoul dnotbe
    expectedt oresul ti
    nbi l
    ater
    alpul monar yi nfi
    lt
    ratesonchestX- ray.

    90.A30- year-
    oldmanpr esentstoyouf orcar
    diol
    ogyconsul
    tati
    on.Hewasor i
    ginal
    ly
    eval
    uatedbyhi si
    nter
    nistforchestpainandshort
    nessofbreathwit
    hexerci
    se.His
    i
    nterni
    stchecked an el ectr
    ocardi
    ogram,which demonstrated l
    eftventr
    icul
    ar
    hypert
    rophy(LVH)wit
    hst r
    ainpatt
    ern.
     

    Thepati
    entreport
    sexert
    ionalchestdiscomfortanddyspneaf orthepast3mont hs.
    Hehasnopastmedi calhistoryandt akesnomedi cat
    ions.Hisfatherdiedi nacar
    acci
    dentattheageof45,andhi smotherisali
    veandwel l.Onexami nat
    ion,hisheart
    rat
    eis76bpm andbl oodpr essur
    ei s110/70mm Hg.Ther ei sal ate-peaki
    ng
    syst
    oli
    cejecti
    onmurmurhear dbestatthelef
    tuppersternalborder.
      
    Echocardi
    ogram r
    evealsLVHwi t
    hanLVsept um andpost
    eri
    orwal
    lthi
    cknessof17
    cm and18mm,r especti
    vely.TheLVeject
    ionfr
    actioni
    s65%,andt
    hecavitysi
    zeis
    normal.ThepeakgradientacrosstheLVoutf
    lowtracti
    s28mm Hg.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nhi
    scar
    e?

    a.Stressechocardiogr am.
    b.Leftandrightheartcat het
    eri
    zat
    ion.
    c.Cardiacmagnet i
    cr esonanceimaging.
    d.Exerciset
    olerancet est.
    e.Transesophagealechocar diogr
    am (TEE)
    .

    Answer

    A.St
    ressechocar
    diogr
    am

    Thecl i
    nicaldiagnosi
    sofhyper tr
    ophi
    ccardiomyopat hy(HCM)i sconvent i
    onal l
    y
    made mostcommonl y witht wo-di
    mensionalechocar di
    ography.Mor phologic
    diagnosisisbasedont hepresenceofahyper trophiedandnondi l
    atedLVi nt he
    absence ofanot hercar di
    ac orsyst emic disease capable ofpr oducing t he
    magni t
    udeofhyper tr
    ophyevi dentinapatient( usuall
    y≥15mm i nadul ts)
    .Thi s
    patient
    ,whohasnopasthi st
    oryandnohyper tension,afamilyhist
    oryconsi stent
    withsuddendeat h,andsi gnifi
    cantLVH onechocar diogr
    am,hasapr esentation
    consist
    entwithHCM.
     
    Identi
    ficationoft hepr esenceandmagni tudeofout f
    low obst r
    uct i
    oni sessent i
    alin
    guidi
    ngpr ognosi sandt her apy.Thepr esenceandmagni t
    udeofout f
    lowobst ruction
    are usual ly assessed wi tht wo-di mensi onalechocar diography and cont i
    nuous
    waveDoppl er.Itisal ate-peakingsyst ol
    icvelocitythatr efl
    ect st heoccur renceof
    subaor ti
    cobst r
    uct i
    onlatei nsyst ol e,andt hepeaki nstantaneousgr adientder i
    ved
    from t he peak vel oci
    ty shoul d be r eported.A peak gr adient>30 mm Hg i s
    consider edsi gnif
    icant.Themeangr adientdoesnothavephysi ologicsi gnifi
    cance
    anddoesnotaf f
    ectt reatment ,andt husi snotassessed.I ft her est ingout f
    low
    gradienti s≤50mm Hg,pr ovocativemeasur esmaybeusedt oascer taini fhi gher
    gradients can be el icit
    ed, pr eferably wi t
    h physi ologic exer cise ( stress
    echocar diography) ,butal t
    ernati
    vel ywi ththeVal salvamaneuverorsel ect i
    velywi t
    h
    amylni trit
    e.Int hi
    spat i
    ent ,provocat ivetestingisimpor tantbecauset hepat ienthas
    sympt omst hatappearoutofpr opor t
    iontot herestinggr adient ,andt her ef
    or e,the
    presence of a physi ol
    ogical ly pr ovoked obst r
    uct ion shoul d be
    assessed.  Provocat i
    onwi thdobut ami neinfusiondur ingDoppl erechocar diogr aphy
    i
    snol ongerr ecommendedasast rat egytoinduceout fl
    owgr adi entsinHCM.  
    TEEi susef ulint
    raoper ati
    velytoguideal coholsept alablati
    onormyomect omyori n
    caseswher ethereisconcer nformi tr
    alval vepathol ogyorf ixedoutflowobst r uction
    notwel lcharacteri
    zedont ransthoracicechocar diogram.I nthi
    scase,adequat e
    i
    nformat ionhasnotyetbeenobt ainedf rom at ranst horacicechocar diogram,and
    thus,TEE i s notwar r
    anted.I n equivocalcases,car diac catheterizati
    on wi th
    i
    sopr oterenolinfusionmayf ur
    therai dinel ici
    ti
    ngapr ovocabl egr adient.Invasi ve
    cardiaccat heter
    izationtodocumentout f
    lowgr adient sisnecessar yonl ywhent here
    aredi scordantdat af r
    om Doppl erechocar di
    ographyandt hephysi calexami nat i
    on.
    Furthermor e,coronar yangiographyi sindicatedonl yincaseswher et hereisahi gh
    l
    ikeli
    hoodofcor onar yarter
    ydi sease,whi chisnott hecasei nthisyoungpat i
    ent
    withnor i
    skfactors.

    91.A30- year-ol
    dmanwi thahi storyofhyper trophiccar diomyopat hy( HCM)pr esent sto
    youf oranopi niononani mpl antablecar diovert
    er-def i
    br i
    ll
    ator( I
    CD)pl acementf or
    suddencar di
    acdeat h(SCD)r i
    sk.Hewasr ecent l
    ydi agnosedbyanot hercardiologist
    .
    Thepat ientreportsnosympt oms.Thedi agnosi swasmadeaf terhisinter
    nisthear da
    systol
    ic mur muron exami nation,and an el ectrocar diogram ( ECG)showed l ef
    t
    ventri
    cular(LV)hypertr
    ophywi thst r
    ainpattern.Heexer cisesbywal kingatabr iskpace
    for30 mi nut
    esdai l
    ywi thoutl imit
    ati
    ons,and hewor ksf ullt i
    measan i nsur ance
    executive.Het akesnomedi cations.Hehasnopasthi story.Hi spar entsandt wool der
    sibl
    ingsar eali
    veandwel l
    .Ther eisnof amil
    yhi st
    oryofSCD.  

    Onexami nation,hishear tr
    atei s68bpm, andhisbloodpr
    essur eis106/64mm Hg.He
    hasahar sh,late-peakingsyst ol
    icej
    ectionmur murheardbestatther i
    ghtupperst er
    nal
    border.Hisechocar diogram demonst ratesnormalLVcavit
    ysi zewithejectionfract
    ion
    of68%.LVsept um andpost eriorwallare20mm and18mm,r espectively.TheLV
    outfl
    ow tract( LVOT)gr adientatr estis40mm Hg.Onst ressechocar diogram,he
    exerci
    sesf or13:00ont heBr uceprotocol,st
    oppingduetofatigue.Hisbloodpr essure
    atrestis110/ 70mm Hgandr i
    sesto180/ 60mm Hg.TheLVOTgr adientroset o60mm
    Hgatpeakexer cise.

    Whi
    choft
    hef
    oll
    owi
    ngdoyour
    ecommendnext
    ?

    a.Foll
    ow- upeval uat
    ioni n1year
    .
    b.El
    ectrophysiologyst udy.
    c.Ambul ator
    yECGmoni tor
    .
    d.Proceedwi t
    hI CDpl acement.
    e.Echocardiogram wi t
    ht i
    ssueDoppl
    eri
    magi
    ng.

    Answer
    C.Ambul
    ator
    yECGmoni
    tor

    Thedeci siont oplaceanI CDi npatient


    swi thHCM shoul dincl
    udeappl icati
    onof
    indivi
    dualclinicaljudgment ,aswel lasat horoughdi scussionoft hestrengthof
    evidence,benef i
    ts,andr i
    skst oal
    low theinformedpat ient’
    sacti
    vepar ti
    cipati
    oni n
    decisionmaki ng.ICDpl acementisr ecommendedf orpatientswit
    hHCM wi thpr i
    or
    document edcar di
    acarrest,ventr
    icularfi
    bri
    ll
    ati
    on,orhemodynami callysignifi
    cant
    vent r
    icul
    artachycardia(VT).Itisr
    easonablet orecommendanI CDf orpati
    ent swith
    HCM wi t
    hsuddendeat hpr esumabl ycausedbyHCM i noneormor efi
    rst-degree
    relati
    ves,a maxi mum LV wal lthickness of30 mm,orone ormor er ecent
    unexpl ai
    nedsyncopalepi sodes.

    Ast hispat i
    enthasnoper sonalorf amilyhi st
    oryofSCD, LVwal lthickness<30mm,
    andnosyncope,I CDi snotwar rantedwi t
    houtf urtheri nformat i
    on.AnI CDcanbe
    usefulinsel ectpatientswi thnonsust ainedVT( NSVT) ,parti
    cul arlythosepat ients
    withar estingLVOTgr adi ent>30mm Hg,LV api calaneur ysm,l ategadolinium
    enhancementoncar diacmagnet icresonancei magi ng,ordoubl eorcompound
    genet i
    cmut ations.Thispat ienthasar estingLVOTgr adient>30mm Hg,sof urther
    i
    nvest i
    gationi swar rantedt odet ermineifanI CDshoul dbeconsi dered.Thefactt hat
    hei sasympt omat i
    cdoesnoti mpactt hedeci si
    on t or i
    sk- stratif
    yhi m forI CD
    placementf orpr i
    mar ypr event ionofSCD,sosi mpl yrecommendi ngannualf ollow-
    upi snotsuf fi
    cientwi t
    houtf i
    rstobt ai
    ningmor ei nformat i
    on.Thi spat i
    entdoesnot
    haveanabnor malbloodpr essur eresponset oexer cise, defi
    nedasei therafai
    lur eto
    i
    ncr easethesyst oli
    cbl oodpr essureby20mm Hgoradr opof20mm Hgdur ing
    effort
    .However ,thet est ing donepr ovidesno i nfor mat i
    on on t hepr esenceor
    absenceofNSVT,whi chwoul dr equireambul atoryECGmoni t oring.Othertest i
    ng,
    suchasel ect r
    ophysiologyst udiest oinduceVTort issueDoppl erimagi ngtoassess
    fordyssynchr ony,doesnotof ferhelpfulinformationf orr iskstrat i
    fi
    cat i
    onofSCD.

    92.A59- year-oldwomani sadmit


    tedtot hehospitalforatr
    ialfi
    bri
    ll
    ati
    on(AF)after
    presenting wit
    h palpit
    ati
    onsand shortnessofbr eath.Shehasapastmedi cal
    historyofhypertension,t
    ype2diabetes,chroni
    cki dneydi
    sease(stageIII
    ),anda
    prior episode of AF. Thr ee months ago she under went tr
    ansesophageal
    echocar di
    ogram (TEE),dir
    ectcurr
    entcar di
    over
    sion( DCCV),andwasst artedon
    war far
    in. 

    Curr
    enthomemedi cati
    onsi ncludewar farin 5 mg dail
    y,li
    sinopril40 mg daily,
    hydr
    ochlor
    othi
    azi
    de25mgdai ly,aml odi
    pine5mgdai ly,omeprazole20mgdai ly,
    si
    mvastati
    n40mgdai l
    yandgl yburi
    de5mgt wicedai l
    y.Laboratorydatareveal:
    sodi
    um 138mmol /L,potassi
    um 4. 2mmol /L,magnesium 2.2mg/ dl,cr
    eati
    nine1.6
    mg/dl(esti
    mated creati
    nine clearance [
    Cr Cl
    ]of45 ml /min),and inter
    nati
    onal
    normal i
    zedrati
    o2.2.Thepati
    ent
    ’screati
    ninehasbeenstableovert
    hepast2years.
    Electr
    ocardi
    ogram onadmissi
    onrevealsAFwi t
    haventri
    cularr
    ateof112bpm anda
    calculat
    ed QTc of420 msec.TEE and DCCV wi t
    h subsequentinit
    iat
    ion of
    antiar
    rhythmicdrugther
    apyarepl
    anned.

    Whichofthef
    oll
    owingismostl
    ikel
    ytocont
    ri
    but
    etoQTpr
    olongat
    ioni
    ntheset
    ti
    ng
    ofdof
    eti
    li
    deadmini
    str
    ati
    oni
    nthi
    spat i
    ent
    ?

    a.Li
    sini
    pr i
    l.
    b.Amlodipine.
    c.Si
    mvast ati
    n.
    d.Omepr azole.
    e.Hydrochlorot
    hiazi
    de.

    Answer

    E.Hydr
    ochl
    orot
    hiazi
    de

    Currentmanuf acturerrecommendat i
    onsf orini ti
    ationofdof eti
    li
    deincludeabasel ine
    QTi ntervalorQTcof<440msec( oraQTi nter valorQTcof<500mseci npat i
    ents
    with an i ntraventr
    icul arconduct ion del ay).Recommendat i
    ons fort he use of
    dofetil
    idei npat i
    ent swi t
    hchr onickidneydi seasei ncl
    udeacont r
    aindi cationf or
    usingt hedr uginpat ientswithaCr Cl<20ml /mi n.Dat aonf il
    ewiththemanuf acturer
    showasi gnif
    icantphar macokineti
    caswel lasphar macodynami cinteract i
    onwhen
    dofetil
    idei sused concomi tantl
    ywi t
    h hydr ochl orothi
    azide.Co- administ ration of
    dofetil
    ide500mcgt wicedai l
    ywi thhydr ochl orothiazide50mgdai lyresul t
    edi nan
    i
    ncr ease i n dofeti
    lide ar ea undert he pl asma dr ug concentrati
    on- ti
    me cur ve
    (appropriateusecr iteri
    a)by27%andpeakconcent rati
    on(Cmax)by21%.I naddi ti
    on,
    thephar macodynami cef f
    ectofdof eti
    li
    dei ncr eased197%( asmeasur edbyt heQTc
    i
    ncr ease over t i
    me) and a 95% i ncrease i nt he maxi mum QTc i ncr ease.
    Phar macoki neti
    c st udies in healthy volunt eer s did notsuggestaml odipine or
    omepr azol ehadasi gnifi
    canteffectont hephar macoki net i
    csofdof et
    ili
    de,andno
    currentr ecommendat i
    onsexi stforavoi dingi nit
    iatingdof eti
    li
    deinpat ientst aking
    thesemedi cati
    ons. 

    93.A65- year-ol
    dwomanwi thahi storyofdi abetesmel l
    it
    ust ype2,hyper t
    ensi
    on,and
    chronicki dneydi seasest age4( glomerularf i
    lt
    rat
    ionrate22ml /min)pr esent
    stot he
    emer gencydepar tmentwi thacut eleft
    -sidedhemi paresis.Shei sdiagnosedwi than
    acuter ight-si
    dedmi ddlecerebralart
    eryst rokeandr eceivest hr
    ombolytics.Daysl at
    er,
    whilebei ngmoni toredi nthestrokeuni t
    ,shei snotedont el
    emetrytohaveanepi sode
    ofatrialfibr
    ill
    ati
    on( AF)wi thventri
    cularratesof130bpm.Shei sasympt omat i
    cdur i
    ng
    thi
    s epi sode. Tr ansthor
    acic echocar diogr am r eveal
    s moder at
    e l eft ventr
    icular
    hyper
    trophyandmoderatel
    eftatr
    ialdil
    ati
    on.Ther
    ear
    enoval
    vul
    arabnor
    mal
    it
    iesnot
    ed.
    Thepatienthasnopr
    iorhi
    storyofbleedi
    ng.

    Whichofthef
    oll
    owi
    ngwoul
    dbet
    hemostappr
    opr
    iat
    ether
    apyf
    orsecondar
    yst
    roke
    pr
    event
    ion?

    a.Dabi
    gatran150mgbymout ht
    wicedail
    y.
    b.Warf
    arintotar
    geti
    nter
    nat
    ionalnormali
    zedr
    ati
    o(INR)of2-
    3.
    c.Ri
    varoxaban20mgbymout hdai
    ly.
    d.Aspi
    rin325mgdaily.
    e.Aspi
    rin325mgdailyandclopi
    dogrel75mgdail
    y.

    Answer

    B.War
    far
    int
    otar
    geti
    nter
    nat
    ionalnor
    mal
    izedr
    ati
    o(NR)of2-
    3.

    Thispat i
    enthasaCHA2DS2  VAScscor eof5( hyper t
    ension,di abetesmel l
    it
    ust ype2,
    diastoli
    chear tfail
    ure,cer ebr ovascul aracci dent )andhashi ghr i
    skoff uturest roke
    duet oAF.Gi venherCHA2DS2  VAScscor eof5  andl ackofpr iormaj orbl eeding,a
    vi
    tami nKant agoni st,adi rectt hrombi ni nhi bitor,oraf actorXai nhi bitorwoul dbe
    appr opri
    ateandwoul dpr ovi debet terpr otect ionagai nstst roket hanaspi ri
    nal one.
    Addi ti
    onally,anor alant icoagul antwoul dpr ovidebet terstrokepr otect i
    ont hant he
    combi nationofaspi ri
    nandcl opidogr el(asseeni ntheACTI VE  W[ AtrialFibril
    lation
    ClopidogrelTr ialWi t
    hI rbesar tanf orPr event i
    onofVascul arEvent s]t ri
    al),andt he
    patienthasnocont r
    aindi cationst oor alant icoagul ati
    on.However ,bot hdabi gat ran
    andr ivar
    oxabanar eprimar i
    lyexcr etedi nt heki dneys, andt hispat ient’smoder atet o
    sever echronicki dneydi seaseneedst obeconsi dered.Dabi gatranusehasnotbeen
    studiedinpat i
    ent swithcr eat i
    ninecl earance<30ml /
    mi nandshoul dbeavoi ded.I n
    patientswi thcr eati
    ninecl ear anceof15- 50ml /mi n,r
    ivaroxabancanbeconsi der ed,
    butatar educeddoseof15mgdai ly.Ther efore, t
    hemostappr opr iate optionint his
    scenar i
    o iswar fari
    nwi thgoalI NRof2- 3.

    94.A 59 year -
    old woman i s admi t
    ted t
    ot he hospitalwith a chi efcomplaintof
    palpitat
    ions,shortnessofbr eat
    h, andfastheartrat
    e.Thepat ienthasapastmedi cal
    historythatissigni f
    icantforhyper tensi
    on,type2di abetes,chr oni
    ckidneydisease
    (stage3) ,andapr eviousepi sodeofat ri
    alfi
    bril
    lat
    ion3mont hspr iorf
    orwhi chthe
    patientunder wentsuccessf ultransesophagealechocar di
    ographyanddi rectcurr
    ent
    cardioversion.Thepat ientreceivedwar f
    ari
    nf or4weeksf oll
    owi ngthecardi
    oversi
    on.
    Currenthomemedi cati
    onsincludeaspiri
    n 81 mg dail
    y,li
    sinopr
    il40 mg dai
    ly,
    hydrochl
    orot
    hiazi
    de(HCTZ)25mgdai l
    y,amlodi
    pine5mgdaily,omeprazol
    e20mg
    dail
    y,si
    mvastati
    n40mgdai l
    y,andglyburi
    de5mgt wi
    cedai
    ly.

    Laboratorydat afrom todayr evealsodium 138mmol /L,pot


    assium 4.2mmol /L,
    magnesi um 2.2mg/ dl
    ,andcr eati
    nine1.6mg/ dl( givesanest i
    mat edcr eat
    ini
    ne
    clear
    ance[ CrCl]of45ml /
    min) .Thepatient
    ’screatininehasbeenst abl
    eovert he
    past2year s.Anel ectr
    ocardiogram onadmi ssi
    onr evealedat
    ri
    alfibri
    ll
    ati
    onwi tha
    ventr
    icularresponserateof112bpm andacal culatedQTcof420msec.Thepl anis
    for t
    ransesophagealechocar diography and directcur r
    entcardioversi
    on wi t
    h
    subsequenti ni
    ti
    ati
    onofant i
    arrhythmicdrugther
    apy.

    Whichoft
    hef ol
    lowingwouldbet
    hebestchoi
    ceast
    owhydof
    eti
    li
    deshoul
    dnotbeused
    i
    nthispat
    ientatthecurr
    entti
    me?

    a. Thedrugi
    nter
    acti
    onwi t
    haml odi
    pine.
    b. Thedrugi
    nter
    acti
    onwi t
    hHCTZ.
    c. Thedrugi
    nter
    acti
    onwi t
    homepr azole.
    d. TheCrCli
    stoolowtoinit
    iat
    edofeti
    lidetherapy.
    e. Thebasel
    ineQTcistoolongtoinit
    iatedofeti
    li
    dether
    apy.

    Answer

    B.Thedr
    ugi
    nter
    act
    ionwi
    thHCTZ.

    Currentmanuf act ur
    err
    ecommendat ionsf orini
    ti
    ationofdof eti
    li
    deincludeabasel ine
    QTi ntervalorQTc<440msec( oraQTi nt er
    valorQTc<500mseci npat ientswithan
    intr
    avent r
    icularconduct iondel ay).Recommendat ionsf ortheuseofdof et
    il
    idei n
    patientswi t
    hchr oni
    ckidneydi seasei ncludeacont raindicati
    onforusi ngt hedrugi n
    patients with a Cr Cl<20 ml /min.Dat a on f i
    le wi t
    ht he manuf act urershow a
    signif
    icant phar macokineti
    c as wel las phar macodynami ci nteract i
    on when
    dofetil
    ideisusedconcomi t
    ant l
    ywi t
    hHCTZ.Co- admi nist
    rati
    onofdof etili
    de500mcg
    twicedai l
    ywi t
    hHCTZ50mgdai lyr esultedinani ncreasei ndofeti
    lideappr opr i
    ate
    usecr iter
    iaby27%andCmaxby21%.I naddi t
    ion,t hephar macodynami ceff
    ectof
    dofetil
    ideincreased197%( asmeasur edbyt heQTci ncr
    easeovert ime)anda95%
    increase int he maximum QTc i ncrease.Phar macoki net
    ic studies i n healthy
    volunteersdidnotsuggestaml odipineoromepr azolehadasi gnif
    icantef f
    ectont he
    phar macokinet i
    csofdof eti
    lide,andnocur rentrecommendat i
    onsexi stf oravoiding
    init
    iati
    ngdof etil
    ideinpatientstakingt hesemedi cations.

    95.A69- year
    -ol
    dwomanpr esentedtotheemer
    gencydepar
    tmentwi
    thnew onsetof
    shor
    tnessofbreat
    hthathaslast
    edfor2daysandaninabi
    li
    tyt
    opart
    ici
    patei
    nher
    usualday-to-dayacti
    viti
    es.Sher epor
    tsthatshefeel
    slikeherhear ti
    sraci
    ngand
    shecannotcat chherbreat
    h.Thepat i
    enthasahistor
    yofhypertensionanddi
    abet
    es.
    Shehasahi storyofgastr
    ointest
    inal(
    GI)bleedi
    ngwhil
    et aki
    ngababyaspi ri
    nand
    anover-the-counternonsteroi
    dalanti
    -inf
    lammatorydrug,sot hesearenotbei
    ng
    used.
     

    An echocardi
    ogram is obtained that reveal
    s car di
    ac normal functi
    on. An
    el
    ect
    rocardi
    ogram demonstr
    at esnew- onsetatr
    ialfibri
    ll
    ati
    on (
    AF).Thepat i
    ent’
    s
    l
    abor
    atorydataar eobtai
    nedandar ewi thi
    nnor malr ange,exceptforaserum
    cr
    eat
    inineof2.
    6mg/ dlandcalculat
    edcreati
    nineclear
    anceof20ml /min. 

    Thepat ientwei ghs58kg.Shei shemodynami cal


    lystabl
    ewi t
    habl oodpr essureof
    110/ 70mm Hgandhear tr at
    eof110- 130bpm andi sstart
    edonmet oprolol
    .On
    met oprolol,herheartrat esdropt othe90sbpm,butshecont inuest or emain
    sympt omat i
    cal
    lyuncomf ort
    ablewithshortnessofbr eat
    h.Thepat i
    entunder goes
    directcur rentcardi
    oversionandi sinit
    iat
    edondr onedaronetomai nt
    ainnor mal
    sinusrhyt hm.Shehasr emai nedinnormalsinusrhyt
    hm ondr onedaronefor3days.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthebestant
    icoagul
    antchoi
    cef
    ort
    hispat
    ient
    ?

    a.Apixaban5mgt wi
    cedaily.
    b.Dabigatran75mgt wicedail
    y.
    c.Ri
    var oxaban20mgoncedai l
    y.
    d.Dose- adjust
    edwarf
    arin.
    e.Aspirin81mgaday.

    Answer

    D.Dose-
    adj
    ust
    edwar
    far
    in.

    HerCHA2DS2- VAScscor eis4.Thepat i


    enthasacal cul
    atedcreatinineclearanceof
    20ml /
    min.Itisrecommendedt hatthedoseofr ivaroxabanber educedt o15mg
    dail
    yf oracr eati
    nineclearanceof15- 50ml /min,so20mgdai lywoul dnotbe
    recommended.Al ternati
    vel
    y,reduceddoses( 2.5mgt wicedaily)wer epr ovidedif
    patientshadtwoormor eofthef ol
    lowingcrit
    eri
    a:age80year s,bodywei ght60kg,
    orser um creati
    nineof1. 5 mg/ dl
    .Theuseofdose- adjust
    ed war fari
    n maybe
    preferr
    ed int hi
    s pat i
    entwi t
    h a hi stor
    y ofgast roi
    ntesti
    nal( GI)bl eeding on
    combi nati
    onaspiri
    nandnonst er
    oidalanti-
    infl
    ammat orydrugther apybecauset he
    i
    ncidenceofGIbl eedingwasgr eaterwi t
    hdabi gatranandr i
    varoxabancompar ed
    withwar f
    arinintheclini
    caltri
    alsoftheseagent sf orAF.Undert heci rcumst ances
    presentedinthiscaseandt hechoi cespresented,closelymanagedwar far
    ini sthe
    bestchoi
    cef
    orant
    icoagul
    ati
    onf
    ort
    hispat
    ient
    . 

    96.Inpatient
    swithatr
    ialf
    ibr
    il
    lati
    on( AF)
    ,ther
    ear etwomnenomi cst
    hathavebeen
    devel
    opedtohel
    prememberr i
    skfactor
    sforst
    roke/
    transi
    enti
    schemi
    cat
    tack(
    TIA)
    . 
    Forwhichofthefol
    lowi
    ngpatient
    swouldanti
    coagul
    ati
    onber
    ecommendedbyt
    he
    CHA2DS2-VAScscor
    e,butnotbytheCHADS2 
    scor
    e?

    a.A 79- year


    -old man wi
    th hypert
    ension and di abetes and 6 years of
    persi
    stentAF.
    b.A66-year -
    oldwomanwithoutpri
    ormedicalhistoryandnew- onsetAF.
    c.A69- year-
    oldwomanwi t
    hahi st
    oryofrheumat i
    cmi tralstenosi
    sandnew-
    onsetAF.
    d.A25-year -
    oldmanwithahist
    oryofdrugabuseandcocai ne-i
    nducedAF.
    e.A42-year -
    oldmanwithnew-onsethypert
    hyroidism andAF.
    Answer

    B.A66-
    year
    -ol
    dwomanwi
    thoutpr
    iormedi
    calhi
    stor
    yandnew-
    onsetAF.

    The66- year -oldwomanhasaCHADS2  scor eof0andaCHA2DS2- VAScscor eof2.


    Shepi cksup2poi nt sintheCHA2DS2- VAScsyst em forbeingf emaleandherage.
    The CHADS2  scori
    ng syst em i ncludes 1 poi nt for congest i
    ve hear tf ai l
    ure,
    hypertension,age>75,anddi abetesand2poi ntsf orstrokeorTI A.TheCHA2DS2-
    VAScscor ei s1poi ntf orcongesti
    vehear tfail
    ure,hypertension,age>65,di abet es,
    vasculardi sease( historyofmyocar dialinfarcti
    on,cor onaryarterydisease,pl aque
    oni maging,orper ipheralvasculardisease) ,andf emal esex,and2poi ntsf orage
    >75andst roke.Basedont hecur rentguidel i
    nes,therapyf oraCHA2DS2  scor eof0
    requir
    esnot herapy.Ascor eof1r equiresnoneoraspi r
    in,orantithr
    ombi nther apy
    may be used.A scor e of≥2 r equires ant i
    thrombi nt herapy.Thi s applies to
    nonvalvularAF.

    97.A26- year-
    oldwomanwi thnopastmedi calhist
    orycomestoseeyoui nclini
    cforfoll
    ow
    -upaf t
    eranemer gencydepartmentvi si
    tforanepisodeofsyncope.Shesayst hatshe
    wasexer ci
    singwhenshebeganf eeli
    ngdizzyandnauseated.Shet r
    iedtowal ktothe
    bathroom andt henlostconsciousness.Herhusbandr ant ohersideandf oundher
    awakeandor i
    ented,butwit
    har apidpulse.Bytheti
    meemer gencymedi calt
    echnici
    ans
    arr
    ived,hervitalsi
    gnswer enormal ,andherevaluati
    onintheemer gencydepar t
    ment
    wasunr emarkable. 

    Onphysicalexaminati
    ontoday,herheartrat
    ewas66bpm,andbl oodpressur
    ewas
    108/
    72mm Hg.Sheappear swel l.Jugul
    arvenouspressurei
    snormal,andlungsare
    cl
    ear. There are no mur mur s. She has no l ower ext
    remity edema. Her
    el
    ect
    rocardi
    ogram (ECG)demonstratesnormalsinusrhyt
    hm andrightbundl
    ebranch
    block(RBBB)withQRSdur ationof128msec.El ectrolytesar ewi t
    hinnormallimit
    s.
    Echocardi
    ogram showsnormalleftventr
    icular(
    LV)f unction,mi l
    drightventr
    icul
    ar(RV)
    enlar
    gement,mi l
    d RV dysfuncti
    on,and mi ldtricuspidr egurgi
    tati
    on.An exercise
    tr
    eadmillt
    estinwhichthepati
    enthasmul t
    ipler
    unsoft her hythm i
    sshowni nFigure1.
    Thereisnofamil
    yhistor
    yofsyncope, car
    diacarrhythmia, orsuddendeat h. 

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    enextst
    ep?

    a.Cardi
    acmagnet icresonancei
    magi
    ng(
    MRI
    ).
    b.Cardi
    accatheteri
    zati
    on.
    c.Endomyocardialbi
    opsy.
    d.Geneti
    ctest
    ing.

    Answer

    A.Car
    diacmagnet
    icr
    esonancei
    magi
    ng(
    MRI
    ).
    The concer nist hatt his young woman has ar rhythmogenicrightvent ricular
    cardi
    omyopat hy(ARVC)becauseshehasexer ci
    se-inducedventri
    culartachycar dia
    andRVenl ar
    gementonechocar di ogram,aswel lasRBBBonECG.I nor dertomeet
    cri
    ter
    iaforARVC,t hereshouldbet womaj orcri
    teri
    a,oronemaj orandt womi nor
    cri
    ter
    iai nt he cat egori
    es ofvent ri
    cul
    ar dysfunction,ti
    ssue char acteri
    zat ion,
    arr
    hythmias,andECGde/ repolarizationcri
    teri
    a.TheMRIwi llal
    lowbot heval uat i
    on
    ofventr
    iculardysfunctionandsi ze,aswel last hetissueandf i
    brofattyinfil
    tration.
    Endomyocar di
    albi opsywoul dal sobehel pfulfort i
    ssuecharacterizati
    on,buti s
    i
    nvasiveandsubj ecttosampl i
    nger ror.MRIprovidesmor edatawithlessr isktot he
    pati
    ent.Once t he di agnosisi s made,you can r eferforgenet i
    ct esti
    ng f or
    confi
    rmationandf ami l
    yplanning.
    Coronary Artery Disease ( ACCSAP-9 2016 )

    1. A 19-year-old African-American male college soccer player is referred to see you in clinic for
    screening prior to participation in collegiate athletics. He has a history of childhood asthma, but is
    otherwise healthy and takes no medications. There is no family history of cardiomyopathy,
    coronary artery disease, or sudden cardiac death. His physical examination is normal. He hands you
    an electrocardiogram (ECG) that his primary care physician performed.
    Which of the following findings, if present, would be of most concern?

    a. Left ventricular hypertrophy (LVH) by the limb-lead voltage criteria (R in lead aVL of 13 mm).
    b. 0.5 mm ST depressions in leads I and aVL.
    c. Wenckebach pattern (Mobitz I second-degree atrioventricular [AV] block).
    d. Domed/convex upsloping ST elevation with T-wave inversions in V2-V3.
    e. Right-axis deviation of QRS complex to 105 degrees.
    1. b. 0.5 mm ST depressions in leads I and aVL

    Elite athletes may demonstrate ECG changes that overlap with findings seen with cardiomyopathy.
    Several criteria, including the European Society of Cardiology criteria, Seattle criteria, and recently
    published “refined criteria” aim to distinguish between normal ECG changes seen with athletic
    adaptation versus those that may be associated with increased risk for sudden death. Importantly,
    ECG changes may be more common in athletes of African/Caribbean ancestry. Right-axis deviations
    of the QRS complex up to 115 degrees, type 1 second-degree AV block, and LVH by voltage criteria
    alone (without evidence of axis changes, repolarization changes, atrial enlargement, or increased
    QRS width) can be seen in healthy athletes. In addition, healthy black athletes may have convex ST-
    segment elevation associated with T-wave inversions in leads V1-V4. However, ST-segment
    depression ≥0.5 mm in two or more leads is considered an abnormal finding.
    2. A 74-year-old man with hypertension and hyperlipidemia presents to your office with chest
    discomfort on exertion. Exercise nuclear stress test demonstrates minimal inferior ischemia and
    transient ischemic dilatation, with a left ventricular ejection fraction (LVEF) of 38%. Coronary
    angiography reveals a 60% proximal left anterior descending artery (LAD) stenosis, 90% left
    circumflex stenosis, and 70% mid right coronary artery stenosis. Fractional flow reserve (FFR)
    evaluation of the LAD lesion is 0.72.

    Which of the following is the most appropriate next step in his treatment?

    a. Coronary artery bypass surgery.


    b. Percutaneous coronary intervention (PCI) of the angiographically significant lesions.
    c. LAD PCI and medical management of the remaining coronary artery disease.
    d. Metoprolol and sublingual nitroglycerin.
    e. Increase atorvastatin to 80 mg daily.
    2. a. Coronary artery bypass surgery

    This patient presents with multivessel coronary artery disease on coronary angiography including
    the proximal LAD, based on an FFR <0.8. Regardless of stable anginal symptoms, surgical
    revascularization of severe left main disease or proximal LAD with multivessel disease, in the
    setting of reduced LVEF, has a proven mortality benefit and is recommended. The preferred
    method would be surgical revascularization in the absence of contraindications. Optimal medical
    therapy should be initiated in conjunction with revascularization, not as stand-alone therapy.
    3. A 56-year-old man with a history of hypertension and hyperlipidemia is evaluated for
    symptoms of progressive chest discomfort. He has increasing substernal chest tightness with
    associated shortness of breath when he walks five blocks or climbs two flights of stairs.

    On physical exam, his heart rate is 58 bpm, blood pressure is 132/82 mm Hg, and cardiac
    examination is normal. His current medications include aspirin 81 mg daily, metoprolol 25 mg twice
    daily, and simvastatin 20 mg daily. An exercise nuclear stress test reveals mild inferior ischemia and
    a normal left ventricular ejection fraction. Coronary angiography reveals a 70% stenosis of the mid
    right coronary artery (RCA) and no other obstructive lesions.

    Which of the following is the most appropriate next step in his management?

    a. Fractional flow reserve (FFR) of the RCA.


    b. Isosorbide mononitrate 30 mg daily.
    c. Intravascular ultrasound (IVUS) of the RCA.
    d. Percutaneous coronary intervention (PCI) to the RCA.
    e. Clopidogrel 75 mg daily.
    3. b. Isosorbide mononitrate 30 mg daily.

    This patient has angina with a low-risk stress test, low-risk angiographic findings, and is not on
    optimal medical therapy. Based on the Appropriate Use Criteria guidelines for revascularization,
    this patient should have a trial of optimal medical therapy, which is defined as treatment with at
    least two maximally-tolerated antianginal medications (beta-blockers, calcium channel blockers,
    long-acting nitrates, and ranolazine).

    In this patient, the addition of a second antianginal medication is the most appropriate next step,
    before PCI would be performed. FFR or IVUS is not recommended in the setting of a stress test that
    has already demonstrated ischemia in the territory of the angiographically abnormal lesion.

    Clopidogrel does not have antianginal properties, and there are no data for its use in this scenario.
    4. A 48-year-old man is seen for cardiovascular (CV) risk assessment. He has a history of tobacco
    use, but quit 15 years ago. His father underwent coronary artery bypass grafting at age 47. He is
    active, but does not exercise regularly. He has no other significant health issues. His blood pressure
    is 135/80 mm Hg in both arms, and his exam is unremarkable.

    His 10-year risk of atherosclerotic CV disease (ASCVD) based on the Pooled Cohort Equation is
    7.8%. He states an interest in alternative medicine and prefers supplements over conventional
    medicines. He is concerned about his CV health and would like advice. He tells you that he does not
    like traditional medications and prefers a more natural approach.

    In addition to encouraging lifestyle changes, which of the following should be initiated?

    a. Vitamin D supplementation 2000 international units.


    b. Atorvastatin 40 mg.
    c. Daily multivitamin.
    d. Red yeast rice 1200 mg.
    e. Vitamin E 400 international units and beta-carotene 15 mg.
    4. b. Atorvastatin 40 mg.

    Based on his risk factors, this patient’s 10-year risk of ASCVD based on the Pooled Cohort Equation
    is 7.8%. According to the most recent guidelines, the initiation of a moderate- or high-intensity
    statin is appropriate. Supplements such as red yeast rice contain varying amounts of monacolin K,
    the active ingredient in lovastatin. As with many supplements, they are not well regulated, and
    therefore the amount of active ingredients may vary considerably.

    Although vitamin D deficiency is a significant concern for many Americans, to date, there are no
    data to support its use for prevention of CVD. The Physicians’ Health Study randomized 14,641
    male physicians, the large majority without coronary artery disease, to either multivitamin daily or
    placebo. No benefit was seen with taking multivitamins. The U.S. Preventive Services Task Force
    has recommended against use of vitamin E and beta-carotene for CV prevention.
    5. A 50-year-old man presents to the emergency department with an acute inferior myocardial
    infarction. A drug-eluting stent is placed in the mid right coronary artery, and he recovers well. The
    patient remarks, "I just had a stress test last week and passed with flying colors. How can I have
    had a heart attack?" You explain that atherosclerotic plaques may be too small to induce ischemia
    on stress testing, but may be vulnerable to rupture and result in acute thrombotic arterial
    occlusion.

    Which of the following features is such vulnerable plaques most likely to have?

    a. Increased smooth muscle proliferation.


    b. Reduced inflammatory markers.
    c. Large lipid-filled cores.
    d. Thick overlying fibrous caps.
    e. Low macrophage content.
    5. c. Large lipid-filled cores.

    Vulnerable plaques are most often plaques with lipid-rich cores, evidence of inflammation, and thin
    fibrous caps. Therefore, an exercise stress test may not predict the presence of such a plaque,
    because they are not necessarily flow limiting. These plaques typically have a high macrophage
    content relative to smooth muscle cells.
    6. A 55-year-old man who is a smoker but otherwise healthy presents to the emergency
    department with several hours of stuttering chest and left arm pain. He is on no medications at
    home but took an aspirin before he came to the emergency department, and his pain was
    somewhat reduced by the time of arrival. His blood pressure is 135/87 mm Hg and heart rate is 90
    bpm. Physical examination is otherwise normal. His electrocardiogram shows T-wave inversions
    and 1 mm ST depressions in the inferior and lateral precordial leads. His point of care troponin is
    elevated. He is initially treated with oxygen, metoprolol, and intravenous nitroglycerin and started
    on systemic anticoagulation.

    Which of the following physiologic components of this patient's acute coronary syndrome explains
    why the aspirin has helped improve his pain?

    a. Inhibition of thrombin.
    b. Inhibition of antithrombin III.
    c. Inhibition of the cyclooxygenase-1 enzyme.
    d. Inhibition of the P2Y12 receptor.
    e. Inhibition of glycoprotein IIb/IIIa interaction with fibrinogen.
    6. c. Inhibition of the cyclooxygenase-1 enzyme.

    Aspirin inhibits platelet activation by irreversibly targeting the cyclooxygenase-1 enzyme.


    Clopidogrel, prasugrel, and ticagrelor target the P2Y12 adenosine diphosphate receptor.
    Glycoprotein IIb/IIIa inhibitors include eptifibatide, abciximab, and tirofiban. Bivalirudin is the only
    intravenous direct thrombin inhibitor used in the treatment of acute coronary syndrome. Heparins
    inhibit the activity of antithrombin III.
    7. The critical step in platelet aggregation involves which of the following receptors?

    a. Glycoprotein Ib/IX.
    b. Thrombin.
    c. Glycoprotein IIb/IIIa.
    d. Inositol trisphosphate 3.
    e. Actin.
    7. c. Glycoprotein IIb/IIIa.

    Platelets have four major functions: adherence, activation, aggregation, and interaction with
    coagulation factors. Platelet activation occurs when platelets are exposed to soluble factors such as
    adenosine diphosphate or thrombin at the site of vascular injury. This initiates a shape change in
    the platelet, and multiple filopodial projections are formed by rearrangements in the cytoskeleton.
    These cytoskeletal changes open the extracellular side of the glycoprotein (GP) IIb/IIIa receptor and
    allow it to bind to fibrinogen. The binding of fibrinogen allows connections between platelets and is
    critical for platelet aggregation. Therefore, the receptor critical to platelet aggregation is the GP
    IIb/IIIa receptor.

    GP Ib/IX is cleaved during the process of platelet activation, but does not have a role in
    aggregation. Inositol trisphosphate 3 receptors are involved in the calcium signaling required for
    activation, but do not have a role in aggregation. Thrombin is responsible for initiation of platelet
    activation, and its receptor on the platelet surface is protease-activated receptor 1. Actin is a
    cytoskeletal protein.
    8. A 59-year-old woman presents to the emergency department with a 3-month history of
    exertional chest pain. Her physical exam is unremarkable. Her resting electrocardiogram (ECG) and
    cardiac biomarkers are normal. She experiences chest pain during a stress test with associated ST-
    segment depression. However, perfusion imaging is normal. Subsequent coronary angiography
    demonstrates mild luminal irregularities.

    Which of the following is the most likely explanation for her chest pain?

    a. Hypertrophic cardiomyopathy.
    b. Noncardiac chest pain.
    c. Coronary microvascular dysfunction.
    d. Coronary vasospasm.
    e. Atherosclerotic coronary artery disease (CAD).
    8. c. Coronary microvascular dysfunction.

    Coronary microvascular dysfunction is diagnosed based on the findings of typical anginal symptoms
    and noncritical epicardial CAD usually associated with abnormal exercise treadmill stress testing.
    Women with normal or near normal coronary arteries with evidence of ischemia and angina have
    an overall higher risk of adverse cardiovascular events compared with patients without angina and
    without CAD. The prognosis of this patient would not be expected to be better than patients
    without cardiovascular disease. In general, patients with angina and fixed obstructive CAD have a
    worse outcome than patients with angina and without fixed obstructive CAD.

    Vasospasm is typically diagnosed with ST-segment elevation at the time of symptoms, but stress
    testing is not sensitive for the diagnosis. Hypertrophic cardiomyopathy can cause chest pain, but
    would be expected to be associated with ECG changes, as well as physical exam findings suggestive
    of outflow obstruction. Atherosclerotic CAD is unlikely to be an adequate explanation, based on the
    findings described on her angiogram.
    9. A 53-year-old woman with hypertension, hyperlipidemia, diabetes, and smoking history has
    progressively worsening exertional jaw discomfort for the past 6 months. She is generally
    sedentary, has not seen a physician in many years, and is presently taking aspirin and atorvastatin
    80 mg daily for medications. Blood pressure in the office is 145/78 mm Hg and pulse is 82 bpm. Her
    low-density lipoprotein (LDL) returned at 137 mg/dl and her glycated hemoglobin is 7.5%.

    She was referred for a pharmacologic myocardial perfusion imaging scan (MPS), which showed a
    reversible defect in the mid to distal anterior wall. Coronary angiography shows diffuse plaque in
    the mid right coronary artery with only 20% narrowing and serial 20-30% lesions in the mid left
    anterior descending artery (LAD).

    Which of the following is the next most appropriate step in the patient's management, in addition
    to aggressive risk factor modification and medical therapy with a beta-blocker, angiotensin-
    converting enzyme inhibitor, and statin?

    a. Percutaneous coronary intervention (PCI) of the LAD.


    b. Isosorbide mononitrate.
    c. Ranolazine.
    d. Extracorporeal counterpulsation.
    e. Fractional flow reserve (FFR).
    9. b. Isosorbide mononitrate.

    The prognosis for patients with coronary microvascular dysfunction is not benign and may be
    similar to selected age- and sex-matched patients with epicardial coronary artery obstructive
    disease. This finding of no obstructive disease should not lead to complacency relative to
    management. The first line of management should be risk factor modification beginning with
    lifestyle modification. The patient should be encouraged to increase her daily activities, and if
    possible, begin a regular exercise program like walking. She should also understand that if angina is
    induced with light exercise, such as walking, it is not dangerous and titration of isosorbide
    mononitrate may permit her to walk comfortably without angina. The goal is to work toward the
    American Heart Association recommended 10,000 steps per day, achieve excellent blood pressure
    control (<120/90 mm Hg), LDL-lowering, and optimal management of glycemia.

    PCI of a nonobstructive lesion will not result in symptom relief. However, her MPS defect and serial
    stenoses are colocalized to the same coronary distribution, and serial stenoses in the 30% diameter
    range could contribute to important obstruction. Thus, if her symptoms persist, FFR would be
    helpful to assess the functional significance of the serial stenoses. If these lesions are confirmed to
    be truly nonobstructive, coronary flow reserve measurements would be useful to assess for
    coronary microvascular dysfunction. Ranolazine and extracorporeal counterpulsation should not be
    the first line of management.
    10. A 49-year-old woman with a history of diabetes and hypertension, and a family history of
    coronary artery disease (CAD) presents to her physician with the chief complaint of chest pain and
    heaviness that occurs with exertion and infrequently at rest. Her symptoms have been persistent
    for nearly a year. She initially attributed her symptoms to acid reflux.

    She is referred for an exercise treadmill test. Her body mass index is 30 kg/m2. She is able to
    exercise for 8 metabolic equivalents (METs) on a standard Bruce protocol, but exercise is limited by
    her typical angina. Her electrocardiogram shows 3-4 mm ST-downsloping segment depressions in
    the lateral leads. She is referred for coronary angiography that shows no obstructive CAD and no
    luminal irregularities.

    Which of the following is the most appropriate next best step in the patient's management?

    a. Esophagogastroduodenoscopy (EGD).
    b. Intravascular ultrasound (IVUS).
    c. Ergonovine challenge.
    d. Coronary flow reserve measurement.
    e. Assess response to empiric antispasm medication.
    10. d. Coronary flow reserve measurement.

    This patient has multiple cardiovascular risk factors and evidence of ischemia on stress testing. She
    has no obstructive CAD on coronary angiography. The most likely diagnosis is coronary
    microvascular dysfunction (CMD). The exact mechanism of CMD is not entirely clear. From a
    pathophysiological view, CMD as reduced coronary flow reserve (CFR) most often results from a
    combination of different alterations, such as impaired vasodilation, enhanced vasoconstrictor
    responsiveness, and/or structural remodeling of the coronary microvasculature. CMD can cause
    abnormalities in stress testing indicative of ischemia without obstructive epicardial CAD.

    CFR measurement either invasively (intracoronary Doppler catheter) or noninvasively (positon


    emission tomography, cardiac magnetic resonance imaging, or transthoracic Doppler), can be very
    helpful in determining if CMD is present. There is no role for IVUS in this setting, nor does
    "prophylactic" stenting of borderline plaques improve outcomes and may be harmful. Coronary
    spasm is not the likely etiology in this case, particularly given the appearance of smooth coronaries
    on angiography and lack of prominent component of her symptoms occurring at rest. Nevertheless,
    testing with intracoronary acetylcholine would exclude spasm with a high degree of certainty and
    perhaps avoid need to expose her to multiple calcium antagonists and nitrates.
    11. A 90-year-old man with hypertension and hyperlipidemia had previously enjoyed a good
    quality of life without symptoms secondary to cardiovascular disease. However, over the last 3
    months, he has noted the progressive onset of symptoms consistent with exertional angina. He
    generally enjoys taking walks around a pond near his home. However, he now notes that after 100
    yards, he develops heaviness in the center of his chest that resolves with rest. He was started on a
    beta-blocker, aspirin, and a statin, but continues to have lifestyle-limiting angina.

    He is referred for an exercise tolerance test, where he is able to perform 5 METs of exercise prior to
    developing limiting angina and 3 mm ST depressions in the lateral leads. He is referred for cardiac
    catheterization, where he is found to have a 90% focal lesion in the mid left anterior descending
    artery (LAD), a 50% lesion in the first obtuse marginal artery (OM1), and a focal 99% stenosis of the
    right coronary artery (RCA) with collaterals to the distal RCA from the LAD.

    Which of the following is the most appropriate next step for this patient?

    a. Medical therapy.
    b. Hybrid CABG/percutaneous coronary intervention (PCI).
    c. Referral for coronary artery bypass grafting (CABG).
    d. PCI of the RCA and LAD.
    e. PCI of the RCA, OM, and LAD.
    11. d. PCI of the RCA and LAD.

    The patient's age is not a limitation to revascularization. With advancements in both surgical and
    interventional techniques, the safety of revascularization procedures has improved over time and
    the elderly have as much to gain by revascularization as the nonelderly. This patient has a low
    SYNTAX score, which would suggest that the outcomes of multivessel PCI are comparable with
    CABG in terms of death and myocardial infarction out to 5 years.

    PCI likely offers a reduced risk of stroke. Therefore, PCI is the preferred revascularization strategy
    for this patient given that it is less invasive. Fractional flow reserve of the OM lesion may be
    reasonable to show that the lesion is not hemodynamically significant. At this time, there are no
    definitive outcome data to support routine use of hybrid revascularization procedures.
    12. A 57-year-old man with hypertension, tobacco use, and diabetes presents with 3 weeks of
    exertional chest tightness. An exercise treadmill stress test is notable for reproducible chest
    discomfort associated with 2 mm inferolateral ST-segment depressions and ST-segment elevation
    in lead aVR.

    He is started on aspirin, simvastatin, and metoprolol and referred for cardiac catheterization, which
    demonstrates a right-dominant system with focal 90% proximal left anterior descending artery
    (LAD), 80% mid left circumflex, and 80% mid right coronary artery stenoses. You discuss with him
    the options of surgical versus percutaneous revascularization.

    Which of the following outcomes is associated with surgical revascularization in this patient?

    a. Decreased bleeding risk.


    b. Increased need for repeat revascularization.
    c. Decreased stroke risk.
    d. Improved ejection fraction.
    e. Improved survival.
    12. e. Improved survival.

    In patients with diabetes and significant left main coronary artery disease (=50%) or severe
    coronary artery disease (=70%) in three major coronary arteries or involving the proximal LAD plus
    one other coronary artery, coronary artery bypass grafting is the recommended revascularization
    strategy and has been shown to improve survival. In contrast, while percutaneous coronary
    intervention (PCI) may improve anginal symptoms in patients with stable ischemic heart disease, no
    studies to date have demonstrated that PCI confers a survival advantage without recent acute
    coronary syndrome. Stroke risk is increased in CABG versus PCI.
    13. A 52-year-old man with hypertension and hyperlipidemia is referred for cardiac stress testing
    due to atypical chest pain and recently declining exercise tolerance. He completes 7 minutes of a
    standard Bruce protocol and stops due to fatigue and chest burning. Perfusion imaging reveals a
    moderately severe, reversible apical defect. He is started on aspirin 81 mg daily, simvastatin 20 mg
    daily, metoprolol 25 mg daily, and amlodipine 5 mg daily, but his symptoms persist. He is referred
    for cardiac catheterization, which reveals a 70% mid left anterior descending artery stenosis
    treated successfully with percutaneous coronary intervention (PCI).

    Which of the following best describes the long-term outcomes of PCI versus coronary artery bypass
    grafting (CABG) in this patient?

    a. No difference.
    b. Decreased mortality with PCI.
    c. Improved left ventricular ejection fraction with CABG.
    d. Decreased target vessel revascularization with PCI.
    e. Increased recurrent myocardial infarction (MI) with CABG.
    13. a. No difference.

    More than 20 randomized controlled trials have compared CABG with balloon angioplasty or
    stenting in patients with single-vessel coronary artery disease, demonstrating similar outcomes
    regarding survival and recurrent MI. CABG has a significantly higher rate of stroke, but lower repeat
    revascularization rate compared with PCI. In this patient with one significant stenosis amenable to
    revascularization and unacceptable angina despite guideline-directed medical therapy, PCI or CABG
    are both beneficial to improve anginal symptoms.
    14. A 62-year-old man with a history of smoking, hypercholesterolemia, and obesity is being
    evaluated for progressive dyspnea on exertion. He denies chest pain, orthopnea, or peripheral
    edema. An echocardiogram demonstrates left ventricular ejection fraction (EF) of 35% with global
    hypokinesis and no significant valvular dysfunction. Coronary angiography reveals significant three-
    vessel coronary artery disease (CAD) with an occluded but well-collateralized dominant right
    coronary artery, and calculated SYNTAX score of 35.

    Which of the following is the most appropriate next step?

    a. Hybrid CABG/PCI.
    b. Implantable cardioverter-defibrillator (ICD).
    c. Coronary artery bypass grafting (CABG).
    d. Medical therapy alone.
    e. Multivessel percutaneous coronary intervention (PCI).
    14. c. Coronary artery bypass grafting (CABG).

    The SYNTAX trial randomized 1,800 patients with left main or three-vessel CAD to revascularization
    with drug-eluting stents or CABG. Overall, at 3 years, major adverse cardiac events were lower for
    CABG over PCI (20.2% vs. 28.0%), driven by decreased recurrent myocardial infarction and repeat
    revascularization in the CABG arm.

    In a post hoc analysis, an angiographic SYNTAX score was derived for each patient as a surrogate
    measure of the CAD complexity, based on the location, severity, and extent of CAD (low SYNTAX
    score, 22; intermediate, 23-32; and high, 33). While patients with a low SYNTAX score had similar
    outcomes with PCI or CABG, those with intermediate and high SYNTAX scores treated with CABG
    exhibited lower mortality at 3 years compared with PCI, with significantly decreased target vessel
    revascularization.

    In summary, the SYNTAX results suggest that PCI or CABG is comparable in less complex disease,
    while in patients with more complex disease, CABG is the preferred revascularization strategy.
    There are no data as of yet to support use of hybrid CABG/PCI. Medical therapy alone is not
    sufficient in the setting of reduced EF. ICD is warranted only if EF remains <35% at 3 months after
    revascularization.
    15. An 82-year-old man with a history of coronary artery disease (CAD) status/post percutaneous
    coronary intervention (PCI) to the left anterior descending artery (LAD) 10 years ago, chronic
    obstructive pulmonary disease, obesity, and chronic kidney disease develops progressive angina on
    exertion. He has been managed successfully for many years on a combination of aspirin,
    atorvastatin, and atenolol. Echocardiography reveals preserved left ventricular function.

    He is referred for coronary angiography, which demonstrates 60% ostial left main coronary
    stenosis, a widely patent LAD stent with diffuse luminal irregularities, no significant left circumflex
    disease, and focal 70% mid-right coronary artery stenosis.

    Which of the following is the next best step in this patient's management?

    a. Heart Team evaluation.


    b. Multivessel PCI.
    c. Medical therapy alone.
    d. Coronary artery bypass grafting (CABG).
    e. PCI to the left main coronary artery.
    15. a. Heart Team evaluation.

    The current stable ischemic heart disease guideline recommends that patients with significant left
    main or complex multivessel CAD be evaluated by a multidisciplinary Heart Team to determine the
    most appropriate method of revascularization. This strategy mimics typical protocols used in
    clinical trials, where a Heart Team, composed of an interventional cardiologist and cardiac surgeon,
    review all available patient data and discuss potential treatment options with the patient.
    Calculation of the Society of Thoracic Surgeons (STS) and SYNTAX scores assist in determining the
    surgical risk category and complexity of CAD.

    While PCI may be a reasonable strategy in patients with amenable coronary anatomy, high surgical
    risk, or other considerations, in general, ad hoc PCI immediately following diagnostic coronary
    angiography is discouraged in patients with complex multivessel CAD.

    Although escalation of medical therapy may improve angina, if the patient is a candidate for
    revascularization, a Heart Team evaluation would be beneficial.
    16. A 65-year-old man with diabetes controlled with medications comes to you for evaluation of
    exertional chest pain. He has been appropriately managed for chronic stable angina with beta-
    blockers, statin, nitrates, and aspirin.

    The patient is able to exercise 7 minutes on a Bruce protocol, his classic chest pain recurs at stage
    3, and there are 2 mm ST depressions in the anterolateral leads with reversible perfusion defects
    anteriorly. His left ventricular ejection fraction (LVEF) is 50%. Cardiac catheterization reveals 90%
    promimal left anterior descending artery (LAD), 70% first obtuse marginal, 80% mid left circumflex,
    and 90% mid right coronary artery stenoses.
    Which of the following is the next best step in the management of this patient?
    a. Ranolazine extended-release 500 mg PO daily.
    b. Coronary artery bypass grafting (CABG) revascularization.
    c. LAD PCI revascularization only.
    d. Increase metoprolol.
    e. Multivessel percutaneous coronary intervention (PCI) revascularization.
    16. b. Coronary artery bypass grafting (CABG) revascularization.

    This patient has diabetes, severe multivessel coronary artery disease (CAD), and a reduced LVEF. He
    should undergo complete revascularization with CABG.

    Recently, results from the FREEDOM trial in patients with diabetes and multivessel CAD treated
    with CABG had a significantly lower composite rate of death from any cause, nonfatal myocardial
    infarction, or nonfatal stroke when compared with diabetic patients treated with PCI.

    An analysis performed in 2009 of data in 7,812 patients (1,233 with diabetes) in 10 randomized
    clinical trials demonstrated a worse long-term survival rate in patients with diabetes after balloon
    angioplasty or bare-metal stent implantation than after CABG.
    The BARI 2D trial randomly assigned 2,368 patients with type 2 diabetes and CAD to undergo
    intensive medical therapy or prompt revascularization with PCI or CABG, according to whichever
    was thought to be more appropriate. By study design, those with less extensive CAD more often
    received PCI, whereas those with more extensive CAD were more likely to be treated with CABG.
    The study was not designed to compare PCI with CABG. At 5-year follow-up, no difference in rates
    of survival or major adverse cardiac events (MACE) between the medical therapy group and those
    treated with revascularization was noted. In the PCI stratum, no significant difference in MACE
    between medical therapy and revascularization was demonstrated (drug-eluting stent in 35%;
    bare-metal stent in 56%); in the CABG stratum, MACE occurred less often in the revascularization
    group.
    17. A 73-year-old morbidly obese woman with insulin-dependent diabetes, dyslipidemia, and
    severe ambulatory dysfunction is sent to you for preoperative assessment before total knee
    replacement. She has chronic kidney disease with a creatinine of 2.1 mg/dl. Her heart rate is 80
    bpm, blood pressure is 150/80 mm Hg, and respiratory rate is 20 breaths/minute. She has no
    evidence of heart failure.

    Her electrocardiogram (ECG) reveals sinus rhythm with inferior Q waves noted. The patient's
    echocardiogram is normal. She is on insulin, losartan 100 mg PO daily, and atorvastatin 40 mg PO
    daily.
    Which of the following is the next best step in the preoperative cardiac risk assessment for this
    patient?
    a. Pharmacologic nuclear stress test.
    b. Coronary computed tomographic angiography.
    c. Cardiac catheterization.
    d. No further cardiac evaluation is necessary.
    e. Exercise ECG stress test.
    17. a. Pharmacologic nuclear stress test.

    This patient has several risk factors for coronary artery disease. While knee replacement is not a
    high-risk surgery compared with vascular surgery and head and neck surgery, this patient has
    several concerning clinical features, including an abnormal resting ECG, increased creatinine, insulin
    therapy, uncontrolled blood pressure, and unclear functional capacity.

    Multivariate risk indices such as the revised cardiac risk index (RCRI) and 2014 American College of
    Cardiology (ACC)/American Heart Association (AHA) perioperative cardiovascular evaluation
    guideline can be applied to determinate the major adverse cardiac event (MACE) risks. Her RCRI
    risk is 11% for MACE (includes possible myocardial infarction, insulin use, and creatinine >2.0
    mg/dl).

    According to the ACC/AHA 2014 guideline for perioperative cardiovascular evaluation for
    noncardiac surgery, this is a Class IIa indication:

    "It is reasonable for patients who are at an elevated risk for noncardiac surgery and have poor
    functional capacity (<4 METs) to undergo noninvasive pharmacological stress testing (either
    dobutamine stress echocardiogram or pharmacological stress perfusion imaging) if it will change
    management. (Level of Evidence: B)"

    Figure 1 outlines the ACC/AHA perioperative guideline. A pharmacologic stress test is appropriate
    in someone who cannot exercise.
    (Figure 1)
    18. A 55-year-old man comes to you for preoperative cardiovascular risk stratification for inguinal
    hernia repair. The patient has hypertension and takes atenolol 25 mg PO daily. He has a strong
    history of smoking 30 pack-years and has not had his lipid profile evaluated for 2 years. He has a
    family history of coronary artery disease; his father had a myocardial infarction at 53 years of age.
    The patient notices pain and discomfort in the groin area while walking. However, he is able to
    walk up a hill and mow the lawn.

    On examination, heart rate is 53 bpm, blood pressure is 120/83 mm Hg, and respiratory rate is 15
    breaths/minute. His electrocardiogram shows sinus rhythm at 54 bpm with an incomplete right
    bundle branch block.

    Based on these findings, which of the following is your next best step in evaluating this patient?

    a. Transthoracic echocardiogram.
    b. Exercise treadmill stress testing.
    c. Proceed with surgery.
    d. Dobutamine stress echocardiography.
    e. Coronary computed tomography angiography.
    18. c. Proceed with surgery.

    Functional status is a reliable predictor of perioperative and long-term cardiac events. Patients with
    reduced functional status preoperatively are at increased risk of complications. Conversely, those
    with good functional status preoperatively are at lower risk. Moreover, in highly functional
    asymptomatic patients, it is often appropriate to proceed with planned surgery without further
    cardiovascular testing, as outlined in the 2014 perioperative cardiovascular evaluation guideline
    (Figure 1).
    19. A 63-year-old woman comes to your office for preoperative clearance for a hysterectomy. The
    patient has been complaining of dysfunctional uterine bleeding and was found to have multiple
    uterine fibriods that have not improved with embolization. She has history of insulin-dependent
    diabetes, hypertension, and chronic kidney disease (stage 3). Her medications include lisinopril 40
    mg daily, ferrous sulfate, and insulin. She can do her activities of daily living, but becomes short of
    breath climbing a flight of stairs.

    On exam, her heart rate is 88 bpm and blood pressure is 133/83 mm Hg, respiration rate is 15
    breaths/minute, and conjunctiva are pale. Cardiovascular examination reveals soft systolic flow
    murmur in the left sternal border. There are no rales or rhonchi and no pedal edema.

    An electrocardiogram in your office shows sinus rhythm with left bundle branch block (LBBB). Her
    most recent labs include glycated hemoglobin of 8.9%, hemoglobin of 9.0 mg/dl, and creatinine of
    2 mg/dl.
    Which of the following is the next best step in her management?
    a. Pharmacologic nuclear stress test.
    b. Exercise treadmill stress test.
    c. Proceed with surgery.
    d. Dobutamine stress echo.
    e. Start beta-blockers.
    19. c. Proceed with surgery.

    This patient has several cardiovascular risk factors and evidence of an LBBB. She can, however,
    climb a flight of stairs, and thus has a functional capacity >4 METs. She does not require stress
    testing prior to undergoing medically necessary surgery.

    Functional status is a reliable predictor of perioperative and long-term cardiac events. Patients with
    reduced functional status preoperatively are at increased risk of complications. Conversely, those
    with good functional status preoperatively are at lower risk. Moreover, in highly functional
    asymptomatic patients, it is often appropriate to proceed with planned surgery without further
    cardiovascular testing.

    If a patient has not had a recent exercise test before noncardiac surgery, functional status can
    usually be estimated from activities of daily living. Functional capacity is often expressed in terms
    of METs, where 1 MET is the resting or basal oxygen consumption of a 40-year-old man who weighs
    70 kg. In the perioperative literature, functional capacity is classified as excellent (>10 METs), good
    (7-10 METs), moderate (4-6 METs), poor (<4 METs), or unknown.
    Perioperative cardiac and long-term risks are increased in patients unable to perform 4 METs of
    work during daily activities. Examples of activities associated with <4 METs are slow ballroom
    dancing, golfing with a cart, playing a musical instrument, and walking at approximately 2-3 mph.
    Examples of activities associated with >4 METs are climbing a flight of stairs or walking up a hill,
    walking on level ground at 4 mph, and performing heavy work around the house.
    20. A 65-year-old man with intermittent bilateral lower-extremity claudication, hypertension, and
    diabetes presents to your office for assessment prior to planned femoral-popliteal bypass surgery.
    He denies chest pain, but is significantly limited by his claudication and cannot walk more than a
    block without stopping. A pharmacologic stress test reveals a large area of ischemia in the anterior
    wall; left ventricular ejection fraction is 40%. Coronary angiography reveals three-vessel coronary
    artery disease.
    Which of the following is the most appropriate next step in his management?
    a. Maximize medical therapy and proceed with vascular surgery.
    b. Multivessel percutaneous coronary intervention (PCI) with drug-eluting stents.
    c. Maximize medical therapy and cancel surgery.
    d. Multivessel PCI with bare-metal stents.
    e. Coronary artery bypass grafting.
    20. e. Coronary artery bypass grafting.

    This patient has significant ischemic disease, reduced left ventricular function, and diabetes.
    Assessment of his functional status is limited by his significant claudication, but he has a high-risk
    nuclear perfusion scan and multivessel coronary artery disease. Regardless of the plans for elective
    surgery, revascularization of his coronary artery disease is indicated.

    Coronary artery bypass grafting is preferable to PCI in light of his diabetes, as shown in the
    FREEDOM trial.
    21. A 60-year-old woman with hypertension presents to the emergency room with chest pain.
    She describes acute onset of chest pain radiating to her back associated with leg weakness and
    presyncope. Blood pressure is 162/100 mm Hg, pulse is 100 bpm, and respiratory rate is 20
    breaths/minute. Cardiac exam reveals an S4 gallop with no murmur. She has no known drug
    allergies. Her electrocardiogram (ECG) is shown in Figure 1.
    Which of the following is the most appropriate next step?
    a. Coronary angiography.
    b. Chest computed tomography angiography (CTA).
    c. Transthoracic echocardiogram.
    d. Thrombolytics.
    e. Chest X-ray.
    21. b. Chest computed tomography angiography (CTA).

    The patient's symptoms of chest pain radiating to the back and weakness of the lower extremities
    are classic for aortic dissection, in this case complicated by extension of the dissection into the
    ostium right coronary artery, as evidenced by the inferior injury current on the ECG, which may be
    present in 7% of dissections. This combination may lead to misdiagnosis and delayed therapy.
    Because the symptoms are so suggestive of dissection, emergent CTA of the chest or
    transesophageal echocardiography imaging of the aorta and cardiac surgical consultation for the
    life-threatening dissection is more appropriate than CTA (see management algorithm in Figure 2).
    Chest X-ray may show a widened mediastinum, which is not very sensitive or specific and would
    not provide enough information to proceed with surgery. Thrombolytic therapy would be
    contraindicated, with the patient's symptoms the central factor in making the correct diagnosis.
    22. Which of the following patients most likely has a myocardial infarction (MI), according to the
    Third Universal Definition of MI?
    a. A 48-year-old woman with 2 weeks of chest pain, palpitations, progressive dyspnea, and volume
    overload. Echocardiogram reveals diffuse hypokinesis with left ventricular ejection fraction of 25%.
    Endomyocardial biopsy shows diffuse necrosis, multinucleated cells, and lymphocytic and
    eosinophilic infiltrates.

    b. A 38-year-old obese man with 10-year tobacco history, recent upper respiratory symptoms, 2 days of
    pleuritic chest pain, and diffuse ST elevations; troponin values are 0.10, 0.11, and 0.09.

    c. A 56-year-old male unrestrained driver with hypertension after a motor vehicle accident and steering
    wheel trauma to the chest. His echocardiogram shows anterior wall hypokinesis.

    d. A 61-year-old woman with noninsulin-dependent diabetes, obesity, and sleep apnea presents with
    new-onset atrial fibrillation, heart rate 130 bpm, and ST depressions in leads II, III, and aVF.

    e. A 68-year-old woman with hypertension, diabetes, and end-stage renal disease presents with
    shortness of breath after missing two hemodialysis sessions. Serial troponin values are 0.05, 0.04,
    0.06, and 0.03. Her electrocardiogram shows left ventricular hypertrophy, but no ST/T wave changes.
    22. d.A 61-year-old woman with noninsulin-dependent diabetes, obesity, and sleep apnea
    presents with new-onset atrial fibrillation, heart rate 130 bpm, and ST depressions in
    leads II, III, and aVF.

    The Third Universal Definition of MI requires elevation in cardiac troponins, with a rise and/or fall
    in levels over serial measurement, together with symptoms or signs of cardiac ischemia. These may
    include new significant ST-segment T-wave changes, new left bundle branch block, new pathologic
    Q waves, imaging evidence of new regional wall motion abnormalities or new loss of viable
    myocardium, or intracoronary thrombus demonstrated by angiography or autopsy. Many
    conditions other than cardiac ischemia may lead to elevation in troponins. Moreover, MI may be
    due either to plaque rupture (type 1 MI) or due to supply-demand mismatch, with or without
    underlying coronary artery disease (type 2 MI).

    The patient presenting with atrial fibrillation and rapid ventricular response with
    electrocardiographic evidence of ischemia most likely has a type 2 MI. The other clinical scenarios
    most likely represent giant cell myocarditis, myopericarditis, troponin elevation without clear rise
    and fall in the setting of renal disease, and myocardial injury due to contusion. If no active ischemia
    is suspected, then these would not be considered instances of MI, according to the Third Universal
    Definition of MI. Troponin elevations due to defibrillation shocks, receipt of cardiotoxic
    chemotherapeutic agents, and rhabdomyolysis with cardiac involvement are other examples where
    myocardial injury occurs apart from ischemia and which would not be considered MI.
    (Figure 2)
    23. A 53-year-old man presents to the emergency room with 1 hour of chest pain. Current vital
    signs are pulse 122 bpm and irregular, blood pressure 178/102 mm Hg, respiratory rate 18
    breaths/minute, Saturation of peripheral oxygen is 98% on room air. The neck veins are flat. The
    lungs are clear and there is no murmur or gallop.

    His electrocardiogram reveals atrial fibrillation with rapid ventricular response and 1 mm ST-
    elevations in leads I and aVL.
    Which of the following is most appropriate to manage his atrial fibrillation?
    a. Oral or intravenous metoprolol.
    b. Intravenous diltiazem.
    c. Intravenous ibutilide.
    d. Sublingual nifedipine.
    e. Oral amiodarone.
    23. a. Oral or intravenous metoprolol.

    In the setting of ST-segment elevation myocardial infarction (STEMI), beta-blockers are the
    preferred rate control agent for atrial fibrillation. Routine use of intravenous beta-blockers for
    STEMI is not recommended, but it may be used in a hypertensive urgency or tachyarrhythmia in
    the absence of other contraindications. Oral beta-blockade within 24 hours of presentation
    remains a Class I indication in STEMI. Calcium channel blockers have no demonstrated benefit in
    STEMI, although they could be considered for rate control in atrial fibrillation, but not if systolic
    dysfunction is present.

    Short-acting nifedipine for hypertension is harmful because of the potential for hypotension and
    reflex tachycardia. Oral amiodarone would not be useful acutely in this setting. Ibutilide would be
    inappropriate, as this patient has no indication for emergent cardioversion and the duration of
    atrial fibrillation is unknown.
    24. A 58-year-old woman with rheumatoid arthritis presents with 1 week of intermittent nausea
    and exertional chest pressure and 30 minutes of constant intense chest pressure. Her
    electrocardiogram is notable for up to 2.5 mm ST elevations in leads I, aVL, and V5-V6. She is found
    to have occlusion of a large second obtuse marginal coronary artery branch and undergoes drug-
    eluting stent placement. Follow-up testing shows normal cardiac function and hemoglobin A1c of
    5.3%.
    Which of the following is most likely to be beneficial for chronic outpatient therapy for this patient?
    a. Isosorbide mononitrate 30 mg daily.
    b. Verapamil sustained release 180 mg daily.
    c. Metoprolol succinate 50 mg daily.
    d. Enalapril 10 mg bid.
    e. Spironolactone 25 mg daily.
    24. c. Metoprolol succinate 50 mg daily.

    Beta-blockers have a Class I indication for continuation during and after hospitalization for all
    patients with ST-segment elevation myocardial infarction (STEMI) in the absence of
    contraindications. Certain conditions warrant caution or avoidance of beta-blocker therapy:
    decompensated heart failure, low-output states, high risk of cardiogenic shock, reactive airways
    disease or active bronchospasm, and prolonged first-degree or high-grade atrioventricular block.

    Angiotensin-converting enzyme (ACE) inhibitors have a Class I indication for use in patients with
    STEMI with anterior involvement, heart failure, and left ventricular ejection fraction (LVEF) ≤40% in
    the absence of contraindications. Angiotensin-receptor blockers may be used for patients who are
    intolerant of ACE inhibitors.

    For patients such as this one, who do not have anterior involvement, heart failure, or low EF, ACE
    inhibitors have a Class IIa indication. Aldosterone antagonists should be used (Class I indication) in
    patients with STEMI and no contraindications who are already receiving an ACE inhibitor and beta-
    blocker and who have LVEF ≤40% AND either symptomatic heart failure or diabetes. This patient
    would not meet these criteria.

    Nitrates are not indicated for routine use after STEMI. Calcium channel blockers have not been
    shown to reduce infarct size or rate of reinfarction, but may be helpful in the treatment of
    ischemia, hypertension, or rapid ventricular rate in patients with atrial fibrillation who are
    intolerant of beta-blockers.
    25. A 53-year-old man with diabetes is admitted with an acute inferoposterior ST-segment
    elevation myocardial infarction (STEMI). He undergoes primary percutaneous coronary
    intervention with placement of a drug-eluting stent to the proximal left circumflex artery. He has
    single-vessel disease, left ventricular end-diastolic pressure of 14 mm Hg, and an ejection fraction
    (EF) of 35%.
    According to the 2013 STEMI guideline, which of the following is a Class I indication for initiating an
    angiotensin-converting enzyme (ACE) inhibitor within 24 hours in this patient?
    a. EF of 35%.STEMI.
    b. Culprit lesion location.
    c. Chronic kidney disease.
    d. Diabetes.
    25. a. EF of 35%.

    An ACE inhibitor should be administered within the first 24 hours to all patients with STEMI with an
    anterior location, heart failure, or EF of ≤40%, unless contraindicated (Class I, Level of Evidence A).
    Oral ACE inhibitors reduce fatal and nonfatal major cardiovascular events in patients with STEMI.
    The magnitude of clinical benefit is greatest in high-risk patient subgroups. Demonstration of an
    early benefit (within the first 24 hours) supports the prompt use of these agents in patients without
    existing contraindications (e.g., hypotension, shock, bilateral renal artery stenosis, or history of
    worsening of renal function with ACE inhibitor/angiotensin-receptor blocker exposure, renal
    failure, or drug allergy). The role of routine long-term ACE inhibitor therapy in low-risk patients
    after STEMI who have been revascularized and treated with aggressive lipid-lowering therapies is
    less certain.
    26. A 60-year-old woman presents to the office for follow-up after cardiac catheterization. She
    had single-vessel disease with a moderate 50% stenosis and noncritical fractional flow reserve
    (0.84). Her medical history is significant for treated hyperlipidemia. Her blood pressure is 120/60
    mm Hg with a heart rate of 70 bpm, and her exam is normal. She is asymptomatic on aspirin, statin,
    and beta-blocker. She asks about her risk of myocardial infarction.

    Which of the following best correlated with her risk of plaque rupture?
    a. High cholesterol.
    b. Plaque macrophage content.
    c. Plaque calcium content.
    d. It is unpredictable.
    e. Stenosis severity.
    26. b. Plaque macrophage content.

    The conversion of a stable plaque-to-plaque rupture or erosion does not have much to do with the
    stenosis severity. Plaque rupture is predicted by several anatomic and systemic factors, including
    inflammation, integrity of the fibrous cap, plaque lipid content, and plaque location.
    27. A 40-year-old woman presents to the emergency department with chest discomfort. She
    describes sharp chest pain that lasts for less than a minute and occurs at various times during the
    day. Her exam is unremarkable. Her electrocardiogram is normal.
    Which of the following risk scores should be used to best guide management in the emergency
    department?
    a. Duke treadmill score.
    b. Framingham Coronary Heart Disease Risk Score.
    c. HEART (History, Electrocardiogram, Age, Risk factors, and Troponin) score.
    d. GRACE (Global Registry of Acute Coronary Events) score.
    e. TIMI (Thrombolysis in Myocardial Infarction) score.
    27. c. HEART (History, Electrocardiogram, Age, Risk factors, and Troponin) score.

    Risk scores can be used to determine the short-term risk of adverse events in patients with chest
    pain or definite acute coronary syndrome (ACS). The HEART score is a prospectively studied scoring
    system to help emergency departments risk-stratifiy chest pain patients according to risk of major
    adverse cardiac events within 6 weeks. The HEART score includes history, electrocardiogram, age,
    risk factors, and troponin.

    TIMI and GRACE scores are used to estimate risk of death or MI for patients with ACS, and are not
    as useful for patients with chest pain of unclear etiology. The Framingham Coronary Heart Disease
    Risk Score estimates risk of heart attack in 10 years in a stable patient. The Duke treadmill score is
    specific to predicting coronary artery disease in a patient undergoing stress testing.
    28. A 47-year-old woman presents to the emergency department with 2 days of substernal chest
    pressure radiating to the jaw with minimal exertion relieved with rest. The last episode was 1 hour
    prior to presentation and lasted 15 minutes. She has no medical history and takes no medication.
    Her resting electrocardiogram is normal.
    Which of the following is the most accurate biomarker strategy for diagnosing myocardial
    infarction (MI) in this patient?
    a. High-sensitivity troponin at time 0 hours.
    b. Creatine kinase-myocardial isoenzyme (CK-MB) at time 0 and 6 hours.
    c. Cardiac-specific troponin at time 0 and 6 hours.
    d. B-type natriuretic peptide (BNP) after 6 hours of observation.
    e. Myoglobin at the time of presentation (time 0).
    28. c. Cardiac-specific troponin at time 0 and 6 hours.

    Cardiac biomarkers are part of the universal definition of MI. Although the specificity of cardiac-
    specific and high-sensitivity troponin assays are of concern, they are the biomarker of choice in
    patients with suspected acute coronary syndrome (ACS). The current American Heart
    Association/American College of Cardiology guideline recommends that cardiac-specific troponin
    (troponin I or T when a contemporary assay is used) levels should be measured at presentation and
    3-6 hours after symptom onset in all patients who present with symptoms consistent with ACS to
    identify a rising and/or falling pattern (Class I).

    Although high-sensitivity troponin may be positive earlier, a single measure at presentation is not
    sufficient to exclude MI. With contemporary troponin assays, creatine kinase myocardial isoenzyme
    (CK-MB) and myoglobin are not useful for diagnosis of ACS (Class III). Use of selected newer
    biomarkers, especially BNP, may be reasonable to provide additional prognostic information (Class
    IIb), but are not used for the initial diagnosis.
    29. A 68-year-old man presents to the emergency department with two episodes of resting chest
    pressure radiating to the jaw and arm and lasting 15 minutes in the 6 hours prior to presentation.
    His pain resolved without treatment and he is now pain free. His medical history is significant for
    hyperlipidemia, hypertension, and tobacco abuse. His medications include aspirin, diltiazem, and
    atorvastatin. His initial high-sensitivity troponin is negative and his electrocardiogram is normal.
    Which of the following is the most appropriate management for this patient?
    a. Triage to observation unit for serial biomarkers.
    b. Discharge with outpatient stress testing within 48 hours.
    c. Admission for stress testing.
    d. Dual antiplatelet therapy and catheterization within 24 hours.
    e. Initiation of a glycoprotein IIb/IIIa inhibitor.
    29. d. Dual antiplatelet therapy and catheterization within 24 hours.

    Patients with acute coronary syndromes (ACS) can be risk stratified with clinical risk scores
    including the TIMI (Thrombolysis in Myocardial Infarction) and GRACE (Global Registry of Acute
    Coronary Events) scores. Although this patient has no objective ischemia, his TIMI risk score is 4
    (age over 64, severe angina, three cardiac risk factors, and aspirin use), which predicts a 20% risk of
    all-cause mortality, new or recurrent MI, or severe recurrent ischemia requiring urgent
    revascularization at 14 days. Several randomized trials have compared an early invasive strategy
    with a delayed, selective, or conservative strategy in patients with ACS.

    In the TIMACS trial, patients with a GRACE score >140, but not those with a GRACE score <140, had
    a reduction in the ischemic endpoint of death, MI, or stroke. Also in the TIMACS trial, death, MI,
    and rehospitalization from ACS was lower with an invasive strategy in patients with positive
    troponin, ST deviation, or a TIMI risk score >3.

    Upstream glycoprotein inhibitor use does not improve outcomes compared to selective use at the
    time of percutaneous coronary intervention. This patient should not be discharged from the
    emergency room without further cardiovascular evaluation.
    30. A 45-year-old male active smoker with diabetes and hypertension presents to the emergency
    room with chest pain. An urgent electrocardiogram demonstrates 4 ml of ST-segment elevation in
    leads V1-V4. Emergent coronary angiography identifies acute plaque rupture in the ostial left
    anterior descending coronary artery with hazy thrombus and Thrombolysis In Myocardial Infarction
    (TIMI) grade 1 coronary flow. After export thrombectomy, the ruptured plaque is treated with
    direct stenting with a 3.5 ml x 18 ml drug-eluting stent, which is post-dilated at 18 atm.

    Which of the following statements is true about the pathobiology of acute plaque rupture?
    a. The majority of coronary artery atherosclerotic plaque rupture occurs at the middle portion
    of the plaque away from the plaque shoulder because the middle portion of the plaque
    experiences greater tensile force from flowing blood.
    b. Platelets are the major source of the myeloperoxidase enzyme, which generates free radicals
    and increases inflammation in rupture-prone coronary artery atherosclerotic plaques.
    c. Coronary calcium does not participate in the pathobiology of coronary artery atherosclerotic
    plaque rupture, and calcification is rarely present in ruptured plaques.
    d. Branch points at coronary bifurcations experience high shear stress conditions that promote
    coronary artery atherosclerotic plaque inflammation and infiltration of monocytes that
    promote plaque rupture.
    e. Macrophage-derived matrix metalloproteinases degrade the fibrous cap and promote
    coronary artery atherosclerotic plaque rupture.
    30. d. Branch points at coronary bifurcations experience high shear stress conditions
    that promote coronary artery atherosclerotic plaque inflammation and infiltration of
    monocytes that promote plaque rupture.

    The majority of coronary artery atherosclerotic plaque rupture occurs at the plaque shoulder,
    which experiences greater tensile force from flowing blood.

    Branch points at coronary bifurcations experience low shear stress conditions that promote
    coronary artery atherosclerotic plaque inflammation and infiltration of monocytes that promote
    plaque rupture.

    Neutrophils and macrophages are the major sources of the myeloperoxidase enzyme, which
    generates free radicals and increases inflammation in rupture-prone coronary artery
    atherosclerotic plaques.

    Coronary calcium participates prominently in the pathobiology of coronary artery


    atherosclerotic plaque rupture, and calcification is present in 80% of ruptured plaques.
    31. A 65-year-old woman with hypertension and hyperlipidemia developed chest pain and
    collapsed while walking her dog. Emergency medical responders used an automated external
    defibrillator to administer one shock, which converted the patient from ventricular fibrillation to
    sinus rhythm.
    The patient is treated emergently for an ST-segment elevation myocardial infarction (STEMI) with
    primary percutaneous coronary intervention, where a stent is used to treat a thrombotic occlusion
    of the left anterior descending artery.Which of the following statements is correct regarding
    mechanisms of coronary artery disease that led to arterial thrombosis and MI in this patient?
    a. Coronary artery atherosclerotic plaque rupture is frequently clinically silent; however, silent
    plaque rupture events speed plaque growth and promote luminal narrowing.
    b. Coronary artery atherosclerotic plaque neovascularization increases plaque stability and
    reduces plaque inflammation.
    c. Superficial plaque erosion-induced coronary artery thrombosis occurs most often at sites of
    macrophage-laden coronary artery atherosclerotic plaques that have a low content of smooth
    muscle cells.
    d. Ischemic preconditioning increases the size of the infarct zone in patients presenting with
    STEMIs.
    e. Distal embolization of platelet aggregates rarely occurs in non-STEMI patients.
    31. a. Coronary artery atherosclerotic plaque rupture is frequently clinically silent;
    however, silent plaque rupture events speed plaque growth and promote luminal narrowing.

    Ischemic preconditioning reduces the size of the infarct zone in patients presenting with STEMI.
    Distal embolization of platelet aggregates frequently occurs in non-STEMI patients, and
    embolization is a major cause of myocardial necrosis. Superficial plaque erosion-induced
    coronary artery thrombosis occurs most often within atherosclerotic plaques that have a high
    content of smooth muscle cells and a low lipid content.

    Coronary artery atherosclerotic plaque neovascularization decreases plaque stability and


    increases plaque inflammation. Neovascularization likely increases risk of plaque rupture.
    32. A 69-year-old man with a history of hypertension and stroke was admitted with a non–ST-
    segment elevation myocardial infarction (NSTEMI). After medical stabilization, he was managed
    with an early invasive strategy and a drug-eluting stent was placed into a thrombotic 80% stenosis
    in the right coronary artery.
    Which of the following regimens would be part of the optimal medical management for this patient
    following drug-eluting stent implantation to treat an NSTEMI?
    a. Aspirin 325 mg daily and ticagrelor 90 mg twice daily.
    b. Aspirin 325 mg daily and prasugrel 10 mg daily.
    c. Aspirin 81 mg daily, ticagrelor 90 mg twice daily, and rivaroxaban 5 mg twice daily.
    d. Aspirin 81 mg daily and prasugrel 10 mg daily.
    e. Aspirin 81 mg daily and ticagrelor 90 mg twice daily.
    32. e. Aspirin 81 mg daily and ticagrelor 90 mg twice daily.

    Prasugrel should not be administered to patients with a prior history of stroke or transient ischemic
    attack. Aspirin 70-100 mg is the optimal dose when aspirin is combined with ticagrelor. Triple
    therapy with aspirin, ticagrelor, and rivaroxaban has not been studied in acute coronary syndrome
    management. Rivaroxaban reduces adverse cardiovascular events in acute coronary syndrome
    patients when added to aspirin and clopidogrel.
    33. A 63-year-old woman with a 2-day history of intermittent chest pain, sometimes responsive
    to belching, presents to the emergency department for evaluation. Her medical history is
    significant for hypertension. Her medications include amlodipine, hydrochlorothiazide, and aspirin.

    Her physical examination reveals blood pressure 128/82 mm Hg, heart rate 82 bpm, and oxygen
    saturation 99% on room air. Her jugular venous pressure is 6 cm water, lungs are clear, and
    cardiovascular exam is normal. Her electrocardiogram shows normal sinus rhythm with nonspecific
    T-wave changes. Her chest x-ray is normal. Laboratory values include two serial troponin I values of
    <0.01 ng/L, normal electrolytes, creatinine 0.8 mg/dl, D-dimer 130 ng/ml, and normal blood cell
    count.
    Which of the following is most appropriate in her care?
    a. No further testing is needed.
    b. Transthoracic echocardiogram.
    c. Invasive coronary angiography.
    d. Ventilation/perfusion (V/Q) scan.
    e. Exercise myocardial perfusion.
    33. e. Exercise myocardial perfusion.

    In this patient with suspected non-ST-segment elevation acute coronary syndrome, further risk
    stratification is warranted. The history, physical exam, and findings are important to consider in the
    initial risk stratification. This patient's Thrombolysis in Myocardial Infarction (TIMI) risk score is 1,
    which gives her a risk of major adverse cardiac events of 5% in the next 14 days. Noninvasive stress
    testing can be used to further risk stratify this patient. Resting transthoracic echocardiogram will
    not provide information about inducible ischemia. With a normal D-dimer and low pretest
    probability of pulmonary embolism, a V/Q scan is not indicated.
    34. A 61-year-old woman presents to the emergency department with 2 hours of chest pain
    associated with shortness of breath. Her medical history is significant for hypertension and
    hyperlipidemia. Her medications include lisinopril 20 mg and hydrochlorothiazide 25 mg daily.

    On exam, her blood pressure is 122/84 mm Hg, heart rate is 94 bpm, oxygen saturation is 98% on
    room air, and body mass index is 24 kg/m2. Jugular venous pressure is 7 cm H2O, and cardiovascular
    exam reveals normal S1 and S2 without murmurs. Lungs are clear and there is no peripheral edema.

    Her electrocardiogram shows sinus rhythm with 0.5 mm ST depression in leads V4-V6. Laboratory
    values include serum creatinine 1.4 mg/dl, troponin I 0.8 ng/ml, hemoglobin 12 g/dl, and N-
    terminal pro-B-type natriuretic peptide 202 ng/L. She is chest-pain free on intravenous
    nitroglycerin and heparin. Repeat troponin I 6 hours later is 1.1 ng/ml.
    Which of the following is the most appropriate management strategy in this patient's care?
    a. Pharmacologic nuclear stress test.
    b. Coronary angiography.
    c. Exercise stress test.
    d. Coronary computed tomography (CT) angiography.
    e. Transthoracic echocardiogram.
    34. b. Coronary angiography.
    Optimal risk stratification of patients with suspected non-ST elevation acute coronary syndrome
    should include risk stratification models such as the Global Registry of Acute Coronary Events
    (GRACE) or Thrombolysis in Myocardial Infarction (TIMI) scores, which employ multiple
    prognostic factors to help determine management strategies. This patient's GRACE score is 159,
    which places her in the high risk category for in-hospital mortality. Therefore, she should be
    managed aggressively with an early invasive strategy.

    Stress testing in this patient with rising troponin is not appropriate. CT angiography may be
    performed in patients with intermediate risk. A normal echocardiogram will not obviate the
    need for cardiac catheterization.
    35. A 57-year-old woman presents to the emergency room with new-onset chest pressure that
    has been escalating for the last 2 hours.
    Her medical history is only remarkable for hypertension and obesity. Initial
    electrocardiogram demonstrates ST-segment elevation in leads V1-V4 with associated changes
    inferiorly.
    She is urgently taken to cardiac catheterization where a mid left anterior descending subtotal
    occlusion is successfully revascularized using a drug-eluting stent, restoring Thrombolysis in
    Myocardial Infarction (TIMI) III flow.
    Following percutaneous coronary intervention, a transthoracic echocardiogram demonstrates left
    ventricular ejection fraction (LVEF) of 25-30% with severe hypokinesis of the anterior wall LV.
    Medical therapy is initiated with atorvastatin, metoprolol, lisinopril, aspirin, clopidogrel, and
    eplerenone. Telemetry on hospital day 2 reveals several brief runs of asymptomatic accelerated
    idioventricular rhythm.Which of the following do you recommend for subsequent risk stratification
    of sudden cardiac death?
    a. Reassessment of LVEF at least 40 days post MI.
    b. Invasive electrophysiology (EP) testing prior to hospital discharge.
    c. Cardiac magnetic resonance imaging (MRI) prior to hospital discharge.
    d. Invasive EP testing at least 40 days post MI.
    e. Reassessment of LVEF at least 90 days post MI.
    35. a. Reassessment of LVEF at least 40 days post MI.

    The correct answer is reassessment of LVEF at least 40 days post MI. Invasive EP testing has no role
    in the immediate post MI period in the absence of significant ventricular arrhythmias. The slow
    idioventricular rhythm is likely related to myocardial reperfusion and does not require EP testing.
    Invasive EP testing >40 days post MI may be considered for moderately decreased LVEF (35-40%) in
    patients with evidence of nonsustained ventricular tachycardia detected on noninvasive
    monitoring. Cardiac MRI to define scar burden has been found to be useful to predict ventricular
    arrhythmias in cardiomyopathic patients. However, cardiac MRI has not yet been integrated into
    the guidelines for risk stratification post MI.

    The 2013 guideline for the management of ST-elevation myocardial infarction indicates that repeat
    assessment of LVEF at least 40 days post MI carries a Class I indication for risk stratification of
    sudden cardiac death. Primary prevention implantable cardioverter-defibrillator (ICD) implantation
    during the infarct-related hospitalization has not been demonstrated to be beneficial (DEFINITE
    trial). Allowing for a period of myocardial healing post MI may avert the need for subsequent ICD
    implantation.

    Greater than 40 days post MI, LVEF should be reassessed. If the LVEF does not improve remains </=
    35% with class II or III symptoms, or remains < 30% independent of symptoms, despite guidelines
    directed medical therapy, then this patient would become a candidate for pr primary prevention
    ICD implant.
    36. A 52-year-old man presents to the emergency room after 3 hours of intermittent sharp
    stabbing chest pain noted when he was raking leaves. His medical history is significant for
    hypertension. He denies tobacco, alcohol, or drug use. His current medications include
    hydrochlorothiazide.

    His physical exam reveals blood pressure of 148/94 mm Hg and heart rate of 72 bpm. His
    cardiovascular exam is unremarkable. His electrocardiogram shows normal sinus rhythm without
    ST- or T-wave changes. His chest x-ray shows normal cardiac silhouette and clear lung fields.
    Which of the following is the most appropriate next step?
    a. Creatine kinase-myocardial band (CK-MB).
    b. N-terminal pro-B-type natriuretic peptide (NT-proBNP).
    c. Urine toxicology.
    d. High-sensitivity C-reactive protein (hs-CRP).
    e. Troponin I.
    36. e. Troponin I.

    Cardiac-specific troponin should be performed in patients with clinical findings or symptoms that
    may be related to potential acute coronary syndrome (ACS) (Class Ia). It should be measured at
    presentation and 3-6 hours after symptom onset in all patients with suspected ACS. If it is negative
    within the first 6 hours of onset of symptoms, it should be repeated in patients with
    electrocardiographic changes and/or intermediate/high risk clinical features. In order to diagnose
    myocardial necrosis, it is important to determine both the peak troponin level and the pattern of
    change.

    CK-MB and myoglobin are not useful for diagnosis of ACS (Class III). NT-proBNP may be reasonable
    for additional prognostic information (Class IIb). Urine toxicology should be performed in patients
    with suspected drug use, as this may be a causal contributor to ACS.
    37. A 62-year-old Caucasian woman with type 2 diabetes presents to the emergency department
    with complaints of constant substernal chest pressure at rest for the last hour, briefly relieved by
    nitroglycerin. She is not on antiplatelet therapy. An electrocardiogram shows lateral precordial ST-
    segment depressions and T-wave inversions. She has no known drug allergies. The troponin I level
    is 2.12 ng/ml.
    Which of the following pharmacotherapeutic strategies is the most appropriate next step for this
    patient?
    a. Ticagrelor 180 mg.
    b. Aspirin 325 mg and clopidogrel 600 mg.
    c. Immediate eptifibatide bolus followed by infusion as monotherapy.
    d. Aspirin 162 mg and prasugrel 60 mg.
    e. Clopidogrel 600 mg.
    37. b. Aspirin 325 mg and clopidogrel 600 mg.

    This woman is experiencing a non-ST-segment elevation myocardial infarction (NSTEMI).


    Clopidogrel and ticagrelor at the described loading and maintenance doses are both reasonable
    therapies for NSTEMI. However, they have been studied in conjunction with and should be
    administered along with aspirin. Prasugrel may be given to patients undergoing percutaneous
    coronary intervention (PCI) in the setting of NSTEMI, but is not guideline-recommended to be
    administered until the anatomy is known and it is certain that the patient will be underoing PCI. In
    the ACCOAST trial, treatment with prasugrel in NSTEMI before PCI did not reduce ischemic events
    and was associated with more bleeding. The best answer is aspirin in conjunction with clopidogrel.
    Glycoprotein IIb/IIIa antagonists are only administered on top of oral antiplatelet therapy.
    38. A 40-year-old man with a history of type 2 diabetes is seen in the office. His blood pressure is
    123/75 mm Hg. Labs include a total cholesterol of 130 mg/dl and high-density lipoprotein
    cholesterol of 40 mg/dl. He is a lifelong nonsmoker. He is active, but overweight with a body mass
    index of 29 kg/m2. He is interested in reducing his risk of developing complications of
    atherosclerotic cardiovascular disease (ASCVD), but wants to be sure any new medications are
    worth the potential side effects.
    Which of the following do you recommend to reduce the risk of ASCVD in this patient?
    a. High-intensity statin therapy.
    b. Dietary modifications alone.
    c. Fenofibrate.
    d. Moderate-intensity statin therapy.
    e. Ezetimibe.
    38. d. Moderate-intensity statin therapy.

    Using the ASCVD risk calculator (estimator), this patient has a 10-year calculated risk of 1.2% and a
    50% lifetime risk. Although primary prevention is reserved for nondiabetic patients with a 10-year
    risk ≥7.5%, the fact that this patient has diabetes means that moderate-intensity statin therapy is
    recommended (Class I, Level of Evidence A). High-intensity statin therapy would be indicated in this
    diabetic patient if the 10-year risk was ≥7.5%.y.
    39. A 66-year-old man is seen in clinic for follow-up after hospitalization for an acute coronary
    syndrome. Current medications include atorvastatin 80 mg, ticagrelor 90 mg bid, aspirin 81 mg,
    metoprolol 25 mg bid, and lisinopril 10 mg daily. He smoked one-half pack of cigarettes daily for
    the past 40 years.

    His current lipid panel includes total cholesterol 150 mg/dl, triglycerides 199 mg/dl, low-density
    lipoprotein 61 mg/dl, and high-density lipoprotein 49 mg/dl. Hemoglobin A1c is 6.0%.
    Which of the following steps will best reduce his risk of future myocardial infarction (MI)?
    a. Ezetimibe.
    b. Omega-3 fatty acids.
    c. Varenicline.
    d. Coenzyme Q10.
    e. Metformin.
    39. c. Varenicline.

    Lifestyle modification including smoking cessation can result in significant improvement in


    atherosclerotic cardiovascular risk. A meta-analysis of smoking cessation in patients with MI found
    it was associated with a 50% reduction in cardiovascular risk. Therefore, varenicline is the best
    answer, because it has been proven to be efficacious for smoking cessation. Ezetimibe in addition
    to statin was associated with an approximately 2% absolute risk reduction (number needed to treat
    = 50) in atherosclerotic cardiovascular disease events in the IMPROVE-IT trial; given his lipid panel,
    this would not likely be as large a benefit as smoking cessation. Adding metformin is not indicated
    with a hemoglobin A1c of 6% and would not be expected to reduce his MI risk. Coenzyme Q10 and
    omega-3 fatty acids have not been shown to reduce global cardiovascular risk.
    40. A 63-year-old woman with a history of hypertension presents with an acute coronary
    syndrome. Coronary angiography demonstrates a 90% lesion in her posterior descending artery.
    She subsequently undergoes stent placement.

    Labs include peak troponin of 1.2 ng/ml and hemoglobin A1c of 5.6%. Fasting lipid profile includes
    total cholesterol of 160 mg/dl, high-density lipoprotein (HDL) of 38 mg/dl, low-density lipoprotein
    (LDL) of 67 mg/dl, and triglyceride (TG) of 240 mg/dl.
    Which of the following is the most appropriate lipid management strategy?
    a. Fenofibrate 145 mg qd.
    b. Fish oil 2 g qd.
    c. Ezetimibe 10 mg qd.
    d. Niacin 500 mg qd.
    e. Atorvastatin 80 mg qd.
    40. d. Niacin 500 mg qd.

    It is important to obtain a fasting lipid profile on all patients presenting with acute coronary
    syndrome. High-intensity statin therapy is indicated for all patients ages <75 years with
    atherosclerotic cardiovascular disease (ASCVD), even with a "normal" LDL. Despite low HDL and
    elevated TG, initial therapy with statin is preferred over the other options.

    When added to statin monotherapy, the addition of niacin or fenofibrate has not been shown to
    reduce CV events despite improvement in lipid profile. While ezetimibe as add-on therapy to statin
    reduced CV events in the IMPROVE-IT trial, it should not be used as monotherapy in a patient who
    is statin naive. To date, fish oil has not been definitively shown to reduce CV events in patients with
    ASCVD and should not be used over statin therapy.
    41. You are counseling a 58-year-old man prior to discharge from the hospital following an acute
    myocardial infarction. He received primary percutaneous coronary intervention with a drug-eluting
    stent to the left anterior descending artery. Left ventricular ejection fraction is 55%. He had no
    known medical history prior to admission. His current medications include atorvastatin 80 mg,
    lisinopril 5 mg, metoprolol succinate 25 mg, aspirin 81 mg, and ticagrelor 90 mg bid.
    In addition to reviewing the importance of taking all his medications, which of the following
    recommendations is the most appropriate?

    a. Limit total calories to <2000 per day.


    b. Reduce saturated fats, trans fatty acid, and cholesterol intake.
    c. Recommend antioxidant vitamin supplements.
    d. Increase monounsaturated fat intake and reduce cholesterol intake.
    e. Limit sodium intake to <2000 mg per day.
    41. b. Niacin 500 mg qd.

    Dietary modification is recommended for all patients with acute coronary syndrome (ACS).
    Reducing saturated fats to <7% of total calories, eliminating or reducing trans fatty acids, and
    limiting dietary cholesterol to <200 mg daily are all likely to improve cardiovascular health.

    Limiting total calories alone is not specific enough to reduce saturated fat intake. Sodium
    restriction to <2000 mg/day is not indicated, as he does not have left ventricular systolic
    dysfunction or heart failure, although lowering sodium intake by 1000 mg/day from baseline or to
    approximately 2400 mg/day with the DASH diet may reduce hypertension.

    Antioxidants, including vitamin E, vitamin C, and beta carotene, have not been shown to confer any
    benefit in secondary prevention of ACS. Increased monounsaturated fat alone will not ensure a
    reduction in dietary saturated fat and trans fatty acid intake.
    42. A 72-year-old man with persistent atrial fibrillation presents to the emergency room with a
    non–ST-segment elevation myocardial infarction. He has a history of hypertension and diabetes.

    The patient undergoes angiography, and a drug-eluting stent is placed in the left circumflex to treat
    a hazy area of acute plaque rupture.
    Which of the following is the best maintenance therapy for this patient?
    a. Aspirin 81 mg, clopidogrel 75 mg, and oral anticoagulation.
    b. Aspirin 325 mg.
    c. Aspirin 325 mg and clopidogrel 75 mg therapy.
    d. Clopidogrel 75 mg.
    e. Aspirin 325 mg and oral anticoagulation.
    42. a. Aspirin 81 mg, clopidogrel 75 mg, and oral anticoagulation.

    In the presence of atrial fibrillation and an acute myocardial infarction, the addition of an oral
    anticoagulant remains controversial following percutaneous coronary intervention. The addition of
    an oral anticoagulation should be guided by use of the CHA2DS2-VASc score. Individualization can
    also be determined by the HAS-BLED scoring system for risk of bleeding.
    43. A 70-year-old man on the trauma service is being evaluated because of a positive troponin.
    He was in a motor vehicle accident yesterday and fractured his femur. He underwent surgical open
    reduction and internal fixation this morning. He has diabetes and hypertension, but no known
    coronary artery disease. There was no steering wheel contact; he was wearing his seat belt. He has
    no symptoms.

    His examination is normal except for pallor and his now casted left leg. His electrocardiogram
    shows sinus rhythm and nonspecific T-wave flattening over the precordial leads. His laboratory
    tests are notable for a hemoglobin of 7.5 mg/dl. The troponin is 1.2 ng/dl.
    Which of the following is the most appropriate next step?
    a. Enoxaparin 40 mg daily.
    b. Aspirin 325 mg daily.
    c. Clopidogrel 300 mg loading dose.
    d. Heparin 60 U/kg bolus.
    e. Ticagrelor 180 mg loading dose.
    43. a. Enoxaparin 40 mg daily.

    This patient has an asymptomatic rise in his troponin in the absence of symptoms and nonspecific
    changes on his electrocardiogram. Moreover, he has undergone significant trauma and is very
    anemic. The low-grade troponin is most likely due to demand ischemia. The clinical scenario is not
    consistent with an acute coronary syndrome and therefore does not require treatment for an acute
    coronary syndrome (e.g., antiplatelet agents, intravenous antithrombins). His greatest risk is deep
    venous thrombosis, and he should receive deep vein thrombosis prophylaxis (e.g., enoxaparin).
    44. A 50-year-old woman presents with chest pain. It occurs with exertion and is relieved by rest.
    Her history is notable for hypertension; her father died suddenly at 55 years of age of unknown
    causes. She completes 6 minutes of a Bruce protocol stress test with myocardial perfusion (MIBI)
    that demonstrates 2 mm ST-depressions in the lateral leads and a reversible defect in the
    inferolateral wall. Her blood pressure and heart rate responses are normal. She undergoes
    coronary angiography that is notable for a left dominant coronary circulation with a 70% mid left
    anterior descending (LAD) lesion and luminal irregularities of the first obtuse marginal branch.
    Fractional flow reserve of the LAD lesion is 0.85.
    Which of the following is the most likely cause of her chest pain?
    a. Coronary vasospasm.
    b. 70% mid LAD lesion.
    c. Pericarditis.
    d. Coronary dissection.
    e. Microvascular angina.
    44. e. Microvascular angina.

    Coronary microvascular dysfunction is an important prognostic factor in a wide range of diseases.


    In this case, microvascular angina is the manifestation of her atherosclerotic coronary artery
    disease. Evidence for ischemia includes her electrocardiographic ST depressions and stress MIBI
    changes. Pericarditis would not produce the ST changes or the stress MIBI changes. Coronary
    vasospasm generally is not provokable with exercise stress testing and typically occurs in the early
    morning hours; it classically involves the epicardial coronary arteries, although microvascular
    spasm has been speculated. Coronary dissection usually presents as a myocardial infarction, and
    the diagnosis is generally apparent on coronary angiography, although intravascular ultrasound and
    ocular coherence tomography may be required for definitive diagnosis.
    45. A 45-year-old woman presents to your office with a 6-month history of chest pain. She
    reports episodes of chest pain lasting 10-15 minutes that occur with exertion. The pain radiates to
    her left shoulder and she becomes short of breath. She has no family history of coronary artery
    disease and she has smoked for 10 years. She does not have a history of diabetes or hypertension.

    Her physical examination is unremarkable, except for a body mass index of 32. A 12-lead
    electrocardiogram (ECG) is normal. A previous cardiologist had performed a treadmill stress test,
    during which she developed chest pain and a 2 mm ST-depression in leads V5 and V6. She undergoes
    diagnostic cardiac catheterization, and her coronary arteries are free of stenosis except for a 20%
    lesion in the circumflex. Echocardiogram shows normal left ventricular and right ventricular (RV)
    function and normal RV systolic pressure.
    What is the most likely cause of her symptoms?
    a. Gastroesophageal reflux disease (GERD).
    b. Stress-induced cardiomyopathy.
    c. Chronic thromboembolic pulmonary hypertension (CTEPH).
    d. Pericarditis.
    e. Coronary microvascular dysfunction.
    45. e. Gastroesophageal reflux disease (GERD).

    Her history is consistent with angina. Although she does not have any significant coronary artery
    stenosis expected to lead to flow limitation, coronary microvascular dysfunction is the most likely
    cause of her symptoms. This syndrome occurs in women more than men, can present with classical
    angina, and can be associated with ST depression provoked by exercise, and it occurs in the
    absence of significant epicardial coronary stenoses.

    CTEPH is not typically associated with anginal type symptoms or with exercise-induced ischemia.
    Stress-induced cardiomyopathy (Takotsubo) results in wall motion abnormalities on
    echocardiography, usually apical ballooning. There is no evidence of pericarditis, because her ECG
    is normal and chest pain is only exertional. While GERD is a common cause of chest pain, it would
    not result in exercise-induced symptoms or ECG changes.
    46. A 50-year-old woman presents to your office for a second opinion. She reports a 3-year
    history of exertional chest discomfort. Her previous cardiologist had performed a treadmill stress
    test during which she developed a 1.5 mm ST-depression in 3 leads, after which he recommended
    the patient undergo a cardiac catheterization. Her coronary arteries had no epicardial stenoses and
    the cardiologist attributed the chest pain to anxiety. The patient continues to have exertional chest
    pain, and she is willing to undergo additional noninvasive diagnostic testing, because she remains
    concerned about this symptom. Her physical examination is unremarkable.
    Which of the following noninvasive diagnostic tests do you recommend?
    a. Computed tomography (CT) angiography of the coronary arteries.
    b. Exercise thallium.
    c. Resting transthoracic echocardiogram.
    d. Assessment of coronary artery calcium by CT.
    e. Repeat stress treadmill with electrocardiogram (ECG) monitoring.
    46. b. Exercise thallium.

    The patient may be presenting with coronary microvascular dysfunction. Patients with this
    condition can develop ischemia in the absence of significant epicardial coronary artery stenosis.
    Such patients may have a reversible perfusion defect as assessed by stress thallium perfusion
    study, though absence of this finding does not exclude that diagnosis. There would be little utility in
    repeating the treadmill test with ECG monitoring, because this was already positive. Neither CT
    angiography or assessment of coronary artery calcium would be helpful given the recent
    demonstration of no significant stenosis at left heart catheterization. A resting transthoracic
    echocardiogram would not establish the diagnosis of coronary microvascular dysfunction.
    47. A 48-year-old woman presents with exertional chest pain with associated dyspnea. Following
    a stress perfusion study showing a reversible defect consistent with ischemia, she undergoes
    cardiac catheterization, including assessment of hemodynamics. Her pulmonary artery pressure
    (PAP) is 30/15/22 mm Hg and cardiac index is 2.5 L/min/m2. Coronary angiography reveals no
    significant epicardial stenoses. The ratio of the coronary flow following administration of
    adenosine, to that at baseline, is 2. A catheter is placed into her left ventricle, and the left
    ventricular end-diastolic pressure (LVEDP) is 12 mm Hg.
    Which of the following diagnoses would be most consistent with these findings?
    a. Coronary microvascular dysfunction.
    b. Noncardiac chest pain.
    c. Pulmonary embolism.
    d. Heart failure.
    e. Pulmonary hypertension.
    47. a. Coronary microvascular dysfunction.

    A coronary flow reserve (CFR) of 2.5 is abnormal and consistent with coronary microvascular
    dysfunction. Her LVEDP is low, which is not consistent with heart failure. Her mean PAP is 25 mm
    Hg, so she does not have pulmonary hypertension. While we cannot exclude pulmonary embolism
    to be the cause of her symptoms, she does not have associated pulmonary hypertension. The
    finding of a low CFR makes coronary microvascular dysfunction a more likely explanation. The
    patient has abnormal CFR and a positive stress test, making noncardiac chest pain less likely.
    48. You are asked to consult on a 55-year-old man in the emergency department with chest pain.
    He describes a dull chest discomfort that started while he was climbing the attic stairs to put away
    some boxes about 2 hours ago. He was sweating and breathing heavily from the work when the
    pain started. The discomfort became so intense that he thought he was going to pass out and
    gradually resolved over 10 minutes when he sat down to catch his breath. Medical history includes
    hypertension managed with amlodipine and gastroesophageal reflux disease managed with
    omeprazole.

    His electrocardiogram is shown in Figure 1. Blood work drawn on arrival in the emergency
    department included chemistries, which were normal, and cardiac troponin I, which was
    undetectable.

    Which of the following laboratory tests should be obtained within the next 6 hours?
    a. Creatine kinase-myocardial band.
    b. High-sensitivity cardiac troponin I.
    c. Heart-type fatty acid binding protein.
    d. Myoglobin.
    e. Lactate dehydrogenase.
    48. b. High-sensitivity cardiac troponin I.

    Injury to cardiac myocytes results in loss of cell membrane integrity and subsequent diffusion of
    intracellular proteins into the extracellular space, where they are detectable by laboratory
    assays on plasma. These biomarkers of myocyte injury include myoglobin (present in all muscle
    cells), lactate dehydrogenase (present in all muscle cells), creatine kinase (present in all muscle
    cells but with subtypes that are more prevalent in cardiac muscle cells), heart-type fatty acid
    binding protein (a subtype of a low molecular weight protein specific to cardiac muscle), and
    cardiac troponin I (present only in cardiac muscle cells). Troponin T may be expressed by some
    skeletal muscle cells, but in most clinical settings will have similar specificity to troponin I.

    The high specificity of cardiac troponin for cardiac muscle injury and predictable kinetics make it
    the preferred biomarker to confirm or exclude the diagnosis of myocardial infarction. Cardiac
    troponins generally will be detectable first in the blood 2-3 hours after the event in 80% of
    patients and within 6 hours of the event in essentially all patients. Serial measurements, as in
    this patient with undetectable troponin immediately after the event, are therefore critical for
    ruling out the diagnosis of myocardial infarction and for ruling in the diagnosis by demonstrating
    the characteristic rise and fall of troponin in the blood.
    49. A 60-year-old man with a 60 pack-year history of smoking presents to the emergency
    department with 2 hours of crushing substernal chest pain. His electrocardiogram shows 3 mm ST
    elevation in the anterior leads. He is taken urgently to the cardiac catheterization laboratory.
    Which of the following strategies would require additional antithrombotic therapy during primary
    percutaenous coronary intervention (PCI)?
    a. Unfractionated heparin.
    b. Bivalirudin.
    c. Fondaparinux.
    d. Unfractionated heparin with eptifibatide.
    e. Unfractionated heparin with abciximab.
    49. c. Fondaparinux.

    Fondaparinux is not recommended as the sole anticoagulant during primary PCI due to an
    increased risk of catheter thrombosis (Class III recommendation). Unfractionated heparin with or
    without concomitant intravenous glycoprotein IIb/IIIa therapy (including abciximab and
    eptifibatide), and bivalirudin, are acceptable anticoagulant therapies during primary PCI.
    50. A 31-year-old man with no significant medical history presents to the emergency department
    with sudden-onset severe substernal chest pain that began 15 minutes prior to presentation. His
    friend admits that they had been smoking marijuana that was laced with cocaine. The patient
    appears somewhat disheveled and irritable. His pupils are dilated, heart rate is 105 bpm, and blood
    pressure is 163/106. He was started on nitroglycerin, but has persistent chest pain. An
    electrocardiogram shows ST elevations in leads V3-V6.
    Which of the following medications would be appropriate to administer?
    a. Flumazenil.
    b. Lorazepam.
    c. Naloxone.
    d. Metoprolol.
    e. Dabigatran.
    50. b. Lorazepam.

    Benzodiazepines with or without nitroglycerin may be used to manage hypertension and


    tachycardia in patients who present with non-ST elevation acute coronary syndromes (NSTE-ACS)
    and signs of acute cocaine or methamphetamine intoxication. For STE-ACS, lorazepam would be
    the most reasonable choice of the options listed, although the primary focus would be on
    emergent coronary angiography and percutaneous coronary intervention, if indicated.

    Per the NSTE-ACS guidelines, "Beta-blockers should not be administered to patients with ACS with
    a recent history of cocaine or methamphetamine use who demonstrate signs of acute intoxication
    due to the risk of potentiating coronary spasm." Naloxone is used to treat opioid overdose and
    flumazenil is used to treat benzodiazepine overdose, so neither would be appropriate here.
    Dabigatran is not indicated for the management of ACS.
    51. A 67-year-old woman with history of diabetes and asthma is admitted to the cardiac intensive
    care unit after percutaneous intervention with drug-eluting stent placement for an ST-elevation
    myocardial infarction (STEMI) involving the right coronary artery. She has not had any recurrent
    chest discomfort since her procedure. Her vital signs are temperature 37.5°C, heart rate 116 bpm,
    blood pressure 153/73 mm Hg, respiratory rate 24 breaths/minute, and oxygen saturation 96%.
    Physical examination is notable for an irregularly irregular heart rhythm, no jugular venous
    pressure, and moderate expiratory wheezing. Electrocardiogram demonstrates atrial fibrillation
    with a rapid ventricular response, but isoelectric ST segments and no Q waves. Her medications
    include aspirin, clopidogrel, and atorvastatin.
    Which of the following would be the next best medication to consider?
    a. Spironolactone.
    b. Metoprolol.
    c. Amiodarone.
    d. Diltiazem.
    e. Nitroglycerin.
    51. d. Diltiazem.

    Certain calcium channel blockers may be useful for the treatment of angina, hypertension, and
    atrial tachyarrhythmias in select patients after STEMI when beta-blockers (or nitrates) are
    ineffective, not tolerated, or contraindicated and in patients who have no signs of congestive heart
    failure, left ventricular dysfunction, or atrioventricular block. In this patient with recent STEMI,
    atrial fibrillation with rapid ventricular response, and elevated blood pressure, diltiazem would be a
    good choice to slow her ventricular rate and help control blood pressure. There is no evidence of
    active ischemia, and thus immediate electrical cardioversion is not necessary.

    Metoprolol is contraindicated given the history of asthma and evidence of active bronchospasm.
    The duration of atrial fibrillation is unknown, thus amiodarone would not be a good choice at this
    point, as it also can cause cardioversion and other attempts at rate control have not been made.
    Nitroglycerin is not ideal in the setting of tachycardia and would not help to control heart rate.
    Aldosterone antagonists are recommended for patients with STEMI who are already receiving an
    angiotensin-converting enzyme inhibitor and beta-blocker and who have a left ventricular ejection
    fraction ≤40% and either symptomatic heart failure or diabetes. This patient would not qualify for
    an aldosterone antagonist at this time.
    52. A 51-year-old woman is admitted to the cardiac intensive care unit (ICU) immediately
    following primary percutaneous coronary intervention for an anterior wall myocardial infarction
    (MI). She was intubated for respiratory distress en route to the hospital and no history is available.
    Current vital signs are pulse 108 bpm, respiratory rate 12 breaths/minute with 100% fraction of
    inspired oxygen from the ventilator, blood pressure 98/70 mm Hg, and oxygen saturation 99%.
    Weight is 240 lbs. Physical exam reveals acanthosis of the neck and bilateral rales; the peripheral
    pulses are weak.

    Lab exam results were remarkable for random glucose 264 mg/dl; there was no anion gap.
    Creatinine and other chemistries were within normal limits. An infusion with insulin is started for
    control of hyperglycemia.
    Which of the following is the most appropriate target of glucose in this patient?
    a. 181-220 mg/dl.
    b. <80 mg/dl.
    c. 221-280 mg/dl.
    d. 81-110 mg/dl.
    e. 111-180 mg/dl.
    52. e. 111-180 mg/dl.

    Nearly one-quarter of patients with ST-elevation MI (STEMI) have diabetes, and up to one-third of
    those may be diagnosed at the time of hospitalization for STEMI. Diabetic patients have higher
    mortality from STEMI, and hyperglycemia is a predictor of early mortality. However, there is a U- or
    J-shaped relationship between serum glucose and death, with the risk of mortality similar for either
    hypoglycemia (random glucose <70 mg/dl) or hyperglycemia (variously defined as random glucose
    >140, >180, or <200 mg/dl).

    The NICE-SUGAR trial randomized 6,104 ICU patients to either intensive blood glucose control
    (target blood glucose 81-108 mg/dl) or conventional blood glucose control (target blood glucose
    <180 mg/dl) and found lower mortality (24.9% vs. 27.5%, p = 0.02) for the conventional glucose
    control strategy, with fewer episodes of hypoglycemia (0.5% vs. 6.8%, p < 0.001).

    Therefore, "modest" rather than "intensive" glucose control, that is, target <180 mg/dl with
    avoidance of hypoglycemia, is the current recommendation for critically ill patients with STEMI.
    53. A 68-year-old Caucasian man is seen in the clinic for cardiovascular risk assessment. He has a
    history of hypertension and type 2 diabetes . He has never smoked. His medications include
    metformin 500 mg bid and lisinopril 10 mg qd. His blood pressure is 130/80 mm Hg. His
    examination is otherwise unremarkable. His lipid profile shows total cholesterol 161 mg/dl, high-
    density lipoprotein 45 mg/dl, low-density lipoprotein 80 mg/dl, and triglyceride 180 mg/dl. His
    hemoglobin A1c is 6.4%.
    Which of the following is the most appropriate next step?
    a. Start glipizide 5 mg qd.
    b. Start fenofibrate 145 mg qd.
    c. No additional therapy.
    d. Start atorvastatin 40 mg qd.
    e. Increase lisinopril to 20 mg qd.
    53. d. Start atorvastatin 40 mg qd.

    Initiating statin therapy is appropriate for diabetics 40-75 years of age with low-density lipoprotein
    cholesterol >70 mg/dl. In this patient whose 10-year risk of atherosclerotic cardiovascular disease is
    11.2% based on pooled cohort equation, high-intensity statin therapy is recommended. In the
    ACCORD trial, intensifying glycemic control to target A1c <6% was associated with higher rates of
    hypoglycemia and increased mortality and did not significantly reduce major cardiovascular events.
    Similarly, the addition of fenofibrate was not associated with significant reduction in rate of
    cardiovascular events. This patient's blood pressure is at goal; up-titration of lisinopril is not
    indicated.
    54. A 74-year-old man with a history of hypertension is brought to the emergency department
    with chest pain and an acute inferior wall myocardial infarction. His only medication on admission
    is lisinopril 40 mg daily. He undergoes drug-eluting stent placement without complications and is
    placed on aspirin 81 mg daily, clopidogrel 75 mg daily, atorvastatin 80 mg daily, and metoprolol 50
    mg twice daily. Prior to discharge, he experiences similar chest pain and diaphoresis. His
    electrocardiogram shows ST elevation in the inferior leads. Stent thrombosis is diagnosed at
    catheterization and successfully remedied.
    Which of the following factors may have contributed to development of subacute stent
    thrombosis?
    a. Inadequate dosing of aspirin.
    b. Heparin-induced thrombocytopenia.
    c. Nickel allergy.
    d. Resistance to clopidogrel.
    e. Resistance to aspirin.
    54. d. Resistance to clopidogrel.

    On March 12, 2010, the Food and Drug Administration approved a new label for clopidogrel with a “boxed
    warning” about the diminished effectiveness of clopidogrel in patients with impaired ability to convert the drug
    into its active metabolite. Patients with decreased cytochrome P450 2C19 (CYP2C19) function because of genetic
    polymorphisms metabolize clopidogrel poorly and have higher rates of cardiovascular events after acute coronary
    syndrome and percutaneous coronary intervention (PCI) than patients with normal CYP2C19 function. The
    warning also notes that tests are available to identify patients with genetic polymorphisms and that alternative
    treatment strategies should be considered for patients who are poor metabolizers. The clopidogrel boxed
    warning leaves the issue of whether to perform CYP2C19 testing up to the individual physician. It does not
    specifically require genetic testing or other changes in evaluation or treatment and does not imply that there are
    solid evidence-based reasons for such actions. Rather, it serves to inform clinicians of genetic variations in
    response to clopidogrel and to emphasize that clinicians should use this knowledge to make decisions about how
    to treat individual patients. At the present time, the evidence base is insufficient to recommend routine genetic
    testing in patients undergoing PCI. There may be a potential role for genetic testing for patients undergoing
    elective high-risk PCI procedures (e.g., unprotected left main, bifurcating left main, or last patent coronary
    artery).

    The recommended maintenance dose of aspirin is 70-100 mg following stent implantation. Higher doses have
    been shown to increase bleeding risk without reducing major adverse cardiac events. The prevalence of aspirin
    resistance is controversial, but has not been linked to stent thrombosis. Heparin-induced thrombocytopenia
    increases thrombosis risk in general, but has not been linked to subacute stent thrombosis. Most modern stents
    are constructed of cobalt-chromium alloys rather than with nickel titanium; furthermore, there is no proven
    association between nickel allergy and stent thrombosis.
    55. A 69-year-old man is hospitalized for primary percutaneous coronary intervention for an ST-
    segment elevation myocardial infarction. His medical history includes hypertension and a previous
    ischemic stroke. His current medications include aspirin 81 mg, carvedilol 12.5 mg bid, lisinopril 20
    mg daily, and atorvastatin 80 mg daily.
    Which of the following best explains the benefits of ticagrelor over clopidogrel?
    a. Ticagrelor is associated with lower rates of side effects.
    b. Ticagrelor is associated with lower stroke risk.
    c. Ticagrelor is associated with lower rates of stent thrombosis.
    d. Ticagrelor is associated with fewer drug-drug interactions.
    e. Ticagrelor is associated with lower bleeding risk.
    55. c. Ticagrelor is associated with lower rates of stent thrombosis.

    In the PLATO trial, ticagrelor was associated with lower rates of death, stroke, and stent thrombosis
    compared with clopidogrel in acute coronary syndrome patients. However, non-coronary artery
    bypass grafting major bleeding rates were higher with ticagrelor compared with clopidogrel,
    although overall bleeding rates were similar. Ticagrelor and clopidogrel were associated with a
    similar risk of stroke, although there were more hemorrhagic strokes with ticagrelor (0.2% vs.
    0.1%). Ticagrelor is metabolized through cytochrome P450 3A and cannot be combined with strong
    inducers or inhibitors of that enzyme. Ticagrelor is associated with more side effects, including
    dyspnea and bradycardia. Because of increased bleeding when combined with higher doses of
    aspirin, ticagrelor should only be combined with aspirin 81 mg.
    56. A 65-year-old retired biology professor presents for cardiac catheterization in the setting of a
    recently positive stress test. You discuss the procedure in detail and obtain informed consent for
    coronary angiography plus percutaneous intervention if needed. He has been reading about
    antiplatelet therapy and asks if you will screen him for genetic mutations related to clopidogrel
    metabolism.
    Which of the following is appropriate routine use of genetic testing to screen patients treated with
    clopidogrel after percutaneous coronary intervention?
    a. Recommended in those receiving drug-eluting stents only.
    b. Recommended, as the evidence suggests that this reduces adverse outcomes.
    c. Recommended in those with concomitant atrial fibrillation.
    d. Recommended in patients who develop a rash after taking clopidogrel.
    e. Not recommended, as the evidence to support this is insufficient.
    56. e. Not recommended, as the evidence to support this is insufficient.

    Clopidogrel is a prodrug that requires conversion into an active metabolite. The major enzyme
    involved in the generation of the active metabolite is cytochrome P450 2C19 (CYP2C19). Among
    several common polymorphisms of CYP2C19 are loss of function mutations that result in a
    premature stop codon and a truncated protein. In theory, patients with these polymorphisms who
    are taking clopidogrel would have a reduced amount of the active metabolite present for platelet
    inhibition.

    Because of concerns over reduced activity in these patients, the Food and Drug Administration
    issued a boxed warning for clopidogrel in 2010. Multiple studies since then have evaluated the
    relationship between the presence of these polymorphisms and adverse outcomes in patients, and
    the data are inconclusive. Therefore, the routine use of genetic screening in patients undergoing
    percutaneous coronary intervention is not recommended.

    Genetic testing for CYP2C19 mutations has nothing to do with allergy or rash to clopidogrel.
    Screening is not recommended in patients receiving bare metal or drug-eluting stents. The
    presence of atrial fibrillation does not affect the recommendation against screening.
    57. A 45-year-old man presents to the emergency department with crushing substernal chest
    pain and ST elevation in the inferior leads on the electrocardiogram. His blood pressure is 185/100
    mm Hg and his heart rate is 100 bpm. The cardiac catheterization laboratory is activated, aspirin
    325 mg is administered orally, and a heparin bolus and drip are started. The patient is anxious and
    reports no medical history, no medication allergies, and he takes a multivitamin daily and sildenafil
    100 mg as needed for erectile dysfunction (most recently the evening prior to presentation). A
    urinary toxicology screen returns that is positive for cocaine.

    Which of the following medications would be appropriate to treat the patient's hypertension, while
    waiting for coronary angiography?
    a. Sodium nitroprusside.
    b. Nitroglycerin.
    c. Lorazepam.
    d. Nifedipine.
    e. Metoprolol.
    57. c. Lorazepam.

    Cocaine-induced chest pain may be related to myocardial infarction (MI), aortic dissection, or
    anxiety. Among those with MI, this may be due to coronary vasospasm and/or thrombotic
    occlusion of one or more coronary vessels. Patients with acute coronary syndromes and severe
    hypertension upon presentation should be treated appropriately with aspirin, heparin (assuming
    aortic dissection has been ruled out or is considered unlikely), and benzodiazepenes to control
    central sympathetic outflow and anxiety.

    Beta-blockers are contraindicated in cocaine-related MI, as they may result in increased coronary
    vasospasm and decreased coronary blood flow due to unopposed alpha activity. Combined alpha-
    and beta-blocker agents, such as labetalol or carvedilol, may be acceptable alternatives. Short-
    acting nifedipine is contraindicated in acute MI. While nitrates to control blood pressure and chest
    pain would be appropriate in cocaine-associated MI, they are contraindicated in this patient due to
    recent use of sildenafil.
    58. A 55-year-old man presents to the emergency department with progressive fatigue and
    shortness of breath for the past 3 weeks. In the past 2 days he has also developed some lower
    extremity edema and feels short of breath in bed at night.

    His medical history is notable for deep vein thrombosis (DVT), for which he is currently maintained
    on apixaban, and he has not missed any doses. He had a recent echocardiography, demonstrating a
    left ventricular ejection fraction of 35%. On examination, his heart rate is 165 bpm and irregularly
    irregular. His blood pressure is 105/75 mm Hg, jugular venous pressure is 7 cm, and there are
    bibasilar crackles on lung exam.
    Cardiac exam is notable for the irregularly irregular rhythm, without appreciable murmur, rub, or
    gallop. Extremities are warm with 1+ bilateral edema to his calves. There are no palpable cords or
    focal tenderness. Electrocardiogram reveals atrial fibrillation with a rapid ventricular response, and
    nonspecific T-wave changes. Laboratory values show a normal troponin, normal basic metabolic
    panel, and an elevated brain natriuretic peptide.
    Which of the following treatments is contraindicated?
    a. Amiodarone.
    b. Esmolol.
    c. Diltiazem.
    d. Dofetilide.
    e. Digoxin.
    58. c. Diltiazem.

    This patient is presenting with signs of acute heart failure in the setting of atrial fibrillation with
    a rapid ventricular response. Rate control is an important step in management, in addition to
    diuresis in light of his signs of volume overload. All of the listed agents may provide rate control
    and are indicated for the acute treatment of supraventricular tachycardia. However,
    nondihydropyridine calcium channel antagonists are contraindicated in the setting of left
    ventricular systolic dysfunction or congestive heart failure, and should be avoided. Cautious use
    of beta-blockers is more appropriate, although monitoring for exacerbation of cardiac function is
    also warranted when they are used in this setting.

    Amiodarone use may be appropriate acutely in this patient, because despite his unknown
    duration of atrial fibrillation, he is already anticoagulated for a history of DVT. Therefore, the risk
    of stroke from cardioversion is low. Dofetilide is not contraindicated, because he has been
    anticoagulated, but will not help with rate control.
    59. A 76-year-old man is brought to the emergency room by ambulance with an acute anterior
    wall myocardial infarction. He has a history of hypertension and permanent atrial fibrillation for
    which he takes metoprolol succinate 100 mg daily and warfarin to maintain an international
    normalized ratio (INR) between 2.0 and 3.0. His creatinine clearance is 65 ml/min. A sirolimus-
    eluting stent is placed in his proximal left anterior descending coronary artery. He was given aspirin
    and clopidogrel at loading doses, and the interventional cardiologist recommends continuing
    aspirin at 81 mg daily and clopidogrel 75 mg daily.

    Which of the following medical therapy adjustments should also be made?


    a. Warfarin should be discontinued.
    b. Change warfarin to rivaroxaban 15 mg daily.
    c. Change warfarin to dabigatran 75 mg twice daily.
    d. Target INR should be 1.5-2.0.
    e. Target INR should be 2.0-2.5.
    59. e. Target INR should be 2.0-2.5.

    Due to his elevated CHA2DS2-VASc score (4, due to age, hypertension, and vascular disease) and
    CHADS2 score (2, due to age and hypertension), anticoagulation with warfarin or a novel oral
    anticoagulant is indicated. Setting a target INR below the therapeutic window is not advised.
    Setting the target INR at 2.0-2.5 in the lower therapeutic range is recommended to decrease the
    risk of bleeding while keeping the risk of stroke and systemic emboli low. There is no current
    recommendation to use non-vitamin K oral anticoagulants as part of a triple therapy strategy.
    60. A 60-year-old woman with a history of nicotine dependence, hypertension, diabetes, and
    right common iliac artery stenting presents to the emergency department with a 3-day history of
    mild exertional substernal chest pain relieved by rest. Her brother underwent coronary artery
    bypass graft surgery at age 55 years. She takes aspirin 81 mg daily, clopidogrel 75 mg daily,
    metoprolol 50 mg twice daily, lisinopril 20 mg daily, and metformin 500 mg twice daily.

    In the emergency department, her blood pressure is 120/70 mm Hg and her heart rate is 65 bpm.
    Electrocardiogram shows normal sinus rhythm with evidence of left ventricular hypertrophy.
    Laboratory values reveal of creatinine 1.2 mg/dl, and the initial troponin is elevated. Sublingual
    nitroglycerin completely resolves her chest pain. She is admitted to the inpatient ward overnight,
    with a plan for coronary angiography in the morning.
    Which of the following medications is most appropriate, in addition to aspirin 324 mg?
    a. IV nitroglycerin.
    b. IV abciximab.
    c. No additional therapy.
    d. Intravenous (IV) unfractionated heparin.
    e. IV fibrinolytics.
    60. d. Intravenous (IV) unfractionated heparin.

    This patient presents with a non-ST-elevation myocardial infarction (NSTEMI). Her TIMI risk score is
    >3. The correct answer is IV unfractionated heparin (Class I, Level of Evidence B).

    In patients with NSTEMI, anticoagulation in addition to antiplatelet therapy is recommended for all
    patients, if there are no contraindications. Anticoagulant options include subcutaneous enoxaparin
    1 mg/kg every 12 hours (reduce dose to 1 mg/kg subcutaneously daily if creatinine clearance is <30
    ml/min). IV bivalirudin 0.1 mg/kg loading dose, followed by 0.25 mg/kg/hr can be administered in
    patients being managed with an early invasive strategy, that is, within 24 hours (Class IB).
    Fondaparinux 2.5 mg subcutaneously daily can be administered either for the duration of the
    hospitalization or until percutaneous coronary intervention (PCI) is performed (Class IB). IV
    fibrinolytics are contraindicated in NSTEMI (Class III). Glycoprotein IIb/IIIa inhibitors can be
    considered, in addition to aspirin and P2Y12 inhibitors in high-risk NSTEMI patients. IV nitroglycerin
    is recommended for persistent ischemia, heart failure, or hypertension (Class IB).
    61. A 60-year-old man with a history of hypertension and diabetes mellitus was admitted to your
    hospital for management of a non–ST-segment elevation myocardial infarction (NSTEMI). His
    coronary angiogram revealed three-vessel coronary artery disease. Coronary artery bypass graft
    (CABG) surgery was recommended. His medications include aspirin 81 mg daily, clopidogrel 75 mg
    daily, enoxaparin subcutaneous 70 mg twice daily (weight is 75 kg and creatinine is normal), and
    metoprolol 25 mg orally twice daily. His clopidogrel is to be discontinued 5 days prior to surgery.
    Which of the following is the appropriate timing to discontinue his enoxaparin prior to surgery?
    a. 36 hours.
    b. 9 hours.
    c. 6 hours.
    d. 1 hour.
    e. 12 hours.
    61. e. 12 hours.

    The correct answer is 12 hours. The half-life for enoxaparin is 4-6 hours. Enoxaparin should be
    discontinued 12- 24 hours prior to CABG, and substituted with intravenous unfractionated heparin.
    Compared with unfractionated heparin, the use of enoxaparin <12 hours prior to CABG is
    associated with lower postoperative hemoglobin and a higher risk of blood transfusion.
    62. A 56-year-old man with a history of nicotine dependence, diabetes, and hypertension
    presents to the emergency department (ED) with a 10-hour history of severe exertional shoulder
    pain. His father underwent three-vessel coronary artery bypass graft (CABG) surgery at age 60
    years.

    The patient takes aspirin 81 mg daily and metformin 500 mg twice daily. In the ED, his blood
    pressure is 100/70 mm Hg, and heart rate 90 bpm. His electrocardiogram (ECG) is shown (Figure
    1).

    His initial troponin is negative. His pain does not improve with sublingual nitroglycerin. Aspirin 324
    mg orally, intravenous (IV) unfractionated heparin, and clopidogrel 600 mg are initiated. Your
    facility is a percutaneous coronary intervention (PCI)-capable hospital.
    Which of the following is the most appropriate next step?
    a. Intra-aortic balloon pump (IABP).
    b. IV metoprolol.
    c. IV Reteplase.
    d. IV tenecteplase.
    e. Emergent PCI.
    62. e. Emergent PCI.

    The correct answer is emergent PCI. His ECG shows an ST-elevation myocardial infarction (STEMI),
    which is defined by the ESC/ACCF/AHA/World Heart Federation Task Force as a new ST elevation at
    the J-point in at least two contiguous leads of ≥2 mm in men or ≥1.5 mm in women; in leads V2 -
    V3 and/or 1 mm in other contiguous chest or limb leads. New left bundle branch block is considered
    an STEMI equivalent, and may interfere with ST-elevation analysis.

    Reperfusion therapy should be administered to all eligible patients with STEMI with symptom onset
    within the prior 12 hours (Class IA). Primary PCI is the recommended method of reperfusion when
    it can be performed in a timely fashion by experienced operators (Class IA). Fibrinolytics, such as
    tenecteplase and reteplase, are not correct because the question states that the hospital is PCI-
    capable. If the hospital is not PCI-capable, and the patient is greater than 120 minutes away from a
    PCI-capable center, then fibrinolytic therapy would be indicated. IABP is not indicated, because the
    patient is hemodynamically stable and needs urgent PCI. IV metoprolol is not the best answer,
    because the patient has ST elevation and needs urgent reperfusion.
    63. A 59-year-old farmer with a history of hypertension and hyperlipidemia presents with
    crushing substernal chest discomfort that started approximately 1 hour prior to arrival in the local
    emergency department. An electrocardiogram demonstrates 2 mm ST-elevations in V1-V3 with
    reciprocal ST depressions in the inferior leads. He continues to have 7/10 chest pain. The closest
    percutaneous coronary intervention-(PCI) capable facility is 3 hours away. He has no
    contraindications to thrombolysis, so intravenous alteplase is administered. His chest discomfort
    and ST elevations resolve, and he remains hemodynamically stable.
    Which of the following is the best next step in this patient's management?
    a. Emergent coronary angiography.
    b. Transfer to facility with cardiac surgery capability.
    c. Transfer to facility with PCI capability.
    d. Echocardiogram.
    e. Admit to the intensive care unit (ICU) for close monitoring.
    63. c. Transfer to facility with PCI capability.

    Patients who present to a non–PCI-capable hospital with ST-elevation myocardial infarction


    (STEMI) within 12 hours of symptom onset should be immediately transferred to a PCI-capable
    hospital for primary PCI, if the time from first medical contact to intervention will be less than 120
    minutes. If the anticipated time exceeds this threshold, then thrombolysis within 30 minutes of
    arrival should be considered if there are no contraindications.

    For patients receiving fibrinolysis, transfer to a PCI-capable facility is reasonable even when they
    are hemodynamically stable and have clinical evidence of successful reperfusion therapy, as in this
    case (Class IIa). In this patient population, angiography should be performed when logistically
    feasible at the receiving hospital (ideally within the first 24 hours), but not within the first 2-3 hours
    following fibrinolysis because of increased bleeding risk. This “pharmacoinvasive” approach has
    been demonstrated in clinical trials to decrease the risk of recurrent MI and death compared with a
    conservative strategy. Although cardiac surgery backup may be necessary, the patient primarily
    needs PCI capability. Admission to the ICU and echocardiography are warranted, but should not
    delay transfer to a PCI facility.
    64. An 82-year-old active, thin woman with a history of remote tobacco use and hypertension
    presents with new-onset chest pain. The symptoms began 2 weeks prior, initially occurring with
    exertion climbing a flight of stairs, but gradually have became more progressive. On the day of
    presentation, she developed an episode of chest discomfort at rest and her husband brought her to
    the emergency department for evaluation.

    On arrival, she was pain free and her electrocardiogram demonstrated inferolateral T-wave
    inversions. She was admitted to the hospital where serial cardiac biomarkers revealed moderately
    elevated troponin levels. Her other blood work was normal, aside from a mild chronic anemia.
    Based on these findings, an early invasive strategy was planned with cardiac catheterization the
    next day.
    Which of the following management strategies would offer the best risk profile in this patient?
    a. Aspirin, clopidogrel, and enoxaparin.
    b. Aspirin, clopidogrel, and unfractionated heparin.
    c. Aspirin, prasugrel, and unfractionated heparin.
    d. Aspirin, clopidogrel, unfractionated heparin, and glycoprotein (GP) IIb/IIIa receptor inhibitor.
    e. Aspirin, prasugrel, unfractionated heparin, and GP IIb/IIIa receptor inhibitor.
    64. b. Aspirin, clopidogrel, and unfractionated heparin.

    In patients with non-ST-elevation acute coronary syndrome (NSTE-ACS), bleeding is associated with
    worse clinical outcomes. Therefore, the choice of antiplatelet and antithrombotic agents must be
    considered carefully. In fact, the ACUITY trial suggested that the mortality risk associated with
    significant bleeding may be at least as great as that related to the myocardial infarction.

    This patient has multiple bleeding risk factors, including female sex, age, low body weight, and
    anemia. Of the available choices, the combintation of aspirin, clopidogrel, and unfractionated
    heparin would likely incur the lowest bleeding risk.

    All NSTE-ACS patients should receive aspirin. Compared with clopidogrel, prasugrel is associated
    with higher rates of bleeding and should also be avoided in patients >75 years old or low body
    weight, as well as those with a history of prior cerebrovascular accident. The addition of GP IIb/IIIa
    receptor inhibitors upstream of percutaneous intervention would significantly increase the
    bleeding risk and has not been shown to have significant clinical benefit. Enoxaparin was associated
    with increased major bleeding compared with unfractionated heparin in NSTE-ACS patients treated
    with an early invasive strategy in the SYNERGY trial.
    65. A 66-year-old male smoker with a history of diabetes mellitus, hyperlipidemia, and
    gastroesophageal reflux disease (GERD) presents with central chest discomfort occurring at rest.
    The pain began nearly 10 hours before, but he believed it was related to a severe flare of his GERD
    and initially avoided seeking medical attention until the following morning. On arrival in the
    emergency department, his electrocardiogram (ECG) demonstrated Q waves with ST elevations in
    V2-V3. However, he is now free of chest pain. Urgent coronary angiography demonstrated occlusion
    of the mid left anterior descending (LAD) without collaterals.

    Which of the following strategies is the best next step to reduce the risk of cardiac rupture related
    to myocardial infarction?
    a. Intra-aortic balloon pump.
    b. Glycoprotein (GP) IIb/IIIa receptor inhibitor.
    c. Angiotensin-converting enzyme inhibitor (ACEI).
    d. Percutaneous coronary intervention.
    e. Beta-blocker.
    65. d. Percutaneous coronary intervention.

    All patients who present with ST-elevation myocardial infarction (STEMI) within 12 hours of
    symptom onset should receive urgent reperfusion therapy. The risk factors for free wall rupture are
    female sex, older age, presence of Q waves on ECG indicating completed infarct, LAD involvement,
    absence of collaterals, no prior history of MI, hypertension during the acute phase of STEMI, use of
    steroids or nonsteroidal anti-inflammatory drugs, and fibrinolytic therapy greater than 14 hours
    after symptoms onset.

    Reperfusion therapy within 12 hours can decrease this risk. An intra-aortic balloon pump and GP
    IIb/IIIa receptor inhibitors do not decrease the risk of free wall rupture. Medical management with
    ACEIs and beta-blockers are likely warranted in this patient, but would be instituted after
    reperfusion therapy when the patient is hemodynamically stable.
    66. A 69-year-old woman with hypertension and hyperlipidemia presents to the emergency room
    with acute shortness of breath. Two nights ago she had the onset of flu-like symptoms. She has no
    other significant past medical history. On exam she is sitting upright. Her blood pressure is 80/50
    mm Hg, her heart rate is 110 bpm, and her oxygen saturation is 88% on 6-liter nasal cannula. Her
    jugular venous pressure is 15 cm. Lung exam reveals rales to the mid lung fields bilaterally.
    Cardiovascular exam reveals tachycardia without murmur or rub appreciated. Extremities are cool.
    Electrocardiogram shows a 1 mm ST elevation in leads II, III, and a ventricular fibrillation.
    Which of the following is the most likely explanation of her clinical presentation?
    a. Contained free wall rupture.
    b. Right ventricular (RV) infarct.
    c. Ventricular septal rupture.
    d. Papillary muscle rupture.
    e. Giant cell myocarditis.
    66. d. Papillary muscle rupture.

    Mechanical complications of acute myocardial infarction (MI) that can result in shock include
    papillary muscle rupture, ventricular septal rupture, free wall rupture, and RV infarct. In this patient
    presenting with an inferior MI and acute pulmonary edema, the most likely etiology would be
    papillary muscle rupture and severe mitral regurgitation. In the acute setting, a murmur may not be
    heard. This typically occurs from 2 to 7 days post MI. Ventricular septal rupture may result in a
    similar presentation, but usually occurs at 3-5 days and occurs more commonly with anterior MIs.
    RV infarct typically presents with hypotension but clear lung fields. Giant cell myocarditis would not
    be expected to be associated with inferior ST elevations.
    67. A 75-year-old woman presents to the emergency department (ED) 4 days after the onset of chest pain. She
    lives in a remote area and did not initially seek medical attention. Today her family visited her and found her
    barely responsive in her home. Upon arrival to the ED, she is cool, clammy, and confused.

    Her blood pressure is 80/50 mm Hg, heart rate is 110 bpm in sinus rhythm, and oxygen saturation is 90%. She has
    bibasilar fine rales, and elevated jugular venous pressure and a thrill felt along the left sternal border. On
    auscultation, there is an audible grade 4/6 holosystolic murmur and an S3. She has no edema. Her initial 12-lead
    electrocardiogram reveals evidence of an acute anterior myocardial infarction (MI). Her initial cardiac enzymes
    are abnormal.

    An echocardiogram confirms your suspicion of an acute ventricular septal defect (VSD) with anterior akinesia and
    left ventricular ejection fraction of 30%. She is taken quickly to the cardiac catheterization laboratory, where a
    total occlusion of the proximal left anterior descending is found, along with a 70% lesion in a large circumflex
    obtuse marginal. Urgent surgical consultation is obtained.

    Which of the following is the best timing to consider operative repair of the VSD?
    a. In more than 28 days.
    b. The risk is unrelated to the time period after the infarction.
    c. In 15-28 days.
    d. In 7-14 days.
    e. In less than 7 days.
    67. e. In less than 7 days.

    The correct answer is less than 7 days. In post MI VSD, overall surgical mortality is 42.9%,
    according to the Society of Thoracic Surgeons (STS) database. The mortality rate is highly
    associated with the timing of surgery post MI. In the STS database, if repair was performed in
    less than 7 days post MI, operative mortality was 54.1%, while it was 18.4% if surgery was more
    than 7 days post MI.

    Additional independent risk factors for mortality include female sex, presence of shock, older
    age, preoperative balloon pump, hemodialysis, moderate to severe mitral regurgitation, and
    whether the surgery is a re-do cardiac surgery.

    The remaining answers are incorrect because the highest mortality is seen early in the post MI
    course. The progressively lower odds of mortality is due to subselection of a healthier cohort
    and healing of the myocardium with time, which improves surgical outcomes. Percutaneous
    closure of the VSD may be considered in high-risk patients who do not require additional surgical
    procedures, such as coronary bypass or valve replacement, within the acute time frame.
    However, the issue of post-MI friable myocardium still applies to this intervention.
    68. A 55-year-old man is shoveling snow when he is seen grabbing his chest and falls to the
    ground. Bystander cardiopulmonary resuscitation (CPR) is performed until emergency medicine
    services (EMS) arrives. An automated external defibrillator (AED) is attached and shock is advised
    and delivered. CPR is continued and there is no return of spontaneous circulation. Awaiting
    advanced cardiac life support (ACLS), the AED advises another shock, which is administered and
    followed by return of a palpable carotid pulse. He is intubated on scene, after the administration of
    5 mg of midazolam. Prior to intubation, there is no witnessed spontaneous limb movement.

    In the hospital emergency department, an electrocardiogram (ECG) is performed that


    demonstrates 2 mm inferolateral ST-segment depressions. Norepinephrine is initiated for
    hypotension and cardiogneic shock. His vital signs are stable and he is cooled to a temperature of
    35 degrees Centigrade. On neurologic examination, the pupils are fixed and nonreactive. He has no
    spontaneous movements, nor does he withdraw or grimace to noxious stimulus. He is
    overbreathing the ventilator. Aspirin is administered through an orogastric tube. A noncontrast
    head computed tomography is unremarkable.
    Which of the following is the best next step in this patient's management?
    a. Immediate coronary angiography.
    b. Coronary angiography only if patient can follow commands.
    c. Coronary angiography only if cardiac-specific troponin is elevated.
    d. Coronary angiography only if ST elevations develop on ECG.
    e. Coronary angiography only if pupils become reactive to light.
    68. a. Immediate coronary angiography.

    Out-of-hospital cardiac arrest is often caused by acute coronary syndromes. Patients with ST-
    elevation myocardial infarction (STEMI) by ECG after return of spontaneous circulation should go
    emergently for coronary angiography. Similarly, patients with non-STEMI or other evidence of
    acute coronary syndromes with electrical or hemodynamic instability should go emergently for
    coronary angiography.

    Recommendations for emergent coronary angiography are independent of neurologic status, as


    the neurologic exam is unreliable early post arrest. The administration of sedatives or paralytics
    further confounds neurologic prognostication. The absence of spontaneous movement post
    arrest should not be interpreted as poor neurologic prognosis. Similarly, pupillary reactivity early
    post arrest lacks sensitivity or specificity for a poor neurologic outcome. Neurologic
    prognostication is improved at 72 hours post return of spontaneous circulation. If the patient
    was cooled, neurologic examination and prognostication should be delayed until 72 hours post
    rewarming.
    69. During acute coronary syndromes, there is thrombus formation at the site of plaque rupture.
    Which of the following patient factors contributes to the formation of thrombus on a ruptured
    coronary plaque?
    a. A thick fibrous cap.
    b. Laminar flow in the culprit vessel.
    c. Cigarette smoking.
    d. Branch point coronary anatomy.
    e. Increased high-density lipoprotein cholesterol (HDL-C).
    69. c. Cigarette smoking.

    Cigarette smoking is the correct answer, because it has been shown to correlate with increased
    systemic thrombotic propensity in patients. Increased thrombotic propensity is one of three factors
    in Virchow’s triad that contributes to thrombus formation in acute plaque rupture. Laminar flow
    would not increase the risk of thrombosis. Branch point areas may have increased plaque
    formation, but not necessarily plaque rupture. Thickness of the fibrous cap correlates with risk of
    plaque rupture, but not directly with thrombus formation. Increased HDL-C does not increase foam
    cell formation as opposed to increased low-density lipoprotein cholesterol.
    70. A 66-year-old man presents with substernal chest pain suspicious for myocardial ischemia
    that began approximately 45 minutes ago, but has now subsided. He has a past history of heavy
    smoking and carries the diagnosis of chronic obstructive pulmonary disease, for which he is being
    treated with inhalers that he intermittently uses. He has been noncompliant with medications in
    the past and has been homeless at various times in his life. He has hypertension and borderline
    hyperlipidemia.

    His examination reveals normal blood pressure with a heart rate of 102 bpm. His oxygen saturation
    is 89%. He has reduced breath sounds throughout, but a normal cardiac exam. His initial
    electrocardiogram (ECG) reveals sinus tachycardia with left ventricular hypertrophy and secondary
    repolarization changes.
    Which of the following is the most sensitive and specific laboratory test (or tests) for the diagnosis
    of myocardial infarction (MI) in this situation?
    a. Cardiac-specific troponin plus creatine kinase-myocardial band (CK-MB).
    b. Cardiac-specific troponin plus D-dimer.
    c. Cardiac-specific troponin plus N-terminal pro-brain natriuretic peptide (NT-proBNP).
    d. Cardiac-specific troponin plus CK total.
    e. Cardiac specific troponin only.
    70. e. Cardiac specific troponin only.

    In the appropriate clinical context, an MI is diagnosed when there is an elevation of cardiac-specific


    biomarkers >99% above the upper reference limit and at least one of the following: 1) symptoms of
    ischemia, 2) new or presumed significant ST-segment–T wave (ST–T) changes or new left bundle
    branch block (LBBB), 3) development of pathological Q waves in the ECG, 4) imaging evidence of
    new loss of viable myocardium, 5) a new regional wall motion abnormality, or 6) identification of
    an intracoronary thrombus by angiography or autopsy.

    The definition revolves around an elevation in cardiac-specific troponin (the preferred biomarker),
    as it is the most sensitive and specific marker of myocardial necrosis. If troponin is unavailable, CK-
    MB would be the next most sensitive biomarker and may be used. Creatine phosphokinase (CPK) is
    nonspecific and released by skeletal and cardiac muscle breakdown; therefore it is unreliable as a
    biomarker of myocardial necrosis. NT-proBNP is a biomarker that reflects myocardial wall stress
    and has been shown to be related to prognosis in acute MI, but is not a specific marker of
    myocardial necrosis. D-dimer is nonspecific, although very sensitive for thrombus, and does not
    reflect myocardial necrosis.
    71. A 28-year-old woman who is 32 weeks pregnant presents to the emergency department with
    1 hour of chest pressure and dyspnea. She has no prior history of cardiac disease. She is tachycardic
    with a heart rate of 120 bpm and a blood pressure of 150/60 mm Hg. Her oxygen saturation is 95%
    on 2 liters of nasal cannula supplemental oxygen. She has a 1/6 early peaking systolic murmur
    across the precordium. Her jugular venous pressure is elevated. There are faint rales at the bases of
    her lungs bilaterally. Her electrocardiogram (ECG) demonstrates sinus tachycardia at 120 bpm with
    3 mm of ST-elevation in leads V1-V4.
    Which of the following is the most likely etiology for her presentation?
    a. Coronary artery dissection.
    b. Pneumothorax.
    c. Amniotic fluid embolism.
    d. Pulmonary embolism.
    e. Eclampsia.
    71. a. Coronary artery dissection.

    The correct answer is coronary artery dissection. There is a risk for coronary artery dissection
    during pregnancy and shortly after delivery in the postpartum period. It is a rare, but well
    recognized complication of pregnancy. Her presentation is most consistent with this diagnosis
    given the clinical features of chest pain, mild pulmonary edema on examination, and ST-segment
    elevation in the left anterior descending territory.

    The ECG findings and clinical features are not characteristic for pericarditis. There is a risk of
    pulmonary embolism during pregnancy and in the postpartum period due to the hypercoagulability
    of pregnancy. However, the features of her presentation are not consistent with this diagnosis.
    Likewise, pneumothorax is also on the differential diagnosis for chest pain and dyspnea, but her
    physical exam is not consistent with this, because there is no history of trauma and there is no
    increased risk of pneumothorax during pregnancy. Amniotic fluid embolus would occur postpartum
    and presents with shock. Eclampsia presents with significant hypertension and seizures and would
    not cause ST elevation.
    72. A 78-year-old man is seen in the office 2 weeks after an anterior ST-segment elevation MI
    (STEMI). He underwent primary percutaneous coronary intervention with a drug-eluting stent to
    the left anterior descending. His ejection fraction is 40%. His medical history is significant for a
    transient ischemic attack (TIA) 5 years ago, chronic kidney disease stage 3b, and peripheral arterial
    disease with mild intermittent calf claudication. He was discharged on dual antiplatelet therapy
    with ticagrelor 90 mg twice daily and aspirin 81 mg daily.
    Which of the following is a contraindication to vorapaxar in this patient?
    a. History of cerebrovascular event.
    b. Concomitant use of ticagrelor.
    c. Chronic kidney disease.
    d. Age greater than 75 years.
    e. Recent STEMI.
    History of cerebrovascular event.

    Vorapaxar is an antiplatelet drug that inhibits PAR-1, the thrombin receptor on platelets. The TRA
    2°P-TIMI 50 (Thrombin Receptor Antagonist inSecondary Prevention of Atherothrombotic Ischemic
    Events Thrombolysis in Myocardial Infarction) trial randomized 26,449 patients who had a history
    of MI, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or
    matching placebo. Cardiovascular death, MI, or stroke was significantly lower in the vorapaxar
    group compared with the placebo group. Moderate or severe bleeding occurred in 4.2% of patients
    who received vorapaxar and 2.5% of those who received placebo.

    There was an increase in the rate of intracranial hemorrhage in the vorapaxar group. Patients with
    a history of stroke had an excessive risk of intracranial hemorrhage. Therefore, the drug is
    contraindicated in patients with a history of a TIA or stroke. In the TRA 2°P-TIMI 50 trial, the use
    andtype of P2Y12 inhibitor was left to the discretion of the physician. There are no specific data on
    the risk of vorapaxar in patients treated with clopidogrel compared with more potent agents. A
    small number of patients (0.7%) received prasugrel during the study. Ticagrelor is not
    contraindicated, but may alter the efficacy or safety. Because of liver metabolism, vorapaxar can be
    used in patients with chronic kidney disease.
    73. A 58-year-old man presents to your office to establish cardiovascular (CV) care. He has a
    history of myocardial infarction (MI) treated with a drug-eluting stent 2 years ago. At that time, he
    had single-vessel disease and a preserved ejection fraction. He was treated with dual antiplatelet
    therapy for 12 months and he has been on low-dose aspirin since that time. He has diabetes
    requiring oral medication and hypercholesterolemia. He has no history of stroke or bleeding. He is
    asymptomatic and has not had recurrent ischemia.
    Which of the following do you recommend to decrease the risk of major adverse CV events?
    a. Clopidogrel 75 mg daily.
    b. Ticagrelor 90 mg twice daily.
    c. Prasugrel 10 mg daily.
    d. Ticagrelor 60 mg twice daily.
    e. Prasugrel 5 mg daily.
    73. d. Ticagrelor 60 mg twice daily.

    The PEGASUS-TIMI 54 (Prevention of Cardiovascular Events in Patients with Prior Heart Attack
    Using Ticagrelor Compared to Placebo on a Background of Aspirin Thrombolysis in Myocardial
    Infarction 54) trial randomly assigned in a 1:1:1 double-blind fashion, 21,162 patients who had an
    MI in the past 1 to 3 years to ticagrelor 90 mg twice daily, ticagrelor 60 mg twice daily, or placebo.
    Ticagrelor reduced the rate of the primary efficacy endpoint (death, MI, or stroke), with Kaplan-
    Meier rates at 3 years of 7.85% for ticagrelor 90 mg twice daily, 7.77% for ticagrelor 60 mg twice
    daily, and 9.04% for placebo group. For ticagrelor 90 mg versus placebo, the hazard ratio (HR) was
    0.85 and the confidence interval (CI) was 0.75 to 0.96 (p = 0.008), and for ticagrelor 60 mg versus
    placebo the HR was 0.84 and the CI was 0.74 to 0.95 (p = 0.004). The rates of TIMI major bleeding
    were higher with ticagrelor (2.60% with 90 mg and 2.30% with 60 mg) than with placebo (1.06%).
    74. A 74-year-old woman is referred to you with indigestion, belching, and mild exertional
    “discomfort,” but no chest pain. She is overweight and has hypertension, diabetes (non-insulin
    dependent), and sleep apnea. There is a family history of coronary artery disease (CAD) in an older
    brother who had successful percutaneous coronary intervention (PCI).

    Her current medications include chlorthalidone 25 mg, lisinopril 40 mg, metformin 500 mg twice
    daily, and a multivitamin. Her baseline labs are normal, including her lipid profile and HbA1c. Her
    electrocardiogram (ECG) is normal. Physical examination reveals a body mass index of 34.5, heart
    rate of 78 bpm and regular, blood pressure of 135/85 mm Hg, and oxygen saturation of 94%. She
    has an auscultatory S4 and a soft grade 2/6 aortic flow murmur, but no bruits, and a negative
    cardiac exam otherwise.

    Which of the following do you recommend as the next step in her work-up?
    a. Nuclear exercise stress test.
    b. No further cardiac workup necessary.
    c. Echocardiogram.
    d. Gastrointestinal (GI) referral and possible endoscopy.
    e. Coronary computed tomographic angiography (CTA).
    74. a. Nuclear exercise stress test.

    While she does not have classic angina, she has multiple features that make her presentation
    suggestive of atypical angina. Atypical angina may present as indigestion, belching, and exertional
    dyspnea, and it is more common in women, older patients, and those with diabetes.

    Her baseline ECG is normal and the first test to be considered should be a stress ECG with imaging.
    In women, the use of imaging improves diagnostic accuracy when compared with standardized ECG
    stress testing. An echocardiogram to assess left ventricular function might be useful, but her exam
    and ECG is normal. GI endoscopy might be a consideration as well, but the exertional component to
    her chest “discomfort” warrants further evaluation. Coronary CTA and a calcium score might also
    be helpful, because a negative study at her age would suggest there is little chance that CAD is
    present. Because angina can be difficult to diagnose in this population, some effort to exclude a
    coronary source should be undertaken.
    75. A 57-year-old man is referred to you with shortness of breath. He has not been followed
    regularly and he says he was told he had a murmur as a teenager, but that he would likely
    “outgrow it.” He works in heating and air conditioning and has a fairly physical work environment.
    He does not smoke and is on no medication.
    Which of the following could be considered an etiology for cardiac-related dyspnea?
    a. A left-to-right intracardiac shunt Qp/Qs of 2.1:1.
    b. Pulmonary capillary wedge pressure (PCWP) of 11 mm Hg.
    c. A distal left circumflex coronary lesion of 60%.
    d. Cardiac index of 3.0 L/m2.
    e. Mean pulmonary artery pressure of 28 mm Hg during exercise.
    75. a. A left-to-right intracardiac shunt Qp/Qs of 2.1:1.

    The correct answer is a left-to-right cardiac shunt with its associated volume overload.

    Cardiac-related dyspnea can occur when there is an elevated PCWP with resultant stimulation of
    the interstitial J receptors and/or pulmonary edema. Usually there is associated orthopnea or
    paroxysmal nocturnal dyspnea (PND), which occurs 2-4 hours after the onset of sleep and subsides
    minutes after sitting upright or standing. The PCWP of 11 mm Hg is normal in this situation.

    Patients with low cardiac output (cardiac index of 3.0 L/m2) experience dyspnea on exertion and
    fatigue in the absence of orthopnea or PND. Dyspnea may also be due to ischemia during exercise,
    but it is very unlikely to be associated with the degree of coronary disease that jeopardizes only a
    small amount of myocardium as noted.
    76. The jugular venous pressure (JVP) reflects the right atrial (RA) pressure. It is a critical
    component of the cardiac examination, as an elevation suggests an elevated RA pressure and has
    prognostic importance.
    Which of the following is correct regarding the assessment of an elevated JVP?
    a. It is best measured as the vertical distance above the clavicle in the upright position.
    b. It is best measured as the vertical distance between the top of the pulsation and the angle of
    c. Louis.
    d. It can best be assessed with the patient lying at a 20 degree elevation.
    e. The degree of elevation cannot be reliably assessed during atrial fibrillation.
    f. Either the external or internal jugular veins can be assessed reliably.
    76. a. It is best measured as the vertical distance above the clavicle in the upright position.

    The height of the JVP is reflective of RA pressure. The best answer is to measure the height of the
    JVP in the upright position above the clavicle. Using that as a reference point is effective, because
    the RA pressure must be at least 10 cm high for the waveforms to be visible in that position. Thus,
    any evidence of waveforms in the upright position means the JVP is elevated.

    While either the external or the internal jugular can be used, the jugular vein valves may interfere
    with accuracy and the internal jugular vein is preferred. Using the angle of Louis (the sternal
    inflection point where the manubrium meets the sternum), a distance >3 cm has been considered
    abnormal. However, the distance from the sternal angle and the RA is quite variable among
    patients, and this leads to an underestimation of the venous pressure. Atrial fibrillation will affect
    the waveforms observed, but the total height of the JVP column will still reflect mean RA pressures.
    The height of the JVP cannot be reliably assessed with the patient in a semisupine position.
    76. A number of early diastolic heart sounds may be audible in certain patients. These include an
    S3 in young patients and in older patients suffering from heart failure, a pericardial knock in those
    with constrictive pericarditis, and a mitral opening snap in patients with rheumatic mitral stenosis.
    The timing from S2 of each of the early diastolic heart sounds varies, depending on the origin of the
    sound.
    Which of the following is the correct sequence one could expect these heart sounds to occur if they
    were present, from a timing perspective in early diastole?
    a. Opening snap, followed by pericardial knock, followed by an S3.
    b. Opening snap, followed by an S3, followed by pericardial knock.
    c. Pericardial knock, followed by an S3, followed by opening snap.
    d. Pericardial knock, followed by opening snap, followed by an S3.
    e. S3, followed by an opening snap, followed by a pericardial knock.
    77. a. Opening snap, followed by pericardial knock, followed by an S3.
    These early diastolic sounds reflect the hemodynamic changes in early diastole. The opening snap is
    a high-pitched sound occurring shortly after S2 and reflects the abrupt opening of a mobile but
    stenotic mitral valve. The interval between the S2 and opening snap decreases as the left atrial (LA)
    pressure rises (worsening mitral stenosis). It is the first sound heard in early diastole, as it reflects
    the mitral valve opening prior to the initiation of left ventricular (LV) filling. The second possible
    sound is the pericardial knock. It occurs once the mitral valve is open and is a high-pitched sound
    reflecting the impact of the cessation of rapid filling on the LV wall. In constriction, the LV fills
    rapidly from the elevated LA pressure, to the point it cannot expand further due to the restriction
    placed on it from the constrictive pericarditis.

    An S3 is a low-pitched sound that reflects the rapid filling phase of diastolic LV filling and occurs
    later than the impact sound from a pericardial knock. An S3 may be normal in children, adolescents,
    and young adults, but implies heart failure in adults. It can also be heard in severe mitral
    regurgitation. Thus, the correct answer is opening snap, followed by pericardial knock, followed by
    an S3.
    78. The Valsalva maneuver can help distinguish the origin of some cardiac murmurs and is known
    to be abnormal in heart failure. For patients with an intact autonomic nervous system, when the
    Valsalva maneuver is performed there are four phases evident from the hemodynamic tracings.

    Which of the following occurs during phase 3 of the Valsalva maneuver?


    a. The systemic pressure declines and the heart rate (HR) increases.
    b. The systemic pressure increases due to increased blood pressure return.
    c. The systemic pressure increases with slowing of the HR.
    d. The systemic pressure declines in response to a decrease in intrathoracic pressure.
    e. The systemic pressure increases transiently due to an increase in intrathoracic pressure.
    78. d. The systemic pressure declines in response to a decrease in intrathoracic pressure.

    The four phases of the Valsalva maneuver are shown in Figure 1, where the relative HR and aortic
    pressure are outlined. In phase 1, with the initiation of the Valsalva, the intrathoracic pressure
    increases and blood is forced out of the pulmonary circuit. There is an increase in left ventricular
    (LV) filling and stroke volume and the systemic blood pressure rises. In phase 2, with the
    maintenance of the Valsalva, the LV filling declines as the increased intrathoracic pressure impedes
    venous return and stroke volume drops, resulting in vasoconstriction with a compensatory
    tachycardia.

    In phase 3, with release of the Valsalva, the aortic pressure declines further in response to the
    decreased intrathoracic pressure and decreased left atrial return associated with the increased
    aortic volume and the delay before venous return catches up to the LV. In phase 4, the LV preload
    increases with the return of the venous flow; stroke volume increases rapidly into the
    vasoconstricted aortic system and the blood pressure overshoots and the baroreceptors are
    stimulated with a subsequent reduction in the HR. Some have noted that when the ratio of the the
    fastest HR (during Valsalva) divided by the slowest HR (upon release) is <1.4, there is evidence for
    autonomic impairment.
    (Figure 1)
    79. The use of the Valsalva maneuver can help differentiate the origin of certain cardiac
    murmurs. The four phases of the Valsalva maneuver also may be abnormal in patients with
    autonomic dysfunction and in heart failure.
    Which of the following summarizes the abnormality in the phases of the Valsalva maneuver that
    occurs in heart failure?
    a. There is an increase in BP with little change in heart rate (HR) during phase 2.
    b. There is a decrease in blood pressure with no change in HR during phase 3.
    c. There is an increase in BP and bradycardia during phase 4.
    d. There is an increase in blood pressure (BP) and bradycardia during phase 2.
    e. There is a decrease in BP with little change in HR during phase 2.
    79. d. There is an increase in blood pressure (BP) and bradycardia during phase 2.

    There is an increase in BP with little change in HR during phase 2 of the Valsalva maneuver in
    patients with significant heart failure. This is shown graphically in Figure 1. As opposed to the
    normal phase 4 of the Valsalva, in patients with severe heart failure there is a “square wave”
    response with an initial increase in BP (phase 1) that remains elevated during the entire strain
    period (phase 2) and returns to resting levels in phase 3. This is thought to be due to maintenance
    of the left ventricular (LV) filling during the strain phase, despite the decrease in venous return. This
    is presumably due to the increased central blood volume that serves as a reservoir to maintain LV
    preload. This can be detected with BP monitoring during Valsalva or by an abnormal response as
    assessed by the Korotkoff sounds as shown in Figure 2. In the latter figure, the loss of the
    overshoot in BP has been correlated with loss of systolic function and the square root response has
    been correlated with an elevated pulmonary capillary wedge.
    (Figure 1)
    (Figure 2)
    80. A 65-year-old woman with hypertension is admitted to a rural hospital with chest pain for 1
    hour and an ST-segment elevation myocardial infarction (STEMI). She immediately undergoes
    therapy with tenecteplase.

    On arrival to the tertiary referral center, she is comfortable without chest pain, her
    electrocardiogram is now normal, and she is hemodynamically stable. Her exam is only remarkable
    for S4.
    Which of the following is the next most appropriate step?
    a. Emergent coronary angiography.
    b. Coronary computed tomography angiography.
    c. Elective coronary angiography.
    d. Cardiac magnetic resonance imaging.
    80. c. Elective coronary angiography.

    Assessment of clinical reperfusion following lytic therapy for STEMI is essential to guiding the
    urgency of subsequent coronary angiography. Resolution of symptoms, improvement of ST-
    segment elevation by at least 50%, and reperfusion arrhythmias (e.g., accelerated idioventricular
    rhythm) are indicative of epicardial coronary patency. If there is clinical uncertainty about the
    status of reperfusion, emergent coronary angiography is warranted (e.g., rescue percutaneous
    coronary intervention). Most patients following STEMI treated with lytic therapy will undergo
    elective coronary angiography to define the coronary anatomy within a day of presentation (Class
    IIa). In high-risk scenarios like shock, heart failure, or recurrent chest pain, urgent coronary
    angiography is recommended (Class I).
    81. A 49-year-old man with no significant medical history presents with 1 week of intermittent
    chest pain that worsened over the 2 hours prior to presentation.

    Blood pressure measures 84/43 mm Hg with a pulse of 113 bpm. Oxygen saturation on 2 liters of
    nasal cannula is 91%. He is tachycardic with an S3 and rales on lung exam. Initial electrocardiogram
    demonstrates ST-segment elevation (STE) in leads V1-V5.

    The patient undergoes urgent cardiac catheterization with placement of a drug-eluting stent in the
    proximal left anterior descending artery. His blood pressure improves post revascularization and he
    is admitted to the coronary care unit. A post-percutaneous coronary intervention echocardiogram
    shows severe hypokinesis of the anterior and anterolateral wall. Left ventricular ejection fraction is
    25%.

    On day 2 of hospitalization, the patient develops dyspnea and the rhythm seen in Figure 1.

    Which of the following best describes the incidence and degree of myocardial injury associated
    with the rhythm seen in Figure 1 in an anterior as compared with inferior myocardial infarction
    (MI)?
    a. The incidence during MI is lower, the degree of myocardial injury is lower, and the location of
    block is at the AV node.
    b. The incidence during MI is greater, the degree of myocardial injury is lower, and the location
    of block is at the atrioventricular (AV) node.
    c. The incidence during MI is the same, the degree of myocardial injury is greater, and the
    location of block is below the AV node.
    d. The incidence during MI is lower, the degree of myocardial injury is greater, and the location
    of block is below the AV node.
    81. d. The incidence during MI is lower, the degree of myocardial injury is greater, and the
    location of block is below the AV node.

    The rhythm strip reveals the development of complete heart block (CHB) occurring in the setting of
    recent anterior wall MI. This is a serious complication of anterior MI, which occurs in roughly 1% of
    cases. CHB in anterior MI is associated with poorer short-term outcomes, including survival, as
    compared with anterior MI patients who do not develop CHB.

    The incidence of CHB in inferior distribution ST-elevation (STEMI) is higher, approximately 4%, and
    may be transient. CHB occurring in inferior STEMI patients is associated with a higher location of AV
    block (typically the AV node), whereas in anterior wall MI, the location of block is usually below the
    AV node, resulting in higher long-term block.

    The degree of myocardial injury in anterior wall STEMI exhibiting CHB is greater than the amount of
    myocardial injury observed in inferior STEMI complicated by CHB.
    82. A 75-year-old woman with diabetes is admitted to the coronary care unit after a drug-eluting
    stent (DES) placement in her mid right coronary artery following an acute inferior wall myocardial
    infarction (MI). Earlier, she had received 600 mg of clopidogrel in the emergency department and
    had been administered a bolus of bivalirudin followed by an intravenous infusion. She has a history
    of a prior ischemic stroke and has been a lifelong asthmatic.

    Her electrocardiogram shows sinus rhythm at 50 bpm, and inferior Q waves with almost complete
    resolution of her inferior ST elevation. Her body mass index is 20 kg/m2, blood pressure is 148/70
    mm Hg, and lungs are clear to auscultation. Cardiac examination reveals a fourth heart sound and a
    loud aortic component of the second heart sound.
    At discharge, which of the following medications is the most appropriate choice?
    a. Ticagrelor.
    b. Ticlopidine.
    c. Prasugrel.
    d. Cangrelor.
    e. Clopidogrel.
    82. d. Cangrelor.

    The choice of antiplatelet agents following DES placement for acute MI should be guided by specific
    patient characteristics outlined by clinical trials. Prasugrel is contraindicated in this patient due to
    her size, age, and previous stroke. Ticagrelor is not preferred due to the history of asthma and
    bradycardia on exam. Ticlopidine is no longer a first-line choice due to its numerous adverse
    effects, including rash, diarrhea, and neutropenia. Cangrelor is only available intravenously.
    83. Mr. K is a 76-year-old man who presents to the emergency department. He complains of
    epigastric pressure, shortness of breath, nausea, and fatigue, all of which suddenly started about 2
    hours earlier. He has been in good health in the past and his history is remarkable only for diabetes
    treated with oral hypoglycemic medication. He is clinically stable with a blood pressure of 112/78
    mm Hg, heart rate of 75 bpm, S02 of 96%, and temperature of 36.4°C. His electrocardiogram
    (ECG) is normal. An initial set of cardiac biomarkers turns out to be negative. After a tablet of
    sublingual nitroglycerin, he says that his symptoms are slightly improved.
    Which of the following is the most appropriate next step for management?
    a. Transesophageal echocardiography.
    b. Outpatient stress test.
    c. ECG with posterior leads.
    d. Ventilation/perfusion scan.
    e. Coronary computed tomography angiography (CTA).
    83. c. ECG with posterior leads.

    This patient presents with strong pretest probability for an acute ischemic syndrome, although
    the ECG is normal. Posterolateral infarctions are often electrocardiographically silent and should be
    considered in these situations. Presence of ST-segment elevation in V7-V9 will confirm the diagnosis
    of true posterior ST-segment elevation myocardial infarction and the need to perform urgent
    reperfusion.

    Outpatient stress testing would not be appropriate in a patient with high pretest probability of an
    acute ischemic syndrome. Coronary CTA performs best in intermediate-risk patients. The pretest
    probability for pulmonary embolism and aortic disease is sufficiently low such that they would not
    be appropriate when the most likely diagnosis is still an acute coronary syndrome.
    84. Which of the following phrases best describes tenecteplase?
    a. Nonantigenic, administered as a single bolus, fibrin specific.
    b. Nonantigenic, administered as two boluses 10 minutes apart, fibrin specific.
    c. Antigenic, administered as a single bolus, fibrin specific.
    d. Antigenic, administered as two boluses 10 minutes apart, not fibrin specific.
    e. Nonantigenic, administered as single bolus, not fibrin specific.
    84. a. Nonantigenic, administered as a single bolus, fibrin specific.

    Tenecteplase, or TNK, is a fibrin-specific, nonantigenic fibrinolytic. Although its administration is


    weight based, its main advantage is that it can be administered as a single bolus. Reteplase, or
    Retavase, has limited fibrin specificity. It is given as two boluses 10 minutes apart, but does not
    have to be adjusted for weight. Tissue plasminogen activator has moderate fibrin specificity, but is
    administered as a drip. Streptokinase has no fibrin specificity and is highly antigenic.
    85. A 63-year-old man presents with chief complaints of chest heaviness. He tells you about an
    episode in the morning that subsided spontaneously after 10 minutes, and a new episode 2 hours
    before presentation that lasted about 30 minutes. Now he is asymptomatic, but his wife insisted on
    bringing him to the emergency department. He has been diabetic for the last 15 years and treated
    with metformin and glimepiride. He has also been prescribed amlodipine to control his blood
    pressure.

    His blood pressure is now 145/90 mm Hg, his heart rate is 62 bpm, and creatinine is 1.12 mg/dl.
    The physical exam is unremarkable. He smokes about 10 cigarettes per day. His electrocardiogram
    is normal and on the first set, his troponin T is 0.06 ng/ml (99th percentile, 0.01 ng/ml). You
    calculate a GRACE score of 106 and TIMI score of 3.
    Which of the following is the optimal management for this patient?
    a. Emergent coronary angiography.
    b. Coronary angiography within 24 hours.
    c. No further diagnostic testing.
    d. Coronary computed tomography angiography.
    e. Stress test.
    85. b. Coronary angiography within 24 hours.

    The risk profile of this patient does not warrant an emergent catheterization. The 2011 focused
    update of the Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation
    Myocardial Infarction (NSTEMI) considers an early invasive management strategy within 24 hours
    reasonable in the case of high-risk criteria or clinical instability. This patient is diabetic and has
    positive troponin, both of which favor an invasive approach within 24 hours.

    This patient has a confirmed NSTEMI, and a stress test to provoke ischemia in this setting is not
    diagnostically useful and is unsafe. Coronary computed tomography angiography is predominantly
    useful when there is diagnostic uncertainty and the pretest probability is either low or
    intermediate.
    86. A 50-year-old man with diabetes mellitus and a history of cigarette smoking underwent
    percutaneous coronary intervention of his mid left anterior descending artery 2 months ago. At the
    time of his procedure, he was noted to have a total cholesterol of 350 mg/dl, low-density
    lipoprotein cholesterol (LDL-C) of 180 mg/dl, high-density lipoprotein cholesterol (HDL-C) of 20
    mg/dl, and triglycerides of 280 mg/dl. He was placed on atorvastatin 40 mg daily, and repeat
    laboratory tests obtained today show a total cholesterol of 200 mg/dl, LDL-C of 120 mg/dl, HDL-C
    of 23 mg/dl, and triglycerides of 250 mg/dl. The patient is compliant with his medical regimen.

    Which of the following is the most appropriate next step for this patient?
    a. Add niacin.
    b. Increase atorvastatin dose to 80 mg daily.
    c. Add omega-3 fatty acids.
    d. Add ezetimibe.
    e. Add gemfibrozil.
    86. b. Increase atorvastatin dose to 80 mg daily.

    For individuals with established coronary artery disease and diabetes, an LDL-C reduction of at least
    50% is the recommended therapeutic strategy. Although administration of a statin reduced the
    patient's LDL-C, since it is not at goal, the statin dose should be increased.

    Gemfibrozil is used primarily to treat hypertriglyceridemia, and an increased incidence of myositis


    is observed when it is used concomitantly with a statin. The addition of niacin to a statin is
    attractive because it may further increase HDL and reduce triglycerides, but it has not been shown
    to reduce cardiovascular events. Ezetimibe and omega-3 fatty acids are not indicated without
    maximizing statin therapy.
    87. Which of the following findings is most useful for establishing or excluding the diagnosis of ST-
    segment elevation myocardial infarction (STEMI)?
    a. Normal cardiac troponin 1 hour after symptom onset.
    b. ECG with 100% ventricular pacing and 3 mm of ST-segment elevation in precordial leads.
    c. ECG with 1 mm of ST-segment elevation in leads V2-V3 in an asymptomatic 44-year-old man.
    d. Electrocardiogram (ECG) with left bundle branch block (LBBB) and 2 mm of concordant ST-
    segment elevation in two leads with a positive QRS deflection.
    87. d. Electrocardiogram (ECG) with left bundle branch block (LBBB) and 2 mm of concordant
    ST-segment elevation in two leads with a positive QRS deflection.

