Short notes

Cardiology

Archan
คำนำ

– Short notes เล่มนี้จัดทำขึ้นระหว่าง training cardiology fellow เนื่องจากตระหนักว่าศักยภาพ

และความจำของเรานั้นมีจำกัด เพื่อสะดวกในการ recall ในสถานะที่เร่งรีบและความปลอดภัยกับ
ผู้ป่วย โดยจะสำเร็จไม่ได้เลย ถ้าไม่ได้อาจารย์ทั้งในสถาบันและต่างสถาบันค่อยสอน โดยความรู้
ทั้งหมดล้วนมาจากเพื่อนๆและอาจารย์ได้สอนมาทั้งสิ้น รูปภาพหรือเนื้อหาหลายๆอย่างนำมาจาก
slide ที่จากอาจารย์จากหลายสถาบัน โดยหลายๆอันผมก็จำไม่ได้ว่าอ้างอิงมาจากอาจารย์ท่าน
ใดเลยไม่ได้ติด reference ไว้ด้วย ซึ่งต้องขออภัยเป็นอย่างสูง โดยไม่ได้มีจุดมุ่งหมายอื่น
นอกจากส่งมอบความรู้ที่อาจารย์เคยสอนให้คนรุ่นต่อไป ซึ่งความรู้ก็เปรียบเสมือนแสงเทียนส่อง
สว่าง เมื่อใดที่เราจุดแสงเทียนผู้อื่นให้ส่องสว่าง ก็ยิ่งทำให้มองเห็นทางเดินในค่ำคืนที่มืดมิดได้
ชัดเจนขึ้น
– สุดท้ายนี้อย่ายึดถือและใช้ short notes นี้เป็นสารณะเด็ดขาด ถ้ามีข้อมูลผิดพลาดประการใด
แจ้งมาหลังไมค์ก็ดีครับ ขอบคุณครับ

อาชัญ เจษฎ์พัฒนานนท์
สารบัญ

!. Valvular heart disease

○ Aortic stenosis : หน้า 6
○ Aortic regurgitation : หน้า 19
○ Mitral regurgitation : หน้า 27
○ Mitral stenosis : หน้า 41
○ Rheumatic fever : หน้า 48
○ Tricuspid valve : หน้า 52
○ Pulmonic valve : หน้า 60
○ Prosthesis valve : หน้า 67
#. Congenital heart disease
○ General congenital heart disease : หน้า 85
○ ASD : หน้า 109
○ VSD & AVSD : หน้า 116
○ PDA : หน้า 123
○ TOF: หน้า 127
○ Ebstein anomaly : หน้า 133
○ TGA : หน้า 139
$. Myocardium & Pericardium
○ Heart failure & Cardiogenic shock : หน้า 147
○ Inotrope & Vasopressor : หน้า 173
○ Cardiomyopathy : หน้า 180
○ Myocarditis : หน้า 195
○ Cardiac amyloid : หน้า 200
○ HCM : หน้า 204
○ ARVD : หน้า 213
○ EMF : หน้า 217
○ Pericarditis : หน้า 221
○ RCM & CP & Tamponade : หน้า 227
○ Cardiac mass : หน้า 238
○ Athlete heart : หน้า 243
%. Arrhythmia
○ Bradycardia : หน้า 246
○ Tachycardia : หน้า 256
○ Ventricular tachycardia : หน้า 267
○ PVC : หน้า 279
○ SVT : หน้า 282
○ Atrial fibrillation : หน้า 289
 ○ Sudden cardiac death : หน้า 299
○ WPW & Bypass tract : หน้า 302
○ Brugada syndrome : หน้า 307
○ Short QT syndrome : หน้า 313
○ Long QT syndrome : หน้า 316
○ CPVT : หน้า 323
○ Early repolarization : หน้า 325
○ Antiarrthythmic drug : หน้า 330
○ Basic EP : หน้า 340
X. Non-invasive test & Imaging
○ CXR : หน้า 365
○ Basic echocardiogram : หน้า 375
○ TEE : หน้า 400
○ M-mode & Doppler : หน้า 408
○ EST & CPET : หน้า 448
○ Stress imaging : หน้า 457
○ Syncope & Tilt table test : หน้า 471
○ Holter monitoring : หน้า 485
Y. CAD & Hemodynamic
○ Stable coronary artery disease : หน้า 493
○ NSTEMI : หน้า 508
○ STEMI : หน้า 516
○ Anti-platelet : หน้า 527
○ Anomalous coronary origin: : หน้า 538
○ Coronary spasm : หน้า 545
○ CAG & PCI : หน้า 549
○ Hemodynamic : หน้า 574
○ PV loops : หน้า 608
Z. Device & Advance HF
○ Temporary pacing : หน้า 621
○ Device indication : หน้า 625
○ Pacing mode & ICD : หน้า 639
○ Cardiac device programming : หน้า 662
○ Mechanical support : หน้า 672
○ IABP : หน้า 676
○ ECMO : หน้า 680
○ LVAD : หน้า 685
○ Heart transplant : หน้า 689
[. Prevention & Metabolic disease
○
 ○ Primary prevention : หน้า 696
○ DM : หน้า 711
○ Dyslipidemia : หน้า 723
○ Hypertension : หน้า 744
○Hypertensive emergency : หน้า 761
c. Vascular disease
○ Aortic disease : หน้า 766
○ PAD : หน้า 783
○ Coarctation of aorta : หน้า 801
○ Cardioembolism : หน้า 807
○ Pulmonary embolism : หน้า 812
○Pulmonary hypertension : หน้า 820
!d. General cardiology & Stat
○ Approach to cardiology : หน้า 835
○ Physical exam : หน้า 844
○ EKG : หน้า 866
○ Statistics : หน้า 889
○ Key investigation : หน้า 911
!!. Other
○ Pre-op evaluation : หน้า 920
○ NOAC : หน้า 940
○ Pregnancy & heart disease : หน้า 958
○ Infective endocarditis : หน้า 970
○ CPR : หน้า 981
○ Cardiac surgery : หน้า 991
○ Cardiac rehabilitation : หน้า 994
○ Therapeutic hypothermia : หน้า 1003
Aortic stenosis
Aortic stenosis

Approach AS
Supravalve AS
– Williams syndrome, familial hypercholesterolemia, coarctation of aorta, takayasu

disease.
Valvular AS
– Calcific AS : leaflet calcification, Rheumatic AS : commissural calcification with/

without leaflet calcification

– Bicupid AS (ดูตอน opening AV) with/without raphe
– Unicuspid AS

– Quadricuspid AV (ass. aortic regurgitation, not AS)

Subvalvular AS
– Fix : early systolic closure (SEM and fix murmur but no radiate to neck)

– Ass. 50%AR, shone complex, VSD, CoA

– Two morphology : membrane/ridge (90%) vs muscular type

– Surgery : modified Konno procedure

– Dynamic : HCOM, Post MV repair, Takotsubo, Hypovolumia

Physical exam
– Systolic ejection murmur is preserved for only semilunar valve (not used in high flow
murmur)
– Aortic sclerosis : Best heard at RUSB, must normal S2, no radiation
– Severe : Pulsus parvus et tardus, Systolic thrill, Late peaking murmur, single or
paradoxical split S2
– Gallavadin murmur = calcific aortic stenosis (แยกจาก MR โดยเสียงจะดังต่อเนื่องไม่มี
เสียงขาดถ้าไล่ฟังจาก AV area to MV area)
Echo
– AS with LVOT obstruction
– Calculated Pressure gradient across AV : 4(V2 of AV-V2 of LVOT)

– PSLX : posteromedial papillary muscle = Non-cusp, No papillary muscle = Lt or Non

cusp
– LV systolic pressure = SBP - mean AV gradient (not peak gradient)
– Mean gradient = 2/3 of peak gradient

– RUPS view for alternate choice to obtain peak gradient

Calcified aortic valve

– Degenerative aortic stenosis : direct correlation with atherosclerosis but statin does

not decrease progression

Grade of AS
– Normal AV : AVA > 3 cm2, Vmax < 2, mean gradient < 10
– Mild AS : AVA > 1.5 cm2, mean gradient < 20, Vmax < 3, DVI > 0.5
 – Severe AS : AVA < 1 or AVAi < 0.6, Mean Gd > 40, Vmax > 4, DVI < 0.25
Gradient in AS
– Mean gradient AS : doppler = cath
– Peak gradient : doppler = peak instantaneous in cath
– Peak to peak gradient in cath ~ 75% of peak gradient in cath
– Mean gradient = 2/3 of peak gradient

State AS
– A : risk : bicuspid AV, aortic sclerosis (No AS : must Vmax < 2)
– B : progressive : mild to moderate AS
– C : asymtomatic severe
– C1 : normal EF

– C2 : EF < 50%

– D : symtomatic
– D1 : high gradient AS

– D2 : low flow/low gradient AS

– D3 : paradoxical low-flow severe AS, EF >= 50% but SVi < 35

Four categories of AS
 – High gradient AS : AVA < 1 & mean gradient > 40 mmHg (Classical AS)
– Classical low-flow, low-gradient AS with reduced EF : AVA < 1, mean gradient < 40
mmHg, EF < 50%, SVI < 35
– Paradoxical low-flow, low-gradient AS with preserved EF : AVA < 1, mean gradient
< 40 mmHg, EF >= 50%, SVI < 35
– Normal-flow, low-gradient AS with preserved EF : AVA < 1, mean gradient < 40
mmHg, EF >= 50%, SVI >= 35 (moderate AS or measurement error)

General
– Progression of AS : decrease AV area 0.1 cm2 per year
– True AVA < 1 cm2 = severe AS
– Except คนไข้ตัวเล็ก = moderate AS
– AVA < 1 cm2, gradient < 40 (must EF >= 50% and SVi > 35)

– Gradient is specific for AS after exclude high flow state (irrespective AVA)
– High flow state (early peak shape of CW) : anemia, hyperthyroid, AV shunt

– Low flow & low gradient AS (must AVA < 1 cm2; AVAi =< 0.6, SVi =< 35)
– EF < 50% —> dobutamine echo

– after test SVi > 35

– AVA > 1 cm2 with low gradient = pseudo severe AS (poor EF)

– AVA < 1 cm2 but high gradient : true severe AS

– AVA > 1 cm2 with high gradient = ให้ dobutamine มากไป

– after test SVi < 35

– Sent calcium score CT

– If contractile reserve (DeltaPeak vel > 0.6, Delta SV > 20%,

DeltaMeanPG > 10)

– Projected AVA (target flow 250)

– EF >= 50% —> calcium score CT severe AS : men >= 2000, women >= 1200, not

severe AS : men < 1600, women < 800

– Paradoxical low flow, low gradient severe AS : small LV chamber
– AVA < 1 cm2, gradient < 40 (must EF >= 50% and SVi =< 35)

– W/U calcium score

Indication for intervention/surgery
No benefit of medication
– Severe AS (AVA < 1 cm2, Vmax > 4 m/s, Gradient > 40 mmHg)

– Symptomatic : DOE, excertional angina/syncope/presyncope

– Asymtomatic

– EF < 50% (I)

– Other cardiac surgery, recommend in at least moderate AS (I)

– Abnormal EST : decrease BP from baseline (I)

– Low risk surgery (STS or EuroScore II < 4% or EuroScore I < 10%) plus one

of following (IIa)
– Vmax > 5.5 m/s

– Vmax progress >= 0.3 m/s/year

– Elevate BNP > 3 เท่าของช่วงอายุ

– Systolic PA (RVSP) > 60 mmHg by cath
Surgical AVR vs TAVI/TAVR (life expectacy > 1 year)
– Surgery if low risk surgery (STS or EuroScore II < 4%) : not cut-point for high risk,
clinical trial High risk > 10%
– Favor TAVI : Age >= 75, severe comorbidity, restricted mobility, frailty

– Screening PAD if plan TAVI (I)

– TAVI only symptomatic patient

– TAVI if increase risk surgery and anatomy suitable & after correct CAD (correct

proximal lesion >= 70%)

– Adequate annulus 18-29 mm

– Valve morphology : less calcify, non bicuspid

– Porcelain aorta prefer TAVI

– Adequate vascular access

– No active IE, No LV thrombus

– No elevated risk of coronary ostium obstruction

Complication
– Mortality 3-4%

– Aortic dissection 0.15%

– High degree AV block 10%, upto 20% in self expandable valve

– Risk for PPM : Depth of implatation, RBBB, Valve type (Old > New self

expandable > New > Old balloon expandable)

– Stroke more than in TAVI > SAVR

Self expandable valve : risk for AV block

Post TAVI : DAPT 3-6 months (AHA : DAPT 6 months) and then single anti-Plt lifelong
– add warfarin during 3 months after TAVI (IIb)
Severe AS with elective surgery
– symptoms : แก้ valve ก่อน
– Asymtomatic
– Low to moderate risk for surgery —> go on surgery

– High risk surgery

– Low risk AVR : แก้ valve ก่อน

– High risk AVR —> go on non cardiac surgery with strict monitor

Frailty index (KATZ score)

– 6 หัวข้อ ข้อละ 1 คะแนน คือ ทำได้ หรือ ทำไม่ได้ ประกอบด้วย
– 1.bathing

– 2.dressing

– 3.toileting

– 4.transferring เดินในบ้าน
–5.continence (อุจจาระ/ปัสสาวะ)
– 6.feeding

– Score 6 : independent, Score 0 : very dependent

Canadian clinical frailty scale

Follow up
– Asymptomatic severe AS : echo q 6 months
– Moderate AS : echo q 1 year
– Mild AS : echo q 2 years

Subaortic stenosis
Indication for surgical intervention
– Peak gradient >= 50 mmHg plus symptoms

– Peak gradient 30-49 mmHg plus (attributable to subAS)

– Ischemia symptoms

– HF

– LV dysfunction
 – Progressive AR from barotrauma (turbulent flow) (IIb,C)

Bicupid AS : Coexisting coronary artery anomaly (LCx from Rt cusp), 50% have root/
ascending aortic dilatation, 10% found coarctation
– Most common is Rt & Lt fusion

– Gene : NOTCH1 gene

– Echo

– PLAX - systolic doming, diatolic prolapse, eccentric valve closure

– SAX : Two cusp & commissures, Raphe, oval opening

– M-mode : eccentricity index > 1.5 (0.5xA/a)

– Screening echo in 1st relatives : bicuspid AV & aortopathy

– Screening first degree relatives (IIb)

M-mode : Normal leaflet separation 2 cm

Unicuspid AS : ass. Ascending aortic aneurysm

– 2 type : Unicommissural unicuspid, Acommissural unicuspid

Quadricuspid AV : risk for AR, no AS, No ass. with aortopathy

 – Ass. PDA, HCM, subaortic stenosis, EHlerz-Danlos syndrome, coronary ostium
displacement, VSD

Supravalvular aortic stenosis

– Etiology : Williams syndrome (AD), familial hypercholesterolemia
– William syndrome : elfin face, low nasal bridge, unusually cheerful, ease with

strangers, developed delay but strong language skills, hypercalcemia

– 3 type : hourglass (common), membranous,Hypoplastic
– Association : coronary ostial stenosis
– PE : Suprasternal thrill, BP at Rt arm > Lt arm, left carotid thrill
– Surgical intervention with patch aortoplasty : symptoms, decrease LV systolic
function

Clinical trial in TAVI

PARTNER B
– Population : severe symptomatic AS with prohibitive risk (super-high risk)

– Intervention : TAVR SAPIEN vs conservative

– Outcome : decrease all death (30% vs 50%, RRR 40%), increase stroke (10% vs

4.5%)
PARTNER A
– Population : severe symptomatic AS with high risk Sx (STS score > 10%)

– Intervention : TAVR SAPIEN vs SAVR

– Outcome : same all death at 1 years, increase stroke (8.3% vs 4.3%), increase

paravalve leakage, less major bleeding & AF

PARTNER 2
– population : severe symptomatic AS with intermediated risk Sx (STS score 4-8%)

– Intervention : TAVR SAPIEN XT vs SAVR

– Outcome : same all death at 2 years, same stroke, increase major vascular

complication, less major bleeding & AF & AKI

PARTNER 3
– Population : symptomatic severe AS with low risk surgery

– Age 73, STS 1.9

– Exclude : bicuspid AV

– Intervention : SAPIEN-3 (balloon expandable valve vs Surgical AVR)