    Neither cardiac troponin nor creatine kinase-myocardial band (CK-MB) are sufficiently sensitive
    within the first 1-2 hours after symptom onset to exclude a diagnosis of MI.

    The multisociety Task Force for the Universal Definition of MI has defined the diagnostic criteria for
    STEMI (at the J point) as follows: ≥2 mm in men or ≥1.5 mm in women in leads V2-V3 and/or ≥1 mm
    in at least two other contiguous chest leads or two limb leads. Moreover, particularly in young
    men, a multisociety scientific statement recommends a higher threshold of ≥2.5 mm in leads V2-V3.

    The Sgarbossa criteria for diagnosis of MI emphasize concordant ST-segment elevation in two leads
    with a positive QRS as most indicative of STEMI in the setting of an LBBB. It is challenging to
    diagnose STEMI in the setting of ventricular pacing.
    88. A 60-year-old businessman has a history of obesity, with a body mass index of 32 kg/m2. His
    history includes prior cigarette smoking, hypertension, and hyperlipidemia. Six months ago, he
    decided to start climbing three flights of stairs to his office each morning. When performing this
    activity, he notes a pressure sensation localized to his substernal region that resolves within 2-3
    minutes once he sits down at his desk. He describes this symptom to his physician, who orders an
    exercise treadmill test. The results are as follows: exercise duration 8 minutes of the Bruce
    protocol; the patient requests to stop because of his chest pressure; exercise electrocardiogram
    (ECG) is negative for ischemia.
    Based on the ECG stress results, his post-test probability of coronary disease is which of the
    following?
    a. >90%.
    b. 60-90%.
    c. 0-30%.
    d. 30-60%.
    88. a. >90%.

    A 60-year-old man with typical angina has a pretest probability of coronary artery disease (CAD)
    that is >90%. According to Bayes Theorem, a negative exercise ECG shifts this probability very little,
    and the post-test probability of CAD remains >90%. This patient’s Duke treadmill score can be
    calculated as 0: 8 minutes Bruce protocol – 0 (for no ST-segment depression) – 8 (4 x 2, for test-
    limiting angina). A Duke treadmill score of zero places a patient into the intermediate-risk category
    for cardiac death, where annual cardiac mortality ranges between 1-3%.
    89. Ionizing radiation can result in cellular DNA injury. A stochastic injury from medical radiation
    exposure results in which of the following consequences?
    a. Carcinogenesis.
    b. Nausea and vomiting.
    c. Skin injury.
    d. Hair loss.
    e. Cellular death.
    89. a. Carcinogenesis.

    Stochastic injuries can occur after a single exposure to the cell. It is therefore not threshold
    dependent. The DNA injury that results does not kill the cell, but rather the cell lives on mutated.
    This can eventually lead to cancers later in life. A deterministic injury results when the cell dies
    from the DNA damage. If enough cells of an organ die, then the organ becomes dysfunctional. This
    is seen most often in skin damage, but can result in hair loss, or if extensive (such as acute radiation
    injury), can result in sloughing of the gastrointestinal tract. Deterministic injury only occurs after a
    threshold level of radiation exposure has occurred.
    90. A 65-year-old active woman has a history of type 2 diabetes and uncomplicated inferior wall
    myocardial infarction treated with lytic therapy therapy 10 years ago. She has experienced a dozen
    episodes of interscapular back and chest discomfort over the past month. This discomfort usually
    occurs while gardening. She has tried nitroglycerin twice and thinks that it has helped. Her
    electrocardiogram (ECG) shows old Q waves in the inferior leads and is otherwise normal.
    Which of the following is the procedure of choice for this woman?
    a. Standard treadmill test.
    b. Coronary angiogram.
    c. Regadenoson single-photon emission computed tomography (SPECT).
    d. Dobutamine ECG.
    90. a. Standard treadmill test.

    This patient is describing atypical angina and is therefore a candidate for noninvasive assessment,
    rather than proceeding directly to coronary angiography. The multisociety stable ischemic heart
    disease guideline recommends consideration of three criteria for deciding between the standard
    treadmill test and stress imaging: a history of prior coronary revascularization, ability to adequately
    exercise, and findings on a resting ECG.

    ECG abnormalities that warrant proceeding with stress imaging instead of the standard treadmill
    test include pre-excitation, left bundle branch block, paced ventricular rhythm, or >1 mm of ST-
    segment depression. The presence of Q waves is not an indication to proceed with stress imaging
    instead of the standard exercise treadmill test. Although this patient has risk factors that place her
    at a higher risk (i.e., history of established coronary artery disease and the presence of diabetes),
    the standard treadmill test would still be the procedure of choice in this setting, according to the
    guideline.
    91. Which of the following procedures results in the highest potential effective radiation dose
    being delivered to the patient?
    a. Technetium-99m sestamibi rest-stress scan.
    b. Thallium-201 rest-stress scan.
    c. Diagnostic coronary angiogram.
    d. CT coronary angiogram.
    e. Coronary calcium computed tomography (CT).
    91. b. Thallium-201 rest-stress scan.

    Diagnostic coronary angiography, technectium-99m scans, and CT angiography (if the newest
    techniques are applied) result in similar effective dose exposure to patients. Increased dose occurs
    with percutaneous coronary intervention because of the time, angulated views, the use of
    magnified views, etc. Thallium-201 has a long half-life and slow excretion, resulting in the greatest
    exposure compared to the other agents.
    92. A 65-year-old man presents for cardiac computed tomography (CT) due to a myocardial
    perfusion study in which the imaging and electrocardiogram findings are discordant.
    Which of the following presenting conditions should lead to cancellation of the cardiac CT order?
    a. Use of sildenafil 24 hours ago.
    b. Body weight 42 kg/m2.
    c. Sinus bradycardia at 40 bpm.
    d. Atrial fibrillation, rate 80-110 bpm.
    92. d. Atrial fibrillation, rate 80-110 bpm.

    Atrial fibrillation due to the extreme R-R variability causes motion artifacts on cardiac CT that lead
    to an unacceptable rate of nondiagnostic examinations. Although some scan modes can enable
    moderately accurate cardiac CT angiography in the setting of atrial fibrillation (e.g., helical CT
    without tube current modulation or single-beat wide-area detector CT), atrial fibrillation represents
    a strong contraindication to the test. Bradycardia is not a contraindication. Increased body mass
    index can lead to noisy cardiac CT images and will necessitate higher radiation exposure. Sildenafil
    use contraindicates use of nitroglycerin, but scanning can proceed without its use.
    93. You are called to see a patient in the emergency room 2 days after percutaneous coronary
    intervention, who has low-grade fever, nausea, diffuse pruritus, and a maculopapular rash on the
    trunk and upper extremities. The patient was initiated on clopidogrel after the procedure.
    Which of the following is your next step in management of this patient?
    a. Intravenous (IV) immunoglobulin (IG).
    b. IV steroids.
    c. Diphenhydramine therapy.
    d. Stop the clopidogrel.
    93. c. Diphenhydramine therapy.

    Late contrast reactions are T-cell mediated and are more common with nonionic dimers. If a
    patient has a prior history of such a reaction, choosing a contrast other than a nonionic dimer, such
    as a nonionic monomer (iopamidol), is advised. This is a self-limiting condition and symptomatic
    treatment is all that is required. This is not a reaction to the clopidogrel and thus should not be
    discontinued.
    94. In a patient who receives enoxaparin with the electrocardiogram shown in Figure 1, which of
    the following conditions would indicate antifactor Xa (anti-Xa) level monitoring?

    a. Liver disease.
    b. Concomitant warfarin
    therapy.
    c. Renal insufficiency.
    d. Diabetes.
    e. Stroke.
    94. c. Renal insufficiency.

    The patient’s degree of renal dysfunction warrants anti-Xa monitoring. According to the
    current American Heart Association/American College of Cardiology guideline, low molecular
    weight heparin agents should be avoided in patients with severe renal dysfunction (creatinine >2.5
    in men, >2.0 in women). In patients with moderate renal dysfunction, dose adjustment should be
    considered and anti-Xa monitoring may be necessary.

    Enoxaparin is not hepatically metabolized; liver function testing abnormalities do not necessitate
    dose adjustment or anti-Xa monitoring. Dose adjustment and anti-Xa monitoring are indicated in
    patients with a weight exceeding 100 kg, but at weights below that standard dosing is appropriate
    and anti-Xa monitoring is not necessary, independent of body mass index.

    While the use of chronic warfarin causes concern for the possibility of increased bleeding risk in the
    setting of enoxaparin, it does not affect dosing or the role of anti-Xa monitoring. Management of
    enoxaparin in the cardiac catheterization laboratory is based on the time from the last dose
    administered, not anti-Xa level.
    95. A 79-year-old man presents to his local community hospital with substernal chest pain lasting
    3 hours. His resting electrocardiogram (ECG) shows 3 mm ST elevation across the anterior
    precordium with presence of QS complexes in V1-V4. His resting heart rate is 96 bpm, and his blood
    pressure in the right upper limb in the supine position is 100/70 mm Hg.

    Physical examination reveals an apical third heart sound, a soft systolic murmur in the aortic area
    that increases with expiration, and crepitations in bilateral lung bases. His respiratory rate is 20
    breaths/minute, and a pulse oximetry on room air is 92%. The emergency department physician
    activates the catheterization laboratory planning for primary percutaneous coronary intervention
    (PCI) and places a nasal cannula delivering oxygen at 4 L/min.
    Which of the following medical interventions is the most appropriate?
    a. Reteplase.
    b. Diltiazem.
    c. Enalaprilat.
    d. Isosorbide.
    e. Furosemide.
    95. e. Furosemide.

    The use of intravenous (IV) enalaprilat in the CONSENSUS 2 trials was not associated with a
    mortality benefit. This lack of benefit was attributed to hypotension in the early postreperfusion
    setting. The borderline blood pressure, high resting heart rate, and evidence of pulmonary
    congestion in this elderly patient with an extensive anterior myocardial infarction (MI) on ECG are
    likely due to a significant acute decrease in stroke volume.

    Treatment with IV beta-blockade as noted in the COMMIT 2 trial increases the risk of precipitating
    cardiogenic shock in this setting and should be avoided. The dosage of unfractionated IV heparin in
    the setting of ST elevation MI should be weight-adjusted with a bolus dose of 60 U/kg not to
    exceed 4000 U, and an infusion rate of 12 U/kg not to exceed 1000 U/h.
    96. A 78-year-old woman presents with resting chest pain and anterior T-wave inversions on
    electrocardiogram (ECG). Her cardiac enzymes are normal. She has no cardiac history, no history of
    diabetes, and no known allergies. She is treated with aspirin and subcutaneous enoxaparin and
    remains chest pain free. However, 6 hours after admission, she develops massive hematemesis.
    Which of the following is the next best step in her management?
    a. Fresh frozen plasma (FFP).
    b. Cryoprecipitate.
    c. Protamine.
    d. Lepirudin.
    96. c. Protamine.

    Although protamine incompletely reverses the effect of enoxaparin on factor Xa, it does reverse its
    effect on thrombin (factor IIa), and as such, is indicated for patients with bleeding complications
    due to enoxaparin. Adverse reactions to protamine can be seen among patients who are allergic to
    fish or who have received pork insulin. Cryoprecipitate and FFP do not reverse the effects of
    indirect thrombin inhibitors such as heparins. A direct thrombin inhibitor, such as lepirudin, is
    contraindicated in the presence of active bleeding.
    97. A 52-year-old man develops intermittent chest pain while on a business trip and presents to
    the emergency department for evaluation. He does not have diabetes and is a nonsmoker. His
    outpatient medical regimen includes atorvastatin 40 mg, and lisinopril 20 mg daily. His exam is
    normal. His electrocardiogram (ECG) shows nonspecific flattening of the T waves in the lateral
    leads, and serial cardiac enzymes are normal. He is treated with aspirin and unfractionated heparin
    for 24 hours and his chest pain has not recurred. He is anxious to return home and asks if he can
    catch his flight later that afternoon.

    Which of the following is most appropriate for the care of this patient?
    a. Exercise treadmill test.
    b. Coronary angiography.
    c. No further testing prior to travel.
    d. Heparin for additional 24 hours.
    97. a. Exercise treadmill test.

    The patient presents with a symptom complex consistent with possible unstable angina. However,
    there are no objective signs of ischemia, the clinical presentation is low risk given his young age, his
    cardiac enzymes are normal, and there is an absence of diagnostic ECG changes. In low-risk
    patients, an initial conservative (ischemia-guided) approach is reasonable in which the patient is
    treated medically and undergoes risk stratification prior to discharge. Although 48-72 hours of
    medical therapy prior to stress testing is recommended when definite acute coronary syndrome
    (ACS) is present, stress testing can be performed safely earlier in low-risk patients with possible
    ACS, and exercise stress testing provides a prudent solution that meets the wishes of the patient
    and avoids excessive testing. Exercise stress testing prior to discharge would be recommended
    because the patient has planned air travel.
    98. A 60-year-old woman with atypical chest pain undergoes a treadmill stress test. The stress
    test findings are:
     Heart rate response: 64-127 bpm
     Blood pressure (BP) response: 132/66 to 174/80 mm Hg
     Symptoms: Mild fatigue at peak
     Electrocardiogram (ECG): 2 mm of horizontal ST-segment depression in leads V5-V6 at peak
    exercise
     Exercise duration: 3.0 minutes on Bruce protocol
     Perfusion images: Reversible apical ischemia

    Otherwise, it was a normal study.

    Which of the following findings best correlate with a highest risk for cardiac death?
    a. Perfusion ischemia.
    b. Poor functional capacity.
    c. Hypertensive BP response.
    d. Heart rate response.
    e. ECG ischemia with 2 mm ST-segment depression.
    98. b. Poor functional capacity.

    Poor functional capacity is the best predictor of cardiac death. Perfusion images or ECG ischemia
    predict ischemic events, but are less predictive of death than exercise duration. Neither her heart
    rate response nor BP response is particularly concerning.
    99. A 65-year-old woman with a history of coronary artery disease is admitted with a 3-day
    history of chest pain, nausea, and vomiting. Her electrocardiogram shows ST elevation in inferior
    leads. She is taken to the cardiac catheterization laboratory and undergoes percutaneous coronary
    intervention of the right coronary artery. In the cardiac care unit, she is somnolent, and her blood
    pressure is 88/60 mm Hg, heart rate is 92 bpm, and oxygen saturation is 96% on room air. Jugular
    venous pressure is 10 cm H2O. Lung fields are clear, and cardiovascular examination has normal
    S1and S2 without murmurs appreciated. Extremities are cool.
    Which of the following is the most likely diagnosis?
    a. Papillary muscle rupture.
    b. Ventricular septal defect (VSD).
    c. Free wall rupture.
    d. Right ventricular (RV) infarct.
    e. Pulmonary embolism.
    99. d. Right ventricular (RV) infarct.

    The patient has signs of RV involvement in her inferior myocardial infarction (MI) with hypotension
    and evidence of poor perfusion. With hypotension and inferior MI, clinical suspicion of RV
    involvement should be high. While other etiologies of her hypotension could include over-sedation,
    bleeding, and cardiogenic shock, management is quite different for an RV infarct and needs to be
    identified early.

    Papillary muscle rupture and VSD are later mechanical complications of MIs. A post-MI VSD may be
    accompanied by a thrill along the left sternal edge in 90% of cases, and the murmur would be
    holosystolic. Free wall rupture is more common in anterior MIs and is more commonly seen in first
    presentation of coronary disease and in elderly women. Pulmonary embolism is less likely given her
    normal oxygen saturation.
    100. A 58-year-old man presents to a community hospital 90 minutes from the nearest cardiac
    catheterization laboratory with 2 hours of substernal chest pain. He is noted on electrocardiogram
    to have marked ST elevation in leads V1-V5, with reciprocal ST depression in the inferior leads,
    consistent with an evolving anterior ST-segment elevation myocardial infarction (STEMI).

    Two years previously, he underwent an aortic valve replacement with a St. Jude mechanical
    prosthesis, due to chronic aortic insufficiency. Prior to the aortic valve replacement, his coronary
    angiogram revealed a 30% stenosis in the proximal left anterior descending coronary artery, which
    was not bypassed. He is taking warfarin, and 3 days ago his international normalized ratio (INR) was
    3.2.
    Which of the following is the most appropriate treatment in this patient's care?
    a. Aspirin, clopidogrel, intravenous unfractionated heparin, and tenecteplase.
    b. Aspirin, clopidogrel, half-dose tenecteplase, followed by transfer for PCI.
    c. Aspirin, clopidogrel, and transfer for primary percutaneous coronary intervention (PCI).
    d. Aspirin plus tirofiban.
    100. c. Aspirin, clopidogrel, and transfer for primary percutaneous coronary intervention
    (PCI).

    Transfer to a primary PCI-capable facility is indicated if first medical contact to device time is <120
    minutes, as in this case. Transfer should also be considered for those at high risk of bleed or signs
    of shock. His risk for bleeding is higher with thrombolytics given his chronic anticoagulation. Even if
    there was a time delay for primary PCI, one might consider transfer since bleeding risk increases
    with a higher INR and thrombolytics. Aspirin plus tirofiban is not definitive reperfusion. Facilitated
    PCI has not been demonstrated to improve outcomes.
    101. An 82-year-old man presents with a non-ST elevation myocardial infarction, complicated by
    congestive heart failure. His initial laboratory values are notable for a serum creatinine of 3.0
    mg/dl, a creatine kinase-myocardial band of 147 mg/dl, and a cardiac troponin I of 23 mg/dl. He is
    treated with aspirin, heparin, and eptifibatide and undergoes cardiac catheterization on hospital
    Day 2. He has successful percutaneous transluminal coronary angioplasty and stenting of a 90%
    stenosis in the proximal left anterior descending artery, and initially does well.

    After the procedure, unfractionated heparin was discontinued, and the patient was maintained on
    aspirin and a tirofiban infusion, which finished 1 hour ago. Sheaths were successfully removed soon
    after the procedure. Later that evening, he is noted to be confused and agitated. On examination,
    his heart rate is 116 bpm, blood pressure 88/58 mm Hg, and respirations are 20 breaths/minute.
    His peripheral pulses are intact, and there is no groin hematoma. His electrocardiogram (ECG) is
    unchanged.
    In addition to intravenous saline, which of the following is the next best step in his care?
    a. Urgent repeat coronary angiography.
    b. Abdominal/pelvic computed tomography.
    c. Platelet transfusion.
    d. Intravenous Solu-Medrol.
    101. b. Abdominal/pelvic computed tomography.

    The most likely diagnosis is retroperitoneal hemorrhage, as a complication of cardiac


    catheterization and antiplatelet therapy. Importantly, the patient has a significant renal
    dysfunction, which will potentiate the antiplatelet effects of tirofiban. Since tirofiban and
    eptifibatide are reversible inhibitors of the glycoprotein IIb/IIIa receptor and have a short half-life,
    platelet infusions are rarely necessary or helpful in patients receiving these agents.

    In contrast, abciximab binds avidly to the receptor and thus has a very prolonged effect on platelet
    aggregation (despite low free abciximab levels). Thus, platelet transfusions may be considered in
    patients with bleeding complications following abciximab administration. The presentation is not
    consistent with allergic reaction, therefore, steroids are not indicated. Repeat ECG is unchanged,
    therefore a repeat catheterization is not indicated.
    102. A 54-year-old man is brought to the emergency department (ED) by his coworker with acute-
    onset dyspnea and syncope. He lost consciousness at work for approximately 15 seconds, but was
    spontaneously revived after falling to the floor. His medical history includes hypertension, active
    smoking, diabetes, and chronic kidney disease. He took an aspirin while on route to the ED.

    His heart rate is 92 bpm and regular, blood pressure is 156/88 mm Hg, and respiration rate is 24
    breaths/minute. Jugular venous pressure is normal, lung fields have scant bibasilar crackles, and he
    has no cardiac murmur. Initial cardiac enzymes are negative, blood urea nitrogen is 42, and
    creatinine is 2.6 mg/dl. Electrocardiography shows normal sinus rhythm with 2-4 mm ST elevation
    in V2-V4. Symptoms began 45 minutes before arrival. In traffic, the nearest percutaneous coronary
    intervention (PCI)-capable facility is 2.5 hours away at this time of day. Helicopter transport is not
    available due to ocean fog.
    Which of the following treatment strategies would you choose prior to transfer?
    a. Tirofiban, half-dose tenecteplase, IV UFH, aspirin.
    b. Full-dose tenecteplase, intravenous (IV) unfractionated heparin (UFH), aspirin, clopidogrel.
    c. IV UFH, aspirin, clopidogrel.
    d. Abciximab, half-dose tenecteplase, IV UFH, aspirin.
    e. Full-dose tenecteplase, IV low molecular weight heparin (LMWH), aspirin, clopidogrel.
    b. Full-dose tenecteplase, intravenous (IV) unfractionated heparin (UFH), aspirin,
    clopidogrel.

    Given the time constraints associated with transfer for primary PCI (i.e., first medical contact to
    device time >120 minutes), full-dose lytic therapy with transfer is the single best choice (Class I). IV
    UFH is preferred over LMWH in the setting of renal insufficiency of this magnitude. Combination
    reperfusion therapy with abciximab and half-dose tenecteplase is not recommended by the current
    ST-segment elevation myocardial infarction (STEMI) guideline. The use of heparin, aspirin, and
    clopidogrel alone is not appropriate for treatment of a STEMI.
    103. A 74-year-old man presents with pain in the toes of his right foot. The pain is most severe at
    night when he is in bed, such that he often sits up and dangles his foot over the side of the bed for
    relief.
    On examination, there is a fissure at the tip of the right great toe that is tender to touch. There is
    mild bilateral ankle edema. The dorsalis pedis and posterior tibial pulses are not palpable in either
    foot.
    Which the following diagnostic tests should be performed to determine appropriate treatment for
    this patient?
    a. Magnetic resonance (MR) angiogram.
    b. Venous duplex ultrasound.
    c. Foot X-ray.
    d. Computed tomography (CT) angiogram.
    103. a. Magnetic resonance (MR) angiogram.

    This patient presents with symptoms and findings of peripheral arterial disease (PAD). Ischemic
    pain in the right foot is exacerbated when he is in bed, so he dangles the foot to improve perfusion
    pressure (via gravitational effects) and reduce his pain. The finding of a skin lesion is consistent
    with severe ischemia. The ankle swelling reflects the prolonged periods of putting his feet in a
    dependent position; it is not a consequence of venous thrombosis. Therefore, a venous ultrasound
    examination is not required.

    A foot X-ray might useful to detect osteomyelitis, but these are not diagnostic for PAD. An
    arteriogram is indicated to define his vascular anatomy and plan a revascularization procedure. MR
    imaging is preferred (Class I, Level of Evidence A) versus CT angiogram (Class IIb, Level of Evidence
    B) to diagnose the anatomic location of the lesion.
    104. A 24-year-old woman with mixed connective tissue disease is admitted with weakness and
    dizziness. Her blood pressure is 105/70 mm Hg, neck veins are elevated, chest is clear, cardiac exam
    is normal, and there is no edema. She is referred to the cardiac catheterization laboratory. An intra-
    arterial catheter yields the pressure tracing shown in Figure 1.
    Which of the following hemodynamic abnormalities is demonstrated?

    a. Pulsus parvus et tardus.


    b. Pulsus paradoxus.
    c. Wide pulse pressure.
    d. Pulsus alternans.
    104. b. Pulsus paradoxus.

    There is marked (>10 mm Hg) variation in the systolic arterial pressure. This finding indicates
    exaggerated variation in systolic arterial pressure with the respiratory cycle, and is known as pulsus
    paradoxus.

    Pulsus parvus et tardus, a low pulse pressure with a slow upstroke, is observed in severe aortic
    stenosis. Pulsus alternans, in which there are alternating strong and weak beats with alternating
    higher and lower systolic arterial pressure, is seen in severe left ventricular systolic dysfunction. A
    wide pulse pressure is observed in aortic regurgitation.
    105. A 78-year-old woman with an anterior ST-segment elevation myocardial infarction (STEMI) is
    treated with fibrinolysis, low molecular weight heparin (LMWH), aspirin, and clopidogrel, beginning
    42 minutes after onset of pain. She is transported to the nearest percutaneous coronary
    intervention center. Two hours later, she develops severe headache and is less responsive. A head
    computed tomography scan shows a right frontal lobe hemorrhage.
    In addition to neurosurgical consultation, which of the following treatments would you
    recommend?
    a. Epsilon aminocaproic acid.
    b. Platelet transfusion.
    c. Aprotinin.
    d. Vitamin K.
    e. Desmopressin acetate (DDAVP).
    105. b. Platelet transfusion.

    This woman has suffered a fibrinolytic-related intracranial hemorrhage. Risk factors for bleeding
    after thrombolytics include age, sex, small body size, and wide pulse pressure, in addition to the
    particular agent used.

    Recommended treatments include:

     Cessation of fibrinolytic, antithrombin, and antiplatelet therapies


     Protamine to reverse the effects of heparin or LMWH
     Fresh frozen plasma to provide clotting factors V and VIII
     Prothrombin complex concentrate to provide additional clotting factors
     Platelets
     Elevation of the head of the bed, hyperventilation, mannitol, and neurosurgical evacuation if
    indicated

    The other choices listed are not recommended. DDAVP is not indicated in the treatment of
    bleeding after thrombolytics. Aprotinin, an antifibrinolytic agent, was withdrawn from the US
    market in May 2008 due to adverse findings in a study of patients undergoing cardiac surgery.
    Epsilon aminocaproic acid is not approved for this indication. Vitamin K is used for reversal of
    bleeding related to vitamin K antagonists such as warfarin.
    106. A 62-year-old woman is admitted with progressive angina, ST depression in leads V4-V6, and a
    cardiac troponin value that peaks at twice the upper reference limit. Invasive therapy is
    recommended, but declined by the patient. She stabilizes after treatment with intravenous
    heparin, aspirin 81 mg, atorvastatin 80 mg, and metoprolol 25 mg bid. At the time of discharge, she
    is chest-pain free while walking around the unit. Her echocardiogram demonstrates normal left
    ventricular function.
    Which of the following do you recommend for medical therapy, in addition to the medications
    listed above?
    a. Cilostazol 100 mg twice daily for 30 days.
    b. Enoxaparin 1.0 mg/kg twice daily for 14 days.
    c. Ticagrelor 90 mg BID for 14 days.
    d. Clopidogrel 75 mg daily for 1 year.
    e. Prasugrel 10 mg daily for 14 days.
    106. c. Ticagrelor 90 mg BID for 14 days.

    For patients with unstable angina/non-ST-segment elevation myocardial infarction (NSTEMI) for
    whom a conservative strategy is chosen, aspirin (75-162 mg) is continued indefinitely (Class I).
    Antithrombin therapy with either unfractionated heparin, enoxaparin, or fondaparinux can be
    given for the duration of hospitalization or up to 8 days (Class I). Based on the CURE trial, the
    unstable angina/NSTEMI clinical practice guideline recommends clopidogrel 75 mg daily for at least
    30 days and ideally for up to 1 year after presentation (Class I).

    Cilostazol has been used as an alternative to thienopyridine therapy in allergic patients after
    percutaneous coronary intervention, but has not been studied in this setting. Prasugrel has not
    been studied in a conservative management strategy. Ticagrelor is an option for conservative
    management therapy, but the duration should be for 1 year. Enoxaparin might be used, but not for
    14 days.
    107. A 62-year-old man with diabetes and dyslipidemia is hospitalized with recurrent angina 4
    months after percutaneous coronary intervention (PCI) with deployment of a bare-metal stent for
    treatment of a 90% mid left anterior descending stenosis. During his previous admission, he
    developed a deep vein thrombosis and was treated with intravenous unfractionated heparin. His
    platelet count fell from 223,000 to 62,000, and a platelet factor (PF4) assay at time of discharge
    was positive. He was discharged on warfarin, aspirin, clopidogrel, atorvastatin, and metoprolol.

    He was readmitted with chest pain and ST-segment depression 3 months later. His hepatic function
    and cardiac enzymes are normal, but he has stage III kidney disease. His pain resolves and his
    electrocardiogram normalizes after 2 hours.

    A repeat cardiac catheterization reveals a 70% in-stent stenosis.


    Which of the following medications would you consider for adjunctive therapy at the time of
    repeat PCI?
    a. Unfractionated heparin.
    b. Bivalirudin.
    c. Fondaparinux.
    d. Enoxaparin plus a glycoprotein IIb/IIIa receptor antagonist.
    107. b. Bivalirudin.

    This man developed heparin-immune thrombocytopenia during his first admission. Unfractionated
    heparin and low molecular weight heparin are contraindicated in this situation. Upstream use of
    fondaparinux has been associated with higher rates of catheter thrombus at time of PCI,
    necessitating the use of heparin.
    108. Which of the following is the correct order of events in the ischemic cascade?
    a. ECG changes, perfusion defects, systolic dysfunction, diastolic dysfunction, chest pain.
    b. Diastolic dysfunction, perfusion defects, ECG changes, chest pain, systolic dysfunction.
    c. Perfusion defects, diastolic dysfunction, systolic dysfunction, electrocardiogram
    (ECG) changes, chest pain.
    d. Perfusion defects, diastolic dysfunction, systolic dysfunction, chest pain, ECG changes.
    e. Diastolic dysfunction, systolic dysfunction, perfusion defects, chest pain, ECG changes.
    108. c. Perfusion defects, diastolic dysfunction, systolic dysfunction, electrocardiogram (ECG)
    changes, chest pain.

    Understanding the order of events that occur in the ischemic cascade is important in understanding
    how stress testing can detect subclinical disease. Single-photon emission computed tomography
    (SPECT) myocardial perfusion imaging (MPI) unmasks exercise- or pharmacologic-induced
    differences in perfusion, revealing subtle patterns of perfusion defects and early atherosclerotic
    disease. This explains why nuclear perfusion-based techniques, which typically detect abnormalities
    in coronary flow reserve even in the absence of ischemia, are more sensitive than contractile
    dysfunction-dependent techniques, like stress or dobutamine echocardiography, which require
    subendocardial ischemia to be abnormal. ECG changes and chest pain are relatively late
    presentations of ischemia, which explains why the sensitivities of coronary artery disease detection
    are lower than with imaging techniques.
    109. A 60-year-old man underwent bare-metal stenting of a discrete left anterior descending
    artery lesion after non-ST-segment elevation myocardial infarction and was placed on aspirin and
    clopidogrel. One week after the procedure, he presents with a lower gastrointestinal bleed and is
    found to have a previously undetected colon cancer that requires resection. Because of the
    extensive surgical exploration that is anticipated, the surgeon requests that the clopidogrel be
    stopped prior to surgery.
    Which of the following is the most appropriate length of clopidogrel therapy in this setting?
    a. 9 months.
    b. 12 months.
    c. 1 week.
    d. 6 months.
    e. 4 weeks.
    109. e. 4 weeks.

    The issue in this clinical situation is a tension between stent thrombosis, which is reduced by dual
    antiplatelet therapy, versus periprocedural bleeding, which is accentuated with antiplatelet
    therapy. For truly elective yet major surgery, studies suggest that waiting for 4-6 weeks after bare-
    metal stenting allows the coronary stent to endothelialize so that perioperative stent thrombosis
    off dual antiplatelet drugs is rare. Operating on dual antiplatelet therapy would expose the patient
    to unacceptable bleeding risk. To stop clopidogrel now would increase the risk of stent thrombosis.
    Heparin has not been shown to reduce the risk of early stent thrombosis. The risk of waiting 6
    months to resect the colon cancer outweighs the benefits of 6 months of dual antiplatelet therapy.
    110. In a patient with hypertrophic obstructive cardiomyopathy, which of the following
    combinations is true of the post-extrasystolic beat?
    a. The gradient increases and the pulse pressure decreases.
    b. The gradient and pulse pressure both decrease.
    c. The gradient decreases and the pulse pressure increases.
    d. The gradient and pulse pressure both increase.
    110. a. The gradient increases and the pulse pressure decreases.

    This is the Brockenbrough sign. The decrease in pulse pressure following a premature ventricular
    contraction is caused by a reduced stroke volume that results from increased dynamic obstruction,
    as evidenced by an increase in the gradient.
    111. A 56-year-old woman presents for evaluation of 8 months of shortness of breath. Her exam
    shows blood pressure 150/80 mm Hg, heart rate 78 bpm, and her body mass index is 40 kg/m2.
    Jugular venous pressure is mildly elevated with clear lungs. No murmur is heard. She has an
    S4 gallop and trace peripheral edema.

    A transthoracic echocardiogram is performed, but is of limited quality due to body habitus. Her left
    ventricular ejection fraction appears grossly normal. She undergoes right and left heart
    catheterization for further evaluation of her symptoms. There is no significant coronary artery
    disease on angiography. Right heart catheterization shows the following: right atrium 10 mm Hg,
    pulmonary artery 55/25 mm Hg (mean 35), and pulmonary capillary wedge pressure 23 mm Hg
    with prominent V waves.
    Which of the following is the most likely cause of her symptoms?
    a. Precapillary pulmonary hypertension.
    b. Mitral regurgitation.
    c. Obesity.
    d. Heart failure with preserved ejection fraction (HFpEF).
    111. d. Heart failure with preserved ejection fraction (HFpEF).

    The hemodynamics shown are consistent elevated filling pressures in a noncompliant left atrium.
    This constellation of symptoms and hemodynamic findings are most compatible with HFpEF.

    Mitral regurgitation would be expected to be associated with a systolic murmur in most cases.
    While obesity may be a cause of her symptoms, it would not necessarily explain the
    hemodynamics. Precapillary pulmonary hypertension would result in a significant transpulmonary
    gradient that is not present here.
    112. A 44-year-old woman is in the coronary care unit following presentation with an inferior
    myocardial infarction. She was treated with primary angioplasty and stenting to a lone proximal
    right coronary artery (RCA) stenosis.

    Upon returning to the coronary care unit, she develops mild palpitations. She has no further chest
    discomfort. Her blood pressure is 110/70 mm Hg and heart rate is 90 bpm. The 12-lead
    electrocardiogram is shown in Figure 1.
    Which of the following is the best management for this rhythm?

    a. Atropine.
    b. Synchronized direct current cardioversion.
    c. No therapy required.
    d. Repeat percutaneous coronary intervention (PCI).
    e. Lidocaine.
    112. c. No therapy required.

    The rhythm strip shows a sinus beat with inferior Q waves followed by an accelerated
    idioventricular rhythm. In the context of PCI to the RCA, this represents a reperfusion rhythm; this
    is self-limiting and does not require treatment.
    113. A 17-year-old is referred by his pediatric cardiologist for advanced cardiovascular imaging
    after a classic tetralogy of Fallot repair at the age of 2 months. His exercise tolerance is normal, and
    he is not cyanotic. An echocardiogram reveals right ventricular enlargement and pulmonic
    regurgitation.
    Which of the following is most appropriate at this time to further assess the status of his congenital
    heart disease?
    a. Radionuclide angiography.
    b. Computed tomographic angiography.
    c. Magnetic resonance imaging (MRI).
    d. Transesophageal echocardiography.
    e. Right-heart catheterization.
    113. c. Magnetic resonance imaging (MRI).

    Cardiac MRI is the only test that can provide all the components needed to quantify all the
    parameters necessary, including right ventricular and right atrial volumes, valvular regurgitation,
    and residual shunting. The right ventricular structures are difficult to quantify by echocardiography,
    and computed tomography does not provide dynamic flow information. Right-heart catheterization
    will not provide volumes or accurate quantification of valvular regurgitation.
    114. A 25-year-old college basketball player is referred to see you due to an abnormal screening
    electrocardiogram (ECG) obtained during basketball practice (Figure 1). He has no complaints, has a
    normal physical examination, and has no family history of arrhythmias or sudden death.
    Which of the following is the next most appropriate step in his management?

    a. Repeat electrocardiogram (ECG).


    b. Cardiac catheterization.
    c. Echocardiogram.
    d. Stress test.
    e. Holter monitor.
    114. a. Repeat electrocardiogram (ECG).

    This ECG is normal except for limb lead reversal. This can be seen by the negative P wave QRS
    complex and T wave in lead I, as well as a total lack of voltage in lead II. It can be repeated with the
    limb leads correctly placed to document the lack of underlying pathology. Other imaging or
    diagnostic studies are not indicated in an asymptomatic patient with an otherwise normal ECG
    without a family history of arrhythmias or premature death.
    115. Which of the following patients has the highest probability of coronary artery disease (CAD)?
    a. A 65-year-old woman with atypical angina and a positive exercise ECG.
    b. A 65-year-old man with typical angina and a negative exercise electrocardiogram (ECG).
    c. A 45-year-old man with atypical angina and a positive exercise ECG.
    d. A 45-year-old woman with typical angina and a positive exercise ECG.
    115. b. A 65-year-old man with typical angina and a negative exercise electrocardiogram
    (ECG).

    According to the Bayes Theorem, the post-test probability that a patient has CAD depends on both
    the pretest probability of the patient having CAD, and the results of the exercise test (Figure 1).
    Pretest probability of CAD depends on age, sex, and character of chest pain, and can be determined
    for an individual patient from published tables.

    For patients at the extreme (low <10%, high >90%), the results of the exercise test shift post-test
    probability of CAD very little (<10%). The 45-year-old man with atypical angina and a positive
    exercise ECG, still has a post-test probability of CAD that exceeds 85-90%, because pretest
    probability is so high. This patient has a pretest probability of CAD that exceeds 90%.

    The other patients described all have a pretest probability of CAD of approximately 50%. A positive
    exercise test shifts their post-test probability to approximately 75-80%.
    (Figure 1)
    116. A 48-year-old African American man presents to your office with palpitations. He is otherwise
    healthy and has no other complaints. His physical examination is unremarkable. His
    electrocardiogram shows sinus rhythm with a PR interval of 230 msec. On Holter evaluation, he has
    6,000 multifocal premature ventricular contractions (PVCs) over a 24-hour period. Transthoracic
    echocardiography reveals normal biventricular function without valvular abnormalities.
    Which of the following is the next best step in his care?
    a. Left-heart catheterization.
    b. Cardiac computed tomographic angiography.
    c. Cardiac magnetic resonance imaging (MRI).
    d. Single-photon emission computed tomography (SPECT) myocardial perfusion imaging (MPI).
    e. Transesophageal echocardiography.
    116. c. Cardiac magnetic resonance imaging (MRI).

    This patient's clinical presentation is most consistent with sarcoidosis. Given his race, high PVC
    burden, and conduction system disease, excluding this diagnosis is essential. Cardiac MRI and
    fluorodeoxyglucose (FDG) PET are two modalities that can help establish the diagnosis of sarcoid.

    He has no cardiovascular symptoms of ischemia. Thus, cardiac catheterization and SPECT MPI are
    not indicated. Transesophageal echocardiography will not add additional information.
    117. A 75-year-old woman was admitted 4 days after the onset of substernal chest pain. The patient is an active
    smoker and has a history of high cholesterol, hypertension, and diabetes. On admission, she was free of chest and
    epigastric pain and had a blood pressure of 142/70 mm Hg with a heart rate of 89 bpm.

    Laboratory testing revealed that the troponin I was elevated at 20 ng/ml and the creatine kinase-myocardial band
    was within normal limits. The patient's electrocardiogram had Q waves in leads II, III, and aVF and there were no
    other ischemic changes. Diagnostic angiography demonstrated an occluded right coronary artery (RCA),
    nonobstructive left anterior descending artery disease, and a 70% proximal left circumflex artery.

    The patient was managed conservatively and medical therapy was implemented. Two days later in the cardiac
    telemetry unit, the patient became acutely hypoxic, hypotensive, and required intubation. On examination, she
    appears acutely ill with bilateral rales and a loud systolic murmur is present, which was not heard on admission.
    Her blood pressure is 85/60 mm Hg and her heart rate is 110 bpm. An echocardiogram reveals an acute
    ventricular septal defect (VSD). An intra-aortic balloon pump is placed and her hemodynamics stabilize.
    Which of the following is the next appropriate management step?

    a. PCI of the RCA.


    b. Implant a left ventricular assist device (LVAD).
    c. Stabilize for 4 weeks, then cardiovascular surgery.
    d. Urgent surgical VSD repair.
    e. Percutaneous coronary intervention (PCI) of the left circumflex artery.
    117. d. Urgent surgical VSD repair.

    Post-infarct VSDs typically occur 2-8 days after a myocardial infarction (MI). This is often after a
    first MI. Medical management of post-MI VSDs have very high mortality rates (>90%) and even
    with cardiac surgical or percutaneous repair, the mortality rates are >50%. Patients who survive
    do better with early surgical VSD repair, as the ruptured site can expand abruptly. Percutaneous
    closure is an emerging potential option, but early results suggest that residual shunting persists.
    As device development improves, this may become a viable option. PCI alone would not correct
    the hemodynamic situation, and an LVAD will not address the shunting problem.
    118. A 45-year-old woman presents to the emergency department with 2 weeks of intermittent
    rest substernal chest pain, which she describes as sharp. It is not provoked by exercise and has
    lasted up to 30 minutes. There are no cardiac risk factors, her electrocardiogram (ECG) and cardiac
    enzymes are normal, and she is able to exercise.

    Which of the following is most appropriate in this patient's care?


    a. Coronary angiogram.
    b. Exercise stress echocardiogram.
    c. Cardiac computed tomography (CT) angiography.
    d. Exercise myocardial perfusion imaging.
    e. Exercise stress test.
    118. e. Exercise stress test.

    In this low-risk patient with a normal ECG and ability to exercise, exercise stress testing is the most
    appropriate first step. Cardiac CT angiography may be helpful in patients who are at intermediate
    risk. This patient with atypical nonexertional chest pain is low risk. With a baseline normal ECG,
    stress testing with additional imaging should be reserved for equivocal exercise stress testing
    results, inability to exercise, or high-risk exercise features.
    119. An 89-year-old woman residing at a nursing home comes to the emergency department of your hospital with a 24-hour
    history of dyspnea and confusion. The patient has significant dementia, as well as hypertension, heart failure with preserved ejection
    fraction, and insulin-dependent diabetes. She is agitated and disoriented, and unable to answer questions.

    Her electrocardiogram demonstrates a heart rate of 72 bpm, with a normal axis, PR interval of 155 msec, a narrow QRS complex,
    and inferior ST elevation. Her troponin T is 1.6 ng/ml and her creatinine is 2.8 mg/dl; her creatinine clearance is calculated as 25
    ml/min. She weighs 60 kg.

    Initial treatment and response: Emergency Medical Service has already given the patient 325 mg of aspirin. As you are preparing to
    wheel the patient to the cardiac catheterization laboratory, her daughter arrives, who holds medical power of attorney. She tells you
    that her mother has a Do Not Resuscitate, Do Not Intubate (DNR/DNI) document and would not want to undergo a procedure.
    However, she agrees to the administration of fibrinolytic therapy.

    In addition to giving fibrinolytics and aspirin 81 mg qd, which of the following do you recommend as additional antiplatelet and
    anticoagulant therapy?

    a. Give a clopidogrel dose of 75 mg orally, followed by 75 mg daily. Also initiate unfractionated heparin with weight-based
    dosing.
    b. Give a clopidogrel load of 300 mg orally, followed by 75 mg daily. Also initiate enoxaparin 60 mg subcutaneously twice daily.
    c. Give a clopidogrel dose of 75 mg orally, followed by 75 mg daily. Also initiate enoxaparin 60 mg subcutaneously twice daily.
    d. Give a clopidogrel load of 300 mg orally, followed by 75 mg daily. Also initiate unfractionated heparin with weight-based
    dosing.
    e. Give a prasugrel load of 60 mg orally, followed by 10 mg daily. Also initiate unfractionated heparin with weight-based dosing.
    119. a. Give a clopidogrel dose of 75 mg orally, followed by 75 mg daily. Also initiate
    unfractionated heparin with weight-based dosing.

    The correct answer is to give 75 mg of clopidogrel, followed by 75 mg a day, followed by the use of
    unfractionated heparin. In this elderly patient with central nervous system symptoms and renal
    dysfunction, adjunctive antithrombotic therapy is limited following fibrinolytic therapy.

    Prasugrel is not recommended in patients over 75 years of age. Enoxaparin dosing is complex in
    patients with chronic kidney disease and every 24-hour dosing is recommended if creatinine
    clearance is <30 cc/min. In patients over the age of 75 years, no loading dose of clopidogrel should
    be used. Fondaparinux is also contraindicated if the creatinine clearance is <30 cc/min.
    120. A 62-year-old woman presented to the emergency department with 2 hours of crushing
    substernal chest pain. An electrocardiogram obtained demonstrates sinus rhythm at 95 bpm with
    1-2 mm of ST elevation in leads II, III, and aVF. Her medical history is significant for dyslipidemia
    and a possible transient ischemic attack. Her current medications include simvastatin. The patient
    receives aspirin and is taken to the catheterization laboratory.
    Which of the following agents confers the greatest survival advantage?
    a. Prasugrel 60 mg orally.
    b. Enoxaparin 1 mg/kg.
    c. Clopidogrel 600 mg orally.
    d. Intravenous heparin 70 U/kg.
    e. Ticagrelor 180 mg orally.
    120. e. Ticagrelor 180 mg orally.

    Either clopidogrel or ticagrelor are Class I recommendations. Prasugrel should be administered


    after the anatomy is known and it is certain that the patient will be undergoing percutaneous
    coronary intervention (PCI). In patients with non-ST-elevation acute coronary syndrome (NSTE-ACS)
    and high-risk features (e.g., elevated troponin) and not adequately pretreated with clopidogrel or
    ticagrelor, it is useful to administer a glycoprotein IIb/IIIa inhibitor (abciximab, double-bolus
    eptifibatide, or high-dose bolus tirofiban) at the time of PCI (Class I).

    Ticagrelor therapy was associated with less cardiovascular mortality than clopidogrel in the PLATO
    trial. Prasugrel therapy was associated with fewer ischemic events than clopidogrel in the TRITON
    trial, but mortality did not differ between treatment groups. Pretreatment with heparin or
    bivalirudin has never been shown to reduce death.
    121. There are multiple centers in Gotham City that perform >500 percutaneous coronary
    interventions (PCIs) per year. Two of these centers spend significant resources advertising their
    expertise in radial access.
    PCI performed via radial access has a demonstrated mortality benefit compared with femoral
    access when performed for which of the following indications?
    a. Non–STEMI.
    b. Assessment of valvular heart disease.
    c. Chronic stable angina.
    d. Unstable angina with negative biomarkers.
    e. ST-segment elevation myocardial infarction (STEMI).
    121. e. ST-segment elevation myocardial infarction (STEMI).

    The mortality benefit of radial access PCI has been demonstrated specifically in STEMI. While there
    are multiple other benefits of radial access over femoral access, including greater patient
    satisfaction and lower access site complications such as bleeding, mortality benefit has not been
    demonstrated in the other clinical situations listed.
    122. A thin 62-year-old man is referred by the patient’s family practitioner for preoperative
    assessment of a large (5.8 cm) abdominal aortic aneurysm. He has a medical history of chronic
    obstructive pulmonary disease (COPD) treated with inhalers, a left hemispheric stroke with little
    residual, diabetes requiring insulin, and chronic renal insufficiency. The patient has one-block
    claudication.

    On exam, his vital signs are normal, and he has no evidence of cardiac murmurs, rubs, or gallops.
    Chest examination reveals bilateral wheezes. There is no lower extremity edema. The
    electrocardiogram (ECG) is normal.
    Which of the following would be your next step in this man’s preoperative evaluation?
    a. Dobutamine echocardiography.
    b. Exercise ECG stress testing.
    c. Resting echocardiogram.
    d. No additional studies are indicated.
    e. Pharmacologic stress testing using regadenoson.
    122. a. Dobutamine echocardiography.

    A vasodilator study would not be wise in this patient, because there is evidence of wheezes on the lung exam.
    Adenosine may induce bronchoconstriction and respiratory compromise by activating the A2B and/or
    A3 receptors, resulting in mast cell degranulation, immunoglobulin E, and histamine release. Regadenoson is an
    A2A-receptor agonist, which theoretically does not appreciably agonize A2B and/or A3 receptors, but as per the
    American Society of Nuclear Cardiology imaging guidelines for nuclear cardiology procedures, patients with
    bronchospasm are considered a contraindication to the use of regadenoson, because there are inadequate data
    regarding its safety with active wheezing. In a recent publication of 356 patients with asthma or COPD undergoing
    stress testing with regadenoson, however, there was no evidence of severe bronchoconstriction; despite this, the
    authors still advised caution in these patients.

    Exercise ECG stress testing is unlikely to have diagnostic value because the likelihood of achieving an adequate
    heart rate and blood pressure response is low due to his disabling claudication.

    His abdominal aneurysm is considered large. Aneurysm diameter is the most important factor predisposing to
    rupture. Based on this patient’s aneurysm diameter, his annual rate of rupture is 3-15%, as per the Joint Council
    of the American Association for Vascular Surgery and Society for Vascular Surgery. This patient should undergo
    repair of his aneurysm.
    According to the guideline on perioperative cardiovascular evaluation and management of noncardiac surgery
    patients, those with high cardiovascular risks with functional status <4 metabolic equivalents should have stress
    testing if it would alter preoperative management by the identification of severe coronary artery disease. A
    dobutamine echocardiogram is therefore the best available test in this situation.

    The patient does not require a resting echocardiogram, as there are no signs of fluid overload and the cardiac
    physical exam is normal. In the absence of history of heart failure or ischemic heart disease, there would be no
    indication for the resting echocardiogram.
    123. A 51-year-old woman is diagnosed with breast cancer. She will undergo a mastectomy with
    adjuvant chemotherapy with doxorubicin hydrochloride. The hospital protocol requires the patient
    to have periodic evaluations of cardiac ejection fraction (EF).

    An echocardiogram is performed and her EF cannot be evaluated despite the use of echo contrast
    due to body habitus. The patient is extremely claustrophobic. The electrocardiogram (ECG) reveals
    criteria for left ventricular (LV) hypertrophy.
    Which of the following is the best imaging alternative in the care of this patient?
    a. A gated single-photon emission CT (SPECT) study.
    b. A radionuclide ventriculography (RVG).
    c. Computed tomography (CT) angiogram.
    d. A 3D echocardiogram.
    e. Cardiac magnetic resonance imaging (MRI).
    123. b. A radionuclide ventriculography (RVG).

    As cardiologists, our role is to provide the oncologist with the necessary information to make therapeutic decisions. It is up to the
    oncologist to decide if an alternative to the doxorubicin hydrochloride is as effective in this type of malignancy.

    Gated-equilibrium RVG is a procedure in which the patient’s red blood cells (RBCs) are radiolabeled and ECG-gated cardiac
    scintigraphy is obtained. Single or multiple measurements of LV and/or right ventricular function are determined. Data are
    collected from several hundred cardiac cycles to generate an image set of the beating heart that is presented as a single,
    composite cardiac cycle. The method provides the clinician with regional and global wall motion, cardiac chamber size and
    morphology, and ventricular systolic and diastolic function, including LV and right ventricular EFs. The most common clinical
    settings in which RVG may be useful include: known or suspected coronary artery disease, distinguishing systolic from diastolic
    causes of congestive heart failure, evaluating cardiac function in patients undergoing chemotherapy, and assessing ventricular
    function in patients with valvular disease. There are certain potential sources of error for this technique, which include red blood
    cell labeling (certain medications alter the labeling efficiency of the isotope), patient positioning, gating errors, and image
    statistics. Since this technique involves radiation, its use has decreased (but it is still a viable alternative to other modalities).

    Cardiac MRI would have been a good alternative, because it is considered a gold standard for evaluation of the EF, but the patient
    is claustrophobic, which is a major limitation of this technique.

    LV chamber and mass quantification have been studied extensively using 3D echocardiography. This method has been shown to
    be more accurate and reproducible than 2D, but the accuracy of the volume calculations is highly dependent on image quality.
    The patient had a 2D echocardiogram performed, but image quality was poor despite the use of echo contrast. A 3D echo would
    have the same issues.

    The accuracy of EF measurement from gated-SPECT has been validated with respect to a variety of radiopharmaceuticals and
    against a large number of gold standards (MRI, 3D multigated acqusition scan, electron beam CT, etc.). EF can be underestimated
    in patients with LV hypertrophy, though, because algorithms are either calibrated for the range of thickness most typically
    encountered in clinical practice or assume a fixed myocardial thickness. The reported discrepancy in EF may be up to 4 points.
    This suggests the RVG would provide a more accurate EF determination in this setting.
    124. For a patient with aortic stenosis and 3+ aortic regurgitation (AR), you are asked to provide an
    aortic valve area (AVA) to help decide about surgical intervention.

    The following data are obtained at cardiac catheterization:

     Peak aortic gradient 50 mm Hg


     Mean aortic gradient 36 mm Hg
     Fick cardiac output 3 L/min
     Thermodilution cardiac output 3.2 L/min

    Based just on these data, which of the following is correct regarding the determination of the
    estimated AVA?
    a. It cannot be determined in the catheterization laboratory because of significant AR.
    b. The AVA will be falsely smaller using the Fick cardiac output.
    c. The AVA can be determined using the thermodilution cardiac output.
    d. The AVA can be determined using the Fick cardiac output.
    124. a. It cannot be determined in the catheterization laboratory because of significant AR.

    One can estimate the AVA by use of the Hakki equation. It is defined by:
    flow past the valve (L/min) / square root of the mean gradient (mm Hg). The Fick cardiac output
    and the thermodilution cardiac output describe the forward flow through the heart to the
    periphery (actually pulmonary flow, but it should equal systemic flow if no shunt). The flow past
    the aortic valve, though, includes both the forward flow and the regurgitant flow due to the AR,
    and this is what is needed to do the calculations.

    In this case, the estimated AVA would be: 6 L/min / 6 mm Hg or an AVA of 1.0 cm2. Using the Fick
    output, the flow would erroneously be less than actual, resulting in a falsely low AVA.
    125. A 75-year-old man with a medical history of hypertension, hyperlipidemia, diabetes, and a
    remote history of neck injury after a fall, presents to the emergency department with vertigo and
    blurred vision that lasted 20 minutes and resolved spontaneously. His symptoms started
    immediately after turning his head to the right. Physical examination is normal except for a bruit on
    the left side of his neck. Noncontrast computed tomography (CT) of the brain is normal.
    Which of the following is the most appropriate test for this patient?
    a. Dix-Hallpike test.
    b. Carotid Doppler ultrasonography.
    c. Cerebral angiogram.
    d. Head and neck CT angiography (CTA).
    125. d. Head and neck CT angiography (CTA).

    The patient’s symptoms are consistent with posterior circulation cerebrovascular syndrome (or
    vertebrobasilar insufficiency). Typical symptoms of posterior circulation ischemia can include
    vertigo, presyncope, syncope, diplopia, blurred vision, perioral numbness, tinnitus, ataxia, or
    bilateral sensory deficits. His symptoms began with turning his head. Posterior circulation ischemia
    can be caused by vessel impingement from the transverse processes in the cervical spine that
    occurs with head movement. Given the patient’s history of neck injury, it is possible that an
    unrecognized neck fracture of the transverse process could have occurred. Vertigo that occurs with
    head movement is typically due to benign paroxysmal positional vertigo and can be assessed using
    the Dix-Hallpike maneuver. However, blurred vision is unlikely to occur with benign paroxysmal
    positional vertigo, thus the response Dix-Hallpike test is incorrect.

    Despite having a left carotid bruit, the patient's symptoms are not consistent with anterior
    circulation ischemia. For vertebral artery disease, the sensitivity and specificity of CTA or magnetic
    resonance angiography is 94% and 95%, respectively, and significantly better than carotid Doppler
    ultrasonography (sensitivity = 70%). Therefore, carotid Doppler ultrasonography is incorrect.
    Cerebral angiography should be reserved for patients that require revascularization based on
    noninvasive imaging. Thus, cerebral angiogram is incorrect. CTA is the correct answer.
    126. You are the preceptor of a cardiology clinic in a university hospital setting. One of the
    residents is evaluating a middle-aged woman with intermediate risk for having coronary artery
    disease and an abnormal resting electrocardiogram (ECG). She has poor echocardiographic
    windows and requires a nuclear stress test.
    Which of the following protocols results in the LEAST radiation exposure to the patient?
    a. One-day rest/stress with technetium-99m.
    b. Stress only with technetium-99m.
    c. Dual isotope (thallium and technetium).
    d. PET scan using rubidium-82.
    e. A positron emission tomography (PET) scan with fluorodeoxyglucose (FDG) and ammonia.
    126. e. A positron emission tomography (PET) scan with fluorodeoxyglucose (FDG) and
    ammonia.

    Ammonia-13 (N-13) is a blood flow tracer and has a half-life of 10 minutes. It is generated in a cyclotron and the
    average effective dose resulting from one of these studies is 2 mSv, making this stress protocol the correct
    answer. The dosimetry is relatively low due to the short half-life of N-13 and the low energy of the emitted
    positrons: 1.48 mSv in 20 mCi (usually cardiac studies utilize 10-20 mCi/study). The 1-day rest/stress protocol with
    technetium is linked to an average effective dose of about 12 mSv. This protocol is one of the most frequently
    used protocols in single-positron emission computed tomography (SPECT).

    Rubidium-82 is a perfusion isotope used in PET. The half-life is 75 seconds and is produced in a generator. The
    average effective dose generated by this protocol (rest/stress) is about 15 mSv. In an average study, 1.75-7.5 mSv
    in 60 mCi (usually cardiac studies utilize 20-40 mCi/study) is used.
    The purpose of a rest image on a nuclear stress test is to define reversibility of stress-induced perfusion
    abnormalities. In more than 50% of the patients, rest imaging is redundant, and does not provide additional
    diagnostic or prognostic information. The average effective dose obtained from a stress-only study using
    technetium-99m is 9 mSv. The ideal candidate for this study has a low pretest probability for coronary artery
    disease, weighs between 120-250 lbs, and has had a normal stress test in the past 3 years. Potential drawbacks
    include the inability to assess ventricular size and function, both at rest and after stress. Transient ischemic
    dilation will not be seen, but the likelihood is very low in patients with normal stress perfusion. There are
    prognostic and long-term data that suggest that this approach is effective. This would be a reasonable alternative
    in the absence of a PET camera.
    The average effective dose obtained from a dual isotope study is 35 mSv, which is one of the reasons (if not the
    main reason) why this test is rarely used anymore. The half-life of thallium is 73.1 hours and the patient is given
    between 2.5-4 mCi per study in addition to the technetium. Thallium thus results in the highest radiation
    exposure.
    127. During a routine cardiac catheterization procedure, which of the following will DECREASE the
    total X-ray dose produced by the X-ray system during a procedure?
    a. Using magnified views.
    b. Panning over the bony structures compared with the lung fields.
    c. Using angulated views.
    d. Using lower framing rates.
    e. Increasing the source-to-image distance.
    127. d. Using lower framing rates.

    Only lowering the acquisition framing rate will help lower the X-ray dose among these scenarios.
    The X-ray exposure equation must be satisfied for each frame imaged, and while the dose per
    frame may be similar, reducing the number of frames per second reduces the overall dose
    delivered during a case.

    X-rays are divergent, and increasing the source-to-image distance results in magnification of the
    image onto the face of the image detector and also loss of X-rays that diverge outside the face of
    the image receptor. Since there are fewer X-rays that strike the image detector due to this loss
    outside, more X-rays are needed to produce a satisfactory image on the detector, and the dose
    necessarily increases.

    Similarly, magnified views are created by using less of the face of the image receptor and, again to
    produce a satisfactory image, more X-rays are needed. Panning over bony structures compared
    with the lung fields also requires more X-rays because of the differences in density of the materials
    and the resultant effect on attenuation of the X-ray beam. Angulated views result in an increase in
    the source-to-image distance and require a greater X-ray dose.
    128. A 68-year-old man (weight 87 kg) with a history of type 2 diabetes, hypertension,
    gastroesophageal reflux disease, and seizure disorder presented to the emergency department
    (ED) with complaints of chest pain and diaphoresis. The patient first noticed the onset of the chest
    pressure the night prior to admission while he was walking on his treadmill. The pain resolved with
    rest and recurred while he was getting dressed on the morning of admission.

    In the ED, laboratory data were notable for a serum creatinine of 1.9 mg/dl and cardiac biomarkers,
    including a troponin T of 0.6 ng/ml and a creatine kinase-myocardial band of 24 U/L. The
    electrocardiogram revealed 1 mm of new ST depression in the inferior leads. Current home
    medications include simvastatin 40 mg daily, lisinopril 10 mg daily, lansoprazole 30 mg daily, and
    phenytoin 300 mg at bedtime. The patient was scheduled for a cardiac catheterization in the
    morning.
    Which of the following medications would preclude the use of ticagrelor therapy in this patient?
    a. Phenytoin.
    b. Lisinopril.
    c. Simvastatin.
    d. Lansoprazole.
    e. Metoprolol.
    128. a. Phenytoin.

    Ticagrelor is metabolized by the hepatic cytochrome P450 (CYP) 3A4 enzyme. Based on this (and
    the observation in pharmacokinetic studies of reduced antiplatelet effect when ticagrelor was
    given concomitantly with drugs that induce the CYP 3A4 isoenzyme such as rifampin), the
    manufacturer currently recommends avoiding the use of ticagrelor with strong inducers of the CYP
    3A4 enzyme, including rifampin, phenytoin, carbamazepine, phenobarbital, and dexamethasone.
    129. A 62-year-old financial planner with a history of hypertension, diabetes, and peptic ulcer
    disease comes to your office for evaluation. She describes nausea and abdominal discomfort that
    has been bothering her for several months. She reports that this has been increasingly bothersome
    to her despite frequent use of antacids. She notes some relation to consumption of large meals or
    at the beginning of exercise. It lasts for several minutes then abates spontaneously. She denies
    dyspnea, orthopnea, palpitations, or lightheadedness. She has no other medical conditions.

    On physical exam, there is point tenderness located over the left sternum, but otherwise is normal.
    Her resting electrocardiogram is normal.

    Which of the following options is the most appropriate next step?


    a. Cardiac catheterization.
    b. Reassurance.
    c. Referral for gastrointestinal source of symptoms.
    d. Exercise stress testing.
    e. Echocardiography.
    129. d. Exercise stress testing.

    This woman has atypical symptoms, but has several features consistent with ischemic heart disease
    and has risk factors for coronary artery disease. The relation of symptoms to exercise and after
    meals is consistent with angina. While typical angina pain is described as heaviness, squeezing, or
    tightness, atypical symptoms are common in women and the elderly. Nausea and difficult to
    characterize discomfort is common in these groups.

    In the WISE (Women's Ischemic Syndrome Evaluation) study, 65% of women with ischemia
    presented with atypical symptoms. Pain reproduced by palpation is suggestive of a musculoskeletal
    etiology, but does not exclude the possibility of her other symptoms being related to ischemic
    heart disease. She has diabetes, and gastroparesis may be contributing.

    The next appropriate study would be stress testing to assess for coronary artery disease.
    130. A 77-year-old man comes to the office to discuss an upcoming cardiac catheterization
    procedure that will be performed for angina that is refractory to medical therapy. He has
    hypertension, hyperlipidemia, and no other chronic medical conditions. His laboratory tests include
    hemoglobin 12 g/dl, creatinine 1.1 mg/dl, and international normalized ratio (INR) 1.0.
    You tell him the most common complication of cardiac catheterization with coronary angiography
    is which of the following?
    a. Vascular access complication.
    b. Anaphylactoid reaction to contrast agent.
    c. Stroke.
    d. Myocardial infarction.
    e. Acute renal failure.
    130. a. Vascular access complication.

    Myocardial infarction, stroke, and death are infrequent complications with a frequency of <0.1%.
    More common complications are tachy- or bradyarrhythmias, acute renal failure, and vascular
    complications. Vascular access site bleeding is the most common complication of cardiac
    catheterization, occurring in 1.5-2.0% of patients. The Registry of the Society for Cardiac
    Angiography and Interventions reported 519 major contrast media complications (0.23%) with four
    deaths (1 in 55,000) in 222,553 patients undergoing selective coronary cineangiography.

    While the radial approach has gained wider acceptance and has fewer bleeding complications
    compared with the femoral approach, the incidence of radial artery occlusion is approximately 1-
    4%, but this is generally asymptomatic. Although major access site complications are rare,
    atrioventricular fistula, nerve injury, radial artery dissection and perforation, hematomas, and
    pseudoaneurysm still occur with the radial approach at a rate that exceeds the other listed
    complications.
    131. An 82-year-old man with diabetes, hypertension, hyperlipidemia, and stable angina comes to
    your office for routine follow-up. He has no change in his angina pattern. He plays tennis 3 times
    per week with no symptoms. His blood pressure is 140/95 mm Hg and heart rate is 67 bpm. His
    glycated hemoglobin is 7%. Urinalysis shows 1+ proteinuria. He is currently only on metoprolol 25
    mg bid, atorvastatin 20 mg, and aspirin 81 mg.
    Which of the following should be initiated?
    a. Sliding scale insulin.
    b. Metformin 500 mg daily.
    c. Lisinopril 5 mg daily.
    d. Hydrochlorothiazide 12.5 mg daily.
    e. Clopidogrel 75 mg daily.
    131. c. Lisinopril 5 mg daily.

    Angiotensin-converting enzyme (ACE) inhibitors are indicated in many patients with stable ischemic
    heart disease, especially those with diabetes or left ventricular dysfunction. Weight loss, aerobic
    exercise, an American Heart Association Step II diet, and ACE inhibitors decrease the risk of
    microvascular complications and potentially cardiac events in patients with diabetes. Tight glycemic
    control does not reduce the risk of macrovascular complications in patients with type 2 diabetes; it
    may actually increase the risk of cardiovascular death and complications. According to the
    guidelines, the goal blood pressure is <140/90 mm Hg in patients with diabetes or chronic kidney
    disease. An ACE inhibitor or angiotensin-receptor blocker is first-line therapy in diabetes to prevent
    progression of renal disease.
    132. A 78-year-old man with peripheral arterial disease is referred to your clinic for preoperative
    evaluation prior to femoral-popliteal bypass. He currently can only walk 1-2 blocks due to
    claudication. He underwent percutaneous coronary intervention with a bare-metal stent for single-
    vessel coronary disease affecting the right coronary artery 2 years ago. He denies angina or
    shortness of breath.

    A persantine sestamibi stress test demonstrates a small area of ischemia at the apex without
    angina. Medications include aspirin 81 mg daily and metoprolol tartrate 50 mg twice daily. Blood
    pressure is 112/72 mm Hg, and heart rate is 62 bpm. Creatinine is 1.5 mg/dl. His low-density
    lipoprotein is 65 mg/dl, high-density lipoprotein is 45 mg/dl, and triglycerides are 100 mg/dl.
    Which of the following do you recommend?
    a. Add nitrates.
    b. Increase beta-blocker.
    c. Proceed with surgery.
    d. Coronary revascularization.
    e. Full-dose aspirin.
    132. c. Proceed with surgery.

    This patient is at elevated risk for perioperative cardiac events for a moderate-risk surgery, but in
    the face of appropriate medical therapy including aspirin and beta-blockade, there is no evidence
    that revascularization will mitigate this risk. Results from the randomized, prospective CARP
    (Coronary Artery Revascularization Prophylaxis) trial demonstrated that coronary artery
    revascularization before elective major vascular surgery did not improve long-term survival or alter
    early postoperative outcomes, including death, myocardial infarction, and length of the hospital
    stay among patients with stable coronary artery disease. This patient’s heart rate suggests that he
    is well beta-blocked, and you would not change the dose just prior to surgery. The patient should
    proceed with surgery on current medical therapy. There is no evidence that an increased dose of
    aspirin or nitrates will reduce perioperative events. The small amount of ischemia would not justify
    revascularization.
    133. A 47-year-old male smoker with hyperlipidemia calls for emergency medical services after
    developing substernal chest pressure while watching television. Emergency medical technicians
    arrive and administer sublingual nitroglycerin, which completely relieves his symptoms.

    Upon arrival to the emergency department, the patient notes recurrent chest pressure with pain,
    and his electrocardiogram shows 2.5 mm ST-segment elevation in V2-5. Both resolve with
    administration of sublingual nitroglycerin. He is given aspirin, heparin, morphine, and intravenous
    nitroglycerin. Coronary angiography reveals minimal nonobstructive plaque in the left anterior
    descending artery and right coronary artery. Toxicology screening is negative.
    In addition to smoking cessation, which of the following is the next most appropriate course of
    action?
    a. Metoprolol.
    b. Niacin.
    c. Omega-3 fatty acids.
    d. Prazosin.
    e. Diltiazem.
    133. e. Diltiazem.

    While the clinical findings suggest coronary spasm, the diagnosis is assumed, but not proven, as
    spasm was not actually observed. Coronary vascular smooth muscle hyper-reactivity is a key factor
    in the pathogenesis of coronary artery spasm. Cigarette smoking is a major risk factor for variant
    angina and endothelial dysfunction; patients should be counseled to avoid tobacco use.

    Diltiazem, a nondihydropyridine agent, is often first-line therapy for coronary spasm, but if
    symptoms recur, spasm testing with intracoronary acetylcholine is indicated.

    Treatment with either niacin or omega-3 fatty acids is not indicated here, as they have not been
    shown to improve coronary spasm. Patients should not be treated with beta-1 and beta-2 selective
    agents, because of the possibility of unopposed alpha-adrenergic activity. If beta-blockade is
    needed for management, the new agents with vasodilator activity (nebivolol, carvedilol, etc.) would
    be better choices.
    134. A 62-year-old man comes to your office with 3 months of dyspnea on exertion. He has a
    medical history of hypertension treated with a calcium channel blocker, hyperlipidemia treated
    with atorvastatin, and long-standing asthma well controlled with theophylline. He also has been
    complaining of severe knee pain that he mitigates with nonsteroidal anti-inflammatory drugs.

    On exam, his blood pressure is 98/65 mm Hg. His cardiovascular exam is unremarkable and lungs
    are clear to auscultation bilaterally. His electrocardiogram (ECG) shows sinus rhythm with first-
    degree atrioventricular (AV) block.

    You decide he needs a pharmacologic nuclear stress test.


    Which of the following factors would contraindicate using adenosine as your stress of choice?
    a. Use of calcium channel blocker.
    b. Low normal blood pressure.
    c. First-degree AV block on ECG.
    d. History of asthma.
    e. Theophylline use.
    134. e. Theophylline use.

    Adenosine is a vasodilator agent that works by producing stimulation of A2A receptors.


    Methylxanthines (caffeine, theophylline, and theobromine) are competitive inhibitors of this effect,
    which require withholding prior to testing. Second- or third-degree AV block is a contraindication;
    first-degree is not. Systolic blood pressure <90 mm Hg is another contraindication.

    Asthmatic patients with ongoing wheezing should not undergo adenosine stress testing. However,
    it has been reported that patients with adequately controlled asthma can undergo an adenosine
    stress test and can have pretreatment with two puffs of an inhaled bronchodilator. This patient had
    clear lungs on auscultation. Another contraindication to adenosine is unstable acute myocardial
    infarction or acute coronary syndrome. The patient was admitted and had negative cardiac
    enzymes.
    135. A 45-year-old man discharged from the hospital 6 weeks ago following an admission for
    unstable angina during which he undergoes stenting of the right coronary artery presents to the
    clinic. He reports no history of diabetes, smoking, hypertension, or a family history of premature
    heart disease. Discharge daily medications include metoprolol succinate 25 mg, aspirin 81 mg,
    atorvastatin 20 mg, and clopidogrel 75 mg. His body mass index is 27 kg/m2, waist circumference is
    42 inches, and blood pressure is 135/85 mm Hg.

    His laboratory results (on admission) were:


     Total cholesterol 230 mg/dl
     Triglycerides 350 mg/dl
     High-density lipoprotein 35 mg/dl
     Low-density lipoprotein 125 mg/dl
     Fasting glucose 99 mg/dl

    Which of the following is the most appropriate next step for this patient?
    a. Add fenofibrate.
    b. Increase atorvastatin to 80 mg.
    c. Continue current therapy.
    d. Add ezetimibe.
    135. b. Increase atorvastatin to 80 mg.

    Current guidelines recommend that this patient with atherosclerotic cardiovascular disease should
    be on a high-dose statin for maximal effect. He had elevated triglycerides on admission, but these
    should be reassessed on a higher-dose statin and with lifestyle changes prior to addition of any
    other pharmacologic therapy such as fenofibrate. This patient is not on a maximal dose of statin.
    Therefore, addition of ezetimibe at this time is not appropriate.
    136. A 43-year-old man is referred for dyslipidemia. He has no history of hypertension or diabetes.
    His father had a myocardial infarction at the age of 38. The patient is a nonsmoker who exercises
    regularly and eats a vegetarian diet.

    Body mass index is 20 kg/m2, waist circumference is 30 inches, blood pressure is 110/80 mm Hg,
    and heart rate is 48 bpm.

    The patient’s internist provides the following lab results:


     Total cholesterol 395 mg/dl
     Low-density lipoprotein (LDL) 321 mg/dl
     High-density lipoprotein 54 mg/dl
     Triglycerides 100 mg/dl

    Which of the following is the appropriate next step?


    a. Exercise treadmill stress test.
    b. Coronary artery calcium score.
    c. Statin therapy.
    d. Genetic testing.
    136. c. Statin therapy.

    For an initial evaluation of hyperlipidemia, testing for secondary causes of elevated cholesterol is
    usually indicated, as disorders such as hypothyroidism, nephrotic syndrome, and medications can
    be secondary causes of dyslipidemia and should be screened for too. In this patient who is likely to
    have the heterozygous form of familial hypercholesterolemia, the most appropriate next step is
    treatment with a statin.

    Familial hypercholesterolemia is an autosomal-dominant disorder, caused by defective LDL-


    receptors. Total cholesterols are usually in the 300-500 mg/dl range in many patients. Tendon
    xanthomas on the Achilles tendon and extensor tendons of the hands are often present. These
    patients carry a risk of premature coronary heart disease, as evidenced by the family history for
    this patient. The prevalence is approximately 1:500 in the United States. This patient should be
    started on lipid-lowering therapy along with continuation of therapeutic lifestyle changes, diet, and
    physical activity. Furthermore, lipid testing is recommended for offspring.

    Stress testing in this asymptomatic patient is not indicated. Calcium scoring does not change the
    management in this patient, as he is already in one of the four statin treatment groups.
    137. A 69-year-old woman sees you in the office for evaluation of fatigue with exertion for the past
    6 months. She says that when she is climbing stairs, especially if she is carrying something, she is
    more tired than usual. Symptoms resolve within 5 minutes of rest. She has hypertension, treated
    with losartan and a diuretic. She reports numerous food allergies and she once had an episode of
    wheezing and nasal congestion after taking aspirin.

    You order a nuclear stress test, which reveals a small, mild reversible inferior perfusion abnormality
    with a normal left ventricular ejection fraction.
    Which of the following should be added to her medical regimen?
    a. Prasugrel.
    b. Cilostazol.
    c. Dipyridamole.
    d. Clopidogrel.
    e. Ticlopidine.
    137. d. Ticlopidine.

    Ordinarily, aspirin (75-162 mg/day) would be recommended for antiplatelet therapy to prevent
    myocardial infarction in patients with established atherosclerotic disease. However, this patient
    has an indication of an aspirin allergy. Aspirin therapy is therefore contraindicated. Clopidogrel has
    proven efficacy for prevention of ischemic events based on the CAPRIE trial, and therefore can be
    used in place of aspirin.

    Cilostazol is a phosphodiesterase-3 inhibitor that acts as both an arterial dilating agent and an
    antiplatelet agent; it can increase symptom-free walking distance in patients with intermittent
    claudication, but has no proven benefit in preventing ischemic coronary events. Dipyridamole in
    combination with aspirin has been shown to reduce subsequent strokes and transient ischemic
    attacks in patients with cerebrovascular disease, but not ischemic coronary events. Ticlopidine is an
    adenosine diphosphate (ADP)-receptor inhibitor similar in mechanism of action to clopidogrel, but
    has more serious side effects, including neutropenia and thrombotic thrombocytopenic purpura,
    thus has been essentially replaced by clopidogrel. Prasugrel is an ADP-receptor inhibitor that is
    approved for patients with acute coronary syndrome. This patient has chronic angina.
    138. A 67-year-old man is seen in the cardiology clinic for a routine follow-up visit. He currently has
    no symptoms of angina, dyspnea, orthopnea, or ankle swelling. He plays golf for exercise, saying
    that he walks all 18 holes four times a week. He suffered an inferior wall myocardial infarction 4
    years ago, which was treated with primary percutaneous coronary intervention. Nonobstructive
    stenoses were noted in the left anterior descending artery at the time, but a total occlusion of the
    right coronary artery was deemed to be the culprit lesion and received treatment with a drug-
    eluting stent. He received medical therapy for lipids and hypertension as well as dual antiplatelet
    therapy for 1 year following his myocardial infarction. An echocardiogram 1 year ago demonstrated
    normal left ventricular systolic function. He is currently taking aspirin 81 mg daily,
    hydrochlorothiazide 25 mg daily, atorvastatin 40 mg daily, and lisinopril 20 mg daily.

    Which of the following interventions should you recommend at this time to reduce morbidity and
    mortality for this patient?
    a. Depression screening.
    b. Cardiac rehabilitation.
    c. Aldosterone antagonist therapy.
    d. Influenza vaccination.
    e. Beta-blocker therapy.
    138. d. Influenza vaccination.

    Vaccination against influenza has been shown to reduce morbidity and mortality in both patients
    with acute coronary syndrome and in patients with prior cardiovascular events. Beta-blocker
    therapy has not been studied in patients with a normal ejection fraction more than 3 years after a
    coronary event. Depression screening may be important for quality of life, assuming supports to
    treat depression are available, but has not been proven to reduce morbidity and mortality among
    patients with coronary artery disease. Aldosterone antagonists are only proven to be beneficial in
    patients with reduced ejection fraction following coronary events. Cardiac rehabilitation is
    important following acute events and for the management of symptoms including angina, but
    neither apply to this patient.
    139. A 61-year-old woman presents for follow-up after a recent hospitalization for a non-ST-
    segment elevation myocardial infarction (NSTEMI). She has type 2 diabetes, hypertension, and
    stage 2 chronic kidney disease. Six weeks ago, she went to the emergency department with chest
    pressure and underwent coronary angiography, which revealed a focal stenosis in the left anterior
    descending coronary artery, for which she received a single drug-eluting stent. Her medications
    include aspirin 81 mg daily, clopidogrel 75 mg daily, and simvastatin 20 mg daily, glargine insulin,
    metoprolol succinate 25 mg qd, amlodipine 5 mg qd, and lisinopril 20 mg qd.

    Today, she reports feeling well, has had no recurrent chest pressure or dyspnea, and is
    participating in cardiac rehabilitation. Her blood pressure is 122/76 mm Hg and heart rate is 68
    bpm. Her lipid profile shows total cholesterol of 210 mg/dl, low-density lipoprotein of 120 mg/dl,
    high-density lipoprotein of 40 mg/dl, and triglycerides of 200 mg/dl.
    Which of the following is the most appropriate next step, in addition to lifestyle modification?
    a. Change simvastatin to atorvastatin 40 mg.
    b. Add ezetimibe 10 mg daily.
    c. Add fenofibrate 145 mg daily.
    d. Add fish oil 3 g daily.
    e. Increase simvastatin to 40 mg.
    139. a. Change simvastatin to atorvastatin 40 mg.

    This patient has established coronary artery disease and had a recent acute coronary syndrome.
    High-intensity statin therapy should be continued in all patients with NSTEMI and with no
    contraindications to its use (Class I, Level of Evidence A). Replacement of simvastatin with
    atorvastatin 80 mg daily is supported by several large randomized trials. High-intensity statin
    therapy used in randomized controlled trials includes atorvastatin 40-80 mg and rosuvastatin 20-40
    mg. Adding ezetimibe, fenofibrate, fish oil, and niacin is not indicated, as the primary goal is high-
    intensity statin therapy.
    140. A 43-year-old man without any significant medical history presents for an office visit to
    discuss prevention of cardiovascular disease (CVD). He is a nonsmoker. He takes no medications
    and exercises 2-3 times per week at the local gym.

    On physical examination, his weight is 220 lbs, blood pressure is 136/84 mm Hg, and pulse is 76
    bpm. His body mass index is 33 kg/m2 and waist circumference is 40 inches. His physical
    examination is otherwise unrevealing. Laboratory studies reveal a total cholesterol of 190 mg/dl,
    low-density lipoprotein cholesterol of 130 mg/dl, high-density lipoprotein cholesterol of 39 mg/dl,
    triglycerides of 209 mg/dl, and a fasting glucose of 110 mg/dl.

    Which of the following is the most appropriate next step?


    a. Start aspirin.
    b. Recommend lifestyle modification.
    c. Start statin.
    d. Measure carotid intima-media thickness (CIMT).
    e. Obtain exercise stress test.
    140. b. Recommend lifestyle modification.

    This patient's risk of atherosclerotic CVD (ASCVD) is low (<5%). Current CVD risk guidelines stress
    the importance of lifestyle modifications to lower CVD risk. This includes eating a heart-healthy
    diet, regular aerobic exercises, maintenance of desirable body weight, and avoidance of tobacco
    products.

    Due to his low risk, he would not benefit from statin or aspirin therapy. Further risk assessment
    may be considered if a treatment decision is uncertain. Assessment of one or more of the
    following–family history, high-sensitivity C-reactive protein, coronary artery calcium score, or ankle
    brachial index—may be considered to inform treatment decision -aking (Class IIb, Level of Evidence
    B). However, measurement of CIMT is not recommended for risk assessment for ASCVD (Class III,
    Level of Evidence B). In a low risk, asymptomatic patient, stress testing is inappropriate.
    141. A 67-year-old Spanish-speaking man from Mexico comes to the hospital for evaluation of
    chest pain that occurred previously with exertion and now at rest. He has a history of hypertension,
    hyperlipidemia, and diabetes. His admission electrocardiogram was notable for 1 mm ST
    depression in the inferior leads. His initial troponin level was 0.2 ng/dl (normal <0.04 ng/dl). His
    chest pain was relieved in the emergency room with sublingual nitroglycerin and morphine.

    You believe that the next appropriate step is coronary angiography and would like to discuss the
    risks/benefits of this invasive procedure with him in order to obtain consent. He speaks broken
    English, but appears to understand much of what you say.
    Which of the following is the most appropriate method to communicate this information to the
    patient?
    a. Having his bilingual daughter translate, who is with him now.
    b. Giving him a copy of the consent form in Spanish to read on his own.
    c. Referring him to your colleague who speaks Spanish and who will be on service tomorrow.
    d. Explaining in English and having him nod to ensure understanding.
    e. Requesting and waiting for a hospital interpreter in person or by phone
    141. e. Requesting and waiting for a hospital interpreter in person or by phone

    In cases of patients whose English skills are limited, an official medical interpreter is the best choice
    for conveying accurate medical information, especially when it concerns an invasive procedure with
    risks of serious complications. A family member is generally only acceptable in emergencies or if
    the patient specifically requests him or her to interpret for a small matter. Minors (<18 years old)
    should be avoided, and the age of the patient's daughter is unknown. Relying on nodding to convey
    understanding of the nature of a complex procedure is not sufficient in this patient with limited
    English skills. Reading and signing the consent form alone is not adequate for obtaining informed
    consent and provides no opportunity for the patient to ask questions. Delaying care of a non-ST-
    elevation myocardial infarction by a day or more to involve your colleague is providing suboptimal
    care and not an acceptable option.
    142. A 68-year-old man with a history of ongoing tobacco use, hypertension, and a 4.2 cm
    abdominal aortic aneurysm (AAA) is seen for scheduled follow-up. His AAA has been followed with
    yearly ultrasounds and is stable in size. He is retired and walks for 30 minutes each morning with
    his dog. Medications include lisinopril, aspirin, and a multivitamin.

    On examination, his blood pressure is 128/82 mm Hg and pulse is 88 bpm. There is a soft
    abdominal bruit and an accentuated abdominal aortic pulsation. A fasting lipid profile reveals total
    cholesterol of 220 mg/dl, high-density lipoprotein (HDL) of 31 mg/dl, and triglycerides of 316
    mg/dl.
    Which of the following is the most appropriate recommendation?
    a. Losartan.
    b. Fenofibrate.
    c. Atorvastatin.
    d. Fish oil.
    e. Niacin.
    142. c. Atorvastatin.

    This patient presents with dyslipidemia with elevated total cholesterol and triglycerides and low
    HDL. The first step in management of dyslipidemia includes assessing patient risk. This patient’s
    AAA places him in the highest risk category for future cardiac events. Other coronary risk
    equivalents include the presence of peripheral arterial disease, diabetes, or cerebrovascular
    disease.

    Given his high risk, moderate- to high-intensity statin therapy is recommended. Fenofibrate is
    effective at lowering triglycerides. However, in this patient, the non-HDL cholesterol should be
    treated first. If triglycerides remain elevated despite non-HDL cholesterol at goal, therapy directed
    toward hypertriglyceridemia is reasonable, although concurrent fibrate and statin therapy increase
    the risk of statin-induced myopathy. Fish oil can also be useful in management of
    hypertriglyceridemia, but should not be used as the initial therapy in this case. Niacin is effective at
    raising HDL. However, the incremental value of raising low HDL with pharmacotherapy has not
    been proven in several large randomized trials, and is an area of ongoing study and debate. Finally,
    addition of a second antihypertensive agent is not indicated, as his blood pressure is well controlled
    to <130/80 mm Hg.
    143. A 48-year-old man presents for follow-up. He feels well and recently completed his first 5k
    road race. His medical history includes dyslipidemia managed with atorvastatin. Physical
    examination is normal. He obtained laboratory work at a recent “employee health fair,” which he
    brings for review. The total cholesterol is 160 mg/dl, high-density lipoprotein cholesterol is 48
    mg/dl, and triglycerides are 102 mg/dl. The high-sensitivity C-reactive protein level is within the
    normal range. Serum chemistries including creatinine are normal. Dipstick urinalysis is negative for
    blood, protein, and glucose. Serum creatine kinase (CK) level is 301 U/L (reference range, 26-192).
    Liver function tests are normal.
    Which of the following is the best next step in management of this patient?
    a. Decrease frequency of atorvastatin to every-other-day dosing.
    b. Decrease the dose of atorvastatin and add ezetimibe.
    c. Stop atorvastatin and prescribe cholestyramine.
    d. Stop atorvastatin and prescribe rosuvastatin.
    e. Continue atorvastatin and check CK in 3 months.
    143. e. Continue atorvastatin and check CK in 3 months.

    This patient is asymptomatic and presents with a slightly increased CK level while on statin therapy.
    Guidelines recommend checking a single CK level upon initiation of statin therapy to obtain a
    baseline value for comparison, should myopathic symptoms develop. CK should be rechecked with
    any new muscle symptoms, but routine monitoring of CK in asymptomatic patients is not
    recommended. Statin therapy should be stopped in patients with severe myopathic symptoms
    regardless of CK level and if the CK is greater than 10-times the upper limit of normal. For this
    asymptomatic patient with a slightly elevated CK, no change in therapy is needed and he can be
    followed serially. The elevations in CK are exacerbated by his training/running.

    Cholestyramine can be used in lieu of statin therapy in statin-intolerant patients, as there are data
    for an improvement in mortality in the primary prevention setting. Rosuvastatin and pravastatin
    are both more hydrophilic than atorvastatin, and in some patients with statin myalgia (not
    myopathy), transition to a more hydrophilic statin can result in symptom improvement. Similarly,
    for statin-intolerant patients, an every other day dosing regimen can allow for some statin therapy.
    A combination of simvastatin and ezetimibe was not superior to simvastatin alone in a randomized
    controlled trial, and no change in therapy is indicated for this patient.
    144. A 55-year-old woman with stable anginal chest pain on no cardiac medication underwent a
    computed tomography (CT) coronary angiogram to assess for possible coronary artery disease
    (Figure 1). Her electrocardiogram (ECG) showed no acute ischemic changes and is normal. Her
    blood pressure is normal and she has no diabetes.
    Based on the CT image shown in Figure 2, which of the following is the next best step?

    Figure 2
    a. An exercise ECG stress test.
    b. Cardiac catheterization.
    c. Begin medical therapy for coronary disease.
    d. An exercise nuclear stress test.
    144. c. Begin medical therapy for coronary disease.

    The CT suggests a mid left anterior descending artery lesion and single-vessel disease. She needs
    initial treatment with medical therapy for stable angina before further testing is indicated.
    145. A 58-year-old man presents to the emergency department with a 5-hour history of crushing, substernal
    chest pain. The patient history is significant for type 2 diabetes, hypertension, dyslipidemia, and coronary artery
    disease with stenting of his proximal left anterior descending artery 3 years ago.

    Admission electrocardiogram shows anterior ST-segment elevation, including ST elevation in lead aVR. The
    patient is referred for emergent cardiac catheterization. Initial coronary angiography shows a 95% ostial left main
    stenosis with thrombus. An intra-aortic balloon pump (IABP) is inserted and successful stenting of the left main is
    performed with 0% residual stenosis and TIMI 3 flow throughout the left coronary system. The right coronary
    artery is widely patent. The IABP is continued at a 1:1 counterpulsation ratio.

    One hour after the procedure, the patient develops atrial fibrillation with a rapid ventricular response. The
    patient remains asymptomatic. Hemodynamic variables after percutaneous coronary intervention (PCI) are
    shown in the table in Figure 1.
    Which of the following choices would be the best next step in the management of this patient?
    a. Add flecainide.
    b. Repeat coronary angiography.
    c. Add amiodarone.
    d. Insert an Impella 5.0 left percutaneous device.
    e. Add dobutamine.
    145. c. Add amiodarone.

    The IABP is a catheter-mounted balloon that augments pulsatile blood flow by inflating during
    diastole, which displaces blood volume in the descending aorta and increases mean aortic
    pressure, thereby augmenting coronary perfusion. Upon deflation, during systole, the IABP
    generates a pressure sink, which is filled by ejecting blood from the heart. The net effect of IABP
    therapy is an increase in mean arterial pressure and augmented ventricular stroke volume. For
    this reason, proper IABP function depends on native contractile function of the heart. During
    periods of tachycardia, the IABP is unable to adequately inflate, and therefore cannot augment
    mean arterial pressure.

    Thus, pharmacological management of reducing the heart rate is a reasonable next step to
    optimize IABP function and stabilize the patient’s hemodynamics. Escalating mechanical support
    to an Impella, which requires surgical vascular access, is not required. There is no indication that
    the patient has developed recurrent thrombosis of the left main artery. Initiation of inotropes
    and vasopressors may worsen the tachycardia and lead to further decompensation. Direct
    current cardioversion may be appropriate but is not listed as an option. Flecainide is
    contraindicated in patients with coronary artery disease.
    146. A 65-year-old woman was admitted with an anterior ST-segment elevation myocardial
    infarction (STEMI). She was taken urgently to the catheterization laboratory, where she underwent
    placement of two bare-metal stents to the proximal and mid-left anterior descending coronary
    artery. Forty-eight hours later, she complains of shortness of breath and chest pain of a different
    quality than her presenting symptoms. On examination, her blood pressure is 80/57 mm Hg, heart
    rate is 102 bpm, and oxygen saturation is 94% on room air. Her jugular venous pressure (JVP) is
    elevated to the angle of the jaw. Lung exam is clear.
    What is the most likely finding on cardiovascular examination?
    a. Loud pansystolic murmur.
    b. Muffled heart sounds.
    c. Displaced point of maximal impulse.
    d. Loud S4.
    146. a. Loud pansystolic murmur.

    The patient is expected to have muffled heart sounds secondary to free wall rupture and increased
    pericardial fluid. This diagnosis is consistent with elevated JVP and clear lungs, and occurs more
    frequently in the setting of an anterior wall MI. It is considered a surgical emergency with a high
    mortality.

    A loud pansystolic murmur at the lower left sternal border, accompanied by a thrill, is consistent
    with ventricular septal defect and is usually accompanied by pulmonary congestion. The treatment
    is urgent surgery. There is a higher mortality in patients with inferior MI compared with those with
    anterior MI. A fourth heart sound may be heard in the setting of an acute MI, but given signs
    consistent with pericardial effusion, this is likely not to be audible. A displaced apex is most
    consistent with chronic systolic heart failure.
    147. A 57-year-old man has had 2 years of progressively worsening angina with exertion. He was
    initially managed with medical therapy, but has had progressively worsening angina despite
    maximization of two antianginal therapies. A stress test showed moderate exercise tolerance, and
    nuclear imaging suggested a large area of inferior ischemia involving >10% of the left ventricular
    muscle mass. A diagnostic cardiac catheterization was performed and showed a chronic total
    occlusion of the right coronary artery, as shown in Figure 1.

    Given his lifestyle-limiting symptoms despite maximal medical therapy, you have referred him for
    percutaneous coronary intervention (PCI). You have obtained careful consent and have advised him
    of the risk of radiation-induced skin injury. You have assured him that you will take every
    precaution to minimize the radiation exposure to the patient during what may be a lengthy
    procedure.

    Which of the following techniques will increase radiation exposure to the patient?
    Figure 1
    a. Use of less magnified views.
    b. Use of fluoroscopy storage instead of cine storage.
    c. Use of collimation.
    d. Steep imaging intensifier angles.
    e. Use of fluoroscopy frame rate of 7.5 frames per second (FPS).
    147. d. Steep imaging intensifier angles.

    Patients with cardiovascular disease are exposed to a wide array of diagnostic and therapeutic procedures that
    result in a significant cumulative exposure of ionizing radiation. There is a growing awareness of this cumulative
    exposure, and every effort should be made in the catheterization laboratory to minimize the radiation exposure
    to the patient (and the operator). The majority of PCI procedures can be completed, as most modern imaging
    equipment in the catheterization laboratory has a fluoroscopy storage function where a maneuver performed
    under fluoroscopy can be permanently stored and recorded. In many cases, the fluoro image will provide
    diagnostic grade imaging so that cine-angiography will not be necessary and further radiation exposure can be
    reduced. On average, cine radiation doses can be as much as 20-times higher than fluoroscopy doses.

    Reducing the frame rate for image acquisition will also significantly reduce radiation exposure during fluoroscopy.
    While many operators prefer using 15 FPS, a frame rate of 7.5 FPS is sufficient in most patients for effective
    imaging and will reduce radiation use by 50% compared to 15 FPS. Collimation and use of lower magnified
    imaging fields are also critical for reduction of radiation exposure.

    Use of steep imaging angles will increase the radiation exposure to the patient. With steep angulation, fewer X-
    rays reach the image intensifier, resulting in feedback to the radiation generator to generate greater energy in
    order to provide a sufficient image as the source-to-image distance is increased. Every effort should be made to
    use angles as shallow as possible during PCI, and to use multiple angles so as not to concentrate the radiation
    beam to one area.
    148. A 76-year-old man with atrial fibrillation presents to clinic with a 2-year history of chest pain
    at rest located in the mid-epigastrium radiating to the mid-substernal region. Computed
    tomography (CT) angiography of the chest reveals the finding shown in Figure 1.

    Which of the following is the abnormality shown in Figure 1?


    Figure 1

    a. Primary cardiac tumor.


    b. Coronary artery aneurysm.
    c. Pericardial cyst.
    d. Atrial appendage thrombus.
    148. b. Coronary artery aneurysm.

    The abnormality shown on the CT image has peripheral calcifications with central contrast and
    surrounding soft tissue density. It is continuous with the atherosclerotic coronary artery and
    consistent with coronary artery aneurysm, rather than a pericardial cyst or primary cardiac tumor.
    Neither of these would be expected to have peripheral calcification. Pericardial cysts are generally
    benign and usually right-sided, often in the atrioventricular groove.

    The abnormality is anterior to the left atrium and not consistent with an atrial appendage
    thrombus.
    149. A 75-year-old man is found by his family, unresponsive and crumpled over in the bathroom.
    Emergency medical service is called, but no bystander cardiopulmonary resuscitation (CPR) is
    attempted. Upon arrival 7 minutes later, emergency medical service personnel begin CPR, and after
    2 minutes the initial rhythm is ventricular fibrillation. After a 20-minute period of CPR effort,
    including epinephrine and repeated shocks, spontaneous circulation is established. He is intubated.
    Upon arrival at the emergency department, the patient has a weak pulse and blood pressure of
    95/65 mm Hg. He remains unresponsive, without spontaneous movement. The monitor reveals a
    wide QRS complex tachycardia at 100 bpm.
    Which of the following is the next most appropriate postresuscitation therapy?
    a. Discuss with the family withdrawal of therapy.
    b. Therapeutic hypothermia.
    c. Electroencephalogram.
    d. Cardioversion for wide QRS tachycardia.
    149. b. Therapeutic hypothermia.

    This patient’s prognosis is poor but not futile. Since he remains comatose, hypothermia is the best
    chance to limit long-term neurological damage. Long-term survival can be improved with
    hypothermia, generally from previous improvement rates of 1-2% to an improvement rate of 5-
    20%. Recent data suggest this may not be the case in children. It is important to realize that in
    order to achieve these improved survival rates, adequate time after rewarming must be allowed
    before reliable prognostication can be done and further efforts terminated. There is no need for
    cardioversion of his postresuscitation wide QRS rhythm since it is providing a current acceptable
    blood pressure and most certainly represents a transient epinephrine/norepinephrine response. An
    electroencephalogram may be important later to help assess his neurologic status.
    150. A 42-year-old man with a long-standing human immunodeficiency virus (HIV) infection comes
    to your office out of concern of his cardiovascular risk. He is on antiretroviral drugs. He smokes half
    a pack per day and drinks 1-2 drinks per week. Pertinent routine tests show a blood pressure of
    127/88 mm Hg, low-density lipoprotein 177 mg/dl, high-density lipoprotein 27 mg/dl, and
    triglycerides 334 mg/dl.
    Which of the following is an appropriate therapy for this patient, in addition to smoking cessation?
    a. Ezetimibe 10 mg a day.
    b. Begin 2 g fish oil daily.
    c. Rosuvastatin 20 mg a day.
    d. Atorvastatin 10 mg a day.
    e. Fenofibrate 150 mg a day.
    150. d. Atorvastatin 10 mg a day.

    HIV-infected individuals have high rates of smoking, and smoking cessation is perhaps the most
    modifiable risk factor to minimize cardiovascular disease risk in these persons. While this patient
    requires antiretroviral drugs and needs to improve his lipid profile, smoking cessation would have
    the most immediate effect on his overall health and cardiovascular disease risk. He warrants
    therapy for his hyperlipidemia. Because of the interaction with antiretroviral drugs, a low-dose
    statin is recommended.
    151. A 57-year-old man with a history of hypertension, hyperlipidemia, and a prior stent to the
    right coronary artery is seen for routine follow-up. Although he does not exercise regularly, he
    denies anginal symptoms during daily activities. He drinks one glass of wine daily and does not
    smoke. His medications are aspirin 81 mg qd, metoprolol succinate 25 mg qd, lisinopril 10 mg qd,
    and atorvastatin 40 mg qd. His blood pressure is 112/75 mm Hg. His most recent lipid panel shows
    a low-density lipoprotein (LDL) of 68 mg/dl and high-density lipoprotein (HDL) of 25 mg/dl. He
    wants to know how to best improve his cardiovascular risk profile.

    Which of the following is the most appropriate recommendation?


    a. Add colesevelam 3750 mg qd.
    b. Start a regular aerobic exercise program.
    c. Add niacin 500 mg bid.
    d. Increase daily alcohol intake to 3-4 drinks.
    e. Change to simvastatin 80 mg daily.
    151. b. Start a regular aerobic exercise program.

    Abundant epidemiologic evidence supports the relationship between increased physical activity
    and reduced cardiovascular risk. Currently, the best advice for patients is to perform regular
    aerobic exercise, which has beneficial effects on cardiovascular health. While niacin is effective at
    raising HDL levels, recent trials have shown that the addition of niacin fails to reduces
    cardiovascular events in patients with well-controlled LDL levels on background statin therapy.

    The AIM-HIGH trial tested the effects of adding niacin for patients with low HDL levels already on a
    statin. Despite increasing HDL levels, there was no benefit with niacin for reducing cardiovascular
    events and there was a question of a signal of increased stroke.

    The HPS2-THRIVE trial also examined the effects of niacin/laropiprant in patients with well-
    controlled LDL levels on a statin. There was no difference in rates of cardiovascular events, and
    niacin treatment was associated with more side effects. Given these results, it is not clear that
    niacin provides any additional benefit in a patient such as this who already is on a statin and at
    target LDL.

    Initiation of simvastatin at 80 mg or uptitration to 80 mg dose is contraindicated in patients due to


    risks of muscle injury. Colesevelam is a bile acid sequestrant that has primarily LDL-lowering effects.
    While moderate alcohol intake (especially red wine) may have beneficial cardiovascular effects,
    consuming more than 1-2 drinks daily has been shown to have detrimental effects on health.
    152. A 45-year-old man presents with substernal chest discomfort that comes on predictably with
    walking two blocks. The discomfort is alleviated with rest. He has a long-standing history of
    hypertension and was diagnosed with diabetes and dyslipidemia 6 months earlier. Current
    medications include metoprolol, lisinopril, simvastatin, and baby aspirin.

    A stress myocardial perfusion imaging study is ordered. He is unable to complete stage 2 of the
    standard Bruce protocol due to recurrence of chest discomfort. At peak stress and 2 minutes into
    recovery, 1.5-2 mm ST-segment depression is noted in the anterolateral leads. His imaging study is
    inconclusive due to submaximal workload.

    The most appropriate next test that also minimizes radiation exposure would be which of the
    following?
    a. Pharmacologic myocardial perfusion imaging.
    b. Diagnostic cardiac catheterization.
    c. Coronary computed tomography (CT) angiography.
    d. Dobutamine stress echocardiography.
    e. Stress echocardiography.
    152. b. Diagnostic cardiac catheterization.

    This patient has a high pretest likelihood of coronary artery disease based on his risk factors and
    characteristics of typical angina. Electrocardiographic changes during peak stress are suggestive of
    inducible ischemia, even though imaging was “inconclusive.” Risk-benefit ratio must be taken into
    account with diagnostic imaging studies. Although repeating the stress test would probably confirm
    the clinical suspicion, he will still need further evaluation of the coronary arteries.

    Coronary CT angiography is an excellent tool in patients with equivocal or nondiagnostic stress


    tests. However, in patients with a high pretest likelihood of coronary artery disease, coronary CT
    angiography is considered an inappropriate test, without added value of layered testing. Among
    the choices provided, triage to diagnostic cardiac catheterization with the option for
    revascularization based on anatomy would be the most appropriate decision in order to avoid
    additional radiation exposure.
    153. A 48-year-old man with a history of hypertension comes to your clinic to establish care. He
    states that he was told a few years ago that he had high cholesterol but he did not take further
    action. He does not smoke and drinks alcohol rarely. He states he eats a balanced diet with limited
    carbohydrates. His only medication is amlodipine. His blood pressure is 129/81 mm Hg, heart rate
    is 76 bpm, and the remainder of his exam is unremarkable. His body mass index is 24.8 and his
    glycated hemoglobin is normal.

    A fasting lipid panel from this morning reveals a total cholesterol of 210 mg/dl, triglycerides 630
    mg/dl, high-density lipoprotein (HDL) 42 mg/dl. His low-density lipoprotein (LDL) cannot be
    calculated. His thyroid-stimulating hormone is normal.
    In addition to recommending therapeutic lifestyle changes, which of the following is the next most
    appropriate step in his care?

    a. Recheck lipids in 3 months.


    b. Start low-dose aspirin.
    c. Switch amlodipine to hydrochlorothiazide.
    d. Start atorvastatin.
    e. Start fenofibrate.
    153. e. Start fenofibrate.

    The patient has very high triglyceride level, as defined by a level >500 mg/dl in the Adult Treatment
    Panel III guidelines. Such a severe elevation in triglycerides can lead to pancreatitis, so priority
    should be made to reduce levels as quickly as possible with effective triglyceride-lowering
    medications. Appropriate first-line choices include fibrates and niacin. Statins are less efficacious on
    this front, and would only be considered for LDL-lowering purposes once triglyceride levels are
    below 500 mg/dl.

    Therapeutic lifestyle changes should be recommended, but are not adequate to prevent
    pancreatitis in such a setting. Certain cardiovascular medications, such as hydrochlorothiazide, can
    increase triglyceride levels, thus would be detrimental in this case. Amlodipine has no such effects.
    The calculated LDL value in a lipid panel will be falsely low in the setting of elevated triglycerides,
    thus cannot be properly interpreted. Alternative approaches are repeating the lipid panel when
    triglycerides are better-controlled, measuring direct LDL, or following a non-HDL cholesterol
    treatment goal.
    154. A 50-year-old man with hypertension comes to your office for consultation on management
    of his cardiovascular risk. He has no symptoms suggestive of cardiovascular disease. His
    hypertension has been treated with hydrochlorothiazide and lisinopril, and his treated resting
    blood pressure is 130/80 mm Hg. His fasting lipid profile reveals a total cholesterol of 170 mg/dl,
    low-density lipoprotein (LDL) of 110 mg/dl, high-density lipoprotein of 45 mg/dl, and triglycerides
    of 75 mg/dl. His fasting glucose is 90 mg/dl. He does not smoke cigarettes. He has no family history
    of early-onset atherosclerotic cardiovascular disease (ASCVD).

    Which of the following therapeutic options is supported by the risk profile?


    a. Omega-3 fatty acids.
    b. Statin therapy.
    c. No lipid-lowering medications.
    d. Nicotinic acid.
    e. Fibrate therapy.
    154. c. No lipid-lowering medications.

    The 2013 American College of Cardiology (ACC)/American Heart Association (AHA) cholesterol
    guideline identified four major statin benefit groups. Using the 2013 ACC/AHA algorithm, this
    patient does not have clinical ASCVD, LDL ≥190 mg/dl, or diabetes. Using the Pooled Cohort
    Equation, his 10-year risk of coronary death, nonfatal myocardial infarction, fatal stroke, and
    nonfatal stroke is 3.7%. This risk level falls below the 7.5% threshold at which the benefit of statin
    therapy significantly exceeds the risk of incident diabetes. While further risk assessment may be
    considered, such as coronary artery calcium scoring, based on the available risk profile, no lipid-
    lowering medications are recommended. There is no randomized clinical trial evidence that
    initiation of a fibrate, niacin, or fatty acids would be beneficial in primary prevention in this patient.
    155. A 65-year-old woman with hypertension comes to your office to seek consultation on
    management of her cardiovascular risk factors. She has no history or symptoms suggestive of
    cardiovascular disease. Her hypertension has been treated with hydrochlorothiazide and lisinopril
    and her resting blood pressure is 130/80 mm Hg. On fasting laboratories, she has a total cholesterol
    of 190 mg/dl, low-density lipoprotein (LDL) of 120 mg/dl, high-density lipoprotein (HDL) of 40
    mg/dl, triglycerides of 150 mg/dl, and glucose of 90 mg/dl. She currently smokes half a pack per
    day of cigarettes.
    After counseling her on smoking cessation and discussing the risks and benefits of testing, you
    recommend that she consider which of the following?
    a. Obtain an exercise stress test.
    b. Measure high-sensitivity C-reactive protein (hs-CRP) level.
    c. Start moderate- to high-intensity statin therapy.
    d. Measure glycated hemoglobin (HbA1c) level.
    155. c. Start moderate- to high-intensity statin therapy.

    The 2013 American College of Cardiology (ACC)/American Heart Association (AHA) cholesterol
    guideline identified four major statin benefit groups. Using the 2013 ACC/AHA algorithm, this
    patient does not have clinical atherosclerotic cardiovascular disease, does not have familial
    hyperlipidemia with an LDL above 190, and does not have diabetes. She is between the age of 40
    and 75 years, and therefore, the Pooled Cohort Equation should be used to estimate her 10-year
    atherosclerotic risk. This calculated to a 10-year atherosclerotic risk of 15.4%, well above the
    recommended 7.5% risk threshold for initiating statin therapy, and therefore, additional testing
    with hs-CRP is not needed.

    She has already had appropriate screening for diabetes with a fasting glucose level, therefore,
    HbA1c is not necessary. The patient has no symptoms suggestive of ischemic heart disease, and
    therefore, stress testing in this asymptomatic patient is not appropriate.
    156. A 55-year-old woman is seen for a second opinion on her lipid management. She has a recent
    diagnosis of non–insulin-dependent diabetes and no known history of cardiovascular disease. At
    the time of the diagnosis of her diabetes 6 months ago, her fasting lipid profile revealed a total
    cholesterol of 200 mg/dl, low-density lipoprotein (LDL) of 110 mg/dl, high-density lipoprotein of 45
    mg/dl, and triglycerides of 225 mg/dl. Although pharmacotherapy for her lipids was recommended
    by her primary care physician, she opted for lifestyle changes first.

    After 6 months of therapy for her diabetes and diet modification, her lipid profile is unchanged. Her
    body mass index is 28 kg/m2 and her glycated hemoglobin is 6.9%. She has a blood pressure of
    135/80 mm Hg and does not smoke. No proteinuria noted on urinalysis.
    In addition to continued lifestyle modification with regular exercise, diet, and modest weight loss
    for a body mass index goal <25, which of the following do you recommend as the next step for this
    patient?
    a. Amlodipine 5 mg.
    b. Atorvastatin 20 mg.
    c. Niacian ER 500 mg bid.
    d. Fenofibrate 145 mg.
    e. No change in medications at this time.
    156. b. Atorvastatin 20 mg.

    The 2013 American College of Cardiology (ACC)/American Heart Association (AHA) cholesterol
    guideline identified four major statin benefit groups. Using the 2013 ACC/AHA algorithm, this
    patient has diabetes with a Pooled Cohort Equation estimated 10-year atherosclerotic risk of 4.4%.
    As per the 2013 ACC/AHA algorithm, in diabetics (40-75 years, LDL 70-189 mg/dl), with a 10-year
    atherosclerotic cardiovascular disease risk <7.5%, a moderate-intensity statin should be initiated.

    This patient's blood pressure is <140 mm Hg, and antihypertensive medication is not indicated. The
    2013 guideline did not find data supporting the routine use of nonstatin drugs combined with
    statin therapy to reduce further atherosclerotic cardiovascular events. Because her risk is <7.5%, a
    high-intensity statin is not indicated.
    157. A 56-year-old African American woman with a history of hypertension treated with
    hydrochlorothiazide, and a family history of premature coronary disease presents to your clinic.
    She is a current smoker. Her blood pressure is 140/70 mm Hg, heart rate is 55 bpm, and body mass
    index is 28.9.

    Her lipid profile after a 10-week very low fat diet with increased physical activity is as follows:
     Total cholesterol 240 mg/dl
     Triglycerides 450 mg/dl
     High-density lipoprotein (HDL) 50 mg/dl
     Low-density lipoprotein (LDL) 145 mg/dl

    Which of the following is the first therapy to initiate?


    a. Omega-3 fatty acids.
    b. Fibrate.
    c. Statin.
    d. Nicotinic acid.
    157. c. Statin.

    The 2013 American College of Cardiology (ACC)/American Heart Association (AHA) cholesterol
    guideline identified four major statin benefit groups. Using the 2013 ACC/AHA algorithm, this
    patient does not have clinical atherosclerotic cardiovascular disease, does not have familial
    hyperlipidemia with an LDL above 190 mg/dl, and does not have diabetes. She is between the age
    of 40 and 75 years, and therefore, the Pooled Cohort Equation should be used to estimate her 10-
    year atherosclerotic risk. This calculated to a 10-year atherosclerotic risk of 10.6%, and is probably
    even higher given her family history of premature coronary artery disease, thus warrants treatment
    with a statin to reduce this risk.
    158. Effective dose-reduction strategies include appropriate patient selection.
    For which of the following patients is coronary computed tomography angiography (CCTA)
    appropriate?
    a. A 68-year-old man with high risk for coronary disease with acute chest pain.
    b. A 50-year-old man unable to undergo risk assessment.
    c. An asymptomatic 59-year-old man with a history of coronary artery bypass grafting surgery 2
    years ago.
    d. A 51-year-old woman with low risk for coronary disease and typical angina.
    e. A 45-year-old male executive with intermediate risk for coronary disease and worsening chest
    pain with activity.
    158. d. A 51-year-old woman with low risk for coronary disease and typical angina.

    Appropriate patient selection is an important first step in dose reduction. In general, due to its high
    sensitivity and negative predictive value, CCTA performs well in ruling out coronary artery disease
    in low-to-intermediate risk individuals. In patients with a high likelihood of coronary disease
    needing triage to invasive assessment, CCTA results in unnecessary radiation exposure with little
    added value. In such patients, CCTA is considered inappropriate.
    159. A 53-year-old woman presents to the heart failure clinic for evaluation and management. She experiences
    angina on minimal exertion despite medical therapy. She had an implantable cardioverter-defibrillator (ICD)
    inserted 3 months after her most recent myocardial infarction (MI). She had suffered two prior MIs and had a
    percutaneous coronary intervention (PCI) of the left anterior descending (LAD) and right coronary artery. Her
    most recent ejection fraction is 25% with a dilated left ventricle and no valvular abnormalities. Her
    electrocardiogram shows normal sinus rhythm with a QRS of 110 msec and Q waves in the inferior leads and
    precordial leads.

    A coronary angiogram shows patent right and left circumflex coronary arteries with a subtotal highly calcified
    occlusion of the proximal LAD. The distal LAD is collateralized from the right and left circumflex coronary arteries.

    PCI was not technically feasible. She undergoes rest/4-hour redistribution thallium. Results show 60%
    redistribution in the distal half of the anterior wall and septum.
    Which of the following is the next best step in this patient's care?

    a. Surgical revascularization.
    b. Biventricular ICD.
    c. Intensify medical treatment.
    d. Transplant evaluation.
    e. Cardiac magnetic resonance imaging (MRI).
    159. a. Surgical revascularization.

    This patient is presenting with ischemic cardiomyopathy and New York Heart Association class III-IV
    heart failure. She has advanced left ventricular dysfunction. On the single-photon emission
    computed tomography images, there is evidence of thallium uptake at 4 hours in her LAD
    distribution. Therefore, this area may improve with revascularization.

    In a meta-analysis comparing all imaging modalities that can identify hibernating myocardium and
    predicting recovery of regional function after revascularization, positron emission tomography
    (PET) using fluorodeoxyglucose (FDG) was the most sensitive, while dobutamine was the most
    specific, but when global recovery after revascularization was analyzed, thallium and PET were very
    similar.

    She does not meet criteria for upgrading to a biventricular ICD based on her QRS. An MRI would
    not provide further information and is contraindicated in patients with an ICD. If she does not
    improve with revascularization, then cardiac transplant should be considered.

    Treatment of triglycerides and non-HDL is secondary to initiating a statin, and there has been no
    evidence to support treatment with a fibrate or nicotinic acid to optimize non-HDL levels.
    160. A 68-year-old woman with hypertension and diabetes is being referred to the nuclear
    laboratory for a myocardial perfusion study. The nurse asks you to choose the imaging protocol for
    the patient. The patient’s body mass index (BMI) is 38 kg/m2. The patient walks her dog routinely.
    The patient lives close to the clinic where you would perform the test and is retired.

    Which of the following protocols would optimize patient images?


    a. One-day low-dose rest/high-dose stress with technetium.
    b. Two-day high-dose rest/stress imaging with technetium.
    c. One-day rest/stress dual-isotope imaging.
    d. One-day low-dose stress/high-dose rest with technetium.
    e. One-day stress/redistribution/reinjection with thallium.
    160. b. Two-day high-dose rest/stress imaging with technetium.

    Ideally, stress and rest imaging with technetium-99 agents should be performed on two separate
    days to avoid having residual activity from the first study contaminating the second study in
    overweight patients (i.e., >250 lbs. or body mass index >30 kg/m2) or in women where significant
    breast attenuation is anticipated. A low dose of technetium-99 radiotracer may result in
    suboptimal images and a 2-day imaging protocol is preferred in this patient population.

    The effective dose of radiation is higher with dual-isotope and should be avoided. The rest-stress
    protocol is a good option if the patient could not have a 2-day protocol. The patient does not
    require an assessment for myocardial viability. The low-dose stress should not be performed in this
    population because of the potential poor quality images on the stress study.
    Coronary Artery Disease ( ACCSAP-9 2016 )

    1.

    A 19-year-old African-American male college soccer player is referred to see you in clinic for

    screening prior to participation in collegiate athletics. He has a history of childhood asthma, but is
    otherwise healthy and takes no medications. There is no family history of cardiomyopathy,

    coronary artery disease, or sudden cardiac death. His physical examination is normal. He hands you
    an electrocardiogram (ECG) that his primary care physician performed.

    Which of the following findings, if present, would be of most concern?

    a. Left ventricular hypertrophy (LVH) by the limb-lead voltage criteria (R in lead aVL of 13 mm).

    b. 0.5 mm ST depressions in leads I and aVL.

    c. Wenckebach pattern (Mobitz I second-degree atrioventricular [AV] block).

    d. Domed/convex upsloping ST elevation with T-wave inversions in V2-V3.

    e. Right-axis deviation of QRS complex to 105 degrees.

    1.
    b.
    0.5 mm ST depressions in leads I and aVL

    Elite athletes may demonstrate ECG changes that overlap with findings seen with cardiomyopathy.

    Several criteria, including the European Society of Cardiology criteria, Seattle criteria, and recently
    published “refined criteria” aim to distinguish between normal ECG changes seen with athletic

    adaptation versus those that may be associated with increased risk for sudden death. Importantly, ECG
    changes may be more common in athletes of African/Caribbean ancestry. Right-axis deviations

    of the QRS complex up to 115 degrees, type 1 second-degree AV block, and LVH by voltage criteria

    alone (without evidence of axis changes, repolarization changes, atrial enlargement, or increased
    QRS width) can be seen in healthy athletes. In addition, healthy black athletes may have convex ST-
    segment elevation associated with T-wave inversions in leads V1-V4. However, ST-segment

    depression ≥0.5 mm in two or more leads is considered an abnormal finding.

    2.

    A 74-year-old man with hypertension and hyperlipidemia presents to your office with chest

    discomfort on exertion. Exercise nuclear stress test demonstrates minimal inferior ischemia and

    transient ischemic dilatation, with a left ventricular ejection fraction (LVEF) of 38%. Coronary

    angiography reveals a 60% proximal left anterior descending artery (LAD) stenosis, 90% left

    circumflex stenosis, and 70% mid right coronary artery stenosis. Fractional flow reserve (FFR)

    evaluation of the LAD lesion is 0.72.

    Which of the following is the most appropriate next step in his treatment?

    a. Coronary artery bypass surgery.

    b. Percutaneous coronary intervention (PCI) of the angiographically significant lesions.

    c. LAD PCI and medical management of the remaining coronary artery disease.

    d. Metoprolol and sublingual nitroglycerin.

    e. Increase atorvastatin to 80 mg daily.

    2.

    a.
    Coronary artery bypass surgery
    This patient presents with multivessel coronary artery disease on coronary angiography including

    the proximal LAD, based on an FFR <0.8. Regardless of stable anginal symptoms, surgical

    revascularization of severe left main disease or proximal LAD with multivessel disease, in the

    setting of reduced LVEF, has a proven mortality benefit and is recommended. The preferred

    method would be surgical revascularization in the absence of contraindications. Optimal medical

    therapy should be initiated in conjunction with revascularization, not as stand-alone therapy.

    3.

    A 56-year-old man with a history of hypertension and hyperlipidemia is evaluated for

    symptoms of progressive chest discomfort. He has increasing substernal chest tightness with

    associated shortness of breath when he walks five blocks or climbs two flights of stairs.

    On physical exam, his heart rate is 58 bpm, blood pressure is 132/82 mm Hg, and cardiac

    examination is normal. His current medications include aspirin 81 mg daily, metoprolol 25 mg twice
    daily, and simvastatin 20 mg daily. An exercise nuclear stress test reveals mild inferior ischemia and a
    normal left ventricular ejection fraction. Coronary angiography reveals a 70% stenosis of the mid
    right coronary artery (RCA) and no other obstructive lesions.

    Which of the following is the most appropriate next step in his management?

    a. Fractional flow reserve (FFR) of the RCA.

    b. Isosorbide mononitrate 30 mg daily.

    c. Intravascular ultrasound (IVUS) of the RCA.

    d. Percutaneous coronary intervention (PCI) to the RCA.

    e. Clopidogrel 75 mg daily.

    3.

    b.
    Isosorbide mononitrate 30 mg daily.
    This patient has angina with a low-risk stress test, low-risk angiographic findings, and is not on
    optimal medical therapy. Based on the Appropriate Use Criteria guidelines for revascularization,

    this patient should have a trial of optimal medical therapy, which is defined as treatment with at least
    two maximally-tolerated antianginal medications (beta-blockers, calcium channel blockers,

    long-acting nitrates, and ranolazine).

    In this patient, the addition of a second antianginal medication is the most appropriate next step,
    before PCI would be performed. FFR or IVUS is not recommended in the setting of a stress test that
    has already demonstrated ischemia in the territory of the angiographically abnormal lesion.

    Clopidogrel does not have antianginal properties, and there are no data for its use in this scenario.

    4.

    A 48-year-old man is seen for cardiovascular (CV) risk assessment. He has a history of tobacco

    use, but quit 15 years ago. His father underwent coronary artery bypass grafting at age 47. He is
    active, but does not exercise regularly. He has no other significant health issues. His blood pressure is
    135/80 mm Hg in both arms, and his exam is unremarkable.

    His 10-year risk of atherosclerotic CV disease (ASCVD) based on the Pooled Cohort Equation is

    7.8%. He states an interest in alternative medicine and prefers supplements over conventional

    medicines. He is concerned about his CV health and would like advice. He tells you that he does not
    like traditional medications and prefers a more natural approach.

    In addition to encouraging lifestyle changes, which of the following should be initiated?

    a. Vitamin D supplementation 2000 international units.

    b. Atorvastatin 40 mg.

    c. Daily multivitamin.

    d. Red yeast rice 1200 mg.

    e. Vitamin E 400 international units and beta-carotene 15 mg.

    4.

    b.
    Atorvastatin 40 mg.
    Based on his risk factors, this patient’s 10-year risk of ASCVD based on the Pooled Cohort Equation
    is 7.8%. According to the most recent guidelines, the initiation of a moderate- or high-intensity statin
    is appropriate. Supplements such as red yeast rice contain varying amounts of monacolin K, the active
    ingredient in lovastatin. As with many supplements, they are not well regulated, and

    therefore the amount of active ingredients may vary considerably.

    Although vitamin D deficiency is a significant concern for many Americans, to date, there are no

    data to support its use for prevention of CVD. The Physicians’ Health Study randomized 14,641

    male physicians, the large majority without coronary artery disease, to either multivitamin daily or
    placebo. No benefit was seen with taking multivitamins. The U.S. Preventive Services Task Force

    has recommended against use of vitamin E and beta-carotene for CV prevention.

    5.

    A 50-year-old man presents to the emergency department with an acute inferior myocardial

    infarction. A drug-eluting stent is placed in the mid right coronary artery, and he recovers well. The
    patient remarks, "I just had a stress test last week and passed with flying colors. How can I have had a
    heart attack?" You explain that atherosclerotic plaques may be too small to induce ischemia on stress
    testing, but may be vulnerable to rupture and result in acute thrombotic arterial

    occlusion.

    Which of the following features is such vulnerable plaques most likely to have?

    a. Increased smooth muscle proliferation.

    b. Reduced inflammatory markers.

    c. Large lipid-filled cores.

    d. Thick overlying fibrous caps.

    e. Low macrophage content.

    5.
    c.
    Large lipid-filled cores.

    Vulnerable plaques are most often plaques with lipid-rich cores, evidence of inflammation, and thin
    fibrous caps. Therefore, an exercise stress test may not predict the presence of such a plaque,

    because they are not necessarily flow limiting. These plaques typically have a high macrophage

    content relative to smooth muscle cells.

    6.

    A 55-year-old man who is a smoker but otherwise healthy presents to the emergency

    department with several hours of stuttering chest and left arm pain. He is on no medications at

    home but took an aspirin before he came to the emergency department, and his pain was

    somewhat reduced by the time of arrival. His blood pressure is 135/87 mm Hg and heart rate is 90

    bpm. Physical examination is otherwise normal. His electrocardiogram shows T-wave inversions

    and 1 mm ST depressions in the inferior and lateral precordial leads. His point of care troponin is
    elevated. He is initially treated with oxygen, metoprolol, and intravenous nitroglycerin and started on
    systemic anticoagulation.

    Which of the following physiologic components of this patient's acute coronary syndrome explains

    why the aspirin has helped improve his pain?

    a. Inhibition of thrombin.

    b. Inhibition of antithrombin III.

    c. Inhibition of the cyclooxygenase-1 enzyme.

    d. Inhibition of the P2Y12 receptor.

    e. Inhibition of glycoprotein IIb/IIIa interaction with fibrinogen.

    6.
    c.
    Inhibition of the cyclooxygenase-1 enzyme.

    Aspirin inhibits platelet activation by irreversibly targeting the cyclooxygenase-1 enzyme.

    Clopidogrel, prasugrel, and ticagrelor target the P2Y12 adenosine diphosphate receptor.

    Glycoprotein IIb/IIIa inhibitors include eptifibatide, abciximab, and tirofiban. Bivalirudin is the only
    intravenous direct thrombin inhibitor used in the treatment of acute coronary syndrome. Heparins

    inhibit the activity of antithrombin III.

    7.

    The critical step in platelet aggregation involves which of the following receptors?

    a. Glycoprotein Ib/IX.

    b. Thrombin.

    c. Glycoprotein IIb/IIIa.

    d. Inositol trisphosphate 3.

    e. Actin.

    7.
    c.
    Glycoprotein IIb/IIIa.

    Platelets have four major functions: adherence, activation, aggregation, and interaction with

    coagulation factors. Platelet activation occurs when platelets are exposed to soluble factors such as
    adenosine diphosphate or thrombin at the site of vascular injury. This initiates a shape change in the
    platelet, and multiple filopodial projections are formed by rearrangements in the cytoskeleton.

    These cytoskeletal changes open the extracellular side of the glycoprotein (GP) IIb/IIIa receptor and
    allow it to bind to fibrinogen. The binding of fibrinogen allows connections between platelets and is
    critical for platelet aggregation. Therefore, the receptor critical to platelet aggregation is the GP

    IIb/IIIa receptor.

    GP Ib/IX is cleaved during the process of platelet activation, but does not have a role in

    aggregation. Inositol trisphosphate 3 receptors are involved in the calcium signaling required for
    activation, but do not have a role in aggregation. Thrombin is responsible for initiation of platelet
    activation, and its receptor on the platelet surface is protease-activated receptor 1. Actin is a
    cytoskeletal protein.

    8.

    A 59-year-old woman presents to the emergency department with a 3-month history of

    exertional chest pain. Her physical exam is unremarkable. Her resting electrocardiogram (ECG) and
    cardiac biomarkers are normal. She experiences chest pain during a stress test with associated ST-
    segment depression. However, perfusion imaging is normal. Subsequent coronary angiography

    demonstrates mild luminal irregularities.

    Which of the following is the most likely explanation for her chest pain?

    a. Hypertrophic cardiomyopathy.

    b. Noncardiac chest pain.

    c. Coronary microvascular dysfunction.

    d. Coronary vasospasm.

    e. Atherosclerotic coronary artery disease (CAD).

    8.

    c.
    Coronary microvascular dysfunction.
    Coronary microvascular dysfunction is diagnosed based on the findings of typical anginal symptoms
    and noncritical epicardial CAD usually associated with abnormal exercise treadmill stress testing.

    Women with normal or near normal coronary arteries with evidence of ischemia and angina have

    an overall higher risk of adverse cardiovascular events compared with patients without angina and
    without CAD. The prognosis of this patient would not be expected to be better than patients

    without cardiovascular disease. In general, patients with angina and fixed obstructive CAD have a
    worse outcome than patients with angina and without fixed obstructive CAD.

    Vasospasm is typically diagnosed with ST-segment elevation at the time of symptoms, but stress

    testing is not sensitive for the diagnosis. Hypertrophic cardiomyopathy can cause chest pain, but
    would be expected to be associated with ECG changes, as well as physical exam findings suggestive
    of outflow obstruction. Atherosclerotic CAD is unlikely to be an adequate explanation, based on the
    findings described on her angiogram.

    9.

    A 53-year-old woman with hypertension, hyperlipidemia, diabetes, and smoking history has

    progressively worsening exertional jaw discomfort for the past 6 months. She is generally

    sedentary, has not seen a physician in many years, and is presently taking aspirin and atorvastatin 80
    mg daily for medications. Blood pressure in the office is 145/78 mm Hg and pulse is 82 bpm. Her
    low-density lipoprotein (LDL) returned at 137 mg/dl and her glycated hemoglobin is 7.5%.

    She was referred for a pharmacologic myocardial perfusion imaging scan (MPS), which showed a

    reversible defect in the mid to distal anterior wall. Coronary angiography shows diffuse plaque in the
    mid right coronary artery with only 20% narrowing and serial 20-30% lesions in the mid left

    anterior descending artery (LAD).

    Which of the following is the next most appropriate step in the patient's management, in addition to
    aggressive risk factor modification and medical therapy with a beta-blocker, angiotensin-converting
    enzyme inhibitor, and statin?

    a. Percutaneous coronary intervention (PCI) of the LAD.

    b. Isosorbide mononitrate.

    c. Ranolazine.

    d. Extracorporeal counterpulsation.
    e. Fractional flow reserve (FFR).

    9.

    b.
    Isosorbide mononitrate.
    The prognosis for patients with coronary microvascular dysfunction is not benign and may be

    similar to selected age- and sex-matched patients with epicardial coronary artery obstructive

    disease. This finding of no obstructive disease should not lead to complacency relative to

    management. The first line of management should be risk factor modification beginning with

    lifestyle modification. The patient should be encouraged to increase her daily activities, and if
    possible, begin a regular exercise program like walking. She should also understand that if angina is
    induced with light exercise, such as walking, it is not dangerous and titration of isosorbide

    mononitrate may permit her to walk comfortably without angina. The goal is to work toward the

    American Heart Association recommended 10,000 steps per day, achieve excellent blood pressure

    control (<120/90 mm Hg), LDL-lowering, and optimal management of glycemia.

    PCI of a nonobstructive lesion will not result in symptom relief. However, her MPS defect and serial
    stenoses are colocalized to the same coronary distribution, and serial stenoses in the 30% diameter
    range could contribute to important obstruction. Thus, if her symptoms persist, FFR would be

    helpful to assess the functional significance of the serial stenoses. If these lesions are confirmed to be
    truly nonobstructive, coronary flow reserve measurements would be useful to assess for

    coronary microvascular dysfunction. Ranolazine and extracorporeal counterpulsation should not be

    the first line of management.

    10. A 49-year-old woman with a history of diabetes and hypertension, and a family history of

    coronary artery disease (CAD) presents to her physician with the chief complaint of chest pain and
    heaviness that occurs with exertion and infrequently at rest. Her symptoms have been persistent

    for nearly a year. She initially attributed her symptoms to acid reflux.

    She is referred for an exercise treadmill test. Her body mass index is 30 kg/m2. She is able to

    exercise for 8 metabolic equivalents (METs) on a standard Bruce protocol, but exercise is limited by
    her typical angina. Her electrocardiogram shows 3-4 mm ST-downsloping segment depressions in

    the lateral leads. She is referred for coronary angiography that shows no obstructive CAD and no

    luminal irregularities.

    Which of the following is the most appropriate next best step in the patient's management?
    a. Esophagogastroduodenoscopy (EGD).

    b. Intravascular ultrasound (IVUS).

    c. Ergonovine challenge.

    d. Coronary flow reserve measurement.

    e. Assess response to empiric antispasm medication.

    10. d.
    Coronary flow reserve measurement.
    This patient has multiple cardiovascular risk factors and evidence of ischemia on stress testing. She
    has no obstructive CAD on coronary angiography. The most likely diagnosis is coronary

    microvascular dysfunction (CMD). The exact mechanism of CMD is not entirely clear. From a

    pathophysiological view, CMD as reduced coronary flow reserve (CFR) most often results from a

    combination of different alterations, such as impaired vasodilation, enhanced vasoconstrictor

    responsiveness, and/or structural remodeling of the coronary microvasculature. CMD can cause

    abnormalities in stress testing indicative of ischemia without obstructive epicardial CAD.

    CFR measurement either invasively (intracoronary Doppler catheter) or noninvasively (positon

    emission tomography, cardiac magnetic resonance imaging, or transthoracic Doppler), can be very

    helpful in determining if CMD is present. There is no role for IVUS in this setting, nor does

    "prophylactic" stenting of borderline plaques improve outcomes and may be harmful. Coronary
    spasm is not the likely etiology in this case, particularly given the appearance of smooth coronaries
    on angiography and lack of prominent component of her symptoms occurring at rest. Nevertheless,

    testing with intracoronary acetylcholine would exclude spasm with a high degree of certainty and

    perhaps avoid need to expose her to multiple calcium antagonists and nitrates.

    11. A 90-year-old man with hypertension and hyperlipidemia had previously enjoyed a good

    quality of life without symptoms secondary to cardiovascular disease. However, over the last 3

    months, he has noted the progressive onset of symptoms consistent with exertional angina. He

    generally enjoys taking walks around a pond near his home. However, he now notes that after 100

    yards, he develops heaviness in the center of his chest that resolves with rest. He was started on a beta-
    blocker, aspirin, and a statin, but continues to have lifestyle-limiting angina.

    He is referred for an exercise tolerance test, where he is able to perform 5 METs of exercise prior to
    developing limiting angina and 3 mm ST depressions in the lateral leads. He is referred for cardiac
    catheterization, where he is found to have a 90% focal lesion in the mid left anterior descending
    artery (LAD), a 50% lesion in the first obtuse marginal artery (OM1), and a focal 99% stenosis of the
    right coronary artery (RCA) with collaterals to the distal RCA from the LAD.

    Which of the following is the most appropriate next step for this patient?

    a. Medical therapy.
    b. Hybrid CABG/percutaneous coronary intervention (PCI).

    c. Referral for coronary artery bypass grafting (CABG).

    d. PCI of the RCA and LAD.

    e. PCI of the RCA, OM, and LAD.

    11. d.

    PCI of the RCA and LAD.

    The patient's age is not a limitation to revascularization. With advancements in both surgical and
    interventional techniques, the safety of revascularization procedures has improved over time and

    the elderly have as much to gain by revascularization as the nonelderly. This patient has a low

    SYNTAX score, which would suggest that the outcomes of multivessel PCI are comparable with

    CABG in terms of death and myocardial infarction out to 5 years.

    PCI likely offers a reduced risk of stroke. Therefore, PCI is the preferred revascularization strategy
    for this patient given that it is less invasive. Fractional flow reserve of the OM lesion may be

    reasonable to show that the lesion is not hemodynamically significant. At this time, there are no
    definitive outcome data to support routine use of hybrid revascularization procedures.

    12. A 57-year-old man with hypertension, tobacco use, and diabetes presents with 3 weeks of
    exertional chest tightness. An exercise treadmill stress test is notable for reproducible chest

    discomfort associated with 2 mm inferolateral ST-segment depressions and ST-segment elevation

    in lead aVR.

    He is started on aspirin, simvastatin, and metoprolol and referred for cardiac catheterization, which
    demonstrates a right-dominant system with focal 90% proximal left anterior descending artery

    (LAD), 80% mid left circumflex, and 80% mid right coronary artery stenoses. You discuss with him

    the options of surgical versus percutaneous revascularization.

    Which of the following outcomes is associated with surgical revascularization in this patient?

    a. Decreased bleeding risk.

    b. Increased need for repeat revascularization.

    c. Decreased stroke risk.

    d. Improved ejection fraction.


    e. Improved survival.

    12. e.
    Improved survival.
    In patients with diabetes and significant left main coronary artery disease (=50%) or severe

    coronary artery disease (=70%) in three major coronary arteries or involving the proximal LAD plus
    one other coronary artery, coronary artery bypass grafting is the recommended revascularization

    strategy and has been shown to improve survival. In contrast, while percutaneous coronary

    intervention (PCI) may improve anginal symptoms in patients with stable ischemic heart disease, no
    studies to date have demonstrated that PCI confers a survival advantage without recent acute

    coronary syndrome. Stroke risk is increased in CABG versus PCI.

    13. A 52-year-old man with hypertension and hyperlipidemia is referred for cardiac stress testing due
    to atypical chest pain and recently declining exercise tolerance. He completes 7 minutes of a standard
    Bruce protocol and stops due to fatigue and chest burning. Perfusion imaging reveals a

    moderately severe, reversible apical defect. He is started on aspirin 81 mg daily, simvastatin 20 mg


    daily, metoprolol 25 mg daily, and amlodipine 5 mg daily, but his symptoms persist. He is referred
    for cardiac catheterization, which reveals a 70% mid left anterior descending artery stenosis

    treated successfully with percutaneous coronary intervention (PCI).

    Which of the following best describes the long-term outcomes of PCI versus coronary artery bypass
    grafting (CABG) in this patient?

    a. No difference.

    b. Decreased mortality with PCI.

    c. Improved left ventricular ejection fraction with CABG.

    d. Decreased target vessel revascularization with PCI.

    e. Increased recurrent myocardial infarction (MI) with CABG.

    13. a.
    No difference.
    More than 20 randomized controlled trials have compared CABG with balloon angioplasty or

    stenting in patients with single-vessel coronary artery disease, demonstrating similar outcomes

    regarding survival and recurrent MI. CABG has a significantly higher rate of stroke, but lower repeat
    revascularization rate compared with PCI. In this patient with one significant stenosis amenable to
    revascularization and unacceptable angina despite guideline-directed medical therapy, PCI or CABG

    are both beneficial to improve anginal symptoms.

    14. A 62-year-old man with a history of smoking, hypercholesterolemia, and obesity is being

    evaluated for progressive dyspnea on exertion. He denies chest pain, orthopnea, or peripheral

    edema. An echocardiogram demonstrates left ventricular ejection fraction (EF) of 35% with global

    hypokinesis and no significant valvular dysfunction. Coronary angiography reveals significant three-
    vessel coronary artery disease (CAD) with an occluded but well-collateralized dominant right

    coronary artery, and calculated SYNTAX score of 35.

    Which of the following is the most appropriate next step?

    a. Hybrid CABG/PCI.

    b. Implantable cardioverter-defibrillator (ICD).

    c. Coronary artery bypass grafting (CABG).

    d. Medical therapy alone.

    e. Multivessel percutaneous coronary intervention (PCI).

    14. c.

    Coronary artery bypass grafting (CABG).

    The SYNTAX trial randomized 1,800 patients with left main or three-vessel CAD to revascularization
    with drug-eluting stents or CABG. Overall, at 3 years, major adverse cardiac events were lower for
    CABG over PCI (20.2% vs. 28.0%), driven by decreased recurrent myocardial infarction and repeat

    revascularization in the CABG arm.

    In a post hoc analysis, an angiographic SYNTAX score was derived for each patient as a surrogate

    measure of the CAD complexity, based on the location, severity, and extent of CAD (low SYNTAX
    score, 22; intermediate, 23-32; and high, 33). While patients with a low SYNTAX score had similar
    outcomes with PCI or CABG, those with intermediate and high SYNTAX scores treated with CABG

    exhibited lower mortality at 3 years compared with PCI, with significantly decreased target vessel
    revascularization.

    In summary, the SYNTAX results suggest that PCI or CABG is comparable in less complex disease,

    while in patients with more complex disease, CABG is the preferred revascularization strategy.

    There are no data as of yet to support use of hybrid CABG/PCI. Medical therapy alone is not

    sufficient in the setting of reduced EF. ICD is warranted only if EF remains <35% at 3 months after
    revascularization.

    15. An 82-year-old man with a history of coronary artery disease (CAD) status/post percutaneous

    coronary intervention (PCI) to the left anterior descending artery (LAD) 10 years ago, chronic

    obstructive pulmonary disease, obesity, and chronic kidney disease develops progressive angina on
    exertion. He has been managed successfully for many years on a combination of aspirin,

    atorvastatin, and atenolol. Echocardiography reveals preserved left ventricular function.

    He is referred for coronary angiography, which demonstrates 60% ostial left main coronary

    stenosis, a widely patent LAD stent with diffuse luminal irregularities, no significant left circumflex
    disease, and focal 70% mid-right coronary artery stenosis.

    Which of the following is the next best step in this patient's management?

    a. Heart Team evaluation.

    b. Multivessel PCI.

    c. Medical therapy alone.

    d. Coronary artery bypass grafting (CABG).

    e. PCI to the left main coronary artery.

    15. a.
    Heart Team evaluation.
    The current stable ischemic heart disease guideline recommends that patients with significant left
    main or complex multivessel CAD be evaluated by a multidisciplinary Heart Team to determine the

    most appropriate method of revascularization. This strategy mimics typical protocols used in

    clinical trials, where a Heart Team, composed of an interventional cardiologist and cardiac surgeon,
    review all available patient data and discuss potential treatment options with the patient.

    Calculation of the Society of Thoracic Surgeons (STS) and SYNTAX scores assist in determining the
    surgical risk category and complexity of CAD.

    While PCI may be a reasonable strategy in patients with amenable coronary anatomy, high surgical

    risk, or other considerations, in general, ad hoc PCI immediately following diagnostic coronary

    angiography is discouraged in patients with complex multivessel CAD.

    Although escalation of medical therapy may improve angina, if the patient is a candidate for

    revascularization, a Heart Team evaluation would be beneficial.

    16. A 65-year-old man with diabetes controlled with medications comes to you for evaluation of

    exertional chest pain. He has been appropriately managed for chronic stable angina with beta-

    blockers, statin, nitrates, and aspirin.

    The patient is able to exercise 7 minutes on a Bruce protocol, his classic chest pain recurs at stage 3,
    and there are 2 mm ST depressions in the anterolateral leads with reversible perfusion defects
    anteriorly. His left ventricular ejection fraction (LVEF) is 50%. Cardiac catheterization reveals 90%

    promimal left anterior descending artery (LAD), 70% first obtuse marginal, 80% mid left circumflex,
    and 90% mid right coronary artery stenoses.

    Which of the following is the next best step in the management of this patient?

    a. Ranolazine extended-release 500 mg PO daily.

    b. Coronary artery bypass grafting (CABG) revascularization.

    c. LAD PCI revascularization only.

    d. Increase metoprolol.

    e. Multivessel percutaneous coronary intervention (PCI) revascularization.

    16. b.
    Coronary artery bypass grafting (CABG) revascularization.

    This patient has diabetes, severe multivessel coronary artery disease (CAD), and a reduced LVEF. He
    should undergo complete revascularization with CABG.

    Recently, results from the FREEDOM trial in patients with diabetes and multivessel CAD treated

    with CABG had a significantly lower composite rate of death from any cause, nonfatal myocardial

    infarction, or nonfatal stroke when compared with diabetic patients treated with PCI.

    An analysis performed in 2009 of data in 7,812 patients (1,233 with diabetes) in 10 randomized

    clinical trials demonstrated a worse long-term survival rate in patients with diabetes after balloon
    angioplasty or bare-metal stent implantation than after CABG.

    The BARI 2D trial randomly assigned 2,368 patients with type 2 diabetes and CAD to undergo

    intensive medical therapy or prompt revascularization with PCI or CABG, according to whichever

    was thought to be more appropriate. By study design, those with less extensive CAD more often

    received PCI, whereas those with more extensive CAD were more likely to be treated with CABG.

    The study was not designed to compare PCI with CABG. At 5-year follow-up, no difference in rates

    of survival or major adverse cardiac events (MACE) between the medical therapy group and those

    treated with revascularization was noted. In the PCI stratum, no significant difference in MACE

    between medical therapy and revascularization was demonstrated (drug-eluting stent in 35%;

    bare-metal stent in 56%); in the CABG stratum, MACE occurred less often in the revascularization

    group.

    17. A 73-year-old morbidly obese woman with insulin-dependent diabetes, dyslipidemia, and

    severe ambulatory dysfunction is sent to you for preoperative assessment before total knee

    replacement. She has chronic kidney disease with a creatinine of 2.1 mg/dl. Her heart rate is 80

    bpm, blood pressure is 150/80 mm Hg, and respiratory rate is 20 breaths/minute. She has no

    evidence of heart failure.

    Her electrocardiogram (ECG) reveals sinus rhythm with inferior Q waves noted. The patient's

    echocardiogram is normal. She is on insulin, losartan 100 mg PO daily, and atorvastatin 40 mg PO


    daily.

    Which of the following is the next best step in the preoperative cardiac risk assessment for this
    patient?

    a. Pharmacologic nuclear stress test.

    b. Coronary computed tomographic angiography.

    c. Cardiac catheterization.

    d. No further cardiac evaluation is necessary.

    e. Exercise ECG stress test.

    17. a.
    Pharmacologic nuclear stress test.
    This patient has several risk factors for coronary artery disease. While knee replacement is not a
    high-risk surgery compared with vascular surgery and head and neck surgery, this patient has

    several concerning clinical features, including an abnormal resting ECG, increased creatinine, insulin
    therapy, uncontrolled blood pressure, and unclear functional capacity.

    Multivariate risk indices such as the revised cardiac risk index (RCRI) and 2014 American College of
    Cardiology (ACC)/American Heart Association (AHA) perioperative cardiovascular evaluation

    guideline can be applied to determinate the major adverse cardiac event (MACE) risks. Her RCRI

    risk is 11% for MACE (includes possible myocardial infarction, insulin use, and creatinine >2.0

    mg/dl).

    According to the ACC/AHA 2014 guideline for perioperative cardiovascular evaluation for

    noncardiac surgery, this is a Class IIa indication:

    "It is reasonable for patients who are at an elevated risk for noncardiac surgery and have poor
    functional capacity (<4 METs) to undergo noninvasive pharmacological stress testing (either

    dobutamine stress echocardiogram or pharmacological stress perfusion imaging) if it will change

    management. (Level of Evidence: B)"

    Figure 1 outlines the ACC/AHA perioperative guideline. A pharmacologic stress test is appropriate in
    someone who cannot exercise.
    (Figure 1)

    18. A 55-year-old man comes to you for preoperative cardiovascular risk stratification for inguinal
    hernia repair. The patient has hypertension and takes atenolol 25 mg PO daily. He has a strong

    history of smoking 30 pack-years and has not had his lipid profile evaluated for 2 years. He has a
    family history of coronary artery disease; his father had a myocardial infarction at 53 years of age.

    The patient notices pain and discomfort in the groin area while walking. However, he is able to

    walk up a hill and mow the lawn.

    On examination, heart rate is 53 bpm, blood pressure is 120/83 mm Hg, and respiratory rate is 15

    breaths/minute. His electrocardiogram shows sinus rhythm at 54 bpm with an incomplete right

    bundle branch block.

    Based on these findings, which of the following is your next best step in evaluating this patient?

    a.
    Transthoracic echocardiogram.

    b.

    Exercise treadmill stress testing.

    c.

    Proceed with surgery.

    d.

    Dobutamine stress echocardiography.

    e.

    Coronary computed tomography angiography.

    18. c.
    Proceed with surgery.
    Functional status is a reliable predictor of perioperative and long-term cardiac events. Patients with
    reduced functional status preoperatively are at increased risk of complications. Conversely, those
    with good functional status preoperatively are at lower risk. Moreover, in highly functional

    asymptomatic patients, it is often appropriate to proceed with planned surgery without further

    cardiovascular testing, as outlined in the 2014 perioperative cardiovascular evaluation guideline


    (Figure 1).

    19. A 63-year-old woman comes to your office for preoperative clearance for a hysterectomy. The
    patient has been complaining of dysfunctional uterine bleeding and was found to have multiple

    uterine fibriods that have not improved with embolization. She has history of insulin-dependent

    diabetes, hypertension, and chronic kidney disease (stage 3). Her medications include lisinopril 40

    mg daily, ferrous sulfate, and insulin. She can do her activities of daily living, but becomes short of
    breath climbing a flight of stairs.
    On exam, her heart rate is 88 bpm and blood pressure is 133/83 mm Hg, respiration rate is 15

    breaths/minute, and conjunctiva are pale. Cardiovascular examination reveals soft systolic flow

    murmur in the left sternal border. There are no rales or rhonchi and no pedal edema.

    An electrocardiogram in your office shows sinus rhythm with left bundle branch block (LBBB). Her

    most recent labs include glycated hemoglobin of 8.9%, hemoglobin of 9.0 mg/dl, and creatinine of

    2 mg/dl.

    Which of the following is the next best step in her management?

    a. Pharmacologic nuclear stress test.

    b. Exercise treadmill stress test.

    c. Proceed with surgery.

    d. Dobutamine stress echo.

    e. Start beta-blockers.

    19. c.
    Proceed with surgery.
    This patient has several cardiovascular risk factors and evidence of an LBBB. She can, however,

    climb a flight of stairs, and thus has a functional capacity >4 METs. She does not require stress testing
    prior to undergoing medically necessary surgery.

    Functional status is a reliable predictor of perioperative and long-term cardiac events. Patients with
    reduced functional status preoperatively are at increased risk of complications. Conversely, those
    with good functional status preoperatively are at lower risk. Moreover, in highly functional

    asymptomatic patients, it is often appropriate to proceed with planned surgery without further

    cardiovascular testing.

    If a patient has not had a recent exercise test before noncardiac surgery, functional status can

    usually be estimated from activities of daily living. Functional capacity is often expressed in terms of
    METs, where 1 MET is the resting or basal oxygen consumption of a 40-year-old man who weighs

    70 kg. In the perioperative literature, functional capacity is classified as excellent (>10 METs), good
    (7-10 METs), moderate (4-6 METs), poor (<4 METs), or unknown.

    Perioperative cardiac and long-term risks are increased in patients unable to perform 4 METs of

    work during daily activities. Examples of activities associated with <4 METs are slow ballroom
    dancing, golfing with a cart, playing a musical instrument, and walking at approximately 2-3 mph.

    Examples of activities associated with >4 METs are climbing a flight of stairs or walking up a hill,
    walking on level ground at 4 mph, and performing heavy work around the house.

    20. A 65-year-old man with intermittent bilateral lower-extremity claudication, hypertension, and
    diabetes presents to your office for assessment prior to planned femoral-popliteal bypass surgery.

    He denies chest pain, but is significantly limited by his claudication and cannot walk more than a
    block without stopping. A pharmacologic stress test reveals a large area of ischemia in the anterior
    wall; left ventricular ejection fraction is 40%. Coronary angiography reveals three-vessel coronary
    artery disease.

    Which of the following is the most appropriate next step in his management?

    a. Maximize medical therapy and proceed with vascular surgery.

    b. Multivessel percutaneous coronary intervention (PCI) with drug-eluting stents.

    c. Maximize medical therapy and cancel surgery.

    d. Multivessel PCI with bare-metal stents.


    e. Coronary artery bypass grafting.

    20. e.
    Coronary artery bypass grafting.
    This patient has significant ischemic disease, reduced left ventricular function, and diabetes.

    Assessment of his functional status is limited by his significant claudication, but he has a high-risk
    nuclear perfusion scan and multivessel coronary artery disease. Regardless of the plans for elective
    surgery, revascularization of his coronary artery disease is indicated.

    Coronary artery bypass grafting is preferable to PCI in light of his diabetes, as shown in the

    FREEDOM trial.

    21. A 60-year-old woman with hypertension presents to the emergency room with chest pain.

    She describes acute onset of chest pain radiating to her back associated with leg weakness and

    presyncope. Blood pressure is 162/100 mm Hg, pulse is 100 bpm, and respiratory rate is 20

    breaths/minute. Cardiac exam reveals an S4 gallop with no murmur. She has no known drug

    allergies. Her electrocardiogram (ECG) is shown in Figure 1.

    Which of the following is the most appropriate next step?


    a. Coronary angiography.

    b. Chest computed tomography angiography (CTA).

    c. Transthoracic echocardiogram.

    d. Thrombolytics.

    e. Chest X-ray.

    21. b.

    Chest computed tomography angiography (CTA).

    The patient's symptoms of chest pain radiating to the back and weakness of the lower extremities

    are classic for aortic dissection, in this case complicated by extension of the dissection into the ostium
    right coronary artery, as evidenced by the inferior injury current on the ECG, which may be present
    in 7% of dissections. This combination may lead to misdiagnosis and delayed therapy.

    Because the symptoms are so suggestive of dissection, emergent CTA of the chest or
    transesophageal echocardiography imaging of the aorta and cardiac surgical consultation for the

    life-threatening dissection is more appropriate than CTA (see management algorithm in Figure 2).

    Chest X-ray may show a widened mediastinum, which is not very sensitive or specific and would

    not provide enough information to proceed with surgery. Thrombolytic therapy would be

    contraindicated, with the patient's symptoms the central factor in making the correct diagnosis.

    22. Which of the following patients most likely has a myocardial infarction (MI), according to the
    Third Universal Definition of MI?

    a.

    A 48-year-old woman with 2 weeks of chest pain, palpitations, progressive dyspnea, and volume

    overload. Echocardiogram reveals diffuse hypokinesis with left ventricular ejection fraction of 25%.

    Endomyocardial biopsy shows diffuse necrosis, multinucleated cells, and lymphocytic and

    eosinophilic infiltrates.

    b.

    A 38-year-old obese man with 10-year tobacco history, recent upper respiratory symptoms, 2 days of
    pleuritic chest pain, and diffuse ST elevations; troponin values are 0.10, 0.11, and 0.09.

    c.

    A 56-year-old male unrestrained driver with hypertension after a motor vehicle accident and steering
    wheel trauma to the chest. His echocardiogram shows anterior wall hypokinesis.

    d.

    A 61-year-old woman with noninsulin-dependent diabetes, obesity, and sleep apnea presents with

    new-onset atrial fibrillation, heart rate 130 bpm, and ST depressions in leads II, III, and aVF.

    e.

    A 68-year-old woman with hypertension, diabetes, and end-stage renal disease presents with

    shortness of breath after missing two hemodialysis sessions. Serial troponin values are 0.05, 0.04,
    0.06, and 0.03. Her electrocardiogram shows left ventricular hypertrophy, but no ST/T wave changes.

    22. d. A 61-year-old woman with noninsulin-dependent diabetes, obesity, and sleep apnea
    presents with new-onset atrial fibrillation, heart rate 130 bpm, and ST depressions in

    leads II, III, and aVF.


    The Third Universal Definition of MI requires elevation in cardiac troponins, with a rise and/or fall
    in levels over serial measurement, together with symptoms or signs of cardiac ischemia. These may
    include new significant ST-segment T-wave changes, new left bundle branch block, new pathologic

    Q waves, imaging evidence of new regional wall motion abnormalities or new loss of viable

    myocardium, or intracoronary thrombus demonstrated by angiography or autopsy. Many

    conditions other than cardiac ischemia may lead to elevation in troponins. Moreover, MI may be

    due either to plaque rupture (type 1 MI) or due to supply-demand mismatch, with or without

    underlying coronary artery disease (type 2 MI).

    The patient presenting with atrial fibrillation and rapid ventricular response with

    electrocardiographic evidence of ischemia most likely has a type 2 MI. The other clinical scenarios
    most likely represent giant cell myocarditis, myopericarditis, troponin elevation without clear rise
    and fall in the setting of renal disease, and myocardial injury due to contusion. If no active ischemia is
    suspected, then these would not be considered instances of MI, according to the Third Universal
    Definition of MI. Troponin elevations due to defibrillation shocks, receipt of cardiotoxic

    chemotherapeutic agents, and rhabdomyolysis with cardiac involvement are other examples where

    myocardial injury occurs apart from ischemia and which would not be considered MI.
    (Figure 2)

    23. A 53-year-old man presents to the emergency room with 1 hour of chest pain. Current vital signs
    are pulse 122 bpm and irregular, blood pressure 178/102 mm Hg, respiratory rate 18

    breaths/minute, Saturation of peripheral oxygen is 98% on room air. The neck veins are flat. The

    lungs are clear and there is no murmur or gallop.

    His electrocardiogram reveals atrial fibrillation with rapid ventricular response and 1 mm ST-

    elevations in leads I and aVL.

    Which of the following is most appropriate to manage his atrial fibrillation?

    a. Oral or intravenous metoprolol.

    b. Intravenous diltiazem.

    c. Intravenous ibutilide.
    d. Sublingual nifedipine.

    e. Oral amiodarone.

    23. a.
    Oral or intravenous metoprolol.
    In the setting of ST-segment elevation myocardial infarction (STEMI), beta-blockers are the

    preferred rate control agent for atrial fibrillation. Routine use of intravenous beta-blockers for
    STEMI is not recommended, but it may be used in a hypertensive urgency or tachyarrhythmia in

    the absence of other contraindications. Oral beta-blockade within 24 hours of presentation

    remains a Class I indication in STEMI. Calcium channel blockers have no demonstrated benefit in

    STEMI, although they could be considered for rate control in atrial fibrillation, but not if systolic
    dysfunction is present.

    Short-acting nifedipine for hypertension is harmful because of the potential for hypotension and

    reflex tachycardia. Oral amiodarone would not be useful acutely in this setting. Ibutilide would be
    inappropriate, as this patient has no indication for emergent cardioversion and the duration of

    atrial fibrillation is unknown.

    24. A 58-year-old woman with rheumatoid arthritis presents with 1 week of intermittent nausea

    and exertional chest pressure and 30 minutes of constant intense chest pressure. Her

    electrocardiogram is notable for up to 2.5 mm ST elevations in leads I, aVL, and V5-V6. She is found
    to have occlusion of a large second obtuse marginal coronary artery branch and undergoes drug-
    eluting stent placement. Follow-up testing shows normal cardiac function and hemoglobin A1c of

    5.3%.

    Which of the following is most likely to be beneficial for chronic outpatient therapy for this patient?

    a.

    Isosorbide mononitrate 30 mg daily.

    b.

    Verapamil sustained release 180 mg daily.

    c.

    Metoprolol succinate 50 mg daily.

    d.

    Enalapril 10 mg bid.
    e.

    Spironolactone 25 mg daily.

    24. c.
    Metoprolol succinate 50 mg daily.
    Beta-blockers have a Class I indication for continuation during and after hospitalization for all
    patients with ST-segment elevation myocardial infarction (STEMI) in the absence of

    contraindications. Certain conditions warrant caution or avoidance of beta-blocker therapy:

    decompensated heart failure, low-output states, high risk of cardiogenic shock, reactive airways

    disease or active bronchospasm, and prolonged first-degree or high-grade atrioventricular block.

    Angiotensin-converting enzyme (ACE) inhibitors have a Class I indication for use in patients with
    STEMI with anterior involvement, heart failure, and left ventricular ejection fraction (LVEF) ≤40% in
    the absence of contraindications. Angiotensin-receptor blockers may be used for patients who are

    intolerant of ACE inhibitors.

    For patients such as this one, who do not have anterior involvement, heart failure, or low EF, ACE

    inhibitors have a Class IIa indication. Aldosterone antagonists should be used (Class I indication) in
    patients with STEMI and no contraindications who are already receiving an ACE inhibitor and beta-
    blocker and who have LVEF ≤40% AND either symptomatic heart failure or diabetes. This patient

    would not meet these criteria.

    Nitrates are not indicated for routine use after STEMI. Calcium channel blockers have not been

    shown to reduce infarct size or rate of reinfarction, but may be helpful in the treatment of

    ischemia, hypertension, or rapid ventricular rate in patients with atrial fibrillation who are

    intolerant of beta-blockers.

    25. A 53-year-old man with diabetes is admitted with an acute inferoposterior ST-segment elevation
    myocardial infarction (STEMI). He undergoes primary percutaneous coronary

    intervention with placement of a drug-eluting stent to the proximal left circumflex artery. He has
    single-vessel disease, left ventricular end-diastolic pressure of 14 mm Hg, and an ejection fraction
    (EF) of 35%.

    According to the 2013 STEMI guideline, which of the following is a Class I indication for initiating
    an angiotensin-converting enzyme (ACE) inhibitor within 24 hours in this patient?

    a.

    EF of 35%.STEMI.

    b.
    Culprit lesion location.

    c.

    Chronic kidney disease.

    d.

    Diabetes.

    25. a.

    EF of 35%.

    An ACE inhibitor should be administered within the first 24 hours to all patients with STEMI with an
    anterior location, heart failure, or EF of ≤40%, unless contraindicated (Class I, Level of Evidence A).

    Oral ACE inhibitors reduce fatal and nonfatal major cardiovascular events in patients with STEMI.

    The magnitude of clinical benefit is greatest in high-risk patient subgroups. Demonstration of an


    early benefit (within the first 24 hours) supports the prompt use of these agents in patients without
    existing contraindications (e.g., hypotension, shock, bilateral renal artery stenosis, or history of
    worsening of renal function with ACE inhibitor/angiotensin-receptor blocker exposure, renal

    failure, or drug allergy). The role of routine long-term ACE inhibitor therapy in low-risk patients
    after STEMI who have been revascularized and treated with aggressive lipid-lowering therapies is

    less certain.

    26. A 60-year-old woman presents to the office for follow-up after cardiac catheterization. She

    had single-vessel disease with a moderate 50% stenosis and noncritical fractional flow reserve

    (0.84). Her medical history is significant for treated hyperlipidemia. Her blood pressure is 120/60

    mm Hg with a heart rate of 70 bpm, and her exam is normal. She is asymptomatic on aspirin, statin,
    and beta-blocker. She asks about her risk of myocardial infarction.

    Which of the following best correlated with her risk of plaque rupture?

    a. High cholesterol.

    b. Plaque macrophage content.

    c. Plaque calcium content.

    d. It is unpredictable.

    e. Stenosis severity.
    26. b.
    Plaque macrophage content.
    The conversion of a stable plaque-to-plaque rupture or erosion does not have much to do with the

    stenosis severity. Plaque rupture is predicted by several anatomic and systemic factors, including
    inflammation, integrity of the fibrous cap, plaque lipid content, and plaque location.

    27. A 40-year-old woman presents to the emergency department with chest discomfort. She

    describes sharp chest pain that lasts for less than a minute and occurs at various times during the day.
    Her exam is unremarkable. Her electrocardiogram is normal.

    Which of the following risk scores should be used to best guide management in the emergency

    department?

    a. Duke treadmill score.

    b. Framingham Coronary Heart Disease Risk Score.

    c. HEART (History, Electrocardiogram, Age, Risk factors, and Troponin) score.

    d. GRACE (Global Registry of Acute Coronary Events) score.

    e. TIMI (Thrombolysis in Myocardial Infarction) score.

    27. c.

    HEART (History, Electrocardiogram, Age, Risk factors, and Troponin) score.

    Risk scores can be used to determine the short-term risk of adverse events in patients with chest pain
    or definite acute coronary syndrome (ACS). The HEART score is a prospectively studied scoring
    system to help emergency departments risk-stratifiy chest pain patients according to risk of major
    adverse cardiac events within 6 weeks. The HEART score includes history, electrocardiogram, age,

    risk factors, and troponin.

    TIMI and GRACE scores are used to estimate risk of death or MI for patients with ACS, and are not as
    useful for patients with chest pain of unclear etiology. The Framingham Coronary Heart Disease Risk
    Score estimates risk of heart attack in 10 years in a stable patient. The Duke treadmill score is specific
    to predicting coronary artery disease in a patient undergoing stress testing.

    28. A 47-year-old woman presents to the emergency department with 2 days of substernal chest

    pressure radiating to the jaw with minimal exertion relieved with rest. The last episode was 1 hour
    prior to presentation and lasted 15 minutes. She has no medical history and takes no medication.

    Her resting electrocardiogram is normal.


    Which of the following is the most accurate biomarker strategy for diagnosing myocardial

    infarction (MI) in this patient?

    a. High-sensitivity troponin at time 0 hours.

    b. Creatine kinase-myocardial isoenzyme (CK-MB) at time 0 and 6 hours.

    c. Cardiac-specific troponin at time 0 and 6 hours.

    d. B-type natriuretic peptide (BNP) after 6 hours of observation.

    e. Myoglobin at the time of presentation (time 0).

    28. c.

    Cardiac-specific troponin at time 0 and 6 hours.

    Cardiac biomarkers are part of the universal definition of MI. Although the specificity of cardiac-
    specific and high-sensitivity troponin assays are of concern, they are the biomarker of choice in
    patients with suspected acute coronary syndrome (ACS). The current American Heart

    Association/American College of Cardiology guideline recommends that cardiac-specific troponin

    (troponin I or T when a contemporary assay is used) levels should be measured at presentation and 3-
    6 hours after symptom onset in all patients who present with symptoms consistent with ACS to

    identify a rising and/or falling pattern (Class I).

    Although high-sensitivity troponin may be positive earlier, a single measure at presentation is not
    sufficient to exclude MI. With contemporary troponin assays, creatine kinase myocardial isoenzyme
    (CK-MB) and myoglobin are not useful for diagnosis of ACS (Class III). Use of selected newer

    biomarkers, especially BNP, may be reasonable to provide additional prognostic information (Class
    IIb), but are not used for the initial diagnosis.

    29. A 68-year-old man presents to the emergency department with two episodes of resting chest

    pressure radiating to the jaw and arm and lasting 15 minutes in the 6 hours prior to presentation.

    His pain resolved without treatment and he is now pain free. His medical history is significant for
    hyperlipidemia, hypertension, and tobacco abuse. His medications include aspirin, diltiazem, and

    atorvastatin. His initial high-sensitivity troponin is negative and his electrocardiogram is normal.

    Which of the following is the most appropriate management for this patient?

    a.

    Triage to observation unit for serial biomarkers.


    b.

    Discharge with outpatient stress testing within 48 hours.

    c.

    Admission for stress testing.

    d.

    Dual antiplatelet therapy and catheterization within 24 hours.

    e.

    Initiation of a glycoprotein IIb/IIIa inhibitor.

    29. d.

    Dual antiplatelet therapy and catheterization within 24 hours.

    Patients with acute coronary syndromes (ACS) can be risk stratified with clinical risk scores

    including the TIMI (Thrombolysis in Myocardial Infarction) and GRACE (Global Registry of Acute

    Coronary Events) scores. Although this patient has no objective ischemia, his TIMI risk score is 4

    (age over 64, severe angina, three cardiac risk factors, and aspirin use), which predicts a 20% risk of
    all-cause mortality, new or recurrent MI, or severe recurrent ischemia requiring urgent

    revascularization at 14 days. Several randomized trials have compared an early invasive strategy

    with a delayed, selective, or conservative strategy in patients with ACS.

    In the TIMACS trial, patients with a GRACE score >140, but not those with a GRACE score <140, had
    a reduction in the ischemic endpoint of death, MI, or stroke. Also in the TIMACS trial, death, MI, and
    rehospitalization from ACS was lower with an invasive strategy in patients with positive

    troponin, ST deviation, or a TIMI risk score >3.

    Upstream glycoprotein inhibitor use does not improve outcomes compared to selective use at the

    time of percutaneous coronary intervention. This patient should not be discharged from the

    emergency room without further cardiovascular evaluation.

    30. A 45-year-old male active smoker with diabetes and hypertension presents to the emergency

    room with chest pain. An urgent electrocardiogram demonstrates 4 ml of ST-segment elevation in

    leads V1-V4. Emergent coronary angiography identifies acute plaque rupture in the ostial left
    anterior descending coronary artery with hazy thrombus and Thrombolysis In Myocardial Infarction

    (TIMI) grade 1 coronary flow. After export thrombectomy, the ruptured plaque is treated with

    direct stenting with a 3.5 ml x 18 ml drug-eluting stent, which is post-dilated at 18 atm.

    Which of the following statements is true about the pathobiology of acute plaque rupture?

    a. The majority of coronary artery atherosclerotic plaque rupture occurs at the middle portion

    of the plaque away from the plaque shoulder because the middle portion of the plaque

    experiences greater tensile force from flowing blood.

    b. Platelets are the major source of the myeloperoxidase enzyme, which generates free radicals

    and increases inflammation in rupture-prone coronary artery atherosclerotic plaques.

    c. Coronary calcium does not participate in the pathobiology of coronary artery atherosclerotic

    plaque rupture, and calcification is rarely present in ruptured plaques.

    d. Branch points at coronary bifurcations experience high shear stress conditions that promote

    coronary artery atherosclerotic plaque inflammation and infiltration of monocytes that

    promote plaque rupture.

    e. Macrophage-derived matrix metalloproteinases degrade the fibrous cap and promote

    coronary artery atherosclerotic plaque rupture.

    30. d.

    Branch points at coronary bifurcations experience high shear stress conditions

    that promote coronary artery atherosclerotic plaque inflammation and infiltration of


    monocytes that promote plaque rupture.
    The majority of coronary artery atherosclerotic plaque rupture occurs at the plaque shoulder,

    which experiences greater tensile force from flowing blood.

    Branch points at coronary bifurcations experience low shear stress conditions that promote

    coronary artery atherosclerotic plaque inflammation and infiltration of monocytes that promote

    plaque rupture.

    Neutrophils and macrophages are the major sources of the myeloperoxidase enzyme, which

    generates free radicals and increases inflammation in rupture-prone coronary artery

    atherosclerotic plaques.

    Coronary calcium participates prominently in the pathobiology of coronary artery

    atherosclerotic plaque rupture, and calcification is present in 80% of ruptured plaques.

    31. A 65-year-old woman with hypertension and hyperlipidemia developed chest pain and

    collapsed while walking her dog. Emergency medical responders used an automated external

    defibrillator to administer one shock, which converted the patient from ventricular fibrillation to
    sinus rhythm.

    The patient is treated emergently for an ST-segment elevation myocardial infarction (STEMI) with

    primary percutaneous coronary intervention, where a stent is used to treat a thrombotic occlusion of
    the left anterior descending artery.Which of the following statements is correct regarding

    mechanisms of coronary artery disease that led to arterial thrombosis and MI in this patient?

    a. Coronary artery atherosclerotic plaque rupture is frequently clinically silent; however, silent
    plaque rupture events speed plaque growth and promote luminal narrowing.

    b. Coronary artery atherosclerotic plaque neovascularization increases plaque stability and

    reduces plaque inflammation.

    c. Superficial plaque erosion-induced coronary artery thrombosis occurs most often at sites of

    macrophage-laden coronary artery atherosclerotic plaques that have a low content of smooth

    muscle cells.
    d. Ischemic preconditioning increases the size of the infarct zone in patients presenting with

    STEMIs.

    e. Distal embolization of platelet aggregates rarely occurs in non-STEMI patients.

    31. a.

    Coronary artery atherosclerotic plaque rupture is frequently clinically silent;

    however, silent plaque rupture events speed plaque growth and promote luminal narrowing.

    Ischemic preconditioning reduces the size of the infarct zone in patients presenting with STEMI.

    Distal embolization of platelet aggregates frequently occurs in non-STEMI patients, and

    embolization is a major cause of myocardial necrosis. Superficial plaque erosion-induced

    coronary artery thrombosis occurs most often within atherosclerotic plaques that have a high

    content of smooth muscle cells and a low lipid content.

    Coronary artery atherosclerotic plaque neovascularization decreases plaque stability and

    increases plaque inflammation. Neovascularization likely increases risk of plaque rupture.

    32. A 69-year-old man with a history of hypertension and stroke was admitted with a non–ST-segment
    elevation myocardial infarction (NSTEMI). After medical stabilization, he was managed

    with an early invasive strategy and a drug-eluting stent was placed into a thrombotic 80% stenosis in
    the right coronary artery.

    Which of the following regimens would be part of the optimal medical management for this patient

    following drug-eluting stent implantation to treat an NSTEMI?

    a. Aspirin 325 mg daily and ticagrelor 90 mg twice daily.

    b. Aspirin 325 mg daily and prasugrel 10 mg daily.

    c. Aspirin 81 mg daily, ticagrelor 90 mg twice daily, and rivaroxaban 5 mg twice daily.

    d. Aspirin 81 mg daily and prasugrel 10 mg daily.

    e. Aspirin 81 mg daily and ticagrelor 90 mg twice daily.

    32. e.

    Aspirin 81 mg daily and ticagrelor 90 mg twice daily.


    Prasugrel should not be administered to patients with a prior history of stroke or transient ischemic
    attack. Aspirin 70-100 mg is the optimal dose when aspirin is combined with ticagrelor. Triple

    therapy with aspirin, ticagrelor, and rivaroxaban has not been studied in acute coronary syndrome
    management. Rivaroxaban reduces adverse cardiovascular events in acute coronary syndrome

    patients when added to aspirin and clopidogrel.

    33. A 63-year-old woman with a 2-day history of intermittent chest pain, sometimes responsive

    to belching, presents to the emergency department for evaluation. Her medical history is

    significant for hypertension. Her medications include amlodipine, hydrochlorothiazide, and aspirin.

    Her physical examination reveals blood pressure 128/82 mm Hg, heart rate 82 bpm, and oxygen

    saturation 99% on room air. Her jugular venous pressure is 6 cm water, lungs are clear, and

    cardiovascular exam is normal. Her electrocardiogram shows normal sinus rhythm with nonspecific

    T-wave changes. Her chest x-ray is normal. Laboratory values include two serial troponin I values of

    <0.01 ng/L, normal electrolytes, creatinine 0.8 mg/dl, D-dimer 130 ng/ml, and normal blood cell
    count.

    Which of the following is most appropriate in her care?

    a. No further testing is needed.

    b. Transthoracic echocardiogram.

    c. Invasive coronary angiography.

    d. Ventilation/perfusion (V/Q) scan.

    e. Exercise myocardial perfusion.

    33. e.
    Exercise myocardial perfusion.
    In this patient with suspected non-ST-segment elevation acute coronary syndrome, further risk

    stratification is warranted. The history, physical exam, and findings are important to consider in the
    initial risk stratification. This patient's Thrombolysis in Myocardial Infarction (TIMI) risk score is 1,
    which gives her a risk of major adverse cardiac events of 5% in the next 14 days. Noninvasive stress
    testing can be used to further risk stratify this patient. Resting transthoracic echocardiogram will not
    provide information about inducible ischemia. With a normal D-dimer and low pretest

    probability of pulmonary embolism, a V/Q scan is not indicated.

    34. A 61-year-old woman presents to the emergency department with 2 hours of chest pain

    associated with shortness of breath. Her medical history is significant for hypertension and

    hyperlipidemia. Her medications include lisinopril 20 mg and hydrochlorothiazide 25 mg daily.

    On exam, her blood pressure is 122/84 mm Hg, heart rate is 94 bpm, oxygen saturation is 98% on

    room air, and body mass index is 24 kg/m2. Jugular venous pressure is 7 cm H2O, and
    cardiovascular exam reveals normal S1 and S2 without murmurs. Lungs are clear and there is no
    peripheral edema.

    Her electrocardiogram shows sinus rhythm with 0.5 mm ST depression in leads V4-V6. Laboratory

    values include serum creatinine 1.4 mg/dl, troponin I 0.8 ng/ml, hemoglobin 12 g/dl, and N-

    terminal pro-B-type natriuretic peptide 202 ng/L. She is chest-pain free on intravenous

    nitroglycerin and heparin. Repeat troponin I 6 hours later is 1.1 ng/ml.

    Which of the following is the most appropriate management strategy in this patient's care?

    a. Pharmacologic nuclear stress test.

    b. Coronary angiography.

    c. Exercise stress test.

    d. Coronary computed tomography (CT) angiography.

    e. Transthoracic echocardiogram.

    34.

    b.
    Coronary angiography.
    Optimal risk stratification of patients with suspected non-ST elevation acute coronary syndrome

    should include risk stratification models such as the Global Registry of Acute Coronary Events

    (GRACE) or Thrombolysis in Myocardial Infarction (TIMI) scores, which employ multiple

    prognostic factors to help determine management strategies. This patient's GRACE score is 159,

    which places her in the high risk category for in-hospital mortality. Therefore, she should be

    managed aggressively with an early invasive strategy.

    Stress testing in this patient with rising troponin is not appropriate. CT angiography may be

    performed in patients with intermediate risk. A normal echocardiogram will not obviate the

    need for cardiac catheterization.

    35. A 57-year-old woman presents to the emergency room with new-onset chest pressure that

    has been escalating for the last 2 hours.

    Her medical history is only remarkable for hypertension and obesity. Initial

    electrocardiogram demonstrates ST-segment elevation in leads V1-V4 with associated changes

    inferiorly.

    She is urgently taken to cardiac catheterization where a mid left anterior descending subtotal

    occlusion is successfully revascularized using a drug-eluting stent, restoring Thrombolysis in

    Myocardial Infarction (TIMI) III flow.

    Following percutaneous coronary intervention, a transthoracic echocardiogram demonstrates left

    ventricular ejection fraction (LVEF) of 25-30% with severe hypokinesis of the anterior wall LV.

    Medical therapy is initiated with atorvastatin, metoprolol, lisinopril, aspirin, clopidogrel, and
    eplerenone. Telemetry on hospital day 2 reveals several brief runs of asymptomatic accelerated

    idioventricular rhythm.Which of the following do you recommend for subsequent risk stratification
    of sudden cardiac death?

    a. Reassessment of LVEF at least 40 days post MI.

    b. Invasive electrophysiology (EP) testing prior to hospital discharge.


    c. Cardiac magnetic resonance imaging (MRI) prior to hospital discharge.

    d. Invasive EP testing at least 40 days post MI.

    e. Reassessment of LVEF at least 90 days post MI.

    35. a.

    Reassessment of LVEF at least 40 days post MI.

    The correct answer is reassessment of LVEF at least 40 days post MI. Invasive EP testing has no role
    in the immediate post MI period in the absence of significant ventricular arrhythmias. The slow

    idioventricular rhythm is likely related to myocardial reperfusion and does not require EP testing.

    Invasive EP testing >40 days post MI may be considered for moderately decreased LVEF (35-40%) in
    patients with evidence of nonsustained ventricular tachycardia detected on noninvasive

    monitoring. Cardiac MRI to define scar burden has been found to be useful to predict ventricular

    arrhythmias in cardiomyopathic patients. However, cardiac MRI has not yet been integrated into

    the guidelines for risk stratification post MI.

    The 2013 guideline for the management of ST-elevation myocardial infarction indicates that repeat
    assessment of LVEF at least 40 days post MI carries a Class I indication for risk stratification of
    sudden cardiac death. Primary prevention implantable cardioverter-defibrillator (ICD) implantation
    during the infarct-related hospitalization has not been demonstrated to be beneficial (DEFINITE

    trial). Allowing for a period of myocardial healing post MI may avert the need for subsequent ICD

    implantation.

    Greater than 40 days post MI, LVEF should be reassessed. If the LVEF does not improve remains </=

    35% with class II or III symptoms, or remains < 30% independent of symptoms, despite guidelines
    directed medical therapy, then this patient would become a candidate for pr primary prevention

    ICD implant.

    36. A 52-year-old man presents to the emergency room after 3 hours of intermittent sharp

    stabbing chest pain noted when he was raking leaves. His medical history is significant for

    hypertension. He denies tobacco, alcohol, or drug use. His current medications include

    hydrochlorothiazide.

    His physical exam reveals blood pressure of 148/94 mm Hg and heart rate of 72 bpm. His
    cardiovascular exam is unremarkable. His electrocardiogram shows normal sinus rhythm without

    ST- or T-wave changes. His chest x-ray shows normal cardiac silhouette and clear lung fields.

    Which of the following is the most appropriate next step?

    a. Creatine kinase-myocardial band (CK-MB).

    b. N-terminal pro-B-type natriuretic peptide (NT-proBNP).

    c. Urine toxicology.

    d. High-sensitivity C-reactive protein (hs-CRP).

    e. Troponin I.

    36. e.
    Troponin I.
    Cardiac-specific troponin should be performed in patients with clinical findings or symptoms that
    may be related to potential acute coronary syndrome (ACS) (Class Ia). It should be measured at

    presentation and 3-6 hours after symptom onset in all patients with suspected ACS. If it is negative
    within the first 6 hours of onset of symptoms, it should be repeated in patients with

    electrocardiographic changes and/or intermediate/high risk clinical features. In order to diagnose


    myocardial necrosis, it is important to determine both the peak troponin level and the pattern of
    change.

    CK-MB and myoglobin are not useful for diagnosis of ACS (Class III). NT-proBNP may be
    reasonable

    for additional prognostic information (Class IIb). Urine toxicology should be performed in patients
    with suspected drug use, as this may be a causal contributor to ACS.

    37. A 62-year-old Caucasian woman with type 2 diabetes presents to the emergency department

    with complaints of constant substernal chest pressure at rest for the last hour, briefly relieved by
    nitroglycerin. She is not on antiplatelet therapy. An electrocardiogram shows lateral precordial ST-
    segment depressions and T-wave inversions. She has no known drug allergies. The troponin I level

    is 2.12 ng/ml.

    Which of the following pharmacotherapeutic strategies is the most appropriate next step for this

    patient?

    a. Ticagrelor 180 mg.

    b. Aspirin 325 mg and clopidogrel 600 mg.

    c. Immediate eptifibatide bolus followed by infusion as monotherapy.

    d. Aspirin 162 mg and prasugrel 60 mg.

    e. Clopidogrel 600 mg.

    37. b.

    Aspirin 325 mg and clopidogrel 600 mg.

    This woman is experiencing a non-ST-segment elevation myocardial infarction (NSTEMI).

    Clopidogrel and ticagrelor at the described loading and maintenance doses are both reasonable

    therapies for NSTEMI. However, they have been studied in conjunction with and should be
    administered along with aspirin. Prasugrel may be given to patients undergoing percutaneous

    coronary intervention (PCI) in the setting of NSTEMI, but is not guideline-recommended to be

    administered until the anatomy is known and it is certain that the patient will be underoing PCI. In the
    ACCOAST trial, treatment with prasugrel in NSTEMI before PCI did not reduce ischemic events

    and was associated with more bleeding. The best answer is aspirin in conjunction with clopidogrel.

    Glycoprotein IIb/IIIa antagonists are only administered on top of oral antiplatelet therapy.

    38. A 40-year-old man with a history of type 2 diabetes is seen in the office. His blood pressure is
    123/75 mm Hg. Labs include a total cholesterol of 130 mg/dl and high-density lipoprotein

    cholesterol of 40 mg/dl. He is a lifelong nonsmoker. He is active, but overweight with a body mass
    index of 29 kg/m2. He is interested in reducing his risk of developing complications of

    atherosclerotic cardiovascular disease (ASCVD), but wants to be sure any new medications are

    worth the potential side effects.

    Which of the following do you recommend to reduce the risk of ASCVD in this patient?

    a. High-intensity statin therapy.

    b. Dietary modifications alone.

    c. Fenofibrate.

    d. Moderate-intensity statin therapy.

    e. Ezetimibe.

    38. d.

    Moderate-intensity statin therapy.

    Using the ASCVD risk calculator (estimator), this patient has a 10-year calculated risk of 1.2% and a
    50% lifetime risk. Although primary prevention is reserved for nondiabetic patients with a 10-year
    risk ≥7.5%, the fact that this patient has diabetes means that moderate-intensity statin therapy is
    recommended (Class I, Level of Evidence A). High-intensity statin therapy would be indicated in this
    diabetic patient if the 10-year risk was ≥7.5%.y.

    39. A 66-year-old man is seen in clinic for follow-up after hospitalization for an acute coronary
    syndrome. Current medications include atorvastatin 80 mg, ticagrelor 90 mg bid, aspirin 81 mg,

    metoprolol 25 mg bid, and lisinopril 10 mg daily. He smoked one-half pack of cigarettes daily for the
    past 40 years.
    His current lipid panel includes total cholesterol 150 mg/dl, triglycerides 199 mg/dl, low-density
    lipoprotein 61 mg/dl, and high-density lipoprotein 49 mg/dl. Hemoglobin A1c is 6.0%.

    Which of the following steps will best reduce his risk of future myocardial infarction (MI)?

    a. Ezetimibe.

    b. Omega-3 fatty acids.

    c. Varenicline.

    d. Coenzyme Q10.

    e. Metformin.

    39. c.
    Varenicline.
    Lifestyle modification including smoking cessation can result in significant improvement in

    atherosclerotic cardiovascular risk. A meta-analysis of smoking cessation in patients with MI found it


    was associated with a 50% reduction in cardiovascular risk. Therefore, varenicline is the best answer,
    because it has been proven to be efficacious for smoking cessation. Ezetimibe in addition to statin was
    associated with an approximately 2% absolute risk reduction (number needed to treat

    = 50) in atherosclerotic cardiovascular disease events in the IMPROVE-IT trial; given his lipid panel,
    this would not likely be as large a benefit as smoking cessation. Adding metformin is not indicated
    with a hemoglobin A1c of 6% and would not be expected to reduce his MI risk. Coenzyme Q10 and

    omega-3 fatty acids have not been shown to reduce global cardiovascular risk.

    40. A 63-year-old woman with a history of hypertension presents with an acute coronary

    syndrome. Coronary angiography demonstrates a 90% lesion in her posterior descending artery.

    She subsequently undergoes stent placement.

    Labs include peak troponin of 1.2 ng/ml and hemoglobin A1c of 5.6%. Fasting lipid profile includes
    total cholesterol of 160 mg/dl, high-density lipoprotein (HDL) of 38 mg/dl, low-density lipoprotein
    (LDL) of 67 mg/dl, and triglyceride (TG) of 240 mg/dl.

    Which of the following is the most appropriate lipid management strategy?

    a. Fenofibrate 145 mg qd.

    b. Fish oil 2 g qd.

    c. Ezetimibe 10 mg qd.

    d. Niacin 500 mg qd.

    e. Atorvastatin 80 mg qd.

    40. d.
    Niacin 500 mg qd.
    It is important to obtain a fasting lipid profile on all patients presenting with acute coronary

    syndrome. High-intensity statin therapy is indicated for all patients ages <75 years with

    atherosclerotic cardiovascular disease (ASCVD), even with a "normal" LDL. Despite low HDL and
    elevated TG, initial therapy with statin is preferred over the other options.

    When added to statin monotherapy, the addition of niacin or fenofibrate has not been shown to

    reduce CV events despite improvement in lipid profile. While ezetimibe as add-on therapy to statin
    reduced CV events in the IMPROVE-IT trial, it should not be used as monotherapy in a patient who

    is statin naive. To date, fish oil has not been definitively shown to reduce CV events in patients with
    ASCVD and should not be used over statin therapy.

    41. You are counseling a 58-year-old man prior to discharge from the hospital following an acute
    myocardial infarction. He received primary percutaneous coronary intervention with a drug-eluting
    stent to the left anterior descending artery. Left ventricular ejection fraction is 55%. He had no known
    medical history prior to admission. His current medications include atorvastatin 80 mg,

    lisinopril 5 mg, metoprolol succinate 25 mg, aspirin 81 mg, and ticagrelor 90 mg bid.

    In addition to reviewing the importance of taking all his medications, which of the following

    recommendations is the most appropriate?

    a. Limit total calories to <2000 per day.

    b. Reduce saturated fats, trans fatty acid, and cholesterol intake.

    c. Recommend antioxidant vitamin supplements.

    d. Increase monounsaturated fat intake and reduce cholesterol intake.

    e. Limit sodium intake to <2000 mg per day.

    41. b.
    Niacin 500 mg qd.
    Dietary modification is recommended for all patients with acute coronary syndrome (ACS).

    Reducing saturated fats to <7% of total calories, eliminating or reducing trans fatty acids, and
    limiting dietary cholesterol to <200 mg daily are all likely to improve cardiovascular health.

    Limiting total calories alone is not specific enough to reduce saturated fat intake. Sodium

    restriction to <2000 mg/day is not indicated, as he does not have left ventricular systolic

    dysfunction or heart failure, although lowering sodium intake by 1000 mg/day from baseline or to

    approximately 2400 mg/day with the DASH diet may reduce hypertension.

    Antioxidants, including vitamin E, vitamin C, and beta carotene, have not been shown to confer any
    benefit in secondary prevention of ACS. Increased monounsaturated fat alone will not ensure a

    reduction in dietary saturated fat and trans fatty acid intake.

    42. A 72-year-old man with persistent atrial fibrillation presents to the emergency room with a

    non–ST-segment elevation myocardial infarction. He has a history of hypertension and diabetes.

    The patient undergoes angiography, and a drug-eluting stent is placed in the left circumflex to treat a
    hazy area of acute plaque rupture.

    Which of the following is the best maintenance therapy for this patient?

    a. Aspirin 81 mg, clopidogrel 75 mg, and oral anticoagulation.

    b. Aspirin 325 mg.

    c. Aspirin 325 mg and clopidogrel 75 mg therapy.

    d. Clopidogrel 75 mg.

    e. Aspirin 325 mg and oral anticoagulation.

    42. a.

    Aspirin 81 mg, clopidogrel 75 mg, and oral anticoagulation.

    In the presence of atrial fibrillation and an acute myocardial infarction, the addition of an oral
    anticoagulant remains controversial following percutaneous coronary intervention. The addition of
    an oral anticoagulation should be guided by use of the CHA2DS2-VASc score. Individualization can

    also be determined by the HAS-BLED scoring system for risk of bleeding.


    43. A 70-year-old man on the trauma service is being evaluated because of a positive troponin.

    He was in a motor vehicle accident yesterday and fractured his femur. He underwent surgical open

    reduction and internal fixation this morning. He has diabetes and hypertension, but no known

    coronary artery disease. There was no steering wheel contact; he was wearing his seat belt. He has no
    symptoms.

    His examination is normal except for pallor and his now casted left leg. His electrocardiogram

    shows sinus rhythm and nonspecific T-wave flattening over the precordial leads. His laboratory

    tests are notable for a hemoglobin of 7.5 mg/dl. The troponin is 1.2 ng/dl.

    Which of the following is the most appropriate next step?

    a. Enoxaparin 40 mg daily.

    b. Aspirin 325 mg daily.

    c. Clopidogrel 300 mg loading dose.

    d. Heparin 60 U/kg bolus.

    e. Ticagrelor 180 mg loading dose.

    43. a.
    Enoxaparin 40 mg daily.
    This patient has an asymptomatic rise in his troponin in the absence of symptoms and nonspecific

    changes on his electrocardiogram. Moreover, he has undergone significant trauma and is very

    anemic. The low-grade troponin is most likely due to demand ischemia. The clinical scenario is not
    consistent with an acute coronary syndrome and therefore does not require treatment for an acute

    coronary syndrome (e.g., antiplatelet agents, intravenous antithrombins). His greatest risk is deep
    venous thrombosis, and he should receive deep vein thrombosis prophylaxis (e.g., enoxaparin).

    44. A 50-year-old woman presents with chest pain. It occurs with exertion and is relieved by rest.

    Her history is notable for hypertension; her father died suddenly at 55 years of age of unknown

    causes. She completes 6 minutes of a Bruce protocol stress test with myocardial perfusion (MIBI)

    that demonstrates 2 mm ST-depressions in the lateral leads and a reversible defect in the

    inferolateral wall. Her blood pressure and heart rate responses are normal. She undergoes

    coronary angiography that is notable for a left dominant coronary circulation with a 70% mid left
    anterior descending (LAD) lesion and luminal irregularities of the first obtuse marginal branch.

    Fractional flow reserve of the LAD lesion is 0.85.

    Which of the following is the most likely cause of her chest pain?

    a. Coronary vasospasm.

    b. 70% mid LAD lesion.

    c. Pericarditis.

    d. Coronary dissection.

    e. Microvascular angina.

    44. e.
    Microvascular angina.
    Coronary microvascular dysfunction is an important prognostic factor in a wide range of diseases.

    In this case, microvascular angina is the manifestation of her atherosclerotic coronary artery

    disease. Evidence for ischemia includes her electrocardiographic ST depressions and stress MIBI

    changes. Pericarditis would not produce the ST changes or the stress MIBI changes. Coronary

    vasospasm generally is not provokable with exercise stress testing and typically occurs in the early
    morning hours; it classically involves the epicardial coronary arteries, although microvascular

    spasm has been speculated. Coronary dissection usually presents as a myocardial infarction, and

    the diagnosis is generally apparent on coronary angiography, although intravascular ultrasound and
    ocular coherence tomography may be required for definitive diagnosis.

    45. A 45-year-old woman presents to your office with a 6-month history of chest pain. She

    reports episodes of chest pain lasting 10-15 minutes that occur with exertion. The pain radiates to her
    left shoulder and she becomes short of breath. She has no family history of coronary artery

    disease and she has smoked for 10 years. She does not have a history of diabetes or hypertension.

    Her physical examination is unremarkable, except for a body mass index of 32. A 12-lead

    electrocardiogram (ECG) is normal. A previous cardiologist had performed a treadmill stress test,
    during which she developed chest pain and a 2 mm ST-depression in leads V5 and V6. She undergoes

    diagnostic cardiac catheterization, and her coronary arteries are free of stenosis except for a 20%

    lesion in the circumflex. Echocardiogram shows normal left ventricular and right ventricular (RV)
    function and normal RV systolic pressure.

    What is the most likely cause of her symptoms?

    a. Gastroesophageal reflux disease (GERD).

    b. Stress-induced cardiomyopathy.

    c. Chronic thromboembolic pulmonary hypertension (CTEPH).

    d. Pericarditis.

    e. Coronary microvascular dysfunction.

    45. e.
    Gastroesophageal reflux disease (GERD).

    Her history is consistent with angina. Although she does not have any significant coronary artery
    stenosis expected to lead to flow limitation, coronary microvascular dysfunction is the most likely
    cause of her symptoms. This syndrome occurs in women more than men, can present with classical

    angina, and can be associated with ST depression provoked by exercise, and it occurs in the

    absence of significant epicardial coronary stenoses.

    CTEPH is not typically associated with anginal type symptoms or with exercise-induced ischemia.

    Stress-induced cardiomyopathy (Takotsubo) results in wall motion abnormalities on

    echocardiography, usually apical ballooning. There is no evidence of pericarditis, because her ECG

    is normal and chest pain is only exertional. While GERD is a common cause of chest pain, it would
    not result in exercise-induced symptoms or ECG changes.

    46. A 50-year-old woman presents to your office for a second opinion. She reports a 3-year history
    of exertional chest discomfort. Her previous cardiologist had performed a treadmill stress test during
    which she developed a 1.5 mm ST-depression in 3 leads, after which he recommended

    the patient undergo a cardiac catheterization. Her coronary arteries had no epicardial stenoses and the
    cardiologist attributed the chest pain to anxiety. The patient continues to have exertional chest pain,
    and she is willing to undergo additional noninvasive diagnostic testing, because she remains
    concerned about this symptom. Her physical examination is unremarkable.

    Which of the following noninvasive diagnostic tests do you recommend?

    a. Computed tomography (CT) angiography of the coronary arteries.

    b. Exercise thallium.

    c. Resting transthoracic echocardiogram.

    d. Assessment of coronary artery calcium by CT.

    e. Repeat stress treadmill with electrocardiogram (ECG) monitoring.

    46. b.
    Exercise thallium.
    The patient may be presenting with coronary microvascular dysfunction. Patients with this

    condition can develop ischemia in the absence of significant epicardial coronary artery stenosis.

    Such patients may have a reversible perfusion defect as assessed by stress thallium perfusion

    study, though absence of this finding does not exclude that diagnosis. There would be little utility in
    repeating the treadmill test with ECG monitoring, because this was already positive. Neither CT

    angiography or assessment of coronary artery calcium would be helpful given the recent

    demonstration of no significant stenosis at left heart catheterization. A resting transthoracic

    echocardiogram would not establish the diagnosis of coronary microvascular dysfunction.

    47. A 48-year-old woman presents with exertional chest pain with associated dyspnea. Following

    a stress perfusion study showing a reversible defect consistent with ischemia, she undergoes

    cardiac catheterization, including assessment of hemodynamics. Her pulmonary artery pressure

    (PAP) is 30/15/22 mm Hg and cardiac index is 2.5 L/min/m2. Coronary angiography reveals no

    significant epicardial stenoses. The ratio of the coronary flow following administration of

    adenosine, to that at baseline, is 2. A catheter is placed into her left ventricle, and the left

    ventricular end-diastolic pressure (LVEDP) is 12 mm Hg.

    Which of the following diagnoses would be most consistent with these findings?

    a. Coronary microvascular dysfunction.

    b. Noncardiac chest pain.

    c. Pulmonary embolism.

    d. Heart failure.

    e. Pulmonary hypertension.

    47. a.
    Coronary microvascular dysfunction.
    A coronary flow reserve (CFR) of 2.5 is abnormal and consistent with coronary microvascular

    dysfunction. Her LVEDP is low, which is not consistent with heart failure. Her mean PAP is 25 mm

    Hg, so she does not have pulmonary hypertension. While we cannot exclude pulmonary embolism

    to be the cause of her symptoms, she does not have associated pulmonary hypertension. The

    finding of a low CFR makes coronary microvascular dysfunction a more likely explanation. The

    patient has abnormal CFR and a positive stress test, making noncardiac chest pain less likely.

    48. You are asked to consult on a 55-year-old man in the emergency department with chest pain.

    He describes a dull chest discomfort that started while he was climbing the attic stairs to put away
    some boxes about 2 hours ago. He was sweating and breathing heavily from the work when the

    pain started. The discomfort became so intense that he thought he was going to pass out and

    gradually resolved over 10 minutes when he sat down to catch his breath. Medical history includes
    hypertension managed with amlodipine and gastroesophageal reflux disease managed with

    omeprazole.

    His electrocardiogram is shown in Figure 1. Blood work drawn on arrival in the emergency

    department included chemistries, which were normal, and cardiac troponin I, which was

    undetectable.

    Which of the following laboratory tests should be obtained within the next 6 hours?
    a. Creatine kinase-myocardial band.

    b. High-sensitivity cardiac troponin I.

    c. Heart-type fatty acid binding protein.

    d. Myoglobin.

    e. Lactate dehydrogenase.

    48.

    b.

    High-sensitivity cardiac troponin I.

    Injury to cardiac myocytes results in loss of cell membrane integrity and subsequent diffusion of
    intracellular proteins into the extracellular space, where they are detectable by laboratory

    assays on plasma. These biomarkers of myocyte injury include myoglobin (present in all muscle
    cells), lactate dehydrogenase (present in all muscle cells), creatine kinase (present in all muscle cells
    but with subtypes that are more prevalent in cardiac muscle cells), heart-type fatty acid

    binding protein (a subtype of a low molecular weight protein specific to cardiac muscle), and

    cardiac troponin I (present only in cardiac muscle cells). Troponin T may be expressed by some

    skeletal muscle cells, but in most clinical settings will have similar specificity to troponin I.

    The high specificity of cardiac troponin for cardiac muscle injury and predictable kinetics make it the
    preferred biomarker to confirm or exclude the diagnosis of myocardial infarction. Cardiac

    troponins generally will be detectable first in the blood 2-3 hours after the event in 80% of

    patients and within 6 hours of the event in essentially all patients. Serial measurements, as in

    this patient with undetectable troponin immediately after the event, are therefore critical for

    ruling out the diagnosis of myocardial infarction and for ruling in the diagnosis by demonstrating the
    characteristic rise and fall of troponin in the blood.

    49. A 60-year-old man with a 60 pack-year history of smoking presents to the emergency

    department with 2 hours of crushing substernal chest pain. His electrocardiogram shows 3 mm ST

    elevation in the anterior leads. He is taken urgently to the cardiac catheterization laboratory.

    Which of the following strategies would require additional antithrombotic therapy during primary

    percutaenous coronary intervention (PCI)?

    a. Unfractionated heparin.

    b. Bivalirudin.

    c. Fondaparinux.

    d.

    Unfractionated heparin with eptifibatide.

    e.

    Unfractionated heparin with abciximab.

    49. c.
    Fondaparinux.
    Fondaparinux is not recommended as the sole anticoagulant during primary PCI due to an

    increased risk of catheter thrombosis (Class III recommendation). Unfractionated heparin with or

    without concomitant intravenous glycoprotein IIb/IIIa therapy (including abciximab and

    eptifibatide), and bivalirudin, are acceptable anticoagulant therapies during primary PCI.

    50. A 31-year-old man with no significant medical history presents to the emergency department

    with sudden-onset severe substernal chest pain that began 15 minutes prior to presentation. His

    friend admits that they had been smoking marijuana that was laced with cocaine. The patient

    appears somewhat disheveled and irritable. His pupils are dilated, heart rate is 105 bpm, and blood
    pressure is 163/106. He was started on nitroglycerin, but has persistent chest pain. An

    electrocardiogram shows ST elevations in leads V3-V6.

    Which of the following medications would be appropriate to administer?

    a. Flumazenil.

    b. Lorazepam.

    c. Naloxone.

    d. Metoprolol.

    e. Dabigatran.

    50. b.
    Lorazepam.
    Benzodiazepines with or without nitroglycerin may be used to manage hypertension and

    tachycardia in patients who present with non-ST elevation acute coronary syndromes (NSTE-ACS)

    and signs of acute cocaine or methamphetamine intoxication. For STE-ACS, lorazepam would be

    the most reasonable choice of the options listed, although the primary focus would be on

    emergent coronary angiography and percutaneous coronary intervention, if indicated.

    Per the NSTE-ACS guidelines, "Beta-blockers should not be administered to patients with ACS with a
    recent history of cocaine or methamphetamine use who demonstrate signs of acute intoxication

    due to the risk of potentiating coronary spasm." Naloxone is used to treat opioid overdose and
    flumazenil is used to treat benzodiazepine overdose, so neither would be appropriate here.

    Dabigatran is not indicated for the management of ACS.

    51. A 67-year-old woman with history of diabetes and asthma is admitted to the cardiac intensive care
    unit after percutaneous intervention with drug-eluting stent placement for an ST-elevation

    myocardial infarction (STEMI) involving the right coronary artery. She has not had any recurrent

    chest discomfort since her procedure. Her vital signs are temperature 37.5°C, heart rate 116 bpm,
    blood pressure 153/73 mm Hg, respiratory rate 24 breaths/minute, and oxygen saturation 96%.

    Physical examination is notable for an irregularly irregular heart rhythm, no jugular venous

    pressure, and moderate expiratory wheezing. Electrocardiogram demonstrates atrial fibrillation

    with a rapid ventricular response, but isoelectric ST segments and no Q waves. Her medications

    include aspirin, clopidogrel, and atorvastatin.

    Which of the following would be the next best medication to consider?

    a. Spironolactone.

    b. Metoprolol.

    c. Amiodarone.

    d. Diltiazem.

    e. Nitroglycerin.

    51. d.
    Diltiazem.
    Certain calcium channel blockers may be useful for the treatment of angina, hypertension, and

    atrial tachyarrhythmias in select patients after STEMI when beta-blockers (or nitrates) are

    ineffective, not tolerated, or contraindicated and in patients who have no signs of congestive heart
    failure, left ventricular dysfunction, or atrioventricular block. In this patient with recent STEMI, atrial
    fibrillation with rapid ventricular response, and elevated blood pressure, diltiazem would be a good
    choice to slow her ventricular rate and help control blood pressure. There is no evidence of active
    ischemia, and thus immediate electrical cardioversion is not necessary.

    Metoprolol is contraindicated given the history of asthma and evidence of active bronchospasm.

    The duration of atrial fibrillation is unknown, thus amiodarone would not be a good choice at this
    point, as it also can cause cardioversion and other attempts at rate control have not been made.

    Nitroglycerin is not ideal in the setting of tachycardia and would not help to control heart rate.

    Aldosterone antagonists are recommended for patients with STEMI who are already receiving an

    angiotensin-converting enzyme inhibitor and beta-blocker and who have a left ventricular ejection
    fraction ≤40% and either symptomatic heart failure or diabetes. This patient would not qualify for an
    aldosterone antagonist at this time.

    52. A 51-year-old woman is admitted to the cardiac intensive care unit (ICU) immediately

    following primary percutaneous coronary intervention for an anterior wall myocardial infarction

    (MI). She was intubated for respiratory distress en route to the hospital and no history is available.

    Current vital signs are pulse 108 bpm, respiratory rate 12 breaths/minute with 100% fraction of

    inspired oxygen from the ventilator, blood pressure 98/70 mm Hg, and oxygen saturation 99%.

    Weight is 240 lbs. Physical exam reveals acanthosis of the neck and bilateral rales; the peripheral
    pulses are weak.

    Lab exam results were remarkable for random glucose 264 mg/dl; there was no anion gap.

    Creatinine and other chemistries were within normal limits. An infusion with insulin is started for
    control of hyperglycemia.

    Which of the following is the most appropriate target of glucose in this patient?

    a. 181-220 mg/dl.

    b. <80 mg/dl.
    c. 221-280 mg/dl.

    d. 81-110 mg/dl.

    e. 111-180 mg/dl.

    52. e.

    111-180 mg/dl.

    Nearly one-quarter of patients with ST-elevation MI (STEMI) have diabetes, and up to one-third of
    those may be diagnosed at the time of hospitalization for STEMI. Diabetic patients have higher

    mortality from STEMI, and hyperglycemia is a predictor of early mortality. However, there is a U- or
    J-shaped relationship between serum glucose and death, with the risk of mortality similar for either
    hypoglycemia (random glucose <70 mg/dl) or hyperglycemia (variously defined as random glucose

    >140, >180, or <200 mg/dl).

    The NICE-SUGAR trial randomized 6,104 ICU patients to either intensive blood glucose control

    (target blood glucose 81-108 mg/dl) or conventional blood glucose control (target blood glucose

    <180 mg/dl) and found lower mortality (24.9% vs. 27.5%, p = 0.02) for the conventional glucose
    control strategy, with fewer episodes of hypoglycemia (0.5% vs. 6.8%, p < 0.001).

    Therefore, "modest" rather than "intensive" glucose control, that is, target <180 mg/dl with avoidance
    of hypoglycemia, is the current recommendation for critically ill patients with STEMI.

    53. A 68-year-old Caucasian man is seen in the clinic for cardiovascular risk assessment. He has a
    history of hypertension and type 2 diabetes . He has never smoked. His medications include

    metformin 500 mg bid and lisinopril 10 mg qd. His blood pressure is 130/80 mm Hg. His

    examination is otherwise unremarkable. His lipid profile shows total cholesterol 161 mg/dl, high-

    density lipoprotein 45 mg/dl, low-density lipoprotein 80 mg/dl, and triglyceride 180 mg/dl. His

    hemoglobin A1c is 6.4%.

    Which of the following is the most appropriate next step?

    a. Start glipizide 5 mg qd.

    b. Start fenofibrate 145 mg qd.

    c. No additional therapy.

    d. Start atorvastatin 40 mg qd.


    e. Increase lisinopril to 20 mg qd.

    53. d.
    Start atorvastatin 40 mg qd.
    Initiating statin therapy is appropriate for diabetics 40-75 years of age with low-density lipoprotein
    cholesterol >70 mg/dl. In this patient whose 10-year risk of atherosclerotic cardiovascular disease is
    11.2% based on pooled cohort equation, high-intensity statin therapy is recommended. In the

    ACCORD trial, intensifying glycemic control to target A1c <6% was associated with higher rates of
    hypoglycemia and increased mortality and did not significantly reduce major cardiovascular events.

    Similarly, the addition of fenofibrate was not associated with significant reduction in rate of

    cardiovascular events. This patient's blood pressure is at goal; up-titration of lisinopril is not
    indicated.

    54. A 74-year-old man with a history of hypertension is brought to the emergency department

    with chest pain and an acute inferior wall myocardial infarction. His only medication on admission is
    lisinopril 40 mg daily. He undergoes drug-eluting stent placement without complications and is
    placed on aspirin 81 mg daily, clopidogrel 75 mg daily, atorvastatin 80 mg daily, and metoprolol 50

    mg twice daily. Prior to discharge, he experiences similar chest pain and diaphoresis. His

    electrocardiogram shows ST elevation in the inferior leads. Stent thrombosis is diagnosed at

    catheterization and successfully remedied.

    Which of the following factors may have contributed to development of subacute stent

    thrombosis?

    a. Inadequate dosing of aspirin.

    b. Heparin-induced thrombocytopenia.

    c. Nickel allergy.

    d. Resistance to clopidogrel.

    e. Resistance to aspirin.

    54. d.

    Resistance to clopidogrel.

    On March 12, 2010, the Food and Drug Administration approved a new label for clopidogrel with a
    “boxed warning” about the diminished effectiveness of clopidogrel in patients with impaired ability
    to convert the drug into its active metabolite. Patients with decreased cytochrome P450 2C19
    (CYP2C19) function because of genetic polymorphisms metabolize clopidogrel poorly and have
    higher rates of cardiovascular events after acute coronary syndrome and percutaneous coronary
    intervention (PCI) than patients with normal CYP2C19 function. The warning also notes that tests are
    available to identify patients with genetic polymorphisms and that alternative treatment strategies
    should be considered for patients who are poor metabolizers. The clopidogrel boxed warning leaves
    the issue of whether to perform CYP2C19 testing up to the individual physician. It does not
    specifically require genetic testing or other changes in evaluation or treatment and does not imply
    that there are solid evidence-based reasons for such actions. Rather, it serves to inform clinicians of
    genetic variations in response to clopidogrel and to emphasize that clinicians should use this
    knowledge to make decisions about how to treat individual patients. At the present time, the evidence
    base is insufficient to recommend routine genetic testing in patients undergoing PCI. There may be a
    potential role for genetic testing for patients undergoing elective high-risk PCI procedures (e.g.,
    unprotected left main, bifurcating left main, or last patent coronary artery).

    The recommended maintenance dose of aspirin is 70-100 mg following stent implantation. Higher
    doses have been shown to increase bleeding risk without reducing major adverse cardiac events. The
    prevalence of aspirin resistance is controversial, but has not been linked to stent thrombosis. Heparin-
    induced thrombocytopenia increases thrombosis risk in general, but has not been linked to subacute
    stent thrombosis. Most modern stents are constructed of cobalt-chromium alloys rather than with
    nickel titanium; furthermore, there is no proven association between nickel allergy and stent
    thrombosis.

    55. A 69-year-old man is hospitalized for primary percutaneous coronary intervention for an ST-

    segment elevation myocardial infarction. His medical history includes hypertension and a previous
    ischemic stroke. His current medications include aspirin 81 mg, carvedilol 12.5 mg bid, lisinopril 20

    mg daily, and atorvastatin 80 mg daily.

    Which of the following best explains the benefits of ticagrelor over clopidogrel?

    a. Ticagrelor is associated with lower rates of side effects.

    b. Ticagrelor is associated with lower stroke risk.

    c. Ticagrelor is associated with lower rates of stent thrombosis.

    d. Ticagrelor is associated with fewer drug-drug interactions.

    e. Ticagrelor is associated with lower bleeding risk.

    55. c.

    Ticagrelor is associated with lower rates of stent thrombosis.

    In the PLATO trial, ticagrelor was associated with lower rates of death, stroke, and stent thrombosis
    compared with clopidogrel in acute coronary syndrome patients. However, non-coronary artery

    bypass grafting major bleeding rates were higher with ticagrelor compared with clopidogrel,

    although overall bleeding rates were similar. Ticagrelor and clopidogrel were associated with a
    similar risk of stroke, although there were more hemorrhagic strokes with ticagrelor (0.2% vs.

    0.1%). Ticagrelor is metabolized through cytochrome P450 3A and cannot be combined with strong

    inducers or inhibitors of that enzyme. Ticagrelor is associated with more side effects, including
    dyspnea and bradycardia. Because of increased bleeding when combined with higher doses of

    aspirin, ticagrelor should only be combined with aspirin 81 mg.

    56. A 65-year-old retired biology professor presents for cardiac catheterization in the setting of a
    recently positive stress test. You discuss the procedure in detail and obtain informed consent for
    coronary angiography plus percutaneous intervention if needed. He has been reading about

    antiplatelet therapy and asks if you will screen him for genetic mutations related to clopidogrel
    metabolism.

    Which of the following is appropriate routine use of genetic testing to screen patients treated with
    clopidogrel after percutaneous coronary intervention?

    a. Recommended in those receiving drug-eluting stents only.

    b. Recommended, as the evidence suggests that this reduces adverse outcomes.

    c. Recommended in those with concomitant atrial fibrillation.

    d. Recommended in patients who develop a rash after taking clopidogrel.

    e. Not recommended, as the evidence to support this is insufficient.

    56. e.

    Not recommended, as the evidence to support this is insufficient.

    Clopidogrel is a prodrug that requires conversion into an active metabolite. The major enzyme

    involved in the generation of the active metabolite is cytochrome P450 2C19 (CYP2C19). Among

    several common polymorphisms of CYP2C19 are loss of function mutations that result in a

    premature stop codon and a truncated protein. In theory, patients with these polymorphisms who

    are taking clopidogrel would have a reduced amount of the active metabolite present for platelet

    inhibition.

    Because of concerns over reduced activity in these patients, the Food and Drug Administration

    issued a boxed warning for clopidogrel in 2010. Multiple studies since then have evaluated the

    relationship between the presence of these polymorphisms and adverse outcomes in patients, and
    the data are inconclusive. Therefore, the routine use of genetic screening in patients undergoing
    percutaneous coronary intervention is not recommended.

    Genetic testing for CYP2C19 mutations has nothing to do with allergy or rash to clopidogrel.

    Screening is not recommended in patients receiving bare metal or drug-eluting stents. The

    presence of atrial fibrillation does not affect the recommendation against screening.

    57. A 45-year-old man presents to the emergency department with crushing substernal chest

    pain and ST elevation in the inferior leads on the electrocardiogram. His blood pressure is 185/100

    mm Hg and his heart rate is 100 bpm. The cardiac catheterization laboratory is activated, aspirin 325
    mg is administered orally, and a heparin bolus and drip are started. The patient is anxious and reports
    no medical history, no medication allergies, and he takes a multivitamin daily and sildenafil 100 mg
    as needed for erectile dysfunction (most recently the evening prior to presentation). A

    urinary toxicology screen returns that is positive for cocaine.

    Which of the following medications would be appropriate to treat the patient's hypertension, while
    waiting for coronary angiography?

    a. Sodium nitroprusside.

    b. Nitroglycerin.

    c. Lorazepam.

    d. Nifedipine.

    e. Metoprolol.

    57. c.
    Lorazepam.
    Cocaine-induced chest pain may be related to myocardial infarction (MI), aortic dissection, or

    anxiety. Among those with MI, this may be due to coronary vasospasm and/or thrombotic

    occlusion of one or more coronary vessels. Patients with acute coronary syndromes and severe

    hypertension upon presentation should be treated appropriately with aspirin, heparin (assuming

    aortic dissection has been ruled out or is considered unlikely), and benzodiazepenes to control

    central sympathetic outflow and anxiety.

    Beta-blockers are contraindicated in cocaine-related MI, as they may result in increased coronary
    vasospasm and decreased coronary blood flow due to unopposed alpha activity. Combined alpha-and
    beta-blocker agents, such as labetalol or carvedilol, may be acceptable alternatives. Short-

    acting nifedipine is contraindicated in acute MI. While nitrates to control blood pressure and chest
    pain would be appropriate in cocaine-associated MI, they are contraindicated in this patient due to
    recent use of sildenafil.

    58. A 55-year-old man presents to the emergency department with progressive fatigue and

    shortness of breath for the past 3 weeks. In the past 2 days he has also developed some lower

    extremity edema and feels short of breath in bed at night.

    His medical history is notable for deep vein thrombosis (DVT), for which he is currently maintained
    on apixaban, and he has not missed any doses. He had a recent echocardiography, demonstrating a

    left ventricular ejection fraction of 35%. On examination, his heart rate is 165 bpm and irregularly
    irregular. His blood pressure is 105/75 mm Hg, jugular venous pressure is 7 cm, and there are

    bibasilar crackles on lung exam.

    Cardiac exam is notable for the irregularly irregular rhythm, without appreciable murmur, rub, or
    gallop. Extremities are warm with 1+ bilateral edema to his calves. There are no palpable cords or
    focal tenderness. Electrocardiogram reveals atrial fibrillation with a rapid ventricular response, and
    nonspecific T-wave changes. Laboratory values show a normal troponin, normal basic metabolic

    panel, and an elevated brain natriuretic peptide.

    Which of the following treatments is contraindicated?

    a. Amiodarone.

    b. Esmolol.
    c. Diltiazem.

    d. Dofetilide.

    e. Digoxin.

    58.

    c.
    Diltiazem.
    This patient is presenting with signs of acute heart failure in the setting of atrial fibrillation with a
    rapid ventricular response. Rate control is an important step in management, in addition to

    diuresis in light of his signs of volume overload. All of the listed agents may provide rate control and
    are indicated for the acute treatment of supraventricular tachycardia. However,

    nondihydropyridine calcium channel antagonists are contraindicated in the setting of left

    ventricular systolic dysfunction or congestive heart failure, and should be avoided. Cautious use of
    beta-blockers is more appropriate, although monitoring for exacerbation of cardiac function is also
    warranted when they are used in this setting.

    Amiodarone use may be appropriate acutely in this patient, because despite his unknown

    duration of atrial fibrillation, he is already anticoagulated for a history of DVT. Therefore, the risk of
    stroke from cardioversion is low. Dofetilide is not contraindicated, because he has been

    anticoagulated, but will not help with rate control.

    59. A 76-year-old man is brought to the emergency room by ambulance with an acute anterior wall
    myocardial infarction. He has a history of hypertension and permanent atrial fibrillation for which he
    takes metoprolol succinate 100 mg daily and warfarin to maintain an international

    normalized ratio (INR) between 2.0 and 3.0. His creatinine clearance is 65 ml/min. A sirolimus-

    eluting stent is placed in his proximal left anterior descending coronary artery. He was given aspirin
    and clopidogrel at loading doses, and the interventional cardiologist recommends continuing

    aspirin at 81 mg daily and clopidogrel 75 mg daily.

    Which of the following medical therapy adjustments should also be made?

    a. Warfarin should be discontinued.

    b. Change warfarin to rivaroxaban 15 mg daily.

    c. Change warfarin to dabigatran 75 mg twice daily.

    d. Target INR should be 1.5-2.0.

    e. Target INR should be 2.0-2.5.

    59. e.

    Target INR should be 2.0-2.5.

    Due to his elevated CHA2DS2-VASc score (4, due to age, hypertension, and vascular disease) and
    CHADS2 score (2, due to age and hypertension), anticoagulation with warfarin or a novel oral

    anticoagulant is indicated. Setting a target INR below the therapeutic window is not advised.

    Setting the target INR at 2.0-2.5 in the lower therapeutic range is recommended to decrease the

    risk of bleeding while keeping the risk of stroke and systemic emboli low. There is no current

    recommendation to use non-vitamin K oral anticoagulants as part of a triple therapy strategy.

    60. A 60-year-old woman with a history of nicotine dependence, hypertension, diabetes, and

    right common iliac artery stenting presents to the emergency department with a 3-day history of

    mild exertional substernal chest pain relieved by rest. Her brother underwent coronary artery

    bypass graft surgery at age 55 years. She takes aspirin 81 mg daily, clopidogrel 75 mg daily,

    metoprolol 50 mg twice daily, lisinopril 20 mg daily, and metformin 500 mg twice daily.

    In the emergency department, her blood pressure is 120/70 mm Hg and her heart rate is 65 bpm.

    Electrocardiogram shows normal sinus rhythm with evidence of left ventricular hypertrophy.

    Laboratory values reveal of creatinine 1.2 mg/dl, and the initial troponin is elevated. Sublingual
    nitroglycerin completely resolves her chest pain. She is admitted to the inpatient ward overnight, with
    a plan for coronary angiography in the morning.

    Which of the following medications is most appropriate, in addition to aspirin 324 mg?

    a. IV nitroglycerin.

    b. IV abciximab.

    c. No additional therapy.

    d. Intravenous (IV) unfractionated heparin.

    e. IV fibrinolytics.

    60. d.

    Intravenous (IV) unfractionated heparin.

    This patient presents with a non-ST-elevation myocardial infarction (NSTEMI). Her TIMI risk score
    is

    >3. The correct answer is IV unfractionated heparin (Class I, Level of Evidence B).

    In patients with NSTEMI, anticoagulation in addition to antiplatelet therapy is recommended for all
    patients, if there are no contraindications. Anticoagulant options include subcutaneous enoxaparin 1
    mg/kg every 12 hours (reduce dose to 1 mg/kg subcutaneously daily if creatinine clearance is <30

    ml/min). IV bivalirudin 0.1 mg/kg loading dose, followed by 0.25 mg/kg/hr can be administered in

    patients being managed with an early invasive strategy, that is, within 24 hours (Class IB).

    Fondaparinux 2.5 mg subcutaneously daily can be administered either for the duration of the

    hospitalization or until percutaneous coronary intervention (PCI) is performed (Class IB). IV

    fibrinolytics are contraindicated in NSTEMI (Class III). Glycoprotein IIb/IIIa inhibitors can be

    considered, in addition to aspirin and P2Y12 inhibitors in high-risk NSTEMI patients. IV


    nitroglycerin is recommended for persistent ischemia, heart failure, or hypertension (Class IB).

    61. A 60-year-old man with a history of hypertension and diabetes mellitus was admitted to your

    hospital for management of a non–ST-segment elevation myocardial infarction (NSTEMI). His

    coronary angiogram revealed three-vessel coronary artery disease. Coronary artery bypass graft

    (CABG) surgery was recommended. His medications include aspirin 81 mg daily, clopidogrel 75 mg

    daily, enoxaparin subcutaneous 70 mg twice daily (weight is 75 kg and creatinine is normal), and

    metoprolol 25 mg orally twice daily. His clopidogrel is to be discontinued 5 days prior to surgery.

    Which of the following is the appropriate timing to discontinue his enoxaparin prior to surgery?

    a. 36 hours.

    b. 9 hours.

    c. 6 hours.

    d. 1 hour.

    e. 12 hours.

    61. e.
    12 hours.
    The correct answer is 12 hours. The half-life for enoxaparin is 4-6 hours. Enoxaparin should be

    discontinued 12- 24 hours prior to CABG, and substituted with intravenous unfractionated heparin.

    Compared with unfractionated heparin, the use of enoxaparin <12 hours prior to CABG is

    associated with lower postoperative hemoglobin and a higher risk of blood transfusion.

    62. A 56-year-old man with a history of nicotine dependence, diabetes, and hypertension

    presents to the emergency department (ED) with a 10-hour history of severe exertional shoulder

    pain. His father underwent three-vessel coronary artery bypass graft (CABG) surgery at age 60

    years.

    The patient takes aspirin 81 mg daily and metformin 500 mg twice daily. In the ED, his blood

    pressure is 100/70 mm Hg, and heart rate 90 bpm. His electrocardiogram (ECG) is shown (Figure

    1).

    His initial troponin is negative. His pain does not improve with sublingual nitroglycerin. Aspirin 324

    mg orally, intravenous (IV) unfractionated heparin, and clopidogrel 600 mg are initiated. Your

    facility is a percutaneous coronary intervention (PCI)-capable hospital.

    Which of the following is the most appropriate next step?


    a. Intra-aortic balloon pump (IABP).

    b. IV metoprolol.

    c. IV Reteplase.

    d. IV tenecteplase.

    e. Emergent PCI.

    62. e.
    Emergent PCI.
    The correct answer is emergent PCI. His ECG shows an ST-elevation myocardial infarction (STEMI),

    which is defined by the ESC/ACCF/AHA/World Heart Federation Task Force as a new ST elevation at

    the J-point in at least two contiguous leads of ≥2 mm in men or ≥1.5 mm in women; in leads V2 -

    V3 and/or 1 mm in other contiguous chest or limb leads. New left bundle branch block is considered
    an STEMI equivalent, and may interfere with ST-elevation analysis.

    Reperfusion therapy should be administered to all eligible patients with STEMI with symptom onset
    within the prior 12 hours (Class IA). Primary PCI is the recommended method of reperfusion when

    it can be performed in a timely fashion by experienced operators (Class IA). Fibrinolytics, such as
    tenecteplase and reteplase, are not correct because the question states that the hospital is PCI-capable.
    If the hospital is not PCI-capable, and the patient is greater than 120 minutes away from a PCI-capable
    center, then fibrinolytic therapy would be indicated. IABP is not indicated, because the patient is
    hemodynamically stable and needs urgent PCI. IV metoprolol is not the best answer,

    because the patient has ST elevation and needs urgent reperfusion.

    63. A 59-year-old farmer with a history of hypertension and hyperlipidemia presents with crushing
    substernal chest discomfort that started approximately 1 hour prior to arrival in the local emergency
    department. An electrocardiogram demonstrates 2 mm ST-elevations in V1-V3 with

    reciprocal ST depressions in the inferior leads. He continues to have 7/10 chest pain. The closest
    percutaneous coronary intervention-(PCI) capable facility is 3 hours away. He has no

    contraindications to thrombolysis, so intravenous alteplase is administered. His chest discomfort and


    ST elevations resolve, and he remains hemodynamically stable.

    Which of the following is the best next step in this patient's management?

    a. Emergent coronary angiography.

    b. Transfer to facility with cardiac surgery capability.

    c. Transfer to facility with PCI capability.

    d. Echocardiogram.

    e. Admit to the intensive care unit (ICU) for close monitoring.

    63. c.

    Transfer to facility with PCI capability.

    Patients who present to a non–PCI-capable hospital with ST-elevation myocardial infarction


    (STEMI) within 12 hours of symptom onset should be immediately transferred to a PCI-capable

    hospital for primary PCI, if the time from first medical contact to intervention will be less than 120

    minutes. If the anticipated time exceeds this threshold, then thrombolysis within 30 minutes of

    arrival should be considered if there are no contraindications.

    For patients receiving fibrinolysis, transfer to a PCI-capable facility is reasonable even when they are
    hemodynamically stable and have clinical evidence of successful reperfusion therapy, as in this case
    (Class IIa). In this patient population, angiography should be performed when logistically

    feasible at the receiving hospital (ideally within the first 24 hours), but not within the first 2-3 hours
    following fibrinolysis because of increased bleeding risk. This “pharmacoinvasive” approach has

    been demonstrated in clinical trials to decrease the risk of recurrent MI and death compared with a
    conservative strategy. Although cardiac surgery backup may be necessary, the patient primarily

    needs PCI capability. Admission to the ICU and echocardiography are warranted, but should not

    delay transfer to a PCI facility.

    64. An 82-year-old active, thin woman with a history of remote tobacco use and hypertension

    presents with new-onset chest pain. The symptoms began 2 weeks prior, initially occurring with

    exertion climbing a flight of stairs, but gradually have became more progressive. On the day of

    presentation, she developed an episode of chest discomfort at rest and her husband brought her to the
    emergency department for evaluation.

    On arrival, she was pain free and her electrocardiogram demonstrated inferolateral T-wave

    inversions. She was admitted to the hospital where serial cardiac biomarkers revealed moderately

    elevated troponin levels. Her other blood work was normal, aside from a mild chronic anemia.

    Based on these findings, an early invasive strategy was planned with cardiac catheterization the

    next day.

    Which of the following management strategies would offer the best risk profile in this patient?

    a. Aspirin, clopidogrel, and enoxaparin.

    b. Aspirin, clopidogrel, and unfractionated heparin.

    c. Aspirin, prasugrel, and unfractionated heparin.

    d. Aspirin, clopidogrel, unfractionated heparin, and glycoprotein (GP) IIb/IIIa receptor inhibitor.
    e. Aspirin, prasugrel, unfractionated heparin, and GP IIb/IIIa receptor inhibitor.

    64. b.

    Aspirin, clopidogrel, and unfractionated heparin.

    In patients with non-ST-elevation acute coronary syndrome (NSTE-ACS), bleeding is associated with
    worse clinical outcomes. Therefore, the choice of antiplatelet and antithrombotic agents must be

    considered carefully. In fact, the ACUITY trial suggested that the mortality risk associated with
    significant bleeding may be at least as great as that related to the myocardial infarction.

    This patient has multiple bleeding risk factors, including female sex, age, low body weight, and

    anemia. Of the available choices, the combintation of aspirin, clopidogrel, and unfractionated

    heparin would likely incur the lowest bleeding risk.

    All NSTE-ACS patients should receive aspirin. Compared with clopidogrel, prasugrel is associated

    with higher rates of bleeding and should also be avoided in patients >75 years old or low body
    weight, as well as those with a history of prior cerebrovascular accident. The addition of GP IIb/IIIa
    receptor inhibitors upstream of percutaneous intervention would significantly increase the

    bleeding risk and has not been shown to have significant clinical benefit. Enoxaparin was associated
    with increased major bleeding compared with unfractionated heparin in NSTE-ACS patients treated

    with an early invasive strategy in the SYNERGY trial.

    65. A 66-year-old male smoker with a history of diabetes mellitus, hyperlipidemia, and

    gastroesophageal reflux disease (GERD) presents with central chest discomfort occurring at rest.

    The pain began nearly 10 hours before, but he believed it was related to a severe flare of his GERD

    and initially avoided seeking medical attention until the following morning. On arrival in the

    emergency department, his electrocardiogram (ECG) demonstrated Q waves with ST elevations in

    V2-V3. However, he is now free of chest pain. Urgent coronary angiography demonstrated occlusion

    of the mid left anterior descending (LAD) without collaterals.

    Which of the following strategies is the best next step to reduce the risk of cardiac rupture related to
    myocardial infarction?

    a. Intra-aortic balloon pump.

    b. Glycoprotein (GP) IIb/IIIa receptor inhibitor.


    c. Angiotensin-converting enzyme inhibitor (ACEI).

    d. Percutaneous coronary intervention.

    e. Beta-blocker.

    65. d.
    Percutaneous coronary intervention.
    All patients who present with ST-elevation myocardial infarction (STEMI) within 12 hours of

    symptom onset should receive urgent reperfusion therapy. The risk factors for free wall rupture are
    female sex, older age, presence of Q waves on ECG indicating completed infarct, LAD involvement,

    absence of collaterals, no prior history of MI, hypertension during the acute phase of STEMI, use of
    steroids or nonsteroidal anti-inflammatory drugs, and fibrinolytic therapy greater than 14 hours

    after symptoms onset.

    Reperfusion therapy within 12 hours can decrease this risk. An intra-aortic balloon pump and GP

    IIb/IIIa receptor inhibitors do not decrease the risk of free wall rupture. Medical management with
    ACEIs and beta-blockers are likely warranted in this patient, but would be instituted after

    reperfusion therapy when the patient is hemodynamically stable.

    66. A 69-year-old woman with hypertension and hyperlipidemia presents to the emergency room

    with acute shortness of breath. Two nights ago she had the onset of flu-like symptoms. She has no
    other significant past medical history. On exam she is sitting upright. Her blood pressure is 80/50

    mm Hg, her heart rate is 110 bpm, and her oxygen saturation is 88% on 6-liter nasal cannula. Her

    jugular venous pressure is 15 cm. Lung exam reveals rales to the mid lung fields bilaterally.

    Cardiovascular exam reveals tachycardia without murmur or rub appreciated. Extremities are cool.

    Electrocardiogram shows a 1 mm ST elevation in leads II, III, and a ventricular fibrillation.

    Which of the following is the most likely explanation of her clinical presentation?

    a. Contained free wall rupture.

    b. Right ventricular (RV) infarct.

    c. Ventricular septal rupture.

    d. Papillary muscle rupture.

    e. Giant cell myocarditis.

    66. d.
    Papillary muscle rupture.
    Mechanical complications of acute myocardial infarction (MI) that can result in shock include

    papillary muscle rupture, ventricular septal rupture, free wall rupture, and RV infarct. In this patient
    presenting with an inferior MI and acute pulmonary edema, the most likely etiology would be

    papillary muscle rupture and severe mitral regurgitation. In the acute setting, a murmur may not be
    heard. This typically occurs from 2 to 7 days post MI. Ventricular septal rupture may result in a
    similar presentation, but usually occurs at 3-5 days and occurs more commonly with anterior MIs.

    RV infarct typically presents with hypotension but clear lung fields. Giant cell myocarditis would not
    be expected to be associated with inferior ST elevations.

    67. A 75-year-old woman presents to the emergency department (ED) 4 days after the onset of chest
    pain. She lives in a remote area and did not initially seek medical attention. Today her family visited
    her and found her barely responsive in her home. Upon arrival to the ED, she is cool, clammy, and
    confused.

    Her blood pressure is 80/50 mm Hg, heart rate is 110 bpm in sinus rhythm, and oxygen saturation is
    90%. She has bibasilar fine rales, and elevated jugular venous pressure and a thrill felt along the left
    sternal border. On auscultation, there is an audible grade 4/6 holosystolic murmur and an S3. She has
    no edema. Her initial 12-lead electrocardiogram reveals evidence of an acute anterior myocardial
    infarction (MI). Her initial cardiac enzymes are abnormal.

    An echocardiogram confirms your suspicion of an acute ventricular septal defect (VSD) with anterior
    akinesia and left ventricular ejection fraction of 30%. She is taken quickly to the cardiac
    catheterization laboratory, where a total occlusion of the proximal left anterior descending is found,
    along with a 70% lesion in a large circumflex obtuse marginal. Urgent surgical consultation is
    obtained.

    Which of the following is the best timing to consider operative repair of the VSD?

    a. In more than 28 days.

    b. The risk is unrelated to the time period after the infarction.

    c. In 15-28 days.

    d. In 7-14 days.

    e. In less than 7 days.

    67.

    e.
    In less than 7 days.
    The correct answer is less than 7 days. In post MI VSD, overall surgical mortality is 42.9%,

    according to the Society of Thoracic Surgeons (STS) database. The mortality rate is highly

    associated with the timing of surgery post MI. In the STS database, if repair was performed in

    less than 7 days post MI, operative mortality was 54.1%, while it was 18.4% if surgery was more

    than 7 days post MI.

    Additional independent risk factors for mortality include female sex, presence of shock, older

    age, preoperative balloon pump, hemodialysis, moderate to severe mitral regurgitation, and

    whether the surgery is a re-do cardiac surgery.

    The remaining answers are incorrect because the highest mortality is seen early in the post MI

    course. The progressively lower odds of mortality is due to subselection of a healthier cohort

    and healing of the myocardium with time, which improves surgical outcomes. Percutaneous

    closure of the VSD may be considered in high-risk patients who do not require additional surgical
    procedures, such as coronary bypass or valve replacement, within the acute time frame.

    However, the issue of post-MI friable myocardium still applies to this intervention.

    68. A 55-year-old man is shoveling snow when he is seen grabbing his chest and falls to the ground.
    Bystander cardiopulmonary resuscitation (CPR) is performed until emergency medicine

    services (EMS) arrives. An automated external defibrillator (AED) is attached and shock is advised
    and delivered. CPR is continued and there is no return of spontaneous circulation. Awaiting

    advanced cardiac life support (ACLS), the AED advises another shock, which is administered and

    followed by return of a palpable carotid pulse. He is intubated on scene, after the administration of 5
    mg of midazolam. Prior to intubation, there is no witnessed spontaneous limb movement.

    In the hospital emergency department, an electrocardiogram (ECG) is performed that

    demonstrates 2 mm inferolateral ST-segment depressions. Norepinephrine is initiated for

    hypotension and cardiogneic shock. His vital signs are stable and he is cooled to a temperature of 35
    degrees Centigrade. On neurologic examination, the pupils are fixed and nonreactive. He has no
    spontaneous movements, nor does he withdraw or grimace to noxious stimulus. He is

    overbreathing the ventilator. Aspirin is administered through an orogastric tube. A noncontrast


    head computed tomography is unremarkable.

    Which of the following is the best next step in this patient's management?

    a. Immediate coronary angiography.

    b. Coronary angiography only if patient can follow commands.

    c. Coronary angiography only if cardiac-specific troponin is elevated.

    d. Coronary angiography only if ST elevations develop on ECG.

    e. Coronary angiography only if pupils become reactive to light.

    68.

    a.
    Immediate coronary angiography.
    Out-of-hospital cardiac arrest is often caused by acute coronary syndromes. Patients with ST-

    elevation myocardial infarction (STEMI) by ECG after return of spontaneous circulation should go

    emergently for coronary angiography. Similarly, patients with non-STEMI or other evidence of

    acute coronary syndromes with electrical or hemodynamic instability should go emergently for

    coronary angiography.

    Recommendations for emergent coronary angiography are independent of neurologic status, as

    the neurologic exam is unreliable early post arrest. The administration of sedatives or paralytics
    further confounds neurologic prognostication. The absence of spontaneous movement post

    arrest should not be interpreted as poor neurologic prognosis. Similarly, pupillary reactivity early
    post arrest lacks sensitivity or specificity for a poor neurologic outcome. Neurologic

    prognostication is improved at 72 hours post return of spontaneous circulation. If the patient

    was cooled, neurologic examination and prognostication should be delayed until 72 hours post

    rewarming.

    69. During acute coronary syndromes, there is thrombus formation at the site of plaque rupture.

    Which of the following patient factors contributes to the formation of thrombus on a ruptured

    coronary plaque?

    a. A thick fibrous cap.

    b. Laminar flow in the culprit vessel.

    c. Cigarette smoking.

    d. Branch point coronary anatomy.

    e. Increased high-density lipoprotein cholesterol (HDL-C).

    69. c.
    Cigarette smoking.
    Cigarette smoking is the correct answer, because it has been shown to correlate with increased

    systemic thrombotic propensity in patients. Increased thrombotic propensity is one of three factors in
    Virchow’s triad that contributes to thrombus formation in acute plaque rupture. Laminar flow

    would not increase the risk of thrombosis. Branch point areas may have increased plaque

    formation, but not necessarily plaque rupture. Thickness of the fibrous cap correlates with risk of
    plaque rupture, but not directly with thrombus formation. Increased HDL-C does not increase foam

    cell formation as opposed to increased low-density lipoprotein cholesterol.

    70. A 66-year-old man presents with substernal chest pain suspicious for myocardial ischemia

    that began approximately 45 minutes ago, but has now subsided. He has a past history of heavy

    smoking and carries the diagnosis of chronic obstructive pulmonary disease, for which he is being
    treated with inhalers that he intermittently uses. He has been noncompliant with medications in

    the past and has been homeless at various times in his life. He has hypertension and borderline

    hyperlipidemia.

    His examination reveals normal blood pressure with a heart rate of 102 bpm. His oxygen saturation is
    89%. He has reduced breath sounds throughout, but a normal cardiac exam. His initial

    electrocardiogram (ECG) reveals sinus tachycardia with left ventricular hypertrophy and secondary
    repolarization changes.

    Which of the following is the most sensitive and specific laboratory test (or tests) for the diagnosis of
    myocardial infarction (MI) in this situation?

    a. Cardiac-specific troponin plus creatine kinase-myocardial band (CK-MB).

    b. Cardiac-specific troponin plus D-dimer.

    c. Cardiac-specific troponin plus N-terminal pro-brain natriuretic peptide (NT-proBNP).

    d. Cardiac-specific troponin plus CK total.

    e. Cardiac specific troponin only.

    70. e.
    Cardiac specific troponin only.
    In the appropriate clinical context, an MI is diagnosed when there is an elevation of cardiac-specific
    biomarkers >99% above the upper reference limit and at least one of the following: 1) symptoms of
    ischemia, 2) new or presumed significant ST-segment–T wave (ST–T) changes or new left bundle

    branch block (LBBB), 3) development of pathological Q waves in the ECG, 4) imaging evidence of

    new loss of viable myocardium, 5) a new regional wall motion abnormality, or 6) identification of an
    intracoronary thrombus by angiography or autopsy.

    The definition revolves around an elevation in cardiac-specific troponin (the preferred biomarker),
    as it is the most sensitive and specific marker of myocardial necrosis. If troponin is unavailable, CK-
    MB would be the next most sensitive biomarker and may be used. Creatine phosphokinase (CPK) is

    nonspecific and released by skeletal and cardiac muscle breakdown; therefore it is unreliable as a
    biomarker of myocardial necrosis. NT-proBNP is a biomarker that reflects myocardial wall stress

    and has been shown to be related to prognosis in acute MI, but is not a specific marker of

    myocardial necrosis. D-dimer is nonspecific, although very sensitive for thrombus, and does not

    reflect myocardial necrosis.

    71. A 28-year-old woman who is 32 weeks pregnant presents to the emergency department with

    1 hour of chest pressure and dyspnea. She has no prior history of cardiac disease. She is tachycardic
    with a heart rate of 120 bpm and a blood pressure of 150/60 mm Hg. Her oxygen saturation is 95%

    on 2 liters of nasal cannula supplemental oxygen. She has a 1/6 early peaking systolic murmur

    across the precordium. Her jugular venous pressure is elevated. There are faint rales at the bases of
    her lungs bilaterally. Her electrocardiogram (ECG) demonstrates sinus tachycardia at 120 bpm with 3
    mm of ST-elevation in leads V1-V4.

    Which of the following is the most likely etiology for her presentation?

    a. Coronary artery dissection.

    b. Pneumothorax.

    c. Amniotic fluid embolism.

    d. Pulmonary embolism.

    e. Eclampsia.

    71. a.
    Coronary artery dissection.
    The correct answer is coronary artery dissection. There is a risk for coronary artery dissection

    during pregnancy and shortly after delivery in the postpartum period. It is a rare, but well

    recognized complication of pregnancy. Her presentation is most consistent with this diagnosis

    given the clinical features of chest pain, mild pulmonary edema on examination, and ST-segment

    elevation in the left anterior descending territory.

    The ECG findings and clinical features are not characteristic for pericarditis. There is a risk of
    pulmonary embolism during pregnancy and in the postpartum period due to the hypercoagulability

    of pregnancy. However, the features of her presentation are not consistent with this diagnosis.

    Likewise, pneumothorax is also on the differential diagnosis for chest pain and dyspnea, but her

    physical exam is not consistent with this, because there is no history of trauma and there is no

    increased risk of pneumothorax during pregnancy. Amniotic fluid embolus would occur postpartum

    and presents with shock. Eclampsia presents with significant hypertension and seizures and would

    not cause ST elevation.

    72. A 78-year-old man is seen in the office 2 weeks after an anterior ST-segment elevation MI

    (STEMI). He underwent primary percutaneous coronary intervention with a drug-eluting stent to

    the left anterior descending. His ejection fraction is 40%. His medical history is significant for a
    transient ischemic attack (TIA) 5 years ago, chronic kidney disease stage 3b, and peripheral arterial
    disease with mild intermittent calf claudication. He was discharged on dual antiplatelet therapy

    with ticagrelor 90 mg twice daily and aspirin 81 mg daily.

    Which of the following is a contraindication to vorapaxar in this patient?

    a. History of cerebrovascular event.

    b. Concomitant use of ticagrelor.

    c. Chronic kidney disease.

    d. Age greater than 75 years.

    e. Recent STEMI.
    History of cerebrovascular event.

    Vorapaxar is an antiplatelet drug that inhibits PAR-1, the thrombin receptor on platelets. The TRA
    2°P-TIMI 50 (Thrombin Receptor Antagonist inSecondary Prevention of Atherothrombotic Ischemic

    Events Thrombolysis in Myocardial Infarction) trial randomized 26,449 patients who had a history

    of MI, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or

    matching placebo. Cardiovascular death, MI, or stroke was significantly lower in the vorapaxar

    group compared with the placebo group. Moderate or severe bleeding occurred in 4.2% of patients

    who received vorapaxar and 2.5% of those who received placebo.

    There was an increase in the rate of intracranial hemorrhage in the vorapaxar group. Patients with a
    history of stroke had an excessive risk of intracranial hemorrhage. Therefore, the drug is

    contraindicated in patients with a history of a TIA or stroke. In the TRA 2°P-TIMI 50 trial, the use
    andtype of P2Y12 inhibitor was left to the discretion of the physician. There are no specific data on
    the risk of vorapaxar in patients treated with clopidogrel compared with more potent agents. A

    small number of patients (0.7%) received prasugrel during the study. Ticagrelor is not

    contraindicated, but may alter the efficacy or safety. Because of liver metabolism, vorapaxar can be
    used in patients with chronic kidney disease.

    73. A 58-year-old man presents to your office to establish cardiovascular (CV) care. He has a

    history of myocardial infarction (MI) treated with a drug-eluting stent 2 years ago. At that time, he
    had single-vessel disease and a preserved ejection fraction. He was treated with dual antiplatelet
    therapy for 12 months and he has been on low-dose aspirin since that time. He has diabetes

    requiring oral medication and hypercholesterolemia. He has no history of stroke or bleeding. He is


    asymptomatic and has not had recurrent ischemia.

    Which of the following do you recommend to decrease the risk of major adverse CV events?

    a. Clopidogrel 75 mg daily.

    b. Ticagrelor 90 mg twice daily.

    c. Prasugrel 10 mg daily.

    d. Ticagrelor 60 mg twice daily.

    e. Prasugrel 5 mg daily.

    73. d.
    Ticagrelor 60 mg twice daily.
    The PEGASUS-TIMI 54 (Prevention of Cardiovascular Events in Patients with Prior Heart Attack

    Using Ticagrelor Compared to Placebo on a Background of Aspirin Thrombolysis in Myocardial

    Infarction 54) trial randomly assigned in a 1:1:1 double-blind fashion, 21,162 patients who had an MI
    in the past 1 to 3 years to ticagrelor 90 mg twice daily, ticagrelor 60 mg twice daily, or placebo.

    Ticagrelor reduced the rate of the primary efficacy endpoint (death, MI, or stroke), with Kaplan-

    Meier rates at 3 years of 7.85% for ticagrelor 90 mg twice daily, 7.77% for ticagrelor 60 mg twice
    daily, and 9.04% for placebo group. For ticagrelor 90 mg versus placebo, the hazard ratio (HR) was
    0.85 and the confidence interval (CI) was 0.75 to 0.96 (p = 0.008), and for ticagrelor 60 mg versus
    placebo the HR was 0.84 and the CI was 0.74 to 0.95 (p = 0.004). The rates of TIMI major bleeding
    were higher with ticagrelor (2.60% with 90 mg and 2.30% with 60 mg) than with placebo (1.06%).

    74. A 74-year-old woman is referred to you with indigestion, belching, and mild exertional

    “discomfort,” but no chest pain. She is overweight and has hypertension, diabetes (non-insulin

    dependent), and sleep apnea. There is a family history of coronary artery disease (CAD) in an older
    brother who had successful percutaneous coronary intervention (PCI).

    Her current medications include chlorthalidone 25 mg, lisinopril 40 mg, metformin 500 mg twice

    daily, and a multivitamin. Her baseline labs are normal, including her lipid profile and HbA1c. Her
    electrocardiogram (ECG) is normal. Physical examination reveals a body mass index of 34.5, heart

    rate of 78 bpm and regular, blood pressure of 135/85 mm Hg, and oxygen saturation of 94%. She

    has an auscultatory S4 and a soft grade 2/6 aortic flow murmur, but no bruits, and a negative

    cardiac exam otherwise.

    Which of the following do you recommend as the next step in her work-up?

    a. Nuclear exercise stress test.

    b. No further cardiac workup necessary.

    c. Echocardiogram.

    d. Gastrointestinal (GI) referral and possible endoscopy.

    e. Coronary computed tomographic angiography (CTA).

    74. a.
    Nuclear exercise stress test.
    While she does not have classic angina, she has multiple features that make her presentation

    suggestive of atypical angina. Atypical angina may present as indigestion, belching, and exertional
    dyspnea, and it is more common in women, older patients, and those with diabetes.

    Her baseline ECG is normal and the first test to be considered should be a stress ECG with imaging.

    In women, the use of imaging improves diagnostic accuracy when compared with standardized ECG

    stress testing. An echocardiogram to assess left ventricular function might be useful, but her exam
    and ECG is normal. GI endoscopy might be a consideration as well, but the exertional component to
    her chest “discomfort” warrants further evaluation. Coronary CTA and a calcium score might also

    be helpful, because a negative study at her age would suggest there is little chance that CAD is

    present. Because angina can be difficult to diagnose in this population, some effort to exclude a
    coronary source should be undertaken.

    75. A 57-year-old man is referred to you with shortness of breath. He has not been followed

    regularly and he says he was told he had a murmur as a teenager, but that he would likely

    “outgrow it.” He works in heating and air conditioning and has a fairly physical work environment.

    He does not smoke and is on no medication.

    Which of the following could be considered an etiology for cardiac-related dyspnea?

    a. A left-to-right intracardiac shunt Qp/Qs of 2.1:1.

    b. Pulmonary capillary wedge pressure (PCWP) of 11 mm Hg.

    c. A distal left circumflex coronary lesion of 60%.

    d. Cardiac index of 3.0 L/m2.

    e. Mean pulmonary artery pressure of 28 mm Hg during exercise.

    75. a.

    A left-to-right intracardiac shunt Qp/Qs of 2.1:1.

    The correct answer is a left-to-right cardiac shunt with its associated volume overload.

    Cardiac-related dyspnea can occur when there is an elevated PCWP with resultant stimulation of

    the interstitial J receptors and/or pulmonary edema. Usually there is associated orthopnea or
    paroxysmal nocturnal dyspnea (PND), which occurs 2-4 hours after the onset of sleep and subsides

    minutes after sitting upright or standing. The PCWP of 11 mm Hg is normal in this situation.

    Patients with low cardiac output (cardiac index of 3.0 L/m2) experience dyspnea on exertion and

    fatigue in the absence of orthopnea or PND. Dyspnea may also be due to ischemia during exercise,

    but it is very unlikely to be associated with the degree of coronary disease that jeopardizes only a
    small amount of myocardium as noted.

    76. The jugular venous pressure (JVP) reflects the right atrial (RA) pressure. It is a critical

    component of the cardiac examination, as an elevation suggests an elevated RA pressure and has

    prognostic importance.

    Which of the following is correct regarding the assessment of an elevated JVP?

    a. It is best measured as the vertical distance above the clavicle in the upright position.

    b. It is best measured as the vertical distance between the top of the pulsation and the angle of c. Louis.

    d. It can best be assessed with the patient lying at a 20 degree elevation.

    e. The degree of elevation cannot be reliably assessed during atrial fibrillation.

    f. Either the external or internal jugular veins can be assessed reliably.

    76. a. It is best measured as the vertical distance above the clavicle in the upright position.

    The height of the JVP is reflective of RA pressure. The best answer is to measure the height of the
    JVP in the upright position above the clavicle. Using that as a reference point is effective, because the
    RA pressure must be at least 10 cm high for the waveforms to be visible in that position. Thus, any
    evidence of waveforms in the upright position means the JVP is elevated.

    While either the external or the internal jugular can be used, the jugular vein valves may interfere
    with accuracy and the internal jugular vein is preferred. Using the angle of Louis (the sternal

    inflection point where the manubrium meets the sternum), a distance >3 cm has been considered

    abnormal. However, the distance from the sternal angle and the RA is quite variable among

    patients, and this leads to an underestimation of the venous pressure. Atrial fibrillation will affect the
    waveforms observed, but the total height of the JVP column will still reflect mean RA pressures.

    The height of the JVP cannot be reliably assessed with the patient in a semisupine position.

    76. A number of early diastolic heart sounds may be audible in certain patients. These include an S3 in
    young patients and in older patients suffering from heart failure, a pericardial knock in those with
    constrictive pericarditis, and a mitral opening snap in patients with rheumatic mitral stenosis.

    The timing from S2 of each of the early diastolic heart sounds varies, depending on the origin of the
    sound.

    Which of the following is the correct sequence one could expect these heart sounds to occur if they
    were present, from a timing perspective in early diastole?

    a. Opening snap, followed by pericardial knock, followed by an S3.

    b. Opening snap, followed by an S3, followed by pericardial knock.

    c. Pericardial knock, followed by an S3, followed by opening snap.

    d. Pericardial knock, followed by opening snap, followed by an S3.

    e. S3, followed by an opening snap, followed by a pericardial knock.

    77. a.

    Opening snap, followed by pericardial knock, followed by an S3.

    These early diastolic sounds reflect the hemodynamic changes in early diastole. The opening snap is
    a high-pitched sound occurring shortly after S2 and reflects the abrupt opening of a mobile but

    stenotic mitral valve. The interval between the S2 and opening snap decreases as the left atrial (LA)
    pressure rises (worsening mitral stenosis). It is the first sound heard in early diastole, as it reflects the
    mitral valve opening prior to the initiation of left ventricular (LV) filling. The second possible sound
    is the pericardial knock. It occurs once the mitral valve is open and is a high-pitched sound reflecting
    the impact of the cessation of rapid filling on the LV wall. In constriction, the LV fills rapidly from
    the elevated LA pressure, to the point it cannot expand further due to the restriction placed on it from
    the constrictive pericarditis.

    An S3 is a low-pitched sound that reflects the rapid filling phase of diastolic LV filling and occurs
    later than the impact sound from a pericardial knock. An S3 may be normal in children, adolescents,
    and young adults, but implies heart failure in adults. It can also be heard in severe mitral

    regurgitation. Thus, the correct answer is opening snap, followed by pericardial knock, followed by
    an S3.

    78. The Valsalva maneuver can help distinguish the origin of some cardiac murmurs and is known

    to be abnormal in heart failure. For patients with an intact autonomic nervous system, when the

    Valsalva maneuver is performed there are four phases evident from the hemodynamic tracings.

    Which of the following occurs during phase 3 of the Valsalva maneuver?

    a. The systemic pressure declines and the heart rate (HR) increases.
    b. The systemic pressure increases due to increased blood pressure return.

    c. The systemic pressure increases with slowing of the HR.

    d. The systemic pressure declines in response to a decrease in intrathoracic pressure.

    e. The systemic pressure increases transiently due to an increase in intrathoracic pressure.

    78. d. The systemic pressure declines in response to a decrease in intrathoracic pressure.

    The four phases of the Valsalva maneuver are shown in Figure 1, where the relative HR and aortic

    pressure are outlined. In phase 1, with the initiation of the Valsalva, the intrathoracic pressure
    increases and blood is forced out of the pulmonary circuit. There is an increase in left ventricular
    (LV) filling and stroke volume and the systemic blood pressure rises. In phase 2, with the

    maintenance of the Valsalva, the LV filling declines as the increased intrathoracic pressure impedes
    venous return and stroke volume drops, resulting in vasoconstriction with a compensatory

    tachycardia.

    In phase 3, with release of the Valsalva, the aortic pressure declines further in response to the
    decreased intrathoracic pressure and decreased left atrial return associated with the increased

    aortic volume and the delay before venous return catches up to the LV. In phase 4, the LV preload
    increases with the return of the venous flow; stroke volume increases rapidly into the

    vasoconstricted aortic system and the blood pressure overshoots and the baroreceptors are

    stimulated with a subsequent reduction in the HR. Some have noted that when the ratio of the the

    fastest HR (during Valsalva) divided by the slowest HR (upon release) is <1.4, there is evidence for
    autonomic impairment.
    (Figure 1)

    79. The use of the Valsalva maneuver can help differentiate the origin of certain cardiac

    murmurs. The four phases of the Valsalva maneuver also may be abnormal in patients with

    autonomic dysfunction and in heart failure.

    Which of the following summarizes the abnormality in the phases of the Valsalva maneuver that

    occurs in heart failure?

    a. There is an increase in BP with little change in heart rate (HR) during phase 2.

    b. There is a decrease in blood pressure with no change in HR during phase 3.

    c. There is an increase in BP and bradycardia during phase 4.

    d. There is an increase in blood pressure (BP) and bradycardia during phase 2.

    e. There is a decrease in BP with little change in HR during phase 2.


    79. d. There is an increase in blood pressure (BP) and bradycardia during phase 2.

    There is an increase in BP with little change in HR during phase 2 of the Valsalva maneuver in

    patients with significant heart failure. This is shown graphically in Figure 1. As opposed to the
    normal phase 4 of the Valsalva, in patients with severe heart failure there is a “square wave”

    response with an initial increase in BP (phase 1) that remains elevated during the entire strain

    period (phase 2) and returns to resting levels in phase 3. This is thought to be due to maintenance of
    the left ventricular (LV) filling during the strain phase, despite the decrease in venous return. This is
    presumably due to the increased central blood volume that serves as a reservoir to maintain LV

    preload. This can be detected with BP monitoring during Valsalva or by an abnormal response as

    assessed by the Korotkoff sounds as shown in Figure 2. In the latter figure, the loss of the

    overshoot in BP has been correlated with loss of systolic function and the square root response has
    been correlated with an elevated pulmonary capillary wedge.

    (Figure 1)
    (Figure 2)

    80. A 65-year-old woman with hypertension is admitted to a rural hospital with chest pain for 1

    hour and an ST-segment elevation myocardial infarction (STEMI). She immediately undergoes

    therapy with tenecteplase.

    On arrival to the tertiary referral center, she is comfortable without chest pain, her

    electrocardiogram is now normal, and she is hemodynamically stable. Her exam is only remarkable

    for S4.

    Which of the following is the next most appropriate step?

    a. Emergent coronary angiography.

    b. Coronary computed tomography angiography.

    c. Elective coronary angiography.


    d. Cardiac magnetic resonance imaging.

    80. c.
    Elective coronary angiography.
    Assessment of clinical reperfusion following lytic therapy for STEMI is essential to guiding the

    urgency of subsequent coronary angiography. Resolution of symptoms, improvement of ST-

    segment elevation by at least 50%, and reperfusion arrhythmias (e.g., accelerated idioventricular
    rhythm) are indicative of epicardial coronary patency. If there is clinical uncertainty about the status
    of reperfusion, emergent coronary angiography is warranted (e.g., rescue percutaneous

    coronary intervention). Most patients following STEMI treated with lytic therapy will undergo

    elective coronary angiography to define the coronary anatomy within a day of presentation (Class

    IIa). In high-risk scenarios like shock, heart failure, or recurrent chest pain, urgent coronary

    angiography is recommended (Class I).

    81. A 49-year-old man with no significant medical history presents with 1 week of intermittent

    chest pain that worsened over the 2 hours prior to presentation.

    Blood pressure measures 84/43 mm Hg with a pulse of 113 bpm. Oxygen saturation on 2 liters of

    nasal cannula is 91%. He is tachycardic with an S3 and rales on lung exam. Initial electrocardiogram
    demonstrates ST-segment elevation (STE) in leads V1-V5.

    The patient undergoes urgent cardiac catheterization with placement of a drug-eluting stent in the
    proximal left anterior descending artery. His blood pressure improves post revascularization and he
    is admitted to the coronary care unit. A post-percutaneous coronary intervention echocardiogram

    shows severe hypokinesis of the anterior and anterolateral wall. Left ventricular ejection fraction is
    25%.

    On day 2 of hospitalization, the patient develops dyspnea and the rhythm seen in Figure 1.

    Which of the following best describes the incidence and degree of myocardial injury associated

    with the rhythm seen in Figure 1 in an anterior as compared with inferior myocardial infarction

    (MI)?
    a. The incidence during MI is lower, the degree of myocardial injury is lower, and the location of
    block is at the AV node.

    b. The incidence during MI is greater, the degree of myocardial injury is lower, and the location of
    block is at the atrioventricular (AV) node.

    c. The incidence during MI is the same, the degree of myocardial injury is greater, and the

    location of block is below the AV node.

    d. The incidence during MI is lower, the degree of myocardial injury is greater, and the location of
    block is below the AV node.

    81. d. The incidence during MI is lower, the degree of myocardial injury is greater, and the
    location of block is below the AV node.

    The rhythm strip reveals the development of complete heart block (CHB) occurring in the setting of
    recent anterior wall MI. This is a serious complication of anterior MI, which occurs in roughly 1% of
    cases. CHB in anterior MI is associated with poorer short-term outcomes, including survival, as

    compared with anterior MI patients who do not develop CHB.

    The incidence of CHB in inferior distribution ST-elevation (STEMI) is higher, approximately 4%,
    and may be transient. CHB occurring in inferior STEMI patients is associated with a higher location
    of AV

    block (typically the AV node), whereas in anterior wall MI, the location of block is usually below the
    AV node, resulting in higher long-term block.
    The degree of myocardial injury in anterior wall STEMI exhibiting CHB is greater than the amount
    of myocardial injury observed in inferior STEMI complicated by CHB.

    82. A 75-year-old woman with diabetes is admitted to the coronary care unit after a drug-eluting stent
    (DES) placement in her mid right coronary artery following an acute inferior wall myocardial
    infarction (MI). Earlier, she had received 600 mg of clopidogrel in the emergency department and

    had been administered a bolus of bivalirudin followed by an intravenous infusion. She has a history
    of a prior ischemic stroke and has been a lifelong asthmatic.

    Her electrocardiogram shows sinus rhythm at 50 bpm, and inferior Q waves with almost complete

    resolution of her inferior ST elevation. Her body mass index is 20 kg/m2, blood pressure is 148/70

    mm Hg, and lungs are clear to auscultation. Cardiac examination reveals a fourth heart sound and a
    loud aortic component of the second heart sound.

    At discharge, which of the following medications is the most appropriate choice?

    a. Ticagrelor.

    b. Ticlopidine.

    c. Prasugrel.

    d. Cangrelor.

    e. Clopidogrel.

    82. d.
    Cangrelor.
    The choice of antiplatelet agents following DES placement for acute MI should be guided by specific
    patient characteristics outlined by clinical trials. Prasugrel is contraindicated in this patient due to her
    size, age, and previous stroke. Ticagrelor is not preferred due to the history of asthma and

    bradycardia on exam. Ticlopidine is no longer a first-line choice due to its numerous adverse

    effects, including rash, diarrhea, and neutropenia. Cangrelor is only available intravenously.

    83. Mr. K is a 76-year-old man who presents to the emergency department. He complains of epigastric
    pressure, shortness of breath, nausea, and fatigue, all of which suddenly started about 2

    hours earlier. He has been in good health in the past and his history is remarkable only for diabetes
    treated with oral hypoglycemic medication. He is clinically stable with a blood pressure of 112/78

    mm Hg, heart rate of 75 bpm, S02 of 96%, and temperature of 36.4°C. His electrocardiogram

    (ECG) is normal. An initial set of cardiac biomarkers turns out to be negative. After a tablet of
    sublingual nitroglycerin, he says that his symptoms are slightly improved.

    Which of the following is the most appropriate next step for management?

    a. Transesophageal echocardiography.

    b. Outpatient stress test.

    c. ECG with posterior leads.

    d. Ventilation/perfusion scan.

    e. Coronary computed tomography angiography (CTA).

    83. c.
    ECG with posterior leads.
    This patient presents with strong pretest probability for an acute ischemic syndrome, although

    the ECG is normal. Posterolateral infarctions are often electrocardiographically silent and should be
    considered in these situations. Presence of ST-segment elevation in V7-V9 will confirm the diagnosis
    of true posterior ST-segment elevation myocardial infarction and the need to perform urgent

    reperfusion.

    Outpatient stress testing would not be appropriate in a patient with high pretest probability of an acute
    ischemic syndrome. Coronary CTA performs best in intermediate-risk patients. The pretest

    probability for pulmonary embolism and aortic disease is sufficiently low such that they would not be
    appropriate when the most likely diagnosis is still an acute coronary syndrome.

    84. Which of the following phrases best describes tenecteplase?

    a. Nonantigenic, administered as a single bolus, fibrin specific.

    b. Nonantigenic, administered as two boluses 10 minutes apart, fibrin specific.

    c. Antigenic, administered as a single bolus, fibrin specific.

    d. Antigenic, administered as two boluses 10 minutes apart, not fibrin specific.

    e. Nonantigenic, administered as single bolus, not fibrin specific.

    84. a.

    Nonantigenic, administered as a single bolus, fibrin specific.

    Tenecteplase, or TNK, is a fibrin-specific, nonantigenic fibrinolytic. Although its administration is


    weight based, its main advantage is that it can be administered as a single bolus. Reteplase, or

    Retavase, has limited fibrin specificity. It is given as two boluses 10 minutes apart, but does not have
    to be adjusted for weight. Tissue plasminogen activator has moderate fibrin specificity, but is
    administered as a drip. Streptokinase has no fibrin specificity and is highly antigenic.

    85. A 63-year-old man presents with chief complaints of chest heaviness. He tells you about an

    episode in the morning that subsided spontaneously after 10 minutes, and a new episode 2 hours

    before presentation that lasted about 30 minutes. Now he is asymptomatic, but his wife insisted on
    bringing him to the emergency department. He has been diabetic for the last 15 years and treated

    with metformin and glimepiride. He has also been prescribed amlodipine to control his blood

    pressure.
    His blood pressure is now 145/90 mm Hg, his heart rate is 62 bpm, and creatinine is 1.12 mg/dl.

    The physical exam is unremarkable. He smokes about 10 cigarettes per day. His electrocardiogram

    is normal and on the first set, his troponin T is 0.06 ng/ml (99th percentile, 0.01 ng/ml). You

    calculate a GRACE score of 106 and TIMI score of 3.

    Which of the following is the optimal management for this patient?

    a. Emergent coronary angiography.

    b. Coronary angiography within 24 hours.

    c. No further diagnostic testing.

    d. Coronary computed tomography angiography.

    e. Stress test.

    85. b.
    Coronary angiography within 24 hours.
    The risk profile of this patient does not warrant an emergent catheterization. The 2011 focused

    update of the Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation

    Myocardial Infarction (NSTEMI) considers an early invasive management strategy within 24 hours

    reasonable in the case of high-risk criteria or clinical instability. This patient is diabetic and has
    positive troponin, both of which favor an invasive approach within 24 hours.

    This patient has a confirmed NSTEMI, and a stress test to provoke ischemia in this setting is not
    diagnostically useful and is unsafe. Coronary computed tomography angiography is predominantly

    useful when there is diagnostic uncertainty and the pretest probability is either low or

    intermediate.

    86. A 50-year-old man with diabetes mellitus and a history of cigarette smoking underwent

    percutaneous coronary intervention of his mid left anterior descending artery 2 months ago. At the
    time of his procedure, he was noted to have a total cholesterol of 350 mg/dl, low-density

    lipoprotein cholesterol (LDL-C) of 180 mg/dl, high-density lipoprotein cholesterol (HDL-C) of 20

    mg/dl, and triglycerides of 280 mg/dl. He was placed on atorvastatin 40 mg daily, and repeat

    laboratory tests obtained today show a total cholesterol of 200 mg/dl, LDL-C of 120 mg/dl, HDL-C

    of 23 mg/dl, and triglycerides of 250 mg/dl. The patient is compliant with his medical regimen.

    Which of the following is the most appropriate next step for this patient?

    a. Add niacin.

    b. Increase atorvastatin dose to 80 mg daily.

    c. Add omega-3 fatty acids.

    d. Add ezetimibe.

    e. Add gemfibrozil.

    86. b.

    Increase atorvastatin dose to 80 mg daily.

    For individuals with established coronary artery disease and diabetes, an LDL-C reduction of at least
    50% is the recommended therapeutic strategy. Although administration of a statin reduced the
    patient's LDL-C, since it is not at goal, the statin dose should be increased.

    Gemfibrozil is used primarily to treat hypertriglyceridemia, and an increased incidence of myositis is


    observed when it is used concomitantly with a statin. The addition of niacin to a statin is

    attractive because it may further increase HDL and reduce triglycerides, but it has not been shown to
    reduce cardiovascular events. Ezetimibe and omega-3 fatty acids are not indicated without

    maximizing statin therapy.

    87. Which of the following findings is most useful for establishing or excluding the diagnosis of ST-
    segment elevation myocardial infarction (STEMI)?

    a. Normal cardiac troponin 1 hour after symptom onset.

    b. ECG with 100% ventricular pacing and 3 mm of ST-segment elevation in precordial leads.

    c. ECG with 1 mm of ST-segment elevation in leads V2-V3 in an asymptomatic 44-year-old man.

    d. Electrocardiogram (ECG) with left bundle branch block (LBBB) and 2 mm of concordant ST-

    segment elevation in two leads with a positive QRS deflection.

    87. d. Electrocardiogram (ECG) with left bundle branch block (LBBB) and 2 mm of concordant
    ST-segment elevation in two leads with a positive QRS deflection.

    Neither cardiac troponin nor creatine kinase-myocardial band (CK-MB) are sufficiently sensitive

    within the first 1-2 hours after symptom onset to exclude a diagnosis of MI.

    The multisociety Task Force for the Universal Definition of MI has defined the diagnostic criteria for
    STEMI (at the J point) as follows: ≥2 mm in men or ≥1.5 mm in women in leads V2-V3 and/or ≥1
    mm

    in at least two other contiguous chest leads or two limb leads. Moreover, particularly in young

    men, a multisociety scientific statement recommends a higher threshold of ≥2.5 mm in leads V2-V3.

    The Sgarbossa criteria for diagnosis of MI emphasize concordant ST-segment elevation in two leads
    with a positive QRS as most indicative of STEMI in the setting of an LBBB. It is challenging to

    diagnose STEMI in the setting of ventricular pacing.

    88. A 60-year-old businessman has a history of obesity, with a body mass index of 32 kg/m2. His

    history includes prior cigarette smoking, hypertension, and hyperlipidemia. Six months ago, he

    decided to start climbing three flights of stairs to his office each morning. When performing this
    activity, he notes a pressure sensation localized to his substernal region that resolves within 2-3
    minutes once he sits down at his desk. He describes this symptom to his physician, who orders an

    exercise treadmill test. The results are as follows: exercise duration 8 minutes of the Bruce

    protocol; the patient requests to stop because of his chest pressure; exercise electrocardiogram

    (ECG) is negative for ischemia.

    Based on the ECG stress results, his post-test probability of coronary disease is which of the

    following?

    a. >90%.

    b. 60-90%.

    c. 0-30%.

    d. 30-60%.

    88. a.

    >90%.

    A 60-year-old man with typical angina has a pretest probability of coronary artery disease (CAD)

    that is >90%. According to Bayes Theorem, a negative exercise ECG shifts this probability very little,
    and the post-test probability of CAD remains >90%. This patient’s Duke treadmill score can be

    calculated as 0: 8 minutes Bruce protocol – 0 (for no ST-segment depression) – 8 (4 x 2, for test-


    limiting angina). A Duke treadmill score of zero places a patient into the intermediate-risk category
    for cardiac death, where annual cardiac mortality ranges between 1-3%.

    89. Ionizing radiation can result in cellular DNA injury. A stochastic injury from medical radiation
    exposure results in which of the following consequences?

    a. Carcinogenesis.

    b. Nausea and vomiting.

    c. Skin injury.

    d. Hair loss.

    e. Cellular death.

    89. a.

    Carcinogenesis.
    Stochastic injuries can occur after a single exposure to the cell. It is therefore not threshold

    dependent. The DNA injury that results does not kill the cell, but rather the cell lives on mutated.

    This can eventually lead to cancers later in life. A deterministic injury results when the cell dies from
    the DNA damage. If enough cells of an organ die, then the organ becomes dysfunctional. This

    is seen most often in skin damage, but can result in hair loss, or if extensive (such as acute radiation
    injury), can result in sloughing of the gastrointestinal tract. Deterministic injury only occurs after a
    threshold level of radiation exposure has occurred.

    90. A 65-year-old active woman has a history of type 2 diabetes and uncomplicated inferior wall

    myocardial infarction treated with lytic therapy therapy 10 years ago. She has experienced a dozen
    episodes of interscapular back and chest discomfort over the past month. This discomfort usually

    occurs while gardening. She has tried nitroglycerin twice and thinks that it has helped. Her

    electrocardiogram (ECG) shows old Q waves in the inferior leads and is otherwise normal.

    Which of the following is the procedure of choice for this woman?

    a. Standard treadmill test.

    b. Coronary angiogram.

    c. Regadenoson single-photon emission computed tomography (SPECT).

    d. Dobutamine ECG.

    90. a.

    Standard treadmill test.

    This patient is describing atypical angina and is therefore a candidate for noninvasive assessment,
    rather than proceeding directly to coronary angiography. The multisociety stable ischemic heart

    disease guideline recommends consideration of three criteria for deciding between the standard

    treadmill test and stress imaging: a history of prior coronary revascularization, ability to adequately
    exercise, and findings on a resting ECG.

    ECG abnormalities that warrant proceeding with stress imaging instead of the standard treadmill

    test include pre-excitation, left bundle branch block, paced ventricular rhythm, or >1 mm of ST-
    segment depression. The presence of Q waves is not an indication to proceed with stress imaging

    instead of the standard exercise treadmill test. Although this patient has risk factors that place her at a
    higher risk (i.e., history of established coronary artery disease and the presence of diabetes), the
    standard treadmill test would still be the procedure of choice in this setting, according to the
    guideline.

    91. Which of the following procedures results in the highest potential effective radiation dose

    being delivered to the patient?

    a. Technetium-99m sestamibi rest-stress scan.

    b. Thallium-201 rest-stress scan.

    c. Diagnostic coronary angiogram.

    d. CT coronary angiogram.

    e. Coronary calcium computed tomography (CT).

    91. b.

    Thallium-201 rest-stress scan.

    Diagnostic coronary angiography, technectium-99m scans, and CT angiography (if the newest

    techniques are applied) result in similar effective dose exposure to patients. Increased dose occurs
    with percutaneous coronary intervention because of the time, angulated views, the use of

    magnified views, etc. Thallium-201 has a long half-life and slow excretion, resulting in the greatest
    exposure compared to the other agents.

    92. A 65-year-old man presents for cardiac computed tomography (CT) due to a myocardial

    perfusion study in which the imaging and electrocardiogram findings are discordant.

    Which of the following presenting conditions should lead to cancellation of the cardiac CT order?

    a. Use of sildenafil 24 hours ago.

    b. Body weight 42 kg/m2.

    c. Sinus bradycardia at 40 bpm.

    d. Atrial fibrillation, rate 80-110 bpm.

    92. d.

    Atrial fibrillation, rate 80-110 bpm.

    Atrial fibrillation due to the extreme R-R variability causes motion artifacts on cardiac CT that lead to
    an unacceptable rate of nondiagnostic examinations. Although some scan modes can enable
    moderately accurate cardiac CT angiography in the setting of atrial fibrillation (e.g., helical CT

    without tube current modulation or single-beat wide-area detector CT), atrial fibrillation represents a
    strong contraindication to the test. Bradycardia is not a contraindication. Increased body mass index
    can lead to noisy cardiac CT images and will necessitate higher radiation exposure. Sildenafil use
    contraindicates use of nitroglycerin, but scanning can proceed without its use.

    93. You are called to see a patient in the emergency room 2 days after percutaneous coronary

    intervention, who has low-grade fever, nausea, diffuse pruritus, and a maculopapular rash on the

    trunk and upper extremities. The patient was initiated on clopidogrel after the procedure.

    Which of the following is your next step in management of this patient?

    a. Intravenous (IV) immunoglobulin (IG).

    b. IV steroids.

    c. Diphenhydramine therapy.

    d. Stop the clopidogrel.

    93. c.
    Diphenhydramine therapy.
    Late contrast reactions are T-cell mediated and are more common with nonionic dimers. If a

    patient has a prior history of such a reaction, choosing a contrast other than a nonionic dimer, such as
    a nonionic monomer (iopamidol), is advised. This is a self-limiting condition and symptomatic

    treatment is all that is required. This is not a reaction to the clopidogrel and thus should not be
    discontinued.

    94. In a patient who receives enoxaparin with the electrocardiogram shown in Figure 1, which of

    the following conditions would indicate antifactor Xa (anti-Xa) level monitoring?

    a. Liver disease.

    b. Concomitant warfarin

    therapy.
    c. Renal insufficiency.

    d. Diabetes.

    e. Stroke.

    94. c.
    Renal insufficiency.
    The patient’s degree of renal dysfunction warrants anti-Xa monitoring. According to the

    current American Heart Association/American College of Cardiology guideline, low molecular

    weight heparin agents should be avoided in patients with severe renal dysfunction (creatinine >2.5

    in men, >2.0 in women). In patients with moderate renal dysfunction, dose adjustment should be
    considered and anti-Xa monitoring may be necessary.

    Enoxaparin is not hepatically metabolized; liver function testing abnormalities do not necessitate dose
    adjustment or anti-Xa monitoring. Dose adjustment and anti-Xa monitoring are indicated in

    patients with a weight exceeding 100 kg, but at weights below that standard dosing is appropriate and
    anti-Xa monitoring is not necessary, independent of body mass index.

    While the use of chronic warfarin causes concern for the possibility of increased bleeding risk in the
    setting of enoxaparin, it does not affect dosing or the role of anti-Xa monitoring. Management of
    enoxaparin in the cardiac catheterization laboratory is based on the time from the last dose

    administered, not anti-Xa level.

    95. A 79-year-old man presents to his local community hospital with substernal chest pain lasting 3
    hours. His resting electrocardiogram (ECG) shows 3 mm ST elevation across the anterior

    precordium with presence of QS complexes in V1-V4. His resting heart rate is 96 bpm, and his blood
    pressure in the right upper limb in the supine position is 100/70 mm Hg.

    Physical examination reveals an apical third heart sound, a soft systolic murmur in the aortic area that
    increases with expiration, and crepitations in bilateral lung bases. His respiratory rate is 20

    breaths/minute, and a pulse oximetry on room air is 92%. The emergency department physician

    activates the catheterization laboratory planning for primary percutaneous coronary intervention

    (PCI) and places a nasal cannula delivering oxygen at 4 L/min.

    Which of the following medical interventions is the most appropriate?

    a. Reteplase.

    b. Diltiazem.

    c. Enalaprilat.

    d. Isosorbide.

    e. Furosemide.
    95. e.
    Furosemide.
    The use of intravenous (IV) enalaprilat in the CONSENSUS 2 trials was not associated with a

    mortality benefit. This lack of benefit was attributed to hypotension in the early postreperfusion
    setting. The borderline blood pressure, high resting heart rate, and evidence of pulmonary

    congestion in this elderly patient with an extensive anterior myocardial infarction (MI) on ECG are
    likely due to a significant acute decrease in stroke volume.

    Treatment with IV beta-blockade as noted in the COMMIT 2 trial increases the risk of precipitating
    cardiogenic shock in this setting and should be avoided. The dosage of unfractionated IV heparin in
    the setting of ST elevation MI should be weight-adjusted with a bolus dose of 60 U/kg not to

    exceed 4000 U, and an infusion rate of 12 U/kg not to exceed 1000 U/h.

    96. A 78-year-old woman presents with resting chest pain and anterior T-wave inversions on

    electrocardiogram (ECG). Her cardiac enzymes are normal. She has no cardiac history, no history of
    diabetes, and no known allergies. She is treated with aspirin and subcutaneous enoxaparin and

    remains chest pain free. However, 6 hours after admission, she develops massive hematemesis.

    Which of the following is the next best step in her management?

    a. Fresh frozen plasma (FFP).

    b. Cryoprecipitate.

    c. Protamine.

    d. Lepirudin.

    96. c.
    Protamine.
    Although protamine incompletely reverses the effect of enoxaparin on factor Xa, it does reverse its
    effect on thrombin (factor IIa), and as such, is indicated for patients with bleeding complications due
    to enoxaparin. Adverse reactions to protamine can be seen among patients who are allergic to

    fish or who have received pork insulin. Cryoprecipitate and FFP do not reverse the effects of

    indirect thrombin inhibitors such as heparins. A direct thrombin inhibitor, such as lepirudin, is
    contraindicated in the presence of active bleeding.

    97. A 52-year-old man develops intermittent chest pain while on a business trip and presents to

    the emergency department for evaluation. He does not have diabetes and is a nonsmoker. His

    outpatient medical regimen includes atorvastatin 40 mg, and lisinopril 20 mg daily. His exam is

    normal. His electrocardiogram (ECG) shows nonspecific flattening of the T waves in the lateral

    leads, and serial cardiac enzymes are normal. He is treated with aspirin and unfractionated heparin
    for 24 hours and his chest pain has not recurred. He is anxious to return home and asks if he can catch
    his flight later that afternoon.

    Which of the following is most appropriate for the care of this patient?

    a. Exercise treadmill test.

    b. Coronary angiography.

    c. No further testing prior to travel.

    d. Heparin for additional 24 hours.

    97. a.

    Exercise treadmill test.

    The patient presents with a symptom complex consistent with possible unstable angina. However,

    there are no objective signs of ischemia, the clinical presentation is low risk given his young age, his
    cardiac enzymes are normal, and there is an absence of diagnostic ECG changes. In low-risk

    patients, an initial conservative (ischemia-guided) approach is reasonable in which the patient is


    treated medically and undergoes risk stratification prior to discharge. Although 48-72 hours of

    medical therapy prior to stress testing is recommended when definite acute coronary syndrome

    (ACS) is present, stress testing can be performed safely earlier in low-risk patients with possible
    ACS, and exercise stress testing provides a prudent solution that meets the wishes of the patient and
    avoids excessive testing. Exercise stress testing prior to discharge would be recommended

    because the patient has planned air travel.

    98. A 60-year-old woman with atypical chest pain undergoes a treadmill stress test. The stress

    test findings are:

     Heart rate response: 64-127 bpm

     Blood pressure (BP) response: 132/66 to 174/80 mm Hg

     Symptoms: Mild fatigue at peak

     Electrocardiogram (ECG): 2 mm of horizontal ST-segment depression in leads V5-V6 at peak

    exercise

     Exercise duration: 3.0 minutes on Bruce protocol

     Perfusion images: Reversible apical ischemia

    Otherwise, it was a normal study.

    Which of the following findings best correlate with a highest risk for cardiac death?

    a. Perfusion ischemia.

    b. Poor functional capacity.

    c. Hypertensive BP response.

    d. Heart rate response.

    e. ECG ischemia with 2 mm ST-segment depression.

    98. b.
    Poor functional capacity.
    Poor functional capacity is the best predictor of cardiac death. Perfusion images or ECG ischemia
    predict ischemic events, but are less predictive of death than exercise duration. Neither her heart rate
    response nor BP response is particularly concerning.

    99. A 65-year-old woman with a history of coronary artery disease is admitted with a 3-day

    history of chest pain, nausea, and vomiting. Her electrocardiogram shows ST elevation in inferior
    leads. She is taken to the cardiac catheterization laboratory and undergoes percutaneous coronary
    intervention of the right coronary artery. In the cardiac care unit, she is somnolent, and her blood
    pressure is 88/60 mm Hg, heart rate is 92 bpm, and oxygen saturation is 96% on room air. Jugular

    venous pressure is 10 cm H2O. Lung fields are clear, and cardiovascular examination has normal

    S1and S2 without murmurs appreciated. Extremities are cool.

    Which of the following is the most likely diagnosis?

    a. Papillary muscle rupture.

    b. Ventricular septal defect (VSD).

    c. Free wall rupture.

    d. Right ventricular (RV) infarct.

    e. Pulmonary embolism.

    99. d.

    Right ventricular (RV) infarct.

    The patient has signs of RV involvement in her inferior myocardial infarction (MI) with hypotension
    and evidence of poor perfusion. With hypotension and inferior MI, clinical suspicion of RV

    involvement should be high. While other etiologies of her hypotension could include over-sedation,
    bleeding, and cardiogenic shock, management is quite different for an RV infarct and needs to be

    identified early.

    Papillary muscle rupture and VSD are later mechanical complications of MIs. A post-MI VSD may be

    accompanied by a thrill along the left sternal edge in 90% of cases, and the murmur would be

    holosystolic. Free wall rupture is more common in anterior MIs and is more commonly seen in first
    presentation of coronary disease and in elderly women. Pulmonary embolism is less likely given her
    normal oxygen saturation.
    100. A 58-year-old man presents to a community hospital 90 minutes from the nearest cardiac

    catheterization laboratory with 2 hours of substernal chest pain. He is noted on electrocardiogram to


    have marked ST elevation in leads V1-V5, with reciprocal ST depression in the inferior leads,

    consistent with an evolving anterior ST-segment elevation myocardial infarction (STEMI).

    Two years previously, he underwent an aortic valve replacement with a St. Jude mechanical

    prosthesis, due to chronic aortic insufficiency. Prior to the aortic valve replacement, his coronary
    angiogram revealed a 30% stenosis in the proximal left anterior descending coronary artery, which
    was not bypassed. He is taking warfarin, and 3 days ago his international normalized ratio (INR) was
    3.2.

    Which of the following is the most appropriate treatment in this patient's care?

    a. Aspirin, clopidogrel, intravenous unfractionated heparin, and tenecteplase.

    b. Aspirin, clopidogrel, half-dose tenecteplase, followed by transfer for PCI.

    c. Aspirin, clopidogrel, and transfer for primary percutaneous coronary intervention (PCI).

    d. Aspirin plus tirofiban.

    100. c. Aspirin, clopidogrel, and transfer for primary percutaneous coronary intervention (PCI).

    Transfer to a primary PCI-capable facility is indicated if first medical contact to device time is <120

    minutes, as in this case. Transfer should also be considered for those at high risk of bleed or signs of
    shock. His risk for bleeding is higher with thrombolytics given his chronic anticoagulation. Even if
    there was a time delay for primary PCI, one might consider transfer since bleeding risk increases
    with a higher INR and thrombolytics. Aspirin plus tirofiban is not definitive reperfusion. Facilitated
    PCI has not been demonstrated to improve outcomes.

    101. An 82-year-old man presents with a non-ST elevation myocardial infarction, complicated by

    congestive heart failure. His initial laboratory values are notable for a serum creatinine of 3.0

    mg/dl, a creatine kinase-myocardial band of 147 mg/dl, and a cardiac troponin I of 23 mg/dl. He is
    treated with aspirin, heparin, and eptifibatide and undergoes cardiac catheterization on hospital Day 2.
    He has successful percutaneous transluminal coronary angioplasty and stenting of a 90%

    stenosis in the proximal left anterior descending artery, and initially does well.

    After the procedure, unfractionated heparin was discontinued, and the patient was maintained on

    aspirin and a tirofiban infusion, which finished 1 hour ago. Sheaths were successfully removed soon
    after the procedure. Later that evening, he is noted to be confused and agitated. On examination, his
    heart rate is 116 bpm, blood pressure 88/58 mm Hg, and respirations are 20 breaths/minute.
    His peripheral pulses are intact, and there is no groin hematoma. His electrocardiogram (ECG) is

    unchanged.

    In addition to intravenous saline, which of the following is the next best step in his care?

    a. Urgent repeat coronary angiography.

    b. Abdominal/pelvic computed tomography.

    c. Platelet transfusion.

    d. Intravenous Solu-Medrol.

    101. b.

    Abdominal/pelvic computed tomography.

    The most likely diagnosis is retroperitoneal hemorrhage, as a complication of cardiac

    catheterization and antiplatelet therapy. Importantly, the patient has a significant renal

    dysfunction, which will potentiate the antiplatelet effects of tirofiban. Since tirofiban and

    eptifibatide are reversible inhibitors of the glycoprotein IIb/IIIa receptor and have a short half-life,
    platelet infusions are rarely necessary or helpful in patients receiving these agents.

    In contrast, abciximab binds avidly to the receptor and thus has a very prolonged effect on platelet
    aggregation (despite low free abciximab levels). Thus, platelet transfusions may be considered in
    patients with bleeding complications following abciximab administration. The presentation is not

    consistent with allergic reaction, therefore, steroids are not indicated. Repeat ECG is unchanged,
    therefore a repeat catheterization is not indicated.

    102. A 54-year-old man is brought to the emergency department (ED) by his coworker with acute-
    onset dyspnea and syncope. He lost consciousness at work for approximately 15 seconds, but was

    spontaneously revived after falling to the floor. His medical history includes hypertension, active
    smoking, diabetes, and chronic kidney disease. He took an aspirin while on route to the ED.

    His heart rate is 92 bpm and regular, blood pressure is 156/88 mm Hg, and respiration rate is 24

    breaths/minute. Jugular venous pressure is normal, lung fields have scant bibasilar crackles, and he
    has no cardiac murmur. Initial cardiac enzymes are negative, blood urea nitrogen is 42, and

    creatinine is 2.6 mg/dl. Electrocardiography shows normal sinus rhythm with 2-4 mm ST elevation

    in V2-V4. Symptoms began 45 minutes before arrival. In traffic, the nearest percutaneous coronary
    intervention (PCI)-capable facility is 2.5 hours away at this time of day. Helicopter transport is not
    available due to ocean fog.

    Which of the following treatment strategies would you choose prior to transfer?

    a. Tirofiban, half-dose tenecteplase, IV UFH, aspirin.

    b. Full-dose tenecteplase, intravenous (IV) unfractionated heparin (UFH), aspirin, clopidogrel.

    c. IV UFH, aspirin, clopidogrel.

    d. Abciximab, half-dose tenecteplase, IV UFH, aspirin.

    e. Full-dose tenecteplase, IV low molecular weight heparin (LMWH), aspirin, clopidogrel.

    b.

    Full-dose tenecteplase, intravenous (IV) unfractionated heparin (UFH), aspirin,


    clopidogrel.
    Given the time constraints associated with transfer for primary PCI (i.e., first medical contact to
    device time >120 minutes), full-dose lytic therapy with transfer is the single best choice (Class I). IV

    UFH is preferred over LMWH in the setting of renal insufficiency of this magnitude. Combination

    reperfusion therapy with abciximab and half-dose tenecteplase is not recommended by the current

    ST-segment elevation myocardial infarction (STEMI) guideline. The use of heparin, aspirin, and

    clopidogrel alone is not appropriate for treatment of a STEMI.

    103. A 74-year-old man presents with pain in the toes of his right foot. The pain is most severe at
    night when he is in bed, such that he often sits up and dangles his foot over the side of the bed for
    relief.

    On examination, there is a fissure at the tip of the right great toe that is tender to touch. There is mild
    bilateral ankle edema. The dorsalis pedis and posterior tibial pulses are not palpable in either foot.

    Which the following diagnostic tests should be performed to determine appropriate treatment for

    this patient?

    a. Magnetic resonance (MR) angiogram.

    b. Venous duplex ultrasound.

    c. Foot X-ray.

    d. Computed tomography (CT) angiogram.

    103. a.

    Magnetic resonance (MR) angiogram.

    This patient presents with symptoms and findings of peripheral arterial disease (PAD). Ischemic

    pain in the right foot is exacerbated when he is in bed, so he dangles the foot to improve perfusion
    pressure (via gravitational effects) and reduce his pain. The finding of a skin lesion is consistent with
    severe ischemia. The ankle swelling reflects the prolonged periods of putting his feet in a

    dependent position; it is not a consequence of venous thrombosis. Therefore, a venous ultrasound

    examination is not required.

    A foot X-ray might useful to detect osteomyelitis, but these are not diagnostic for PAD. An

    arteriogram is indicated to define his vascular anatomy and plan a revascularization procedure. MR
    imaging is preferred (Class I, Level of Evidence A) versus CT angiogram (Class IIb, Level of
    Evidence B) to diagnose the anatomic location of the lesion.

    104. A 24-year-old woman with mixed connective tissue disease is admitted with weakness and

    dizziness. Her blood pressure is 105/70 mm Hg, neck veins are elevated, chest is clear, cardiac exam
    is normal, and there is no edema. She is referred to the cardiac catheterization laboratory. An intra-
    arterial catheter yields the pressure tracing shown in Figure 1.

    Which of the following hemodynamic abnormalities is demonstrated?

    a. Pulsus parvus et tardus.

    b. Pulsus paradoxus.

    c. Wide pulse pressure.

    d. Pulsus alternans.

    104. b.
    Pulsus paradoxus.
    There is marked (>10 mm Hg) variation in the systolic arterial pressure. This finding indicates
    exaggerated variation in systolic arterial pressure with the respiratory cycle, and is known as pulsus
    paradoxus.

    Pulsus parvus et tardus, a low pulse pressure with a slow upstroke, is observed in severe aortic

    stenosis. Pulsus alternans, in which there are alternating strong and weak beats with alternating higher
    and lower systolic arterial pressure, is seen in severe left ventricular systolic dysfunction. A wide
    pulse pressure is observed in aortic regurgitation.

    105. A 78-year-old woman with an anterior ST-segment elevation myocardial infarction (STEMI) is

    treated with fibrinolysis, low molecular weight heparin (LMWH), aspirin, and clopidogrel, beginning
    42 minutes after onset of pain. She is transported to the nearest percutaneous coronary

    intervention center. Two hours later, she develops severe headache and is less responsive. A head
    computed tomography scan shows a right frontal lobe hemorrhage.

    In addition to neurosurgical consultation, which of the following treatments would you

    recommend?

    a. Epsilon aminocaproic acid.

    b. Platelet transfusion.

    c. Aprotinin.

    d. Vitamin K.

    e. Desmopressin acetate (DDAVP).

    105. b.
    Platelet transfusion.
    This woman has suffered a fibrinolytic-related intracranial hemorrhage. Risk factors for bleeding
    after thrombolytics include age, sex, small body size, and wide pulse pressure, in addition to the
    particular agent used.

    Recommended treatments include:

    Cessation of fibrinolytic, antithrombin, and antiplatelet therapies

    Protamine to reverse the effects of heparin or LMWH

    Fresh frozen plasma to provide clotting factors V and VIII

    Prothrombin complex concentrate to provide additional clotting factors

    Platelets

    Elevation of the head of the bed, hyperventilation, mannitol, and neurosurgical evacuation if

    indicated

    The other choices listed are not recommended. DDAVP is not indicated in the treatment of

    bleeding after thrombolytics. Aprotinin, an antifibrinolytic agent, was withdrawn from the US

    market in May 2008 due to adverse findings in a study of patients undergoing cardiac surgery.

    Epsilon aminocaproic acid is not approved for this indication. Vitamin K is used for reversal of

    bleeding related to vitamin K antagonists such as warfarin.

    106. A 62-year-old woman is admitted with progressive angina, ST depression in leads V4-V6, and a
    cardiac troponin value that peaks at twice the upper reference limit. Invasive therapy is

    recommended, but declined by the patient. She stabilizes after treatment with intravenous
    heparin, aspirin 81 mg, atorvastatin 80 mg, and metoprolol 25 mg bid. At the time of discharge, she is
    chest-pain free while walking around the unit. Her echocardiogram demonstrates normal left

    ventricular function.

    Which of the following do you recommend for medical therapy, in addition to the medications

    listed above?

    a. Cilostazol 100 mg twice daily for 30 days.

    b. Enoxaparin 1.0 mg/kg twice daily for 14 days.

    c. Ticagrelor 90 mg BID for 14 days.

    d. Clopidogrel 75 mg daily for 1 year.

    e. Prasugrel 10 mg daily for 14 days.

    106. c.

    Ticagrelor 90 mg BID for 14 days.

    For patients with unstable angina/non-ST-segment elevation myocardial infarction (NSTEMI) for

    whom a conservative strategy is chosen, aspirin (75-162 mg) is continued indefinitely (Class I).

    Antithrombin therapy with either unfractionated heparin, enoxaparin, or fondaparinux can be

    given for the duration of hospitalization or up to 8 days (Class I). Based on the CURE trial, the
    unstable angina/NSTEMI clinical practice guideline recommends clopidogrel 75 mg daily for at least
    30 days and ideally for up to 1 year after presentation (Class I).

    Cilostazol has been used as an alternative to thienopyridine therapy in allergic patients after

    percutaneous coronary intervention, but has not been studied in this setting. Prasugrel has not

    been studied in a conservative management strategy. Ticagrelor is an option for conservative

    management therapy, but the duration should be for 1 year. Enoxaparin might be used, but not for

    14 days.

    107. A 62-year-old man with diabetes and dyslipidemia is hospitalized with recurrent angina 4

    months after percutaneous coronary intervention (PCI) with deployment of a bare-metal stent for

    treatment of a 90% mid left anterior descending stenosis. During his previous admission, he

    developed a deep vein thrombosis and was treated with intravenous unfractionated heparin. His
    platelet count fell from 223,000 to 62,000, and a platelet factor (PF4) assay at time of discharge was
    positive. He was discharged on warfarin, aspirin, clopidogrel, atorvastatin, and metoprolol.

    He was readmitted with chest pain and ST-segment depression 3 months later. His hepatic function

    and cardiac enzymes are normal, but he has stage III kidney disease. His pain resolves and his

    electrocardiogram normalizes after 2 hours.

    A repeat cardiac catheterization reveals a 70% in-stent stenosis.

    Which of the following medications would you consider for adjunctive therapy at the time of

    repeat PCI?

    a. Unfractionated heparin.

    b. Bivalirudin.

    c. Fondaparinux.

    d. Enoxaparin plus a glycoprotein IIb/IIIa receptor antagonist.

    107. b.
    Bivalirudin.
    This man developed heparin-immune thrombocytopenia during his first admission. Unfractionated

    heparin and low molecular weight heparin are contraindicated in this situation. Upstream use of

    fondaparinux has been associated with higher rates of catheter thrombus at time of PCI,

    necessitating the use of heparin.

    108. Which of the following is the correct order of events in the ischemic cascade?

    a. ECG changes, perfusion defects, systolic dysfunction, diastolic dysfunction, chest pain.

    b. Diastolic dysfunction, perfusion defects, ECG changes, chest pain, systolic dysfunction.

    c. Perfusion defects, diastolic dysfunction, systolic dysfunction, electrocardiogram

    (ECG) changes, chest pain.

    d. Perfusion defects, diastolic dysfunction, systolic dysfunction, chest pain, ECG changes.

    e. Diastolic dysfunction, systolic dysfunction, perfusion defects, chest pain, ECG changes.

    108. c. Perfusion defects, diastolic dysfunction, systolic dysfunction, electrocardiogram (ECG)


    changes, chest pain.

    Understanding the order of events that occur in the ischemic cascade is important in understanding
    how stress testing can detect subclinical disease. Single-photon emission computed tomography

    (SPECT) myocardial perfusion imaging (MPI) unmasks exercise- or pharmacologic-induced

    differences in perfusion, revealing subtle patterns of perfusion defects and early atherosclerotic
    disease. This explains why nuclear perfusion-based techniques, which typically detect abnormalities
    in coronary flow reserve even in the absence of ischemia, are more sensitive than contractile

    dysfunction-dependent techniques, like stress or dobutamine echocardiography, which require

    subendocardial ischemia to be abnormal. ECG changes and chest pain are relatively late

    presentations of ischemia, which explains why the sensitivities of coronary artery disease detection
    are lower than with imaging techniques.

    109. A 60-year-old man underwent bare-metal stenting of a discrete left anterior descending

    artery lesion after non-ST-segment elevation myocardial infarction and was placed on aspirin and

    clopidogrel. One week after the procedure, he presents with a lower gastrointestinal bleed and is
    found to have a previously undetected colon cancer that requires resection. Because of the
    extensive surgical exploration that is anticipated, the surgeon requests that the clopidogrel be

    stopped prior to surgery.

    Which of the following is the most appropriate length of clopidogrel therapy in this setting?

    a. 9 months.

    b. 12 months.

    c. 1 week.

    d. 6 months.

    e. 4 weeks.

    109. e.
    4 weeks.
    The issue in this clinical situation is a tension between stent thrombosis, which is reduced by dual
    antiplatelet therapy, versus periprocedural bleeding, which is accentuated with antiplatelet

    therapy. For truly elective yet major surgery, studies suggest that waiting for 4-6 weeks after bare-
    metal stenting allows the coronary stent to endothelialize so that perioperative stent thrombosis off
    dual antiplatelet drugs is rare. Operating on dual antiplatelet therapy would expose the patient to
    unacceptable bleeding risk. To stop clopidogrel now would increase the risk of stent thrombosis.

    Heparin has not been shown to reduce the risk of early stent thrombosis. The risk of waiting 6

    months to resect the colon cancer outweighs the benefits of 6 months of dual antiplatelet therapy.

    110. In a patient with hypertrophic obstructive cardiomyopathy, which of the following

    combinations is true of the post-extrasystolic beat?

    a. The gradient increases and the pulse pressure decreases.

    b. The gradient and pulse pressure both decrease.

    c. The gradient decreases and the pulse pressure increases.

    d. The gradient and pulse pressure both increase.

    110. a.

    The gradient increases and the pulse pressure decreases.

    This is the Brockenbrough sign. The decrease in pulse pressure following a premature ventricular

    contraction is caused by a reduced stroke volume that results from increased dynamic obstruction, as
    evidenced by an increase in the gradient.

    111. A 56-year-old woman presents for evaluation of 8 months of shortness of breath. Her exam

    shows blood pressure 150/80 mm Hg, heart rate 78 bpm, and her body mass index is 40 kg/m2.

    Jugular venous pressure is mildly elevated with clear lungs. No murmur is heard. She has an

    S4 gallop and trace peripheral edema.

    A transthoracic echocardiogram is performed, but is of limited quality due to body habitus. Her left
    ventricular ejection fraction appears grossly normal. She undergoes right and left heart

    catheterization for further evaluation of her symptoms. There is no significant coronary artery

    disease on angiography. Right heart catheterization shows the following: right atrium 10 mm Hg,
    pulmonary artery 55/25 mm Hg (mean 35), and pulmonary capillary wedge pressure 23 mm Hg

    with prominent V waves.

    Which of the following is the most likely cause of her symptoms?

    a. Precapillary pulmonary hypertension.

    b. Mitral regurgitation.

    c. Obesity.

    d. Heart failure with preserved ejection fraction (HFpEF).

    111. d.

    Heart failure with preserved ejection fraction (HFpEF).

    The hemodynamics shown are consistent elevated filling pressures in a noncompliant left atrium.

    This constellation of symptoms and hemodynamic findings are most compatible with HFpEF.

    Mitral regurgitation would be expected to be associated with a systolic murmur in most cases.

    While obesity may be a cause of her symptoms, it would not necessarily explain the

    hemodynamics. Precapillary pulmonary hypertension would result in a significant transpulmonary

    gradient that is not present here.


    112. A 44-year-old woman is in the coronary care unit following presentation with an inferior

    myocardial infarction. She was treated with primary angioplasty and stenting to a lone proximal

    right coronary artery (RCA) stenosis.

    Upon returning to the coronary care unit, she develops mild palpitations. She has no further chest
    discomfort. Her blood pressure is 110/70 mm Hg and heart rate is 90 bpm. The 12-lead

    electrocardiogram is shown in Figure 1.

    Which of the following is the best management for this rhythm?

    a. Atropine.

    b. Synchronized direct current cardioversion.

    c. No therapy required.

    d. Repeat percutaneous coronary intervention (PCI).


    e. Lidocaine.

    112. c.
    No therapy required.
    The rhythm strip shows a sinus beat with inferior Q waves followed by an accelerated

    idioventricular rhythm. In the context of PCI to the RCA, this represents a reperfusion rhythm; this is
    self-limiting and does not require treatment.

    113. A 17-year-old is referred by his pediatric cardiologist for advanced cardiovascular imaging
    after a classic tetralogy of Fallot repair at the age of 2 months. His exercise tolerance is normal, and
    he is not cyanotic. An echocardiogram reveals right ventricular enlargement and pulmonic

    regurgitation.

    Which of the following is most appropriate at this time to further assess the status of his congenital
    heart disease?

    a. Radionuclide angiography.

    b. Computed tomographic angiography.

    c. Magnetic resonance imaging (MRI).

    d. Transesophageal echocardiography.

    e. Right-heart catheterization.

    113. c.

    Magnetic resonance imaging (MRI).

    Cardiac MRI is the only test that can provide all the components needed to quantify all the

    parameters necessary, including right ventricular and right atrial volumes, valvular regurgitation, and
    residual shunting. The right ventricular structures are difficult to quantify by echocardiography, and
    computed tomography does not provide dynamic flow information. Right-heart catheterization

    will not provide volumes or accurate quantification of valvular regurgitation.


    114. A 25-year-old college basketball player is referred to see you due to an abnormal screening
    electrocardiogram (ECG) obtained during basketball practice (Figure 1). He has no complaints, has a
    normal physical examination, and has no family history of arrhythmias or sudden death.

    Which of the following is the next most appropriate step in his management?

    a. Repeat electrocardiogram (ECG).

    b. Cardiac catheterization.

    c. Echocardiogram.

    d. Stress test.

    e. Holter monitor.

    114. a.

    Repeat electrocardiogram (ECG).

    This ECG is normal except for limb lead reversal. This can be seen by the negative P wave QRS
    complex and T wave in lead I, as well as a total lack of voltage in lead II. It can be repeated with the
    limb leads correctly placed to document the lack of underlying pathology. Other imaging or

    diagnostic studies are not indicated in an asymptomatic patient with an otherwise normal ECG

    without a family history of arrhythmias or premature death.

    115. Which of the following patients has the highest probability of coronary artery disease (CAD)?

    a. A 65-year-old woman with atypical angina and a positive exercise ECG.

    b. A 65-year-old man with typical angina and a negative exercise electrocardiogram (ECG).

    c. A 45-year-old man with atypical angina and a positive exercise ECG.

    d. A 45-year-old woman with typical angina and a positive exercise ECG.

    115. b. A 65-year-old man with typical angina and a negative exercise electrocardiogram (ECG).

    According to the Bayes Theorem, the post-test probability that a patient has CAD depends on both

    the pretest probability of the patient having CAD, and the results of the exercise test (Figure 1).

    Pretest probability of CAD depends on age, sex, and character of chest pain, and can be determined
    for an individual patient from published tables.

    For patients at the extreme (low <10%, high >90%), the results of the exercise test shift post-test
    probability of CAD very little (<10%). The 45-year-old man with atypical angina and a positive
    exercise ECG, still has a post-test probability of CAD that exceeds 85-90%, because pretest

    probability is so high. This patient has a pretest probability of CAD that exceeds 90%.

    The other patients described all have a pretest probability of CAD of approximately 50%. A positive
    exercise test shifts their post-test probability to approximately 75-80%.
    (Figure 1)

    116. A 48-year-old African American man presents to your office with palpitations. He is otherwise
    healthy and has no other complaints. His physical examination is unremarkable. His

    electrocardiogram shows sinus rhythm with a PR interval of 230 msec. On Holter evaluation, he has
    6,000 multifocal premature ventricular contractions (PVCs) over a 24-hour period. Transthoracic

    echocardiography reveals normal biventricular function without valvular abnormalities.

    Which of the following is the next best step in his care?

    a. Left-heart catheterization.

    b. Cardiac computed tomographic angiography.

    c. Cardiac magnetic resonance imaging (MRI).

    d. Single-photon emission computed tomography (SPECT) myocardial perfusion imaging (MPI).

    e. Transesophageal echocardiography.
    116. c.

    Cardiac magnetic resonance imaging (MRI).

    This patient's clinical presentation is most consistent with sarcoidosis. Given his race, high PVC

    burden, and conduction system disease, excluding this diagnosis is essential. Cardiac MRI and

    fluorodeoxyglucose (FDG) PET are two modalities that can help establish the diagnosis of sarcoid.

    He has no cardiovascular symptoms of ischemia. Thus, cardiac catheterization and SPECT MPI are

    not indicated. Transesophageal echocardiography will not add additional information.

    117. A 75-year-old woman was admitted 4 days after the onset of substernal chest pain. The patient is
    an active smoker and has a history of high cholesterol, hypertension, and diabetes. On admission, she
    was free of chest and epigastric pain and had a blood pressure of 142/70 mm Hg with a heart rate of
    89 bpm.

    Laboratory testing revealed that the troponin I was elevated at 20 ng/ml and the creatine kinase-
    myocardial band was within normal limits. The patient's electrocardiogram had Q waves in leads II,
    III, and aVF and there were no other ischemic changes. Diagnostic angiography demonstrated an
    occluded right coronary artery (RCA), nonobstructive left anterior descending artery disease, and a
    70% proximal left circumflex artery.

    The patient was managed conservatively and medical therapy was implemented. Two days later in the
    cardiac telemetry unit, the patient became acutely hypoxic, hypotensive, and required intubation. On
    examination, she appears acutely ill with bilateral rales and a loud systolic murmur is present, which
    was not heard on admission.

    Her blood pressure is 85/60 mm Hg and her heart rate is 110 bpm. An echocardiogram reveals an
    acute ventricular septal defect (VSD). An intra-aortic balloon pump is placed and her hemodynamics
    stabilize.

    Which of the following is the next appropriate management step?

    a. PCI of the RCA.

    b. Implant a left ventricular assist device (LVAD).

    c. Stabilize for 4 weeks, then cardiovascular surgery.

    d. Urgent surgical VSD repair.

    e. Percutaneous coronary intervention (PCI) of the left circumflex artery.

    117.

    d.
    Urgent surgical VSD repair.
    Post-infarct VSDs typically occur 2-8 days after a myocardial infarction (MI). This is often after a
    first MI. Medical management of post-MI VSDs have very high mortality rates (>90%) and even

    with cardiac surgical or percutaneous repair, the mortality rates are >50%. Patients who survive do
    better with early surgical VSD repair, as the ruptured site can expand abruptly. Percutaneous

    closure is an emerging potential option, but early results suggest that residual shunting persists.

    As device development improves, this may become a viable option. PCI alone would not correct

    the hemodynamic situation, and an LVAD will not address the shunting problem.

    118. A 45-year-old woman presents to the emergency department with 2 weeks of intermittent rest
    substernal chest pain, which she describes as sharp. It is not provoked by exercise and has

    lasted up to 30 minutes. There are no cardiac risk factors, her electrocardiogram (ECG) and cardiac
    enzymes are normal, and she is able to exercise.

    Which of the following is most appropriate in this patient's care?

    a. Coronary angiogram.

    b. Exercise stress echocardiogram.

    c. Cardiac computed tomography (CT) angiography.

    d. Exercise myocardial perfusion imaging.

    e. Exercise stress test.

    118. e.
    Exercise stress test.
    In this low-risk patient with a normal ECG and ability to exercise, exercise stress testing is the most
    appropriate first step. Cardiac CT angiography may be helpful in patients who are at intermediate
    risk. This patient with atypical nonexertional chest pain is low risk. With a baseline normal ECG,
    stress testing with additional imaging should be reserved for equivocal exercise stress testing

    results, inability to exercise, or high-risk exercise features.

    119. An 89-year-old woman residing at a nursing home comes to the emergency department of your
    hospital with a 24-hour history of dyspnea and confusion. The patient has significant dementia, as
    well as hypertension, heart failure with preserved ejection fraction, and insulin-dependent diabetes.
    She is agitated and disoriented, and unable to answer questions.

    Her electrocardiogram demonstrates a heart rate of 72 bpm, with a normal axis, PR interval of 155
    msec, a narrow QRS complex, and inferior ST elevation. Her troponin T is 1.6 ng/ml and her
    creatinine is 2.8 mg/dl; her creatinine clearance is calculated as 25

    ml/min. She weighs 60 kg.

    Initial treatment and response: Emergency Medical Service has already given the patient 325 mg of
    aspirin. As you are preparing to wheel the patient to the cardiac catheterization laboratory, her
    daughter arrives, who holds medical power of attorney. She tells you that her mother has a Do Not
    Resuscitate, Do Not Intubate (DNR/DNI) document and would not want to undergo a procedure.

    However, she agrees to the administration of fibrinolytic therapy.

    In addition to giving fibrinolytics and aspirin 81 mg qd, which of the following do you recommend
    as additional antiplatelet and anticoagulant therapy?

    a. Give a clopidogrel dose of 75 mg orally, followed by 75 mg daily. Also initiate unfractionated


    heparin with weight-based dosing.

    b. Give a clopidogrel load of 300 mg orally, followed by 75 mg daily. Also initiate enoxaparin 60 mg
    subcutaneously twice daily.

    c. Give a clopidogrel dose of 75 mg orally, followed by 75 mg daily. Also initiate enoxaparin 60 mg


    subcutaneously twice daily.

    d. Give a clopidogrel load of 300 mg orally, followed by 75 mg daily. Also initiate unfractionated
    heparin with weight-based dosing.

    e. Give a prasugrel load of 60 mg orally, followed by 10 mg daily. Also initiate unfractionated


    heparin with weight-based dosing.

    119. a. Give a clopidogrel dose of 75 mg orally, followed by 75 mg daily. Also initiate


    unfractionated heparin with weight-based dosing.
    The correct answer is to give 75 mg of clopidogrel, followed by 75 mg a day, followed by the use of
    unfractionated heparin. In this elderly patient with central nervous system symptoms and renal

    dysfunction, adjunctive antithrombotic therapy is limited following fibrinolytic therapy.

    Prasugrel is not recommended in patients over 75 years of age. Enoxaparin dosing is complex in

    patients with chronic kidney disease and every 24-hour dosing is recommended if creatinine

    clearance is <30 cc/min. In patients over the age of 75 years, no loading dose of clopidogrel should
    be used. Fondaparinux is also contraindicated if the creatinine clearance is <30 cc/min.

    120. A 62-year-old woman presented to the emergency department with 2 hours of crushing
    substernal chest pain. An electrocardiogram obtained demonstrates sinus rhythm at 95 bpm with

    1-2 mm of ST elevation in leads II, III, and aVF. Her medical history is significant for dyslipidemia
    and a possible transient ischemic attack. Her current medications include simvastatin. The patient
    receives aspirin and is taken to the catheterization laboratory.

    Which of the following agents confers the greatest survival advantage?

    a. Prasugrel 60 mg orally.

    b. Enoxaparin 1 mg/kg.

    c. Clopidogrel 600 mg orally.

    d. Intravenous heparin 70 U/kg.

    e. Ticagrelor 180 mg orally.

    120. e.

    Ticagrelor 180 mg orally.

    Either clopidogrel or ticagrelor are Class I recommendations. Prasugrel should be administered

    after the anatomy is known and it is certain that the patient will be undergoing percutaneous

    coronary intervention (PCI). In patients with non-ST-elevation acute coronary syndrome (NSTE-
    ACS) and high-risk features (e.g., elevated troponin) and not adequately pretreated with clopidogrel
    or ticagrelor, it is useful to administer a glycoprotein IIb/IIIa inhibitor (abciximab, double-bolus
    eptifibatide, or high-dose bolus tirofiban) at the time of PCI (Class I).

    Ticagrelor therapy was associated with less cardiovascular mortality than clopidogrel in the PLATO

    trial. Prasugrel therapy was associated with fewer ischemic events than clopidogrel in the TRITON

    trial, but mortality did not differ between treatment groups. Pretreatment with heparin or
    bivalirudin has never been shown to reduce death.

    121. There are multiple centers in Gotham City that perform >500 percutaneous coronary

    interventions (PCIs) per year. Two of these centers spend significant resources advertising their
    expertise in radial access.

    PCI performed via radial access has a demonstrated mortality benefit compared with femoral

    access when performed for which of the following indications?

    a. Non–STEMI.

    b. Assessment of valvular heart disease.

    c. Chronic stable angina.

    d. Unstable angina with negative biomarkers.

    e. ST-segment elevation myocardial infarction (STEMI).

    121. e.

    ST-segment elevation myocardial infarction (STEMI).

    The mortality benefit of radial access PCI has been demonstrated specifically in STEMI. While there
    are multiple other benefits of radial access over femoral access, including greater patient

    satisfaction and lower access site complications such as bleeding, mortality benefit has not been
    demonstrated in the other clinical situations listed.

    122. A thin 62-year-old man is referred by the patient’s family practitioner for preoperative

    assessment of a large (5.8 cm) abdominal aortic aneurysm. He has a medical history of chronic

    obstructive pulmonary disease (COPD) treated with inhalers, a left hemispheric stroke with little
    residual, diabetes requiring insulin, and chronic renal insufficiency. The patient has one-block

    claudication.

    On exam, his vital signs are normal, and he has no evidence of cardiac murmurs, rubs, or gallops.

    Chest examination reveals bilateral wheezes. There is no lower extremity edema. The

    electrocardiogram (ECG) is normal.

    Which of the following would be your next step in this man’s preoperative evaluation?

    a. Dobutamine echocardiography.
    b. Exercise ECG stress testing.

    c. Resting echocardiogram.

    d. No additional studies are indicated.

    e. Pharmacologic stress testing using regadenoson.

    122. a.
    Dobutamine echocardiography.
    A vasodilator study would not be wise in this patient, because there is evidence of wheezes on the lung
    exam.

    Adenosine may induce bronchoconstriction and respiratory compromise by activating the A2B
    and/or

    A3 receptors, resulting in mast cell degranulation, immunoglobulin E, and histamine release.


    Regadenoson is an A2A-receptor agonist, which theoretically does not appreciably agonize A2B
    and/or A3 receptors, but as per the American Society of Nuclear Cardiology imaging guidelines for
    nuclear cardiology procedures, patients with bronchospasm are considered a contraindication to the
    use of regadenoson, because there are inadequate data regarding its safety with active wheezing. In a
    recent publication of 356 patients with asthma or COPD undergoing stress testing with regadenoson,
    however, there was no evidence of severe bronchoconstriction; despite this, the authors still advised
    caution in these patients.

    Exercise ECG stress testing is unlikely to have diagnostic value because the likelihood of achieving
    an adequate heart rate and blood pressure response is low due to his disabling claudication.

    His abdominal aneurysm is considered large. Aneurysm diameter is the most important factor
    predisposing to rupture. Based on this patient’s aneurysm diameter, his annual rate of rupture is 3-
    15%, as per the Joint Council of the American Association for Vascular Surgery and Society for
    Vascular Surgery. This patient should undergo repair of his aneurysm.

    According to the guideline on perioperative cardiovascular evaluation and management of


    noncardiac surgery patients, those with high cardiovascular risks with functional status <4 metabolic
    equivalents should have stress testing if it would alter preoperative management by the identification
    of severe coronary artery disease. A dobutamine echocardiogram is therefore the best available test
    in this situation.

    The patient does not require a resting echocardiogram, as there are no signs of fluid overload and the
    cardiac physical exam is normal. In the absence of history of heart failure or ischemic heart disease,
    there would be no indication for the resting echocardiogram.

    123. A 51-year-old woman is diagnosed with breast cancer. She will undergo a mastectomy with
    adjuvant chemotherapy with doxorubicin hydrochloride. The hospital protocol requires the patient

    to have periodic evaluations of cardiac ejection fraction (EF).

    An echocardiogram is performed and her EF cannot be evaluated despite the use of echo contrast

    due to body habitus. The patient is extremely claustrophobic. The electrocardiogram (ECG) reveals
    criteria for left ventricular (LV) hypertrophy.

    Which of the following is the best imaging alternative in the care of this patient?

    a. A gated single-photon emission CT (SPECT) study.


    b. A radionuclide ventriculography (RVG).

    c. Computed tomography (CT) angiogram.

    d. A 3D echocardiogram.

    e. Cardiac magnetic resonance imaging (MRI).

    123. b.

    A radionuclide ventriculography (RVG).

    As cardiologists, our role is to provide the oncologist with the necessary information to make
    therapeutic decisions. It is up to the oncologist to decide if an alternative to the doxorubicin
    hydrochloride is as effective in this type of malignancy.

    Gated-equilibrium RVG is a procedure in which the patient’s red blood cells (RBCs) are
    radiolabeled and ECG-gated cardiac scintigraphy is obtained. Single or multiple measurements
    of LV and/or right ventricular function are determined. Data are collected from several hundred
    cardiac cycles to generate an image set of the beating heart that is presented as a single,
    composite cardiac cycle. The method provides the clinician with regional and global wall motion,
    cardiac chamber size and morphology, and ventricular systolic and diastolic function, including
    LV and right ventricular EFs. The most common clinical settings in which RVG may be useful
    include: known or suspected coronary artery disease, distinguishing systolic from diastolic
    causes of congestive heart failure, evaluating cardiac function in patients undergoing
    chemotherapy, and assessing ventricular function in patients with valvular disease. There are
    certain potential sources of error for this technique, which include red blood cell labeling
    (certain medications alter the labeling efficiency of the isotope), patient positioning, gating
    errors, and image statistics. Since this technique involves radiation, its use has decreased (but it
    is still a viable alternative to other modalities).

    Cardiac MRI would have been a good alternative, because it is considered a gold standard for
    evaluation of the EF, but the patient is claustrophobic, which is a major limitation of this
    technique.

    LV chamber and mass quantification have been studied extensively using 3D echocardiography.
    This method has been shown to be more accurate and reproducible than 2D, but the accuracy of
    the volume calculations is highly dependent on image quality.

    The patient had a 2D echocardiogram performed, but image quality was poor despite the use of
    echo contrast. A 3D echo would have the same issues.

    The accuracy of EF measurement from gated-SPECT has been validated with respect to a
    variety of radiopharmaceuticals and against a large number of gold standards (MRI, 3D
    multigated acqusition scan, electron beam CT, etc.). EF can be underestimated in patients with
    LV hypertrophy, though, because algorithms are either calibrated for the range of thickness
    most typically encountered in clinical practice or assume a fixed myocardial thickness. The
    reported discrepancy in EF may be up to 4 points.
    This suggests the RVG would provide a more accurate EF determination in this setting.

    124. For a patient with aortic stenosis and 3+ aortic regurgitation (AR), you are asked to provide an
    aortic valve area (AVA) to help decide about surgical intervention.

    The following data are obtained at cardiac catheterization:

     Peak aortic gradient 50 mm Hg

     Mean aortic gradient 36 mm Hg

     Fick cardiac output 3 L/min

     Thermodilution cardiac output 3.2 L/min

    Based just on these data, which of the following is correct regarding the determination of the

    estimated AVA?

    a. It cannot be determined in the catheterization laboratory because of significant AR.

    b. The AVA will be falsely smaller using the Fick cardiac output.

    c. The AVA can be determined using the thermodilution cardiac output.

    d. The AVA can be determined using the Fick cardiac output.

    124. a.

    It cannot be determined in the catheterization laboratory because of significant AR.

    One can estimate the AVA by use of the Hakki equation. It is defined by:

    flow past the valve (L/min) / square root of the mean gradient (mm Hg). The Fick cardiac output

    and the thermodilution cardiac output describe the forward flow through the heart to the

    periphery (actually pulmonary flow, but it should equal systemic flow if no shunt). The flow past the
    aortic valve, though, includes both the forward flow and the regurgitant flow due to the AR,

    and this is what is needed to do the calculations.

    In this case, the estimated AVA would be: 6 L/min / 6 mm Hg or an AVA of 1.0 cm2. Using the Fick

    output, the flow would erroneously be less than actual, resulting in a falsely low AVA.

    125. A 75-year-old man with a medical history of hypertension, hyperlipidemia, diabetes, and a

    remote history of neck injury after a fall, presents to the emergency department with vertigo and
    blurred vision that lasted 20 minutes and resolved spontaneously. His symptoms started
    immediately after turning his head to the right. Physical examination is normal except for a bruit on
    the left side of his neck. Noncontrast computed tomography (CT) of the brain is normal.

    Which of the following is the most appropriate test for this patient?

    a. Dix-Hallpike test.

    b. Carotid Doppler ultrasonography.

    c. Cerebral angiogram.

    d. Head and neck CT angiography (CTA).

    125. d.

    Head and neck CT angiography (CTA).

    The patient’s symptoms are consistent with posterior circulation cerebrovascular syndrome (or

    vertebrobasilar insufficiency). Typical symptoms of posterior circulation ischemia can include

    vertigo, presyncope, syncope, diplopia, blurred vision, perioral numbness, tinnitus, ataxia, or

    bilateral sensory deficits. His symptoms began with turning his head. Posterior circulation ischemia
    can be caused by vessel impingement from the transverse processes in the cervical spine that

    occurs with head movement. Given the patient’s history of neck injury, it is possible that an

    unrecognized neck fracture of the transverse process could have occurred. Vertigo that occurs with
    head movement is typically due to benign paroxysmal positional vertigo and can be assessed using

    the Dix-Hallpike maneuver. However, blurred vision is unlikely to occur with benign paroxysmal

    positional vertigo, thus the response Dix-Hallpike test is incorrect.

    Despite having a left carotid bruit, the patient's symptoms are not consistent with anterior

    circulation ischemia. For vertebral artery disease, the sensitivity and specificity of CTA or magnetic
    resonance angiography is 94% and 95%, respectively, and significantly better than carotid Doppler
    ultrasonography (sensitivity = 70%). Therefore, carotid Doppler ultrasonography is incorrect.

    Cerebral angiography should be reserved for patients that require revascularization based on

    noninvasive imaging. Thus, cerebral angiogram is incorrect. CTA is the correct answer.

    126. You are the preceptor of a cardiology clinic in a university hospital setting. One of the

    residents is evaluating a middle-aged woman with intermediate risk for having coronary artery

    disease and an abnormal resting electrocardiogram (ECG). She has poor echocardiographic
    windows and requires a nuclear stress test.

    Which of the following protocols results in the LEAST radiation exposure to the patient?

    a. One-day rest/stress with technetium-99m.

    b. Stress only with technetium-99m.

    c. Dual isotope (thallium and technetium).

    d. PET scan using rubidium-82.

    e. A positron emission tomography (PET) scan with fluorodeoxyglucose (FDG) and ammonia.

    126. e. A positron emission tomography (PET) scan with fluorodeoxyglucose (FDG) and
    ammonia.

    Ammonia-13 (N-13) is a blood flow tracer and has a half-life of 10 minutes. It is generated in a
    cyclotron and the average effective dose resulting from one of these studies is 2 mSv, making this
    stress protocol the correct answer. The dosimetry is relatively low due to the short half-life of N-13
    and the low energy of the emitted positrons: 1.48 mSv in 20 mCi (usually cardiac studies utilize 10-20
    mCi/study). The 1-day rest/stress protocol with technetium is linked to an average effective dose of
    about 12 mSv. This protocol is one of the most frequently used protocols in single-positron emission
    computed tomography (SPECT).

    Rubidium-82 is a perfusion isotope used in PET. The half-life is 75 seconds and is produced in a
    generator. The average effective dose generated by this protocol (rest/stress) is about 15 mSv. In an
    average study, 1.75-7.5 mSv in 60 mCi (usually cardiac studies utilize 20-40 mCi/study) is used.

    The purpose of a rest image on a nuclear stress test is to define reversibility of stress-induced
    perfusion abnormalities. In more than 50% of the patients, rest imaging is redundant, and does not
    provide additional diagnostic or prognostic information. The average effective dose obtained from a
    stress-only study using technetium-99m is 9 mSv. The ideal candidate for this study has a low pretest
    probability for coronary artery disease, weighs between 120-250 lbs, and has had a normal stress test
    in the past 3 years. Potential drawbacks include the inability to assess ventricular size and function,
    both at rest and after stress. Transient ischemic dilation will not be seen, but the likelihood is very low
    in patients with normal stress perfusion. There are prognostic and long-term data that suggest that this
    approach is effective. This would be a reasonable alternative in the absence of a PET camera.

    The average effective dose obtained from a dual isotope study is 35 mSv, which is one of the reasons
    (if not the main reason) why this test is rarely used anymore. The half-life of thallium is 73.1 hours
    and the patient is given between 2.5-4 mCi per study in addition to the technetium. Thallium thus
    results in the highest radiation exposure.

    127. During a routine cardiac catheterization procedure, which of the following will DECREASE the
    total X-ray dose produced by the X-ray system during a procedure?

    a. Using magnified views.


    b. Panning over the bony structures compared with the lung fields.

    c. Using angulated views.

    d. Using lower framing rates.

    e. Increasing the source-to-image distance.

    127. d.
    Using lower framing rates.
    Only lowering the acquisition framing rate will help lower the X-ray dose among these scenarios.

    The X-ray exposure equation must be satisfied for each frame imaged, and while the dose per

    frame may be similar, reducing the number of frames per second reduces the overall dose

    delivered during a case.

    X-rays are divergent, and increasing the source-to-image distance results in magnification of the
    image onto the face of the image detector and also loss of X-rays that diverge outside the face of the
    image receptor. Since there are fewer X-rays that strike the image detector due to this loss

    outside, more X-rays are needed to produce a satisfactory image on the detector, and the dose

    necessarily increases.

    Similarly, magnified views are created by using less of the face of the image receptor and, again to
    produce a satisfactory image, more X-rays are needed. Panning over bony structures compared

    with the lung fields also requires more X-rays because of the differences in density of the materials
    and the resultant effect on attenuation of the X-ray beam. Angulated views result in an increase in the
    source-to-image distance and require a greater X-ray dose.

    128. A 68-year-old man (weight 87 kg) with a history of type 2 diabetes, hypertension,

    gastroesophageal reflux disease, and seizure disorder presented to the emergency department

    (ED) with complaints of chest pain and diaphoresis. The patient first noticed the onset of the chest
    pressure the night prior to admission while he was walking on his treadmill. The pain resolved with
    rest and recurred while he was getting dressed on the morning of admission.

    In the ED, laboratory data were notable for a serum creatinine of 1.9 mg/dl and cardiac biomarkers,
    including a troponin T of 0.6 ng/ml and a creatine kinase-myocardial band of 24 U/L. The

    electrocardiogram revealed 1 mm of new ST depression in the inferior leads. Current home

    medications include simvastatin 40 mg daily, lisinopril 10 mg daily, lansoprazole 30 mg daily, and


    phenytoin 300 mg at bedtime. The patient was scheduled for a cardiac catheterization in the

    morning.

    Which of the following medications would preclude the use of ticagrelor therapy in this patient?

    a. Phenytoin.

    b. Lisinopril.
    c. Simvastatin.

    d. Lansoprazole.

    e. Metoprolol.

    128. a.
    Phenytoin.
    Ticagrelor is metabolized by the hepatic cytochrome P450 (CYP) 3A4 enzyme. Based on this (and

    the observation in pharmacokinetic studies of reduced antiplatelet effect when ticagrelor was

    given concomitantly with drugs that induce the CYP 3A4 isoenzyme such as rifampin), the

    manufacturer currently recommends avoiding the use of ticagrelor with strong inducers of the CYP

    3A4 enzyme, including rifampin, phenytoin, carbamazepine, phenobarbital, and dexamethasone.

    129. A 62-year-old financial planner with a history of hypertension, diabetes, and peptic ulcer

    disease comes to your office for evaluation. She describes nausea and abdominal discomfort that

    has been bothering her for several months. She reports that this has been increasingly bothersome to
    her despite frequent use of antacids. She notes some relation to consumption of large meals or at the
    beginning of exercise. It lasts for several minutes then abates spontaneously. She denies

    dyspnea, orthopnea, palpitations, or lightheadedness. She has no other medical conditions.

    On physical exam, there is point tenderness located over the left sternum, but otherwise is normal.

    Her resting electrocardiogram is normal.

    Which of the following options is the most appropriate next step?

    a. Cardiac catheterization.

    b. Reassurance.

    c. Referral for gastrointestinal source of symptoms.

    d. Exercise stress testing.

    e. Echocardiography.

    129. d.
    Exercise stress testing.
    This woman has atypical symptoms, but has several features consistent with ischemic heart disease
    and has risk factors for coronary artery disease. The relation of symptoms to exercise and after

    meals is consistent with angina. While typical angina pain is described as heaviness, squeezing, or
    tightness, atypical symptoms are common in women and the elderly. Nausea and difficult to

    characterize discomfort is common in these groups.

    In the WISE (Women's Ischemic Syndrome Evaluation) study, 65% of women with ischemia

    presented with atypical symptoms. Pain reproduced by palpation is suggestive of a musculoskeletal


    etiology, but does not exclude the possibility of her other symptoms being related to ischemic

    heart disease. She has diabetes, and gastroparesis may be contributing.

    The next appropriate study would be stress testing to assess for coronary artery disease.

    130. A 77-year-old man comes to the office to discuss an upcoming cardiac catheterization

    procedure that will be performed for angina that is refractory to medical therapy. He has

    hypertension, hyperlipidemia, and no other chronic medical conditions. His laboratory tests include
    hemoglobin 12 g/dl, creatinine 1.1 mg/dl, and international normalized ratio (INR) 1.0.

    You tell him the most common complication of cardiac catheterization with coronary angiography

    is which of the following?

    a. Vascular access complication.

    b. Anaphylactoid reaction to contrast agent.

    c. Stroke.

    d. Myocardial infarction.

    e. Acute renal failure.

    130. a.
    Vascular access complication.
    Myocardial infarction, stroke, and death are infrequent complications with a frequency of <0.1%.

    More common complications are tachy- or bradyarrhythmias, acute renal failure, and vascular

    complications. Vascular access site bleeding is the most common complication of cardiac

    catheterization, occurring in 1.5-2.0% of patients. The Registry of the Society for Cardiac

    Angiography and Interventions reported 519 major contrast media complications (0.23%) with four

    deaths (1 in 55,000) in 222,553 patients undergoing selective coronary cineangiography.

    While the radial approach has gained wider acceptance and has fewer bleeding complications

    compared with the femoral approach, the incidence of radial artery occlusion is approximately 1-

    4%, but this is generally asymptomatic. Although major access site complications are rare,

    atrioventricular fistula, nerve injury, radial artery dissection and perforation, hematomas, and

    pseudoaneurysm still occur with the radial approach at a rate that exceeds the other listed

    complications.

    131. An 82-year-old man with diabetes, hypertension, hyperlipidemia, and stable angina comes to

    your office for routine follow-up. He has no change in his angina pattern. He plays tennis 3 times per
    week with no symptoms. His blood pressure is 140/95 mm Hg and heart rate is 67 bpm. His

    glycated hemoglobin is 7%. Urinalysis shows 1+ proteinuria. He is currently only on metoprolol 25

    mg bid, atorvastatin 20 mg, and aspirin 81 mg.

    Which of the following should be initiated?

    a. Sliding scale insulin.

    b. Metformin 500 mg daily.

    c. Lisinopril 5 mg daily.

    d. Hydrochlorothiazide 12.5 mg daily.

    e. Clopidogrel 75 mg daily.

    131. c.
    Lisinopril 5 mg daily.
    Angiotensin-converting enzyme (ACE) inhibitors are indicated in many patients with stable ischemic
    heart disease, especially those with diabetes or left ventricular dysfunction. Weight loss, aerobic
    exercise, an American Heart Association Step II diet, and ACE inhibitors decrease the risk of

    microvascular complications and potentially cardiac events in patients with diabetes. Tight glycemic
    control does not reduce the risk of macrovascular complications in patients with type 2 diabetes; it
    may actually increase the risk of cardiovascular death and complications. According to the

    guidelines, the goal blood pressure is <140/90 mm Hg in patients with diabetes or chronic kidney
    disease. An ACE inhibitor or angiotensin-receptor blocker is first-line therapy in diabetes to prevent
    progression of renal disease.

    132. A 78-year-old man with peripheral arterial disease is referred to your clinic for preoperative
    evaluation prior to femoral-popliteal bypass. He currently can only walk 1-2 blocks due to

    claudication. He underwent percutaneous coronary intervention with a bare-metal stent for single-

    vessel coronary disease affecting the right coronary artery 2 years ago. He denies angina or

    shortness of breath.

    A persantine sestamibi stress test demonstrates a small area of ischemia at the apex without

    angina. Medications include aspirin 81 mg daily and metoprolol tartrate 50 mg twice daily. Blood

    pressure is 112/72 mm Hg, and heart rate is 62 bpm. Creatinine is 1.5 mg/dl. His low-density

    lipoprotein is 65 mg/dl, high-density lipoprotein is 45 mg/dl, and triglycerides are 100 mg/dl.

    Which of the following do you recommend?

    a. Add nitrates.

    b. Increase beta-blocker.

    c. Proceed with surgery.

    d. Coronary revascularization.

    e. Full-dose aspirin.

    132. c.
    Proceed with surgery.
    This patient is at elevated risk for perioperative cardiac events for a moderate-risk surgery, but in the
    face of appropriate medical therapy including aspirin and beta-blockade, there is no evidence that
    revascularization will mitigate this risk. Results from the randomized, prospective CARP

    (Coronary Artery Revascularization Prophylaxis) trial demonstrated that coronary artery

    revascularization before elective major vascular surgery did not improve long-term survival or alter
    early postoperative outcomes, including death, myocardial infarction, and length of the hospital

    stay among patients with stable coronary artery disease. This patient’s heart rate suggests that he is
    well beta-blocked, and you would not change the dose just prior to surgery. The patient should
    proceed with surgery on current medical therapy. There is no evidence that an increased dose of

    aspirin or nitrates will reduce perioperative events. The small amount of ischemia would not justify
    revascularization.

    133. A 47-year-old male smoker with hyperlipidemia calls for emergency medical services after
    developing substernal chest pressure while watching television. Emergency medical technicians

    arrive and administer sublingual nitroglycerin, which completely relieves his symptoms.

    Upon arrival to the emergency department, the patient notes recurrent chest pressure with pain,

    and his electrocardiogram shows 2.5 mm ST-segment elevation in V2-5. Both resolve with

    administration of sublingual nitroglycerin. He is given aspirin, heparin, morphine, and intravenous


    nitroglycerin. Coronary angiography reveals minimal nonobstructive plaque in the left anterior

    descending artery and right coronary artery. Toxicology screening is negative.

    In addition to smoking cessation, which of the following is the next most appropriate course of

    action?

    a. Metoprolol.

    b. Niacin.

    c. Omega-3 fatty acids.

    d. Prazosin.

    e. Diltiazem.

    133. e.
    Diltiazem.
    While the clinical findings suggest coronary spasm, the diagnosis is assumed, but not proven, as

    spasm was not actually observed. Coronary vascular smooth muscle hyper-reactivity is a key factor
    in the pathogenesis of coronary artery spasm. Cigarette smoking is a major risk factor for variant
    angina and endothelial dysfunction; patients should be counseled to avoid tobacco use.

    Diltiazem, a nondihydropyridine agent, is often first-line therapy for coronary spasm, but if

    symptoms recur, spasm testing with intracoronary acetylcholine is indicated.

    Treatment with either niacin or omega-3 fatty acids is not indicated here, as they have not been

    shown to improve coronary spasm. Patients should not be treated with beta-1 and beta-2 selective

    agents, because of the possibility of unopposed alpha-adrenergic activity. If beta-blockade is

    needed for management, the new agents with vasodilator activity (nebivolol, carvedilol, etc.) would
    be better choices.

    134. A 62-year-old man comes to your office with 3 months of dyspnea on exertion. He has a

    medical history of hypertension treated with a calcium channel blocker, hyperlipidemia treated

    with atorvastatin, and long-standing asthma well controlled with theophylline. He also has been

    complaining of severe knee pain that he mitigates with nonsteroidal anti-inflammatory drugs.

    On exam, his blood pressure is 98/65 mm Hg. His cardiovascular exam is unremarkable and lungs

    are clear to auscultation bilaterally. His electrocardiogram (ECG) shows sinus rhythm with first-

    degree atrioventricular (AV) block.

    You decide he needs a pharmacologic nuclear stress test.

    Which of the following factors would contraindicate using adenosine as your stress of choice?

    a. Use of calcium channel blocker.

    b. Low normal blood pressure.

    c. First-degree AV block on ECG.

    d. History of asthma.

    e. Theophylline use.
    134. e.
    Theophylline use.
    Adenosine is a vasodilator agent that works by producing stimulation of A2A receptors.

    Methylxanthines (caffeine, theophylline, and theobromine) are competitive inhibitors of this effect,
    which require withholding prior to testing. Second- or third-degree AV block is a contraindication;
    first-degree is not. Systolic blood pressure <90 mm Hg is another contraindication.

    Asthmatic patients with ongoing wheezing should not undergo adenosine stress testing. However,

    it has been reported that patients with adequately controlled asthma can undergo an adenosine

    stress test and can have pretreatment with two puffs of an inhaled bronchodilator. This patient had
    clear lungs on auscultation. Another contraindication to adenosine is unstable acute myocardial

    infarction or acute coronary syndrome. The patient was admitted and had negative cardiac

    enzymes.

    135. A 45-year-old man discharged from the hospital 6 weeks ago following an admission for
    unstable angina during which he undergoes stenting of the right coronary artery presents to the

    clinic. He reports no history of diabetes, smoking, hypertension, or a family history of premature


    heart disease. Discharge daily medications include metoprolol succinate 25 mg, aspirin 81 mg,

    atorvastatin 20 mg, and clopidogrel 75 mg. His body mass index is 27 kg/m2, waist circumference is
    42 inches, and blood pressure is 135/85 mm Hg.

    His laboratory results (on admission) were:

     Total cholesterol 230 mg/dl

     Triglycerides 350 mg/dl

     High-density lipoprotein 35 mg/dl

     Low-density lipoprotein 125 mg/dl

     Fasting glucose 99 mg/dl

    Which of the following is the most appropriate next step for this patient?

    a. Add fenofibrate.

    b. Increase atorvastatin to 80 mg.

    c. Continue current therapy.

    d. Add ezetimibe.
    135. b.
    Increase atorvastatin to 80 mg.
    Current guidelines recommend that this patient with atherosclerotic cardiovascular disease should be
    on a high-dose statin for maximal effect. He had elevated triglycerides on admission, but these should
    be reassessed on a higher-dose statin and with lifestyle changes prior to addition of any

    other pharmacologic therapy such as fenofibrate. This patient is not on a maximal dose of statin.

    Therefore, addition of ezetimibe at this time is not appropriate.

    136. A 43-year-old man is referred for dyslipidemia. He has no history of hypertension or diabetes.

    His father had a myocardial infarction at the age of 38. The patient is a nonsmoker who exercises
    regularly and eats a vegetarian diet.

    Body mass index is 20 kg/m2, waist circumference is 30 inches, blood pressure is 110/80 mm Hg,

    and heart rate is 48 bpm.

    The patient’s internist provides the following lab results:

     Total cholesterol 395 mg/dl

     Low-density lipoprotein (LDL) 321 mg/dl

     High-density lipoprotein 54 mg/dl

     Triglycerides 100 mg/dl

    Which of the following is the appropriate next step?

    a. Exercise treadmill stress test.

    b. Coronary artery calcium score.

    c. Statin therapy.

    d. Genetic testing.

    136. c.
    Statin therapy.
    For an initial evaluation of hyperlipidemia, testing for secondary causes of elevated cholesterol is
    usually indicated, as disorders such as hypothyroidism, nephrotic syndrome, and medications can

    be secondary causes of dyslipidemia and should be screened for too. In this patient who is likely to
    have the heterozygous form of familial hypercholesterolemia, the most appropriate next step is

    treatment with a statin.

    Familial hypercholesterolemia is an autosomal-dominant disorder, caused by defective LDL-

    receptors. Total cholesterols are usually in the 300-500 mg/dl range in many patients. Tendon

    xanthomas on the Achilles tendon and extensor tendons of the hands are often present. These

    patients carry a risk of premature coronary heart disease, as evidenced by the family history for this
    patient. The prevalence is approximately 1:500 in the United States. This patient should be

    started on lipid-lowering therapy along with continuation of therapeutic lifestyle changes, diet, and
    physical activity. Furthermore, lipid testing is recommended for offspring.

    Stress testing in this asymptomatic patient is not indicated. Calcium scoring does not change the
    management in this patient, as he is already in one of the four statin treatment groups.

    137. A 69-year-old woman sees you in the office for evaluation of fatigue with exertion for the past 6
    months. She says that when she is climbing stairs, especially if she is carrying something, she is more
    tired than usual. Symptoms resolve within 5 minutes of rest. She has hypertension, treated

    with losartan and a diuretic. She reports numerous food allergies and she once had an episode of

    wheezing and nasal congestion after taking aspirin.

    You order a nuclear stress test, which reveals a small, mild reversible inferior perfusion abnormality
    with a normal left ventricular ejection fraction.

    Which of the following should be added to her medical regimen?

    a. Prasugrel.

    b. Cilostazol.

    c. Dipyridamole.

    d. Clopidogrel.

    e. Ticlopidine.

    137. d.
    Ticlopidine.
    Ordinarily, aspirin (75-162 mg/day) would be recommended for antiplatelet therapy to prevent

    myocardial infarction in patients with established atherosclerotic disease. However, this patient has an
    indication of an aspirin allergy. Aspirin therapy is therefore contraindicated. Clopidogrel has proven
    efficacy for prevention of ischemic events based on the CAPRIE trial, and therefore can be used in
    place of aspirin.

    Cilostazol is a phosphodiesterase-3 inhibitor that acts as both an arterial dilating agent and an
    antiplatelet agent; it can increase symptom-free walking distance in patients with intermittent

    claudication, but has no proven benefit in preventing ischemic coronary events. Dipyridamole in

    combination with aspirin has been shown to reduce subsequent strokes and transient ischemic

    attacks in patients with cerebrovascular disease, but not ischemic coronary events. Ticlopidine is an
    adenosine diphosphate (ADP)-receptor inhibitor similar in mechanism of action to clopidogrel, but
    has more serious side effects, including neutropenia and thrombotic thrombocytopenic purpura,

    thus has been essentially replaced by clopidogrel. Prasugrel is an ADP-receptor inhibitor that is
    approved for patients with acute coronary syndrome. This patient has chronic angina.

    138. A 67-year-old man is seen in the cardiology clinic for a routine follow-up visit. He currently has
    no symptoms of angina, dyspnea, orthopnea, or ankle swelling. He plays golf for exercise, saying

    that he walks all 18 holes four times a week. He suffered an inferior wall myocardial infarction 4

    years ago, which was treated with primary percutaneous coronary intervention. Nonobstructive

    stenoses were noted in the left anterior descending artery at the time, but a total occlusion of the right
    coronary artery was deemed to be the culprit lesion and received treatment with a drug-eluting stent.
    He received medical therapy for lipids and hypertension as well as dual antiplatelet therapy for 1 year
    following his myocardial infarction. An echocardiogram 1 year ago demonstrated normal left
    ventricular systolic function. He is currently taking aspirin 81 mg daily,

    hydrochlorothiazide 25 mg daily, atorvastatin 40 mg daily, and lisinopril 20 mg daily.

    Which of the following interventions should you recommend at this time to reduce morbidity and

    mortality for this patient?

    a. Depression screening.

    b. Cardiac rehabilitation.

    c. Aldosterone antagonist therapy.

    d. Influenza vaccination.
    e. Beta-blocker therapy.

    138. d.
    Influenza vaccination.
    Vaccination against influenza has been shown to reduce morbidity and mortality in both patients

    with acute coronary syndrome and in patients with prior cardiovascular events. Beta-blocker

    therapy has not been studied in patients with a normal ejection fraction more than 3 years after a
    coronary event. Depression screening may be important for quality of life, assuming supports to

    treat depression are available, but has not been proven to reduce morbidity and mortality among

    patients with coronary artery disease. Aldosterone antagonists are only proven to be beneficial in
    patients with reduced ejection fraction following coronary events. Cardiac rehabilitation is

    important following acute events and for the management of symptoms including angina, but

    neither apply to this patient.

    139. A 61-year-old woman presents for follow-up after a recent hospitalization for a non-ST-

    segment elevation myocardial infarction (NSTEMI). She has type 2 diabetes, hypertension, and

    stage 2 chronic kidney disease. Six weeks ago, she went to the emergency department with chest

    pressure and underwent coronary angiography, which revealed a focal stenosis in the left anterior
    descending coronary artery, for which she received a single drug-eluting stent. Her medications

    include aspirin 81 mg daily, clopidogrel 75 mg daily, and simvastatin 20 mg daily, glargine insulin,
    metoprolol succinate 25 mg qd, amlodipine 5 mg qd, and lisinopril 20 mg qd.

    Today, she reports feeling well, has had no recurrent chest pressure or dyspnea, and is

    participating in cardiac rehabilitation. Her blood pressure is 122/76 mm Hg and heart rate is 68

    bpm. Her lipid profile shows total cholesterol of 210 mg/dl, low-density lipoprotein of 120 mg/dl,
    high-density lipoprotein of 40 mg/dl, and triglycerides of 200 mg/dl.

    Which of the following is the most appropriate next step, in addition to lifestyle modification?

    a. Change simvastatin to atorvastatin 40 mg.

    b. Add ezetimibe 10 mg daily.

    c. Add fenofibrate 145 mg daily.

    d. Add fish oil 3 g daily.

    e. Increase simvastatin to 40 mg.


    139. a.

    Change simvastatin to atorvastatin 40 mg.

    This patient has established coronary artery disease and had a recent acute coronary syndrome.

    High-intensity statin therapy should be continued in all patients with NSTEMI and with no

    contraindications to its use (Class I, Level of Evidence A). Replacement of simvastatin with

    atorvastatin 80 mg daily is supported by several large randomized trials. High-intensity statin

    therapy used in randomized controlled trials includes atorvastatin 40-80 mg and rosuvastatin 20-40

    mg. Adding ezetimibe, fenofibrate, fish oil, and niacin is not indicated, as the primary goal is high-
    intensity statin therapy.

    140. A 43-year-old man without any significant medical history presents for an office visit to

    discuss prevention of cardiovascular disease (CVD). He is a nonsmoker. He takes no medications

    and exercises 2-3 times per week at the local gym.

    On physical examination, his weight is 220 lbs, blood pressure is 136/84 mm Hg, and pulse is 76

    bpm. His body mass index is 33 kg/m2 and waist circumference is 40 inches. His physical

    examination is otherwise unrevealing. Laboratory studies reveal a total cholesterol of 190 mg/dl,
    low-density lipoprotein cholesterol of 130 mg/dl, high-density lipoprotein cholesterol of 39 mg/dl,
    triglycerides of 209 mg/dl, and a fasting glucose of 110 mg/dl.

    Which of the following is the most appropriate next step?

    a. Start aspirin.

    b. Recommend lifestyle modification.

    c. Start statin.

    d. Measure carotid intima-media thickness (CIMT).

    e. Obtain exercise stress test.

    140. b.
    Recommend lifestyle modification.
    This patient's risk of atherosclerotic CVD (ASCVD) is low (<5%). Current CVD risk guidelines stress
    the importance of lifestyle modifications to lower CVD risk. This includes eating a heart-healthy diet,
    regular aerobic exercises, maintenance of desirable body weight, and avoidance of tobacco

    products.

    Due to his low risk, he would not benefit from statin or aspirin therapy. Further risk assessment may
    be considered if a treatment decision is uncertain. Assessment of one or more of the

    following–family history, high-sensitivity C-reactive protein, coronary artery calcium score, or


    ankle brachial index—may be considered to inform treatment decision -aking (Class IIb, Level of
    Evidence B). However, measurement of CIMT is not recommended for risk assessment for ASCVD
    (Class III,

    Level of Evidence B). In a low risk, asymptomatic patient, stress testing is inappropriate.

    141. A 67-year-old Spanish-speaking man from Mexico comes to the hospital for evaluation of chest
    pain that occurred previously with exertion and now at rest. He has a history of hypertension,
    hyperlipidemia, and diabetes. His admission electrocardiogram was notable for 1 mm ST

    depression in the inferior leads. His initial troponin level was 0.2 ng/dl (normal <0.04 ng/dl). His
    chest pain was relieved in the emergency room with sublingual nitroglycerin and morphine.

    You believe that the next appropriate step is coronary angiography and would like to discuss the

    risks/benefits of this invasive procedure with him in order to obtain consent. He speaks broken

    English, but appears to understand much of what you say.

    Which of the following is the most appropriate method to communicate this information to the

    patient?

    a. Having his bilingual daughter translate, who is with him now.

    b. Giving him a copy of the consent form in Spanish to read on his own.

    c. Referring him to your colleague who speaks Spanish and who will be on service tomorrow.

    d. Explaining in English and having him nod to ensure understanding.

    e. Requesting and waiting for a hospital interpreter in person or by phone

    141. e.

    Requesting and waiting for a hospital interpreter in person or by phone


    In cases of patients whose English skills are limited, an official medical interpreter is the best choice
    for conveying accurate medical information, especially when it concerns an invasive procedure with
    risks of serious complications. A family member is generally only acceptable in emergencies or if
    the patient specifically requests him or her to interpret for a small matter. Minors (<18 years old)
    should be avoided, and the age of the patient's daughter is unknown. Relying on nodding to convey
    understanding of the nature of a complex procedure is not sufficient in this patient with limited
    English skills. Reading and signing the consent form alone is not adequate for obtaining informed
    consent and provides no opportunity for the patient to ask questions. Delaying care of a non-ST-
    elevation myocardial infarction by a day or more to involve your colleague is providing suboptimal
    care and not an acceptable option.

    142. A 68-year-old man with a history of ongoing tobacco use, hypertension, and a 4.2 cm

    abdominal aortic aneurysm (AAA) is seen for scheduled follow-up. His AAA has been followed with

    yearly ultrasounds and is stable in size. He is retired and walks for 30 minutes each morning with his
    dog. Medications include lisinopril, aspirin, and a multivitamin.

    On examination, his blood pressure is 128/82 mm Hg and pulse is 88 bpm. There is a soft

    abdominal bruit and an accentuated abdominal aortic pulsation. A fasting lipid profile reveals total
    cholesterol of 220 mg/dl, high-density lipoprotein (HDL) of 31 mg/dl, and triglycerides of 316

    mg/dl.

    Which of the following is the most appropriate recommendation?

    a. Losartan.

    b. Fenofibrate.

    c. Atorvastatin.

    d. Fish oil.

    e. Niacin.

    142. c.
    Atorvastatin.
    This patient presents with dyslipidemia with elevated total cholesterol and triglycerides and low HDL.
    The first step in management of dyslipidemia includes assessing patient risk. This patient’s AAA
    places him in the highest risk category for future cardiac events. Other coronary risk

    equivalents include the presence of peripheral arterial disease, diabetes, or cerebrovascular

    disease.

    Given his high risk, moderate- to high-intensity statin therapy is recommended. Fenofibrate is

    effective at lowering triglycerides. However, in this patient, the non-HDL cholesterol should be

    treated first. If triglycerides remain elevated despite non-HDL cholesterol at goal, therapy directed
    toward hypertriglyceridemia is reasonable, although concurrent fibrate and statin therapy increase the
    risk of statin-induced myopathy. Fish oil can also be useful in management of

    hypertriglyceridemia, but should not be used as the initial therapy in this case. Niacin is effective at
    raising HDL. However, the incremental value of raising low HDL with pharmacotherapy has not

    been proven in several large randomized trials, and is an area of ongoing study and debate. Finally,
    addition of a second antihypertensive agent is not indicated, as his blood pressure is well controlled
    to <130/80 mm Hg.

    143. A 48-year-old man presents for follow-up. He feels well and recently completed his first 5k road
    race. His medical history includes dyslipidemia managed with atorvastatin. Physical

    examination is normal. He obtained laboratory work at a recent “employee health fair,” which he

    brings for review. The total cholesterol is 160 mg/dl, high-density lipoprotein cholesterol is 48

    mg/dl, and triglycerides are 102 mg/dl. The high-sensitivity C-reactive protein level is within the
    normal range. Serum chemistries including creatinine are normal. Dipstick urinalysis is negative for
    blood, protein, and glucose. Serum creatine kinase (CK) level is 301 U/L (reference range, 26-192).

    Liver function tests are normal.

    Which of the following is the best next step in management of this patient?

    a. Decrease frequency of atorvastatin to every-other-day dosing.

    b. Decrease the dose of atorvastatin and add ezetimibe.

    c. Stop atorvastatin and prescribe cholestyramine.

    d. Stop atorvastatin and prescribe rosuvastatin.

    e. Continue atorvastatin and check CK in 3 months.


    143. e.

    Continue atorvastatin and check CK in 3 months.

    This patient is asymptomatic and presents with a slightly increased CK level while on statin therapy.

    Guidelines recommend checking a single CK level upon initiation of statin therapy to obtain a

    baseline value for comparison, should myopathic symptoms develop. CK should be rechecked with

    any new muscle symptoms, but routine monitoring of CK in asymptomatic patients is not

    recommended. Statin therapy should be stopped in patients with severe myopathic symptoms

    regardless of CK level and if the CK is greater than 10-times the upper limit of normal. For this
    asymptomatic patient with a slightly elevated CK, no change in therapy is needed and he can be

    followed serially. The elevations in CK are exacerbated by his training/running.

    Cholestyramine can be used in lieu of statin therapy in statin-intolerant patients, as there are data for
    an improvement in mortality in the primary prevention setting. Rosuvastatin and pravastatin

    are both more hydrophilic than atorvastatin, and in some patients with statin myalgia (not

    myopathy), transition to a more hydrophilic statin can result in symptom improvement. Similarly,

    for statin-intolerant patients, an every other day dosing regimen can allow for some statin therapy.

    A combination of simvastatin and ezetimibe was not superior to simvastatin alone in a randomized

    controlled trial, and no change in therapy is indicated for this patient.


    144. A 55-year-old woman with stable anginal chest pain on no cardiac medication underwent a

    computed tomography (CT) coronary angiogram to assess for possible coronary artery disease

    (Figure 1). Her electrocardiogram (ECG) showed no acute ischemic changes and is normal. Her

    blood pressure is normal and she has no diabetes.

    Based on the CT image shown in Figure 2, which of the following is the next best step?

    Figure 2

    a. An exercise ECG stress test.

    b. Cardiac catheterization.

    c. Begin medical therapy for coronary disease.

    d. An exercise nuclear stress test.

    144. c.
    Begin medical therapy for coronary disease.

    The CT suggests a mid left anterior descending artery lesion and single-vessel disease. She needs
    initial treatment with medical therapy for stable angina before further testing is indicated.

    145. A 58-year-old man presents to the emergency department with a 5-hour history of crushing,
    substernal chest pain. The patient history is significant for type 2 diabetes, hypertension, dyslipidemia,
    and coronary artery disease with stenting of his proximal left anterior descending artery 3 years ago.

    Admission electrocardiogram shows anterior ST-segment elevation, including ST elevation in lead


    aVR. The patient is referred for emergent cardiac catheterization. Initial coronary angiography shows
    a 95% ostial left main stenosis with thrombus. An intra-aortic balloon pump (IABP) is inserted and
    successful stenting of the left main is performed with 0% residual stenosis and TIMI 3 flow
    throughout the left coronary system. The right coronary artery is widely patent. The IABP is
    continued at a 1:1 counterpulsation ratio.

    One hour after the procedure, the patient develops atrial fibrillation with a rapid ventricular response.
    The patient remains asymptomatic. Hemodynamic variables after percutaneous coronary intervention
    (PCI) are shown in the table in Figure 1.

    Which of the following choices would be the best next step in the management of this patient?
    a. Add flecainide.

    b. Repeat coronary angiography.

    c. Add amiodarone.

    d. Insert an Impella 5.0 left percutaneous device.

    e. Add dobutamine.

    145.

    c.
    Add amiodarone.
    The IABP is a catheter-mounted balloon that augments pulsatile blood flow by inflating during

    diastole, which displaces blood volume in the descending aorta and increases mean aortic

    pressure, thereby augmenting coronary perfusion. Upon deflation, during systole, the IABP

    generates a pressure sink, which is filled by ejecting blood from the heart. The net effect of IABP

    therapy is an increase in mean arterial pressure and augmented ventricular stroke volume. For

    this reason, proper IABP function depends on native contractile function of the heart. During

    periods of tachycardia, the IABP is unable to adequately inflate, and therefore cannot augment

    mean arterial pressure.

    Thus, pharmacological management of reducing the heart rate is a reasonable next step to

    optimize IABP function and stabilize the patient’s hemodynamics. Escalating mechanical support

    to an Impella, which requires surgical vascular access, is not required. There is no indication that the
    patient has developed recurrent thrombosis of the left main artery. Initiation of inotropes

    and vasopressors may worsen the tachycardia and lead to further decompensation. Direct

    current cardioversion may be appropriate but is not listed as an option. Flecainide is

    contraindicated in patients with coronary artery disease.

    146. A 65-year-old woman was admitted with an anterior ST-segment elevation myocardial

    infarction (STEMI). She was taken urgently to the catheterization laboratory, where she underwent
    placement of two bare-metal stents to the proximal and mid-left anterior descending coronary

    artery. Forty-eight hours later, she complains of shortness of breath and chest pain of a different
    quality than her presenting symptoms. On examination, her blood pressure is 80/57 mm Hg, heart

    rate is 102 bpm, and oxygen saturation is 94% on room air. Her jugular venous pressure (JVP) is

    elevated to the angle of the jaw. Lung exam is clear.

    What is the most likely finding on cardiovascular examination?

    a. Loud pansystolic murmur.

    b. Muffled heart sounds.


    c. Displaced point of maximal impulse.

    d. Loud S4.

    146. a.
    Loud pansystolic murmur.
    The patient is expected to have muffled heart sounds secondary to free wall rupture and increased
    pericardial fluid. This diagnosis is consistent with elevated JVP and clear lungs, and occurs more
    frequently in the setting of an anterior wall MI. It is considered a surgical emergency with a high
    mortality.

    A loud pansystolic murmur at the lower left sternal border, accompanied by a thrill, is consistent with
    ventricular septal defect and is usually accompanied by pulmonary congestion. The treatment

    is urgent surgery. There is a higher mortality in patients with inferior MI compared with those with
    anterior MI. A fourth heart sound may be heard in the setting of an acute MI, but given signs

    consistent with pericardial effusion, this is likely not to be audible. A displaced apex is most

    consistent with chronic systolic heart failure.


    147. A 57-year-old man has had 2 years of progressively worsening angina with exertion. He was

    initially managed with medical therapy, but has had progressively worsening angina despite

    maximization of two antianginal therapies. A stress test showed moderate exercise tolerance, and

    nuclear imaging suggested a large area of inferior ischemia involving >10% of the left ventricular
    muscle mass. A diagnostic cardiac catheterization was performed and showed a chronic total

    occlusion of the right coronary artery, as shown in Figure 1.

    Given his lifestyle-limiting symptoms despite maximal medical therapy, you have referred him for

    percutaneous coronary intervention (PCI). You have obtained careful consent and have advised him

    of the risk of radiation-induced skin injury. You have assured him that you will take every

    precaution to minimize the radiation exposure to the patient during what may be a lengthy

    procedure.
    Which of the following techniques will increase radiation exposure to the patient?

    Figure 1

    a. Use of less magnified views.

    b. Use of fluoroscopy storage instead of cine storage.

    c. Use of collimation.

    d. Steep imaging intensifier angles.

    e. Use of fluoroscopy frame rate of 7.5 frames per second (FPS).

    147. d.

    Steep imaging intensifier angles.

    Patients with cardiovascular disease are exposed to a wide array of diagnostic and therapeutic
    procedures that result in a significant cumulative exposure of ionizing radiation. There is a growing
    awareness of this cumulative exposure, and every effort should be made in the catheterization
    laboratory to minimize the radiation exposure to the patient (and the operator). The majority of PCI
    procedures can be completed, as most modern imaging equipment in the catheterization laboratory
    has a fluoroscopy storage function where a maneuver performed under fluoroscopy can be
    permanently stored and recorded. In many cases, the fluoro image will provide diagnostic grade
    imaging so that cine-angiography will not be necessary and further radiation exposure can be
    reduced. On average, cine radiation doses can be as much as 20-times higher than fluoroscopy doses.

    Reducing the frame rate for image acquisition will also significantly reduce radiation exposure
    during fluoroscopy.

    While many operators prefer using 15 FPS, a frame rate of 7.5 FPS is sufficient in most patients for
    effective imaging and will reduce radiation use by 50% compared to 15 FPS. Collimation and use of
    lower magnified imaging fields are also critical for reduction of radiation exposure.

    Use of steep imaging angles will increase the radiation exposure to the patient. With steep angulation,
    fewer X-rays reach the image intensifier, resulting in feedback to the radiation generator to generate
    greater energy in order to provide a sufficient image as the source-to-image distance is increased.
    Every effort should be made to use angles as shallow as possible during PCI, and to use multiple
    angles so as not to concentrate the radiation beam to one area.
    148. A 76-year-old man with atrial fibrillation presents to clinic with a 2-year history of chest pain at
    rest located in the mid-epigastrium radiating to the mid-substernal region. Computed

    tomography (CT) angiography of the chest reveals the finding shown in Figure 1.

    Which of the following is the abnormality shown in Figure 1?

    Figure 1

    a. Primary cardiac tumor.

    b. Coronary artery aneurysm.

    c. Pericardial cyst.

    d. Atrial appendage thrombus.

    148. b.

    Coronary artery aneurysm.

    The abnormality shown on the CT image has peripheral calcifications with central contrast and

    surrounding soft tissue density. It is continuous with the atherosclerotic coronary artery and

    consistent with coronary artery aneurysm, rather than a pericardial cyst or primary cardiac tumor.

    Neither of these would be expected to have peripheral calcification. Pericardial cysts are generally
    benign and usually right-sided, often in the atrioventricular groove.

    The abnormality is anterior to the left atrium and not consistent with an atrial appendage

    thrombus.

    149. A 75-year-old man is found by his family, unresponsive and crumpled over in the bathroom.

    Emergency medical service is called, but no bystander cardiopulmonary resuscitation (CPR) is

    attempted. Upon arrival 7 minutes later, emergency medical service personnel begin CPR, and after 2
    minutes the initial rhythm is ventricular fibrillation. After a 20-minute period of CPR effort,
    including epinephrine and repeated shocks, spontaneous circulation is established. He is intubated.

    Upon arrival at the emergency department, the patient has a weak pulse and blood pressure of

    95/65 mm Hg. He remains unresponsive, without spontaneous movement. The monitor reveals a

    wide QRS complex tachycardia at 100 bpm.

    Which of the following is the next most appropriate postresuscitation therapy?


    a. Discuss with the family withdrawal of therapy.

    b. Therapeutic hypothermia.

    c. Electroencephalogram.

    d. Cardioversion for wide QRS tachycardia.

    149. b.
    Therapeutic hypothermia.
    This patient’s prognosis is poor but not futile. Since he remains comatose, hypothermia is the best
    chance to limit long-term neurological damage. Long-term survival can be improved with

    hypothermia, generally from previous improvement rates of 1-2% to an improvement rate of 5-

    20%. Recent data suggest this may not be the case in children. It is important to realize that in order to
    achieve these improved survival rates, adequate time after rewarming must be allowed

    before reliable prognostication can be done and further efforts terminated. There is no need for

    cardioversion of his postresuscitation wide QRS rhythm since it is providing a current acceptable
    blood pressure and most certainly represents a transient epinephrine/norepinephrine response. An

    electroencephalogram may be important later to help assess his neurologic status.