– Outcome : proved superiority primary endpoint (death, stroke, rehospitalization at 1

year)
– Pre-specified subgroup : Reduced stroke, AF, short hospitalization.
 Aortic
regurgitation
Aortic regurgitation

General
– Moderate AR ส่วนใหญ่ไม่มีอาการจนกว่าจะ severe
– Severe AR : must low DBP
– Medication : ACEI/ARB, betablock in severe symptomatic AR or LV dysfunction

Approach AR
– Valve AR : Rhuematic, Calcific, IE, Trauma, Congenital (Bicuspid, Unicommissural,
Quadricuspid), Drug (anorectics, serotoninergics), CNT (RA, SLE), radiation, VSD
with cusp prolapse
– Root AR (“MRSA”) : Marfan, rheumatologic disease (ankylosing, takayasu), syphylis,
aortic dissection, annuloaortic ectasia

Echo
– Marfan syndrome : annuloaortic ectasia and loss of sinotubular junction +/- Intimal
flap

Physical exam
– Soft S1, decrease A2 in valve, normal/increase A2 in root, S3 gallop
– Valve : murmur at 3-4th LUPS (erbʼs), Root : murmur at RPSB
– To & fro murmur, DBM early peak, decrescendo pattern
– Austin Flint murmur (Relative MS) : Begin after S3, No OS, soft S1, maneuvers aid to
differentiate from MS
– Severe : long duration of DBM, Austin flint murmur (Normal S1, no OS), peripheral
sign, pulsus magnus
– Peripheral sign of AR
○ Corriganʼs pulse: A rapid and forceful distension of the arterial pulse with a quick
 collapse
○ De Mussetʼs sign: Bobbing of the head with each heartbeat (like a bird walking)
○ Mullerʼs sign: Visible pulsations of the uvula
○ Quinckeʼs sign: Capillary pulsations seen on light compression of the nail bed
○ Traubeʼs sign (pistol shots): Systolic and diastolic sounds heard over the femoral
artery
○ Duroziezʼs sign: Gradual pressure over the femoral artery leads to a systolic and
diastolic bruit
○ Hillʼs sign: Popliteal systolic blood pressure exceeding brachial systolic blood
pressure by ≥ 60 mmHg (most sensitive sign for aortic regurgitation)
○ Shellyʼs sign: Pulsation of the cervix
○ Rosenbachʼs sign: Hepatic pulsations
○ Beckerʼs sign: Visible pulsation of the retinal arterioles
○ Gerhardtʼs sign (aka Sailerʼs sign): Pulsation of the spleen in the presence of
splenomegaly
○ Mayneʼs sign: A decrease in diastolic blood pressure of 15 mmHg when the arm
is held above the head (very non-specific)
○ Landolfiʼs sign: Systolic contraction and diastolic dilation of the pupil

Grade of AR
– Mild : jet/LVOT < 25%, vena contracta < 0.3, Jet area/LVOT area < 5%, Rvol < 30 ml,
RF < 30%
– Support : pressure half time > 500 ms, normal LV size

– Severe : jet/LVOT < 65% within 1 cm from vena contracta (annulus), vena contracta >

0.6, Rvol >= 60, RF >= 50%, Jet area/LVOT area >= 60%
– Support : pressure half time < 200 ms, LV enlarge, aortic reversal flow in

descending (PW) : VTI DAo > 15 (point just below left subclavian)
Specific criteria for severe AR (>= 4 criteria definitively severe)
– Flail valve

– VC > 0.6 cm

– Jet/LVOT >= 65%

– Large flow convergence

– Pressure half time < 200 ms

– Aortic reversal flow in descending (PW) : VTI DAo > 15

– Enlarge LV with normal function

Siriraj grade of AR
– Trivial : jet/LVOT < 17%

– Mild : jet/LVOT < 47%

– Severe : jet/LVOT > 62%

Grade AR by aortogram
based on the amount of opacification of the left ventricle, two complete cardiac cycles
after injection compared to that of the aortic root.
– Grade 1 : Brief and incomplete ventricular opacification. Clears rapidly.

– Grade 2 : Moderate opacification of the ventricle that clears in less that 2 cycles.

Never greater than aortic root opacification.

 – Grade 3 : Opacification of the ventricle equal to aortic root opacification within
2 cycles. Delayed clearing of ventricle over several cycles.
– Grade 4 : Opacification of the ventricle almost immediately that is greater than
that of the aortic root with delayed clearing of the ventricle.

Indication for surgery in severe AR (must severe AR) : Exclude root AR

– Symptomatic
– Asymtomatic
– EF =< 50% (I)

– EF > 50% (IIa)

– LVESD > 50 mm or > 25 mm/BSA : reflex contractile reserve

– LVEDD > 70 mm (ESC) : reflex degree of volume overload

– LVEDD > 65 mm (AHA) with low risk surgery

– Other cardiac surgery in asymtomatic severe AR or progressive AR (moderate)

(I)

Indication for surgery for root AR (irrespective of severity AR)

: prefer repair in root AR
– >= 55 mm In normal or bicuspid aortic

– Bicuspid 50 mm with risk : family Hx, HT, coartation, incease diameter > 3 mm/year

Marfan or marfanoid
– >= 50 mm

– 45 mm with risk : family Hx of dissection, increase size > 3 mm/year, severe AR/MR,
 desire pregnancy, TGFBR1 or 2 include loey-dietz syndrome

Other imaging
– If inconclusive severity from TEE (Eccentric jet), prefer TEE or MRI

Repair situation
– In young patient with aortic root dilatation and tricuspid valve in experienced

surgeons

Follow up
– Asymptomatic severe AR
– LVD or LVEF close to threshold : echo 3-6 months

– No close threshold : echo 1 year

– Mild to moderate AR : echo 2 years

Rupture sinus of Valsava

– Etiology : IE, RA, EDS, Marfan, Turner, Loeys-Diet, degenerative, trauma
– Ass. VSD (perimembranous/subarterial VSD)

– Echo : Short axis view at great vessel level : “wind sock”

Example echo finding

– Filamentous structure protruding from Rt sinus of valsava into RVOT (Windsock

appearance). Color & Doppler showed continuous flow across Rt sinus of valsava
into RV outflow tact
– Drop out of interventricular septum size ... at 10 oʼclock compatible with

perimembranous VSD with Lt to Rt shunt

– Mx : surgical vs transcather closure,

– conservative in asymptomatic type B-1 with anticoaggulant
Mitral regurgitation
Mitral regurgitation

General
– Mitral valve prolapse

– Systolic mitral leaflet displacement >= 2 mm above annular plane

– If billowing < 2 mm

– Etiology : Barlowʼs disease, Fibroelastic deficiency (old age)

– Prognosis correlated with regurgitation volume > ERO

– Flail mitral valve leaflet : tip mitral leaflet into LA

– Pseudo-prolapse in rheumatic MR : excessive anterior leaflet tip motion & restrict

posterior leaflet
– Barlow's valve : degenerative mitral valve, Difficult to repair

– Mitral coaptation zone 7-10 mm

– Mitral annulus วัดท่า PSLA แต่ท่า bicommissural view จะได้ annulus กว้างสุด
– Mitral A1/P1 : lateral, Mitral A3/P3 : medial
– 4 chamber : A3P1, 3 chamber : A2P2, 2 chamber : A1P3, bicommis view : P1A2P3
– Lateral side is A1 & P1
– Aortomitral curtain connect with AV (Lt & non cusp)

Chordae
Primary chordae at tip leaflet : if rupture = fail leaflet
Secondary chordae at mid leaflet
Tertiary cordae at base of post. Leaflet
Papillary muscle
– Anterolateral : one head, give chords to A1/P1, half A2/P2
 – Vascular supply : LAD & LCx
– Inferomedial :
– Vascular supply : RCA

Approach MR
– Annulus : dilatation, abscess

– Leaflet : Myxomatous (MVP), endocarditis, calcific, rheumatic, valvulitis, congenitial

(cleft), Anorectic drug (phen-fen), radiation

– Chordae tendinae : rupture (mostly partial rupture), myxomatous, endocarditis,

trauma
– Papillary muscle : dysfunction, rupture

– Ventricular : cardiomyopathy

Functional MR : low closing force, tethering force, annular dilatation, dyssynchrony

Carpentierʼs classification
– Type I : normal leaflet

– : Annular dilatation, perforation, cleft

– Type II : Excessive leaflet

– Type III : Restricted leaflet motion (leaflet thickening)

– Restricted opening (diastole) : rheumatic MV, carcinoid

– Restricted closure (systole)

– Asymmetrical tethering : ICM

– Symmetrical tethering : DCM

Physical exam
– PSM : common is anterior leaflet
– Mid to late systolic murmur : common is posterior leaflet

– MVP : Valsalva (Strain phase : increase murmur, Release phase decrease murmur),
Increase regurgitation in maneuver that decrease LV volume
– MR : Valsalva (Strain phase : decrease murmur, Release phase increase murmur)
– Severe : S3, PHT
Echo
Echo finding in secondary MR
– Isolated inferolateral or posterobasal wall abnormality

– Ant. leaflet override due to post. leaflet restriction

Echo finding in ruptured papillary muscle

: common is posterior medial papillary muscle
– Severe MR due to Flail posterior mitral leaflet. Homogeneous hypermobile mass

attach to cordae tendinae of posterior MV and protruding into LV. Presented/

absence of posterior/anterior papillary muscle
– Good LVEF with inferior wall akinesia

– Dx : Inferior wall MI with Severe MR due to partial ruptured of posteromedial papillary

muscle.

Grade for primary MR

– Mild : ERO < 20 mm2, Rvol < 30 ml, RF < 30%
– Vena contracta < 0.3 cm. Jet area < 4 cm2 or < 20% of LA area.

– Severe : ERO >= 40 mm2 (PISA radius >= 1 cm), Rvol >= 60 ml, RF >= 50
– Vena contracta >= 0.7 cm (PSLX). Jet area >= 40% of LA area.

– Prominent fail leaflet or ruptured papillary muscle

– Pulmonary vein systolic reversal

Definition severe secondary MR

 – ESC : ERO >= 20 mm2, Rvol >= 30 ml. Due to poor prognosis when ERO >= 20
– ACC : Surgical intervention still define ERP >= 40 mm2 for more specificity
– Severe : ERO >= 40 mm2, Rvol >= 60 ml, RF >= 50%

Formula parameter MR
– Simplified ERO (set aliasing 40) = (r^2)/2 (r = หน่วยเป็น cm)
– Vena contracta : evaluate in parasternal long axis
– MR Vmax : mostly 5 m/s, not relate to severity MR
– ความเข้มของ MR VTI ยิ่งเข้มมากยิ่ง severe
Formula (ทุกอย่างเป็น cm)
– r = หน่วยเป็น cm
– Aliasing velocity = cm/s เช่น เลข 37-40
– MR velocity = หน่วยเป็น cm
– EROA = 2π(R^2 of Pisa)xAliasing velocity/Vmax
– Regurgitation volume = EROAxVTI(MR)

Grade angiogram (Sellars criteria)

– 1 : contrast not complete fill LA

– 2 : contrast complete fill LA but not reach intensity in LV

– 3 : contrast complete fill LA and reach intensity in LV after several beats

– 4 : contrast complete fill LA and reach intensity in LV after first beat, reflux to

pulmonary vein
Indication for surgery in primary MR (repair when possible)
– Symptomatic with EF > 30%

– Symptomatic with EF < 30% or LVESD > 55 mm with refractory med with durable

valve repair with low comorbidity

– high risk surgery with suitable echo : MV clip (llb)

– Asymtomaitc
 – EF < 60% or LVESD >= 45 mm (ESC class I)
– LVESD >= 40 mm (AHA class I)

– Systolic PA > 50 mmHg (IIa)

– New onset AF (IIa)
– Low risk valve repair with LVESD 40-44 mm plus one risk factor (IIa)
– Fail leaflet

– LA volume index >= 60 in sinus rhythm

Feasibility for MV repair

– Feasible for repair : Posterior leaflet prolapse, mild annular dilatation, no
calcification
– Repair is less likely : moderate calcification, rheumatic MV, bileaflet prolapse/severe
barlow, severe annular dilatation
– Controversy for repair : perforation, cleft MV, anterior leaflet prolapse, moderate
annular dilatation

Indication for surgery in severe secondary MR

– Undergoing CABG with EF > 30% (I), if EF < 30% (lla)

– Fail med FC III-IV and CRT with EF > 30% with low surgical risk (IIb)

– If increase surgical risk, any EF —> MV clip (IIb)

Surgical in secondary MR
– Restrictive annuloplasty ring or chord-sparing valve replacement

Post MV clip : DAPT 1 months and ASA lifelong

Follow up echo in moderate MR q 1-2 years

New concept

DOMV (double orifice mitral valve)

– Symptoms : MR (common), MS, combine MS/MR
– Ass. AVSD, obstructive left side lesion, cyanotic heart disease
Clinical trial
COAPT trial (NEJM 2018)
– Population : HF with At least moderate to severe secondary MR with optimize

medication, N 614
– mean Age 70, High STS 40%, NYHA II-III, mean-EF 30%

– Intervention : Mitral clip vs medication

– Outcome : Decrease HF hospitalization (NNT 3 in 2 years), Death from any cause.

Mitral stenosis
Mitral stenosis

Cause of LV inflow obstruction

– Pulmonic vein stenosis

– LA : Supravalve stenosis ring (beneath LA appendage), Cor triatriatum (thin echo

density plate like at traversing LA, divide LA to two chamber), LA myxoma

– MV : Parachute MV, MAC (elderly, ESRD, hyperparathyroid), Rheumatic MS, Myxoma,

mucopolysaccharidosis (course face, short stature)

General
– Rheumatic mitral stenosis : symptoms in age 30-40, F > M, 25% pure MS, 40% MS/

MR
– Atypical presentation : intractable asthma, dysphagia, hoarseness (ortnerʼs

syndrome)

Physical exam
– Pliability of valve : loud S1, OS (same as fix split), presystolic accentuation

– Increase intensity : tachycardia, exercise, nitrate

– Severity : long murmur, short A2-OS, loud P2, RVH

Ortnerʼs syndrome : LA enlarge compress recurrent laryngeal nerve

Definition
– Significant MVA < 1.5 cm2,

– Very severe = MVA < 1 cm2

Grade
– Mild MS : MVA > 2 cm2, Systolic PA < 30

– Severe : MVA < 1.5 cm2, Mean gd > 5, pressure half time > 150, sys PA > 30

– Very severe : MVA < 1, mean Gd > 10, pressure half time > 220, sys PA > 50

Echo
– MVA by 220/pressure half time, limitation in MR (overestimate), ASD
(underestimate), immediate post PTMC, elevate LVEDP
– Pressure half time = 0.3xDT (measure second slope)

– Rheumatic MS

– Calcified MV leaflet and Limited MV excursion with diastolic doming (hockey-

stick appearance)
– PSAX : MV showed commissural fusion MV (fish-mouth appearance)

– Wilkinʼs score

– Mean gradient across MV and Pressure half time

– Severe LAE with SEC/thrombus

– PHT, Enlarged RV & RV function

Picture 3 : measure Pressure half time for MVA

Picture 2 : measure deceleration time of diastolic function

Stress echo
– Indication : severity not matching with symptoms, asymptomatic significant MS
– Positive stress echo : symptoms, BP drop, exercise tolerance
– Poor prognosis : MPG >= 15 mmHg

Indication for intervention or surgery in significant MS

– Symptomatic

– Prefer PMC if suitable

– Surgery (Not suitable PMC) in FC III or more

– If surgery prefer surgical commissurotomy

– Asymptomatic with suitable for PMC or low risk surgery (IIa)

– High risk embolism : Hx of embolism, dense spont. contrast, new AF

– High risk hemodynamic decompensation

– Systolic PA > 50 mmHg (ESC), PCWP > 25 with excercise (AHA)

– Plan pregnancy

– Plan high risk non cardiac surgery

– Exercise test : symptoms at low level of exercise

– Stress echo : Systolic PA > 60 mmHg

Contraindication for PMC

– LA thrombus

– More than mild MR

– Severe or bi-commissural calcification

– Absence commissural fusion

– Wilkins score > 8

Wilkins score
Mobile
c. Highly mobile
d. Restrict tip leaflet
e. Restrict all leaflet but preserve forward move
f. No/minimal forward move
Thickening
c. Normal < 4 mm
d. Tip & mid leaflet
e. Total leaflet =< 8 mm
f. Total leaflet > 8 mm
Chordal involvement (subvalve thickness)
c. Normal
d. Upper 1/3 chord
e. Upper 2/3 chord
f. Total chord to papillary muscle, shortening
Calcification
c. Single
d. Scatter at tip (leaflet margin)
e. Tip & mid leaflet
f. Total leaflet

Good predictor for PBMV

Complication of PBMV
– Mortality 1-2%

– Cardiac perforate 1%

– Embolic stroke 1-2%

– Severe MR 2%

– ASD 5%
Follow echo in Moderate MS q 2-3 years
Time to follow echo in VHD

Parachute mitral valve

– Asymmetrical congenital MS, unifocal attachment of MV chordae,
– Independent number of papillary muscles

– Associate : Lt side obstruction (Coarctation, Bicuspid AV), ASD, PDA, VSD

– Echo : Eccentric opening of MV orifice, thickened and restricted MV leaflet/chordae,
Unbalanced cordal attachment, Cordal tendinaes converge to single papillary muscle
(usually posteriormedial), Variable-sized anterolateral papillary muscle.

Cor Triatriatum
– Term
– Cor Triatriatum sinister : Lt side

– Cor Triatriatum dexter : Rt side

– General : no progression, not associated PHT

– Association : ASD, VSD, Anomalous pulmonary venous connection, shone complex
– Cor triatriatum connect between opening of LA appendage to opening upper part of
fossa ovalis
– Prior cor triatriatum sinister & recurrent symptoms : evaluate PV stenosis
– Echo : thin membrane separate LA into two chamber, connect between opening of
LA appendage to opening upper part of fossa ovalis
– Time of surgery : mean gradient at least 8 mmHg, evaluate PV stenosis before Sx
Rheumatic fever
Rheumatic fever
– 50% no history of pharyngitis
– Patho : Aschoff body (granulomatous with fibrinoid change and lymphocytic
infiltration, necrotic center), Antischkow cell
– Evidence of chronic : Chronic RHD, Jaccoud arthropathy (non erosive)

Rheumatic MS : commissural fusion, female 2/3, onset symptom 30-40 years

Jone criteria (First : 2 major or 1 major + 2 minor, Recurrent with RHD : 2 minor)
– Must evidence of recent GAS infection : Throat swab GAS culture, Anti-DNase B

(peak 6-8 wks), ASO titer (peak at 5 wk) : titer at 2 wks with rising/falling 2 folds
– Major (ข้อ คอ คา คิว ผิวแดง)
– Sydenhamʼs Chorea : มักมี weakness ร่วมด้วยและส่วนใหญ่ criteria อื่นมักไม่ค่อยมี
เพราะ inflammation ดีขึ้นแล้ว, spontaneous resolution, control symptom with
valproate/carbamazipine
– Carditis : consider pancarditis involve from endocardial (regurgitation) to

pericardial consequence and MV before AV

– Subcutaneous nodule at elbow, occiput, knee (painless) : 1.5%

– Erythema marginatum

– Arthritis 80-100%, migratory or additive polyarthritis

– Minor
– Fever : < 2-3 wks

– Arthralgia
– Elevate ESR/CRP
– Prolong PR
Manage Acute rheumatic fever
– Antibiotic : Benzathine 1.2 mU IM single dose, PenV 500 mg tid total 10 days,

erythromycin/azithromycin total 10 days

– Salicylate and steroid : no long term benefit, may consider steroid 2 MKday for 2-3

wks in severe carditis, mild carditis/arthritis : salicylate

Secondary prophylaxis
– PenV 250 mg bid, Benzathine 1.2 mU IM. monthly.

– Penicillin allergy : sulfadiazine 1 gm OD, Erythromycin 250 mg bid.

– Duration (whichever is longer)

– No residual valve damage : until 21 years or 10 years after onset

– Residual valve damage : until 40 years or or 10 years after onset

– No carditis : until 21 years or 5 years after onset

Tricuspid valve
Tricuspid valve disease

General
– TV nearly AV node
– TR is load dependent, severity depend on preload & RV function

Echo view
– Apical 4 chamber/RV focus view : Ant- septal leaflet
– Parasternal short axis view : post leaflet + Ant or septal leaflet

Tricuspid regurgitation
Etiology
– Functional TR ไม่เท่ากับ TR with PHT
– Pacemaker induced TR : prevalence 30%
General
– 3/4 secondary TR : RVSP > 55

– 1/4 Primary TR : RVSP < 40

Primary or secondary TR by echo

Physical exam
– Soft, holosystolic murmur with caravalloʼs sign, if prolapse systolic click, cavello sign

positive, vitums sign (Increase intensity when push on liver), wood sign (winking
earlobe sign)
– Secondary TR from PHT : pansystolic murmur

– Primary TR : mid-late systolic murmur

– JVP with Giant c-v wave (lancisiʼs sign)

Grade
– Mild : is physiologic

– VC < 3 mm

– Jet area < 5 cm2

– Incomplete or faint CW jet

– PISA radius < 4 mm at Nyquist 40 cm/s

– EROA < 20 mm2, RVol < 30 mL

– Severe :

– Dilated annulus without coaptation or flail

– VC >= 7 mm, Jet > 50% of RA, Jet area > 10 cm2

– Systolic hepatic reversal flow, triangular CW jet (underestimate RVSP)

– PISA radius > 9 mm at Nyquist 28 cm/s

– EROA > 40 mm2, RVol > 45 mL

New grading of TR
– แบ่ง severe TR ออกเป็นอีก 3 grade
Indication for surgery : prefer TV repair > TVR, TV annulus ใหญ่สุด in 4 chamber
– Left side valve surgery

– Severe TR (primary or secondary)

– Mild to moderate TR

– Tricuspid annulus dilatation >= 40 mm or 21 mm/m2

– Intra-op TV annulus dimeter >= 7 cm

 – Recent sign of RV failure
– Only severe TR
– Primary severe TR

– Markedly symptoms

– Progressive RV dilatation/dysfunction

– Secondary severe TR without LV severe RV/LV dysfunction or PHT

– Markedly symptoms

– Progressive RV dilatation/dysfunction

Tricuspid stenosis
Most common acquire TS with PS : carcinoid syndrome, endomyocardial fibrosis,
systemic lupus erythematosus, and congenital tricuspid atresia
– PE : Giant A wave , Loss of Y descend, Kuassmall sign (Increase JVP when inspire),

Positive cavello sign

Echo finding
– EKG in Tricuspid atresia : Lt axis deviation, RAE with LVH

– Significant stenosis : mean gradient >= 5 mmHg, PHT > 190.

– Indication for percutaneous tricuspid dilatation (if anatomy suit) : risk for TR

– Symptomatic despite medical therapy

Carcinoid syndrome
– Serotonin destroy in Liver, lung, brain
– Rt side heart valve involvement in liver metastasis
– Lt side heart valve involvement in lung metastasis or presence of Rt to Lt shunt

– Echo : Thickening and retraction of TV with severe TR +/- TS, PV thickening and
retraction with PS, RV dilatation and preserve/impaired RV function.
Pulmonic valve
Pulmonic valve disease

Pulmonic regurgitation
Etiology : post TOF repair, congenital, endocarditis, carcinoid
PE : Graham steell murmur due to PHT (High pitched and blowing, early diastolic
decrescendo, begin with P2 but PR without PHT (Diastolic murmur begin after P2)
Grade : except acute PR
– Mild : is physiologic

– Jet length < 10 mm

– Regurgitation fraction < 20% (MRI)

– Severe :

– RV dilatation

– Steep deceleration (DT < 260 ms, Pressure half time < 100 msec), early

termination
– Jet/RVOT > 0.7

– Regurgitation fraction > 40% (MRI)

RV dilatation : RV focus view

– > 41 mm at base, > 35 mm at mid level

– RV EDVs : male 87 ml/m2, female 74 ml/m2

– RV ESVs : male 44 ml/m2, female 36 ml/m2

RVOT obstruction/Pulmonic stenosis
General
– PS : Decrease intensity during inspiration

– Subinfundibular stenosis = Double chamber RV (DCRV) ass. VSD

– Supravalve PS : Noonan syndrome, William, TOF

– Peripheral PS : maternal rubella, William, Alagille

– Valve PS

– Dome-shaped PV, Dysplastic PV (only in Noonan), Unicuspid PV, Bicuspid PV

– Peripheral narrow > 50% = significant stenosis

– PS without shunt = normal pulmonary blood flow

– DCRV : anomalous muscle bundle between RV body & RV outlet

Physical exam DDx AS

– Normal carotid pulse

– Soft P2 in valve PS

– Respiratory variation

– Radiate along left sternal border

– SEM at LUPS : moderate degree - splitting S2, severe degree - single S2

– Mid-systolic click is decrease on inspiration (due to partial opening PV), absence in

Noonan (Dysplastic PV)

– Common is no heave but RVH

– If RV heave ddx combine PS with VSD

– Thrill prefer valvular PS > ASD

– Subvalular PS : no thrill

CXR : mPA enlarge but normal RDPA (Chenʼs sign)

Grade
– Moderate : Peak gradient 36-64 mmHg (Velocity 3-4 m/s)
– Severe : peak gradient > 64 mmHg (mean gradient > 35 mmHg, AHA)
Indication for repair
Pulmonic stenosis
– Asymptomatic severe valvular PS : พิจารณาแก้ไขทุกเคส (IIa)
– Valvular PS : balloon valvotomy

– Valve PS : balloon dilatation, size Max 140% of PV diameter

– Peripheral PS : balloon dilatation, size Max 200% of site stenosis

– If fail ballon valvotomy with RVSP > 80 : surgery

– Moderate valve/subvalve PS with one of following (IIaj

– Unexplained symptoms : If failed balloon valvuloplasty, surgical repair

– HF

– cyanosis

– Exercise intolerance

– Only suitable for balloon valvotomy

– Decrease RV function

– DCRV

– Important arrhythmia

– Rt to Lt shunt via ASD/VSD

– Peripheral PS with narrow > 50% and RVSP > 50 : Balloon angioplasty or stenting

of a peripheral PA is effective
Isolated PR after repair PS
– Indication for PV replacement (at least moderate PR)

– Symptoms (I)

– Asymptomatic (IIb)

– Exercise intolerance attributable to PR

– RV dilation

– RV dysfunction

– After transcatheter PV replacement : ASA lifelong (prevent platelet aggregation to

decrease risk IE)

Syndrome
Straight Back Syndrome
– Pseudo-heart disease, mimic ASD, Ddx Pectus excavatum

– Benign disease, Association with MVP.

– DOE from restrictive ventilatory impairment

– PE : SEM at LUPSB with fix split S2 and decrease murmur on inspiration. No PHT

– EKG : incomplete RBBB and a vertical QRS axis (early transition at chest lead)

– CXR lateral/PA

– ratio of the distance between the anterior body of T8 and the posterior sternum

to the transverse diameter of the thorax measured at the level of the diaphragm
is less than 1/3.
– Loss of kyphotic curve of the thoracic spine.
– Echo : highly turbulent flow at RVOT and decrease systolic flow velocity at end
inspiration
Prosthesis valve
Prosthesis valve

Type of prosthetic valve

– Biologic : Stent (D,E), Stentless (F), Percutaneous (G,H)

– Profile : Good hemodynamic profile but late central valvular AR

– Homograft AV : more resistance to infection, more physiologic, low thrombotic

– Stentless : better hemodynamic profile but require surgical skill

– Mechanical : Bileaflet, single tilting disc, caged-ball

No. of prosthesis depend on external circumferential

– AV prosthesis : most used in Thai No.19, 21

– MV prosthesis : most used in Thai No.25-30

– GOA (Geometric orifice area) > EOA

Prefer Mechanical prosthesis
– Age < 50 years (AHA)

– AVR < 60, MVR < 65 (ESC)

Prefer Bioprosthesis valve

– Contraindication for OAC

– Age > 70 years (AHA)

– AVR > 60, MVR > 65 (ESC)

Bioprosthesis valve degeneration

– MV ~ 6-8 years

– AV ~ 8-10 years

MRI & Prosthetic valve

http://mrisafety.com
– MRI 1.5T : safety in all prosthetic valve & safety after immediate valve surgery

– MRI 3T : possible safety in all prosthetic valve

Evaluate post valve surgery at 1 month

No. of valve is outer ring
Bileaflet : open angle > 75 degree
View magnify 15
– AV in LAO cranial

– MV ปรับจน valve ขนาน

Normal in prosthesis valve
– 2 wall layer

– Closing volume (watching jet < 50% of phase systole/diastole) : up to 5 cm but

narrow, no tubulent
– Bileaflet : 3 jet

– Tilting disc : central jet

Key evaluate prosthesis dysfunction

– Increase gradient : exclude high flow state

– Thrombus

– size > 8-10 mm prefer Sx,

– size < 8-10 mm prefer UFH +/- ASA, if failure —> fibrinolytic/surgery

– Pannus

– Prosthesis valve mismatch

– Aortic EOA index =< 0.85

– Mitral EOA index =< 1.2

– Degenerative

– Regurgitation

– Physiologic : watching jet

– Pathologic

– Intravalvular

– Paravalvular (% leakage of circumferential)

– Grade

– < 10% : mild

 – 10-20% : moderate
– > 20% : severe

– Rocking motion > 40% dehiscence

– Paravalvular leakage with intractable hemolysis

– Surgical (I)

– Catheter base treatment (IIa)

– Endocarditis : Paravavular abscess/pseudoaneurysn, vegetation

Echo
Example
– Position & type of Prosthesis valve : MV or AV, Bileaflet/Tilting disc/Cage-ball

– Rocking motion of prosthesis valve, severe paravalvular leakage with eccentric jet

regurgitation.
– Combine with infective endocarditis : abscess, pseudoaneurysm, vegetation

– Dx : Prothesis valve dehiscence with infective endocarditis

– Limited opening and closure of prosthesis valve leaflet with forward turbulent flow

across prosthesis valve (mean gradient ...mmHg) with severe eccentric jet
regurgitation.
– Combine with thrombus or pannus

– Dx : Prothesis valve thrombosis

Thrombus vs Pannus
CT
– HU >= 145 : prefer pannus
– HU < 145 : prefer thrombus
– HU < 90 : good outcome for thrombolytic (complete resolution)
Prosthetic valve EOA
Formula for EOA
– EOA = 0.785x(LVOTdiameter)^2x(LVOT VTI)/(AV VTI)

– EOA = 0.785 x LVOTdiameter^2 x DVI

– EOA = SV/(AV VTI)

Mitral prosthesis dysfunction
– Regurgitation
– Paravalvular leakage

– Intravalvular regurgitation

– Watching jet

– Trapped (ปิดไม่สนิท)
– Stenosis (CW via MV) : Key is PHT > 130 (High PPV), Peak E vel >= 1.9 (High

NPV)
– Peak velocity > 1.9 m/s if > 2.5 = significant stenosis
– Mean gradient > 5 mmHg if > 10 = significant stenosis
– Pressure half time > 130 if > 200 = significant stenosis
– TVI : MV/LVOT VTI > 2.2. if > 2.5 = significant stenosis
– EOA < 2 cm2. by cont. equation if < 1 = significant stenosis
– MV E >= 1.9 m/s (if bileaflet >=2.4]

Diagram for MV prosthesis stenosis

– High mean gradient > 5 mmHg
Aortic prosthesis dysfunction
Limit in TEE
Stenosis : Key is AT > 100
– Peak velocity > 3 m/s

– Mean gradient > 20

– DVI < 0.3 (VTI of LVOT/AV)