    150. A 42-year-old man with a long-standing human immunodeficiency virus (HIV) infection comes

    to your office out of concern of his cardiovascular risk. He is on antiretroviral drugs. He smokes half
    a pack per day and drinks 1-2 drinks per week. Pertinent routine tests show a blood pressure of

    127/88 mm Hg, low-density lipoprotein 177 mg/dl, high-density lipoprotein 27 mg/dl, and

    triglycerides 334 mg/dl.

    Which of the following is an appropriate therapy for this patient, in addition to smoking cessation?

    a. Ezetimibe 10 mg a day.

    b. Begin 2 g fish oil daily.

    c. Rosuvastatin 20 mg a day.

    d. Atorvastatin 10 mg a day.

    e. Fenofibrate 150 mg a day.

    150. d.
    Atorvastatin 10 mg a day.
    HIV-infected individuals have high rates of smoking, and smoking cessation is perhaps the most

    modifiable risk factor to minimize cardiovascular disease risk in these persons. While this patient
    requires antiretroviral drugs and needs to improve his lipid profile, smoking cessation would have
    the most immediate effect on his overall health and cardiovascular disease risk. He warrants

    therapy for his hyperlipidemia. Because of the interaction with antiretroviral drugs, a low-dose

    statin is recommended.

    151. A 57-year-old man with a history of hypertension, hyperlipidemia, and a prior stent to the

    right coronary artery is seen for routine follow-up. Although he does not exercise regularly, he

    denies anginal symptoms during daily activities. He drinks one glass of wine daily and does not

    smoke. His medications are aspirin 81 mg qd, metoprolol succinate 25 mg qd, lisinopril 10 mg qd,

    and atorvastatin 40 mg qd. His blood pressure is 112/75 mm Hg. His most recent lipid panel shows

    a low-density lipoprotein (LDL) of 68 mg/dl and high-density lipoprotein (HDL) of 25 mg/dl. He

    wants to know how to best improve his cardiovascular risk profile.

    Which of the following is the most appropriate recommendation?

    a. Add colesevelam 3750 mg qd.

    b. Start a regular aerobic exercise program.

    c. Add niacin 500 mg bid.

    d. Increase daily alcohol intake to 3-4 drinks.

    e. Change to simvastatin 80 mg daily.

    151. b.

    Start a regular aerobic exercise program.

    Abundant epidemiologic evidence supports the relationship between increased physical activity

    and reduced cardiovascular risk. Currently, the best advice for patients is to perform regular

    aerobic exercise, which has beneficial effects on cardiovascular health. While niacin is effective at
    raising HDL levels, recent trials have shown that the addition of niacin fails to reduces
    cardiovascular events in patients with well-controlled LDL levels on background statin therapy.

    The AIM-HIGH trial tested the effects of adding niacin for patients with low HDL levels already on a
    statin. Despite increasing HDL levels, there was no benefit with niacin for reducing cardiovascular
    events and there was a question of a signal of increased stroke.

    The HPS2-THRIVE trial also examined the effects of niacin/laropiprant in patients with well-

    controlled LDL levels on a statin. There was no difference in rates of cardiovascular events, and
    niacin treatment was associated with more side effects. Given these results, it is not clear that niacin
    provides any additional benefit in a patient such as this who already is on a statin and at target LDL.

    Initiation of simvastatin at 80 mg or uptitration to 80 mg dose is contraindicated in patients due to


    risks of muscle injury. Colesevelam is a bile acid sequestrant that has primarily LDL-lowering
    effects.

    While moderate alcohol intake (especially red wine) may have beneficial cardiovascular effects,

    consuming more than 1-2 drinks daily has been shown to have detrimental effects on health.

    152. A 45-year-old man presents with substernal chest discomfort that comes on predictably with
    walking two blocks. The discomfort is alleviated with rest. He has a long-standing history of

    hypertension and was diagnosed with diabetes and dyslipidemia 6 months earlier. Current

    medications include metoprolol, lisinopril, simvastatin, and baby aspirin.

    A stress myocardial perfusion imaging study is ordered. He is unable to complete stage 2 of the

    standard Bruce protocol due to recurrence of chest discomfort. At peak stress and 2 minutes into

    recovery, 1.5-2 mm ST-segment depression is noted in the anterolateral leads. His imaging study is
    inconclusive due to submaximal workload.

    The most appropriate next test that also minimizes radiation exposure would be which of the

    following?

    a. Pharmacologic myocardial perfusion imaging.

    b. Diagnostic cardiac catheterization.

    c. Coronary computed tomography (CT) angiography.

    d. Dobutamine stress echocardiography.

    e. Stress echocardiography.

    152. b.
    Diagnostic cardiac catheterization.
    This patient has a high pretest likelihood of coronary artery disease based on his risk factors and
    characteristics of typical angina. Electrocardiographic changes during peak stress are suggestive of
    inducible ischemia, even though imaging was “inconclusive.” Risk-benefit ratio must be taken into
    account with diagnostic imaging studies. Although repeating the stress test would probably confirm
    the clinical suspicion, he will still need further evaluation of the coronary arteries.

    Coronary CT angiography is an excellent tool in patients with equivocal or nondiagnostic stress

    tests. However, in patients with a high pretest likelihood of coronary artery disease, coronary CT

    angiography is considered an inappropriate test, without added value of layered testing. Among

    the choices provided, triage to diagnostic cardiac catheterization with the option for

    revascularization based on anatomy would be the most appropriate decision in order to avoid

    additional radiation exposure.

    153. A 48-year-old man with a history of hypertension comes to your clinic to establish care. He
    states that he was told a few years ago that he had high cholesterol but he did not take further

    action. He does not smoke and drinks alcohol rarely. He states he eats a balanced diet with limited
    carbohydrates. His only medication is amlodipine. His blood pressure is 129/81 mm Hg, heart rate

    is 76 bpm, and the remainder of his exam is unremarkable. His body mass index is 24.8 and his

    glycated hemoglobin is normal.

    A fasting lipid panel from this morning reveals a total cholesterol of 210 mg/dl, triglycerides 630

    mg/dl, high-density lipoprotein (HDL) 42 mg/dl. His low-density lipoprotein (LDL) cannot be

    calculated. His thyroid-stimulating hormone is normal.

    In addition to recommending therapeutic lifestyle changes, which of the following is the next most
    appropriate step in his care?

    a. Recheck lipids in 3 months.

    b. Start low-dose aspirin.

    c. Switch amlodipine to hydrochlorothiazide.

    d. Start atorvastatin.

    e. Start fenofibrate.
    153. e.
    Start fenofibrate.
    The patient has very high triglyceride level, as defined by a level >500 mg/dl in the Adult Treatment
    Panel III guidelines. Such a severe elevation in triglycerides can lead to pancreatitis, so priority
    should be made to reduce levels as quickly as possible with effective triglyceride-lowering

    medications. Appropriate first-line choices include fibrates and niacin. Statins are less efficacious on
    this front, and would only be considered for LDL-lowering purposes once triglyceride levels are

    below 500 mg/dl.

    Therapeutic lifestyle changes should be recommended, but are not adequate to prevent

    pancreatitis in such a setting. Certain cardiovascular medications, such as hydrochlorothiazide, can


    increase triglyceride levels, thus would be detrimental in this case. Amlodipine has no such effects.

    The calculated LDL value in a lipid panel will be falsely low in the setting of elevated triglycerides,
    thus cannot be properly interpreted. Alternative approaches are repeating the lipid panel when

    triglycerides are better-controlled, measuring direct LDL, or following a non-HDL cholesterol

    treatment goal.

    154. A 50-year-old man with hypertension comes to your office for consultation on management of
    his cardiovascular risk. He has no symptoms suggestive of cardiovascular disease. His

    hypertension has been treated with hydrochlorothiazide and lisinopril, and his treated resting

    blood pressure is 130/80 mm Hg. His fasting lipid profile reveals a total cholesterol of 170 mg/dl,
    low-density lipoprotein (LDL) of 110 mg/dl, high-density lipoprotein of 45 mg/dl, and triglycerides
    of 75 mg/dl. His fasting glucose is 90 mg/dl. He does not smoke cigarettes. He has no family history
    of early-onset atherosclerotic cardiovascular disease (ASCVD).

    Which of the following therapeutic options is supported by the risk profile?

    a. Omega-3 fatty acids.

    b. Statin therapy.

    c. No lipid-lowering medications.

    d. Nicotinic acid.

    e. Fibrate therapy.

    154. c.

    No lipid-lowering medications.
    The 2013 American College of Cardiology (ACC)/American Heart Association (AHA) cholesterol

    guideline identified four major statin benefit groups. Using the 2013 ACC/AHA algorithm, this

    patient does not have clinical ASCVD, LDL ≥190 mg/dl, or diabetes. Using the Pooled Cohort

    Equation, his 10-year risk of coronary death, nonfatal myocardial infarction, fatal stroke, and

    nonfatal stroke is 3.7%. This risk level falls below the 7.5% threshold at which the benefit of statin
    therapy significantly exceeds the risk of incident diabetes. While further risk assessment may be
    considered, such as coronary artery calcium scoring, based on the available risk profile, no lipid-
    lowering medications are recommended. There is no randomized clinical trial evidence that

    initiation of a fibrate, niacin, or fatty acids would be beneficial in primary prevention in this patient.

    155. A 65-year-old woman with hypertension comes to your office to seek consultation on

    management of her cardiovascular risk factors. She has no history or symptoms suggestive of

    cardiovascular disease. Her hypertension has been treated with hydrochlorothiazide and lisinopril and
    her resting blood pressure is 130/80 mm Hg. On fasting laboratories, she has a total cholesterol of
    190 mg/dl, low-density lipoprotein (LDL) of 120 mg/dl, high-density lipoprotein (HDL) of 40

    mg/dl, triglycerides of 150 mg/dl, and glucose of 90 mg/dl. She currently smokes half a pack per

    day of cigarettes.

    After counseling her on smoking cessation and discussing the risks and benefits of testing, you

    recommend that she consider which of the following?

    a. Obtain an exercise stress test.

    b. Measure high-sensitivity C-reactive protein (hs-CRP) level.

    c. Start moderate- to high-intensity statin therapy.

    d. Measure glycated hemoglobin (HbA1c) level.

    155. c.

    Start moderate- to high-intensity statin therapy.

    The 2013 American College of Cardiology (ACC)/American Heart Association (AHA) cholesterol

    guideline identified four major statin benefit groups. Using the 2013 ACC/AHA algorithm, this

    patient does not have clinical atherosclerotic cardiovascular disease, does not have familial

    hyperlipidemia with an LDL above 190, and does not have diabetes. She is between the age of 40
    and 75 years, and therefore, the Pooled Cohort Equation should be used to estimate her 10-year

    atherosclerotic risk. This calculated to a 10-year atherosclerotic risk of 15.4%, well above the

    recommended 7.5% risk threshold for initiating statin therapy, and therefore, additional testing

    with hs-CRP is not needed.

    She has already had appropriate screening for diabetes with a fasting glucose level, therefore,

    HbA1c is not necessary. The patient has no symptoms suggestive of ischemic heart disease, and

    therefore, stress testing in this asymptomatic patient is not appropriate.

    156. A 55-year-old woman is seen for a second opinion on her lipid management. She has a recent

    diagnosis of non–insulin-dependent diabetes and no known history of cardiovascular disease. At

    the time of the diagnosis of her diabetes 6 months ago, her fasting lipid profile revealed a total
    cholesterol of 200 mg/dl, low-density lipoprotein (LDL) of 110 mg/dl, high-density lipoprotein of 45

    mg/dl, and triglycerides of 225 mg/dl. Although pharmacotherapy for her lipids was recommended

    by her primary care physician, she opted for lifestyle changes first.

    After 6 months of therapy for her diabetes and diet modification, her lipid profile is unchanged. Her
    body mass index is 28 kg/m2 and her glycated hemoglobin is 6.9%. She has a blood pressure of

    135/80 mm Hg and does not smoke. No proteinuria noted on urinalysis.

    In addition to continued lifestyle modification with regular exercise, diet, and modest weight loss for
    a body mass index goal <25, which of the following do you recommend as the next step for this
    patient?

    a. Amlodipine 5 mg.

    b. Atorvastatin 20 mg.

    c. Niacian ER 500 mg bid.

    d. Fenofibrate 145 mg.

    e. No change in medications at this time.

    156. b.
    Atorvastatin 20 mg.
    The 2013 American College of Cardiology (ACC)/American Heart Association (AHA) cholesterol

    guideline identified four major statin benefit groups. Using the 2013 ACC/AHA algorithm, this

    patient has diabetes with a Pooled Cohort Equation estimated 10-year atherosclerotic risk of 4.4%.

    As per the 2013 ACC/AHA algorithm, in diabetics (40-75 years, LDL 70-189 mg/dl), with a 10-year

    atherosclerotic cardiovascular disease risk <7.5%, a moderate-intensity statin should be initiated.

    This patient's blood pressure is <140 mm Hg, and antihypertensive medication is not indicated. The
    2013 guideline did not find data supporting the routine use of nonstatin drugs combined with

    statin therapy to reduce further atherosclerotic cardiovascular events. Because her risk is <7.5%, a
    high-intensity statin is not indicated.

    157. A 56-year-old African American woman with a history of hypertension treated with

    hydrochlorothiazide, and a family history of premature coronary disease presents to your clinic.

    She is a current smoker. Her blood pressure is 140/70 mm Hg, heart rate is 55 bpm, and body mass

    index is 28.9.

    Her lipid profile after a 10-week very low fat diet with increased physical activity is as follows:

     Total cholesterol 240 mg/dl

     Triglycerides 450 mg/dl

     High-density lipoprotein (HDL) 50 mg/dl

     Low-density lipoprotein (LDL) 145 mg/dl

    Which of the following is the first therapy to initiate?

    a. Omega-3 fatty acids.

    b. Fibrate.

    c. Statin.

    d. Nicotinic acid.

    157. c.
    Statin.
    The 2013 American College of Cardiology (ACC)/American Heart Association (AHA) cholesterol

    guideline identified four major statin benefit groups. Using the 2013 ACC/AHA algorithm, this

    patient does not have clinical atherosclerotic cardiovascular disease, does not have familial

    hyperlipidemia with an LDL above 190 mg/dl, and does not have diabetes. She is between the age

    of 40 and 75 years, and therefore, the Pooled Cohort Equation should be used to estimate her 10-

    year atherosclerotic risk. This calculated to a 10-year atherosclerotic risk of 10.6%, and is probably
    even higher given her family history of premature coronary artery disease, thus warrants treatment
    with a statin to reduce this risk.

    158. Effective dose-reduction strategies include appropriate patient selection.

    For which of the following patients is coronary computed tomography angiography (CCTA)

    appropriate?

    a. A 68-year-old man with high risk for coronary disease with acute chest pain.

    b. A 50-year-old man unable to undergo risk assessment.

    c. An asymptomatic 59-year-old man with a history of coronary artery bypass grafting surgery 2

    years ago.

    d. A 51-year-old woman with low risk for coronary disease and typical angina.

    e. A 45-year-old male executive with intermediate risk for coronary disease and worsening chest

    pain with activity.

    158. d.

    A 51-year-old woman with low risk for coronary disease and typical angina.

    Appropriate patient selection is an important first step in dose reduction. In general, due to its high
    sensitivity and negative predictive value, CCTA performs well in ruling out coronary artery disease
    in low-to-intermediate risk individuals. In patients with a high likelihood of coronary disease

    needing triage to invasive assessment, CCTA results in unnecessary radiation exposure with little
    added value. In such patients, CCTA is considered inappropriate.

    159. A 53-year-old woman presents to the heart failure clinic for evaluation and management. She
    experiences angina on minimal exertion despite medical therapy. She had an implantable
    cardioverter-defibrillator (ICD) inserted 3 months after her most recent myocardial infarction (MI).
    She had suffered two prior MIs and had a percutaneous coronary intervention (PCI) of the left
    anterior descending (LAD) and right coronary artery. Her most recent ejection fraction is 25% with a
    dilated left ventricle and no valvular abnormalities. Her electrocardiogram shows normal sinus
    rhythm with a QRS of 110 msec and Q waves in the inferior leads and precordial leads.

    A coronary angiogram shows patent right and left circumflex coronary arteries with a subtotal highly
    calcified occlusion of the proximal LAD. The distal LAD is collateralized from the right and left
    circumflex coronary arteries.

    PCI was not technically feasible. She undergoes rest/4-hour redistribution thallium. Results show 60%

    redistribution in the distal half of the anterior wall and septum.

    Which of the following is the next best step in this patient's care?

    a. Surgical revascularization.

    b. Biventricular ICD.

    c. Intensify medical treatment.

    d. Transplant evaluation.

    e. Cardiac magnetic resonance imaging (MRI).

    159. a.
    Surgical revascularization.
    This patient is presenting with ischemic cardiomyopathy and New York Heart Association class III-IV

    heart failure. She has advanced left ventricular dysfunction. On the single-photon emission

    computed tomography images, there is evidence of thallium uptake at 4 hours in her LAD

    distribution. Therefore, this area may improve with revascularization.

    In a meta-analysis comparing all imaging modalities that can identify hibernating myocardium and

    predicting recovery of regional function after revascularization, positron emission tomography

    (PET) using fluorodeoxyglucose (FDG) was the most sensitive, while dobutamine was the most

    specific, but when global recovery after revascularization was analyzed, thallium and PET were very
    similar.

    She does not meet criteria for upgrading to a biventricular ICD based on her QRS. An MRI would

    not provide further information and is contraindicated in patients with an ICD. If she does not

    improve with revascularization, then cardiac transplant should be considered.

    Treatment of triglycerides and non-HDL is secondary to initiating a statin, and there has been no
    evidence to support treatment with a fibrate or nicotinic acid to optimize non-HDL levels.

    160. A 68-year-old woman with hypertension and diabetes is being referred to the nuclear

    laboratory for a myocardial perfusion study. The nurse asks you to choose the imaging protocol for
    the patient. The patient’s body mass index (BMI) is 38 kg/m2. The patient walks her dog routinely.

    The patient lives close to the clinic where you would perform the test and is retired.

    Which of the following protocols would optimize patient images?

    a. One-day low-dose rest/high-dose stress with technetium.

    b. Two-day high-dose rest/stress imaging with technetium.

    c. One-day rest/stress dual-isotope imaging.

    d. One-day low-dose stress/high-dose rest with technetium.

    e. One-day stress/redistribution/reinjection with thallium.

    160. b.
    Two-day high-dose rest/stress imaging with technetium.

    Ideally, stress and rest imaging with technetium-99 agents should be performed on two separate

    days to avoid having residual activity from the first study contaminating the second study in

    overweight patients (i.e., >250 lbs. or body mass index >30 kg/m2) or in women where significant
    breast attenuation is anticipated. A low dose of technetium-99 radiotracer may result in

    suboptimal images and a 2-day imaging protocol is preferred in this patient population.

    The effective dose of radiation is higher with dual-isotope and should be avoided. The rest-stress
    protocol is a good option if the patient could not have a 2-day protocol. The patient does not

    require an assessment for myocardial viability. The low-dose stress should not be performed in this
    population because of the potential poor quality images on the stress study.
    Hear
    tFai
    lur
    eandCar
    diomyopat
    hies

    QUESTI
    ONS:

    1. A35- year-ol
    dmanpr esent
    sf orevaluat
    ionofhear
    tfail
    ure.Hi
    swor kuphasincludedan
    echocardiogram t
    hatdemonstrat
    esadi lat
    edcar di
    omyopathywithanej ecti
    onfract
    ionof25%,
    l
    eftventricul
    ar(LV)end-
    diastol
    icdimensionof6. 5cm,andmi ldmitralregurgi
    tati
    on.Cardi
    ac
    cathet
    erizati
    ondemonstr
    atedangiographicall
    ynormalcor
    onaryarter
    ies. 

    Laborator
    yr esult
    s,i ncl
    udingthyroid-sti
    mul at
    inghormone,humani mmunodefi
    ciencyvir
    us,
    completebloodcel lcount,
    metabolicpanel ,andfer
    ri
    ti
    n,ar
    eallwithi
    nnor
    malli
    mits.Hisbrot
    her
    wasr ecentl
    ydi agnosedwi thheartf ail
    ure,hisfat
    herunderwentaheartt
    ransplant,andhis
    pater
    nalgrandfatherdiedsuddenlyatt heageof30ofa“ hear
    tattack.
    ”

    Whichoft
    hef
    oll
    owi
    ngi
    srequi
    redt
    omakeadi
    agnosi
    soff
    ami
    li
    alcar
    diomyopat
    hyi
    nthi
    s
    pat
    ient
    ?

    a. Echocardiographyofhisfi
    rst-
    degr
    eerelat
    ives.
    b. Endomy ocardialbi
    opsy.
    c. Cardiacmagnet icr
    esonanceimaging(MRI).
    d. Genetictesti
    ngofhisbrother.
    e. Nof urt
    herdiagnosti
    cstudies.

    ANSWER:

    1. e. Nof
    urt
    herdi
    agnost
    icst
    udi
    es.

    Thedi agnosisoff ami li


    alcar di
    omyopat hyst i
    llremai nsaclinicaldiagnosisandr equir
    est hr
    ee
    generati
    onst obeaf fect ed.Itisusual l
    yaut osomaldomi nant.Genet i
    ct esti
    ngcanbeusef ulbut
    i
    snotcur rentl
    ynecessar ytoestablishthedi agnosi sofaf amili
    alcardiomyopat hy.Mut ati
    onsin
    sarcomer i
    cproteins,t hecyt oskeleton,calcium fluxpr ot
    eins,andmet aboli
    cpat hwayshaveal l
    beendescr i
    bed.Ifgenet ictesti
    ngi sconsider ed( alt
    houghnotr equir
    edf ordiagnosis),t
    hemost
    aff
    ected proband shoul d be tested.Ther e ar e no specifi
    c pat hologicfindings atbi opsy,
    alt
    hough genet ict esting ofcar diomyocyt es coul d be performed.Si mil
    arly,there are no
    pathognomoni ccar diacMRIpat t
    ernsf orfami li
    alcardiomyopat hy.Althoughechocar di
    ography
    ofallhisfir
    st-degreer elat
    iveswoul dbeadvi sabl e,i
    tisnotr equiredt omaket hediagnosisof
    famili
    alcardi
    omyopat hy.

    2. Whi
    chofthef
    oll
    owi
    ngechocar
    diogr
    aphi
    cfi
    ndi
    ngsi
    smostconsi
    stentwi
    thadi
    lat
    ed
    car
    diomyopat
    hy?
     

      Endsyst
    oli
    c(mm) Enddi
    ast
    oli
    c(mm) Post
    eri
    orwal
    l(mm) Sept
    alwal
    l(mm)
    A.2.
    0 5.
    0 0.
    8 0.
    8
    B.2.
    0 3.
    5 2.
    0 2.
    0
    C.5.
    0 6.
    5 1.
    0 1.
    0
    D.1.
    0 3.
    5 1.
    0 2.
    5
    E.2.
    0 6.
    0 1.
    4 1.
    4
    a.RowA.
    b.RowC.
    c. RowD.
    d.RowB.
    e. RowE.

    ANSWER

    2. b. RowC.

    Dil
    atedcar diomyopathies( opti
    onC)ar echaracteri
    zedbyani ncr
    easedend- diastol
    icvolume,
    decreasedej ect
    ionfraction,andi ncr
    easedeccent r
    icmyocar di
    almass.Opt i
    onA i snor mal
    dimensi ons.OptionB i sconsi stentwithar estr
    ictivecardiomyopat hywithl eftventr
    icul
    ar
    hypertrophy (e.
    g.,amyl oid).Opt ion D demonstrates a smal lventricl
    e with supranormal
    contractil
    it
    y and asymmet r
    ic hypertr
    ophy (e.
    g.,hyper t
    rophic cardiomyopathy).Opt i
    on E
    demonst r
    atesalargehear tbutnor malcontr
    acti
    li
    tywi thconcentri
    cleftventr
    icularhypert
    rophy
    consistentwithanathlete’sheart.

    3. A58- year
    -ol
    dwomanpr esentswit
    hacuteshor t
    nessofbreathandchestpain.Shehad
    j
    ustlefthomeaf t
    err
    ecei
    vingacal
    lthatherhusbanddiedsuddenlyatwork.
     Shehasneverbeen
    hospit
    alizedandhasnocardi
    ovascularhi
    stor
    yorriskfact
    ors.Shelooksanxiousonexam and
    di
    aphor eti
    c. 

    Herbl oodpr essurei s170/80mm Hg,herhear trateis110bpm,andherr espir


    atoryr at
    eis18
    breaths/mi nute.Venouspr essur
    esar enotel evat
    ed;lungsarecl ear
    ;S4 on cardiacexam.
    Abdomenandext remiti
    esareunremar kable.Tr
    oponi nIi
    s1.0ng/dl;B-t
    ypenatriur
    et i
    cpeptide
    (BNP)i s500 pg/ ml.Herel ectr
    ocardiogram showsdeep ant er
    iorT- waveinver si
    ons.Her
    echocar diogram demonst r
    atesleftventri
    cular(
    LV)dysfuncti
    onwit
    hanej ecti
    onfraction(EF)of
    30%.Car diaccatheteri
    zati
    onshowsnor malcoronariesandLVapicalaneurysm.Thepat i
    entis
    start
    edonmet oprolol.

    Whi
    choft
    hef
    oll
    owi
    ngt
    her
    api
    esi
    smostappr
    opr
    iat
    eint
    hispat
    ient
    ?

    a. Apixi
    ban.
    b. Colchi
    cine.
    c. Sacubit
    ril
    /val
    sart
    an.
    d. Implant
    ablecardi
    over
    ter
    -def
    ibr
    il
    lat
    or(
    ICD)i
    mpl
    ant
    ati
    on.
    e. Lisi
    nopril
    .

    ANSWER:

    3. e. Li
    sinopr
    il
    .

    Thispati
    entmostl
    ikelyhasTakotsubocar diomyopat hy,whichi sclassi
    cal
    lyseeni
    nmi ddle-
    agedwomenwhoexper i
    encesevereemot ionaldi st
    ress,althoughanysi tuati
    ont
    hatcoul d
    resul
    tinamassivecat echol
    aminereleasecanr esultinthi
    st ypeofmyocar di
    ali
    nsult
    .The
    ventr
    icul
    arwal
    lmot i
    onabnor mali
    tyisdisti
    nctivewi t
    hpr eservationofthebaseandal arge
    segmentofapi
    calball
    ooning.Othert
    ypesofwal lmot ionabnor mali
    tieshavebeendescri
    bed,
    butaregenerall
    ynotincoronar
    yvasculardi st
    ri
    buti
    ons.Characteri
    sti
    cal
    ly,t
    heBNPelevat
    ionis
    greatl
    youtofproporti
    ontothet
    roponi
    nr elease,whichisgener
    allymodest.Despi
    tet
    heseverit
    y
    oft he wal
    lmot ion abnor
    mali
    ty,myocar dialscarri
    ng is di
    ff
    icultto documentbycar di
    ac
    magnet i
    cresonance.Commonly,compl
    et enormalizati
    onofLVf uncti
    onisexpect
    ed.

    Alt
    hough there are no speci f
    ic guidelines to di
    rectt herapy,medi cati
    ons thatt argett he
    neurohormonalaxi s and car di
    ac r emodel ing are appr opr i
    atei nt his pat
    ientpopul ati
    on.
    Therefor
    e, angiot
    ensin- conver t
    ing enzyme ( ACE) i nhibitors woul d be i ndicated her e.
    Anti
    coagulati
    onwi t
    hnovelant icoagulant s,suchasapi xibani npat i
    entswi thapicalaneurysms,
    hasnotbeenst udied.Ther eisnoevi denceofper i
    carditis;therefore,t
    reatmentwi thcolchicine
    i
    snoti ndi
    cated.Sacubit
    r il
    /valsartanhasnotbeenst udi edi npat i
    entswi t
    hacutehear tfail
    ureor
    i
    nt hosewhohavenotpr eviouslyt oleratedACEi nhibitors.I CDi mplantati
    onisnoti ndicated
    heresincethisisthefirstdemonst rationofl ow EFint hispat i
    entandmyocar dialrecover yi s
    common.

    4. A25- year-
    oldmanpr esentsforevaluat
    ionofhypert
    rophiccardiomyopathy(HCM) .He
    hasnoexer t
    ionalsymptoms.Hi sf
    atherdiedsuddenlyattheageof40year s.AHol t
    ermoni t
    or
    showsoccasi onalpremat
    urevent r
    icul
    arcompl exes(PVCs),butnononsust ainedventr
    icul
    ar
    tachycar dia(NSVT).OnaBr uceprotocolstr
    esstest,
    hehasSTdepr essionswithexer
    ciseanda
    hypot ensiver esponseto exerci
    se.Theaor t
    icoutfl
    ow vel
    ocityis4 msec;t heseptalwall
    thicknessi s30mm.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    ether
    apy?

    a. Al
    coholsept alabl
    ati
    on.
    b. Surgicalmyect omy.
    c. Me t
    opr ol
    ol.
    d. Disopyrami de.
    e. Animpl antablecardi
    over
    ter
    -def
    ibr
    il
    lat
    or.

    ANSWER:

    4. e. Ani
    mpl
    ant
    abl
    ecar
    diover
    ter
    -def
    ibr
    il
    lat
    or.

    Theassessmentofsuddendeat hr
    iski
    nHCM i spar toft
    herout
    ineevaluati
    onofapatientwi
    th
    thi
    sdiagnosis.Thefi
    vetradi
    ti
    onalri
    skfact
    orsincludesyncope,
    familyhist
    oryofsuddendeat
    h,
    sever
    eleftventr
    icul
    arhypert
    rophy(
    30mm) ,hypotensionwit
    hexerci
    se,andNSVT. 

    Interesti
    ngly,aseverer esti
    nggr adi
    enthasnotbeenest abli
    shedasar iskfactorforsudden
    cardiacdeat h(SCD).Lategadol i
    nium enhancementsuggest i
    veoffi
    brosi
    sandscaroncar di
    ac
    magenet i
    cr esonanceimagi ngmayal sobepr edi
    cti
    veofSCD overandabovecl ini
    calri
    sk
    factors.Inthispati
    ent,
    SCDpr eventi
    onisparamountsincehehast hreeri
    skfactorsforSCD,f
    or
    exampl e,fami l
    yhistor
    y,sever eleftventr
    icul
    arhypertrophy,andahypot ensi
    ver esponseto
    exercise.ThePVCsandr est
    inggradientar
    enotpredi
    ctive. 

    Medicaland/orsurgi
    calther
    apyaregeneral
    lyreservedforsymptomati
    cpat
    ient
    sandmost
    aut
    hor i
    ti
    esfavormyectomyingoodsur
    gicalcandidatesoverabl
    ati
    on,i
    fmedi
    calt
    her
    apyf
    ail
    s
    tor
    elievesymptoms.
    5. A60-year -
    oldmani sadmit
    tedtot hehospi
    talwi
    thdyspneaandabdomi nalbloati
    ng.He
    hasbeenadmittedtwot i
    mesthisyearforacutedecompensatedheartfai
    lur
    e.Therehadbeen
    nopri
    orcar
    diovascularhi
    stor
    y.Heistakingfur
    osemide,di
    goxi
    n,warfari
    n,andmetoprolol
    . 

    Onexami nation,
    heappear schroni
    cal l
    yil
    l.Hisbloodpressureis95/75mm Hgandhear tr
    ateis
    95bpm wi thani rr
    egul
    arr hyt
    hm.Thecent r
    alvenouspr essureistothemandi bl
    eintheseated
    posit
    ion;thecar oti
    dupstrokesareweak.Ral esar epresentinthel ungbases.Auscultat
    ion
    notablef
    orr espi
    rophasicholosyst
    olicmur muroverprecor di
    um andS3 gal
    lop.Theabdomeni s
    di
    stended;li
    verisenlarged.Theextremiti
    esar ecool
    ,andt helegsareedematous. 

    TheB-typenatri
    uret
    icpepti
    de( BNP)is1400pg/ ml,f
    erri
    ti
    nis89mcg/ L,t
    ransferri
    nsaturation
    i
    s32%,bl oodureani t
    rogenis60mg/ dl
    ,andcr eati
    nineis2.5mg/ dl
    .Anel ectrocar
    diogram
    showsatri
    alfi
    bri
    ll
    ati
    on,ri
    ghtwardaxis,andnarrowQRSwi thprecordialQRSampl i
    tudeof4mV.
    Anechocardi
    ogram demonst r
    atesanej ecti
    onfract
    ionof50%wi thleftventr
    icularhypertr
    ophy
    (LVH;20 mm post eri
    orwal l
    ),moder atemi t
    ralregurgi
    tati
    on,tricuspidregur gi
    tati
    on,smal l
    peri
    car
    dialef
    fusi
    on,andseverebiatr
    ialenlar
    gement .

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    ydi
    agnosi
    s?

    a. Cardi
    acamyl oi
    dosi s.
    b. Hypert
    rophiccardiomyopathy.
    c. Heartf
    ail
    urewi t
    hpr eser
    vedeject
    ionf
    ract
    ion(
    HFpEF)
    .
    d. Constr
    ict
    ivepericardi
    ti
    s.
    e. Hemochromat osis.

    ANSWER:

    5. a. Car
    diacamyl
    oidosi
    s.

    HFpEFi sadi agnosisofexclusi


    on.Thispat i
    enthassever ebiventricul
    arheartfai
    lur
    e,alow
    bloodpr essur ei ntheabsenceofvasodi l
    ators,andaver yelevatedBNPdespi t
    et henormal
    eject
    ion f raction.Moreover,the elect
    rocardiogram shows low vol t
    age and an anteri
    or
    myocar dialinfarcti
    ondespi
    tetremendousLVH, noanter
    iorwallmotionabnor mali
    ty,
    andsevere
    biatr
    ialenlar gement.Thesefindi
    ngsar eallhighlysuggest
    iveofar estr
    ict
    ivecardi
    omyopathy
    (e.g.
    ,amyl oidosis).
     

    Hemochr omat osi


    sdoesnottypi
    cal
    lypr esentwit
    har estri
    cti
    vecardi
    omyopathy,butratherwi
    th
    adi l
    atedcardiomyopathy.I
    naddit
    ion,thet r
    ansf
    er r
    insat urati
    onof32%i snotconsistentwi
    th
    thisdiagnosis.Theveryelevat
    edBNPi snotchar acteri
    sticofeit
    herconstri
    cti
    onorHFpEF.
    Hypertrophiccardi
    omyopathycanpr esentinit
    sl atest ageswi t
    hsevereheartfai
    lur
    e,butthe
    eject
    ionfracti
    onisgeneral
    lyi
    mpair
    ed, alt
    houghthehear tmaynotbedilated.

    6. A 60-year-ol
    d woman pr esentst o your off
    ice on advi
    ce ofher brother
    ,who
    recommendst hatshebeeval
    uat edforhypertr
    ophiccardiomyopat
    hy(HCM).Shebringscopies
    ofhi s medi
    calr ecor
    ds.He had an out -of
    -hospitalcardi
    ac arr
    estand for
    tunatel
    y was
    resusci
    tat
    edsuccessfull
    y.Hi
    sechocar di
    ogram demonst r
    atedHCM wit
    ha1. 8cm ventricul
    ar
    septum.Shehasnothadgenot ypingper f
    ormed. 

    Yourpat
    ienti
    sasympt
    omat
    icandherexam,i
    ncl
    udi
    ngcar
    diovascul
    ar,i
    sunr
    emar
    kabl
    e.You
    obtainanechocardi
    ogram,whichistechni
    cal
    lyverydiff
    icul
    t,butyouareconf
    identt
    hather
    septum i
    snotthi
    ck,al
    thought
    heotherlef
    tvent
    ri
    cularwall
    sarenotwellseen.
     
    Atthispoi
    nt,
    yourecommendshehavewhi chofthefol
    lowing?

    a. Cardiacmagnet i
    cresonancei
    maging(MRI
    ).
    b. Exercisestr
    esstest.
    c. 24-hourHol t
    ermonitor
    .
    d. Genetictest
    ingusinganHCM panel.
    e. El
    ectrophysiol
    ogystudy.

    ANSWER

    a. Car
    diacmagnet
    icr
    esonancei
    magi
    ng(
    MRI
    ).

    HCM hashet
    erogeneousphenot ypi
    cexpr essi
    on.Alt
    houghyoucanexcl udesept alhyper
    trophy,
    shemaymanifestHCM throughhypertrophyinotherpart
    sofherleftvent
    ricle.Cardi
    acMRIhas
    aClassIi
    ndi
    cati
    ontoassessf orHCM whenechocar di
    ographyi
    sinconclusiveofthediagnosis.
    Nei
    theraHol
    ternorexer
    cisestresstestwi l
    lconf
    ir
    m orref
    utethediagnosisofHCM.  

    I
    fgenetictest
    ing i
    s desir
    ed,itwould be more appropri
    atet otestt
    he brot
    herwho has
    documentedHCM,andt hengenotypeyourpat
    ientf
    orani dent
    if
    iedmutat
    ion.Fur
    thert
    est
    ingi
    s
    i
    ndicat
    edbecauseyourpati
    entcouldbeatri
    skforsuddendeathifsheisf
    oundtohaveHCM.

    7. A17-year-ol
    dwomanwhoi sahi ghschoolsoccerpl
    ayerpresent
    st otheemergency
    room wi
    threport
    sofchestpainfor1week.Shereport
    shavingalow-gradefeveranddi
    arr
    hea.
    Sheisschedul
    edtoplayinherteam’sst
    atechampionshi
    psoccergamenextweek.  

    Herphysi calexaminati
    onshowshert obeinnoappar entdistressthoughsomewhatanxi ous,
    herpulsei s100bpm wi t
    hsomepr emat urebeat
    s,andherbl oodpr essur
    ei s110/70mm Hg.
    Shehasanor malS1 andS2 withnoS3 ormur mur,herneckvei nsar enotdi st
    ended,andt he
    remainderofherexami nationisunr
    emar kabl
    e.Herelectrocardiogram isnotableforpremature
    ventr
    icularcont r
    acti
    onsand l ow volt
    age.Hercar diact roponi nisundet ectabl
    e.A limited
    echocardiogram intheemer gencyroom showsal eftventricularejecti
    onfracti
    onof50%wi th
    noper i
    cardialef
    fusi
    on.

    Whi
    choft
    hef
    oll
    owi
    ngi
    syourbestcour
    seofact
    ion?

    a. Dischar
    gehomeonl ow-dosebet
    a- bl
    ocker
    s,butadviseshenotplayinthesoccergame.
    b. Dischar
    gehomewi t
    hnomedi cat
    ionsandcleartoplayinthesoccergame.
    c. Admi ttothe hospit
    alforfurt
    herdi agnost
    ictest i
    ng,incl
    uding cardi
    ac magneti
    c
    r
    esonancei
    magi
    ng(
    MRI
    ).
    d. Admi
    ttoobser
    vat
    ionst
    atusover
    nightanddi
    schar
    gei
    fser
    ialcar
    diacenzymesr
    emai
    n
    negat
    ive.
    e. Di
    schar
    gehomeonl
    ow-
    dosebet
    a-bl
    ocker
    swi
    thcl
    ear
    ancet
    opl
    ayi
    nthesoccergame.

    ANSWER

    c. Admi
    ttot
    he hospi
    talf
    orf
    urt
    herdi
    agnost
    ict
    est
    ing,i
    ncl
    udi
    ng car
    diac magnet
    ic
    r
    esonancei
    magi
    ng(
    MRI
    ).

    Myocar di
    ti
    scanpr esenti nvariablef ashion.Shef ul
    fil
    scriteriaproposedbyt heEuropean
    SocietyofCar di
    ologyf ormyocar diti
    s.Sheshoul dnotpar ticipateincompeti
    ti
    vesportswith
    possibl
    eacut emyocar dit
    is,evenwhi leonbet a-bl
    ockers.Furtherdiagnost
    ict
    esti
    ngtoconfir
    m
    whethershehasmyocar dit
    isiswar ranted,anditwouldber easonabl et
    oobtai
    nacar di
    acMRI
    wit
    hgadol i
    nium.Anendomyocar dialbiopsyshouldalsobeconsi der
    ed. 

    8. A17-year-oldmalehighschoolstudenti
    nDall
    as,Texas,whowaspr evi
    ouslyhealt
    hy
    present
    edwithacut esyst
    oli
    cheartf
    ail
    ureintheset
    ti
    ngofaf ebr
    il
    eill
    nessinthesummer .He
    doesnotdri
    nkal cohol
    ,smoke,orusedrugsandisnotsexual
    lyacti
    ve.Endomyocar
    dialbi
    opsy
    confi
    rmedt
    hedi agnosisofmyocardi
    ti
    s.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    yvi
    ralet
    iol
    ogyofhi
    sil
    lness?

    a. I
    nfl
    uenzaB.
    b. Par
    vovirusB19.
    c. CoxsackieB.
    d. Humani mmunodef
    ici
    encyvi
    rus(
    HIV)
    .
    e. Adenovir
    us.

    ANSWER

    c. Admittothe hospi
    talf
    orf
    urt
    herdi
    agnost
    ict
    est
    ing,i
    ncl
    udi
    ng car
    diac magnet
    ic
    resonancei
    magi
    ng(MRI).

    Myocar di
    ti
    scanpr esenti nvariablef ashion.Shef ul
    fil
    scriteriaproposedbyt heEuropean
    SocietyofCar di
    ologyf ormyocar diti
    s.Sheshoul dnotpar ticipateincompeti
    ti
    vesportswith
    possibl
    eacut emyocar dit
    is,evenwhi leonbet a-bl
    ockers.Furtherdiagnost
    ict
    esti
    ngtoconfir
    m
    whethershehasmyocar dit
    isiswar ranted,anditwouldber easonabl et
    oobtai
    nacar di
    acMRI
    wit
    hgadol i
    nium.Anendomyocar dialbiopsyshouldalsobeconsi der
    ed. 

    9. Youareevaluati
    nga25- year-ol
    dAf r
    ican-Ameri
    canmani nt heemergencydepart
    ment
    (ED)
    .Hehadbeenwat chinghisnephewpl ayfootbal
    landhadsyncopeandcol l
    apsedwhenhe
    waswalking up t
    hestadium steps.When t hepar amedicsarri
    ved,theynoted hewasi n
    i
    nter
    mit
    tenthi
    gh-gradeatri
    ovent
    ri
    cular(AV)blockandtranspor
    tedhimtoyourhospital
    .

    Anelectrocar
    diogram i
    ntheEDconfir
    mstheirf
    indi
    ngs.I
    nt al
    kingwithhim,herepor
    tshehas
    beenmor eshor tofbr
    eaththepast2monthscomparedwithhisbaseli
    ne.Onexaminat
    ion,he
    hadjugularvenouspressur
    eof12cm andanaudibl
    eS3.ChestX-rayshowedcardi
    omegalybut
    noinfi
    lt
    rates.

    Youobt
    ainanechocardi
    ogr
    am,whichr
    eveal
    shislef
    tvent
    ri
    cul
    ar(LV)eject
    ionf
    ract
    ioni
    s25%
    wit
    hanLVdiast
    oli
    cdimensi
    onof6.
    5cm.Cardi
    acenzymesarenegat
    ive.

    Whi
    choft
    hef
    oll
    owi
    ngdi
    agnost
    ict
    est
    swoul
    dyounextr
    ecommend?

    a. Exer
    ciseper
    fusi
    oni
    magi
    ng.
    b. 48-hourHoltermoni tor
    .
    c. Endomy ocardialbi
    opsy.
    d. Lef
    t-heartcatheter
    izati
    on.
    e. El
    ectrophysi
    ology( EP)test
    ing.

    ANSWER

    9. c. Endomyocar
    dialbi
    opsy.

    Thepr esentationofacutesyst oli


    chear tfail
    urewi thhigh- gradeAVbl ockr aisesthespecterof
    myocar di
    tiscausedbygi antcel lmyocar di
    t i
    sorani nf
    il
    trati
    vepr ocesssuchassar coi
    dosis.The
    AHA/ ACC/Eur opeanSociet yofCar di ologysci entif
    icst atementont heroleofendomyocar dial
    biopsyi nt hemanagementofcar diovascul ardi seasehasa Cl assIr ecommendat ion f
    or
    endomyocar di
    albiopsyf ornew- onsethear tfai
    lureof2weekst o3mont hsdur at
    ionwi t
    ha
    dil
    atedLVandnew vent ricul
    arar rhyt hmi as,second-ort hi
    rd-degreehear tblock,orfail
    ureto
    respondt ousualcar ewithin1t o2weeks.Atage25,cor onaryarterydiseasewoul dbemuch
    l
    essl ikel
    y.Ther eisnoi ndicati
    onf oradi agnosticEPst udyor48- hourHol termonitorinthe
    setti
    ngofacut emyocar diti
    s. 

    10. A 38- year-ol


    d woman pr esentstot he emergency depar
    tmentwi t
    h 5 days of
    progressiveexer
    t i
    onaldyspnea,fati
    gue,andmildl
    owerext r
    emityedema.Shehadprevi
    ously
    beenf eel
    ingwell.Hermedi calhi
    stor
    yi snot
    abl
    eforhypothyr
    oidi
    sm secondar
    ytoHashi
    moto's
    thyroi
    diti
    s.Heronl ymedi cati
    onisl evot
    hyr
    oxi
    ne.Herhear trat
    ei s105bpm andherblood
    pressureis92/68mm Hg.  

    Onphysi calexamination,ther
    ei smoder atejugularvenousdi stent
    ion,t
    achycardicbutregular
    rhythm withoccasionalprematurebeat s, anS3, bi
    basil
    arral
    es, andcoolperi
    pher alext
    remit
    ies.
    Shei sadmi t
    tedtot hecar di
    aci ntensivecar eunitforfurtherwor kup.Anechocar diogram
    demonst ratessevereleftventr
    iculardysf unctionwithanej ectionfract
    ionof23%.Thenur se
    notif
    iesyout hatthepat i
    entishavi ngmul tiplerunsofmul ti
    focalnonsustai
    nedvent ri
    cular
    tachycardia.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    yet
    iol
    ogyoft
    hepat
    ient
    'scar
    diomyopat
    hy?

    a. Cardiacamyloi
    dosis.
    b. Takotsubo(str
    ess)cardi
    omyopat
    hy.
    c. Chagasdisease.
    d. Cardiacsar
    coidosi
    s.
    e. Giantcel
    lmyocarditi
    s.

    ANSWER:

    10. e. Gi
    antcel
    lmyocar
    dit
    is.

    Thispatient'
    spr esentat
    ion i snotableforr apidl
    ypr ogressi
    veheartfai
    luresymptomsand
    ventr
    icul
    arar rhythmi as.Takot subo (st
    ress)car di
    omyopat hytendsto presentin an ol
    der
    pati
    entpopulat i
    on( cl
    assicallypostmenopausalwomen)andmaybepr ecededbyanacut e
    emotionalorphysi calstress;neitherisment ionedher e.Cardi
    acamyloi
    dosisalsot endsto
    aff
    ectol derindividuals.Al though cardiac sarcoi
    dosis may be associ
    ated both withlef
    t
    ventr
    icul
    ar dysf unct i
    on and ar r
    hythmias,i ti s usuall
    y seen inindi
    viduals wit
    h other
    manifestat
    ionsofsarcoi
    dosi
    s.Chagasdiseaseisani
    mportantcauseofcar
    diomyopathyin
    Centr
    al and Sout h Amer i
    ca, usual
    ly devel
    opi
    ng year
    s or decades after i
    nfect
    ion
    wit
    h Trypanosomacruzi.
     

    Giantcellmyocardit
    isiscommonl yseeni nyoungeri ndi
    vidual
    s,i
    sr api
    dlyprogressi
    ve,andi s
    often associ
    ated wit
    h ventr
    icul
    ararrhythmias.Ther eisa hi gh f
    requencyofaut oi
    mmune
    disordersini
    ndivi
    dualswithgiantcel
    lmyocar di
    ti
    s.Thus,gi antcel
    lmyocar dit
    isisthecorrect
    opt i
    on.Endomyocardialbi
    opsyisindicat
    edf orpatientswithrapi
    dlyprogressi
    ve,unexplai
    ned
    cardiomyopathyasgiantcel
    lmyocarditi
    smayber esponsivetoimmunosuppr essi
    on. 

    11. Whi
    choft
    hef
    oll
    owi
    ngi
    sTRUEr
    egar
    dingt
    heepi
    demi
    ologyofhear
    tfai
    lur
    e(HF)
    ?

    a. Atage40year
    s,t
    heli
    fet
    imeriskofdevel
    opi
    ngHFis20%.
    b. Thebenef
    it
    sofbloodpressurecontroli
    nreduci
    nginci
    dentHFar
    eseenpr
    imar
    il
    yin
    youngerandmi ddl
    e-agedadults,withnosi gnif
    icanteffectamongadults>80year
    sof
    age.
    c. Theinci
    denceandpr eval
    enceofHFar eincreasi
    ng, butonlyintheWesternhemi
    spher
    e
    andinhigh-
    income/developedcount r
    ies.
    d. HFamongadul ts<50yearsofagei smor ecommoni nwhi test
    hanblacks.
    e. Amongadults>65year sofage,theincidenceofHFi shigherinwoment hanmen.

    ANSWER

    11. a. Atage40year
    s,t
    hel
    if
    eti
    mer
    iskofdevel
    opi
    ngHFi
    s20%.

    HFamongadul t
    s<50year sofagei smor ecommoni nblackst hanwhi t
    es.Thei nci
    denceofHF
    i
    smor ecommoni nolderment hanolderwomen.I ntheHyper tensi
    onint heVer yEl
    derlyTr i
    al,
    amongadul ts>80yearsofagewi t
    habasel i
    nesystol
    icbloodpr essure=160mm Hg, tr
    eat ment
    wit
    hindapami deorperindopri
    lwasassoci atedwit
    ha64%r elativeri
    skr educti
    oninther ateof
    HF.Althoughtheeti
    ologyofHFvar i
    esaroundtheworld,HFisawor ldwidepandemi cwithbot h
    i
    ncreasinginci
    denceandpr evalence,especi
    all
    yintheelderl
    y.Atage40year s,t
    heli
    fet
    imer i
    sk
    ofdevelopi
    ngHFi sapproximately20%.Ther i
    skofnewHFatage80year sisalso20%. 

    12. Amongi ndi


    vidual
    snewlydi
    agnosedwi
    thhear
    tfai
    lur
    e,t
    he5-
    yearmor
    tal
    it
    yrat
    eis
    cl
    osestt
    owhi
    chofthefol
    lowi
    ng?

    a. 20%.
    b. 40%.
    c. 50%.
    d. 30%.
    e. 60%.

    ANSWER: 

    12. c. 50%.

    The 5-
    year mor
    tal
    it
    yrat
    e among i
    ndi
    vidual
    s newl
    y di
    agnosed wi
    th hear
    tfai
    lur
    eis
    appr
    oxi
    matel
    y50%.

    13. Hear
    tfai
    lur
    e(HF)r
    epr
    esent
    sAmer
    ica'
    slar
    gestdi
    agnosi
    s-r
    elat
    edgr
    oup,l
    eadi
    ngt
    othe
    f
    actt
    hatmor
    eMedi
    car
    edol
    lar
    sar
    espentonHFt
    hanonanyot
    herdi
    agnosi
    s.

    Which ofthe f
    oll
    owi
    ng condi
    ti
    ons r
    epr
    esentt
    he hi
    ghestpopul
    ati
    on at
    tr
    ibut
    abl
    eri
    sk f
    or
    devel
    opingHF?

    a. Micr
    oalbuminuri
    aandl eftvent
    ri
    cularhypert
    rophy.
    b. Di
    abetesandobesi t
    y.
    c. Hypert
    ensionandcor onaryart
    erydisease.
    d. Smok i
    ngandchr oni
    cki dneydi
    sease.
    e. Peri
    pheralar
    ter
    ialdi
    seaseandhypot hyr
    oidi
    sm.

    ANSWER: 

    13. c. Hyper
    tensi
    onandcor
    onar
    yar
    ter
    ydi
    sease.

    Alloftheriskf
    actorslist
    edhavebeenassoci
    atedwit
    hHFinselectpopulat
    ions.Thegr
    eatest
    ri
    skf act
    orsfordevelopmentofHFacrossallpopul
    ati
    onsi
    ncl
    udehypertensionandcoronary
    arter
    ydisease.

    14. A 56- year-


    old patient wit
    hl ong-standing heartf ailur
    e( HF) from nonischemi
    c
    cardiomyopathypr esent
    st ot heemergencyr oom with dyspneaand pr esyncope.Hehas
    recentl
    yexper i
    enced shocksf rom hi
    si mplantablecardi
    over ter-
    def
    ibri
    ll
    ator(ICD)and now
    presentswit
    hdyspneaatr est,dif
    fi
    cul
    tyconcentrati
    ng,anddecr easeduri
    neout put.
     

    Onexami nat
    ion,heisi
    nmoder atedistr
    esssecondarytobreat
    hlessness.Hi
    sbloodpressur
    eis
    88/62mm Hgandhi sheartr
    ateis100bpm.Jugul arvenouspressureisel
    evat
    ed,andhehasa
    prominentS3 gal
    lop.Dist
    alextremit
    iesarecoolt ot ouch,and thereis2+ pit
    ti
    ng edema.
    Creat
    ininei
    selevatedt
    o2.1mg/ dlfr
    om abaseli
    neof1. 3mg/dl.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextmostappr
    opr
    iat
    ether
    apy?

    a. Dobutamine.
    b. Bet
    a-blockers.
    c. I
    ntr
    avenous( IV)f
    lui
    ds.
    d. Ni
    troprussi
    de.
    e. Amiodarone.

    ANSWER: 

    14. a. Dobut
    ami
    ne.

    Thepat i
    entisin car
    diogenicshockwi t
    h evidenceofend- organ hypoper f
    usi
    on (el
    evated
    creati
    nineandchangesinment alstat
    us).Despi
    tehypotension,therei
    sevi denceofanincrease
    inintr
    acardiacfi
    ll
    ingpressures,andt herapyshouldfocusonbot hincreasingperf
    usionand
    decreasingvolumeoverload.Bet a-
    blockersarecontr
    aindicatedbecauseofshockdespi tehis
    ventri
    cularect
    opyandICDshocks.  

    Nit
    roprusside mi
    ghtbe appropr
    iatein a hypotensi
    ve pati
    entifi nvasi
    ve hemodynami cs
    demonst r
    ateaseverel
    yelevat
    edsystemicvascularresist
    ance.Inthiscase,theeti
    ologyof
    hypotensi
    oni suncl
    ear,andempi r
    icni
    tr
    oprussideint hissett
    ingcouldwor senthe 
    cli
    nical
    situati
    on. I
    Vfluidswouldnotbehel pfulsincet heover allpictureisoneofvolumeover loadand
    reduced car diac output.His nonsust ained vent riculart achycar
    dia and subsequentI CD
    dischargesar emor elikel
    yar eflecti
    onof  
    hiswor seningHF.I Vamiodaronelikel
    ywi l
    lwor sen
    hisHFduet obet a-
    blockeref
    fect .
     Thebestopt i
    oni sdobut ami nebecauseitmostr apidlywill
    i
    mpr ovehiscar di
    acoutputandaddr esshi scar di
    ogeni cshock.
    15. A42- year-ol
    dmal epatientwi thahi storyofhyper t
    ensi onandrecentdiagnosisofhear t
    fail
    ure( HF)pr esent
    st oyourof ficef orfur t
    hereval uat ion.Hehasal eftventri
    cul
    arej ect
    ion
    fracti
    on( EF)of35%.Hi smedicalr egimeni ncludescar vedilol25mgbi d,li
    sinopri
    l10mgdai l
    y,
    furosemi de20mgdai l
    ywhennecessar y,andamul t
    ivitami n. 

    Pri
    orwor kup f
    orhis cardiomyopathy di
    d notshow a r ever sible cause,and coronar
    y
    angi
    ogr aphydemonst
    ratednocoronar yl
    esi
    ons.Hehasnopr oteinur ia,hemogl
    obinA1cis5.2,
    andl ow-densi
    tyli
    poprotei
    nwasf oundtobe80mg/ dl
    .Hecur rent l
    yhasNew Yor kHear t
    Associati
    on(NYHA)classIsympt oms,anormalphysi
    calexami nat ion,andbloodpressur
    eof
    128/92mm Hg.

    Whichofthefol
    lowingisthenextbestst
    epi
    nmanagementpr
    iort
    oeval
    uat
    ionf
    ori
    mpl
    ant
    abl
    e
    car
    diover
    ter
    -def
    ibri
    ll
    ator(
    ICD)?

    a. Eplerenone25mgdai l
    y.
    b. Digoxin0. 125mgdai ly.
    c. As pi
    rin81mgdai ly.
    d. Increaselisinopr
    ildose.
    e. Ros uvastati
    n10mgdai ly.

    ANSWER: 

    15. d. I
    ncr
    easel
    isi
    nopr
    ildose.

    Inthispati
    entwithrecentlydiagnosedcar diomyopathy,opti
    mizati
    onofmedi calt
    herapyshould
    beper f
    ormedpr i
    ortoconsi derati
    onforICDpl acementforprimarypreventi
    onofsuddencar diac
    death.Eplerenonehasbestbeenst udiedi nthepost- myocardi
    alinfarcti
    onpopul at
    ionand
    chronicHFpat i
    entswi thNYHA cl assI I-I
    Vf uncti
    onalclass(thi
    spat ienti sclassI)
    .Int he
    absenceofanot herindicat
    ion,therei
    snoevi denceofbenefitf
    oruseofst ati
    nsoraspi r
    ini
    nt he
    HFwi thpreservedEFpopul ati
    on.Ther oleofdi goxi
    nint heHFwi thpr eservedEFpopulati
    on
    remainscont r
    oversi
    al,butmayr educehospi t
    ali
    zat
    ions.

    16. A62- year-


    oldmanpresentstothehospi
    talwith2weeksofprogr
    essi
    vemid-ster
    nal
    chestpr
    essurewhenwalki
    ngatanor malpaceonlevelgr
    ound.Pr
    iort
    o1mont hago,hewas
    worki
    ng12hour s/
    dayasaroofer
    .Hisvi
    talsi
    gnsarebloodpr
    essur
    e123/84mm Hgandhear t
    rat
    e88bpm.  

    Onexam,hehasnosi gnsoff l
    uidoverl
    oad.Laboratori
    esarenor malwi t
    ht heexceptionofan
    el
    evatedB- typenatri
    ureticpepti
    de.Hisechocar di
    ogram showsgl oballeftventri
    cular(LV)
    hypokinesi
    swi t
    hanLVej ect
    ionfr
    acti
    on(LVEF)of20%, LVdiastol
    icdiamet erof6cm, andmi l
    d
    concentri
    cLVhyper tr
    ophy.Coronaryangiographydemonstratesmul ti
    vesselcoronarydisease
    wit
    hf ocalpr
    oximalstenosesof70%i nthecir
    cumflex,70%i
    nt heleftanteri
    ordescendingar t
    ery,
    and80%i ntherightcoronaryart
    ery.
     

    Hei
    sst
    art
    edonaspi
    ri
    n81mg,
    lisi
    nopr
    il10mg/
    day,
    ator
    vast
    ati
    n80mgPOqhs,
    andcar
    vedi
    lol
    12.
    5mgbi
    d.Af
    tersever
    alweeksont
    her
    apy,
    hisexer
    ti
    onalangi
    naper
    sist
    s.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextst
    epi
    nmanagementoft
    hispat
    ient
    ?

    a. LVas si
    stdevi ce(LVAD)implant
    .
    b. Coronaryarterybypasssurgery(CABG).
    c. Nuclearvi
    abi l
    itystudy.
    d. Hearttr
    anspl antli
    sti
    ng.
    e. Magne t
    icresonancei maging(MRI)vi
    abil
    it
    yst
    udy.

    ANSWER: 

    16. b. Cor
    onar
    yar
    ter
    ybypasssur
    ger
    y(CABG)
    .

    Theuseofcor onar yrevasculari


    zation(surgicalorper cutaneous)i
    naddi ti
    ont oguideli
    ne-
    di
    rectedmedi caltherapyi npat ient
    swi thhear tf
    ail
    ure( HF)andr educedLVEFshoul dbe
    i
    ndividual
    ized.Inthiscase, i
    tisaCl assIrecommendat i
    ont oproceedwithrevascul
    ari
    zati
    onf or
    i
    mpr ovementofangi nalsympt omsi n a pat i
    entwith HF and suit
    ablecor onar
    yanat omy.
    Furt
    hermor e,surgicalrevascul
    arizati
    onisr easonabletoimpr ovemorbidi
    tyandcardiovascular
    mortali
    tyforpat i
    entswi t
    hsever eLVdysf unction(EF<35%) ,HF,andsigni
    fi
    cantcoronaryartery
    di
    sease( ClassIIa).
     

    Myocardialvi
    abil
    it
    ytesti
    nghasar oleincer t
    ainpat i
    ents.However ,inthiscase,i ti
    sunlikelyto
    changemanagement .Further,inananal ysisoft heSTI CH (
    Sur gicalTr eatmentforIschemi c
    HeartFail
    ure)t
    ri
    alofsurgicalr evasculari
    zati
    oni npatientswit
    hsever eLVsyst ol
    icdysf
    unct i
    on,
    theassessmentofmyocar dialviabil
    itydidnoti dentifypat
    ientswi thadi f
    fer
    enti
    alsur vival
    benefi
    tfrom CABG,as compar ed wi t
    h medi calther apyalone.Ref erralforadvanced HF
    ther
    apiesincl
    udingLVADandhear ttransplantisreasonableinpat ientswi thsevereLVsyst olic
    dysf
    unctionwhohaveexhaust edconvent ionaltherapiesincl
    udinggui deline-
    dir
    ectedmedi cal
    ther
    apyandconvent i
    onalcar diacsurgery.Inthiscase, suchar ef
    erralwoul dbepremature.

    17. A 58- year-ol


    d man wi th a strong family histor
    y ofhear tfail
    ure( HF)has an
    echocar diogram per formedbyhi spr i
    mar ycarephysician.Theechocardiogram showsal ef
    t
    ventricul
    arej ect i
    onfract i
    on(EF)of35%.Hei sanact ivenonsmokerwhoexer ci
    sesr egul
    arl
    y
    withoutdi ff
    iculty.Exami nati
    onisunremar kabl
    eexceptf orabloodpressureof144/ 92mm Hg
    andhear trateof74bpm.Labor atorytestsareunremar kabl
    e.Heprefer
    snott otakeanymor e
    medi cati
    onsandcont rolhypert
    ensionwi t
    hdietandexercise.

    Whi
    choft
    hef
    oll
    owi
    ngi
    syourr
    ecommendat
    ionf
    ort
    hispat
    ient
    ?

    a. Nome dicalt
    herapyunl
    essHFsymptoms.
    b. Angi
    otensin-
    convert
    ingenzymei
    nhi
    bit
    orsandbeta-blocker
    s.
    c. Angi
    otensin-
    convert
    ingenzymei
    nhi
    bit
    orsanddigoxin.
    d. Nome dicalt
    herapyunl
    essEFremai
    nsdepressedat90days.
    e. Cal
    cium channelbl
    ocker
    .

    ANSWER: 

    17. b. Angi
    otensi
    n-conver
    ti
    ngenzymei
    nhi
    bit
    orsandbet
    a-bl
    ocker
    s.
    Asympt omaticdecr easesinEF( StageBHF)shoul dbet reatedwi thangiotensin-convert
    ing
    enzymei nhi
    bitortherapyandabet a-bl
    ockertherapyasanaddi tionaldrug.Therapyshoul dnot
    bedel ayedwhi l
    eawai ti
    ngi mprovement .Whil
    eappr opri
    ateforhyper t
    ension,calcium channel
    blockerther
    apyi snotindicatedasaf ir
    st-l
    inetherapyf
    orpatientswithreducedEF.  

    18. A68- year


    -oldmal epati
    entwithahistor
    yofhypert
    ension, di
    abet
    es,andmorbi
    dobesity
    present
    stoyourcli
    nicwithcomplaint
    sofdyspneaonexerti
    onf orthepast2months.Hedenies
    chestdiscomfor
    t,orthopnea,paroxysmalnocturnaldyspnea,l owerext
    remit
    yswel l
    ing,or
    abdominalbl
    oati
    ng.Her eport
    sheisr el
    ati
    vel
    ysedentar
    yandhasbeenmor esosincetheonset
    ofsymptoms.Hehasa20pack- yearhist
    oryofsmokingandqui t20year
    sago. 

    Onexami nati
    on, hisbloodpr essur eis150/ 90mm Hgandhi shear trateis78bpm.Hi soxygen
    saturationi s98%onr oom airatr estandwi thambul ati
    on.Thej ugularvenouspr essureis6cm
    H2O.Thecar diacexami nati
    onr evealsar egularr ateandr hythm wi t
    hagr ade2/6hol osystoli
    c
    mur muratt he rightl owerst ernalborder .The abdomen i s notdi st
    ended wi t
    houtany
    appreci ableasci t
    es.Thel ungsar ecleartoauscul t
    ation.Theext r
    emi t
    iesar ewarm andwi thout
    edema.Theel ectrocar di
    ogram demonst ratesl eftvent ri
    cularhyper t
    rophy( LVH)byvol tage
    cri
    teria.Theechocar diogram repor tsnormalbi ventricularfuncti
    on,mi ldLVH,mi ldleftatri
    um
    enl
    ar gement ,and mi ld mitralr egurgi
    tati
    on.A phar macol ogi
    c nucl earper f
    usion study is
    negat i
    vef ori nducibleischemi a.Amonghi slabor atoryevaluati
    on,hi sN- ter
    minalpro–B- type
    natri
    ur eti
    cpept ide( NT-proBNP)i s100pg/ ml.

    Whichofthef
    oll
    owi
    ngoft
    hef
    oll
    owi
    ngi
    smostl
    ikel
    ytobehel
    pfuli
    nest
    abl
    ishi
    ngt
    hecor
    rect
    di
    agnosi
    s?

    a. Cardiacmagnet i
    cr esonanceimagi
    ng.
    b. Transesophagealechocar di
    ogram.
    c. Ri
    ght -heartcatheterizat
    ionwit
    hexerci
    se.
    d. Coronaryangi ography.
    e. Treadmi l
    lstresstest.

    18. c. Ri
    ght
    -hear
    tcat
    het
    eri
    zat
    ionwi
    thexer
    cise.

    Hear tfail
    urewi t
    hpr eser
    vedeject
    ionf
    ract
    ion( HFpEF)ist hecli
    nicaldi
    agnosis.Pat i
    ent
    soft
    en
    presentwi thsignsandsympt omsofcongesti
    on.Typicalfeatur
    esonechocar diographyi
    ncl
    ude
    LVH,l eftatri
    alenlargement
    ,andabnormalE/ e'values.Thenat r
    iuret
    icpept
    idel evelsmaybe
    onlymi l
    dlyelevated.Hehasnor malNT- pr
    oBNPl evel
    s,butt hi
    scanbeconf oundedbyhis
    mor bidobesity. 

    Inthiscase, thedi agnosi


    sismoredi f
    fi
    cultasthi
    spatientiseuvol emiconexami nat i
    onandhas
    sympt oms onl y with exer
    ti
    on.Ther ei s a wi
    derdi f
    ferentialdiagnosis,i
    ncludi ng chr
    onic
    obstructi
    vepul monar ydisease(given hissmoking history)and decondi t
    ioning (gi
    ven his
    sedentaryl i
    festyl
    e and mor bi
    d obesity).Inthese cases,r i
    ght-heartcat
    heter i
    zati
    on may
    demonst ratenor malhemodynami csatr est
    ,butanexagger atedincreaseinfil
    lingpressures
    wit
    hexer ci set hatmaybeaccompani edbyabl unt
    edi ncreasei ncar di
    acoutput ,whichhelp
    establi
    sht hedi agnosisofHFpEF. 

    Whileacardi
    acmagneticr
    esonancemaybeusefultoeval
    uat
    ecardi
    acfuncti
    onandassessfor
    scarandotherpot
    ent
    ialet
    iol
    ogi
    esofHFpEF,i
    tsuti
    li
    tyi
    nmakingadiagnosisofHFpEFi
    slow.A
    tr
    ansesophagealechocar
    diogr
    am is unli
    kel
    yt o yiel
    d addi
    ti
    onalinformati
    on.Coronary
    angi
    ogr
    am maybehel pfuli
    fhisshort
    nessofbreathi
    sthoughttobeanangi
    nalequi
    val
    ent
    ,but
    hi
    snegati
    veperfusi
    oni magingmakest hi
    sl essli
    kel
    y.Ast andar
    dtr
    eadmil
    ltesti
    sli
    kel
    yt o
    i
    nducedyspnea,
    butthiswil
    lnotident
    if
    yeti
    ology.
     

    19. A54- year


    -oldmanwi thahi stor
    yofhear tfai
    lur
    ewi t
    hpr eser
    vedej
    ect
    ionf r
    act
    ionis
    ref
    err
    edtoyouf orrefr
    act
    oryvolumeover load.Onexami nat
    ion,hehasanelevatedjugul
    ar
    venouspr
    essure,
    clearl
    ungs,
    regularheartr
    atewithS4,
    andpi t
    ti
    ngedemat ot
    het
    highs. 

    Your evi
    ew hi sdi agnosti
    cst udiesincludi
    nganel ectr
    ocar diogr am (ECG)t hatdemonstr ates
    sinusr hyt
    hm, l
    owvol t
    ageinthel i
    mbl eads,andnonspeci f
    icl ateralST-Twavechanges, andan
    echocar di
    ogr am t hatdemonst ratesconcent r
    icleftvent
    ricul arhyper t
    rophy,al ef
    tventri
    cul ar
    eject
    ion fraction of50%,sever ebi atr
    ialenlargement,and an est i
    mat ed pulmonar
    yar tery
    systolicpressureof50mm Hg.Apr iorri
    ght
    - heartcat
    heterizat i
    ondemonst r
    atesequali
    zati
    onof
    diastoli
    cpr essures, aprominentYdescenti nther i
    ghtatri
    altr acing,anda" square-
    root"signi n
    therightvent ri
    culartraci
    ng.

    I
    nadditi
    ontoi
    ntensi
    fyi
    ngt
    hepat
    ient
    'sdi
    uret
    icr
    egi
    men,whi
    choft
    hef
    oll
    owi
    ngshoul
    dbe
    per
    for
    med?

    a. Comput edtomogr aphycoronaryangiogr


    am.
    b. Coronaryangi ogr
    aphy.
    c. Endomy ocardialbiopsy.
    d. Chestcomput edtomographywithoutcont
    rast
    .
    e. Exerci
    senucl earperfusi
    onimaging.

    ANSWER: 

    19. c. Endomyocar
    dialbi
    opsy.

    This pati
    ent '
    s exam and di agnost i
    c studies are highly suggestive of an infil
    tr
    ati
    ve
    cardi
    omyopat hy resulti
    ng i nar estri
    cti
    ve cardi
    omyopat hy.Despi tet hi
    ckened walls on
    echocardi
    ogr aphy,thel owvol t
    agei nt helimbleadsont heECGi ssuggest i
    veofaninfil
    tr
    ati
    ve
    process.Bi atri
    alenl argementwi thoutval vulardi
    sease i s also suggestive ofrest
    ri
    cti
    ve
    physiol
    ogy.Hi sr i
    ght-heartcatheterizati
    onisconsist
    entwi theitherarestr
    icti
    veorconstri
    cti
    ve
    processgivenequal izationofpr essures,rapidYdescent,andt hesquar erootsignsuggesti
    ng
    earl
    yequalizat i
    onofpr essuresbet weent heatri
    aandventricl
    es. 

    Givent hisconstell
    ati
    onoff i
    ndings,amyloidcar diomyopat hywoul dbehi ghl
    ysuspect ed.The
    goldst andardfordi agnosisisendomyocar dialbi opsy.Gi venthedi f
    fusenatureofamyl oid
    deposition,di
    agnosticyiel
    dfrom biopsyishigh.I naddition,ti
    ssueallowsforthedeterminati
    on
    ofamyl oidsubt ypeandpot ential
    lyaff
    ectsmanagement .Whi l
    ecar di
    acmagnet i
    cr esonance
    maybehi ghl
    ysuggest i
    veofamyl oidversusot herpot enti
    aletiol
    ogies,inthi
    srel
    ativel
    yyoung
    pati
    ent, wherethereisahi ghsuspici
    onforcardi acamyl oid,atissuediagnosisi
    sbestt ogui de
    therapy.

    Eval
    uationf ori
    schemi cdisease,suchasexer ci
    senucl earperfusionimagingandcor onary
    angi
    ogr aphy,i
    sl essl
    ikel
    ytobehel pfulint
    hesett
    ingofot herf
    indingssuggestiveofinfil
    trat
    ive
    heartdisease.Anoncont rastchestcomput edtomographywoul dbeusef ult oevaluatet he
    peri
    cardium inthesetti
    ngofconstricti
    veperi
    car
    dit
    is,butinthi
    scase,t heevidencepoi nt
    st oa
    myocar
    dialpr
    ocess.
     

    20. A75- year-oldmanwi t


    hahi storyofhypert
    ensionanddi abet
    esisseenbyyoui nfol
    low-
    up.Athisl astvisit
    ,hecompl ai
    nedofpr ogr
    essi
    veshor t
    nessofbr eath,ort
    hopnea,andlower
    extr
    emityswel li
    ng.Hewashyper tensive,andtherewasevi denceofvolumeover l
    oad.Hewas
    star
    tedonl i
    sinopri
    l10mgandf urosemi de20mgdai ly.Anechocar di
    ogram demonstrat
    ed
    normalbi ventri
    cular f
    uncti
    on,2+ t r
    icuspidregurgit
    ation,and moder ateleftventri
    cular
    hypert
    rophy.At readmil
    lnucl
    earperfusionstudydemonst ratednofi
    xedorrever
    sibl
    edefects.
     

    Onexami nati
    ontoday,hi
    sbloodpressur
    eis150/95mm Hg,hi shear
    trat
    eis72bpm,andhis
    j
    ugularvenouspressureis8cm H2O.Hehasar egul
    arheartr
    atewit
    hgrade2/6hol
    osyst
    oli
    c
    murmuratt heri
    ghtlowerst
    ernalborder
    ,hi
    slungsareclear
    ,andhehastracel
    owerext
    remit
    y
    edema.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    einhi
    scar
    e?

    a. I
    ncreasel isinopril
    .
    b. Adddi goxin.
    c. Adds pironol act
    one.
    d. Addme toprol ol
    .
    e. Addval sartan.

    ANSWER: 

    20. a. I
    ncr
    easel
    isi
    nopr
    il
    .

    Nopr ovent herapi esexisttor educemor bidi


    tyormor tal
    it
    yint hegr oupofpat i
    entswi t
    hheart
    fai
    lur
    ewi thpr eservedej ecti
    onf ract
    ion(HFpEF) .Guideli
    nesrecommendcont rol
    li
    ngcongest ion
    wit
    h di ureti
    cs,r uling outi schemia,and cont rol
    li
    ng blood pr essure and rate cont r
    ol(or
    considerati
    on ofcar diover
    sion)when at ri
    alf ibri
    ll
    ati
    on is present.A r ecentst udy ofa
    pharmacol ogicagentf orHFpEFwasTOPCAT( TreatmentofPr eservedCardiacFunct ionHeart
    Fai
    lureWi thanAl dosteroneAnt agonist
    ),whichl ookedatspironolactoneversusplacebowi t
    ha
    pri
    mar ycomposi teout comeofcar diovasculardeath,abortedsuddencar diacdeat h,orheart
    fai
    lur
    ehospi tali
    zat ion.Thisstudywasneut r
    al. 

    Ofnote,givensigni
    ficantdif
    fer
    encesi neventrat
    esi nNor
    thAmer i
    cacomparedwit
    htherestof
    thewor l
    d,asubgr oupanal ysisofpat i
    entsinNor thAmeri
    cademonst r
    atedabenef
    itforthe
    aldost
    erone antagonistoverpl acebo.However ,since t
    his anal
    ysi
    s was posthoc,t he
    hypothesi
    st hataldosteroneantagonistsar eeff
    icaci
    ousinthetreat
    mentofHFpEFr emains
    unproven.Therefor
    e, t
    reatmentofhishypertensi
    oni st
    hepri
    marygoal.
     

    Thelow doseofli
    sinopr
    ilshoul
    dbet it
    ratedbef or
    et headditi
    onofasecondagent .Bet
    a-
    bl
    ocker
    sar ef
    ourt
    h-li
    netherapyforthet r
    eat mentofhypertensi
    on,andangi
    otensi
    n-r
    ecept
    or
    bl
    ocker
    sshouldnotbeaddedtoangiotensin-convert
    ingenzymeinhi
    bit
    ors.
     

    21. Youar eadmitti


    nga65-year-oldwomant othehospitalbecauseofdyspnea,orthopnea,
    andedema.Shei swell-
    knowntoyourpr act
    icebecauseofl ong-standi
    nghear tf
    ailur
    ewi t
    h
    eject
    ionfract
    ion(EF)
     of45%andhyper tensi
    on.Hermedi cat
    ionsincludeli
    sinopr
    il2.
    5mgdai l
    y,
    carvedi
    lol12.
    5mgbi d,andfur
    osemi de40mgdai l
    y.Vit
    alsignsaret emperatur
    e36.9°C,heart
    rate110bpm, bloodpressur
    e160/100mm Hg, and 
    oxygensaturati
    oni s88%onr oom air
    . 
    Herphysicalexam i
    sr emarkablef
    orelevat
    edj ugul
    arvenouspr essureandanS3 gal
    lop.She
    has3+edemat oherkneesandoverthesacr um.Extremi
    tiesarewar m.Labor
    ator
    yevaluati
    on
    i
    ssignif
    icantforsodium 134mEq/ L,creat
    inine2.0mg/ dl(baseli
    ne1.2mg/ dl
    ),andB- t
    ype
    nat
    ri
    uret
    icpeptide3400pg/ml .

    Whi
    choft
    hef
    oll
    owi
    ngf
    indi
    ngsi
    nthi
    spat
    ienti
    sthemostl
    ikel
    yet
    iol
    ogyofherr
    enalf
    ail
    ure?

    a. Angiot
    ensin-
    converti
    ngenzyme(
    ACE)i
    nhi
    bit
    oruse.
    b. Hypoxemia.
    c. Lef
    tventri
    cul
    arejecti
    onf
    racti
    on(
    LVEF)
    .
    d. Lowc ar
    diacout
    put .
    e. Venouscongesti
    on.

    ANSWER: 

    21. e. Venouscongest
    ion.

    Cardi
    orenalsyndrome,especial
    lytype1( acut
    e)car
    diorenalsyndr
    ome,compli
    cates25-30%of
    hospit
    alizat
    ionsforacutedecompensat edhear tf
    ail
    ure.Changesassmal las0. 3mg/ dlin
    ser
    um cr eati
    nine have been associ
    ated wi t
    h prol
    onged hospit
    ali
    zat
    ion and increased
    mortal
    ity. 

    Multi
    plef act
    ors have been post ul
    ated to contr
    ibut
    et othis syndrome,incl
    udi ng venous
    congest
    ion,lowr enalper
    fusion,anddysfunctionalaut
    oregul
    ati
    onoft heki
    dney.Int hi
    spat i
    ent
    ,
    ther
    eisclearevidenceofvenouscongest i
    onandvol umeoverl
    oad.Herphysicalexam doesnot
    suggestlow cardiacoutput.Further
    ,int heESCAPE( EndovascularTreat
    mentf orSmal lCore
    andProximalOccl usi
    onIschemi cStroke)tr
    ial
    , t
    herewasnocor r
    elati
    onbetweenr enalfunct
    ion
    andcardiacindex. 

    LVEFi snotconsider
    edar i
    skfact
    orf orcardi
    orenalsyndrome,andcardi
    orenalsyndromei s
    seeni ncasesofhear
    tfail
    urewithpreservedorreducedEF.Whi l
    eACEinhi
    bitor
    scandecr ease
    glomer ul
    arfi
    lt
    rat
    ion r
    ate,they do notdecr ease renalblood fl
    ow and arether
    efore not
    responsibl
    eforrenalfai
    lur
    ei nthi
    spat ient
    .Hypoxemi aini sol
    ati
    onisnotacauseofr enal
    fail
    ure.
     

    22. Youar epl anningtodischar gea55-year-oldmanf rom thehospi


    talaft
    ertreat
    mentfor
    acut edecompensat edheartfail
    ure( HF)
    .Hewasadmi t
    ted5daysagowi t
    hdyspnea, decr
    eased
    exercisetol
    erance,andedema.Thi swashissecondadmi ssionforHFwit
    hinayear .Hismedial
    historyincl
    udesanant eri
    orwal lmyocardialinfar
    cti
    on3year sagowi t
    hal ef
    tventri
    cul
    ar
    ejectionf
    ract
    ionof30%, hypert
    ension,andat
    r i
    alfi
    bri
    ll
    ati
    on,whi chisnowratecontr
    oll
    ed. 

    Hehasasi ngl
    e- l
    ead,pri
    marypr eventi
    on implantablecardioverter
    -defi
    bri
    ll
    ator
    .Dur
    ing the
    hospit
    ali
    zati
    on,hisweighthasdecreased7pounds, andhi ssymptomsofdyspneaandf at
    igue
    arenow consistentwithNew YorkHear tAssociat
    ionf uncti
    onalclassII.Curr
    entmedicat
    ions
    i
    ncludecarvedil
    ol,l
    isi
    nopr
    il
    ,spi
    ronolactone,
    furosemi de,at
    orvastat
    in,aspi
    ri
    n,andwarf
    arin.

    I
    naddit
    iontogui
    deli
    ne-di
    rect
    edmedi calt
    herapy,
    whi
    choft
    hef
    oll
    owi
    ngi
    nter
    vent
    ionshasbeen
    pr
    oventohelpr
    educerehospi
    tal
    izat
    ionsforHF?
    a. Exerci
    setrai
    ningpr ogram.
    b. Enroll
    mentinadi seasesuppor tgr
    oup.
    c. Cogniti
    vebehavioraltherapy.
    d. Standardi
    zeddiseaseeducat i
    on.
    e. Telemonit
    ori
    ngofsympt oms.

    ANSWER: 

    22. d. St
    andar
    dizeddi
    seaseeducat
    ion.

    HFpat i
    entsr emai ni navul ner ableperi
    odf ol lowingdi schargef r
    om t hehospi tal
    .Impr oved
    communi cati
    onbet weencl iniciansandnur ses,medi cationr econci l
    iation,careful
    lypl anned
    transit
    ionsbet ween car eset t
    ings,and consi stentdocument ation ar eexampl esofpat i
    ent
    safetystandar dst hatshouldbeensur edforpat ientswithHFdi schar gedf r
    om thehospi t
    al(see
    theHFgui deli
    ne) .Theaddi ti
    onofa1- hournur seeducat or-deli
    ver edt eachi ngsessionatt he
    ti
    meofhospi taldi scharger esultedinimpr ovedcl i
    nicalout comes,i ncr easedself-careand
    treatmentadher ence,andreducedcostofcar e.Educat i
    onwhi l
    ei nthehospi t
    alal
    ongwi thear l
    y
    foll
    ow- upandenr oll
    menti nanout pati
    entdi seasemanagementpr ogram shoul dbeusedt o
    address pat i
    ent -specifi
    c bar ri
    erst o guideline- di
    rected medi calt her apy and bar ri
    erst o
    behavioralchange, asdescribedi ntheHFgui del ine.

    Randomi zed,control
    ledtri
    alsoft el
    emonitori
    ngandexer ci
    set rai
    ninghavenotpr ovent hat
    theseint
    erventi
    onsr educereadmissi
    ons,althoughexercisetr
    ainingmayhaveot herbenef i
    cial
    eff
    ectsforHFpat ients,i
    ncl
    udingimprovedheal t
    h- r
    elat
    edqualit
    yofl if
    e.Enr
    ollmenti ndisease
    supportgroupsmayhavepsychosoci albenefit
    sf orpati
    entswithmanychr oni
    cdi seases,but
    hasnotbeenpr ovent or
    educereadmissionsinprospectivecl
    inicalt
    rial
    s.Cognit
    ivebehavi oral
    therapyi
    snotat reatmentforHF. 

    23. You ar easked to seea 59- year-


    old man recent
    lydi
    agnosed wit
    h non-Hodgki
    n’s
    l
    ymphomai n consult
    ati
    on regar
    ding thecardi
    acrisksofanthracycl
    inechemother
    apy.He
    speci
    fi
    cal
    lyasksaboutcardiactoxici
    tyoftheproposedchemotherapyregi
    menbecausehi s
    fat
    herdi
    edsuddenlyofaheartatt
    ackathisage.

    Whichofthef
    oll
    owi
    ng,i
    fpr
    esent
    ,mostl
    ikel
    ywoul
    dincr
    easet
    her
    iskofant
    hracycl
    ine-
    induced
    car
    diomyopat
    hy?

    a. Personalhi
    stor
    yofper i
    cardit
    is.
    b. Personalhi
    stor
    yofradiati
    ont reat
    ment.
    c. Presenceofsel
    enium defi
    ciency.
    d. Presenceofhematologi
    cmal ignancy.
    e. Familyhist
    oryofheartf
    ail
    ure.

    ANSWER: 

    23. b. Per
    sonalhi
    stor
    yofr
    adi
    ati
    ont
    reat
    ment
    .

    Riskf actor
    sforanthracycl
    ine t
    oxi
    cit
    yinclude:1)t ot
    alli
    fet
    ime dose ofanthracycl
    ine;2)
    i
    ntravenous bol
    us administ
    rati
    on;3)highersingl
    e doses;4)historyofpr i
    ormedi ast
    inal
    i
    rradiati
    on;5)useofot herconcomit
    antagentsknownt ohavecardiot
    oxicef
    fects,suchas
    cyclophosphami
    de,trast
    uzumab,andpaclit
    axel;6)femalesex;7)underlyi
    ngcardiovascular
    disease;8)extr
    emesofpat i
    entage(
    bot
    hver
    yyoungandol
    dage)
    ;and9)i
    ncr
    easedl
    engt
    hof
    ti
    mesi nceanthracycl
    inecompl
    eti
    on.
     

    Per icardit
    isisgeneral
    lysel f
    -li
    mitedandnotspeci fical
    lydemonstrat
    edt oincreaser i
    sksof
    car diotoxi
    cit
    y of chemot herapy. Tot aldose of chemotherapeuti
    c agent and t ype of
    chemot herapeuti
    cagentarebot himpor tantf
    act
    orsinthedevel
    opmentofcar di
    omyopat hy,but
    typeofcancerbei ngtreat
    edbeyondt heagentusedi snot.Caseser i
    eshavesuggest eda
    relationshipbetweenselenium defici
    encyanddevelopmentofcardiomyopathy,butthesehave
    notbeenval idat
    edinprospectivestudies. 

    24. A72- year


    -oldwomani sreferr
    edt oyourclinicforconsultat
    ionregar
    dingthecar di
    ac
    ri
    sksofchemot herapyf
    orherbreastcancer.Shehasahi storyofhyper
    tensi
    oncontroll
    edwith
    li
    sinopr
    ilandamlodipi
    neandcoronaryarterydi
    seasef orwhi chsheunderwentstent
    ingseveral
    yearsago.Shehasneverhadacl i
    nicalmyocardi
    alinfarct
    ion. 

    Ar ecentechocar di
    ogram document edlef
    tventricularejecti
    onf ract
    ionof55%.Sher ecentl
    y
    wasdi agnosedwi thbr eastcancer,andpathologicr esult
    si ndicat
    edt hetumorwast ripl
    e
    negative fort he est
    rogen r ecept
    or,the pr
    ogest erone receptor,and t HER2/
    he  neu 
    gene.
    Therefore,heroncologistrecommendsacombi nationofchemot herapeuti
    cagent
    s,incl
    uding
    anant hracycl
    ine.

    I
    nadditi
    ontol
    imi
    tingthetot
    aldoseofant
    hracycl
    ineagents,
    whichofthefol
    lowi
    ngst
    rat
    egi
    esi
    s
    mostl
    ikel
    ytomit
    igateherri
    skofdevel
    opi
    nganthracycl
    inecardi
    otoxi
    cit
    y?

    a. Useofradiat
    ioninaddi t
    iontochemot her
    apy.
    b. Addi
    ti
    onofcycl ophosphami detothechemot herapyregi
    men.
    c. Addi
    ti
    onofpr ednisonetothechemot herapyregimen.
    d. Admini
    strati
    onofbol usrathert
    hancont i
    nuousant hr
    acycli
    nei
    nfusi
    ons.
    e. Admini
    strati
    onofal i
    posomalant hracycl
    inepreparat
    ion.

    ANSWER: 

    24. e. Admi
    nist
    rat
    ionofal
    iposomalant
    hracycl
    inepr
    epar
    ati
    on.

    Thelar
    gestsingleriskfact
    orf
    ordevel
    opingcardi
    otoxi
    cit
    yiscumul ati
    vedoseofant
    hracycli
    ne.
    2
    Thecumulat
    ivepr obabil
    it
    yofdoxor
    ubi
    cin-i
    nducedheartfai
    lur
    e i
    s 3-5%wit
    h400mg/ m, 7-
    26%
    at550mg/m2, and18- 48%at700mg/m2. 

    Otherriskfactor
    sf oranthr
    acycli
    net oxicityinclude:1)i ntravenousbol usadmi nistr
    ati
    on,2)
    highersingl
    edoses,3)hi stor
    yofpr iormedi astinalir
    radiation,4)useofot herconcomi t
    ant
    agentsknown t o havecar di
    otoxi
    cef fect s,such ascycl ophosphami de,trast
    uzumab,and
    pacli
    taxel
    ,5)femalesex,6)underl
    yingcar diovasculardisease, 7)extremesofpatientage(both
    veryyoungandol dage),and8)incr
    easedl engthoft i
    mesi nceant hracycl
    inecompl eti
    on.

    Preventionst
    rat
    egiesincl
    udeco-admi ni
    strat
    ionofcardi
    oprotect
    antssuchasdexr azoxane,use
    ofli
    posomalanthracycli
    nepreparat
    ions,anduseofpr ol
    ongedcont i
    nuousinfusionsratherthan
    boluses.Angiotensi
    n-convert
    ing enzyme inhibit
    ors and beta-bl
    ockers also may have a
    protect
    iveeff
    ectbutarenoteffecti
    veinallpatient
    s.Predni
    soneandot hersteroi
    ds,whi chare
    partofmanychemot herapyregimens,donothaveani nt
    eracti
    onwi t
    hant hracycli
    nesi nthe
    myocar dium.
     
    25. A 55- year-ol
    d man withi schemi
    c car
    diomyopat
    hy pr
    esent
    s wi
    th compl
    aint
    s of
    pal
    pit
    ati
    ons,f
    atigue,andheadaches.Heusuall
    ycanexerciseupto30mi nut
    esatat ime
    wal
    kingonatreadmillbr
    iskl
    ywi
    thoutsympt
    oms. 

    Curr
    entdai
    lymedi
    cat
    ionsi
    ncl
    udecarvedi
    lol12.
    5mgor
    all
    ybi
    d,l
    isi
    nopr
    il10mg,aspi
    ri
    n81mg,
    at
    orvast
    ati
    n80mg,andhydr
    ochl
    orot
    hiazi
    de25mg. 

    Exami nati
    onr evealshisbloodpressureis131/ 65mm Hg, pulseis79bpm r egular,
    andoxygen
    saturati
    onis96%onr oom air
    .Hisbodymassi ndexis34.Car diacauscult
    ati
    onr evealsasof tS1,
    physiologi
    callyspl i
    tS2,andasof tapi calS3.Nomur murswer eheard.Lungswer eclear.
    Extremiti
    esr evealmi ni
    maledema.An el ectrocardiogr
    am r evealssinusr hythm wi t
    hr ight
    bundlebr anchbl ockandQRS dur ationof121msec.Hi smostr ecentechor evealedl ef
    t
    ventri
    cular ejection fract
    ion of34%.I nterrogati
    on ofhi s singl
    e chamber i mplantable
    cardiovert
    er-defibri
    ll
    ator(I
    CD)revealssever alelevatedventri
    cularhigh-rat
    eepi sodesthatar e
    ir
    regular.Not herapieshavebeendelivered.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nthi
    spat
    ient
    'seval
    uat
    ion?

    a. Invasi
    veelectrophysi
    ologicstudy.
    b. Upgradet odual-chamberI CD.
    c. Echowi thdyssynchronyanal ysi
    s.
    d. Noc t
    urnalpolysomnogr aphy.
    e. My ocardi
    alperfusi
    onimagi ngstudy.

    ANSWER: 

    25. d. Noct
    urnalpol
    ysomnogr
    aphy.

    Ther ei
    sahi ghpreval
    enceofsleepdi
    sorderedbreathi
    ng(eit
    herobstructi
    vesleepapnea[ OSA]
    orcent r
    alsleepapnea)inpatientswit
    hcongest iveheartfai
    lure(approximatel
    y60%) .Thi s
    patient
    'ssymptomsar ehighl
    ysuggesti
    veofsl eepapnea( headaches/f
    atigue).I
    nadditi
    ont o
    theassociat
    ionbetweencongesti
    veheartf
    ailur
    eandOSA, OSAi salsothoughttobeapot ential
    tri
    ggerofatri
    alfi
    bri
    ll
    ati
    on(AF)insomeaf f
    ectedindivi
    dual
    s.Thispatient
    'sdeviceint
    err
    ogation
    i
    ssuggest i
    veofAF. 

    Thetreatmentofsl
    eepapneai sdependentupont henat ureoft heapnea.OSAsar ebestt reated
    withCPAP.Cent r
    alapneasar ebestt r
    eatedwi thopt i
    mi zingvolumest atusandhear tfai
    lure
    ther
    apy.Whileaddinganat ri
    alleadmayhel pquant ifyhisbur denofAF,thisdoesnotappeart o
    beindicat
    edatthepr esentti
    me.Echowi thevaluationofdyssynchr onyisofverylimitedut il
    it
    y
    andnotwi delyacceptedf ordecisionmaki ngf orupgr adi ngtoacar diacresynchronization
    ther
    apydevice.Therei snoi ndicati
    onf orelectrophysiol ogictest
    ingint hi
    spat i
    ent,andhi s
    symptomsar enonangi nal
    .Ther ef
    ore,thecor r
    ectopt ioni ssleepstudyt oevaluat
    ef orsl eep
    apnea. 

    26. A69- year-


    oldmanwi t
    hahi st
    oryofpr i
    ormyocardi
    alinfarcti
    onpresentsafterr ecent
    hospi
    tal
    izat
    ion forcongestiveheartf
    ail
    ure( CHF)
    .Echocardiographyduring hospi
    t ali
    zation
    demonstrat
    edwor senedlef
    tventr
    icul
    arfuncti
    onwi t
    hanej ecti
    onf ract
    ionof30%.Cor onary
    angi
    ography demonst r
    ated no fl
    ow-li
    miti
    ng or obstr
    uctive lesi
    ons. At dischar ge,hi s
    medi
    cati
    onsincl
    udedat
    orvast
    ati
    n80mg,
    aspi
    ri
    n81mg,
    li
    sinopr
    il40mg,
    andcar
    vedi
    lol25mg
    t
    wicedai
    ly.
     

    Laborator
    yvaluesincl
    udest
    abl
    ecreati
    nineof1.
    4mg/dlandpotassi
    um of4.
    4mEq/L.Because
    ofnocturnalapneathatwasnotedduri
    nghishospi
    tal
    izat
    ion,heunder
    wentout
    pati
    entsleep
    studythatwasconsist
    entwi
    thcent
    ralsl
    eepapnea(
    CSA).

    Whichofthefoll
    owi
    ngt her
    api
    eshasbeendemonst
    rat
    edt
    obeoft
    hegr
    eat
    estbenef
    iti
    nthe
    t
    reatmentoft
    hispat
    ient
    'sCSA?

    a. Ref
    erralforuvulect
    omy.
    b. Addi
    ti
    onofspi ronolact
    one.
    c. Cont
    inuousposi ti
    veairwaypr
    essur
    e.
    d. Addi
    ti
    onoft heophylli
    ne.
    e. Noct
    ur naloxygentherapy.
    ANSWER: 

    26. b. Addi
    ti
    onofspi
    ronol
    act
    one.

    Therear everylimiteddat asuppor ti


    ngtheuseofsuppl ementalt
    herapi
    esf orthetreatmentof
    CSA/ obstr
    ucti
    vesl eepapneai npat i
    entswithCHF.Whi l
    eli
    mitedtr
    ial
    shavesuggest edabenef i
    t
    fortheophylli
    neandoxygent herapy,thesedat aareveryl i
    mit
    ed.TheCANPAP ( Canadian
    ContinuousPosi t
    iveAi rwayPressur eforPati
    entsWithCentr
    alSleepApneaandHear tFai
    lur
    e)
    studyshowedsomebenef iti
    nt er
    msofi mprovementoflef
    tventr
    icul
    arejecti
    onfractioninthe
    treat
    edar m ofthest udy.However, at2yearsoffoll
    ow-up,mortal
    it
    yandtransplantratesinthe
    twogr oupswer esimi l
    ar. 

    Cardiacr esynchronizati
    ont her apyandat ri
    alpacingar enotconclusivelyi ndicat
    edi nt his
    population. Hence, t he gui deline continues to r ecommend f i
    rst-l
    ine t herapy to be
    compr ehensive and pr ogressive managementofCHF medi caltherapy int hese patients.
    Additi
    onofal dosteroner eceptorantagoni stinthissympt omati
    cpatienti sindicatedashi s
    ser
    um cr eat
    ini
    nei s<2. 5mg/ dlandpot assium islessthan5.0mEq/ L.Car efulmoni t
    ori
    ngof
    potassium andr enalf uncti
    oni si mport
    antwi t
    hiniti
    ati
    onofaldoster
    oner eceptorantagonist.
    Uvulectomyi snoti ndi
    catedinpat i
    ent
    swi thCSA.  

    27. A44- year-


    ol dmanhasa5- yearhistor
    yofnonischemiccar diomyopathy.Hepresents
    toyouroff
    icefoll
    owi nghisthir
    dhospi t
    ali
    zati
    oninthepastyearforvolumeoverload.Heisshort
    ofbreath with mi nimalexer t
    ion,butappear s euvol
    emic on exam.Hi s echocardi
    ogram
    demonstratesaleftventri
    culareject
    ionfr
    actionof20%,t
    heleftventr
    icularcavi
    tysizei
    sdilat
    ed,
    andtherearenomaj orvalvul
    arabnor mal
    iti
    es.

    Pr
    ognosi
    sint
    hispat
    ienti
    sbestdet
    ermi
    nedbywhi
    choft
    hef
    oll
    owi
    ng?

    a. Ri
    ght-heartcat
    heterizat
    ion.
    b. Cardi
    opulmonaryexer ci
    setest
    ing.
    c. 6-minut
    ewal ktest
    .
    d. Seatt
    leHeartFail
    ureScor e.
    e. Cardi
    acmagnet icresonanceimaging(
    MRI
    ).
    ANSWER: 

    27. b. Car
    diopul
    monar
    yexer
    ciset
    est
    ing.

    Prognosisin heartf
    ail
    ureisbestdet ermined byassessmentoffuncti
    onalcapaci
    ty.The
    acceptedindi
    cati
    onforheartt
    ranspl
    antationisanoxygenconsumpt
    ionof<14cc/ kg/
    min(or
    12cc/kg/minint hepr
    esenceofbeta-blocker
    s)measuredduri
    ngacardiopul
    monaryexerci
    se
    test
    . 

    TheSeat t
    leHeartFai
    lureScoreisknownt ounder esti
    mat eri
    skinpati
    entswi t
    hadvancedhear t
    fai
    lur
    e,suchast heonedescr ibedi
    nt hisquest i
    on.Whi l
    ethe6-minutewal ktestdoesconvey
    prognosti
    cinformati
    on,itisnotasi nfor
    mat i
    veascar di
    opulmonarystresstestingandisnot
    usedasani ndicat
    ionfortr
    ansplant
    ation.CardiacMRImaybehel pf
    ulinidenti
    fyi
    ngt heeti
    ology
    ofnonischemiccardiomyopathyandcanconveypr ognosti
    cinf
    ormati
    onbasedont heamount
    ofdelayedenhancement,butisnotaswel lval
    idatedascar di
    opul
    monar ystr
    esst esti
    ng.
     

    28. A 62- year


    -ol
    d woman with chr
    onic heartfai
    lur
    e wit
    hr educed ej
    ecti
    on fr
    acti
    on i
    s
    transfer
    redtothecoronar
    ycareuni
    t.Shewasst artedonmilr
    inonewhenshewasadmi tt
    edto
    thefloor3daysagowher eshewasawaiti
    nghear tt
    ranspl
    ant
    ation.Apulmonaryart
    erycat
    het
    er
    i
    spl aced. 

    Thehemodynami
    csar
    e(i
    nmm Hgwher
    eappr
    opr
    iat
    e):

     Ri
    ghtatr
    ialpressure:20
     Pul
    monar ycapil
    lar
    ywedgepr essure:30
     Pul
    monar yarter
    ypr essur
    e:60/30/40
     Car
    diaci
    ndex:1. 5L/ mi m2
    n/
     Bl
    oodpressure:80/ 50/65

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextmostappr
    opr
    iat
    est
    ep?

    a. I
    sosor bidetri
    nit
    r at
    e.
    b. Referralforaleftvent
    ri
    cul
    arassi
    stdevi
    ce(
    LVAD)
    .
    c. Removef rom tr
    ansplantl
    ist
    .
    d. Phe nylephri
    ne.
    e. Si
    ldenaf il
    .

    ANSWER: 

    28. b. Ref
    err
    alf
    oral
    eftvent
    ri
    cul
    arassi
    stdevi
    ce(
    LVAD)
    .

    Themostcommoni ndicati
    onf oranLVADi sasabr i
    dget ohear ttr
    anspl antati
    on.Thi spati
    ent
    remai nsinseveredecompensat edhear tfail
    uredespi tei nt
    ravenousi notropicsuppor t(i.
    e.,
    mi l
    ri
    none). Because t he t i
    ming of t ransplantati
    on cannot be det ermi ned, adequate
    hemodynami csupportofthepat i
    entmustbemai ntai
    nedi nor dertoopt imizet hepreoperati
    ve
    stateofthetranspl
    antcandi dat
    e.Phenylephrinewi l
    lprovidevasoconst r
    icti
    on, butwillnottr
    eat
    thel ow outputstate.Sil
    denaf i
    lcan increaset hepul monar ycapi l
    larywedgepr essureby
    decreasingthepulmonar yvascularresist
    anceandover whelmt heleftventricularcompliance
    from theincr
    easedflowacr ossthepulmonar ycirculati
    on.Ni t
    rateswoul dbepoor l
    ytoler
    atedin
    thesetti
    ngofhypot ensi
    on.Removalf
    rom t
    het r
    anspl
    antli
    sti
    spri
    maril
    yindi
    cat
    edwhenthe
    patientis nota tr
    ansplantcandi
    dat
    e due t
    o sever
    e comor
    bidi
    ti
    es t
    hatcompromi
    se t
    he
    transpl
    antprocedur
    e.

    29. A24- year-oldwomanpr esentswit


    h2weeksofpr ogr essiveshor t
    nessofbreath,fat
    igue,
    ort
    hopnea,andsyncopeaf t
    erar ecentvirali
    ll
    ness.Thei ni
    ti
    alechocar di
    ogram evaluati
    on
    demonstrat
    esanor malheartsizeandleftventri
    cularejecti
    onf ractionof20%.Despi teinit
    ial
    att
    emptsatst abili
    zat
    ion ofacutedecompensat ed heartf ai
    lurewi t
    h medicaltherapy,the
    pati
    ent’
    sconditi
    oncont i
    nuestodet er
    ior
    ate.Onexami nation,herbl oodpr essurei
    s82/ 67mm
    Hgwi t
    hahear trateof115bpm.Herpul monar yar t
    eryoxygensat urati
    onf el
    lfr
    om 45%t o37%
    aft
    er12hoursofhi gh-
    doseintr
    avenousinotropes.

    Hercr
    eati
    ninei
    s2.6mg/dl
    ,andsheisol
    igur
    ic.Herment
    alst
    atusdecl
    ines.Shei
    sint
    ubat
    ed
    andpl
    acedonextr
    acor
    por
    ealmembr
    aneoxygenati
    on.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextmostappr
    opr
    iat
    edi
    agnost
    ict
    est
    ?

    a. Endomy ocardialbiopsy.
    b. Coronar
    yangi ogr ams.
    c. Cardi
    acmagnet icresonanceimaging(MRI
    ).
    d. Geneti
    ct est
    ing.
    e. Cardi
    accomput edt omography(CT).

    ANSWER: 

    29. a. Endomyocar
    dialbi
    opsy.

    Thispat i
    enthascar diogenicshocknotr esponsi
    vet omedicalther apyandi sappropri
    atel
    y
    placedonmechani calsupport.Endomyocar di
    albi
    opsyshouldbeconsi deredinpati
    entswi t
    h
    rapidlypr ogressi
    veclini
    calhear tfail
    ureandi sespecial
    lyhelpfult oevaluat
    eforgi antcell
    myocar di
    tis,whichmayr espondtoi mmunosuppr essi
    vetherapies.CardiacCT, 
    cardiacMRI ,
    andcor onaryangiogramsar econtrai
    ndicatedbecauseofacut er enalfai
    lur
    eandwoul dnot
    provideadef ini
    ti
    vediagnosis.Genet i
    ctestingisnotusefulwithoutapr i
    orfamil
    yhi st
    oryof
    i
    diopat hiccardiomyopathy. 

    30. A 64- year


    -ol
    d man wi thi schemic car di
    omyopathy is admit
    ted wi t
    h wor seni
    ng
    short
    nessofbr eat
    handl owerextremityedema.Hei sonfurosemide40mgperday, aspir
    in81
    mg,atorvastati
    n80mgatbedt i
    me,andl i
    sinopr
    il40mgperday.Onexami nati
    on,heisi nno
    acutedistr
    ess.Hi sbloodpr essureis115/ 75mm Hg,hear trateis72bpm,andoxygen
    satur
    ati
    onis96%.Hi sjugularvenouspr essureiselevat
    ed,l
    ungsar ecl
    ear,andheartisregul
    ar
    wit
    hnor malS1 andS2 
    andgr ade3/ 6hol osystol
    icmur muratapex.Ext
    remi t
    iesarewarm wi t
    h
    2+edema.  

    Anelect
    rocar
    diogr
    am showsnormalsinusrhythm wit
    hQwavesinV1-V4.QRSdur ati
    onis110
    msec.Echodemonstr
    ateseject
    ionfr
    acti
    on( EF)of30%wit
    hlef
    tvent
    ri
    cul ar(LV)end-di
    ast
    oli
    c
    di
    mensionof6.0cm,moderate-
    sever
    emi t
    ralregur
    git
    ati
    on(
    MR),andl
    eftatri
    alenlar
    gement.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostef
    fect
    ivewayt
    odecr
    easeMR?

    a. Dobut
    ami
    ne.
    b. Mit
    ralvalverepair.
    c. Car
    diacr esynchroni
    zati
    ontherapy-
    def
    ibr
    il
    lat
    or(
    CRT-
    D).
    d. Sur
    gicalventricul
    arreduct
    ion.
    e. Car
    vedilol.

    ANSWER: 

    30. e. Car
    vedi
    lol
    .

    Secondar yMR i scommonandassoci atedwi thwor seout comesi n  heartfail


    ur e(HF)wi th
    reducedEF.Thepr imaryappr oacht othetreatmentofMRi nt hi
    ssettingi nvolvesopt imizat
    ion
    ofmedi calt herapy f or reduced EF.The i mprovementi nr emodel ing associ ated with
    opti
    mi zati
    onofmedi cati
    onwi llresul
    tindecr easedMR.CRT- Dalsowi llreducef unctionalMR
    duet oimpr ovedr emodeling, buti nthiscase,CRT- Disnotindicatedbecauset hepat ientisnot
    onopt imalmedi caltherapyandhasanar r
    owQRS.Sur gi
    calther
    apiesf ortheMRi nt hissett
    ing
    havenotbeenpr ovent oimpr ovemor tal
    it
    yandar eonl yusedasapal li
    ati
    onf orrefract
    ory
    sympt oms.  
    Inot
    ropesi nchr oni cHFar eonlyusedaspal l
    iati
    onorasabr idget oadvanced
    therapies.
     Theaddi tionofbet a-blockerstot hispatient'
    sregimenof fer sthebestst rategyto
    i
    mpr ovehisMRt hroughLVr emodel i
    ngandpr ovidesmor tal
    it
    ybenef i
    t.
     

    31. Whi
    choft
    hef
    oll
    owi
    ngi
    sthel
    ikel
    ihoodofsur
    vivalat5year
    saf
    terhear
    ttr
    anspl
    ant
    ati
    on?

    a. 90%.
    b. 70%.
    c. 60%.
    d. 80%.
    e. 50%.

    ANSWER: 

    31. b. 70%.

    Sur vivalafterhearttranspl
    antat
    ionhasi ncreasedsteadi
    lysincethe1980s.Accor dingtothe
    Internat i
    onalSociet
    yofHear tandLungTr ansplantat
    ion,t
    hesurvivalaf
    terhear
    ttransplant
    ati
    on
    is90%at1year ,
    70- 75%at5year s,
    and50%beyond10year s.Incontr
    ast,inthe1980s, t
    he5-
    year sur vival r
    ate af t
    er hearttransplantati
    on was 65%. The medi an survi
    val after
    transpl antati
    onint he1980swasappr oximately8yearsandi scurrent
    lyapproximately11
    year s. 

    32. Whi choft


    hef
    oll
    owi
    ngi
    sthemostcommoncauseofdeat
    hint
    hef
    ir
    stmont
    haf
    terhear
    t
    tr
    anspl
    ant
    ati
    on?

    a. Malignancy.
    b. Rej
    ect i
    on.
    c. I
    nfection.
    d. Cardiacall
    ograf
    tvascul
    opat
    hy.
    e. Pri
    mar ygraftf
    ail
    ure.

    ANSWER: 
    32. e. Pr
    imar
    ygr
    aftf
    ail
    ure.

    Themostcommoncauseofdeat hinthefi
    rst30dayspostcardi
    actranspl
    anti
    spri
    mar
    ygraft
    fai
    lur
    e,def
    inedasdysfunct
    ionoft
    hetransplant
    edorganwi
    thinthefi
    rst24hour
    s.Ri
    skf
    actors
    forthedevelopmentofpri
    marygraftdysfunct
    ionmayincludeolderdonorageandlonger
    i
    schemicti
    mes.  

    Whiletherei sasignif
    icantriskofinfect
    ionimmedi at
    elypostt r
    anspl
    ant,i
    tisnotascommona
    causeofdeat hwithi
    n30daysaspr i
    marygr af
    tdysfunction( 13%vs.39%,respect
    ivel
    y).Acute
    cel
    lularrejecti
    onisseeni nthef i
    rstyearposttransplant,buthyperacuterej
    ect
    ionimmedi at
    ely
    aft
    ersur geryisrar
    elyani ssue.Malignancyandvascul opathyar enotcommoncausesofdeat h
    wit
    hint hefirst30days,butar esi
    gnifi
    cantlong-t
    erm compl icati
    ons. 

    33. A57- year-oldmanpr esent


    sf orhi
    st hi
    rdhear tfai
    lure(HF)hospital
    izat
    ionint hepast
    year.Hehadal argeant eri
    ormyocardiali
    nfar
    ction(MI)3year sagoandhasanej ecti
    onf r
    acti
    on
    of20%.Hi s medi calregimen incl
    udes met oprol
    olext ended-rel
    ease 100 mg once dai ly,
    li
    sinopr
    il40mgdai ly,
    furosemide120mgt wi
    cedai l
    y,atorvastat
    in80mgoncedai ly,aspir
    in81
    mgoncedai ly,andwar fari
    n5mgdai l
    y. 

    He had an i mplantabl
    e cardi
    overt
    er-def
    ibri
    ll
    ator(ICD)pl aced 1 yearafterhi
    s MI .His
    el
    ectrocardi
    ogram showsat r
    ialf
    ibri
    ll
    ati
    onandaQRSdur ati
    onof110msec.Hi sbloodurea
    nit
    rogeni s80mg/ dl
    ,andhi screati
    nineis1. 9mg/ dl.Echoshowsadi l
    atedlef
    tventri
    cle,
    moder at
    ely severe mi t
    raland tri
    cuspidr egurgi
    tat
    ion,leftatri
    alenlar
    gement,and large
    hypokinet
    icrightventri
    cle.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    enextst
    ep?

    a. Cardi
    acresynchronizati
    ontherapy.
    b. Ref
    erralf
    ormitralvalverepl
    acement.
    c. Ref
    erralf
    orhearttransplant
    .
    d. Hydral
    azi
    ne.
    e. Dobutamine.

    ANSWER: 

    33. c. Ref
    err
    alf
    orhear
    ttr
    anspl
    ant
    .

    Ani mportantaspectofchr oni


    cHFmanagementi stherecogni
    ti
    onofadvancedHFandt he
    tr
    igger
    sf or ref
    err
    alf or advanced therapies such as hearttranspl
    ant
    ati
    on.Fr equent
    hospit
    ali
    zations,car
    diorenalsyndrome,r ecurr
    entICD shocks,and poorfunct
    ionalstatus
    despit
    eopt i
    malmedi calther
    apyareconsideredmilest
    onesofworseni
    ngadvancedHFandar e
    associat
    edwi thhi
    ghmor tali
    ty.
     

    34. A 55- year


    -oldmanwi thchroni
    chear
    tfai
    lur
    e( HF)withreducedej
    ect
    ionf
    ract
    ioni
    s
    admitt
    edwit
    hper si
    stentdyspnea.Duri
    nghi
    shospit
    ali
    zati
    on,hi
    ssympt omsar
    eref
    ract
    oryt
    o
    i
    ncreasi
    ngdosesofdiuret
    ics.
     

    Onexami nati
    on,hi
    sbodymassi ndexis38kg/m2,bl
    oodpressur
    eis90/
    70mm Hg,andhear t
    rat
    eis100bpm.Hi svenouspressur
    ecannotbeassessed.Hisl
    ungsar
    eclear
    ,heartsounds
    aredi
    stant,andabdomenisobese.Hisext
    remi
    ti
    esareedematouswi
    thbr
    awnydiscol
    orat
    ionof
    t
    heover
    lyi
    ngski
    n. 

    Hislabor
    atori
    es(mg/dl)ar
    enot
    abl
    eforasodi
    um of134,
    pot
    assi
    um of5.
    0,bl
    oodur
    eani
    tr
    ogen
    of70,andcreati
    nineof2.
    5.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextmostappr
    opr
    iat
    est
    ep?

    a. Cardi
    opulmonar yexercisetesti
    ng.
    b. Echocar
    diography.
    c. Pulmonaryarterycatheteri
    zati
    on.
    d. ChestX-r
    ay.
    e. Brai
    nnatri
    ureticpeptidelevel.

    34. c. Pul
    monar
    yar
    ter
    ycat
    het
    eri
    zat
    ion.

    Thispatientwithacut edecompensatedhear tfail


    ure(ADHF)i sfai
    li
    ngtoi mprovewit
    hempi ri
    c
    diuret
    icmanagementandhasanuncl earhemodynami cpr of
    il
    efrom bedsideassessment .
    Althoughal ow out putsyndromei spossible,themostcommonhemodynami cabnormalit
    y
    associatedwi t
    hADHFi sanel evat
    edcentralvenouspr essure.I
    nordertodeterminethecause
    oft his pat
    ient'
    sr efract
    ory HF and cardiorenalsyndr ome,invasive measurementoft he
    hemodynami csar erequired.However,ther outi
    neuseofpul monaryar t
    ery(PA)catheter
    -
    guidedtherapyf orADHFi snotrecommendedasnot edi ntheESCAPEt r
    ial
    . 

    Thepr imaryindicati
    onsforPAcat heterizationinHFi ncludediagnost i
    cuncer taintywithrespect
    tot hehemodynami cprofi
    le,conf irmat ionofWor ldHeal thOr ganizati
    onGr oup1pul monary
    arteri
    alhypertension,andinpr eparationf oradvancedt herapi
    es,suchashear ttransplantat
    ion
    orvent ri
    cularassistdevices.Theot herchoi cesar elimitedbyt heirindir
    ectassessmentof
    hemodynami cs,whi charecommonl yi nsensiti
    vetosubt l
    echangesi nhemodynami cstatus.B-
    typenat r
    iuret
    icpept ide(
    BNP)canbef alselylowinobesi t
    yduet oi ncreasedcl earanceofBNP
    byendopept i
    dases.Echocar diographyr equirescertain assumpt ionsi n ordert o determine
    absolute r at
    her t han relative hemodynami c values ( e.
    g., assessment of pul monary
    hypertension).

    35. Admi ni
    str
    ation ofwhich ofthe fol
    lowi
    ng agent
    s shoul
    d be accompani
    ed by an
    assessmentofl
    eftvent
    ricul
    ar(
    LV)funct
    ion?

    a. Dexrazoxane.
    b. Suni
    tinib.
    c. Radi
    at i
    on.
    d. 5-Fl
    uorouracil(
    5-FU)
    .
    e. Cort
    icoster
    oids.

    ANSWER

    35. b. Suni
    ti
    nib.

    Cancerchemot her
    apyi scommonl yassociat
    edwi t
    hcardiovascul
    aradver
    seeff
    ects.Alt
    hough
    anthracycli
    nes(e.
    g.,doxor
    ubici
    n)andt r
    astuzamab( Hercept
    in)ar
    egenerall
    ywell
    -recogni
    zed
    agentst hatcausemyocar di
    aldysfunct
    ion,manyot heragentsrequi
    reclosecardi
    ovascul
    ar
    surveil
    lance.Suni
    ti
    nib(Sutent)
    ,at yr
    osi
    neki naseinhi
    bitor
    ,iscommonl yusedforrenalcel
    l
    carcinomaandgast r
    icst romaltumor sandmaycauseLVdysf uncti
    on,part
    icul
    arl
    yi fpat ient s
    experiencehyper tensiondur i
    ngt her
    apy.Dexrazoxaneisusedt opr ot
    ectagainstanthracycl i
    ne
    cardiotoxici
    tythroughf reer adi
    calscavenging.Radiati
    onmaypr oduceaccelerat
    edcor onar y
    art
    ery di sease,val vulari nj
    ury,and per i
    cardi
    tis,butgener all
    y only pr
    oduces syst oli
    c LV
    dysfunction int he set ting ofr eceivi
    ng anothercardiotoxic agentsuch as doxor ubi cin.
    Surveill
    anceechocar diographyi sgenerall
    ynotneededdur ingchestr adiat
    ionadministrationi n
    theabsenceofsympt oms.St eroidshavenodi rectcardiotoxicit
    y.5-FUmaycausecor onar y
    vasospasm, butdoesnotgener all
    ycausedi r
    ectmyocardialinjury. 

    36. A45- year-ol


    dmanwaspr evi
    ousl
    yhospit
    ali
    zedforbiopsy-
    provenacutelymphocyti
    c
    myocar dit
    is.Initi
    alechocar diogr
    am demonst r
    ated bi
    ventr
    icul
    ar dysfunct
    ion wi
    thal ef
    t
    ventr
    icularejecti
    onf r
    acti
    on(LVEF)of25%andnor malcavi
    tydimensions.Hewasdi schar
    ged
    withNewYor kHear tAssoci
    ation(NYHA)classI
    Isymptoms. 

    Ona6- mont hfoll


    ow-upvisi
    t,heendor sesNYHAcl assI Isympt
    oms.Anechocardi
    ogr
    am is
    obtainedthatdemonst r
    atesrightventri
    culardysfuncti
    on,anLVEFof20%,andamoder at
    ely
    di
    latedleftvent
    ricl
    e.Hiscurr
    entmedi cati
    onsincludel i
    sinopri
    l20mgqd,car
    vedi
    lol25mgbid,
    andspi r
    onolact
    one25mgqd.
     
    Whichoft hefol
    lowingisthemostappr opri
    atenextstepinmanagementofthi
    spatient
    ?

    a. Ref
    erralf
    orleftvent
    ricul
    arassi
    stdevi
    ce(LVAD)pl
    acement.
    b. St
    artrosuvastati
    n.
    c. St
    artwarfarin.
    d. St
    artprednisone.
    e. Ref
    erralf
    orimpl ant
    ablecardi
    over
    ter
    -def
    ibr
    il
    lat
    or(
    ICD)pl
    acement
    .

    ANSWER: 

    36. e. Ref
    err
    alf
    ori
    mpl
    ant
    abl
    ecar
    diover
    ter
    -def
    ibr
    il
    lat
    or(
    ICD)pl
    acement
    .

    Pat
    ient
    swit
    hnonischemiccar
    diomyopat
    hywit
    hEF<35% andNYHAclassIIorIIIsymptoms
    whoareongui
    del
    ine-di
    rect
    edmanagementf
    oratl
    east6mont
    hshavesur
    vivalbenef
    itwi
    thICD
    pl
    acement
    . 

    Therei sl it
    tl
    eevidencet hata  denovo  presentationofvi r
    alorl ymphocyt i
    cmyocar dit
    isi s
    responsive t o st
    eroids.However ,evidence suggest sthatsome pat i
    ents wi th chronic
    i
    nflammat ory myocar dit
    is such as ongoi ng l ymphocyt i
    c myocar dit
    is may r espond t o
    i
    mmunosuppr essi
    on,especi all
    yt hat subgroup wi t
    hout evidence ofcar di
    otropic viral
    ly
    medi at
    edmyocar dit
    is.Ingener al,pati
    entspr esentingwithfulminantlymphocyticmyocar dit
    is
    presentmor edramat i
    call
    yandar emor el i
    kelytoneedmechani calsuppor t
    ,butar ealsomor e
    l
    ikelytor ecovermyocar dialfunctionversust heacut epresentat
    ion.Giantcellmyocar dit
    isisa
    parti
    cularly mor bid i nflammat ory myopat hy. Whi l
    e i t may r espond t o mul ti
    ple
    i
    mmunosuppr essi
    veagent s,transplant
    -freesur vivalisparti
    cularl
    ylow;t hus,diagnosisand
    earlytr
    eat mentisrequired. 

    Therearenodatatosuppor
    ttheuseofwarf
    ari
    ninpati
    entswit
    hdil
    atedcardi
    omyopat
    hyi
    nthe
    absenceofat
    ri
    alfi
    bri
    ll
    ati
    on,
    LVthrombus,
    orotheri
    ndi
    cati
    onforant
    icoagul
    ati
    on.
     

    St
    ati
    nshavenotdemonst
    rat
    edbenef
    iti
    npat
    ient
    swi
    thnoni
    schemi
    ccar
    diomyopat
    hy.LVADs
    ar
    eindi
    cat
    edf
    ormor
    eadvancedhear
    tfai
    lur
    e. 

    37. A 78- year


    -old woman presentsto youroffi
    ce f
    orconsul
    tat
    ion.She complains of
    dyspneawi
    thexert
    ionandlowerextremi
    tyswelli
    ng.Hermedi
    calhi
    stor
    yincl
    udesdiabetesand
    dysl
    ipi
    demi
    a. 

    Onexami nat
    ion,shehasanel evatedjugularvenouspul sat
    ion,ar egul
    arrat
    eandr hyt
    hm,faint
    crackl
    esatt hel ungbases,and2+l owerext remit
    yedema.Shehashadanechocar di
    ogram
    thatdemonstratesanor mall
    eftvent
    ri
    cularejecti
    onfracti
    on( EF).Youtel
    lherthatshehasheart
    fail
    urewith preserved EF(HFpEF).Sheasksyou f oraddi t
    ionalinf
    ormati
    on regar
    ding her
    diagnosi
    s.

    Whi
    choft
    hef
    oll
    owi
    ngbestdescr
    ibeschar
    act
    eri
    sti
    csofHFpEFi
    nthegener
    alpopul
    ati
    on?

    a. Malesexisar i
    skfact
    orforHFpEF.
    b. Mortal
    it
    yissimi l
    artoHFwi threservedEF(HFr
    EF).
    c. Angi
    otensin-converti
    ngenzymei nhibi
    tor
    sareassoci
    atedwi
    thr
    educt
    ioni
    nmor
    tal
    it
    y.
    d. Overal
    lprevalanceofHFpEFi sdeclini
    ng.
    e. Approxi
    mat el
    y25%ofpat ientswithHFhaveHFpEF.

    ANSWER: 

    37. b. Mor
    tal
    it
    yissi
    mil
    art
    oHFwi
    thr
    eser
    vedEF(
    HFr
    EF)
    .

    PatientswithHFpEFver susanHFr EFar eaboutequali nprevalence,withsi milarmortal


    it
    y
    outcomes.HFpEFpat ient
    s,however ,aremor eoft
    enf emale,older,andhypert ensive.Wi
    ththe
    agingoft hepopulation,thepr eval
    enceofHFpEFi sincr
    easing.Ot herassociatedconditi
    ons
    seenwi thHFpEFi ncludeobesi ty,atr
    ialfi
    bri
    ll
    ati
    on,dysl i
    pidemia,anddi abetes.Whi leuseof
    medi cat
    ionsfortr
    eatmentf orbloodcontrolandvolumemanagementi sappropr i
    ate,atpr
    esent,
    therearenodr ugsthathavepr ovenbenefitoncardiovascul
    arout comes. 

    38. A65- year


    - ol
    dwomanpr esent
    stoyouwi thcomplai
    ntsofdyspneaonexerti
    on.She
    deni
    es dyspnea atrest
    ,or t
    hopnea,orparoxysmalnoctur
    naldyspnea.She deni
    es lower
    ext
    remi
    tyedema.Hermedi calhi
    storyi
    sonl
    ynotablef
    orhyper
    tensi
    onandhyper
    li
    pidemia.
     

    Onphysi calexaminati
    on,herbloodpr essurei s154/ 90mm Hgandot her
    wiseunr emarkable.
    HerN- ter
    minalpro–B-typenatriuret
    icpept ideis150pg/ ml.Anexerci
    semyocar dialperf
    usion
    i
    magi ngstudyisperformed.Sheexer ci
    ses4mi nutesonast andardBruceprotocol,andstops
    duet odyspnea.Herst r
    esselectrocardiogram iswi t
    houtischemicchangesandt heper f
    usion
    i
    magesdonotshow evi denceofi nfarctori schemi a.Yoususpectshehashear tfail
    urewith
    preservedeject
    ionfr
    acti
    on( HFpEF)andor derar ight-hear
    tcathet
    eri
    zat
    ionwi t
    hexercise.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    yfi
    ndi
    ngwi
    thexer
    cise?

    a. Inappr opr
    iat
    eincreaseinheartrat
    e.
    b. Exagger at
    edincreaseinpulmonaryart
    erypressur
    es.
    c. Increaseinthemi xedvenousoxygensatur
    ation.
    d. De creaseinpulmonar ycapi
    ll
    arywedgeV-waveamplit
    ude.
    e. Sy st
    emi chypotension.
    ANSWER: 

    38. b. Exagger
    atedi
    ncr
    easei
    npul
    monar
    yar
    ter
    ypr
    essur
    es.

    HFpEFi sadi ffi


    cul tdiagnosi st omakeandi soccasi onal l
    yoneofexcl usionifpat i
    entsarenot
    clearl
    y congest ed atr est.Whi lear i
    ght -
    heartcat heteri
    zation may demonst r
    ate normal
    hemodynami cs,ar ight- heartcat heteri
    zati
    onwi t
    hexer cisecanof t
    enconf i
    rm asuspect ed
    diagnosi
    sbyshowi nganexagger atedelevat i
    oninsyst emicbl oodpressureandi nt
    racardi
    ac
    fi
    lli
    ng pressurer esponset o exercise.Forpat i
    entswi th normalhemodynami csatr est,a
    pulmonar yarterysyst olicpr essurewi thexerciseof>45mm Hgsuggest sadi agnosisofHFpEF
    withhighsensi ti
    vi t
    y.Of tentimes,augment ationincar diacout putisbluntedandi nsuff
    ici
    entto
    supporttheexer ciseandl owert hansi milarpatientswi t
    houtHFpEF,l ikel
    yr el
    atedt olackof
    systol
    icanddi ast oli
    cr eserve.HFpEFi softenassoci atedwi thlackofchronotropicresponse. 

    39. Tr
    oponi
    nisnecessar
    yforwhi
    choft
    hef
    oll
    owi
    ngf
    unct
    ionswi
    thi
    nthehear
    t?

    a. Mitochondri
    alel
    ectront r
    ansport.
    b. Propagati
    onoftheact ionpotential
    .
    c. DNAr epli
    cat
    ionandmyocar dialcelldivi
    sion.
    d. Cardiomyocytecontracti
    onandr elaxat i
    on.
    e. Maintenanceofcellmembr anef l
    uidity.

    ANSWER: 

    39. d. Car
    diomyocyt
    econt
    ract
    ionandr
    elaxat
    ion.

    Myosin,actin,t
    ropomyosin,and t
    hetroponi
    nsaresarcomericprotei
    nsthatinteractwi
    th
    cal
    cium andadenosinetri
    phosphat
    etoproducemyocar
    dialcontr
    act
    ionandrelaxati
    on.None
    oft
    heot heranswerchoi
    cesarecorr
    ect
    .

    40. Exci t
    ati
    on-cont
    ract
    ioncoupl
    ingdescr
    ibesthepr
    ocessbywhi chelect
    ri
    calact
    ivat
    ionof
    thecar
    diomyocyt
    eviaanacti
    onpotenti
    alr
    esult
    sinmyocar
    dialcont
    ract
    ion.

    Whi
    choft
    hef
    oll
    owi
    ngoccur
    sfi
    rstwi
    thi
    nthepr
    ocessofexci
    tat
    ion-
    cont
    ract
    ioncoupl
    ing?

    a. Entryofcalci
    um i
    ntot hecell
    .
    b. Displacementoftr
    opomyosi nf rom acti
    n-bindingsit
    es.
    c. Releaseofcalci
    um from thesar coplasmicreti
    culum.
    d. Mov ementofmyosinheadsal ongt heactinfi
    lament.
    e. Dissociat
    ionofcal
    cium from troponin.

    ANSWER: 

    40. a. Ent
    ryofcal
    cium i
    ntot
    hecel
    l.

    Entryofcalci
    um intothecelloccur
    sf i
    rst
    .Subsequent l
    y,t
    herei
    sr el
    easeofcalci
    um f rom t
    he
    sarcoplasmicreti
    culum (cal
    cium-i
    nduced calci
    um r el
    ease)
    .Cal cium binds t
    ot roponin C,
    i
    nducing conformati
    onalchangest hatdisplacetr
    opomyosi nfrom t heacti
    n-binding si
    tes.
    Therei s cr
    oss bri
    dge formati
    on bet
    ween myosi n and act
    in with adenosi
    ne tri
    phosphat e
    hydrolysi
    s.Thepowerst r
    okeconsistsoft hemovementofmyosi nheadsalongt heacti
    n
    fi
    lament .Adenosi
    netr
    iphosphate-bi
    ndi ngisneededf orreleaseofmyosinheadsfrom t
    heactin
    fi
    lament .Thiscycl
    econt i
    nuesunt i
    lintracell
    ularcalcium level
    sfalll
    ow enoughthatcalci
    um
    dissociatesfr
    om tr
    oponin,causi
    ngar eturntot heori
    ginalconformati
    onoftropomyosi
    nwher e
    i
    tbl ocksmyosi nfr
    om accessingtheact in-bi
    ndi ngsi
    tes.Thismar kstheendofthecontr
    acti
    le
    cycle.

    41. Fi gur
    e1depict
    sapressur
    e-vol
    umel
    oopoft
    hel
    eftvent
    ri
    cleatr
    est(
    cur
    veA)andaf
    ter
    ani
    nter
    venti
    on(
    curveB).

    Whi
    choft
    hef
    oll
    owi
    ngi
    smostl
    ikel
    ytor
    epr
    esentt
    hei
    nter
    vent
    iont
    hatwasadmi
    nist
    ered?

    a. Metoprolol.
    b. Norepi
    nephr ine.
    c. Phenylephrine.
    d. Fur
    osemi de.
    e. Dobutami ne.

    ANSWER: 

    41. e. Dobut
    ami
    ne.

    Pressure-vol
    umel oopsdepi ctchangesi n vent
    ri
    cularpressureagai nstvent r
    icularvol
    ume
    duri
    ngasi nglecardiaccycle.Thest rokeworkoft hevent r
    icl
    ei srepresentedbyt hearea
    enclosedbyt hepr essur
    e-volumel oop.Changesi nstr
    okewor karei nfl
    uencedbypr el
    oad,
    aft
    erload,andint
    ri
    nsiccontracti
    li
    tyofthemyocardium.Thepr essure-
    volumel oopcanbeused
    todescribethecompl i
    anceandener geti
    cstat
    eoftheventri
    cle.CurveBdemonst ratesashif
    tin
    theend- systol
    icpr essur
    e-vol
    umer elati
    onshi
    p( ESPVR)t hatisconsistentwit
    hani ncreasei n
    cont r
    acti
    li
    ty.Al soseeni sani ncreasei nstr
    okevol ume( t
    hedifferencebetweent heend-
    diastoli
    candend- systol
    icvol
    umes) .Theshif
    tf r
    om cur veAt ocurveBi sconsi
    stentwi t
    ht he
    effectsofdobut amine,whichactsprimaril
    yasabet a-1adr ener
    gicagoni st
    .Theend- diastoli
    c
    volumei sr educed,becausethei ncreasedcontract
    il
    ityoftheleftvent r
    icl
    ehasr esul
    tedi na
    lowerend- systoli
    cvolumebeforeonsetofdiastoli
    cfi
    ll
    ing. 

    Fur osemide woul d show a decr ease in preload,but woul d not affect contractil
    ity.
    Phenyl ephri
    nei sadi rectalphaagonistthatresultsinar t
    eri
    alvasoconstr
    ict
    ionandi ncreased
    afterload,butdoesnotaf fecttheESPVR ( contractil
    it
    y).Norepi
    nephri
    nehaspr edomi nant ly
    alpha- 1 adrenergic acti
    vit
    yal ong withal owercomponentofbet a-1 adrenergic act
    ivity,
    resulting i
    ni ncreased afterl
    oad and a smal lincreasei n cont
    ract
    il
    it
    y.No i ncr
    easei nt he
    afterloadisseeni nthisdiagram.Metoprololwouldr esul
    tinadecreaseincontracti
    li
    ty,depicted
    byacl ockwiseshift
    /lesssteepESPVRcur ve.

    42. Youar eseeinga63- year


    -ol
    dwomani ncl i
    nicforfollow- upaftershewashospi tali
    zed
    l
    ast week wi t
    h an ant erior wal
    lST- segment myocar di ali nf
    arcti
    on ( MI)
    .Dur i
    ng t he
    hospit
    ali
    zation,sher eceivedt wodrug-eluti
    ngst ent
    st oherl eftanteriordescendingar t
    ery.
    Bipl
    ane vent ri
    cul
    ogr aphy at t he ti
    me of pr imar y percut aneous cor onaryi nter
    vent i
    on
    demonstratedanterior,l
    ateral,andapicalhypokinesi
    swi t
    hl ef tventri
    culareject
    ionfractionof
    40%.Herel ectr
    ocardiogram i sshowninFi gure1.Hercar diacmedi cati
    onsincludeaspi rin81
    mg,clopidogrel75mg,met oprol
    olsuccinate100mg,l isi
    nopr i
    l10mg,spi r
    onolactone25mg,
    andatorvastati
    n80mg.

    Whichoft
    hef
    oll
    owi
    ngneur
    ohor
    monesi
    smostl
    ikel
    ytopr
    eventmal
    adapt
    iver
    emodel
    ingi
    nthi
    s
    pat
    ient
    ?
    a.Endotheli
    n-1.
    b.Norepinephri
    ne.
    c. Al
    doster
    one.
    d.Atri
    alnatri
    uret
    icpepti
    de.
    e. Ar
    gini
    ne-vasopressi
    n.

    ANSWER: 

    42. d. At
    ri
    alnat
    ri
    uret
    icpept
    ide.

    Acommonset tingformyocar di
    alremodel ingisMI ,especiall
    yoft heanteri
    orwal l
    .Persist
    ent
    acti
    vationoft hesympat heticnervoussyst em,partl
    ymedi at
    edt hroughnorepi
    nephr i
    ne,aswell
    asact ivati
    onoft her eni n-
    angiotensin-al
    doster
    onesyst em resultinincreasedendot heli
    n-1
    product i
    on,col l
    agen t urnover,reduced ni t
    ri
    coxi deact ivi
    ty,and cell
    ularapopt osi
    s.These
    cell
    ularphenomena t ranslat
    ei ntoi ncreased ventricularsize and spher i
    cit
    y,decr eased
    contractil
    eper formance,andevent uall
    yhear tfai
    lurei nmanypat i
    ent
    s.Theneur ohormonal
    mediator s(norepinephrine,angiotensin,al
    dosterone,andvasopr essi
    n)arealltar
    getsofdr ugs
    thatreduceorevenr ever seremodel i
    ngandl eadtoi mprovedcl i
    nicalout
    comesaf terMI. 

    Endot
    hel
    ini
    sact
    ivat
    edbyangi
    otensi
    nandr
    educedbyangi
    otensi
    n-conver
    ti
    ngenzymei
    nhi
    bit
    or
    andangi ot
    ensi
    n- r
    eceptorbl ockert herapy;specif
    icendothel
    ininhi
    bit
    orshavebeenshownt o
    reduceremodelinginani malmodel saswel l.Natri
    ureti
    cpepti
    desar evasodi
    lat
    orsthatalso
    maydi rectl
    yinhibitmyocyt ehyper tr
    ophy.Ani malmodel sand smal lhuman studi
    eshave
    demonst r
    atedreducedr emodel ingaf terMIwi t
    hi nf
    usionsofbothbrainandat r
    ialnat
    ri
    ureti
    c
    pepti
    des.However ,theonecl inicalstudytodat edidnotfindanychangeincli
    nicalout
    comes
    suchasdeat horrehospital
    ization.

    43. A68- year-


    oldwomanpr esent
    st oyourcl inicforevaluationofherpr ogressivelower
    extr
    emityedemaanddyspneaonexer tion.Hermedi calhist
    oryincludeshypert
    ension,diabetes,
    andchronickidneydi
    sease.Sheisonl isinopri
    l,hydrochlorot
    hiazide,andinsul
    in.Transthoraci
    c
    echorevealslef
    tventr
    icul
    ar(LV)eject
    ionf ract
    ionof65%, moder ateconcentr
    icLVhyper trophy,
    normalvalvul
    arfunct
    ion,pul
    monar yarterysystoli
    cpr essureof45mm Hg, andE/ e'rat
    ioof18.

    Whicht
    hefol
    lowingther
    api
    eshavebeenprovenef
    fect
    ivet
    oreducehermor
    tal
    it
    yfr
    om herhear
    t
    f
    ail
    urewit
    hpreservedej
    ect
    ionf
    ract
    ion(
    HFpEF)?

    a. Not herapyr educesmortal


    it
    y.
    b. Diureti
    cs.
    c. Beta-blocker s.
    d. Angiotensin- conver
    ti
    ngenzymei
    nhi
    bit
    ors.
    e. Spironolactone.

    ANSWER: 

    43. a. Not
    her
    apyr
    educesmor
    tal
    it
    y.

    Unfort
    unat
    ely,noneofthecurrentther
    api
    esusedforheartf
    ail
    urewithreducedejecti
    onf r
    acti
    on
    havebeenshownef f
    ect
    iveforHFpEF.Cli
    nicalt
    ri
    alsi
    nHFpEFhavepr oducedneutralresult
    sto
    date,andt
    reatmenti sl
    argelydirect
    edtowardassoci
    atedcondit
    ions( e.
    g.,hyper
    tension)and
    symptoms(e.g.,edema).
     

    44. A40- year-oldmani sreferr


    edforeval
    uationofexerti
    onalchestpai nandshor t
    nessof
    breat
    h.Hismedicalhist
    oryisnotablef
    orhypercholest
    erol
    emia,forwhi chhetakesrosuvast
    at i
    n
    20mgqhs.Hei sal if
    eti
    menonsmokeranddoesnotdr inkal cohol.Ther
    ei snohi stor
    yof
    hypert
    ensi
    on.Thef amil
    yhistor
    yi snot
    ableforhismat er
    nalgrandfatherandhisbrotherhaving
    devel
    opedheartfail
    ure(HF)i
    nt hei
    r50s. 

    Hisexaminati
    onreveal
    sabloodpressureof110/
    70mm Hg,ahear tr
    ateof80bpm,jugul
    ar
    venousdist
    enti
    onat16cm H20,cl
    earlungsonauscul
    tat
    ion,anS4 
    gall
    op,andmi
    ldper
    ipher
    al
    edema. 

    Anelectrocardi
    ogr am revealssinusrhythm,withgeneral
    lylowQRSvol tageandnoevi denceof
    apr i
    ormyocar dialinfarcti
    on.Hisechocar di
    ogram showsmoder ateconcentri
    cleftvent ri
    cul
    ar
    (LV)hyper t
    rophywi t
    hanej ecti
    onf r
    action(EF)of50% andnoval vul
    arabnormal i
    ties.Init
    ial
    l
    aboratoriesarenot ableforasodi um l
    evelof132mEq/ L,serum creati
    nineof1.8mg/ dl ,
    andan
    N-terminalpro-brainnat r
    iuret
    icpepti
    de( NT-proBNP)of1800pg/ ml .Hi
    scompl et
    ebl oodcount
    wasnor malwi t
    hanor malwhi tebloodcountdiffer
    ent
    iati
    on. 

    Atcar
    diaccat
    heteri
    zat
    ion,hi
    scoronar
    yar t
    eri
    esarenor
    mal
    .Thepressur
    emeasur ement
    sare:
    meanrightat
    ri
    al,10mm Hg;r i
    ghtventr
    icl
    e,55/
    14mm Hg;pulmonaryart
    ery,55/25mm Hg
    wit
    hmeanof35mmHg;andpulmonar
    ycapi
    ll
    arywedge,
    25mm Hgwi
    thaVwaveof32mm Hg.
    Cardi
    acout
    putwas4.
    0L/
    min.

    Whichofthefol
    lowi
    ngi
    sthemostr
    easonabl
    euni
    fyi
    ngdi
    agnosi
    sfort
    hispat
    ientwi
    thHFand
    pr
    eservedEF?

    a. Amy loi
    dosis.
    b. Glycogenst oragedisease.
    c. Fabry'sdisease.
    d. Loeffl
    erendocar di
    ti
    s.
    e. Sarcoidosis.

    ANSWER: 

    44. c. Fabr
    y'sdi
    sease.

    ThecorrectanswerisFabry'sdisease,analpha-gal
    act
    osi daseAdef i
    ciency.Thispresentat
    ion
    wit
    hHFi nthesett
    ingofreasonablypreservedEFassociatedwi t
    hchestpai n,normalcoronary
    art
    eri
    es,LVhyper tr
    ophy,andr enaldysfuncti
    onismostt ypicalofFabry'sdisease.Thefami l
    y
    hi
    stor
    yi sconsi st
    entwi t
    h at ransmission ofan X-l
    inked disorder
    .Si ncet hebrotherand
    maternalgrandf
    atherwerealsoaffect
    ed, hi
    smothermayhavebeenanunaf f
    ectedcarri
    erofthe
    mutati
    on.Ar epl
    acementtherapyisavailabl
    eatahighcost . 

    Theechocar diographi cfindingsandr enalinsuffi


    ciencyar eatypicalforpat ientswi t
    hLoef f
    ler
    endocar dit
    is,whi ch isnoti nherit
    ed,and i schar acteri
    sti
    cal
    lyassoci ated wi t
    h endocar dial
    thickeningandmur althrombiaswel lasper ipher
    aleosi nophi
    li
    a.Car di
    acsar coidosisisal soan
    acqui r
    edr athert hani nher i
    teddi sorder,andi scommonl yassociatedwi t
    hat rioventr
    icularblock
    orvent r
    icularar rhythmi asi naddi ti
    ont oHF.Whi l
    efami li
    alamyloidosisrelatedt oelaborationof
    mut antt r
    anst hyretinal somaybeassoci atedwi t
    hcar diacandr enalinvolvement ,autosomal
    domi nanti nher i
    tancei st ypicalandusual lymani f
    estsatanol derage.Pat i
    ent swithgl ycogen
    storagedi seasest ypicall
    ypr esentwi t
    hHFatayoungage,andevenwi thappr opri
    atet herapy,
    rarelysurvivet oadul thood.

    45. A50- year


    -ol
    dmanwi thnosi gnif
    icantmedi calhi
    storypresent
    swit
    hpalpi
    tat
    ions.On
    examinat
    ion,
    hehasami l
    dlyelevatedjugularvenouspressureat10cm H20,
    afai
    ntparast
    ernal
    l
    ift
    ,andaprobabl
    eri
    ghtventr
    icular(RV)S3 
    gallop.

    Hisel ectr
    ocar diogr am isnot ablef orsinusrhyt
    hm,wi thani ncompl eter ightbundl ebr anch
    block.AHol termoni torrevealsf requentr unsofnonsustai
    nedvent riculart achycardiawi t
    ha
    lef
    tbundl e br anch bl ock pattern.Cor onaryangi
    ographyr eveals no si gnificantepicardial
    coronar yarterydi sease.Echocar di ographysuggestsRVcavitydilat
    ionandmoder at
    etri
    cuspid
    valver egurgitati
    on.Magnet icr esonancei magi
    ngi ssuggesti
    veoff at t
    yi nfil
    trationoftheRV,
    consistentwi thar rhyt
    hmogeni cRVcar diomyopathy(ARVC).

    Whi
    choft
    hef
    oll
    owi
    ngpr
    otei
    nsmostl
    ikel
    yhasadef
    ecti
    nit
    sgeneencodi
    ng?

    a. Lami nAandC.
    b. Tafazzin.
    c. My osinheavychai
    n.
    d. Plakoglobi
    n.
    e. Dyst
    rophi
    n.

    ANSWER: 

    45. d. Pl
    akogl
    obi
    n.

    Thecor rectansweri splakoglobin.ARVCi sanaut osomaldomi nantfamil


    ialdi seaseoft he
    desmosome,l i
    nkedt omut ati
    onsi nseveralgenesencodi ngdesmosomalpr oteins,including
    j
    unctionalplakoglobin.Myosinheavychai nmut at
    ionsmaybeassoci at
    edwi thbot hdi l
    ated
    cardi
    omyopat hyandhyper trophiccardi
    omyopat hy.Similar
    ly,mutati
    onsindyst rophinmaybe
    associat
    edwi t
    hmuscul ardyst r
    ophyanddi l
    atedcar di
    omyopat hy,andmutat i
    onsi nt afazzin
    havebeenassoci atedwith dil
    atedcardiomyopathyandl eftventri
    cul
    arnoncompact i
    on,but
    neit
    heristypicalofARVC.

    46. A 62-year-
    oldmanwi t
    hahistor
    yofhypert
    ensi
    onisref
    erredwit
    hadecreasedlef
    t
    vent
    ri
    cul
    arej
    ect
    ionfr
    act
    ion(
    LVEF)
    .Hehasahi
    stor
    yofpoorcompl
    iancet
    ohismedi
    cat
    ions.
     

    Hisli
    stedmedicat
    ionsi
    ncludeval
    sart
    an80mgdai
    ly,at
    enol
    ol50mgdail
    y,andf
    urosemide40
    mgdai ly.Hi
    sbloodpressureis130/85mm Hgandhisheartr
    atei
    s80bpm andr egul
    ar.
    Cardi
    acexaminati
    onisnormal.

    Echocar
    diogr
    aphyr
    esul
    tsshowamoder
    atel
    ydi
    lat
    edLV,
    LVhyper
    trophy,
    andanLVEFof30%.

    Which oft
    he f
    oll
    owing i
    sthe mostappr
    opri
    ate nexttherapeut
    ic step,based on cur
    rent
    gui
    deli
    nesf
    ort
    hetreat
    mentofasympt
    omati
    csystol
    icvent
    ricul
    ardysfuncti
    on?

    a. Changeatenololtocarvedil
    ol.
    b. Beginadiuret
    ic.
    c. Changevalsartantoli
    sinopri
    l.
    d. Referf
    orprophylacti
    cimplantabl
    ecar
    diover
    ter
    -def
    ibr
    il
    lat
    or(
    ICD)
    .
    e. Beginanaldosteroneblocker.

    ANSWER: 

    46. a. Changeat
    enol
    olt
    ocar
    vedi
    lol
    .

    Thecorrectansweri st ochanget hebeta-blockertoapr ovenone.Al t


    houghat enol
    olisan
    ef
    fect
    ivebet a-
    blocker,
    ithasnotbeenst udi
    edi nheartf
    ailur
    e.Theref
    ore,t
    heef f
    icacyandother
    cl
    ini
    call
    yrelevantissues,suchast ar
    getdose,ar enotknown.Most ,butnotall
    ,beta-bl
    ockers
    havebeenf oundtobeef fect
    iveinchr
    onicsystoli
    cheartfail
    ure.Gui
    deli
    nesrecommendt heuse
    ofagent
    st hathavebeenst udiedincl
    ini
    calt
    rials.
     

    Angiot
    ensin- r
    eceptorbl ockersappeart obeatl eastasef f
    ecti
    veasangi otensi
    n-conver t
    ing
    enzymei nhibit
    orsandar eacceptablechoi ces,parti
    cularlyinpatient
    sal r
    eadyr eceivi
    ngt hem
    fort
    het r
    eatmentofhyper tensi
    on.Aldosteronebl ockadeisnotr ecommended, unlessadequat e
    l
    aboratoryfollow-upcanbeensur ed.Diur eti
    csanddi goxinareusef ulonlyf orsympt omat i
    c
    heartfail
    ure.The i ndications f
    oran I CD,based on t he Amer i
    can College ofCar diology
    Foundati
    on/ Amer i
    canHear tAssoci
    ation/Hear t
    hRhyt hm Soci ei
    tyguideli
    nes,i ncl
    udeanLVEF
    <35%wi t
    hNewYor kHear tAssociati
    oncl assII-I
    IIheartfail
    ure(ClassI,LevelofEvidence[ LOE]
    B).Thepat i
    enti scurrentlyasymptomat i
    c,butanI CDcoul dbeconsidered( ClassIIb,LOEC) .
    Thebestanswert
    houghi
    stoensur
    ethepat
    ienti
    songui
    del
    ine-
    dir
    ect
    edmedi
    calt
    her
    apy.
     

    47. A62- year-


    oldAfr
    ican-Americanmanwi thahi stor
    yofhypert
    ensionwasr efer
    redwitha
    decreasedl
    eftventri
    cul
    areject
    ionfr
    action(LVEF).Hedeniesdyspnea,f
    atigue,chestpain,li
    ght-
    headedness,orsyncope.Heseeshi sint
    erni
    stsporadical
    lyandhasnotf oll
    owedt heprevi
    ous
    recommendat i
    ont oseeacar diol
    ogist.Hel i
    ves50mi lesawayandhasdi f
    ficul
    tygetting
    transpor
    tat
    ion. 

    Hismedicati
    onsi ncludevalsart
    an80mgdai ly,at
    enolol50mgdaily,andf
    urosemide,which
    wasdisconti
    nuedi nt hepast.Hisbloodpressureis130/85mm Hg,hishear
    trateis80bpm
    andregular
    ,hiscar diacexaminati
    oni snormal,andhehasnosi gnsofheartfai
    lur
    eorfluid
    over
    load.Echocardiographyresult
    sshow amoder at
    elydi
    lat
    edLV,withanLVEFof30%.You
    swit
    chhisatenololtoanotherbeta-bl
    ocker
    . 

    Hefai
    lstokeephi s1-monthscheduledfol
    low-upappointment.Sixmonthslater,hepresents
    wit
    hincreaseddyspnea.Hisint
    erni
    stmadef ur
    thermedicat
    ionchangesandr eferredhim back
    t
    oyou,st i
    llsympt
    omatic.Hisdail
    ymedicat
    ionsarelong-acti
    ngmet opr
    ololsuccinate100mg,
    l
    isi
    nopri
    l20mg, andfurosemide40mg.Hehasgai ned6poundssi ncehispri
    orvisit.
     

    Hisbloodpressureis120/80mm Hg,hi sheartr


    ateis50bpm andregul
    ar,hi
    sjugularvenous
    pressur
    eismi l
    dlyelevat
    ed,andasof tS3 gal
    lopi
    spresent.Hehast
    raceedema.Hislaboratory
    resul
    tsaresodium 138mEq/ L,potassium 4.
    8mEq/ L,bl
    oodureani
    tr
    ogen32mg/ dl,creat
    inine
    1.2mg/ dl
    ,andB-typenatri
    uret
    icpeptide150pg/ml.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    enextst
    ep?

    a. I
    ncreasehisli
    sinoprildose.
    b. I
    nit
    iateanaldosteronebl ocker
    .
    c. Ref
    erforcardi
    act ransplant.
    d. I
    nit
    iatehydral
    azineandi sosorbidedi
    nit
    rat
    e.
    e. I
    ncreasehismet oprololdose.

    ANSWER: 

    47. d. I
    nit
    iat
    ehydr
    alazi
    neandi
    sosor
    bidedi
    nit
    rat
    e.

    Thecor rectansweristoaddhydr al
    azineand i
    sosor bidedinitrat
    eandt i
    tr
    atetothetar
    getblood
    pressur e.The combi nati
    on ofhydr alazi
    ne and i sosorbide dinit
    ratel owers mort
    ali
    ty and
    decreaseshear tfail
    urehospital
    izat
    ionsi nAfrican-Amer icanpat i
    ent swithchronicsystolic
    heartf ailur
    e( New YorkHear tAssociati
    onclassI II-
    IV)whoar ealreadyonopt imalmedi cal
    therapy.The pat ient’
    sr est
    ing heartr at
    e of50 bpm makes i ncreasing his bet
    a-bl
    ocker
    impr actical
    .Analdosterone-r
    eceptorblockerrequirescar efulfol
    low- up,whichisprobl
    emat ic
    inapat ientwhomi ssesappointments.Transplantati
    onispr ematurei npati
    ent
    swhohavenot
    yetexhaust edmedicalt
    herapy. 

    48. A74- year-


    oldwomanwi t
    hnoni schemicdilat
    edcardiomyopathyisseen1weekaf ter
    hert hi
    rd hospi
    tal
    ization i
    n 6 monthsf orprogressi
    vewei ghtgain,peripheraledema,and
    reduced uri
    neout put,each ti
    mer api
    dl yresponsivetointravenousfurosemi de.Di
    schar
    ge
    medicati
    onswer el i
    sinopri
    l20mgdai ly,carvedi
    lol25mgt wicedail
    y,spironolact
    one25mg
    dail
    y,andfurosemide120mgt wicedai
    ly.
    Sincedi
    scharge,
    shehasgai
    ned10pounds.Herdaught
    erconf
    ir
    msshei
    scompl
    iantwi
    thal
    lof
    hermedicat
    ionsandsodi
    um r
    est
    ri
    cti
    on.

    Whi
    chofthefol
    lowi
    nginter
    venti
    onsismostl
    ikel
    ytobesuccessf
    uli
    nrest
    ori
    ngf
    lui
    dbal
    ance
    wi
    ththemi
    nimum adver
    sepotent
    ial
    ?

    a. Substi
    tutetorsemideforfur
    osemi
    de.
    b. I
    ncreasespi ronol
    actonedose.
    c. I
    ncreasefurosemi dedose.
    d. I
    ncreaselisinopri
    ldose.
    e. Addme tolazone.

    ANSWER: 

    48. a. Subst
    it
    utet
    orsemi
    def
    orf
    urosemi
    de.

    Thecorrectansweri stochanget otorsemide.Thegreat


    eroralbioavai
    labi
    li
    tyoftorsemide( e.g.,
    approachingi tsi
    ntravenousaction)provi
    desbenef i
    tsoverfurosemide,whichhassi gnif
    icant
    vari
    ableor alabsorpti
    on.Alloft
    heot herchoicesaremor eli
    kelytoproduceunt owardadver se
    eff
    ects,suchashypokal emia(
    e.g.,metol
    azone),wit
    houtsigni
    ficantcl
    ini
    calbenefi
    t,part
    icular l
    y
    si
    ncet hepat ient
    ’sbasel i
    nemedi cat
    ionsareal r
    eadyatthet argetdosesusedi nt heclinical
    tr
    ial
    s. 

    49. A 73- year


    -oldwomanwi thhyper t
    ension,di
    abetes,andhear tfai
    lurewi t
    hpreser ved
    ejecti
    onf r
    acti
    onpr esent
    st ot heemergencydepar t
    mentwi t
    ha2- weekhistoryofprogressive
    dyspnea on exer tion,wei ghtgai n,and lower extremit
    y edema.A di agnost
    ic cardiac
    catheter
    izati
    on 1 year ear l
    ier demonstrat
    ed normalcor onary ar
    teri
    es.Her out patient
    medi cat
    ionsi ncl
    udel i
    sinopril5 mg oncedai l
    y,metoprol
    olsuccinate100 mg oncedai ly,
    furosemide40mgoncedai l
    y,andmet for
    min500mgt wicedaily.
     

    Herphysi
    calexaminati
    onisnotabl
    eforajugularvenouspressureof14cm ofwat er
    ,bibasi
    lar
    i
    nspir
    ator
    yrales,
    and2+l owerextr
    emit
    yedemat othekneesbil
    ater
    ally.HerchestX-rayshows
    mil
    dcardi
    omegal ywit
    hpulmonaryvascul
    arredist
    ri
    buti
    onandasmal llef
    tpleur
    aleff
    usion.
     

    Sheisadmi
    tt
    edt
    othehospi
    talser
    vicewi
    thadi
    agnosi
    sofacut
    edecompensat
    edhear
    tfai
    lur
    e
    (ADHF)
    .

    Whi
    chofthefol
    lowingabnormal
    it
    iesi
    st hemostimport
    antpredi
    ctorofhospi
    talmor
    bidi
    tyand
    mor
    tal
    it
    yinthi
    ssituat
    ion,
    inaddi
    ti
    ontolowsystol
    icbl
    oodpressure?

    a. Serum creati
    nine.
    b. Heartr
    ate.
    c. Oxygensat ur
    ation.
    d. Serum sodium.
    e. Hematocr i
    t.

    ANSWER: 

    49. a. Ser
    um cr
    eat
    ini
    ne.
    Thecor r
    ectansweri sthecr eati
    nine.Cl i
    nicalinformationobtainedatthet i
    meofadmi ssioncan
    helpt opr edi
    ctout comesdur i
    ngt hehospi tali
    zationandf ol
    lowingdischarge.TheADHERE
    (AcuteDecompensat edHear tFailur eNationalRegi str
    y)foundt hatthesinglebestpredictorfor
    mor tal
    itywasanel evatedbl oodur eani t
    rogen( ≥43mg/ dl)
    ,foll
    owedbyl owSBP( <115mm Hg) ,
    and hi gh ser um cr eatini
    ne ( ≥2.75 mg/ dl)
    . A subsequentmodelf rom t he OPTI MIZE-HF
    (OrganizedPr ogram t oInit
    iateLifesavi ngTr eatmenti nHospi t
    ali
    zedPatientsWi t
    hHear tFail
    ure)
    registr
    yal sofoundSBP ( ≤100mm Hg)andser um creati
    nine( ≥2.
    0mg/ dl)tobepower ful
    predictors ofi n-hospitalmor tality. 
    Hyper t
    ensi on is associated wit
    hi mpr oved outcomes.
    Anemi aandhyponat remiaar ecommoni npat ientswithadvancedHFandpr edictadverselong
    -ter
    m out comesandnotshor tter m.Tachycar di
    ahasnotbeenshownt opr edi
    ctei t
    herin-
    hospi t
    alorpost di
    schar gemor t
    alityi npatientswi thADHF.  

    50. A56- year-oldmanst atus/postanter


    iormyocardialinfarcti
    onwi t
    hanej ect
    ionfract
    ion
    of25% andmi ldrightventri
    culardysfuncti
    onpresent
    sur gentlytocl i
    nicwithcomplaintsof
    ort
    hopnea,par oxysmalnoct urnaldyspnea,andabdomi nalbl oati
    ngf or2days.Her ecentl
    y
    tr
    aveledtovisi
    tfami l
    yforthehol i
    daysandadmi t
    tedtohavingdi ffi
    cult
    ymai nt
    aini
    ngthesodium
    andf l
    uidrestr
    icti
    on,althoughhewasadher entwit
    hhi smedi cati
    ons.Uponr etur
    nhome,he
    notedthathisweighthadi ncreased10poundsandhi slegswer eswollen. 

    Hisout pati
    entmedi calregi
    meni ncludesenalapril10mgtwi cedail
    y,car vedil
    ol12. 5mgt wice
    daily,spi
    ronolactone25mgoncedai l
    y,fur
    osemi de80mgt wicedaily,
    at orvastati
    n40mgonce
    daily,
    andaspi ri
    n81mgoncedai ly.Hedoesnotsmokeci garettesordrinkalcohol .Hisphysical
    exami nati
    onreveal sabloodpr essureof130/80mm Hg,hear trat
    eof88bpm,j ugularvenous
    pressureof14cm H2O,decr easedbr eat
    hsoundsatt hel eftbase,andasof thol osystoli
    c
    mur muratt hel eftl
    owersternalborder.Theliveredgei
    spal pablethreef i
    nger breadthsbelow
    ther i
    ghtcostalmar gi
    n,andthel owerextremiti
    esarewarm wi th1+pi tt
    ingedemat ot hemi d
    calvesbilat
    erall
    y. 

    Youdeci
    detoadmitthi
    spat
    ientdir
    ectl
    ytothei
    npat
    ientcar
    diol
    ogyser
    vicef
    ormanagementof
    acut
    edecompensat
    edhear
    tfail
    ure(ADHF)
    .

    Whi
    ch ofthe fol
    lowi
    ng woul
    d be the saf
    estand mostef
    fect
    ive i
    nit
    ialor
    derf
    orvol
    ume
    management
    ,inaddit
    iont
    oa2-li
    terf
    lui
    drestr
    ict
    ion?

    a. Bedsidevenovenousul
    traf
    il
    tr
    ati
    onat100ml/h.
    b. Furosemide80mgi nt
    ravenousbol
    usevery12hour
    s.
    c. Furosemide40mgi nt
    ravenousbol
    usevery12hour
    s.
    d. Bedsidevenovenousul
    traf
    il
    tr
    ati
    onat200ml/h.
    e. Bume tani
    de2mgor all
    yevery12hours.

    ANSWER: 

    50. b. Fur
    osemi
    de80mgi
    ntr
    avenousbol
    usever
    y12hour
    s.

    Thecor r
    ectansweri sl argerdosesofi ntr
    avenous( I
    V)f ur
    osemi de.Thispatientpresents
    urgent
    lywit
    hsympt omsandsi gnsofcongest i
    onandnor malsyst emicperfusi
    on.Thel i
    kely
    preci
    pit
    antt
    ot hi
    sadmi ssionisnonadherencewiththesodi um andf l
    uidrest
    ri
    cti
    on,whichoften
    canoccurduringtr
    avelawayf rom home.Whenpat ientsareadmi tt
    edtot hehospi
    talwit
    hADHF,
    i
    niti
    ati
    ng an eff
    ecti
    vedi uresi
    swi thIVl oop diur
    eticsiscr i
    ticaltol oweri
    ng cardi
    acf i
    ll
    ing
    pressur esandr eli
    evingcongest i
    vesympt oms.Accor dingt otheACCF/ AHA2013Gui deli
    nef or
    theManagementofHear tFai l
    ure, 
    ifpati
    entsareal r
    eadyr eceivi
    ngl oopdiureti
    cs,t heini
    tialIV
    doseshoul dequalorexceedt hechr oni
    coraldose( f
    urosemi de80mg, not40mg) .Bumet anide
    i
    sa mor epotentl oop di ureticthan furosemide,but2 mg t wicea dayi sequi valentt o
    furosemi de80mgt wiceadayandshoul dbegi venintravenously,perguideli
    nes.Ther ecent
    DOSE( Diur
    eti
    cOpt i
    mi zat
    ionSt r
    ategiesEvaluat
    ioni nAcut eHear tFail
    ure)studyshowedno
    benefitofacont inuousi nf usion, 
    andwhi lepil
    otst udiessuggestt hatearl
    yul trafi
    lt
    rat
    ioni s
    associ atedwithgr eaterfl
    uidr emovalt hanmedi caltherapyal one, 
    theHeartFailureSoci etyof
    Amer icagui del
    inesr aiseconcer nsaboutsaf et
    y,cost,andneedf orspeciali
    zedmedi caland
    nursingsuppor t. 

    51. An83- year-oldmanwi t


    hatri
    alf
    ibr
    il
    lat
    ionandnoni schemicdi
    latedcardi
    omyopat hyis
    admi t
    tedt othehospi talwithacutedecompensatedhear tfai
    lur
    e(ADHF) .Hi
    smedi calhist
    ory
    i
    ncludest ype2di abetes,chronicki
    dneydisease,andgout .Hisadmissionbl
    oodpr essureis
    90/
    76mm Hg,andhi shear tratei
    s94bpm andi rregul
    ar.Bumetani
    dei sadmini
    steredasa4
    mgi ntravenous(IV)bol usevery12hours.

    Despi
    tehigh-
    doseIVdiuret
    ics,hisur
    ineoutputr
    emains<70ml/h,hiswei
    ghtdecreases<0.
    5kg,
    andhisserum creat
    ini
    neincreasesf r
    om 1.4mg/dlto2.1mg/ dloverthefir
    st48hour s.I
    n
    addi
    ti
    on,shortr
    unsofnonsustainedventr
    icul
    art
    achycar
    diaar
    enot edontel
    emetry.

    Whi
    choft
    hef
    oll
    owi
    ngwoul
    dbear
    easonabl
    enextst
    epi
    nthemanagementoft
    hispat
    ient
    ?

    a. Bedsidevenovenousul traf
    il
    trat
    ionat200ml /h.
    b. Dopami ne2mcg/ kg/minbycont i
    nuousinfusion.
    c. Mil
    rinone0. 25mcg/ kg/minbycont i
    nuousinfusion.
    d. Ni
    troprusside20mcg/ minbycont i
    nuousinfusion.
    e. Obtainright
    - hear
    tcatheter
    izati
    onbeforechangingther
    apy.

    ANSWER: 

    51. b. Dopami
    ne2mcg/
    kg/
    minbycont
    inuousi
    nfusi
    on.

    Thecor r
    ectansweri stoassesshemodynami cs.Cardior enalsyndr ome, orco- existentcar di
    ac
    andr enaldysf unct i
    on, i
    scommoni npat i
    ent swi thHF.  
    Fur ther mor e,dur inganHF
    hospit al
    izati
    on, 15- 30%ofpat i
    entswi lldevelopwor seni ngr enalf unct ion.Thi spat i
    enthas
    severalindependentr i
    skfact orsforthedevel opmentofwor seningr enalf unct ion,including
    olderage, di
    abet es,andbasel i
    ner enaldysf unct i
    on.Di uret i
    cr esi
    st ancemaybecont ri
    but i
    ngt oo.
    Addingal ow- dosei notrope( dopami ne)ori nodi lat
    or( mi lr
    inone)hasnotbeenshownt o
     
    i
    mpr oveshor t
    -term outcomesandmayexacer batethispat i
    ent ’
    sar rhyt hmi as. Empi ri
    c
    admi nistrati
    onofni tr
    oprussidewi thoutar terialmoni toringmaybedi ffi
    cul tgivent hepat i
    ent’
    s
    relat
    ivelylowbl oodpr essure.TheCARRESS- HF( Cardior enalRescueSt udyi nAcut e
    Decompensat edHear tFail
    ur e)tr
    ialtestedt hesaf etyandef ficacyoful trafilt
    rationasar escue
    strat
    egyi nthisset t
    ingandf oundnocl ini
    calbenef i
    twi thwor seningr enalf unct ioncompar ed
    withst eppedphar macol ogiccar e. 
    Whi letherei snor olef orr outinepul monar yar t
    er y
    cathet er
    izationint hemanagementofADHF, theAmer i
    canCol l
    egeofCar diol
    ogy
    Foundat ion/Amer i
    canHear tAssoci ati
    on2013Gui del
    inef ortheManagementofHear tFai l
    ure
    suggest st hathemodynami cmeasur ement smayhel pi nt hechoi ceandt itr
    ationofpar enteral
    agent s,especi all
    yinpat i
    entswhoar er ef
    ractor ytoinitialther apy, i
    ncl udinghi gh-doseor
    combi nat i
    ondi uretics(Table1) .
    52. A71- year-ol
    dwomanpr esent
    st otheoutpati
    entcli
    nicwi thexerti
    onaldyspneafort he
    past6months.Thereisnoorthopneaorchestdiscomfort
    .Shei sal i
    fet
    imenonsmokerandhas
    hi
    stor
    yofhypertensi
    onandpar oxysmalatri
    alf
    ibri
    ll
    ati
    on.Currentmedi cati
    onsincludeli
    sinopri
    l
    20mgandat enolol50mg.Herhear trateis55bpm andr egular,herbloodpressureis165/ 90
    mm Hg,andherjugularvenouspressureis12cm. 

    Cardiopulmonar y exami nat


    ion is unr
    emar kable,and ther
    ei s 1+ pret
    ibi
    aledema.Chest
    radi
    ogr aphyisunr emar kabl
    e.Echocardiographyshowsnor mallef
    tventr
    icl
    esizeandmass,
    witheject i
    onfract
    ionof66%.Ther eismi l
    dl ef
    tatri
    alenl
    argementandmi l
    d( Gr
    adeI)di
    ast
    olic
    dysfunct i
    on,withanest imatedpulmonar yar t
    erysystol
    icpressur
    eof45mm Hg.Mi l
    dmitral
    i
    nsuf f
    iciencyandmi ld-
    moder at
    etri
    cuspi
    di nsuff
    ici
    encyarepresent
    .

    Whi
    choft
    hef
    oll
    owi
    ngdoyour
    ecommend?

    a. St
    artdigoxi
    n0.125mgqd.
    b. St
    artsil
    denafi
    l20mgt i
    d.
    c. I
    ncreaseatenololt
    o100mgqd.
    d. St
    artchlort
    hali
    done25mgqd.
    e. St
    artbosentan62.5mgbid.

    ANSWER: 
    52. d. St
    artchl
    ort
    hal
    idone25mgqd.

    Thecor rectanswerist ostartchlor


    thal
    idone.Basedont hepatient’shi
    stor
    y,demogr aphics,
    exam, andechocar diogram, t
    hemostl i
    kelydiagnosisisheartf
    ailurewit
    hapr eser
    vedejecti
    on
    fr
    action( HFpEF).Pulmonar yhypert
    ensioniscommonl yseeninHFpEFandi sr el
    atedt
    o
    elevatedleft
    -heartfi
    ll
    ingpressures.Thefir
    ststepi str
    eatmentoft heunder
    lyingcauseoft he
    HFpEF, thatis,
    thesyst emicelevati
    oninbloodpr essure.
     

    Inthissituation,t
    henextopt i
    oni stoaddadi uret
    icsuchaschl or t
    hali
    done.Increasingthe
    atenololwoul dnotbeasef fecti
    veandherhear tr
    atesarelowal ready.Whilestudiesare
    underway, thereisnocur r
    entevi denceforpulmonary-specif
    icvasodilator
    sinHFpEF, andther
    e
    i
    spot entialforwor seningleft
    -sidedcongest i
    onwi t
    hisolatedpulmonar yvasodilati
    onwi t
    h
    bosent anorsi l
    denaf i
    linHFpEF.Di goxinwasnotassoci atedwithi mprovedoutcomesi nan
    ancil
    laryanal ysi
    soft heDI Gtri
    al.Digoxinisusefultohelpcontroltheventri
    cularresponsein
    atri
    alfibr
    ill
    ation,butthepat i
    entisi nsi
    nusr hyt
    hm.  

    Whi l
    ethereisnopr oventherapyforHFpEF, theAmer icanCollegeofCar di
    ology
    Foundation/AmericanHear tAssociat
    iongui delinerecommendscont rolofbloodpr essureand
    volumest at
    us(Classl )
    ,andbot hcanbeef f
    ect ivelyaccompl i
    shedbyaddi ngchl ort
    halidoneto
    theregimen.Inananci ll
    aryanalysisf
    rom theALLHAT( Ant
    ihypert
    ensiveandLi pid-Lowering
    TreatmenttoPreventHear tAttack)tr
    ial
    ,chlorthalidonewasassoci atedwithal oweri nci
    dence
    ofnew- onsetHFpEF, al
    thoughef f
    ectsonpr eval entHFpEFmor bi
    dit
    yandmor tali
    tyhavenot
    beenassessed. 

    53. A50- year


    -oldmanpr esent
    st otheoutpati
    entcli
    nicwi
    thcomplai
    ntsofdyspneaand
    fat
    iguewi t
    h anyact i
    vit
    y.Hehasa di st
    ant20- packperyearsmoking hi
    story,and mi l
    d
    control
    ledhypert
    ension.Onexami nati
    on,hi
    shear trateis60bpm andr egular,hi
    sbl ood
    pressureis105/85mm Hg,andhi sjugul
    arpressureis20cm wit
    hprominentVwaves.Hi s
    hearthasar egul
    arrateandr
    hythm,wi t
    hathi
    rdsoundandgr adeIhol
    osyst
    oli
    cmur muratthe
    l
    eftster
    nalborder.
     

    Liveredgeispulsat
    il
    eandpalpabl
    eatfourf
    ingerbr
    eadt
    hsbel
    owthecost
    almargi
    n,andt
    herei
    s
    a positi
    ve flui
    d wave.Lowerext r
    emiti
    es are coolwit
    h 3+ edema.Chestfil
    m shows
    cardiomegalyandpulmonar
    yvenoushypertensi
    on. 

    Theel
    ectr
    ocardi
    ogram (
    Figur
    e1)showsnor mall eftvent
    ri
    cul
    ar(
    LV)si
    zeandf
    unct
    ion,wi
    th
    moder
    ateconcent
    ri
    cLVhypertrophyandbi
    atr
    ialenlar
    gement.

    Whi
    choft
    hef
    oll
    owi
    ngwoul
    dyour
    ecommend?
    a. I
    nvasi vehemodynami csatrestandwit
    hexerci
    se.
    b. Startli
    sinopri
    l5mgperday.
    c. Coronar yangiography.
    d. Cardiopulmonar yexerci
    setesti
    ng.
    e. Ri
    ght -heartcatheter
    izat
    ionwithvent
    ri
    cularbi
    opsy.

    ANSWER: 

    53. e. Ri
    ght
    -hear
    tcat
    het
    eri
    zat
    ionwi
    thvent
    ri
    cul
    arbi
    opsy.

    Thecor r
    ectanswerisright-heartbi
    opsyf orhi
    ghsuspicionofamyl oi
    dheartdiseasegivenhi
    s
    symptoms, age,
    andl owvol tageonelectrocar
    diogram despi
    tehisLVhyper t
    rophy.Thi
    s
    suggestsaninfi
    lt
    rat
    ivedisease.Hehashear tfai
    lur
    ewithsignif
    icantvol
    umeover l
    oad,
    as
    evi
    dencedbysever ejugulardistent
    ion,pulsat
    il
    ehepatomegaly,ascit
    es,edema, andathir
    d
    heartsound. 

    Cardiopul
    monar yexercisetest
    ingandinvasi
    veexer
    cisehemodynami csarever
    yusefult
    o
    assessforheartfai
    lurewithpreservedej
    ecti
    onfr
    act
    ion( HFpEF)whenhist
    oryandexam
    fi
    ndingsareequivocal.Inthispat
    ientwhois50yearsold,themostli
    kel
    ydiagnosi
    sisli
    ght-
    chain(AL)
    -typeamyl oid. 

    Angi
    otensi
    n-conver
    ti
    ngenzymeinhi
    bit
    orshavenotbeenshowntobeeff
    ect
    ivei
    nHFpEFor
    i
    nfi
    lt
    rat
    ivecardi
    omyopat
    hies,
    andgivenhisl
    owbloodpressur
    e,t
    hiscoul
    dcausesever
    e
    hypotensi
    onorazotemia.Thereisnot
    hinginthehi
    stor
    ytosuggestacti
    veischemiaint
    he
    presentat
    ion;t
    her
    efor
    e,coronaryangi
    ographywoul
    dnotbethefir
    sttestofchoice.
     

    54. A68- year-ol dwomanpr esentstot heemer gencyr oom wi t


    hsever eor thopneaf ort he
    past12hour s.Shehasahi storyofhyper tension,ost eoarthr
    iti
    s,andbor der l
    inedi abetes.
    Examinationr evealsi r
    regularrateandr hythm,wi t
    hahear trateof115bpm,bl oodpr essureof
    2
    190/100 mm Hg,j ugularpr essureof14 cm,and bodymassi ndexof38 kg/ m .Chest
    auscult
    ationshowsbi l
    ateralrales,whilet hepr ecordialexam r eveal sani rr
    egul arandr apid
    heartr
    atewi thdi stanthear tsoundsandnodi scerniblegal l
    op.Thepat ienti
    sgiveni nt
    ravenous
    fur
    osemide,di lt
    iazem,ni tr
    oglycerininfusions,and hepar i
    n,wi th pr omptimpr ovementi n
    symptoms.Hert ransthoracicechocar diogr am showsnor malbi ventri
    cularsizeandf unct i
    on,
    mildmitralregur gitati
    on,andmi ldlef
    tatrialenlargement .Theel ectrocardi
    ogram showsat rial
    fi
    bri
    ll
    ati
    onandvol t
    agecr iteri
    aforleftventr
    icularhyper trophy. 

    Fort
    y-ei
    ghthour slater
    ,shei sonor allosar
    tan,di
    lt
    iazem,ri
    var
    oxaban,andf ur
    osemide.Her
    heartr
    ateisnowi r
    regularat70bpm,bloodpressurei
    s130/65mm Hg, and venouspressur
    eis
    normal,butshesti
    llcomplainsofmoderatedyspneaonexert
    ion.

    Whi
    choft
    hef
    oll
    owi
    ngwoul
    dyour
    ecommend?

    a. Switchdilt
    iazem t
    oatenol
    ol.
    b. Transesophagealechocar
    diogr
    am-guidedcar
    diover
    sion.
    c. Continuouspositi
    veair
    waypressur
    e(CPAP).
    d. Holtermoni t
    or.
    e. Adddr onedarone.

    ANSWER: 

    54. b. Tr
    ansesophagealechocar
    diogr
    am-
    gui
    dedcar
    diover
    sion.

    Thisisatypicalpresent ationofacut ehyper tensi vepulmonar yedemai nawomanwi thhear t


    fail
    urewithpreservedej ect i
    onf r
    action( HFpEF) .Shepr esentedinr apidatri
    alfi
    bril
    lati
    on, which
    mayhavepr ecipi
    tatedt hedecompensat ion.Thesepat ientstypicallyrespondfairl
    yqui cklywit
    h
    goodcont rolofbloodpr essur eandvent ricularr esponse.Atrialfi
    bril
    lati
    onisextremely
    commoni nHFpEF, notedi n30- 40%ofpat i
    ents.I ncontrasttohear tfail
    urewithreduced
    ejecti
    onfracti
    on(HFr EF) ,therearenot ri
    alscompar i
    ngr ateversusr hythm contr
    oli nHFpEF.
    However ,becauset herei sthepot entialforincr easedrel i
    anceonat ri
    alsystol
    eintheset tingof
    diastol
    icdysfunction,theACC/ AHAgui deliner ecommendsst rongconsi derat
    ionof
    cardiover
    sionforat ri
    alfibril
    lati
    on( Classl l
    b,LevelofEvi denceC) .

    Becauset hisisthefir
    stepisodei nthispati
    ent,t
    hel i
    kel i
    hoodt ohaveadur abl erest orat i
    onof
    sinusrhythm isenhanced.Ther eisnoevi dencet osuppor tatenol oloverdil
    tiazem orl isinopril
    overlosartani nHFpEF,asnot reatmentshavebeenpr ospect ivelyshownt obeef fecti
    vei nl arge
    randomizedt rial
    s.Thepat i
    ent’
    sbodyhabi t
    usandat r
    ialfibr i
    ll
    ationincreaset her iskofsl eep-
    disorder
    edbr eathing,andthisshouldbeeval uated,butsheshoul dnotbest artedonCPAPi n
    theabsenceofadi agnosisofsleepapnea.AHol termoni torcanbeusef ultodet ermi ne
    adequater atecontrol
    ,butthispatientissymptomat icdespi t
    er at econtr
    ol.Ther efor e,an
    attemptatr estor
    ingsinusrhythm isappr opr
    iat
    e.Dr onedar onei snotindicatedi npat i
    ent swi th
    decompensat edheartfai
    lurewithinthepast4weeks, andi sunl ikel
    ytocar diover tthispat ient. 
    55. A25- year
    -oldcoll
    egestudentwasplayi
    ngwit
    hhisyoungnephew,whohadafeverand
    aner yt
    hematousrash.Subsequenttot hatvi
    sit
    ,hedevel
    opsdyspnea,rash,andf
    ever.An
    echocardi
    ogr
    am reveal
    edhisej
    ectionf
    racti
    ontobe25%.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    ycauseofmyocar
    dit
    isi
    nthi
    spat
    ient
    ?

    a. Mumps .
    b. Al
    cohol.
    c. Chagasdisease.
    d. Parvovi
    rusB19.
    e. Adenovir
    us.

    ANSWER: 

    55. d. Par
    vovi
    rusB19.

    Themostcommonvi ralet
    iol
    ogyofmyocarditi
    satpresenti
    sparvovi
    rus.Rashesar
    ecommon
    withal
    ltypesofvi
    ruses,andaresuggesti
    veofavirus-r
    elat
    edmyocarditi
    sinthi
    sscenari
    o.
    Adenovir
    usandmumpsmaycausemyocar di
    ti
    s,butarerar
    eeti
    ologi
    es.Thereisnoreduvi
    id-
    organi
    sm exposur
    et osuggestChagas,whichisendemictoCentr
    alandSouthAmer i
    ca. 

    56. A55- year-


    oldtruckdri
    verwhoseonlymedicalhi
    stor
    ywasunt reatedhyper
    tensi
    onwas
    di
    agnosedwi t
    hdilat
    edcar di
    omyopathyandNew Yor kHeartAssoci
    ationclassII
    Isymptoms.
    Hisendomyocardi
    albiopsyisposi
    ti
    veforl
    ymphocyti
    cmyocar di
    ti
    s.