– Jet contour : round shape = stenosis, triangular = normal

– Acceleration time > 100 or Acceleration time/Ejection time > 0.4

– EOA < 1.2 cm2 or EOAi < 0.85 cm2/m2

Diagram for AV prosthesis stenosis (exclude homografts, stentless valve, percutaneous

prosthesis)
Management prosthetic valve thrombosis
Prefer fibrinolysis in Right side valve > Lt side valve
– Critically ill : Surgical immediately, if not available —> Fibrinolytic

– Non critical ill

– Recent inadequate anticoagulant : try UFH +/-ASA

– If failure : Surgery but If high risk for surgery—>fibrinolytic

– Previous adequate anticoagulant

 – Surgery but If high risk for surgery—> fibrinolytic
– Embolism with residual thrombus >= 10 mm : surgery

Fibrinolytic for prosthetic valve thrombosis

– rTPA 10 mg bolus then 90 mg in 90 mins with UFH

– SK 1.5 mU in 60 mins without UFH

Pulmonic prosthetic dysfunction
– Regurgitation
– Mild : jet width/pulmonary annulus =< 25%

– Severe : jet width/pulmonary annulus > 50%, RV dilatation, valve dehiscence

– Stenosis
– Morphology : thickening & immobility, new RV systolic hypertension

– Doppler : Peak PV vel > 3 m/s or > 2 m/s in homograft

Tricuspid prosthetic dysfunction

– Regurgitation
– Mild : normal RA, Jet area < 5 cm2

– Severe : markedly dilated RA, holosytolic reversal of hepatic flow, Jet area > 10

cm2, VC > 0.7

– Stenosis
– Peak vel > 1.7 m/s

– Mean gradient >= 6 mmHg

– Pressure half time >= 230 ms

Anti-thrombotic in prosthesis heart

– All mechanical MV : keep INR = 3
– High thrombotic risk : tilting-disc valve, ball-cage
– Low thrombotic risk : bi-leaflet valve
– Add low dose ASA ontop VKA after adequate INR
– Thromboembolism (IIa)
 – Concomitant CAD (IIb)
– On-X valve (Aortic valve prosthesis) : can keep INR 1.5-2 after 3 months implatation
 General
congenital heart
diseases
Congenital heart disease

Cyanotic heart disease

Hypoxemia : rest O2sat =< 90%
– Central cyanosis or severe hypoxemia : define O2sat < 85% (can visual diagnosis)

– Clubbing of finger : cyanotic more than 3 months

– หัวใจ รับ pressure load ได้ดีกว่า volume load

Key approach : Cyanosis onset & Loud P2

Cyanosis onset (5T2E1S)
– Onset at Child : shunt dependence (ASD, VSD, PDA)

– Decrease pulmonary blood flow

– TOF, CXR : boot shape (narrow mediastinal, apex upward)

– Ebsteinʼs anomaly

– Tricuspid atresia with shunt

– Pulmonary atresia with shunt

– Increase pulmonary blood flow (loud P2)

– TAPVR (shunt dependence : ASD, VSD) : loud P2

– CXR: snow man (widening mediastinal)

– Truncus arteriosus

– CXR : Egg on a string (narrow mediastinal, apex downward)

– Transposition of great arteries : loud A2

– HLHS (common combine with ASD, PDA)

– Onset at Adolescent
– Loud P2
– Eisenmengerʼs syndrome: ASD at 40 yr, VSD/PDA at 20 yr

– Normal P2
– Pink TOF

– ASD/VSD plus

– PS

– Preferential TR

– CTEPHT

– Prominent eustachian valve

– Ebsteinʼs anomaly

– Single ventricle/hypoplastic left heart syndrome

EKG approach in cyanotic heart with surgical scar
– Rt axis

– RBBB : post TOF repair

– Reverse R progression : D-TGA

– Lt axis

– LVH +/- LAE : Tricuspid atresia, S/P fontan procedure

– Q in V1 & inferior lead (pseudoinfarction) : L-TGA

Adult congenital heart disease (AHA)
– Congenital heart disease : mostly < 5 years
– Acquire heart disease
– Abnormal murmur
– Shunt murmur : onset > 2 months age

– Obstructive murmur : onset after birth

Syndromes ass. with congenital heart

– Down syndrome : AVSD, primum ASD, VSD
– Turner syndrome : coartation, bicuspid aortic valve

– Holt-Oram : secondum ASD

– Marfan syndrome : aortic dilatation, dissection, MVP

– Noonan syndrome (chromosome 12/PTPN11 gene) : PS, HCM

– Williams syndrome : supravalve AS, supravalve PS, coartation, renal artery stenosis

Syndrome & Gene associated valvular stenosis

– Alagilleʼs syndrome : associate cardiac condition PS, TOF, VSD

– Dysmorphic feature : Prominent forehead, Deep set eyes (ตาลึกโหล่), pointed

chin, bolbous tip of nose
Operation (surgical scar)
Left lateral thoracotomy
– Left Blalock-Taussig shunt

– Pulmonary artery band

– Coarctation repair

– PDA ligation

– Potts shunt (create PDA)

– Closed mitral commissurotomy

Right lateral thoracotmy

– Right Blalock-Taussig shunt

– Mitral valve repair

– ASD repairs
Fontan operation : SVC and IVC to pulmonary artery (by pass RV)
– Palliative surgery

– Tricuspid atresia, pulmonic atresia, hypoplastic right/left heart, double outlet LV/RV

– Candidate for fontan: PA endiastolic pressure < 10, mPAP < 15, PVR < 2.5 wood unit

– Contraindication : high PVR

– Complication : chronic systemic venous hypertension

– Arrhythmia : IART is common (Intraartrial reentry tachycardia)

– New onset or worsening atrial arrhythmia : search for potential hemodynamic

abnormality
– Prevent thromboembolism (OAC)

– Arrhythmia control : ablation (IIa), medication

– Late : protein losing enteropathy (High alpha1-antitrypsin stool clearance), plastic

bronchitis : poor prognosis

– Treatment : Budesonide, consider octreotide

– Definite is Transplant

– Suggestion

– Annual lab : LFT, Renal function

– Imaging of liver (U/S, MRI, CT) : cirrhosis & HCC

– In case with atrial arrhythmia, suspected thrombus/embolic event

– Warfarin (I)

– ASA (IIb)
Congenital heart procedure
– Ross procedure : aortic valve replacement with own pulmonic valve
– Norwood procedure : PA connect to Ao (Hypoplastic left heart syndrome)
– Fontan requirement
– mPAP < 15 mmHg

– PVR < 4 wood unit

– PA/Ao diameter < 0.75

– EF > 60% and LVEDP < 12 mmHg

– After Fontan procedure

– Imaging for evaluated cirrhosis & HCC

– Risk for protein losing enteropathy

– Waterston shunt: Ascending Ao to RPA

– Potts shunt: Descending Ao to LPA
Common arrhythmia in congenital heart
– Rt side WPW : Ebsteinʼs anomaly
– IART (intra-atrial re-entry tachycardia) : atriotomy
– Sinus bradycardia or junctional rhythm : S/P Fontan, Mustard, Senning, TOF
– AV block : correct L-TGA, AV septal defect
Complication of cyanotic heart disease
– Hyperviscosity (symptoms : headache, fatique, other)
– therapeutic thrombectomy in symptom of hyperviscosity without dehydration

(Hb > 20 or Hct > 65%)

– Initial management is hydration

– Bleeding and thrombotic diathesis

– Paradoxical emboli
– IDA from inappropriate phlebotomy
Complication of surgical correction
DORV
– Vary physiology : VSD/TOF/TGA/PS, Single ventricle physiology
– 5 basic types
– VSD type (no PS)

– TOF type

– TGA type (with or without PS)

– Remote VSD (with or without PS)

– DORV with AVSD

– Ass. AVSD, arch obstruction, Heterotaxy syndrome, ventricular hypoplasia, PS/PA,

MV straddling/stenosis/atresia
– Indication for surgical repair : HF, cyanosis, limited exercise
– Treat as TOF
DCRV
Double chamber RV
– RV outlet obstruction

– Commonly associate VSD

– VSD above obstructive lesion (distal VSD)--> left to right

– VSD below obstructive lesion (proximal VSD)--> right to left

– EST performed in asymptomatic patient : decrease exercise capacity

Treatment
– Surgical repair (transatrial or transventricular ressection of obstructing muscle

bundles +- VSD closure) in moderate to greater outflow obstruction in pt. with

unexplained symptoms of HF, cyanosis or exercise limitation
– Asymptomatic Severe gradient (ไม่มีตัวเลข)
Pulmonic atresia with VSD
– Shunt : PDA, MAPCAs, shunt, bronchial artery, RV coronary fistula
Treatment
– No MAPCAs: Tx as TOF

– MAPCAs

– Palliative with BT shunt

– Unifocisation: single stage repair, Two stage repair

Tricuspid atresia
– Ass. VSD, TGA
– EKG in Tricuspid atresia : Lt axis deviation, RAE with LVH

Persistant of left SVC

– Associate : ASD, AV septal defect, Herotaxy

TAPVR/TAPVC
– Total anomalous pulmonary venous connection
– most common shunt is ASD
– Cat-eye syndrome : TAPVR plus vertical colobomas (Cat eye)
– O2 step up at upper SVC to lower SVC
– If shunt is ASD : Same O2 at RA/LA/RV/LV

– Adult : TAPVR without obstructive pulmonary venous obstruction (if pulmonary

venous obstruction, developed pulmonary edema at born)
Univentricular heart

– Approach : pulmonary blood flow & Heterotaxy

– Non-heterotaxy
– Heterotaxy syndrome
– Right isomerism : Asplenia, unroof CS, bilateral SVC, TAPVR, common atrium,

complete AVSD, TGA, DORC, PS/PA

– Left isomerism : Polysplenia, interuptted IVC (ipsilateral hepatic vein), common

atrium, complete AVSD

– Physiology minic : Hypoplastic left or Right heart
Principle of management
Staged repair is unavoidable - palliation
• Protect lung if pulmonary blood flow is high —> PA banding
• Provide adequate pulmonary blood flow —> systemic-to-pulmonary shunt
• Relieve systemic ventricular outflow tract obstruction
• Correction of anomalous pulmonary venous connection
 • Prevent AV valve regurgitation
• Adequate mixing of blood: atrial septostomy
Treatment
– Cyanosis with decrease PBF

– < 3 months : systemic-pulmonary shunt

– 4-6 months : bidirectional Glenn

– > 2 years : fontan

– Cyanosis with increase PBF

– < 3 months : pulmonary banding

– >= 4 months : bidirectional Glenn

– > 2 years : fontan

Anticoagulant
– Fontan with atrial arrhythmia

Truncus arteriosus
– Hemitruncus arteriosus : ass. PDA
– Finding : both ventricles connected to common arterial trunk via single tri-leaflet
truncal valve and PA arises from common arterial trunk, non restricted VSD beneath
truncus with bidirectional shunt. Moderate truncal valve regurgitation
– Sx : Rastelli repair with patch septum abs new pulmonary valve/artery

AP window
– Similar to truncus arteriosus but present of Aortic & pulmonic valve
Treatment : rastelli operation

Shoneʼs complex
– Typical consists of 4 obstruction of Lt side heart
– Parachute MV
 – Supravalve mitral ring
– Subaortic stenosis

– Coartation of aorta

– Incomplete forms (2-3 lesion)

– MV anomaly

– LVOT obstruction

– Coarctation of aorta

Uhlʼs anomaly
– Thin Rt ventricle
– partial/complete absence of myocardium (trabeculation).
– Mimic severe type of Ebsteinʼs anomaly: nearly complete atrialisation of RV

Eisenmenger syndrome
– Advanced form of PAH ass. Congenital heart
– Exclude other potential right to left shunt (RVOT obstruction) or other PHT

– Confirm diagnosis by imaging and cardiac cath

– Sequelae : stroke, brain abscess, osteoarthropathy, iron def, pulmonary artery

thrombosis, hemoptysis, pneumonia, AKI/CKD, SCD
– Palliative therapy
– Drug specific for PAHT : 1. Bosentan 2. PDE-5i

– Systemic anticoagulant (IIb)

– Avoid : Pregnancy, dehydration, high altitude (5000 feet above sea level), O2

supplement during on airplane, High heat (vasodilation), CCB

– Prevention : IE prophylaxis, IV filter, Vaccination

– Alert : ถ้ามีปวดหัวให้ระวังและรีบมา รพ. (brain abscess)

– Definite therapy : heart-lung transplantation

ICD indication in ACHD

Secondary prevention
– Abort SCD

– Sustained VT

Primary prevention
– EP study : inducible sustained VT/VF

– Indication : Frequent PVCs or non-sustained VT plus high risk feature

– QRS duration ≥180 ms

– Decreased LVEF or diastolic dysfunction

– Dilated right ventricle

– Severe pulmonary regurgitation or stenosis

– Prior palliative systemic to pulmonary shunts

– Unexplained syncope

– Atrial tachycardia
 – Elevated levels of BNP

Genetic consultation
General in congenital heart
– Father transmission rate ~ 3%

– Mother transmission rate ~ 6%

ASD
ASD
Type
– Secundum : most common, must see limbus

– Ass. Mitral valve prolapse

– Holt-Oram syndrome (fingerized thumb)

– Primum : MV & TV continuation

– Ass. Cleft mitral valve, AVSD, Down syndrome in complete AVSD

– Sinus node displacement (may be Pw negative in inferior lead)

– Sinus venosus

– Ass. PAPVR, Common PAPVR (RUPV to Innominate vein)

– Coronary sinus defect

– Ass. Persistent Lt SVC

– Isolated Lt SVC : ass dextrocardia or complete situs inversus

– Atypical Lt SVC (drain to LA) : cause cyanosis and paradoxical emboli

General
– Small secundum ASD < 3-5 mm in diameter

– ASD < 5 mm and Age < 5 years : can spontaneous closure

– Significant ASD > 1 cm in diameter

– Large ASD >= 2 cm in diameter

– significant shunt : Qp/Qs >= 1.5 or RV volume overload

Approach
ASD with hypoxemia
– Eisenmenger ASD

– Non-eisenmenger

– ASD with preferential TR

– ASD with large eustachian valve

– ASD with TAPVR

– PHT : CTEPH, PPAH

ASD with PHT

– Eisenmenger syndrome

– PAHT

– Association : MR, MS, P/TAPVR

Physical exam
– Slightly increase JVP

– RV heave

– SEM at LUPSB with fixed split S2

– Fix split S2 found in Qp:Q2 > 1.5

– Tricuspid diastolic rumble

– found in Qp:Q2 > 1.5

EKG : incomplete RBBB

– Secundum ASD : incomplete RBBB, RAD, RVH

– ASD sinus venosus type : same EKG as secundum ASD plus negative inferior Pw

– Primun ASD : incomplete RBBB plus Lt axis (LAFB), RVH

– Crochetage : notch near apex of R wave in Inferior lead, corrrelated with shunt

severity
– One inferior lead : Sense 70%, specific 90%

– Three inferior lead : specific 100%

Echo
– Secundum ASD : no LA enlarge until age > 40, IAS drop-out size ... mm with left to

right shunt, CS dilatation, +/- MVP

– Primum ASD : lowest part of IAS drop-out, LA enlarge, TV-MV continuation (AV valve

at same level), Groove neck deformity

– Sinus venosus ASD with PAPVR : TEE showed abnormal pulmonary vein connection,

PAPVR : fuse SVC with RUPV (tear drop sign : RUPV-SVC/Ao)

– Coronary sinus ASD with persistent Lt SVC : confirm by contrast echo injection at Lt

arm : first visualized in CS and then RA

– PW across ASD
Benefit at time of correction
– before 25 years - decrease mortality

– before 40 years - decrease RV failure but increase atrial arrhythmia

Indication for closure

Goal : reduced RV volume & FAC
– Symptoms : Paradoxical embolism, Rt side symptoms, exercise induced cyanosis

– Asymptom/symptoms

– Significant shunt (Qp:Qs > 1.5)

 – AHA : PA systolic pressure < 50% of SBP & PVR < 1/3 of SVR (I)
– RA/RV volume overload

Contraindication
– Eisenmenger syndrome

– PVR > 2/3 of SVR at baseline or vasodilator

– PA systolic pressure > 2/3 of SBP.