    I
    naddi
    ti
    ont
    obet
    a-bl
    ocker
    sanddi
    uret
    ics,
    whi
    choft
    hef
    oll
    owi
    ngi
    sappr
    opr
    iat
    einhi
    scar
    e?

    a. Prednisone.
    b. Angiotensin- conver
    ti
    ngenzymei
    nhi
    bit
    or. 
    c. Betainterferon.
    d. Spir
    onol actone.
    e. Me t
    hot r
    exate.

    ANSWER: 

    56. b. Angi
    otensi
    n-conver
    ti
    ngenzymei
    nhi
    bit
    or. 

    Themainstayoft reatmentformyocardit
    isisst
    andardheartf
    ail
    uret
    herapy.Diur
    eti
    ctherapy
    al
    oneisinsuff
    icient.Thereisnoevidencethatr
    outi
    neimmunosuppressionisofbenefi
    t.Ther
    e
    aresomedatat hatpat i
    entswithchroni
    clymphocyti
    cmyocardit
    iswit
    houtevidenceofaviral
    et
    iol
    ogymaybenef i
    tfr
    om steroi
    dtherapy,butt
    hisi
    snotfir
    st-
    li
    netherapy.
     

    57. I
    nwhi
    choft
    hef
    oll
    owi
    ngcl
    ini
    calscenar
    iosshoul
    danendocar
    dialbi
    opsybeper
    for
    med?

    a. A20-
    year
    -ol
    dwomanwi
    thacut
    ehear
    tfai
    lur
    e,ej
    ect
    ionf
    ract
    ion(
    EF)of25%,andt
    hir
    d-
    degr
    eeat
    ri
    ovent
    ri
    cul
    arbl
    ock.
    b. A 65-
    year
    -ol
    d man wi
    th cr
    ushi
    ng chest pai
    n,or
    thopnea,l
    eg edema,and an
    el
    ect
    rocar
    diogr
    am showi
    ngaQRSdur
    ati
    onof150msec.
    c. A65-
    year
    -ol
    dmanwi
    that
    ypi
    calchestpai
    nanddel
    ayedgadol
    ini
    um enhancementi
    n
    t
    helater
    alwall
    s.
    d. A35-year-
    oldmanwhocomplai
    nsofacut
    epl
    eur
    it
    icchestpai
    nwi
    thanor
    malej
    ect
    ion
    f
    ract
    iononechocar
    diogr
    am.

    ANSWER: 

    57. a. A20-year
    -ol
    dwomanwi thacutehear
    tfai
    lur
    e,ej
    ect
    ionf
    ract
    ion(
    EF)of25%,
    andt
    hird-
    degreeat
    ri
    ovent
    ri
    cularbl
    ock.

    Thecor rectansweri sthepatientwi thacutehear tfail


    ure, at
    ri
    oventr
    icularblock,andr educed
    l
    eftventricularEF.I
    tiscrit
    icaltoident i
    fycausesofl i
    fe-threat
    eningmyocar diti
    swhosecour se
    couldbeal teredbyearlyinterventi
    on, suchasgi antcel lmyocar di
    ti
    soreosi nophil
    ic
    myocar diti
    s.Thepat i
    entpresent i
    ngt otheemer gencydepar t
    mentwi thcrushingchestpai n,
    orthopnea, etc.
    ,hascoronarydi seaseunt i
    lprovenot her wise.Thepat i
    entcompl ai
    ningofacut e
    pleuri
    ti
    cchestpai nwi t
    hanor malEFonechocar diogr am hasnoevi denceofmyocar dial
    dysfunction.Thepat i
    entwithat ypicalchestpainanddel ayedgadolini
    um enhancementi nthe
    l
    at er
    alwal l
    shasevi denceofcor onar ydisease.
     

    Endomyocardi
    albi
    opsyisaClassIrecommendat ioninpatientswhodevelopnew-onsethear
    t
    fai
    lur
    eandheartbl
    ock.Inthi
    ssit
    uati
    on,i
    nfil
    trat
    ivedisorder
    si ncl
    udi
    ngsarcoidneedtobe
    consider
    ed,
    andthediagnosi
    sisbestestabl
    ishedbybi opsy.

    58. A43- year


    -ol
    dwomanwi tha6-yearhist
    oryofnonischemicdilat
    edcardi
    omyopat
    hy,
    paroxysmalatri
    alfi
    bri
    ll
    ati
    on,andanimplant
    abledefi
    bri
    ll
    atorisref
    erredtothehear
    tfail
    ure
    cl
    inic.Shehashadprogressi
    vesympt
    omsdespiteopt
    imalmedicalt
    herapy.

    I
    nr evi
    ewinghermedi calhist
    ory,whi
    choft
    hef
    oll
    owi
    ngwoul
    dbeassoci
    atedwi
    thawor
    se
    pr
    ognosisforherhear
    tfail
    ure?

    a. Sinusbr adycardi
    a.
    b. Lowc holest
    erol.
    c. Femal esex.
    d. Obe si
    ty.
    e. Hy pouricemia.

    ANSWER: 

    58. b. Lowchol
    est
    erol
    .

    Lowercholester
    olhasbeenl i
    nkedt oworseprognosisi
    nhear tfai
    lurepati
    ent
    sandi sli
    kely
    rel
    atedtopoornutri
    ti
    onalstatus(cardi
    accachexia)andelevatedcircul
    ati
    nginfl
    ammat or
    y
    cyt
    okines.I
    ngeneral,pat
    ientsrequir
    inghigherdosesofloopdi ur
    eti
    cshavewor seoutcomes,
    sothefactthatt
    hecasepat i
    entdoesnotr equir
    eloopdiureti
    cspor t
    endsabet t
    erprognosi
    s. 

    The“ obesi
    typaradox”suggest
    sthatobesepati
    entshavebett
    eroutcomescomparedwit
    hthei
    r
    thincounter
    part
    s.Hyperuri
    cemiahasbeenassociatedwithworseoutcomes,
    ashasrest
    ing
    sinustachycar
    dia.Womenwi thheartf
    ail
    urehaveabetterpr
    ognosisthanmen.
    59. An 86- year-old woman wi th noni schemic cardiomyopat hy and type 2 diabet
    es
    complicatedbychr onickidneydisease(creat i
    nineclear
    ance22ml /min)i
    shospi t
    ali
    zedwith
    worsening cr eati
    nine,decr eased appeti
    te/ f
    ail
    uret ot hrive,cooll ower extr
    emiti
    es,and
    confusionbyf ami l
    yr epor
    t.Herelect
    rocar
    di ogram showedar i
    ghtbundlebranchblock(RBBB)
    wit
    haQRSdur ati
    onof136msec.Homemedi cati
    onsincludel i
    sinopr
    il20mgdai l
    y,carvedi
    lol
    12.5mgbi d,
    andspi ronolact
    one25mgdai ly. 

    ASwan- Ganzcatheterizat
    ionisperfor
    med,whi chreveal
    sar i
    ghtatr
    ialpressureof24mm Hg,
    pulmonarycapi
    ll
    ar ywedgepr essure(PCWP)of34mm Hg,andcar diacindexof1. 4L/min/m2.
    Milr
    inoneisi
    nstit
    utedwi thadecr easeofPCWPt o22mm Hgandani mpr ovementincardi
    ac
    2
    i
    ndext o1.9L/mi n/m .Ment at
    ioni mprovesandshei seati
    ngandabl et ointer
    actwithher
    famil
    y.However,wi t
    hin24hour sofweani ngtheinotr
    ope,thepat
    ientisnot edtobeconfused
    andhercreat
    ini
    nei ncreasedfurt
    her.

    Whi
    choft
    hef
    oll
    owi
    ngwoul
    dbet
    henextst
    epf
    ort
    hispat
    ient
    ?

    a. I
    nit
    iationofanangi ot
    ensin-receptorblocker(
    ARB).
    b. I
    nit
    iationofdialysis.
    c. Continuousinfusionofinot r
    ope.
    d. Useofi nt
    ermittentintr
    avenous( IV)inotr
    ope.
    e. I
    mpl antat
    ionofacar di
    acr esynchronizati
    onther
    apy(CRT)
    .

    ANSWER

    59. c. Cont
    inuousi
    nfusi
    onofi
    not
    rope.

    Thedecisi
    ontousechronici
    nfusionsofinot
    ropi
    ct her
    apyiscli
    nicalandmustt
    akeinto
    accountpat
    ientpr
    efer
    encesandcost .Themajorreasontoini
    ti
    atetherapyi
    spal
    li
    ati
    on.
    Mortal
    it
    yisveryhi
    ghinthispati
    entcohort.
     

    Implant
    ationofaCRThasnotbeenr igorousl yst
    udi edininotrope-dependentpat ientsandis
    notindi
    cat edinpatient
    swi t
    hanRBBBandQRSdur ati
    onof<150msec.Useofi ntermitt
    entIV
    i
    notropicagent sisaClassI IIrecommendat ion;therear enodoubl e-bl
    indedcl i
    nicaltri
    alst
    o
    supportthepr act
    ice.Dialysi
    sshoul donl ybeconsi deredunderext enuatingcircumst ances
    duri
    ngt er
    mi nalcare.Dialysiswi l
    lnotchanget henat uralhi
    storyofhear tfai
    lur
    ei nthissett
    ing.
    Theaddi t
    ionofanARBwhent hepat ientisal r
    eadyonanangi otensi
    n-conver t
    ingenzyme
    i
    nhibit
    orandspi r
    onolactonei saCl assIIIrecommendat i
    on.
     

    60. Accor di
    ngt otheFr amingham Hear
    tSt
    udy,t
    heli
    feti
    mer i
    skatage40year
    sfort
    he
    devel
    opmentofheartf
    ail
    ureforbothmenandwomeniswhichoft
    hefol
    lowi
    ng?

    a. 1i
    n5.
    b. 1i
    n2.
    c. 1i
    n20.
    d. 1i
    n15.
    e. 1i
    n10.

    ANSWER: 

    60. a. 1i
    n5.
    Accor
    dingt
    otheFramingham Hear
    tSt
    udy,
    thel
    if
    eti
    mer
    iskatt
    heageof40year
    sfort
    he
    devel
    opmentofhear
    tfai
    lur
    eforbot
    hmenandwomenis1in5.

    61. A67- year


    -oldmanwi t
    hatri
    alfi
    bri
    ll
    ati
    onandnoni schemicdil
    atedcardi
    omyopat
    hyi s
    admitt
    edtot
    hehospitalwit
    hacutedecompensatedheartfail
    ure(ADHF).Hi
    smedicalhi
    story
    i
    ncludest
    ype2diabetesandchroni
    ckidneydisease.Hi
    sadmi ssi
    onbloodpressur
    eis82/ 66
    mm Hgandhisheartr
    ateis94bpm andir
    regul
    ar. 

    A uri
    nar ycatheterispl acedf oraccur ateassessmentoffluidbalance,andbumet ani
    dei s
    administer
    edasa4mgi ntr
    avenous( IV)bol
    usevery12hours.Despitehigh-doseIVdiur
    etics,
    hi
    sur ineout putr emains<70mlperhour ,hisweightdecreases<0.5kg,andhi sserum
    creat
    inineincreasesfr
    om 1. 4mg/ dlto2.1mg/dloverthef
    ir
    st48hour s.Inaddit
    ion,
    shortruns
    ofnonsustainedventri
    cul artachycardiaarenot
    edont el
    emetr
    y.

    Whi
    choft
    hef
    oll
    owi
    ngwoul
    dbear
    easonabl
    enextst
    epi
    nthemanagementoft
    hispat
    ient
    ?

    a. Mil
    rinone0.25mcg/ kg/minbycont i
    nuousinfusion.
    b. Sendbloodf orB-t
    ypenat r
    iuret
    icpepti
    demeasur ement .
    c. Pulmonaryar t
    erycathet
    erforassessmentofcent ralhemodynami
    cs.
    d. Bedsidevenovenousul t
    raf
    ilt
    rat
    ionat200mlperhour .
    e. Nit
    roprussi
    de20mcg/ minbycont i
    nuousinfusion.

    ANSWER: 

    61. c. Pul
    monar
    yar
    ter
    ycat
    het
    erf
    orassessmentofcent
    ralhemodynami
    cs.

    Cardiorenalsyndrome,orco- exi
    stentcardi
    acandr enaldysf
    uncti
    on,iscommoni npatient
    s
    withHF.Fur ther
    more,duri
    ngaHFhospi tal
    izat
    ion,15-30%ofpat i
    entswil
    ldevelopwor seni
    ng
    renalfuncti
    on.Thispati
    enthassever alindependentr i
    skfactor
    sforthedevelopmentof
    worseni ngrenalf
    uncti
    on,includi
    ngol derage,diabetes,andbaseli
    nerenaldysfuncti
    on.Diuret
    ic
    resi
    stancemaybecont ri
    butingaswel l,andthenextst epinmanagementi scri
    tical
    ,but
    empiric. 

    Addingalow-doseinot
    ropeorinodil
    atorhasnotbeenshownt oimproveshort
    -term out
    comes,
    andmayexacer bat
    ethi
    spati
    ent'sarrhyt
    hmi as.Empiri
    cadmi ni
    str
    ati
    onofnit
    roprussi
    dewi t
    hout
    art
    erialmoni
    tor
    ingmaybediff
    icultgi
    vent hepatient
    'srel
    ati
    velyl
    owbl oodpr
    essure.

    Thesafetyandeffi
    cacyoful
    traf
    il
    tr
    ati
    onasar escuestrat
    egyi
    nt hi
    ssetti
    nghasnotbeent est
    ed,
    andcli
    nicalr
    eportsrai
    seconcernsaboutf
    urtherworseni
    ngofrenalfunct
    ion.Inaddi
    ti
    on,the
    CARRESS- HFtri
    alshowednobenefitoful
    tr
    afil
    tr
    ati
    oninpati
    ent
    swi thcardior
    enalsyndr
    ome
    duetoADHF.  

    Whi l
    ether
    ei snor oleforrouti
    nepulmonaryar t
    erycatheter
    izati
    oninthemanagementofADHF,
    the2013HFgui delinegivesaClassII
    arecommmendat i
    onf ori
    nvasi
    vehemodynamic
    moni t
    ori
    nginpat i
    entswi t
    hacuteHFwi t
    hper si
    stentsymptomsdespi teempi
    ri
    cadjust
    mentof
    standardtherapieswi t
    hwor seni
    ngrenalfuncti
    on.

    62. A53- year


    -ol
    dmanwi t
    hischemiccar
    diomyopat
    hyandaleftventr
    icul
    ar 
    eject
    ionfract
    ion
    (EF)of26% i
    shospit
    ali
    zed wi
    th acut
    edecompensated hear
    tf ai
    lur
    e( HF),hist hi
    rd such
    admi
    ssi
    oni
    nthel
    ast6mont
    hs.
     

    Medicat
    ionsi
    ncl
    udeaspir
    in81mgqd,warf
    ari
    n,furosemide40mgqd,car
    vedi
    lol25mgbi
    d,
    l
    isi
    nopri
    l20mgqd,spi
    ronol
    act
    one25mgqd,andatorvast
    ati
    n40mgqd.
     

    Hehadadual
    -chamberi
    mpl
    ant
    abl
    ecar
    diover
    ter
    -def
    ibr
    il
    lat
    or 
    (I
    CD)i
    mpl
    ant
    ed18mont
    hsago.
     

    Onphysi
    calexaminati
    on,hi
    sheartrateis 
    75bpm and  ir
    regular.Hisbloodpressur
    eis 110/75
    mm Hg.Jugul
    arvenouspressur
    eis 15cm H20. 
    Ther earecracklesovertwo-
    thirdsofbothlung
    f
    iel
    ds.Hehasa+S3  gal
    lopand 
    grade3/ 6holosystoli
    cmur muratt heapex.Abdomenshows
    mil
    dhepatomegal
    y. 
    Hehas 3+bil
    aterall
    owerextremityedema.  

    Laborat
    oryresul
    ts 
    i
    nclude:troponi
    n I0. 54 ng/
    ml,B-type natr
    iur
    eti
    c pept
    ide 1523 pg/
    ml,
    creat
    ini
    ne 1.
    8 mg/dl,and inter
    nati
    onalnor mali
    zed r
    atio 2.
    3.Compl et
    e blood cel
    lcount
    shows hemogl
    obi
    nof7. 0 
    g/dl
    . 
    Recent 
    glycat
    edhemoglobin 
    is7.3%. 

    Hi
    select
    rocar
    diogr
    am (
    ECG)shows at
    ri
    alf
    ibr
    il
    lat
    ionwi
    thhear
    trateof75bpm,and 
    l
    eftbundl
    e
    br
    anchblockwit
    hQRSdurat
    ionof165msec(nochangefr
    om pri
    orECG).

    Af
    terdi
    uresi
    s,whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nhi
    smanagement
    ?

    a. Er
    ythropoi
    etin.
    b. Ref
    erforventri
    cularassistdevi
    ce.
    c. Per
    cutaneousmi t
    ralval
    verepair.
    d. Addangiotensi
    n- r
    eceptorblocker.
    e. Upgradetoabi ventri
    cul
    arICD.

    ANSWER: 

    62. e. Upgr
    adet
    oabi
    vent
    ri
    cul
    arI
    CD.

    AnacuteHFadmi ssionof fersanimportantopportunityt


    oadjustoralmedi cati
    ons,toaddress
    probl
    emsassoci atedwi thr educedEFsuchasar rhythmiaandthromboembol icri
    sk,andto
    managecomor biditi
    esi ncludingdiabet
    es,anemia, andchroni
    ckidneydi sease.Thispati
    entis
    onguidel
    ine-di
    rectedmedi caltherapy,
    incl
    udingbet a-bl
    ocker
    ,angiotensin-conver
    tingenzyme
    (ACE)i
    nhibi
    tor,
    andal dactone.However ,hi
    stherapyi snotopt
    imizedbecausehehasaCl assI
    i
    ndicat
    ionforbiventri
    cul arpacing.

    Mit
    ralval
    verepai
    risaClassII
    bindicat
    ionformi
    tr
    alr
    egurgi
    tat
    ionaft
    eral
    lothert
    herapi
    esar
    e
    i
    mplemented,i
    ncl
    udingbivent
    ri
    cularpaci
    ng,whi
    chcanreducethesever
    it
    yofmitral
    r
    egurgit
    ati
    on.

    HeisonACEinhibi
    torsandaldactone.Thus,theadditi
    onofanangiotensi
    n-receptorblocker
    wouldputhi
    m atsignif
    icantr
    iskofhyperkal
    emia.Alt
    houghr epeat
    edhospit
    alizat
    ionssuggest
    hehasadvancedHF, youwoul dupgradetoabiventr
    iculardevi
    cepri
    ortoconsiderati
    onofmor e
    advancedt
    herapi
    essuchasvent r
    icul
    arassi
    stdeviceort r
    anspl
    ant.
     

    Whil
    eanemiaisassociatedwithworseout
    comesi
    nHFpat
    ient
    s,cl
    ini
    calt
    ri
    aldat
    ahavenot
    shownbenef
    itf
    rom erythropoi
    eti
    nther
    apy.
     
    63. A35- year-ol
    dmanwi thanonischemi
    ccardiomyopathyof10yearsdurat
    ionwit
    hal eft
    ventri
    culareject
    ionfract
    ion(
    LVEF)of15% wasreferr
    edtoyourcar di
    actranspl
    antcent
    erf or
    progressivesymptomsofhear tf
    ail
    ure.Aspar
    tofthisevaluat
    ion,heunderwentari
    ght-heart
    catheter
    izati
    on. 

    Inthecat heter
    izati
    onlaborat
    ory,hi
    sini
    tialhemodynamicsincludedar i
    ghtatr
    ialpressur eof  
    15
    mm Hgandpul monarycapill
    arywedgepr essure(PCWP)of 35mm Hg.Thecar diologistwas
    carefultodef l
    atetheballoonfoll
    owingmeasur ementofthePCWP.Addi ti
    onalmeasur ement s
    2
    i
    ncludedacar diacindexbyt her
    modiluti
    onof2. 4L/min/m  andaFi ckcardiacindexof1. 5
    L/min/m2.Oxygen consumpt ion wasmeasur ed f
    ortheFickcar diacindex.Syst oli
    cbl ood
    pressurewas80mm Hgandsyst emicvascul arr
    esi
    stancewas1800dyne- sec-cm5.Bl ood
    obtainedf r
    om t heri
    ghtatri
    um hadasat urati
    onof48%,andf rom thepulmonar yartery( PA),a
    saturati
    onof35%.  

    Thepat ientwasstart
    edonsodium ni
    tr
    oprussideat0.5mcg/kg/
    minandtransf
    erredbackt o
    theintensivecar
    eunit(I
    CU),wher
    eanothersampleofPAbloodwasobtai
    ned1houraf terthe
    i
    niti
    almeasur ement,andfoundtohaveasat urat
    ionof95%.Thepat
    ient
    ’scli
    nicalcondit
    ion
    remainedunchanged.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    yexpl
    anat
    ionf
    ort
    hechangei
    nPAsat
    urat
    ion?

    a. Theri
    ghtheartcat
    hetercreatedaventri
    cul
    arseptaldef
    ect.
    b. Thei
    niti
    alPAsaturat
    ionwaser r
    oneousl
    ylow.
    c. Thepati
    enthascyanidetoxicit
    y.
    d. ThesampleofPAbl oodint heI CUwaserroneouslyobt
    ainedf
    rom t
    hepr
    oxi
    malpor
    tof
    t
    her
    ighthear
    tcat
    het
    er.
    e. Ther
    ighthear
    tcat
    het
    ermi
    grat
    eddi
    stal
    lydur
    ingt
    ranspor
    tbackt
    otheI
    CU.

    ANSWER: 

    63. e. Ther
    ighthear
    tcat
    het
    ermi
    grat
    eddi
    stal
    lydur
    ingt
    ranspor
    tbackt
    otheI
    CU.

    Itwouldbeunl i
    kelyforthepatienttodevel opsodi um ni
    tr
    opr ussi
    detoxicit
    yorani ntr
    acar di
    ac
    shuntwithin1hour .Dependingonwher ebloodi ssampledint heri
    ghtat r
    ium,it
    ssat urati
    on
    canbehi gherthanthePA.Typi cal
    ly,infer
    iorvenacavabl oodhasahi gheroxygensat urati
    on
    thansuperiorvenacavaorcor onarysi nusblood.Evenifbloodwer esampl edfrom thepr oxi
    mal
    port,i
    twouldbeunl ikel
    yforrightatrialorsuper i
    orvenacavabl oodtohaveasat urati
    onashi gh
    as95%.Ri ghtheartcatheter
    scanmi gratedistal
    lyduri
    ngt r
    ansportintothewedgeposi ti
    on
    evenwi t
    hthebal l
    oondef l
    ated.Ifthisoccur s,aswasl i
    kel
    yi nthiscase,thebloodsampl ewill
    refl
    ectpulmonaryvenousO2  sat ur
    ation.

    64. A 56- year-


    old woman wi th a hi
    storyofbr eastcancerwho is curr
    entl
    yreceivi
    ng
    doxorubicinchemot her apyisref
    erredtothecar di
    ologycli
    nicbyheroncol
    ogistf
    orchangesin
    l
    eftventricul
    arejectionf ract
    ion(LVEF)not edbyser i
    almulti
    gatedacqui
    sit
    ion(MUGA)scans.
    Thepatientisduet or eceiveaddi
    tionaldosesofchemot her
    apy,pendi
    nghercardi
    aceval
    uation.
    Herbasel ineLVEFpr iortodoxorubicintherapywas64%,andhermostr ecentLVEFaftera
    cumulativedoxorubicindoseof400mg/ m2 isnow58%.  

    Thepatientappearswell
    ,isinnodist
    ress,
    anddeni
    escomplai
    ntsofexer
    ti
    onalorrestdyspnea,
    chestpain,noct
    urnaldyspnea,orl
    owerextr
    emi
    tyswel
    li
    ng.Onexaminati
    on,herbl
    oodpr essur
    e
    i
    s122/ 70mm Hg,herpul
    seis88bpm andr egul
    ar,andherjugul
    arvenouspressurei
    s5cm
    H2O.Cardi
    acandpulmonaryexaminat
    ionsarenormal.A12- l
    eadelect
    rocar
    diogram shows
    normalsi
    nusr
    hythm wi
    thnonspeci
    fi
    cSTandTabnor mali
    ti
    es.

    Whi
    choft
    hef
    oll
    owi
    ngwoul
    dyour
    ecommend?

    a. Troponinlevel.
    b. Disconti
    nuedoxorubici
    n.
    c. Serum B-typenatr
    iuret
    icpept
    ide.
    d. Echocardiogram.
    e. Continuedoxorubi
    cin.

    ANSWER: 

    64. e. Cont
    inuedoxor
    ubi
    cin.

    Chemot herapy- i
    nducedcar diomyopat hyhasbeenvar iablydef i
    ned, butadefinit
    iont hatisoften
    referencedi sonedevel opedbyt hecardiacr eviewandeval uationcommi t
    teeover seeing
    trastuzumabt ri
    als.Thecommi tt
    eedef inedcar diacdysf uncti
    oni nt
    heset t
    ingofchemot herapy
    useasanyoneoft hefollowing:1)car diomyopat hychar act
    erizedbyadecr easei ncar di
    ac
    LVEFt hatwasei therglobalormor esevereint hesept um;2)sympt omsofcongest ivehear t
    fail
    ur e(CHF) ;3)associat
    edsi gnsofCHF, includingbutnotl i
    mi tedtoS3 gall
    op, t
    achycar dia,or
    bot h;and4)decl ineinLVEFof≤5- 55%wi thaccompanyi ngsignsorsympt omsofCHFora
    decl i
    nei nLVEFof≤10- 55%wi t
    houtaccompanyi ngsignsorsympt oms.However ,recent
    evidencesuggest sthatchangesi nlongitudinalstrai
    nmaybemor esensiti
    vet oearly
    myocar dialdamage.  

    Althoughther estingEFislowert hanpr iorEF,i


    tisstilli
    nt henormalrangeandt hepat i
    entby
    histor
    yandcl inicalexaminationhasnosi gnsofhear tfailur
    e.Therearenocl eargui del
    inesas
    touseofbi omar kerstoguidemanagementi nasympt omat icpati
    entswithnor malEF
    undergoingchemot herapy,andunl esst heMUGAscanwasofquest i
    onablequal i
    ty,an
    echocardiogram woul dnotbei ndicated.Basedont heFoodandDr ugAdmi nistr
    ation-approved
    l
    abel i
    ngfordoxor ubici
    n,anEFdr opof≥10%t oanabsol utelevel<50%shoul dprompt
    disconti
    nuationofchemot herapyandconsi derat
    ionfori nit
    iat
    ionofangiotensin-converti
    ng
    2
    enzymei nhibit
    or sorbeta-blockers.Afteracumul ati
    vedoseof500mg/ m, repeatevaluati
    on
    shouldbeconsi der edforeveryaddi t
    ional50mg/ m2 ofdoxor ubi
    cinadministered.

    65. A63- year-


    oldCaucasi anwomani sevaluatedinthehear tf
    ai l
    urecli
    nicf
    orconsi
    deration
    ofadvanced t her
    apies,including possi
    blehear ttransplantat
    ion.Shehasal ong-standing
    hist
    oryofi schemiccar di
    omyopat hywi thal eftventri
    cularejectionf r
    acti
    onof15% despi t
    e
    ther
    apywi thbeta-bl
    ockers,angiot
    ensin-converti
    ngenzymei nhi
    bitors,al
    doster
    oneantagonists,
    anddi uret
    ics.Shei saf or
    mersmokerwi tha60pack- yearhistoryofsmoki ng,andhas
    hypert
    ensionanddi et-control
    leddiabetes.Shehadabi ventri
    cularimplantabl
    ecardiovert
    er-
    defi
    bri
    llat
    orplaced2year sago. 

    Herpr imary cardiol


    ogistwas concerned aboutherwor sening f
    uncti
    onalstatus,as she
    becomesdyspnei cwi t
    hmi ni
    malact i
    vit
    y.Sheper f
    ormed" poorl
    y"ona6- mi
    nutewal ktest
    ,
    pri
    mar i
    lylimited by dyspnea.A car di
    opulmonar y exer
    cise testreveal
    s peak VO2 of9.9
    ml/kg/min.Sheal sohadar i
    ght-hear
    tcatheter
    izat
    ion,whichdemonst rat
    edacardiacindex(CI
    )
    of1.8.Shewaspl acedoni nt
    ravenousmilri
    noneandherCIi mpr oved.
    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nhercar
    e?

    a. Referfortr
    ansplant
    .
    b. Ri
    ghthear tcat
    heteri
    zation.
    c. Continuemedicaltherapy.
    d. Destinat
    ionlef
    tventri
    cularassi
    stdevi
    ce.

    ANSWER: 

    65. a. Ref
    erf
    ort
    ranspl
    ant
    .

    Pati
    ent
    sgenerallyareconsideredcandidatesforhearttransplantationwhent hei
    rpeakVO2 i
    s
    <14ml/kg/
    min( or<12ml /kg/minonbet a-bl
    ockers).Shehaspr ogressivesymptomsdespite
    opt
    imalmedicaltherapy.Shemaybeacandi dat
    ef ordestinati
    onl eftvent
    ricul
    arassi
    stdevi
    ceif
    sheisdeemednott obeat ranplantcandidat
    e,butsheshoul dunder goaf ullwor
    kupto
    det
    erminebestavail
    abletherapy.Ar epeatri
    ght-heartcatheter
    izationwi l
    lnotaddtohercare.
     

    66. A50- year -


    ol dmani sr eferr
    edt oyourcl i
    nicf orevaluat
    ionofexertionaldyspnea.Over
    thepast3mont hs, hehasnot edi ncreasingshortnessofbr eathduringdailyacti
    vit
    ies,suchas
    walking shortdistancesorcar ryi
    ng lightbundles.Hehasno pr iorhistoryofmyocar dial
    i
    nfarcti
    onanddeni eschestpai n.Hi spastmedi calhistoryisnotableonlyforhypertensionand
    hypercholest
    erolemi a.Hisonl ymedi cat
    ionsareat enolol25mgoncedai l
    yandsi mvast at
    in20
    mgoncedai l
    y.Hedr inks t
    wo gl assesofwi newithdi nnereachni ghtanddeni esuseoftobacco
    oril
    li
    citdrugs.Hisfami l
    yhistoryi snotableforapat ernalunclewhodi edsuddenlyinhis50s. 

    Hisexaminationisnotablef orbloodpr essure170/ 80mm Hg,pul se80bpm,mi ldjugular


    venousdist
    ent i
    onat12cm H2O,cl earlungst oauscul t
    at i
    on,andmi l
    dper ipher
    aledema.S1 is
    normal,
     
    S2 i
    spar adoxi
    cal
    lyspl it
    ,andt her eisasof t S3 gall
    opwithagr ade2/ 6holosyst
    olic
    murmuratt heapex.Hiselectrocar
    diogram reveal
    ssi nusr hythm,wit
    hl eftbundl
    ebranchblock
    (LBBB)andaQRSdur ati
    onof150msec.Echocar diogr am reveal
    sadi latedlef
    tventr
    icl
    ewi th
    eccent
    ri
    chyper tr
    ophy,
    anteriorhypokinesis,andej
    ectionf r
    acti
    on(EF)25%.

    Whi
    choft
    hef
    oll
    owi
    ngf
    act
    orsi
    sthemostl
    ikel
    yet
    iol
    ogyofhi
    scar
    diomyopat
    hy?

    a. Alcoholuse.
    b. Fami li
    aldil
    atedcardi
    omyopat
    hy.
    c. Cor onaryart
    erydisease(
    CAD).
    d. Hy pertensi
    on.
    e. Viralmyocar di
    ti
    s.

    ANSWER: 

    66. c. Cor
    onar
    yar
    ter
    ydi
    sease(
    CAD)
    .

    Thispatientpresentswi thnew- onsetheartfai


    lure(HF)inthesetti
    ngoflef
    tventr
    icular(
    LV)
    cavit
    ydi l
    ati
    onandr educedEF.Ther egionalwallmotionabnormalit
    yandLBBBi nt hepresence
    ofcardiacriskfact
    or s,includi
    nghyper t
    ensionandhyper li
    pidemia,makeCADt hemostl i
    kely
    eti
    ology.Hypertensioni tself
    ,ifuncontroll
    ed,mayl eadtothedevelopmentofLVhyper tr
    ophy
    andHF, wi
    theitherpr eservedorr educedEF.Thef amilyhi
    storyofsuddendeathhintsata
    potent
    ialgeneti
    ccontr
    ibutortohisi
    ll
    ness,butgi
    ventheri
    skf act
    orsf
    orCAD,thi
    sismoreli
    kely
    acauseofsuddencar diacdeath.Myocardit
    isi
    snotsuggestedspeci
    fi
    cal
    lybythehi
    stor
    y,buta
    typi
    calvir
    alprodromeisfrequent
    lyabsent.Modestal
    coholconsumpti
    onisunli
    kel
    ytobe
    associ
    atedwi t
    hthedevelopmentofcardiomyopathy.

    67. A55- year-


    oldmanwi t
    hahistoryofaleftanteri
    ordescendinginf
    arcti
    on( l
    eftventr
    icul
    ar
    eject
    ionfr
    acti
    on[LVEF]of15%,andLVend- diast
    olicdimensionof7. 8cm)i nt hesetti
    ngof
    cocaineuse12yearspriort
    opresentat
    ionisadmi t
    t edwithincreasi
    ngshor t
    nessofbr eathin
    thesett
    ingofnoncompli
    ancewit
    hdietaryrecommendat ions.Hisbloodpressureonadmi ssion
    i
    s90/ 50mm Hg. 

    HisB- t
    ypenat r
    iuret
    icpepti
    deis2235pg/ mlandserum sodi
    um is128mEq/L.Hemoglobi
    nis
    7.9 g/dl
    .He was di ur
    esed and sodi
    um nor mali
    zed t
    o 136 mEq/L.He did nottol
    erat
    e
    angiot
    ensin-convert
    ing enzyme (ACE)inhi
    bit
    ors due t
    o symptoms ofdi
    zziness.He was
    ther
    eforedischargedoncarvedi
    lol3.
    125mgor al
    lybidandfur
    osemide80mgorall
    ybid.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sassoci
    atedwi
    thawor
    sepr
    ognosi
    sfort
    hispat
    ient
    ?

    a. Fur
    osemidedose>60mgbi d.
    b. Ser
    um sodium <140mEq/L.
    c. Hypot
    ension.
    d. Anemia.
    e. Lef
    tvent
    ricul
    ardiast
    oli
    cdi
    mensi
    on>7.
    0cm.

    ANSWER: 

    67. c. Hypot
    ensi
    on.

    Inpati
    entswi t
    hhear tfailurewi t
    hreducedEF, t
    her ear eanumberofadver seprognosti
    c
    i
    ndicator
    s, andthispatienthasmanyoft hem,includinghyponat remia,anemia,diur
    eticdose,
    anddilat
    edLV.However ,noneoft hem isassociatedwi thashi ghamor tali
    tyrat
    east hatseen
    i
    npat i
    entswhocannott olerateACEinhibit
    orsduet oeitherhypotensi
    onorr enalf
    ail
    ure
    (ci
    rcul
    atoryrenalli
    mi t
    ation) .Inanobservati
    onalst udy,patient
    swi thadvancedheartfailure
    whoar edischargedoffACEi nhi
    bit
    orsduet ocirculatoryrenalli
    mitati
    onhaveamor tal
    ityrateof
    57%at8. 5mont hs.

    68. A55- year


    -ol
    dtruckdr i
    verwhoseonl ymedicalhistor
    yi ncl
    udesunt r
    eatedhypertensi
    on
    presentswit
    h3weeksofNewYor kHeartAssociati
    onclassIIIheartfai
    lur
    e( HF)symptoms.An
    echocardi
    ogram demonstratesl eftventr
    iculardil
    atati
    on with an eject
    ion fract
    ion of26%.
    Cardiaccat
    heteri
    zat
    ionisnegativeforobstructi
    vecoronaryarterydi
    sease.

    I
    naddi
    ti
    ont
    otr
    eat
    mentofhi
    sHF,
    whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nhi
    scar
    e?

    a. Continuecurrenttherapy.
    b. Leftventr
    icul
    arassi stdevice.
    c. Endoc ar
    dialbiopsy.
    d. Implantablecardiovert
    er-defi
    bri
    ll
    ator(
    ICD)
    .
    e. Prednisone.
    ANSWER: 

    68. a. Cont
    inuecur
    rentt
    her
    apy.

    Themai nstayoftr
    eatmentf ormyocardit
    isisst
    andar
    dHFt herapy.I
    mmunosuppr essi
    onmaybe
    ofbenefi
    tforgiantcel
    lmyocar dit
    is,
    buthis3-weekpresentati
    oni si
    nconsi
    stentwi thgi
    antcell
    .
    Endomyocar di
    albiopsyisindicat
    edfordiagnosi
    sifi
    tinf
    luencesmanagement .Thepatienti
    s
    notacandidateforICDbecausehehasnotbeenopt imallymedi cal
    lytr
    eat
    ed.Althoughsome
    pati
    entswithacutemyocar diti
    smayr equir
    emechanicalsuppor t
    ,nothi
    nginthisquesti
    on
    suggeststhatthepatienti
    si l
    ltot
    hatextent.
     

    69. Thel ef
    tvent
    ri
    cul
    arandsyst
    emi
    car
    ter
    ialpr
    essur
    etr
    aci
    ngsshowni
    nFi
    gur
    e1ar
    e
    obt
    ained.

    I
    nwhi
    choft
    hef
    oll
    owi
    ngcondi
    ti
    on(
    s)ar
    ethesef
    indi
    ngsexpect
    ed?

    a. Supraval
    vul
    araort
    icstenosi
    s.
    b. Subaorti
    cmembrane.
    c. Val
    vularaor
    ti
    cstenosis.
    d. Hypertr
    ophi
    cobstruct
    ivecar
    diomyopat
    hy(
    HOCM)
    .
    ANSWER: 

    69. d. Hyper
    trophi
    cobst
    ruct
    ivecar
    diomyopat
    hy(
    HOCM)
    .

    Inthepost extrasystol
    icbeat(foll
    owingavent r
    icul
    arpr emat urebeat),ther
    eisani ncreasei nt
    he
    pressuregr adient.Thisfi
    ndingisobser vedinaor t
    icst enosis( AS),subaorti
    cmembr ane, and
    HOCM, anddoesnothel pdi st
    inguishamongt hethree.However ,i
    nHOCM, t
    heincreased
    contracti
    litythatcharacter
    izesthepost ext
    rasystoli
    cbeatcausesgr eaterapposit
    ionoft he
    i
    nterventricularseptum totheant eri
    orleaf
    letofthemi tralvalve,i
    ncreasingthedegr eeof
    obstructi
    on.Thi seffectoverwhelmsanybenef itobtainedf rom thehi gherend-diastol
    icvolume
    thatcharact eri
    zesthepost ext
    rasystoli
    cbeat .Therefore, t
    hest rokevolume, andhence, the
    aorti
    cpul sepr essurefal
    ls.Thisphenomenoni sknownasaBr ockenbr oughsign. 

    I
    nval vul
    arAS, supr
    aval
    vul
    arAS, 
    andsubaor t
    icmembr ane,t
    heincr
    easedprel
    oadinthe
    postextr
    asystoli
    cbeati
    ncr
    easesstr
    okevolume,result
    inginbot
    hani ncr
    easeingr
    adientduet
    o
    thehigherfl
    owandani ncr
    easeinaort
    icpulsepressur
    eduet ot
    hehigherstr
    okevolume.

    70. Youar ewalki


    ngthr
    oughthecar
    diaccathet
    eri
    zat
    ionl
    abor
    ator
    yandseeat
    raci
    ngofr
    ight
    atr
    ial(
    RA)pr
    essur
    eonthemonit
    or(Fi
    gure1).

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    ydi
    agnosi
    s?
    a. Pulmonaryhypert
    ensi
    on.
    b. Peri
    cardi
    altamponade.
    c. Constr
    icti
    on.
    d. Tri
    cuspidregur
    git
    ati
    on.

    ANSWER: 

    70. b. Per
    icar
    dialt
    amponade.

    TheRApr essur
    eishigh(mean=appr
    oximatel
    y15mm Hg, wi
    thnormal=6mm Hg).Ther
    eare
    normalAwaves, Xdescent
    s,andVwaves,
    buttheYdescenti
    sblunt
    ed.Thi
    sist
    ypi
    call
    yseeni
    n
    tamponade. 

    Inconst
    ri
    cti
    veperi
    cardi
    ti
    s,t
    heRApressuremaybeel evat
    ed,butthewavefor
    msshowst eepX
    andYdescents.RApressur
    emaybehighi npulmonaryhypert
    ension,
    butapulmonaryar
    ter
    y
    tr
    acingi
    salsoneededtomakethi
    sdiagnosis.Youwouldnotexpecttohaveablunt
    edY
    descent
    . 

    Inthesett
    ingoft
    ricuspi
    dregur
    git
    ati
    on,
    theRAt
    raci
    ngwi
    lldemonst
    rat
    eal
    argeCVwavedur
    ing
    ventr
    icul
    arsyst
    ole. 

    CannonAwavesareobser
    vedwhenthereisanarrhyt
    hmi
    acharact
    eri
    zedbysi
    multaneous
    depol
    ari
    zat
    ionoft
    heatr
    iaandvent
    ri
    cles.Pr
    ominentXandYdescentsar
    eseeninperi
    cardi
    al
    const
    ricti
    on.Lar
    geV,
    or,
    mor
    eaccur
    atel
    y,r
    egur
    git
    ant(
    CV)wavesar
    eobser
    vedi
    ntr
    icuspi
    d
    regur
    gitat
    ion.

    71. Yourpat ientwithprevi


    ouslystableNewYor kHeartAssociat
    ionclassIIheartfai
    lur
    eand
    ast
    hmar eturnstoyourof f
    icewithorthopnea,par oxysmalnoct ur
    naldyspnea,andnoct uria.He
    hasbeent akingfurosemide40mgdai ly,met oprololsucci
    nate50mgdai l
    y,li
    sinopri
    l20mg
    dai
    ly,anddigoxin0.125mgdai l
    y.Themet oprololwasbegun3weeksago.Onexam,hi shear t
    rat
    ei s110bpm,bl oodpressureis100/ 70mm Hg,andvenouspr essureis15cm ofwat er.
    Cardi
    ovascularexam revealsamitralregurgi
    tationmur murthatislouderthanpreviousl
    yhear d.
    Hehasanor malS1, S2,andanS3 isheard.Hisl ungsar ecl
    ear,andthereisnoper i
    pheraledema.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    ep?

    a. St
    artaldost
    eroneantagonist.
    b. I
    ncreaseli
    sinopri
    l.
    c. I
    ncreasehisfurosemide.
    d. Decreasehi
    sbet a-bl
    ocker.

    ANSWER: 

    71. c. I
    ncr
    easehi
    sfur
    osemi
    de.

    Volumeretenti
    onisacommoncompl i
    cati
    onofbet a-bl
    ockert
    herapyandshoul dbetreated
    wit
    hani ncreaseindiuret
    ict
    oachievecli
    nicaleuvolemi
    a.Generall
    y,beta-blockerdosesdonot
    needtobedecr easedunlessther
    eishypotensionordiuret
    icr
    esistance.Aldosterone
    antagoni
    stsandl i
    sinopri
    lwouldnotbeexpectedtoachieveapromptandadequat ediur
    esis.

    72. A 55- year-oldmanwi thischemi csystol


    ichear tfai
    lur
    e( HF)wi thbasel
    ineeject
    ion
    fract
    ionof30%i sbeingseeni nfol
    low- upafterarecentadmissionfordecompensatedHF.He
    reportsthatheget sshor tofbreathwal kingupt hethreestepsi ntohishouse.Hisdai l
    y
    medicat i
    onsi
    ncludemet oprol
    olsuccinate200mg, li
    sinopri
    l20mg, furosemide120mg,aspiri
    n
    81mg, andat
    orvastati
    n40mg.  

    Onexam,hi sbloodpressureis95/ 65mm Hgandhear trateis62bpm.Hi sjugularvenous


    pressur
    eis7cm H2O.Hi sl ungsar ecl
    ear
    ,andcar di
    ovascularexaminati
    onr evealsnormal
    S1 andS2 
    andgrade2/ 6holosystol
    icmurmur.Hisextr
    emi ti
    esshow tr
    aceedema.Sodi um i
    s
    136mg/ dl,pot
    assi
    um is4. 2mEq/ L,andserum creati
    nineis1. 4mg/ dl
    .Electr
    ocardiogram
    showsnormalsinusrhythm withevi
    denceofpr
    iorant
    eri
    ori nf
    arct
    ion.

    Whi
    choft
    hef
    oll
    owi
    ngshoul
    dbeaddedt
    ohi
    smedi
    cat
    ionr
    egi
    men?

    a. Warfar
    in.
    b. Angi
    otensin-
    receptorbl
    ocker(
    ARB)
    .
    c. Amiodarone.
    d. Al
    dosteroneantagonist
    .

    ANSWER: 

    72. d. Al
    dost
    eroneant
    agoni
    st.
    Thepat i
    enti
    stolerati
    nganangi otensin-
    conver
    ti
    ngenzymeinhibi
    tor,
    soaddi ti
    onofanARBor
    substit
    uti
    onofanARBi snotindicated.Hisr
    enalf
    uncti
    onandpotassium level
    swoul dall
    owfor
    additi
    onofaldosteroneantagonistinthi
    spati
    entwit
    hclassI
    IIheartf
    ail
    ure.Ami odar
    one,
    war f
    ari
    n,andserum level
    sofdigoxinhavenotbeenshownt oextendsurvivalorimprovehear
    t
    fai
    luremorbi
    dity.

    73. A33- year-


    oldwomanwi t
    hahistoryofperi
    part
    um cardi
    omyopat hy(PPCM)comest o
    youst at
    ingthatshewant stohaveanotherbaby.Anechocar
    diogram i
    nt heoff
    icer
    eveal
    sthat
    hercur r
    entleftventri
    cularej
    ect
    ionfr
    act
    ion( LVEF)i
    s55%.Sheisonl i
    sinopri
    l20mgadayand
    carvedil
    ol12.5mgt wiceaday.

    Whi
    choft
    hef
    oll
    owi
    ngi
    scor
    rectr
    egar
    dingherr
    iskwi
    thsubsequentpr
    egnancy?

    a. Herr
    iskofrecur
    renthear
    tfai
    lur
    ewi
    thasubsequentpregnancyi
    sapproxi
    matel
    y20%.
    b. She shoul
    d conti
    nue curr
    entmedi
    cat
    ions dur
    ing pregnancytoreduce t
    he r
    iskof
    r
    ecur
    renthear
    tfai
    lur
    e.
    c. Sheisnotatriskofr
    ecurrentheartf
    ail
    ure.
    d. Recurr
    entpregnancyisassociat
    edwi t
    h80%mat
    ernalmor
    tal
    it
    y.

    ANSWER: 

    73. a. Herr
    iskofr
    ecur
    renthear
    tfai
    lur
    ewi
    thasubsequentpr
    egnancyi
    s
    appr
    oxi
    mat
    ely20%.

    Inallwomenwi thahi storyofPPCM, anextensi


    vedi scussionabouttherisksofasubsequent
    chil
    disimportant.Thispat i
    ent'
    sLVEFhasr etur
    nedt onor mal,butshesti
    llhasar i
    skofrel
    apse
    withsubsequentpr egnancy.Basedonast udyof44womenwi thahistor
    yofPPCM, women
    whor ecover
    edtheirLVEFhada21%r i
    skofrecurrencewithsubsequentpr egnancy,butt
    here
    werenomat ernaldeat hs.Inthepati
    entswithpersist
    entLVdysf uncti
    on,therewasa44%r i
    skof
    recurr
    entheartf
    ailureanda19%r iskofmaternalmor tal
    it
    ywi t
    hsubsequentpr egnancy.

    Bothangiot
    ensi
    n-convert
    ingenzymeinhi
    bit
    orsandangiot
    ensin-
    recept
    orbl
    ockersar
    e
    ter
    atogeni
    candtheref
    orenotsafedur
    ingpregnancy;medi
    cat
    ionsshouldberevi
    ewedifa
    pati
    entdeci
    destoproceed.

    74. A 45- year-ol


    d man wi th known hyper trophic obstr
    uctive cardi
    omyopat
    hy and
    signifi
    cantoutf
    low tr
    actgr adi
    enti
    sadmi tt
    edt othei ntensi
    vecareuni twit
    hhypot
    ensi
    onaft
    er
    receivi
    ngspinalanesthesia.Hewasgi ven3liter
    soff luidinthepost-anest
    hesi
    acareuni
    tand
    stil
    lremainshypotensive.Hehasalsodevelopedralesonexam.
     
    Whi chofthefol
    lowingwoul dyourecommendt or ai
    sehi sbloodpressure?

    a. Dobut ami ne.


    b. Epinephr i
    ne.
    c. Phe nylepinephr
    ine.
    d. Dopami ne.
    e. Isoprotenol.

    ANSWER: 
    74. c. Phenyl
    epi
    nephr
    ine.

    Whent r
    eati
    nghypotensioninpati
    entswi thobst
    ructivecar di
    omyopathy,inot
    ropesthat
    i
    ncreasecontr
    acti
    li
    tyshouldbeavoided, astheywillincreasethel
    eftventri
    cularout
    fl
    owt r
    act
    gr
    adientandreducecardiacoutput
    .Instead,agentst hatincr
    easeaf
    terloadandhavel i
    tt
    le
    ef
    fectonmyocardialcontr
    acti
    li
    tyshouldbepr ef
    erent i
    all
    yused. 

    Phenylepi
    nephr
    inehaspot
    entalpha-adrenergi
    cacti
    vit
    yandlit
    tl
    ebeta-
    adrenergi
    cacti
    vity,
    and
    i
    stherefor
    eagoodchoicei
    nt hi
    sset t
    ing.Al
    loftheotherchoi
    ceshavesi
    gnif
    icantbet
    a-recept
    or
    act
    ivi
    tyandwoul dwor
    senthepatient
    'soutfl
    owt r
    actgradi
    ent
    .

    75. A30- year-oldmancomest oyourcl


    ini
    cwit
    ha1- yearhistor
    yofexer t
    ionalchestpai
    n,
    dyspnea,andpal pitat
    ions.Hehashadaknownhear tmurmurf orseveralyears.Hedoesnot
    takeanymedi cationsorsupplementsanddeni
    esanyrecr
    eationalsubstanceabuse.Thereare
    nocardiacri
    skf actorsorhist
    oryofpr
    ematur
    ecardi
    acdeathinthefamily.
     

    Hisphysi
    calexam demonstrat
    esaheartrat
    eof56bpm andbloodpressurei
    nt hel
    eftar
    m of
    115/78mm Hg.Agr ade3/6di amond-
    shapedsystol
    icmurmuri
    sappr eci
    atedovertheleft
    l
    owersternalbor
    der;i
    tislouderduri
    ngthestr
    ainphaseoft
    heValsal
    vamaneuverandsof ter
    wit
    hsquatti
    ng.

    Forwhichofthef
    oll
    owi
    ngr
    iskf
    act
    orsi
    sitr
    easonabl
    etoi
    mpl
    antani
    mpl
    ant
    abl
    ecar
    diover
    ter
    -
    def
    ibr
    il
    lat
    or(I
    CD)?

    a. Fami l
    yhistor
    yofsyncope.
    b. Leftventri
    cul
    ar(LV)wal lt
    hicknessof>30mm.
    c. Re pet
    iti
    venonsustainedVT( NSVT)onHoltermonitor
    .
    d. Inducibl
    eventri
    culartachycardi
    a(VT)onelect
    rophysi
    ologyst
    udy(
    EPS)
    .

    ANSWER

    75. b. Lef
    tvent
    ri
    cul
    ar(
    LV)wal
    lthi
    cknessof>30mm.

    I
    npat i
    entswithhypert
    rophiccardi
    omyopathy( HCM)andaper sonalhistoryofsuddencardiac
    deat h(SCD),vent
    ri
    cularfi
    bri
    ll
    ati
    on,orhemodynami call
    ysignifi
    cantVT, implantat
    ionofanICD
    i
    saCl assIrecommendat i
    on.However,guidelinessurroundingt hedecisionforpri
    mary
    preventionI
    CDsi nthesetti
    ngofHCM ar edrivenpredomi natelybyexper tconsensus.Cl
    assI I
    a
    recommendat i
    ons(LevelofEvi
    denceC)includef i
    rst-degr
    eer elati
    vewithSCD, maximum wal l
    thickness>30mm, andoneormor erecentsyncopalepi sodes.

    I
    nHCM pat i
    entswithNSVTorabnor malbl oodpressureresponset oexerci
    se,otherr
    iskfact
    ors
    mustbepr esenttowar r
    antimplant
    ationofanI CD.Theseot herr
    iskfactorsincl
    uderesti
    ngLV
    outfl
    owt r
    actobstruct
    ion>30mm Hg, gadoli
    nium enhancementr epresenti
    ngmyocar di
    al
    fi
    brosisbycardiacmagneticresonance,andLVapi calaneurysm.

    Thereisnorol
    eforEPSinthedecisi
    onaboutpri
    marypreventi
    onICDsinHCM.Fami
    lyhi
    stor
    yof
    syncopeisnotanindi
    cati
    onforICD(asopposedtof
    amilyhist
    oryofSCD)
    .NSVTonHolt
    er
    monitorr
    equir
    esotherri
    skfact
    orstobepresent
    ,asdescr
    ibedabove.
     
    76. A55- year-ol
    dwhi tewomanwi t
    ha4- mont hhistoryofnoni schemiccar di
    omyopat hy
    comesi nforfoll
    ow- upofherhear tfai
    lure.Shewal ksone- halfmilebeforesheget sshor tof
    breath,anddeni esdi zzi
    ness,palpi
    tat
    ions,orthopnea,orpar oxysmalnoct urnaldyspnea.Her
    l
    eftvent r
    icul
    arejecti
    onf r
    actionwhenassessedl astmont hwas32%.Onexami nat
    ion,herblood
    pressurei s104/70mm Hg,andpul se72bpm.Herj ugularvenouspr essur
    ei snotel evated,
    normalS1  andS2 withoutmur mursorgal lop,andt hereisnoper ipheraledema.Medi cat
    ions
    i
    ncludel i
    sinopri
    l5mgdai ly,car
    vedil
    ol12.5mgt wicedaily,andfurosemide40mgt wicedai l
    y.
    Herser um creat
    inineis2.5mg/ dl
    .

    Whi
    chi
    sthenextmostappr
    opr
    iat
    est
    epi
    nhercar
    e?

    a. Adds pironol
    actone12. 5daily.
    b. Decreaset heli
    sinoprilt
    o2.5mgaday.
    c. I
    ncreasecar vedil
    olto18. 75mgt wicedail
    y.
    d. Adddi goxin0.125dai l
    y.
    e. Addisor di
    l20mg/ hydral
    azine37.5mgt hreet
    imesdai
    ly.

    ANSWER: 

    76. c. I
    ncr
    easecar
    vedi
    lolt
    o18.
    75mgt
    wicedai
    ly.

    Beta-blockerdoseshoul dbeescal atedtoachievet argetdoses( e.g.,


    carvedilol25mgt wice
    dai
    lyormet oprololsuccinat
    e200mgdai l
    y)intheabsenceofcont rai
    ndicati
    on.Spironol
    actone
    shouldnotbest artedgivenhercr eatini
    neof2.5mg/ dl.Digoxinwoul dnotbei ni
    ti
    atedgi
    venher
    cl
    assI Isympt omsbef or
    eoptimizationofot hermedi caltherapy.Isordil
    -hydralazi
    neisnot
    i
    ndicatedi nclassIIwhi t
    epatients.Ther eisnor easont oreducet hedoseoft heangi ot
    ensin-
    convertinginhibi
    tor .
     

    77. A75- year


    - ol
    dmanwi t
    ha10- yearhist
    oryofnonischemiccar di
    omyopathy(
    eject
    ion
    fr
    acti
    on25%)i sadmi t
    tedwit
    hacut
    edecompensat edheartf
    ail
    ure.Hehasbeenunablet
    oaf f
    ord
    hismedicati
    onsf orthelastmont
    h.Hehadgai ned30poundsovert heprecedi
    ng2weeks.
    Overni
    ght,hewasgi venonedoseofi
    ntravenous(I
    V)fur
    osemide60mgandhemade3l it
    ersof
    uri
    ne. 

    Onexami nat
    ion,hi
    sbloodpressur
    ewas105/ 78mm Hg,pul sewas90bpm andr egul
    ar,and
    respir
    atoryratewas20br eat
    hs/minute.Hedidnotappearacut el
    yil
    l.Hi
    sj ugularvenous
    pressurewasatt heangleoft
    hejaw,lungshaddimini
    shedbreathsoundsatt
    her i
    ghtbase,and
    hehadasof tS3.Hehadasci t
    es,andt her
    ewas3+pi t
    ti
    ngedemat othethigh.Laborat
    ory
    analysi
    sshowedanel evat
    edN- t
    erminalpro–B-t
    ypenatri
    ur et
    icpepti
    de(2500pg/ ml),and
    hyponatremia(130mmol /L)
    .Hiscr
    eatini
    newaselevat
    edat2.6mg/ dl.

    Whi
    choft
    hef
    oll
    owi
    ngwoul
    dyour
    ecommendf
    ort
    hispat
    ient
    ?

    a. Mil
    rinone.
    b. ContinueIVfur
    osemi
    de.
    c. Carvedil
    ol.
    d. Nesiri
    ti
    de.
    e. Metolazone.
    ANSWER: 

    77. b. Cont
    inueI
    Vfur
    osemi
    de.

    Thepatienti
    srespondi
    ngappropriat
    elytoIVdi ur
    eti
    csandt heseshouldbecont i
    nuedsi
    ncethe
    pat
    ientismarkedlyvol
    umeoverloaded.Neithernesir
    iti
    denormi lr
    inonehavebeenshownt o
    i
    mpr oveoutcomesinpati
    entswithdecompensat edhear tf
    ail
    ure.Beta-blocker
    sshouldnotbe
    i
    nit
    iatedinpati
    entswhoareacutelydecompensat ed,butshouldbeconsi deredoncethepati
    ent
    i
    scompensat ed.Metol
    azoneisnotindicat
    ed, asthi
    spat i
    enti
    sr espondingwelltofur
    osemide. 

    78. A76- year-oldmanwi thischemiccar diomyopathyand r


    ecur r
    entadmi ssionsf orhear
    t
    fail
    ure despite excell
    entmedi caland di etary compli
    ance presentst o yourof f
    ice f
    ora
    consul t
    ati
    on.Hei saccompani edbyhi swi feanddaught er.Hedeniesangi nalsympt omsand
    under wentcor onary angiography 1 yearago t hatshowed pat entbypass  gr
    afts.He has
    dyspneawi thmi nimalexer t
    ion.Hisangi ot
    ensi n-
    convert
    ingenzymei nhibi
    tor(ACEI)andbet a-
    blockerhavebeendownt i
    tr
    atedovert helastfewmont hs,andult
    imatelyhadt obedi sconti
    nued.
    Hehasani mplantablecardiovert
    er-defi
    bri
    llator(I
    CD)inplaceandr ecei
    vedashock2mont hs
    agof orventri
    culartachycardia.
     

    Onexami nat i
    on,hisbl oodpressureis80/60mm Hg, hispulse98bpm, andhi sr
    espir
    atoryrate
    is16br eaths/mi nute.Hei snotacut el
    yill
    .Hehasmi l
    dbi t
    empor alwast i
    ngpresent.Jugular
    venouspr essur eis12cm,auscul t
    at i
    onrevealsS1 andS2  wi
    thgr ade2/ 6mur murofmi t
    ral
    regurgitat
    ion at t he apex.Hi sliver is not distended,and he has 1+ edema.Hi s
    electr
    ocar diogram showssi nusrhythm,withar ightbundlebranchbl ock( RBBB),QRSof110
    msec,wi th deep Q wavesacr osst heprecordium.Echocar di
    ogr am showsl eftventri
    cular
    diastol
    icdi mensi on( LVDd) 
    tobe 7.
    8cm, l
    eftventr
    icul
    arejecti
    onfracti
    on( LVEF)20%,moder ate
    mi t
    ralregurgitati
    on( MR) ,
    andhi sri
    ghtventri
    cularfuncti
    onwasmi ldlydepressed.

    Whi
    choft
    hef
    oll
    owi
    ngwoul
    dbeappr
    opr
    iat
    einhi
    scar
    e?

    a. Mit
    ralval
    ver epai
    r.
    b. Upgradefr
    om I CDtocardi
    acresynchr
    oni
    zati
    ont
    her
    apydef
    ibr
    il
    lat
    or(
    CRT-
    D).
    c. Repeatcoronaryangiogr
    aphy.
    d. Desti
    nati
    onvent r
    icul
    arassi
    stdevice(
    VAD).
    e. Metoprol
    olsuccinate12.
    5mg/ day.

    ANSWER: 

    78. d. Dest
    inat
    ionvent
    ri
    cul
    arassi
    stdevi
    ce(
    VAD)
    .

    Thepat i
    enthasmul ti
    plemarker sofadvancedhear tf
    ail
    ure,i
    ncl
    udingr ecurr
    enthospi
    tali
    zati
    on,
    i
    ntolerancetoACEIandbet a-blocker,ICDshock,andcachexia(manifestasbitemporal
    wasting).Heappearstohavegoodf amil
    ysupportandtobecompl iant.Overall
    ,hei
    sa
    candidateforadvancedheartfailuretherapi
    es.Hi
    sagei sabovethecut offf
    orconsi
    derati
    onfor
    cardiactranspl
    antat
    ion,buthemi ghtbenefi
    tfr
    om desti
    nati
    on-t
    herapyVAD.  

    I
    niti
    ati
    onofbet
    a-bl
    ocker
    swouldnotbeindicat
    edatthi
    spoint
    ,becauseher
    emains
    decompensat
    ed.Amitr
    alval
    verepai
    rwouldnotbethepref
    err
    edtreat
    mentgi
    venhisi
    schemi
    c
    cardi
    omyopathywithamar kedlyenlar
    gedLVDd, onl
    ymoder ateMR,andhistwopriorcor
    onary
    art
    erybypassgraf
    ts.Bi
    ventricul
    arpacingisunli
    kel
    ytobenefithi
    m,gi
    venhisQRSi s110msec
    i
    nanRBBBpat t
    ern.Thepatientdoesnothavechestpain,hadacardiaccat
    heter
    izati
    onwith
    patentgr
    aft
    s1yearago, andar epeatcoronar
    yangiogr
    am isnotindi
    cated.
     

    79. A40- year-oldmanwi t


    ha5- yearhistor
    yoff amil
    ialdil
    atedcar di
    omyopathyandhear t
    fai
    lur
    e( HF)presentst ot he emergency departmentwi t
    hi ncreased short
    ness ofbreath,
    parti
    cul
    arl
    ywhenhet ri
    est osleepatni ght.Hi
    smedi calhist
    oryissi gni
    fi
    cantforanxi
    ety.On
    examinati
    on,
    hewasi nnoacut edist
    ress,hadbloodpressureof110/ 80mm Hg, hadapulseof
    98bpm, andwasaf ebri
    le.Hisbodymassi ndexwas25kg/ m2. 

    Hisjugul
    arvenouspulsationswerevi si
    blej
    ustbelowhi searlobeswhi l
    ehewassitt
    ingupright
    .
    Oncar di
    acauscult
    ati
    on, t
    herewasnoS3  ormur mur.Auscultati
    onrevealedcl
    earl
    ungfiel
    ds.His
    abdomenwasbeni gnwithouttendernessorflui
    dshift.Hisextremit
    ieswerewarm andwithout
    peri
    pheraledema.Hi selectr
    ocardiogram showedsi nusr hythm,leftvent
    ri
    cul
    arhypertr
    ophy,
    andnoot herabnor
    mal i
    ty.ChestX-rayshowedmi ldcar di
    omegal y.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthel
    ikel
    yet
    iol
    ogyofhi
    ssympt
    oms?

    a. Sl
    eepapnea.
    b. Myocar
    diali
    nfar
    cti
    on.
    c. Decompensat
    edHF.
    d. Pul
    monaryembolus.
    e. Pani
    catt
    ack.

    ANSWER: 

    79. c. Decompensat
    edHF.

    Thepat i
    entpr esentswithorthopnea, whichisamar kerofelevatedfil
    li
    ngpressuresi npatient
    s
    withHF.Hi sjugularvenouspr essurewasel evatedwi t
    hpulsationsvisi
    blebyhisear lobesinthe
    uprightposit
    ion.Itisimportantt orecognizethatrales,l
    egedema, andpulmonar yedemaon
    chestX- r
    aycanal lbeabsenti npat i
    ent
    swi thdecompensat edHF.Hi sbodymassi ndexwas
    normal ,
    maki ngsleepapneal esslikel
    y.Giventhathehadobj ecti
    veevidenceofel evatedjugul
    ar
    venouspr essure,itisl
    ikel
    ythathi ssympt omswer esecondar ytodecompensat edHFandnota
    panicattack,despitehishistoryofananxi etydisorder.

    80. A 25- year


    - old Af ri
    can- Amer i
    can man wi t
    h a 3- year history of noni schemic
    cardiomyopat hypresent stoyourof f
    iceforfoll
    ow- up.Her eports 
    shortnessofbreat hwit hl
    ess
    thanonef l
    ightofst airs.Hiscur rentmedi calr egimeni ncludescar vedil
    ol25mgt wicedaily,
    aldactone 25 mg dai l
    y,l i
    sinopril40 mg t wi ce dai ly,furosemi de 80 mg t wice daily,and
    potassium 40mEqt wicedai ly.Hishomesyst olicbl oodpr essuresar ebetween145and160
    mm Hg.Onexami nat i
    on,heappear scomf ortabl e.Vitalsignsar ebloodpr essure150/ 100mm
    Hg,pul se78bpm,r espirat
    oryr ate16br eaths/mi ntut e.Perti
    nentf i
    ndingsonhi sexami nati
    on
    i
    ncludedcl earlungf i
    elds,jugularvenouspr essur eof8cm,anor malS1 andS2 wi t
    houtS3 or
    mur mur ,and hisl owerext remiti
    esar ewar m wi thoutedema.Hi sbasicmet aboli
    cpanel
    revealedanor malpot assium andcr eatini
    neval ues.  

    Whi
    choft
    hef
    oll
    owi
    ngi
    smostappr
    opr
    iat
    einhi
    scar
    e?
    a. Dil
    ti
    azem sustai
    ned-r
    elease120mgdaily.
    b. CoenzymeQ10100mgdai ly.
    c. I
    sosorbidedini
    tr
    ate20mg/ hydral
    azi
    ne37.
    5mgt
    hreet
    imesdai
    ly.
    d. Candesart
    an4mgdai l
    y.
    e. Cl
    onidine0.1mgt wi
    cedai l
    y.

    ANSWER: 

    80. c. I
    sosor
    bidedi
    nit
    rat
    e20mg/
    hydr
    alazi
    ne37.
    5mgt
    hreet
    imesdai
    ly.

    TheA- HeFT(African-Amer i
    canHear tFail
    ureTr i
    al)trialdemonst rat
    edsignif
    icantreduct i
    onin
    mortal
    itywhent hecombi nationofisosorbi
    dedi nitrate-hydr
    al azi
    newasi ncorporatedint ot
    he
    medicalregi
    menofsel f-
    ident if
    iedAfri
    can-Amer i
    canswi t
    hsyst ol
    icheartf
    ail
    ur eandNewYor k
    HeartAssociat
    ioncl assIII-I
    Vsympt oms.Thecombi nationofanangi ot
    ensin- convert
    ing
    enzymei nhi
    bit
    or, al
    dactone, andanangi otensin-recept orbl
    ockershoul dnotbeusedt oget
    her
    duetother i
    skofhyper kalemi a.Theuseofanondi hydr opyr
    idinecalci
    um channelbl ocker
    (har
    m)ornut ri
    ti
    onalsuppl ement s(nobenefit
    )car ryacl assIIIrecommendat ion.Clonidinehas
    notbeenadequat el
    ytestedi nsystoli
    cheartfail
    ure. 

    81. A25- year -


    oldmandevel opeddyspneaonexer ti
    on2mont hsago.Eval
    uationbyanother
    physici
    ani ncludedanel ectr
    ocardiogram wit
    hleftbundlebr anchblockat160msecandan
    echocardi
    ogr am thatshowedal eftventri
    cul
    areject
    ionfract
    ionof25%wi thglobalhypoki
    nesis
    andnoval vularabnormalit
    ies.Anexer ci
    seperf
    usionstudydemonst rat
    ednoischemi a.Hewas
    star
    tedonenal apr
    il5mgbi dandf urosemide20mgbi d.
     

    Youal sot r
    eathisfather,whohasanoni schemiccar diomyopathy;thus,t
    hepat ientpr
    esentst
    o
    yourof f
    iceforasecondopi nion.Her eport
    songoi ngdyspneaatone- hal
    fmi le.Hedeniedany
    chestpai n,pal
    pitat
    ions,syncope,or thopnea,par oxysmalnocturnaldyspnea,orl egedema.On
    examinat i
    on,hewasi nnoacut edistress.Hisbl oodpr essur
    eis110/ 80mm Hg, hispul
    seis72
    bpm,andhi srespirati
    onis16br eaths/minute.Ther ewasnoj ugularvenousdi st
    enti
    onor
    hepatojugularrefl
    ux.AuscultationrevealedS1 andS2  arenormalwithasof tS3 andnomur mur.
    Extr
    emi ti
    eswer ewar m,andt herewasnoedema.Your evi
    ewedt heout si
    deechocar di
    ogram
    andagr eewi t
    ht hepreviousinterpr
    etat i
    on.

    Whi
    choft
    hef
    oll
    owi
    ngdoyour
    ecommend?

    a. Ref
    erforcardiacresynchronizati
    ont her
    apy-def
    ibr
    il
    lat
    or(
    CRT-
    D).
    b. Per
    form anendomyocar dialbiopsy.
    c. St
    artcarvedi
    lol3.125mgbi d.
    d. Ref
    erforimplantablecardiovert
    er-defi
    bri
    ll
    ator(
    ICD).
    e. Ref
    erforcoronaryangiography.

    ANSWER: 

    81. c. St
    artcar
    vedi
    lol3.
    125mgbi
    d.

    Thepatientpr
    esent
    swithnew- onsetsyst ol
    icheartfai
    lur
    e,possi
    blyfr
    om afamili
    al
    cardi
    omyopathy,gi
    venhisfat
    her’sil
    lness.Hecur rentl
    yisNewYor kHeartAssociat
    ioncl
    assI
    I,
    appearscompensatedonexami nat
    ion, andaddingabet a-bl
    ockertohisangi
    otensin-
    convert
    ingenzymeinhi
    bit
    orwoul dbei ndicated.
     
    Anendomyocar di
    albiopsyshoul dnotbeper for
    medi nther out
    ineeval
    uati
    onofpatientswit
    h
    heartfail
    ure(Cl
    assIIIi
    ndicati
    oni nthehear tf
    ail
    ureguideline).BothICDandCRT- Dshouldbe
    i
    mpl antedfoll
    owingat ri
    alofguidel
    ine- basedmedicaltherapy, whichwoul
    dincludebeta-
    bl
    ocker s,f
    orthispharmacologicaltherapycouldpromot er everseremodel
    ingandthereby
    obviat
    et heneedforeitherICDorCRT- D.Givenhisage, absenceofchestpain,andnegative
    str
    essper fusi
    onstudy,coronaryangi ographyisnotindicated. 

    82. A56- year-oldmanwi t


    hani schemi ccar di
    omyopat hyandsympt omati
    chear tfailur e
    presentstoyourof ficeforaconsul tati
    vevi sitafterar ecenthospit
    alizationforheartfai
    lure.He
    underwentcor onar yarterybypassgr afting2year sagoi nt hesett
    ingofanacut emyocar di al
    infar
    cti
    on.Hehasbeenhospi tal
    izedt wi cei nt helast  
    3mont hsf oracut eheartfail
    ureand
    ventri
    cular tachycar di
    a( treat
    ed wi thi mpl antable car di
    over
    ter-defibri
    ll
    ator [
    ICD]shock) .
    Echocardiographicassessmentdur ingt hel asthospi tali
    zati
    onshowedl ef
    tventri
    cularejection
    fract
    ion(LVEF)of  
    15%wi thmoder atemi tralr egurgit
    ationandLVend- diastol
    icdi
    mensi onof  
    7
    cm.Dur ing the hospi tali
    zati
    on f or vent ricul
    ar t achycardi
    a,cor onary angiography had
    demonst rat
    edpat encyofhi sbypassgr aftsandher epor t
    snochestpai n. 

    Her eportsdyspneawi th minimalexer t


    ion such aswal ki
    ng t othebathroom.Her eports
    compliancewi t
    hhismedi cati
    onandpr escribedlow-sodium dietandstoppedt obaccouseat
    theti
    meofhi smyocar dialinf
    arct
    ion.Thisisconf i
    rmedbyhi swi fewhoaccompani eshimt o
    thi
    svisit.Duetosympt omat ichypotensi
    onandacut ekidneyinjurydur
    ingthel astadmissi
    on,
    hisangiotensi
    on-converti
    ngenzyme( ACE)inhibi
    torandaldactonehavebeendi sconti
    nued,but
    heistakingcarvedi
    lol3.125mgPObi d.
     

    Onexami nation,his 
    bloodpr essure i
    s92/ 71mm Hg,hispul
    seis100bpm,andhi srespi
    rator
    y
    2
    rateis16br eaths/minute;bodymassi ndexi
    s24kg/ m ;heisinnodist
    ress.Jugularvenous
    pressureis14cm,auscul t
    ationrevealsanS3 wi
    thgrade3/6mur murofmit
    ralregurgi
    tat
    ionat
    theapex.Hisl i
    verisnotdi stended,andhehas1+edema.Cr eat
    ini
    neis1.
    3mg/ dl.Youperform
    acardiopulmonar yexercisetestandf i
    ndhehasapeakoxygenconsumpt i
    onof10ml /kg/
    mi n.

    Hieel
    ect
    rocardi
    ogram shows 
    normalsi
    nusrhythm,ant
    eri
    orQwaves,andaQRSdur
    ati
    onof
    100msec. 
    Right
    -hear
    tcathet
    eri
    zat
    iondemonst
    ratest
    hefol
    lowi
    ngr
    esul
    ts:
     

     Ri
    ghtatr
    ialpressure:12mm Hg
     Pul
    monar yarter
    ypr essur
    e(PAP):45/20mm Hgwi
    thameanPAP32mm Hg
     Pul
    monar ycapil
    lar
    ywedgepr essure:25mm Hg
     Car
    diacoutput:4L/ min
     Car
    diaci
    ndex:1. 8L/ mi m2
    n/

    Att
    hispoi
    nt,
    whi
    choft
    hef
    oll
    owi
    ngwoul
    dbeappr
    opr
    iat
    e?

    a. Ref
    erhimforupgradetobi ventr
    icularICD.
    b. Ref
    erhimforcardi
    actranspl ant
    ation.
    c. I
    nit
    iat
    ether
    apywi t
    hmi l
    rinone0. 25mcg/ kg/min.
    d. Ref
    erhimf orconsider
    at i
    onofal eftvent
    ri
    cularassi
    stdevi
    ce(
    LVAD)asdest
    inat
    ion
    t
    her
    apy.
    e. Ref
    erhi
    mforconsi
    der
    ati
    onofmi
    tr
    alval
    ver
    epai
    r.
    ANSWER: 

    82. b. Ref
    erhi
    mforcar
    diact
    ranspl
    ant
    ati
    on.

    Thepat ienthasmul tiplemar kersofadvancedhear tfai


    lur e,i
    ncl udingr ecur renthospi talizat
    ion,
    nar r
    owpul sepr essur e,restingt achycar dia,i
    ntolerancet oACEi nhibitor ,
    dilatedvent ri
    cl e,and
    electri
    calinst abil
    ity.Car diopulmonar yexerci
    set estingcanpr ovidei mpor tantpr ognost ic
    i
    nf ormation, andapeakoxygenconsumpt ion<14ml /
    kg/ mi nsuggest s>50%1- yearmor tal
    it
    y
    andconsi derat i
    onofcar diact ranspl antati
    on.Heappear st ohavegoodf ami lysuppor tandt o
    becompl iantanddoesnotappeart ohavemedi calcont raindicationst ot ransplantationsuch
    asongoi ngsubst anceabuse, pul monar yhyper t
    ensi on, advancedage, obesi t
    y,orpoorr enal
    function.Ther efore, hewoul dnotbeconsi deredf ordest inationt herapyLVADi mplant ation,
    whi chisgener all
    yr eservedf ornont ransplantcandi dates.Hei snotacandi datef orcar diac
    resynchr onizationt herapybecausehi sQRSdur ationi s<120msec.Ami t
    ralvalver epai rwould
    notbet hepr eferr
    edt r
    eat mentgi venhi sischemiccar diomyopat hy, EF<30%wi t
    hamar kedly
    enlargedLVdi astoli
    c- dimensi on, andonl ymoder atemi tr
    alregur gitation.Al thoughi not ropi
    c
    suppor tmaybeusedaf terlisti
    ngf orcardiactranspl antation, thereisnour gentneedf ort hi
    s
    therapyint heabsenceofend- organdysf unction. 

    83. A45- year-


    oldmanwi thahistoryofi
    schemiccardi
    omyopathyandal ef
    tventr
    icul
    ar
    ej
    ectionfr
    action(LVEF)of25% presentsforr
    outi
    nefoll
    ow-up.Hedeniesor
    thopnea,edema,
    paroxysmalnocturnaldyspnea,
    orangina.Hehasdyspneawhenwalkingt
    woblocksorupone
    fl
    ightofst
    air
    s. 

    Onexamination,hi
    sbloodpr
    essureis145/90mm Hgandhi shear
    trateis80bpm.Hisj
    ugul
    ar
    venouspressureis7cm withouthepato-j
    ugul
    arr
    efl
    ux.Hehasal ateral
    lydi
    spl
    acedpoi
    ntof
    maximum impulse(PMI),
    noS3,cl
    earlungs,
    andnolowerext
    remit
    yedema.  

    Hi
    scurr
    entmedi cati
    onsincl
    udecarvedi
    lol25mgt wicedai
    ly,
    li
    sinopri
    l40mgdai l
    y,f
    urosemide
    40mgtwicedai l
    y,aspi
    ri
    n81mgdai l
    y,andsimvast ati
    n40mgdai ly.Hi
    slabor
    atorydatareveal
    anN-t
    erminal-probrai
    nnatri
    uret
    icpept i
    de(NT- pr
    oBNP)levelof1232pg/ ml,sodi
    um of134
    mmol/
    L,potassium of4.
    2mEq/ L,
    andcr eati
    nineof1.4mg/dl.

    Whi
    choft
    hef
    oll
    owi
    ngwoul
    dbet
    hemostappr
    opr
    iat
    eforhi
    scar
    e?

    a. Addaml odipi
    ne10mgdai l
    y.
    b. I
    ncreasefurosemideto60mgt wicedail
    y.
    c. Adds pi
    ronolact
    one12.5mgdaily.
    d. Addlosartan25mgdai ly.
    e. Addisosorbidedini
    tr
    ate10mgpl ushydral
    azi
    ne12.
    5mgt
    hreet
    imesdai
    ly.

    ANSWER: 

    83. c. Addspi
    ronol
    act
    one12.
    5mgdai
    ly.

    Thispati
    enthasNewYorkHeartAssoci ati
    on(NYHA)classIIIsympt omsandareducedLVEF.
    Aldost
    erone-r
    ecept
    orant
    agoni
    stsar erecommendedi npat i
    entswi t
    hNYHAclassII-I
    Vheart
    fai
    lur
    ewi t
    hanLVEFof35%orless, unl
    esscont r
    aindi
    cated,t
    or educemorbidi
    tyandmor t
    ali
    ty.
    Thispati
    ent’
    screat
    ini
    neandpotassium level
    sarewellbelowther ecommendedthreshol
    dsf or
    i
    nit
    iat
    inganaldost
    eroneantagoni
    st.Cr
    eat
    ini
    neshoul
    dbe<2.
    5mg/
    dli
    nmenand<2.
    0mg/
    dli
    n
    women, andpot
    assium <5mEq/L.
     

    Althoughhehasdyspneawi thexert
    ionandanelevat
    edNT-proBNP,heappear seuvolemicon
    exami nat
    ion.Thus,
    incr
    easingfur
    osemidewouldbenotbeappropri
    ate.Calci
    um channel
    blockingdrugsarenotrecommendedasr out
    inetr
    eatmentf
    orpati
    entswithheartfai
    lureand
    reducedEF. 

    Acombi nati
    onofisosorbidedini
    trateandhydr alazineisrecommendedf orself
    -report
    ed
    Afri
    can-Americanpatientswit
    hNYHAcl assI I
    I-I
    Vhear tfail
    ureandreducedEFonopt i
    mal
    ther
    apywi t
    hanangi otensin-
    conver ti
    ngenzymei nhibi
    tor(ACEI)andbet
    a-blocker,orf
    orany
    pati
    entwithsymptomat icheartf
    ailurewit
    hr educedEFwhocannotbegi venanACEIor
    angiot
    ensin-r
    eceptorblocker(ARB) .However,thispatientisCaucasi
    anandi staki
    nganACEI,
    makingthischoicelessappropriate. 

    TheadditionofanARBt oanACEIandbeta-
    blockerf
    oraper
    sist
    entl
    ysymptomati
    cpatientwi
    th
    heartfai
    lureandreducedEFshouldonl
    ybeconsider
    edwhenanaldost
    eroner
    eceptor
    antagonistisnoti
    ndicat
    edortol
    erat
    ed.

    84. Youhavef oll


    owedan89- year
    -ol
    dpat i
    entformanyyearsinyourpractice.Hehashad
    stableangina,whi chhasbeenmanagedmedi call
    y.Hehasbeent r
    eatedforpr ost
    atecancer
    ,
    hypertensi
    on, hyperl
    ipi
    demi
    a,andhashaddi abetescontr
    oll
    edwit
    hmedi cat
    ions.Hei sbr
    ought
    tot hehospitalbyambul anceafterst
    affathisassistedli
    vingf
    acil
    it
    ynot edt hathelooked
    "gray.
    " 

    Uponar r
    ivaltot hehospi t
    al,hei sment ati
    ngandcompl ai
    nsofchestpai n.Hehasabl ood
    pressureof82/ 40mm Hg, heartrateof100bpm, andanoxygensaturat
    ionof89%on6l it
    ersof
    nasalcannul a.Hislungsar econgest edonexam andyouhearanS3  aswel lasaholosystol i
    c
    mur mur.Hi sextremitiesarecool.Hisel ect
    rocardi
    ogram demonstr
    ates4mm STel evationi n
    theant eri
    orpr ecordium.You r ecommend ur gentcardi
    accatheteri
    zati
    on,butyourpat ient
    ref
    usesi nvasivepr ocedures,avi ew hehasexpr essedtoyoui nthepast .Youcont actt he
    assist
    edl i
    vingfacil
    ityanddet er
    mi nethatthepati
    enthasahome" donotr esusci
    tat
    e"order.

    Whi
    choft
    hef
    oll
    owi
    ngi
    syournextst
    epi
    nthemanagementoft
    hispat
    ient
    ?

    . Admi
    tthepat
    ientt
    othegener
    almedi
    cineuni
    t,pr
    ovi
    desuppor
    ti
    vemeasur
    es,consul
    t
    pal
    li
    ati
    vecar
    eteam.
    b. Pr
    oceedt
    othecat
    het
    eri
    zat
    ionl
    abor
    ator
    yforur
    gentper
    cut
    aneouscor
    onar
    yint
    ervent
    ion
    wit
    ht wophysicianconsent ssi
    ncehisconditi
    onisli
    fe-t
    hreat
    ening.
    c. Contactthepsychiatri
    stoncallforur
    gentevaluat
    ionofpati
    entcompetency.
    d. Cal
    lhi sspouset or equestherconsentf ort heproceduregiventhelif
    e-t
    hreat
    ening
    nat
    ureofhi ssi
    tuation.
    e. Documentt hatthepat ientisnotcompetentandobt ai
    nawi tnesstosigntheconsent
    andpr oceedwit
    ht heprocedureunderemer gencycir
    cumstances.

    ANSWER: 

    84. a. Admitt
    hepatienttot
    hegener
    almedi
    cineuni
    t,pr
    ovi
    desuppor
    ti
    vemeasur
    es,
    consul
    tpal
    li
    ativecar
    eteam.
    Thi
    spat ienthassignsofseverecardiacdysfuncti
    onandacutemyocar dialinf
    arcti
    on.Whi l
    e
    car
    diaccat het
    erizati
    onandrevasculari
    zati
    onar ei
    ndi
    catedandnecessar ytostabi l
    izethe
    pat
    ient,hedoesnotwantsuchpr ocedures.Despit
    ederangementinvitalsigns,thereisno
    evi
    dencet hatthepatienti
    snotcompet enttomakemedi caldeci
    sions.Hisdecisiont oavoid
    i
    nvasivemedi caltherapi
    esshoul
    dbehonor ed.

    Alt
    houghgr avel
    yil
    l,
    heappearscompetent,
    sother
    eisnoindi
    cati
    ontocallpsychi
    atr
    y.Nei
    ther
    spousalconsentnortwophysi
    cianconsent
    sshouldover
    ri
    dehispref
    erence.I
    tisnot
    appropri
    atetofi
    ndawi t
    nesstosignt
    heconsentbecausehei
    scompet enttomakehisown
    deci
    sions. 

    85. Youar econsul t


    edtoseea36- year-
    oldAf r
    ican-Amer icanwomanont hepostpart
    um
    unitforevaluati
    onofdyspneaandedema.Shehasahi st oryofchr onichyper t
    ensionand
    cocaineabuse.Twodaysago,shedel i
    veredtwi ni nfants,andsi ncet henhasdevel oped
    worseningdyspnea,or t
    hopnea,andlowerextremityedema.Herbl oodpr essureis110/82mm
    Hg,herhear trat
    eis118bpm,andheroxygensat urati
    oni s90%on6l i
    terspernasalcannul a.
    Sheappear sfati
    gued,isinmoderaterespi
    ratorydistress,andhasj ugularvenousdi st
    entionto
    themandi ble.Cardiacauscultat
    ion r
    evealstachycar dia,r egularr hyt
    hm,and an S3  gall
    op.
    Cracklesar
    ehear dinthelowerhalfoft
    helungf i
    eldsbi l
    aterally.Theext r
    emi t
    iesarecooland3+
    pit
    ti
    ngedemai spresentuptotheknees. 

    Laborator
    yf i
    ndingsr evealasodi um of132mmol /L,potassi
    um 4.2mmol /L,creati
    nine 
    1.7
    mg/ dl
    ,magnesi um 2.
    4mg/ dl,aspart
    atetransaminase32U/ L,alani
    netr
    ansaminase28U/ L,
    hemoglobin11.4g/ dl,andpl atel
    etcountof280, 000/ mm3.Anechocardiogr
    am isper f
    ormed
    showingnor mallef
    tvent r
    icul
    arsize,butseverel
    ydepr essedsystol
    icf
    unct
    ion,est
    imatedat10-
    15%wi thglobalhypokinesis.Cardiaccatheteri
    zat
    ionshowsnor malcor
    onari
    es,withelevated
    2
    bivent
    ri
    cularfi
    ll
    ingpressures,andcardiacindexof1.2L/ min/
    m.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sLEASTl
    ikel
    ytobeofpot
    ent
    ialt
    her
    apeut
    icbenef
    iti
    nthi
    scondi
    ti
    on?

    a. Anti
    coagul ati
    on.
    b. Angiotensin-convert
    ingenzymeinhi
    bit
    or(
    ACEI
    ).
    c. Considerationforcardiactr
    anspl
    ant
    ati
    on.
    d. Magne sium.
    e. Mechani calcir
    culat
    or ysuppor
    t.

    ANSWER: 

    85. d. Magnesi
    um.

    Thiscasei
    ll
    ustr
    atesthepresentati
    onofawomanwi t
    hper i
    partum cardiomyopathy(PPCM).
    Advancedmaternalage,
    mul t
    iparousst
    atus,
    mult
    i-f
    etalgest
    ation,
    Af r
    icandescent,hist
    oryof
    hypert
    ensi
    on/pr
    e-eclampsia,andcocai
    neabusehavebeenr eport
    edt obepot enti
    alr
    isk
    fact
    ors.
     

    Magnesium i
    samainst
    ayoft herapyf
    orpre-eclampsia,butnoti
    nperi
    part
    um car
    diomyopat
    hy.
    Furt
    hermore,
    magnesi
    um levelsarenormali
    nt hiscase;ther
    efor
    e,magnesi
    um
    repl
    acement/
    suppl
    ementati
    oni snoti
    ndicat
    ed. 

    Convent
    ionalt
    her
    api
    es,
    suchasbet
    a-bl
    ocker
    sandACEI
    s,shoul
    dbei
    nit
    iat
    edoncet
    hepat
    ient
    i
    sdeemedhemodynami
    cal
    lyst
    abl
    e. 

    Advancedheartfai
    lur
    etherapi
    esoflef
    tvent
    ri
    cul
    arassi
    stdevi
    cesandcar
    diact
    ransplant
    ati
    on
    arepotent
    ialt
    herapeut
    icopti
    onsforsomepati
    ent
    swi t
    hsever
    ePPCM wit
    houtrecoveryof
    vent
    ri
    cularfunct
    ion.

    Duet othehighi ncidenceoft hromboembol ism i nPPCM, anti


    coagulati
    oni sat herapeut i
    c
    considerati
    on, especiall
    yduringpr egnancyandi nthefirst6-8weekspost par t
    um duet o
    hypercoagulabi l
    it
    ydur i
    ngtheset i
    meper iods.Dat afrom smallstudieshavedemonst ratedt
    hat
    additi
    onofbr omocr ipti
    netost andar dheartfailuret her
    apiesmayi mprovel eftventr
    icular
    ejecti
    onfractionandcomposi teclinicaloutcomesi nwomenwi t
    hPPCM.Thepost ulated
    mechani sm ofact i
    oni sthr
    oughsuppr essionofpr olacti
    n, whi
    chi nits16-kDaant i
    -angiogeni
    c
    andpr oapoptot i
    cform mayl eadtoendot helialinfl
    ammat i
    on,impairedcardi omyocyt e
    met abol
    ism, andr educedmyocar dialcontractioni nPPCM.However ,t
    histher apyisnotyet
    recommended.

    86. A79- year-ol


    dwomanpr esent
    stothecl i
    nicwithshor t
    nessofbr eathonexer ti
    on.She
    hasNew Yor kHeartAssociat
    ionclassIIheartfail
    ure.Hermedi calhistoryincludesahear t
    murmur, poor l
    y controll
    ed hyper t
    ensi
    on, and hyper l
    ipi
    demi a. A t wo- di
    mensional
    echocar
    diogram showspr eser
    vedejecti
    onfract
    ion,moder at
    eleftventr
    icularhypertr
    ophy,mil
    d
    aort
    icstenosis,andanormalpulmonaryarterypressure.Theimagesf r
    om t heechoar eshown
    i
    nFigures1, 2,and3.

    Whi
    choft
    hef
    oll
    owi
    ngbestdef
    inest
    hegr
    adeofdi
    ast
    oli
    cfunct
    ion?
     
     
    Fi
    gur
    e1
    Fi
    gur
    e2
    Fi
    gure3
    a. Gr
    adeI
    II
    b.
    b. Gr
    adeI
    .
    c. Gr
    adeI
    I.
    d. Gr
    adeI
    II
    .

    ANSWER: 

    85. d. Magnesi
    um.

    Thiscasei
    ll
    ustr
    atesthepresentati
    onofawomanwi t
    hper i
    partum cardiomyopathy(PPCM).
    Advancedmaternalage,
    mul t
    iparousst
    atus,
    mult
    i-f
    etalgest
    ation,
    Af r
    icandescent,hist
    oryof
    hypert
    ensi
    on/pr
    e-eclampsia,andcocai
    neabusehavebeenr eport
    edt obepot enti
    alr
    isk
    fact
    ors.
     

    Magnesium i
    samainst
    ayoft herapyf
    orpre-eclampsia,butnoti
    nperi
    part
    um car
    diomyopat
    hy.
    Furt
    hermore,
    magnesi
    um levelsarenormali
    nt hiscase;ther
    efor
    e,magnesi
    um
    repl
    acement/
    suppl
    ementati
    oni snoti
    ndicat
    ed. 

    Convent
    ionalt
    her
    api
    es,
    suchasbet
    a-bl
    ocker
    sandACEI
    s,shoul
    dbei
    nit
    iat
    edoncet
    hepat
    ient
    i
    sdeemedhemodynamical
    lyst
    abl
    e. 

    Advancedhear
    tfai
    lur
    ether
    api
    esofl
    eftvent
    ri
    cul
    arassi
    stdevi
    cesandcar
    diact
    ranspl
    ant
    ati
    on
    arepot
    entialt
    herapeut
    icopt
    ionsf
    orsomepat
    ient
    swi
    thsever
    ePPCM wi
    thoutr
    ecover
    yof
    vent
    ri
    cularfunct
    ion.

    Duet othehighi ncidenceoft hromboembol ism i nPPCM, anti


    coagulati
    oni sat herapeut i
    c
    considerati
    on, especiall
    yduringpr egnancyandi nthefirst6-8weekspost par t
    um duet o
    hypercoagulabi l
    it
    ydur i
    ngtheset i
    meper iods.Dat afrom smallstudieshavedemonst ratedt
    hat
    additi
    onofbr omocr ipti
    netost andar dheartfailuret her
    apiesmayi mprovel eftventr
    icular
    ejecti
    onfractionandcomposi teclinicaloutcomesi nwomenwi t
    hPPCM.Thepost ulated
    mechani sm ofact i
    oni sthr
    oughsuppr essionofpr olacti
    n, whi
    chi nits16-kDaant i
    -angiogeni
    c
    andpr oapoptot i
    cform mayl eadtoendot helialinfl
    ammat i
    on,impairedcardi omyocyt e
    met abol
    ism, andr educedmyocar dialcontractioni nPPCM.However ,t
    histher apyisnotyet
    recommended.

    87. A 25- year-old woman pr esentst othe emergency departmentwi th progressively


    wor seni
    ngdyspneaovert hepastweek.Sympt omswer einit
    ial
    lyassoci
    atedwithaf ever,
    rigors,
    andnasalcongest ionf ort hefir
    st2days.Thepat i
    enthasnoknownpr i
    ormedi calhistory.
    Admi ssi
    onel ectrocardiogr am isnor
    mal.Thepat i
    entisafebril
    e.Herheartrat
    eis100bpm.Her
    bloodpr essur eis90/ 70mm Hg.I nit
    ialphysi
    calexami nati
    onshowedanel evatedjugul ar
    venouspr essure,bi l
    ateralr al
    es,anS3/ S4 
    summati
    ongal lop,and2+pi t
    ti
    nglowerext remi ty
    edemabi laterall
    y. 

    Admission echocardi ogram shows a l eftventri


    cular( LV) 
    ejecti
    on fract
    ion of20%,gl obal
    hypokinesis,novalvul ardisease,andnoper icardi
    alef fusi
    on.Ri ghtvent r
    icul
    arfuncti
    oni s
    normal.I ntr
    avenous di ureti
    cs arei niti
    ated wi t
    h minimalr esponse.Wi t
    hin 24 hours of
    admission,t he pat
    ientdevel ops hypot ension and pr ogressive heartfail
    urer ef
    ract
    oryt o
    i
    notropesandvasopr essors.Thepatienti sref
    erredforacut emechani calci
    rculat
    orysupport
    .A
    prei
    mpl anttwo-dimensi onalechocar
    di ogram oftheLVi sshown( Fi
    gur e1).

    Whichoft
    hef
    oll
    owi
    ngper
    cut
    aneousmechani
    calsuppor
    tdevi
    cesi
    scont
    rai
    ndi
    cat
    edi
    nthi
    s
    pat
    ient
    ?
    Fi
    gur
    e1

    a. TandemHeart.
    b. I
    ntra-
    aorti
    cballoonpump( I
    ABP)
    .
    c. I
    mpella.
    d. Veno-ar
    teri
    alextracor
    por
    ealmembr
    aneoxygenat
    ion(
    VA-
    ECMO)
    .

    ANSWER: 

    87. c. I
    mpel
    la.

    Thi
    spati
    enthasanapi
    calLVthr
    ombusseenonechocar
    diogr
    aphy.Ofthesuppor
    tdevi
    ces
    l
    ist
    ed,
    theImpell
    aispl
    acedi
    ntheLVvi
    aretr
    oaor
    ti
    capproach,andther
    efor
    e,maycause
    embol
    ism oft
    heLVthr
    ombus.

    Intr
    a-aor
    ticbal
    looncounterpul
    sat
    ionpumpsareplacedi
    ntothedescendi
    ngaor t
    aanddispl
    ace
    bloodvolumefrom thedescendi
    ngaort
    abyinfl
    ati
    ngduri
    ngdiast
    oleanddeflat
    ingduri
    ng
    systol
    e.Anabsolutecontr
    aindi
    cati
    ontotheI
    ABPismoderateorsevereaort
    icregur
    git
    ati
    on.

    TheTandemHear tdevi
    ceisanextracor
    por
    ealcent
    rif
    ugalpumpt hatusestwopercut
    aneously
    del
    iveredcannulastopumpoxygenat edbl
    oodfrom t
    heleftat
    rium t
    othesystemicci
    rcul
    ati
    on
    vi
    at hefemoralarter
    y.Forl
    efthear
    tsuppor
    t,t
    hedevicerequir
    esat r
    ans-sept
    alpunct
    urefor
    del
    iver
    yoft
    he21- Fr
    enchinf
    lowcannul
    aandaseparat
    ear
    ter
    ialaccesssi
    tefora15-,
    17-,or19
    -Fr
    enchart
    eri
    alcannul
    a.Anabsolut
    econt
    rai
    ndi
    cat
    iontot
    heTandemHear tdevi
    ceisl
    eftat
    ri
    al
    thr
    ombus.

    TheImpell
    apumpsareaxial
    -fl
    owcathet
    ersthatdi
    rectl
    ydispl
    acebloodfrom t
    heLVintothe
    ascendi
    ngaort
    a.Thedevi
    cescanbeplacedviafemoralart
    eri
    alaccessinret
    rogr
    adefashion
    acrosst
    heaort
    icval
    veint
    othelef
    tventr
    icl
    e.Anabsolutecont
    rai
    ndicat
    iontotheImpel
    lapumps
    i
    sLVt hr
    ombus.

    VA-ECMOisplacedvi
    aper
    ipheralcannul
    asinthevenousandar t
    eri
    alsyst
    em.A
    cont
    rai
    ndi
    cat
    iontoVA-ECMOi ssevereperi
    pheralvascul
    ardi
    sease.
     
    Mi
    scel
    laneous
    Quest
    ion:

    1. A28-year-ol
    dmanpr esentst oyourofficeforgeneticcounseling.Hehasaknown
    hist
    oryofaort
    icdi
    latati
    on,
    mi tralvalveprol
    apse, andocul arlensdisplacement
    .Onexami
    nati
    on,
    younotepectusexcavatum andmar kedjointlaxit
    y.Hei saccompani edbyhiswif
    ewhois
    normalappeari
    ngandhasnof ami lyhist
    oryofcar diovasculardisease.Theywantt
    oknowthe
    li
    kel
    ihoodofthei
    rchildr
    eninher i
    ti
    ngt hei
    rfather'scardi
    ovascul arconditi
    on.

    Whi
    choft
    hef
    oll
    owi
    ngi
    syourr
    esponse?

    a. Lowr
    isk,
    ashi
    sdi
    seasei
    scausedbymul
    ti
    plegenes,
    wit
    hgene-
    envi
    ronment
    i
    nter
    act
    ions.
    b. Unli
    kel
    y,ashi
    sdi seasei scausedbyanaut osomalrecessivegene.
    c. 0%ofhisdaughters, ashisdiseaseiscausedbyanX- l
    inkedrecessivegene.
    d. 50%ofhischi
    ldr
    en, ashisdiseaseiscausedbyanaut osomaldomi nantgene.
    e. 100%ofhisdaught ers,ashisdiseaseiscausedbyanX- li
    nkeddomi nantgene.

    Answer
    :

    1. d. 50%ofhi
    schi
    ldr
    en,
    ashi
    sdi
    seasei
    scausedbyanaut
    osomaldomi
    nantgene.

    Thi spat ienthasMar f


    ansyndr ome, whichi soneoft hemostcommonMendel i
    andi sor ders,
    wi thapr eval
    enceofappr oximat ely1in5, 000indivi
    duals.Marfansyndr omei scausedby
    mut ati
    onsi nthefibril
    li
    n-1geneandi si nheri
    tedinanaut osomaldomi nantfashion.Ther efore,
    50%oft heof f
    spri
    ngofanaf f
    ectedpar entwoul dbeexpectedtoi nheritt
    heabnor malgene.
    Ot hercar diovasculardiseasest hatdemonst r
    ateMendel i
    aninher i
    tanceincludefami lialdilat
    ed
    car diomyopat hy,whi chhasdi f
    ferentmodesofi nherit
    ancebasedont hegenemut ati
    on
    i
    nvol vedbutmostcommonl yisaut osomaldomi nant;f
    amili
    alhyper tr
    ophiccardiomyopat hy,
    whi chhasaut osomaldomi nanti nheri
    tancecausedbyoneof>900i denti
    fi
    edmut ati
    onsi none
    oft he14genesencodi ngcomponent soft hesarcomere;andl ongQTsyndr ome, whi ch
    typical l
    yshowsanaut osomaldomi nantmodeofi nherit
    ancebutwi t
    hvar i
    ablepenet rance.
    Thesedi seaseswi thMendel ianinher i
    tanceshoul dbecont r
    astedwi thcommon, compl ex
    diseasessuchasat heroscleroti
    ccar diovasculardisease,whichhasmul ti
    plegenesconf erri
    ng
    risk, wit
    honl ymodestef fect,oft
    enwi t
    hmul t
    ipl
    egene- geneandgene- envir
    onmenti nteract i
    ons.

    Quest
    ion:

    2. A27-year-oldwomanpr esent stoyouroffi


    cef orgenet
    iccounseling.Herf
    atherdiedof
    anaor t
    icdissect
    ionatage45year s.Herolderbrotherhasbeendi agnosedwi t
    hMar fan
    syndrome.Thepat ientisrecent
    lymar ri
    edandt hi
    nki ngofhavingchildr
    en.Shedeniesany
    histor
    yofeyepr oblems.Onexami nat
    ion,shehasapect usexcavatum andstri
    aeonher
    abdomen, butotherwisehasnoscol i
    osisorarachnodact yl
    yandhasanegat i
    vewristand
    thumbsi gn.Echocardiogr
    am showsnor malaorti
    cr ootandascendi ngaortasi
    ze,wit
    hout
    evidenceofmi t
    ralortri
    cuspidvalveprolapse.

    Sheisi
    nter
    est
    edinundergoi
    nggenet
    icscr
    eeni
    ngt
    oknowwhetherherfut
    urechi
    ldr
    enwoul
    dbe
    atr
    iskf
    orMarfansyndr
    omeandwantstoknowhowli
    kel
    ygenet
    icscreeni
    ngtest
    saret
    opick
    upt
    hedi
    sease.
     

    Your
    espondt
    hatgenet
    ict
    est
    ingwi
    lli
    dent
    if
    yacausat
    ivemut
    ati
    oni
    nwhi
    choft
    hef
    oll
    owi
    ng?

    a. Appr
    oxi
    mat el
    y30%ofcases.
    b. Appr
    oxi
    mat el
    y70%ofcases.
    c. <10%ofcases.
    d. >90%ofcases.
    e. Appr
    oxi
    mat el
    y50%ofcases.

    Answer
    :

    2. d. >90%ofcases.

    Mar fansyndr omei saconnect i


    vet issuedi sorderchar act er
    izedbycar di ovascular( aorti
    c
    dil
    at at i
    onanddi ssect ion,mitralandt ricuspi dvalvepr olapse) ,ocular(lensdi splacementand
    retinaldet achment ),andmuscul oskel etal(jointlaxi t
    y, l
    ongboneover gr owt h,scoliosis,pect us
    excavat um orcar inatum)mani f
    est ations.Ther evisedGhentscor eprovi desascor i
    ngsyst em
    tohel pmakeacl ini
    caldi agnosi sofMar fansyndr ome.Ourpat i
    enthasaGhentscor eof3( 2
    point sf orpect usexcavat um and1poi ntforski nst ri
    ae) .Whi leshehasaf amilyhi stor
    yof
    Mar fansyndr ome, herscor eof3i sbel owt hesyst emi cscor eof7neededt odiagnoseMar fan
    syndr ome.Mar f
    ansyndr omei sinher it
    edi nanaut osomaldomi nantfashi on,andi scausedby
    mut ationsi nt hef i
    brill
    in-1extracel l
    ul armat ri
    xpr ot ei
    ngene.Upt o30%ofcasesdonothave
    affect edpar ent sandar efel
    ttor epr esent  denovo  mut ations.Genet i
    ct estingisavai l
    able,and
    thel ikelihoodoff indingacausat i
    vemut ationi sappr oximat ely95%i npat ientswi thMar fan
    syndr ome.Genet ictest i
    ngisnotr equi redf orconf irmi ngdi agnosi sint hei ndexcase( whichi s
    madecl inically), butcanbehel pfulf orot herf amilymember swhoneedt obescr eened.These
    resul tscanhel pdet ermi newhet hert heyneedt ohavel ongi t
    udi nalcli
    nicalmoni tor i
    ngor
    whet hert heycanber eassuredt hatt heyhavenoti nheritedt hepat hologi cmut ation.

    Quest
    ion:

    3. A35-year-ol
    dmanpr esent
    stoyouroff
    iceforadvi
    ceregar
    dinggeneticscr
    eeni
    ng.His
    40-year-ol
    dbr ot
    herwasdi agnosedrecentl
    ywithanidi
    opathi
    cnonischemiccardi
    omyopathy.
    Hisfatherhadahear tt
    ransplantatage48.Hehasr eadontheInt
    ernetthatgenet
    ict
    est
    ingis
    avail
    ableandiswonder i
    ngi fiti
    scorr
    ectforhi
    m.

    Whi
    chofthefol
    lowi
    ngbestrepr
    esent
    sthesensi
    ti
    vit
    yforcur
    rentgenet
    ict
    est
    ingf
    orpat
    ient
    s
    wi
    thfami
    li
    alcar
    diomyopat
    hy?

    a. 10-20%.
    b. <10%.
    c. 30-40%.
    d. >90%.
    e. 50-60%.
    Answer
    :

    3. c. 30-
    40%.

    Fami li
    aldilat
    edcardi
    omyopat hy(FDC)isacl i
    nicaldiagnosi swheni di
    opathicdil
    ated
    cardiomyopat hyoccursi natleasttwocloselyrelatedfami lymember s.About80-90%ofcases
    areinheritedintheautosomaldomi nantfashi
    on.I tisrarelyinherit
    edi nautosomalrecessiveor
    X-li
    nkedf ashion.Mutationsi n>30geneshavebeenf oundt ocauseFDC.I fgeneti
    ctesti
    ngi s
    considered, i
    tshoul
    dfirstbeper for
    medi nthemostcl earlyaffectedper soninthefamil
    y.FDCi s
    ahet erogeneousgeneticdi sease,wit
    hvar i
    ablepresent ati
    ons, r
    educedpenet r
    ance,and
    dif
    ferentmodesofi nheritance.Theknownmut at
    ionsaccountf oronl y40-50%ofcases;t hus,
    theroleofr outi
    negenetictest i
    ngisunclear.

    Quest
    ion:

    4. Youar easkedtoconsultona45- year-ol


    dmanhospi tal
    izedwithaf i
    rstepisodeofhear t
    fail
    ure.Hehasnoknownpastmedi calhi
    story.Headmitstoasedent arylif
    estyl
    e.Exami nati
    on
    disclosesbloodpressureof118/70mm Hg, el
    evatedj
    ugularvenouspr essure,clearlungfi
    elds,
    normal lyspli
    t 
    S1 
    andS2,and2+edemat otheleveloft
    hepost er
    iorthi
    ghsbi l
    aterall
    y.His
    electrocardi
    ogram i
    sshowni nFigure1.Hisechocardi
    ogram demonst ratedconcent ri
    clef
    t
    ventricular(
    LV)hypert
    rophywithwallthi
    ckness1. 5cm andincreasedLVmassi ndex;normal
    systolicfunct
    ionwithLVeject
    ionfract
    ionis60%.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    ydi
    agnosi
    s?
    a. Hyper t
    ensiveheartdi
    sease.
    b. Athl
    ete'sheart.
    c. Hyper t
    rophiccardi
    omyopathy.
    d. Cardiacamyl oi
    d.
    e. Fabry'sdisease.

    Answer
    :

    4. c. Hyper
    trophi
    ccar
    diomyopat
    hy.

    Hyper t
    rophi
    ccardi omyopat hymustbedi ff
    erentiatedfrom inf
    ilt
    rativeandmet aboliccondi t
    ions
    thatalsocancausel eftvent r
    icularwallthickening, suchasFabr y'sdi seaseorPompe' s
    disease.Thi
    spat ienti
    sol derthanexpect edf orpresentati
    onf orFabr y'sdisease, whi chtypical
    ly
    presentswithneur ol
    ogicsignsandhear tdiseasei nchi l
    drenandadol escents.Thedi agnosis
    woul dbemadewi thalphagal actosidaseact ivit
    yandendomyocar dialbiopsy.Amyl oidosis
    woul dbeexpectedt ocausenor malorl owvol t
    ageont heelectrocar diogram witht hi ckened
    wallsonechocar diographyandwoul dbeconf i
    rmedwi thmyocar dialbiopsy.At hlete'shear t
    changescani ncludewal lthickeningandi ncreasedchambersi zeandi sseeni nhi ghl ytrai
    ned
    athlet
    es,whichthispat i
    entisnot .Thispat ientdoesnothaveahi storyoforcur rent
    hypertensi
    ontoexpl ai
    nhyper tensivehear tdisease.

    Quest
    ion:

    5. A22- year
    -oldcoll
    egeat hleteisbeingeval uatedafteranepisodeofsyncopeonhi sway
    toclass.Hehasnosi gnif
    icantpastmedi calhist
    or yanddeni estobacco,drug,andsoci al
    alcoholuse.Hei sonnomedi cat i
    onsanddeni esuseofanyher balornutri
    tionalsupplement s.
    Hisfami lyhistoryi
    sunr emar kabl e.Hisexami nationreveal
    sbl oodpressureof110/ 68mm Hg,
    heartrate66bpm, bodymassi ndex21, andbeni gnexami nat i
    on.Echocardiogram r
    eveals
    normall eftventri
    clesizeandt hickness,normalr ightventr
    icle,andnovalvularabnormal i
    ties.
    Elect
    rocar diogram showssi nusr hyt
    hm andQTi nter
    valof492msec.Toxi cologyscreeningi s
    negative.

    I
    naddi
    ti
    ont
    oini
    ti
    ati
    onofbet
    a-bl
    ocker
    s,whi
    choft
    hef
    oll
    owi
    ngi
    smostappr
    opr
    iat
    einhi
    scar
    e?

    a. Car diacmagnet icresonancei


    maging.
    b. Electrophysiologi
    cst udy.
    c. Impl antablelooprecorder.
    d. Ge neticscreening.
    e. Impl antati
    onofi mplantabl
    ecar
    diover
    ter
    -def
    ibr
    il
    lat
    or.

    Answer
    :

    5. d. Genet
    icscr
    eeni
    ng.

    Geneticanalysisisimportantt
    oidentif
    yal ongQTsyndromemutati
    ontoal
    lowforri
    sk
    str
    atif
    icat
    ionandt herapeuti
    cdecisionsandt oeval
    uat
    efamil
    ymemberstoident
    if
    ysilent
    carr
    iers.I
    mpl antablecar
    diover
    ter
    - defi
    bri
    ll
    atori
    mplant
    ati
    onshouldber
    eser
    vedforthosewho
    hadpr evi
    ouscar diacarr
    est(Cl
    assI )andcanbeconsideredi
    nthosewhohavesyncopeor
    ventri
    culartachycardi
    awhi l
    eonbeta-bl
    ockers.Hehadnotbeentreatedyetwithbet
    a-bl
    ockers.
    Patientsundergoingmoni t
    ori
    ngshouldhaveexter
    nalmonitori
    ngpriort
    oimplantabl
    eloop
    recorders.El
    ectrophysi
    ologi
    cstudyandmagnet i
    cresonanceimagingarenotindi
    catedatthi
    s
    ti
    me.Thi spatientalsoshouldunder
    golif
    estyl
    echanges,i
    ncludi
    ngavoidanceofcompetit
    ive
    sportsandavoi danceofdrugsthatprol
    ongQT.

    Quest
    ion:

    6. A45-year
    -oldwomanpr esentstoyouroff
    iceforadviceregar
    dingherri
    skofdeepvein
    thr
    ombosis(DVT).Herbrot
    herhadaDVTandwasdi agnosedashavi ngfact
    orVLeiden.She
    wantstoknowherriskofhavi
    ngt hediseaseandwhet hersheshouldbetaki
    nglif
    elong
    anti
    coagul
    ati
    on.

    Youadvi
    set
    hatf
    act
    orVLei
    deni
    swhi
    choft
    hef
    oll
    owi
    ng?

    a. X-l
    inkeddominantwit
    hlowlif
    eti
    mer i
    skofDVT.
    b. Aut
    osomalrecessivewit
    hhighli
    fet
    imeriskofDVT.
    c. Aut
    osomalrecessivewit
    hlowlif
    eti
    mer i
    skofDVT.
    d. Aut
    osomaldomi nantwit
    hlowlif
    eti
    mer i
    skDVT.
    e. Aut
    osomaldomi nantwit
    hhighli
    fet
    imeriskofDVT.

    Answer
    :

    6. d. Aut
    osomaldomi
    nantwi
    thl
    owl
    if
    eti
    mer
    iskDVT.

    FactorVLei denisanaut osomaldomi nantgeneticdisorderinwhi chamut at i


    onoff act
    orV
    cannotbei nacti
    vatedbyact i
    vatedpr otei
    nC, r
    esult i
    nginani ncreasedriskoft hrombosis.
    Therefore,herri
    skofhavi ngthemut ationis50%.Whi l
    eappr oxi
    mat ely20%ofpat i
    entswithDVT
    willbefoundt ohavefactorVLei den,theli
    feti
    mer iskofDVTi napat i
    entwi thfactorVLeidenis
    onlyappr oximat
    ely5%.Thepr evalenceoft hefactorVLei denmut at
    ionisappr oximatel
    y5%i n
    CaucasianAmer i
    cans,2%i nHispanicAmer i
    cans, 1%inbot hAfricanAmer icansandNat i
    ve
    Amer i
    cans, and0.5%i nAsi anAmer i
    cans.Whi lethispatientshouldnotbepl acedon
    prophylacticant
    icoagulation,l
    if
    est yl
    emodi fi
    cation,suchasmai ntai
    ningnor malbodywei ght
    ,
    avoidanceofsuppl ementalest r
    ogen, andavoi danceoft obaccopr oducts,shouldbe
    encouraged.

    Quest
    ion:

    7. A78- year-
    oldmani sadmi t
    tedt othecoronarycar euni taft
    erpr esenti
    ngwi t
    hanacut e
    anter
    iormyocar di
    alinfarcti
    on.Heunder goessuccessf ultreatmentofapr oximall ef
    tant eri
    or
    descendingocclusi
    onwi thadr ug-eluti
    ngst ent
    .Af ol
    low- upechocar diogram r evealsant er
    ior
    andapicalhypokinesis,withanej ectionfracti
    onof40%.Hi spastmedi calhistoryisnot ablefor
    hypert
    ension,hyperl
    ipidemi awithhismostr ecentlow-densi tyli
    poprotein120mg/ dl,r
    ecurrent
    ki
    dneyst ones,andpr i
    orgast r
    ointestinal(
    GI )bl
    eedingfrom duodenalul cers.I
    naddi t
    iont o
    conti
    nuinghishomemedi cati
    onsofaspi r
    in81mg, atorvastatin40mg, andallopur i
    nol,his
    l
    isi
    noprilisi
    ncreasedt o20mgdai l
    y,andhei sstar
    tedoncl opidogrel75mgdai l
    y.

    Whichofthefol
    lowi
    ngi
    scor
    rectr
    egar
    dinghi
    str
    eat
    mentf
    oll
    owi
    ngper
    cut
    aneouscor
    onar
    y
    i
    ntervent
    ion(
    PCI)?
    a. Routi
    negenet i
    ctestingforclopi
    dogr
    elmetabol
    ism i
    srecommended.
    b. Cl
    opidogrelshouldbechangedt opr
    asugr
    el.
    c. Prot
    onpumpi nhi
    bitor(PPI)ther
    apyshoul
    dbeadded.
    d. Pl
    atel
    etfuncti
    ont estingisrecommended.
    e. Aspi
    rinshouldbei ncreasedto325mgdaily.

    Answer
    :

    7. c. Pr
    otonpumpi
    nhi
    bit
    or(
    PPI
    )ther
    apyshoul
    dbeadded.

    In2010, theFoodandDr ugAdmi nistrati


    onappr ovedanewl abelf orclopidogr elwi t
    haboxed
    war ningaboutt hedi mi ni shedef fectivenessofcl opidogr elinpat ientswi thimpai r
    edabi lityto
    conver tt hedr ugintoi tsact ivemet abol i
    te.Pat ientswi thdecr easedcyt ochromeP4502C19
    (CYP2C19)f unctionbecauseofgenet icpolymor phi smsmet abol izecl opidogr elpoor l
    yandhave
    higherr at esofcar di
    ovascul arevent saf teracut ecor onar ysyndr omeandPCIt hanpat ient swith
    normalCYP2C19f unct i
    on.Thewar ningal sonot est hatt estsar eavai lablet oi dentifypat ients
    withgenet i
    cpolymor phi smsandt hatal ternat ivet reat mentst rategiesshoul dbeconsi der edfor
    patient swhoar epoormet abolizers.Thecl opi dogr elboxedwar ningl eavest hei ssueofwhet her
    toper form CYP2C19t est i
    ngupt ot hei ndividualphysi cian.Itdoesnotspeci fical l
    yrequi re
    genet i
    ct est i
    ngorot herchangesi neval uationort reat mentanddoesnoti mpl yt hatt herear e
    solidevi dence- basedr easonsf orsuchact ions.Rat her ,itservest oinform cl iniciansofgenet ic
    variationsi nresponset ocl opidogr elandt oemphasi zet hatcl i
    niciansshoul duset his
    knowl edget omakedeci sionsabouthowt ot r eati ndi vidualpat i
    ent s.Atthepr esentt ime, the
    evidencebasei sinsuf ficienttor ecommendr out inegenet ictestingi npat ientsunder goi ngPCI .
    The2011ACCF/ AHA/ SCAIPCIgui del i
    net her ef oregi vest her outinecl i
    nicaluseofgenet i
    c
    testingf orclopidogr elmet abolism aCl assI IIindi cat ion( nobenef it).Similarly, routi
    nepl atel
    et
    funct i
    ont est
    ingal soisnotr ecommended.  

    TheCOGENTt rialrandomi zedpat i


    entswi t
    hdualant iplatelettherapy( DAPT)t ocl opidogreland
    omepr azol
    eorcl opidogrelandpl acebo.Althought herewasnodi f
    ferencei ncar di
    ovascul ar
    event sbetweent het wogr oups,GIevent swer ehalvedi nt hoser andomi zedt oomepr azole.Iti
    s
    reasonabl etocar eful
    lyevaluatetheindicationforPPIt her apyinpat ientstreatedwi th
    clopidogrelbasedont hepr esenceorabsenceoft her i
    skf actors.Theneedf orGIpr otection
    i
    ncr easeswi t
    ht henumberofr i
    skfactorsforbleeding.Pr iorupperGIbl eedingi sthest rongest
    andmostconsi stentri
    skfact orf
    orGIbl eedingonant iplatelettherapy.Pat ientswi t
    hacut e
    cor onarysyndromeandpr iorupperGIbl eedingareatsubst antialcar di
    ovascul arrisk,soDAPT
    withconcomi t
    antuseofaPPImaypr ovidetheoptimalbal anceofr iskandbenef i
    t.Prasugrelis
    relati
    velycontraindicatedandhasabl ackboxwar ningi npat ientsabovet heageof75year s, a
    priorhistoryofstroke,orwi thweight.Aspirinatdoses>100mgi snotr ecommendedaspar tof
    DAPTf oll
    owingPCI .

    Quest
    ion:

    8. Upto30%ofbi cuspidaorti
    cvalve(BAV)patientswil
    lhaveafirst
    -degr
    eerelati
    vewit
    h
    associ
    atedaort
    opathy.Thisincl
    udescoar ctat
    ionoftheaort
    aoranascendi nganeurysm.At
    ti
    mes,theaort
    opathymaybedet ectedindependentofthepresenceofaBAV.

    Whichoft
    hefoll
    owi
    nggenet
    icabnor
    malit
    iesi
    srecognizedasbei
    ngr
    esponsi
    blef
    ort
    he
    devel
    opmentofaBAVandit
    sassoci
    atedaort
    opathy?
    a. Transf
    orminggrowthfactor
    -beta1(TGF-
    beta1)mutat
    ion.
    b. NOTCH1ge nemut at
    ion.
    c. Noge nehasbeenidenti
    fi
    ed.
    d. Absenceofanabnormal i
    tyofoneoftheXchromosomes.
    e. Fi
    bril
    li
    n-1mutat
    ion.

    Answer
    :

    8. c. Nogenehasbeeni
    dent
    if
    ied.

    Thecor rectansweri sthatnogeneti


    cmut ati
    onhasbeeni dent
    ifiedtodat e.Whileitisknown
    thatNOTCH1mut ationsareassoci
    atedwi thearlydevelopment aldefectsintheaor ti
    cvalveand
    possiblyaBAV, thepr esenceofthi
    smut ationalsohasbeenl i
    nkedt ohypopl asti
    cl ef
    theartand
    tocalcium deposi ti
    oni nboththeaorti
    cval veandaor ta.Thefi
    br il
    li
    n-1mut ati
    oni sassociated
    withtheMar f
    ansyndr ome.Theabsenceoranabnor mal i
    tyintheXchr omosomei sassociated
    withTur ner'
    ssyndr ome.Aorti
    caneurysmsmaybepr esentinbot htheMar fanandTur ner'
    s
    syndrome.Tur ner'ssyndromepat i
    entsfrequentl
    yhaveabi cuspi dvalveaswel lasaor ti
    c
    coarctation.TheTGF- beta1genemut at
    ioni sassociatedwithLoeys- Dietzsyndr omeand
    multipl
    eaor ti
    caneur ysms.

    Quest
    ion:

    9. An18- year-ol
    dmani srefer
    redtoyouroffi
    ceforaf ami
    lyhist
    oryofhyper
    trophi
    c
    cardi
    omyopat hy(HCM) .Heplayshighschoolsport
    s,isasymptomatic,hasnoothermedical
    hist
    ory,andhasaf amilyhi
    storyofHCM.Hi sfat
    herwasdi agnosedwithHCM atage30year s,
    andatage45year sisasymptomaticonabet a-bl
    ocker.Thepati
    enthasnoheartmur murat
    restorwithValsal
    va,andhiselectr
    ocardi
    ogram isnormal.Yourecommendgenet ict
    esti
    ng.

    Thei
    nter
    valf
    orcl
    ini
    calscr
    eeni
    ngf
    orHCM i
    nthi
    spat
    ientdependsonwhi
    choft
    hef
    oll
    owi
    ng?

    a. I
    ndependentofgenet i
    ctest
    ing.
    b. Predi
    ctedri
    skofsuddendeat h.
    c. Genotypeofthepatient
    .
    d. Phenotypeofthefather.
    e. Genotypeofthefather.

    Answer
    :

    9. c. Genot
    ypeoft
    hepat
    ient
    .

    Hyper trophiccardiomyopat hy( HCM)i scausedbyanaut osomaldomi nantmut ati


    oni ngenes
    encodi ngsar comer epr oteinsorsar comere-associ
    atedpr oteins.Geneticorcl i
    nicalscreening
    ofal lfirst-
    degr eefami l
    ymember sofpat i
    entswithHCM i sindicatedinthosewi thunrecognized
    disease.Rel ati
    veswi thover tHCM wi l
    lhavethesamepat hogeni cHCM mut ati
    onast heindex
    pat i
    ent .Thesemut ationcar r
    iersshouldbeevaluatedbyphysi calexaminat i
    on,
    electrocar diography, andt wo- dimensionalechocardi
    ography.I fHCM isi dentif
    ied,these
    i
    ndi vidual sshoul dunder gor i
    skstrati
    fi
    cati
    on.Genetictesti
    ngpr ovi
    desdef i
    niti
    vedi agnosisof
    affect edgenet icstatus, andcur rentl
    yisusedmostef fecti
    velyi ntheidentif
    icati
    onofaf fected
    relativesi nfami l
    iesknownt ohaveHCM.Mut at
    ion-negati
    vef ami l
    ymember sandt heir
    descendant shavenor iskf ordevelopingHCM anddonotneedf urt
    hereval uati
    on.The
    phenotypi
    cexpr
    essi
    onofHCM isvar
    iabl
    e,evenamongf
    ami
    lymember
    swi
    tht
    hesame
    genotype,
    anddoesnoti
    nfl
    uencescr
    eening.

    Quest
    ion:

    10. A47- year-ol


    dmanwi t
    ht hehumani mmunodef ici
    encyvirus(HIV)presentswithan
    acut eanteri
    ormyocar diali
    nfarction.Hehasnoot hersi gnif
    icantpastmedicalhist
    ory.Heison
    highlyact i
    veantir
    etr
    oviraltherapy, butnoothermedi cat i
    ons.Heunder goesasuccessf ul
    per cutaneouscoronaryinterventionofhisproximallef tanteri
    ordescending.Hislaborator
    y
    valuesatt hetimeofpr esentati
    oni ncludeHbA1cof5. 9%, CD4countof330, andadet ectable
    viralload.Totalchol
    esterolis195mg/ dl
    ,l
    ow- densit
    yl ipoprotei
    ncholester
    olis110mg/ dl
    ,hi
    gh
    -densi tyl
    ipoprot
    eincholesterolis40mg/ dl
    ,andt r
    igl
    ycer idesare225mg/ dl
    .

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    yexpl
    anat
    ionf
    orhi
    sacut
    eevent
    ?

    a. Anti
    ret
    rovi
    ralplat
    eletacti
    vat
    ion.
    b. Vi
    ralmyocardialt
    oxicit
    y.
    c. Vi
    ralendothel
    ialt
    oxicit
    y.
    d. Vascul
    arinfl
    ammat ion.
    e. Anti
    ret
    rovi
    ral-
    inducedvasospasm.

    Answer
    :

    10. d. Vascul
    ari
    nfl
    ammat
    ion.

    Car di
    ovascularcompl icationsar emor ecommoni nHI V- i
    nfectedindivi
    dualsthani nage-
    mat cheduni nfectedindividual s.Ant i
    ret r
    ovir
    alther apyr educest heriskofcardiovascul ar
    compl icati
    ons, suggest i
    ngt hatvi ralreplicat
    iondi rectlyori ndi
    rect
    lycausesvascul ardisease.
    Long- term ef
    fectiveant i
    retrovi ralther apydoesnotf ul
    lyr estor
    evascul arheal
    th, andtreated
    adul t
    scont i
    nuet ohavehi gher -than- expectedr atesofdi seaseprogression.Althought his
    excessr iskdur i
    ngt herapyi sl ikelyduet omul ti
    plef actors, agrowingbodyofevi dence
    suggest sthatchr onicinflammat ion, whichper sistsdur ingef f
    ecti
    veant i
    ret
    roviralther
    apy, i
    s
    directl
    yandcausal lyassoci atedwi thvascul ardysf unctionandt heaccel er
    ateddevel opmentof
    atherosclerosi
    s.LowCD4count s, asevi dencedbyt heD: A:Dstudy,arear i
    skf orcardiovascul
    ar
    diseasei nHIVpat i
    ents.Vi remi aaf fectst hemyocar dium andcancausecar diomyopat hy,but
    woul dnotbeexpect edt ocauseat hrombot i
    ceventorvasospasm.

    Quest
    ion:

    11. A55- year-


    oldmanwi t
    hthehumani mmunodefi
    ciencyvir
    us(HIV)pr
    esentsfor
    eval
    uat
    ionofhi
    sriskofcor
    onaryar
    ter
    ydisease.Hehasneversmokedandhi stot
    alchol
    est
    erol
    i
    s134mg/ dl
    .Hedoesnothavehypert
    ension.Heexer
    cisesregul
    arl
    y.

    Whi
    choft
    hef
    oll
    owinghasbeenshowntoi
    mprovecardiovascul
    arr
    iskpr
    edi
    cti
    oni
    npat
    ient
    s
    wi
    thHI
    V,i
    naddi
    ti
    ontotradi
    ti
    onalFr
    ami
    ngham r
    iskf
    actors?

    a. Durat
    ionofdiabet
    es.
    b. CD4c ounts.
    c. Useoffusioninhi
    bit
    ors.
    d. Useofintegr
    aseinhibi
    tor
    s.
    e. Tr
    igl
    ycer
    idel
    evel
    .
    Answer:

    11. b. CD4count
    s.

    TheFr ami ngham modelforglobalcar diovasculardisease( CVD)r i


    skmaysi gnif
    icantl
    y
    underest i
    mat et
    helikel
    ihoodofCVevent sinHI V-inf
    ectedpat ient
    s.Abet t
    ermodelhasbeen
    deri
    vedf rom theD:A:D(DataCol l
    ect i
    ononAdver seEvent sofAnt i-
    HI VDrugs)study, whi
    chalso
    consider sCD4cellcountsandadmi nist
    rati
    onofant iret
    roviralagents.TheD: A:
    Dmodeli s
    basedonobser vati
    onsin32,663HI V-positivepersonsf rom 20Eur opeancount ri
    esand
    Australi
    awhower efreeofCVDatst udyent ryandwhopr ovidedthoroughi nfor
    mat iononCV
    ri
    skfact ors.Therat
    eofacomposi teCVDendpoi nt,
    compr i
    singmyocar dialinf
    arcti
    on(MI),
    str
    oke, coronaryart
    eryrevascularization,caroti
    dendar terectomy,oranyCVDdeat h,was
    assessedover186, 364.5person- years. 

    FullandreducedD:A:Dmodel
    swer edevelopedtocalcul
    ateesti
    mat ed5-yearrisksofCVD.
    Therewer e1,
    010compositeCVDevents,givi
    ngarateof5.42per1, 000person- years.Near
    ly
    one-halfoft
    heeventswereMIs(493/1010),f
    oll
    owedbyst roke(295/1010),angioplasty
    (129/1010),
    coronaryar
    ter
    ybypass,carot
    idendart
    erectomy,andot herevents.
     

    Thef i
    nalfullD:A:Dmodeli ncludedtradi
    ti
    onalCVDr iskf
    actors,
    aswel lasCD4counts,
    combi nati
    onant ir
    et r
    oviraltherapy(cART),cumulat
    iveexposuretoprotease-andnucleosi
    de-
    reverse-t
    ranscriptasei nhibit
    ors,andcurrentuseofabacavir
    .Othersingl
    e-classt
    herapi
    eswere
    notassociat edwithi ncreasedr i
    sk.Thereducedmodeldoesnoti ncludeuseofART.Dur at
    ion
    ofHIVi nf
    ectionisassoci atedwithhigherri
    skofeventsinthi
    sstudy.Dur at
    ionofdi
    abeteswas
    evaluatedint hi
    sst udy.

    Quest
    ion:

    12. A32- year-oldunrestrainedpassengerisbroughtt otheemer gencyr oom f


    oreval uat
    ion
    aft
    eranaut omobi l
    eaccident .Heisaler
    tandor i
    ented, andhei scompl ai
    ningofleftlegpai nand
    chestpainafterairbagdepl oyment .Hi
    sbloodpressur e145/ 75mm Hg, andhi shear trate105
    bpm.Lungsoundsar eclearandequalt hr
    oughout .Cardiovascularexam reveal
    sdi stanthear t
    soundswi t
    houtr ub.Otherfindingsarechestwallwi t
    hmi lderythemaandear l
    ybruising, anda
    ri
    ghtfemurwi thobviousdef ormityandnormalper ipheralpulses.ChestX- r
    ayrevealscl ear
    l
    ungf i
    elds,normalmedi asti
    num, andfr
    actureofther i
    ght10thand11t hri
    bs.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthebestnextst
    epi
    nthecar
    diaceval
    uat
    ionoft
    hispat
    ient
    ?

    a. Evaluatet
    roponinandmyogl obi
    n.
    b. Transesophagealechocardi
    ogram.
    c. Cardiaccomput edtomographyangi
    ogr
    aphy.
    d. Transthor
    acicechocardiogr
    am.
    e. 12-leadelect
    rocardi
    ogram

    Answer
    :

    12. e. 12-
    leadel
    ect
    rocar
    diogr
    am

    Thor
    aci
    cinj
    uri
    esar
    ethet
    hir
    dmostcommoni
    njur
    iesi
    npol
    ytr
    aumapat
    ient
    s.The12-
    lead
    electrocar di
    ogram ( ECG)i sthebestnextst epinthemanagementoft hepat i
    entt oruleout
    evidenceofmyocar dialinjur
    y.Al thoughECGchangesar enonspeci f
    icandar enotr egardedas
    ast r
    ongi ndicatorofmyocar dialcontusioni ntr
    aumacases, t
    heycani ndi
    cat ecardiac
    i
    nvol vementandcer t
    aincompl i
    cati
    ons,suchasr uptureofthecoronaryar t
    eriesleadingto
    massi vemyocar di
    alinf arcti
    on( MI )
    .Amet a-analysisbyMaenzaandcol l
    eaguesshoweda
    concor dancebet weeni mpor tantcardiaccompl i
    cat i
    onsandabnor malECGf indings.Cardiac
    contusi onsanddi rectinjurywi thdissectionoft hecor onaryarter
    iesandsecondar yMImustbe
    routi
    nel yconsi deredi naddi tiontoacut eMI .Alongwi t
    htypicalaccompanyi nginjuries,
    arrhythmi asof t
    enoccuri nconj uncti
    onwi thcar diaccontusions.Attenhoferandcol leagues
    foundECGchangesi n32%ofpat ientsafterbluntt horaci
    ctrauma, pri
    marilytachycar di
    a,ST
    segmentchanges, andbundl ebr anchbl ocks. 

    Myogl obinisexpect edtobeabnor mal.Determinati


    onofmyocar dialmar kersincasesofsever e
    thoracictraumadoesnotper mi tanyval i
    ddiff
    erenti
    ati
    onoftheet iol
    ogy.Car diacenzymel evel
    s
    serveasani ndicat
    orofcar diacpat hology,thoughindivi
    duallaboratoryvaluesar eless
    signif
    icantindet er
    mi ni
    ngadi agnosist hanthepat i
    ent
    'scourseandcl inicalconditi
    on.
    Echocar di
    ogr aphycanbeusef ultoevaluatewallmot i
    onabnor malit
    ies,pericardi
    alinvolvement,
    andaor ta,buttheECGshoul dbeper formedf i
    rst.Si
    milar
    ly,
    car di
    accomput edt omogr aphy
    angiographycanbeusef ultoeval uat
    ecor onaryvesselsandaor ta,butECGshoul dbe
    performedf ir
    st. 

    Quest
    ion:

    13. A68- year-


    oldwomanwhohasbeenondi al
    ysisf
    ormanyyear sisadmi tt
    edfr
    om home
    wit
    hdi zzinessandhypotensi
    on.Sheunder wentherrout
    inedi
    alysisyester
    day.Shehadbeen
    welluntil3hour spri
    ort
    oadmi ssi
    on,whenshehadashaki ngchillandcomplainedof
    headache, butonlyvaguechestdiscomfort
    .Shehaslong-st
    andingdiabetes,butnoprior
    cardiachistoryexceptf
    orl
    eftbundlebranchblock(
    LBBB)onherel ectr
    ocardi
    ogram (ECG).She
    i
    sal ertbutanxiousandmildl
    ydyspneic. 

    Herbloodpr essureis85/60mm Hg, temperat


    ur eis38. 2degr eesCent i
    grade,andhear tr
    ateis
    103bpm andr egular
    .Herlungsrevealafewmi norcr acklesbilaterall
    y.Hercar diac
    examinationrevealsthefuncti
    oni
    ngshunti nt
    hel eftarm, mi l
    dj ugularvenousdi stenionwi t
    ha
    posit
    ivehepatojugularref
    lux,anS4 
    andS3,butonlyagr ade1/ 6aor ticfl
    owmur mur .Thereisno
    edema, butshei scoolandclammy.AnECGi sobt ainedr eveali
    ngt heLBBB, butnonew
    changessi ncetheECGobt ai
    ned1yearago.Theacut emyocar dialinfarct
    ion(MI)pr otocoli
    s
    acti
    vated,andyouar easkedt oconsideremergentcar diaccat heteri
    zation.

    Whichoft
    hefoll
    owi
    ngwoul
    dmostl
    ikel
    yresul
    tint
    heneedf
    orur
    gentcar
    diaccat
    het
    eri
    zat
    ioni
    n
    t
    hissit
    uat
    ion?

    a. Elevat
    edcreati
    ninekinase-
    myocardi
    alband.
    b. Ne wwallmotiononherechocardi
    ogram.
    c. Elevat
    edD- di
    mer .
    d. S3 gal
    loponexami nat
    ion.
    e. Elevat
    edtroponi
    nT.
    Answer
    :

    13. b. Newwal
    lmot
    iononherechocar
    diogr
    am.

    Thecor rectansweri snewwal lmotionont heechocar diogr am.Shei sf ebr i


    leandot hercauses
    ofherhypot ensionandshockshoul dbequi ckl
    yexcl udedpr i
    ortoconsi der ationf orcardi
    ac
    catheteri
    zat i
    onandcor onaryangi ography.Herpr esentationi spossibl yr elatedt osepsisor
    shock, andyourdeci sionmustt henr elyonwhet herthishasl edtoaMI .Shei scol dand
    cl
    ammy, suggest i
    ngt hecausei scardi ogenic.Thet r
    oponi nTandcr eat inineki nasemaybe
    el
    evatedi npat ientsondi al
    ysisandcanbeconf usingint hisset t
    ing.Theel evat edwhi t
    eblood
    countismor el
    ikelyassoci atedwi thheri nfecti
    ouspr ocesst hanapot ent i
    alMI .TheS3 gall
    op
    suggest sleftventri
    cul ardysfunction, butdoesnothel pdi ff
    er ent
    iateacauseofherhypot ension
    i
    nt hi
    sset t
    ing.Theechocar diogram sept alwallmot i
    onmaybeaf fectedbyt heLBBB, butthe
    presenceofanewwal lmot i
    onabnor mal it
    yisofconcer nandi sthest rongesti ndicati
    onofa
    myocar dialeventr equi r
    ingur gentintervention.

    Quest
    ion:

    14. A75- year


    -oldwomanpr esent st othehospi t
    alafter2- 3daysoff eel i
    ngunwel l,
    fati
    gue,
    nausea, andvomi ti
    ng.Herbl oodpr essur ei
    s70/ 40mm Hgandt heelectrocar diogram
    demonst r
    atedQwavesandSTel evationsinleadsV1- V4 
    andST- segmentdepr essionsi nthe
    i
    nf er
    iorleads.Sheistakent ot hecar diaccathet eri
    zati
    onl aborat
    or yandf oundt ohavea
    thrombot i
    cocclusionofthepr oximall eftant
    eriordescendi ngartery.Percut aneouscor onary
    i
    nt er
    ventionisperformedwi thpl acementofadr ug-eluti
    ngst ent.Ventr
    icul ography
    demonst r
    atesanteri
    orhypoki nesi sandapi caldyskinesiswi thanej ect
    ionf ractionof35%on
    dopami ne.Laterthateveningt hepat i
    entbecomessuddenl ypale,diaphor etic,andi ncreasingl
    y
    hypotensive.Anewsyst olicmur muri shear datt heleftl
    owerst ernalborder .Nor epinephrineis
    start
    ed.Ast atechocardiogram i sor dered.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    ycauseofhersuddendet
    eri
    orat
    ion?

    a. Acut
    emi t
    ralregurgi
    tati
    on.
    b. Lef
    tventr
    icul
    arpseudoaneur ysm f
    ormat
    ion.
    c. Vent
    ri
    cularseptaldefect
    .
    d. Myocardi
    alfreewallruptur
    e.
    e. Ri
    ghtventri
    culari
    nfarcti
    on.

    Answer
    :

    14. c. Vent
    ri
    cul
    arsept
    aldef
    ect
    .

    Whi l
    elesscommont hani npriorer as,mechanicalcompl i
    cationsaf t
    erat r
    ansmur almyocar di
    al
    i
    nfarction(MI )sti
    lloccur ,
    especi allyinthosewithal ate-presentingMI .I
    nt hi
    spatient,sudden
    hemodynami cdet eri
    or ati
    oni ntheset ti
    ngofal ate-presenting,leftanter
    iordescending(LAD) -
    rel
    atedMIwi thanewwel l-heardmur murismostconsi stentwi thanacut eventr
    icularseptal
    defect.Whi l
    eLADi nf
    ar cti
    oncanbeassoci atedwi t
    hacut emi tralregurgi
    tati
    on(MR) ,the
    mur murofacut eMRi squitedifficulttoheargivenrapi dequal i
    zationofchamberpr essures,
    andt hislesi
    oni susual lyassociat edwi t
    hflashpulmonar yedemaandhypoxemi a.Inaddi t
    ion,
    ther
    ei sdualbl
    oodsuppl
    ytot
    heanterol
    ater
    alpapi
    ll
    arymuscle,whi
    let
    hepost
    eromedi
    al
    papil
    larymusclehasasi
    ngl
    ebloodsupplyf
    rom whateverar
    ter
    ysuppl
    iest
    heinf
    eri
    orwal
    l.
     

    Freewal lr
    upt
    ureismostcommonl yassociatedwit
    hlate-presenti
    nglef
    tci
    rcumflex-
    relat
    edMI,
    al
    thoughi tmaybeassoci at
    edwi t
    hinfar
    cti
    oni nanyterri
    tor
    y.Thisisusual
    lyacatastr
    ophic
    compl i
    cati
    onassociatedwitheff
    usiononechocardiogram, unl
    esscontai
    nedbyt he
    pericar
    dium.Rightventr
    icul
    arinf
    arcti
    onisaconsequenceofpr oxi
    maltomidrightcoronary
    arteryoccl
    usi
    onandwoul dnotsuddenlypresenti
    nal atefashion.

    Quest
    ion:

    15. A72- year-oldmanwi thahi st


    oryofcor onar yar t
    erydisease(CAD) ,pri
    orper cutaneous
    coronaryi nt
    ervention( 16mont hsago)onaspi ri
    n81mgdai l
    yandcl opidogrel75mgdai lywas
    admittedt ohospital.Hehasnochestpai n.Hehaschr onicatri
    alfi
    bril
    lati
    on(AF)forwhi chhe
    takeswar fari
    n.Hewasadmi t
    tedfordizzi
    nessandf oundt ohaveanacut egastrointesti
    nal
    bleedandhypot ension.Hi swarfari
    nandbet a-blockersar eheld.Heisr esuscit
    atedwi thbl ood
    productsandf r
    eshf rozenplasmai sadmi ni
    stered.Anur gentendoscopydemonst r
    ateda
    gastri
    cul certhatiscaut eri
    zed.Atthet i
    meofadmi ssionhewast achycardicandanemi c.An
    elect
    rocar di
    ogram ( ECG)demonst ratedAFwi t
    har apidvent r
    icul
    arresponseandi nferolateral
    downsl oping1.5mm ST- segmentdepr essions.Att het i
    meofadmi ssion,atroponinTi s
    checkedandr eturnsat0. 08ng/ ml.Sixhoursl aterthet r
    oponi nTreturnsat0.13ng/ ml( cut-of
    f
    foracutemyocar dialinfar
    cti
    oni s0.1ng/ml ).

    Whichoft
    hef
    oll
    owi
    ngi
    sthebestnextbestst
    epi
    nthecar
    diovascul
    armanagementoft
    his
    pat
    ient
    ?

    a. Resumebeta-bl
    ocker
    s.
    b. Pr
    oceedwi t
    hcoronar
    yangiography.
    c. Resumeaspiri
    nandclopi
    dogrel.
    d. I
    niti
    ateahepari
    ndri
    p.
    e. Resumewar f
    ari
    n.

    Answer
    :

    15. a. Resumebet
    a-bl
    ocker
    s.

    Thispatientl
    ikel
    yhasat ypeIImyocar dialinfarction(MI )duetot heacut
    ebl oodloss,
    hypotension,andt achycardi
    aincreasi
    ngmyocar dialoxygendemandanddecr easi
    ngoxygen
    deli
    very.Hehasnochestpai n.Thispr esentationi snotconsi stentwit
    hat ypeIMI( acute
    coronarysyndrome) .Theut i
    li
    tyofchecki ngcar diacbi omarkersint hi
    ssetti
    ngwher etherei
    sa
    cl
    earet i
    ologyforthepat i
    ent'
    ssympt oms( acut ebloodl oss,hemodynami call
    ysignifi
    cant
    bleedi
    ng)i sl
    ow, yetfrequent
    lyresult
    si ncar diologyconsul tat
    ion. 

    Themosti mpor tantconsiderat


    ioni storestoreadequateoxygenat iont othemyocar di
    um
    throughbl oodr esusci
    tati
    on,and, oncest able,
    resumptionofr atecont rolmedicationsforat
    rial
    fi
    brill
    ation.Asthistroponinelevationisnotr el
    atedtoacutepl aquer upture,thereisnoutil
    it
    yf or
    i
    ni t
    iati
    onofant icoagulati
    onorcor onaryangi ography.Whileresumpt ionofaspi rin81mgdai ly
    i
    sappr opriat
    eaf t
    ergastroint
    estinal(GI)i
    nterventi
    on,giventhepat ient'
    sr equir
    ementf or
    war far
    in,theclopidogrelshouldbedi scontinuedgivenhisrecentGIbl eedandl engthoftime
    sincehi sstentplacement .Whilewar f
    arin(ortarget
    edant i
    coagul ants)shoul deventuall
    ybe
    r
    esumedforst
    rokeprophyl
    axi
    s,t
    heper-dayriskofst
    rokeissmallanditwouldber
    easonabl
    e
    t
    oholdr
    esumptionofanti
    coagul
    ati
    onuntili
    tiscl
    earthepati
    enti
    snol ongerbl
    eedi
    ng.

    Quest
    ion:

    16. A42- year


    - ol
    dwomani sbeingtreat
    edwi t
    hchemot herapy,i
    ncludingdoxor ubicin,f
    or
    recentlydiagnosedmet astat
    icosteosarcoma.Asidefrom legpainatthesi t
    eofhert umor ,she
    hasbeenwel landhasnosympt omswi thphysicalexert
    ion.Shehadbeenexer cisi
    ngr egularl
    y
    untilherrecentdiagnosis.Heroncologi
    stperf
    ormedabasel i
    neelectr
    ocar di
    ogram thatwas
    normal ,aswellasamut li
    gat
    edacqui st
    ionscanthatshowedal ef
    tventri
    cularejecti
    onf racti
    on
    of65%.

    Whichofthefol
    lowi
    ngstagesofhear
    tfai
    lur
    e,byAmer
    icanCol
    legeofCar
    diol
    ogy/
    Amer
    ican
    HeartAssoci
    ati
    oncri
    ter
    ia,
    doesshehave?

    a. St
    ageE.
    b. St
    ageA.
    c. St
    ageD.
    d. St
    ageC.
    e. St
    ageB.

    Answer
    :

    16. b. St
    ageA.

    Whil
    ethispat
    ientcurrentl
    yhasanor malhear
    t,shei
    sbeingtr
    eatedwit
    hanant hr
    acycl
    ine
    chemother
    apeuticagent.Exposuret
    opotenti
    all
    ycar
    diot
    oxiccancert
    herapyagent
    sis
    cl
    assi
    fi
    edasst ageAhear tfai
    lur
    e(HF).

    St
    ageA:AthighriskforHF,butwit
    houtstruct
    uralheartdi
    seaseorsympt
    omsofHF.
    St
    ageB:Str
    ucturalheartdi
    sease,
    butwithoutsignsorsympt omsofHF.
    St
    ageC:Str
    ucturalheartdi
    seasewithpr
    iororcurrentsymptomsofHF.
    St
    ageD:Refr
    actoryHFr equi
    ri
    ngspecial
    izedinter
    venti
    ons.

    Ther
    eisnoAmer
    icanCol
    legeofCar
    diol
    ogy/
    Amer
    icanHear
    tAssoci
    ati
    onst
    ageE.

    Quest
    ion:

    17. A42- year-


    oldwomani sevaluatedforacutelef
    tlowerextremit
    yischemia.Herpast
    medi
    calhist
    or yi
    ssigni
    fi
    cantforhypert
    ensionandchr onicmyelogenousleukemia.Her
    medi
    cati
    onsi ncl
    udeamlodipi
    ne,hydrochlorot
    hiazi
    de,ethi
    nylestr
    adiol
    /norgest
    rel
    ,andnil
    oti
    nib.
    Sheunder
    goessuccessfullef
    tfemoralarter
    yembol ectomywithrestor
    ationoffl
    ow.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    ycont
    ri
    but
    ingf
    act
    ort
    othedevel
    opmentofhert
    hrombus?

    a. Oralcontracepti
    ve.
    b. Tyrosinekinaseinhibi
    tor.
    c. Hypertension.
    d. Vascularspasm.
    e. Atheroscl
    er ot
    icplaqueruptur
    e.
    Answer
    :

    17. b. Tyr
    osi
    neki
    nasei
    nhi
    bit
    or.

    Certai
    nBCR- ABLt yrosi
    neki naseinhibitorsareassociat
    edwi thani ncr
    easedri
    skoft hromboti
    c
    events.Thesecond-andt hird-generationagents,suchasnilotinibandponat i
    nib,havea
    higherriskofthiscompl i
    cat i
    on.Ponat i
    nibhasblackboxwar ningr egar di
    ngcardiovascul
    ar,
    cerebrovascular,andperipher alvasculararter
    ialthr
    ombosis.Al thought hi
    spati
    enthas
    hypertension,atherage, t
    her i
    skofpl aqueruptureandper i
    pher althrombosisi
    sl essli
    kely.
    Spasm issi mil
    arlylessli
    kelyt ooccuri nthispatient
    .Oralcontracept i
    vesaremostcommonl y
    associatedwi t
    hvenoust hr ombosi s.

    Quest
    ion:

    18. A54- year-ol


    dmanwi t
    hmet astat
    icprostatecancerunder
    goesradi
    calprostatect
    omy.
    Heisstart
    edonadj uvantther
    apywiththeandr ogen-depri
    vat
    ionagentl
    euprol
    ide.Hehasno
    hist
    oryofhyper
    tension,di
    abetes,
    orhyperli
    pidemia.Hei sanonsmoker.Arecentli
    pidprofi
    le
    showedat ot
    alcholester
    olof166mg/ dlandlow- densit
    yli
    poprot
    einchol
    ester
    olof85mg/ dl
    .

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    eti
    mingf
    orf
    utur
    ecar
    diovascul
    arr
    iskassessment
    ?

    a. 2year
    s.
    b. 1month.
    c. 1year
    .
    d. 5year
    s.
    e. 3months.

    Answer
    :

    18. e. 3mont
    hs.

    Patient
    sr eceivi
    ngandr ogen-depri
    vati
    ontherapyshouldbeevaluatedper
    iodi
    cal
    lyforblood
    pressure,li
    pids,andfastingglucose.I
    ngeneral,
    patient
    sshouldbeseenbyt hei
    rphysician
    within3-6mont hsofinit
    iati
    onoftherapybecausethefi
    rstef
    fectsofandr
    ogen-deprei
    ation
    therapytypicall
    yoccuri nthi
    st i
    mef r
    ame.

    Quest
    ion:

    19. A75- year-oldmanhasahi storyofcoronaryart


    erydisease,stat
    us/postpercutaneous
    coronaryi
    nterveniontotheri
    ghtcoronar yar
    tery2yearsagof orexert
    ionalangina,mil
    dCl assII
    systol
    icheartfai
    lure,di
    abet
    es,hyperl
    ipidemia,andarecentdiagnosisofmul t
    iplemyeloma.  

    Heret
    urnstothecardi
    ologycl
    ini
    ctodayafterarecentemer
    gencyroom vi
    sitf
    orr
    ightcal
    fpai
    n
    andswell
    ing.Hewasdiagnosedwithadeepvei nthr
    ombosisoft
    herightl
    owerextr
    emityand
    i
    nit
    iat
    edonant i
    coagul
    ationwi
    thri
    varoxaban. 
    Hiscardi
    ovascularmedicat
    ionsincludemet oprol
    olsuccinat
    e25mgoncedai l
    y,met
    for
    min
    1000mgoncedai ly,
    andali
    rocumab( proprotei
    nconvertasesubti
    li
    sin–kexintype9[
    PCSK9]
    i
    nhibit
    or),
    ivabradi
    ne5mgt wi cedai
    ly,sacubitr
    il
    /val
    sart
    an50mgt wicedaily,
    andaspir
    inonce
    dail
    y.Hismultipl
    emyelomai sbeingtreat
    edwi thpredni
    sone,thal
    idomide,andasneeded
    ondansetronfornausea.
     

    Hisbloodpr essureis120/70mm Hg,heartrate70bpm, oxygensaturati


    on99%onr oom ai
    r.
    Onexami nat
    ion,hisjugul
    arvenouspr
    essureis2cm abovet hecl
    avi
    clewhi l
    elyi
    ngat45
    degrees.Nor malS1andS2 wit
    hnomur murs,rubs,
    orgallops.Lungsarecleartoauscult
    ati
    on
    bi
    lat
    er al
    ly.Hehasasymmet ri
    cedemainther i
    ghtlowerextremit
    ywithintactpul
    ses.

    Whichoft
    hefol
    lowi
    ngmedi
    cat
    ionsi
    sassoci
    atedwi
    thi
    ncr
    easedr
    iskofvenous
    t
    hromboemboli
    sm?

    a. Sacubit
    ril
    /val
    sart
    an.
    b. I
    vabradine.
    c. Ondansetron.
    d. Ali
    rocumab( PCSK9)i
    nhi
    bit
    or.
    e. Thali
    domi de.

    Answer
    :

    19. e. Thal
    idomi
    de.

    Thecor rectansweri st hali


    domi de.Orali
    mmunomodul ator
    ydrugs, suchast halidomideand
    l
    enalidomi de, haveadocument edassoci
    ationwi thincr
    easedr i
    skf orvenoust hromboembolic
    events.Theot hermedi cati
    onsar enotassociatedwi thincr
    easedr i
    skoft hromboembol i
    sm.
    Pati
    entswi t
    hmul tiplemyel omaar egenerall
    yol derandmayhavepr e-exist
    ingcar diac
    conditi
    ons.Ther efor e,theymayber eferr
    edt othecar di
    ologyclinicforf oreval uati
    onoflower
    extr
    emi tyedema, asi spr esentinthiscase,orfordyspneai ntheeventofvenous
    thr
    omboembol i
    sm l eadi ngtopul monaryembol ism.Hence, cardiologistsshoul dbeawar eof
    thi
    spot entialsideef fectoft heseagentsusedt otreatmul t
    ipl
    emyel oma.Nei therivabradi
    neor
    sacubitri
    l/valsartanhavebeenshownt oincreaser i
    skofvenoust hromboembol ism.

    Quest
    ion:

    20. Your eviewanarti


    clet
    hatsuggestsanovelserum biomarkerexcl
    udesthepresenceof
    cor
    onaryar
    terydi
    sease(CAD).I
    nthearti
    cle,ser
    um samplesofthenovelbiomarkerare
    cor
    rel
    atedwit
    hsubsequentangi
    ographi
    callydefi
    nedpresenceorabsenceofCAD.

    Ther
    esul
    tsoft
    hisst
    udyar
    edepi
    ctedi
    nFi
    gur
    e1.

    Whichoft
    hef
    oll
    owi
    ngi
    sthecor
    rectnegat
    ivepr
    edi
    cti
    veval
    ue(
    NPV)oft
    hebi
    omar
    keri
    nthi
    s
    st
    udy?
    a. 67%.
    b. 15%.
    c. 90%.
    d. 20%.
    e. 53%.

    Answer
    :

    20. c. 90%.

    Thecor
    rectansweri
    s90%.

    NPViscalcul atedbythef ormula:(TrueNegat ives)


    /(TrueNegat i
    ves+FalseNegati
    ves)
    .
    Inthiscase45/ (5+45)=0. 9or90%.
    67%represent sthesensitivi
    tyofthet est:(Tr
    uePositives)/
    (TruePositi
    ves+Fal
    se
    Negat
    ives).
    10/(10+5)=67.
    53%represent sthespecifici
    tyofthet est:(Tr
    ueNegat ives)
    /(TrueNegati
    ves+False
    Posi
    ti
    ves).
    45/(45+40)=0. 53.
    15%represent stheprevalenceoft hedi sease:(Tot
    alwi thDisease)
    /(Tot
    alSampl
    e).
    15/100=0. 15.
    20%r epresentsthepositi
    vepredi
    cti
    vevalueofthetest
    :(Tr
    uePositi
    ves)
    /(TruePosi
    ti
    ves
    +FalsePosi ti
    ves).
    10/(
    10+40)=0. 2.
    Consequentl
    y, fr
    om thisstudy,wewouldconcludethatthi
    sbiomarkerhasahighNPV, and
    thosepati
    entswhoar ebiomarkernegati
    veareveryli
    kelyt
    onothaveangiographical
    lypr
    oven
    CAD.

    Quest
    ion:

    21. Youar easkedt oseea19- year- ol


    dmanaspar tofhi
    sscreeningphysicalpri
    orto
    playi
    ngcol l
    egebasket ball
    .Hehasnopastmedi calhistoryandhasbeenpl ayi
    ngbasket ballat
    thehighschooll evelfor4year s.Herepor tsnochestpai nordyspnea, andcankeepupwi thhi
    s
    teammat esduringdr i
    ll
    sandcondi ti
    oni ngexercises.Hehasnopal pitat
    ions.Hedoesnot
    smoke.Hi sfamilyhi storyisnegati
    vef orarrhythmia, congenit
    alheartdisease,aneur
    ysm, or
    unexplaineddeat hs.Onexam, heis6f eet4i nchest allandweighs190pounds.Vi t
    alsignsar e
    heartrate55bpm, bloodpr essure115/ 65mm Hg, andoxygensat urati
    on99%.Jugul arvenous
    pressureisnormalandhehasnocar diacmur mur s.Lungsar eclearandhehasno
    muscul oskel
    etalabnor mali
    ti
    es.

    Whi
    choft
    hef
    oll
    owi
    ngst
    udi
    esdoyouper
    for
    m bef
    orecl
    ear
    inghi
    mforspor
    tspar
    ti
    cipat
    ion?

    a. El
    ectrocardiogr
    am.
    b. ChestX- r
    ay.
    c. Echocardiogram.
    d. Nofurthertesti
    ngneeded.
    e. Exerci
    setreadmill
    test
    ing.

    Answer
    :

    21. d. Nof
    urt
    hert
    est
    ingneeded.

    Cardiovascularscreeningofathletesi
    sperfor
    medinonlythreecountr
    ies:theUni t
    edSt at
    es,
    It
    aly,andI sr
    ael.I
    nt heUnitedStates,t
    hescreeni
    ngconsist
    sofat hor
    oughhi storyanda
    compl etephysicalexam.Ital
    yhasadvocat edfort
    headditi
    onofanelectrocardiogram (
    ECG),
    andIsr aelhasadpot edthi
    sstrategytoo.Ther
    eissti
    llaf
    airamountofdebat eaboutt heopti
    mal
    str
    ategy.  

    Whenconsi deri
    ngt headditi
    onoft heECG, onemustconsidertheresourcesi
    nvolvedandthe
    i
    mpactoff alsel
    yposi ti
    vetest
    ing.Af ewimpor t
    antpoi
    ntst
    hatsuppor tt
    heuseofhi stor
    yand
    physicalonlyare:1)t heuseofECGsasascr eeni
    ngtesti
    nheal t
    hypopulati
    onshasnotbeen
    proven,2)thebenef it
    sofECGscr eeninghaveonlybeendemonst rat
    edinonedat abasefr
    om a
    smallregioni nIt
    aly,and 3)theser esul
    tshavenotbeenrepli
    catedinotherareas.
     

    Ther ef
    ore,thecur
    rentrecommendat i
    onsint heUni
    tedStat
    esforscreeningofathletesi
    ncl
    udea
    thoroughhi st
    oryandphysi calexaminati
    on( Ameri
    canHeartAssociati
    on's14-pointscr
    eeni
    ng
    guideli
    nes;Amer i
    canAcademyofPedi at
    rics’Pr
    epart
    ici
    pat
    ionPhysicalEvaluati
    on).Mass
    screeningofyoungat hlet
    eswi thECGsi snotrecommended.Similarl
    y,i
    nanasympt omati
    c
    patientwithnosignif
    icantfamilyhist
    ory,exerci
    setr
    eadmil
    ltest
    ing,chestX- r
    ay,and
    echocar di
    ographyarenotnecesssar y.
    Quest
    ion:

    22. A19- year


    - ol
    dmancomest oyouf orasecondopi nionaboutpar ti
    cipati
    ngincollege
    basketball.Hi sbrotherwasr ecentlydiagnosedwi t
    hhyper tr
    ophi ccardi
    omyopat hy(HCM)af t
    er
    hehadchestpai nwhi lerunning.Thepat ienthasbeengenet icall
    yscreenedandi sfoundt o
    havehi sbr other'
    sdi sease-causingmut ation.Yourpat i
    entunder wentechocar di
    ography, which
    wasnor mal .Therewasnol eftventri
    cularhyper tr
    ophyandnor est
    ingorprovokableleft
    ventr
    icularout fl
    owt ractgradient.Cardiacmagnet i
    cresonancedemonst ratednomyocar dial
    fi
    brosis.Yourpat ienthasneverhadsympt omsandhaspl ayedonhi shighschoolbasket ball
    team wi t
    houti nci
    dent .Thereisnof ami l
    yhi storyofsuddencar di
    acdeath.Hisprimarycar e
    physicianr ecommendedt hathenotpar t
    icipateincoll
    egeat hleti
    cs.Thepat i
    entisanxi
    oust o
    playandcomest oyouf orasecondopi nion.

    Whi
    choft
    hef
    oll
    owi
    ngdoyour
    ecommend?

    a. Al
    lowhimtoparti
    cipateaf
    teri
    niti
    ati
    onofbeta-
    blockers.
    b. Al
    lowhimtoparti
    cipateaf
    ter48-hourHolt
    ermonitor
    ingshowsnoar rhyt
    hmi
    a.
    c. Cl
    earhimforcompetiti
    vesport
    s. 
    d. Al
    lowhimtoparti
    cipateaf
    teri
    mpl ant
    ati
    onofcardi
    overter
    -def
    ibr
    il
    lat
    or.
    e. Noclear
    anceforpart
    ici
    pati
    ngincompet i
    ti
    vesport
    s.

    Answer
    :

    22. c. Cl
    earhi
    mforcompet
    it
    ivespor
    ts.
     

    Patient swi t
    hadiagnosisofhyper t
    rophi ccardiomyopat hy(HCM)andcl inicalexpressi onofthe
    phenot ypeshouldnotpar t
    ici
    pateincompet it
    ivesports,exceptf orlow- i
    ntensityactivities,
    i
    ndependentofage, sex,magnitudeofl eftventri
    cularhypertr
    ophy( LVH) ,specif
    icmut ation,
    presenceorabsenceofLVout f
    lowtractobst ructionatrestorexer cise,fi
    br osi
    soncar di ac
    magnet i
    cresonance(CMR) ,absenceofpr i
    orsympt oms, andhi storyofmyect omyorsept al
    ablation.Phar macologicagentsandi mpl antablecardiover
    ter-def i
    bril
    lat
    or sshouldnotbe
    uti
    li
    zedf orthesolepurposeofpar t
    ici
    pat ioninhi gh-i
    ntensit
    yspor t
    s.Pat i
    ent swhoar egenot ype
    -posi t
    iveandasympt omaticwithnoevi denceofLVHbyechocar di
    ogram andCMRi nt he
    absenceofaf amil
    yhistoryofHCM- relatedsuddendeat hhavenocont r
    aindicati
    ont o
    participation(Cl
    assIIa).

    Quest
    ion:

    23. An85- year-oldwomani sseeni nthehospi talforapr eoperativecardi


    acevaluat
    ion.She
    wasadmi t
    tedear l
    ierinthedaywi t
    haf emor alheadf racturesustaineddur i
    ngawi t
    nessed
    mechani calf
    al lonherwaybackf r
    om thegym.Hercar diacexami nationisnotabl
    eforanor mal
    S1 andsoftS2, anda3/ 6systoli
    cmur murt hatr adi
    atest ohercar oti
    dsand2/ 6api
    calsystol
    ic
    mur mur.Herj ugul arvenouspr essureisnotel evated.Theel ectrocardiogr
    am showsshei sin
    si
    nusr hythm, withleftventr
    icularhypertr
    ophy.Labor at oryvaluesrevealtroponi
    nis0.01ng/ ml
    ,
    creati
    nineis1. 7mg/ dl,andbrainnatri
    ureticpept i
    deis109pg/ ml.

    Theor
    thopedi
    csur
    geonwoul
    dli
    ket
    otakehert
    osur
    ger
    yassoonaspossi
    ble.Abedsi
    de
    echocar
    diogr
    am i
    sobt
    ained(
    Videos1and2)
    .

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    enextst
    ep?
     

    ht
    tp:
    //cdn.
    mycr
    owdwi
    sdom.com/acc/questions/9dd124a7-3ae1-
    4cf6-bc9f
    -
    1cf066238bf4.mp4
    ht
    tp:
    //medi
    a.mycrowdwi
    sdom.
    com.
    s3.amazonaws. com/ acc/accsap9/
    Questi
    on1524%20Vi
    deo
    2.
    mp4

    a. Per
    for
    mr ightandleftheartcathet
    eri
    zati
    on.
    b. Per
    for
    m coronarycomput edt omographyangiography.
    c. Ref
    erforvalver
    eplacementpr iort
    ohipsurgery.
    d. Per
    for
    m myocar di
    alperfusionimaging(si
    ngle-photonemi
    ssi
    oncomput
    edt
    omogr
    aphy)
    .
    e. Pr
    oceedwi t
    hhipsur gery.

    Answer
    :

    23. e. Pr
    oceedwi
    thhi
    psur
    ger
    y.

    Thispat i
    enthaswhatappearstobeasympt omaticsever
    eaor t
    icst
    enosis.Whil
    ethemost
    approriatel
    ong-ter
    mtherapyfortheaorti
    cstenosi
    smayi nfactbeaort
    icvalverepl
    acement
    (ei
    thertranscut
    aneousorsurgical
    ),shehasahipfract
    urethatmaywellrequir
    emor eurgent
    att
    ention. 

    Af r
    ankdi scussionwi t
    ht hepat i
    entandwi tht
    hesur gicalandanesthesiat
    eamsi sappr opri
    ate.
    Stresstestinginanact ivewomenf orpreoperati
    ver i
    skassessmentisunneccessar y.I
    nvasive
    cardiaccatheterizati
    on,includi
    ngcor onaryangiographyandmeasur ementofi nt
    racardiac
    pressures,maybehel pfulformanagi ngahemodynami cal
    lyunstabl
    epatient
    ,butwoul dnotbe
    neededi nthispat i
    ent(asidefrom cardiaccatheter
    izati
    ontodef i
    necoronaryanatomypr iort
    o
    valvereplacement ).Simil
    arly,acoronarycomput edt omorgraphyangiogr
    aphywoul daddl it
    tle
    tothispatient'
    smanagement .

    Quest
    ion:

    24. A70- year-


    oldreti
    redinternistpresent
    st oyourofficeaskingforyouropinionabouther
    ri
    skofhavingacardi
    accompl i
    cationfrom anupcomi ngf emoral-popli
    tealbypasssurger
    y
    bei
    ngperformedtorel
    ievesever eclaudicati
    on.Indiscussingthis,shetellsyouthatsherecal
    ls
    usi
    ngtheGol dmanri
    skscor ewhenshepr act
    icedtoassessoper at
    iverisk.

    Whichoft
    hefoll
    owingwouldbet
    hemostaccur
    atechar
    act
    eri
    zat
    ionofmul
    ti
    var
    iabl
    etool
    sfor
    pr
    eoperat
    iver
    iskassessment
    ?

    a. Val
    idat
    edmul
    ti
    var
    iabl
    eri
    sk-
    predi
    cti
    ont
    ool
    srecei
    veaCl
    ass1i
    ndi
    cat
    ioni
    nthe
    pr
    eoper
    ati
    veassessmentofnoncar
    diacsur
    ger
    y.
    b. Nat
    ri
    uret
    icpept
    idet
    est
    inghassuppl
    ant
    edt
    heuseofmul
    ti
    var
    iabl
    eri
    skt
    ool
    sint
    he
    pr
    eoper
    ati
    veset
    ti
    ng.
    c. TheGol
    dmanr
    iskscor
    eremai
    nst
    hepr
    efer
    redmul
    ti
    var
    iabl
    escor
    eforpr
    eoper
    ati
    ver
    isk
    assessment.
    d. Dobutaminestr
    essechocar
    diogr
    aphyhassuppl
    ant
    edt
    heuseofmul
    ti
    var
    iabl
    eri
    skt
    ool
    s
    i
    nthepr
    eoper
    ati
    veset
    ti
    ng.
    e. Sever
    almul
    ti
    var
    iabl
    eri
    skscor
    esar
    enowavai
    labl
    eforpr
    eoper
    ati
    ver
    iskassessment
    .

    Answer
    :

    24. e. Sever
    almul
    ti
    var
    iabl
    eri
    skscor
    esar
    enowavai
    labl
    eforpr
    eoper
    ati
    ver
    isk
    assessment
    .

    Ther
    eareseveralmult
    ivari
    abl
    etoolsavail
    ableforpreoper
    ati
    veriskassessment.Theseincl
    ude:
    1)Ameri
    canCollegeofSurgeonsNationalQuali
    tyImprovementProgram (ACS-NSQIP)surgi
    cal
    ri
    skcal
    culat
    or,
    2)RevisedCardiacRiskIndex(RCRI),and3)VascularSt
    udyGr oupofNew
    Engl
    and(VSGNE)r i
    skindex.
     

    TheACS- NSQIPof fersaWeb- basedcal culat


    or(www. r
    iskcal
    culator.
    facs.
    org).Recent
    guideli
    nesst at
    et hataval i
    datedr i
    sk-predicti
    ontoolcanbeusef ulinpredicti
    ngtheriskof
    perioperati
    vemaj oradver secardiacevent sinpati
    entsundergoingnoncar diacsurgery(Class
    II
    a,notCl assI).Neitherdobutami nestressechocar di
    ographynornat ri
    ureti
    cpeptidetesti
    ng
    hasr epl
    acedt heser iskscores.Inpatientswithoutacar di
    achistorywhohaveno
    cardiopulmonar ysympt oms, nofurtherr i
    skstrat
    if
    icat
    ionisnecessary.TheGol dmanr iskscore
    hasbeensuppl antedbyt hesemor emoder ntool
    s.

    Quest
    ion:

    25. A60- year -


    oldmanhasahi storyofabaremetalst
    entimplant
    edinhismidlef
    tant
    eri
    or
    descendi
    ng3year sagoforangina.Sincethenhehasbeenchest-pai
    nfree.Heissomewhatof
    avaguehistorian, buthi
    swife,whoisi ngoodhealt
    h,conf
    ir
    mshewasabl etokeepupwit
    hher
    astheywalkedt hr
    ought heshoppingmal lovert
    heholi
    dayseason,andoftenhel
    pswit
    h
    vacuumingthei rhouse.Heisanavi dgolferandcanwalkan18-holecourse. 

    Onemont hago,hehadmil
    dhemopt ysi
    sandwasf oundtohavea1-cm lungcancerintheright
    upperlobe.Hi
    soncol
    ogi
    strepor
    tsthatheisanexcell
    entcandi
    dat
    eforcurat
    iveresect
    ion.The
    pati
    entnowpresent
    stoyouforpreoper
    ati
    veclear
    ance. 

    Onexami nati
    on,hi
    sbloodpr essureis120/80mm Hg, heartrate74bpm, andbodymassi ndex
    35kg/m2.Hehasnor malS1 andS2 heartsoundswit
    hnoS3  ormur mur,cl
    earlungs,noedema,
    andotherwisehasanormalexami nati
    on.Onelect
    rocardi
    ography, t
    hereisl
    eftvent
    ricul
    ar
    hyper
    trophywi t
    hstr
    ain,butotherwiseiti
    snormal.Hiscreati
    nineleveli
    s1.2mg/ dl
    .

    Whi
    choft
    hef
    oll
    owi
    ngwoul
    dyour
    ecommendaspar
    tofyourpr
    eoper
    ati
    vepl
    an?

    a. Left
    -heartcatheteri
    zat
    ion.
    b. Nofurthertesti
    ngisneeded.
    c. Dobutaminest ressechocardi
    ography.
    d. Exerci
    setreadmi l
    lstr
    esstest.
    e. Exerci
    senucl earperf
    usiontest
    .

    Answer
    :

    25. b. Nof
    urt
    hert
    est
    ingi
    sneeded.
    TherecentAmer i
    canCol legeofCar diology/Amer icanHear tAssociati
    onguideli
    nerecommends
    nofurt
    herpreoperativetesti
    ngi fpati
    ent shavemoder ateorgr eat
    er(≥4METS)f uncti
    onal
    capaci
    ty.Addit
    ionall
    y,nof urtherpreoper at
    ivetestingisadvisedifitwil
    lnotchange
    managementdeci sions.Inthiscase, eveni ft
    hepat i
    entwasf oundt ohavecoronarydisease,
    rout
    inecoronaryrevascularizati
    onbef orenoncar diacsur ger
    yexclusivel
    ytoreduce
    peri
    operat
    ivecardiacevent sisNOTi ndi cat
    ed( ClassI I
    I:nobenefi
    t).

    Quest
    ion:

    26. A29- year


    -ol
    dwomanwi thahistor
    yoftr
    icuspi
    datresi
    awhounder wentaFontan
    procedur
    eyearsagoisconsi
    der
    ingbecomingpregnantagai
    nsthercar
    diol
    ogist
    'sadvi
    ce.

    I
    fshei
    sabl
    etosust
    ainapr
    egnancyi
    ntot
    het
    hir
    dtr
    imest
    er:
     

    Whi
    choft
    hef
    oll
    owi
    nghemodynami
    cchangeswi
    llmostl
    ikel
    yoccuri
    nthi
    spat
    ient
    ?

    a. Systemicvascul arresi
    stancewi lldecrease.
    b. Fontanejecti
    onf racti
    onwi l
    lincrease.
    c. E/E'rat
    iowi l
    ldecrease.
    d. Leftventr
    icularmasswi lldecrease.
    e. Leftventr
    icularejecti
    onfract
    ionwi l
    ldecrease.

    Answer
    :

    26. e. Lef
    tvent
    ri
    cul
    arej
    ect
    ionf
    ract
    ionwi
    lldecr
    ease.

    Manywomenwi thst ructuralheartdiseasereachr eproduct


    iveageandcont emplate
    mot herhood.Pregnancyi nducesandr equiresmaj orhemodynami cchanges.Pregnantwomen
    withstructuralhear tdiseasemayhavear educedcar diacreserve.Cardiacoutput,
    stroke
    volume, lef
    tventricularmass, andE/E' r
    ati
    oi ncr
    easesi gni
    fi
    cantly,andejecti
    onfracti
    onand
    fr
    act i
    onalshor t
    eningdecr easedur i
    ngpr egnancy.Cor net
    teandcol leaguesshowedt hatt
    here
    wasast ati
    sti
    callysi gnif
    icantdiff
    erenceinej ect
    ionfracti
    on,fr
    actionalshort
    ening,andE/E'r
    ati
    o
    beforeandaf terpr egnancy.

    Quest
    ion:

    27. A36- year-oldwomanunder goesinvitr


    ofer
    til
    izati
    onandbecomespregnantwi
    thtwins.
    Herpregnancyi scompl i
    cat
    edbygest ati
    onalhyper
    tension.Shei
    str
    eatedwit
    hbeta-bl
    ocker
    s
    anddeli
    verst woheal t
    hysons.Duri
    ngt henextmonths, herbl
    oodpr
    essurer
    eturnst
    onormal,
    andshenol ongert akesanymedicati
    ons.

    Whi
    choft
    hef
    oll
    owi
    ngi
    srecommendedf
    orherf
    oll
    ow-
    up?

    a. Surveill
    anceechocar di
    ogr
    aphy.
    b. Ongoi ngcoronaryarter
    ydiseaser
    iskf
    act
    orscr
    eeni
    ng.
     
    c. Dai
    lyaspi ri
    n.
    d. Cardiacrehabil
    itat
    ion.
    e. Geneticscreening.
    Answer
    :

    27. b. Ongoi
    ngcor
    onar
    yar
    ter
    ydi
    seaser
    iskf
    act
    orscr
    eeni
    ng.
     

    Womenwi thahistoryofgest
    ati
    onalhypert
    ensionorpr e-ecl
    amspi aareatatwofoldincreased
    ri
    skofcardi
    ovasculardi
    seaseandshouldhaveaggr essiveri
    skf actorscr
    eeni
    ngf orcoronary
    art
    erydi
    seaseastheyage.Nei t
    hergeneti
    cscreeni
    ngf ormut at
    ionsorechocardiographyar e
    i
    ndicat
    ed.Alt
    houghhercar di
    ovascul
    arri
    skiselevat
    ed, prophyl
    act i
    caspiri
    nisnotindicated.

    Quest
    ion:

    28. A27- year


    -oldwomani sseenint heemergencydepar t
    ment(ED)forseveraldaysof
    progressivedyspnea, orthopnea,paroxysmalnocturnaldyspnea,
    andper i
    pheraledema.She
    hadasi mi l
    arpresentationtotheED3weeksagoandwasgi venaprescri
    pti
    onfor40mgdai l
    y
    offurosemideandmet oprol
    ol12.5mgt wicedai
    ly.Sheis25weekspr egnant.Vi
    talsignsare
    heartrate102bpm, bloodpr essure100/60mm Hg, andoxygensaturat
    ion100%on2l i
    ter
    s
    nasalcannul aoxygen. 

    Physicalexami nati
    ondemonst r
    ateselevatedjugularvenouspr essuretot heangleofthe
    mandi blelyingat45degr ees,aregulartachycardi
    cr hythm wi
    tha1/ 6hol osystoli
    cmur murat
    theapexwi tha2/ 4diastolicmurmuratt heapex;anopeni ngsnapi spresent .Ther
    eare
    bil
    ateralralesfortwo- t
    hirdsofthepost eri
    orlungfiel
    dswi thtr
    aceper ipheraledema.
    Echocar di
    ogr am revealsnor mallef
    tventri
    cularfunctionwithameanmi tr
    alvalvegradi
    entof16
    mm Hgwi t
    ht ri
    vialmitr
    alr egur
    git
    ation.Valveismobi lewithminimalcal ci
    ficati
    on.The
    esti
    mat edr ightventri
    cularsystol
    icpressureis50mm Hg.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthebestnextst
    epi
    nhermanagement
    ?

    a. Del
    iverynow, t
    henmitralvalverepl
    acementsurgeryshort
    lyt
    her
    eaft
    er.
    b. Mit
    r alval
    verepl
    acementsur gery.
    c. Percutaneousmitr
    alcommi ssurotomy(val
    vuloplast
    y).
    d. Percutaneousmitr
    aledge-to-edgemitr
    alvalverepair(
    Mit
    ra-
    Cli
    p).
    e. Cont i
    nuemedicalt
    herapy.

    Answer
    :

    28. c. Per
    cut
    aneousmi
    tr
    alcommi
    ssur
    otomy(
    val
    vul
    opl
    ast
    y).

    Percutaneousmitralval
    vecommi ssur
    otomy(valvul
    oplasty)i
    saCl assIIar
    ecommendat i
    onin
    theabsenceofsignifi
    cantmitralregur
    git
    ati
    onandf avorableanatomicfeat
    uresinthe2014
    Amer i
    canCollegeofCardiol
    ogy/ Ameri
    canHear tAssociat
    ionvalvul
    arheartdiseaseguidel
    ines
    f
    orpr egnantpati
    entswithClassI I
    IorI
    Vheartfail
    uresympt omsdespitemedicaltherapy. 

    Cardiothoraci
    csurgerycarri
    esa30%r iskoff et
    allossandi sthereforeavoi
    dedduring
    pregnancy, i
    fpossi
    ble.Deli
    veryandthensur gerywoul dnotbeopt i
    malmanagementatt his
    point
    , unlessforaspecif
    icobstetr
    ici
    ndicati
    onduet oissuesrelatedtoprematur
    it
    y.Her
    sympt omshavepr ogresseddespitedi
    uretictherapy,thus,conti
    nuedmedi calt
    herapywould
    notbet hebestchoice.Percutaneousmitraledge-to-edgemi tr
    alvalverepai
    r(Mit
    raCli
    p)isnot
    i
    ndi
    cat
    edast
    hepat
    ienthasmi
    tr
    alst
    enosi
    snotmi
    tr
    alr
    egur
    git
    ati
    on.

    Quest
    ion:

    29. A32- year-ol


    dwomanwi t
    hahi st
    oryofbicuspidaort
    icvalvepresentsf
    orevaluationof
    aorti
    cstenosis.Sher eport
    ssomer ecentdyspneawi t
    hexerti
    on,buthasnothadsyncopeor
    chestpain.Echocardiographyrevealsnormalleftventr
    icul
    arfuncti
    on,andameangr adient
    acrossheraor t
    icvalveof52mm Hg.Herascendi ngaortaisnormalinsize.Shei
    sr ecently
    mar r
    ied,andisanxioust ostar
    taf amily.

    Whi
    choft
    hef
    oll
    owi
    ngdoyour
    ecommend?

    a. Exercisetreadmil
    ltest
    ing.
    b. Surgicalaorti
    cvalverepair
    .
    c. Aorti
    cval verepl
    acementpr i
    ortopregnancy.
    d. Transcatheteraorti
    cvalverepl
    acementpriort
    opr
    egnancy.
    e. Noint er
    ventionpri
    ortopregnancy.