Surgery in sinus venosus ASD with PAPVR : Warden operation (pulmonary baffle)
ASD device : only ASD secundum
– diameter size < 38 mm

– rim > 5 mm (Must too closed to AV valve, coronary sinus, Lt & Rt vena cava, Rt PV) -

except aortic rim

– Key is SVC & IVC rim

– IE prophylaxis 6 months and ASA at least 100 mg/day

TEE for evaluated rim for device (ช่วง systolic รูใหญ่สุด)

Mid esophageal view
– 0 degree : AV valve-posterior rim

– 45 degree : aortic-posterior rim

– 90 degree : SVC-IVC rim

Routine follow screening

Syndrome
– Holt-Oram syndrome : AD (TBX-5 mutation), cardiac limb syndrome (fingerized
thumb, absence radial bone)
– Lutembacher syndrome : congenital/acquire MS with secundum ASD
– Ellis van creveld syndrome : short limb dwafism, polydactyly
– ASD is common, single atrium, VSD, PDA
VSD & AVSD
VSD

Type
– Perimembranous type : most common, MV&TV continuation

– Muscular type : common spontaneous closure

– Inlet/AV canal type

– Outlet type (AV&MV continuation): Infracristal (subaortic type), Supracristal

(subpulmonic type)

General
– Can spontaneous closure < 8 years
– Significant VSD >= 1 cm
– Restrictive VSD : small shunt (Qp:Qs < 1.4), Risk IE
– Non-restrictive VSD (Qp/Qs > 2.2)
– Size of VSD (compared to aortic annulus)
– Large > 50%

– Medium 25-50%

– Small < 25%

– Ruptured sinus of valsava ass. with Outlet VSD, IE

– Mean age of death 37 years
– 25 years survival in large VSD ~ 60%

– Gerbode defect : ventriculo-atrial defect (common LV to RA)

CXR & EKG
– CXR : LAE&LVE, pulmonary plethora, normal Ao

– EKG : Biventricular hypertrophy (Katz Wachtel sign) : Tall Rw + Deep Sw in V2-4 >=

50 mm
AR : Prolapsed aortic cusp from venturi effect (common is Rt cusp & non cusp) in
perimembranous or supracristal VSD (subaortic) ~ 6%

Physical exam
Small VSD
– palpable thrill, normal P2, pansystolic murmur at LLSB

Large VSD with PHT

– Prominent A wave, loud P2, no VSD murmur, PR & TR murmur

– Relative MS : found in Qp:Qs > 2

Echo
PLAX : color flow across ventricular septum
– Outlet or Perimembranous VSD

PSAX at great vessel view

– Color flow via aortic valve at 8 Oʼclock = Gerbode defect, rupture sinus of valsava

– Color flow via aortic valve at 10 Oʼclock = perimembranous VSD

– Color flow via aortic valve at 12 Oʼclock = outlet VSD (Infracristal/subaortic)

– Color flow via pulmonic valve at 2 Oʼclock = outlet VSD (Supracristal/subpulmonic)

Ddx rupture sinus of Valsalva, coronary AV fistula, abnormal coronary origin

PSAX at MV & mid level : color flow across ventricular septum

– Inlet VSD : flow at inferior septum

– Muscular type VSD : flow at superior septum

A4C : color flow across ventricular septum
– Inlet VSD : flow at basal part ventricle

– Muscular type : flow at mid-apex part of ventricle

Low velocity diastolic left to right is normal finding in restrictive VSD

Echo description
– IVS drop out size... at ...Oʼclock, compatible with perimembranous VSD with left to

right shunt, +/- prolapsed Rt/non-cusp of AV leaflet

– Dx restrictive perimembranous VSD with Lt to Rt shunt and moderate AR due to AV

leaflet prolapse

Indication for closure

– Symptomatic VSD (I)
– Asymptomatic VSD
– LV volume overload (I)

– Qp:Qs > 1.5

– AHA : PA systolic pressure < 50% of SBP & PVR < 1/3 of SVR
 – Hx of IE (ESC IIa, AHA IIb), common site PV & TV
– VSD (outlet/perimem VSD) ass. Prolapsed aortic cusp causing progressive AR (Rt or

Non cusp)
Contraindication
– Eisenmenger syndrome

– PVR > 2/3 of SVR at baseline or vasodilator, PA systolic pressure > 2/3 of SBP.

Contraindication for closure

– Eisenmenger or excercise induced desaturation
– Small VSD : does not leading LV load or PHT without Hx of IE

Procedure
– Surgical with pericardial patch

– Device closure only in muscular VSD (must remote to TV & Ao), perimembranous

– IE prophylaxis 6 months after procedure, lifelong if residual defect

Routine follow up

VSR (Ventricular septal rupture)

General
– Anterior infarct : apical defect

– Inferior or lateral infarct : basal defect

– Inferior infarct : basal inferoseptum

– Subacute process require 3-5 days

Example echo finding

– Serpiginous septal tear, irregular border, disrupted interventricular septum with thin

wall myocardium at apical septum/basal-inferoseptum, compatible with VSR with Lt

to Rt shunt (peak PG ... Hg)
– LV function and regional function

Management
– Delay surgery at least 7 days (Full mechanical support) in ESC

– Role percutaneous VSR closure

– Defect < 15 mm

– Adequate rim : lack adequate rim in most of inferior/posterior defect

AVSD
(atrioventricular septal defect)

Partial AVSD : defect only atrial level

– most in primum ASD with mitral valve cleft

Complete AVSD : defect in crux of heart

– 4 component

– Septum primum ASD

– Cleft mitral valve

– Inlet VSD

– Widened antero-septal tricuspid commisure

– PE : single S1, mid diastolic murmur (augmented AV inflow)

– Complete AVSD : 75% ass. Down syndrome

ECG :
– Lt axis deviation

– LAFB in ASD primum & AVSD

– 1st AV block

Echo finding
– Common AV valve at same level

– Gooseneck deformity (elongated Lt ventricular outflow tract)

Treatment in no Eisenmenger
– Partial AVSD —> Treat as ASD

– AV valve regurgitation

– Symptomatic with at least moderate AV valve

– Asymptomatic with moderate to severe AV valve

– EF < 60%

– LVESD > 45 mm

– AHA depend on MR guideline

– LVOT obstruction (Peak gradient > 50 mmHg) or HF

– Cause from Gooseneck deformity

– No treatment in Eisenmenger, PVR >= 2/3 of SVR

Routine follow up
PDA
PDA

– Ddx coronary AV fistula, ARCAPA

– Differential cyanosis (pink hand but blue feet) : PDA with reverse shunt, Interrupted
aortic arch
– Reverse differential cyanosis (blue hand but pink feet) : D-TGA with PDA with

severe PHT
– Pre-ductal type PDA with Rt to Lt shunt : clubbing finger at 3 extremity (spare Rt

hand)

General
– Ass. Maternal rubella
– Ass. Coarctation of aorta
– Cont. flow increase load heart
– Unlikely spontaneous closure after 3 months
– Closing all detect murmur case except Eisenmenger
– Large nonrestrictive PDA > 0.6 cm (AHA)

Physical exam
– Differential cyanosis : measure O2 sat feet & hands
– Bounding pulse and wide pulse pressure
– Cont. murmur with systolic accentuation (at S2) at Lt ICS 2 or Lt subclavicle

Echo
– Measure defect size (significant > 6 mm) and gradient across PDA, PHT
– Turbulent high velocity from descending Ao to left PA with Lt to Rt flow
– Cont flow with systolic accentuation
– Look for PA endarteritis (vegetation at PA)
Doppler in PDA with severe PHT
– Low velocity continuous Lt to Rt flow with diastolic accentuation

Indication for closure

Device closure is method of choice
– Sign of LV or LA volume overload

– PHT : PA systolic pressure < 50% of SBP and PVR < 1/3 of SVR
 – Suitable for device : small PDAs with cont. flow
– Closed PDA in non-significant shunt for decrease risk of endarteritis (~ 1% per

year)
Silent PDA : no required closure
Contraindication
– Eisenmenger syndrome

– PVR > 2/3 of SVR at baseline or vasodilator, PA systolic pressure > 2/3 of SBP.

– Exercise-induced lower limb desaturation.

– Very small : no murmur

CTA or MRA for evaluated device closured

– Surgical PDA closure : risk for recurrent laryngeal nerve injury

**High pressure : DDx High flow or High resistance —> Try occlude PDA for exclude High
flow —> Reevaluated pressure

Routine follow up as ASD

Syndrome
– Char syndrome : PDA + 5th finger abnormalities (absent of fifth middle phalanges) +
Facial dysmorphism (Short philtrum, prominent lips, flat nasal bridge with upturned
nares and ptosis)
TOF
TOF
Comprises
– RVOT obstruction (most subvalve PS)

– No restrictive VSD (most is subaortic VSD)

– Overriding of aorta (< 50%)

– Must see stradding valve (cordae attach in opposite site of septum)

– Ddx DORV : Overriding of aorta > 50% & mitral-aortic discontinuity

– RV hypertrophy

Physiology
– Anterior displacement : Size Ao > PA
– TOF: More severe PS, less intensity of murmur
– Isolated PS: More severe PS, more intensity of murmur

General
– Rt to Lt shunt from PS ไม่ใช่ Eisenmenger syndrome
Ddx 1. VSD with PS : no overriding aorta. 2. DORV : Ao & PA from RV
– 15% ass. DiGeorge syndrome (22q11 deletion) : suspected in TOF with Rt side aortic

arch
– CXR : Ascending Ao enlarge, mPA absence

– Associated anomaly : Valvular PS 50%, ASD 15%, Rt aortic arch 25%, Persistent Lt

SVC, Anomalous coronary artery crossing RVOT ~ 5% (LAD from RCA, pre-pulmonic
type) or dual LAD
Long case : cyanotic at birth & cont. murmur at Lt subclavian (BTS)

Echo
– TOF : non-restrictive VSD with bidirectional shunt, overriding aorta (Ddx DORV),
Right side aortic arch, subvalve PS, small PA, RV thickness, preserved aortic-mitral
continuity. Ass. ASD
– Post TOF repair : increase echogenicity at IVS near AV (patch VSD)

Repair
– Palliative surgery in severe symptoms & low BW < 8 kg (siriraj)
– Waterston shunt & Potts shunt (in infant) : High pulmonary blood flow—>

Increase risk PHT

– BTS (modified Blalock–Taussig shunt)

– Primary repair in first year of life (6-18 months) : VSD closure & relief RVOT
obstruction
– Increase RVOT by patch augmentation or transannular patch : risk PR

– Pink TOF : total repair —> ระวัง MAPCAs (major aortopulmonary collateral artery)
เพราะหลัง total correction ถ้าปิด MAPCAs ไม่หมดจะเกิด severe PHT
– MAPCAS : originated from descending Ao or subclavain
 – PVOD develops in unrestricted blood flow MAPCAS
– Siriraj plan total correction BW > 10 kg
– Evaluate PA before total correction

– McGoon ratio [Diameter of (RPA+LPA)/Descending Ao]

– McGoon ratio : Normal 2g1, > 1.4 suitable for total correction, < 0.8 not-

suitable for total correction

– Nakata index: summation of area of RPA and LPA divided by BSA (< 150

precluded definitive repair)

– Surgery with VT ablation if present VT (IIb)
– Surgical PVR mortality 1-4%
– EKG post TOF repair : RBBB ~ 90%

Late complication repair TOF

– Pulmonic regurgitation (severe PR : P1/2 time < 100, density of PR same antegrade
flow, PRi (regurgitation time/diastolic time) < 0.77) —> RV dilation/dysfunction
– Indication for PV Replacement (surgical or percutaneous) in severe PR/PS

– Symptom PR. If PS (RVSP > 60 mmHg, TR vel > 3.5 m/s)

– Asymptomatic : two of following (AHA 2018)

– Decrease objective exercise capacity

– Progressive RV dilatation (RVEDV index >= 160 ml/m2 or RVESV >= 80

ml/m2)
– RVEDV >= 2 times of LVEDV

– RV dysfunction (RVEF < 40%) or LV dysfunction

– RVSP 2/3 of SBP

– Add on ESC (one of following criteria)

– RVOTO with > 80 mmHg (TR vel > 4.3 m/s)

– Sustained atrial/ventricular arrhythmia

– Progress TR at least moderate

– Aortic root dilatation with AR (relates to intrinsic abnormal aorta & increase flow) :
rarely to aortic dissection
– TR mechanism : annular dilatation, Disruption of septal-anterior commissure by VSD
patch
– AT/VT & SCD
– VT/SVT in Repair TOF: 30% with hemodynamic abnormalities (seek for

hemodynamic abnormalities)
Transcatheter PV replacement
– Coronary compression test ก่อนเสมอ (I)
– Type of transcatheter valve

– Melody valve (Medtronic): Bovine jugular vein valve, Platinum iridium Fame

– SAPIEN-3 valve (Edwards): Bovine pericardial tissue

– Venus P-valve (China): Porcine pericardial valve, self expandable

Medication : ASA after transcatheter PV replacement

Follow up CMR evaluate RV before surgery
– 3 years F/U in Stable patient

– 1 years F/U in RV volume index >= 150 or progressive RV volume (increase > 25 ml/

m2) or RV dysfunction (RV EF =< 48% or decrease 6%)

ICD indication
Secondary prevention
– Sustained VT

– Abort SCD

Primary prevention
– LVEF =< 35% with NYHF II-III

– In selected case with multiple risk factor (AHA, IIa)

Risk of SCD after correction : primary prevention for ICD still controversial, 0.2% per
year
– Reduced LV systolic or diastolic dysfunction (Add RV dysfunction, ESC)

– QRS >= 180 ms

– High grade ectopy (non-sustained VT) on holter

– Extensive RV scarring (AHA)

– Inducible sustained VT/VF at EPS

– Indication for EPS

– LV systolic or diastolic dysfunction

– Non sustained VT, QRS >= 180

– Extensive RV scarring

– Residual PR/RVOT obstruction (ESC)

Routine Follow up

Syndrome
– Pentalogy of Cantrel
– Omephalocele

– Anterior diapharmgmatic hernia

– Sternal cleft (หัวใจเต้นข้างนอก)

– Ectopic cordis

– Intracardiac defect : TOF, AVSD, VSD, LV diverticulum

– DiGeorge syndrome (22q11 deletion): Velocardiofacial syndrome, underdeveloped

chin, low-set ears, wide-set eyes or a narrow groove in the upper lip, gap in the roof
of the mouth (cleft palate) or other problems with the palate
Ebstein anomaly
Ebstein anomaly

– Ass. 50% ASD/PFO, 25% Right side bypass tract (Posterior & septal aspect of TV
ring), RVOT obstruction from ant TV leaflet redundant
– Drug ass. Lithium or benzodiazepines

Classification

Physical exam
– +/- cyanosis/clubbing
– Quiet precordium
– No RV heave/thrill + Parasternal heave in severe case
– Normal PMI
– Sail sound(multiple T1 คล้ายๆ multiple click), very late Tricuspid OS
– Normal JVP (good RA compliance)
– Pansystolic murmur at LLSB with carvalloʼs sign (severe TR)
– Widely split S1

EKG
– 80%RBBB (If no bypass tract) with fragmented QRS, TWI in V1-V4 and inferior lead
– Polyphasic or splintered QRS in chest lead

– Qw in inferior lead
 – Pre-excitation. Tall P pulmonary, AF/flutter
– DDx from ARVD from Pw (Himalayan Pw > 5 mm)

– Absence of RBBB is specific for presence of accessory pathway (Rt side bypass)
– PR prolong in no accessory pathway (Intra-atrial conduction delay)

Echo (key)
– Apical displacement > 8 mm/m2 of septal & post leaflets
– Fenestration, Redundant, Elongated, Sail like with Tethering (FREST) of ant. leaflet
– Abnormal chordal attachment
– Atrialization of RV
– Poor coaptation of TV : moderate to severe TR
– RV function
– Small PA
– Ass. Anomalies : ASD/PFO

Predict mortality for surgery (GOSE score)

– RA area/other 3 chamber area in apical 4 chamber view in diastole

– Grade I : ratio < 0.5

– Grade II : ratio 0.5-1.0, mortality 10%

 – Grade III : ratio 1.0-1.49, mortality 44%
– Grade IV : ratio >= 1.5, mortality 100%

Indication for surgery

Surgery : correct TR in significant TR (at least moderate TR) and ASD/PFO closure
– Symptomatic

– HF with NYHC FC II (I)

– Objective evidence of worsening exercise capacity (I)

– Systemic desaturation (Rt to Lt at atrial shunt) (IIa)

– Paradoxical emboli

– If no symptom of TR : ASD/PFO device closure

– Asymptomatic

– Progressive RV dysfunction (I)

– Progressive RV dilatation (IIa)

– Atrial tachyarrhythmias (IIa)

EPS before surgery in all case even in absence preexcitation

– look for bypass tact/atrial arrhythmia

– Ablation before surgery or intra-op ablation

Surgical technique
– TV replacement or TV repair in significant TR
– Palliative shunt : bidirectional Glenn in child
Routine follow up
 Transposition
of great arteries
Segmental approach
– Cardiac position and axis
– Position : Levo/Meso/Dextroposition

– Axis (Apex) : Levo/Meso/Dextrocardia

– Determine of situs : (most abdomen & atria is same site)

– Abdominal situs

– Solitus

– Inversus

– Ambiguous (IVC & aorta at same side)

– Rt isomerism (double SVC, IVC still anterior to aorta)

– Lt isomerism (Interupted IVC, IVC posterior to aorta)

– Atrial situs : Solitus/Inversus/Ambiguous

– Segment : Great vein, Atrial, Ventricules, Great arteries

– Atrial morphology

– Determine RA : connect to IVC (Not rely on SVC), Board base appendage,

Pectinated muscles, Crista terminalis

– Determine LA : Narrow base appendage, smooth muscle, received PV, PFO

flap in LA side
– Ventricle morphology

– Determine RV (must connect with TV) : TV more apical insertion, RV

trabeculated wall, Chordal insertion in septum

– Determine LV (must connect with MV) : Less trabeculated wall, papillary

muscle
– Great vessel

– Pulmonary artery : PA bifurcation

– Aorta : Arch with neck vessels, coronary artery

– Connection :
– Veno-Atrial : PAPVR, Lt side SVC

– Atrio-Ventricular : Double(LV > RV)/single/common inlet

– Ventriculo-Arterial : Concordant, Discordant (D or L loop TGA)

– Relation of ventricles : Depend on RV morphology

– D-loop : RV morphology in Rt side of LV

– L-loop : RV morphology in Lt side of LV

– หลักการ : นิ้วโป้ง = inflow, 4 นิ้ว = outflow, D-loop = มือขวาวางได้ (normal)

– Outlet : double outlet(RV > LV)
General
– D-TGA : A-V concordance but V-a discordance

– Association : VSD ~ 90%, PS/PA ~ 60%, coronary anomaly, LVOT obstruction,

coarctation
Physical exam
– Loud A2 in TGA (AV closed to chest wall)

Echo
 – Parallel of great vessel in PSLA
– TGA : Short axis showed Ao is anterior and mPA is posterior.
– Ao is left : L-loop

– L-TGA: Ventricular inversion (Atrioventricular discordance &

Ventriculoarterial discordance), Morphologic LA connect to systemic RV,

apical displacement of left side TV with moderate/severe TR
– Ao is right : D-loop

– L-TGA (Atrial & Ventricle switch) : 90% isolated dextrocardia/dextroposition/

abdominal solitus **present with left side HF**

ECG
– AV block ~ 2% per years in L-TGA with situs solitus, less in L-TGA with situs inversus

– L-TGA : *Lt axis*, Q in V1 & inferior lead (pseudoinfarction)

– In Dextrocardia : Absence/reverse R progression

– Situs inversus : Pw negative in lead I, aVL

– Situs solitus : Pw positive in lead I, aVL

– d-TGA with atrial switch : sinus node dysfunction

Operation :
– Stage of operation

– One stage arterial switch operation : age less than 3 weeks

– Two stage arterial switch : age more than 3 weeks

– 1) PA banding (train LV)

– 2) Arterial switch operation

– L-TGA : double switch operation (arterial & atrial switch)

– Atrial switch procedure (Old surgery) Complication : late systemic RV failure (60% at

25 years), SSS, atrial reentry tachycardia, obstruction of pathway (edema), leakage

of buffle (cyanosis)
– Mustard (pericardial or prosthesis)

– Senning (atrial wall : high risk arrythmia)

– Arterial switch (Current surgery) in a month of life

– Jatene arterial switch

– look for outflow stenosis/obstruction before plan surgery

 – Long term complication : AR, coronary ostial stenosis
– LeCompte procedure

– Long term complication in non surgical case : RV dysfunction due to systemic

ventricle
Indication for intervention after atrial switch
– Valve repair or replacement in severe symptomatic systemic (tricuspid) AV valve

regurgitation
– No ventricular dysfunction (RVEF >= 45%), I level C

– Ventricular dysfunction (RVEF < 45%), IIa level C

– Symptomatic baffle stenosis/leak

– 1st : intervention stent

– 2nd : surgery if not amenable for intervention

Role anticoagulant
– d-TGA with atrial switch with atrial arrhythmia (I, B)

Late complication
Atrial switch
– Complication

– Systemic RV dysfunction ~ 90% : CMR for RV size & function

– Systemic AV regurgitation (PR) ~ 40% : prefer TV replacement than TV repair in

symptomatic moderate to severe TR with ventricular dysfunction

– No surgery in severe TR with more than mildly systemic ventricular

dysfunction
– Baffle problem

– obstruction : 30%

– Leak : 25% : detect by agitated saline contrast echo

– Subpulmonic stenosis

– Sinus node dysfunction : suggest ambulatory monitory for bradycardia in case

treated with beta-block

– Atrial arrhythmia : anticoagulant (I,B)

Arterial switch
– Complication

– Neo-aortic root dilation

– Neo-valve AR or Neo-valve PR

– Supravalvular AS or Branch PS

– Coronary artery abnormalities or stenosis

– Suggestion :

– Imaging (CAG, CT, MRA) in Symptomatic/Asymptomatic for evaluation coronary

anatomy (IIa)
– EST for symptomatic case

Routine follow up
Atrial switch

Arterial switch
CCTGA
 Heart failure
Cardiogenic shock
Heart failure & Cardiogenic shock

– HF : abnormal cardiac structure or function —> leading poor tissue O2 delivery OR

increase filling pressure
– Definition advance HF (despite optimal treatment)
– LVEF < 30% plus all of following

– Symptoms : NYHA III-IV or HF hospitalization > 1 in last 6 months

– Objective evidence of impair function capacity : 6MWTD =< 300 (FC IIIb),

peak VO2 < 12-14

– Episode of diuretic resistance or malignancy arrhythmia in last 12 months

– Hypotension is not hypoperfusion

– Term : new-onset HF, chronic HF (at least 1 month), Decompensated HF
– HF is clinical diagnosis
– BNP/NT-proBNP is screening

– Echo is conformation test

– Cardiogenic shock : PCWP > 15 plus CI =< 2.0-2.2 with support/CI =< 1.8 without
support
– Cardiac power (CPO) < 1 W (CPO = MAP x CO/451)

– Pulmonary Artery Pulsatility Index (PAPi) < 1 : PAPi = (Systolic PAP-diastolic

PAP)/RA
– Normal CO 4-8 LPM
– 5 years survival 50% in HFpEF/HFrEF
– 20% Lifetime risk at age 40 years for HF
– Not recommend in FC IV : ACEI/ARB, ARNI, ICD, Ivabradine

Classification & Stage

– Stage A (Risk) : DM, HT, obesity, CAD
– Stage B (Asymptomatic, FC I) : Prior MI, LV dysfunction, valvular heart
General
– Diagnosis chronic HF : BNP > 35 pg/ml, NT-proBNP > 125 pg/ml (For diagnosis and
prognosis)
– Diagnosis acute HF :
– NT-proBNP

– Age <50 : >= 450

– Age 50 to 75 : >= 900

– Age >75 : >= 1800

– Exclude BNP <100 pg/mL or NT-proBNP <300 pg/mL.

 – False low natriuretic peptide : Flash pulmonary edema, HF at the level of LA, morbid
obesity, treat with ARNI (low NT-proBNP)
– Morbid obesity : 4% reduction in BNP/NT-proBNP cutoff for every increase of 1

kg/m2 in BMI > 20 kg/m2

– NYHA IIIb = severe exercise capacity = low 6MWTD (< 300 m)
– Role natriuretic peptide
– Diagnosis acute/chronic HF (I)

– Exclusion of HF (I)

– Prognosis & severity in chronic/acute decompensated HF (I)

– Natriuretic peptide predischarge (IIa)

– Screening patient at risk of developing HF (IIa) : screening in stage A HF, cut of

BNP >= 50 underwent echo & refer cardiologist

Poor prognosis
– Low BP

– Low BMI

– Low Peak VO2

– Increase uric

– Low cholesterol

Best correlated with prognosis : V(E)/VO2 slope during exercise

Physiology
– Hemodynamic change
– Neurohormonal system : via Adrenergic activation —> Cardiac remodeling

– Down regulation of B1 receptor

– Upregulation of beta2 receptor

– Uncoupling of B1&2 receptor

– Up regulation of B1-ARK

– Increase Gi protein

– Decrease Gs protein

Concept treatment
– Beta-block : reverse remodeling

– ACEI/ARB : slow remodeling

Sympatholytic drug : increase mortality

Clinical & Physical exam
– Trepopnea : dyspnea in lateral decubitus
– Bendopnea : dyspnea within 30 sec when bending forward
– JVP >= 12 and orthopea >= 2 pillows (associated with PCWP > 30 mmHg)
– PCWP > 18 : interstitial edema (Kerley B line)

– PCWP > 25 : alveolar edema

– Proportional pulse pressure = pulse pressure/systolic BP (< 25% associated with low
cardiac index)
– Chronic venous congestion : pigmented purpuric dermatosis
– Cheyne-Stroke respiration : sign of hypoperfusion
Identification cause of acute HF
Stem treatment
CHF : inotrope in CHF, most is level IIb due to trend increase mortality
– Wet & cold (PCWP > 15, Cardiac index < 2.0)

– SBP > 90 —> vasodilator (IIa) & diuretic

 – SBP < 90 —> inotrope (IIb) then diuretic
– Wet & warm
– Hypertension (fluid redistribution) : vasodilator > diuretic

– Congestion (fluid overload) : diuretic > vasodilator

– Wet & warm HF

– No ass. between cardiac output and renal function

– ass. with renal congestion

– Congestion ass. mortality more than AKI

– Dry & cold

– Hypovolumia : fluid challenge

– Poor pumping : inotropic

– Dry & warm : compensated is goal (PCWP < 15, Cardiac index > 2.2)
HFpEF
– Definition : Clinical HF + EF >= 50% + Elevate natriuretic peptides (BNP > 35 pg/ml,
NT-proBNP > 125 pg/ml) + one of two (LVH/LAE, diastolic dysfunction)
Approach HFpEF
– H2FpEF score for probability diagnosis HFpEF
– Screen CAD (IIa, C)
– Coronary revascularization in angina or evidence of ischemia (IIa)

– Main-treatment
– Control BP & comorbid

– ARB or MRA : decrease hospitalization (IIb, B)

HFiEF : Improved LVEF 40-50% and increase EF > 10%
– Good predictor : Female, Non-ischemic, short duration of HF, less cardiac

remodeling, LBBB in CRT responder

– Myocardial remission (สงบ) vs recovery

Summary guideline
– HFpEF : keep SBP < 130, ARB or MRA for decrease hospitalization (IIb,B)
INTERMACS (NYHA III-IV) : severity of CHF 7 level
– Level 1 : critical cardiogenic shock, die in hours

– Mx : Balloon pump, ECMO, short term LVAD

– Level 2 : progressive decline despite inotropic support

– Level 3 : inotropic dependence

– INTERMACS 2-3 : appropriate for long term LVADs or transplant

– Level 4-5 : resting symptoms

– Level 6-7 : NYHA III

– INTERMACS 4-7 : LVADs not improved survival

– : LVAD, improved QoL (increase 6MWT) but risk complication

Timing for management acute HF
– Echo with in 48 hr in unstable hemodynamic acute HF (I)

– Immediate stabilization & transfer intensive care unit within 60-120 mins

Initial betablock or ACEI

– Initial betablock : decrease sudden death but increase rate HF

– Initial ACEI : decrease HF but increase sudden death

– Should be combine low dose > high dose monotherapy

Drug & Dose

Diuretic
– Torsemide : good absorption compare with furosemide
Diuretic resistance : lasix > 160 mg with persistant HF
– Rx : HCTZ 50-100 mg or Tolvaptan if hyponatremia

Inotrope
– Low cardiac output : used inotrope —> not improve renal function but increase
mortality (ref : OPTIME-CHF trial, ROSE-AHF trial)
BetaBlock : In sinus, decrease mortality in HFrEF, In AF : same mortality but improved
LVEF
 – General concept
– Add beta-block after euvolumia, avoid in FC IV

– No clearance by H/D : carvedilol & propranolol

– Selective beta1 : Nebivolol > Bisoprolol > Metoprolol > Carvedilol

– Effect inverse agonism (up regulation B1 receptor) : Metoprolol > Nebivolol >

Bisoprolol = Carvedilol
– Tolerability : Carvedilol > Metoprolol > Bisoprolol

– Carvedilol : effect antioxidants, vasodilator effect

– Max dose 25 mg bid (up to 50 mg bid in BW > 85 kg)

– Nebivolol : effect vasodilator via NO, B3 agonist

– Neutral mortality in HF

– Target HR : sinus rate 50-60 bpm, AF rate 60-110

ACEI : most is clearance by H/D

ARB : no clearance by H/D
– used in FC II-III

– First ARBs of choice of HF: Valsartan, Candesartan, Losartan.

– First ARBs of choice for CV prevention: Telmisartan

– Losartan : dose 100 mg, start 50 mg OD, max 150 mg OD

– Neutral mortality in HF

– Valsartan (Diovan): dose 80, 160, 320 mg

– Start dose for HF: 40 mg bid, max 160 mg bid

– Start dose for HT: 80 mg OD, max 320 mg OD

– Candesartan (Blopress): dose 8, 16 mg, start 4 mg OD, max 32 mg OD.