    Answer
    :

    29. c. Aor
    ti
    cval
    ver
    epl
    acementpr
    iort
    opr
    egnancy.

    ThispatienthasaCl assIindi
    cati
    onforaor t
    icvalver epl
    acement(AVR)becauseshei s
    sympt omat i
    cwithsevereaort
    icstenosis(AS)andwant stobecomepr egnant
    .Valveselect
    ion
    i
    nt hi
    spopul ati
    oniscontroversi
    alandallpatientsshouldbecounsel edbycar
    diol
    ogistswith
    experti
    sei nval
    vularheartdi
    seaseaboutt herisksandbenef i
    tsofallopt
    ionsf
    oroperative
    i
    ntervention,i
    ncl
    udingmechani calprost
    hesis,bioprosthesi
    s,andtheRossprocedure.
     

    AVRi sanapplicabl
    eopt
    ionforsomepatientswit
    haorti
    cvalveregur
    gitat
    ion,
    butisnotan
    optioninpat
    ientswit
    hAS.Transcat
    heterAVRisnotapprovedforpati
    entswithbicuspi
    dval
    ve,
    andt hi
    spati
    enthasaverylowSocietyofThoraci
    cSurgeonsscore.Treadmil
    ltesti
    ngisnot
    recommendedbecauseshei ssymptomat i
    cwithsever
    eAS.

    Quest
    ion:

    30. A38- year-ol


    dmanwi
    thmetastat
    ict
    esti
    cularcancerunder
    goessurgi
    calresect
    ion,
    foll
    owedbyt
    reat
    mentwit
    haci
    spl
    atin-
    basedregimen.Hehasnoot hersi
    gnif
    icantmedical
    histor
    y.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    ycar
    diovascul
    arcompl
    icat
    ionofhi
    schemot
    her
    apy?

    a. Venoust hrombosi s.
    b. Arter
    ialthrombosis.
    c. Cardiomyopat hy.
    d. Premat ureatheroscl
    erosi
    s.
    e. Hyper t
    ension.
    Answer
    :

    30. e. Hyper
    tensi
    on.

    Thegreatestcardi
    ovascul arr
    iskofplatinum-basedchemother
    apyisassociat
    edwiththe
    devel
    opmentofhyper tension.Ar t
    eri
    althromboti
    criski
    sassoci
    atedwithtyr
    osineki
    nase
    i
    nhibit
    orssuchasni l
    otinib.Cardiomyopat hi
    esaremostcommonl yassoci
    atedwit
    h
    anthr
    acycli
    ne-basedther apy.Venoust hrombosismayberelat
    edtothehypercoagul
    abil
    it
    y
    associ
    atedwi t
    hunderlyingmal ignancy.

    Quest
    ion:

    31. Youar eseei ngi ntheoffi


    cea45- year
    -oldwhi temal enonsmokerwi thtype2diabetes
    andhumani mmunodef i
    ciencyvir
    us( HIV).Hehasat otalcholesterolof190mg/ dl,l
    ow-densi
    ty
    l
    ipoprot
    eincholesterolof101mg/ dl,andasyst ol
    icbloodpr essur eof125mm Hgonno
    medicat
    ionsforhyper tension.HisHIVi swellcontroll
    edonapr oteasei nhi
    bit
    or-basedregi
    men
    wit
    hanundet ectableviralload.Previouslyhi
    sHI Vhadnotbeenwel lcontr
    oll
    ed.Youwoul dli
    ke
    himtobeonopt i
    malmedi cati
    ont oreducehisr i
    skf orcardiovascular(CV)events.

    Whichofthefoll
    owingchangesi
    npharmacot
    her
    apydoyour ecommendasthebestst
    rat
    egy
    f
    orreduci
    ngt heCVr i
    skforat
    her
    oscl
    erot
    icCVdi
    seaseevent
    swhi l
    emai
    ntai
    ningef
    fi
    cacyof
    t
    reatmentforHIV?

    a. Changeanti
    retr
    oviralagentt
    oanon-nucleosi
    derever
    set
    ranscr
    ipt
    asei
    nhi
    bit
    or.
    b. I
    nit
    iat
    efenofi
    brate145mgperday.
    c. Changeanti
    retr
    oviralagentt
    oani
    ntegraseinhi
    bit
    or.
    d. I
    nit
    iat
    eatorvast
    atin10mgperday.
    e. I
    nit
    iat
    esimvastati
    n40mgperday.

    Answer
    :

    31. d. I
    nit
    iat
    eat
    orvast
    ati
    n10mgperday.

    I
    niti
    at i
    ngmedi cati
    ons,li
    kestat
    insandf i
    shoi l,
    whicharedesignedtoi mprovel
    ipi
    dsand
    tr
    iglyceri
    des,isli
    kelyabett
    eroptionfordecreasingCVrisk,r
    atherthanchangingantir
    etr
    ovi
    ral
    s.
    Proteaseinhibit
    ordrugsworsenlipidprofi
    les,moresothanintegraseinhibi
    tor
    sornon-
    nucleoside-r
    everse-tr
    anscri
    ptaseinhibi
    torregimens.However,switchingfr
    om astabl
    e
    proteaseinhibit
    orregi
    ment oanal t
    ernati
    ver egimenmaybeassoci atedwi t
    hvir
    ologi
    c
    breakthrough. 

    Inar andomi zedtr


    ialofli
    pidlower i
    ng,pravast
    atinandbezaf i
    br at
    epr ovedsigni f
    icantlymor e
    eff
    ectivei nthemanagementofhi ghlyacti
    veant ir
    etroviraltherapy- r
    elatedhyper l
    ipidemi athan
    switchingt her
    apyfrom proteaseinhibit
    orstonevi rapineoref avirenz.However ,
    large-scaleCV
    outcomespr event
    iondataar elacking.Simvastatinandl ovastati
    nar econtraindicatedf oruse
    withpr oteaseinhi
    bitor
    s.Preferr
    edst art
    ingdosesofast atininHI Vpat i
    entstakingpr otease
    i
    nhibitorr egi
    mensi ncl
    udeat or
    vastatin10mgdai lyorr osuvast ati
    n10mgdai ly)Inthisvignett
    e,
    thepat ientwouldmeetgui deli
    nesforamoder ate-intensitystatinbyvi r
    tueofhi sdiabet es.
    Quest
    ion:

    32. A36- yearoldwomanpr esent


    stoyouf orcar
    diol
    ogyconsul
    tat
    ion.Her42-yearol
    d
    brot
    herwasrecent
    lydiagnosedwithhyper
    trophiccar
    diomyopat
    hy(HCM) ,andhetoldhert
    hat
    sheneededt
    obescr eenedbyacar di
    ologi
    st.
     

    Thepati
    ent’
    sbr otherwasdi agnosedafterar
    outi
    neelect
    rocardi
    ogr
    am (ECG)showedlef
    t
    vent
    ri
    cular(LV)hypertrophywithastrai
    npatter
    n.Herbrot
    herhadanechocar di
    ogr
    am
    conf
    ir
    mi ngthediagnosi s,
    andheunder wentgenet
    iccounsel
    ingandtesti
    ng.Hewastoldthat
    nopathogenicmut ati
    onswer eident
    if
    ied. 

    Thepati
    enthasnosympt oms.Sheexerci
    sesbywal kingatabriskpacefor30minutesdai
    ly
    wit
    houtli
    mitat
    ionsandworksful
    lti
    measahi gh-
    schoolalgebrateacher
    .Shetakesno
    medicat
    ionsandhasnopastmedi calhi
    stor
    y.Herfatherdiedattheageof42inacaraccident
    .
    Hermotherisali
    veandwell
    ,andshei snotsurei
    fhermot herorhertwosister
    shavebeen
    scr
    eened.Onexaminati
    on,herheartr
    ateis72bpm andherbl oodpressurei
    s108/70mm Hg.
    Shehasnomur mur
    s. 

    Youperform a12-l
    eadECGt hatshowsnormalsinusrhyt
    hm, withnormalaxi
    sandinter
    vals
    andnoST- Tchanges.Youper f
    orm anechocar
    diogr
    am thatshowsnor malLVfunct
    ion,noLV
    hyper
    trophy,nor
    malvalvul
    arfuncti
    on,andnopulmonaryhypertensi
    on.

    Whi
    choft
    hef
    oll
    owi
    ngt
    est
    sdoyouadvi
    se?

    a. 24-hourambul at
    or yECGmoni t
    oring.
    b. Cardiacmagnet i
    cr esonanceimagi ng.
    c. Not esti
    ngnow;r epeatechocardiogram i
    n5year
    s.
    d. Geneticcounseli
    ngandt est
    ing.
    e. Exercisest
    resstest.

    Answer
    :

    32. c. Not
    est
    ingnow;r
    epeatechocar
    diogr
    am i
    n5year
    s.

    Hypertrophiccardiomyopat hy(HCM)iscausedbyanaut osomaldomi nantmut ationingenes


    thatencodesar comer eprotei
    nsorsar comere-associatedpr oteins.Geneticand/ orclinical
    screeningofallfi
    rst-degreefamilymember sofpatientswi thHCM i simpor tanttoi dentif
    ythose
    withunr ecogni
    zeddi sease.Ont hebasisoffamil
    yhi st
    or y,cli
    nicalscreening,andpedi gree
    analyses, t
    hepatternofinherit
    anceisascertai
    nedtoi dent i
    fyandcounselr elat
    ivesatr i
    sk.
    Becausef amili
    alHCM i sadomi nantdisorder,
    theriskthatanaf fectedpatientwilltransmi t
    diseaset oeachof f
    springis50%.  

    Whenapat hogenicmut at
    ionisi denti
    fi
    edinanindexpatient,t
    hegenet i
    cstatusofeachf amil
    y
    membercanber eadi
    lyascer t
    ained.BecauseHCM mut ationsarehighlypenetrant,amutati
    on
    conveyssubstanti
    al(
    95%)r iskoveral if
    eti
    mefordevelopingcli
    nicaland/orphenotypic
    evi
    denceofHCM.However ,
    whent hereisnoi
    dentif
    iabl
    epat hogenicmutati
    oni ntheindex
    pati
    ent,
    therei
    snoi ndicat
    ionf orfurt
    hergenet
    ictesti
    ngofot herfamil
    ymember s. 
    Exer cisest resst estingisusef ulinpat i
    entswi t
    hHCM t oassessf unctionalcapaci tyand
    responset ot herapy, performr i
    skst r
    atif
    icati
    onf orsuddencar di
    acdeat h,andt oassessf oran
    exerci se- induceddynami cleftventri
    cularout f
    lowt ractgr adient
    .However ,thispatienthasno
    evidenceofHCM onechocar diogram, sotherei snoi ndicat i
    onforstr
    esst est i
    ng.Car diac
    magnet icr esonancei maging( MRI)isusef ulinpatientswi thHCM whent heechocar di ogram is
    i
    nconcl usi vef orthedi agnosisormor einformat i
    onr egardi ngthemitralval veappar at usis
    requi red.However ,cardiacMRIcur rentl
    ydoesnotpl ayar oleinthescr eeni ngoffirst-degr ee
    rel
    at ivesofpat i
    entswi thHCM.Twent y-four-hourambul at oryel
    ectr
    ocar diographicmoni tori
    ng
    i
    sr ecommendedf orpat i
    entswi thHCM whohavepal pit
    at ionsorli
    ghtheadedness( ClassI )
    ,as
    ani nitialscr eeningf orvent r
    iculartachycardiatodet ermi net heneedf orplacementofan
    i
    mpl ant edcar di
    over ter-
    def i
    bri
    ll
    ator(ClassI )
    ,andever y1- 2yearstor eassessr i
    skofsudden
    cardi acdeat h( ClassI I
    a).However ,allofthesei ndicati
    onsar especif
    ictopat i
    entswhoal ready
    carryadi agnosi sofHCM, andt heyarenoti ndicatedaspar toft
    hescr eeningal gorithm f or
    unaf fect edf irst-degreer elati
    ves. 

    Seri
    alechocardiogramsar ereasonabl
    e(ClassII
    a)forcli
    nical
    lyunaffectedpatient
    swhohavea
    fi
    rst
    -degreerel
    at i
    vewi t
    hHCM whengenet i
    cstatusi
    sunknown.Suchf oll
    ow-upmaybe
    consider
    edevery12t o18mont hsforchil
    drenoradolescentsfrom high-ri
    skfamil
    iesandever
    y
    5year sf
    oradultfami l
    ymember s.Thus,notesti
    ngnowandaf oll
    ow-upechocar diogr
    am i
    n5
    yearsisthecorr
    ectr esponse.

    Quest
    ion:

    33. A60- year-


    oldmancol l
    apsesatal ocalfit
    nesscent er
    .Bystandershavewi tnessedthe
    col
    lapse,911iscalled,andchestcompr essionsar eini
    ti
    ated.Paramedicsar r
    ivewi t
    hin5
    minutes.Ventri
    cul
    arf i
    bri
    ll
    ati
    on( VF)i
    sseenont hemoni tor,a200Jbi phasicshocki sdeli
    ver
    ed,
    andchestcompr essionsareresumedf or2mi nutes.VFremains,anda200Jbi phasicshockis
    del
    ivered,f
    oll
    owedbyanot her2mi nut
    esofchestcompr essions.VFst i
    llr
    emai nsont he
    monitor.

    Whi
    choft
    hef
    oll
    owi
    ngshoul
    dbet
    henextst
    epi
    nmanagement
    ?

    a. Hol
    dcar di
    opulmonaryresusci t
    ati
    onandi nt
    ubatethepat
    ient
    .
    b. Est
    abli
    shIVaccessanddel iverami odar
    one300mg.
    c. Del
    iveranotherimmedi
    ate(st acked)shock.
    d. Del
    iverepi
    nephr i
    ne1mgi ntraosseousandcont i
    nuechestcompressi
    ons.
    e. Est
    abli
    shintravenous(
    IV)accessanddel i
    verl
    idocai
    ne1mg/ kg.

    Answer
    :

    33. d. Del
    iverepi
    nephr
    ine1mgi
    ntr
    aosseousandcont
    inuechestcompr
    essi
    ons.

    Accordingt o2010advancedcar di
    aclifesupportguideli
    nes,thenextstepinmanagementi
    sto
    del
    iverepinephrinebyeitheranIVorintraosseousroute,butavoidint
    errupti
    oninchest
    compr essions.Vasopressi
    nisanalternati
    ve.Avasopr essorshouldbegi venbef
    ore
    anti
    arrhythmictherapyisini
    ti
    ated.
    PERI
    CARDI
    ALDI
    SEASE

    1. A49-
    year
    -ol
    dmanwi
    thahi
    stor
    yofhyper
    tensi
    onandobesi
    typr
    esent
    stot
    he
    emer
    gencydepar
    tmentf
    oll
    owi
    ngar
    ecentvi
    ralsyndr
    ome.Onexami
    nat
    ion,
    hei
    spal
    e
    andappearsuncomfor
    table,wi
    thel
    evatedj
    ugularvenouspressur
    e,clearlungf
    iel
    ds,
    andnocardiacmurmurs,rubs,
    orgall
    ops.Hi
    ssystoli
    cbloodpressurefall
    s20mm Hg
    wit
    hinspi
    rati
    on.Hi
    ssaturati
    onsare91%onr oom ai
    r. 

    Anelect
    rocar
    diogram demonstr
    atessinustachycar
    diaandbor der
    li
    nelowvol tages,
    buti
    sotherwi
    senor mal.Labor
    atori
    esretur
    nwi t
    hhemat ocri
    t29%,potassium 3.3
    mEq/L,andcreati
    nine1.0mg/dl.Whil
    eadditi
    onaleval
    uationisbei
    ngpur sued, a
    nursecheckingonthepat
    ientobservesthathesuddenlybecomesunr esponsi
    ve.
    Sinustachycar
    diai
    snotedont hecardi
    acmoni t
    or,butheiswithoutdetect
    ablepul
    se
    andtherefor
    ecardi
    opulmonaryresusci
    tati
    onispromptlyi
    niti
    ated.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    yet
    iol
    ogyoft
    hepat
    ient
    ’scar
    diacar
    rest
    ?

    a. Pul
    monar yemboli
    sm.
    b. Hypokalemia.
    c. Anemia.
    d. Myocardialinf
    arct
    ion.
    e. Cardi
    act amponade.

    ANSWER

    E.Car
    diacTamponade

    Inpatientswithtachycar
    dia, jugulardistenti
    on,orpulselesselectri
    calacti
    vity,cardi
    ac
    tamponadeshoul dbehighlysuspect ed.Whencar diacar r
    estoccur ssecondar yto
    tamponade, retur
    nofspont aneousci rculat
    ionisoft
    ennotpossi bleunti
    lperforming
    emergentper icar
    diocent
    esi stoabr uptlydecreasepericardialpr
    essur esandal low
    vent
    ricularfi
    ll
    ing.Alt
    houghaddi ti
    onalcausesofpul selessel ect
    ricalacti
    vit
    yi nthi
    s
    pati
    entmustbeconsi dered, basedont heinfor
    mationpr ovided,theotheranswer
    choi
    cesar el
    essl i
    kel
    yetiologiesthancar di
    actamponade.
    2. A64- year-ol
    dmanpr esentswit
    hnewonsetofpal pitati
    ons,substernalchest
    discomf ort
    ,anddyspnea.Hef el
    twellunti
    labout5daysagowhenhet houghthehad
    theflu.Hei sonnomedi cati
    onexceptforover-the-count
    erpseudoephedr i
    neand
    i
    bupr ofen.Onexami nat
    ion,heisanxious,
    inmoder atedistress,andtachypneic.He
    hasahear trateof122bpm, bl
    oodpressureof90/ 55mm Hg, andtemper atureof
    37.2°C.Hisl ungsarecl
    ear,andther
    ei sanelevatedjugularvenouspr essure.A
    pulsuspar adoxusismeasur edat18mm Hg.Hei scoolandcl ammy.

    Per
    ti
    nentl
    aborator
    ydatarevealahemat
    ocr
    itof28%,
    whi
    tebl
    oodcel
    lcountof12,
    500,
    andcr
    eati
    nineof1.2mg/dl.
     

    Anelectrocardi
    ogram reveal
    sanarrowcomplext achycar
    dia.Abedsi de
    echocardiogram conf
    ir
    msamoder ateperi
    car
    dialeff
    usionwithrightventr
    icul
    ar
    diast
    oli
    ccol l
    apse,substanti
    almi
    tr
    alinfl
    owvariabil
    it
    y,andinfer
    iorvenacavapl et
    hor
    a.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nthi
    spat
    ient
    ’smanagement
    ?

    a. Dopami neinfusion.
    b. Peri
    cardiocentesis.
    c. Dir
    ectcur r
    entcar di
    oversi
    on.
    d. I
    ntravenousfur osemide.
    e. Bedsideadenosi netesti
    ng.

    ANSWER

    B.Per
    icar
    diocent
    esi
    s

    Thepat i
    entisincar diactamponadeandcar diogenicshockandi sinurgentneedof
    defi
    nit
    ivetreatmentwi t
    hemer gentper i
    cardiocentesi
    stor eli
    eveper i
    cardi
    alpressur
    e
    andimpr ovethehemodynami cinstabili
    ty.Whilesorti
    ngouthi stachycardiaand
    i
    mpr ovinghishear tratewillbenecessar y,dir
    ectcurrentcardioversi
    onwoul dnot
    l
    ikel
    yimpr ovehi sacut ehemodynami cpicture,andheneedsf ir
    sttohavet he
    peri
    cardialfl
    uidremoved.Dopami nemayhel phisbloodpr essureatt heexpenseof
    i
    ncreasinghist achycar di
    a.Diur
    eticslikelywoul dworsenhi slowout putstat
    e.

    3. A57- year-ol
    dwomanwi t
    hal ongsmoki nghist
    orypresentswi t
    hfever,mal
    aise,
    anddyspnea.Onexami nat
    ion,hervi
    tal
    sincludetemperatur
    e37. 9°C,hear
    trate110
    bpm, andbloodpressure98/64mm Hg.Scat t
    eredwheezesar enotedonl ung
    auscultat
    ion.Heartsoundsaredist
    antbutregularandtachycardicwithnomur murs,
    rubs,orgal
    lops.Anel
    ect
    rocar
    diogram demonstrat
    essinust
    achycardiaandl ow
    volt
    ages.Thepulsuspar
    adoxusismeasur edat17mm Hg.Ast atechocar di
    ogram i
    s
    perfor
    medandshowsnosi gnif
    icantperi
    cardi
    aleff
    usi
    onandnor malleftventr
    icul
    ar
    functi
    on.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    yexpl
    anat
    ionf
    orherpul
    suspar
    adoxus?

    a. Chronicobstruct
    ivepulmonar
    ydi
    seaseexacer
    bat
    ion.
    b. Thyrotoxi
    cosis.
    c. Restri
    cti
    velungdi sease.
    d. Pneumomedi ast
    inum.
    e. Anorexianervosa.

    ANSWER

    A.Chr
    oni
    cobst
    ruct
    ivepul
    monar
    ydi
    seaseexacer
    bat
    ion

    Inpat i
    ent swi thsuspect edper icar di
    altamponade, document ati
    onofanel evat ed
    pulsuspar adoxusi sakeyexami nat i
    onfinding.Pul suspar adoxusismeasur edusing
    slowdef lationofamanualbl oodpr essurecuf fandcal culati
    ngt hepressur e
    diff
    erencebet weent hef ir
    stauscul tatedKor otkoffsoundst hatoccuronl yi n
    expirati
    onandt hepr essur eatwhi chKor ot
    kof fsoundsar eaudi bleforallhear tbeats.
    Normal ly,thepul suspar adoxusi s<10mm Hg.I nper i
    cardialtamponade, const rai
    nts
    onvent ricularfill
    ingleadt or espi rophasi ci
    nt erventriculardependencet hatenhances
    fl
    uctuationsi nleftventri
    cul arst rokevol ume.However , anelevatedpulsuspar adoxus
    i
    snotl imi tedt oper i
    cardialt amponade, butcanal sobeobser vedi npati
    ent swi t
    h
    obstructivel ungdi sease, obesi ty,obst r
    uctivesl eepapnea, andt ension
    pneumot hor ax.Inthispat ient ,t
    heai rtr
    appingandi ncreasedwor kofbreat hinglead
    towi deswi ngsi nintrat
    hor aci cpr essureandcr eatet heel evatedpulsuspar adoxus.

    4. A52- year-ol dwomanwi t


    hahi st
    oryofmetastaticbreastcanceron
    chemot herapypr esentswithsl
    owlyprogressi
    vedyspneaonexer ti
    onoverthepast
    month.Shedeni esfeverorchestpain,buthasbeeni ncreasi
    nglyfat
    igued.On
    physicalexam, herhear tr
    ateis115bpm wi t
    hbloodpr essure102/70mm Hgand
    ther
    ei sevidenceofel evat
    edjugularvenouspressure. 

    Achestcomputedtomographi
    c(CT)scandemonst r
    atesa“l
    argeper
    icar
    dialeff
    usi
    on”
    prompti
    nganurgentbedsi
    deechocardi
    ogram thatr
    eveal
    snormalbi
    ventr
    icular
    funct
    ionanda1.7cm ci
    rcumfer
    enti
    alef
    fusion.
    I
    naddit
    iont
    or i
    ghthear
    tdi
    astol
    iccol
    lapse,whichoft
    hefol
    lowi
    ngechocar
    diogr
    aphi
    c
    f
    indi
    ngswouldbemostsuggesti
    veofpericar
    dialt
    amponade?

    a. I
    nferi
    orvenacavacol l
    apse.
    b. Mitr
    alDoppl erfl
    owvar iat
    ion40%.
    c. Paradoxicalint
    erventr
    icularseptalmot
    ion.
    d. Atr
    ialseptaldefectfl
    owr eversal.
    e. Tri
    cuspidDoppl erinf
    lowvar i
    ation40%.

    ANSWER

    B.Mi
    tr
    alDoppl
    erf
    lowvar
    iat
    ion40%

    Thispat i
    enti ssuf fer
    ingf r
    om per i
    cardialtamponadeandr equi resur gentdiagnost i
    c
    andt herapeut icper i
    cardiocentesis.I
    tisessent i
    altounder standt hef undament al
    echocar diographi cfi
    ndingsoft amponade, ofwhicht hehal l
    mar kisrightheart
    diastoli
    cchambercol lapseduet ocompr essionoft hecar diacchamber sbyel evated
    pericardialpressur eleadingtoi mpairedf i
    ll
    ing.I
    naddi t
    ion, patientsintamponade
    oftendemonst rateexagger at
    edf l
    owvar iati
    onacr osst heat rioventri
    cularvalvesasa
    resultofr espirophasicvent ri
    cularinter
    dependence, defi
    nedas>30%mi t
    ralf
    low
    variati
    onand>60%t ri
    cuspi dfl
    owvar i
    ati
    on, andinferiorvenacavadi lat
    ationreflecti
    ng
    mar kedlyel evatedcent ralvenouspr essures.Paradoxi calint er
    vent r
    icularseptal
    mot ionandat rialseptaldefectfl
    owr eversalarenotchar act eri
    sticfi
    ndi ngsin
    tamponade.

    5. A49- year-
    oldwomanwi t
    hahistor
    yofsystemiclupuserythematosuspresent
    s
    foreval
    uationofint
    ermit
    tentshar
    pchestpainforthepast3days.Sher eport
    sthe
    discomfortcameonsuddenl y,
    isl
    ocatedattheanteri
    orchestwallwi
    thr adi
    ati
    onto
    theshoulders,
    andfeelsworsewithdeepbreathi
    ng.Onexami nati
    on,t
    hehear ti
    s
    regul
    arwit
    hasof tsystol
    icmurmuratthelef
    tst
    ernalbor
    der
    .Anelectrocar
    diogr
    am
    (ECG)demonstr
    atessinustachycardi
    awit
    hmi l
    ddiff
    useSTelevat
    ion.AchestX-ray
    showsclearl
    ungf i
    eldsandcardiomegal
    y.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestdi
    agnost
    icmodal
    it
    y?

    a. Cardiacmagnet i
    cr esonancei
    magi
    ng(
    MRI
    ).
    b. High-sensiti
    vitytroponin.
    c. Coronaryangi ography.
    d. Echocar di
    ogram.
    e. Exercisetr
    eadmi lltest.
    ANSWER

    B. Echocar
    diogr
    am

    Peri
    cardialef
    fusioncanbecausedbyanydi sorderoftheper i
    cardi
    um andis
    suspectedbyhi story,
    physi cal
    ,ECG,andchestX- r
    ayfindings.Thispat
    ientdescr
    ibes
    thecharacter
    ist
    icshar p,pleuri
    ti
    csubst er
    nalchestdiscomf ortassoci
    atedwith
    peri
    cardiali
    nfl
    ammat ion.Oftenthediscomfortisalsowor sewhenl yi
    ngdownand
    i
    mpr ovedwhensi tt
    inguprightandforwar d,
    andmayr adiatetotheshouldersdueto
    i
    nvolvementoft hephr enicnerveasittraversesthepericardi
    um.  

    Examinati
    onmayr evealapericardi
    alfri
    ct i
    onr ub,whichisahi ghlysensiti
    vefi
    nding.
    Earl
    yinthediseasecour se,t
    heECGof tenshowsdi f
    fuseSTel evat
    ion(concaveup)
    andPRdepr essioninmostl eadsexceptf orleadaVR, whichmayr evealPRelevati
    on
    andSTdepr ession.However ,
    afterthefirstweek,thechar acteri
    sti
    cSTandPR
    changesmaynor malize.Whil
    et hechestX- r
    ayisoftenwit houtacuteabnor mali
    ti
    es,
    l
    argerperi
    cardialeff
    usions(>200mlf luid)maydemonst rat ecardi
    omegal y.
     

    Asthispat i
    entpresentswi thacl i
    nicalsyndr omesuggest i
    veofper i
    cardialdisease
    andenl argementoft hecardiacsilhouet t
    eonchestX- rayi mplyinganunder lyi
    ng
    peri
    car dialeff
    usion,anechocar di
    ogr am isthenextbestst epint hepat i
    ent’
    s
    eval
    uat ion.High-sensiti
    vitytroponi nwoul dbehelpf
    ultoeval uat eforevidenceof
    myocar dialinfl
    ammat i
    onbuti ssecondar ytoechocardiography, whichcandet ermi ne
    thesizeandhemodynami csi gnif
    icanceoft heperi
    cardialeffusion.Thepat ientisl ess
    l
    ikel
    yt ohaveobst ructi
    vecor onarydi sease,andtheref
    or e,exercisetreadmillstress
    test
    ingandcor onar yangiographyar enotindicat
    ed.CardiacMRImaybebenef icial
    oncet hedi agnosisisestablished, butwoul dnotbethef ir
    st-li
    net est.

    6. A50- year
    -oldwomanpr esent swi t
    hevaluat i
    onofcar diomegalyonr outinechest
    X- ray.Shei sacti
    vewi t
    houtsympt oms.Herr eviewofsympt omsisnot abl
    eforcold
    i
    nt olerance.Herhistoryisnotablef orhypothyroidism anddi abet
    es.Shei stakingno
    medi cat i
    ons.Onexami nati
    on, herbl oodpressurei s140/ 100mm Hg, heartratei
    s50
    bpm, andt emperatureis35°C.Shei swearingawi g.Thereisnoj ugularvenous
    distention,andlungsar eclear.Ther eisnoadenopat hypalpable.Breastexami nat
    ion
    i
    snor mal .Heartsoundsaredi stant.Abdomeni sobese, andt her
    eis1+l ower
    extremi tyedema.Ther earebrawnyski nchangesoverherl owerextremiti
    es.

    Anel
    ect
    rocar
    diogr
    am (
    Figur
    e1)andechocar
    diogr
    am (
    Figur
    e2)ar
    eshown.
    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextmostappr
    opr
    iat
    edi
    agnost
    icst
    ep?

    Fi
    gur
    e1.

    Fi
    gur
    e2.
    a. Thyroid-st
    imulatinghormone.
    b. Cardiaccathet
    er i
    zati
    on.
    c. Chestcomput edt omography.
    d. Cardiacmagnet icresonancei
    magi
    ng(
    MRI
    ).
    e. Peri
    car di
    ocentesis.

    ANSWER

    A. Thyr
    oid-
    sti
    mul
    ati
    nghor
    mone.

    Themanagementofper i
    cardialeffusionsdependsupont heetiology, i
    ts
    hemodynami cconsequences, andt hepat i
    ent'
    ssympt oms.Int heabsenceof
    symptomsorhemodynami csequel ae,thet r
    eatmentshoul dbebasedupont he
    underlyi
    ngetiol
    ogy.Inthiscase, thepat ient'
    sunder lyi
    nghypothyr oidism likely
    explai
    nshermyxedemat ousst ateandconsequentl argeperi
    car dialeffusion.Since
    shehasnosympt omsandt herei snoevi denceforhemodynami ccompr omi seby
    examinationorecho, t
    hereisnoi ndi cati
    onf orpericardi
    ocentesisf ortherapeut i
    c
    reasons.Otherconsiderati
    onsi ncludeaut oi
    mmunecondi ti
    ons, medi cati
    ons( e.
    g.
    hydral
    azine),Dr
    essler'
    s,radiati
    on, uremi a,malignancy,andinfections. 

    Mostper icar di
    alef f
    usionsareeit
    herviralori
    diopat
    hicineti
    ology.Di
    agnosti
    c
    peri
    car di
    ocent esiscanbeconsi deredwhent hereisconcernformali
    gnancyor
    nonvirali
    nf ections.However ,
    pericar
    dialti
    ssuegenerall
    yprovidesgr
    eaterdi
    agnosti
    c
    uti
    li
    ty.Car diaccat heteri
    zat
    ionisnotli
    kelytobeusefulintheabsenceofsymptoms, a
    normalcar diovascularexaminati
    on,andnoevi denceforhemodynami ccompromise
    onecho.Car di
    acMRIwouldbel i
    kelytoonlyconf
    irmtheechocardiogr
    aphicfi
    ndings;
    therearenoMRIf i
    ndi
    ngsthatarepathognomonicofaspecifi
    cdiagnosis.A
    screeni
    ngchestcomputedtomogr aphyformali
    gnancycouldbeofusei fthecl
    ini
    cal
    diagnosisofhypot
    hyr
    oidi
    sm isnotconfi
    rmedbyt hyr
    oid-
    sti
    mul at
    inghormone.

    7. A65- year-
    oldmanunder goespericar
    diocentesi
    sforalargeeffusion.Fluid
    analysisi snotableforadenosi
    nedeami naselevel100U/L,protei
    n3g/ dl
    ,glucose30
    mg/ dl,lactatedehydrogenase(LDH)120mg/ dl
    ,andspecif
    icgravit
    y1. 020.Numer ous
    atypicalandmesot heli
    alcel
    lsareseen.Theserum glucoseis120mg/ dl,pr
    ot ei
    nis4
    g/dl,lactatedehydrogenase(LDH)is150mg/ dl,
    andwhi t
    ecountis15, 000wi tha
    normaldi f
    ferent
    ial
    .

    Wi
    thwhi
    choft
    hef
    oll
    owi
    ngar
    ethesef
    indi
    ngsmostconsi
    stent
    ?

    a. I
    diopathic.
    b. Hypothyroidism.
    c. Malignant.
    d. Tuberculosis.
    e. Autoimmune.

    ANSWER

    D.Tubecul
    osi
    s

    Whenper icardialfl
    uidisobt ai
    neddur ingper i
    cardiocentesis,i
    tshoul
    dber outi
    nel
    y
    sentforbot hchemi calandcyt ologicalexami nation.However ,theet
    iologyof
    peri
    cardialeffusionsisrarelyestabl i
    shedt hroughexami nati
    onofpericardialf
    lui
    d;
    sampl i
    ngoft heper i
    cardium itselfistypicall
    yneeded.Unf ort
    unatel
    y,mal i
    gnant
    eff
    usionsr arelydemonst ratemal ignantcells.Ahi ghtri
    glyceri
    decontentofan
    eff
    usionischar act
    eri
    sti
    cofmyxedema.Anadenosi nedeami naselevelof>40U/ L,
    el
    evatedpr otein,andLDHl evelsar esuggest i
    veoft uberculosis.

    8. A21- year
    - ol
    df emal estudentwithrecentupperrespirat
    orysymptomspr esent
    s
    compl ai
    ningof12hour sofleft
    -sidedchestpain.Thepai nisdescri
    bedasshar p,
    worsenswi t
    hbr eathing,andimpr oveswithleaningforward.Thereisnochangewi t
    h
    eat
    ing.Shehaspr eviouslybeenact i
    ve,exerci
    singregular
    lywithoutsymptoms.Her
    el
    ectrocardiogram (ECG)i sshowni nFi
    gur e1.

    Whi
    choft
    hef
    oll
    owi
    ngwoul
    dbet
    henextappr
    opr
    iat
    edi
    agnost
    ict
    est
    ?
    a. Hepatobil
    iaryult
    rasound.
    b. Comput edtomogr aphyangi
    ographyofchest
    .
    c. Esophagogast r
    oduodenoscopy.
    d. Exerci
    sest r
    esstest.
    e. Echocardi
    ogr am.

    ANSWER

    E. Echocar
    diogr
    am

    Thispat i
    entpr esentswi thclassicsymptomsofpericardi
    tiswi t
    hpl euri
    ti
    cshar pchest
    pain,betterleaningf orward.HerECGshowst ypi
    caldif
    fuseSTel evati
    ons,wi t
    hPR
    depressional sonot ed.Anechocar di
    ogr
    am wouldbehel pful,bothinconf i
    rmingt he
    diagnosisofper i
    carditi
    sbypr esenceofapericar
    dialeff
    usion( seeni napproximat el
    y
    60%ofpat ients)andi nruli
    ngoutt amponade.Withthispatient'
    scl assi
    csympt oms
    andECGf indings, t
    hereisnor easonatthi
    sti
    met opursueal ternateeti
    ologieswith
    esophagogast roduodenoscopy, st
    resst
    esti
    ng,hepatobil
    iaryultrasound,orcomput ed
    tomogr aphyangi ographyoft hechest.

    9. A60- year
    -ol
    dwomanwi t
    hdiabet
    esmel l
    it
    usandahistor
    yofmant elradi
    ati
    on
    forl
    ymphomaatage15present
    stoyouroff
    iceforeval
    uat
    ionofpr
    ogressivedyspnea
    onexer
    ti
    on.Onexami
    nati
    on,herbl
    oodpressureis90/70mm Hgwithapul sus
    paradoxusof8andahear trat eof80bpm.Shehasj ugul
    arvenousdistensionwit
    h
    posit
    iveKussmaul’ssign,
    clearlungs,normalhear
    tsoundswithoutmur mur,pal
    pabl
    e
    enl
    argedliverwit
    hnoappr eciableasci
    tes,and2+pit
    ti
    ngedemabi l
    ateral
    ly.An
    el
    ectrocar
    diogram demonstratesinf
    eri
    orQwavesandl owQRSvol tage.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    ydi
    agnosi
    s?

    a. Peri
    cardialeffusion.
    b. Tri
    cuspidst enosis.
    c. I
    schemi ccar diomyopat hy.
    d. Constr
    ictiveper i
    cardit
    is.
    e. Pulmonar yhyper tensi
    on.

    ANSWER

    D.Const
    ri
    cti
    veper
    icar
    dit
    is

    Basedont hehi st
    oryandphysi calexami nation, themostl ikel
    ydi agnosi si s
    const ri
    ct i
    veper i
    cardi
    tis.Constrict
    iveper icardit
    isf rom chr onicinflammat ioncauses
    i
    mpai redf il
    li
    ngoft hevent ri
    clesandr educedvent r
    icularfunction.I ncreased
    pericar dialthicknessi sgenerall
    ypr esentbutnotr equi r
    edf orthedi agnosisor
    treatment .Historycanr evealcommonr iskf actors, i
    ncludingpr iorcomput ed
    tomogr aphysur gery,chestradiati
    on, andr ecurr entper i
    car dit
    is.Onhi st
    ory, pat
    ients
    mayr epor tfatigue,edema, dyspnea, andabdomi nalswel l
    ing.Typi cal l
    y,thereisa
    l
    ongdel aybet weent hei ni
    ti
    alper i
    cardialinflammat ionandconst ri
    ct i
    vedi sease.On
    exami nat ion,Kussmaul ’
    ssignandot herf indingsofr i
    ghthear tfai
    lur earepr esent.
     

    Dif
    ferentialdiagnosisincludesr i
    ghthear tfail
    uresuchasf rom acut eri
    ghtventri
    cul
    ar
    myocar dialinfarct
    ion,tri
    cuspidst enosis, orrestri
    cti
    vecar diomyopat hy.
    Echocar diographyisusef ulf
    ordi agnosi s, canassessf orthickenedorcal ci
    fied
    pericardium, andcanexcl udeot hercauses.Car di
    accat heterizati
    onhas
    hemodynami cwavef ormschar acteri
    sticofconst ri
    cti
    onandi susef ulf
    or
    dif
    ferentiati
    ngr estr
    icti
    vecardiomyopat hy.Pat ient
    swi thprevi ouschestradiati
    onare
    atincreasedr iskforcoronaryar terydiseaseandval vularhear tdi
    sease,butthat
    woul dnotr esultintheexami nationfindingsseeni nthispat ient.Asympt omatic
    pericardialeffusi
    onwoul dbeexpect edt obeassoci atedwi thapul susparadoxus.

    10. A57- year-ol


    dwomani sseeingyouf orthefi
    rstt
    imeandhasbeenr efer
    red
    becauseofdyspneaandedema.Shehadr adi
    ati
    ontherapytoherchestforHodgkin'
    s
    lymphomawhenshewas17year sold.Shehasdonewel lunti
    labout6monthsago,
    whenshenot edtheonsetofexer
    cise-rel
    atedshort
    nessofbr eathandmildbil
    ater
    al
    l
    owerextr
    emit
    yedema.Overthelastf
    ewweeks,t
    hishaswor senedandshenowhas
    pi
    tt
    ingedematohermi
    dcalves.Shedeni
    espalpi
    tat
    ions,
    fever,cough,
    orabdomi
    nal
    bl
    oati
    ng. 

    Onexami nat
    ion, sheappearswel lwit
    habl oodpressur
    eof120/80mm Hgwi th
    minimalchangewi t
    hinspir
    ation.Herheartr at
    eis78bpm andr egular
    .Herlungsare
    cl
    ear.Herjugularvenouspr essureiselevatedtoherearlobeswhilesit
    ti
    ngupright
    andtherearepr ominentwavef or
    msobser ved.Therearenomur mursandnoext ra
    cardi
    acheartsounds.Herabdomeni snor malexceptforali
    veredgefeltt
    wof i
    ngers
    bel
    owt hecostalmar gin.Theedemai sevi dent.
     

    Youor deranelectr
    ocar diogr
    am thatreveal
    snormalsi nusr hythm andborderl
    inelow
    volt
    age,butisotherwisenor mal.Anecho/ Doppl
    erisobt ai
    nedandt heresul
    tsare
    showni nFigure1andVi deo1.Perti
    nentadditi
    onalresultsincludeamaxi mal
    tr
    icuspidregurgi
    tantjetveloci
    tyof3.0msec.Leftventricular(LV)andrightventr
    icul
    ar
    systol
    icfuncti
    onar enor mal.

    Basedonthecl
    ini
    calhist
    oryandechocar
    diogr
    ams,
    whi
    choft
    hef
    oll
    owi
    ngi
    sthemost
    l
    ikel
    ycauseofherr
    ightheartf
    ail
    uresympt
    oms?

    Fi
    gur
    e1.
    Vi
    deo1.

    htt
    p:/
    /media.
    mycrowdwisdom.com.s3.
    amazonaws.com/
    acc/
    quest
    ions/
    asset
    _per
    ica
    rdi
    al/
    1754b2ae-
    b00e-4571-aca2-
    49b1f2747c77.
    mp4

    a. Restri
    cti
    vecar di
    omyopathy.
    b. Radiati
    on-inducedtri
    cuspi
    dregurgi
    tati
    on.
    c. Chronicthromboembol i
    cpulmonarydisease.
    d. Constri
    cti
    veper i
    cardi
    ti
    s.
    e. Pulmonar yfi
    brosi
    sandcorpulmonal e.

    ANSWER

    D.Const
    ict
    ivePer
    icar
    dit
    is
    Thecor rectansweri sconst
    rictivepericarditi
    s.Theevidenceofr ighthear tfail
    urein
    associat ionwi t
    ht heechocar diographicf i
    ndingsconfirmt hediagnosi s.I
    n
    const r
    iction, t
    herightatri
    alpr essuresar eelevatedandt hereisveryr apidear l
    yfill
    ing
    ofther ightvent r
    icle(rapi
    dydescent ).Ther eisoftenevidenceofasept al"bounce, "
    correspondi ngtot hehighimpact  earl
    yr apidfi
    lli
    ngoftheLVbef orethel i
    mi tsofthe
    LVdi mensi onresul t
    sinstoppageofi nfl
    owt ot heLV.Pat i
    entswi t
    hconst ricti
    ve
    pericarditisusuallyhavenor malpul monar ypressures,anda>25%r eductionint he
    mitralinfowDoppl ervelocit
    ieswi thinspirati
    on.Thevi deoandf iguredemonst rate
    thesef i
    ndi ngs. 

    Thel ackofpul monaryhypert


    ensioninthiscaseisi nconsistentwit
    ht hediagnosesof
    rest
    ricti
    vecar di
    omyopathy,chronicthr
    omboembol i
    cpul monar ydisease,andcor
    pulmonal e.Radiat
    ionheartdi
    seasecani ncludethef ormat i
    onoffi
    brosi st
    hataffects
    theper i
    cardium,myocardium,conductionsystem, orcar di
    acvalves.Itcanalsor esult
    i
    nsi gnif
    icantlunginj
    ury.Whil
    et heseareallrel
    evanti nthiscase,t
    hef indi
    ngsont he
    echo/ Dopplerconfi
    rmthediagnosisofconst ri
    cti
    veper i
    car di
    ti
    s.

    11. A26- year-oldmanpr esentswi t


    hchestpai n.Heexper i
    encedanupper
    respirat
    oryinfection2weeksago.Fort hepastweek, hehashadchestpai nt hatgets
    wor sewi t
    hinspirati
    onandsupi neposi t
    ion.Therei snoexerti
    onalquali
    tytot hepain;
    otherwise,onseti sunpredi
    ctable.Hehashadnof evers,
    chil
    ls,orsweats.Hehasno
    cough.Onexami nati
    on,helookswel l
    .Hisbloodpr essur
    eis118/ 70mm Hg, hisheart
    rateis70bpm, andhei safebril
    e.Lungsar eclear.Ani nt
    ermitt
    entperi
    cardialrubis
    noted.ChestX- rayi snormal.Hiselectr
    ocardiogram intheoffi
    ceshowssi nusr hyt
    hm,
    buti sotherwisenor mal.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    ether
    apeut
    icst
    rat
    egyatt
    hist
    ime?

    a. I
    buprofenf
    or8- 12weeks;colchi
    cinefor1-2weeks.
    b. Predni
    sonefor8-12weeks;colchici
    nefor1-2weeks.
    c. Oxycodonefor1-2weeks;prednisonefor8-12weeks.
    d. I
    buprofenf
    or1- 2weeks;col
    chici
    nef or8-12weeks.
    e. Predni
    sonefor1-2weeks;oxycodonef or8-12weeks.

    ANSWER

    D.I
    bupr
    ofenf
    or1-
    2weeks;col
    chi
    cinef
    or8-
    12weeks.
    Thisyoungmanhasper i
    car diti
    s.Itismostl ikelyidiopat hi corviralinli
    ghtofhi s
    recentupperr espiratoryinfection.Thepr edominantt her apeuticconcer nsarer el
    iefof
    sympt omsandpr eventi
    ngr ecur rence.Nonst eroidalant i- i
    nflammat orydrugs( NSAI Ds)
    areveryeffectiveati mmedi at epainr eli
    efandshoul dbeconsi der edfi
    rstli
    ne.The
    additi
    onofcol chicinehasbeenshownt opreventr ecurr encesi nsever alprospective
    randomizedt ri
    als.Pr ednisonehasl it
    tleroleinthepr imar ycontempor ary
    managementofper i
    carditi
    sandmaybedi ff
    icul
    tt oweanoverext endedper iodsof
    ti
    me, notwithstandingt hesi gnifi
    cantsi deeffectsofchr oni csteroids.Narcoticshave
    nospecificant i
    -infl
    ammat or yactionsandar einferiortoant i
    -i
    nflammat ory
    approaches.NSAI Dsshoul dbeusedf orsympt om sever ity,gener al
    lyabout2weeks.
    Colchici
    neshoul dbecont i
    nuedf or2- 3mont hst opr eventr ecurr
    ence.

    12. A20- year


    -ol
    dmanpr esent
    swit
    ha1- weekhi
    stor
    yofrhi
    niti
    s,myalgi
    a,f
    ever
    ,and
    chestpain.Hisexaminati
    onisnot
    abl
    eforaneasi
    lyaudi
    bleper
    icar
    dialf
    ri
    cti
    onruband
    isother
    wi seunremarkabl
    e.

    Whichofthefol
    lowi
    ngagent
    smaycont
    ri
    but
    etoani
    ncr
    easedr
    iskofr
    ecur
    rent
    per
    icar
    dit
    is?

    a. Aspiri
    n.
    b. I
    bupr ofen.
    c. Corti
    cost er
    oids.
    d. Colchicine.
    e. I
    ndomet hacin.

    ANSWER

    C. Cor
    ti
    cost
    eroi
    ds

    Thi
    spatientmostli
    kelyhasvi r
    alpericardi
    ti
    s.Whi
    lecorti
    costeroi
    dsmaybeef f
    ecti
    ve
    att
    reat
    ingacutepericardi
    ti
    s,theyshouldnotbeusedasf irst
    -li
    netherapyasthey
    mayleadt oanincr
    easedr i
    skofr ecurr
    ence.Theotheragentsdonoti ncr
    easetherisk
    ofr
    ecurrence,
    andinf act,
    colchici
    nehasbeenshownt oreducetheriskofrecurr
    ent
    per
    icar
    diti
    s.
    13. A65-
    year
    -ol
    dwomani
    sbr
    oughtt
    othecat
    het
    eri
    zat
    ionl
    abf
    ort
    reat
    mentof
    car
    diact
    amponade.Shei
    suncomf
    ort
    abl
    eandsi
    tt
    ingat45degr
    eesont
    hegur
    ney.
    Herbl oodpressur
    eis100/85mm Hg, herheartr
    ateis110bpm, andherbreat
    hingi
    s
    rapid.Thevenouspressurei
    svisi
    bleatthejaw,r
    alesarepresenti
    nthelungbases,
    heartsoundsar edi
    stant
    ,andther
    earenopr ecordi
    alimpul
    ses.Herpulsesare
    thready.

    Underf
    luoroscopi
    cguidance,
    aperi
    cardi
    ocentesisneedl
    eisplacedint
    heepigast
    ri
    um
    anddir
    ectedposter
    ior
    lytowardt
    helef
    tshoulder.Wit
    hneedleaspir
    ati
    on,bl
    oodis
    obt
    ained.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextmostappr
    opr
    iat
    est
    ep?

    a. Transducepressuref r
    om per
    icar
    diocent
    esi
    sneedl
    e.
    b. Sendbloodforanal ysi
    s.
    c. Placeperi
    car
    di aldrai
    n.
    d. Perfor
    mr i
    ght-heartcathet
    eri
    zati
    on.

    ANSWER

    A.Tr
    ansducepr
    essur
    efr
    om per
    icar
    diocent
    esi
    sneedl
    e.

    Duringur gentper icardiocentesi s,eit


    herechocar diogr aphicorf l
    uor oscopi cguidance
    canbeusedt ofaci l
    it
    atet hepr ocedur e.Whent heaspi ratedf l
    uidi ssangui nous, i
    tmay
    beduet oeitherhemoper i
    cardi um (e.g.,
    foll
    owingat r
    ialf i
    brill
    ationabl ation)or
    myocar dialpunct ure,awel l
    -recogni zedcompl icationofper i
    cardiocent esis.Themost
    expedi t
    iousmet hodf ori dentifyingthesour ceoft hesangui nousaspi r
    at eisto
    tr
    ansducet hepr essur efrom theneedl e.Inthecaseofmyocar dialpunct ure,the
    wavef ormt ransducedwi llbechar acteri
    sti
    cofint ravent ri
    cularpr essur e;ifinthe
    peri
    car dialspace, thewavef or m wi l
    lnotdemonst ratet hewavef ormsofi ntracardiac
    pressur es.Echocar diographicgui dancemaydecr easet hispar ticularcompl i
    cationof
    peri
    car diocentesiswhencompar edwi t
    hf l
    uoroscopi c- guidedper i
    cardi ocentesis.
    Placingadr ai
    nwi thoutconf irmat ionoft helocationoft heneedl eiscont raindicated.
    Theot herdi agnost i
    copt ionswoul dnotbet i
    mel yint hisur gentsi tuati
    on.

    14. A60-
    year
    -ol
    dobesemal
    esmokerpr
    esent
    swi
    thsubst
    ernalpl
    eur
    it
    icchestpai
    n.
    Onemont hago, herecall
    sasever eepi sodeofhear tburnaftereati
    ngal ar
    gemeal .His
    wiferecallshi
    m sweat i
    ngpr ofusel
    y.Hef el
    tpoor lyandf ati
    guedf orthedayafter.I
    n
    thepastweek, hi
    schestpai nhasbeenwor sewhi l
    esupineandwi thdeepinspirat
    ion.
    Hishistoryisnotabl
    ef orpoorlycont r
    olleddi abetes,hypertensi
    on, anddysli
    pidemia.
    Onexami nati
    on,heisuncomf or
    table.Hisbl oodpr essureis160/ 110mm Hg, hi
    s
    heartrateis85bpm, andhi stemperatur ei
    s37. 9° C.Jugularvenousdi st
    enti
    oni snot
    visi
    ble.Lungsar ecl
    ear .Scrat
    chymur muri saudi ble.Abdomeni sobese.Venous
    stasi
    schangesar eappar entoverthelowerext remities.

    Hi
    sel
    ect
    rocar
    diogr
    am i
    sshown(
    Figur
    e1)
    .

    Whi
    choft
    hef
    oll
    owi
    ngwoul
    dbet
    henextmostappr
    opr
    iat
    edi
    agnost
    icst
    ep?

    a. Anti
    nuclearanti
    body.
    b. Venti
    lat
    ion-perf
    usionscan.
    c. Coronar
    yangi ography.
    d. Chestcomput edtomography.
    ANSWER

    C. Cor onaryAngiography
    Thi spatientpresentswi t
    hsympt omsconsi stentwi t
    hper i
    carditi
    s,butalsohas
    car di
    ovascul arri
    skfactorsforcoronaryart
    erydi sease.Thehi storyofheartburn,
    diaphor esis,andfeel
    ingpoor l
    yforadayi sstrongl ysuggest i
    veofamyocar di
    al
    i
    nf arcti
    on( MI)athome, forwhichhedi dnotseekmedi calat t
    ention.The
    electrocardiogram i
    salsosuggest iveofapr i
    orant eri
    orMI .Thisclini
    calscenarioi
    s
    highlysuggest i
    veofpostinf
    arcti
    onper i
    cardit
    is(e.g.,Dressler'
    ssyndrome) .Dressl
    er'
    s
    syndr omehasbecomeanuncommoncompl icationofST- segmentel evati
    onMIi n
    themoder ner aduetot herapidtri
    ageandr eperfusiont r
    eatmentf orMI. 

    Abr oaddi f
    ferent i
    alshouldal waysbeentert
    ainedwhenadi agnosisofper icardi
    ti
    sis
    suggest edbycl inicalevaluati
    on.Otherdi
    agnost i
    cconsi
    derati
    onsi ncludepul monary
    embol ism withr esulti
    ngpl euri
    sy,
    aorti
    cdissecti
    onwithproxi
    malext ensi
    onr esul
    ti
    ng
    i
    nper icardi
    albl ood, andacut ecoronar
    ysyndromes.Inthispatient
    , anunr ecogni
    zed
    MIist hemostl i
    kel ydiagnosisandisbestconf i
    rmedwithcoronaryangi ography.I
    f
    coronar yangiogr aphyi snotdiagnosti
    c,t
    heot herdi
    agnosti
    copt i
    onswoul dbe
    reasonablet opur sue.

    15. A45- year-ol


    dmani sadmi tt
    edt ot hehospi t
    alaf t
    ersuf f
    eri
    ngsuddencar diac
    arrestathiswor kpl
    ace.Acowor kersuccessf ull
    yut i
    li
    zedthewor kplaceautomat ed
    externaldefibr
    il
    lat
    or,whi
    chr ecordedvent r
    iculartachycardia.Hishospit
    alevaluati
    on
    revealsapr evi
    ouslyundiagnosednoni schemi cdilat
    edcar diomyopathy.Heist r
    eated
    forsignsandsympt omsofhear tfail
    ure, andonhospi t
    alday3her ecei
    vesan
    i
    mpl antablecardiover
    ter
    -defibr
    il
    lator(ICD) .
     

    Thatnightyouarecall
    edbythefloornursewhoisconcernedthathi
    sbloodpressur
    e
    hasdroppedandhi shear
    trat
    ehasi ncreased.Hecomplai
    nsofchestti
    ghtnessand
    short
    nessofbreath.Hehasclearlungs,buthisj
    ugul
    arvenouspressur
    eiselevat
    ed.
    Hi
    sbl
    oodpr
    essur
    eis80/
    50mm Hgandhi
    shear
    trat
    eis120bpm.

    Hi
    select
    rocardiogr
    am showsnoi
    schemi
    cpat
    ter
    ns.Anechocar
    diogr
    am r
    eveal
    sa
    smal
    lperi
    cardialef
    fusi
    on. 

    Youtr
    ansferhimtothei
    ntensi
    vecar
    eunitandplaceacentr
    alvenouscat
    het
    eri
    nhi
    s
    ri
    ghti
    nter
    naljugul
    arvei
    ntomeasurehi
    srightheartpr
    essur
    es.
     

    Youobt
    aint
    her
    ightat
    ri
    al(
    RA)pr
    essur
    etr
    aci
    ngf
    rom yourcent
    rall
    ine(
    Figur
    e1)
    .

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    enextst
    ep?

    a. Pericar
    diocentesis.
    b. Thrombol yt
    ictherapy.
    c. Bloodtransfusion.
    d. Aggressi
    vediur
    esis.
    e. Surgi
    calper
    icar
    dialwindow.

    ANSWER

    A.Per
    icar
    diocent
    esi
    s

    TheRApr essuretracingi sconsi stentwithcardiact amponade,andt hepatientneeds


    pericardi
    ocentesi
    s.Thi sscenariodescr ibesapr obabl eri
    ghtventri
    cular(RV)
    perforati
    onfrom theICDpr ocedur e.Becausei tisacut e,t
    heamountofper i
    cardi
    al
    fl
    uidmaybesmal l.TheRAt racingshowsabl untedydescentconsi stentwithcardi
    ac
    tamponade.Thi sisduet othei nabi l
    it
    yoft heRVt of il
    linear
    lydiast
    oleoncet he
    tri
    cuspidvalvehasopenedast heRVdi astoli
    cpr essureisbeingaffectedbythe
    elevatedpericar
    dialpr essure. 

    Hissyst emicbl oodpr essur eisl


    ow, andapar adoxicalpul semaybedi f
    fi
    culttodet ect.
    Althoughabl oodt r
    ansf usionmi ghtbehel pf ulinthisinstance,itshouldnotbet he
    fi
    rststepaf t
    err ecognizingcar di
    act amponadei spr esent.Ifanythi
    ng,heneedsf l
    uids
    andi notropicsuppor t.Aggr essi
    vedi uresiswoul dr educepr eloadandmaywor senhi s
    signif
    icanthemodynami ccompr omi sebyr educingvent r
    icularfil
    li
    ng.Thrombol yt
    ic
    therapyhast hepot enti
    alt oworsent hesi tuation.Sur gi
    calconsul t
    ati
    onfora
    pericardialwindowmaybeconsi der
    ed, butt hef i
    rststepshoul dbeper i
    cardiocentesis,
    ast hi
    si susuallyallthati srequi
    r edtost abili
    zet hepat i
    entandr e-establ
    ishhis
    hemodynami cstatus.

    16. A20- year


    -oldwomanunder goessur gicalr
    epai rofalargesecundum at r
    ial
    septaldef
    ectviaamedi anster
    notomy.Twoweeksl ater
    ,shepr esentswithcli
    nical
    si
    gnsandsympt omsofl ar
    geperi
    cardialeff
    usion.Sheunder goesper icar
    diocentesi
    s,
    whichrevealsopalescentmil
    kyfl
    uid,
    whi chbyanal ysisishighint r
    igl
    yceri
    desand
    prot
    ein.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    eini
    ti
    alr
    ecommendat
    ioni
    nthi
    spat
    ient
    ?

    a. Di
    etwi
    thmedi
    um-
    chai
    ntr
    igl
    ycer
    ides.
    b. Colchicine.
    c. Steroids.
    d. Surgicalthoraci
    cductl
    igat
    ion.
    e. Pericardiect
    omy.
    ANSWER

    A. Di
    etwi
    thmedi
    um-
    chai
    ntr
    igl
    ycer
    ides.

    Thecor rectanswerf orachyl opericardialeffusioni stot rydi et


    aryeffortsbef ore
    surgery.Chyl oper i
    cardium i sararecompl icat i
    onofcar diacsur geryandt endst obe
    rel
    at edtodi sruptionoft horacicductt ri
    butaries.Per i
    cardi ocentesisisi ndicatedin
    thesepat i
    ent s.Becausemedi um chai ntri
    glycer i
    desar eabsor beddi rectl
    yi ntothe
    portalsystem andnott hroughl ymphat i
    cs,al ow- fatdiett hatincludesonl yt hesefats
    i
    st hemostappr opriatefirstli
    neoft r
    eatment .I nthemaj orityofcases, thisal ongwit
    h
    drainageoft hefluidwillallowcl osur eofthef istul
    ousconnect ionandavoi dmor e
    i
    nvasi vether apies.Surgicalper i
    car dialwindowandl igationandr esect i
    onoft he
    thoracicductj ustabovet hedi aphr agm havebeenr epor tedasef fectivetreatment
    optionsint hiscondi ti
    on, butusual lyar ereser vedforper sistentorr ecur r
    entchyl ous
    pericardi
    alef fusions.Phar macol ogi ctherapiesar enoti ndi catedint het r
    eat mentof
    thi
    scondi ti
    on.

    17. A70- year-


    oldwomanwi t
    hahi st
    oryofhypert ensi
    onanddysl i
    pidemiapresents
    wit
    hst utteri
    ngsubst er
    nalchestpai noverseveraldays.Ont hedayofadmi ssi
    on,she
    devel
    ops10/ 10chestpai natrest.Herinit
    ialvi
    talsar eabl oodpressureof160/90
    mm Hgwi t
    hahear trateof40bpm i ncompl etehear tblock.Hercardiacenzymesar e
    posit
    ive.Herelectrocardiogr
    am (ECG)demonst ratesdiffuseST-segmentdepr ession.
    Sheisdi agnosedwi thanon- STel evati
    onmyocar di ali
    nfarcti
    on,
    andi sr
    eferr
    edtot he
    cardi
    accat heteri
    zati
    onl aborat
    ory. 

    Atempor ar
    ypacingwireisimplanted.Diagnosti
    cangiographyviather i
    ghtfemoral
    ar
    teryreveal
    sobstruct
    ivediseaseinther i
    ghtcoronar
    yartery.Percutaneouscoronary
    i
    ntervent
    ion(PCI)i
    spursuedandi sdiff
    icultduetothetor
    tuosityofthetargetvessel
    .
    Postprocedure,
    thepatienti
    schest-painfree.Unfr
    acti
    onatedhepar i
    nandt icagr
    elor
    ar
    eadmi nist
    eredfol
    lowingPCI. 

    Thepatientisadmit
    tedtothecoronar
    ycareuni t
    .Approxi
    mat el
    y10-12hour slater
    ,
    thenursecallst
    oinfor
    m youthatthepati
    entishypot ensi
    ve.Thepatientreport
    smi ld
    dizzi
    ness,short
    nessofbreat
    h,chestpai
    nwi thdeepi nspir
    ati
    onandleaningf orward,
    andmi l
    dnausea.Shehasasupi nebloodpr essureof80/60mm Hg, wi t
    hapul serate
    of80bpm ( vent
    ri
    cul
    arl
    ypaced).Thecatheterizati
    ongroinsit
    elooksokay.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nhermanagement
    ?
    a. Incr
    easepaci
    ngrate.
    b. ECG.
    c. Echocar
    diogr
    am.
    d. Computedtomographyoft
    hechest
    .
    e. Computedtomographyoft
    heabdomen.

    ANSWER

    C. Echocar
    diogr
    am

    Thecor r
    ectansweri sanechocardiogram.Thi spati
    enthasdevel opedat raumati
    c
    i
    at rogenicper
    icardialef
    fusi
    onandt amponadeasal atecompl i
    cationofPCIort he
    tempor arypacemakeri mplant
    ation.Althoughtheincidenceislowf ol
    lowi ngPCI(0.2-
    0.4%) ,pr
    omptr ecogniti
    onisessentialsothatpreventi
    onoft hetransitionf rom
    effusiontotamponadecanbeat tempt ed(e.g.
    ,byreversinganticoagulat ion)ort
    he
    hemodynami ccollapsecaneitherbeaver tedortr
    eated( per
    icardiocent esis).
     

    Thepr esentat
    iondependsonseveralfactors,i
    ncludi
    ngthestr
    uctur
    ethati
    s
    perfor
    ated,thedevi
    cethatcausedtheper forat
    ion,t
    hebasel
    inehemodynamicstat
    us
    ofthepat i
    ent,
    andthelevelofant
    icoagulationpresent
    .Symptomscanbefair
    ly
    nonspecifi
    c. 

    I
    nt hi
    svignette,r
    iskfactor
    sincludethediffi
    cul
    tyofthePCIandt hetemporarypacer
    pl
    acementi nassociationwit
    ht heuseofpot entanti
    coagul
    ant s.Thispati
    entli
    kel
    y
    developedadi st
    alcoronarywireperfor
    ationorar i
    ghtvent
    ricularperf
    orati
    on
    unrecognizedatthetimeofthepr ocedure,butthentheper
    icar di
    aleff
    usionworsened
    i
    nt hesett
    ingofcontinuedanticoagulat
    ion. 

    AlthoughanECGcanbeconsi der
    ed, sheisbei ngpacedandhersympt omsar eoutof
    propor ti
    onf oranischemi ccauseoft hehypot ensi
    on.Similar
    ly,thereissomeover l
    ap
    i
    nsympt omat ol
    ogywi t
    ht hedevelopmentofacut epulmonaryembol i
    sm, butthi
    sis
    l
    oweront hedi f
    fer
    entialinwhatwasot herwiseanambul ator
    ypat ient
    .Hersympt oms
    al
    socoul dbeamani festati
    onofretroper i
    tonealhemor rhage(aconcer nthatwould
    promptr eturntothecar diaccatheterizati
    onl aborator
    y),butinthissettingan
    emer gencyechocar diogram shouldbet hef i
    rststudyordered.Admi nisteri
    ng
    i
    ntr avenousf lui
    dsisessent ialtotempor aril
    yr esuscit
    atethepatient.I
    ncr easi
    ngthe
    paci ngratewoul dlikelynotbeofmuchval ue.

    18. A24- year-ol


    dmanpr esent
    stot
    heemergencyroom withtheonsetofchestpai
    n
    over1day.Hedescr i
    besthepainasshar
    pandstabbing,wit
    hsomer adiat
    iontohis
    lef
    tshoul
    der.Hisbreathi
    ngalsoisal
    it
    tl
    eshall
    ow.Her epor
    tsfeverwi
    thchill
    sfort
    he
    past24hours.Heiscur r
    entl
    yonnomedicat
    ionsandhasnoknownal l
    ergi
    es. 

    Onadmi
    ssi
    on,
    hei
    sfebr
    il
    eto37.
    9ºC.Hi
    swei
    ghti
    s65kg.Hi
    sbl
    oodpr
    essur
    eis
    140/92mm Hg, heartrateis104bpm andregul
    ar,andrespir
    ator
    yratei
    s22
    breat
    hs/min.Hisphysicalexaminati
    onisnor
    mal,exceptforathr
    ee-component
    peri
    cardi
    alrub.Hi
    sel ect
    rocardi
    ogram i
    sshowninFigure1.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nmanagement
    ?

    a. I ndomethaci
    n50mgbidwithcolchicine0.6mgdai lyfor6weeks.
    b. Aspi r
    in800mgtidf
    or6weekswi thcol chi
    cine0.6mgbi dfor3months.
    c. Aspi r
    in325mgbidwit
    hcolchi
    cine0. 6mgbi df
    or4weeks.
    d. Pr edni
    sone60mgdail
    ywit
    hcol chicine0.6mgdai l
    yfor6weeks.
    e. I bupr
    ofen800mgti
    dfor7-
    10dayswi thcolchi
    cine0.6mgbi df
    or3
    mont
    hs.
    ANSWER

    E. I
    bupr
    ofen800mgt
    idf
    or7-
    10dayswi
    thcol
    chi
    cine0.
    6mgbi
    dfor3mont
    hs.

    Thecorr
    ectopti
    oni sibuprofen800mgt i
    df or7-
    14dayspluscolchi
    cine0.
    6mgbi d
    for3months.Thispatienthasclassi
    csympt omsofacut
    eperi
    cardit
    isconf
    irmedby
    hisel
    ect
    rocardi
    ogram wi t
    hSTel evat
    ionandPRdepressi
    oninmul ti
    plel
    eads.Thefi
    rst
    -li
    net
    reatmentishigh-doseaspirin(
    650-975mgt i
    d)ori
    buprofen(800mgt i
    d)for7-
    10days,al
    ongwi thcolchici
    nefor6mont hs. 

    I
    nt heICAP( I
    nvest i
    gat iononColchicineforAcut ePericar
    diti
    s)trial
    , addi
    ngcol chici
    ne
    for3mont hst ost andar danti
    -i
    nfl
    ammat oryregimens( ei
    therhigh- doseaspi ri
    nor
    nonsteroidalant i-infl
    ammat orydrugs[NSAI Ds])reducedther elati
    ver i
    skofi ncessant
    orrecurrentper icar dit
    isby44%.Thest andar dhigh-doseanti-infl
    ammat ori
    eswer e
    usedonl yf orthef irst7- 14days,withtaperingbyt heendof3- 4weeks.Thebenef i
    ts
    ofcolchicinewer ei ndependentoft heuseofei theraspiri
    norNSAI Ds.Pr ednisone
    generall
    yi sr eservedf orthoseall
    ergictoori nt
    olerantofaspir
    inorNSAI Ds, and
    i
    ncreasest her i
    skofr ecur r
    entperi
    cardit
    is.Apr otonpumpi nhibitorshoul dbeadded
    totheant i
    - infl
    ammat oryregimen.

    19. A50- year-oldwomanwi t


    hahi storyofbr eastcancer,di
    abetes,hypertensi
    on,
    andcor onaryarterydiseasepresentst otheemer gencyroom withprogressive
    shortnessofbreath.Shehadbeenf eel
    ingwel lunt i
    labout6mont hsagowhenshe
    noti
    cedshehadbegunt oloseweightwi thouttryingtodoso.Shenowcompl ai
    nsofa
    2-weekper i
    odwi t
    hwor seningdyspneaevenatr est.Hermedicati
    onsinclude
    metformin500mgbi d,l
    isi
    nopril20mg, aspi
    ri
    n81mg, clopi
    dogrel75mg, metoprol
    ol
    25mgbi d,l
    evothyroxine125mcg/ kg,andchl orthali
    done25mgeachday.  

    Onexami nat
    ion,herbloodpressureis90/70mm Hgandhear trat
    eis100bpm.She
    isaf
    ebril
    e.Herbodymassi ndexis28.3.Shehasclearl
    ungfi
    elds,
    butherj
    ugul
    ar
    venouspressureiselevat
    edabovet heclavi
    cleupr
    ight,
    butt
    hereisnoedema.The
    heartsoundsaredistant,
    butnomur mur sareaudi
    ble.

    Anelectrocar
    diogram i
    snormalexceptf
    orl
    owvoltage.HerchestX-
    rayi
    sclear
    exceptforcardi
    omegaly.Youobtai
    nanechocar
    diogram thatr
    eveal
    sevi
    dencefora
    peri
    cardialef
    fusi
    on(Figur
    es1and2) .
    Fi
    gur
    e1.
    Fi
    gur
    e2.

    Basedont hepr
    evi
    ousi
    nfor
    mation,
    whichofthefoll
    owingchar
    act
    eri
    sti
    csoft
    he
    present
    ati
    onwouldwar
    rantur
    gentper
    icar
    diocentesi
    s?

    a. Thefactt
    hatthecausei slikel
    ymal ignancy.
    b. Thehemodynamici nstabil
    ity.
    c. Thel
    ikeli
    hoodthi
    sisper icardialhemorrhage.
    d. Theechocardi
    ographicfindings.

    ANSWER

    B. Thehemodynami
    cinst
    abi
    li
    ty

    Thecorrectopti
    oni
    sthehemodynami cinst
    abil
    it
    y.Whiletheechocardiogram reveal
    s
    ther
    eisnotonlyperi
    car
    dialef
    fusi
    onpresentbutalsorightvent
    ri
    cul
    ardi astol
    ic
    coll
    apse(Figur
    e3)and>25%mi tr
    ali
    nfl
    owvar i
    abil
    ityconsist
    entwit
    ht amponade, thi
    s
    wouldnotdictateanur gentresponseift
    hepat i
    entwer ehemodynami cal
    lyst
    abl e.Her
    weightlossandlargeef f
    usionsuggestthi
    spr ocesshasbeengoi ngonf oralongt i
    me
    andthecausei shighlyli
    kelyrelat
    edtoherpr i
    ormal i
    gnancy.Whil
    eitispossiblethe
    charact
    eroftheper i
    cardialfl
    uidishemorrhagic(especi
    all
    ygivenit
    slikel
    ycauseand
    theuseofdualant i
    platel
    ettherapy),
    thi
    sshoul dhavenobear i
    ngont heurgencyofa
    peri
    cardialt
    ap.

    Fi
    gur
    e3.
    20. A52- year
    -oldmanpresent
    stotheemergencyroom wi
    thabdomi nalpainand
    bl
    oati
    ng,lowerextremi
    tyedema,anddecr
    easedappetit
    eofseveralmonthsdurati
    on.
    Onexaminat i
    on,heisf
    oundtohavemarkedjugul
    arvenousdistenti
    on,asci
    tes,
    and
    per
    ipher
    aledema.

    Echofindi
    ngsar
    eshown(
    Figur
    es1,
    2,3,
    4).Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    y
    diagnosi
    s?

    Fi
    gur
    e1.
    Fi
    gur
    e2.
    Fi
    gur
    e3.
    Fi
    gur
    e4.

    a. Restri
    cti
    vecardi
    omyopathy.
    b. Chronicobst
    ruct
    ivepulmonarydi
    sease(
    COPD)
    .
    c. Constri
    cti
    veperi
    cardi
    ti
    s.
    d. Dil
    atedcardi
    omyopathy.

    ANSWER

    C. Const
    ri
    cti
    veper
    icar
    dit
    is

    Theinferiorvenacava( IVC)isdilat
    ed, asignofel
    evatedr i
    ghtatri
    alpressure.Mitral
    inf
    lowvar iabi
    li
    ty(i
    nspirator
    yf al
    loft hepeakEwavevel ocityof>25%ont hefir
    stbeat
    fol
    lowingt heonsetofinspirati
    on)isar efl
    ecti
    onofthedi ssoci
    ati
    onofi nt
    r at
    horacic
    andintracardiacpressures.Oni nspirat
    ionthewedgepr essurefal
    ls,butleft
    ventr
    icular(LV)diastol
    icpressur eremainsconstant
    ,hencet heleftatr
    ial
    / LVpressure
    gradientdecreases.Expirator
    yfl
    owr eversalinthehepat
    icveinsisalsoaref
    lect
    ionof
    thedissociat
    ionofpr essuresdescr
    ibedear l
    ierandventr
    iculari
    nter
    dependence.The
    l
    ow- veloci
    tysuperiorvenacava( SVC)flowwi thminimalrespir
    ator
    ychangeisalso
    characteri
    sti
    cofconst ri
    ction.
     

    COPDandast hmaexacer bati


    onbot hhavemi tr
    alinfl
    owvari
    abil
    it
    y,butt hesedonot
    conformt othefi
    rstbeatfol
    lowingtheonsetofi nspi
    rati
    onandexpir
    ation.Int hese
    scenarios,t
    hereismar kedrespi
    ratoryvar
    iat
    ioni nSVCf l
    ow.I
    nrestri
    ctive
    cardi
    omyopat hy,ther
    ei snovariabi
    li
    tyofmit
    ralandt ri
    cuspi
    dinf
    lows, noexpi rat
    ory
    fl
    owr eversali
    nthehepat i
    cveinsandt hemitrale'vel
    ocit
    yismarkedlydecr eased.
    Pul
    monar
    yCi
    rcul
    ati
    onDi
    sor
    der
    s
    Quest
    ion:

    1. A65- year -oldmanwi thsystemi chypertensionandpar oxysmalat r


    ialfi
    bril
    lati
    onis
    hospitalizedf orshor tnessofbr eath.Onphysi calexam, hisHRi s75, BPi s155/88, andoxygen
    saturationi s95%onr oom air.Hiscar diovascularexam isnot ablef oraJVPof10cm H20,
    heartexam i sr egul arwi thaf aintS3,S4, andaI I/
    VIholosystolicej ecti
    onmur muratt heapex.
    Cracklesar ehear di nbot hlungbases, andhehast racebilaterallowerext r
    emi t
    yedema.Hi s
    echocar diogr am demonst r
    atesanEFof65%, LVH, mil
    d-moder atemi tr
    alregurgitat
    ion,and
    pulmonar yar terysyst oli
    cpr essur eesti
    mat edat48mmHg.Hi sECGdemonst r
    atesnor mal
    si
    nusr hythm wi thl eftventri
    cul arhypertrophy.ChestCTshowedmi ldbibasil
    arpulmonar y
    i
    nfil
    trates, butot herwi senor mall ungpar enchymaandnoPE.Bedsi dePFTswer enor mal
    exceptf ormi ldr educt ionindi f
    fusioncapaci t
    y.BNPi s135ng/ L.Hei scurrentl
    ytaki ng
    met prololsucci nate50mgdai ly,amiodar one200mgdai l
    y, l
    asix20mgdai l
    y,andwar f
    ari
    n.

    Whati
    sthenextappr
    opr
    iat
    est
    epi
    nthemanagementofhi
    spul
    monar
    yhyper
    tensi
    on?

    a. Si
    ldenafil20mgt hreeti
    mesdai l
    y.
    b. Disconti
    nueami odarone.
    c. I
    ncr easelasi
    xto40mgdai ly.
    d. Ri
    ghthear tcatheteri
    zat
    ion.
    e. Pulmonar yventi
    lati
    on-perf
    usionscan.

    Answer
    :

    1. c. I
    ncr
    easel
    asi
    xto40mgdai
    ly.

    Whilerecentevi
    dencepointstoani ncreasei
    nthenumberofpatientswit
    hWHOGr oup1
    pulmonaryarter
    ialhypert
    ensi
    on( PAH), t
    henumberofpati
    entswithpulmonar
    yhypert
    ensi
    on
    (PH)relat
    edtochroniclef
    theartdisease(WHOGr oup2)orchronichypoxi
    cst
    ates(WHOGroup
    3)isfargreat
    er.

    Whilet hi
    spatientdoeshavemoder atepul monaryhypertensionbyechocr it
    eria,hepresents
    withmul ti
    plesignsandsympt omsofl eftheartf
    ail
    ure,andthedi agnosti
    ctesti
    ngper f
    ormedso
    farclearl
    ysuggest sthathehasincreasedpulmonar yvenouspr essureli
    kelyrelatedt
    ochr oni
    c
    hyper t
    ension,l
    eftventri
    cul
    arhypert
    rophy, anddiast
    olicdysfunct ion.Thefi
    rststepistomanage
    hisincreasedpulmonar yvenouspressur ewit
    hadditionaldiuresis.

    Intheevaluati
    onofpul monar yhypert
    ension( PH),i
    tisimport
    anttofi
    rstevaluateforl
    eftheart
    diseaseorlungdisease.Iftheseareconf i
    rmedandt r
    eatedwit
    houtimprovement ,orofthe
    sympt omsar eoutofproporti
    ont othedegr eeofdisease,t
    henaddit
    ionalevaluati
    onis
    war r
    anted.Ruli
    ngoutchr onicthromboembol icdiseaseisanappropri
    atenextstep.Oncet hese
    stepshavebeencompl et
    ed, i
    fthepatientremainswi t
    hPHt henadditi
    onaltesti
    ngi swarrant
    ed
    tofurthereval
    uateforpul
    monar yart
    erialhypert
    ension.

    Forthi
    spati
    ent,
    rightheartcathet
    eri
    zati
    onisnotnecessar
    yatt hisst
    ageoftheeval
    uat
    ionunt
    il
    thepati
    enti
    sfurt
    herdiuresed.AV/ Qscani
    salsonotyetindicated;t
    hepat
    ienti
    s
    anti
    coagul
    atedmakingthromboembol icdi
    seaselessli
    kel
    y,andt hemorel
    ikel
    ycauseofhi
    s
    i
    ncreasedpulmonar
    ypr essur
    eshouldfir
    stbetr
    eated,aspulmonaryedemacanr esul
    tin
    abnormalV/Qresul
    ts.Amiodaroneisunl
    ikel
    ytobecont r
    ibut
    ingher
    einlightofthenormallung
    parenchymaandrel
    ativel
    ynormalPFTs:themildl
    yreducedDLCOmayal sobeseenduet o
    pul
    monar yedema.I
    twoul dbeinappropr
    iat
    etobegintreatmentwi
    thsil
    denafi
    lforPAHunt i
    lthe
    di
    agnosisofPAHwer emade.

    Quest
    ion:

    2. A49- year-oldwomanpr esent stoyourcl inicforeval uationofpr ogressivedyspneaon


    exerti
    onoverl ast2year s.Herhi stor yissignifi
    cantf orobesi tytreat edwi t
    h
    fenfl
    uramine/ phentermine20year sago, remotet obaccouse, andr emot eDVTassoci atedwith
    tobaccouseandor alcontraceptivepi ll
    s.Onphysi calexami nat ion,hear tratei
    s72bpm, BP
    142/85, Pulseoximet ryis95%onr oom ai randBMIi s45.Shei sinnoacut edistress.
    Pulmonar yexami nat i
    onisnot ablef orabi basil
    arcr ackleswhi chcl earwi t
    hcough.Car diac
    exami nati
    onr evealsanor malS1/ S2 withaI I
    /VIholosyst ol
    icej ectionmur muratherapex.Ther e
    i
    snoRVheave.Herext r
    emi t
    iesar ewar m, andtherei snoedemaorcl ubbing.HerECG
    demonst ratesnormalsi nusr hythm wi thbor derl
    inel owvol t
    ageQRS.Echocar diogram i sli
    mit
    ed
    butshowsmi l
    dlydilatedRVwi t
    hmi ldl
    yr educedf unct i
    on,traceTR, normalLVf unctionand
    PASPest i
    mat edat25mmHg.HerV/ Qscanshowedsmal lper fusiondef ectint her i
    ghtlower
    l
    obe.HerPFTsshowedmi ldl
    yr educedDLCOandmi ld-moder at erestricti
    on.Ri ghthear t
    catheteri
    zationreveals:RA4mm Hg, RV30/ 4mm Hg, PA33/ 16mean22mmHg, PCWP12
    mmHgandLVEDP11mmHg.HerCOi s5.4L/ min.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nhercar
    e?

    a. Startsi
    ldenaf
    il
    b. Vasodilat
    ortest
    ing
    c. Referforbari
    atr
    icprogram
    d. Pulmonar yangi
    ogram
    e. Repeatechocardiogram i
    n6mont
    hs

    Answer
    :

    2. c. Ref
    erf
    orbar
    iat
    ri
    cpr
    ogr
    am

    Thispat i
    enthassympt omsofwor seni
    ngdyspneaonexerti
    on,andamedi calbackgroundof
    priorDVTwi thl
    ikel
    yPE, signi
    fi
    cantobesi
    ty,
    hyper
    tensi
    on,andprioruseof
    fenfl
    uramine/phenter
    mi ne.Theinci
    denceofPAHisapproxi
    mately0.005%iffenf
    lur
    ami nei
    s
    usedf orgreat
    erthan3mont hs.

    Eval
    uat
    ionf
    orpul
    monar
    yhyper
    tensi
    oni
    swar
    rant
    edher
    ebasedonhersympt
    omsandhi
    stor
    y.

    Cardi
    accat heteri
    zationi nthispat i
    entdemonst
    rat
    edthatwhileshehasmodestsyst
    emicand
    pulmonarypr essureel evation,shedoesnotmeetcrit
    eri
    aforthediagnosi
    sofpul
    monary
    hyper
    tension:thisisdef inedatameanPAP>25mmHgatr estint
    hesetti
    ngofanor
    mal
    pulmonarycapi l
    larywedgepr essure(3Woodunit
    s.Hersympt omsmaybeduet oherobesi
    ty
    andtheref
    or ewei ghtlossi ntervent
    ionsarei
    ndi
    cated.
     

    Acut
    evasodil
    atort
    est
    ingshouldbeperf
    ormedinalli
    diopat
    hicpulmonar
    yart
    erialhyper
    tensi
    on
    (I
    PAH)pat
    ient
    swhomi ghtbeconsi
    der
    edpotent
    ialcandi
    datesforl
    ong-t
    ermtherapywithoral
    cal
    cium channelbl ockers.IPAHpat i
    entsinwhom chr oniccalcium channelblockertherapy
    wouldnotbeconsi dered,suchast hosewi thovertrightheartfail
    ureorhemodynami c
    i
    nstabil
    it
    y,neednotunder goacut evasodi latort
    esting.Thedef ini
    ti
    onofanacut eresponsethat
    maywar rantiniti
    ationoflong-termt herapywi thoralcalcium channelblockersisadecr easein
    mPAPofatl east10mm Hgt oanabsol utemPAPofl essthan40mm Hgwi thoutadecr easein
    car
    diacout put.Acut evasodil
    atortestingisnoti ndi
    cat ed,andmaybehar mful,inpatientswit
    h
    si
    gnifi
    cantl
    yel evatedleftheartfi
    ll
    ingpr essures.

    Tr eatmentwithendot hel i
    nr eceptorant agoni stsorphosphodi est
    eraseinhibi
    torsisoften
    i
    ndi catedinpatientswhohavenegat iver esponset oacut evasoreacti
    vetesti
    ngandar ei nlower
    riskcategori
    es.TheSUPER- 1(Sil
    denaf i
    lUsei nPul monar yAr t
    eri
    alHypertension)studywasa
    randomi zed,doubl e-blind, placebo- cont rolledt r
    ialthatassigned278pat ient
    swi thPAH( either
    IPAHorPAHassoci atedwi thconnect ivet i
    ssuedi seaseorwi threpair
    edcongeni talsystemi c-t
    o
    -pul monaryshunt s)topl aceboorsi ldenaf il(20,40, or80mg)or all
    y3timesdai lyfor12weeks.
    The6MW t estincreasedf rom basel inei nal lsildenaf i
    lgroups,withmeanpl acebo- corr
    ect ed
    treatmenteffectsof45, 46,and50m f or20- ,
    40- ,and80- mgdosesofsi l
    denaf i
    l,r
    espectively.
    Thi sappearedt obeent i
    relyr el
    atedt oi mpr ovement swi thacti
    vetherapy,astherewasl ittle
    changei n6- minut ewal ktesti nthepl acebogr oup.Al lsil
    denafi
    ldosesreducedt hemPAPand
    i
    mpr ovedfunctionalcl ass.Thei ncidenceofcl inicalwor seni
    ngdi dnotdif
    fersignifi
    cantl
    y
    bet weenthepat ientstr eatedwi t
    hsildenaf i
    lver suspl acebo.

    Patientswi t
    hsuspectedPAHshoul dunder goeval uati
    onf orchronicthromboembol i
    c
    pulmonar yhypertension(CTEPH) .Thescreeningt oolofchoicef orCTEPHi sventi
    lat
    ion
    perfusionscanning.Ifindicati
    veofCTEPH, apul monar yangiogram shoul dbeper f
    ormed.
    Patientsareconsideredt obecandi dat
    esforpul monar ythromboendar terectomy(PTE)ift
    hey
    havesur gicall
    yaccessiblediseaseandpr esentaccept ablesurgicalr
    isk.ThegoalofPTEi sto
    removesuf f
    ici
    entmat eri
    alfrom t
    hepul monaryar t
    eriestosubst anti
    all
    yl owerPVRandi mprove
    cardiacout put
    .Thiscompl exandli
    fe-savi
    ngt herapyisbestper formedathi gh-
    volume
    centers. 

    Repeatechocar
    diogr
    am i
    n6mont
    hsi
    snotwar
    rant
    edi
    ntheabsencechangei
    ncl
    ini
    calst
    atus.

    Quest
    ion:

    3. A34- year-ol
    dwomancomest oyourclinicforevaluationofdyspneaonexer t
    ion.She
    hasahi storyofGERD, andapriorDVTduringr ecoveryfrom kneesur gery.Sher epor t
    st hat
    overt hepastyearshehasnot i
    cedincr
    easingfat i
    gue.Sheusedt ojoglastsummerbutst opped
    i
    nt hef al lduet oincr
    easingproblemswithRaynaud' si nherhands.Sheswi t
    chedt oani ndoor
    tr
    eadmi llbuthasbeenget ti
    ngmor eshortofbreathwi ththisandhast ostopear lier.Her
    medi cat ionsi ncl
    udelansoprazoleandanor alcontraceptive.Herphysicalexam i snot ablefora
    HR80, BP135/ 82,pulseoxygenof97%onr oom air.Herpul monar yexami nati
    oni s
    unremar kable.Cardi
    acexami nati
    onisnotableforapr omi nentS2att heapex, andal eft
    parast ernalheave.HerJVPi s6cm H20.Shehasnol owerextr emit
    yedema, not ender nessor
    palpabl evenouscor ds.Herhandsar epuff
    yandt heski nonherdi stalf
    ingersisshi ny.HerECG
    i
    sshowni nFi gur
    e1.
    Whati
    sthemostappr
    opr
    iat
    enextt
    estf
    orhereval
    uat
    ion?

    a. Echocardi
    ogram
    b. Exerci
    sestr
    esstest
    c. V/Qscan
    d. Ri
    ghtheartcatheter
    izati
    on
    e. Pulmonaryfuncti
    ont est
    s

    Answer
    :

    3. a. Echocar
    diogr
    am

    Thispati
    enthasphysicalexami nat
    ionandECGf i
    ndingsconsist
    entwithrightventri
    cular
    hypert
    rophyandpulmonar yhyper t
    ension(l
    oudP2) .Inaddit
    ion,shehasahi storyandphysi
    cal
    exam f
    indingssuggesti
    veofsyst emicscler
    osis.Giventhesefi
    ndings,
    therei ssi
    gnif
    icant
    concernforpul
    monar yart
    erialhypert
    ension(group1pul monaryhypertension).

    Giventhehi ghcl
    inicalsuspicionf orpul monar yhypertensionandt hediagnosisofr i
    ght
    ventri
    cularhypert
    rophyi nthispat ient,anechocar diogram isthemostappr opriatenexttestto
    confir
    mt hediagnosisandeval uatet hedegr eeofsever it
    y.AV/ Qscanmaybeconsi deredat
    somepoi nt,butdespiteherpr iorDVTaf tersurgery,chronicthromboembol i
    cdiseaser emai ns
    lessli
    kelythanpulmonar yar t
    er i
    alhyper tensionassoci atedwithsystemicsclerosisbasedon
    herhistory.Pul
    monar yfunctiont estsar eunlikel
    yt obesi gnif
    icant
    lyabnormalinher ,and
    theref
    orear eunl
    ikelytoaidindet er miningpr ognosisort reat
    mentf orher
    .Anexer cisestress
    testissi milarl
    yunlikelytobehel pfulinhereval uati
    on, ashersympt omsar eunli
    kelyt
    obedue
    toischemi aorarrhythmias.A6- mi nute-walktestwoul dbeabet t
    ertoolatthisstagetohelp
    stratif
    yherr i
    sk.Arightheartcat heterizati
    onisoftenindicatedwhent hediagnosisof
    pulmonar yar t
    eri
    alhypertensioni ssuspect edorknown, butitismor eappropriat
    et of
    ir
    st
    pur suemor enon-invasivetesting.Wi thabet t
    erunder standingofherdi agnosisanddisease
    sever i
    ty,ar i
    ghthear tcathet
    erizationmaybemor eusef uliftheresponset oacutevasodil
    ator
    s
    i
    seval uated,whichcant hengui det herapy.

    Thereare5groupsofpul monaryhypert
    ensionascl assi
    fiedbyt heWHO:gr oup1, pulmonary
    art
    eri
    alhypert
    ension;group2,pulmonaryhypertensionduet olefthear
    tdisease;group3,
    pulmonaryhypertensi
    onassociat
    edwithlungdi seasesand/ orhypoxemia;group4, pulmonary
    hypert
    ensionduet ochroni
    cthromboti
    cand/ orembol i
    cdi sease(CTEPH);andgr oup5,
    miscel
    laneous(sarcoi
    dosis,l
    ymphangiomatosis,compr essionofpulmonaryvessel s)
    .

    Apr i
    mar ypul monaryar teriopathyoccur smostcommonl yi npati
    entswi t
    ht heli
    mi ted
    cutaneousf orm ofsystemi csclerosis,former l
    yref
    erredtoast heCREST( calci
    nosis, Raynaud’s,
    esophagealdysf unction, sclerodactaly,telangect
    asias)variant
    .Alt
    houghataut opsy, 65%t o
    80%ofi ndividual
    shavehi stopathologicalchangesconsi stentwit
    hPAH, lessthan10%devel op
    cl
    inicall
    yappar entdisease.Sur veil
    lanceechocar diographysuggestst hatthereisasubst ant
    ial
    prevalenceofmi ldtomoder atePHi nconnect i
    veti
    ssuedi seasepatients.However , t
    he
    managementandnat uralhi st
    oryofsuchpat i
    entshasnotbeenwel lstudied.Histology
    consistentwi t
    hPAHhasal sobeenobser vedinsystemiclupuserythemat osus, mixed
    connect i
    vetissuedisease, andr heumat oidar t
    hri
    ti
    s.

    I
    naddi t
    iont othescleroderma/ connecti
    vet i
    ssuespectrum ofdiseases,gr
    oup1PHal so
    i
    ncl udes:i
    di opathi
    c,famili
    al(usuallyassociatedwit
    hbonemor phogeni
    cprotei
    nreceptor-2
    [
    BMPR2]aut osomaldomi nantmut ati
    ons),congeni
    tal(systemic-to-pul
    monaryshunts),por
    tal
    hyper t
    ension, HIVi
    nfection,drugsandt oxi
    ns, andotheril
    lnessessuchashemogl obinopathies,
    glycogenst oragediseases, heredit
    aryhemor rhagi
    ctelangiect
    asia,andchronic
    myel oprol
    iferati
    vedisorder.

    Quest
    ion:

    4. A28yearol dwomanpr esent


    stoyourcl i
    nicwitha6monthhistor
    yofprogressi
    ve
    dyspneaandchr onicfat
    igue.Pastmedicalhi
    storyisremar
    kabl
    eforarthr
    it
    is.Hercurr
    ent
    medicati
    onsincludeibuprofenasneeded.Sher epor
    tsexer
    ti
    onaldyspneawhenwal ki
    ng
    dist
    ancesgreaterthan100f eet
    . 

    Onexam, bloodpr essureis112/ 65.Pulsei s76andr egular.Room air02 sat


    ur at
    ionis93%.BMI
    2
    i
    s20kg/ m .Car diacauscultati
    onr evealsasof tsystolicfl
    owmur muratt herightsternalborder
    .
    P2 
    componentoft hesecondhear tsoundi saccentuat ed.Lungexam i sclearbi l
    ater
    all
    y.EKG
    demonst r
    atessinusr hythm wit
    hi ncompl eteRBBB.Tr ansthoraci
    cechocar diogram reveals
    normalleftvent
    ricularsyst
    olicfunction,moder ateTRandami l
    dlyenlargedrightventri
    cleand
    ri
    ghtatr
    ialenlar
    gement .Ri
    ghtvent ri
    cularsystoli
    cpressur esi sesti
    mat edat59mm Hg.
    Agit
    atedsalinei
    nj ecti
    onwasnor malwi thnoevi denceofshunt .

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nhermanagement
    ?

    a. Car
    diacMRI
    b. Myocardi
    alPer
    fusi
    onI
    magi
    ng
    c. Ri
    ghtheartcardiaccat
    heteri
    zati
    on
    d. PEprot
    ocolCTangi ogram ofthechest
    e. Noct
    urnalpolysomnography

    Answer
    :

    4. c. PEpr
    otocolCTangi
    ogr
    am oft
    hechest

    Thedi
    agnosisofpulmonar yhypert
    ensionencompassesWHOcl assesI-V,ofwhi
    chtypeIis
    pul
    monaryarter
    ialhypertensi
    on(PAH).Becauseofheryoungage,lackofcomorbi
    dit
    iesand/or
    si
    gnsofl
    eftheartdisease,wesuspectPAHi nthi
    spati
    ent.

    RHCi sindicatedi npat i


    entswithsuspectedpulmonar yar terialHTNaspar tofthewor kupof
    elevatedrighthear tpressuresdetect
    edonechocar di
    ogr aphy.Al thoughcar di
    acMRIcan
    provideanat omi cinformation,i
    twil
    lnotconfir
    mt hedi agnosi sofPAH.Myocar dialperfusi
    on
    imagingi snoti ndicatedasshei snothavingact iveangi naandherpr etestprobabili
    tyofCADis
    low.CTangi ographymaybehel pf
    ultofurt
    hereluci datetheet i
    ologyofpul monar yHTNwhen
    signif
    icantthromboembol i
    cdiseaseissuspected.However ,thechr onicit
    yoft hispati
    ent's
    sympt omsmakeVQscanmor eappropriat
    efort heeval uationofchr onicthromboembol i
    c
    pulmonar yhyper tension.Sleepstudymaypr ovidei nformat ionaboutet i
    ologyofpul monar y
    hypertension,RHCr epresentstheonlywayt oobt aindi r
    ectmeasur ement sofpul monary
    vascularresistanceandt heref
    oreestabl
    ishadi agnosi sofPAH.

    Quest
    ion:

    5. A72yearol dmanwi thahist


    oryofhypertensi
    onandpr ostat
    ecancerpr esentsfor
    eval
    uationofdyspnea.Threeyear
    sago, thepati
    entunderwentarobot i
    cprostatect
    omyt hat
    wascompl i
    catedbysepsisandapr ol
    ongedI CUcourse.Atthatti
    me, tr
    ansthoracic
    echocardi
    ogram perf
    ormed,demonstratednormalLVsystoli
    cfunction.Fol
    lowingdischarge
    fr
    om thathospit
    ali
    zati
    on,hehashadpr ogressi
    vedyspneaonexer ti
    on.

    Heunder wentmyocar
    dialperf
    usi
    onstudywhichreveal
    ednoevi denceofischemia,
    butshowed
    evidenceofRVhypert
    rophyandRVenlargement.Repeatechocardiogr
    am reveal
    snormalLV
    functi
    on,moderat
    eRVenl ar
    gement,
    moder at
    etri
    cuspidregur
    gitat
    ionrightvent
    ri
    cul
    ar
    hypertr
    ophyandPASPof55mmHg.  

    Uponexam t oday,hisbloodpr essuremeasured145/76,pulse78andr


    egul
    arandO2 sat
    urat
    ion
    =93%onr oom air.Physicalexam demonstratesaquietpr
    ecordi
    um wi
    thnomur mur
    s.S2 
    is
    spl
    itphysiol
    ogically.P2 
    i
    sl oud.Lungsarecl
    ear .Ther
    eisnoedemaperi
    pheral
    ly.Hei
    snoton
    anycardiovascularmedi cati
    ons. 

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextmostappr
    opr
    iat
    est
    epi
    nhi
    scar
    e?

    a. Exerci
    seechocardiogr
    aphy
    b. Nocturnalpol
    ysomnogr aphy
    c. HIVserologi
    es
    d. Pulmonaryventil
    ati
    onper f
    usi
    onscan
    e. Coronaryangiogr
    aphy
    Answer
    :

    5. d. Pul
    monar
    yvent
    il
    ati
    onper
    fusi
    onscan.

    Thecor rectansweri spulmonar yventilati


    onperfusionscan( VQscan) .Thispat i
    ent'
    shi st
    oryof
    cancerandpr ol
    ongedhospitali
    zationsuggest sthathemayhavedevel opedpul monar y
    embol icdi sease.VQscansar ethescr eeningstudyofchoi cet oexcludechr onic
    thromboembol i
    cpulmonarydiseaseasacauseofpul monar yhyper t
    esion.Hissci nti
    graphic
    fi
    ndi ngsar ehighlysuggest
    iveofpul monar yHTN( RVH/RVenl ar
    gement )
    .Exercise
    echocar diographywoul dhavelimitedut il
    it
    yinthiscir
    cumst ance,ashisMPIhasexcl uded
    signifi
    canti schemiaburden.HIVt est
    ingi sreasonable,butgi venhisclini
    calhistory,chronic
    thromboembol i
    cdiseaseseemsmor el i
    kely.Coronaryangiogr aphyisnoti ndicatedashi s
    stresst estshowednoevi denceofi shchemi aandhi sexertionalsympt omsar emor elikel
    y
    relatedt opul monar yhyper
    tension.Noct urnalpolysomnogr aphymaybeconsi deredonce
    chr onict hromboembol icdi
    seasei sexcl uded.

    Quest
    ion:

    6. A39yearoldwomanseeksasecondopi nionregar
    dingherdyspnea.Oneyearago,she
    developedincr
    easingdyspneaonexer t
    ionwi
    thoccasionalpalpit
    ati
    ons.Shewasrefer
    redtoa
    cardiol
    ogistwhoperformedastressechocar
    diogram.Sherelatesthati
    treveal
    edshehadhigh
    pressuresinherheart.Shecur
    rentl
    ytakesdi
    lt
    iazem 120mgdai l
    yandaspiri
    n81mgdai l
    y.

    Physi
    calexam r
    eveal
    sabl oodpressureof108/64andapul seof63bpm.O2 
    sat
    urat
    ionon
    room ai
    rwas93%.Cardiacexam reveal
    edapr ominentsecondheartsoundandaI/I
    Vdiast
    oli
    c
    murmuratthebaseoftheheart.Shehasmoder atepret
    ibialedema.

    Herest
    imatedpul
    monaryarteri
    alsyst
    oli
    cpressur
    eonherrecentechowas76mmHg.Ther
    e
    wasnoevidenceofi
    nter
    atr
    ialshuntbyagit
    atedsal
    inecont
    rast
    . 

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nthi
    spat
    ient
    'smanagement
    ?

    a. Myocar
    dialPerfusionImagingSt udy.
    b. Tr
    ansesophagealechocar di
    ogram.
    c. Lef
    tandrightheartcatheter
    izat
    ion
    d. PEprot
    ocolCTangi ogr
    aphyoft hechest.
    e. Ri
    ghtheartcatheteri
    zati
    onwi t
    hvasodilat
    orchal
    lenge.

    Answer
    :

    6. e. Ri
    ghthear
    tcat
    het
    eri
    zat
    ionwi
    thvasodi
    lat
    orchal
    lenge.

    Thenextbestst
    epint hi
    spati
    ent
    'seval
    uat
    ionwouldberighthear
    tcathet
    eri
    zati
    onwi t
    hplanned
    vasodi
    lat
    orchal
    lenge.Hersympt
    omsandpr iori
    magingstudi
    esallsuppor
    tthediagnosi
    sof
    pulmonar yhyper tension.TheACCF/ AHAgui deli
    nesf ort hetr
    eatmentofpul monar y
    hypertensionf ocusont heimpor tanceofobt aini
    ngar ightheartcardiaccat heteri
    zati
    ont o
    confir
    mt hedi agnosi sofpul monar yHTN.Thi sshoul dincludemeasur ement sofoxygen
    saturati
    onsandr ighthear tchamberpr essuresincludingt hepulmonar yarteryandcal culati
    ons
    ofcardiacout put/indexandpul monar yvascularresistance.Atthet i
    meofr ightheartcardiac
    catheteri
    zation,ther esponset oacut evasodi l
    atorsubst ancesshoul dbeassessedaswel l.
    Furtherevaluat i
    onf orcoronar yarterydiseasewi thmyocar di
    alperfusionimagi ngorl eftheart
    cathisnoti ndicatedatt histimegi venhernor malst ressechocar diogram andherl owpr etest
    probabili
    ty.CTangi ographyoft hechestmaybehel pfulindeterminingt heet i
    ologyofher
    suspectedpul monar yHTN, butthedi agnosisofpul monar yhypertensionneedst obe
    confir
    medi nvasively.TEEmaybeabl etoidentif
    yani nt r
    acardiacshuntt hiswoul dnotconf irm
    thediagnosi sofpul monar yhyper tension.

    Quest
    ion:

    7. A65- year-oldmanpr esentst otheemergencydepar tmentwith2daysofchestpai n


    anddyspnea.Hehasahi stor
    yofhyper t
    ension,
    dysl i
    pidemia,andcoronaryar terydisease
    tr
    eatedwi thcor
    onar yart
    erybypasssur ger
    ysever alyearsago.Hei safebri
    le,buthisoxygen
    satur
    ationis92%onr oom air
    .Jugul arvenouspr essureis6cm H2O.Hi slungsar eclearto
    auscultat
    ionbil
    aterall
    y.Hiselect
    rocar di
    ogram i
    sonl yr emarkabl
    eforsinust achycardi a.
    Cardiacbiomarkers,incl
    udingcardiact r
    oponin,arenor mal.HischestX-rayi sinter
    pr etedas
    normal.

    Basedonthepat
    ient
    ’spr
    esent
    ati
    onandr
    iskf
    act
    ors,
    whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    y
    di
    agnosi
    s?

    a. Gastr
    oesophagealrefluxdi
    sease.
    b. Pulmonaryembol i
    sm (PE).
    c. Congesti
    veheartfai
    lure.
    d. Pneumoni a.
    e. Acutecoronarysyndrome.

    Answer
    :

    7. b. Pul
    monar
    yembol
    ism (
    PE)
    .

    PEi sthecor r
    ectchoicebecauset hepat i
    ent’
    scl i
    nicalpresentat
    ionofchestpai n,dyspnea,
    hypoxemi a,andsinust achycardi
    ai nt hesetti
    ngofanor malchestX- r
    aysuppor t
    st he
    diagnosisofPE.Fur t
    her more,patientswi t
    hatherot hr
    ombot iccardiovasculardiseaseand
    associatedriskfact
    orshaveani ncr easedincidenceofvenoust hromboembol ism.Pneumoni a
    i
    si ncorrectbecauseoft helackoff ever,physi
    calexami nationsignsofconsol idation,andchest
    X- r
    ayfindingsdonotsuppor tadi agnosisofpneumoni aorhear tfail
    ure.Gastroesophageal
    refl
    uxdiseaseshoul dnotr esul
    tinhypoxemi a.Acut ecoronarysyndr omei sincorrectbecause
    thepat i
    entishypoxemi c,withacl earlungexami nat i
    onandchestX- ray,andhasno
    electr
    ocar di
    ographi
    cf i
    ndingsofi schemi a.

    Quest
    ion:

    8. A54-year
    -ol
    dwomanpr esent
    st otheemergencydepart
    mentwit
    h12hoursofpl
    euri
    ti
    c
    pai
    n,cough,
    anddyspnea.Shehasahi stor
    yofhypert
    ensi
    ont r
    eatedwi
    that
    hiazi
    dedi
    uret
    ic.
    Sheisaf
    ebril
    eandhasanoxygensaturati
    onof99%onr oom ai
    r.Herel
    ect
    rocardi
    ogr
    am
    demonstr
    atessi
    nusrhyt
    hm withnoabnormalit
    ies.Car
    diacbiomarker
    s,i
    ncludi
    ngcardi
    ac
    tr
    oponi
    n,arenor
    mal.HerchestX-r
    ayisinter
    pretedasnormal.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    enextst
    epi
    ntheeval
    uat
    ionoft
    hispat
    ient
    ?

    a. D-dimerenzyme- l
    inkedimmunosorbentassay(ELI
    SA)t
    est
    .
    b. Magne ti
    cr esonancepulmonaryangiography.
    c. Contrast-
    enhancedchestcomput edt omography.
    d. Transthoracicechocardiogr
    aphy(TTE).
    e. Venti
    lati
    on- perf
    usionlungscan.

    Answer
    :

    8. a. D-
    dimerenzyme-
    li
    nkedi
    mmunosor
    bentassay(
    ELI
    SA)t
    est
    .

    TheD- dimerELISAt estist hecor r


    ectchoice, becauset hecl inicalprobabi l
    ityofpul
    monar y
    embolism (PE)basedonherpr esentationisl owt omoder ate.Init
    ialevaluationwithD- di
    mer
    ELISAtesti
    ng, i
    fnormal ,avoi dst heneedf orfur t
    hercost lydiagnost icimagi ngbecauseoft he
    test
    ’shighnegat i
    vepr edictiveval ue(99%) .Inaddi t
    ion,D- dimert estingwhenused
    appropri
    atelyavoidsexposi ngt hepatientt oionizi
    ngr adiationandi ntr
    avenouscont r ast
    requi
    redforchestcomput edt omogr aphyeval uati
    onf orPE.Thechoi cesofachestcomput ed
    tomography, l
    ungscan, ormagnet i
    cresonanceangi ographyar eincorrectbecauset hepatient
    doesnothaveahi ghenoughcl inicalprobabi l
    ityofPEt owar rantproceedi ngdirect
    lyt oi
    magi ng.
    TheTTEopt i
    onisincor r
    ectbecauseTTEi snotsensi ti
    vef orthedi agnosi sofPE.

    Quest
    ion:

    9. A48-year-
    oldmanpr esentstotheemer gencydepart
    mentwith3hour sofpr
    ofound
    dyspneaandl i
    ghtheadednessand2daysofr i
    ghtlegpainandswell
    ing.Hehasahi st
    oryof
    diabetesandcoronaryarter
    ydiseasewithapr i
    orlargeant
    eri
    ormyocardiali
    nfar
    cti
    onandal ef
    t
    ventri
    cularej
    ecti
    onfract
    ionof30%.Hei safebri
    lebuthasabl oodpr
    essureof70/30mm Hg
    andanoxygensat ur
    ati
    onof84%onr oom air
    . 

    Hiselectr
    ocar diogram demonst ratessinustachycardiaat120bpm andnoot herchanges
    compar edwi t
    hapr iortracing.Chemi strypanel,
    compl et
    ebloodcount , andcoagulati
    ontests
    arenormal .Car di
    act roponinTi s2ng/ ml(normal<0.2ng/ml).Hi schestX- r
    aydemonst rat
    es
    cardi
    omegal ywi t
    hcl earlungf i
    elds.Bedsideechocar di
    ogram revealsasever el
    ydil
    ated
    hypokineti
    cr i
    ghtvent r
    icle.Contrast-enhancedchestcomput edt omogr aphydemonst r
    ates
    l
    argebi l
    ateralmai npul monar yembol iwit
    hsevereri
    ghtventri
    cul arenlargement.Heis
    i
    mmedi at
    elyst art
    edoni ntravenousunf racti
    onatedhepari
    nasabol usf oll
    owedbyi nf
    usion.

    Whichoft
    hefol
    lowi
    ngi
    sthemostappr
    opr
    iat
    enextst
    epi
    nthemanagementoft
    hispat
    ientwi
    th
    pul
    monaryemboli
    sm?

    a. Cont
    inuesystemi
    canticoagulati
    onwithunfr
    acti
    onat
    edhepar
    in.
    b. Ref
    erthepati
    entf
    oropensur gi
    calpul
    monaryembolect
    omy.
    c. Admini
    sterr
    ecombinanttissue-pl
    asminogenacti
    vat
    or100mg.
    d. Ref
    erthepati
    entf
    orul
    trasound-
    faci
    li
    tated,
    cat het
    er-
    dir
    ect
    ed,
    low-
    dosef
    ibr
    inol
    ysi
    s.
    e. I
    nsertaret
    ri
    evabl
    einf
    eri
    orvenacava( I
    VC)fil
    ter.

    Answer
    :

    9. c. Admi
    nist
    err
    ecombi
    nantt
    issue-
    plasmi
    nogenact
    ivat
    or100mg.

    Administr
    ationofti
    ssue-pl
    asminogenactivatori
    sthecor r
    ectopti
    on,becausethepati
    enthas
    suff
    eredmassi vepulmonaryemboli
    sm, andisatincreasedri
    skofdeathfrom ri
    ghtventr
    icul
    ar
    (RV)fai
    lur
    ei fr
    eperf
    usionther
    apyisnotinstit
    uted.Hehasnoevi denceofacti
    vebleedi
    ng,
    thr
    ombocyt openia,
    orothercont
    rai
    ndicati
    ont ofi
    bri
    nolyti
    ctherapy.
     

    Referri
    ngthepat i
    enttocatheter-
    di r
    ectedfibrinolysi
    sorsur geryisincorrectbecauset hepatient
    doesnothaveanycont rai
    ndicati
    onst of i
    brinolyti
    cther apy.Cat het
    er-basedorsur gical
    pulmonar yembolectomygener allyisreservedf orpatientswi thcontrai
    ndi cati
    onstof i
    bri
    nolyti
    c
    therapyorcatheter-
    basedt echniques.Insertionofar et r
    ievableIVCf i
    lt
    erisi ncor
    rectbecause
    IVCf i
    lt
    erplacementwillnotreversetheRVpr essureover loadthatisresultinginRVf ail
    ureand
    hypotension.Simplyconti
    nuinghepar inther apyi si
    ncor rectbecausesyst emi canti
    coagulation
    alonewi l
    lnotimproveRVf ail
    urer api
    dlyenought oavertfurtherhemodynami ccol
    lapseand
    possiblydeath.

    Quest
    ion:

    10. TheFi f
    thWor l
    dSymposi um onPul monar
    yHypertensi
    on( WSPH)in2013out l
    inedthe
    fi
    vemajorcategori
    es(Groups)ofpathologi
    cmani f
    est
    ati
    onsofpulmonar yar
    ter
    ialhypert
    ension
    (PAH)i
    nanef for
    ttobettercat
    egori
    zet hemanycausesofelevatedpul
    monar yart
    erypressures.
    Whilet
    hedemogr aphics,manif
    est
    ations,andoutcomesmayvar y,t
    hosecausescategorizedin
    Group1refl
    ectedthepresenceofanunder lyi
    ngpulmonaryvascul
    opathy.

    Whichoft
    hefoll
    owi
    ngassociat
    ionswithpul
    monar
    yar
    ter
    ialhyper
    tensi
    onhasbeencl
    assi
    fi
    ed
    asGroup1intheWSPHclassif
    icat
    ion?

    a. Sar
    coidosi
    s.
    b. Sl
    eepapnea.
    c. Chroni
    cthromboemboli
    cdi
    sease.
    d. Mit
    ralval
    vestenosi
    s.
    e. Ei
    senmengersyndrome.

    Answer
    :

    10. e. Ei
    senmengersyndr
    ome.

    Thecor r
    ectanswerisEi senmengersyndr ome.Group1PAHi ncludest hosewithevidencefor
    pulmonar yhypert
    ensionandanunder l
    yingvasculopat
    hy.Group1i ncludesidi
    opathicPAH,
    heri
    tablePAH( themostcommonmut ationbeingbonemor phogenet icprotei
    nreceptortype2
    [
    BMPR2] ),
    drug-ortoxin-inducedPAH( part
    icul
    arl
    ybyappet i
    tesuppr essantdrugs),andthose
    associatedwithconnectivetissuedi
    sorders(par
    ti
    cular
    lyscleroderma) ,human
    i
    mmunodef i
    ciencyvir
    us(HI V)inf
    ecti
    on,port
    alhypert
    ensi
    on,andschi
    stosomiasi
    s,andthose
    relat
    edtocongeni t
    alheartdisease.Whenthereispul
    monaryhypert
    ensionandar esul
    tantr
    ight
    -to-l
    eftshuntwithcyanosis,thecomplexisref
    erredt
    oastheEisenmengercomplexor
    syndrome. 

    Thef i
    veWSPHgr oupsare:Group1, pul
    monar yveno-occlusivediseaseandpul monary
    capil
    laryhemanigomatosis;Group2, PHduet oleft
    -heartdisease, suchasmi t
    ralst
    enosis;
    Group3, PHduet olungdiseaseorhypoxi a,
    suchassl eepapnea;Gr oup4, PHduet ochroni
    c
    thr
    omboembol i
    cdisease;Group5, PHduet ounclearormul ti
    factorialmechanisms,suchas
    sarcoidosi
    s,chr
    onicmyel opr
    olif
    erati
    vediseases,orglycogenstor agediseases.

    Quest
    ion:

    11. A55- year-oldsedentarywomanpr esent sincli


    nicwi thworseni
    ngshortnessofbreath
    overthepastseveralmonths.Shehasahi stor yofhypertension,
    diagnosedat30yearsofage,
    andcutaneoussarcoidosi
    s.Hercur r
    entmedi cationsarelisi
    nopril20mgdailyand
    hydrochl
    orot
    hiazi
    de25mgdai l
    y.Herbloodpr essureis128/ 70mm Hgandhear tr
    ateis75
    bpm.Physicalexaminati
    onr eveal
    sanel evatedj ugularvenouspr essur
    eandahol osystol
    ic
    murmur ,
    bestheardattheleftlowersternalbor der. 

    Anechocar diogram orderedbyherprimarycarephysicianrevealedami ldlydil


    atedatriaand
    ri
    ghtventricl
    e(RV),mi l
    dconcentri
    cleftventr
    icul
    arhypertr
    ophy, andinterventri
    cularseptalwall
    fl
    att
    eninginsyst ol
    ewi thabnormalmot i
    on.Ther i
    ghtandleftventri
    cularsystoli
    cf uncti
    onwas
    normal.Therewasmoder at
    etri
    cuspidregurgit
    ati
    onsecondar ytoadi l
    atedt r
    icuspidvalve
    annulus.TheRVsyst oli
    cpressur
    e(RVSP)wasest i
    mat edtobe40mm Hggr eaterthantheright
    atr
    ialpressure,butmaybeunder esti
    mat ed.Therewasmi ldl
    ydilatedinferi
    orvenacava.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nthi
    spat
    ient
    'scar
    e?

    a. Nuc l
    earperfusi
    oni magi ng.
    b. Ri
    ght -hear
    tcatheterizati
    on.
    c. Cardiacmagnet i
    cr esonancei maging(MRI )
    .
    d. Transesophagealechocar di
    ogram (TEE).
    e. Comput edtomogr aphi cangiography(CTA).

    Answer
    :

    11. b. Ri
    ght
    -hear
    tcat
    het
    eri
    zat
    ion.

    Thispati
    enthaspulmonar yhyper t
    ension(PH) .Thepresenceofaf latt
    enedintervent
    ri
    cular
    septum anddil
    atedri
    ghtatrium andvent ri
    cleinthesettingofshortnessofbreatharemost
    consist
    entwit
    hPH.Al thoughechocar diographycanof tenesti
    mat etheRVSP, asur r
    ogatefor
    pulmonarysystol
    icpressurewhennopul monar yvalvepat hol
    ogyexists,t
    hedi agnosi
    sofPH
    mustbemadevi ari
    ght-heartcatheter
    izati
    onanddi rectmeasur ementofpulmonar yarteri
    al(
    PA)
    pressur
    es. 

    TheRVSPi nthispatienti
    sslightl
    yelevated,
    butcoul
    dbeanunder est
    imationofthetrue
    pulmonarypressure.Theref
    ore,thenextstepshoul
    dbetoreferthepati
    entforr
    ight-
    heart
    cathet
    eri
    zat
    iont odetermi
    nePApr essure.Ameanpulmonarypressure>25mm Hgonr ight
    -
    heartcat
    heteri
    zati
    ondocument sthepresenceofPH. 
    CTAwoul dbeusef ulwhent hereisasuspi cionofpul monar yembol ism ( PE).Inthiscase,the
    chronicityoft hepat i
    ent'ssympt omsgoagai nstanacut ePE.Chr oni ct hromboembol i
    c
    pulmonar yhyper tension(CTEPH)canpr esentmor echronically,butt hegol dstandardfor
    diagnosi ngCTEPHi sviaaVQscan, onlyaf terPHi sdocument edvi ar i
    ght -heartcathet
    eri
    zation.
    CardiacMRIi shelpfulfortheexactquant ifi
    cat i
    onoftheejectionf ract i
    on, toevaluate
    myocar di alfi
    brosis,toassessPAsi ze,andt oquant i
    fythetricuspidr egurgitati
    on,butitwould
    notbeabl et odiagnosePH.TEEwoul dnotof feraddi
    tionalinformat i
    ont odi agnosePH.
    Improvedvi suali
    zat i
    onoft hetricuspidval vei sunnecessary,becauset heet iol
    ogyi sdi
    lat
    ionof
    theannul usrelatedt ori
    ght-sideddilatati
    onf rom PH.Finall
    y, nuclearper fusionimagingwoul d
    behel pfultoassessi schemi aiftheshor tnessofbr eathwast houghtt obeanangi nal
    equivalent ,butthef i
    ndingsonechocar diogr am makePHmuchmor el ikely.

    Quest
    ion:

    12. A43- year-oldwomanwi thafamilyhistor


    yofpul monaryhyper tension(PH)isseenin
    cl
    inicforacompl aintofdyspneaonexer t
    ion.Shet akesadailymul tivi
    tamin.Curr
    entvitalsi
    gns
    areapul seof90bpm, bl
    oodpr essur
    e110/ 76mm Hg, respi
    ratoryrate14, andoxygen
    saturat
    ion99%onr oom air.Herexaminati
    oni sremarkableforpromi nentAwavesi nthe
    j
    ugularveins,apar ast
    ernalli
    ft
    ,asystoli
    cmur mural ongtheleftsternalborder,
    andar ight-
    si
    dedS4  sound.Thereisnohepat omegalyandonl yt r
    aceankleedema.  

    Herechocardiogram r
    evealsnormalleftvent
    ricularsizeandf uncti
    on.Ther i
    ghtventri
    cular(RV)
    basaldi
    amet eris4.
    1cm, andtheRVf r
    eewal lthicknessis8mm.Tr icuspidannularplane
    syst
    oli
    cexcur si
    onis2.0cm.Ther eisseptalflatt
    eningi nbot
    hsyst oleanddi ast
    ole.Thereis
    moderatetr
    icuspidregurgit
    ati
    on(TR),withapeakTRj etvel
    ocityof3.9m/ sec.Theinferi
    or
    venacavaisnor malinsi
    ze, butdoesnotchangesi gnif
    icant
    lywi t
    hrespirat
    ion.Thereisno
    evi
    denceofashunt . 

    Right-
    heartcathet
    eri
    zationr evealstheri
    ghtatr
    ial(RA)pressur
    eis9mm Hg, RVpr essure68/9
    mm Hg, pulmonaryartery(PA)pr essure67/29mm Hgwi thameanof42mm Hg, and
    pulmonarycapill
    arywedgepr essureis12mm Hgmeasur edatend-expir
    ati
    on.Fickcardiac
    2
    outputwas4.5L/ min(cardiaci ndex2.8L/min/
    m) .Fol
    lowingachallengewithi
    nhal ednit
    ri
    c
    oxide,t
    hePApr essureis47/ 23mm Hgwi thameanof31mm Hg, andtheFickcardiacoutput
    i
    s5. 0L/min(cardi
    acindex3. 1L/min/m2).

    Whichofthef
    oll
    owi
    ngt
    her
    api
    esi
    sthemostappr
    opr
    iat
    efori
    nit
    ialt
    reat
    mentofherpul
    monar
    y
    hyper
    tensi
    on?

    a. Sil
    denaf il
    .
    b. Riociguat.
    c. Epopr ostenol
    .
    d. Nifedipine.
    e. Bos entan.

    Answer
    :

    12. d. Ni
    fedi
    pine.

    Thecor
    rectansweri
    sacal
    cium channelbl
    ocker
    .Thi
    spat
    ienthasPH(
    li
    kel
    yWor
    ldHeal
    th
    Organization[WHO]Gr oup1givenherf amilyhi
    stor
    y)withoutsignsofr i
    ghtheartfail
    ure.Her
    ri
    ght-heartcat het
    eri
    zati
    ondemonstratedadr amaticacuteresponset oavasodilatorchall
    enge,
    usuall
    ydef inedasaf al
    linmeanpulmonar yart
    erysyst
    olicpressureofatleast10mm Hgt oa
    val
    uel esst han40mm Hg, wi
    thoutadr opincardi
    acoutput,inresponsetoacut e
    administrationofapulmonaryvasodilatorsuchasinhalednitr
    icoxide,i
    ntravenous(IV)
    epoprostenol ,ori
    ntr
    avenousadenosine. 

    Anacut er esponsei sobservedonl yi


    nami nori
    tyofGr oup1PHpat ients.Anacut er esponse
    predict schr onicresponsetot herapywi thacalcium channelbl ocker ,whichhasf ewersi de
    effectst hanot hermor especifictherapiesforPH.Ni fedipi
    neandaml odipinearemost
    commonl yused.Ver apamilshoul dbeavoi dedbecauseofi tsnegat iveinot r
    opicef f
    ects.
    Prost anoi dssuchasI Vepopr ostenol,
    whi chrequiresacont inuousI Vpump;endot heli
    n- 1
    ant agoni stssuchasbosent an, whichcancausehepat i
    cdysf unction;phosphodi esterase
    i
    nhi bitorssuchassi ldenaf
    il,whichcancausef lushingandepi staxis;orguanyl atecycl ase
    stimul atorssuchasr ioci
    guat, whichcancausesi gnifi
    canthypot ensi on, wouldallbe
    reasonabl echoi cesinapat i
    entwhodi dnothaveanacut eresponset ovasodilators,orf or
    pat i
    ent swhodonothavei mpr ovementi nsympt oms( toNewYor kHear tAssociat i
    oncl assIor
    IIstatus)wi t
    hcal ci
    um channelbl ockers.

    Quest
    ion:

    13. A35- year-oldAf


    rican-Ameri
    canwomanpr esentswit
    h6mont hsofwor seni
    ng
    exertionaldyspnea.Shedeni eschestpai
    n,hypertension,di
    abetes,hyperli
    pidemia,
    jointpai
    ns,
    historyofpulmonar yembol i
    ,orsmokingcigar
    ettes.Onexami nation,herbloodpressureis
    135/ 72mm Hg, pulse86bpm, andt
    emperature98. 6ºF.Shehasj ugularvenousdistenti
    on,
    clearlungf i
    elds,aprominentsecondcomponentofS2, andnoedema.  

    AchestX- rayrevealspromi nentpulmonaryar t


    eri
    es,noinf
    ilt
    rates,andami ldl
    yenl ar
    gedright
    atri
    um (RA)andr i
    ghtventricle(RV).Herel
    ectrocardi
    ogram revealsborderlinerightaxis
    deviati
    onandani ncompl eterightbundlebranchblockinnor malsinusr hythm.Her
    echocardiogr
    am showednor mallef
    tventr
    icularcontr
    acti
    li
    tywithanej ectionfractionof65%,
    RAandRVenl argementwi that ri
    cuspidannularplanesystoli
    cexcur si
    onof14mm, andan
    esti
    mat edpulmonar yart
    ery( PA)systol
    icpressureof70mm Hgmeasur edbyt ricuspi
    d
    regurgi
    tati
    onjetveloci
    ty. 

    Youorderaright
    -heartcat
    het
    eri
    zat
    ionandthemeanRApressur
    ei s6mm Hg, RVpressureis
    73/
    9mm Hg, PApressurei
    s73/18mm Hg( meanof38mm Hg),andpulmonarycapil
    lary
    wedgepressurei
    s13mm Hg.Sher espondsfavor
    abl
    ytoanit
    ri
    coxideinhal
    ati
    onchallenge.

    Inaddi
    ti
    ontoini
    ti
    alt
    her
    apywi
    thacal
    cium channelbl
    ocker
    ,whi
    choft
    hef
    oll
    owi
    ngshoul
    dbe
    consi
    dered?

    a. I
    sosorbidedinatrat
    e/hydr
    alazi
    ne.
    b. Warfar
    in.
    c. I
    vabradine.
    d. Metoprololsucci
    nate.
    e. Sacubi
    tril
    /valsar
    tan.

    Answer
    :
    13. b. War
    far
    in.

    Thecor rectansweri swar fari


    n.Thepat i
    entmostl ikelyhasGr oup1i diopathicpulmonar y
    arterialhyper t
    ension(IPAH) ,althoughot hercausesmustbeexcl uded.Ant i
    coagulantshave
    beenst udiedinfouruncont r
    olledobser vationalser i
    es, twopr ospecti
    veandt woretrospective,
    primar il
    yinI PAHpat i
    ent s.Ani mpr ovementi nsur vivalwasobser vedinal lf
    ourwi t
    ht heuseof
    war fari
    n.Mostgui del
    inesr ecommendwar farinanticoagul ati
    ontitr
    atedt oani nt
    ernational
    nor mal i
    zedr ati
    oof1.5- 2.5inpat i
    entswi t
    hI PAH.Ther earenodat atosuppor ttheother
    optionsi nt hi
    ssituati
    on.Met oprololsuccinat e,i
    vabr adine,sacubitri
    l/
    valsartan,andisosor bide
    dintrate/hydralazi
    nehavebeenshownt obehel pfulwi thleftheartfai
    lureandr educedej ecti
    on
    fr
    act ion,buthavenotbeenst udi edinGr oup1pul monar yarteri
    alhyper t
    ension.

    Quest
    ion:

    14. A51- year


    -ol
    dwomanwi t
    hahi stor
    yofsystemi csclerosispresent
    stoyouroff
    icef
    or
    worseningdyspneaonexer ti
    on.Shereportsthatwithevent hemostmi ni
    malofphysi
    cal
    acti
    vit
    y,suchasgettingdressed,shebecomesmar kedlyshor tofbr
    eath.Onexaminat
    ion,she
    hasanel evat
    edjugularvenouspressure.Shehasapr ominentP2 andar i
    ght-
    sidedpr
    ecordial
    heave.Anechocardiogram suggestsapulmonar yarterysystoli
    cpressureof70mmHg.  

    Youor deraright -heartcat


    heterizationwithpulmonar yvasor eact
    ivit
    ytest i
    ng.Herrightatri
    al
    (RA)pressurei s14mm Hg, andt her i
    ghtventr
    icul
    arsyst ol
    icandend- diastoli
    cpressuresare
    68and14mm Hg, respect
    ivel
    y.Herpul monaryarter
    ialpressur ei
    s68/ 28mm Hgandt he
    pulmonar ycapi l
    larywedgepr essur eis12mm Hg.Thecar diacout putis4.8L/ minandt he
    cardiacindex( CI)is2L/ min(aver ageofthreethermodiluti
    onmet hoddet erminati
    ons).Her
    hemodynami csshownosi gnif
    icantchangeaf teradministr
    ationofni t
    ricoxi de(NO)ateither10
    partspermi l
    lion( PPM)or20PPM.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthebesti
    nit
    ialdr
    ugt
    her
    apyf
    ort
    hispat
    ient
    ?

    a. Oraltadal
    afi
    landoralambri
    sent
    an.
    b. I
    ntravenousepoprost
    enol.
    c. Oraldil
    ti
    azem.
    d. I
    ntravenousepoprost
    enolandoralambr
    isent
    an.
    e. Oraltadal
    afi
    l.

    Answer
    :

    14. d. Intravenousepopr ostenolandor alambr isentan.


    Thispat ienthashi gh-riskprecapil
    larypulmonar yhypertensi
    on.Themostappr opri
    ate
    tr
    eatmentopt i
    ongi venherhi gh-
    risk(highRApr essure,lowCI )andWor ldHealt
    hOr gani
    zati
    on
    (WHO)f unctionalclass4st atus,i
    sacombi nati
    onofi ntr
    avenouspr ostacycli
    nandanor al
    endothel inantagoni st
    .Thecombi nat i
    onofor albosentanandi nt
    ravenousepopr ost
    enolhas
    beenst udi edandappear stohavehemodynami cadvant agesasupf r
    ontt her
    apyforsevere,
    high-
    riskpul monar yarteri
    alhypertension(PAH) .Basedont heEur opeanSoci et
    yof
    Cardi
    ol ogy/ EuropeanRespi rator
    ySoci ety(
    ESC/ ERS)2015gui del
    inef orpulmonary
    hypertensi on,thi
    si saCl assIIar
    ecommendat ion. 

    Theupf
    rontchoi
    ceofdualtherapyfort
    hiscohor
    tist
    heini
    ti
    alrecommendationintheESC/ERS
    tr
    eat
    mentalgori
    thm f
    ort
    hishigh-ri
    skcohort
    .Ahigh-
    dosecalci
    um channelblocker
    ,suchas
    dil
    ti
    azem,wouldbeindicat
    edonlyinpati
    entswhor espondtoNOvasor eacti
    vit
    ytest
    ing.Even
    amongpat i
    entswhodor espond,hi
    gh-dosecalci
    um channelblocker
    sarerecommendedonl y
    fori
    diopat
    hic,
    heri
    tabl
    e,ordrug-i
    nducedPAH, not
    but  connect
    iveti
    ssuedisorder-
    rel
    atedPAH. 

    Upfr
    onttreat
    mentwi thoralagentsislessidealgiventhehigh-r
    isknatureofthi
    spatient'
    s
    hemodynami cf
    indingsandWHOf uncti
    onalclass.Ini
    ti
    almonotherapywithintr
    avenous
    epoprost
    enolwouldbeaconsi derat
    ion,butthefir
    st-l
    inerecommendat i
    onforthispati
    entis
    combinati
    ontherapyofintravenousepopr ost
    enolandor alambrisent
    an.

    Quest
    ion:

    15. A26- year-


    oldwomanwi t
    har ecentdiagnosi sofpulmonaryhyper t
    ension(PH)isunder
    yourcare.Echocardiographyshowsnor mall eftventri
    cular(
    LV)systol
    icfuncti
    on, normall
    eft
    atr
    ial(LA)vol
    umes, severePH, andpreservedr ightventr
    icul
    ar(RV)systoli
    cfunction.A
    venti
    lati
    on-perf
    usion(VQ)scanr evealsnoevi denceoft hromboembolicdisease.Shehasno
    evi
    denceofcongeni talheartdi
    sease,li
    verdisease, humani mmunodef i
    ciencyvirus(HIV)
    ,
    hemat ol
    ogicorrheumat ologi
    cdisease,orsleep- di
    sorderedbreat
    hing.
     

    Youperfor
    m ar i
    ght-hear
    tcatheter
    izati
    onthatreveal
    sthesepressures:ri
    ghtat r
    ial5mm Hg,RV
    90/5mm Hg, pulmonaryarter
    y(PA)90/ 33/52mm Hg, andpulmonar ycapil
    larywedge8mm
    Hg.Thecardiacindexis2.8L/min/m2 (car
    diacoutput5L/min).Thereisnoi ntr
    acardi
    acshunt
    .
    Aft
    er10mi nutesofinhal
    ednitr
    icoxideat40par t
    spermi l
    li
    on,themeanPApr essurei
    s
    88/31/
    50mm Hgandt hecardi
    acout putisunchanged.

    Whi
    choft
    hefol
    lowi
    ngist
    heappr
    opr
    iat
    ecl
    assi
    fi
    cat
    ionaccor
    dingt
    otheFi
    ft
    hWor
    ldSymposi
    um
    onPul
    monar
    yHypert
    ensi
    on?

    a. Gr
    oup1.
    b. Gr
    oup2.
    c. Gr
    oup3.
    d. Gr
    oup5.
    e. Gr
    oup4.

    Answer
    :

    15. a. Gr
    oup1.

    Thewomani nt hi
    svignet
    tehasGroup1pul monaryar
    ter
    ialhypert
    ension(PAH).A
    compr ehensivewor kupdoesnotrevealot
    hercausesofPH.Herhemodynami csrevealsever
    e
    PHt hatisunr esponsivet
    oavasodilat
    orchall
    enge(i
    naposi t
    ivestudy,t
    hemeanpul monar y
    art
    erypr essuremustber educedby10mm Hgt oavalueof40mm Hgorl ess).
     

    Group1PAHi seit
    heridiopathic,her
    it
    able,drug-andtoxin-r
    elat
    ed, orassociatedwi t
    h
    connecti
    veti
    ssuedisease,portalhyper
    tension,HIV,orcongenit
    aldisease.Gr oup2i s
    secondaryt
    oleft
    -heartdisease.Group3i ssecondarytolungdiseaseorhypoxi a.Group4is
    duetothromboembolicandot herpulmonar yarter
    yobstruct
    ivedisease.Gr oup5i sunclear
    and/ormult
    if
    actori
    aleti
    ology,suchashemat ologi
    corsystemicinfl
    ammat orydisorderssuch
    assarcoi
    d.

    Quest
    ion:
    16. A35- year-oldwomanwi thidi
    opathi
    cpulmonaryarter
    ialhyper
    tensi
    on( PAH)(Gr
    oup1)
    i
    sunderyourcare.Atdi
    agnosis,shehadapositi
    vevasodil
    atorstudywithadropinhermean
    pul
    monaryarter
    y(PA)pressurefrom 50mm Hgto38mm Hg, withapreservedcardi
    acindexof
    2.
    6L/min/m2.Shewaspr escr
    ibedlong-act
    ingni
    fedi
    pine.
     

    Sixmont hslater,atar epeatr


    ight-
    hear tcat
    het er
    izat
    ion,herPApr essuresar
    eincreasedtoa
    2
    meanof49mm Hg, withacardi
    acindexof2. 2L/min/ m .Otherwi
    se,shehasWor l
    dHeal t
    h
    Organi
    zat i
    oncl ass2sympt oms,a6- mi nut
    ewal kdistanceof450m, andapeakVO2  of15
    ml/kg/minonacar diopulmonaryexercisetest.Shehaspr eser
    vedri
    ghtventr
    icul
    arfuncti
    onon
    echocardiogram.Youdeci detoini
    tiat
    ecombi nati
    ont herapy.

    Whi
    chofthef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    ether
    apy,
    inaddi
    ti
    ont
    ochangi
    ngni
    fedi
    pinet
    o
    ambr
    isent
    an?

    a. Epoprostenol.
    b. Aml odi
    pine.
    c. Tadalafi
    l.
    d. Verapami l
    .
    e. Treprost
    inil
    .

    Answer
    :

    16. c. Tadal
    afi
    l.

    Thispat i
    enti samongt hemi nor i
    tyofpat i
    entswi t
    hPAHwhor espondt oapul monary
    vasodi latorstudy.Overt ime, however ,herPAHhaswor senedandshei sinneedoff urt
    her
    therapy.Agent sapprovedbyt heFoodandDr ugAdmi ni
    strati
    onf orthispati
    entincl
    ude
    prost acycli
    ns, endothelinrecept orantagonists,andagentstar get i
    ngt henit
    ri
    coxidepat hway
    (phosphodi esterasetype-5i nihibit
    orsandsol ubleguanylycycl asei nhibi
    tor
    s).Verapimili
    s
    gener allyavoi dedinpat i
    entswi thPAHowi ngt oitsnegati
    veinot r
    opicef f
    ect
    s.Further,t
    his
    pati
    enti snotr espondingt ocal cium channelblockers.Therefor e,verapamili
    snotan
    appr opr i
    atechoi ce.Recentevi dencesuppor tstheuseofambr isentanandt adalafi
    linde
    novo  ClassI Ipulmonar yhyper tension.

    Quest
    ion:

    17. A35- year-


    oldwomanwi th6mont hsofdyspneaevenwhendr essingwhoexper i
    enced
    twoepi sodesofsyncopeunder wentanechocar diogram thatrevealedseverepul monar y
    hypertension(PH).Sheult
    imatelyunder wentr i
    ght -
    heartcatheteri
    zationrevealingapulmonar y
    capil
    larywedgepr essureof10mm Hg, rightatrial(RA)pressure18mm Hg, pulmonaryar t
    ery
    meanpr essureof70mm Hg, cardiacout putof5L/ min,andpulmonar yvascularresi
    stanceof
    12Woodsuni t
    s.Therei
    snor esponset oinhaledni tri
    coxide.Furtherevaluati
    ont hatexcluded
    othercausesofPHl edtoadiagnosi sofidiopathicpulmonar yarteri
    alhypertension.Shecomes
    toyouf oranopi ni
    onregardi
    ngt herapeuticopti
    ons.

    Whi
    choft
    hef
    oll
    owi
    ngt
    her
    api
    eswoul
    dyouadvi
    se?

    a. Epoprost
    enolandambri
    sent
    an.
    b. Sil
    denafi
    landri
    oci
    guat
    .
    c. Si
    ldenafi
    l.
    d. Ambrisent
    anandsi
    ldenafi
    l.
    e. Ambrisent
    anandri
    ociguat
    .

    Answer
    :

    17. a. Epopr
    ost
    enolandambr
    isent
    an.

    Thecor r
    ectansweri sepoprost
    enolandambr i
    sentan.Thi
    spatienthasseveralhi
    gh-risk
    featur
    es,i
    ncludingNewYor kHeartAssoci
    ati
    onclass4dyspnea, syncope,andaRApr essure
    >15mm Hg.Ot herhigh-
    riskf
    eaturesarea6-minutewalkdist
    ance<300m, peakVO2 <12
    ml /
    kg/min,cardiacindex≤2L/min/ m2,
    andri
    ghtventri
    cularej
    ecti
    onf r
    acti
    on<35%oncar diac
    magnet i
    cresonance.  

    Thet r
    eatmentofpul monar yar
    teri
    alhypertensi
    onshouldbetail
    oredtot hesever
    ityofi
    ll
    ness.I
    n
    suchhi gh-ri
    skpat ient
    s,epoprostenolshouldbeincl
    udedininit
    ialt
    reatmentplans.Alt
    hough
    highestriskpatientarenotwel lr
    epresentedinrandomizedcl
    ini
    caltri
    als,exper
    topini
    onfavors
    upfrontcombi nationtherapyoftwot othreedrugs,i
    ncl
    udingepoprostenol.

    Quest
    ion:

    18. A42- year-oldmanpr esent


    stoyouroffi
    cet odiscusstr
    eatmentforhisrecently
    diagnosedidiopathi
    cpul monar yart
    eri
    alhypert
    ension( I
    PAH).Hewasdi agnosedaf t
    er
    developingprogressivedyspneaonexer t
    ion,andechocar di
    ographydemonst r
    atednor mallef
    t
    ventri
    cular(
    LV)funct ion,el
    evatedpulmonaryarterypressur
    e,amoder at
    elydil
    atedright
    ventri
    cle(RV)withRVhyper t
    rophyandmoder atelyreducedfuncti
    on,andsigni
    ficanttr
    icuspid
    regurgi
    tati
    onwi t
    hadi lat
    edrightat
    ri
    um (RA).
     

    Hispriorworkuphasdemonst ratednoevi denceofchroni cthromboembol i


    cdisease,anormal
    sl
    eepst udy,andnegativetesti
    ngf orhumani mmuodef iciencyvirusandconnect i
    vetissue
    diseases.Hecurr
    entlygetsshor tofbreathwhenhepl ayswi thhiskidsandisnol ongerableto
    mowhi slawn.Hi
    sphysi calexami nati
    onisnot abl
    eforanaccent uat
    edP2,amidsyst oli
    c
    ejecti
    onmur mur,andleftparasternalheave.Hehasdi stendedj ugul
    arveinsandt r
    acel ower
    extremityedema,buthisextremi t
    iesarewar m andtherei snocyanosisorclubbing. 

    Heper for
    msa6- minut
    ewal kt
    esti
    nyouroffi
    ceandisabletowalk350met er
    s.Aright-heart
    catheteri
    zat
    iondemonstr
    atesLVenddiast
    oli
    cpressureof13mm Hg, meanpulmonar yarter
    y
    pressureof38mm Hg, wit
    hacardiaci
    ndexof2.5L/min/m2,andapulmonaryvascular
    resi
    stance(PVR)of5Wooduni t
    s.Hehasanegativeresponsetovasodi
    lat
    orchal
    lenge.

    Whi
    choft
    hef
    oll
    owi
    ngi
    nit
    ialt
    her
    apeut
    icappr
    oachesi
    sappr
    opr
    iat
    e?

    a. Ri
    ociguatandsil
    denafi
    l.
    b. Si
    ldenafi
    l.
    c. Amlodipine.
    d. Ambr i
    sentanandtadal
    afi
    l.
    e. At
    rialseptost
    omy.
    Answer
    :

    18. d. Ambr
    isent
    anandt
    adal
    afi
    l.

    Thecor r
    ectanswerisambr i
    sentanandtadalafil
    .Si
    ldenaf
    ilhasbeenst udi
    edinarandomized,
    placebo-cont
    rol
    ledtrialandwasf oundtoimpr ove6-minutewalkdistanceandhemodynami cs,
    butnotthesecondar yendpointofti
    met oclini
    calworsening.Gi
    vent hi
    spatient
    ’ssever
    it
    yof
    disease,t
    reat
    mentwi thsildenaf
    ilal
    oneisnotadequat eandcombi nationt
    herapywithan
    endotheli
    nreceptorantagonistoraprostanoidshouldbeconsidered.

    Theseverit
    yofi ll
    nessi nIPAHi sani mportantf
    actorindetermini
    ngtherapy.Thi
    spatient
    demonstratesfindingsofatl eastmoder at
    elyseverePAH( NewYorkHeartAssociat
    ion[NYHA]
    cl
    assII-
    IIIheartfail
    ure, 6-
    mi nutewalkdistanceof350m, RVhypertr
    ophywi t
    hreducedf uncti
    on,
    andPVRof5Wooduni ts)
    .Therear edatashowingthatt heini
    ti
    alcombinati
    onofambr i
    sentan
    andtadalafi
    lli
    ssuper iortoambr isentanortadal
    afil
    laloneinNYHAf uncti
    onalcl
    assIIandI II
    PAHpat i
    ents.Ther ef
    or e,t
    hisini
    tialcombinati
    ontherapywoul dbeagoodchoi ceforthispati
    ent.

    Calci
    um channelbl ockerscanbever yeff
    ecti
    vether
    api
    esforthosefewpati
    entswithavery
    robustresponsetoacut evasodilat
    ortest
    ing.However
    ,becausethi
    spati
    enthadanegat i
    ve
    responsetoavasodi latorchal
    lenge,heshouldnotbetr
    eatedwithacal
    cium channelbl
    ocker
    suchasaml odi
    pine.

    Thesolubleguanylat
    ecyclasesti
    mulat
    orri
    ociguatwasappr ovedbytheFoodandDrug
    Admini
    strationi
    nOctober2013t oimpr
    oveexercisecapaci
    tyandfuncti
    onalcl
    assanddelay
    cl
    ini
    calwor seni
    ngingroup1PAH, buti
    scontraindi
    catedwit
    hphosphodiester
    ase5inhi
    bitor
    s
    suchassildenafi
    lduetohypotensi
    on.

    Atrialseptostomycr eatesar i
    ght-to-lefti
    nt eratr
    ialshunt
    , andsever alcaseserieshaver epor
    ted
    hemodynami candcl i
    nicalimprovement sfol l
    owingthispr ocedure.Whilethecr eatedshunt
    decr easessystemicar teri
    aloxygensat uration,t
    hegoali sani mpr ovementinsyst emicoxygen
    deliverybasedont heimpr ovedcar diacout put.However ,proceduralmor t
    alit
    yishi ghandis
    drivenbyt hesever i
    tyofPAHandr ighthear tfail
    ureinpat i
    entsunder goingthispr ocedure.
    Cur rentl
    y,atr
    ialseptostomyi srecommendedf orpatient
    swi t
    hsever ePAHandi ntractableri
    ght
    hear tfai
    luredespit
    emaxi malmedi calther apy.Thegoal soft hisprocedurearepal li
    ati
    onand
    restorati
    onandmai nt
    enanceofcl inicalstabi l
    it
    yunt i
    latransplantcanbeper f
    ormed.

    Quest
    ion:

    19. A55- year-oldwomanwi t


    hahi st
    oryofexer
    tionaldyspneaandreducedexercise
    capaci
    typresentst oyourcl
    ini
    cforher3mont hfol
    low- upeval
    uati
    on.Hermedicalhistor
    yis
    si
    gnifi
    cantfornicoti
    nedependenceandmor bidobesity. 

    Previ
    ously,
    anextensi
    vediagnosti
    cwork-upwi
    thatr
    anst
    horaci
    cechocardi
    ogram (TTE),
    venti
    lat
    ion-
    per
    fusionscan,chestcomput
    edtomogr
    aphy(CT)
    ,andri
    ght-hear
    tcatheter
    izat
    ion
    reveal
    edsever
    epulmonar
    yhyper
    tensi
    on(PH)secondaryt
    ochr
    onict
    hromboembol
    ic
    pulmonar
    yhypert
    ensi
    on(CTEPH)
    .Warfar
    inwasinit
    iat
    edandshequi
    tsmoking.
     

    Sheunderwentpulmonar yendar t
    erectomy.Anechocardiogram perf
    ormedpri
    ortohospi
    tal
    dischar
    gereveal
    edimpr ovedrighthear themodynamicswithasi gni
    fi
    cantr
    educt
    ioni
    nher
    pulmonaryart
    erypressures.Shepr esentstodayforf
    oll
    ow- up.Shehasnonewsympt omsand
    report
    sfeel
    ingsi
    gnifi
    cantlybetter
    .Vitalsarestabl
    e.

    Whi
    choft
    hef
    oll
    owi
    ngt
    est
    sshoul
    dbeor
    der
    edatt
    oday'
    svi
    sit
    ?

    a. D-di
    mert est.
    b. Lowerextremityvenousdupl
    exscan.
    c. 6-minut
    ewal ktest.
    d. ChestCT.
    e. Exer
    cisestresstest
    .

    Answer
    :

    19. c. 6-
    minut
    ewal
    ktest
    .

    Thecorrectanswerisasi x-minutewal ktest.Surgeryisthedef i


    nit
    ivetherapyforCTEPH.
    Pulmonaryendar t
    erectomyist hesurgicalprocedureofchoi ce.Thebenef i
    cialeff
    ectsof
    pulmonaryendar t
    ectomymaybedet ectedshor t
    lyaft
    ersur geryandincludei mprovedexer ci
    se
    capacit
    y,reducedpulmonar yar t
    erypressure,reducedpul monaryvascul arresi
    stance,and
    reducedmor tal
    it
    y.Echocardiographymayr evealimprovedt r
    icuspidregurgit
    ationandr educed
    ri
    ghtatri
    alandvent r
    icularsi
    ze. 

    Insomepat i
    ents,surgerymayhaveasubopt imaleffectonfuncti
    onalcapacityand
    hemodynami cs.Inthesepat i
    ents,assessmentshoul dbeper for
    medt odeterminewhet hera
    repeatpul
    monar yendar tectomyormedi calmanagementi sappropr
    iate.Thegoalsofmedi cal
    therapywi
    thpul monar yvasodi l
    atorsincludereducti
    onofpul monaryvascularresi
    stanceand
    pulmonaryarter
    ialpressur es,andimpr ovedexercisecapacityandoxygenation.Medications
    i
    ncludeprostanoids,solubleguanyl atecyclasesti
    mul ator
    s,phosphodiester
    ase-5inhibit
    ors,
    andendotheli
    nr eceptorant agonists.
     

    Foll
    owi ngtherapeuti
    cinterventi
    onf orPH, assessmentshoul dbeper for
    medt odet erminethe
    pati
    ent '
    sresponset otherapy.Ateachf ol
    low- upvi sit
    ,a6- minut ewal ktestshoul dbeobt ai
    ned.
    ATTEshoul dbeobt ai
    nedatl eastannual ly,andsooneri findicat ed.Thedeci sionf orar i
    ght-
    heartcatheter
    izati
    onisusual lyperformedonai ndi vi
    duali
    zedbasi s,usuall
    year lyafterther
    apy
    andr epeatedifthepatientdeteri
    orates.Ot herimpor t
    antfoll
    ow- upassessment sincludebrain
    natr
    iureti
    cpept i
    delevelandt readmi l
    ltestforexer cisecapacit y.Thi spat i
    entisclinical
    lystabl
    e.
    Thereisnoi ndicati
    onforD- dimer,chestCT, exercisestresst est ,orvenousdupl exscanatt his
    ti
    me.

    Quest
    ion:

    20. A43- year-oldwomancomest otheemer gencyr oom complai


    ningofa2- mont hhi
    stor
    y
    ofdyspneaonexer t
    ionandbi
    lat
    erall
    owerextremityedema.Shehasahi storyofpulmonary
    emboli,
    fir
    stdiagnosed5year
    sagoandt reat
    edwi th6mont hsofwar f
    arintherapy.Her
    echocardi
    ogram atthatt
    imedemonstrat
    ednosi gnif
    icantval
    vularorotherstr
    ucturalhear
    t
    diseaseandanormalleftventri
    cul
    arfuncti
    on.Therightventr
    icl
    ewasthoughttobemildl
    y
    dil
    atedwithmil
    dlydepressedfuncti
    on.Thereaf
    ter
    ,sheagai nwasdiagnosedwit
    hapulmonar
    y
    embol i
    sm wi
    thi
    n2mont hsofdisconti
    nuingwafar
    in.Sheneverfoll
    owedupwi t
    hthe
    recommendedhemat ol
    ogi standselfdi
    sconti
    nuedwar f
    arinuponleavi
    ngthehospi
    tal
    . 

    Shecur r
    entl
    yt akesbirthcontrolpil
    lsandnoot hermedicat
    ions.Shehasnotseenamedi cal
    professionalinmor ethan4year s.Onexami nat
    ion,
    herbloodpr essurei
    s94/68mm Hg,heart
    rate106bpm andr egular,l
    ungsar eclear
    ,andneckveinsarei ncr
    eased.Hercar
    diac
    exami nati
    ondemonst ratesrightventri
    cul
    arheave,anondisplacedpointofmaxi
    malimpulse,
    andar egul
    art achycardicrhythm withaloudsecondcomponentoft hesecondhear
    tsound.
    Herext remit
    iesdemonst rat
    e2+edemabi lat
    erall
    y.

    Whi
    choft
    hef
    oll
    owi
    ngi
    smostl
    ikel
    ytobeseenonherel
    ect
    rocar
    diogr
    am?

    a. AtallRwavei nleadVI .
    b. Ventri
    cularpre-exci
    tati
    on.
    c. AlongQTi nt
    erval.
    d. NegativePwavesi nleadsI
    IandI
    IIandaVF.
    e. At
    rialfi
    bril
    lat
    ion.

    Answer
    :

    20. a. At
    allRwavei
    nleadVI
    .

    Thecor r
    ectansweri sat al
    lRwavei nleadV1.Thepat i
    enthaspul monaryhyper tension
    secondar yt
    ochroni cpulmonar yembol i
    .AtallRwavei sconsi
    stentwithrightventricul
    ar
    hypertr
    ophyandpul monar yhypertensi
    on.Inacut epulmonaryembol i,onemi ghtexpectanS
    wavei nleadI(duet ori
    ghtaxisf r
    om leftpost
    eriorfascicul
    arblock),
    Qwavei nleadI II
    ,and
    i
    nvertedTwavei nleadIII(McGinn- Whitesi
    gn).Itisfoundinonly10%ofpat i
    entswi thanacute
    pulmonar yemboli.Atri
    alfi
    bril
    lat
    iononlyhasaweakassoci at
    ionwi t
    hpul monar yembol i
    .Long
    QT,Wol f
    f-Parki
    nson- Whitesyndrome, oratri
    alfociarenotclassical
    lyseeninchr onic
    pulmonar yhypert
    ension.

    Quest
    ion:

    21. A33- year


    -oldwomanwi thahi st
    oryofhypertensi
    onpr esentswi
    t hsharpchestpainat
    rest,
    associ at
    edwi thdyspnea.Sheis10dayspost oper at
    ivefr
    om ahyst erectomy.Herresti
    ng
    oxygensat urati
    onis91%.Herexami nati
    onisotherwisenormal .Heronl
    ymedi cati
    onisbirt
    h
    controlpil
    ls.Herelect
    rocardi
    ogram showssi nustachycardiaandT- wavei nversi
    oninthe
    anteri
    orleads.TroponinIiselevatedat0.8ng/L.Shei sgivenaspiri
    nintheemer gencyroom,
    butcont i
    nuest ocompl ai
    nofdyspneaandchestpai n.

    Whi
    choft
    hef
    oll
    owi
    ngshoul
    dbet
    henextst
    ep?

    a. Obtaincomput edtomographypul monar


    yangi
    ogr
    am.
    b. Schedulecardiaccathet
    eri
    zati
    on.
    c. Referforur
    gentcar di
    accatheter
    izat
    ion.
    d. Scheduleexercisestr
    esstest.
    Answer
    :

    21. a. Obt
    aincomput
    edt
    omogr
    aphypul
    monar
    yangi
    ogr
    am.

    Thenonspeci f
    icelectr
    ocardi
    ogram findi
    ngsinayoungpat i
    entwithalowpr etestprobabil
    it
    yfor
    coronaryarter
    ydiseaseshouldpr omptconsider at
    ionofalt
    ernat
    ivediagnoses.Whi letr
    oponin
    el
    evationisspecifi
    cformyocardialinjur
    y,i
    tisnotspeci f
    icf
    ortheetiol
    ogy,andpul monar y
    embolism (PE)isaknowncauseoft roponinelevati
    on.Inpati
    entswithPE,thepr esenceof
    tr
    oponinelevati
    oni sanadversepr ognosti
    cindicatorandshouldpromptanaggr essive
    diagnosti
    candt herapeut
    iccourse.

    Quest
    ion:

    22. A45- year-oldwomanpr esentswith6mont hsofwor seningdyspneaonexer ti


    on.Her
    symptomshavewor senedtothepointthatsheisunabl etoper f
    orm herdail
    yacti
    viti
    es.She
    undergoesechocardiogr
    aphiceval
    uation,ri
    ght-heartcatheterizati
    on,hi
    gh-resol
    utionchest
    computedtomogr aphy(CT),andchestCTwi thapul monar yembol i
    sm (PE)prot
    ocol,which
    reveal
    edadiagnosisofprimarypulmonar yhypertensi
    on( PH) .Bosentantherapyisini
    ti
    ated.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthebesteval
    uat
    iont
    odet
    ermi
    neef
    fi
    cacyoft
    her
    apy?

    a. 6-minutewal kdist
    ance>380met ers.
    b. VO2 great
    erthan18ml /min/
    kg.
    c. Cardiacindex≥3.5L/min/m2.
    d. WorldHeal t
    hOr gani
    zat
    ion(WHO)f uncti
    onalcl
    assIIorI
    IIsympt
    oms.
    e. Brai
    nnat ri
    ureti
    cpepti
    de(BNP)levellessthan500pg/ml.

    Answer
    :

    22. a. 6-
    minut
    ewal
    kdi
    stance>380met
    ers.

    Theabsol uteincreaseinthedistancewalkedf r
    om baseli
    newhi l
    eont reat
    menthasnotbeen
    shownt ocorr
    elatewellwithlong-ter
    m outcomes.However ,anabsolutevalue,thatis,
    a
    thresholddist
    ance, hasbeenshownt opredictsurvi
    val
    .Thisthreshol
    dwas380met ersinone
    studyand440met ersinanother.Achi
    eving6- minutewal
    kdi st
    ancesabovet hisrangeisa
    gener al
    lyacceptedgoalforpatientsontherapiesforpul
    monar yarter
    yhypertension.Other
    predictorsofeff
    icacyincl
    udenor malornearnor malBNP, normalornearnor malr i
    ght
    ventri
    cularfuncti
    on, WHOf uncti
    onalclassIorIIsymptoms, car
    diacindex=2. 5L/mi m2,
    n/ or
    VO2 ≥15ml /min/kg.

    Quest
    ion:

    23. A40- year-


    oldwomani sseen6weekspostdi schargeforpulmonar yhypert
    ension( PH).
    Sincedi
    schar ge,
    herdyspneahasi mproved,butshecont i
    nuest ohaveexerti
    onalfat
    igueand
    mildort
    hopnea.Hermedi calhist
    oryissigni
    ficantf
    ortobaccouse, hyper
    tension,
    andobesi ty.
    Hercurrentmedicati
    onsincludeloopdiuret
    icandanangi otensi
    n-converti
    ngenzymei nhibitor
    .
    Onexami nat
    ion,herbloodpressureis132/78mm Hg, hear
    trate72bpm, andbodymassi ndex
    33.Herjugul
    arvenouspr essureis10cm H2O, andherlungsar ecl
    ear. 

    Car
    diovascul
    arexami
    nat
    ionr
    eveal
    snor
    malS1 
    andS2,
    andr
    ight
    -si
    deS4.Nomur
    mur
    s,r
    ubs,
    or
    heavesappr eciated.Ext
    remi t
    ieshavet raceedema.Echocar di
    ogram att
    hetimeof
    hospitalizationshowedsever econcent r
    iclef
    tventr
    icul
    arhypertr
    ophywithnormalsystol
    ic
    function.Pul monar yart
    erysyst oli
    cpressurewasest i
    mat edat88mm Hg.Sheunder wentright
    -
    heartcat heterizationandherr esult
    sare:ri
    ghtatri
    alpressure15mm Hg;r i
    ghtvent
    ri
    cular
    pressur e90/ 15mm Hg;pul monar yarterypressur
    e90/ 25(47)mm Hg;pulmonarycapill
    ary
    wedgepr essure( PCWP)22mm Hg;aor tapressur
    e150/ 100mm Hg;car di
    acouput3.9L/min;
    2
    cardiaci ndex1. 8L/min/m.

    Basedonther
    ight
    -hear
    tcat
    het
    eri
    zat
    ionhemodynami
    cs,
    whatf
    urt
    herst
    udi
    esshoul
    dbe
    consi
    der
    ed?

    a. Venti
    lati
    on-per
    fusionscan.
    b. Repeatright
    -heartcathet
    eri
    zat
    ionwithacutevasodi
    lat
    orchal
    lenge.
    c. Transesophagealechocardi
    ography(TEE)
    .
    d. Cardiacmagneticresonanceimaging(MRI)
    .

    Answer
    :

    23. a. Vent
    il
    ati
    on-
    per
    fusi
    onscan.

    hecor rectansweri
    savent il
    ati
    on-per
    fusionscant oexcludethr
    omboembolicdi
    sease.Her
    calculatedpulmonar
    yvascul arr
    esist
    ance( PVR)is6.4(normal<2.0)
    .Thi
    sisder
    ivedbydivi
    ding
    thetranspulmonarypressuregradi
    ent/cardiacoutput
    .Thisimpli
    esther
    ecouldbeasecondary
    processbesi dest
    heelevatedPCWPatwor kinthi
    spati
    ent. 

    Thisclini
    calscenarioisanexampl eofreacti
    vepost capill
    aryPH,givent heelevat
    ionofthe
    surrogateofleftatr
    ialpressureandat ranspulmonar ypressuregradient>12mm Hg, i
    mpl yi
    ng
    thatthereisalsoacomponentofl eftheartdiseasepr esent.Gi
    venherobesi tyandsignif
    icant
    tobaccouse, thereareotherdiseaseprocessest hatmaybepl ayi
    ngar olei
    nt hepati
    ent’
    sPH,
    suchas  sleepapneaorchr oni
    cthromboembol i
    cdisease.Comput edt omographyofthechest
    withapul monar yembol i
    sm protocoloraV/ Qscani st henextbestst epinthispati
    ent,
    andt he
    V/Qscani snowpr eferr
    ed. 

    Asleepst udywoul dalsobeappropri


    ate.Acutevasodi
    lat
    ortesti
    ngwi t
    hinhal
    ednitr
    icoxideis
    rel
    ati
    velycontraindi
    cat edi
    npati
    entswithmildlyel
    evat
    edleftheartf
    il
    li
    ngpressur
    es,especiall
    y
    aft
    erar ecentcli
    nicaldecompensati
    onast hi
    scanacut el
    yincreasethePCWPbyi ncreasi
    ng
    pulmonar yfl
    owandl eadtocl
    ini
    caldecompensat i
    onduetopul monaryedema.Thereisnor eal
    advantageineitheraTEEorcar di
    acMRIi nthissit
    uati
    on.

    Quest
    ion:

    24. A45- year


    -ol
    dmani sadmit
    tedt
    ot hehospit
    alwit
    hshort
    nessofbreat
    h.Hi
    shist
    oryi
    s
    si
    gni
    fi
    cantformorbi
    dobesi t
    yandhypert
    ensiondiagnosed15year
    sago.Hedoesnotrecal
    lhi
    s
    bl
    oodpressuremedi
    cations.Hisbl
    oodpressureonadmi ssi
    oni
    s162/100mm Hg,hear
    trat
    e80
    bpm,andbodymassi ndexis41. 

    Anechocardiogram i
    sperformedthat 
    showsl ef
    tventr
    icul
    arhypert
    rophywi t
    hnor mallef
    t
    ventr
    icul
    arsystoli
    cfunct
    ion;theri
    ghtventr
    icl
    eisnormalinsizeandsystoli
    cf unct
    ion,wit
    h
    pulmonaryarter
    ysystoli
    cpressureesti
    matedat59mm Hg.Ar ight
    -heartcatheter
    izat
    ionis
    perf
    ormed,andt hehemodynami csare:r
    ightatr
    ialpr
    essure10mm Hg;r ightventr
    icul
    ar
    pressur
    e62/10mm Hg;
     pul
    monaryar
    ter
    ypr
    essure(PAP)62/
    21(
    35)mm Hg;pulmonar
    y
    capil
    lar
    ywedgepr
    essur
    e(PCWP)17mm Hg;car
    diacouput4.
    1L/
    min,andcar
    diaci
    ndex2.
    2
    2
    L/min/m.

    Whichofthefol
    lowingi
    stheappr
    opri
    atecl
    ini
    calWorl
    dHeal
    thOr
    gani
    zat
    ion(
    WHO)
    cl
    assif
    icat
    ionofthi
    spul
    monaryhyper
    tensi
    on(PH)?

    a. Gr
    oup5.
    b. Gr
    oup4.
    c. Gr
    oup1.
    d. Gr
    oup3.
    e. Gr
    oup2.

    Answer
    :

    24. e. Gr
    oup2.

    Thi
    sclini
    calscenari
    oisanexampl eofPHsecondarytoleftheartdisease,whi chisthemost
    commoncl assofPH( WHOGr oup2).ThePHi saresultofreacti
    vepost capil
    laryPH, given
    el
    evat
    ionofsur r
    ogatelef
    tatr
    ialpressur
    eandat ranspulmonar ypressuregradi ent>12mm Hg.
    Aswit
    hr eacti
    vepostcapi
    ll
    aryPH, passi
    vepostcapil
    lar
    yPHi sdefinedbyameanPAP  ≥25mm
    HgandaPCWP>15mm Hg.However ,thet
    ranspulmonarypr essuregradientis>12mm Hg.  

    Group1ispulmonaryart
    erialhypertensi
    on(PAH),defi
    nedasmeanPAP≥25mm Hgatr estand
    meanPCWP<15mm Hg.Gr oup3i sdef i
    nedasPHduet ochroni
    clungdi
    seaseandor
    hypoxemia.Group4i
    sdefinedasPHsecondar ytochronicthromboembol
    icdi
    sease.Gr
    oup5
    i
    ncludesPHf r
    om mult
    if
    actorialcauseswithoutaclear
    ,unif
    yingdi
    agnosi
    s.
    Syst
    emicDi
    sor
    der
    sAf
    fect
    ingt
    heCi
    rcul
    ator
    y
    Syst
    em
    Quest
    ion:

    1. A44- year-oldwomani sreferredtoyoubyherpr i


    mar ycar ephysi cianduet odyspnea
    onexerti
    on,dizziness,andvaguecompl ai
    ntsforthelast3mont hs.Thepat ienthasno
    signi
    fi
    cantmedi calhist
    or y.Herf atherhadast rokewhenhewas50year sol d.Shet ell
    syou
    thatshehasbeenexper iencingf ever,chil
    ls,
    weightloss,art
    hr algias,andbl uedi scolorat
    ionof
    herfi
    ngersandt oesi nthecol d.Onexami nati
    onherhear tratei s88bpm, bloodpr essure
    133/78mm Hg, andpul seoxygeni s100%onr oom air.Shei sfebr i
    leat101°F, herfingersare
    cyanoti
    c,andt hereisdigitalclubbing.Onauscul tat
    ion,hercar diacexam r evealsal oudS1 and
    asoftdiast
    olicsoundandr umbl eattheapex.Anechocar diogram i sobtained( Figure1).

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    ycauseofhersympt
    oms?

    a. Nonbacteri
    althrombot i
    cendocar
    dit
    is.
    b. Metast
    aticrenalcellcarci
    noma.
    c. SubacuteInfect
    iveendocardi
    ti
    s.
    d. Fungalendocardit
    is.
    e. Cardi
    acmyxoma.
    Answer
    :

    1. e. Car
    diacmyxoma.

    Myxomasaccountf or40- 50%ofpr i


    mar ycardiactumor s.Approximately90%aresol i
    taryand
    pedunculat
    ed,and75- 85%occuri ntheleftatri
    alcavit
    y.Upt o25%ofcasesar efoundi nthe
    ri
    ghtatr
    ium.Mostcasesar esporadic.Approximately10%ar efami l
    ialandaretr
    ansmi ttedi
    nan
    autosomaldominantmode.Mul t
    ipletumor soccurinappr oxi
    mat el
    y50%off amilialcasesand
    aremoref r
    equent
    lylocatedinthevent r
    icl
    e( 13%vs.2%i nsporadiccases).
     

    Symptomsr angefr
    om nonspeci
    fi
    candconst
    ituti
    onaltosuddencardiacdeath.Inabout20%of
    cases,myxomamaybeasympt omati
    canddiscover
    edasani ncident
    alfi
    nding.Const i
    tut
    ional
    symptomst hati
    ncl
    udefever
    ,weightl
    oss,
    art
    hralgi
    as,andRaynaudphenomenonar eobserved
    i
    n50%ofpat i
    ent
    s.Thesesymptomsmayber elat
    edtooverproducti
    onofinterl
    eukin-6. 

    Theechocar diogram clearl


    yshowsawel l-definedcar diacmassobst ruct ingthemi tr
    alor i
    fi
    ce,
    suggesti
    veofl eftat
    rialmyxomawi thahi ghr iskofembol izati
    on.Car diaccomput ed
    tomographyandmagnet icresonancei magi ngcanbeper f
    ormedf ortissuechar act
    er i
    zati
    on.
    Inf
    ecti
    veendocar di
    ti
    sandnonbact eri
    alendocar dit
    isarelesslikel
    ygi vent heechofindingsand
    hersympt omsr elat
    edt oobstructi
    onofbl oodf lowf rom theleftat
    rium t ot heventri
    clebyt he
    mass.Fungalendocar dit
    iscancausel argeveget ati
    onst hatmaybecomeobst r
    uctive,butare
    nottypi
    callyassociatedwi t
    ht hesympt omsdescr i
    bedher ethatarer elatedt otheIL-6secr eti
    on.
    Renalcellcarcinoma, alt
    houghassoci atedwi thsyst emicsympt oms, t
    ypi call
    yspreadst hrough
    theinf
    eri
    orvenacavat otherightheart.Sympt omsar ecausedbyobst ruct i
    onatthemi tral
    valveori
    fi
    ce.Val vedamagemayr esultinmi tralr egurgi
    tati
    on.Sever edi zziness/syncopei s
    experi
    encedbyappr oximately20%ofpat ients.Themostf requentcausei npat i
    entswi t
    hl ef
    t
    atr
    ialmyxomasi sobst r
    ucti
    onoft hemi t
    ralvalve.Sympt omsmaychangeast hepat i
    ent
    changesposi ti
    ons.

    Quest
    ion:

    2. A58- year-oldwomani srefer


    redt
    oyourclini
    cf oreval
    uati
    onandmanagementofat r
    ial
    fi
    bril
    lat
    ion(AF) .Hercomor bi
    ditiesincl
    udehypert
    ension,metaboli
    csyndrome,and
    dysfuncti
    onalut eri
    nebleeding.Shewasf ir
    stdiagnosedwi t
    hparoxysmalAF6year spri
    orto
    presentati
    on.Hersympt omsi ncludeshort
    nessofbreath,dyspneaonexert
    ion,pal
    pit
    ati
    ons,
    andf at
    igue.Herhusbandnot est hatshesnor
    es.Whi l
    eshecanexper i
    enceepisodesatallt
    imes
    oftheday, shenot icest
    hesympt omsmost l
    ywhensheawakens.  

    Onexami nation,herbl
    oodpr essureis132/78mm Hg, herheartr
    ateis78bpm, andherbody
    massi ndexis36.Hercar di
    ovascul arexam i
    sunr emar kabl
    e.Medicati
    onsincludemet oprol
    ol
    succi
    nat e50mgdai l
    y,l
    isi
    nopril20mgdai ly,andr i
    varoxaban20mgdai l
    y.Herwor kupshowsD
    -dimerandt hyroi
    d-sti
    mulatinghormonewi t
    hinthenor malrange.Echocardiogram
    demonst rat
    esanej ect
    ionfr
    act i
    onof55%, septalwal lt
    hicknessof1.6cm, andal ef
    tatri
    um of
    4.4cm.Theel ect
    rocar
    diogram revealsAFatar ateof80bpm andl ef
    tventri
    cularhypert
    rophy
    (LVH).

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nthi
    spat
    ient
    ?

    a. Ami
    odarone200mgdai l
    y.
    b. I
    ncr
    easemetoprol
    oldoseto100mgdai
    ly.
    c. Cat
    heterabl
    ati
    on.
    d. Fl
    ecai
    nide50mgt wicedai
    ly.
    e. Pol
    ysomnography.

    Answer
    :

    2. e. Pol
    ysomnogr
    aphy.

    Thepat i
    enti
    sobeseandherear lymor ningsympt omsmaywel lrepresentAFpr ovokedby
    unt r
    eatedsleepapnea.Treatmentofherunder lyi
    ngsleepapneamayi mpr oveherAFand
    associ at
    edsymptoms.Bef orepursui
    ngphar macologi
    corinvasi
    vether api
    es, t
    her apyshouldbe
    directedattheunderl
    yingcause.Flecainideisnotindi
    catedinpati
    entswi thstructuralhear
    t
    diseaseandLVH.Ami odaroneisnotfir
    st -l
    inet
    herapyinayoungpat ient.Catheterablati
    onis
    usual l
    yreservedf
    orpatientswhof ai
    lmedi calt
    herapy.

    Quest
    ion:

    3. Ther
    eisani
    ncr
    easei
    ncar
    diovascul
    ardi
    seaseassoci
    atedwi
    thobst
    ruct
    ivesl
    eepapnea
    (OSA)
    .

    Whichoft
    hef
    oll
    owi
    ngef
    fect
    shasbeenshownt
    obeexer
    tedupont
    hecar
    diovascul
    arsyst
    em
    byOSA?

    a. Decreasedi
    nflammat orymar ker
    s.
    b. I
    ncreasedparasympat hetict
    one.
    c. Decreasedendot hel
    inlevel
    s.
    d. I
    ncreasedplateletacti
    vati
    on.
    e. Decreasedfi
    brinogenlevels.

    Answer
    :

    3. d. I
    ncr
    easedpl
    atel
    etact
    ivat
    ion.

    Thecor r
    ectansweri sincreasedpl ateletactivati
    on.OSAr esult
    sinani ncreaseinprothrombotic
    acti
    vi t
    yinvivo. 
    Thi sincludesani ncreasei npl atel
    etactivati
    onandani ncreaseinfi
    brinogen
    l
    evel s.Pati
    entswi t
    hOSAal soexhi bitincreasesi nsympat hetictone,leadingt ohi
    gherr est
    ing
    pulsesandal sopot entiall
    yaggravat i
    ngunder lyi
    nghyper tension.Endot heli
    nlevelsare
    i
    ncr easedinpatientswi thOSA, and, inter
    estingly,decreasef ol
    lowingt reatmentwith
    cont i
    nuouspositiveai r
    waypr essur e.Elevatedendot heli
    nl evel
    sar ethoughtt ocontri
    but et
    o
    hyper t
    ensioninunt reatedOSApat i
    ent s.Inf
    lammat or
    ymar kersarealsoi ncreasedinsome
    patients.

    Quest
    ion:

    4. Youar eseei
    nga42- year-ol
    dwomani ncli
    nicforfol
    low-upofstageCdi l
    ated
    cardi
    omyopat hyandNewYor kHeartAssoci
    ati
    on(NYHA)classIIheartfai
    lur
    ewi t
    hal ef
    t
    ventr
    icularejecti
    onfract
    ion(LVEF)of35%.Shedeniesanydyspnea, or
    thopnea,chestpain,
    or
    palpi
    tations.Herhusband,whoaccompani esher,
    expressesconcernthatsheoftenfall
    sasleep
    watchingTVatt heendoftheday.Shewal ks40minuteseveryotherdayforexerci
    se
    (unchangedovert hepast2year s).
     
    Hermedi calhistor yincludespost par
    tum car diomyopat hy,whichhasbecomechr onic.She
    doesnotsmokeordr inkanyal cohol.Shei songui deline-di
    rectlymedi caltherapyf orher
    cardiomyopathy.Physi calexami nati
    oni sremar kableforabodymassi ndexof34. 5,whichis
    stablesi
    nceherl astvisit,bloodpr essure100/ 58mm Hg, heartrate64bpm, respiratoryrat
    e12
    breathspermi nut e,andoxygensat urati
    on99%onr oom ai r
    .Neckvei nsar eflatsi
    t ti
    ngupr i
    ght
    ,
    andt hehepatojugul arreflexisnegat ive.Thel ungsar eclearbilater
    all
    ywi t
    hnor ales.The
    cardiacexaminat iononl yr evealsaI I
    /VIhol osystol
    icmur muratt heapex.Theext r emiti
    es
    revealnoedema.Recentl absincl udeat hyroid-sti
    mulat i
    nghor monel evelof1. 2andnor mal
    compl et
    ebloodcount .

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestt
    estt
    oeval
    uat
    eherongoi
    ngf
    ati
    gue?

    a. Pol
    ysomnogr am.
    b. Car
    diopul
    monar yexer ci
    setest
    ing.
    c. Pul
    monaryf uncti
    ont est
    s.
    d. Car
    diacmagnet i
    cr esonanceimaging(
    MRI
    ).
    e. Ri
    ghtheartcatheteri
    zati
    on.

    Answer
    :

    4. a. Pol
    ysomnogr
    am.

    Sleepdi sordersar ecommoni npat i


    entswi t
    hhear tfailure( HF) ,
    wi thupt o61%ofHFpat ient s
    havingei thercent ralorobst ructivesl eepapnea( OSA) . Despi tehavi ngl esssl eept i
    meand
    sleepef f
    iciencycompar edwi tht hosewi thoutHF, pat i
    ent swi thHF, includi ngthosewi th
    document edsl eepdi sorders, rarel
    yr epor texcessi vedayt i
    mesl eepi ness.  
    Thus, ahi ghdegr ee
    ofsuspi cionforsl eepdi sorder sshoul dbemai ntainedf ort hesepat ients.Inamaj ortrial
    ,
    cont i
    nuousposi ti
    veai rwaypr essur eforOSAwasef fectivei ndecr easingt heapnea–hypopnea
    i
    ndex, i
    mpr ovingnoct urnaloxygenat i
    on, increasingLVEF, loweringnor epinephr i
    nel evels, and
    i
    ncr easingt hedist ancewal kedi n6mi nutes;t hesebenef it
    swer esust ainedf orupt o2year s.
    Smal lerstudiessuggestt hatcont inuousposi tiveai rwaypr essur ecani mpr ovecar diacf unction
    andqual i
    tyofl i
    feinpat i
    entswi t
    hHFandOSA.Manypat ientswi thHFhavecent ralsleepapnea,
    andt herear erecentdat athatsuggestt reatmentwi thser vo- adapt i
    vevent il
    ati
    onmayact uall
    y
    resultinwor secar di
    ovascul arout comes.  Alt
    houghwor seni ngHFcanal socausef atigue, she
    hasnoevi denceofvol umeover loadorl ow- flowst ateonexam, andshehasst ableHF
    sympt omsonar egimenofneur ohor monal -
    modi f
    yi ngdr ugs, sothatr i
    ghthear tcathet erizati
    on,
    cardiopulmonar yexer cisetest i
    ng, orcar diacMRIwoul dnotbeusef ulatt histime.Depr ession
    shoul dalsobeconsi dered,especi allyifthesl eepst udyi snor mal.

    Quest
    ion:

    5. A72- year-oldwomanwi t
    hhist oryofischemi ccar diomyopat hycomeswi thher
    husbandt oyourcar di
    ologyclinicforroutinefollow-up.Thepat i
    entreportsstabledyspnea
    whil
    ecl i
    mbi ngst ai
    rs.Hercurrentmedi cati
    onsi ncludeaspi rin81mgdai ly,at
    or vastati
    n40mg
    dail
    y,carvedilol12.5mgt wicedai l
    y,lisinopri
    l40mgdai ly,andf urosemide40mgdai l
    y.Vi
    tal
    si
    gnsar ehear trate76bpm, bloodpr essur e122/ 65mm Hg, 16r espi
    rat
    ionspermi nut
    e,and
    oxygensat urati
    on96%whi lebr eat
    hingambi entai r
    .Onexam, shei seuvolemic.An
    echocardiogram f r
    om 6mont hsagodemonst ratedal eftvent r
    icularej
    ectionfract i
    onof32%.An
    el
    ectrocardiogram obtainedint heofficeshowssi nusr hythm wi thincompl et
    elef tbundle
    br
    anchbl
    ock(
    LBBB)
    ,QRSdur
    ati
    on110msec,
    andevi
    denceofapr
    iori
    nfer
    iori
    nfar
    ct.

    Herhusbandment
    ionst
    hatwhilehi
    swif
    eissleepi
    ngatni
    ght,hehasnoticedt
    hatshewi
    llst
    op
    br
    eathi
    ngforsometi
    me,fol
    lowedbyper
    iodsofmorerapi
    d,deepbreat
    hing.

    Whi
    choft
    hef
    oll
    owi
    ngdoyour
    ecommendf
    ort
    reat
    mentofhercondi
    ti
    on?

    a. Theophylli
    ne.
    b. Conti
    nuecur renttherapy.
    c. Cardi
    acr esynchronizati
    onther
    apy.
    d. Adapti
    veser voventi
    lati
    on.
    e. Spi
    ronolactone.

    Answer
    :

    5. e. Spi
    ronol
    act
    one.

    Cheynes- Stokesr espirati


    onsareaf orm ofcent
    r alsl
    eepapnea, asubsetofsl eep-di
    sordered
    breathing,t
    hatmaybeseeni npat i
    entwithheartfail
    ure.Thebestt r
    eatmentt odat eis
    optimizati
    onoft her apyforcongest i
    veheartfai
    lure.Adapti
    veser vovent
    ilat
    ionwasassoci ated
    withhar mint heSERVE- HFt r
    ialforpat
    ientswit
    hhear tfail
    ureandcent ralsleepapneaandt hus
    woul dnotbei ndicat ed.Thispati
    enthasani ncompl eteLBBBf orwhichcar diac
    resynchronizati
    ont herapywouldnotbei ndicat
    ed.Theophyl l
    inehasnor oleint hetr
    eatmentof
    Cheynes- Stokesr espirati
    ons.Giventhi
    spat i
    ent'sheartfai
    luresympt oms, additionof
    spironolact
    onei st hebestopt i
    on.

    Quest
    ion:

    6.  
    55-year
    -oldobesemanwi t
    hsympt omaticpar oxysmalatri
    alf
    ibr
    il
    lati
    onpresentsto
    cli
    nicforchroni
    cfati
    gue.Hefeel
    stir
    edal ltheti
    me, andf al
    lsasleepwheneverheiswatching
    TVorr eadi
    ngabook.Hei sfearf
    ulbecausehef ellasleepr ecent
    lywhi
    ledrivi
    ngintr
    affi
    c,which
    result
    edinami normotorvehicl
    eaccident.Hiswifesayst hathesnoresloudlyandhas
    episodeswhenhest opsbreathi
    ngatnight.

    Forwhi
    choft
    hef
    oll
    owi
    ngi
    sthepat
    ientati
    ncr
    easedr
    isk,
    ifl
    eftunt
    reat
    ed?

    a. Al
    teredtestoster
    onelevels.
    b. Atr
    ialf
    ibri
    ll
    ation.
    c. Symptomat icbradycar
    dia.
    d. Val
    vularhear tdi
    sease.
    e. Suddencar diacdeathduringwakef
    ulhour
    s.

    Answer
    :

    6. b. At
    ri
    alf
    ibr
    il
    lat
    ion.

    Thecor r
    ectansweri sincreasedriskofatr
    ialf
    ibr
    il
    lati
    onrel
    atedtountr
    eat edobstructi
    vesleep
    apnea(OSA) .Ithasbeenshownt hatuntr
    eatedOSAi sassociat
    edwithrecurrentatri
    al
    fi
    bri
    ll
    ati
    on,includingaftercardi
    oversi
    on.However, whentr
    eated,t
    heincidenceofr ecurr
    ent
    atr
    ialf
    ibri
    ll
    ationdecreases.Increasedri
    skofsuddencar di
    acdeathistrueinpatientswithOSA,
    buthasbeenf oundtooccurdur ingsleephours,notduringwakef
    ulness.Valvularheartdi
    sease
    i
    snotassociatedwi t
    hthepr esenceofOSA.Longst andingOSAcanl eadtopul monar y
    hypert
    ensi
    onandr esultanttri
    cuspidregurgi
    tat
    ion,buttherei
    snodirectcorrel
    ation.Thereis
    ei
    thernochangeoradecr easeintestoster
    onelevelassociat
    edwiththepresenceofsl eep
    apnea.Whil
    eapnei cepisodescanr esulti
    narrhythmiassuchasbradycardia,theseoccurwhi l
    e
    sl
    eeping,t
    herefor
    ear enotconsideredsympt omat i
    c.WhenOSAi str
    eated,orwhi lethepati
    ent
    i
    sawake, t
    heseapnei c-associat
    edar r
    hythmiasresolve.

    Quest
    ion:

    7. Youar econsultedregardinga40- year-


    oldwomanwhohasknownCushi ng'ssyndr
    ome
    andpresentswi thatransi
    entischemicattack.Herechocardiogr
    am showsalargeleftat
    ri
    al
    myxoma30mm x32mm x28mm.Shet ell
    syouherf at
    herhadat umorcutoutofhisheart
    aroundthesameageasshei snow, butthet umorgrewbackseveralyear
    slat
    er.Sheneeds
    surgi
    calint
    ervention,
    butherr ealconcer
    ni sherchil
    dren,ages24and18years,andt hei
    rri
    skof
    si
    mi l
    arhealt
    hi ssues.

    Whichofthefol
    lowi
    ngdoyour ecommendt
    othepat
    ientr
    egar
    dingt
    heher
    it
    abi
    li
    tyor
    t
    ransmissi
    bil
    it
    yofhercondi
    ti
    on?

    a. Sugge stthatt
    hepatientbet
    estedfortheFBN1genemut at
    ion.
    b. Testthemyxomaf orCongoredstaini
    ngfoll
    owingsurgery.
    c. Obtai
    nechocar di
    ographyonherchi l
    dren.
    d. Reassur ethepat
    ientther
    earenosuchher it
    ablecondit
    ionstoconsi
    der
    .
    e. Sugge stthatt
    hepatientbet
    estedforEpstei
    n-Barrvi
    rus.

    Answer
    :

    7. c. Obt
    ainechocar
    diogr
    aphyonherchi
    ldr
    en.

    Mostmyxomasar esporadic,
    butt
    heymaybef amili
    al.Inpar t
    icular,t
    heCar neyCompl exor
    CarneySyndromei sanautosomaldomi nantfamili
    almyxomasyndr ome.Thi spati
    entscenario
    descri
    bespr i
    marypigmentednodularadrenocorti
    caldi sease(PPNAD) ,whichcanpr oduce
    Cushingsydrome, anendocri
    nedi
    sordercommonl yassoci atedwi thCar neySyndr ome.Gi ven
    thefamil
    ialpatt
    ern,t
    heansweristoexami nethechildrenf orsimilarfeaturesoft hi
    ssyndr ome.
    Epstei
    n-Barrvir
    us,FBN1genemut ati
    ons( Marfansyndr ome) ,andcar diacamyl oidosis(Congo
    redstai
    ning)areunrel
    atedtocar
    diacmyxomas, thereforetestingisnotwar ranted.

    Quest
    ion:

    8. A48-year-oldwomanwi thahi storyofhypertensionandseizur


    esseeksassistance
    withsmoki ngcessation.Shehassmoked1packperdayf ort
    helast25years.Shetr
    iedtoqui
    t
    severalyearsagobyusi nganicoti
    nepat ch,
    butwasunsuccessf ul.Medicati
    onsincl
    ude
    hydrochlorot
    hiazide25mgandl evetir
    acet am 1000mgt wicedai
    ly.Shetel
    lsyouthather
    brotherwasr ecentl
    yabletostopsmoki ngaf t
    erheusedbupr opi
    onpharmacot her
    apyandshe
    woul dli
    ketot r
    ybupr opi
    on.Shedeniesanydepr essi
    vesympt oms.
    Whi
    choft
    hef
    oll
    owi
    ngwoul
    dbet
    hemostappr
    opr
    iat
    erecommendat
    ionf
    ort
    hispat
    ient
    ?

    a. Nicoti
    nenasalspray6dosesdai l
    y.
    b. Bupropion150mgt wicedaily.
    c. Nicoti
    nei nhal
    er10cart
    ri
    dgesdaily.
    d. Nicoti
    negum asneeded.
    e. Varenicl
    ine1mgt wicedail
    y.

    Answer
    :

    8. e. Var
    eni
    cli
    ne1mgt
    wicedai
    ly.

    Thehighestabst i
    nenceratesarewi t
    hvarenicli
    netherapy,andgivenherfailedat t
    empti nthe
    pastwitht
    heni cotinepatch,i
    tisanappropriatetherapy.Bupropi
    oniscont raindi
    cat edwit
    hher
    hi
    storyofseizures.Ofthethreenicoti
    ne-
    replacementt herapi
    es,t
    henicotinei nhalerist
    hemost
    ef
    fecti
    venicoti
    nei nter
    venti
    onbecauseoft heincreaseddependencyr ateswi ththenasalspray,
    butiti
    ssti
    lli
    nferiortovareni
    cli
    net her
    apy.Inaddi t
    iontomedicalther
    apy, patientsshould
    al
    waysbepr ovidedwi thcounseli
    ngandavai lableresources,
    suchast hequi tli
    ne.

    Quest
    ion:

    9. A66-
    year-
    oldr
    ight-
    handedmanpr esentswit
    hdizzi
    nessandri
    ghtarmfati
    guewhil
    e
    painti
    nghisgar
    agedoor.Hehasbil
    ateralcervi
    calandsupracl
    avi
    cul
    arbrui
    ts.Theri
    ghtar
    m
    pressurei
    s100/72mm Hg, andt
    heleftarm pressur
    eis146/80mm Hg.

    Magnet
    icr
    esonanceangiogr
    aphyshowsa90%stenosi
    soft heinnomi
    nateart
    ery,a60%
    st
    enosi
    softher
    ighti
    nter
    nalcarot
    idar
    ter
    y,anda75%stenosisofthel
    efti
    nter
    nalcar
    oti
    dar
    ter
    y.

    Whi
    choft
    hef
    oll
    owi
    ngt
    reat
    ment
    sisi
    ndi
    cat
    edf
    orhi
    ssympt
    oms?

    a. Leftcar
    otidar
    teryendart
    erect
    omy.
    b. Leftcar
    otidar
    terystent
    .
    c. Innominatear
    terystent
    .
    d. Rightcarot
    idart
    eryendart
    erect
    omy.

    Answer
    :

    9. c. I
    nnomi
    nat
    ear
    ter
    yst
    ent
    .

    Thispati
    enthasclassicsymptomsofrightarm claudicati
    onandsubcl avi
    anstealresult
    ing
    fr
    om ahigh-gradestenosisoft
    heinnominateartery.Withrightarm ef
    fort
    ,ther
    eisli
    mb
    vasodi
    lat
    ionandr et
    rogradefl
    owdownt herightvertebralarter
    ytoaccommodat et
    hedi l
    ated
    vessel
    s.Theleftandri
    ghtcaroti
    darter
    ystenosesar enotcausi ngthesesympt oms,ther
    efore
    tr
    eatmentsdir
    ectedatthesearenotthecorrectoptions.
    Quest
    ion:

    10. A63- year-oldmal enonsmokerunder wentcar oti


    dultr
    asonographyaspartofhis
    evaluationforasyncopalevent .Whilediamet erreductionwasnotevi dentduetopoorimage
    quality,
    Doppl errecordi
    ngssuggest edincreasedvel ociti
    esinthelefti
    nter
    nalcar
    oti
    dartery
    l
    eadi ngt oanest i
    mat i
    onof<50%di seaseint herightinternalcar
    otidarter
    yand50-69%
    stenosisi nt
    hel efti
    nternalcar
    otidart
    ery.Carotidultrasonographyperformed2yearsearl
    ier
    suggest ed<50%bi l
    ater
    aldisease,r
    aisi
    ngt heconcer naboutpr ogressivel
    eft
    -si
    dedstenosis.

    Hewasr ef
    err
    edforcaroti
    dart
    eryangiography:magnet
    icresonanceangiogram (MRA)is
    showninFigur
    e1.Serum chemist
    ri
    esi ndicat
    edalow-densityl
    ipoprot
    eincholest
    eroll
    evelof
    63mg/dl,r
    educedfrom 114mg/dlfr
    om 2year spri
    orwit
    hi nsti
    tut
    ionofli
    fest
    ylechangesand
    l
    ow-dosestati
    nther
    apy.

    Whichoft
    hef
    oll
    owi
    ngi
    stheappr
    opr
    iat
    emanagementofcar
    oti
    dar
    ter
    yat
    her
    oscl
    erosi
    sfort
    his
    pat
    ient
    ?

    a. Ref
    erf ori
    nvasiveheadandneckangi
    ogr
    aphy.
    b. Ref
    erf orl
    eftcarot
    idendar
    ter
    ect
    omy.
    c. I
    ncreasestatindose.
    d. Noc hangeinmanagement .

    Answer
    :

    10. d. Nochangei
    nmanagement
    .
    Thecont rast-enhancedMRApr ovidesexcel l
    entvisuali
    zationoft hecar oti
    dar teri
    es, wit
    hno
    evidenceofsi gni f
    icantst enosis, andmi l
    dl uminalirr
    egulari
    tyint heinternalcar oti
    dar t
    er i
    es
    consistentwithhi sor iginaldupl excarotidultr
    asoundexami nation.Thus, invasiveangi ography
    toconf i
    rmt hesef indingsi snotnecessar y.MRAwasusef ulinthisinstancet or esolve
    discordantser ialultr
    asoundf indings;intheabsenceofsympt omsandsi gnif
    icantst enosis,
    endarterectomyi snoti ndicated.Thi spatient’
    slow- densit
    ylipopr ot
    einachi evedwi thst ati
    n
    therapyandl ifestylechangesi swel lbelowt argetforapat i
    entwi thevidentat herosclerosis,and
    managementshoul dr emai nunchanged.

    Quest
    ion:

    11. A56- year-ol


    dwomanpr esentstotheemergencydepart
    mentwi t
    hsympt omsof
    amaur osi
    sfugax.Hersympt omsr esolvewithi
    n15minutesofpresentati
    on.Shehasamedical
    hi
    storyofhypertension,andsheisanact i
    vesmoker.Herheartr
    atei s85bpm andbl ood
    pressurei
    s142/ 84mm Hg.Physi calexami nat
    ioni
    snotabl
    eforar ightcaroti
    dbrui
    t.An
    el
    ectrocar
    diogram revealsnor
    malsi nusrhythm.Headcomputedt omogr aphyisnormal
    .

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    enextst
    ep?

    a. Electr
    oencephal
    ogram.
    b. Dischargehome.
    c. Implantabl
    elooprecorder
    .
    d. Erythr
    ocytesedi
    ment at
    ionrat
    e.
    e. Carotidart
    eryul
    tr
    asonography.

    Answer
    :

    11. e. Car
    oti
    dar
    ter
    yul
    tr
    asonogr
    aphy.

    Thecor rectansweri nt hiscasei stoper form addi t


    ionalevaluationforsuspectedsympt omat i
    c
    caroti
    dar terydiseasewi thul t
    rasonogr aphyorcomput edtomogr aphy/magneticresonance
    angiography.I fsi
    gnificantcarotiddiseasei sfoundi nthi
    spat i
    ent ,i
    twouldwar rant
    considerationofintervention.Itisnotappr opriatetodischarget hispati
    entwit
    houtf ur
    ther
    evaluati
    on, becausei tmaydef errevascul ari
    zat i
    oninsympt omat i
    ccaroti
    dstenosi s.Transient
    i
    schemi cat tackisthemosti mpor tantpredi ctorofstroke,withupt o13%ofpat i
    ent shavinga
    strokewi t
    hin90daysofi nit
    ialpresentati
    onandupwar dof30%wi t
    hin5years.Thi spatient'
    s
    sympt omsofamaur osisfugaxi snotl i
    kelyt obeexpl ainedbyasei zureortempor alarteri
    ti
    s.
    Occultatrialfi
    bril
    lat
    ioni sani mpor t
    antcauseofcr yptogenicstroke,andani mpl antabl
    el oop
    recordermayhel ptomaket hi
    sdi agnosisaf termor eurgentdi seaseshavebeenexcl uded.

    Quest
    ion:

    12. A40- year-


    oldwomanwi thnomedicalhist
    orypresentstotheemer gencyroom with
    progressivel
    eft
    -sidedfacialweaknessof2daysdur ati
    on.Heriniti
    alsymptomsst art
    ed1week
    agowi thneckpain,headache,andsomenausea.Shedeni estakinganynewmedi cati
    onsand
    saidshewasi nami norcaraccident1daypriortoonsetofhersympt oms.Herbloodpr essur
    e
    i
    s142/ 82mm Hgi nbot harmswi thahear
    trateof105bpm onpr esentat
    ion.Examinati
    onis
    notableforpt
    osisoft heri
    ghteyeandconst r
    icti
    onoftherightpupil.
    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    edi
    agnost
    icst
    udyf
    ort
    hispat
    ient
    ?

    a. Chestcomput edtomography(CT)
    .
    b. Caroti
    dcomput edtomographyangiography(CTA)
    .
    c. Transthoracicecho(TTE)withami cr
    ocavit
    ati
    onstudy
    d. TranscranialDoppler
    .
    e. Magne ti
    cr esonanceimaging(MRI)ofthebrai
    n.

    Answer
    :

    12. b. Car
    oti
    dcomput
    edt
    omogr
    aphyangi
    ogr
    aphy(
    CTA)
    .

    Thisyoungpat i
    entwi thantecedentminornecktrauma, pain, andHorner’
    ssyndr ome( ptosi
    s,
    anhydrosis,andmi osi
    s)mostl ikel
    yhasacar ot
    idart
    erydi ssect i
    on.Ei
    therCTAorMR
    angiography(MRA)ar eaccept ablemeanstoevaluatefordi ssecti
    on.Acuteischemi cstroke
    ei
    therfrom vasculardiseaseorembol idoesnotcauseHor ner’ssyndr
    ome.Ther efore,aTTE
    wit
    hmi crocavit
    ationisnothelpf ul
    .APancoasttumorwoul dbeunusuali nthispatientand
    wouldcauseani psil
    ateralHorner’
    ssyndromeresult
    ingi nleft-si
    dedsympt oms.Ther efore,
    the
    chestCTi snotindicated.MRIwoul dnoteval
    uatethevascul atur
    eandanMRAwi l
    lbeneeded.

    Quest
    ion:

    13. An80- year-oldwomanpr esentstotheemer gencyroom (ER)wi thacuteri


    ghtarm
    weaknessandsl urredspeech.Shehasahi st
    oryofpoor l
    ycontr
    olleddiabetesmel l
    it
    us,
    hypertensi
    on, atr
    ialfi
    br i
    ll
    ation,
    andcor onaryart
    erydiseasewit
    hpr eviousstentplacement.The
    pati
    entisaccompani edbyherdaught erwhonot esthathermother ’
    ssympt omsst art
    ed
    approximately90mi nutesago.Shewasseeni ntheER2mont hsear li
    erwi t
    hat r
    ansient
    i
    schemi cattackatwhi cht i
    meherat r
    ialfi
    bri
    ll
    ati
    onwasdi agnosed.Cur rentmedicati
    onsincl
    ude
    i
    nsulin,aspi
    rin81mg, li
    sinopri
    l5mg, warfari
    n5mg, andmetoprolol25mgbi d.
     

    Onexami nation,shei safebri


    le.Herheartrateis88bpm, bl
    oodpr essurei s210/100mm Hg,
    andr espi
    r atoryrateis16br eathspermi nute.Herneur
    ologicexami nati
    oni sconsist
    entwitha
    3
    l
    eftmi ddl
    ecer ebralarter
    ystroke.Plat
    eletcountis239,000mm , i
    nt ernat
    ionalnor mali
    zedrat
    io
    i
    s1. 8,andpar ti
    althromboplastinti
    mei s28seconds.Aheadcomput edt omogr aphyobtai
    ned
    wit
    hi n30mi nutesoft hepatientarr
    ivi
    ngi ntheERshowsal arge, acut e,l
    eft-si
    dedmi ddl
    e
    cerebralar t
    erystroke.Thepat ienthasnohi stor
    yofpri
    orgastroint esti
    nalbleedingor
    i
    ntracranialhemor rhageandhashadnor ecentsurger
    ies.

    Whi
    choft
    hef
    oll
    owi
    ngt
    her
    api
    esi
    smostappr
    opr
    iat
    eatt
    hist
    ime?

    a. Clopidogrel
    .
    b. Full
    -doseaspiri
    n.
    c. Recombi nantti
    ssueplasmi
    nogenact
    ivat
    or.
    d. Argatroban.
    e. Unfracti
    onatedhepari
    n.
    Answer
    :

    13. b. Ful
    l-
    doseaspi
    ri
    n.

    Thepat i
    entishavi nganacut ei schemi cstroke.Despiteherear lypresentati
    on,shehassever al
    contr
    aindicati
    onst olyti
    cs,includi ngelevat
    edbl oodpr essure,recentstrokewithi
    n3mont hs,
    andconcur rentuseofwar farin.Cont raindi
    cationstolyticsincludesystolicbl
    oodpressure>185
    mm Hgordi astoli
    c>110mm Hg, activeint
    ernalbleeding, pl
    ateletcount<100,000mm3, heparin
    administrat
    ionwi t
    hin48hour s,cur r
    entuseofant i
    coagul ants(int
    ernati
    onalnormali
    zedr ati
    o
    >1.7,prothrombint i
    me>15sec) ,currentuseofdi rectthrombini nhi
    bit
    or sordir
    ectf
    actorXa
    i
    nhibi
    tor swithelevatedsensitivel aborator
    yt ests,
    bloodgl ucoseconcent rati
    on<50mg/ dl,and
    comput edtomogr aphydemonst rati
    ngmul til
    obarinfarction.
     

    Atpr esent,theusef ulnessofar gatrobanorot hert hrombi ninhi


    bitor
    sfort r
    eatmentofpat ients
    withacut eischemi cst rokeisnotwel lestablished( ClassI I
    b,LevelofEvidence[LOE]B) .These
    agent sshoul dbeusedi nthesettingofcl ini
    calt ri
    als.Urgentant i
    coagulati
    onwi th
    unfract i
    onatedhepar i
    norl owmol ecul arwei ghthepar i
    n,withthegoalofpr eventi
    ngear ly
    recurrentstroke, halti
    ngneur ologicalwor seni ng,orimpr ovingoutcomesaf teracut eischemi c
    strokei snotr ecommendedf ortreat mentofpat i
    entswi thacuteischemicst r
    oke( ClassI II
    ,LOE
    A).Or aladmi nistr
    ationofaspi ri
    n( initialdose325mg)wi thin24-48hour safterstrokeonseti s
    recommendedf ortr
    eatmentofmostpat ient
    s( Cl
    assI ,LOEA) .Theusefulnessofcl opidogr elf
    or
    thetreat mentofacut eischemi cstrokei snotwel lestabli
    shed( Cl
    assIIb,LOEC) .Fur t
    her
    resear chtestingtheusef ul
    nessoft heemer gencyadmi nist
    rati
    onofclopidogrelint hetreatment
    ofpat ientswithacut est rokeisrequi red.

    Quest
    ion:

    14. A65- year- ol


    dmanpr esentstoar uralur gentcar ecli
    nicwi thsympt omsofper i
    or al
    numbnessandr i
    ghtar mt i
    ngl i
    ngthatst art
    edappr oximat el
    y2hour sagowhi lehewasdr ivi
    ng
    tothest ore.Thepat ienthasnotseenaphysi cianinyear s,deni esanymedi calhi st
    ory,and
    takesnomedi cations.Exami nati
    onatt heur gentcar eclinicreveal sanobesemal einnoacut e
    distr
    ess.Hei saf ebri
    le.Pulsei s128bpm andi rregular.Bloodpr essureis155/ 100mm Hg.
    Respiratoryrateis18br eathspermi nute.Neur ologicalexami nat i
    oni ssigni f
    icantforflattened
    right
    -sidednasol abialfold,lossofsensat ionovert herightforear m, andl ossoft wo- point
    discri
    mi nati
    oni nther i
    ghthand.Labor atorydat a, i
    ncludingabasi cchemi strypanel ,acompl et
    e
    bloodcount ,internati
    onalnor mali
    zedr ati
    o( I
    NR) ,prothrombi nt i
    me, andpar t
    ialthrombopl astin
    ti
    mear eal lwithinnor mallimi t
    s.Electr
    ocar diogram showsat rialfibril
    lat
    ionwi t
    havent ricular
    responseof130bpm.  

    Duetoconcer nsforanacutei
    schemicstroke,
    thepat
    ientistransferr
    edtotheneareststr
    oke
    cent
    er.Thepat i
    entarr
    ivesatt
    hestrokecenter
    ’semergencydepar tment1.
    5hour sl
    ater.An
    i
    mmedi ateheadcomput edtomographyshowsanacut eischemi cstr
    okeinthethalamuswith
    nohemor rhage.Hisneurol
    ogi
    calexaminati
    onandvit
    alsignsar eunchanged.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    ether
    apy?

    a. St
    reptoki
    nase.
    b. Aspi
    rin.
    c. Cl
    opidogrel
    .
    d. Enoxopar
    in.
    e. Recombinantt
    issue-
    typepl
    asmi
    nogenact
    ivat
    or(
    rtPA)
    .

    Answer
    :

    14. e. Recombi
    nantt
    issue-
    typepl
    asmi
    nogenact
    ivat
    or(
    rtPA)
    .

    Thepatientinthi
    sscenariopr
    esentswithacuteischemicstroke.Hispresentationtoast roke
    centeri
    swi t
    hinawi ndowof3-4.5hoursaftersymptom onset.Hisplat
    eletsarenor mal,andhis
    bloodpressureis<185/110mm Hg.Accor dingtotheAmericanHear tAssociation/American
    StrokeAssociati
    on2013guidel
    inesforthemanagementofi schemi cstroke,i
    ntravenousr tPA
    (0.9mg/kg,maxi mum dose90mg)i srecommendedf oradmi nist
    rat
    iont oeli
    giblepati
    entswho
    canbet reat
    edint het
    imeperi
    odof3- 4.5hoursaft
    erstr
    okeonset( ClassI ,
    LevelofEvidence
    B). 

    Quest
    ion:

    15. A65- year-oldmanwi t


    hahi storyoft obaccoabuse, hypert
    ensi
    on,hyper li
    pidemia,
    obesity,andsl eepapneapr esentst ot heemer gencydepar tmentwithlef
    t-si
    dedhemi paresis
    andf aci
    aldr oop.Thesympt omsbegan8hour spri
    ortopr esent
    ati
    onbuthadr esolvedatthe
    ti
    meofeval uationintheemer gencydepar t
    ment .Hiscurrentmedicati
    onsincludeaspi r
    in81mg
    dail
    y, at
    enolol50mgdai l
    y,l
    isinopril20mgdai l
    y,andatorvastat
    in40mgdai ly.Revi ewof
    systemsi sremar kableforoccasi onalepi sodesofleft
    -sidednumbness.Car diacexami nationis
    unremar kableexceptf orbil
    ateralcarot i
    dbr uit
    s. 

    Hisel
    ectr
    ocardi
    ogr
    am showsnor malsinusr
    hythm andi
    snormal
    .Computedtomographi
    c
    angi
    ographyshowedr
    ightinternalcaroti
    dst
    enosi
    sof75%justdi
    stalt
    othebi
    fur
    cati
    onand
    mini
    malplaqueint
    helef
    tinternalcaroti
    d.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    emanagementoft
    hispat
    ient
    ’scar
    oti
    dst
    enosi
    s?

    a. I
    ncreaseaspir
    into325mg.
    b. Beginaspir
    in/
    dipyr
    idamole.
    c. Caroti
    dendarter
    ectomy(CEA).
    d. Beginclopi
    dogrel
    .
    e. Not r
    eatmentneeded.

    Answer
    :

    15. c. Car
    oti
    dendar
    ter
    ect
    omy(
    CEA)
    .

    Thispatienthassi gni
    fi
    cantcar oti
    ddi seaseandi sexperiencingt ransientischemi catt
    acks
    (TIAs)li
    kelyfrom embolizati
    onofcar ot
    idpl aque.Hewar rantst r
    eatmentt opr eventapossibl
    e
    devastati
    ngst rokeinthefuture.Insever alrandomi zedtrialsinvolvingpatientswhohadaTI A
    orstrokeassoci atedwit
    hi psi
    lateralcaroti
    dst enosis,CEAr educedt hesubsequentr i
    skof
    stroke.I
    nt heNASCETst udy,patientswi t
    hst enosisof70%ormor er andoml yassignedtoCEA
    plusmedi caltherapyhada2- yearriskofi psil
    ateralst
    rokeof9%compar edwi t
    h26%i nthe
    groupassi gnedt omedicaltherapyal one.Amet a-analysisoft hemaj ort
    rialsofCEAshowed
    thatthebenef i
    tfrom CEAwasgr eatestwheni twasper formedwi thin2weeksoft heonsetof
    TIAorst r
    oke, rat
    herthanlater.Thepat ientisalreadyonaspi rin,andaddi ngaddi ti
    onal
    ant
    ipl
    atel
    etagent
    sisnotr
    ecommended.

    Quest
    ion:

    16. I r
    respecti
    veofthemet hodf
    orevaluat
    ingcarot
    idart
    erydisease(
    incl
    udingduplex
    ult
    rasonography,computedtomographicangiogr
    aphy,magneti
    cresonanceangiography,and
    cathet
    erangiography)
    ,whichofthefol
    lowingfact
    orsbestcor
    rel
    ateswithri
    skoffuturestr
    oke?

    a. Tortuosit
    yofdistalart
    eries.
    b. Statusofthecont r
    alat
    eralcaroti
    dar
    ter
    y.
    c. Plaqueulcerati
    on.
    d. Percentageofcarotidstenosis.
    e. Extentofplaque

    Answer
    :

    16. d. Per
    cent
    ageofcar
    oti
    dst
    enosi
    s.

    Themosti mpor tantinf


    or mat iongai nedfrom eval uat
    ionofthecar ot
    idarter
    ies,irr
    especti
    veof
    i
    magi ngmodal it
    y,istheper cent ageofcar oti
    dstenosi s.Theprognosisforpatientswithcar
    otid
    diseaseismostcl oselylinkedt ot hedegreeofst enosis,wit
    ha2mm r esidualluminaldiameter
    ora60- 70%r educti
    oni ndi amet erassociatedwi t
    hamar kedincreaseinther i
    skofst r
    oke.
    Plaqueulcerati
    onsar ecommon, butdonotst ronglyassociatewithsubsequenti psil
    ater
    al
    i
    schemi cstroke.Extensivepl aquemayf avorcarot i
    dendar t
    erect
    omyr atherthancar oti
    d
    stenti
    ng.Occludedcont ralat eralcaroti
    dar ter
    iesmayf avorcarot
    idstenti
    ngr at
    hert han
    endarter
    ectomyf ordefiniti
    vet reatment.

    Quest
    ion:

    17. A42- year-


    oldwomanpr esentstoyouroffi
    cewi thcompl
    aint
    soffati
    gue, malai
    se,
    shortnessofbreat
    h,andpr ogressi
    velowerextremityedemaoverthepast2mont hs.Shehas
    nopr i
    orhist
    oryofcardiopulmonarydisease.Examinat i
    onshowsnormaljugularvenous
    pulsati
    on,cl
    earlungs,2+pitti
    ngedemaoft hebi l
    aterall
    owerext
    remit
    ies,
    wi t
    hsever al
    cutaneousgrowths,andpigment edlesi
    onsoft heskin.

    At
    ranst
    hor
    aci
    cechocar
    diogr
    am i
    sshowni
    nFi
    gur
    e1.

    Whichoft
    hef
    oll
    owingcl
    ini
    calsyndr
    omei
    smostl
    ikel
    ytobeassoci
    atedwi
    tht
    heabnor
    mal
    it
    y
    depi
    ctedi
    nFi
    gure1?
    a. Car
    neycompl ex.
    b. VonRe ckl
    inghausen’sdisease.
    c. Loef
    fl
    er’sendocar di
    ti
    s.
    d. Noonan’ssyndr ome.
    e. Car
    cinoidsyndr ome.

    Answer
    :

    17. a. Car
    neycompl
    ex.

    Thecor rectoptionisCar neycompl exwi t


    har i
    ghtatri
    almyxomashown.Thi si
    sar are
    autosomaldomi nantneopl asticdisor derchar acter
    izedbycar diacmyxomas, cutaneous
    myxomasorpi gment edlesions, andendocr inetumor s.Carci
    noidt umor sar eusuall
    ylocatedin
    thegast r
    ointesti
    nalsystem ( 90%)orl esscommonl yi npulmonar yorgeni touri
    narylocations.
    Cardiacinvolvementusual l
    ymani festsasf ibroti
    cchangest or i
    ghthear tstructur
    esr esulti
    ngin
    valvul
    arr egurgit
    ati
    onorst enosi s.Car diacinvolvementi nLoeffl
    er ’
    shyper eosinophil
    ic
    syndromeusual lyisexhibit
    edbyendocar di
    tisorendomyocar di
    t i
    s.Themostcommoncar diac
    abnormal it
    yinNoonan’ ssyndr omei sdysplast i
    cpul monaryvalvest enosis.Von
    Recklinghausen’ sdisease(neur ofibromat osis)isnotknownt obeassoci at edwithcardiac
    tumor sbutmaybeassoci atedwi t
    hcongeni talheartdefect
    s.
    Quest
    ion:

    18. A60- year-oldmani sadmittedwithat r


    ansi
    entischemicattack(TIA).Hehasahi stor
    y
    ofgast roesophagealr efl
    uxdisorderandost eoar
    thr
    it
    isbutnosi gni
    fi
    cantcardiovascularri
    sk
    factors.Histemper atureis98.3°F,bloodpressurei
    s134/ 72mm Hg, heartrateis82bpm, and
    oxygensat ur
    at i
    onis99%onr oom ai r.Hi
    slungsareclear
    , hear
    tsoundsincludeasof tsystol
    ic
    mur mur ,andt herearenoext raheartsounds.Theskinexami nati
    onisunremar kable.Heis
    referr
    edf orachestwal lechocardi
    ogr am,andbecauseofanabnor malit
    y,at ransesophageal
    echocar diogram isperformed( Fi
    gure1) .

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    yet
    iol
    ogyoft
    heabnor
    mal
    it
    yshowni
    nFi
    gur
    e1?

    a. Fi
    br oelast
    oma.
    b. My xoma.
    c. Endoc ardi
    tis.
    d. Bloodcyst s.
    e. Thrombus.
    Answer
    :

    18. a. Fi
    broel
    ast
    oma.

    Thecor rectopt i
    onispapi ll
    aryf i
    broel
    astoma( PFE).Thepr esent ati
    ondescribedand
    abnor malit
    yshownar etypicalofasympt omat i
    cPFE.PFEi sthesecondmostcommonpr i
    mar y
    car diacmass.Appr oximat elythree-f
    ourthsofPFEsor iginatef rom thevalves( aort
    ic44%, mit
    ral
    35%, tr
    icuspid15%, andpul moni c8%).Whi l
    et hemaj orit
    yofpat ientsareasympt omat i
    c,the
    mostcommonpr esent i
    ngsympt omsar et r
    ansientischemi cat t
    ackandst r
    oke, f
    ollowedby
    angi na, myocar di
    alinfarcti
    on, heartf
    ail
    ure, suddendeat h, andsyncope.Tr eatmentofchoi cefor
    sympt omat i
    cPFEi ssurgicalexcision.Cli
    nicalfoll
    ow- upcoul dbeconsi deredf orasympt omat ic
    PFEswhent heyareofl argesi ze(>1cm)andhavehi ghmobi l
    ity.Bloodcyst sarecar di
    ac
    massest hatarecommonl yattachedtoval vularsurfaces.Theyar echaracteri
    zedby
    mi crobubbl econt r
    astent eri
    ngt hedivert
    icularcavityandof tenbecomehear tshapeddur i
    ng
    vent ri
    cularsyst ol
    e.Theyar erarelyseeninadul ts.Surger yisindi catedforbloodcyst swhen
    valvedest r
    uct i
    onispr esent.Thel ackofcl i
    nicalfi
    ndingsofi nfectiveendocarditi
    sandt he
    locat i
    onont heaor t
    icsider atherthanvent r
    icularsideoft hel eaf l
    etmakeendocar dit
    isless
    li
    kel y.Therei snosuggest i
    ont hisisathrombus.

    Quest
    ion:

    19. A64- year


    -ol
    d-manpr esentstoyouroff
    iceforevaluati
    onofaheartmass.Hismedi cal
    hist
    oryincl
    udeshyperl
    ipidemia,t
    obaccoabuse, andchronicobstr
    uct
    ivepulmonarydisease.
    Whileoutoftown2weeksagovi si
    ti
    ngfamily,
    hewasadmi t
    tedtoanoutsi
    dehospitalf
    orfever
    s,
    cough,anddyspnea.Hesayst hathissymptomsi mprovedt osomeextentaft
    err
    eceiving
    anti
    biot
    icsforpneumonia.

    Anechocardiogr
    am i
    sperfor
    med,andacardiacmassisi
    dent
    if
    iedi
    nther
    ightat
    ri
    um t
    hatdoes
    notappeartobeeit
    herveget
    ati
    onorthrombus.
    Whichofthefoll
    owi
    ngisthemostli
    kelycar
    diactumor
    ?

    a. Li
    poma.
    b. Papil
    laryf
    ibr
    oelastoma.
    c. Metastati
    cdisease.
    d. Sarcoma.
    e. Myxoma.

    Answer
    :

    19. c. Met
    ast
    ati
    cdi
    sease.

    Thecor rectopt i
    onismet astati
    cdisease.Excludingthr
    ombiandveget ati
    ons,mal i
    gnant
    met astasesar ethemostcommonl yfoundcar diacmasses,occurr
    ing30-1000timesmor e
    frequentlythanpr i
    marycar diacmasses.Forexampl e,
    inaNor thAmericanstudyincludi
    ng
    >11, 000aut opsiesperf
    ormedbet ween1973and2004, 266cardi
    acmasseswer efound.Of
    these,264wer eduetomal ignantmet astasi
    s.Commonmal i
    gnanciestometastasizetothe
    hear ti
    ncludelung, br
    east,gastroi
    ntesti
    nal,mel anoma,andleukemia/l
    ymphoma.Among
    primar
    ycardi
    acmasses,myxomasarethemostcommon,fol
    lowedbyli
    pomasandpapil
    lar
    y
    fi
    broel
    ast
    omas.Mal
    ignantpri
    marycar
    diacmassesar
    eexceedingl
    yrar
    e;however
    ,among
    these,
    sar
    comasarethemostcommonlyoccurr
    ingmasses.

    Quest
    ion:

    20. A42- year-ol


    dmancomest oyouroff
    iceforeval
    uati
    onofanabnormallipi
    dpanel
    obtainedintheprocessofappl
    yingforl
    if
    einsurance.Hedoesnothaveanysympt omsofchest
    painordyspnea.Hewr estl
    edincoll
    ege,butdoesnotexerci
    seregul
    arl
    yatpresent.Hisbl
    ood
    pressureis142/86mm Hg, hei
    ghtis70inches,weighti
    s209pounds,andwai stci
    rcumfer
    ence
    i
    s42i nches.
     

    Thefasti
    ngli
    pidpanelshowedtotalchol
    ester
    ol201mg/dl
    ,tr
    igl
    yceri
    des196mg/ dl
    ,l
    ow-densi
    ty
    l
    ipoprot
    einchol
    ester
    ol(LDL-C)131mg/ dl
    ,andhigh-
    densi
    tyl
    ipoprot
    einchol
    est
    erol(
    HDL-C)34
    mg/dl.

    Whichofthefol
    lowingdiet
    arychangeswoul
    dyour ecommendforr
    educi
    nghi
    sri
    skf
    orf
    utur
    e
    car
    diovascul
    arevents,
    inaddit
    iontoaregul
    arexer
    cisepr
    ogram?

    a. Di
    etwi
    thsimil
    arcomposi
    ti
    ontopresent
    ,butwi
    thlowertotalcal
    ori
    es.
    b. Di
    etwi
    thfewersi
    mplecar
    bohydr
    atesandlowertotalcal
    ori
    es;addmorepr
    otei
    nfr
    om
    f
    ish.
    c. St
    ri
    ctno-
    carbohydrat
    ediet,butsimil
    arintot
    alcal
    ori
    es;addmoreprot
    einfr
    om fi
    sh.
    d. St
    ri
    ctno-
    carbohydrat
    edietlowerintotalcal
    ori
    es,
    andaddagl assofr
    edwinedaily.
    e. St
    ri
    ctl
    ow-fatdi
    etloweri
    nt otalcal
    ori
    es,andaddaglassofredwine3timesperweek.

    Answer
    :

    20. b. Di
    etwithfewersi
    mpl
    ecar
    bohydr
    atesandl
    owert
    otalcal
    ori
    es;addmor
    e
    pr
    otei
    nfrom fi
    sh.

    Thispatienthast hemet aboli


    csyndrome,def i
    nedast hreeormor eofthef oll
    owing:blood
    pressure≥130/ 85mm Hg, fast
    ingbl
    oodgl ucose≥100mg/ dl
    ,waistci
    rcumf erence>40inches
    i
    nmenor35i nchesinwomen, HDL-C<40mg/ dli nmenor<50mg/ dlinwomen, and
    tri
    glycer
    ides>150mg/ dl.Causesaremul t
    ifactorial,butincl udedailycalori
    ci nt
    akeconsi stent
    ly
    exceedingcal ori
    esburnedbyexer ci
    se,sedentar yl if
    estyles, i
    nsul
    inresistance,andgenet ic
    makeup.I nit
    ialtreat
    mentr evol
    vesaroundexer ciseanddi etmodi fi
    cat
    ion.Low- glycemici ndex
    foodsaret houghtt oavoidthenascenti
    nsul i
    nr esi stance, andlowertotalcal or
    icint
    akeis
    crucial
    .Omega- 3fatt
    yacidsmayal sobebenef i
    ci al;thus, fewersimplecar bohydrat
    es,lower
    totalcal
    oricintake,andmor efishi
    sthebestanswerchoi ce. 

    Low-orno- carbohydratediets(suchasAt ki
    nsorSout hBeach)areunproven,butsimil
    artot
    al
    cal
    ori
    cint
    akei sunli
    kelytosubst ant
    ial
    lyalt
    ertheli
    pidprof
    il
    e.Alt
    houghmoder at
    ealcoholint
    ake
    canrai
    selevelsofHDL- C,pref
    erenti
    almetabolism ofet
    hanoli
    ntheliverwil
    lresulti
    nhigher
    l
    evel
    softriglyceri
    desandwi l
    lnotbehel pf
    ulinthi
    ssyndrome.

    Quest
    ion:

    21. A57- year-


    oldwomanpresentsforaf
    oll
    ow-upoff
    icevi
    sit
    .Shehasahistoryof
    hyper
    tensi
    on,hyperl
    ipi
    demi
    a,di
    abetes,
    andtobaccouseandunderwentper
    cutaneous
    coronar
    yint
    ervent
    iontoherl
    eftci
    rcumfl
    excoronar
    yart
    ery2year
    spr
    ioraf
    terpr
    esent
    ingwi
    tha
    non–ST-segmentelevat
    ionmyocardi
    ali
    nfar
    cti
    on(NSTEMI)
    . 

    Today,shedenieschestpainandshortnessofbreath,
    butrepor
    tshavingtroublesl
    eepi
    ng,
    decreasedappeti
    te,l
    ossoffocus,andlossofi
    nteresti
    nherhobbies.Shehasbeencompl i
    ant
    withhermedicalther
    apy,whichincl
    udesaspir
    in81mgdai l
    y,metoprol
    olsuccinat
    e50mgdaily,
    rosuvastat
    in20mgdai l
    y,andvarenicl
    ine1mgt wicedail
    y. 

    Bloodpr
    essureis132/72mm Hg, pulsei
    s72bpm,andrespi
    rat
    oryr
    atei
    s12br
    eat
    hs/
    minut
    e.
    Theremainderofherphysi
    calexaminati
    oni
    swit
    hinnor
    mallimit
    s.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthebestnextst
    epi
    nmanagementoft
    hispat
    ient
    ?

    a. Di
    sconti
    nuemet oprolol
    .
    b. Di
    sconti
    nuevarenicli
    ne.
    c. St
    artesci
    tal
    opram.
    d. Di
    sconti
    nuerosuvastati
    n.
    e. Ref
    erthepati
    enttoapsychiat
    ri
    st

    Answer
    :

    21. b. Di
    scont
    inuevar
    eni
    cli
    ne.

    Thepatienti
    saf ormersmokerwi t
    hmulti
    pleri
    skfact
    orsf
    orcor onaryarter
    ydi seasewhohad
    anNSTEMI2year spri
    or.Sheisbeingtr
    eatedwit
    hvareni
    cli
    ne,apar ti
    alagonistofthenicoti
    nic
    acet
    ylcholi
    nereceptor
    ,whichbothreducesthesymptomsofnicotinewithdrawalandr educes
    theeff
    ectofcigaret
    tesmoking.Thepati
    entexhi
    bit
    stypi
    calsideeffect
    sofvar enicl
    ine,
    andt hi
    s
    medicati
    onshoul dbediscont
    inued. 

    Thereisnoi ndicati
    onforbegi
    nninganant i
    depressantmedi cati
    onorr eferr
    ingt opsychi
    at r
    y
    unlessthesesympt omsper si
    stedafterdiscont
    inuationofthevar enicli
    ne.Bet a-blocker
    sar e
    l
    essl i
    kelytobet hecul
    pr i
    tandareindicatedinthispost -
    MIpat i
    ent .Ther ehasbeenno
    consist
    ent,rel
    iableevi
    dencetosuggestt hatstatintherapyi
    sr el
    at edtot heset ypesofcentral
    nervoussystem sideeffect
    s.Giventhatthepatienthasknowncor onar yarter
    ydi sease,she
    meet saClassIr ecommendationforlipi
    d- l
    oweringtherapywi t
    hast ati
    n.

    Quest
    ion:

    22. A75- year-


    oldwomanpr esentswithabdomi nalpai
    nandshortnessofbr
    eath.Physi
    cal
    examinati
    oni sunremar
    kable.Echocardi
    ogram showsani l
    l-def
    inedmassintheri
    ght
    vent
    ri
    cularapex.Sheundergoescont r
    ast-enhancedcomput edtomographyoft
    hechestand
    abdomen, showingtheabnormalit
    ydepictedinFigure1.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    ydi
    agnosi
    s?
    a. Intr
    acar
    diacthrombus.
    b. Tumorme t
    astasi
    s.
    c. Lipomatoushypertr
    ophyoft
    heseptum.
    d. Prominentri
    ghtventri
    cul
    art
    rabecul
    ati
    ons.

    Answer
    :

    22. b. Tumormet
    ast
    asi
    s.

    Thisimageshowsal obulatedmassofmi xedatt


    enuat ionintheapexoft heri
    ghtventr
    icle
    (Fi
    gure2) .Thi
    si sanunusuallocati
    onf ort hr
    ombus.Thel argesizeandhet erogeneousdensity
    ismor econsistentwit
    htumor .Li
    pomat oushyper t
    rophyaf f
    ectstheinteratr
    ialsept
    um, notthe
    ventr
    icularseptum,andwoul dbeoff atdensi t
    y,nott hedensityofthelesionshowni nthis
    image.Pr ominenttr
    abeculati
    onstypicallyhaveat ubularandmor eli
    nearappear anceandar e
    ofunifor
    m densi t
    y.Thismassr epr
    esent edamet astasisfr
    om ahepat oma.
    Quest
    ion:

    23. A73- year


    -oldmanpr esentstocli
    nicwithnonspeci
    fi
    csympt omsofmalai
    se,weight
    l
    oss,andlowbackpain.Inspiteofthi
    s,heledanactiveandunrestr
    ict
    edli
    fe.Hi
    smedi cal
    hist
    oryi
    ncludesaremotehistoryofaort
    ocoronarybypassandresecti
    onofalef
    trenalcell
    carci
    noma.Hewasadmi ttedtothehospitalaf
    teranabnormalf
    indingonabdominalultr
    asound.

    Anechocar
    diogram wasor
    der
    ed.Figur
    e1i sasti
    llf
    rameoft
    heapi
    calf
    our
    -chambervi
    ew.
    Fi
    gure2isastil
    lfr
    ameimageoftheinf
    eri
    orvenacava(I
    VC).

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    yet
    iol
    ogyoft
    hiscar
    diacmass?

    Fi
    gur
    e1
    Fi
    gur
    e2

    a. At
    rialmyxoma.
    b. Hepatocell
    ularcar
    cinoma.
    c. Recurrentr
    enalcellcar
    cinoma.
    d. Deepvenoust hrombosisofthel
    owerext
    remi
    ty.

    Answer
    :

    23. c. Recur
    rentr
    enalcel
    lcar
    cinoma.

    Themostcommont umortoi nvadet heheartviat heIVCi sr enalcel


    lcarci
    noma.Intr
    aluminal
    growthoccur sviatherenalvei nsandI VC,of
    teni ntother ightatri
    um.Lesscommonl y,
    theIVC
    maybei nvadedbyhepat ocellularcarci
    noma, uterineleiomyoma, andcancersoftheadrenal
    gland,
    includingpheochromocyt oma.Alt
    houghat ri
    almyxomascanar isefr
    om theri
    ghtatri
    um,
    theyareusual l
    ylocatedont hef ossaovali
    swi thnoext ensionf r
    om theIVCandareof t
    en
    pedunculated.Deepvenoust hrombosi swouldbel essl i
    kelyinanact i
    vepersonwithno
    complaintsoflegpai norswel li
    ng.
    Quest
    ion:

    24. A50- year


    -ol
    dmancomest oyourclini
    cforanewpat i
    entvi
    sit
    .Hehasahi st
    oryof
    hypert
    ensionandhyperl
    ipi
    demi a,
    forwhichheisonaml odi
    pineandrosuvastati
    n.Hehasbeen
    smokingonepackperdayf orthelast35years.Hedoesnotdrinkanyalcohol.Hi
    sexam is
    unremarkabl
    eandar ecentl
    ipi
    dpanelshowedal ow-
    densit
    yl i
    popr
    otei
    n( LDL)of84mg/ dl
    .Hi
    s
    wif
    ehasbeenhoundi nghimt oquitsmoking,buthef
    eels“t
    hedamaget hathasbeendonei s
    done.”

    Whi
    choft
    hef
    oll
    owi
    ngdoyout
    ellhi
    m,r
    egar
    dingt
    heef
    fectofsmoki
    ngcessat
    ion?

    a. I
    twil
    levent
    uall
    yreducehisriskoflungcancertot hatofanonsmoker .
    b. Ther
    eisminimalcar
    diovascularbenefi
    tofcessationforlong-standingheavysmokers.
    c. Swi
    tchi
    ngtochewingtobaccowi llr
    educehiscar diovascularr
    isktot hatofanonsmoker
    .
    d. I
    twil
    levent
    uall
    yreducehisriskofcoronarydiseaset othatofanonsmoker .
    e. Swi
    tchi
    ngtoelect
    roni
    ccigaretteswil
    lreducehiscar diovascul
    arriskt othatofa
    nonsmoker
    .

    Answer
    :

    24. d. I
    twi
    llevent
    ual
    lyr
    educehi
    sri
    skofcor
    onar
    ydi
    seaset
    othatofanonsmoker
    .

    Thebenefi
    tsofsmokingcessati
    onaresignif
    icanti
    nallsmokers,regardlessoflengthof
    smokinghist
    ory.Smokingcessat
    ionleadstodecreasedmor t
    ali
    ty,decreasedcardiovascul
    ar
    event
    s,anddecreasedinci
    denceofcancer.Alt
    houghtheexacttimingvar ies,
    studi
    essuggest
    thatt
    hecoronaryheartdi
    seaseri
    skreturnstobasel
    ine(nonsmokerl evel)wit
    hin15yearsof
    smokingcessati
    on. 

    Althoughthecancerri
    skalsosubst
    antial
    lydecreases,
    itwil
    lalwaysremainel
    evatedcompared
    tononsmokers.TheAmer i
    canHear tAssoci
    ation(AHA)advisesthatsmokel
    esstobacco
    productsareharmfulandshouldbediscouragedbycli
    nici
    ans.Ther i
    skofel
    ectr
    oniccigar
    ett
    es
    i
    suncl ear
    ,buta2014AHApol icyst
    atementdi scour
    agestheuseunt i
    lmoredataareavail
    abl
    e.
    Syst
    emi
    cHyper
    tensi
    onandHypot
    ensi
    on
    Quest
    ion:

    1. A55- year-oldwomanwi t
    ha40- yearhist
    oryofi
    nsuli
    n-dependentdi abet
    esmel li
    tus
    presentstoyourof f
    iceforcareofherhypert
    ension(HTN).Herserum creati
    ninehasbeen
    graduall
    ywor seni
    ngovert hepast10year sfr
    om 1.3to4.2mg/ dl
    .Herbl oodpressur
    e( BP)has
    beenincreasi
    ngovert hepastyearfr
    om 138/84mm Hgt o152/ 90mm Hg.Shehast r
    ied
    l
    if
    estylemodificat
    ion,buthersystol
    icBPhasr emained>150mm Hg.Shedeni essnoring,
    dayti
    mesomnol ence,cigaret
    tesmoking,fr
    equentheadaches,ordiaphoreti
    cspell
    s. 

    Onphysi
    calexamination,herbodymassindexis24andherBPi s154/92mm Hginbotharms.
    Herl
    ungsareclear.Cardiacexaminat
    ionisnot
    ableforanS4.Therearenoabdomi
    nalbrui
    ts.
    Ther
    eistr
    acepr et
    ibi
    aledema.Ther ei
    snor adi
    al-
    femoralpul
    sedelay.Herpot
    assi
    um i
    s5.2
    mmol/L,
    andhercr eati
    nineis4.2mg/dl.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    ycausef
    orherHTN?

    a. Chronickidneydisease(CKD)
    .
    b. Coarctat
    ionoftheaor t
    a.
    c. Pheochromocyt oma.
    d. Obstruct
    ivesleepapnea.
    e. Pri
    mar yhyperaldoster
    onism.

    Answer
    :

    1. a. Chr
    oni
    cki
    dneydi
    sease(
    CKD)
    .

    CKDisbothacauseandaconsequenceofHTN.Mor ethan80%ofpat ientswit


    hCKDhaveHTN.
    Iti
    sthoughtthatthishighrat
    eofHTNi npat
    ient
    swithCKDi smulti
    fact
    orial
    ,buti
    nlargeparti
    s
    duetosodium retenti
    on.Shedoesnothavesignsorsymptomssuggest i
    ngobstruct
    ivesl
    eep
    apnea,aor
    ticcoarctati
    on,orpheochr
    omocytoma.Herpotassi
    um of5.2mmol /Lmakes
    hyperal
    doster
    onism lessli
    kely.

    Quest
    ion:

    2. A50-year-ol
    dmanpr esentstoyouroffi
    cesayinghewant stoseeacardiol
    ogisttocar
    e
    forhishypert
    ension(HTN) .Hisbloodpressure(BP)wasnot edtobeelevat
    edlastyear,andhi
    s
    i
    nternistr
    ecommendedl ifestylemodifi
    cati
    onandl i
    sinopr
    il
    ,whichhasbeent i
    tr
    atedto20
    mg/ day.Wit
    ht hesemedicat i
    ons,hisBPathomehasbeenaver aging132/80mm Hg.He
    deniessnori
    ng, dayt
    imesomnol ence,f
    requentheadaches,ordi
    aphoreti
    cspell
    s.Bothofhis
    parentsdevelopedHTNint hei
    r50s. 

    Onphysi calexaminati
    on,
    hisBPi s136/ 86mm Hgi nbot harms.Hislungsandcardiac
    exami nat
    ionar eunr
    emarkable.Hisabdomeni ssoftwithoutbrui
    ts.Therei
    snoradial-
    femor
    al
    delay.Labsshownor malelectrol
    ytes.Anelect
    rocardi
    ogram showssi nusr
    hyt
    hm and
    i
    ncr easedvoltagewit
    houtsecondar yrepol
    ari
    zati
    onchanges.
    Whi
    choft
    hef
    oll
    owi
    ngdoyour
    ecommend?

    a. Nofurthereval
    uationatt
    hecurrenttime.
    b. Renalmagnet i
    cresonanceangiography.
    c. Comput edtomographyofthethoracicaor
    ta.
    d. Pl
    asmaal dost
    eroneandreni
    nlevels.
    e. Twenty-fourhoururi
    neforfr
    acti
    onatedmet anephr
    inesandcat
    echol
    ami
    nes.

    Answer
    :

    2. a. Nof
    urt
    hereval
    uat
    ionatt
    hecur
    rentt
    ime.

    Whi l
    epr i
    mar yhyperaldoster
    onism, renalarter
    yst enosis,andpheochr omocytomaarethemost
    commoncausesofsecondar yHTN, theseoccuri n<10%ofadul tswithHTN,andthevast
    maj ori
    tyofadultpatientshavepr imar yHTN.Test i
    ngf orsecondar ycausesofHTNistypi
    cal
    ly
    reservedforthosepat ientswit
    hr esist antHTN, new-onsetHTNatayoungage, orsymptoms,
    signs,orlabssuggest ingaspeci f
    iccauseofsecondar yHTN, suchasheadachesand
    diaphoreticspel
    ls,abdomi nalbruits, orserum hypokalemi a.This50-year-
    oldpati
    entwit
    hwell
    -
    cont r
    oll
    edBPonasi ngleanti
    hyper tensi vemedicineandanunr emar kabl
    eexaminati
    onand
    normall absdonotwar r
    antworkupf orsecondar ycausesofHTN.  

    Quest
    ion:

    3. A48- year-ol
    dwomanpr esentsforevaluationofherwor seninghyper
    tension(HTN) .She
    hasbeent r
    eatedwi thaml odi pi
    ne5mgqdandhydr ochlorothi
    azide25mgqdandr eport
    st hat
    hersyst
    olicbloodpr essure( BP)pr evi
    ouslyaveragedi nt he130smm Hgbuti snowaver aging
    i
    nt he150smm Hg.Shest atesshehadbeenpr escribedr amipri
    l,butt
    hiswasdiscontinued
    becausehercr eat
    ininehadi ncreasedfrom 1.4to2. 8mg/ dlwhent aki
    ngramipri
    l.Shedeni es
    snori
    ng,daytimesomnol ence, f
    r equentheadaches, ordiaphor et
    icspell
    s.Shedeniescigarette
    smoking,hyperli
    pidemia, diabetes,orfamilyhistoryofHTN.  

    Onphysi
    calexami
    nati
    on,herBPi s162/74mm Hgi nbotharms.Herl
    ungsareclear.Car
    diac
    exami
    nat
    ionisnot
    ableforanS4 sound.Shehasbi
    later
    almidabdominalsyst
    oli
    cbruit
    s.Ther
    e
    i
    snoradi
    al-f
    emoralpul
    sedelay. 

    Herser
    um pot
    assi
    um i
    s4.
    6mmol
    /L,
    andherser
    um cr
    eat
    ini
    nei
    s1.
    4mg/
    dl.

    Whi
    choft
    hef
    oll
    owi
    ngdoyour
    ecommend?

    a. Computedtomogr aphyangiographyofherrenalart
    eri
    es.
    b. Tri
    alofangiot
    ensin-r
    eceptorbl
    ockade.
    c. Twenty-f
    ourhourur i
    neformetanephri
    nesandcat echol
    ami nes.
    d. Computedtomogr aphyangiographyofthethoraci
    caorta.
    e. Pl
    asmaal doster
    oneandr eninconcent
    rati
    ons.

    Answer
    :
    3. a. Comput
    edt
    omogr
    aphyangi
    ogr
    aphyofherr
    enalar
    ter
    ies.

    Thispati
    ent’spresent at
    ioni ssuggest i
    veofr enalarter
    yst enosis( RAS),withworseningofher
    previ
    ouslycontrolledHTN, wor senedrenalfunctionaftert r
    eatmentwi thanangi otensin-
    convert
    ingenzymei nhibit
    or, andanabdomi nalbr ui
    t.Whi lemostcasesofRASar eduet o
    ather
    osclerosi
    s, approximat ely10%ar eduet ofibromuscul ardysplasi
    a( FMD).FMDi smore
    commoni nfemal es,about90%off emalesinsomeser ies.FMDt endstooccuri nyounger
    women, alt
    hought hemeanagei ntheFMDr egistrywas52year sold.Ther adi
    ogr aphic
    appearanceoft heRAScanhel pdisti
    nguishbetweenat heroscleroti
    candFMDst enosis,wi
    th
    ather
    oscleroti
    cdi seaseusual lyinvolvi
    ngt heostialorpr oximalrenalarterywhil
    eFMDusual ly
    i
    nvolvesthemi ddl eordistalsegment .

    Quest
    ion:

    4. A70- year-ol
    ddiabeti
    c,hyperl
    ipidemicfemalesmokerisrefer
    redfort
    reatmentofher
    hyper
    tension(HTN) .Hercurr
    entmedi cati
    onsincludechlor
    thal
    idone25mgqd, amlodipi
    ne10
    mgqd, candesar t
    an32mgqd, andterazosin2mgqd.Shedeni essnori
    ng,dayti
    me
    somnolence,frequentheadaches,ordiaphoret
    icspell
    s. 

    Onphysicalexaminati
    on,herbodymassi ndexis24,bloodpressureinbotharmsis190/98
    mm Hg, andBPi nherlegsis194/
    104mm Hg.Herl ungsar ecl
    ear.Cardiacexami
    nati
    onis
    notabl
    eforanS4 andagr ade1/6systol
    iceject
    ionmurmur .Shehasar ightmidabdominalbr
    uit
    .
    Therei
    snor adial
    -femoralpul
    sedelay. 

    Herpot
    assi
    um i
    s4.
    2mmol
    /L,
    andhercr
    eat
    ini
    nei
    s1.
    1mg/
    dl.

    Whi
    choft
    hef
    oll
    owi
    ngdoyour
    ecommend?

    a. Pl
    asmaal dosteroneandr eninconcentrations.
    b. Angi
    otensin-convert
    ingenzymei nhi
    bit
    ordi agnost
    icchall
    enge.
    c. Magneti
    cr esonanceangiogr aphyofthet horaci
    caorta.
    d. Uri
    nar
    ysodi um andpot assium level
    s.
    e. Computedt omographyangi ographyoft herenalart
    eries.

    Answer
    :

    4. e. Comput
    edt
    omogr
    aphyangi
    ogr
    aphyoft
    her
    enalar
    ter
    ies.

    Thispatientpresentswi t
    hr efr
    actoryhypertension.Sheishyper tensive,despit
    egooddosesof
    fourantihypert
    ensivemedi cations.Thisshouldl eadtowor kupf orsecondar ycausesof
    hypertension.Shedoesnothavedayt imesomnol enceorhistor yofsnor ingtosuggestsleep
    apnea.Ther eisnodr opinbl oodpr essurebetweent hearmsandl egs, makingcoarctat
    ionless
    l
    ikely.Thispatienthasmul tipl
    er i
    skfactorsforatheroscl
    erot i
    cr enalarterystenosi(
    RAS) ,
    i
    ncludinghersmoki ng,diabetes,andhyper l
    ipi
    demi a.Asyst oli
    cabdomi nallater
    ali
    zingbruiti
    s
    specifi
    cbutnotsensi ti
    vef orRAS, andwar rantsadditi
    onaleval uation.

    Quest
    ion:
    5. A55-year
    -ol dmanisr
    eferredfortreatmentofhi shyper
    tensi
    on( HTN) .Despi
    teramipr
    il
    10mgqd, amlodi
    pi ne10mgqd, andhydr ochlorot
    hiazide25mgqd, hisbl oodpressure(BP)
    hasbeen160/100mm Hg.Hi swi f
    er epor
    tsloudsnor i
    ng.Hedeniescigarettesmokingandno
    di
    abetesorhyperl
    ipidemi
    a.Hedeni esanyot hersystemicsymptoms, suchasdi aphoresi
    s,
    pal
    pit
    ati
    ons,orheadache. 

    Onphysi
    calexaminati
    on,heweighs210poundsandhasabodymassi ndexof27.Hi
    sBPis
    162/
    98mm Hgi nbothar
    ms.Lungsandcardiovascul
    arexami
    nat
    ionar
    eunr emar
    kabl
    e.Ther
    e
    i
    snoabdomi nalbr
    uitorr
    adial
    -femor
    alpul
    sedelay. 

    Labsr
    evealnor
    malel
    ect
    rol
    ytesandr
    enalf
    unct
    ion.

    Whi
    choft
    hef
    oll
    owi
    ngi
    stheappr
    opr
    iat
    enextst
    epi
    nhi
    smanagement
    ?

    a. Twe nt
    y-fourhourur i
    nef ormet anephri
    nesandcat
    echol
    ami
    nes.
    b. Serum aldosteroneandr eninlevels.
    c. Nof ur
    therdiagnostictestsneeded.
    d. Pol
    ysomnogr aphy.
    e. Abdomi nalcomput edangi ogr
    aphy.

    Answer
    :

    5. d. Pol
    ysomnogr
    aphy.

    Thispati
    entmostl i
    kelyhasobst r
    uctivesleepapnea( OSA)basedonhi shistory.Treatmentof
    sleepapneaincludesweightlossandcont i
    nuousposi ti
    veairwaypr essure(CPAP) ,whichhelps
    preventupperairwaycoll
    apsedur i
    ngexpi rat
    ion.CPAPhasbeenshownt olowerBPi npat i
    ents
    withOSA.Thispat i
    entdoesnothaveot herri
    skf actor
    sforatherosclerosisorabdomi nalbruit
    s
    tosuggestrenalarter
    ystenosis.Heisl essli
    kelytohavehyper aldosteronism or
    pheochromocyt omawi t
    hnormalel ectr
    olytesandnopar oxysmalsyst emicsympt oms, suchas
    headaches,diaphoret
    icspel
    ls,orcyclicuncontrolledHTN.

    Quest
    ion:

    6. A42-year-
    oldmanwithahistoryofhypert
    ensionisseeninanur gentcar
    eclini
    cfor
    blur
    ri
    ngofvi si
    on.Hehasbeenonl i
    sinopri
    l40mgaday.Hehadr unoutofhismedicationf
    or
    thepast2weeks.Hi sbl
    oodpressur
    e( BP)is196/132mm Hg, heartr
    ateis78bpm, and
    physicalexaminat
    ioni
    sother
    wisenor malexceptforanS4 
    gall
    oponcar diacauscul
    tati
    on.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextmostappr
    opr
    iat
    est
    epi
    nthemanagementoft
    hispat
    ient
    ?

    a. Hospi
    taladmi
    ssi
    onforrenalarter
    ydenervation.
    b. Hospi
    taladmi
    ssi
    onforintr
    avenousl abet
    alol
    .
    c. Di
    schargehomeincr
    easingli
    sinoprilt
    o80mgdai l
    y.
    d. Di
    schargehomeonpriormedications.
    e. Hospi
    taladmi
    ssi
    onandr esumepr iormedicati
    ons.

    Answer
    :
    6. b. Hospi
    taladmi
    ssi
    onf
    ori
    ntr
    avenousl
    abet
    alol
    .

    Hypertensiveurgencyi sthesit
    uati
    oninwhichapatient'
    sdiast
    oli
    cbl oodpr essure(BP)i
    s>120
    mm Hg.I fthereisacuteorr api
    dlyworseni
    ngtarget
    -organdamage, t
    henthet er
    m usedis
    hypertensi
    veemer gency.Inthi
    scase,hisbl
    urr
    edvisionisconcerningforretinaledemaor
    i
    njury.Hypertensiveurgencycanbemanagedasanout pat
    ient
    ,buthyper t
    ensi veemergency
    requir
    esadmi ssiont oauni twi
    thcardi
    ovascul
    armoni t
    ori
    ngfacil
    iti
    esforpar enteral
    anti
    hyper t
    ensivetherapy.

    Quest
    ion:

    7. A54- year-
    oldwomanwi thahistoryofhyper t
    ension(HTN)isseeni nyourof f
    icef
    ora
    routinevisit
    .Sheof f
    ersnocompl ai
    ns.Herphysi calexaminati
    onisnor malexceptforablood
    pressur e(BP)of172/ 102mm Hg, heartrat
    eof54bpm, anS4 gal
    loponcar diacexami nat
    ion,
    andmi l
    dabdomi nalobesi t
    y.Hercur r
    entmedi cati
    onsincludeextendedr el
    easedil
    tiazem 300
    mgdai l
    y,hydrochlorothi
    azide50mgdai ly,
    andl i
    sinopri
    l40mgdai ly.Shereportsthatsheis
    compl iantwithhermedi cationsandnot esthatherBPsathomear ever ysimil
    artothese
    currentvalues.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextst
    epi
    nhermanagement
    ?

    a. Scheduleforr
    enalar terydenervat
    ion.
    b. I
    ncreasingdil
    ti
    azem t o360mgdai ly.
    c. Addit
    ionofatenolol50mgdai l
    y.
    d. Addit
    ionofspironolactone25mgdai ly.
    e. A1,500calori
    er est
    ricteddiet
    .

    Answer
    :

    7. d. Addi
    ti
    onofspi
    ronol
    act
    one25mgdai
    ly.

    Near l
    yallcaseslabeledr esi
    stantHTNcanhavet hei
    rBPnor mali
    zedwithaggressi
    vemedi cal
    therapy,wit
    hatl eastthreeantihyper
    tensi
    veagentsuptomaximallyapprovedortol
    erated
    doses, andinsomecaseswi t
    hf ourorfi
    vedr
    ugsofdiff
    erentcl
    asses,i
    ncludi
    nganal doster
    one
    antagonistifappropri
    ate.

    Quest
    ion:

    8. A43-year-ol
    dmanwi t
    houtpri
    ormedicalhi
    storyisseeninyourof f
    ice3daysaf ter
    recordi
    ngabloodpressure( BP)of160/110mm Hgwi t
    hanaut omatedmachi neinhi
    s
    pharmacywhileshoppingwi thhiswif
    e.Heisasympt omatic,
    takesnomedi cati
    ons,r
    arelyuses
    alcohol
    ,andusesnoi l
    li
    citdrugs.Hismotherandfatherbothhadhypertension,andhisf at
    her
    died2yearsagoofast roke.Hisphysi
    calexaminati
    oni snormalexceptforaBPof166/ 112
    mm Hg.Ar epeatBPatt heendoft heexaminat
    ionis164/114mm Hg.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    emedi
    calr
    egi
    menf
    ort
    hispat
    ient
    ?
    a. At
    enol olandhydrochlorothiazide.
    b. Li
    sinopr i
    l.
    c. Li
    sinopr i
    landhydrochlorothiazide.
    d. At
    enol ol.
    e. Li
    festylemodif
    icati
    onwi thdai l
    yexer ci
    se.

    Answer
    :

    8. c. Li
    sinopr
    ilandhydr
    ochl
    orot
    hiazi
    de.

    ForpersonswithBP>20/10mm Hgabovegoal ,i
    niti
    alt
    reatmentshouldbewi thtwodrugs
    chosenfrom 1)areni
    n-angi
    otensin-al
    dost eronesystem i
    nhibit
    or(angiot
    ensin-conver
    ti
    ng
    enzymei nhi
    bit
    ororangi
    otensi
    n- r
    ecept orblocker
    ),2)adihydropyr
    idinecalci
    um channel
    blocker
    ,and3)athiazi
    deorthiazi
    de- l
    ikediureti
    c.

    Quest
    ion:

    9. A36-year -oldwoman, 35weekspr egnant,i


    sseenintheemergencydepar tmentwit
    h
    shor t
    nessofbr eath.Herbloodpressure( BP)hasbeenlabil
    eduringherpregnancy, andsheis
    mai ntai
    nedonhydr alazi
    ne50mg3t i
    mesdai ly.HerBPis180/110mm Hg, heartrateis110
    bpm andr egular,andl ungswithbibasil
    arrales.Hercar
    diacexaminati
    onisregular,wit
    haflow
    mur murandl owerext r
    emiti
    eswith2+edema.Shei sgi
    venint
    ravenouslabet
    aloland
    furosemidewi t
    ht her esul
    ti
    ngBPof140/ 95mm Hgandhear trat
    eof95bpm.Aur i
    nalysi
    s
    reveals3+proteinuria.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextmostappr
    opr
    iat
    est
    epi
    nhermanagement
    ?

    a. Oralli
    sinopri
    l.
    b. I
    ntravenousdi goxin.
    c. Renalultraf
    il
    trat
    ion.
    d. I
    nductionofl abor.
    e. I
    ntravenousmagnesi um sul
    fat
    e.

    Answer
    :

    9. d. I
    nduct
    ionofl
    abor
    .

    Urgentdelivery/i
    nduct ionisrecommendedi nwomenwi t
    hgestati
    onalhyper tension(HTN)and
    protei
    nuriaint hesettingofot heradversecondit
    ionssuchaspul monar yedema, coagulopathy,
    orfetaldi
    stress.Pr eeclampsi aisdefi
    nedasbot hHTN( 140/90mm Hg)andpr oteinur
    iaorin
    faceofnewHTNwi thoutpr otei
    nuri
    a:platel
    etcount<100,
    000,serum creatini
    ne>1. 1,pul
    monar y
    edema, li
    verfunctiont estsmor ethantwot i
    mesnor mal,andcerebralorvisualsympt oms.This
    usuallyoccursi nthet hir
    dt ri
    mesterofpregnancy.Eclampsi
    aisdi f
    ferenti
    atedfrom
    preeclampsiabyt headdi t
    ionofseizures.
    Quest
    ion:

    10. A34- year-ol


    dwomanwi thhist
    oryofhypert
    ension(HTN)andobesitypresent stoyour
    off
    iceforevaluat
    iondur ingpregnancy.ShehashadHTNf or9years,
    andwor kupsf or
    secondarycausesi nt hepasthavebeennegat i
    ve.Shewast r
    eatedwithat
    enololi nthepastbut
    waschangedt olabetaloli
    npreparati
    onforpregnancy.Sheisnow22weekspr egnantand
    doingwell.Shebr i
    ngsherhomebl oodpressure(BP)log,whi
    chshowsBPr angi ngfrom 135-
    160systolicover65- 88diast
    olic.Shehasnosympt oms.Medicati
    onsincl
    udepr enatal
    vi
    taminsandl abetalol200mgbi d.
     

    Onexamination,sheiswel
    lappeari
    ng.Herhear
    tr at
    ei s90bpm, BPis155/88mm Hg, and
    oxygensat
    urationis98%.Herjugul
    arvenouspressurei snormal
    ,andlungsarecl
    ear
    .Heart
    hasregul
    arrhythm andnomur murs.Abdomenisgr avid,andext
    remit
    ieswit
    hnoedema.
    Hematocri
    tis34%, andcr
    eati
    nineis0.8mg/dl
    .

    Whi
    choft
    hef
    oll
    owi
    ngi
    stheopt
    imalBPi
    nthi
    spr
    egnantwoman?

    a. 120/
    80mm Hg.
    b. 160/
    100mm Hg.
    c. 130/
    85mm Hg.
    d. 145/
    95mm Hg.
    e. 140/
    90mm Hg.

    Answer
    :

    10. e. 140/
    90mm Hg.

    Thispati
    enthadHTNpr iortopr
    egnancy,andsoherpregnancy-rel
    atedHTNi stermedchr onic
    HTN.Inwomenwi t
    hchr oni
    cHTN, t
    hetreatmentgoal
    sremainthesameaspr i
    ortopr egnancy.
    Gestat
    ionalHTNiselevatedBPthatoccursinwomenafterthe20thweekofgest ati
    on.Inthese
    women, AmericanColl
    egeofObstetr
    ici
    ansandGynecologist
    sguideli
    nesrecommendno
    tr
    eatmentunti
    lBPis>160/ 110mm Hg.

    Quest
    ion:

    11. A65- year-oldpat ientpresentst oyourcar di ologyclini


    cf oraroutinef ol
    low- upvi sit
    .He
    hasahi storyofcor onar yar ter
    ydiseasewi thadr ug- eluti
    ngst enttohisleftanteriordescendi ng
    3year sago, hyperli
    pidemi a,andborder li
    nehyper tensi on(HTN) ,whichhehascont rolledwi t h
    dietf
    ort hepastf ewyear s.Her eport
    st hathehasr ecent l
    ybeendi agnosedwi thmet astatic
    renalcellcarcinomaandi saboutt ost arttherapywi t
    hbevaci zumab.Hedeni esanyr ecent
    cardiovascularsympt omsorchangesi nexercisetol erance.Hei scurrentlytakingaspi ri
    n81
    mgdai l
    y,cl
    opidogr el75mgdai ly,
    andsi mvast at
    in40mgdai l
    y.Onexami nation,hishear trate
    i
    s58bpm andbl oodpr essur eis138/ 88mm Hg.Hi scar diovascularexami nat i
    oni sot herwi se
    unremar kable.Youdi scusst hecardiovascul arri
    sksoft herapywi thvascul arendot helial
    growt hfact
    or( VEGF)i nhibi t
    orswithhi m.

    I
    naddi
    ti
    ont
    othr
    omboembol
    ism,
    whi
    choft
    hef
    oll
    owi
    ngot
    hercar
    diovascul
    arcompl
    icat
    ionsof
    t
    hebevaci
    zumabt
    her
    apyi
    smostl
    ikel
    ytobeseeni
    nthi
    spat
    ient
    ?

    a. Lef
    tventri
    culardysf
    unct
    ion.
    b. Coronaryvasospasm.
    c. HTN.
    d. QTpr ol
    ongation.
    e. Atr
    ialfi
    bri
    ll
    ati
    on.

    Answer
    :

    11. c. HTN.

    Mul ti
    pleinvesti
    gat i
    veandcl inicalobser vat i
    onshavedemonst r
    at edHTNt obeacommoncl ass
    effectresult
    ingf rom tr eat mentwi thVEGFi nhibi tors,occur r
    ingin10- 30%ofpat ient st reated
    withbevaci zumab.Ther atesofsubst ant i
    alHTNappeart odependont heant iangiogeni cagent
    used, t
    het umort ype, andpat ient -r
    elatedf actor s,includingageandcomor bidity.Angi ogenesi s
    i
    nhi bit
    or-rel
    atedHTNi st ypical l
    ymanageabl ewi thear l
    yi ni
    ti
    ati
    onofphar macol ogi ct her apyto
    reachaccept edbl oodpr essur et argets.Pr eferredant i
    hypertensiveagent sf orangi ogenesi s
    i
    nhi bit
    or-associ atedHTNi ncludeangi otensin- conver tingenzymei nhibitorsand
    dihydropyr i
    dinecal cium channelbl ockers, alt
    hought herearemi ni
    maldat at osuggest
    super i
    orit
    yofasi nglecl assofagent s.Earlyandaggr essiveini
    tiationofant ihyper tensi ve
    therapyappear st ohel pmai ntai ntreatmentschedul eandr educet her iskofsubst ant ial
    compl icati
    ons,incl udingmal ignantHTNandr ever sibleposteri
    orl eukoencephal opat hy.
    Bevaci zumabi snotknownt ohaveanysi gni f
    icantr iskofQTpr olongat ionorar rhyt hmi as.
    Ther eisasmal lincreasei ncar diacischemi aint r
    ialsofbevacizumab, whi chi slikel yduet o
    thromboembol iccompl icationsr athert handi rectef f
    ectont hecor onar yar teriesorvasospasm.
    Ther eisanappr oximat e20%i ncidenceofvenoust hromboembol i
    sm andanappr oximat e5- 6%
    i
    nci denceofar terialthr ombosi si npat i
    entst reat edwi thbevacizumab.

    Quest
    ion:

    12. Youar easkedtogiveapr esent


    ationonhyper
    tensi
    on(HTN)toagr
    oupofmedi
    cal
    st
    udents.Thegroupisint
    erestedinoutcomes,pr
    eval
    ence,andt
    reat
    mentofHTNi
    nthegener
    al
    popul
    ati
    onaswel lasseveralethni
    cgroups.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    est
    atement
    ?

    a. Me naremoreli
    kelytobet
    reatedthanwomen.
    b. Pati
    ents>80yearsofageareunli
    kelytobenef
    itf
    rom t
    reat
    ment.
    c. Preval
    enceisgreat
    eramongwoment hanmen.
    d. Preval
    enceisgreat
    estamongnon- Hispani
    cbl
    ackpopulat
    ioncompar
    edwi
    thot
    her
    popul
    ations.
    e. HTNisnotamaj
    orr
    iskf
    act
    orf
    ori
    nci
    denthear
    tfai
    lur
    e.
    Answer
    :

    12. d. Pr
    eval
    enceisgreat
    estamongnon-
    Hispani
    cbl
    ackpopul
    ati
    oncompar
    edwi
    th
    ot
    herpopul
    ati
    ons.

    Basedont hemostr ecentdat


    afrom theNat ionalHealthandNutri
    ti
    onExami nati
    onSur vey,HTN
    prevalenceishighestamongnon- Hispani cblackadultswhencompar edwithot herethnic
    groups.Non- HispanicAsianadult
    shadal owerpr eval
    enceofawarenessthant heot herraces
    andHi spanic-ori
    gingroupsandlowert reatmentthannon- Hi
    spanicwhiteandnon- Hispanic
    blackadults.Menandwomenhaveasi mi l
    arprevalenceandawarenessofHTN.However ,
    mor ewoment hanmenwer etr
    eati
    ngt heirHTNandhadi tundercontr
    ol.TheHYVET
    (HypertensionintheVeryElderl
    yTrial
    )st udydemonst rat
    edthebenefi
    toftreatmentofHTNi n
    patients>80yearsofage.HTNi sthel eadingmodi fi
    ableri
    skfact
    orforthepreventionofhear t
    fail
    ure.

    Quest
    ion:

    13. A65- year-


    oldmalewithhypert
    ensionanddiabet
    esisseenintheoff
    ice.Hi
    s
    medicati
    onsincl
    udeamlodi
    pine10mgqdandmet formin500mgbi d.Hisbl
    oodpressur
    e(BP)
    i
    s145/ 92mm Hg.Cardi
    acexami nat
    ionreveal
    snormalheartsounds.Cr
    eati
    ninecl
    ear
    anceis
    nor
    mal ,andt
    hereisnoprot
    einur
    ia.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    etr
    eat
    mentr
    ecommendat
    ion?

    a. Fur
    osemi de20mgqd.
    b. Noc hangeinmedicat
    ions.
    c. Li
    sinopri
    l10mgqd.
    d. Metoprol
    olsucci
    nate25qd.
    e. Spi
    ronolact
    one25mgqd.

    Answer
    :

    13. c. Li
    sinopr
    il10mgqd.

    Thereismoder ateevidencet osuppor ti


    nit
    iat
    ingdr ugtreatmentwithanangi otensin-converti
    ng
    enzymeinhi bit
    or ,
    angi ot
    ensin-receptorbl
    ocker,calci
    um channelbl ocker
    ,orthiazide-type
    diur
    eti
    cint henonbl ackhypertensivepopulat
    ion,includingthosewithdiabetes.Inthebl ack
    hypert
    ensivepopul ati
    on,incl
    udingt hosewithdiabetes,acal ci
    um channelblockerort hiazi
    de-
    typedi
    ureticisr ecommendedasi niti
    alt
    herapy.Inmanycases, twohypertensivedr ugsar e
    neededforbl oodpr essurecont rol
    .

    Quest
    ion:

    14. A67- year -


    oldfemal ei
    sseenf orevaluati
    onofpal pit
    ations.Shehasahi st
    oryof
    hypert
    ension( HTN)andhyper chol
    esterolemia.Medicati
    onsi ncludelisi
    noprilandat orvastat
    in.
    Onphysicalexami nati
    on,herheartrat
    ei s90bpm andbl oodpr essureis182/ 74mm Hg.
    Cardi
    acexami nati
    oni snormalexceptfora grade3/6cr escendo- decrescendomur muratt he
    l
    eftuppersternalbor derthatr
    adiatesintothecaroti
    dsandagr ade3/ 6apicalsystolicmur mur.
    Anelectr
    ocardi ogram showssi nusrhythm withoccasionalpremat ureventri
    cul arcontracti
    ons
    (PVCs).A24- hourambul atorymoni t
    ordemonst rat
    esmul t
    ipl
    eepi sodesofat rialf
    ibri
    ll
    ation(AF)
    andt
    woepi
    sodesofanar
    rowcompl
    ext
    achycar
    dia.

    Whi
    choft
    hef
    oll
    owi
    ngf
    indi
    ngsi
    nthi
    spat
    ienti
    smostl
    ikel
    yther
    esul
    tofpoor
    lyt
    reat
    edHTN?

    a. Atr
    ioventr
    icul
    arnodalr
    e-ent
    rantt
    achycar
    dia.
    b. AF.
    c. PVCs .
    d. Mit
    ralregurgi
    tat
    ion.
    e. Aorti
    cstenosi
    s.

    Answer
    :

    14. b. AF.

    HTNi sassociat
    edwi t
    hmul ti
    plecardiovascularcomplicati
    ons.Thesei ncludelef
    tventri
    cular
    hypert
    rophy,whichisanear l
    yfindi
    ngi npatientswit
    hHTN, heartfai
    lur
    e( bothwithreducedand
    preser
    vedejecti
    onf r
    acti
    on),str
    oke(ischemi candhemor r
    hagic),i
    schemi cheartdisease,
    chroni
    ckidneydisease,andAF.Ther eisnotacl earincreaseinotherar r
    hythmias,suchas
    PVCsorat r
    ioventr
    icul
    arnodalre-entranttachycardi
    a,orvalvularheartdisease,suchasmi tr
    al
    valveprol
    apseoraor t
    icstenosi
    s.

    Quest
    ion:

    15. A55- year-ol


    dfemal
    eisseeni
    ntheoffi
    ceforcar
    diovascul
    arr
    iskassessment.Herbl
    ood
    pressure(
    BP)is155/92mm Hg.ShechecksherBPatherlocalphar
    macyweekl yandstat
    es
    thatiti
    snormal.

    I
    naddi
    ti
    ontol
    ifest
    ylechanges,
    whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    e
    r
    ecommendat
    ions?

    a. Ambulat
    oryBPmoni t
    ori
    ng.
    b. Nofur
    therrecommendati
    ons.
    c. Ret
    urntooffi
    cein1weekforBPcheck.
    d. Ret
    urntophar macyf
    orr
    epeatBPcheck.
    e. St
    artl
    isi
    nopril10mgdai
    ly.

    Answer
    :

    15. a. Ambul
    ator
    yBPmoni
    tor
    ing.

    Ambul at oryBPmoni toringoffersmanybenef itsandaddspr ognosti


    cval uet oBPr eadi ngs
    obtainedi ntheof fi
    ce.Itpr ovi
    desagr eaterdegr eeofriskassessmentt ot hatofBPsobt ainedin
    theof f
    iceset ti
    ng.Indeed, subclinicalorgandamagei smor eclosel
    ycor relat
    edwi th24- hour
    meant hanwi thof f
    iceBP, and24- hourmeansyst ol
    icordi astoli
    cBPhasast eeperr elationship
    withcar diovascularmor bidorf at
    alevent sthant hecor respondingofficeBPval ues.Itishel pf
    ul
    i
    neval uat i
    ngpat ientswi thsuspect edresistanthyper t
    ensi on(HTN)andpr edi
    ctiveoft hoseat
    ri
    skf orvar i
    ouscompl ications,includi
    ngend- stagekidneydi sease.Absenceofnoct urnal
    decreasei nBP, ornoct urnaldipping,isassoci atedwithmar kersofrenaldysf uncti
    on.
    Repeat ingso- call
    ednor malBPatherl ocalphar macyi soflitt
    leval
    ue.HerBPmayr emai n
    elevateddur ingof f
    iceeval uati
    onbutnor malathome, suggest i
    veof“ whitecoatHTN. ”St arti
    ng
    drugt
    herapymaybepr ematur
    eatt
    hispointandassociatedwi
    thpoorcompl i
    anceift
    hepati
    ent
    i
    snotconvincedshehasHTN.However,tr
    uewhitecoatHTNhasbeenshownt opr
    edictt
    he
    ri
    skofcardi
    ovascul
    arevent
    satanint
    ermediat
    elevelbetweennormalBPandt rueHTN,and
    mostHTNexper t
    swouldrecommendtreat
    mentoncedi agnosi
    sisestabl
    ished.

    Quest
    ion:

    16. A50- year-


    oldmalewi
    thaf
    amil
    yhistor
    yofhyper
    tensi
    on(
    HTN)isaskedtocheckhi
    s
    bl
    oodpr
    essure(BP)athomet
    oeval
    uat
    efor"whit
    ecoatHTN."Hi
    sBPintheoff
    icei
    s160/70
    mm Hg,
    whileBPschecked4ti
    mesdai
    lyathomeforaweekaver
    age130/70mm Hg.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    erecommendat
    ion?

    a. Recommendexer ciselifest
    ylechanges.
    b. St
    artmetopr
    ololsucci nate25mgqd.
    c. St
    arthydr
    ochlor
    ot hiazide25qd.
    d. St
    artaspi
    ri
    n81mgqd.
    e. St
    artl
    isi
    nopri
    l10qd.

    Answer
    :

    16. a. Recommendexer
    cisel
    if
    est
    ylechanges.

    Whi t
    ecoatHTNi snotabeni gncondi ti
    on.Indivi
    dual
    swi t
    hwhi tecoatsyndr omet endt ohavea
    greaterprevalenceofmet abolicri
    skf actor
    sandmor ecommoncoexi stencewi thor gan
    damage, andt heyhaveagr eatertendencyf orBPtoriseovertimeandf orsust ainedHTNand
    diabetesmel l
    itustodevelop.Theyal sohaveal ong-t
    erm cardi
    ovascularriskthati slessthan
    thatofsustainedHTN, butneverthelessgreaterthanthatofindivi
    dualswithin-andout -of-
    offi
    ceBPnor mal i
    ty.Assuch, r
    ecommendat ionsforl
    if
    estylemodi f
    icat
    ionsar ereasonabl eeven
    i
    fphar macologi ctherapyisnotindicated.Aspi r
    ini
    snotindicatedforprimarypr eventioninmen
    <55year sofage.

    Quest
    ion:

    17. A28- year-oldwomencomesi nforevaluationofrecurr


    entheadaches.Shehasbeen
    toldathealthscr eeningsinthepastthatshehasbeenhyper t
    ensive.Sheisonnomedi cati
    ons
    andhasnoheal thproblems.Sheeat saheal thydietandgoest othegym 5days/ week.She
    deniestobaccouseordr uguseanddr inksanoccasi onalglassofwi ne.Onexami nation,her
    bloodpressur eis190/ 100mm Hgont herightand188/ 98mm Hgont helef
    t.Herhear tratei
    s
    76bpm, andbodymassi ndexis22.Fundoscopi cexami nati
    onr eveal
    sarteri
    ovenousni cking
    andnohemor rhages.Lungexami nati
    oni sclear,andcardiovascularexaminati
    onr eveals
    normalS1/ S2,andS4 ispresent.Ext
    remi t
    iesarewi t
    houtedemaandwi t
    hequalpulseswi t
    hout
    delay.Compl etebloodcountandel ectrolyt
    esar enormal.Creati
    nineis1.0mg/ dl.
    Whi
    choft
    hef
    oll
    owi
    ngi
    smostl
    ikel
    ytoi
    dent
    if
    ythecauseofherhyper
    tensi
    on(
    HTN)
    ?

    a. Transt
    horacicechocardiogram.
    b. Abdominalcomput edtomogr aphyangi
    ogr
    aphy.
    c. Renalart
    eri
    alDoppl erst
    udy.
    d. Dexamethasonesuppr essiontest
    .
    e. Urinemetanephri
    nes.

    Answer
    :

    17. c. Renalar
    ter
    ialDoppl
    erst
    udy.

    Thispat i
    entisayoungwomanwi thsever eHTNandevi denceofend- organdamageon
    physicalexami nation.Themostl i
    kelyet i
    ologyisfi
    bromuscul ardyspl
    asia( FMD).Evaluat i
    onfor
    thi
    sr eversibl
    ecausei simportant.Initi
    alscreeni
    ngwi t
    hr enalDopplercanbeacost -effecti
    ve
    screeningt ool
    .Ifthereisevidenceofi ncr
    easedvelocit
    ies, t
    henextstepwoul dbeinvasive
    evaluati
    on.Comput edtomographyangi ographyandabdomi nalmagnet icresonance
    angiographybot hhavehi ghaccur acyt odetectFMD.Thesecanbeusef ulinanondi agnost i
    c
    ult
    rasoundwi t
    hhi ghi ndexofsuspi cion.Echocardi
    ogram maybehel pfultoevaluateleft
    ventri
    cularhyper t
    rophy, butgivenlackofmur murandequalbl oodpressure,identi
    fi
    cationof
    coarctati
    onoft heaor taislessl i
    kely.Shedoesnotr epor tsymptomsoff lushing,pal
    pitati
    ons, or
    sweat i
    ngt hatwoul dsuggestpheochr omocytoma.Sheal sodoesnothavecent r
    alobesi t
    y,
    buffalohump, ormoonf aci
    est hatwoul dsuggestCushing’ ssyndrome.

    Quest
    ion:

    18. A39- year -ol


    dmani sevaluatedinyourof fi
    ceforhyper
    tension.Hehasbeenheal t
    hyand
    i
    sonnomedi cations.Hei sanonsmoker ,eatsaveget ari
    andiet,dr
    inksoccasi
    onalal
    cohol,and
    walks2mi l
    esever yday.Hi sexaminationrevealsbloodpressure(BP)142/92mm Hgont he
    ri
    ght,and144/94mm Hgont hel
    eft.Hishear tr
    ateis58bpm andbodymassi ndexis21.His
    cardi
    ovascul
    arexami nat
    ionisnor mal.Hebr i
    ngsi nrecor
    dingsfrom hi
    shomeBPmoni tor,
    whichyoucalibrateandf i
    ndaccur ate.Hi
    sr eadingsrangefrom 135/88mm Hgt o150/96mm
    Hg.Hiselect
    rolytes,uri
    nalysi
    s,andcr eat
    ini
    near enor mal
    .

    I
    naddit
    iontocont
    inui
    nghi
    sheal
    thyl
    if
    est
    yleandl
    ower
    inghi
    ssal
    tint
    ake,
    whi
    choft
    hef
    oll
    owi
    ng
    doyourecommend?

    a. Metoprol
    olsucci
    nat
    e.
    b. Li
    sinopri
    l.
    c. RepeatBPi n3months.
    d. Amilodi
    pine.
    e. Losart
    an.
    Answer
    :

    18. d. Ami
    lodi
    pine.

    Thispati
    enthasconsi stentBP>140/ 90mm Hgandt hereforewouldbenef i
    tfr
    om
    pharmacologictherapy.Heal r
    eadypr act
    icesahealthyl i
    festyl
    eandhassever alhomer eadi
    ngs
    thatareal
    soel evated.Initi
    altr
    eatmentwi thdihydr
    opyridinecalcium channelblockeror
    thi
    azidedi
    ur et
    icisconsi deredfir
    st-
    li
    net herapy.Angiotensin-conver
    tingenzymei nhibi
    torscan
    beconsideredint hosewi threnaldysfuncti
    on.Beta-blockersar enowf our
    th-l
    inetherapy.

    Quest
    ion:

    19. Manychangesi nl i
    festyl
    esuchaswei ghtl
    oss,maint
    enanceofnormalbodyweight ,
    i
    ncreasedphysi
    calacti
    vit
    y, moderationofal
    coholi
    ntake,
    anddietar
    ymodifi
    cat
    iontoinclude
    morefrui
    ts,
    vegetabl
    es,andl ow-fatdair
    yproduct
    s,andareducti
    oninsodi
    um insal
    t-sensiti
    ve
    i
    ndivi
    dualscanlowerbloodpr essure.

    I
    nwhichofthefoll
    owi
    nggroupshavecl
    ini
    calt
    ri
    alsshownt
    hatt
    hesel
    if
    est
    ylechangescan
    pr
    eventhyper
    tensi
    on(HTN)?

    a. Preecl
    ampsi a.
    b. Prehypertensi
    on.
    c. Chronickidneydisease.
    d. Renalarterystenosi
    s.
    e. Hyperaldoster
    onism

    Answer
    :

    19. b. Pr
    ehyper
    tensi
    on.

    Eachoft hesehealt
    hylif
    estyl
    esshouldbet hebasisfort
    reatmentofallindi
    viduals,especiall
    y
    thoseatincreasedcardi
    ovascularri
    sk.Inpati
    entswithprehyper
    tension,adopti
    onoft hese
    healt
    hylifest
    ylescanreducethedevelopmentofHTN.Pat ientswit
    hpr eecl
    ampsi aar eatriskof
    developi
    ngHTNast heyageandshoul dadoptheal t
    hylif
    estyl
    es,al
    thoughnocl inicaltri
    alsare
    avail
    ableinthispopul
    ation.Healt
    hyli
    festyl
    esalsoshouldbei mpli
    catedinthosewi thHTNf rom
    anycausebutar el
    essli
    kelytoreducebloodpressureinthosewithsecondar yHTN.

    Quest
    ion:

    20. A53- year-


    oldmanisr
    efer
    redt
    oyouformanagementofhyper
    tensi
    on(HTN)
    .Hisbl
    ood
    pressur
    eis163/94mm Hg.Hi
    sheartr
    atei
    s82bpm, hei
    ghti
    s70inches,andwei
    ghti
    s260
    pounds.

    Presenceofwhichoft
    hefol
    lowi
    ngconst
    ell
    ati
    onsofsi
    gnsandsympt
    omswoul
    dbemost
    helpf
    ulini
    denti
    fyi
    ngapossi
    blecont
    ri
    but
    ingfact
    ort
    ohisHTN?

    a. Morningheadachesandwaki ngwi
    thchoki
    ngsensat
    ion.
    b. Photophobi
    aandvi sualaur as.
    c. Epi
    sodiccutaneousflushinganddiarr
    hea.
    d. Ast
    erixi
    sandt el
    angiectasias.
    e. Noct
    uri
    aandpost
    -voi
    ddr
    ibbl
    ing.

    Answer
    :

    20. a. Mor
    ningheadachesandwaki
    ngwi
    thchoki
    ngsensat
    ion.

    Thispatienthasabodymassi ndexof37. 3kg/ m2,i


    denti
    fyinghi m wit
    hCl assIIobesit
    y.Obesit
    y
    i
    sf r
    equent lyassoci atedwi thobstr
    uctivesleepapnea( OSA) . Epi
    demi ological,animal
    ,and
    cli
    nicalstudiesal lsuggestt hatOSAcancauseorcont ri
    but etoHTN.Mor ningheadaches,loud
    snoring,gaspi ngorchoki ngforai
    r,andexcessdayt imef atiguemaybesi gnsofOSAandi nthe
    appropriatecl i
    nicalcont extshoul
    dpr omptconsi derat
    ionf orpolysomnogr aphy( sl
    eep
    study).
    Cirrhosis( asterixi
    sandt el
    angiectasias),
    benignprost ati
    chyper plasia(nocturi
    aandpost
    -voiddribbling),migr aineheadaches( photophobiaandvi sualaur as)
    ,andcar cinoi
    dsyndrome
    (epi
    sodiccut aneousf lushinganddiarrhea)ar enotassociatedwi thHTN.

    Quest
    ion:

    21. A58- year-oldmanpr esentstoyourclinicforevaluati


    onofr esistanthypertension(HTN).
    Hispastmedicalhistor
    yisnot abl
    eforcoronarydi seasewithpri
    ort hree-vesselbypasssur gery
    atage49years.Heexer cisesregul
    arlydespit
    echr onicstableangina.Her eportsoccasional
    ly
    wakingwithachoki ngsensationatnight
    .Heavoi dsexcesssal tandt riestoeataheal thydiet
    .
    Hismedicati
    onsincludeaspirin81mg, ator
    vastat i
    n80mg, hydrochlorothiazide50mg,
    enal
    apri
    l20mg, aml odi
    pine10mg, andmet oprolol100mgdai l
    y.Onexami nati
    on,hisheart
    2
    rat
    eis65bpm, bloodpr essure(BP)is152/75mm Hg, andbodymassi ndexi s36kg/ m.

    Whi
    choft
    hef
    oll
    owi
    ngi
    smostl
    ikel
    ytoi
    mpr
    ovet
    hispat
    ient
    'sBPcont
    rol
    ?

    a. Renalsympatheticdenervati
    on.
    b. Continuouspositi
    veair
    waypr essure(
    CPAP)
    .
    c. Implantabl
    epulmonaryar t
    erypressur
    emoni
    tor
    .
    d. Chelati
    ontherapy.
    e. Enhanc edext
    ernalcounterpul
    sati
    on.

    Answer
    :

    21. b. Cont
    inuousposi
    ti
    veai
    rwaypr
    essur
    e(CPAP)
    .

    Treatmentofobst ructi
    vesleepapnea( OSA)wi t
    hCPAPcani mproveBP, althought heef f
    ect
    maybemodest( adecr easeinsystolicBPofabout3- 6mm Hg) .Thispat ientmostl ikelyhas
    OSA.Ther efore,CPAPi sthecorrectchoi ce.TheSYMPLI CI
    TYHTN- 3(RenalDener vationin
    PatientsWi t
    hUncont roll
    edHyper t
    ensi on)tri
    alf
    ail
    edtoshowbenef itwithr enalsympat heti
    c
    denervat i
    on.Al thoughquest ionsregar dingadequacyofdenervati
    oni nthei nterventionar m
    havebeenr aised,asofOct ober2015, t her
    eisnoroleforsympatheticrenaldener vationout si
    de
    ofthecont extofacl inicalt
    ri
    alfortreatmentofHTN.Enhancedext er nalcount erpulsat i
    onhas
    beenusedt ot r
    eatangi nabutwoul dnotbet hetr
    eatmentofchoiceforHTN.Ther ei snor olef
    or
    chelationther apyint het r
    eatmentofHTN.Ther eisnor ol
    eforimplantablepul monar ypr essure
    moni torsint het r
    eatmentofHTN.
    Quest ion:

    22. A57-
    year
    -ol
    dmanpr
    esent
    stoyourcl
    ini
    cformanagementofHTN.Hi
    smedi
    cat
    ions
    i
    ncludeamlodipine10mg,l
    isi
    nopril40mg, andchlor
    thal
    idone25mg.Onexami nation,hi
    s
    heartr
    ateis78bpm, bl
    oodpressure(BP)is156/93mm Hg, andbodymassindexis42kg/ m2.
    Heartexaminat
    ionisnot
    abl
    ef oranS4 andsustai
    ned,nondisplacedpoi
    ntofmaxi
    mali mpulse.

    Whi
    choft
    hef
    oll
    owi
    ngt
    est
    smaybemostappr
    opr
    iat
    eforeval
    uat
    ionoft
    hispat
    ient
    'sHTN?

    a. Holtermoni t
    or.
    b. Ti
    lttable.
    c. Exercisetol
    erancetest.
    d. Polysomnogr aphy.
    e. 5-Hydr oxyi
    ndoleacet
    icaci
    d(5-
    HIAA)
    .

    Answer
    :

    22. d. Pol
    ysomnogr
    aphy.

    HTNandobst ruct i
    vesleepapnea( OSA)f requent l
    yco- exi
    st,wit
    h50%ofOSApat ientshavi
    ng
    HTN, and30%ofhyper tensivepat i
    ent shavingOSA.I naddi t
    ion,hyper
    tensivepatientswit
    han
    abnormall
    yblunteddi pi nBPwi thsleep( nondi ppers)aremor eli
    kelytohaveOSA.TheSevent h
    Reportoft
    heJoi ntNat i
    onalCommi t
    t eeonPr evention,Detecti
    on,Eval
    uation,andTr eat
    mentof
    HighBloodPressur erecogni zessleepapneaasoneoft heidentif
    iabl
    ecausesofHTN.I n
    pati
    entswit
    hresi stantHTN( elevat
    edBPdespi t eadequatedosesoft hreediff
    erent
    anti
    hypert
    ensi
    veagent s,includingadi ur
    et i
    c),secondar ycausesofHTNshoul dbeconsi der
    ed. 

    Inthispat i
    entwi thClassI I
    Iobesity(bodymassi ndex≥40kg/ m2)
    , eval
    uationforsi
    gnsor
    sympt omsofsl eepapneawoul dbeappr opriat
    e, fol
    lowedbypossi blepolysomnogr am (sleep
    study)i fi
    ndicated.5- HIAAisthebr eakdownpr oductofser otoni
    n, and24- houruri
    nar y5- HIAA
    excretionmaybeusedasascr eenf orcarcinoi
    dsyndr ome.Ther eisnosuspi cionforcar cinoi
    d
    syndromebasedont hei nf
    ormationpr ovided,andcar cinoidsyndr omeismor eoft
    en
    charact er
    izedbyf lushingspell
    saccompani edbyhypot ensionratherthanHTN.Ti lttabl
    et ests,
    exercisetolerancet ests,andHoltermoni torsar enotindicatedfort heevaluat
    ionofHTN.

    Quest
    ion:

    23. A66- year -oldmanwi thhyper tension( HTN)isrefer


    redf orevaluati
    onofr esi
    stant HTN.
    Hispastmedi calhistoryi
    ssignif
    icantf orcoronaryar t
    erydisease,sleepapnea, anddi abetes.
    Hismedi cationsi ncludelisi
    nopri
    l40mg, hydrochlorot
    hiazi
    de25mg, amlodipine10mg, and
    met oprololsucci nate150mg.Hewal ks 2 milesdail
    y,useshi spositi
    vepr essurevent il
    ati
    on
    deviceni ghtl
    y, andf oll
    owsasodi um- restri
    cteddiet.Thephysi calexam revealsabl ood
    pressure( BP)of172/ 90mm Hgont hel eft
    ,168/88mm Hgont heri
    ght,andhear trate58bpm.
    Cardiovascul arexam r eveal
    sanS4.Hi slungsar eclear,andther earenoabdomonalbr ui
    ts.
    Labor at
    or yval uesincludesodium 131mmol /L,potassium 4.
    1mmol /
    L,creati
    tine1. 5mg/ dl,
    andt hyroid-stimulat i
    nghormone1. 5I U/ ml.

    Whichofthef
    oll
    owi
    ngismostappr
    opr
    iat
    einhi
    scar
    e,i
    naddi
    ti
    ont
    orei
    nfor
    cingmedi
    cat
    ion
    compli
    anceandsodi
    um r
    est
    ri
    cti
    on?

    a. I
    ncr
    easemet
    opr
    olol
    succi
    nat
    eto200mgdai
    ly.
    b. Addl
    osartan50mgdai l
    y.
    c. Addspi
    ronolact
    one25mgdai l
    y.
    d. Addcl
    onidine0.
    1mgt wicedai
    ly.
    e. Adddoxazosin1mgatbedtime.

    Answer
    :

    23. c. Addspi
    ronol
    act
    one25mgdai
    ly.

    Resi stanthyper t ensionisdefinedasaBPl evelthatremainsabovegoaldespi t


    et heconcur rent
    useoft hreeant ihyper t
    ensivemedi cati
    ons, incl
    udingat hiazidediuretic.Despit
    eaheal t
    hy
    l
    ifestyleandt akingf ourantihypertensivemedi cations,t
    hisman’ sBPr emainsabovegoal .Whi l
    e
    evaluat i
    onf orrenalar t
    erystenosi smaybeappr opri
    ate,t
    reatmentofhi sBPatt hist imewi than
    addi ti
    onalagenti swar r
    anted.Spi r
    onol actonei sanef f
    ecti
    veadd- ondr uginthet r
    eat mentof
    resistanthyper tension.ThePat hway2st udyexami nedspironolactone, bi
    soprolol,and
    doxazosi nasadd- ontherapyt oat hree-drugr egimen.Oft hoser eceivingspir
    onol act one,58%
    achievedt het argetBP, ascompar edwi t
    h42%oft hoseondoxazosi nand43%oft hoseon
    bisopr olol.Givent hi
    spatient’
    sr estinghear trate,hismetoprololshoul dnotbet it
    rat edf ur
    ther.
    Combi nationt her apywithanangi otensin-conver ti
    ngenzymei nhibi
    torandanangi otensin-
    recept orbl ockeri snotrecommended.

    Quest
    ion:

    24. A22- yearol dmani sref err


    edf orevaluationofhyper tension( HTN)i dent i
    fiedinapr e-
    empl oymentphysi cal.Hehasnosi gnifi
    cantpastmedi calhi story.Hehasaf ami lyhistoryof
    HTN  inhisfat herandpat ernalgr andmot her.Hei sonnomedi cations.Her uns3mi lesdaily,
    eatsavegandi et ,
    isal i
    felongnonsmoker ,anddr inkssoci al l
    y.Physi calexam r evealsabl ood
    pressur eof168/ 92mm Hgont heright,174/88mm Hgont heleftside, heartrate66bpm,
    height75  i
    nches, weight180l bs,andabodymassi ndexof22.Car diovascul arexam r eveals
    normalS1  andanS2  withoutmur mur sappreciated.Lungswer ecl earthroughout .Pulses2+
    andequali nal lextremities.Nobr ui
    tswer enot ed.Labor at oryval uesi ncludesodi um 132
    mmol /L,potassi um 5.4mmol / L,chlori
    de97mmol /L,bicar bonat e28mmol /L,bloodur ea
    nit
    rogen22mg/ dl,andcr eat
    inine0. 7mg/ dl.Urinalysisr eveal snopr ot ei
    n.

    Whi
    choft
    hef
    oll
    owi
    ngi
    smostl
    ikel
    ytor
    evealt
    heet
    iol
    ogyofhi
    sHTN?

    a. Serum renin/
    aldosterone.
    b. Transthoraci
    cechocar diogr
    am.
    c. Renalultr
    asound.
    d. Thoracicmagnet i
    cr esonanceangi
    ogr
    aphy(
    MRA)
    .
    e. Serum catecholamines.

    Answer
    :

    24. a. Ser
    um r
    eni
    n/al
    dost
    erone.
    Inyoungpat i
    entswi t
    hnewl ydiagnosedHTN, i
    tisimportanttobeal ertforsecondar ycausesof
    HTN.I nthispatientwithaf amil
    yhi st
    oryandel evatedser um potassi um, considerati
    onof
    hyperaldosteronism shouldbeent ert
    ained.Ser um reni
    nandal dosteronel evel
    swi llconfi
    rmthi
    s
    diagnosis.Whi l
    eanechocar di
    ogram mayr eveallef
    tventricul
    arhyper t
    rophy, t
    hiswoul dbea
    secondar ymani f
    estati
    onofhi sHTN.Hedoesnothaveevi dencebyexam ofcoar ctati
    onor
    renalarterystenosis;t
    hereforeimaginghi srenalarteri
    esandt hor acicaor taareunl i
    kel
    ytobe
    reveal
    ing.Hedoesnothavesympt omsoff l
    ushi ng,
    headache, palpitati
    ons, ordiarrheathat
    wouldsuggestpheochr omocyt oma.

    Quest
    ion:

    25. A59- year-oldmani sseenforeval uat


    ionofhypertension(HTN) .Hehasnohi stor
    yof
    diabetes,kidneydi sease,orcoronaryarterydisease.Hewasst art
    ed6mont hsagoon
    hydrochlorothiazide25mgdai l
    yandl i
    sinopri
    l20mgdai l
    y.Hisbloodpr essure(BP)i
    s148/ 82
    mm Hgandhear trateis72bpm, whichar econsist
    entwithhomer ecordi
    ngs.Laboratory
    valuesincludeser um pot assi
    um of4.1mmol /L,serum cr
    eatinineof1.0mg/ dl,
    andur i
    nalysi
    s
    withoutevidenceofpr oteinur
    ia.

    Whichoft
    hefol
    lowingi
    sthemostappr
    opr
    iat
    enextst
    ep,
    inaddi
    ti
    ont
    orei
    nfor
    cingdi
    et,
    exer
    cise,
    andsodi
    um r
    estri
    cti
    on?

    a. Addme topr ol
    olsucci
    nate50mgdai ly.
    b. Increaselisinopri
    lto40mgdai l
    y.
    c. Pe r
    form 24- hourambulator
    yBPmoni t
    oring.
    d. Cont i
    nuecur r
    entregi
    men.
    e. Evaluatepl asmar eni
    nandaldoster
    onel evel
    s.

    Answer
    :

    25. b. I
    ncr
    easel
    isi
    nopr
    ilt
    o40mgdai
    ly.

    Themostl ikelyreasonforthepoorcont r
    olofhi sHTNi sinadequatether
    apy.Mostpati
    ents
    requireatl
    easttwo, ifnott
    hree,drugsforadequat eBPcont rol
    .Themaximum recommended
    doseofl i
    sinopri
    lis40mgdai l
    y,andthisisthebestchoi ce.Beta-bl
    ocker
    sarenotfi
    rst-
    li
    ne
    therapyforessentialHTN.Withanor malpot assium level,andinadequat
    emedicalther
    apy,
    thereisnoi ndi
    cationtoobtai
    nr enin/
    aldost
    er onelevels.

    Quest
    ion:

    26. A30- year-oldwomanwi t


    habi cuspidaorti
    cval
    ve,mil
    daor t
    icst
    enosis,andhistoryof
    surgicall
    yr epair
    edcoar ct
    ati
    onoft heaortapresent
    stocli
    nic16weekspr egnant.Physical
    exami nati
    onr evealsapulseof90bpm, bloodpressur
    eof120/80mm Hgi ntherightarm,a
    systoli
    cej ecti
    onclick,aII
    /VIsystoli
    cejecti
    onmur muratt
    heleftupperst
    ernalborder,andmild
    brachialfemor aldelay.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthi
    spat
    ientati
    ncr
    easedr
    iskf
    ordevel
    opi
    ngdur
    ingpr
    egnancy?

    a. Hyper
    tensi
    ve-
    rel
    atedcondi
    ti
    ons.
    b. Atr
    ialarr
    hythmias.
    c. Spontaneousaorticdissect
    iondur
    ingsecondt
    ri
    mest
    er.
    d. Ventri
    cul
    ararrhythmias.
    e. Thromboticevents.

    Answer
    :

    26. a. Hyper
    tensi
    ve-
    rel
    atedcondi
    ti
    ons.

    Althoughpatient
    swi t
    habi cuspidaor t
    icvalvemaydevel opaor t
    icrootdil
    ation,which
    predisposesthem tospontaneousdi ssect
    ion,thismostof t
    enoccur sinlategestati
    onort he
    postpartum peri
    od.Neitheranincreaseinar r
    hythmi corthrombot i
    cevent sisassoci at
    edwith
    theseleft-
    heartl
    esions.However ,
    thereisadef ini
    teincreasei nhypertensi
    ve- r
    elat
    edcondi t
    ions
    duringpregnancyinwomenwi thpr i
    oraorti
    ccoar ctati
    on, despit
    enosi gnif
    icantresidual
    gradient.

    Quest
    ion:

    27. A30- year -oldwomanat26weeksgest ationpresentsf orevaluati


    onofhyper tensi
    on
    (HTN).Shehasnosi gnif
    icantpastmedi calhistory.Physicalexaminat i
    onr eveal
    sapul seof90
    bpm, bloodpressur e(BP)of160/ 90mm Hgi nt her i
    ghtarm, 158/90i nthel ef
    tarm,andaI I
    /VI
    systol
    icejecti
    onmur muratt heleftsternalbor der.Shehassymmet ri
    cpul seswithouta
    brachial-f
    emor aldelay.Bloodwor k,i
    ncludi ngliverfuncti
    ont ests,i
    snor mal .A24-houruri
    ne
    sampl edetected0. 1gramsofpr oteinpr esent.Youf oll
    owedhert hroughoutherpr egnancyand
    postpartum periodandherBPnor malizedwi thin1mont hfollowingdelivery.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthecor
    rectdi
    agnosi
    s?

    a. Aorti
    ccoar ct
    ation.
    b. Preeclampsia.
    c. HELLP( hemolysi
    s,el
    evat
    edl
    iverenzymel
    evel
    s,andl
    owpl
    atel
    etl
    evel
    s)syndr
    ome.
    d. Pregnancy- i
    nducedHTN.
    e. Pre-existi
    ngsystemicHTN.

    Answer
    :

    27. d. Pr
    egnancy-
    inducedHTN.

    Fi
    veper centofpregnantwomenhavepr e-
    existi
    ngHTN, defi
    nedbyel evatedBPsdocument ed
    pri
    orto20weeksgest ation.Morethan10%ofwomenbecomehyper tensiveinthesecondhal f
    ofpregnancy.IftheBP returnstonormalvalueswithi
    n6weeksofdel iver
    y, t
    heyareclassifi
    ed
    ashavingpr egnancy-i
    nducedHTN, whichisthecorrectdi
    agnosi sint hi
    scase.Anaddi ti
    onal
    5%ofwomendevel opHTNi nthesecondhalfofpregnancy,associatedwi th>0.3gramsof
    prot
    einintheur i
    neovera24- hourperi
    od,whichisdefinedaspr eeclampsi a.Aort
    iccoarctati
    on
    i
    sar arecauseofHTN, andi soft
    enaccompani edbyar adial
    -femor aldelayonexami nation.
    HELLPsyndr omeoccur si nwomenwi t
    hpreeclampsia,andincludesel evatedli
    verenzymes,
    hemolyticanemia,andt hrombocytopenia.
    Question:

    28. A29-
    year
    -ol
    dwomanwi
    thani
    ntr
    aut
    eri
    nepr
    egnancyat25weeksgest
    ati
    onpr
    esent
    sto
    theemer gencyr oom wi thincr easedheadachesf or1 week.Herpastmedi calhistor
    yincludes
    type2di abetesmel litusandobesi ty.Atbaseline,shehasheadachesappr oximat el
    yonceor
    twiceamont h,i
    ncr easingi nsever i
    tyovert helastweek.Shehasmi l
    dphot ophobia.Her
    temper atur
    eis37. 2Cel sius, bloodpr essure(BP)168/ 112mm Hg, heartrate86bpm, and
    oxygensat urat
    ionof99%onr oom ai r. 
    Fundoscopi cexami nat i
    oni snor mal .Jugularvenouspul sati
    oni snor mal.Pointofmaxi mal
    i
    mpul seisnondisplaced.Thehear tisr egul
    arwi t
    hnomur mur s,rubs,orgallops.Lungsar e
    clear.Abdomeni sgr avid.Ext remiti
    esshow1+pi tti
    ngedema.Neur ol
    ogicexam i sgrosslyint
    act
    withnor malrefl
    exes.Labor atoryfindi ngsshowahemogl obi
    nof11. 2g/dl,plat
    eletcountof
    199,000cel l
    s/mm3, creatinineof1. 0mg/ dl
    ,andnor maltransami nases,uricacid,andlactate
    dehydr ogenaselevel s.Ur i
    nalysi sreveal sspecif
    icgravit
    yof1. 022,negativeforleukocytes,
    blood, pr
    otei
    n,ket ones, andgl ucose.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    enextst
    epi
    nthemanagementoft
    hispat
    ient
    ?

    a. I
    mmediatedeli
    veryoft
    hefetus.
    b. Admini
    str
    ati
    onoforalat
    enolol.
    c. Pai
    nrel
    iefandcloseBPmoni tor
    ing.
    d. Admini
    str
    ati
    onoforall
    osartan.
    e. Admini
    str
    ati
    onoforalmethyldopa.

    Answer
    :

    28. e. Admi
    nist
    rat
    ionofor
    almet
    hyl
    dopa.

    Methyldopai stheprefer
    redagent ,duet odatademonst r
    atingstableut er
    oplacentalbloodflow
    andfetalhemodynami csinlong- t
    erm studies.Whi l
    elabetalolmaybeoner easonabl e
    alt
    ernati
    ve,otherbeta-blockerssuchasat enololhavebeenassoci atedwithintr
    auterinegrowth
    rest
    rict
    ionandar eoftenavoided, especial
    lyear l
    yinpregnancy.Angi ot
    ensin-converti
    ng
    enzymei nhibit
    orsandangi otensin-recept
    orbl ockersarecont r
    aindicatedduet ofetalgrowth
    rest
    rict
    ion,oli
    gohydramni os,renalfail
    ure,
    anddeat h.
     

    Hal l
    mar ksofpr eeclampsiaincludepr oteinur
    ia(>2.0gin24hour s)
    ,elevatedcreatinineand
    transami nases, l
    owpl at
    eletcount ,andper si
    stentepi
    gastr
    icpai n,f
    indingsnotpr esentinthis
    case.I ndicati
    onsf ordel
    iveryforpreeclampsi aincl
    udegest ati
    on>38weeks, HELLP( hemolysi
    s,
    elevatedliverenzymes, lowplat el
    etcount )syndrome,severefetalgrowthr est
    ricti
    on,
    nonr eassuringfetaltest
    ing,orol i
    gohydr amnios.TheRepor toftheNat i
    onalHighBl ood
    Pr essureEducat i
    onPr ogram Wor kingGr ouponHi ghBloodPr essurei nPregnancy
    recommendst reatmentforBP  l
    evelsabove150- 160/
    100- 110mm Hg, r
    atherthanobser vati
    on
    alone.

    Quest
    ion:

    29. A52- year


    -oldmani sseenincl
    ini
    cforeval
    uationofhypert
    ension(
    HTN)diagnosed1
    yearago.Hei sonnomedi cat
    ions.Hi
    sfather
    ,mother,andtwosibl
    ingshaveHTN.Hehasbeen
    fol
    lowingtheDiet
    aryApproachestoStop Hypert
    snsion(DASH)dietandexer
    cisi
    ng4timesper
    weekf ort
    helastyear.Hehasbeencheckinghisbloodpressur
    e(BP)athomef ort
    helast6
    mont hsandsaysitis“hi
    gh.” 

    Hi
    sBP 
    i
    ncl
    ini
    cis162/
    92mm Hg,
    inbot
    har
    ms,
    andhear
    trat
    eis72bpm.Hi
    scar
    diovascul
    ar
    exam revealsregul
    arratewithanS4, butnomur murs.Pul
    sesaresymmet
    ri
    candequal
    thr
    oughoutandwi t
    houtedema.Hi sel ect
    rocar
    diogr
    am (ECG)showssi
    nusrhyt
    hm wi
    thvol
    tage
    cri
    ter
    iaforleftvent
    ri
    cularhypert
    rophy( LVH).

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextmostappr
    opr
    iat
    est
    epi
    ntr
    eat
    ment
    ?

    a. St
    artchl
    orthali
    done25mgdai l
    y.
    b. Per
    form 24-hourambulat
    oryBPmonit
    ori
    ng.
    c. I
    nit
    iat
    emet oprol
    olsucci
    nate50mgdail
    y.
    d. Per
    form arenalul
    tr
    asound.
    e. Pr
    escri
    beast ri
    ctsodi
    um rest
    ri
    cti
    on(
    <500mgperday)
    .

    Answer
    :

    29. a. St
    artchl
    ort
    hal
    idone25mgdai
    ly.

    Init
    ialhypertensivetreat
    mentshoul dincludeat hiazi
    dediureti
    c,calcium- channelblocker
    ,
    angiotensin-conver t
    ingenzymei nhibi
    tor,orangiotensi
    n-receptorblockeri nthegeneralnon-
    blackpopul ati
    on, whilei
    nt hegeneralblackpopulat i
    on,
    itshouldbeat hiazidediur
    eticor
    calcium channelbl ocker
    .IfthetargetBP isnotreachedwi thi
    n1mont hafteri
    nitat
    ingtherapy,
    thedoseoft heinit
    almedi cati
    onshouldbei ncreasedorasecondmedi cati
    onshoul dbeadded. 

    Thispat i
    ent'
    sphysicalexaminati
    onr evealedevidenceofl ong-st
    andingHTN  (
    S4,LVHonECG) ,
    sot heexpenseofa24- hourambulatory BP monitortoverif
    yHTN  i
    snotj usti
    fi
    ed.Thereisno
    evidencet osuggestthatsuchastrictsodium restri
    cti
    on( <500mgperday)i sbenefici
    ali
    nthi
    s
    setting.I
    fthepati
    enthasanunusual l
    ysever eandsuddenonsetofHTN  orevidenceof
    resistantHTN af
    terini
    ti
    atingpharmacol ogictr
    eatment ,
     furt
    hereval
    uationf orsecondaryHTN,
    i
    ncl udingarenalult
    rasound,wouldbeappr opri
    ate.
    Val
    vul
    arDi
    sease
    Quest
    ion:

    1. A38-year
    -oldAsianwomani sref
    er r
    edtoyouf orthef
    ir
    stti
    mebecauseofper ipheral
    edema.Shemovedt ot
    heUni tedStatesfrom China12yearsagoandunder wentami tr
    alval
    ve
    replacementforrheumaticmitralst
    enosis.Atthetime,shehadmildtr
    icuspi
    dst enosis(TS).
    Shehasdonewel lunti
    labout6mont hsago, whenshebegant onot
    icesomer ecurrentbrief
    palpit
    ati
    onsandsomebi lat
    erallegedema.

    Herexami nati
    onrevealsevi
    dencef orrightheartfail
    urewit
    hanelevatedjugul arvenous
    pressureandapr ominentAwavenot ed.Shehasal oudgrade3/4diastoli
    cr umbleatthef i
    fth
    i
    ntercostalspaceatthelef
    tsternalborderthatincreaseswithi
    nspi
    ration.Mechani calopening
    andclosingsoundsf rom t
    hemi tral
    valveareevi dent.Shehasanenlargedliverabouttwo
    fi
    ngersbelowt hecostalmargin,butnoasci t
    es.Ther eis2+edematoj ustabovet heankles.

    Anecho/ Doppl errevealsevidenceforsevereTSandt ri


    vialt
    ri
    cuspidregurgi
    tat
    ion.Themean
    tr
    icuspidgradientisest i
    matedat12mm Hg, andthetri
    cuspidpressurehalf
    -t
    imei s240msec.
    Ther i
    ghtatri
    um i squiteenlarged.Rightventr
    icul
    arfunct
    ionappearstobenor mal,andthe
    mechani calmitralvalveisfuncti
    oningwel l
    .Thereismini
    malaor t
    icvalvethi
    ckening.

    Youini
    ti
    atemedicalt
    herapybyaddi
    ngtor
    semide40mg/dayandspir
    onolact
    one25mg/dayto
    hermedicalr
    egi
    men, whichi
    ncl
    udeswarf
    ari
    n.Youal
    soobtai
    na24-hourambulat
    orymoni
    tor
    .

    Sher etur
    nsin4weekswi t
    hnoedemabutst
    il
    lwi
    thdyspneaonexer
    ti
    on.Her24-
    hourmoni
    tor
    revealsparoxysmalat
    ri
    alt
    achyar
    rhyt
    hmi
    as.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nhermanagement
    ?

    a. Surgicalt
    ri
    cuspidval
    ve(TV)replacement
    .
    b. Digoxin.
    c. I
    ncreasedi ur
    eti
    cdose.
    d. Percutaneousball
    oontr
    icuspi
    dval vul
    opl
    ast
    y.
    e. Surgicalt
    ri
    cuspidval
    vul
    oplasty.

    Answer
    :

    1. a. Sur
    gicalt
    ri
    cuspi
    dval
    ve(
    TV)r
    epl
    acement
    .

    Thecorr
    ectansweri ssur gi
    caltri
    cuspidvalvereplacement.Thepati
    entwi t
    honlymildto
    moderateTVst enosismayi mprovewi t
    hdi ur
    esis.Furosemideispoorlyabsorbedwhenthere
    i
    sboweledema, andal t
    er nati
    vessuchast orsemideorbumet anide,
    bot hofwhichhavebett
    er
    bowelabsorpti
    on, shouldbeusedi nst
    eadf ormanypat ient
    s(especi
    allyiff
    urosemi
    deistri
    ed
    andnotfoundef fecti
    ve).Overt i
    me, di
    uret
    icsmaynotbeabl etomaintainadequate
    hemodynami csast hepr oblem i
    smechani calobst r
    ucti
    onattheTVl evel.
     

    Thepati
    entpresentedher
    ehassever
    eTSbyal lpar
    ameters.The2014AmericanHear
    t
    Associ
    ati
    on/Amer i
    canColl
    egeofCar
    diol
    ogyvalvul
    arhear
    tdiseasegui
    del
    inedefi
    nessever
    e
    TSasdemonst rati
    ngapr essurehalf
    -t
    ime>190msecandval vear ea<1.0cm2.Neithersurgi
    cal
    norpercut
    aneousval vuloplast
    yhasbeenpr ovenveryeffect
    iveforTS, asbothprocedures
    oft
    enleadtowor seningt r
    icuspi
    dregurgi
    tat
    ion.Tri
    cuspidvalvereplacementisrecommended
    whensympt omsper sistdespiteadequat
    emedi calmanagement .Digoxincanbeusedi n
    sedent
    arypati
    entsf orratecontroli
    natri
    alf
    ibri
    ll
    ati
    on,buthaslit
    tlerolehere.

    Quest
    ion:

    2. A34-year-
    oldisadmitt
    edwi thfeverandanewmur mur.Heisaknownsubst ance
    abuser,
    andhecl ai
    mshehasf eltpoor
    lyforsever
    al mont
    hs.Hehashada10- l
    bweightloss
    andrecurr
    ingnightsweats.I
    nt hepastfewweeks, hehasnot
    edprogressivedyspneaandis
    sl
    eepingon2-3pi l
    lows.Hehasnoedema.Hei sonnomedi cat
    ionsatthisti
    me. 

    Hisexaminati
    onr evealsafri
    ght
    enedyoungmanwi t
    hevidenceofi ntr
    avenousdr uguseon
    botharms.Histemper atur
    eis38.5°C,hear
    trateis103bpm, bloodpr essureis95/ 50mm Hg,
    andresti
    ngsaturationis96%.Hislungsrevealbibasil
    arfinerales.Hisjugularvenouspr essur
    e
    i
    snotelevated,andt herei
    snotri
    cuspidregurgit
    ation.Hisapexi shyperdynami c,andthereisa
    grade1/2aorti
    csyst oli
    cmurmurandgr ade2/ 4diastoli
    cmur mural ongthel ef
    tsternalborder
    .
    AnS3 i
    spresent,andanS1  i
    ssoft
    .Hehasnoedema.  

    Youobtainbloodcultur
    es,anelectr
    ocardiogram (ECG),chestX-ray,
    andanechocardi
    ogram.
    Theecho/ Doppl
    erreveal
    sahyper dynami cleftvent
    ri
    clewithevidencef
    orsever
    eaor t
    ic
    regur
    git
    ation(AR)andvegetat
    ionsconsi stentwithendocardit
    isonhisaor
    ti
    cvalve.Oneofthe
    i
    magesf rom theechocardi
    ogr
    am i sshowni nFi gur
    e1.

    Basedont
    hepr
    ovi
    dedi
    nfor
    mat
    ionandhi
    scur
    rentcl
    ini
    calst
    atus,
    youbegi
    nempi
    ri
    cant
    ibi
    oti
    cs.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextappr
    opr
    iat
    est
    epi
    nhi
    smanagement
    ?
    a. St
    artint
    ravenousaf terl
    oadreductionwi t
    hanangiotensi
    n-conver
    ti
    ngenzymei
    nhi
    bit
    or.
    b. Ur
    gentsur gi
    calconsul t
    ati
    onf oraorti
    cvalverepl
    acement.
    c. St
    artabeta-blockertoreducet achycardi
    a.
    d. Schedul
    eat ransesophageal echocardiogram (
    TEE).
    e. Ur
    gentcardiaccat heter
    izat
    ion.

    Answer
    :

    2. b. Ur
    gentsur
    gicalconsul
    tat
    ionf
    oraor
    ti
    cval
    ver
    epl
    acement
    .

    Thepat ienthasobvi ousi nfecti


    veendocar diti
    sinvolvi
    ngt heaor ti
    cval ve.Heisincongesti
    ve
    heartfailure(CHF),tachycar di
    c, andf ebril
    e.Hisechocar diographyr evealsprecl
    osureofthe
    mi t
    ralvalveduet other apidlyrisingleftvent r
    iculardi
    astolicpressureasar esul
    tofhissevere
    AR.Thi sal soresult
    sint hesof tS1 obser ved.Asopposedt ochr onicAR, thediff
    erence
    betweent heaorti
    candl ef tventri
    cularpr essuresi ndi
    astolemaybesmal li
    nacuteAR, and
    theremaybel i
    tt
    lediastoli
    cmur mur .Likewiset hepulsepr essuremaynotbewi de,andther
    e
    maybenoneoft heclassichemodynami cfindingsofchr onicAR.Schemat ichemodynami c
    traci
    ngsofchr onicversusacut eARar eshowni nFigure2.  

    Inf
    ecti
    veendocar dit
    ispatient
    swi t
    hmi t
    ralval
    vepreclosureandCHFshoul dbeconsideredfor
    eit
    herurgentorearlysurgery.Theyareatriskforsuddentotallossofaort
    icval
    vecompet ence
    andcatastr
    ophicandl et
    halheartfai
    l
    ure.Heneedst obeconsi deredforur
    gent/
    emergency
    surger
    y.Furtherstudiesandt her
    apyshouldnotdelayhi ssurgery.Hedoesnotneeda
    cathet
    eri
    zati
    onathi sageandwi thhist
    enuoushemodynami cs. 
    ATEEwoul dbeast andar dpartoft hi
    ssur gi
    calint
    ervent
    ion,andwhi l
    eitisindicatedin
    pati
    entswithaorti
    cval veendocar diti
    st obet t
    erassesstheveget at
    ionsizesandt ohelpdefine
    thepresenceofanaor ticabscess, thepr ocedureshouldnotdel aysurgicali
    nterventi
    on.There
    i
    sl i
    tt
    lerol
    eforafter
    loadr educti
    oni nt hisacut ephasewithhislowsyst emicbloodpr essur
    e.
    Histachycardi
    aisappr opriateforhisser ioushemodynami cst ate,
    andbet a-
    blockersli
    kewise
    wouldnotbeappr opriate.Inadditi
    on, ther educedheartrat
    ef r
    om abet a-bl
    ockerwoul d
    i
    ncreasediastol
    icti
    meandt hedur ati
    onofARperbeat .

    (
    Figur
    e2)

    Quest
    ion:

    3. A22-year-
    oldwomani sreferr
    edtoyouf oradviceregardinganti
    coagul at
    ion
    managementi fshegetspregnant
    .Shehasahi st
    oryofendocar dit
    isi
    nvolvingbot hhermitr
    al
    andaorti
    cvalves3yearsago.Shehadanaor ti
    cvalver epairandamechani calmi t
    ralval
    ve
    repl
    acementatthatti
    me.Shehasbeenonwar far
    insincet hen.Shehasclinicall
    ydonewel l
    andisasympt omati
    c.Sheisgetti
    ngmar r
    iedthisyearandwant stohavechi ldr
    en.Her
    examinat
    ionisbenignexceptfortr
    ivi
    alaort
    icregurgi
    tationandt hemechani calmitr
    alval
    ve
    sounds.

    Hermedicati
    onsincl
    udebir
    thcontr
    ol pi
    ll
    s,aspi
    ri
    n81mg, andwarfar
    in4mgeacheveni
    ng.She
    hasbeenreli
    abl
    yf ol
    lowi
    ngheri
    nternati
    onalnormal
    izedr
    ati
    os,andtheval
    uesr
    angefr
    om 2.
    5
    to3.
    0mont hl
    y.
    Basedoncurr
    entgui
    del
    ines,
    whichofthef
    oll
    owingmedicalopt
    ionswoul
    dyour
    ecommendt
    o
    heri
    nregar
    dtotheuseofanti
    coagul
    ati
    onduri
    ngpregnancy?

    a. Becauseoftheri
    sksi
    nvolved,permanentster
    il
    izat
    iontopreventapr
    egnancy.
    b. Weight-
    basedlowmolecularweighthepar
    in(LMWH)f ortheenti
    repr
    egnancyandt
    hen
    changetoUFHj ustpri
    ortodeli
    very.
    c. We i
    ght-
    basedLMWHf orthefi
    rsttri
    mest er
    ,warfar
    infort
    hesecondandthi
    rdtri
    mester,
    andthenUFHj ustpri
    ortodeli
    very.
    d. We i
    ght-
    basedUFHdur ingtheentir
    epr egnancy.
    e. Warfar
    intheenti
    repregnancyuntilti
    mef ordeli
    veryandthenchanget
    ounfract
    ionat
    ed
    hepari
    n(UFH).

    Answer
    :

    3. e. Warfar
    intheenti
    repr
    egnancyunt
    ilt
    imef
    ordel
    iver
    yandt
    henchanget
    o
    unf
    racti
    onatedhepar
    in(
    UFH).

    Thecor r
    ectansweri sthatshemaycont i
    nuetouseherl ow-dosewarfari
    nf ort
    heentir
    e
    pregnancyandchanget oUFH( withactivat
    edparti
    althromboplasti
    ntimeofmor ethan
    twofol
    dcont rol
    )justpri
    ortovaginaldeli
    very.Thi
    sisbecauset heembr yopathyfr
    om war f
    arin
    appearstobedosedependent .I
    tisnowaCl assI(LevelofEvidenceB)recommendat ionthat
    thosepatient
    son≤5mg/ dayofwar f
    ari
    nmaysaf elyremainonwar f
    ari
    nt heenti
    repregnancy,
    changingt oUFHj ustpri
    ortodel
    ivery. 

    Theot heropt i
    onsmaybeconsi deredi ft
    hedailydoseofwar f
    ari
    nis>5mg/ day.Inthat
    sit
    uat ion, t
    hewar far
    inshouldbedi sconti
    nuedf orthefi
    rsttri
    mesterandei therUFH( wi
    th
    measur edacti
    vatedparti
    althrombopl ast
    intimeofmor et hantwofol
    dcont r
    ol)orLMWH( wit
    h
    measur edanti
    -Xaof0.8-1.
    2U/ ml4-6hour spostdose)maybeused.Wei ght -
    baseddosi ngof
    UFHandLMWHdoesnotpr ovideadequat eanti
    coagulanteffecti
    nmanycasesbecauseoft he
    i
    ncr easedvol umeofdi stri
    buti
    ont hatoccur sduri
    ngpregnancy.War fari
    nt hencanbe
    reinstitutedforthesecondandt hi
    rdtrimesterandstoppedj ustpr
    iortodel i
    veryandr eplaced
    withUFHasment ionedearli
    er.Ifsheisotherwisehealthy,shewouldnotneedt oconsider
    steril
    izat i
    on.

    Quest
    ion:

    4. Rheumatichear tdi
    seaser emainsamaj orprobl
    em i
    nt hedevel
    opingworld.Acut
    e
    rheumati
    cfevercontinuestopl aguemuchofAf r
    icaandAsia.Iti
    sesti
    mat edt
    hat60%of
    pati
    entswit
    hacut erheumat i
    cf everdevelopcarditi
    sandval
    vul i
    ti
    s,andchroni
    crheumatic
    heartdi
    seasemayf ollow.Mitralvalvestenosi
    s( MS)isthemostcommonoft hesechronic
    l
    esionsandcanhaveamaj orimpactonsur vi
    val.

    Withouti
    nter
    venti
    on,whichoft
    hef
    oll
    owi
    ngi
    stheest
    imat
    ed5-
    yearsur
    vivalr
    atef
    rom t
    heonset
    ofsymptomsi npati
    ent
    swi t
    hMS?

    a. 10%.
    b. 75%.
    c. 25%.
    d. 50%.
    e. 95%.

    Answer
    :

    4. d. 50%.

    Earl
    yst udi
    esofMSsuggest eda10-yearmortal
    it
    yrateof33-70%wi t
    ha20- yearmortali
    tyrat
    e
    of80-87%.Inthesehistori
    calst
    udies,t
    herewasani nci
    denceofhear tf
    ail
    ureinabout60%and
    embol i
    cevent
    si n20%.I na1991review,itwasnotedthati
    npat i
    entswhor ef
    useintervent
    ion,
    the5-yearsur
    vivalrat
    ewasabout50%.I ndevel
    opingcountr
    ies,t
    het i
    mef r
    om theinit
    ialbout
    ofrheumaticfeverandthedevelopmentofsympt omaticMSi sgeneral
    lyaboutthr
    eet ofour
    decades. 

    Quest
    ion:

    5. Percut
    aneousbal l
    oonMVcommi ssurotomy(orvalvul
    oplasty)hasbeenpr oventobe
    asef f
    ectiveassurgi
    calcommi ssurotomyi nthetreat
    mentofr heumat i
    cmi tr
    alst
    enosis.To
    assesst hesuit
    abil
    it
    yforballoonval vul
    oplasty,oneofthemostcommonl yusedcrit
    eri
    aarethe
    Massachuset tsGeneralHospital(MGH)cr iter
    iathati
    nvolvegradingcertainfeat
    uresoftheMV
    andaddi ngtheresult
    stodet er
    mi neanMVscor e.Fourfeatur
    esar eincl
    udedi nt
    hisscori
    ng
    system, andeacharegr aded1- 4.

    Whi
    choft
    hef
    oll
    owi
    ngf
    eat
    uresofr
    heumat
    icMVi
    sNOTi
    ncl
    udedi
    ntheMGHscor
    ingsyst
    em?

    a. Submitralchordalthi
    ckeni
    ngandscar
    .
    b. MVmobi li
    ty.
    c. MVc al
    ci um.
    d. MVt hi
    ckeni ng.
    e. Mit
    ralregur gi
    tat
    ion(MR).

    Answer
    :

    5. e. Mi
    tr
    alr
    egur
    git
    ati
    on(
    MR)
    .

    Theonefeat
    urenotincl
    udedi nt
    hemi t
    ralscor
    ingsyst
    em isMR.Whi lei
    tisacceptedt
    hatmore
    than2+MReliminat
    est hepossi
    bil
    it
    yfortheball
    oonproceduretobeef f
    ective,t
    hedegreeof
    MRwasnotpar toft
    hecr i
    ter
    ia.Atot
    alscoreof<8foreachoftheot herfourfeat
    ureshasbeen
    foundt
    oresul
    tinthehighestrat
    eofsuccessfrom t
    heballoonvalvulopl
    astyprocedur
    e. 

    Cli
    nicalf
    actorssuchasage, NewYor kHear tAssoci
    ationclass,
    andthepr esenceorabsence
    ofatri
    alfi
    bril
    lat
    ionalsohavebeenshownt obepredicti
    veofsuccessfulout comes,ashasthe
    fi
    nalMVar eaandgr adientaft
    erthepr ocedure.I
    npat i
    entswhohaveunder gonesurgical
    commi ssurotomy,balloonvalvulopl
    ast ycanstil
    lbeeffecti
    veusingt
    hesameanat omic
    feat
    urestohel pguideappr opri
    ateness. 

    Quest
    ion:

    6. Mit
    ralr
    egur
    git
    ati
    on(MR)r
    esul
    tswhenther
    eisl
    ossofintegr
    it
    yoft
    hemitr
    alappar
    atus.
    Broadl
    y,t
    hecausesoftheMRaredi
    ff
    erent
    iat
    edastowhet
    hertheyarepr
    imar
    yorsecondaryi
    n
    natur
    e.
    Whichofthef oll
    owinganat omi cf eatur
    esfavor
    ssecondar
    ymi
    tr
    alval
    ve(
    MV)di
    seaseas
    opposedtochr onicprimaryMVdi sease?
    a. Restr
    ictedleafletmobi li
    ty.
    b. Abnormal mi t
    ralchor dallength.
    c. Calci
    um bui l
    d-upint heleaf l
    et.
    d. Excessivemi t
    ralvalvulart i
    ssue.
    e. MVe ndocar di
    tis.

    Answer
    :

    6. a. Rest
    ri
    ctedl
    eaf
    letmobi
    li
    ty.

    Inchr onicsecondaryMR, t
    heMVi susual l
    ynormal ,buttheremaybesever el ef
    tvent ri
    cular
    (LV)syst ol
    icdysfuncti
    onandmal alignmentoft hepapi l
    larymuscles.Thisr esult
    si nabnor mal
    tetheringoftheMVwi t
    hr estri
    ctedl eafletmobil
    ity(orprolapse),
    poorleafletcoapt ati
    on,and
    subsequentMR.Annul ardil
    atati
    onmayal socont r
    ibute.TheCar pent
    ierclassifi
    cationis
    somet imesusedt or ef
    lectthis.TypeIi sduet oannul ardilat
    ati
    on.TypeI Irefl
    ectsatl eastone
    l
    eaf l
    etpr ol
    apsing.TypeIIIaresultswhent herei
    sr estri
    ctedleafl
    etmobi l
    ityinbothsyst oleand
    diastole.TypeIII
    boccur swhent herei srest
    ri
    ctedleaf l
    etmobi l
    it
    yonlyinsyst ole.

    I
    nprimaryMVdi sease,
    ther
    eisanabnormali
    tyi
    ntheval
    veitsel
    fori
    nsomecomponentofthe
    mit
    ralapparatus.Themitr
    alappar
    atuscanbedefi
    nedbyeachoftheval
    vecomponent
    sthat
    f
    uncti
    ont opreventMR.Theseincl
    udetheannul
    us,thel
    eaf
    lets,
    thechor
    dae,
    andthepapi
    ll
    ary
    muscles.
     

    Adescr i
    pti
    onofhowt hesest ructureswor ktogethertopr eventMRi sr el
    evant .Itisi
    mpor tant
    tonotethatbothmi tr
    alleafl
    et sattachviachor daet obot hpapil
    larymuscl es.WhenLV
    contr
    actionbegins,bothpapi ll
    arymuscl escont ractandpul ltheleafletstowar deachot her.As
    contr
    actioncontinues,t
    hel eafletsabutagainsteachot her,andt heLVpr essur eoneachsi de
    oftheleafl
    etstendtohol dthem t ogether.Thisisreferredtoast hekeyst oneef fectasitis
    simil
    artothemi ddlekeystoneatt hetopofanar chway.Wi thcont inuingvent ri
    cular
    contr
    action,t
    hepapi l
    lar
    ymuscl escont i
    nuet opul landt heannuluscont r
    act s.Anyabnor mal i
    ty
    i
    nt hepapill
    arymuscl econtraction,anyabnor mal chordallength, anyexcessi veMVt issue, or
    anyabnor mali
    tyinannul arsizeorcont ri
    butionmayr esultinMR.  

    Themostcommoncauseofpr i
    maryordegener ati
    veMRi sMVpr ol
    apsefoll
    owedbyot her
    s,
    suchasinf
    ecti
    veendocardi
    ti
    s,connect
    ivetissuediseases,rheumat
    icheartdi
    sease,cl
    eftMV,
    cal
    cif
    ici
    nfi
    lt
    rat
    ion,
    andradiat
    ionheartdisease.Obviousl
    y,thesurgi
    calt
    reatmentdif
    fer
    s
    dependi
    ngonwhethertheMRi sprimaryorsecondar yinnature.

    Quest
    ion:

    7. Youhavebeenf oll
    owinga52-year-ol
    dwomanf ormitr
    alprolapseformanyyear s.She
    hasalwaysbeenasympt omat i
    candonexami nationhashadmul ti
    plemi tr
    alcl
    ickswit
    hasof t
    mitr
    alinsuf
    fi
    ciencymur mur.Peri
    odi
    cecho/ Dopplerstudieshaveconf ir
    medmi tr
    alval
    ve
    prol
    apse,mil
    dmi tr
    alregur
    gitat
    ion(MR),andapr eservedleftvent
    ricularej
    ecti
    onfract
    ionwith
    normalchambersizes.

    Whi
    legar
    deni
    ng,
    shenot
    icessudden,
    shar
    pchestpai
    nandt
    hent
    her
    api
    donsetofshor
    tness
    ofbreathandtachycar
    dia.Shei
    sfri
    ghtenedandcall
    s911.Sheistr
    ansport
    edtot
    he
    emergencydepartmentwheresheisinflor
    idpul
    monaryedema.Sheistr
    eatedwi
    th
    i
    ntravenous(I
    V)diuret
    icsandqui
    cklystabi
    li
    zesbutr
    emainsdyspnei
    c.

    Bythetimeyouseeher ,shehasahear trateof110bpm, bloodpressureof90/60mm Hg,and


    room airsaturat
    ionof90%.Shei stachypneicsi
    tt
    ingboltupright
    .Thereareral
    esallt
    hewayup
    onbothsi desofherlungsandagr ade2/6holosyst
    oli
    cmur murwithanassociat
    edS3.She
    i
    mpr ovesqui ckl
    ywithIVfurosemidetherapy.

    Thef
    ourchambervi
    ewsofherecho/
    Doppl
    erst
    udyar
    eshowni
    nVi
    deos1and2.

    Sheunder
    goescar
    diaccat
    het
    eri
    zat
    ionwi
    tht
    hef
    oll
    owi
    ngper
    ti
    nentf
    indi
    ngs:

     Normalcoronaries.Ri
    ghtatri
    alpressur
    emeanof10mm Hg.
     Rightventr
    icul
    arpressure65/35mm Hg( meanof45mm Hg)
    .
     Pulmonarycapill
    arywedgepr essureVwaveof40mm Hg(meanof33mm Hg)
    .
     Aorti
    c100/ 80mm Hg.
     Leftvent
    ri
    cularpressure100/29mm Hg.
     Cardiacoutput3.2L/min.
     Cardiaci
    ndex1. 8L/min/m2.

    Basedont
    hesedat
    a,whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nhermanagement
    ?

     
    htt
    p:/
    /medi a.
    mycrowdwisdom.com.
    s3.amazonaws.
    com/
    acc/
    quest
    ions/
    asset
    _val
    ve/
    a1ea56f
    4-
    9ae0-436d-b015-
    96ecaf
    378850.mp4

    ht
    tp:
    //media.
    mycrowdwisdom.com.
    s3.
    amazonaws.
    com/
    acc/
    quest
    ions/
    asset
    _val
    ve/
    23f
    de7df
    -
    eb2a-46d5-
    bcb9-
    cfcb0cb7762c.
    mp4

    a. I
    Vdopami ne5mcg/ kg/mi n.
    b. Urgentsurgicalmit
    ralvalverepair
    /repl
    acement
    .
    c. Hepari
    nbol usandinfusion.
    d. Ni
    troprussideinf
    usion.
    e. I
    ntra-
    aorti
    cbal l
    oonpumpi nsert
    ion.

    Answer
    :

    7. b. Ur
    gentsur
    gicalmi
    tr
    alval
    ver
    epai
    r/r
    epl
    acement
    .

    Thecor rectansweri sur gentsur gicalinterventi


    on.Whi lecont i
    nueddi uresi
    sandt heuseof
    after
    loadr educti
    ont her apy,suchasi nt ravenousar teri
    alvasodi latorsorani ntra-aorticbal loon
    pump, mayhel pthehemodynami cstransi ent
    ly,asmi ghtani not ropesuchasdopami ne, she
    needsur gentmi t
    ralval ver epairorr eplacement .Shehasal readyst abi
    li
    zedusi ngI Vdi uretics,
    andherhemodynami csandechocar diogramsr eflectthatshehasacut emi tralchor dalr upt ure.
    Asopposedt ochr onicsever eMR, herl eftatr
    ium andl eftventricleareunpr epar edf ort he
    suddeni ncreaseinpr eloadr esulti
    ngf rom t heacuter egurgit
    ation.Herpul monar yhyper t
    ensi on
    i
    ssecondar ytoherhi ghpul monar ycapi ll
    arywedgepr essure,andt hereisnosuggest iont hati t
    i
    sr el
    atedt opulmonar yembol i,ashert ranspul monar ygradienti snor mal.Shet her eforedoes
    notneedhepar i
    nt herapyf orthatpossi bi l
    it
    y.Thefactt hatherMRi sonlygrade2/ 6r eflectst he
    highleftatri
    alpressur ei ntheacut eset ti
    ng.Thehemodynami cdi ffer
    encebet weenchr oni cMR
    andacut
    eMRi
    sschemat
    ical
    lyshowni
    nFi
    gur
    e1.

    (
    Figur
    e1)

    Quest
    ion:

    8. A40-year-oldwomanpr esentswithincreasingdyspneaovert hepast6mont hs.On


    exami nati
    on,shehasabl oodpr essur
    eof130/ 84mm Hg, heartrateof78bpm wi thincreased
    j
    ugul arvenouspr essureto10cm, fewbibasil
    arrales,ear
    lysystoli
    ccl ickwit
    hagr ade3/ 6mi d
    tolatesystoli
    cmur murbesthear dattheapex, andnoper i
    pheraledema.Echocar diography
    showsl eftventr
    iculareject
    ionfracti
    on(LVEF)of75%, wit
    hmoder atelyenlar
    gedLVwi th
    mar kedprolapseoft heposteri
    ormi tr
    alvalveleafl
    etwithseveremi tralregurgi
    tat
    ion( MR)
    extendingintotwopul monar yveins.Herpulmonar yarter
    ypeaksyst olicpr
    essureis45mm Hg.

    Whi
    choft
    hef
    oll
    owi
    ngdoyour
    ecommendi
    sassoci
    atedwi
    thi
    ncr
    easedl
    ongevi
    ty?

    a. Li
    sinopr i
    l.
    b. Mitralvalver epai
    r.
    c. Diureti
    ct herapy.
    d. Carvedilol.
    e. Bosent an.
    Answer
    :

    8. b. Mi
    tr
    alval
    ver
    epai
    r.

    Mi t
    ralvalvesurger y,pr
    eferablywithr
    epair,isaClassIrecommendationforsympt omati
    c
    patientswithchr onicseverepr i
    maryMRandLVEF>30%.Vasodi lat
    ortherapyinnormotensi
    ve
    patientswithchr onicpri
    mar yMRhasnotbeenshownt obeofsigni
    ficantbenefi
    t.Whil
    e
    diureti
    csar ehel
    pf ulintreati
    ngcongestivesympt omsofheartfai
    lur
    e, t
    heyhavenotbeen
    shownt oimprovel ongevity.Thispat
    ient'
    spulmonaryhypertensi
    onissecondaryt oher
    valvularheartdi
    sease, andt heendotheli
    nr ecept
    orantagoni
    stbosentanwoul dnotbe
    appr opri
    atetherapy.

    Quest
    ion:

    9. A64-year-ol
    dwomanwi thahi st
    oryofnonischemi ccar di
    omyopat hy,
    completeheart
    block,andabi ventr
    iculari
    mpl antabl
    ecar di
    overt
    er-defi
    bri
    ll
    atorpl aced4yearsagoisadmi t
    ted
    withrecurr
    entf ever
    sandbact eremiawi t
    hmet hi
    cil
    lin-
    sensit
    iveSt aphyl
    ococcusaureus.Sheis
    tr
    eatedwi t
    hint r
    avenous( I
    V)naf cil
    li
    nandgent amicinwithclinicalimpr
    ovement.
    Transesophagealechocar diography( TEE)doesnotdemonst rateanyevidenceofendocardit
    is.
    After3days, r
    epeatbl oodculturesshowper sist
    entbacteremi a.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    enextst
    ep?

    a. Complete6-
    weeksofIVant i
    bioti
    csfol
    lowedbychr onicanti
    biot
    icsforsuppr
    essi
    on.
    b. Ext
    racti
    onofherbi
    ventri
    cularimplant
    ablecar
    dioverter-
    defi
    bri
    ll
    atorsyst
    em.
    c. Complete6weeksofIVant i
    bioti
    csfol
    lowedbyrepeatbl oodcult
    ures.
    d. RepeatTEE.
    e. Taggedwhit
    ebloodcellscan.

    Answer
    :

    9. b. Ext
    ract
    ionofherbi
    vent
    ri
    cul
    ari
    mpl
    ant
    abl
    ecar
    diover
    ter
    -def
    ibr
    il
    lat
    orsyst
    em.

    Thispatientispresent i
    ngwithpersist
    entbacteremiawithSt aphylococcus,andintheabsence
    ofaclearalternativesource,t
    hereforethei
    mpl anteddevicemustbepr esumedt obethe
    sourceofongoi ngi nf
    ection,
    despi t
    eanegativeTEE.Wi t
    hper si
    stentbacter
    emia,theonly
    vi
    ablest r
    ategyfordef ini
    ti
    veresoluti
    onisextract
    ionoftheimpl anteddevice.Thi
    spatienthas
    compl et
    ehear tblockandi spacemakerdependentandt hereforewillr
    equireatemporary
    pacingsolutionunt i
    lthebacteremiahasclearedandanewper manentdevi cecanbe
    i
    mpl anted. 

    RepeatTEEatt hi
    spoi ntwi l
    lnotl i
    kel
    ychangemanagementandi snotver ysensi t
    iveor
    specifi
    cf ordiagnosingveget at
    ionsondevi celeads.About30%ofpat ient
    swi t
    hi mpl ant
    ed
    devi
    cel eadsmayhavemobi l
    et hrombithataregenerall
    ynotinfected.Taggedwhi tebloodcel
    l
    scansorposi tronemi ssi ontomogr aphyscanshavel owr esol
    utionandwi l
    lagainnotchange
    managementi nthispat i
    ent.Att hi
    spoint,t
    hebact er
    emiaispersistentdespitesever aldaysof
    appropriateant i
    bioti
    ct herapy,andsimpl yconti
    nuingorchangingant ibiot
    icswillbeunl i
    kel
    yto
    achievest er
    il
    izati
    on. 
    Quest
    ion:

    10. A70- year-


    oldmanishospit
    ali
    zedwithsubacutebacteri
    alendocardi
    ti
    s.Bloodcultur
    es
    growSt r
    eptococcusbovi
    s.Echocardi
    ographydemonst rat
    esa3mm mobi levegetat
    iononthe
    anteri
    orleafl
    etofthemit
    ralval
    vewithmildmit
    ralregurgit
    ati
    onandnoot hervalvul
    arlesi
    ons.
    Leftvent
    r i
    cularej
    ecti
    onf
    racti
    onis65%.Examinati
    oni sunremarkable.

    I
    naddi
    ti
    ont
    oant
    ibi
    oti
    cs,
    whi
    choft
    hef
    oll
    owi
    ngi
    smostappr
    opr
    iat
    eforhi
    smanagement
    ?

    a. Surgi
    calconsul
    t.
    b. Uri
    nalysi
    s.
    c. Col
    onoscopy.
    d. DentalX-r
    ays.
    e. Coronaryangi
    ography.

    Answer
    :

    10. c. Col
    onoscopy.

    Strept
    ococcusbovi sendocardit
    isisoft
    enassoci atedwit
    hmal i
    gnancyofthegastr
    ointest
    inal
    tract
    ,socolonoscopyt oevaluatet
    hispossibil
    it
    yshouldbeconsi der
    ed.Thesmallvegetat
    ion
    andmi ldmitralr
    egurgit
    ati
    ondonotr equir
    esur gi
    cal i
    nter
    venti
    on,sotherei
    salsonoindicati
    on
    forcoronaryangiographyatthisti
    me.Streptococcusbovisisnottypi
    call
    yassoci
    atedwi t
    h
    dentalcari
    es.Urinal
    ysistolookforuri
    narytractinvol
    vementwoul dbeindi
    cat
    edfor
    Staphylococcali
    nfecti
    onsbutnotf orStr
    eptococcusbovis.

    Quest
    ion:

    11. A54- year-


    oldmanpr esentsforr out
    ineevaluat
    ionforknownchr onicaorti
    cvalve
    regur
    git
    ati
    onduet obicuspi
    daor ti
    cval vemorphology.Heremai nsasympt omati
    c.Physical
    examinati
    onreveal
    sahear trat
    eof84bpm andbl oodpressureof140/ 50mm Hg.Physi cal
    examinati
    onreveal
    sagr ade2/6syst olicej
    ecti
    onmur mural ongt helef
    tsternalborderanda
    grade3/4diast
    oli
    cflowmur mural ongt hesamear ea.Echocardiogram reveal
    sadi lat
    edlef
    t
    ventr
    icl
    ewithsevereaort
    icregurgit
    ation.

    Whichofthefol
    lowi
    ngechocar
    diogr
    aphi
    cpar
    amet
    erswoul
    dbeani
    ndi
    cat
    ionf
    orsur
    gical
    aor
    ticval
    verepl
    acementatt
    histi
    me?

    a. LVejecti
    onf racti
    on55%.
    b. Venacont ract awidth0.7cm.
    c. Aort
    icregur gitantfract
    ion65%.
    d. Lef
    tventricular( LV)end-syst
    oli
    cdi
    mensi
    on5.
    3cm.
    e. LVend-diast olicdimension6.0cm.
    Answer
    :

    11. d. Lef
    tvent
    ri
    cul
    ar(
    LV)end-
    syst
    oli
    cdi
    mensi
    on5.
    3cm.

    Basedont he2014Amer i
    canCollegeofCardiol
    ogy/AmericanHeartAssociat
    ionvalvularheart
    di
    seasegui del
    ine,t
    hepati
    enthasevidenceforsevereaor
    ticval
    veregurgi
    tati
    on.Surgicalrepai
    r
    i
    sindicat
    edi nanasymptomaticpati
    entwhent hereisevi
    denceforLVdysfunction,
    LVej ection
    fr
    acti
    on5.0cm, LVend-
    diast
    oli
    cdiameter>6.5cm, orwhenundergoingothercardi
    acsur gery.
     

    Quest
    ion:

    12. A32- year-oldwomanpr esentstocli


    nicwithseveralmonthsofpr ogr essivedyspneaon
    exert
    ion,ascites,andlowerext remit
    yedema.At r
    ansthor
    acicechocar di
    ogr am demonst r
    ates
    anestimatedr ightventr
    icular(RV)systol
    icpressureof90mm Hg, RVenl argementand
    dysfuncti
    on, andseveret r
    icuspidregurgi
    tat
    ionwi t
    havenacont ract
    aof0. 8cm.She
    undergoesr i
    ght -
    heartcatheter
    izati
    onthatconfir
    mst hediagnosi
    sofsever epul monar yarter
    ial
    hypertensi
    onwi t
    hapul monar yvascularr
    esistanceof12Wooduni ts.Leftvent r
    icularend-
    diast
    olicpressureis10mm Hg.Hercar diacindexis1.7L/min/m2.Ther eisnor eacti
    vit
    yto
    i
    nhaledni t
    ricoxide.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nhermanagement
    ?

    a. Diureti
    c.
    b. Pulmonar yvasodil
    ator
    .
    c. Calcium channelbl
    ocker.
    d. Tri
    cuspidvalvesurgery.
    e. Digit
    ali
    s.

    Answer
    :

    12. b. Pul
    monar
    yvasodi
    lat
    or.
    Quest
    ion:

    13. A27- year-ol


    dwomani sseeni ntheemergencydepartmentforseveraldaysof
    progressi
    vedyspnea, or
    thopnea,paroxysmalnoctur
    naldyspnea,andper i
    pheraledema.She
    hadasi milarpresentati
    ontotheemer gencydepartment3weeksago, andwasgi vena
    prescri
    pti
    onf or40mgoncedai lyoffurosemideandmet oprol
    ol25mgt wicedail
    y.Sheis25
    weekspr egnant.Hervi t
    alsi
    gnsar eaheartrateof102bpm, bl
    oodpr essure100/60mm Hg,
    andoxygensat ur at
    ion100%on2l it
    ersnasalcannulaoxygen.
     

    Physicalexami nationr evealsat achycardiaat88bpm.Ther earebilat


    eralr
    alest wo-thir
    dsof
    thewayupt hepost er
    iorl ungfiel
    ds.Therei sanelevatedj ugularvenouspressur etot heangle
    ofthemandi bleupr ight, a1/6hol osyst
    olicmur muratt heapexwi t
    ha2/ 4diastolicmur mur,
    andanopeni ngsnapi sal sopresent.Therei str
    aceper ipheraledema.Echocar diogram reveal
    s
    normalleftventricularf uncti
    onwi thrheumat icmit
    ralstenosi sandameanmi t
    ralvalve
    gradientof16mm Hgwi thtri
    vialmitr
    alregurgit
    ati
    on.Theest imatedri
    ghtventricularsystol
    ic
    pressureis50mm Hg.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthebestnextst
    epf
    ormanagement
    ?

    a. Del
    iver ynowandt henmi t
    ralval
    verepl
    acementsur gerysoonther
    eaf
    ter
    .
    b. Mit
    r alvalver
    eplacementsur ger
    y.
    c. Percutaneousmi t
    ralcommi ssurot
    omy(valvulopl
    asty)
    .
    d. Cont i
    nuecurrentobservat
    ionalmanagement .
    e. Percutaneousmi t
    raledge-t
    o-edgemitr
    alvalverepai
    r(Mitr
    aCli
    p).

    Answer
    :

    13. c. Per
    cut
    aneousmi
    tr
    alcommi
    ssur
    otomy(
    val
    vul
    opl
    ast
    y).

    Percutaneousmi tr
    alvalvecommi ssurotomy( val
    vul
    oplasty)isaCl assIIarecommendat ionin
    theabsenceofsi gnif
    icantmi t
    ralregurgitat
    ionandaf avorableWi l
    kinsScorei nthe2014
    AHA/ ACCval vul
    ardiseasegui del
    inesf orpregnantpati
    entswi thClassIIIorIVheartf ail
    ure
    symptomsdespi t
    emedi caltherapy.Del i
    veryandthensur gerywoul dnotbeopt imal
    managementatt hispoint
    ,unlessf oraspeci f
    icobstetr
    icindicati
    on,duet oissuesrelatedto
    prematurit
    y.Hersympt omshavepr ogresseddespit
    edi ur
    eticandbet ablockade, t
    huscur r
    ent
    medicaltherapywoul dnotbet hebestchoi ce.Percutaneousmi traledge-t
    o-edgemi tralvalve
    repai
    r(MitraCli
    p)isnotindicatedast hepat i
    enthasmi tr
    alstenosis,notmi t
    ralregurgitat
    ion. 

    Quest
    ion:

    14. A26- year-


    oldwomani sseeni nconsultati
    onont heobst etr
    icsinpati
    entwar dfor
    eval
    uationofwor seni
    ngdyspnea6hour safterdel i
    veryofaf ull-
    ter
    m healthybabyboy.She
    deni
    eschestpai n.Herexami nationreveal
    sherhear trateis105bpm, bl
    oodpr essureis
    100/60mm Hgandequali nbot hupperextremi ti
    es,andj ugularvenouspr essureiselevated.
    Sheist achycar
    dicwit
    har egul arrhyt
    hm, agrade3/ 6latesystolicmur murwi t
    hami d-syst
    oli
    c
    cl
    ickatt heapex,andral
    es2/ 3oft heposteri
    orl ungf i
    eldsbilateral
    ly.Oxygensat ur
    ationis99%
    on2l i
    terssupplementaloxygen.Theel ectr
    ocar diogram iswithoutanyi schemi cST-Twave
    changes.
    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    ydi
    agnosi
    s?

    a. Mit
    ralr
    egurgit
    ati
    on.
    b. Pul
    monaryembol ism.
    c. Aor
    ticst
    enosis.
    d. Cor
    onarydissect
    ion.
    e. Aor
    ticdi
    ssecti
    on.

    Answer
    :

    14. a. Mi
    tr
    alr
    egur
    git
    ati
    on.

    Regur git
    antval velesions, evenwhensever e,ar egener all
    ywel ltolerateddur i
    ngpr egnancy.
    However , asi nthi
    sscenar i
    o, shortl
    yaf t
    erdeli
    ver ywi t
    hsi gni
    ficantf lui
    dshi f
    tsfrom t he
    placenta,asi gnifi
    cantvol umel oadmayoccur ,leadingt oovertcongest i
    vehear tfail
    ur e.
    Coronar ydi ssecti
    onmayoccurdur ingpregnancyorshor tl
    yaf terdel i
    ver y,
    butwi thoutchest
    painorel ect r
    ocardiographi cchanges, thisi
    snott hebestanswer .Pulmonar yembol ism or
    amni oti
    cf luidembol ism alsomayoccurwi thpr egnancyoraf terdel i
    ver y.However ,thi spati
    ent
    hasevi denceofr i
    ght-andl eft
    -sidedheartfail
    ur eonexami nation, andl eft-
    sidedfailur ewould
    beabsentwi thapul monar yembol i
    sm.Aor ti
    cdi ssectioncanoccurdur ingpr egnancyor
    i
    mmedi atelypost partum int hecont extofMar fansyndr ome, Loeys- Di etzsyndr ome, or
    coarctati
    onoft heaor ta.Thescenar iopresentedi snotconsi stentwi t
    haor ticdissect ion.Her
    exami nationf i
    ndingsar enotsuggest iveofaor ti
    cstenosi s.

    Quest
    ion:

    15. A60- year-ol


    dmani shospital
    izedforfurt
    hereval uat
    ionoffever,chi
    ll
    s, nightsweats,
    andwei ghtl
    oss.Bl oodcultur
    esgrowmet hi
    cil
    li
    n-sensit
    iveStaphyl
    ococcusaur eus.Hei s
    startedonappr opri
    ateanti
    biot
    iccoverage.Transesophagealechocar diogr
    am r evealsnormal
    l
    ef tventri
    cul
    arf uncti
    onwi thabicuspidaort
    icvalvewi t
    hmoder ateaor t
    icvalver egurgi
    tat
    ion
    andan8mm veget ati
    on.Theotherheartvalvesarewi thoutevi
    denceofveget at ionor
    dysf uncti
    on.Thepat ienthasanumberofquest i
    onsr egardi
    nghispr ognosiswi thendocardit
    is,
    i
    ncl udinghisriskofdyi ng.

    Whichofthefol
    lowi
    ngbestdescr
    ibest
    hei
    n-hospi
    tal
    mor
    tal
    it
    yforpat
    ient
    swi
    thi
    nfect
    ive
    endocar
    dit
    is?

    a. 60%.
    b. 80%.
    c. 40%.
    d. 20%.
    e. 5%.

    Answer
    :

    15. d. 20%.

    Avarietyoff
    actor
    shavebeenassoci
    atedwithevenhighermor t
    ali
    tyi
    nselect
    edpatients,such
    asadvancedheartfai
    lur
    esympt
    omsonpr esentati
    onandnotunder goingval
    vesurgery.A
    mult
    idisci
    pli
    nar
    ytreat
    mentappr
    oachinvol
    vingcardiol
    ogy,i
    nfecti
    ondiseasespeci
    ali
    sts,and
    car
    diacsur
    ger
    ytoachi
    eveopt
    imal
    out
    comesi
    srecommended.
     

    Quest
    ion:

    16. A35- year


    -ol
    dmal eintravenousdrugabuserpr esentswit
    hworseningshortnessof
    breathanddyspneaonexer t
    ion.Onexami nati
    on,hi
    sbl oodpressurei
    s120/55mm Hg, heart
    ratei
    s95bpm, andr espi
    rat
    ionr at
    eis20.Oxygensatur ati
    onis93%onr i
    ghtatri
    um.Car di
    ac
    auscultati
    ondemonst rat
    esabl owingdecrescendodiastoli
    cmur murhear
    dovert he
    precordium andalatediast
    olicrumbleattheapexwithnoopeni ngsnap.S1 i
    ssof t
    ,andS2 i
    s
    paradoxicall
    yspl
    it.

    Whi
    choft
    hef
    oll
    owi
    ngi
    stheet
    iol
    ogyoft
    hispat
    ient
    '
    sshor
    tnessofbr
    eat
    h?

    a. Pulmonicregurgi
    tati
    on.
    b. Tri
    cuspidstenosis.
    c. Mitr
    alstenosis(MS).
    d. Mitr
    alregurgi
    tati
    on.
    e. Aorti
    cregurgi
    tati
    on(AR).

    Answer
    :

    16. e. Aor
    ti
    cregur
    git
    ati
    on(
    AR)
    .

    Thephysi calexami nat


    ionfindingsdescr i
    bedar econsistentwi t
    hAR;t heblowingdecr escendo
    diastolicmur muri stheregurgitati
    on, t
    hepar adoxicalsplitS2 i
    sduet odel ayedaor t
    icvalve
    closur efr
    om t hei ncreasedleftvent r
    icularvolume, andthel atediastolicr
    umbl eisconsi st
    ent
    withanAust i
    nFl intmur mur.Aust inFli
    ntmur muri shear dint heset t
    ingofsever eARandi s
    thoughtt obeduet oear l
    yclosur eofthemi t
    ralvalveresulti
    ngi nfunct i
    onalMS.I tisfr
    equent l
    y
    mi stakenf orvalvularMS, butthel ackofopeni ngsnapi sacl uethatt hisi
    snott hecase.S1  i
    s
    sof tinARl ikel
    yduet oear l
    yclosur eofthemi t
    ralvalvefrom theel evatedleftventri
    cul
    arend-
    diastolicpressur e.Ingeneral,S1 invalvularMSi sloudunt i
    lthevalvei sseverelyinvol
    ved.

    Quest
    ion:

    17. A75- year-oldmanpr esentswit


    h3daysofchestpai nandwor seningdyspneaon
    exert
    ion.Onexami nati
    on,hisbloodpressurei
    s125/ 60mm Hg, heartrateis95bpm, and
    j
    ugularvenouspr essureis12cm.Ther eisaharshsystol
    icmur murhear dt hr
    oughoutthe
    precordium wit
    houti nspi
    rator
    yaugment ati
    on.Attheapex,i
    tisnotedt hatfoll
    owinga
    premat urevent
    ricularcontr
    acti
    on,themur murbecomest r
    ansientl
    ylouder .An
    el
    ectrocardiogr
    am showsQwavesi ntheinfer
    iorl
    eads.

    Ift
    hepati
    entunder
    wentahemodynami
    ccar
    diaccat
    het
    eri
    zat
    ion,
    whi
    choft
    hef
    oll
    owi
    ngwoul
    d
    befound?

    a. Larger i
    ghtvent
    ri
    cularoutf
    lowt racttoPApressuregradient.
    b. Increasedpulmonaryart
    ery( PA)oxygensaturat
    ion.
    c. LargeVwaveonpul monarycapi ll
    arywedgepressuretracing.
    d. LargeVwaveonr ightat
    ri
    al pressuretr
    aci
    ng.
    e. Largeleftvent
    ri
    cletoaort
    agr adient.
    Answer
    :

    17. e. Lar
    gel
    eftvent
    ri
    clet
    oaor
    tagr
    adi
    ent
    .

    Thepat i
    enthasdegener ativeorage- rel
    atedAS, themostcommonet i
    ologyofAS.Onphysi cal
    examinat i
    on,hedemonst ratesGal l
    avardinphenomenon—ahar shASmur murhear dbestatthe
    apex.Thisisduet othehigh- f
    requencycomponent soft heASmur murradi atingtot heleft
    ventr
    icularapex.I
    talsocanbedi f
    ferenti
    atedf r
    om MRbynot ingagapbet weenS1, themur mur,
    andthenS2.TheMRmur murst artswi t
    hS1 andcont inuest hr
    oughS2 untilthemi tr
    alvalve
    opens.Themur murofASal soincreaseswi t
    hbr adycardiaorafterapause, suchasaf t
    era
    prematureventri
    cularcontr action;anMRmur murwoul dnotchange.Thi si snott ricuspid
    regur
    gitati
    on,whichwoul dbehol osystoli
    candbesthear datthelef
    tlowerst ernalborder.Nor
    i
    st hi
    spul monicstenosi
    s, whi chwoul dtypical
    lybestbehear dattheleftupperst ernalborder.
     

    Bothoft heser ight-


    sidedmur murswoul dbecomel ouderwithinspirati
    on.Ifahemodynami c
    cardiaccatheter i
    zati
    onwer eperformed, i
    twoul ddemonst r
    ateal argeleftventricl
    etoaor t
    a
    pressuregr adient,consi
    stentwithAS.Al argeVwaveonpul monar ycapi l
    larywedgepr essure
    i
    sconsi stentwi thsignif
    icantMR.Al argeVwaveont heri
    ghtat r
    ium isconsi stentwith
    signifi
    canttri
    cuspi dregurgit
    ati
    on.IncreasedPAoxygensat urati
    onsuggest sthepr esenceofa
    l
    ef t
    -to-
    ri
    ghtshunt ,
    suchasavent ri
    cularseptaldefect.Aventri
    cularsept aldefectmur muri s
    typical
    lycont i
    nuousandhear datt hesternalborder,
    nottheapex.Al arger i
    ghtventricular
    outflowtracttoPApr essuregradientisconsistentwithpul
    moni cst enosis. 

    Quest
    ion:

    18. A35- year-


    oldwomanpr esent
    sforshort
    nessofbreath.Shehasahistor
    yofdiabetes
    andhypertension.Onphysicalexami
    nati
    on,herbloodpr
    essureis140/85mm Hg, hear
    trateis
    88bpm, andbodymassi ndexis38.Herjugul
    arvenouspressurei
    snormal
    , andshehas1- 2+
    bi
    lat
    erall
    owerext remit
    yedema.

    Sherecentlyunderwentanechocardi
    ogram,whichwastechnical
    lydif
    fi
    cul
    t,butshowed
    nor
    malbi ventr
    icul
    arfunct
    ion,mil
    dconcentr
    icl
    eftvent
    ri
    cularhypert
    rophy,
    andmoder at
    e
    pul
    moni cregurgit
    ati
    on.Ventr
    icl
    esarenormali
    nsize.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    ep?

    a. Compr essi
    onstockings.
    b. Transesophagealechocar di
    ogram.
    c. Antibi
    oti
    cprophylaxisfordentalpr
    ocedur
    es.
    d. Repeatechocardiogram in6mont hs.
    e. Chestcomput edtomogr aphyangiogr
    aphy.

    Answer
    :

    18. a. Compr
    essi
    onst
    ocki
    ngs.

    Thismor bidl
    yobesepat
    ienthasani nci
    dentalfi
    ndi
    ngofmoderatepulmonaryregurgi
    tation.
    Thisfi
    ndingiscommonandr equi
    resnoaddi t
    ional
    workuporint
    ervent
    ion.Theref
    ore,repeat
    echocardiographyandt
    ransesophagealechocardi
    ogr
    aphyarenotindi
    cated.Pulmonar y
    regurgit
    ationdoesnotr equireanti
    bioti
    cprophyl axi
    s.Othert hanshortnessofbr eat
    h, t
    he
    patienthasnoot herknownr i
    skfactorsforpulmonar yembol i
    sm andisnottachycar dic,
    thereforecomputedt omogr aphyangiographyi snotindicated.Herlowerextremi t
    yedemai s
    notsecondar ytoright-
    sidedheartfail
    ureint hesett
    ingofanor malj
    ugularvenouspr essure.
    Heredemai ssecondar ytovenousi nsuff
    iciencyintheset t
    ingofmor bidobesity.Compr essi
    on
    stockingsareindicatediftheedemai sbot hersomet othepat ient
    . 

    Quest
    ion:

    19. A35- year


    -oldmanr ecentl
    ymovedt otheUnit
    edStatesandi sseenforshortnessof
    breat
    h.Aftermedi calopti
    mizat
    ionwithdiur
    esisandbeta-
    blockade,echocardi
    ographyr eveal
    s
    thatt
    hemi tr
    alvalveleafl
    etsandapparatusaresever
    elycal
    cifi
    edandl eafl
    etshavedecr eased
    excursi
    on.Themi tralval
    veareais1.4cm2 wit
    hameangr adientof12mm Hgandapr essure
    half
    -t
    ime(PHT)of180msec.Thet ri
    cuspidvalvei
    salsonotablythi
    ckenedwi t
    haval vear eaof
    0.9cm2,ameangr adientof7mm Hg, andaPHTof220msec.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nthi
    spat
    ient
    'smanagement
    ?

    a. Mit
    ralandt r
    icuspi
    dvalvesur
    ger
    y.
    b. Mit
    ralvalvesurger
    y.
    c. Mit
    ralvalvul
    oplast
    y.
    d. Tr
    icuspidvalvesurger
    y.
    e. Mit
    ralandt r
    icuspi
    dvalvul
    opl
    ast
    y.

    Answer
    :

    19. a. Mi
    tr
    alandt
    ri
    cuspi
    dval
    vesur
    ger
    y.

    Thepat ienthassymptomat i
    crheumaticvalvediseasewi thbot hseveremi t
    ralandt r
    icuspi
    d
    stenosis.Severemitr
    alstenosisi
    sdefinedasanabnor malvalvewi thaPHTof150msecand
    aval veareaof1.5cm2.Mi t
    ralval
    vestenosisischar acter
    izedasver ysevereifPHTi s220
    msecandt hevalveareais1cm2.Sever etr
    icuspidst enosisisdefinedasat hickenedvalve
    2
    withaPHTof190msecandaval veareaof1cm .Theonl ydefini
    tivetreatmentf orrheumati
    c
    tr
    icuspidst enosi
    sissurgi
    calrepl
    acement.Dependi ngont heWi l
    kinsscor e,t
    hemi t
    ralval
    ve
    mi ghtbemanagedwi t
    hvalvulopl
    astyorsurgery.

    Quest
    ion:

    20. A66- year-


    oldpati
    entpresent
    switht ypi
    calangina,butnosympt omsofheartfai
    lur
    e.He
    hasahist
    oryofhypertension,
    smoking,type2di abet
    es, andhyper
    li
    pidemia.Healsohasa
    str
    ongfamil
    yhi st
    oryofcoronaryart
    erydisease.Anucl earst
    resst
    estrevealsaposit
    ive
    el
    ectr
    ocardi
    ogram withstr
    ess,chestpai
    n, andtransi
    entischemicdil
    atati
    ononthestress
    i
    mage. 

    Heundergoescar
    diaccatheteri
    zati
    onandsignifi
    cantthr
    ee-
    vesseldi
    seaseisfound.His
    echocar
    diogr
    am r
    evealsanej ect
    ionfr
    act
    ion(EF)of50%andevi denceforseveremit
    ral
    regur
    git
    ati
    on(MR).Thereisanar eaofmi
    ldleftventr
    icul
    arhypoki
    nesi
    alateral
    ly.

    Whi
    choft
    hef
    oll
    owi
    ngmi
    tr
    alval
    veechocar
    diogr
    aphi
    cpar
    amet
    ersshoul
    dpr
    omptr
    epai
    roft
    he
    mit
    ralval
    vei
    ntheset
    ti
    ngofconcomi
    tantcor
    onar
    yar
    ter
    ybypassgr
    aft
    ing(
    CABG)andanEFof
    50%?

    a. MRvenacontr
    acta=0.4cm.
    b. Mi
    tr
    alval
    veeff
    ecti
    veregur
    git
    antor
    if
    i ERO)=42mm2.
    ce(
    c. MRregur
    git
    antvol
    ume=38cc.
    d. MRregur
    git
    antfr
    acti
    on=40%.

    Answer
    :

    20. b. Mi
    tr
    alval
    veef
    fect
    iver
    egur
    git
    antor
    if
    i ERO)=42mm2.
    ce(

    Thecor rectanswerisalargemitralval
    veEROar eaof>40mm2.Hemodynami call
    ysevere
    valvelesionsshouldundergorepairorrepl
    acementatthet
    imeofCABG, evenifpr
    esumably
    asympt omat i
    c.Theli
    keli
    hoodofsympt omsr ef
    erabl
    etoseverel
    esionswi t
    hin2-3year
    softhe
    diagnosisishigh,andthereoperati
    vecardi
    acsurgerymort
    ali
    tyisgreateri
    nthatti
    mef r
    ame
    thanthemor t
    ali
    tyassoci
    atedwithCABGcombi nedwit
    hvalvesurgery.
     

    Thedefinit
    ionofsevereMRbyechocar diogr
    aphiccri
    teri
    aincl
    udesavenacontr
    acta≥0.
    7cm,
    regurgi
    tantvol
    ume≥60cc, regur gi
    tantfr
    acti
    on≥50%, orERO≥40mm2.Themi tr
    alval
    ve(ERO)
    2
    of42mm   isthustheonl
    yr esponset hatdef
    inessevereMRbyt hegui
    del
    ines,
    andthisf
    indi
    ng
    warrantsconcomitantmit
    ralvalverepairwit
    hCABG.

    Quest
    ion:

    21. A74- year


    -ol
    dmanpr esent
    stotheambulator
    ycli
    nicf
    ortheeval
    uationofdyspnea.He
    i
    saf ar
    merwhosesymptomsbeganappr oxi
    mately2monthsago.Hisdyspneaoccursonly
    dur
    ingmoderat
    eorsever
    elevelsofexer
    ti
    on,suchasbai
    li
    nghayorcarryi
    ng50poundsacksof
    dai
    ryfeedi
    nhisdai
    lywork.
     

    Thepat ient’
    smedi calhist
    or yconsistsoft r
    eat edhyper t
    ension,andar emot edeepvenous
    thr
    ombosi sthatoccur r
    edi ntheset t
    ingofkneesur gery.Thef amilyhistoryisunr emarkable.
    Hiscur r
    entmedi cat i
    onsar ehydrochlorothi
    azi de(25mgdai ly)andmet oprolol(
    25mgt wi
    ce
    dail
    y).Onphysi cal exami nation,hisbloodpr essurei s132/74mm Hgandhear trat
    eis64bpm.
    Thel ungsar eclear .Jugularvenouspul seisnor mal.Caroti
    dupst rokehasmi ni
    maldel ay.The
    apicalimpulseisl ocal i
    zedandnotenl arged.Ther eisagr ade3/ 6late-peakingsyst ol
    icejecti
    on
    mur murhear dbestatt her i
    ghtupperst ernal border.Noeject i
    onclickispr esent.Theaor ti
    c
    componentoft hesecondhear tsoundi saudi blebuti ssli
    ghtlydiminished;t hepulmoni c
    componenti snor mal .Peri
    pher alexaminationshowsnoedema.Ther emai nderoft he
    exami nati
    oni snor mal .
     