– Salcubitril/Valsartan (ENTRESTO) : dose 24/26, 49/51, 97/103 mg

– Indication : replacement for an ACEI/ARB in stable patients with HFrEF who

remain symptomatic despite optimal treatment

– Decease CV death 20% compare with Enalapril (NNT 21) & HF hospitalizations

– Avoid : SBP < 90, GFR < 30, K > 5.2, Hx of angioedema

– Before switch to ENTRESTO, stop ACEI 36 hr but ARB not require stop

– If on previous ACEI/ARB, start 100 mg bid. No previous ACEI/ARB, start 50 mg

bid.
– Start 100 mg bid if Losartan >= 50 mg/day, Enalapril >= 10 mg/day, Valsartan >=

160 mg/day
– Titrate double dose q 2-4 weeks

– F/U NT-proBNP, not BNP due to false high

– Safety for used in acute stable decompensated HFrEF

MRA
– Indication : EF =< 35% with symptoms and optimal betablock & ACEI/ARB

– After STEMI : EF =< 40% & HF or DM with optimal betablock & ACEI/ARB (I)

– Spironolactone : max 50 mg/day

– Eplerenone : no gynecomastia side effect

– Caution used in GFR < 45 or K >= 4.5

Ivabradine (Coralan)
– Indication : HF NYHF II-III (EF =< 35%) with sinus rate > 70 after optimal betablock

or contraindication form beta-block

– Outcome : decrease hospitalization HF & CV death

– Dose 5 mg tab : start 2.5 mg bid (Max 7.5 mg bid), Keep HR 50-60

– Side effect : Phosphenes (enhance brightness), bradycardia

Other
– lifestyle modification : no reduced mortality
– Aerobic exercise : Improved FC & Reduced HF hospitalization

– Target BP < 130/80 in HFrEF/HFpEF

– Thromboembolism prophylaxis in acute HF (I,B)
– HFrEF NYHF II-III : IV Iron (Ferric carboxymaltose) to improved functional status &
QoL (AHA IIb, ESC IIa)
– Ferritin <100 ng/mL

– Ferritin 100 to 300 ng/mL plus transferrin saturation is <20%

– Keep Ferritin >= 300 & Transferrin sat >= 20% (IIa, B)
– Thiazolidinediones is contraindication in HF (Increase HF hospitalization)
– Influenza vaccine (I, B)
– NIV in O2sat < 90% with SBP > 85 & consciousness
– Look for associated disease : Sleep disorder (OSA)
– Adaptive servo-ventilator in Central sleep apnea in HFrEF (III) : increase all

death & CV death (CANPAP trial : CPAP)

– Possible explanation : central sleep apnea may be compensate mechanism

of HF (cheyne stroke respiration)

Key advice in HF
 – Drug
– Food
– Exercise
– Avoidance & pregnancy
– Vaccination
– Revascularization
– Device indication : ICD/CRT
– Advance care : LVAD/transplant
– Rehabilitation
– Psychosocial support & End of life care

Summary trial in HF
V-HeFT (1986)
– Population : HF

– Intervention : ISDN/Hydralazine vs Prazosin vs Placebo

– Prazosin : trend to increase mortality

– ISDN/Hydralazine : reduced mortality in black

A-HeFT
– Population : African-American

– Intervention : ISDN/Hydralazine vs placebo

– Result : decrease mortality

CONSENSUS :
– Population : HF, NYHA IV

– Intervention : Enalapril vs placebo

– Result : decrease mortality, NNT 6

SOLVD-T
– Population : HF, NYHA I-III

– Intervention : Enalapril vs placebo

– Result : decrease mortality

V-HeFT II
– Population : HF

– Intervention : ISDN/Hydralzine vs Enalapril

– Result : Enalapril decrease mortality

COPERNICUS
– Population : HF, NYHA III-IV, EF =< 35%

– Intervention : Carvedilol vs placebo

– Result : decrease mortality & HF hospitalization

ARB trial in HFrEF (compare with ACEI)

– ELITE : small study, losartan improve survival compare to captopril

– ELITE II : Losartan is not better than captopril

– VAL-HeFT : Valsartan plus ACEI is not better than ACEI alone

– CHARM-add : add on candesartan improved survival

 – Summary ACEI = ARB
RALES
– Population : HF EF =< 35%, NYHA III-IV

– Intervention : spironolactone vs placebo

– Result : Decrease mortality, NNT 9

EPHESUS
– Population : Post MI within 14 days, EF < 40%

– Intervention : Eplerenone vs placebo

– Result : Decrease mortality

EMPHASIS-HF
– Population : HF, EF < 30%, NYHA II

– Intervention : Eplerenone vs placebo

– Result : Decrease mortality

PARADIGM-HF
– Population : HFrEF

– Intervention : Enalapril 10 mg bid vs Valsartran/ARNI 200 mg bid

– Outcome : Reduced CV death 20%, Reduced first HF hospitalization 21%, reduced

sudden death 19%, reduced all death 16%

SHIFT
– Population : stable chronic HF, EF =< 35%, sinus rhythm rate >= 70

– Baseline : FC II-III, on Beta-block 90%

– Intervention : placebo vs Ivabradine

– Start dose 5 mg bid, titrate up to 7.5 mg bid, target HR 50-60

– RCT superiority trial

– Outcome : Decrease primary outcome (CV death & HF hospitalization) : drive by HF

death & HF hospitalization

 Inotrope
Vasopressor
Inotrope & high alert drug

General
– Inotrope in CHF, most is level IIb due to trend increase mortality
– Inotrope that increase intracellular calcium—> increase risk arrhythmia

– Beta agonist : loss efficacy in chronic betablock, acidosis, hypoxia

– Levophed vs dopamine in Cardiogenic shock : same mortality, less arrhythmia
– Dopamine & Adrenaline : Increase PVR (beware in RV failure)
– Inodilator : Positive inotropic & vasodilator effects
– Adrenergic drugs should not be mixed with sodium bicarbonate (Levophed ผสม
NaHCO2 ได้)
Dopamine (B1 > Alpha1 >> B2) : via catecholamine, adjust q 5-10 mins
– < 5 mcg/kg/min. = renal blood flow

– 5-10 mcg/kg/min. = inotropic effect if

BW 50 kg dose 2Z1 IV rate 7.5-15 ml/hr
If BW 70 kg dose 2Z1 IV rate 10-20 ml/hr
– > 10 mcg/kg/min. = vasopressor

Max dose 50 mcg/kg/min = 5Z1 IV rate 30 ml/hr

Dobutamine (B2 > B1 > A) : B2 vascular smooth muscle ทำให้ vasodilation

– Prefer in cariogenic shock more than dopamine

– Initial 2Z1 IV rate 3 ml/hr

– Max 40 mcg/kg/min, 5Z1 rate 30 ml/hr (BW 70 kg)

Adrenaline : most potent increase Cardiac output and arterial BP

– during CPR via tube 2-2.5 mg q 3 mins

– Dose 0.01-1 mcg/kg/min

– 1Z10 IV rate 5 ml/hr (max 30 ml/hr)

Levophed (vasopressor) with 5%DW (must adequate volume status)

– Effect : headache, AF, tachycardia, hypokalemia

– 4Z250 (16Z1) IV rate 5 ml/hr, 60Z1 IV rate 1 ml/hr (max 100 ml/hr)

– Dose 0.02-2 mcg/kg/min

 – Prefer norepinephrine over dopamine for vasopressor effect in cariogenic shock to
maintain SBP

Milrinone (PDE3 inhibitor : increase cAMP —> release intracelluar Ca2+)

– 50 mcg/kg loading in 10 mins then 0.375-0.75 mcg/kg/min

– Dose 1Z5 IV load 15 ml in 10 mins then 1Z5 IV rate 7-15 ml/hr (BW 60 kg)

– Onset 10 mins duration 5 hr

– Decrease PCWP same as isoproterenol

– Better in chronic betablock therapy

– Require renal adjust dose

Levosimendan (calcium sensitizer), no increase mortality

– Increase contraction without increase O2 consumption, vasodilator, decrease

cardiac cell death by open K+ ATP channels

– Loading 6-24 mcg/kg over 10 mins and then 0.05-0.2 mcg/kg/min for 24 hr

– Dilution 1Z40, 12.5 mg per vial with 5%DW up to 500 ml

– Hemodynamic response within 5 min, Long effect 2 weeks

– Better in chronic betablock therapy

Practicalities of intermittent levosimendan

– Advance HF (LVEF < 35%) : NYHA III-IV, regular hospitalization, highly symptomatic
Digoxin (increase calcium influx from inhibit Na/K ATPase)
– Dose 0.0625 mg, 0.25 mg per tab

– Start 0.25 mg : 0.5 tab po OD, max 2 tab po OD (suggest max 0.125 mg/day for

increase vagal tone)

– Recommend :

– Chronic setting : AF with HFrEF (level IIa), sinus with HFrEF (level IIb)

– Acute setting : Control rate AF in HFrEF

– Digoxin normal level 0.5-0.9 ng/ml and level > 1.2 increase mortality, serum digoxin

level not correlate with toxicity (define intoxication, level > 2)

– Outcome : Reduced HF hospitalization, neutral/increase mortality

Digoxin intoxication
– Risk : CKD, HypoK/Mg, HyperCa, Hypothyroid, BW < 60 kg
– Digoxin effect : Decrease Tw amplitude, Shortening of QT interval, Prominent U

waves
– Intoxication : SVT with block, bidirectional VT

– Increase automaticity : increase intracellular calcium

– Decrease AV conduction : increase vagal effect

– Lesslikely digoxin intoxication : Atrial flutter, Mobitz II (infranodal block)

– Effect : downsloping STD, flat/invert/biphasic T, short QT

Management
Digoxin induced unstable bradycardia
– Atropine IV

– Temporary transvenous pacemaker

– Antidote : Digibind

– Avoid adrenaline and related beta-agonist

Digoxin induced unstable tachycardia

– First-line : Digibind (Digoxin-specific antibody Fab fragments)

– Esp. Digoxin intoxication with hyperkalemia

– Second line : IV xylocaine (Suppress EADs/DADs) or IV dilantin (same dose as

status epilepticcus) plus magnesium sulfate

– Xylocaine : no effect on AV node (benefit more than amiodarone in digoxin

intoxication)
– Avoid inotropic drug & cardioversion

– Amiodarone increase digoxin level

Isoproterenol
– 20-60 mcq IV bolus followed 10-20 mcq or infusion 1-20 mcq/min based on HR

response
Cardiomyopathy
Cardiomyopathy

Reversible cardiomyopathy
A-Alcohol, Amphetamine, Amyloid
B-Beri beri, broken heart syndrome
C-CAD, Cocaine, CNT, Childbirth (peripartum)
D-Doxorubicin and other CMT
E-Endocrine and metabolic, Eosinophilic myocarditis
F-Fast heart rate
G-Glycogen/Lysosomal storage disease
H-HIV, Hypertension, Hemochromatosis
I-infection, inflammation
– History : R/O drug, alcohol/B1, Autoimmune

– Lab : Anti-HIV, TFT, CBC for Eo, SI/TIBC & ferritin (hemochromatosis)

Primary cardiomyopathy

Pathology
General
– Very good prognosis of DCM : peripartum cardiomyopathy
– Very poor prognosis of DCM from HIV

Morphologic characteristics
– HCM
– Dilated cardiomyopathy (DCM)
– ICM
– RCM
– Endomyocardial fibrosis
– ARVD
– Non compaction

ICM
: EF < 40% with one of following
– LM >= 50%

– LAD >= 70%

– Significant two other epicardial vessel

Tachycardia induced cardiomyopathy

– HR > 120 BPM consistent with arrhythmia-induced cardiomyopathy
 – Duration unclear, week to month
– Diagnosis by R/O and recovery after treatment 3-6 months

LV non compaction
– General
– Male > Female, Bimodal age : 5-7 years, 40-50 years

– 2/3 developed HF

– Ass. Neuromuscular disease & congenital heart

– Non genetic LV non compaction that potentially recovery : Athletes, sickle cell
anemia, pregnancy, hematologic disease, chronic renal failure, polycystic kidney
disease
– Diagnosis criteria (non-compact/compact part), Mostly LV dysfunction
– Echo : 2/1 (short axis view in end systole or end diastole)

– CMT : 2.3/1 (long axis view in end diastole), at least 4 segment or trabeculated

mass > 20% of global LV mass

– Presentation : LV dysfunction, embolic phenomenon, Ventricular arrhythmia/sudden
death
– Echo : prominent trabeculation and deep recess of LV (usually apical & lateral LV),
Intertrabecular space filled by direct blood flow (color Doppler flow at intertrabecular
space)
– Primary prevention ICD : EF < 35%, Family Hx of SCD, unexplained syncope, non
sustained VT.
– Barthʼs syndrome (Tafazzin gene mutation in X chromosome) : male, neutropenia,
skeletalmyopathy
– OAC in AF with LVNC (regardless of risk score)

DCM
– Definition : Reduced EF with LV dilatation exclude CAD & loading condition
– Mutation : HCN5A mutation (common in Thai), Truncating variant in TTN gene
(largest single genetic), LMNA (limb Girdle)
– Cardiolaminopathy
– Autosomal dominant familial DCM

– Mutation in the LMNA gene, encoding the nuclear envelope protein lamin A/C.

– Manifestations : conduction system disease, arrhythmias or ventricular

dysfunction.
– Barth syndrome (DCM with LV non compaction) : mutation in TAZ gene
– Clinical : skeletal myopathy, growth retardation, neutropenia, Increase urinary 3-

methylglutaconic acid
– Duchenne muscular dystrophy
– Tall R in V1

– Early cardiac involvement : basal-inferoposterior wall

– Dystrophin gene
Alcoholic cardiomyopathy
– Definition : > 80-90 gm of alcohol per days for > 5 years
– Recovery 1/3

Shoshin syndrome (Beri beri)

– Clue : High output heart failure, Lactic acidosis, Reversible with IV thiamine
– Early sign of improvement : good urine, ECG change from TWI to normal TW

CMT induced cardiomyopathy

– EF < 53% and drop > 10% or GLS > 15% change from baseline
– CMT induced cardiomyopathy : Anthracyclines, HER-2 therapy, VEGFi
– Type 1 : Doxorubicin, Epirubicin, Idarubicin, Mitocantrone

– Mechanism: cellular death, biopsy change, cumulative dose related,

permanent damage
– Dose related cardiotoxicity : Doxorubicin > 450 mg/m2, Idarubicin > 90 mg/

m2 (Induction in AML 60 mg/m2)

– Type 2 : Trastuzamab, lapatinib, pertuzamab, imatinib, sorefenib, sunitinib,

bevacizumab, bortezomib
– Mechanism: cellular dysfunction, No biopsy change, not cumulative dose-

related, reversible
– Drug for prevent Betablock or ACEI in High risk (Trastuzumab + Anthracycline)
– Novel drug : Dexrazoxane (IV iron chelator) in cumulative dose of doxorubicin >

300 mg/m2
Peripartum cardiomyopathy
 – Incidence 1/2000
– Definition : LVEF < 45% in last month before delivery or within 5 months after
delivery & no identifiable cause
– Risk : age > 30, multiple pregnancy, twin pregnancy, african
– 50% improved after 6-12 months
– predictor of poor recovery :at presentation EF < 30%, EDD > 60 mm, RV

involvement
– Biologically active in PPCM : 16kDA prolactin, soluble fms-like tyrosine kinase-1
(sFlt-1)
– Treatment : drug for HFrEF
– Specific treatment

– Uncomplicated case : bromocriptine 2.5 mg OD for 7 days.

– Complicated case (EF < 25% or cardiogenic shock) : bromocriptine 2.5

mg bid for 2 weeks then 2.5 mg OD for 6 weeks.

– Prophylaxis anticoagulant

– Bromocriptine treatment

– PPCM with LVEF =< 30-35%

– Inotrope of choice : levosimandan

– Advice against pregnancy

– EF < 25% at presentation

– Persistent reduced EF

– Expect Improved LV function in 6 months for ICD decision

– Prognosis in next pregnancy
– Persistent LV dysfunction: 50% recurrent & 25% mortality

– Full recovery LV (EF > 50%): 20% recurrent & 0% mortality

Cardiac sarcoidosis
– Disease of ventricle
– Clue : heart block, VT, HF, Involvement IVS (common basal septal thinning &
aneurysm) and LV free wall
– Diagnosis : cardiac tissue proven or other organ tissue proven plus criteria
– Imaging : FDG-PET scan

– Patho : non-caseating granuloma

 – Treatment : Prednisolone 0.5 MKD for 2-3 months and F/U response
– Indication for ICD
– Secondary prevention (I) : SCA survival, sustained VT (spontaneous or inducible)

– Primary prevention

– EF =< 35% regardless of NYHA

– High risk (IIa) : syncope, extensive scar by CMR/PET

– EP study (IIa)

– Candidate for pacemaker (IIa)

Radiation heart disease

– > 30 Gy of radiation, onset 15-20 years after expose
Clinical clue
– Endocardium : Thickening & calcified mitral-aortic intervalvular fibrosa (aorto-mitral

curtain), MAC
– Myocardium : Restrictive cardiomyopathy

– Pericardium : Constrictive pericarditis

– Vascular : Proximal coronary artery stenosis, microvascular disease, calcified aorta

– Electrical : Heart block

Takotsubo cardiomyopathy
Diagnosis
Diagnosis score
General
– excess catecholamine

– Reverse Takotsubo cardiomyopathy : pheochromocytoma, Subarachanoid

– Common in postmenopausal women

– Mimic STEMI/NSTEMI

– RV involvement ~ 10%

Mechanism
Investigation
– EKG : QRS and TW positive in AVR (origin from apex), QTc prolongation > 500 ms

– Echo : support basal hyperkinesia with apical and mid LV ballooning, esp. mid-

inferior ballooning (not exclude in wrap around LAD, multi-vessel disease) +/- LVOT
obstruction
– CMR : Increase extracellular volume without scar

Prognosis
– Good prognosis in takotsubo syndrome related to emotional stress

– 5-year mortality : class IIb > IIa > III > I

Treatment
– Avoid catecholamine inotrope : dopamine, dobutamine, adrenaline

– Acute treatment : Treat cause, IV fluid, Beta-block

– If shock - suggest : milrinone, levosimandan

– If non shock/HF : betablock > phyenylephrine (increase LV cavity size)

– Chronic treatment : prefer ACEI/ARB > beta-block

Chagas disease
– Caused by Trypanosoma cruzi (protozoan parasite)

– Endemic area : Central and South America.