    Thepat
    ientunder
    goesat
    ranst
    hor
    aci
    cechocar
    diogr
    am wi
    tht
    hef
    oll
    owi
    ngr
    esul
    ts:
     

    •Leftventr
    icular(LV)ejecti
    onfracti
    on(calculated):68% 
    •Int
    erventr
    icularseptalwallthi
    ckness:13mm 
    •Meanaor ticvalvegradient:30mm Hg 
    2
    •Aorti
    cvalvear ea:1.3cm  
    •Esti
    mat edpeakr ightventri
    cularsyst
    oli
    cpr essure:32mm Hg
    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    ep?

    a. Comput edtomogr aphicangiogram.


    b. Transcatheteraorti
    cvalvereplacement .
    c. Dobut amineinfusi
    onechocar diography.
    d. Cardiaccatheteri
    zati
    on.
    e. Surgicalaorti
    cvalvereplacement .

    Answer
    :

    21. d. Car
    diaccat
    het
    eri
    zat
    ion.

    Thecor rectansweriscardiaccat heteri


    zat
    ion.Thepatientpresentsforevaluat i
    onof
    sympt omsofexer ti
    onaldyspnea.Thephysi calexaminationsuggestssevereaor t
    icstenosi
    s
    (AS).However ,theechocardiogram showsonl ymoder ateAS.Insympt omat icpat i
    entswitha
    discrepancybetweencl i
    nicalexami nati
    onandt heresult
    soft henoninvasivet esti
    ng,invasi
    ve
    hemodynami ccatheter
    izati
    oni sindicat
    edtodet er
    minet hetrueseveri
    tyoft heaor ti
    cvalve
    l
    esion( ClassIrecommendat ion). 

    Inthispat ient,echocardiographymayhaveunder estimat edtheASbypooral i


    gnmentoft he
    Doppl erpr obewi ththeaor t
    icsyst olicj
    et( i
    .e.,l
    eadingt ounder estimationofthegradient)
    ,and
    bysampl ingt heLVout flowt r
    actt i
    mevel ocityint
    egr altoocloset otheaor t
    icvalve(i
    .e.
    ,leading
    toover estimat i
    onoft het i
    mevel ocityintegr almeasur ement ).I
    nvasi vehemodynami c
    catheterizationforaor t
    icgradienti snotindi catedinpat ientswi t
    hconcor dantresult
    sfrom the
    cli
    nicalexami nati
    onandechocar diogram duet other i
    skoft hepr ocedure,parti
    cular
    lyin
    regardt ost r
    oker iskcrossingthest enot
    icaor t
    icvalve(Cl assIIIrecommendat ion)
    . 

    Neithersurgerynorcat
    heter
    -basedaor
    ti
    cvalvereplacementshoul
    dbeconsi
    deredunti
    lthe
    severit
    yoft heASisdeter
    mined.Adobut aminestudyisnotindi
    cat
    edunl
    essthecardi
    ac
    outputislow. 

    Quest
    ion:

    22. A74- year


    -oldwomanpresentstoyourcl
    ini
    cwit
    ha1- monthhistor
    yofpr ogr
    essive
    shor
    tnessofbr eathandankl
    eedema.ShehasNewYor kHeartAssociati
    on( NYHA)functi
    onal
    cl
    assIIIheartfai
    lur
    e.Hermedicalhi
    stor
    yincl
    udeshypert
    ensi
    onandhyper l
    ipi
    demia,butshe
    hasotherwisebeenhealt
    hy.

    Onexamination,
    hervi t
    alsi
    gnsarenormal.Ther
    eisanel evat
    edjugularvenouspr essuretot
    he
    j
    awwi t
    hnoCVwave.Thecar oti
    dsdonotappeartohaveadel ay.Therewasasi ngl
    esecond
    hear
    tsoundandagr ade3/6late-
    peaki
    ngsystol
    iceject
    ionmur muralongt hesecondr i
    ght
    i
    nter
    costalspaceradiati
    ngtothecarot
    ids.Thel
    eftvent
    ricl
    e(LV)isenlargedwithpalpableA
    wave.Thereisnoedema.

    Atwo-dimensionalechocardi
    ogram r
    eveal
    samoder
    atelydil
    atedLVwithacal
    culat
    edeject
    ion
    fr
    act
    ionof36%.Ther eisglobalhypoki
    nesi
    sandmoderateLVhypertr
    ophy.Aconti
    nuouswave
    Dopplerechocardi
    ogram acrosstheaor
    ti
    cval
    vei
    sshowni nFigure1.
    Cardi
    accathet
    eri
    zat
    ionr
    eveal
    ednosigni
    fi
    cantcoronar
    yarter
    ydiseaseandmi
    ldpul
    monar
    y
    hyper
    tensi
    onduetoanelevat
    edpul
    monarycapil
    larywedgepressur
    e.

    Whi
    choft
    hef
    oll
    owi
    ngwoul
    dyounowr
    ecommend?

    a. Referfortr
    anscathet
    eraorticval
    verepl
    acement(TAVR)
    .
    b. Medicalmanagement .
    c. Referforsurgi
    calaort
    icvalverepl
    acement(SAVR).
    d. Dobutamineechocardiogram.

    Answer
    :

    22. c. Ref
    erf
    orsur
    gicalaor
    ti
    cval
    ver
    epl
    acement(
    SAVR)
    .

    Thecorrectansweri
    sSAVR.Theechor eveal
    sapeakveloci
    tyaort
    icst
    enosi
    s(AS)j
    etofat
    l
    east4msec, confi
    rmingsevereAS.Thus,thi
    spat
    ienthassymptomati
    cASwi t
    hahighmean
    gradi
    entandLVdysf unct
    ion.
     

    Theuseofdobut amineechocar
    diogr
    aphyisreservedforlow-
    gradi
    ent,
    loweject
    ionf
    racti
    on
    (EF)AS(ClassI
    Ia).Iti
    sdefi
    nedasameangr adientof≤30mm HgandanEF<40%.
    Dobutamineisi
    nf usedtoamaximaldoseof20mcg/ kg/
    mi nt
    odisti
    nguishbet
    weentrueAS
    and“pseudo-AS”(i
    .e.,
    severeLVdysfunct
    ionandnotsever
    eAS).I
    fameangradientof>40mm
    Hgcanbeachi evedwi t
    ht hedobut
    amineinf
    usion,t
    henonecanassumet
    hevalveandnotthe
    vent
    ri
    cleistheli
    mitingfactori
    nthecl
    ini
    calsyndrome.
     

    Thispat
    ienthasnosigni
    fi
    cantcomor bi
    dit
    iesi
    nherhi
    stor
    y.Theref
    ore,
    shewouldnotbe
    consi
    deredacandidatef
    orpercutaneousTAVR.Ther
    eisnoroleformedi
    calmanagementof
    sever
    esympt omat
    icAS,excepttoreli
    evesymptomspri
    ortoval
    verepl
    acement
    . 

    Quest
    ion:

    23. A54- year


    -oldwomanpr esentstotheambul at
    orycli
    nicforevaluat
    ionofshor t
    nessof
    breath.Shehasbeenf ol
    lowedf ormitr
    alstenosiswit
    hahistoryofrheumat i
    cfeverattheage
    of14year s.Twomont hsago,shebeganexper ienci
    ngsomemi l
    ddyspneadur inglight
    exercise,suchasj oggi
    ngandi ndoorcycli
    ng.Shewor ksasanur se,andwhileshehasbeen
    abletocont inuetowork,shefeelsmor eti
    redthaninyearspast.Shehasnopal pi
    tati
    onsand
    shedeni esanyot herheartf
    ail
    ur esymptoms. 

    Atranst horacicechocar di
    ogr am showsnor malleftvent
    ricularsystol
    icfuncti
    on( ej
    ecti
    on
    fr
    action65%) .Mitr
    alstenosi sispr esentwithameanmi tralgradientof5mm Hganda
    calculatedvalveareaof1. 9cm2  (atheartrate60bpm) .Theval veappear spli
    ablewithno
    commi ssuralcalci
    fi
    cation( herechoscor e=7).Sheunder goescar di
    accatheteri
    zati
    onandthe
    i
    nvasi vely-
    derivedmitr
    algr adi entmeani s12mm Hgwi thami t
    ralvalveareacalcul
    atedtobe
    0.9cm2.Mi l
    dpul monaryhyper t
    ension(40/ 20withmean29mm Hg)i spresent.Coronary
    angiogr aphyshowsnoat herosclerosis.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epf
    ort
    hispat
    ient
    ?

    a. Cardiopul
    monaryexer ci
    setest
    .
    b. Transesophagealechocardi
    ography(TEE)
    .
    c. Repeatresti
    ngechocar di
    ogram i
    n6mont hs.
    d. Cardiacmagneticresonanceimaging(MRI).

    Answer
    :

    23. a. Car
    diopul
    monar
    yexer
    ciset
    est
    .

    Thecor
    rectansweri
    saf
    unct
    ional
    test(
    car
    diopul
    monar
    yst
    resst
    est
    ).

    Thepat i
    entpresentswi thmi l
    dquest ionabl esympt oms, andherechocar diographi
    cf i
    ndings
    suggestonl ymoder at
    emi t
    ralst
    enosi s.However ,theinvasi vehemodynami cdatasuggest
    moresever edisease.Int hi
    sdiscrepancy, theinvasivedat amaybei ncorrectduetot heuseof
    pulmonar ycapi l
    lar
    ywedgepr essur ef orcal cul
    ati
    onoft hemi tr
    algradient.Pulmonarycapill
    ary
    wedgepr essuresaccur atel
    yreflectmeanl eftat
    rial(
    LA)pr essurei
    nt hevastmaj ori
    tyof
    pati
    ent s.However ,pul
    monar ycapill
    ar ywedgepr essur es( PCWP)cannotal waysber el
    iedupon
    fortheaccur atecalculati
    onoft hemi t
    r algradientduet ot hecharacteri
    sti
    ct emporaldelayand
    dampi ngoft heydescenti nthePCWPt racing.Anat r
    ialt r
    ans-sept
    alpunct uretomeasur etrue
    LApr essureandgr adi
    enti soneopt iont hatcoul dresolvet hegradientdiscrepancyissue. 

    Doppl
    erechocar
    diogr
    aphyi
    snotal
    waysr
    eli
    abl
    eforassessmentoft
    het
    ransmi
    tr
    algr
    adi
    ent
    ei
    ther
    ,andinfactt
    hecur
    rentguidel
    inepref
    erst
    heuseoft
    hepr
    essur
    ehal
    f-
    ti
    met
    odeci
    de
    sever
    it
    y(>220msecisconsi
    deredsevere).
     

    Inthispati
    ent,f
    urthereval uati
    oni sindicat
    edtoassessherf unct
    ionalst atus.Astress
    echocardiogram wouldbeoneopt i
    on,andacar di
    opul monarystresst estanother.Balloon
    mitralval
    vulopl
    astywoul dbei ndicatedinthepresenceofelevatedt ransmi tr
    algradient(>15
    mm Hg)dur i
    nganexer ci
    sest udyori nthepresenceofasi gnifi
    cantcar diaclimit
    ationby
    cardiopul
    monar ystresst esti
    ng.Bal l
    oonmi tr
    alvalvulopl
    astywoul dbepr efer
    redoversur gical
    valverepl
    acementduet othepl i
    ablenat ur
    eofthel esi
    onandt helowechoscor e.Shewoul d
    needaTEEanywaypr i
    ort oaper cutaneousvalvuloplast
    yprocedur e.Car diacMRIwoul dnotbe
    l
    ikelytoaddanyaddi t
    ionalinformat i
    on.

    Quest
    ion:

    24. A22- year-


    oldwomanpr esentsf
    orroutinefol
    low-upinyourmedi caloff
    ice.Whenshe
    was13yearsold,t
    hepati
    entsuffer
    edfrom rheumati
    cf everwi
    thcar di
    ti
    s,andrecoveredful
    ly
    withmedi
    calther
    apyal
    one.Shenowexer cisesregular
    lyasar unnercovering4mi l
    esin35
    minut
    esseveralt
    imesperweek.Thereisnohi st
    oryofatri
    alar
    r hyt
    hmiasorpr i
    orembolic
    event
    s.Sheisonnomedicati
    onexceptbirt
    hcont rol
    pill
    s.

    Onphysicalexaminat
    ion,sheis67i nchestal
    landwei ghs127lbs.Herbloodpressurei s
    122/72mm Hgandhear trat
    eisr egul
    arat76bpm.Lungsar eclear
    .Herr i
    ghtheartpressur
    es
    appearnormal.Thefi
    rstheartsoundi si
    ncreased.Bothcomponentsoft hesecondhear t
    soundarenormal.Asof tear
    lydiastol
    icrumbleispresentt
    hatisprecededbyacr ispopening
    snap.Thereappearst
    obewi deseparati
    onofA2-openingsnapinterval
    .Noper i
    pheraledemais
    present
    . 

    Theechocardi
    ogram showsr heumaticmi t
    ralst
    enosis.Themeant r
    ansmi t
    ralgradi
    entis4mm
    Hg,whichisobservedatahear tr
    ateof88bpm.Byt hepr essurehalf
    -ti
    memet hod,
    themi tral
    2
    val
    veareaiscalculat
    edtobe2. 3cm .Trivi
    al mi
    tralr
    egurgitat
    ionispresent.Themitralvalve
    appearspl
    iabl
    e(echocardi
    ographicscore=2) .Withsupinebicycleexerci
    seandani ncreasein
    herheartr
    ateto122bpm, themeanmi t
    ralgradi
    entincreasest o8mm Hg.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    enextr
    ecommendat
    ionf
    ort
    hispat
    ient
    ?

    a. Vi
    tami nKant agonistt
    herapy.
    b. Transesophagealechocardiography(TEE)
    .
    c. Oralpenici
    ll
    inV250mgt wi cedail
    y.
    d. Surgicalmit
    ralvalverepl
    acement .
    e. Percutaneousballoonmitralval
    votomy.

    Answer
    :

    24. c. Or
    alpeni
    cil
    li
    nV250mgt
    wicedai
    ly.

    Thecorrectansweriscontinuedpeni cil
    li
    nprophylaxis.Fi
    gure1out l
    inestheguidel
    ineoptions
    thati
    ncludeoralpenici
    ll
    inVt wicedaily,monthlybenzathinepenici
    ll
    inGintramuscular
    i
    njecti
    on,ordail
    ysulfadi
    azine.Cur r
    entguideli
    nesal sorecommendcont i
    nuinganti
    biot
    icsfor
    secondarypreventi
    oninpat i
    entswi t
    hr heumaticfeverandcardit
    is(Figure2).Fort
    hose
    pati
    entswithresi
    dualvalvulardisease,therecommendeddur at
    ionistocont i
    nuepenicil
    li
    n
    prophylaxi
    sfor10year sfrom t
    helastepisodeofacuter
    heumat i
    cf everorunt
    ilt
    heageof40.I
    f
    therewasacutecar dit
    is,
    butnor esi
    dualvalvedi
    sease,t
    herecommendat i
    onisfor10year
    sor
    untilage21(whicheverislonger)
    .Ift
    herewasr heumati
    cfeverwithoutcardi
    ti
    s,the
    recommendat i
    onisf or5yearsoruntilt
    heageof21( whicheveri
    sl onger)
    . 

    Thepatienthasevidenceofrheumat icmitr
    alstenosisonphysicalexami nationand
    echocardi
    ography.However ,herl
    esionseveri
    tycur r
    entl
    yismi l
    d,andshei sasympt omatic
    wit
    hnoevi denceforpulmonar yhypertensi
    on.Thus, t
    hereisnoindicati
    onf oreither
    percut
    aneousorsur gi
    caltherapy.TEEwoul dbei ndi
    catedtoruleoutleftatri
    althrombusin
    pati
    entsbeingconsideredforpercut
    aneousbal loonmi t
    ralval
    votomy.Avi taminKant agoni
    st
    wouldber equi
    redifatr
    ialarr
    hythmiaswer epresentortherewasevi dencef orembolioran
    atr
    ialt
    hrombus.

    (
    Figur
    e1)
    (
    Figur
    e2)

    Quest
    ion:

    25. Youareaskedt
    oseea60-year-
    oldmanwhohashadamur mursincehi
    steenageyear
    s.
    Heent
    eredmi
    li
    tar
    yser
    vice,
    however
    ,andhasnotseenacar
    diol
    ogi
    stsi
    ncethen.
     

    Hefinal
    lyhadarout
    inephysi
    cal
    examinati
    onwit
    hhisi
    nter
    nist
    ,whoor
    der
    edan
    echocar
    diogr
    am andDoppler
    ,wi
    ththefol
    lowi
    ngper
    ti
    nentr
    esult
    s: 

    •Leftventriculareject
    ionfracti
    on(LVEF):55% 
    •LVwal lthickness:1.1cm 
    •Esti
    mat edpul monaryarterypressur
    eviatri
    cuspi
    dregur
    git
    ant(
    TR)jetvel
    oci
    ty:40mm Hg 
    •Aorti
    cval vet hickeni
    ng/calci
    fi
    ed 
    •Aorti
    cDoppl er:Peakinstantaneousgradi
    ent:3.
    6msec,meangradi
    ent30mm Hg, est
    imat
    ed
    aort
    icvalvear ea( AVA):1.1cm2 
    •Aorti
    cr ootsize:2. 8cm 
    •Leftatr
    ialsize:3. 8cm 

    Thepat
    ientcl
    aimshehasnot
    icedanincr
    easei
    nexer
    ti
    onaldyspneal
    atel
    yandisunableto
    cl
    imbafli
    ghtofst
    air
    swit
    houtgett
    ing“wi
    nded.
    ”Hehasnothadsyncopeorpr
    esyncope,but
    doeshavesomechestt i
    ght
    nessatt
    imeswithext
    remeexer
    ti
    on.Hedeni
    esanyor
    thopnea,
    paroxysmalnoct
    urnal
    dyspnea,
    edema,orpal
    pit
    ati
    ons.
     

    Onexami nati
    on,hisbl
    oodpr essurei s120/80mm Hgandhear tratei
    s78bpm.Hi slungsare
    cl
    ear .Hehasnoj ugul
    arvenousdi stenti
    onorhepat oj
    ugul
    arrefl
    ux.Hiscarot
    idsuggestslow
    volt
    agewi t
    hdelayandt her
    ei satransmi t
    tedaorticmurmur.HehasamodestLVheavei nthe
    l
    eftlater
    alposi
    tionwithapalpableAwave.Onauscul t
    ati
    on,t
    hereisasystol
    icmur murthatis
    crescendo-
    decrescendoinnat ur
    ewi thmi dpeakingandasingleS2. 
    Noeject
    ioncl
    ickisheard.
    ThereisanS4.Noaor ti
    cregurgit
    ationormi tr
    alregurgi
    tat
    ioni
    saudi bl
    e.Ther
    eisnoedema.

    Whati
    sthenextst
    epi
    nhi
    smanagement
    ?

    a. Car
    diacmagnet
    icresonanceimagi
    ng(MRI)
    .
    b. Car
    diaccat
    het
    eri
    zation.
    c. Car
    diaccomput
    edt omography(
    CT).
    d. Si
    ngle-
    phot
    onemissioncomputedtomogr
    aphy(
    SPECT)myocar
    dialper
    fusi
    on.

    Answer
    :

    25. b. Car
    diaccat
    het
    eri
    zat
    ion.

    Thecor r
    ectanswerist oproceedwithcardiaccathet
    erizat
    iongivenhissympt omat i
    cstatus
    andthedi scr
    epancybet weentheclini
    calfi
    ndingsandt heecho/Doppler
    .Givenhi sage,the
    pati
    entli
    kelyhasabi cuspidaorti
    cvalveandal t
    ernat
    iveimaging,suchascardi acMRIandCT,
    areclear
    lyofvalueindecipheringwhetherhehasanassoci at
    edaorti
    caneur ysm, evenwhen
    theechodoesnotsuggestanenl argedaorta.
     

    CardiacMRImi ghtbeabl etoclar


    ifyt heaorti
    cvalvesever i
    tyandpr ovi
    dequanti
    tat
    iveLV
    functi
    onaldat
    a, buti
    sanunnecessar yst
    epi fyoubelievethepat i
    enthassymptomat i
    caorti
    c
    stenosis(
    AS)basedont hecli
    nical exam (i
    .e.,
    lossofej ect
    ionsound, mi
    d-l
    atepeakingaort
    ic
    mur mur,l
    ossofA2 result
    inginasi nglesecondhear tsound) .Cardi
    acMRIcanal soprovide
    evidenceofpr
    iormyocar diali
    njuryandmyocar dialperfusi
    on.Hedoeshavesomechest
    pressure,
    butamyocar di
    alperf
    usionst udyi snothelpfulindecipheri
    ngtheseveri
    tyofhisAS. 

    Iti
    sconsideredaClassIindi
    cati
    on(LevelofEvi
    denceC)toproceedt
    oaninvasi
    vest
    udyi
    n
    symptomaticpati
    entswherethereappearstobeadiscr
    epancybetweent
    he
    echocar
    diographi
    cfindi
    ngsandt hecl
    ini
    calexam andhi
    stor
    y. 

    Quest
    ion:

    26. A40- year-


    oldwomanpr esentsforrout
    inegener almedi
    calevaluation.Thr
    eeyear
    sago,
    sheunderwentpercutaneousclosureofanostium secundum atr
    ialseptaldefect
    .Att
    hatti
    me,
    ther
    ightventr
    icl
    ewasmoder at
    elydilat
    edanddysfunctional
    ,butshewasasympt omati
    c.She
    hasdonewel lsi
    ncetheprocedure,andreport
    snosympt oms. 

    Herphysi
    calexaminat
    ionisunremarkabl
    e.Transthor
    acicechocardi
    ogr
    aphy(TTE)
    demonstr
    atesnormall
    eftventr
    icul
    ar(LV)f
    unction(ej
    ecti
    onfracti
    on65%).Theri
    ghtvent
    ri
    clei
    s
    mil
    dlyenl
    argedwithmilddepr
    essionofsystol
    icfunct
    ion. 
    Onechocardi
    ography,theatri
    alseptaloccl
    uderi
    swellvi
    sual
    izedattheatr
    ialsept
    um wit
    hno
    evi
    denceofdevi
    ceer osion.Dopplercolorf
    lowacr
    osstheatr
    ialsept
    um showsnor esi
    dual
    shunt
    ing.Abubblestudyi snor
    mal .

    Thepati
    entwi
    llbeunder
    goi
    ngarouti
    necleani
    ngofhert
    eet
    hint
    henextmont
    h.Shewoul
    dli
    ke
    toknowabouttheneedf
    orant
    ibi
    oti
    cprophyl
    axi
    s.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    enextst
    epf
    ort
    hispat
    ient
    ?

    a. Amox i
    cil
    lin2g,30-60minutespriortotheprocedure.
    b. Cl
    indamyci n600mg, 30-60minutespriort
    ot heprocedure.
    c. Peni
    cil
    linG250mg, 30-60minutespr i
    ortotheprocedure.
    d. Noantibioti
    cprophyl
    axisisi
    ndicated.
    e. Amox i
    cil
    lin4g,30-60minutespriortotheprocedure.

    Answer
    :

    26. d. Noant
    ibi
    oti
    cpr
    ophyl
    axi
    sisi
    ndi
    cat
    ed.

    Shedoesnotneedant i
    bioti
    cprophyl axis.Antibioticpr ophylaxisi sindi
    cat edforpat i
    entswi th:
    1)prost
    het i
    ccar diacvalvesorpr osthet i
    cmat eri
    al usedf orvalver epai
    r,2)pr i
    orinfecti
    ve
    endocardit
    is,3)unr epair
    edcyanot iccongeni t
    al hear tdisease, 4)sur gi
    callyorper cutaneously
    repai
    redcongeni talheartdefectsdur ingt hefirst6mont hsaf t
    ert heprocedur e,5)repai r
    ed
    congenit
    alhear tdiseasewi thresidual defectsatt hesi teoradj acenttothesi teofapr osthesis,
    or6)cardiactranspl antreci
    pientswi thval vul
    ardi seaseduet oast r
    ucturallyabnormalval ve.It
    shouldalsobeconsi deredinpat i
    entswhohaveanact ivesour ceofi nfection.Thecor rectdose
    ofamoxicill
    in,whenused, is2g, 20-60mi nutesbef oret heprocedur e.

    Quest
    ion:

    27. Thedeci si
    ont oint
    erveneandtheappropri
    atechoiceofint
    erventi
    oninvalvularhear
    t
    di
    seaseshoul
    dbebasedont heri
    sk-benef
    itanal
    ysi
    sthatincludestheoperat
    ivemor tal
    it
    y,t
    he
    pat
    ient
    ’sdegr
    eeoffrail
    ty,
    thenumberofcur r
    entmajororgansystemst hatar
    edysf uncti
    onal
    ,
    andanyspeci
    ficpr
    oceduralimpedimentsthatwouldl
    imittheli
    keli
    hoodthattheprocedure
    wouldbeasuccess.
     

    Inyourevaluationofan80- year-ol
    dpat ientwithsever eaorti
    cstenosis(AS),youdetermine
    thathi
    sSoci etyofThor aci
    cSur geons( STS)pr edict
    edr i
    skofmor tali
    ty(PROM)i s7.0%.Hei s
    rel
    ati
    velyactive,li
    vesalone,andcont inuest oplaygolfont heweekends.Hehasmoder ate
    chronickidneydiseasewi thacreatinineof1. 9mg/ dl.Thoughapr iorsmoker ,
    hismostr ecent
    pulmonaryf unctiontestshavenotsuggest edsignif
    icantlungdisease.Hehadapr iorbypass
    procedureandabdomi nalaorti
    caneur ysm r epair
    .Heot herwisehasf el
    twellunti
    lrecentl
    y,
    whenhehasnot edsomedyspneaonexer ti
    on.Hi saorti
    cvalvemeangr adi
    entisnow
    esti
    mat edat45mm Hgandt heaorticval vear eais0.7cm2.

    Basedont
    helat
    estguidel
    ines,
    hiscombi
    nedr
    iskassessmentwoul
    dpl
    acehi
    mint
    owhi
    chof
    t
    hef ol
    l
    owi
    ngcategor
    ies?

    a. Hi
    ghri
    sk.
    b. Pr
    ohi
    bit
    iver
    isk.
    c. Lowrisk.
    d. Int
    ermediat
    eri
    sk.

    Answer
    :

    27. d. I
    nter
    medi
    ater
    isk.

    Thecor r
    ectanswerisint
    ermedi
    ater
    isk.Thel
    atestval
    vularhear
    tdi
    seaseguidel
    inessuggest
    thattheri
    sk-
    benefitf
    orpati
    ent
    sneedingaval
    vularint
    ervent
    ioncanbebestdefi
    nedusingthe
    foll
    owingguidel
    ines:
     

    1. Lowr i
    sk:STSPROM <4.0%AND noevidencef
    orfr
    ail
    tyAND 
    noot
    hermaj
    oror
    gan
    syst
    em dysf
    uncti
    onAND noprocedur
    alspeci
    fi
    cimpediment
    . 

    2. Int
    ermedi
    ateri
    sk:STSPROM 4-8%OR atl
    eastonei
    ndexoff
    rai
    lt
    y(mi
    ld)
    OR 
    oneor
    gan
    syst
    em i
    nvol
    vement 
    OR apossi
    blepr
    ocedur
    alimpediment
    . 

    3. Highrisk:STSPROM >8.
    0% 
    OR 
    twoormoreindi
    cesoffrail
    ty(moder
    ate-
    sever
    e) 
    OR 
    up
    tot
    womajororgansyst
    emscompromi
    sedOR 
    probabl
    eprocedurali
    mpediment.
     

    4. Pr
    ohi
    bit
    iver
    isk:Pr
    edi
    ctedsurgical
    riskormaj ormor bi
    dit
    yat1yearof>50% 
    OR 
    thr
    eeor
    moremaj
    oror
    gansystemscompr omised 
    OR  sever
    epr ocedurali
    mpedi
    ment. 

    Inthepat ientdescr ibed,hissur gicalriskf rom t heSTSscor epl aceshi mi nthei ntermedi ate
    ri
    sk.Heal sohassomemi ld-moder atecompr omi seinhi sr enalf unct ion, buthehasnoobvi ous
    frai
    ltydespi tehisageandt her ei snocl earpr ocedur al i
    mpedi ment ,althoughcomput ed
    tomogr aphy( CT)mi ghtbeusef ul t
    odeci dei fhispr i
    orcor onar ygr aftsar eadher i
    ngt ohi s
    sternum.Hewoul dthereforebeconsi der edati ntermedi ater iskbasedont hei nformat ion
    provided.Lowr iskisi ncorrect ,astheSTSscor eistoohi ghandhehasanor gansyst em
    i
    nvol ved.Hi ghr i
    skisi ncorrect ,ashi sSTSscor eisnot>8%andhehasnof railtynort womaj or
    organsyst emsi nvolved.Pr ohi biti
    ver i
    ski si ncor rectfort hesamer easons, ashemeet snone
    ofthemostsever el
    yrest r
    ictivecr it
    eria.Themostdi fficultdeci sioni nt hissi tuationi sof t
    en
    definingf railt
    y.Mostoft heavai l
    ableef fortst oquant i
    fyf rail
    tyt akei ntoaccountt hepat ient
    ’s
    i
    ndependencei ndoi ngr outineact i
    viti
    es, suchaseat ing, bat hing,dr essi ng,transf erri
    ng,
    toil
    eting, i
    ncont inence, ambul ating(wi t
    handwi thoutassi stance) ,andt hedi stanceonecan
    ambul ate.Pr ocedurali mpedi ment scanal sobequi t
    esubj ect i
    ve, buti ncl udet hepr esenceofa
    porcel ainaor ta,lackofvascul araccess, priorchestr adiation, adher entcor onar ygr aftstothe
    sternum, chestmal format i
    on, presenceofat racheost omy, etc. 

    Quest
    ion:

    28. A70- year-


    oldmani sr eferredformanagementofaort
    icstenosi
    s(AS).Heret
    ir
    edthis
    pastyearf
    rom thelocaluniversity.Heandhiswifewalkdai
    l
    yf or30minutesever
    ymor ni
    ng.
    Hedeniesanyexertionall
    imitations,angi
    na,orsyncope.
     
    Anechocar di
    ogram demonst r
    atesanaor ticvelocit
    yof3. 5msec, val
    veareaof1. 0cm2,
    ejecti
    onfract
    ion60%, andmi l
    dleftventr
    icular(LV)hyper t
    rophyi spresent.Hisexam isnotabl
    e
    forthelackofhypertensi
    onorvascul ardisease.Hehasagr ade3/ 6systoli
    cejecti
    onmur mur
    overthebaseoft heheartradi
    atingtothecar oti
    ds, cl
    avicl
    es, andapex.S2 appearspreserved.
    ThereisanS4.Ther eisnoevidenceofr i
    ghtorl eftheartvolumeover load.

    Whi
    choft
    hef
    oll
    owi
    ngdoyour
    ecommend?

    a. Fol
    low-upexam year
    lyandobtai
    nechoonl
    yifexam changes.
    b. Repeatechoin3years.
    c. Fol
    low-uponlyi
    fhedevelopssympt
    oms.
    d. Repeatechoin1year.
    e. Repeatechoin6mont hs.

    Answer
    :

    28. d. Repeatechoi
    n1year
    .

    Thecorrectansweri
    sserialexamsand( year
    ly)echocardi
    ography.Thi
    srecommendati
    oni s
    predi
    cat
    edont hepotent
    ialforsi
    lentandvari
    ableprogressi
    onofAS, andthepot
    enti
    alf
    or
    progr
    essiveLVdysfunct
    ionandt hedevelopmentofotherconcomi t
    antval
    vul
    arhear
    tdisease.
     

    Thef
    requencyoffol
    low-
    upi
    sbasedontheseveri
    tyofdi
    sease:aor
    ti
    cveloci
    ty≥4.
    0msecf
    oll
    ow
    -
    upin1year;>3.
    0-3.
    9msec,
    every1-
    2years;>2.
    0-2.
    9msec,every3-5year
    s. 

    Thispat i
    enthasmoder at
    eAS.Thus, thefol
    low-upechoshoul dbeevery1- 2year
    s.The
    averageannual rat
    eofprogressioninASisani ncr
    easeinaor t
    icveloci
    tyof0.3msec, mean
    gradientof5-10mm Hg, andadecr easei
    naor t
    icvalveareaof0. 1cm2 oncemoder ateASi s
    present.Morerapidprogressi
    oncanbeant i
    cipatedinthepresenceofadvancedageand
    extensiveval
    vularcal
    cifi
    cati
    on,butprogr
    essionishighl
    yvariable.Repeatechocardiographi
    c
    assessmenti sindi
    cat
    edi fsymptomsorachangei nexam develops. 

    Quest
    ion:

    29. Youhavebeenfol
    lowi
    ngf
    oroveradecadea71-
    year-
    oldmanwi t
    hknownbi
    cuspi
    d
    aor
    ti
    cval
    vest
    enosi
    s.Hei
    sacoll
    egeprof
    essorandi
    sveryphysi
    cal
    lyacti
    ve.
     

    Hehadcar di
    acmagnet i
    cresonanceimagingthatreveal
    ednoevi denceforanassociat
    ed
    dil
    atedascendi ngaorta.Hi
    sechoeshaver evealedslowwor seni
    ngoft hesever
    it
    yofhisaorti
    c
    stenosis(AS),andhenowhasapeaki nst
    antaneousDoppl ervel
    ocityof4.
    1msec, an
    estimatedmeanaor t
    icgradientof42mm Hg, andanaor t
    icvalveareaof0.9cm2withnormal
    l
    ef tvent
    ri
    cularfuncti
    on.Hecont inuest
    odenyanyexer ti
    onalsympt omsofchestpressure,
    dyspnea,ordizziness.

    Whi
    choft
    hef
    oll
    owi
    ngi
    stheappr
    opr
    iat
    enextst
    epi
    nhi
    smanagement
    ?

    a. Surgicalaor
    ticval
    vereplacement(
    SAVR).
    b. Exercisestr
    esstest
    .
    c. Transcathet
    eraorti
    cvalverepl
    acement(
    TAVR)
    .
    d. Cont
    inuet
    omoni
    torever
    y6mont
    hs.

    Answer
    :

    29. b. Exer
    cisest
    resst
    est
    .

    Thecorrectanswerisafuncti
    onal
    test
    ,suchasanel
    ectrocardi
    ogram (
    ECG)stresstest
    .The
    pat
    ientnowhasevi denceforsi
    gni
    fi
    cantaor
    ti
    cval
    vestenosis.However,hedeniessymptoms.
     

    Iti
    sr easonabletopr oceeddirectl
    ytosur geryi
    nasympt omaticsevereASi fthegradi
    entis
    “super-severe”(i
    .e.
    ,veloci
    ty>5msecandt hepati
    entisl owrisk(ClassIIaindi
    cati
    on,Levelof
    EvidenceB) ,buthedoesnotmeett hesecrit
    eri
    a.Thus, proceedi
    ngdi r
    ectlytoSAVRi sincorr
    ect
    .
    Hedemonst ratesnohi gh-
    riskfeaturesandhehasabi cuspidaor t
    icvalve,makingan
    evaluationforTAVRi ncor
    rectatthispointtoo.
     

    ASpr ogr essessl owly,andi tissafetomoni torhisechocar di


    ogr amsper iodically,t
    houghever y
    6mont hsmaybet oof requent.Thecor rectansweri s,therefor
    e, toperform anexer ci
    se
    treadmi l
    ltest .Thi
    sshoul dal waysbedoneundert hesupervisi
    onofaphysi cian, wit
    hcl ose
    moni t
    or i
    ngofbot htheECGandbl oodpr essureresponse.Thet estshoul dbeconsi dered
    positi
    vei fanysympt omsar eprovoked, ifthereisanabnor malhemodynami cr esponse
    (hypotensi onoral ackofr ise>20mm Hgi nsystemi cbloodpr essurewi thstress, orST
    abnormal i
    tiesdevelop).Byusi ngthismet hod, upto29%ofpat ientsthoughtt obe
    asympt omat iccanbei dentifi
    edasbei ngl imitedbyt heaorticval vest
    enosi s.Exer ci
    sest ress
    testi
    ngshoul dnotbeper formedi npatientswi thsympt omsofASori nt hosewi th“super-
    severe”AS( meangr adient>55mm Hg) . 

    Quest
    ion:

    30. Youar easkedt oseean87- year-


    oldwomanwhohasknownaor ti
    cstenosi
    s.Shel i
    ves
    i
    nanassi stedlivi
    ngenvi r
    onment ,butisquiteindependentandcont i
    nuestokni
    tandvisitwit
    h
    fri
    endsandf ami l
    y.Shehadapr iorcerebr
    ovascularaccident(
    CVA)2year sago,buthas
    recoveredexceptf orami l
    dr i
    ghtfootdrop,causinghertoambul at
    ewi t
    hacaneorwal ker.Her
    medi calhistoryisalsopositivef
    orhyper t
    ension,mildtype2diabetes,mil
    dobesit
    y,ari
    ghthip
    replacement ,andapr iorcolonresecti
    onf orcoloncancer(12yearsago). 

    Shehasr ecentlynoti
    cedthatherst
    ami
    nahasdecl
    inedandnowshei sdyspnei
    cafter
    ambulati
    ngj ust30-40feet
    .Shehasnoort
    hopneaorpar
    oxysmalnoctur
    naldyspnea,butdoes
    not
    ebilat
    er alankl
    eedema.Shehasnopalpit
    ati
    onsorchestpai
    n,andhasnotfall
    ensinceher
    st
    roke.
     

    Onherexam, shehasobvi oussevereaorti


    cst enosis(AS),andthisi
    sconfirmedbyan
    echocardi
    ogram thatrevealssevereASwi thpr eser
    vedleftvent
    ricul
    arsystol
    icf
    uncti
    on.Her
    peakgradientis4.8m/ secandmeangr adientis50mm Hg, wit
    hanaor ti
    cvalvear
    eaof0.5
    2
    cm .Perti
    nentlaboratorydata,however,r
    eveal hercreati
    ninei
    s3. 2mg/dlandshehasa
    severel
    ycalcifi
    caorta(porcelai
    naorta)onthescr eeningcomput edtomographi
    cangiogr
    am.

    Basedonthepr
    ecedi
    ngf
    indi
    ngs,
    whi
    choft
    hef
    oll
    owi
    ngt
    her
    apeut
    icopt
    ionsdoyou
    recommend?

    a. Per
    cut
    aneousbal
    loonaor
    ti
    cval
    vul
    opl
    ast
    y.
    b. Me di
    caltherapyal
    one.
    c. Transcathet
    eraorti
    cvalverepl
    acement(
    TAVR)
    .
    d. Surgicalaor
    ticval
    vereplacement(
    SAVR).

    Answer
    :

    30. c. Tr
    anscat
    het
    eraor
    ti
    cval
    ver
    epl
    acement(
    TAVR)
    .

    Thecorr
    ectansweri
    sTAVR.Shehassomef r
    ail
    tyandli
    mitedact
    ivi
    ty,
    alt
    houghsheconti
    nues
    toenj
    oyfamil
    yandsedent
    aryact
    ivi
    ty.Percut
    aneousbal
    loonaort
    icval
    vulopl
    ast
    yisnotcorr
    ect
    ,
    asiti
    sareasonabl
    eopt
    iononl
    yasabr idgetoSAVRorTAVR.  

    Shehascr i
    teri
    atobeconsi deredashavi
    ngpr ohi
    bit
    ivesur
    gicalr
    isk,
    givenherpor
    cel
    ainaor
    ta,
    si
    gnif
    icantrenaldisease,
    andCVAwi thr
    esi
    dual.Thishaslef
    therrat
    herfrai
    landwit
    ha
    cal
    culat
    edSoci et
    yofThor acicSurgeon(
    STS)r i
    skof>8%.
    Thesurgicalopti
    onseemsof fthet
    ablef
    orthesereasons.
     

    Shecouldoptf orcontinuedmedicalther
    apyknowingthati
    twi l
    levent
    uallyf
    ailgi
    venthe
    severi
    tyofherAS, orshecoul dbeconsideredacandi
    dateforTAVRi nasetti
    ngwher et
    herei
    s
    ateam ofphysiciansdedicatedtotheprocedur
    e.Basedont henewestguidel
    ines,TAVRis
    recommendedi fpatientshaveanindicati
    onforAVR,buthaveapr ohi
    bit
    iveri
    skforSAVRand
    haveapr edi
    ctedpost -
    TAVRsur vi
    valof>12mont hs.
     

    Quest
    ion:

    31. An84- year-


    oldmanpr esentstothecli
    nicwit
    hmilddyspneaonexer tion.Hismedical
    hist
    oryincludeshypert
    ension,hyperl
    ipi
    demia,chr
    onicki
    dneydisease,andr ecurr
    entgout.Hi
    s
    examinationreveal
    saheartr at
    eof75bpm andabl oodpressur
    eof160/ 65mm Hg.Hehasa
    grade1/6ear l
    ypeakingsystoli
    cejecti
    onmur murinthesecondrighti
    nterspaceandagr ade
    2/4diastoli
    cmur murattheleftst
    ernalborder
    . 

    Theechocardiogr
    am showspr eservedleftventr
    icularej
    ectionf
    racti
    on(
    LVEF)andmoder at
    e
    LVhypert
    rophy.Therewasmoder atelef
    tatrial
    enl ar
    gementandgr ade2di
    astoli
    cdysf
    unct i
    on.
    Theaort
    icvalvewasscleroti
    candt ril
    eafl
    et.Ther egurgi
    tantvol
    umeoftheaorti
    cregur
    gitati
    on
    (AR)i
    sesti
    mat edat35cc/ beatandt hewidthoft hejeti
    s50%oft heLVoutf
    lowt r
    ackdiameter.

    Basedont
    hesedat
    a,whi
    choft
    hef
    oll
    owi
    ngdef
    inest
    hesever
    it
    yofhi
    sAR?

    a. Mil
    d.
    b. Severe.
    c. Tr
    ivial
    .
    d. Mode rat
    e.

    Answer
    :

    31. d. Moder
    ate.

    Asshowninthet
    able(
    Figure1)oft
    hest
    agesofchroni
    cAR, f
    rom t
    he2014AHA/
    ACCval
    vul
    ar
    gui
    del
    ine,
    thi
    spat
    ienti
    swithint
    hemoderat
    erangeofsever
    it
    yofAR.
    (
    Figur
    e1)

    Quest
    ion:

    32. A50- year-


    oldphysi
    cianwitha5-yearhi
    storyofmitralvalveprol
    apsepresentswi
    than
    acutei
    ncreasei nhismurmur .Si
    xweeksagohehadwhathet houghtwasthe"flu"andf
    elt
    poorl
    yforthenextcoupl eweeks.Hehasnowr ecover
    edandi sbackatwor kfullti
    me.Hesays
    hefeel
    swel landnot esnochangeinstamina,chestpain,
    ordyspnea.  

    Hisexam reveal
    sabloodpressur
    eof110/ 76mm Hg, hear
    trat
    eof78bpm, andoxygen
    saturat
    ionof98%.Hisl
    ungsareclearandhiscardi
    acexam reveal
    sagrade4/6holosyst
    oli
    c
    mur muroverthepr
    ecordi
    um andloudestattheapex.Ther
    eisanassoci
    atedS3.
     

    Hisechocardi
    ogram demonstrat
    esaf lail poster
    iorleafl
    etfrom chordalrupt
    ureandan
    2
    eff
    ecti
    veregurgi
    tantori
    fi
    ceof0.35cm , leftventri
    cular(LV)ejecti
    onf r
    acti
    onof60%,end-
    systol
    icdi
    mension4.5cm, andleftatr
    ial dimensionof4. 5cm.Hi select
    rocar
    diogr
    am (
    ECG)
    showssinusrhythm,occasionalpremat ureventricularcontract
    ions,andanarrowQRSwi t
    h
    nonspecif
    icECGchanges.
    Whi
    choft
    hef
    oll
    owi
    ngdoyour
    ecommend?

    a. Li
    sinopril
    .
    b. Carvedil
    ol.
    c. Digoxin.
    d. Surgicalr
    efer
    ral
    .
    e. Continuedobser
    vat
    ion.

    Answer
    :

    32. d. Sur
    gicalr
    efer
    ral
    .

    Thecor rectanswerissurgicalrepai
    r.Al
    thoughthi
    spati
    entclai
    mstobeasympt omati
    c,hehas
    developedacut eseveremi t
    ralregur
    git
    ati
    on(MR)complicatedbyaflai
    lmi t
    ralleaf
    let
    .Hehas
    LVsyst oli
    cdysfuncti
    onexhi bi
    tedbyani ncr
    easedend-
    systoli
    cdimension.Surgical
    managementi sclearl
    yrecommendedatt hi
    sti
    me( Cl
    assI).Ther
    eiscurrentl
    ynocompel l
    ing
    evi
    dencet osupportaft
    erl
    oadr educti
    onorinot
    ropi
    cagents,suchasdigoxin,inanysituat
    ion
    butinacut edecompensat edMR.

    Quest
    ion:

    33. A34- year-oldwomani sref err


    edt oyouwi thshor tnessofbr eathandt henewonsetof
    atr
    ialf
    ibril
    lation.Afteryourexami nationandf oll
    owi ngtheper f
    ormanceoft hechestwall
    echo/Doppl er,youf indshehassi gnificantmi tr
    al stenosis(meangr adient15mm Hg)wi t
    h
    mildmitralregur git
    at i
    on(MR).Herest i
    mat edpul monar ysyst oli
    cpr essur esar eel
    evatedat64
    mm Hgandherl eftatri
    alsi
    zeis5. 0cm.Herval vularleafl
    etsappearf usedont he
    echocardiogr am, butthereissti
    llgoodmobi l
    it
    ywi thmi ld-moder ateval vularthi
    ckeni
    ng,only
    minimalcal cium, andmi ld-
    moder atesubmi tr
    alscarandr etracti
    on.Youconcl udethatherecho
    scoreforthisi sappr oximatel
    y8.However , youar econcer nedr egar dingthesever i
    tyofherMR,
    butthetranst horacicechosuggest sonl ymi l
    dMRt houghi tisclearlyaudi bleonexam.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextappr
    opr
    iat
    est
    udy?

    a. Cardiaccathet
    eri
    zation.
    b. Cardiacmagneticresonanceimaging(MRI)
    .
    c. Cardiaccomputedt omography(CT).
    d. Transesophagealechocardi
    ography(TEE)
    .

    Answer
    :

    33. d. Tr
    ansesophagealechocar
    diogr
    aphy(
    TEE)
    .

    Thecor r
    ectansweri saTEE.Pati
    entswit
    hr heumat i
    cvalvularmi tralstenosi shavebeenshown
    todowel lf
    ollowingper cut
    aneousball
    oonmi tralval
    vulopl
    ast yiftheval veispl i
    abl
    ewith
    commi ssuralfusion.Long-t
    ermresul
    tsmirrorthoseofsur gicalcommi ssur otomy.Thi
    spati
    ent
    hasindicat
    ionsf orinter
    venti
    oninhermitr
    alstenosis,ashermeangr adientis>10mm Hgata
    hear
    trate<70bpm, therei
    spulmonaryhypertensionandat r
    ialfibril
    lati
    on, andsheis
    symptomat i
    c.Themit
    ralvalvei
    ssai
    dtobeamenabl etoapercutaneousapproachwi
    th
    rel
    ati
    velyl
    owechoscor e.Eachcomponentoftheechoscor
    eisgr aded1-4,
    wi t
    h4beingthe
    mostsevere.Thecomponent si
    ncl
    udevalvul
    armobili
    ty,
    val
    vularthi
    ckeni
    ng,theamountof
    cal
    cif
    icati
    on,andtheamountofsubmitr
    alapparat
    usscarandr et
    racti
    on.
     

    Notincludedi nthescor i
    ngsyst em, however,i
    st hedegr eeofMR.Thepr ocedureisineffective
    i
    ftheMRi s>2+.Thenextbestt estt odecidethatist heTEE.Thi swoul dbeneededr egar dl
    ess
    ofwhet herabal loonvalvuloplastypr ocedur
    ei sproposed, sinceanat ri
    althrombusneedst o
    beexcludedbef orethepr ocedurecanbeper formedsaf ely.CardiacMRIcanest imatet he
    degreeofMRbynot i
    ngt heregurgi tantfl
    owand, ifpr operl
    yobt ained,canpr ovi
    desome
    evidencef oranat ri
    alappendaget hrombus;thus, itwoul dbeasecondchoi ceinthissituation.
    Thecar diacCTwoul dnotpr ovidet heMRsever i
    tyi nformation,andcar di
    accat heter
    ization
    shouldber eser
    vedf oreitherresolvingunclearinfor mationf rom thenoninvasivestudiesorf or
    theactualpr ocedure. 

    Quest
    ion:

    34. Youhavebeenaskedt oconsul tona30- year-ol


    dwomanwi thsymptomati
    csevere
    rheumat i
    cmi tr
    alstenosis,whoappear stohavear elat
    ivel
    ylowechoscoreforsuccessusi
    ng
    ball
    oonmi tralvalvul
    oplasty.Priort
    ot hepr ocedure, youobtainatr
    ansesophageal
    echocardiogrm( TEE)thatr evealsaleftatri
    alappendaget hrombus.Shehasneverhada
    cli
    nicalembol i
    ceventandi sinnormal sinusr hythm att heti
    meoftheTEE.Hercurrent
    medi cat
    ionsincludeaspi r
    in81mgdai l
    y,furosemi de40mgdai l
    y,spir
    onol
    actone12.5mgdail
    y,
    andmet oprolol25mgt wicedai l
    y.Shei salsot akingabi rt
    hcontr
    olpil
    l.

    Basedont hi
    sinfor
    mati
    on,
    your
    ecommendr
    epeat
    ingt
    heTEEi
    n4-
    6weeksbef
    oreat
    tempt
    ing
    t
    hemi t
    ralval
    vulopl
    ast
    y.

    Dur
    ingt
    hatt
    ime,
    whi
    choft
    hef
    oll
    owi
    ngdoyoual
    sor
    ecommend?

    a. Di
    sconti
    nuet hebi
    rthcont
    rolpi
    ll
    .
    b. Begi
    ndabi gat
    ranat150mgt wi
    ceaday.
    c. Begi
    nwar fari
    n.
    d. I
    ncreasetheaspir
    indoseto325mgaday.

    Answer
    :

    34. c. Begi
    nwar
    far
    in.

    Thecor rectansweri
    st oini
    ti
    atewarfar
    intherapy.Whilebeingont hebir
    thcontrolpil
    lmay
    contri
    but etoahypercoagul
    ablestat
    e,therearenodat athati
    tsdisconti
    nuati
    onwoul dr esul
    tin
    dissol
    utionoftheappendaget hrombus.Similar
    ly,t
    herearecurrentl
    ynodat athatinapat i
    ent
    withvalvulardi
    seaseandpar oxysmalatri
    alf
    ibri
    llat
    ionthatei
    therincr
    easingtheaspirindose
    ortheuseofotherant
    it
    hrombinagent
    s,suchast henovelant
    icoagul
    ants,
    issuperi
    ortothe
    useofwarfar
    in.I
    ndeed,t
    henoveloral
    anticoagul
    antsarecont
    raindi
    catedforat
    ri
    alfi
    bri
    ll
    ati
    on
    ther
    apyinpati
    entswit
    hmi t
    ral
    stenosi
    s. 

    Theuseofwar fari
    nint hissetti
    nghasaCl assIindi
    cati
    on( LevelofEvi
    denceB) .Avit
    aminK
    antagonistal
    soi sindicatedinmi t
    ral
    stenosispati
    entswithparoxysmal,persi
    stent
    ,or
    permanentat r
    ialfi
    bril
    lati
    on, ori
    nthosewhohavehadapr i
    orembol i
    cevent.Themostr ecent
    guidel
    inealsohasadded, asaClassIIbindi
    cati
    on(LevelofEvidenceC),thatvi
    taminK
    antagonistsbeconsi deredwhent hemi t
    ralval
    veareais55mm byTTE, ori
    ftherei
    s
    spontaneousleftatri
    alappendageoncont rast
    .

    Quest
    ion:

    35. A63- year-


    oldmanwi thNewYorkHear tAssociationclassIheartfail
    urepresentsto
    yourcl i
    nicwi t
    hanewl ydiagnosedhear
    tmur mur .Hisechocar di
    ogram revealsaleftventr
    icul
    ar
    (LV)end- syst ol
    icdiameterof50mm andLVej ect i
    onfraction(EF)of55%.Ther eispost er
    ior
    mitralleafletprolapsewi t
    hcol orf
    lowevi
    dencef orsignif
    icantmi tr
    alr
    egur gi
    tati
    on(MR) .The
    2
    effecti
    ver egur gi
    tantorif
    ice(ERO)ismeasuredat45mm .Hi sbloodpressureduringthe
    exami nationi s140/ 80mm Hg.

    Basedont
    heechocar
    diogr
    aphi
    cfi
    ndi
    ngs,
    whi
    choft
    hef
    oll
    owi
    ngwoul
    dyour
    ecommend?

    a. Mitr
    alvalverepl
    acement.
    b. Repeatechocardi
    ogram i
    n6mont hs.
    c. Mitr
    alvalverepai
    r.
    d. Endovascularmit
    ralval
    verepai
    r.

    Answer
    :

    35. c. Mi
    tr
    alval
    ver
    epai
    r.

    Thecorrectansweri
    smi tr
    alvalverepai
    r.Thepat
    ienthassever
    eMRbyquant i
    tat
    ive
    2
    echocar
    diography(r
    egurgit
    antvolume>60ccandERO>40mm ) .Alt
    houghheis
    asymptomat i
    c,t
    heventr
    icl
    ei sdil
    atedandtheEFisnotnormalint heset
    ti
    ngofsevereMR.
     

    Iti
    saCl assIindicati
    ontoreferforsur
    gicalr
    epairinanasympt omat
    icpat
    ientwi
    thsevereMR
    withanEFbet ween30- 60%and/ oranend-syst
    olicdiamet
    er>40mm.I sol
    atedposter
    iorl
    eaf
    let
    prolapseisi
    dealf orval
    verepairwit
    ha>90%chanceofsuccess.Endovascul armit
    ralval
    ve
    repairi
    snotindicatedinthi
    spat i
    entwhoisnotathi ghsur
    gicalri
    sk.

    Quest
    ion:

    36. A51- year-


    oldwomani sreferr
    edtoyouwi thmi t
    ralval
    vepr ol
    apseandsever emi t
    ral
    regurgi
    tat
    ion( MR).ShehashadknownMRf ormanyyear sandhasbeenf ol
    lowedwi t
    hserial
    echocardi
    ogr aphy.Hermostrecentecho/Dopplerrevealssevereposter
    iorleaf
    letprol
    apse
    withavalvularaneurysmalbul
    geandpossi blet
    or nmi t
    ralchord.Theprolapseinvol
    ves
    approxi
    mat elyone-t
    hirdoft
    hepost er
    iormit
    rall
    eaflet.
     
    Theot
    herf
    eat
    uresofherechocar
    diogr
    am ar
    easf
    oll
    ows:
     

    •Lef
    tvent ri
    cular( LV)end- diastol
    icdimension:5.
    8cm 
    •LVend- systolicdimensi on:4. 1cm 
    •LVejectionf racti
    onest imat e:50% 
    •Eff
    ecti
    ver egur gitantori
    fice( ERO):0.45cm2 
    •Mil
    dt r
    icuspidr egur gi
    tation 
    •Pulmonar ysyst olicpressur eesti
    mat e:45mm Hg 
    •Nomi t
    ralgr adient  
    •Noaorticval vedi sease 
    •Mil
    dLVhyper trophy

    Basedont
    hesedat
    a,whi
    choft
    hef
    oll
    owi
    ngwoul
    dbet
    henextappr
    opr
    iat
    est
    epf
    ort
    hispat
    ient
    ?

    a. Af
    terloadreducti
    on
    b. Mitr
    alvalverepai
    r.
    c. Exerciset
    esti
    ng.
    d. Mitr
    alvalverepl
    acement
    .

    Answer
    :

    36. b. Mi
    tr
    alval
    ver
    epai
    r.

    Thecor r
    ectansweri smi t
    ralval
    verepair.Thepat i
    enthasreachedaClassIindi
    cati
    onforan
    i
    nterventi
    onf orherMR.HerLVej ecti
    onf r
    actionisnowbel ow60%andherLVend- systol
    i
    c
    dimensionis>4.0cm.Shehassever eMR( ERO0. 4cm2).Ther
    eisnoneedt oconsi
    derany
    functi
    onaltesti
    ngint hi
    ssituati
    on.Inadditi
    on, t
    herearenodatathataft
    erl
    oadreducti
    onalter
    s
    thecourseofherdi seaseatthispoint.Sheshoul dundergoaninter
    vent
    ion.
     

    Shedoesnothaveapr ohibi
    tivesurgicalr
    isk.Thus, apercut aneousappr oachi snotwarrant
    ed
    andsheshouldhaveasur gicali
    nterventi
    onei therbyst ernot omyorl imit
    edt horacot
    omy.
    Whent heprol
    apseinvolves<50%oft hepost eriorleaf
    let,thesur gicalapproachshould
    def
    ini
    telybevalverepairandnotr eplacement .Indeed,fort hemostpar t,
    mi t
    ralrepai
    rshould
    al
    waysbeaf i
    rstchoiceinthosewi thdegener ativemitralval vedisease. 

    Cur r
    entguideli
    nesemphasizethati
    tisaClassII
    I(har
    m)indicati
    ontoper f
    orm mitr
    alval
    ve
    replacementinapat i
    entwit
    h<50%oft heposter
    iorl
    eafl
    eti
    nvolved;r
    ather,theyal
    lshoul
    dhave
    mitralrepai
    r.Theonlyexcept
    ionwouldbeinthosesit
    uati
    onswher emitralrepai
    rwas
    attempt edandfai
    led.

    Quest
    ion:

    37. Themostcommoncauseoft
    ri
    cuspi
    dregur
    git
    ati
    on(
    TR)i
    sfunct
    ionali
    nnat
    ure.

    Whichofthefoll
    owi
    ngisconsi
    deredaClassI(
    LevelofEvi
    denceC)i
    ndi
    cat
    ionf
    ort
    ri
    cuspi
    d
    val
    verepairwhensever
    eTRispresent
    ?

    a. Whenapacemakerordef
    ibri
    ll
    atorisrequi
    red.
    b. Att
    heti
    meoflef
    t-si
    dedvalvesurgery.
    c. Whenther
    eareatr
    ialar
    rhythmias.
    d. Whenpulmonar
    yhypertensionispr
    esent
    .

    Answer
    :

    37. b. Att
    het
    imeofl
    eft
    -si
    dedval
    vesur
    ger
    y.

    Thecorrectansweri satthetimeofl ef
    t-sidedvalvesurger y.Inapproximat
    ely80%oft hecases
    ofTR,theanat omi cunderpinningsaref unctionali
    nnat ure.Thi sr
    elat
    estothef actt
    hatchor dal
    att
    achment sf orthethreeleafl
    etsareof tenont heventricularwallandnotspeci f
    icpapill
    ary
    muscles.Ifther i
    ghtventricl
    e(RV)di l
    atesf oranyreason, itresult
    sinpoorleafl
    etcoapt at
    ion
    duetother esultanttet
    heringoft hevalve.Inaddition,
    thet ricuspi
    dannularrevertsfr
    om its
    normalsaddl e-shapedelli
    psoidtoapl anarci rcul
    arstr
    uct urewhent heRVenl arges,f
    ur t
    her
    di
    scouragingappr opri
    ateleaf
    letcoaptation. 

    Thedeci si onast owhent ooper ateinfuncti


    onal TRi snotani nfrequentcl i
    nicaldilemma.I tis
    aCl assIi ndicationt oper f
    ormt ricuspi
    dvalver epairwhenr epai
    ringorr eplacingthemi tr
    alor
    aorticvalveandt hereisassoci atedsevereTR.Whi lepacemaker sand/ ordefibri
    llatorsarea
    sour ceofwor seni ngTRwheni tispresent,t
    herei snoi ndicati
    ont orepairfunctionalTRpr i
    orto
    theirimpl antati
    on.I ngener al,
    funct i
    onalTRr espondst or educingt hepulmonar ypr essures
    whenpul monar yhyper tensionispr esent,
    butitisnoti ndicatedwi thouttreati
    ngt heRV
    afterloadpr oblem.Fi nally,whil
    er educingTRmayr educet hevolumeover l
    oadont her i
    ght
    atri
    um andr educeat ri
    alar r
    hythmi as,i
    tiscurrentlynotconsi deredapr imar yindicat i
    onfor
    i
    nter veningont het r
    icuspidvalvei nfuncti
    onal TR.

    Quest
    ion:

    38. A43- year-


    oldwomanwi t
    hamechani calaor
    ticval vereplacementf orendocar dit
    isis
    admitt
    edwi thpulmonar yedemaf ol
    lowing2weeksofpr ogressivedyspnea.Shehashada
    l
    onghi st
    oryofpoormedi calcompl i
    anceandt headmi ssioninternati
    onalnormalizedr ati
    o(INR)
    was1.0.Onexami nation,sheisanxiousandi nrespiratorydistressandhypot ensive.Shei s
    afebr
    il
    e,withal oudaor t
    icregurgi
    tantmur mur.Shei niti
    allyr
    espondst ocont i
    nuousposi t
    ive
    ai
    rwaypr essure,i
    ntravenous( I
    V)diuresis,andinotropes.Ahepar i
    ndripisstart
    ed.An
    emergencyechocar diogram revealssever eaort
    icstenosi sandr egur
    git
    ation,wit
    ha
    questi
    onablelargemassont heaorti
    cval ve.Afluoroscopi cviewoft heaor t
    icvalvereveals
    oneleafl
    etfrozenint heopenposi ti
    on.

    Basedont
    hecl
    ini
    calsi
    tuat
    ion,
    whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    ep?

    a. Beginstr
    eptoki
    nase.
    b. Beginti
    ssueplasminogenacti
    vat
    or.
    c. Referf
    oremer gencysurger
    y.
    d. Conti
    nueIVhepar i
    n.

    Answer
    :
    38. c. Ref
    erf
    oremer
    gencysur
    ger
    y.

    Thecor rectansweri ssurgicalinterventi


    on.I napat i
    entwi t
    hapr obablelargethrombusbur den
    andevi dencef orsevereprostheticvalvedysf unct ionwi thNewYor kHear tAssociati
    on(NYHA)
    classI I
    IorIVsympt oms, surgical r
    emoval ofthet hrombusi sindicated.Atransesophageal
    echocar di
    ogr am al
    sowoul dhavebeenusef ultochar acteri
    zetheval veandpr ovi
    dean
    estimateoft hethrombussi ze.However ,insomecases, iti
    ssimpl yeasiertousef l
    uoroscopy;
    i
    nt hiscase,itwasdi agnostic.Fibrinol
    ytictherapyi sreasonabl eonlyinthosewi thNYHA
    functionalcl
    assIorI Isympt oms.Ther i
    skoff ibri
    nol yictherapyisembol izat
    ionofthe
    thrombus, andt heri
    skishigheri fthet hrombusi smobi l
    eorover0. 8cm.I Vheparinshouldbe
    continuedunt ilt
    hetimeofsur geryandasabr idget ot herapeuticINR.

    Quest
    ion:

    39. Youar econsul t


    edtoseea58- year-ol
    dmanwhounder wentcar diacsurgeryyester
    day
    forsevere,sympt omat i
    caor t
    icstenosis(AS)duet oabi cuspidval ve.Duringsurgery,he
    recei
    vesamechani calbil
    eafl
    etaor t
    icvalve.Thesurgeonal soper formsr ootrepai
    rt otr
    eat
    milddil
    atationoft hethoracicaorta(mid-ascendingaorticdiamet er,45mm) .Apostoperat
    ive
    echocardiogr am showst hevalvetobef unctioningnormally(meangr adient,9mm Hg)wi tha
    l
    eftventri
    cul arejecti
    onfracti
    on( LVEF)65%.Thepat i
    ent’shospitalcour sehasbeen
    uncompl i
    cat ed.Thereisnohi storyofpri
    orst rokeoratr
    ialfi
    bril
    lation.Thesur gi
    calteam has
    askedyout oi ni
    ti
    ateanti
    thrombot i
    ctherapyf ortheaort
    icvalvepr osthesis.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    enextst
    ep?

    a. Aspi
    ri
    n81mgdai
    lyandwar
    far
    inwi
    thani
    nter
    nat
    ionalnor
    mal
    izedr
    ati
    o(I
    NR)goalof2.
    0
    -
    3.0.
    b. Ri
    varoxaban20mgdai
    ly.
    c. Dabi
    gatran150mgtwi
    cedail
    y.
    d. Warf
    arinwit
    hanINRgoalof2.
    5-3.
    5.
    e. Warf
    arinwit
    hanINRgoalof3.
    5-4.
    5.

    Answer
    :

    39. a. Aspir
    in81mgdail
    yandwar
    far
    inwi
    thani
    nter
    nat
    ionalnor
    mal
    izedr
    ati
    o(I
    NR)
    goalof2.
    0-3.
    0.

    War far
    inisindicatedwi t
    hat argetINRof2. 0-3.
    0inpat i
    entswi thabi leafl
    etorMedt ronic-
    Hal l
    mechani calaor t
    icvalvepr osthesiswhodonothavehi gh-riskfeatures,suchasLVdysf unction,
    atri
    alfibri
    ll
    ati
    on, pri
    orthromboembol ism, andhypercoagul ablecondi ti
    ons.Inpati
    ent swith
    high-ri
    skfeatures,aSt arr-
    Edwar dsval ve,
    oradi scvalveinaddi itontoaMedt r
    onic-Hallvalve,
    war f
    arinisindicatedwi t
    hat argetINRof2. 5-
    3.5.Theaddi tionofl ow-doseaspiri
    nhasbeen
    shownt odecreaset heriskoft hromboembol i
    sm forpatient swit
    hal lprosthet
    icheartvalves.
    Dabigat r
    anandr i
    varoxabanar enotindicatedforanti
    thrombot i
    ct herapyofprostheticheart
    valves.

    Quest
    ion:

    40. A71-
    year
    -ol
    dmanr
    etur
    nsf
    orf
    oll
    ow-
    upofhi
    spr
    ost
    het
    icaor
    ti
    cval
    ve.Hehada23mm
    biopr
    ostheti
    cval veplaced16year sagoforendocar di
    ti
    sandhasdonewel l
    .Hisinit
    ial
    echocardi
    ogramsr eveal
    edmi nimalgradi
    ent,butoverthel
    astfewyears,therehasbeen
    progr
    essiveevidencef orworseningaorti
    cstenosis(AS)wit
    hmi l
    daor t
    icregurgit
    ati
    on(AR).He
    i
    sactiveanddeni esanysympt omsofexer t
    ionaldyspnea,
    chestpressure,ordizzi
    ness.Hehas
    nocardiovascularsympt oms. 

    Hisexami nationisnor
    malexceptf orthemedianst er notomyscarandagr ade3/6mi d-peaking
    systoli
    cejectionmurmurandmi lddi
    astoli
    cmur mur .AnS4  isalsopresent
    .Anechocar diogram
    providesthef ol
    lowi
    nginformation:l
    eftvent
    ri
    culareject ionfracti
    on(LVEF)of55%, LVend-
    diastol
    e4. 9cm, LVend-systol
    e2.3cm, andLVwal lthickness1. 1cm.Thepeaki nstant
    aneous
    aorti
    cgr adienti
    s4.3msecandt hemeanaor ti
    cgr adienti s44mm Hg.Theaor t
    icvalvear eais
    2
    0.9cm , withmi l
    dAR,andt hereisnotri
    cuspidregur gitati
    onjettoesti
    matepulmonar y
    pressures.

    Basedont
    hesedat
    a,whi
    choft
    hef
    oll
    owi
    ngshoul
    dbeyournextst
    epf
    ort
    hispat
    ient
    ?

    a. Exerci
    setest
    ing.
    b. Dobutaminestressechocardi
    ogram.
    c. Referforaor
    ti
    cvalvereplacement(AVR)
    .
    d. Tr
    ansesophagealechocar di
    ogram (
    TEE)
    .

    Answer
    :

    40. a. Exer
    ciset
    est
    ing.

    Pati
    entswit
    hprosthet
    icvalvestenosisaregener all
    yhandledsimilar
    lytot hosewi t
    hnat i
    ve
    val
    vestenosi
    s.Thispati
    enthassever eAS, yetdeniessymptoms.Hi sval vegradientsand
    aort
    icval
    vearea(AVA)areconsi stentwithsevereAS, butar
    enotsuper -severe(peakgr adi
    ent
    of5msec).Thus,anexercisetestisappropriatetoassesswhet herheist rul
    yasympt omatic.
    Thisshoul
    dbedonewi thaphysi cianpresent.Thetestshouldbeconsi deredposi t
    ivei fany
    symptomsareprovoked,ifther
    ei sanabnor mal hemodynami cresponse( i.
    e.,
    hypot ensionor
    l
    ackofar i
    se>20mm Hgi nsystemi cbloodpr essur
    ewi t
    hstress,orSTabnor mali
    ti
    es
    devel
    op).
     

    Byusingthismet hod,upto29%ofpat ientsthoughttobeasympt omati


    cwi l
    ldemonst rate
    funct
    ionalderangement.Attimes, t
    hestenosisobservedaf t
    ersur
    ger
    yissimplyduet otoo
    smallavalvebeingusedatt het i
    meofi mplantati
    on.Thisisref
    err
    edtoas“patient
    -prostheti
    c
    mismatch.”Becauseoft hi
    s,itisimpor
    tanttoal waysobtai
    nanechocardiogram earl
    yaf tert
    he
    surgi
    calprocedure.Severemi smatchi
    sconsi deredpresentinAVRwhent heAVAi s<0. 65
    cm2. 

    Atthecurrentt
    ime,bothsurgi
    calandpercutaneousAVRmaybeconsideredifhebecomes
    sympt omati
    corhasaposi t
    ivefuncti
    onal
    study.Noadditi
    onali
    nfor
    mati
    onislikel
    ytobe
    gleanedfr
    om aTEE, givent
    heresultsoft
    hechestwallechointhi
    spar
    ti
    cularpati
    ent.
    Dobutaminestressechoisnotindicat
    edashehasanel evat
    edmeangradientconsi
    stentwi
    th
    severeASandpr eservedLVfuncti
    on. 

    Quest
    ion:

    41. Youar
    easkedt
    oseea23-
    year
    -ol
    dpr
    egnantwomanwhoi
    snear
    ingt
    heendofher
    secondtri
    mest er.Shehashadcont i
    nuouspr enatalcare,butherphysici
    annotedsheseemst o
    behavingmor er espiratorysymptomst hanhewoul dhaveexpect ed.Heorder
    edacar diac
    echocardi
    ogram, whichr eveal
    edanewdi agnosisofsever emitr
    alstenosi
    s.Sheisst
    ar t
    edon
    hydrochol
    orothiazideandmet oprol
    ol.Herbloodpr essureis115/60mm Hgandhear trateis
    65bpm.Despi tet his,shecontinuestodemonst ratewor seni
    ngdyspnea.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    ep?

    a. I
    ncreasebeta-blockade.
    b. Therapeuti
    cabor t
    ion.
    c. Sur
    gi calmi
    tralvalverepl
    acement
    .
    d. Bal
    loonmi tr
    alvalvulopl
    asty.

    Answer
    :

    41. d. Bal
    loonmi
    tr
    alval
    vul
    opl
    ast
    y.

    Thecorrectanswerisballoonval vuloplast
    y,ift
    hevalvei ssuitabl
    ef orbal
    loonvalvuloplasty,
    ther
    eisnoat r
    ialcl
    ot,andt hereisnosever emi t
    ralregurgit
    ation.Pregnancycompl icatesthe
    careofpati
    entswithvalvularhear tdisease.Asagener ali
    ty,regurgi
    tantvalvularl
    esionsare
    tol
    erat
    edmuchbet terthanst enoticlesions,aspregnancyi ncursamar kedr educt
    ion
    i
    n aft
    erl
    oadandamar kedi ncreasei ncardiacoutputrequirement. 

    Duri
    ngthef i
    rsttwot r
    imesters,muchofthecardiacout
    putisaccomplishedbyi ncreasi
    ngt he
    st
    rokevolume, whilehear
    tr atei
    ncreasesdominatedur
    ingthethi
    rdtri
    mest er
    .Thegr adientin
    mit
    ralstenosisisdependentonbot hthestrokevol
    umet hr
    oughthevalveandt heamountof
    di
    astol
    ictime.Ast heheartrateincr
    easesinthethir
    dtr
    imester
    ,diast
    olicti
    mef all
    s,andt he
    gr
    adientwor sensfurt
    her.
     

    TheFoodandDr ugAdmi nist


    rati
    onconsider shydrocholorothiazi
    deacl assBagentand
    appropri
    ateinpregnancy.Al t
    houghal lofthebet a-
    blockersareconsi deredclassCdr ugs,they
    arerouti
    nelygivenandendor sedbyt hegui deli
    nes.Ther earemanyst udiesvali
    dati
    ngt heuse
    ofpercutaneousmi tralvalvulopl
    astyduringpr egnancy,andt hereisli
    ttl
    er i
    sktothefetusf r
    om
    theprocedureort heradiationduringthesecondandt hi
    rdtrimester.Surgicalmit
    ralvalve
    repl
    acementcanbeper formed, butatani ncreasedfetalri
    sk,wi t
    hthet i
    meper iodbetweent he
    20thand28t hweekr epresentingtheleastrisk.Ift
    heval vei
    samenabl et ocommi ssurotomy,a
    percut
    aneousappr oachi spreferr
    ed.

    Quest
    ion:

    42. A20- year-


    oldwomanwi t
    hahi storyofmitralval
    verepair3yearsprior(formitr
    al
    regur
    gitati
    on[ MR]duet omi tr
    alprolapse)isadmittedwithfeverofunknowncausef orone
    week.Inretrospect,shehasbeenf eeli
    ngpoorlyforatleast2mont hsandnot esher
    temperaturetendstoi ncreaseintheevening.Shegener all
    ycangett hetemperaturereduced
    withacetaminophenandhasbeenabl etoconti
    nuet ogot oschool.Shehasl ostafewpounds,
    buthasnoot herspecifi
    ccompl ai
    nt s.
     

    Sher ecent
    lywentt
    oanur gentcar
    efaci
    li
    ty,
    wher eshewaspr
    escri
    bedazithromycin.Shehas
    takenthisoverf
    ort
    helast3days.Onexami nat
    ion,shei
    smil
    dlyf
    ebril
    e(37.8°C)and
    tachycardi
    cat105bpm.Herbl oodpr
    essureis100/75mm Hg.Herlungsareclear.Cardi
    ac
    exam reveal
    snoj ugul
    arvenousdistenti
    on,noCVwave, andnohepatojugularref
    lux.Her
    carot
    idisnormal.Apexishyperdynami cwithnothri
    ll
    s.Onauscult
    ati
    on,thereisagrade3/6
    MRmur murradi
    at i
    ngtotheaxi
    llaandt othebackwi t
    hanassociat
    edS3.Ther emainderofher
    exam i
    snor mal,
    wi t
    hnoper i
    pheralsti
    gmat aforendocar
    dit
    is.
     

    Anechocar di
    ogr
    am isobtained,anditrevealsmoderatet osevereMRwi t
    habr i
    ghttarget
    observedontheanteri
    orleafl
    etthatisoffi
    ciallyr
    eadasei thercal
    cium orapossibleveget
    ati
    on.
    Leftventr
    icul
    ar(
    LV)functionisnor malasist heLVsize,andt her
    earenoot herabnormali
    ti
    es
    observed.Youordert
    woset sofbl oodculturesandadmi thert ot
    hehospital.Af
    ter24hours,
    nei
    thersetofcul
    turesispositi
    veforanygr owt hofbacteri
    a.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthebestnextst
    ep?

    a. Begi
    nampi ci
    ll
    inandgentami
    cin.
    b. Begi
    nceftr
    iaxone.
    c. Repeatbl
    oodcultur
    es.
    d. Begi
    nvancomyci nandri
    fampi
    n.

    Answer
    :

    42. c. Repeatbl
    oodcul
    tur
    es.

    Thecorr
    ectansweristowaitunti
    lbloodcul
    tur
    escanbeobt ainedof
    fantibi
    oti
    csbefor
    e
    star
    ti
    ngempiri
    ctherapy.Thepati
    enthasevi
    denceforfeverandacli
    nicalscenar
    ioi
    nwhich
    endocar
    dit
    isi
    scertainl
    ypossi
    ble.Youaregi
    vennopr i
    orexamst oknowi ft
    heMRi snewor
    worsefr
    om previ
    ousexams. 

    Thet argetonthemi tralvalvei snotdef i


    niti
    veandat ransesophagealechocar diogr am would
    nowbei ndicat
    edt obet t
    erdef inethel esion.Sher eceivedant ibioti
    csf r
    om theur gentcar evisi
    t.
    Thus, thelackofpositivit
    yoft hei nit
    ial bl
    oodcul t
    uresmaysi mpl ybeduet otheant ibi
    otic
    therapyshehasr ecei
    ved.Sher emainsst able,soant ibioti
    csshoul dnotbei nit
    iat edunt i
    l
    cultureshavebeenobt ainedt hathavenotbeenpot ential
    lyinfluencedbyt hepr iorantibi
    otic
    therapy.Att hi
    sstage, shedoesnotmeett hemodi f
    iedDukecr i
    teriaforendocar dit
    is,anda
    secondsetofcul t
    uresshoul dbeobt ai nedandnot her apyinit
    iatedunt ilt
    heser esultsareback.
    Iftheculturesthenbecomeposi t
    ive,theappr opri
    ateant i
    bioti
    cscanbeadmi nisteredort he
    patientcanbeempi ri
    callytreatedf orcul t
    ur e-negati
    veendocar dit
    is.

    Quest
    ion:

    43. A36- year-


    oldwomani sseenf orevaluati
    onofanewmur mur .Shei sactive,buthas
    milddyspneaonexer t
    ionandmi l
    df atigue.Shehasnothadanor exiaorf ever.Shei sonno
    medications.Sheisafebril
    e,herbloodpr essureis132/ 60mm Hg, andhear trat
    ei s90bpm.
    Shehas5cm j ugularvenousdistenti
    onwhenupr ight.Chestexaminat i
    oniscl ear,andther
    eis
    agrade3/ 6systoli
    cejecti
    onmur muratt heleftuppersternalbor
    der, al
    ongwi thagr ade3/4
    decrescendodiastoli
    cmur muratt heleftlowersternalborder.
     

    Anechocar diogram reveal


    sabicuspidaort
    icval
    vewit
    hsevereaort
    icinsuffi
    ciency.Thelef
    t
    vent
    ricularend-diast
    olicdi
    mension(LVEDD)is6.0cm andl
    eftvent
    ri
    cularend- syst
    oli
    c
    dimension( LVESD)is5. 0cm.Ej
    ecti
    onf r
    acti
    onis55%.Nootherval
    vularlesi
    onsar enoted,and
    t
    heaor
    ti
    crootsi
    zenor
    mal
    .

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthebestnextst
    epf
    ort
    hispat
    ient
    ?

    a. Aorti
    cvalvereplacement.
    b. Nif
    edipi
    nesust ained-
    rel
    easeoral
    ly30mgdai ly.
    c. Tr
    ansesophagealechocar di
    ogram (TEE).
    d. Li
    sinopr
    iloral
    ly5mgdai l
    y.
    e. Repeattr
    ansthor aci
    cechocardi
    ogram (TTE)i
    n6mont
    hs.

    Answer
    :

    43. a. Aor
    ti
    cval
    ver
    epl
    acement
    .

    Thecor
    rectanswerissurgicalaort
    icval
    verepl
    acement.Thecr i
    ter
    iaf
    orsurgicalreplacement
    i
    nsevereaort
    ici
    nsuffi
    ciencyincludeanLVEDD>6. 5cm,LVESD>5. 0cm, andejectionfracti
    on
    <50%orsymptoms.Afterloadreducti
    oninnormotensi
    vepatient
    shasnotbeenshownt o
    i
    mproveoutcomesinpat i
    entswithsevereaort
    icr
    egurgit
    ati
    on.TEEwillnotprovideaddi t
    ional
    i
    nfor
    mationfr
    om thatseenont heTTE.

    Quest
    ion:

    44. Whi l
    etheval vul
    arhear tdiseaseguidel
    inesgener al
    lyfocusont hei nt
    erventi
    oncr i
    ter
    ia
    forindivi
    dualvalvesandindividual l
    esions(ei
    therstenosisorregurgit
    ati
    on) ,somepat i
    ents
    presentwithmi xedvalvul
    ardisease, wherebot hst
    enosisandr egurgitat
    ionar epresent.The
    gradientsandr esult
    antventr
    icularvolumesar egreatl
    yaf f
    ectedbybot hr egurgi
    tati
    onand
    stenosis,makingt hetr
    adit
    ional t
    hresholdsforint
    erventi
    onl i
    kelyunrel
    iableinsomecases.

    Accor
    dingl
    y,t
    hel
    atestval
    vul
    arhear
    tdi
    seasegui
    del
    i
    nesat
    tempt
    edt
    ohel
    presol
    vet
    hei
    ssue.

    Basedont
    hecur
    rentvalvul
    arhear
    tdi
    seasegui
    del
    ines,
    whi
    chgui
    del
    inecr
    it
    eri
    afori
    nter
    vent
    ion
    shoul
    dbeusedi
    npatientswit
    hmixedval
    vul
    ardi
    sease?

    a. Cr
    it
    eri
    afort
    heregurgitantrathert
    hanthestenot
    icl
    esi
    on.
    b. Cr
    it
    eri
    afort
    hestenoticratherthantheregur
    git
    antl
    esi
    on.
    c. Rel
    yonsymptomsal one.
    d. Cr
    it
    eri
    afort
    hedomi nantval vul
    arl
    esion.

    Answer
    :

    44. d. Cr
    it
    eri
    afort
    hedomi
    nantval
    vul
    arl
    esi
    on.

    Thecor rectansweri stouset hecrit


    eriaforthedomi nantabnor mal i
    tyint heval ve.For
    i
    nst ance,ift herei
    ssever eaor t
    icst
    enosis(AS)andonl ymi l
    d-moder ateaor ticregurgit
    ati
    on
    (AR) ,
    thent heAScr it
    eriaprevail
    .Conversely,ifthereismi l
    d-moder ateASwi t
    hsever eAR, t
    hen
    theARcr i
    ter iawouldpr evai
    l.Manypat i
    entswi thmi xedvalvedi seasedevel ophemodynami c
    consequencesear l
    ierthantheseverityofeitherl esi
    onmi ghtpredi ct.Forinst ance,pulmonary
    hyper t
    ensionmi ghtbeexpect edearli
    erinmi xedmi t
    ralstenosisandmi tralregur gi
    tati
    onthan
    wi t
    heitherl esionalone.Simi l
    arl
    y,areducedl eftventri
    cularend- systoli
    cdi mensi onorejecti
    on
    fracti
    onmi ghtbeexpect edearli
    eri
    nmi xedAS/ ARdi seasethanwi theitheral one. 
    Thedeci si
    ontoint
    erveneoftencomesdownt oacl
    ini
    caljudgmentcall.Exerci
    setest
    ingmay
    hel
    pi fcardi
    acli
    mitati
    oncanbedemonst ratedint
    hoseappar ent
    lyasympt omati
    c.Alt
    hough
    unstudiedatthi
    spoint,ot
    herparameter
    s,suchasbiomarkersmayal sobeofval ueinthe
    fut
    uretohel pdi
    sti
    nguishventri
    cul
    ardysfuncti
    oni
    nmi xedvalvul
    ardisease.

    Quest
    ion:

    45. Thehemodynami ct
    raci
    ngshowni
    nFi
    gur
    e1mi
    ghtbeseeni
    nwhi
    choft
    hef
    oll
    owi
    ng
    congeni
    talsyndr
    omes?

    a. Marfansyndrome.
    b. Prader-
    Will
    isyndrome.
    c. Holt-
    Oram syndrome.
    d. Shonec omplex.

    Answer
    :

    45. d. Shonecompl
    ex.
    Thet racingshowni nFigure1depi ctsasi gni
    ficantgr adientbetweent helef tventri
    cleandt he
    femor alar t
    ery.Thi scanbeseenwi thhyper tr
    ophi ccar diomyopat hy,aorticval vestenosis,
    subval vularandsupr aval
    vularaor ticstenosi s,andcoar ctati
    onoft heaor t
    a.Shonecompl exi s
    associ atedwi thl ef
    theartobstructivedi sease, includingsupr avalvularmi tralstenosisand
    parachut emi tralvalve,aswellassubval vularaor ti
    cst enosis,valvul
    araor ticst enosis,
    and
    coarctat i
    onoft heaor ta.Holt-
    Or am syndr omei scausedbyamut ati
    oni nt het ranscri
    pti
    on
    factorTBX5andi sassociatedwi that r
    ial septal defectsandr adioulnardef ect s.Prader-
    Wi l
    liis
    acongeni talsyndr omeassoci atedwi thl ossoff unctionofgenesonchr omosome15, butdoes
    nothavesi gnificantcardiacmani festations.Mar f
    ansyndr omei sadi seaseoft heconnect i
    ve
    ti
    ssuet hataffect smulti
    pleorgansyst ems.Themostsi gnifi
    cantcar diovascul armani f
    estation
    ofMar fansyndr omeisaor t
    opat hy.

    Quest
    ion:

    46. A44- year


    -ol
    dwomanwi
    thr
    heumat
    icmi
    tr
    alst
    enosi
    sisbei
    ngeval
    uat
    edf
    ormi
    tr
    al
    val
    vul
    opl
    ast
    y. 

    Hercardiaccat heteri
    zati
    ondemonst r
    atesthef ol
    lowinghemodynami cs:pulmonaryartery
    90/45mm Hgwi thameanof60mm Hg, pulmonarycapill
    arywedgepr essure30mm Hg, l
    eft
    ventri
    cularend-diastoli
    cpressur
    e5mm Hg, andcar diacoutput3.0l/
    min.Thecalculatedmi t
    ral
    2
    val
    ve( MV)i s1.0cm .Echocar di
    ogram revealsfusedMVcommi ssur
    es, mil
    dthi
    ckeningofthe
    mitrall
    eafletsandchor dalappar
    atus,f
    ocalcal ci
    fi
    cationoft
    ipoft heanteri
    ormit
    rall
    eaf l
    et,
    and
    mildmi t
    ral r
    egurgitat
    ion.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nhercar
    e?

    a. I
    ntr
    avenousepoprostenol
    .
    b. Per
    cutaneousball
    oonmi t
    ral
    val
    vul
    opl
    ast
    y.
    c. Bosent
    antherapy.
    d. Sur
    gicalMVreplacement.

    Answer
    :

    46. b. Per
    cut
    aneousbal
    loonmi
    tr
    alval
    vul
    opl
    ast
    y.

    Herel evatedpulmonar yarter


    ypr essuresarear esul
    tofherchronicall
    yelevatedwedge
    pressur e.Withrel
    iefofhermi t
    ralstenosis,herwedgepressurewillli
    kelynormali
    zeandher
    pulmonar yart
    erypressureswi l
    ldeclineoverthenextseveralmonths.Thi si
    snotnecessar
    ily
    thecasewi thotherval
    vularlesi
    ons.HerMVanat omyisamenabl etoper cut
    aneousther
    apy,
    andt hisisthetreatmentofchoi ce.SurgicalMVr epl
    acementisappr opri
    ateformorecal
    cif
    ied
    valveanat omyorsi gnif
    icantmitralregurgi
    tati
    on. 

    Quest
    ion:

    47. A70- year-


    oldmanwi thhi
    stor
    yofcoronaryart
    erydisease,di
    abet
    es,andhyper
    tensi
    on
    i
    sadmi tt
    edwithfeverandfati
    gue.Hehashadr heumatoi
    dar t
    hri
    ti
    sfor20years,
    whichhas
    resul
    tedinchroni
    cmi t
    ralandaort
    icr
    egurgi
    tat
    ion. 

    Onexami
    nat
    ion,
    hehasaswol
    lenr
    ightkneet
    hati
    swar
    m andt
    ender
    .Car
    diacexami
    nat
    ion
    showsapulseof100bpm.Hisbloodpressur
    eis120/
    60mm Hg,
    andhehasmi
    ldaor
    ti
    cand
    mitr
    alr
    egur
    gitat
    ion.Hi
    stemper
    aturei
    s38.1°C.
     

    Hisbasel
    ineelectrocardiogr
    am (ECG)showssi nusr hyt
    hm andf ir
    st-degr
    eeheartbl
    ock.
    ReviewofpreviousECGshowst hatthef
    ir
    st-degreeheartblockisold.Anechocardiogr
    am is
    done,whi
    chshowsmi l
    dtomoder ateaor
    ti
    cr egurgi
    tati
    on,withanappar entveget
    ati
    onattached
    totheaor
    ticvalve.Bloodcultur
    esar eposit
    iveformet hi
    cil
    li
    n-sensit
    iveStaphyl
    ococcusaureus
    ontwooft wosampl es.Heisstart
    edonnaf cil
    li
    nandgent ami ci
    n. 

    Atransesophagealechocardi
    ogram i
    sperf
    ormed,andt
    herei
    sevidenceforaveget
    ati
    onof0.8
    cm indiameterontheaorti
    cvalve.Ther
    eissi
    gni
    fi
    cantaor
    ti
    cregurgi
    tat
    ionandquesti
    onabl
    e
    evi
    denceofapar avalvul
    arabscess. 

    Thepat i
    entisst
    art
    edonanti
    bioti
    cs.Overthenext3days,
    thetemperatur
    eshowssome
    decrease,andheissympt
    omat i
    call
    yimproved.Onday6,thepat
    ienthasarout
    ineECG(
    Figur
    e
    1).

    Whi
    choft
    hef
    oll
    owi
    ngdoyour
    ecommendatt
    hist
    ime?

    a. Diagnosticel
    ectrophysiologystudy.
    b. Broadenant i
    biot
    iccover age.
    c. Surgicalaort
    icvalvereplacement.
    d. Permanentpacemakeri mpl ant
    ati
    on.
    e. Cont
    inuet
    oobser
    ve.

    Answer
    :

    47. c. Sur
    gicalaor
    ti
    cval
    ver
    epl
    acement
    .

    Thepr esenceofcomplet eheartbl


    ockisl
    ikel
    yduet oi
    nvol vementofconduct i
    onsyst em wit
    h
    perivalvulari
    nvasi
    onorabscess.Thi sisaClassIindi
    cationf orurgentsur gicalinterventi
    on.
    Onewoul dnotpl
    aceaper manentpacemakerinanactivelyinfect
    edpat ientatt hist ime,
    thoughat emporarypacemakermi ghtbeanopt i
    onpriortosur gery.Therei snoval uein
    obser vati
    ononcet hediagnosisofanabscesshasbeenmade.Onemustassumei nfect
    ious
    i
    nvasi onoft heconductionsystem i
    nthepresenceofcompl eteheartblockeveni ft he
    transesophagealechocar diogr
    am doesnotconfir
    m abscess.

    Quest
    ion:

    48. A64- year


    -ol
    dhealthywomanwi t
    haknownhear tmurmurpresent
    swi
    thr
    ecenthi
    stor
    y
    ofdyspneaonexerti
    on(threebl
    ocks).Coronaryangi
    ogr
    aphyperf
    ormed10monthsago
    reveal
    ednoevidenceofcoronar
    yarterydisease.
     

    Echocar di
    ogram datai
    ncludecal culat
    edej
    ect
    ionfract
    ion65%, moderat
    econcentr
    icleft
    vent
    ricularhyper
    trophy(wallthickness15mm) ,
    bicuspidaort
    icvalvewi
    thpeakvelocit
    y5
    m/sec, aort
    icval
    vemeangr adient58mm Hg,andaor ti
    cvalvearea0.9cm2.Midascending
    aort
    ai s5.0cm.

    Whi
    choft
    hef
    oll
    owi
    ngt
    reat
    ment
    swoul
    dyour
    ecommend?

    a. Ball
    oonaor t
    icval
    vulopl
    asty.
    b. Me di
    calmanagement .
    c. Surgicalaor
    ti
    cvalverepl
    acement(
    AVR)andr
    epl
    acementoft
    heascendi
    ngaor
    ta.
    d. Transcathet
    erAVR( TAVR).
    e. SurgicalAVR.

    Answer
    :

    48. c. Sur
    gicalaor
    ti
    cval
    ver
    epl
    acement(
    AVR)andr
    epl
    acementoft
    heascendi
    ng
    aor
    ta.

    Thepatienthasbicuspi
    daorti
    cvalve,severesympt omati
    caorti
    cstenosis(AS),andamaxi
    mal
    ascendi
    ngaor ti
    cdiameterof>4.
    5cm.Sur gicaltr
    eatmentofbot
    hdisordersisaCl assI
    recommendat i
    on.Thereisnorol
    ef ormedi calmanagementinseveresympt omaticAS.
    Bicuspi
    daor t
    icval
    veandassociatedaortopat hyneedtobeaddressedsurgical
    ly.
     

    Currentrecommendati
    onsaret
    orepl
    acetheascendi ngaort
    aif>5.5cm orexhibi
    tsagrowth
    rateof>0.5cm/year.I
    faor
    ti
    cval
    vesurgeryisbei
    ngunder t
    aken,t
    her ecommendat i
    onisto
    replacetheaor
    taif>4.
    5cm.Ball
    oonaorti
    cvalvul
    oplastyi
    ssomet i
    mesr eser
    vedasabr idgeto
    surgeryinunst
    ablepati
    ent
    sorasapall
    iativemeasurefort
    heinoperablepat
    ient(Cl
    assIIb)
    .
    Finall
    y,TAVRhasnotyetbeenappr
    ovedf orcl
    ini
    calusefortr
    eatmentofbicuspidaort
    icvalve.
    Quest
    ion:

    49. A52- year-


    oldwomani sref
    erredf
    oreval
    uat
    ionofahear
    tmur
    mur
    .Ar
    epr
    esent
    ati
    ve
    tr
    ansesophagealechocar
    diogram i
    mageisshowninFigur
    e1.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    ydi
    agnosi
    s?

    a. Parachutemit
    ralval
    ve.
    b. Fl
    ailmitr
    all
    eafl
    et.
    c. Subaorti
    cmembr ane.
    d. Systol
    icant
    eri
    ormot i
    onoft
    hemi
    tr
    alval
    ve.

    Answer
    :

    49. b. Fl
    ailmi
    tr
    all
    eaf
    let
    .

    Thei
    mageshowsf
    lai
    loft
    heA2 
    scal
    lopoft
    hemi
    tr
    alval
    ve.

    Quest
    ion:

    50. A52-year-oldwomani sr
    eferr
    edtotheechocar di
    ographylabor
    ator
    yforahear
    tmurmur
    .
    Shei
    sasymptomat i
    c.Sheisonnomedi cat
    ion.Herbloodpressureis130/
    75mm Hg.Figur
    e1
    i
    sthepar
    ast
    ernallongaxisvi
    ew.Figure2isatransesophagealimage. 
    Theechocar
    diogr
    am showsaf l
    ail
    mi trall
    eafl
    etispresent
    .Leftventr
    icul
    ar(LV)end-
    syst
    oli
    c
    di
    mensionis45mm, LVej ect
    ionfracti
    oni s55%,meangr adienti
    s3mm Hg, peakvel
    oci
    tyis
    1.
    5msec, mitr
    alr
    egurgi
    tantvolumei s100ml /beat,
    effect
    iveregurgi
    tantor
    ifi
    ceareai
    s0.67
    cm2.Est
    imatedpulmonaryart
    erialpressure(r
    est)i
    s45mm Hg.

    Whi
    choft
    hef
    oll
    owi
    ngwoul
    dbet
    heappr
    opr
    iat
    enextst
    ep?

     
    Figur
    e1
    Fi
    gur
    e2
    a. Fol
    lowser ial
    lybyechocar diogr
    aphy.
    b. Surgicalmitr
    alvalverepair.
    c. Percutaneousmi tr
    alvalverepair
    .
    d. Beginlisi
    nopril20mg/ day.

    Answer
    :

    50. b. Sur
    gicalmi
    tr
    alval
    ver
    epai
    r.

    Thepatientmeetsthe2014valvularhear
    tdiseaseguidel
    inecri
    ter
    iaforseveremitr
    alval
    ve
    regur
    git
    ation.Shealsomeet
    sgui deli
    necri
    teri
    aforint
    erventi
    onwithLVend- syst
    oli
    cdimensi
    on
    of>4.0cm andLVej ect
    ionf
    racti
    onof55%.

    Quest
    ion:

    51. A52- year-


    oldwomani srefer
    redtotheechocar
    diogr
    aphyl
    abor
    ator
    yforaheartmurmur.
    Sheisasymptomati
    c.Herbloodpressur
    eis130/75mm Hg.Figur
    e1istheparast
    ernall
    ong-
    axi
    sview.Fi
    gure2isatransesophageali
    mage. 

    Leftventr
    icul
    ar(
    LV)end-syst
    oli
    cdimensi
    onis45mm,LVejecti
    onfracti
    on(EF)is55%,
    mean
    gradienti
    s3mm Hg, peakveloci
    tyi
    s1.5msec,mi
    tr
    alr
    egur
    gitantvolume(RV)is100ml/beat
    ,
    andef f
    ect
    iver
    egurgit
    antori
    fi
    cearea( EROA)i
    s0.67cm2.Est
    imat
    edpul
    monar
    yar
    ter
    ial
    pressure(
    rest
    )is45mm Hg.
    Whichofthefoll
    owingisthebestrecommendati
    onfort
    reatment
    ?
     

    Fi
    gur
    e1
    Fi
    gur
    e2
    a. Referralformit
    ralvalvesurgery.
    b. Continuedsurveil
    lance.
    c. Percutaneousballoonvalvuloplast
    y.
    d. Vasodi l
    atort
    herapy.

    Answer
    :

    51. a. Ref
    err
    alf
    ormi
    tr
    alval
    vesur
    ger
    y.

    TheMRi ssever e(RV>60cc;EROA>0. 40cm2)andsecondar ytoflailanteri


    orleafl
    et.TheEFis
    mildlydepressed,andtheend-
    systol
    icdimensionis>40mm.I nthepr esenceofmi ldly
    depressedEF, therei
    snoadvantaget omedi
    cal management .Thepeakvel oci
    tyacrossthe
    mitralval
    veisincreasedduetosevereMRandnotst enosis,renderingvalvuloplast
    y
    i
    nappr opri
    ate.TheAHA/ ACCguideli
    neonvalvularheartdiseasegivesaCl assIindicati
    onfor
    asympt omatic,sever
    eMRandmi l
    dt omoderateLVdysf unction(EF30- 60%)orLVend- syst
    oli
    c
    dimension>40mm.

    Quest
    ion:

    52. A29- year


    -ol
    dmani st
    ransf
    err
    edwithent
    erococcusfaecal
    isendocar
    dit
    is.Hehasbeen
    onappr
    opr
    iateanti
    biot
    ict
    her
    apyfor3weeks.Hi
    sphysicalexaminat
    ionshowshei saf
    ebri
    le.
    Hi
    shear tr
    atei
    s100bpm, bl
    oodpressurei
    s100/60mm Hg,andjugul
    arvenouspressurei
    s12
    cm H2O.Hehasagrade3/6pansystol
    icmurmuratapexandmil
    dbibasi
    larcr
    ackl
    es.Figur
    es1,
    2,
    and3ar eobtai
    ned.Cal
    cul
    atedej
    ecti
    onfract
    ion(
    EF)is36%.

    Whi
    choft
    hef
    oll
    owi
    ngi
    stheappr
    opr
    iat
    emanagementf
    ort
    hispat
    ient
    ?

    Fi
    gur
    e1
    Fi
    gur
    e2
    Fi
    gur
    e3

    a. Af
    terl
    oadreducti
    ont her
    apy.
    b. Bet
    a-bl
    ockertherapy.
    c. Pr
    omptmi tr
    alvalverepl
    acement.
    d. Fi
    nishthecourseofantibi
    oti
    csandr
    e-eval
    uat
    e.

    Answer
    :

    52. c. Pr
    omptmi
    tr
    alval
    ver
    epl
    acement
    .

    Thepatienthassever emi t
    ralr
    egurgitat
    ion,signi
    fi
    cantlef
    tventr
    icul
    ardysfuncti
    on,
    and
    evi
    dencef orhear
    tf ai
    lure.Thetachycardiaisacompensat orymechanism andshouldnotbe
    tr
    eated.Thereisnor oleforvasodil
    atortherapyinthi
    ssetti
    ngashi ssyst
    olicbl
    oodpressur
    eis
    only100mm Hg, andt r
    eatmentoft hemi t
    ralregurgi
    tat
    ionshoul
    dbesur gi
    cal. 

    Quest
    ion:

    53. A22- year-


    oldmanwi thfamili
    alMarf
    ansyndromepresent
    swithdyspneaonexer
    ti
    on.
    Fouryearspri
    ortopresentat
    ion,heunder
    wentaort
    icrootr
    epairwi
    thaort
    icval
    ve(AV)
    resuspensi
    on(val
    ve-spar
    ingsurgery).
     
    Physicalexami nationreveal
    sahi gharchedpalat
    e,ar
    achnodactyl
    y,andaseverepectus
    excavatum.Bl oodpr essureis134/34mm Hg.Thepoi ntofmaximalimpul
    seisdisplaced
    i
    nferolat
    erall
    y.Ther eisasyst ol
    iccl
    ick.Agrade4/6harsh,l
    ate-
    peaki
    ngsystol
    iceject
    ion
    murmuri sauscul tatedacrosstheprecordi
    um.Thereisagrade4/4holodi
    astoli
    cmur murat
    thelowerleftsternalborder.
     

    Fi
    gur
    e1showsacont
    inuouswaveDoppl
    eracr
    osst
    heAV.
     

    Lef
    tvent
    ri
    cul
    aroutfl
    owt
    ract(
    LVOT)di
    ameteri
    s2.4,LVOTt
    imevel
    oci
    tyi
    ntegr
    al(
    TVI
    )is26,
    meanAVgradienti
    s87mm Hg,andAVTVIis167.

    Yourr
    ecommendat
    iont
    othepat
    ienti
    swhi
    choft
    hef
    oll
    owi
    ng?

    a. Aorti
    cvalver eplacement(AVR)
    .
    b. Rosspr ocedur e.
    c. TranscatheterAVR( TAVR)
    .
    d. Continuedsur veil
    lance.
    Answer
    :

    53. a. Aor
    ti
    cval
    ver
    epl
    acement(
    AVR)
    .

    Thepat i
    enthassevereaorti
    cstenosi
    s(andaort
    icregurgi
    tat
    ion)andissympt omat
    ic,whi
    chi
    s
    aClassIindicat
    ionforAVR.Thereisnorolef
    ormedi calmanagementint hi
    sscenari
    o.ARoss
    procedurewouldbet echni
    call
    yimpossi
    blewi
    thpreviousaorti
    crootsurgery.TAVRisnot
    approvedforthi
    sindicati
    on.

    Quest
    ion:

    54. A22- year-


    oldmanwi thfamili
    alMarf
    ansyndromepresent
    swithdyspneaonexer
    ti
    on.
    Fouryearspri
    ortopresentat
    ion,heunder
    wentaort
    icrootr
    epairwi
    thaort
    icval
    ve(AV)
    resuspensi
    on(val
    ve-spar
    ingsurgery).
     

    Physicalexami nationreveal
    sahi gharchedpalat
    e,ar
    achnodactyl
    y,andaseverepectus
    excavatum.Bl oodpr essureis134/34mm Hg.Thepoi ntofmaximalimpul
    seisdisplaced
    i
    nferolat
    erall
    y.Ther eisasyst ol
    iccl
    ick.Agrade4/6harsh,l
    ate-
    peaki
    ngsystol
    iceject
    ion
    murmuri sauscul tatedacrosstheprecordi
    um.Thereisagrade4/6holodi
    astoli
    cmur murat
    thelowerleftsternalborder.
     

    Fi
    gur
    e1showsacont
    inuouswaveDoppl
    eracr
    osst
    heAV.
     

    Lef
    tvent
    ri
    cul
    aroutfl
    owt
    ract(
    LVOT)di
    ameteri
    s2.4,LVOTt
    imevel
    oci
    tyi
    ntegr
    al(
    TVI
    )is26,
    meanAVgradienti
    s87mm Hg,andAVTVIis167.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthecor
    rectaor
    ti
    cval
    vear
    ea(
    AVA)i
    nthi
    spat
    ient
    ?
    a. 0.
    6cm2.
    b. 1cm2.
    7cm2.
    c. 0.
    9cm2.
    d. 0.

    Answer
    :

    54. c. 7cm2.
    0.

    AVAiscalcul
    atedbythecont
    inui
    tyequat
    ion.(
    ASjet=aor
    ti
    cstenosi
    sjet
    )AVAxTVIASjet=
    LVOTareaxTVILVOT.ThusAVA=LVOTar eaxLVOTTVI/TVIASjet=0.785xD2xTVI
    LVOT/TVIASjet=4.52x26/167=0.7cm2.

    Quest
    ion:

    55. An85- year-


    oldwomanwi thsevereaorticstenosisandmul t
    iplesurgi
    calri
    skfact
    orsis
    dyspneicatr
    est,butmental
    lycompetent.Sheisr efusedcardi
    acsur ger
    yduet othemulti
    ple
    comorbidi
    ti
    esandi sbei
    ngevaluatedforpossibletranscat
    heteraort
    icvalverepl
    acement
    (TAVR).Acoronaryart
    erycomputedtomogr aphicangi ogr
    am ofheraor t
    aandr unof
    fvessel
    sis
    perf
    ormed. 
    Findi
    ngsincl
    udeaort
    icannul
    usdimensionsof21mm x28mm.Mi ni
    mum il
    iof
    emoral
    measurementsare4.8mm ontheleftand5.2mm onther
    ight
    .Therei
    sseverecal
    cif
    icat
    ionof
    theaort
    afrom t
    herenalar
    ter
    iest
    ot heil
    iacbi
    fur
    cat
    ion.

    Whichofthefol
    lowingconcl
    usi
    onscanbedr
    awnf
    rom t
    hesedat
    ainr
    egar
    dtot
    heuseofa
    t
    ranscat
    heterapproacht
    oAVR?

    a. Sur
    gicalAVRi sthebestoption.
    b. Anonfemor alapproachforTAVRisthebestopti
    on.
    c. TAVRispr ecl
    udedbyt hedegreeofaort
    iccal
    cif
    icati
    on.
    d. Astandardfemor alappr
    oachTAVRappr oachisfeasi
    bleandt
    hebestopt
    ion.
    e. TAVRnotf easibl
    eduet otheaort
    icannul
    arsi
    ze.

    Answer
    :

    55. b. Anonf
    emor
    alappr
    oachf
    orTAVRi
    sthebestopt
    ion.

    Comput edtomogr aphicangi ographyisthegoldstandardforannularmeasur ement .The


    pati
    ent’sannularsizewoul dnotpr ecludeTAVR, butherminimum il
    iofemoraldiamet er
    swoul d
    precl
    udet hetr
    ansf emor alapproach.Thedegr eeofcalci
    fi
    cationoftheabdomi nalaor t
    aisnot
    i
    ni t
    selfacontraindicat
    ion,butthepr esenceofextremetortuosi
    tyoraneurysm woul dr equi
    re
    caref
    ulconsideration.Shedoesnotwi shfort
    hesur gi
    calopti
    on.Adi r
    ectaorti
    c,apical,or
    subclavianapproachmi ghtbef easible.

    Quest
    ion:

    56. A35- year


    -oldwomanpr esent
    sat24weeksgest at
    ion,newt oyourpract
    ice.Shehasa
    hi
    storyofr heumaticheartdi
    sease,alt
    houghshecannotr ecallwhichvalveisaf
    fected.She
    stoppedallmedicationsatthetimeofconception.Shewasr eferr
    edduet oincr
    easingf at
    igue
    overthepastmont h.Oneval uati
    on,herhear
    trate(HR)isregularat100bpm andbl ood
    pressureis105/73mm Hg.Acar di
    acexaminationreveal
    sapr ominentS1,anopeningsnap,
    andagr ade2/ 4diastol
    icmur murattheapexthatdoesnotr adiat
    e.HerS2 i
    snor mal,andlungs
    areclear.Noechocar di
    ogram isavail
    abl
    etoday.

    I
    nconsi
    der
    ingt
    het
    her
    apeut
    icopt
    ions,
    whi
    choft
    hef
    oll
    owi
    ngdoyouadvi
    se?

    a. Beginangiotensi
    n- converti
    ngenzymei
    nhi
    bit
    or.
    b. El
    ectivet
    ermi nat
    ionofpr egnancy.
    c. Eme r
    gentbal l
    oonval vuloplast
    y.
    d. Surgi
    calmi tr
    alvalver epair
    .
    e. Beginbeta-bl
    ocker .

    Answer
    :

    56. e. Begi
    nbet
    a-bl
    ocker
    .

    Thi
    spati
    ent'
    sexami nat
    ionfi
    ndingsareconsistentwithmitr
    alst enosi
    s,andthepreferredini
    ti
    al
    managementstrategywoul dbeHRsl owi
    ngwi thabet a-
    blocker.Aspr egnancyprogresses,t
    he
    HRincr
    easesandr esul
    tsindecreaseddi
    astoli
    cf i
    ll
    ingwit
    hi ncreasingleftat
    ri
    alpressures.
    Managementincludesmai ntenanceofsi
    nusr hythm andcont r
    olofHRt opromotetimef or
    adequatefil
    li
    ng.I
    nvasivestr
    ategi
    esarereser
    vedf orsi
    tuat
    ionswi
    thseverecompr
    omi
    se
    unresponsivetomedicalt
    herapy.Angi
    otensi
    n-convert
    ingenzymei
    nhibi
    torsar
    e
    contrai
    ndicat
    edinpregnancy. 

    Quest
    ion:

    57. A55- year-


    oldmanhasahi stor
    yofhypertensi
    on.Overthepast6months,hehas
    noticeddecreasedexer
    cisetol
    erance.Heget sshortofbreathonwalki
    ngamile.On
    exami nat
    ion,hi
    sbloodpressur
    ei s140/ 60mm Hg.Hi spulseis80bpm wi
    thnosignsofhear
    t
    fai
    lure.Hehasamur murofaort
    icr egurgi
    tat
    ion(
    AR) .
     

    Hisel
    ect
    rocar
    diogr
    am showslef
    tventri
    cularhyper
    trophy(
    LVH)
    .Hi
    svent
    il
    ati
    on/
    per
    fusi
    on
    scani
    snormal.Pul
    monaryfunct
    iontestsarenormal. 

    Echocar
    diogr
    aphyshowsmi
    ldLVH,
    sever
    eAR,
    eject
    ionf
    ract
    ionof50%,
    andLVend-
    diast
    oli
    c
    di
    mensionof60mm.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthebestopt
    ion?

    a. Aorti
    cvalvereplacement(AVR)
    .
    b. Li
    sinopri
    l.
    c. Metoprol
    ol.
    d. Conti
    nuedsur veil
    lance.
    e. Nif
    edipi
    ne.

    Answer
    :

    57. a. Aor
    ti
    cval
    ver
    epl
    acement(
    AVR)
    .

    ClassIindicat
    ionsf orAVRar e:1)sympt omati
    cpatientswi t
    hsevereARi r
    respect
    iveofLV
    systol
    icfuncti
    on( Level ofEvidenceB),2)asymptomat i
    cpatientswi
    thchronicsevereARand
    LVsystolicdysfunct i
    on( ej
    ectionfr
    acti
    on<50%)atr est(LevelofEvi
    denceB) ,
    and3)patient
    s
    withchronicsevereARwhi l
    eunder goi
    ngcoronaryarter
    ybypassgr aft
    ingorsurgeryonthe
    aortaorotherhear tvalves(LevelofEvidenceC).
    Quest
    ion:

    58. Whichoft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    ycausef
    ort
    hehemodynami
    cfi
    ndi
    ngsi
    nFi
    gur
    es
    1and2?

    Fi
    gur
    e1
    Fi
    gur
    e2
    a. Peri
    cardi
    altamponade.
    b. Tr
    icuspidregurgi
    tat
    ion.
    c. Pr
    imarypul monaryhypert
    ensi
    on.
    d. Tr
    icuspidstenosi
    s.

    Answer
    :

    58. b. Tr
    icuspi
    dregur
    git
    ati
    on.

    Thesimilar
    it
    ybetweent
    her i
    ghtatri
    alandrightventri
    cularpressur
    etraci
    ngsi
    ndicatesthatt
    he
    tr
    icuspi
    dvalveisal
    mostfuncti
    onall
    yabsent ,meaningthatitisopenduri
    ngbothdiastol
    eand
    systol
    e.Thus,t
    herei
    sseveretr
    icuspidregurgit
    ati
    on.

    Quest
    ion:

    59. A52- year-


    oldwomanpr esent
    sintheambulat
    orycli
    nicf
    orherannualgeneralmedi
    cal
    examinati
    on.Sherepor
    tsnosympt oms.Thepati
    entt
    akeshydrochlor
    othi
    azi
    de( 12.
    5mgdai l
    y)
    forhyper
    tensi
    onandatorvast
    atin(10mgdaily)f
    orahist
    oryofhyperl
    ipi
    demia.Her 
    brot
    herhad
    anaorti
    cvalverepl
    acementatage50year s.

    Onphysi
    calexami
    nat
    ion,
    thebl
    oodpr
    essur
    eis110/
    70mm Hgandhear
    trat
    eis80bpm.The
    headandneckexami nat
    ioni snormal
    .Lungsar ecleartoauscult
    ati
    on.Caroti
    dupst r
    okei s
    normal.Agrade1/ 6earl
    y-peakingsyst
    olicejecti
    onmur murisheardattheleftlowersternal
    border
    .Themur murdi minishessli
    ghtl
    ywi t
    hsquat -
    to-
    standmaneuver.TheS2  isnor
    mal .There
    arenoclicksorrubs.S3 
    andS4  ar
    eabsent.Peripher
    alpulsesareint
    act.Thereisnoper i
    pheral
    edema.
    Thepatientasksaboutherneedf orfurt
    herevaluati
    onandt hepotenti
    alforvalvesurgeryinthe
    fut
    ure.
     

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    ep?

    a. Calcium scoreassessment .
    b. Nof urthert
    estingrequir
    ed.
    c. Exercisestresstest.
    d. Transthoracicechocardiogr
    am.
    e. Cardiacmagnet i
    cresonanceimagi
    ng.

    Answer
    :

    59. d. Tr
    anst
    hor
    aci
    cechocar
    diogr
    am.

    Thepat
    ienti
    sasympt
    omat
    ic,
    andherphysi
    cal
    findi
    ngsar
    econsi
    stentwi
    thani
    nnocent
    murmur.
     

    Charact eri
    sticsofani nnocentmurmurareasof t(gr
    ade1or2)ej ecti
    onmur murt hatpeaks
    earl
    yi nsyst ole,withoutevidencef
    orothercardiacpathol
    ogy(i.
    e.,normalapicalimpulseand
    caroti
    dupst r oke;nodi astoli
    cmurmur,S3 
    orS4,cli
    cksorrubs,si
    gnsorsympt omsofhear t
    fai
    lure).However ,becauseoft hef
    amilyhist
    oryofapr obablebi
    cuspi daort
    icvalveandthe
    mur mur ,sheshoul dbescr eenedf
    orthepresenceofabi cuspi
    dval vewithechocardiogr
    aphy.
    Noneoft heot herst udiesareappr
    opri
    ate.
     

    Quest
    ion:

    60. A55- year-


    oldmani sadmi t
    tedtot hehospi talf
    orevaluationandmanagementof
    fati
    gueandl owerext r
    emi t
    yedema.Hef i
    rstnot edhissympt oms4mont hsago.Thepatient
    beli
    eveshehasgai nedmor ethan25pounds( 11.4kg)sincethattime.Thereisnoassociated
    chestdiscomf or
    t,hist
    oryofpal pi
    tati
    ons, f
    ever ,orconsti
    tuti
    onalsympt oms.Thepati
    entisa
    non-insuli
    n-dependentdi abeti
    c.Hehasbeent r
    eatedforhyper t
    ensionfor8yearsonstable
    dosesofl isi
    nopr i
    l(10mgdai l
    y)andaml odipine(10mgdai l
    y).Twoyear sago,heunderwent
    pacemakerpl acementf orsympt omat i
    cbr adycardia.Thepat i
    entalsohasbeent r
    eat
    edf or
    obstructi
    vesl eepapnea;hi slastevaluati
    on6mont hsagoshowedadequat efitandf
    unct i
    onof
    hiscont i
    nuouspost i
    ti
    veairwaypr essure machi ne.Hisregularphysici
    anprescri
    bedloop
    diureti
    cs2mont hsagowi thoutanybenef icialeff
    ect. 

    Onphysicalexami nati
    on,thepatientisobese( bodymassi ndex35.2kg/ m2).Bloodpressurei
    s
    128/72mm Hgwi thahear trateof72bpm.Thel ungsar eclear.Thejugularvenouspulseis
    l
    ocatedatthel evel ofthejawwi t
    hpat i
    entsitt
    ingupr i
    ght.Ther eisaprominentV  wave.The
    carot
    idcontouri snor mal.Precor
    di al
    palpati
    onr evealsasl i
    ghtlif
    t(1+)attheleftlowerster
    nal
    border
    .A2/ 6bl owi ngholosystol
    icmur murispr esentint hi
    sregionwi t
    hanear lydiast
    oli
    c
    fi
    ll
    ingsoundthataccent uatesduringinspir
    ati
    on.Apul satil
    eli
    verispresent.Onper i
    pheral
    examinati
    on,ther eissevereedema( 3+)invol
    vingt hethighsandl owerlegs. 
    ChestX- rayrevealscardiomegalywi t
    hmi l
    denlargementoftheri
    ghtventr
    icularcontour.The
    l
    ungf ieldsshownoedema.At ransthoracicechocardi
    ogram (
    TTE)showsnor malleft
    ventri
    cul arsystoli
    cfuncti
    on(ej
    ectionfracti
    on65%)andsever etr
    icuspi
    dregur gi
    tat
    ion(TR)by
    colorflowDoppl er
    .Mild-
    moderatesyst ol
    icdysfuncti
    onandenlar
    gementoft herightventri
    cle
    i
    spr esent .Esti
    mat edri
    ghtvent
    ricularsystol
    icpressurei
    s30mm Hg.Doppl er
    echocar diographyofthehepaticveinsshowsnoexpi rat
    oryr
    ever
    sal.

    Whi
    chi
    fthef
    oll
    owi
    ngi
    sthemostl
    ikel
    ycauseoft
    heTR?

    a. Pul
    monar yhypertension.
    b. Restri
    cti
    vecardi
    omyopat hy.
    c. Cons t
    ri
    cti
    veperi
    caridit
    is.
    d. Pacemakerleadimpi ngement.
    e. Ebstei
    n'sanomaly.

    Answer
    :

    60. d. Pacemakerl
    eadi
    mpi
    ngement
    .

    Thepat i
    enthasapr imaryabnor mal it
    yint hetri
    cuspidvalve.Itmayber el
    at edt ori
    ght
    ventri
    cularsystoli
    cdysf unctionwi t
    hr etr
    actionofthetri
    cuspi dval
    vechor daeandi ncreased
    annulus.Thepat i
    entpresentswi thsympt omsandsi gnsofr i
    ghtheartfailur e.Thedifferenti
    al
    diagnosisincl
    udesconst r
    icti
    veper icardi
    tis,astr
    uctural
    lyabnor maltri
    cuspi dval ve(suchas
    Ebstein'
    sorpr olapse),
    andsecondar yTRduet opulmonar yhypertensi
    on( suchassl eepapnea
    orrestri
    cti
    vecar diomyopat hy).Recent l
    y,therehasbeeni ncreasedrecogni tionoft hepot ent
    ial
    forsevereTRcausedbydevi celeadimpl antati
    onintotherightventri
    cle. 

    TTEmaynotdet ectsuchleafletimpingement ,andtransesophagealechocar diographyshould


    bepur suedi nsuspectedpat i
    ents.Inast udyof41pat ientswhounder wenttr
    icuspidsurgery
    fordeviceleafletimpingementatt heMayoCl i
    nic,onlyfive(12%)ofthepat i
    entshadan
    accuratepr eoperati
    vediagnosisonTTE.Dat afrom theDoppl erinter
    rogati
    onoft hehepatic
    veindonotsuppor tthepresenceofconst r
    ict
    ivepericardit
    is.Therewasnocommentabout
    apicaldisplacementoft heseptal orposteri
    ortri
    cuspidleaflet
    sthatwoul dbeseeni nEbstein'
    s
    anomal y.Thepul monar ypressureswer enormal byecho/ Doppler,suggesti
    ngnosecondar y
    causef ortheTR.

    Quest
    ion:

    61. A30- year-


    oldmani sr efer
    redf orevaluationofamur mur .Her eport
    snosympt oms, and
    hasnosi gnifi
    cantmedicalhistory.Onphysi cal exami nati
    on,hishei ghtis69i nchesandwei ght
    i
    s185l bs.Thebl oodpressurei s135/ 70mm Hgwi thar egularhear trateof78bpm.Hi slungs
    areclear.Prominentcarot
    idpul sati
    onsar epr esent.Thej ugularvenouspul seisatthel evelof
    thesternalnotch.Theapicalimpul seisslightlyenlargedandl aterallydisplacedtotheant eri
    or
    axil
    lar
    yl i
    ne.TheS1 andS2 arenor mal ,andanS3  ispresent.Therei sanear lysystol
    icclickthat
    doesnotchangewi thi
    nspiration.Bot hasof t(grade2/ 6)crescendo- decrescendosyst oli
    c
    mur murandasof t(
    grade2/ 4)decr escendodi astoli
    cmur murarepr esentalongtheleftsternal
    border.
    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostl
    ikel
    yval
    vul
    arabnor
    mal
    it
    y?

    a. Patentductusarteri
    osus.
    b. Bi
    cuspidaor t
    icvalve(BAV)wi t
    hregurgit
    ati
    on.
    c. Pul
    moni cvalvestenosiswithregurgi
    tati
    on.
    d. Rheumat i
    cmi t
    ralstenosisandregurgit
    ati
    on.
    e. Degenerati
    veaorticvalvestenosi
    swi t
    hregurgi
    tat
    ion.

    Answer
    :

    61. b. Bi
    cuspi
    daor
    ti
    cval
    ve(
    BAV)wi
    thr
    egur
    git
    ati
    on.

    Pulmoni cvalvestenosisisunl i
    kelybecauset hemur murdoesnotchangewi thr espirationand
    thejugularvenouspul sei snormal .Thei ntensityofthepul moni cejecti
    oncl i
    ckdecr easeswi t
    h
    i
    nspirati
    on.Degener ati
    veaor ti
    cst enosisi snotassoci atedwi t
    hasyst oli
    ccl i
    ck,andhei sonl
    y
    30year sold.Rheumat icmi tr
    alstenosi smaybeassoci atedwi thadi astoli
    cclick,butnotone
    thatoccur sduri
    ngsyst ole.Patentduct usar teri
    osuspr oducesacont inuousmachi ne-l
    ike
    mur murandi snotassoci at
    edwi t
    hacl ickorwi depul sepr essur e.BAVcanbeassoci atedwi t
    h
    suddencessat ionofval veopening, leadingt oanej ecti
    onsyst oli
    ccl i
    ck,andof teni s
    associatedwi t
    hsignif
    icantAVr egurgitation.Findingsofchr onicaor ti
    cr egurgit
    ationwi thlef
    t
    ventri
    cularvolumeover loadincludeanenl ar
    gedandl aterall
    ydi splacedapi calpulse, wide
    aorti
    cpul sepressure,andanS3.

    Quest
    ion:

    62. An80- year-


    oldmani sadmi t
    tedtothehospitalf
    oranacut eexacerbati
    onofhear tfail
    ure.
    Thepat i
    enthasaknownhi st
    oryofaor t
    icstenosis,
    buthasnotsoughtr ecentmedi calcare.For
    thepast3year s,hehashadexer ti
    onaldyspnea.Hissymptomshavei ncreasedsignifi
    cantly
    overthepastmont h,
    andnowar eaccompani edbynoctur
    nalsympt omsandor t
    hopnea.Ther e
    arenocompl aintsofchestdi scomfortorsyncope.Thepatienthasahi st
    oryofpr i
    orst r
    oke,
    diabetesmell
    itus,andt r
    eatedhypertension.Thereisnoknownhi st
    oryofcor onaryartery
    diseaseoratr
    ial ar
    rhythmia. 

    Onphysi calexami nation,heappear sfr


    ail
    .Thepat ientis160cm t al
    landwei ghs70. 2kg.Hi s
    bloodpr essur eis104/ 72mm Hgwi thaheartrateof80bpm.Di ffusecr acklesarepr esentin
    bothl ungf ields.Thej ugularvenouspul seiselevatedtot heangl eoft hej awwitht hepatient
    sitt
    ingupr i
    ght .Thecar oti
    dpul sesarediminishedanddel ayedincont our.Hisapicalimpul sei
    s
    displacedt ot heant er
    ioraxi
    ll
    ar yl
    ine.Asoft,mid-peakingsyst oli
    cej ecti
    onmur muri shear dat
    ther i
    ghtupperst ernalborder.Theaor t
    iccomponentoft hesecondhear tsoundissl ightl
    y
    diminished, whilethepul moniccomponenti ssignifi
    cantl
    yi ncreased.At hir
    dhear tsoundi s
    present .Per i
    pher aledema( 2+)ofbot hlowerext r
    emi t
    iesisnot ed. 

    Transt
    horacicechocardiographyshowsal eftvent
    ri
    cularej
    ectionf r
    acti
    onof35%wi thadi l
    ated
    l
    eftventr
    icle(end-di
    astol
    icdiamet er
    ,58mm) .Themeanaor t
    icval vegradi
    entis24mm Hg
    withavalvear eaof0.7cm2 derivedfrom t
    hecont i
    nui
    tyequation.Car di
    acoutputiscal cul
    ated
    tobe3.2 L/min.Moder at
    etricuspidregur
    gitati
    onispresentwithanest imat
    edr i
    ghtvent ri
    cular
    systol
    icpressureof62mm Hg.Ther emainderoftheechocardi ogram i
    sunremar kable.
    I
    ntr
    avenousdi
    uresi
    sisi
    nit
    iat
    ed,
    andsympt
    omsi
    mpr
    ove.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    enextst
    ep?

    a. Dobut aminest
    ressechocardiogram.
    b. Cardiacmagneticresonancei magi
    ng(MRI)
    .
    c. Rightheartcat
    heteri
    zati
    on.
    d. Transesophagealechocardiogram (
    TEE)
    .
    e. Exercisestr
    essechocardiogram.

    Answer
    :

    62. a. Dobut
    ami
    nest
    ressechocar
    diogr
    am.

    Thepat ienthasevi denceofl ow- out put ,low- gradi entaor t


    icst enosi s.Thi sent itycanbedi fficult
    todi sti
    ngui shf r
    om pat i
    entswhohavemi l
    dormoder ateaor ticst enosiswi thl owcar di
    acout put
    duet oanet iologyothert hant heaor t
    icval velesi on.I ti si mpor tantt onot et hatt heval vear ea
    i
    sf low- dependent .Thel owval vear eai nt hispat ient( 0.7cm2)maybeduet oei ther
    anat omi callysever eaor ti
    cstenosi s,oracar diomyopat hyi nwhi chdecr easedcont ractil
    it
    y
    l
    eadst oadecr easeinaor t
    icvalveopeni ng.Themostappr opr i
    atenextst epi sadobut ami ne
    stressst udy, whichmaybeper formedwi thechocar diogr aphyori nt hecar di accat heter i
    zat i
    on
    l
    abor atory.Thegoaloft hedobut ami nest udyi st oexami net hesever i
    tyoft heaor ti
    cst enosi s
    withani ncr easei ntransvalvularf lowwi thmeangr adi ent>40mm Hg.Pat ient swi thsever e,
    i
    ntr i
    nsi caor ticstenosist ypi
    cal l
    ywi l
    lexhi bitahi ghaor ti
    cgr adientwi thaper sistentlylowval ve
    areawi thdobut amineadmi nistration.Conver sel y,inpat ientswi thoutanat omi callysever e
    aor t
    icst enosi s,theaor t
    icvalvear eawi llincreasesi gni ficant lywi thani ncreasei ncont ract i
    lity
    2
    andcar diacout put(typicall
    y>1. 2cm ) .ATEE, car diacMRI , andonl yright -
    hear t
    cathet erizationwoul dnothel pdi stingui shwhet hert hel owgr adientwasduet ol owout put
    rel
    at edt ot heaor ti
    cst enosisorani nher entcar diomyopat hy.Exer cisest udi esi napat ientwi th
    sever eaor ticst enosisandsympt omsar enotr ecommended. 

    Quest
    ion:

    63. A55- year


    -ol
    dwomani sref
    err
    edtoyouf oreval
    uat
    ionandt reat
    mentofaorti
    c
    regurgi
    tat
    ion(AR).Shehasaknownhi st
    oryofbicuspi
    daort
    icvalve.Thepat
    ientexerci
    sesfour
    tofivet
    imesperweekonanupr i
    ghtst
    ati
    onarybicycl
    eandreport
    snosympt oms.Hermedi cal
    hist
    oryconsistsofmedical
    lyt
    reat
    edhyperl
    ipi
    demi aandahyster
    ect omy.
     

    Onphysicalexaminat
    ion,t
    hebloodpr essureis126/74mm Hgwi thaheartr
    ateof84bpm.
    Lungsarecleart
    oauscultat
    ion.Theleftventr
    icul
    ar(LV)api
    cali
    mpul sei
    snormalandnot
    di
    splaced.Asoft,
    grade2/4diastol
    icdecrescendomur murispresentmaxi
    mall
    yatthelef
    t
    ster
    nalborder
    .Asystoli
    cejecti
    oncli
    cki snoted.Therei
    snoS3 orS4,andnoperi
    pher
    aledema.
     

    Transt
    horaci
    cechocar
    diogr
    am demonst
    rat
    esanLVej
    ecti
    onf
    ract
    ionof59%wi
    thanend-
    systol
    icdi
    mensionof33mm andend-di
    ast
    oli
    cdi
    mensi
    onof50mm.

    Whi
    choft
    hef
    oll
    owi
    ngshoul
    dbepr
    escr
    ibed?

    a. Met
    opr
    ololt
    art
    rat
    e.
    b. Nif
    edipine.
    c. Aspir
    in.
    d. Enal
    apr i
    l.
    e. Nome di
    cati
    oni
    ndi
    cat
    ed.

    Answer
    :

    63. e. Nomedi
    cat
    ioni
    ndi
    cat
    ed.

    Forpat i
    entswi thAR,long-termt herapywithvasodi l
    atorsisindicat
    edi npat i
    ent swit
    hsevere
    regurgit
    ationandsympt omsorLVdysf uncti
    ononl ywhensur gi
    calinterventioncannotbe
    performedduet ocomor bidit
    y.Vasodi l
    atortherapyalsomaybeconsi deredi nasympt omatic
    pati
    entswi thsevereregur git
    ationwhohaveLVdi lat
    ationbutnor malsyst oli
    cf unct
    ion,andas
    abridget oaorticval
    ver eplacementi npatientswithsever eregurgi
    tati
    onanddecompensat ed
    heartfail
    ure.However ,intheabsenceofot herindicati
    ons( e.
    g.,hypertension),vasodil
    ator
    therapyisnoti ndi
    catedi nasympt omati
    cpat i
    entswi t
    hmi l
    dormoder at eARandnor mal
    systoli
    cfunction.Ther eisnoi ndicati
    onforaspirinorbet a-
    blockersformodi f i
    cati
    onofherr i
    sk
    foreventualaor t
    icvalvereplacement .

    Quest
    ion:

    64. Youar easkedt oseea67- year-


    oldmanwhowasadmi tted2daysagot othehospital
    .
    Twomont hsago, t
    hepat i
    entunder wentaorti
    cvalvereplacementwi t
    ha26mm por cine
    bioprosthesi sandcor onaryarterybypassgr aft
    ingwithplacementofal eftinter
    nalmammar y
    arter
    yt othemi ddleleftant
    eriordescending.Thesur ger
    yandhospi talcoursewer e
    uncompl icated, exceptforsternaldehiscencethatoccurredsoonafterthepr ocedure.Overthe
    pastweek, thepat i
    enthashadsympt omsofl et
    hargy,hadpoorappet i
    te,andf el
    tfeveri
    sh.His
    physicianf oundhi mt obef ebril
    e(103°F)andpr omptlyadmitt
    edt hepatienttoyourhospi t
    al
    servi
    ce.Thepat i
    enthasnocompl aint
    sofdyspneaorchestpai n.Therear enogeni touri
    nary
    sympt oms.  

    Onphysi calexamination,t
    hetemper atur
    ei s102.
    5°F.Thehear trateis101bpm withablood
    pressureof110/ 70mm Hg.Thel ungsar ecleart
    oauscultati
    on.Jugul arvenouspul
    seisnot
    elevated.Carot
    idcont our
    sarenor mal.Agr ade2/6earl
    y-peakingsystolicmurmurispresentat
    therightuppersternalborder
    .Ther eisnoS3 orS4.Theperipheralexami nat
    ioni
    sunremarkable.
     
    Hi ssternalwoundl ookswellhealed,butthester
    num wasunst abl
    e.

    AchestX- rayshowsnormalcardiacsil
    houett
    eandbi later
    alinf
    ilt
    rateswit
    hnopl eural
    eff
    usions.Bloodcult
    uresaredrawnandpendi ng.Anel ect
    rocardiogram r
    eveal
    sl ef
    tvent
    ri
    cul
    ar
    hypertr
    ophywi t
    hnormalPRi nt
    erval.Atranst
    horaci
    c echocardiogram wasperformed,and
    no vegetat
    ionsare 
    evi
    dent.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    enextst
    ep?

    a. Posit
    r onemissiontomogr aphycomputedtomogr
    aphy.
    b. Transesophagealechocar diogr
    aphy(TEE)
    .
    c. Chestcomput edt omography.
    d. Cardiacmagnet icresonanceimaging.
    e. Cardiaccatheteri
    zati
    on.
    Answer
    :

    64. b. Tr
    ansesophagealechocar
    diogr
    aphy(
    TEE)
    .

    Inpati
    entswi thapr ostheti
    cval ve,TEEi spreferredtoeval uateforendocar diti
    sasi tismor e
    sensit
    iveindet ectingveget ationsandcompl icationst hant ransthoracicimagi ng.Inpat i
    ents
    withsuspectedendocar di
    tis,bloodculturesshoul dbedr awnusi ngt woset sfrom different
    sit
    es.Surgeryf orpr ostheti
    cval veendocar dit
    isshoul dbeconsi deredwhent hereisevi denceof
    heartfai
    lur
    e, valvedehi scence, progressivevalvedegener at
    ion,compl icat
    ions( e.g.,
    abscess),
    persi
    stentbact eremi a,orrecur r
    entembol i
    .Antimi cr
    obi altherapyf orprostheti
    cval ve
    endocardit
    isshoul dutil
    izevancomyci nunt i
    lsuscept ibili
    tytooxaci ll
    inhasbeendet ermi ned.I
    f
    theTEEi snegat ive,thenot herimagingmodal i
    ti
    esmi ghtbeconsi dered.Ot hersourcesof
    i
    nfecti
    ons,suchasmedi astiniti
    sorpneumoni a,shoul dbesoughti fthereisnoevi dencef or
    endocardit
    is.Ther ei snoindi cati
    onforcor onar yangiogr aphyatt histi
    me. 

    Quest
    ion:

    65. A55year -ol


    dmal efar
    mercomest oseeyouint heoutpatientcl
    ini
    cfornewsympt oms
    ofshortnessofbreath.Thepatienthasal i
    fel
    onghistoryofabi cuspidaor
    ticvalve.Overthe
    past2mont hs,hebegannot i
    ngsympt omsdur i
    ngmoder atelevelsofacti
    vit
    y(e.g.,choppi
    ng
    wood,balinghay).Withsever
    eexer ti
    on,thepati
    entoccasionallyexperi
    enceslightheadedness.
    Thereisnohi st
    oryofchestdiscomf or
    t,coronar
    yarterydisease,hypert
    ension,orcardiac
    arr
    hythmi a.
     

    Hisphysicalexaminat i
    onisremarkableforalate-peakingsystol
    icejecti
    onmur murattheri
    ght
    uppersternalborderandasi ngl
    ecomponentS2.At ranst
    horacicechocardi
    ogram
    demonst r
    atessever e,bi
    cuspidaor
    ticstenosi
    s( valvearea0.7cm2, meangradient56mm Hg) ,
    mildaorti
    cregurgitati
    on,andnormal l
    eftvent
    ricularsystol
    icfuncti
    on( ej
    ect
    ionfract
    ion62%).
     

    Yourecommendsurgi
    calaor
    ti
    cval
    verepl
    acement.Thepati
    entst
    rongl
    ydesi
    resat
    issue
    prost
    hesi
    s,ashewant
    stoavoidt
    heneedforant
    icoagul
    ati
    onwithwarf
    ari
    n.

    Whi
    choft
    hef
    oll
    owi
    ngst
    atement
    siscor
    rectr
    egar
    dingt
    heuseofat
    issuepr
    ost
    het
    icval
    ve?

    a. Autogr
    aft
    shavepoor
    ersurvi
    val
    comparedwit
    htissueval
    ves.
    b. Thehemodynamicpr
    ofi
    leofastent
    edt
    issueval
    veissimi
    lart
    oamechani
    cal
    pr
    osthesis.
    c. Ther i
    skofsurgicalr
    eoper
    ati
    onissimi
    lart
    other
    iskofi
    nit
    ialoper
    ati
    on.
    d. Struct
    uraldegenerat
    ioni
    sage-r
    elat
    ed.

    Answer
    :

    65. d. St
    ruct
    uraldegener
    ati
    oni
    sage-
    rel
    ated.

    Ther
    eisani
    ncreasedriskofst
    ruct
    uraldegener
    ati
    onofatissueprost
    hesi
    sinyoungerpat
    ient
    s
    compar
    edwit
    hol derpati
    ent
    s.Thecauseforthi
    sincr
    easedriski
    snotcomplet
    elyknownbut
    l
    ikelydue, atleasti npart,t
    othehi ghval vestressconf err edbyyounger ,
    relati
    vel
    ymor eactive
    i
    ndi viduals.Theuseofanaut ograft(i.
    e.,Rosspr ocedur e)isnotinferi
    ortoat i
    ssuepr osthetic
    valve.St entedt issuepr ost
    heseshaveasmal leref fectiveor i
    ficeareaandt ypi
    callyhigher
    residualgr adi entst hanmechani cal valves.Stentlesst issuepr ostheseshaveabet t
    er
    hemodynami cpr of i
    lethanstentedval ves,butaret echni call
    ymor echall
    engingt osurgicall
    y
    i
    mpl antast heyar esewnt otheinsi deoft heaorticr oot.Ther i
    skofsurgicalreoperati
    oni s
    significantlyrelat edt opati
    entmor bi di
    ty,buti
    st ypicallyt wof oldt
    ot hr
    eefol
    dhi gherthant he
    ri
    skoft hei nit
    ial surgery.

    Quest
    ion:

    66. Youar eseeinga66- year-ol


    dwomanwhounder wentcardiacsur ger
    yyesterdayfor
    symptomat i
    cmi tr
    alregurgitat
    ion.Duringtheprocedur e,t
    hesur geonpl aceda31mm St .Jude
    mechanicalbileaf
    letprosthesi
    si nthemi t
    ralposi
    ti
    on, inadditi
    ont oper f
    ormingtri
    cuspid
    annul
    oplastyforsever etr
    icuspidregurgit
    ati
    on.Post operati
    veat r
    ialfi
    bril
    lat
    ionoccurredand
    spont
    aneousl yresolvedwi t
    hin24hour s.Hermedi calhistor
    yissi gnif
    icantonlyfor
    hyper
    tension.Apr eoperati
    vecor onaryangiogram haddemonst ratednor malart
    eri
    es.

    Whichoft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    elong-
    ter
    m ant
    it
    hrombot
    ict
    her
    apyf
    ort
    his
    pat
    ient
    ?

    a. Warf
    ari
    nINRgoalof2.5-
    3.5.
    b. Aspi
    ri
    n81mgdaily;warfar
    inint
    ernat
    ionalnormal
    izedr
    ati
    o(I
    NR)goalof2.
    5-3.
    5.
    c. Aspi
    ri
    n81mgdaily;warfar
    inINRgoal of2.
    0-3.
    0.
    d. Dabi
    gatr
    an150mgt wicedail
    y.

    Answer
    :

    66. b. Aspi
    ri
    n81mgdai
    ly;war
    far
    ini
    nter
    nat
    ionalnor
    mal
    izedr
    ati
    o(I
    NR)goalof2.
    5-
    3.5.

    Forpatientswithamechani calvalveprost hesi


    sinthemi t
    ralposition,warfari
    nshoul dbe
    uti
    li
    zedwi thanI NRgoalof2. 5-3.5.Highergoalsmaybeconsi der edinpat i
    entswhohave
    thr
    omboembol iceventswhi l
    eant icoagulatedwithi
    nthisINRr ange.Randomi zedt r
    ial
    shave
    demonst rat
    edr educti
    onoft hromboembol iceventswit
    ht headdi t
    ionofaspi ri
    n( 75-
    100mg
    dai
    ly)t
    owar far
    inanticoagulati
    oni npatientswithmechani calvalves.Clopidogrel,i
    naddi
    tiont
    o
    warfar
    in,shouldbeconsi der
    edi npat i
    entswhocannott akeaspi rin.Aspiri
    nalonei snot
    eff
    ecti
    vef orprophylaxisagainstval vethrombosis.Dabigatr
    ani snotr ecommendedf or
    anti
    thr
    ombot ict her
    apyf ormechani calvalves.

    Quest
    ion:

    67. A65- year-oldmancal l


    syouroffi
    cewithquest i
    onsregardi
    nghismi tr
    alvalveprost
    hesis.
    Twoyear sago, thepat i
    entunder
    wentsurgerywi thpl
    acementofa31mm por ci
    nemi tr
    alval
    ve
    prosthesi
    sf orsympt omatic,
    severer
    egurgi
    tati
    onduet omyxomat ousdisease.Hehasdone
    wellsincesurgery, wit
    hnosympt omsorcompl icati
    onsinfoll
    ow-up.Hislastechocardi
    ogram,
    whichwasper formed2mont hsago,demonstratedameant ransmitr
    algradientof2mm Hg
    andtrivi
    alregurgitati
    on.

    Forwhi
    choft
    hef
    oll
    owi
    ngpr
    ocedur
    esshoul
    dhet
    akeant
    ibi
    oti
    csaspr
    ophyl
    axi
    sagai
    nst
    i
    nfect
    iveendocar
    dit
    is?

    a. Noant i
    bioti
    cprophylaxi
    sneeded.
    b. Transesophagealechocardi
    ography.
    c. Surveil
    lancecol
    onoscopy.
    d. Cystoscopyformalignancyremoval.
    e. Drainageofaskinabscess.

    Answer
    :

    67. e. Dr
    ainageofaski
    nabscess.

    Accor dingtothemostr ecentguideli


    nes,ant ibioti
    cpr ophyl axisagainstendocar dit
    isisl
    imited
    onlytopat ientsathi ghestriskofcompl i
    cat ions.Thesehi gh-ri
    skpatientsincludethosewi t
    h
    prosthet i
    chear tvalves.Ant ibi
    ot i
    cprophylaxi sisr equiredi nthesepat i
    entswhoar eundergoing
    dentalpr ocedur est hatinvolvemani pul
    ationoft hegi ngivaltissues,theper i
    apicalregi
    onoft he
    teet
    h, orper f
    orat i
    onofor almucosa.Ant ibioticpr ophyl axisalsomaybeconsi deredinhigh-ri
    sk
    pati
    ent sforrespi ratoryt r
    actprocedurest hati nvolveinci sionofthemucosa( e.
    g.,
    tonsi
    llectomyoradenoi dectomy)andf orgeni t
    our inary,skin,orgastroint
    est i
    nalprocedures
    thati
    nvol veinfect edar eas.Patientsunder goingdi agnost i
    cpr oceduresint heabsenceoft hese
    conditionsdonotr equireant i
    bioti
    cprophyl axis. 

    Quest
    ion:

    68. A50- year-


    oldmanpr esent
    st oyourambul at
    oryoff
    icef
    orevaluati
    onofaorti
    cstenosi
    s
    (AS)andanaor t
    icaneurysm.Tenyear sago,t
    hepat i
    entwasdiagnosedwithabicuspi
    daor t
    ic
    valve(BAV)duri
    ngar outinegeneralmedicalexaminati
    on.Heisanact i
    veandasymptomat i
    c
    i
    ndi vi
    dualwi
    thgoodexer cisetol
    erance.Thepatientt
    akesnomedi cat
    ions.
     

    Onphysicalexami nat
    ion,t
    hebl oodpressureis110/70mm Hgwi t
    hahear tr
    ateof66bpm.
    Thecaroti
    dcont ourisnormal.Asystoli
    ccl i
    ckandgr ade2/6earl
    y-peaki
    ngsystol
    icej
    ecti
    on
    mur murarepresentattherightuppersternalbor
    der.Theaorti
    ccomponentoft heS2 
    is
    preser
    ved.Thereisnodi ast
    olicmurmurandnoS3  orS4.Per
    ipher
    alexaminati
    onshowsno
    edema. 

    Thepat
    ientunder
    goesanechocar
    diogr
    am,
    whi
    chdemonst
    rat
    esaBAVandt
    hef
    oll
    owi
    ngdat
    a: 

    Lef
    tventr icularejectionfracti
    on:60%. 
    Lef
    tend- diast ol
    icdimensi on:50mm.  
    Ascendingaor t
    adi mension:4.6cm.  
    Aort
    icrootdi amet er:3.
    8cm.  
    Lef
    tatri
    alvol umei ndex:32ml /m2.
    Meanaor ticvalvegr adient:10mm Hg.  
    2
    Aort
    icval vear ea:2.0cm .

    Whichoft
    hef
    oll
    owi
    ngwoul
    dbet
    hemostappr
    opr
    iat
    eti
    met
    oper
    for
    m anechocar
    diogr
    am
    agai
    n?

    a. Ever
    y3year
    s.
    b. Ever
    y2years.
    c. Ever
    yyear
    .
    d. Ever
    y5yearsorl
    ater
    .

    Answer
    :

    68. c. Ever
    yyear
    .

    Forpatientswi t
    haBAVandanascendi ngaor ti
    caneurysm >4.5cm, annuali
    magingofthe
    aneurysm isrecommended.Forpat ient
    swithmi ldASwi t
    houtanascendi ngaort
    icaneurysm,
    seri
    alechocar diographyevery3-5yearsisrecommendedi ntheabsenceofachangei n
    cl
    ini
    calst at
    usorphysi calfi
    ndi
    ngs.Echocardiographyi
    srecommendedannual l
    yfor
    asympt omaticpat i
    entswi t
    hsevereASandever y1-2year
    sint hosewithmoderateAS.
    Pati
    entsshoul dbeadvi sedtor
    eportchangesi nsymptomspr omptly.

    Quest
    ion:

    69. A29- year-ol


    dwomani sref
    erredbyherinter
    nistforeval
    uat
    ionofanewlyident
    ifi
    ed
    murmur.Thepat i
    entrepor
    tsnocardiovascul
    arsymptomsandhasnosi gni
    fi
    cantmedical
    hist
    oryexceptforaknownpenicil
    li
    naller
    gy.Heronlyprescri
    bedmedici
    neisanoral
    contr
    acepti
    ve.Shedeniesrecr
    eati
    onal dr
    uguse. 

    Onphysi calexami nati


    on,thereisasystol
    icclickfol
    lowedbyagr ade2/6lat
    esyst
    oli
    cmur mur,
    consi
    stentwi thmi tr
    alregurgit
    ati
    on.Noot herabnormalf i
    ndingsarepresent
    .Atr
    ansthor
    acic
    echocardiogram demonst ratesmyxomat ousmi tr
    alvalvediseasewithmoderat
    eregurgi
    tat
    ion
    andmi l
    dl ef
    tat r
    ialdil
    atati
    on.Theleftventri
    cul
    arend- syst
    oli
    cdimensionis32mm, and
    ej
    ecti
    onf racti
    oni s65%.

    Whi
    choft
    hef
    oll
    owi
    ngt
    ypesofant
    ibi
    oti
    cpr
    ophyl
    axi
    sisr
    equi
    redpr
    iort
    odent
    alpr
    ocedur
    es?

    a. Noantibi
    oticpr
    ophyl
    axi
    sisr
    equi
    red.
    b. Amox i
    cil
    li
    n2g.
    c. Amox i
    cil
    li
    n4g.
    d. Cl
    indamycin800mg.
    e. Cl
    indamycin600mg.

    Answer
    :

    69. a. Noant
    ibi
    oti
    cpr
    ophyl
    axi
    sisr
    equi
    red.

    Themostcur rentguideli
    nesdonotr ecommendant i
    biot
    icprophylaxi
    sf orendocarditi
    sf or
    myxomat ousmi t
    ralvalvedisease.Endocar di
    tisprophylaxisisonlyrecommendedf or
    condi
    tionsassociatedwiththehi ghestriskofadver seoutcomef rom endocar di
    ti
    s.These
    condi
    tionsare:1)prostheti
    ccar diacvalveorpr osthet
    icvalverepairmat eri
    al,
    2)priorhistor
    yof
    i
    nfect
    iveendocar di
    tis,
    3)car di
    act ransplantr
    ecipientswithvalvul
    opathy, 4)completel
    y
    repairedcongenit
    alheartdi
    seasewithper
    cutaneousorsurgi
    calr
    epairoccurr
    ingwi
    thi
    nt he
    previous6mont hs,5)repai
    redcongeni
    tal
    heartdiseasewi
    thresi
    dualshuntsordef
    ectsthat
    i
    mpai rendot
    heli
    ali
    zat
    ionofprosthet
    icmater
    ial
    ,and6)unrepai
    redcyanoti
    ccongeni
    talheart
    disease. 

    Forpatientswiththeseconditi
    ons, ant
    ibi
    oti
    cpr ophylaxi si
    sr ecommendedf ordental
    proceduresthatinvolvemanipulati
    onoft hegingivaltissues, t
    heper i
    api
    calregionoftheteeth,
    orperforati
    onofor almucosa.Ant i
    biot
    icprophylaxisal somaybeconsi deredforprocedures
    thati
    nvolveincisi
    onoft herespirat
    orymucosa( e.
    g.,tonsil
    lectomyoradenoi dectomy)andf or
    genit
    our i
    nary,
    skin,orgastroi
    ntesti
    nalprocedurest hatinvolveinfectedareas.Pati
    ents
    undergoingdiagnost i
    cproceduresintheabsenceoft hesecondi tionsdonotr equi
    reanti
    biotic
    prophylaxi
    s. 

    Quest
    ion:

    70. A51- year-


    oldmani srefer
    redtoyouforevaluati
    onofachr oni
    cmur mur.At20year sof
    age,heunderwentsurgicalr
    epairofbi
    cuspi
    daor t
    icvalve( BAV)st
    enosi
    s.Thepat i
    enthasbeen
    fol
    lowedint
    ermitt
    entlyandhasnoot hersi
    gnif
    icantmedi calhi
    stor
    y.Heisphysical
    lyacti
    veand
    asymptomatic,
    regularl
    yrunning5mi l
    eswit
    houtlimitat
    ion. 

    Onphysi calexami nati


    on, thepat i
    entis184cm t allandwei ghs84kg.Thehear trateisregul
    ar
    at60bpm wi thabl oodpr essur eof135/ 55mm Hg.Thel ungsar ecleartoauscul tati
    on.The
    l
    ef tventricular(LV)apicalimpul seisenl argedandl ateral
    lydisplacedt otheanterioraxil
    lar
    y
    l
    ine.Agr ade2/ 6ear l
    y-peaki ngsyst oli
    cmur murandadecr escendogr ade2/ 4diastoli
    c
    mur murbot har epresental ongt hel eftsternal border.TheS2Per ipheralexamination
    demonst ratesapul sati
    leuvul aandacol lapsingwat erhammerr adialpulse.
     
    Thepat ientunder goesat ransthor acicechocar diogram thatdemonst ratesBAV.LVend-
    diastoli
    cdi mensionis7. 1cm, LVend- syst oli
    cdi mensi onis4.2cm, andLVej ectionfracti
    on
    (calcul
    ated)i s57%.I ntervent r
    icularsept alwal lthicknessis1. 2cm, LVpost eri
    orwal lthi
    ckness
    i
    s1. 2cm, aort
    icrootdiamet eri s4.2cm, AVr egur gi
    tantvolumei s70ml ,AVregur gi
    tant
    fracti
    oni s60%, andcar di
    acout putis6. 8L/ min.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    ep?

    a. Surgicalaorti
    cvalvereplacement(SAVR).
    b. Seri
    alechocar di
    ography.
    c. Transcatheteraorti
    cvalvereplacement(
    TAVR)
    .
    d. Sympt om-li
    mi t
    edexercisestresstest
    .

    Answer
    :

    70. b. Ser
    ialechocar
    diogr
    aphy.

    Foranasympt omaticpati
    entwithsever
    eAR, SAVRi srecommendedwhent herei
    ssignif
    icant
    LVdil
    atat
    ion( end-
    diast
    oli
    cdimension>6.5cm (Cl
    assI I
    b)orend-syst
    oli
    cdimension>5.0cm
    (Cl
    assII
    ar ecommendat i
    on).SAVRalsomaybeconsi deredatlowerl
    evelsofLVdilat
    ati
    on
    whenthereisevidenceofprogressi
    vecavit
    ydil
    atati
    on,declini
    ngexer
    cisetoler
    ance,or
    abnor
    malhemodynami cresponsestoexerci
    se(ClassIIbrecommendation).
     

    Accor
    dingt
    orecentAmer
    icanHear
    tAssoci
    ati
    on/
    Amer
    icanCol
    legeofCar
    diol
    ogygui
    del
    ines,
    themostappropriat
    ei ni
    ti
    alr
    ecommendat i
    onistorepeattheechocardiogr
    am in6-
    12mont hs
    todetermi
    neiftheLVdi mensionsarestableorenl
    arging.Asympt om-li
    mitedexer
    cisest
    ress
    testisr
    easonabletoclari
    fyf
    unctionalcapaci
    tyi
    npat i
    entswithequivocalsymptoms.TAVR
    current
    lyi
    snotappr ovedaft
    errepair
    edvalveswithAR.

    Quest
    ion:

    71. Youar easkedtoeval uateandmanagea79- year-


    oldwomanwi thaorti
    cstenosis(
    AS).
    Forthepast3mont hs,shehasnot edprogressi
    veshor t
    nessofbreathwithdail
    yhousehold
    chores.Hermedicalhi
    storyissigni
    fi
    cantforhypert
    ension,atr
    ansienti
    schemi catt
    ack(2year
    s
    ago),andchr
    onicrenaldisease.Shecurrentl
    ytakeslosart
    an(50mgdai ly)andaspiri
    n(81mg
    dai
    ly).
     

    Onphysi calexaminati
    on,shei s158cm t al
    l andweighs65kg.Thebl oodpr essureis124/72
    mm Hgwi thahear tr
    ateof84bpm.Thej ugularvei
    nsar enotdistended.Car oti
    dsare2+tardus.
    Herlungsar ecleartoauscultati
    on.Theapi cali
    mpulsei ssustai
    nedanddi splaced2cm tothe
    l
    eftofthemi d-cl
    avicul
    arli
    ne.Agr ade3/6har shlat
    e-peaki
    ngsyst oli
    cejectionmur murisheard
    thr
    oughoutt heprecordium,loudestatther i
    ghtuppersternalborder,andradi at
    estothe
    carot
    ids.Thereisnodi astol
    icmur mur.Ther estofherphysicalexami nat
    ioni snormal.
     

    Laboratoryst
    udiesincl
    udeahemogl obinof12. 1g/ dlandacr eati
    nineof1.6mg/ dl
    .An
    echocardiogr
    am demonst r
    atesconcent r
    icleftventricul
    arhyper t
    rophywithanej ecti
    onfract
    ion
    of65%.Cal ci
    fi
    cASi spresentwithameangr adi entof42mm Hgandacal cul
    atedvalvearea
    of0.7cm2.Thecor onaryangiographyrevealsan80%st enosisintheproxi
    mal  
    leftanter
    ior
    descending(LAD)arter
    yandat otal
     r
    ightcoronar yarter
    yst enosi
    s.Herestimatedoper ati
    ve
    mortali
    tyforcardi
    acsurgeryiscalculat
    edas5. 6%.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    epi
    nthi
    spat
    ient
    ’smanagement
    ?

    a. Surgicalaort
    icvalvereplacement(AVR)withcoronaryar
    ter
    ybypassgr af
    ti
    ng.
    b. Ball
    oonaor ti
    cvalvuloplastyandpercut
    aneouscoronaryi
    ntervent
    ion.
    c. Drug-elut
    ingstentplacementi nt
    heLAD.
    d. Percutaneouscoronar yinter
    vent
    ionandtranscat
    heterAVR.

    Answer
    :

    71. a. Sur
    gicalaor
    ti
    cval
    ver
    epl
    acement(
    AVR)wi
    thcor
    onar
    yar
    ter
    ybypassgr
    aft
    ing.

    Thepatienthassymptomat i
    c,severeASandsi gni
    fi
    cantcoronaryarterydiseaseinvol
    vingher
    LADartery.Hersurgi
    calri
    skisintermediate.Themostappr opr
    iatetherapyissurgicalAVRand
    cor
    onaryar ter
    ybypassgraft
    ing.TranscatheterAVRpr esent
    lyi
    sr estr
    ictedtohigh-r
    iskor
    i
    noperablepat i
    ent
    swithseveresympt omat i
    cAS.Balloonaorti
    cvalvuloplastywouldnotbe
    i
    ndicat
    ed, excepti
    ncri
    ti
    call
    yillpati
    entsasabr idgetoAVRorasapal l
    iati
    veprocedure.

    Quest
    ion:

    72. A56-
    year
    -ol
    dwomani
    sref
    err
    edt
    oyourof
    fi
    cef
    ordyspnea.Hersympt
    omsbegan
    sever
    alyearsago,andhaveprogressedsteadil
    yoverthepast12months.Pr
    esent
    ly,
    she
    cannotwalkmorethan100yar dswithoutpreci
    pit
    ati
    nghersymptoms.Shetakesmetopr
    olol
    50mgdai l
    yforhypert
    ension.
     

    Thejugularvenouspressureiselevat
    edt o9cm H20wi thpr ominentVwaves.Asl i
    ghtl
    eft
    par
    asternalli
    ft(1+)i
    spresent.Thefir
    stheartsoundi snormalinintensit
    y.Thepul moni
    c
    componentoft hesecondhear tsoundisincreased.Bothasof tgrade2/4diastoli
    crumbleand
    a3/6holosystolicmurmurarehear dattheapex.Att heleftst
    ernalborder,
    agrade2/ 6systol
    ic
    ej
    ecti
    onmur murispresentandincreaseswithinspir
    ation.Apulsatil
    eli
    verisevidentwi
    thmi l
    d
    l
    owerext r
    emi t
    yedema( 1+).
     

    At ransthoraci
    cechocardiogram demonst r
    atesnor malleftventri
    cul
    arfuncti
    on(eject
    ion
    fracti
    on65%)andr heumat i
    cmi t
    ralstenosi
    s( meangr adientis14mm Hg;val veareais1.0
    cm2) .Themi tr
    alval
    veispliablewit
    hnocommi ssuralcalci
    ficat
    ion.Moderatetoseveremit
    ral
    regur gi
    tat
    ionandseveret r
    icuspidregurgi
    tati
    onar epresent.Ther i
    ghtventr
    icl
    eismi l
    dlydi
    lat
    ed
    wi t
    hgener ali
    zedhypokinesis.Thepulmonar yarter
    ysyst oli
    cpressureisesti
    matedat60mm
    Hg.Cor onar yangi
    ographydemonst r
    atesmildatherosclerosis.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthenextbestst
    ep?

    a. Opt
    imizedmedi calt
    herapy.
    b. Bal
    loonmitralval
    vulopl
    asty.
    c. Car
    diacsurgery.
    d. Car
    diopul
    monar ystresstest
    .

    Answer
    :

    72. c. Car
    diacsur
    ger
    y.

    Thepat i
    enthassever emi tralstenosisandr egur git
    ationwit
    hseveresympt omsofdypsnea
    (NewYor kHear tAssociationf uncti
    onal cl
    assI II)
    .Althoughhermitralval
    vei spl
    iable,t
    he
    presenceofmoder atetosever emi tr
    alregurgitati
    oni sacontrai
    ndicati
    ont oball
    oon
    valvuloplast
    y.Car diacsurger y,wit
    hmi t
    r alvalvereplacementandt ri
    cuspidvalverepair,i
    s
    i
    ndi catedduet othesever enat ureofhersympt oms, thepr
    esenceofpul monaryhyper t
    ension,
    andheri nel
    igi
    bili
    tyforvalvuloplasty.Acar diopulmonar ystr
    esstestwoul dbeindicatedonlyif
    thereisadi screpancybet weent hecli
    nical f
    indingsandt heresul
    tsoft heechocardiogram. 

    Quest
    ion:

    73. A78- year-ol


    dwomani sr eferr
    edtoyouforevaluati
    onoffat
    igueandshortnessof
    breat
    h.Hersympt omsbegansever almont
    hsago, occurr
    ingatmoderat
    elevel
    sofexer t
    ion.
    Shehasnoot hercompl ai
    nts,
    includingnochestpainorsyncope.Thepati
    entrecei
    vesat enol
    ol
    100mgdai l
    y,li
    sinopri
    l20mgdai l
    y,andhydrochl
    orothi
    azide25mgdai l
    yforl
    ong-standi
    ng
    hypert
    ensi
    on. 

    Onphysi
    calexami
    nat
    ion,
    thebl
    oodpr
    essur
    eis150/
    90mm Hgwi
    thahear
    trat
    eof72bpm.
    Theexaminati
    onisremarkabl
    eforclearl
    ungs,anda2/6mid-
    peakingsyst
    oli
    cej
    ect
    ionmur
    mur
    thati
    sheardbestatther
    ightupperster
    nalbor
    der.Atr
    anst
    horaci
    cechocardi
    ogr
    am
    demonstr
    atesthefol
    lowi
    ngdata: 

    Lef
    tvent r
    icularejectionfraction(LVEF):55% 
    Ventri
    cularsept alwallthickness:13mm 
    Posteri
    orwal lthickness:13mm 
    Meanaor ticvalvegr adient:30mm Hg 
    Peakaor t
    icveloci t
    y:3.4msec 
    Aort
    icvalvear ea:0.7cm2 
    Esti
    mat edrightvent r
    icularpressure:35mm Hg 
    2
    Str
    okevol umei ndex:30ml /
    m 

    Ahemodynami
    ccar
    diaccat
    het
    eri
    zat
    ionconf
    ir
    mst
    heechocar
    diogr
    aphi
    cfi
    ndi
    ngs.

    Whatisthi
    spat
    ient’
    sexpectedmort
    ali
    tyaf
    teraor
    ti
    cval
    verepl
    acement(AVR)compar
    edwi
    th
    pat
    ient
    swithhi
    gh-gradi
    entaort
    icst
    enosi
    sandnormalLVEFwhoundergoAVR?

    a. Unknown.
    b. Simil
    ar.
    c. Higher.
    d. Lowe r
    .

    Answer
    :

    73. d. Lower
    .

    Paradoxicallow-gr
    adient,sever eaorti
    cstenosisandpr eservedLVEFisanewl yr
    ecognized
    cli
    nicalenti
    tythatposesanumberofdi agnosti
    candt herapeuti
    cchall
    enges.Whi
    letheaor t
    ic
    2
    valveareaiswi t
    hinthesever er ange(<1.0cm ) ,
    theaorticgradi
    entisl
    owduet oarelat
    ively
    2
    l
    owst r
    okevol ume(<35ml /m )despi tepreservati
    onoft heLVEF.Thel owstr
    okevolume
    occursduet oavar i
    etyofet iologies,
    suchasanel evat
    edsyst emicaft
    erl
    oadorahypertrophied
    ventri
    cleandsmal lcavit
    ysi ze.  

    Presentl
    y,ther
    eisnocl earconsensusont her ol
    eofaort
    icval
    vereplacement(AVR)inthi
    s
    enti
    ty.Someoft hese“par adoxicallow-
    gradientaor
    ticst
    enosi
    s”pati
    entsmaybenef i
    tfr
    om
    AVR, butcohortst
    udieshavef oundoutcomest obeworseaft
    ersurgeryinlow-gr
    adi
    entnormal
    LVEFpat i
    entscompar edwi thout comesafterAVRi npati
    ent
    swithhigh-gradi
    ent,
    nor
    malLVEF
    andsevereaor t
    icstenosis.

    Quest
    ion:

    74. A28- year-ol


    dwomanpr esentstotheemer gencyroom 26weekspr egnantwith
    progr
    essi
    vedyspneaandpal pi
    tati
    onsint hepast1-2weeks.Shehasahi storyofbeingver
    yill
    asachil
    d.Examinati
    onfi
    ndsani r
    regularheartr
    ateof140bpm wi t
    habl oodpressureof85/60
    mm Hg.Jugularvenouspressureis8cm abovet hesternalangl
    e.Grade2/ 4diast
    oli
    crumble
    i
    sheardatapex.Therearebibasil
    arcrackles.
     

    Shei
    sgivenat
    enolol.Herhear
    tratecomesdownt
    o90bpm,andshefeel
    ssomewhatbett
    er.
    2
    Themeanmitr
    alvalve(MV)gradienti
    s12mm Hg.TheMVar
    eais0.
    85cm .Ther
    eismi l
    d
    mi
    tr
    alregur
    git
    ati
    on.Ej
    ect
    ionf
    ract
    ioni
    spr
    eser
    ved.Thepeakpul
    monar
    yar
    ter
    ypr
    essur
    eis50
    mm Hg.

    Whi
    choft
    hef
    oll
    owi
    ngwoul
    dyoudonext
    ?

    a. Ur
    gentper cut
    aneousball
    oonvalvulopl
    ast
    y.
    b. MVreplacement.
    c. Ur
    gentdirectcur
    rentcar
    dioversi
    on.
    d. Ti
    tr
    atebeta-bl
    ockersandstartant
    icoagul
    ati
    on.

    Answer
    :

    74. d. Ti
    tr
    atebet
    a-bl
    ocker
    sandst
    artant
    icoagul
    ati
    on.

    Thei nit
    ialtreat
    mentwillbemedi calt
    herapywiththepati
    enttreat
    edtohaveasl owerheartr
    ate,
    startanticoagulant
    s,andtreatf
    orcongest i
    veheartfai
    lur
    e.Thereisnorol
    eforcardiover
    sionat
    thistime, assheisnowr easonablyratecontr
    oll
    edwi t
    himprovedsymptoms, shehasnotbeen
    previouslyant i
    coagul
    ated,andthedurationofatr
    ialfi
    bri
    ll
    ati
    onisunknown. 

    Ifsympt omsf ai
    ltoimprovewi thadditionalmedi caltherapy,fut
    ureoptionsi
    nclude
    transesophagealechocar diogram/dir
    ectcur rentcardioversi
    on.Indicat
    ionsfori
    ntervent
    ion
    (eit
    herpercutaneousorsur gi
    cal)aresympt omsr efr
    actorytomedi calmanagement .I
    fmedical
    managementf ail
    s,ball
    oonval vulopl
    ast y(
    wi thpelvicshiel
    ding)woul dbetheprocedureof
    choiceifthevalvemor phologyi sappropriate.Sur gi
    calMVr eplacementduringpregnancy
    carri
    esa30%r i
    skoffetallossandi sthereforeal astresort.

    Quest
    ion:

    75. A31- year-


    oldmanpr esent
    stoyourcli
    nicf
    orannualf oll
    ow-upforhisbicuspidval
    ve
    andsevereaor ti
    cregurgit
    ation.Hehasnoothersigni
    ficantmedicalhist
    oryandi sa
    nonsmoker .Hehasbeenhavi ngyearl
    yechocardi
    ograms, butconti
    nuestof eelwellandhave
    nosympt oms.Hewor ksfullti
    meandr uns3 t
    imesperweekf orabout30mi nutes.Hetel
    lsyou
    thathehasnotnot edanychangei nhisexer
    ciset
    oleranceoverthepastyear .Hehasno
    palpi
    tat
    ions,chestpain,orsyncope. 

    Onexami nati
    on,heiswel lappear i
    ng.Hishei
    ghti
    s72i nchesandweightis180lbs.Hisheart
    rateis62bpm, bloodpressur eis145/50mm Hg, andoxygensatur
    ati
    onis98%.Hi slungsare
    clear
    .Hisjugularvenouspr essureisnormal,
    andhehasanor malS1 
    andS2.Thereisagrade
    1/6systoli
    cmur muratthel eftsternal
    border
    ,fol
    lowedbyagr ade3/4decrescendodiast
    oli
    c
    mur mur.Thereisnolowerext remityedema. 

    Hisechocardiogr
    aphyt odaydemonstr
    atesnormal l
    eftventr
    icul
    ar(LV)funct
    ionandnoLV
    hypertr
    ophy.However ,hi
    sLVend-syst
    olicdimensi
    oni s5.2cm, i
    ncreasedfr
    om 4.7cm t
    he
    yearbeforeand4.4cm f r
    om 2yearsbefore.HisLVejecti
    onfract
    ionis50%.Youtellhi
    mt hati
    t
    i
    sr easonabl
    et oproceedtoaort
    icval
    vereplacementinthenearfuture.

    Youarr
    angeanappoi
    ntmentwi
    tht
    hecar
    diacsur
    geonandor
    derwhi
    choft
    hef
    oll
    owi
    ng
    addi
    ti
    onalt
    est
    ing?

    a. Cor
    onar
    yangi
    ogr
    aphy.
    b. Car
    diopul
    monarystresst
    est
    .
    c. Computedtomographyangi
    ographyofthechest
    .
    d. Magneti
    cresonanceangi
    ographyofthebrai
    nvascul
    atur
    e.

    Answer
    :

    75. c. Comput
    edt
    omogr
    aphyangi
    ogr
    aphyoft
    hechest
    .

    Patientswi t
    hbi cuspidvalveshaveahi ghi ncidenceofascendi ngaor t
    icaneurysm, thought
    secondar ytoi ntr
    insi
    cabnor mali
    ti
    esint heaor ticwallconnectivet i
    ssue.Af ewalsohave
    evidencef orcoar ct
    ati
    on.Thi scanoccuri ntheabsenceofsi gnifi
    cantval vedisease.Itis
    i
    mpor tantt oevaluatethesi zeoftheascendi ngaor t
    apr i
    ortosur gerysincei tmayneedt obe
    repairedatt hesamet i
    meast hevalve.Ther efore,comput edtomogr aphyangiographyoft he
    chesti sthemostappr opri
    at eanswer.Magnet i
    cresonanceangi ogr aphyoft hebrai
    ncoul dbe
    consider edi nLoeys-Dietzsyndr omeort oconsi derrevi
    ewf orcer ebralaneurysms, butthisi
    s
    notindi catedi nthissit
    uation.Hedoesnotneedcor onaryangi ography.

    Quest
    ion:

    76. Youar easkedt oseeayoungwomanwhoi si nthe28thweekofherf i


    rstpr
    egnancy.
    Shehashadver ylit
    tl
    eprenatalcare,buttell
    syout hatsher emember sbeingtoldshehada
    mur murasachi ld.Shehadbeendoi ngfineupunt ilt
    hepastf ewweekswhenshedevel oped
    dyspneaonexer tionandmi l
    dor t
    hopnea.Onexami nati
    on,herheartrateis112bpm and
    regular
    ,bloodpressureis125/72mm Hg, andjugularvenouspr essureismildlyel
    evat
    ed.She
    hasmi nimalbibasil
    arral
    esandagr ade2/ 4diastol
    icmur murhear dattheapex.Shehasno
    l
    owerext remit
    yedema.Anel ectr
    ocar di
    ogram revealssinustachycardia.Anechocardi
    ogram
    demonst rat
    essignifi
    cantrheumaticmi t
    ralstenosiswi t
    hameangr adientof8mm Hg.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthebestmedi
    calt
    her
    apyt
    ohel
    pimpr
    ovehersympt
    oms?

    a. Amiodarone.
    b. Di
    goxin.
    c. Li
    sinopri
    l.
    d. Metoprol
    ol.

    Answer
    :

    76. d. Met
    opr
    olol
    .

    Thisyoungwomanhasnewl ydiscoveredmi t
    ral st
    enosisandisnottolerati
    ngtheincreased
    hear trateandi ncreasedplasmavol umeofpr egnancy.Shei sneari
    ngtheendofhersecond
    tri
    mest erwhenhervol umest atusandcar diacout putreachthei
    rpeak.Thebestopt ionisto
    i
    ncr easeherdi ast
    olicfi
    ll
    ingtimebydecr easingherhear tratewit
    hbeta-blockade.Metoprol
    ol
    i
    swel ltoler
    ateddur ingpregnancyandmi ghtallevi
    atehersympt omsenought ogether
    throught her estofherpr egnancywi t
    houtapr ocedur e.Bal
    loonmitr
    alvalvuloplast
    yissafe
    afterthefi
    rsttrimester
    ,butnotwi t
    houtri
    sk.Bothangi
    otensi
    n-conver
    ti
    ngenzymei nhi
    bit
    ors
    andangi otensin-r
    eceptorblocker
    sareterat
    ogensandshouldnotbeusedi nwomenwhoar e
    pregnantorbr eastfeeding.Sheisinsi
    nusr hyt
    hm,andthereisnoindicat
    ionfordi
    goxi
    n.
    Ami odaroneshoul dnotbeusedi npregnancy. 

    Quest
    ion:

    77. A60- year-


    oldwomancomesf oratr
    ansesophagealechocar diogram (TEE)pri
    ortoa
    pl
    annedmi tralvalvul
    oplastyformitralst
    enosis.Althoughther
    eisnopr i
    orhistor
    yofat r
    ial
    fi
    bri
    ll
    ati
    on( AF),atthetimeofpr esentati
    onfortheTEE, sheisnotedtobei nAF.Shei snoton
    anti
    coagulati
    on.Herl aborat
    orydat aarenormal exceptforacreati
    nineof2.0mg/ dlwit
    h
    gl
    omer ul
    arf i
    lt
    rati
    onrateof30ml /min.TheTEEi sshowni nFigure1.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthebestnextcour
    seofact
    ion,
    basedont
    heTEE?

    a. Aspi
    rinandclopidogr
    el.
    b. Anoveloralant
    icoagulantagent
    .
    c. Unfr
    acti
    onatedheparinandwar f
    ari
    nther
    apy.
    d. Lowmol
    ecul
    arwei
    ghthepar
    in(
    LMWH)andwar
    far
    int
    her
    apy.

    Answer
    :

    77. c. Unf
    ract
    ionat
    edhepar
    inandwar
    far
    int
    her
    apy.

    Thereisclearl
    yal eftatr
    ialappendaget hr
    ombus.Thepat ienthasnew- onsetAFwi thalarge
    appendaget hrombust hatrequir
    esi mmediat
    eant i
    coagulation.Thecorrectansweristoadmi t
    herforheparinandwar f
    arintherapy,anddel
    ayconsiderationofvalvulopl
    astyuntilf
    urt
    her
    i
    magi ngisperformedi n6weeks.Thenovel anti
    coagulantshavenotbeenappr ovedforAF
    rel
    atedtomi tr
    alvalvularstenosi
    s.LMWHshoul dnotbeusedi napatientwiththi
    sdegr eeof
    chronicki
    dneydi sease.Clopidogrelandaspi
    rinhavebeenshownt obei nferi
    ortowar f
    ari
    nfor
    AF. 

    Quest
    ion:

    78. A49- year


    -ol
    dmani seval
    uatedf
    orprogressivedyspneaandedema.Forthepast
    severalmonths,hehasexperi
    encedworseni
    ngdyspneawi t
    hmoderateact
    ivi
    ti
    esand
    worseninglowerextr
    emit
    yedemaandabdomi nalfull
    nessdespi
    teescal
    ati
    ngdosesof
    diur
    etics.
     

    Onphysicalexaminat i
    on, t
    emperaturei snormal,
    bloodpr essureis118/65mm Hg, pulserate
    i
    s88bpm, andrespirationratei
    s18br eaths/mi
    nute.Lungsar eclearbil
    aterall
    y.Thereis
    j
    ugularvenousdistentiontothemandi blewithapromi nentCVwave.Hear trhyt
    hm isregular
    .
    Thereisagrade2/ 6low- pi
    tched,holosystoli
    cmur mural ongt helef
    tsternalborderthat
    i
    ncreasesduringinspirati
    on.Thel i
    verspani senlarged,andt hereisbil
    aterallowerextr
    emity
    edema. 

    Elect
    rocardiogr am showssi nusrhythm at80bpm andi ncompl eteri
    ghtbundlebranchblock.
    Transthoracicechocar diogr aphyshowsnor mal lef
    tventr
    iculardimensionsandsystol
    ic
    functi
    on,butt her i
    ghtvent ri
    cleisdil
    atedwi t
    hreducedsyst oli
    ccont r
    acti
    on.Thereispoor
    coaptati
    onoft hetri
    cuspi dval ve(
    TV)leaflet
    swi thmobil
    e, t
    hickenedleafl
    etsandsevere
    tri
    cuspidregur git
    ati
    on( TR) .Therightventri
    cularsyst
    oli
    cpr essureisesti
    matedat30mm Hg.
    Ther i
    ghtatrium isalsodi lated.Uri
    nedr ugscreenandbloodcul turesarenegati
    ve.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthemostappr
    opr
    iat
    emanagementf
    ort
    hispat
    ient
    ?

    a. Angiot
    ensin-
    convert
    ingenzymei
    nhi
    bit
    or.
    b. TVrepairorr
    eplacement.
    c. Si
    ldenafi
    l.
    d. Di
    goxin.

    Answer
    :
    78. b. TVr
    epai
    rorr
    epl
    acement
    .

    ThispatientwithsevereTRshoul dunder goTVr eplacementsur geryorrepair


    .Thenormal
    esti
    mat edrightventri
    cul
    arsystoli
    cpr essur
    ebyDoppl erechocar diographysuggest
    s
    regur
    gitati
    oncausedbyl eafletormyocar di
    al dysfuncti
    on,rathert hanfunct
    ionalTRdueto
    pulmonar yhypertensi
    on.Hehasevi denceofr i
    ghtventri
    cularvol umeover l
    oad,i
    ncl
    uding
    dil
    ati
    onandr educedsystol
    icfuncti
    on.Theonl ydefini
    ti
    vether apyf orsever
    e,symptomati
    cTR
    i
    ssur gery,eit
    hertri
    cuspi
    dannul oplastyorreplacement. 

    Thet i
    mingofTVsur geryischallengi
    ng, butshoul dbeconsi deredinpatientswi thsevere
    regurgit
    ationandeithersympt omsorevi denceofpr ogressi
    veri
    ghtventricularenlargementor
    dysfunctiondespit
    eadequat ediureti
    ct herapy.Di goxinisincor
    rect.Al
    thought hereisevi
    dence
    ofrightventri
    cul
    ardysf unct
    ion,nost udiesconcl usivelydemonstrateabenef itfordigoxi
    nor
    otherinotropi
    ctherapyf orr
    ight-
    sidedhear tfailur
    e.Ther eisnoindicat
    ionf orsildenafi
    lwit
    h
    normalpul monaryar t
    erypressuresandnocl earadvant ageforangiot
    ensi n-
    conver t
    ingenzyme
    i
    nhibiti
    oni nthesett
    ingofnor mal l
    eftvent r
    icularfunction.

    Quest
    ion:

    79. Youar easkedtoseeayoungwomanwhoi sinthe28thweekofherf ir


    stpregnancy.
    Shehadbeendoingfineupunt i
    lthepastfewweeks, whenshedevelopeddyspneaonexer t
    ion
    andmi l
    dort
    hopnea.Onexami nati
    on,herheartrat
    eis112bpm andr egularandbloodpr essure
    i
    s125/ 72mm Hg.Herj ugularvenouspressureismildl
    yelevat
    ed,shehasmi nimalbi basi
    lar
    ral
    es,andagrade2/4di ast
    olicmurmuri sheardattheapex.Youhavenomedi calrecords
    becauseshegrewupi nSout hAmer i
    ca,butshedoesr ememberapr olongedfebri
    leill
    nessas
    achil
    d.

    Herechocar
    diogr
    am reveal
    sevi
    dencef
    orr
    heumat
    icmi
    tr
    alst
    enosi
    s.Theel
    ect
    rocar
    diogr
    am
    r
    evealssi
    nustachycardi
    a.

    Whi
    choft
    hef
    oll
    owi
    ngi
    sthebestmedi
    calt
    her
    apyt
    ohel
    pimpr
    ovehersympt
    oms?

    a. Di
    goxin0.25mgqd.
    b. Li
    sinopri
    l5mgqd.
    c. Hydral
    azine25mgt
    id.
    d. Metoprol
    ol12.
    5mgbid.

    Answer
    :

    79. d. Met
    opr
    olol12.
    5mgbi
    d.

    Thisyoungwomanhasnewl ydiscoveredmi t
    ralst
    enosis.Whileshemayneedf urosemide,
    the
    bestopti
    oni st
    oincreaseherdiastoli
    cfill
    ingt
    imebydecr easingherheartrat
    ewi thbeta-
    bl
    ockade.Noneoft heotheroptionswoul dimproveherhemodynami csinthi
    ssituati
    on.
    Pregnancyresult
    sinmar kedaft
    er l
    oadr educt
    ionandani ncreaseincardi
    acoutputandpr el
    oad.
    Oftenapatient
    'scli
    nical
    classwor sensbyoneNewYor kHear tAssociati
    onclassdur i
    ng
    pregnancy.Shehasnowdevel opedmi ldcongest i
    veheartfail
    ure.
     

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