– Manifestation :

– Gastrointestinal dysmotility.

– Cardiac involvement : conduction disease, apical aneurysm, VT.

Myocarditis
Myocarditis

General
– Presentation : Preceded by flu-like symptoms
– ACS-like

– Acute HF

– Chronic HF

– Life threatening arrhythmia/SCD

– Etiology : Infection, Autoimmune, Drug/toxic

– Cause of fulminant myocarditis : Giant cell myocarditis, Necrotizing esosiophilic
myocarditis, Peripartum cardiomyopathy, Immune check point inhibitor (PD-L1)

Diagnosis
– Definition: Inflammatory disease of myocardium diagnosed by established
histological Dallas criteria, immunological and immunohistochemical criteria (WHO/
ISFC1)
– ≥14 leucocytes/mm2 including up to 4 monocytes/mm2 with the presence of CD

3 positive T-lymphocytes ≥7 cells/mm2.

– Diagnosis criteria (One clinical plus one lab)
 – Diagnosis by CMR
– CMR: positive 2/3 (Myocardial edema, Hyperemia, Myocardial necrosis), sense

76% spec 96% accuracy 85%.

– Updated Lake Louise criteria

– Main criteria: myocardial edema, non-ischemic myocardial injury

– Supportive criteria: pericarditis, LV dysfunction

– Biopsy proven fulminant myocarditis >= 50 cells/m2

Classification
Treatment
– Role of immunosuppressive drug : Giant cell myocarditis , cardiac sarcoidosis,
myocarditis ass. extra-cardiac autoimmune disease, refractory infection-negative
lymphocytic myocarditis
– Role only steroid : infective-negative eosinophilic or toxic myocarditis with HF/

Arrhythmia
– Immunosuppressive drug
– Cyclosporin + steroid +/- AZA (Giant cell myocarditis)

– AZA + steroid

– Steroid alone

Role ICD
– Only giant cell myocarditis with VF or unstable VT (IIb)

Other
– Restricted physical activity at least 6 months in Myocarditis

Role of endomyocardial biopsy

– Before endomyocardial biopsy must exclude other cause : CAD, Endocrine (TFT)
Cardiac amyloid
Cardiac amyloid

Type of amyloid
– AA : Autoimmune/Chronic infection/Inflammation
– AL (Ig light chain from plasma cell)
– Clinical : Macroglossia or periorbital purpura

– ATTR (amyloid tetrameric transthyretin protein from liver)

– Clinical : bilateral CTS, lumbar stenosis, biceps tendon rupture, low-flow low

gradient AS
– EKG : may be normal QRS voltage

– Wild type : senile systemic amyloidosis

– Mutant : familial amyloid cardiomyopathy, autosomal dominant

General
– Pathogenesis : misfolding peptide
– Two type from plasma cell & liver

– Low voltage EKG ~ 2/3 of AL

– Favor AL type (plasma cell) : amyloid purpura
– Favor TTR type (Liver) : Bilateral carpal tunnel syndrome, Lumbar spinal stenosis,
Biceps tendon rupture.
– Bleeding from factor Xa deficiency
– Clue cardiac amyloid : HFpEF with normal BP plus
– Unexplained weight loss

– Peripheral or autonomic neuropathy

– Nephrotic syndrome

– Unexplained hepatomegaly

– Intolerance of ACEi, BB

Diagnosis
Amyloid cardiomyopathy
– Require proved tissue biopsy from non-cardiac or cardiac tissue

Poor prognosis factor by echo

– LV thickness >= 15 mm

– RV thickness > 7 mm

– Mitral inflow deceleration time < 150 msec

– LV dysfunction, RV enlarge

– global longitudinal strain < 11.78

– Tei index > 0.77 (Sum of Isovolumic contraction time + Isovolumic relaxation time /

ejection time)

Investigation
– UA, LFT, CBC, Renal function, Calcium
 – Serum & urine immunofixation, serum free light chain assay
– Tissue patho (congo red stain) : apple green birefigrence
– Abdominal fat aspiration : low yield in wide type ATTR

– EKG : Pseudoinfarction (QS in V1-3), 1st AV block, AF/flutter

– Specific 91% if low voltage ECG with septal wall thickness > 19.8 mm

– (S in V1 + R in V5 or 6)/(myocardial mass) < 1.5, sense & spec 80%

– Echo : Biatrial enlargement, Increase LV/RV wall thickness (not used hyperthrophy),
Granular sparking appearance of myocardium (Non harmonic imaging), Thickness of
valve/interatrial septum (> 6 mm), pericardial effusion, diastolic dysfunction,
pericardial effusion, Decrease GLS and apical sparing pattern (Cherry on top)
– CMR : Diffuse subendocardial delay enhancement with zebra pattern at LV/RV, IAS &
RA/LA
– Tc99mPYP scan (Technetium Pyrophosphate) if strongly positive (grade 2 or 3) =
ATTR both wild/mutant type
– Adapt from bone scan : positive uptake at cardiac

– H/CL ration at 1 hr (heart/rib in contralateral lung ratio) > 1.5

Treatment
– Patisiran in (Hereditary=mutant) ATTR amyloid : RNA interference therapy

– Tafamidis for wild/mutant ATTR amyloid : stabilization of transthyretin tetramer

– Liver transplantation in ATTR amyloid

If require PPM due to AV block : add defibrillator (IIa)

 Hypertrophic
cardiomyopathy
HCM

General
– Other name : Teareʼs disease, Brockʼs disease
– Must R/O AS, hypertensive heart, athlete heart, cardiac amyloid
– Sarcomeric protein gene mutation (35% MYBPC3, 35% MYH7, 15% Troponin/TNNT2)
– AD with incomplete penetrace
– Patho : myocardium disarrangment > 10%, intramural coronary ischemia
– Found in Anderson-Fabry disease, Noonan syndrome, Friedreich ataxia

– mycardial crypt (ร่องใน myocardium), sign developed HCM

– Type reverse curve HCM (septal hypertrophy) : positive 80% myofilament gene
– AF in HCOM : anticoagulant in all case regardless of CHADsVAS
Presentation & physical exam
– Presentation : dyspnea, angina, syncope on exertion, palpitation (AF, VT), SCD
– Physical exam : prominent A in JVP, Bisferiens carotid pulse (Spike & dome), double
apical impulses, systolic thrill at 4 Lt ICS, mid to late SEM at LLSB with dynamic
maneuvers (ยืนดัง นั่งเบา handgrip เบา), MR radiated to PSB, delay A2 (paradoximal
split S2), S4
– Ddx AS : systolic thrill at 2nd Rt ICS, radiate to neck (not found in HCM)

Investigation
– ECG : LVH with strain, septal Qw in inferolateral lead
– Apical HCM (Yamaguchi cardiomyopathy) : LVH with giant TWI (> 10 mm) at

V4-6
– Echo : wall thickness >= 15 mm (>= 3 segments), ratio >= 1.3 in normotensive, 1.5 in
hypertensive
– SAM, MR posterior jet, RV thickness, mid systolic AV closure

– Pathogenesis of SAM : Elongation of leaflets, Abnormal papillary muscle &

insertion
– Burnt-out HCM : EF < 50%

– LV thickness > 13 mm less athlete heart, 13 wk deconditioning prefer athlete

heart.
– HCOM : define peak LVOT gradient > 30 mmHg
– LVOT obstruction : 1.Septal hyperthrophy 2.Elongation of MV & cord 3.Apical

insertion of papillary muscle

– Start Tx if peak LVOT gradient >= 50 mmHg —> betablock/verapamil/

disopyramide
– Betablock (non-vasodilator) : atenolol, metoprolol, propanolol

– If symptoms but Gr < 50 —> stress echo

– Role myocardium biopsy (IIb) : สงสัยโรคอื่น เช่น infiltrative, inflam, storage

– 48 hr holter monitoring in all HCM
– Pompeʼs disease : HCM with short PR
– Patho : Myocardial disarray, interstitial fibrosis, myocardial hypertrophy.

Echo
– Septal type HCM : concentric LVH with asymmetrical septal hypertrophy, small LV
cavity, SAM with posterior eccentric jet leading to mild/moderate MR, LVOT
obstruction with peak gradient ... mmHg, LA dilatation.
– Apical type HCM : concentric LVH with spade shape of LV, apical pseudo aneurysm
+/- thrombus, LV dilatation
– CW : Dragger shape +/- diastolic forward flow from high apical LV chamber pressure
in diastole
– PW : Lobster claw found in mid LV obstruction, apical HCM with aneurysm
– Reverse pulsus paradoxus
Treatment
Asymptomatic : no treatment
– Consider medical treatment in significant gradient (IIb)

If symptoms : first-line betablock (Decrease LVOT gradient, no decrease SCD)

- New drug proven reduced LVOT gradient : Mavacamten
Septal reduction therapy : no decrease mortality
 – Gr >= 50 and failure medication plus FC III-IV/excertional syncope
– Surgical myectomy > alcohol ablation

– Sx : Morrow procedure (ขุดร่องน้ำ), extended septal myectomy, Resection-

Plication-Release repair (Resection of septum + Mitral leaflet Plication +
Release of abnormal muscle attachment)
– Risk pacemaker Sx 4% (risk LBBB) vs Ablation 20% (risk RBBB)
– Anatomic require for alcohol septal ablation : Septum > 18 mm, No intrinsic MV
disease, relative normal coronary artery, proper septal perforation size &
location
– Procedure : alcohol injection to 1st septal branch

– Response immediate after myectomy, response 8-12 wk after alcohol ablation

– Dual chamber pacing : response 4 wks

– Indication (IIb) : contraindication for myectomy or ablation, ICD indication

– AF on HCM : all case require OAC include NOAC (I)

– Prefer rhythm control : amiodarone, If failure AF ablation.

Role AICD for primary prevention

– ESC HCM risk-SCD score : 5 years risk of SCD >= 4% (IIb), >= 6% (IIa)
 – ประกอบด้วย 7 อย่าง : age, max LV thickness, Lt LA size (M-mode), Max LVOT
gradient, Fm Hx of SCD, non-sustained VT, unexplained syncope.
– SCD survivor or Sustained VT (I)

– FH of SCD from HCM (IIa)

– LV wall >= 30 mm (IIa)

– Unexplained syncope within 6 months (IIa)

– Non sustained VT or Abnormal BP response (SBP drop > 20) with exercise plus high

risk feature (6L)

– Age < 30 (Late adolescent)

– Delayed hyperenhancement on CMR (LV scar > 15%)

– LVOT obstruction

– LV aneurysm

– Syncope > 5 year ago (Late syncope)

– +/- LV EF < 50%

EP study for evaluate before ICD is harm (III)

Advice exercise
– recommend IA sport (low dynamic & static component) : bowling, cricket คล้าย bat-
ball, hockey on ice sket, ยิงปืน, Yoga, golf
– Non recommend competitive sport : bicycle is harm
Family screening for HCM
Genetic counseling in all HCM patient (I)
– EKG in first degree relatives

– Screening echo since 12-21 years every 12-18 months

– If age > 18-21 years : screening echo q 5 years

– จำ age 12-21 years screening yearly, after 21 years q 5 years

– genetic testing in questionable case or for family screening (index case HCM with
gene+ve if first degree relative negative gene, no require screenings)

Syndromic HCM
– Noonan syndrome
– AD : chromosome 12/PTPN11 Gene mutation

– Clinical feature : male infertility, short sature, Webbed neck, learning difficulties

– Face : Prominent nasolabial folds, triagular-shaped head, High anterior

hairline, Transparent/wrinkled skin

– Cardiac involvement: PS, HCM
 – Leopard : Lentigines, Electrical conduction anomalies, Ocular hypertelorism (ตาห่าง),
Pulmonic stenosis, Abnormal of genitalia, Retarded growth, Deafness
– Common mutation :PTN11, RAF1, BRAF

– Friedreichʼs ataxia : Autosomal recessive, hammer toes, LV posterior thickness

– Mucopolysaccharidoses : Asymmetrical septal hypertrophy, Thickening of valves
– Costello syndrome : large mouth, thick lips, excessive skin dorsum, deep palmar
crease
Non-sarcomeric mutation
– Febry disease : X-link recessive, GLA mutation
– Deficiency of the enzyme alpha-galactosidase A.

– Manifestations : HT, mitral valve prolapse, restrictive cardiomyopathy, corneal

opacities (conjunctival vessel tortuosity).

– EKG : high voltage

– Angiokeratoma at genitalia, cornea verticilata, MRI brain : T1 hypersensitivity of

pulvinar nuclei
– Echo : bright inner and mid myocardium, strain show double peak sign of basal

lateral wall
– Treatment : recombinant human alpha-galactosidase A

– Danon : Lamp2 mutation, X-link dominant

– Key is large LVH > 3 cm, extreme LVH with WPW, Ventricular arrhythmia

refractory to ICD, intellectual disability

– Treatment : heart transplant

– AMP-Kinase (PRKAG2) : AD
– Key : progressive heart block, LVH with WPW
ARVD
ARVD

– Arrhythmogenic right ventricular cardiomyopathy

– Cause by desmosomal protein dysfunction (cell to cell adhesion)
– AD with incomplete penetrance
– heritable progressive replacement of RV by fibrofatty tissue (progressive from
epicardium to myocardium) —> wall thinning and aneurysm dilatation
– Male > Women (3C1)
– Onset young or middel-aged (20-40 years)
– Presentation : syncope, palpitation from VT (epicardium), HF, SCD
– Area involvement RV : triangle of dysplasia (inferior, apex, infundibulum)
– EKG : epsilon wave (up or downward) in V1-3 with TWI (พบ 30%)
– Terminal activation duration (TAD) in V1-3 without RBBB : Initial S to end S wave

> 55 ms
– If presence, investigation for ARVD

– Epsilon (postexcitation of myocyte) Ddx : Posterior wall MI, sickle cell disease

with RVH from PHT, RV infarct, Infiltrative disease, sarcoidosis

– Fontaine bipolar precordial leads

– Echo : Reduced RV function, Aneurysm/dyskinesia/akinesia of RV free wall, RV apex

dilatation, prominent RV trabeculation
 – MRI : predictor Ventricular arrhythmia
– Finding fatty infiltration (LV posterolateral), fibrosis

– Fatty or scar in MRI ไม่อยู่ใน criteria

– Regional RV เช่น accordion sign
– RV angiogram : stag of horn of RV

Criteria 6 categories : การ diagnosis ต้องใช้ต่าง categories กัน

Family screening
– Gene screening in first degree & Risk stratification

– Mutation in genes encoding desmosome protein

Management
– AICD as indication of arrhythmia (gene carrier or just diagnosis ARVD is low risk)

– Survival SCA (I)

– Sustained VT (I)

– RVEF or LVEF =< 35% (I)

– Syncope presumed due to ventricular arrhythmia (IIa)

– EP for risk stratification in asymptomatic (IIb)

– PVC or non sustained VT : 1.betablock. 2.amiodarone

– Avoid competitive sport for decrease progression of disease

Syndrome
Naxos disease (cardio-cutaneous syndrome)
– AR, found in Greek

– Presentation : Diffuse non-epidermolytic palmopanta keratoderma, wooly hair, ARVD

– Varient : Carvajal syndrome

EMF
EMF (Endomyocardial fibrosis)

4 stage
– Acute inflammation

– Rich thrombus deposition

– Endocardial thickening (valve involve)

– Fibrosis

Involvement
– 50% LV & RV involvement

– 40% LV involvement alone

– 10% RV involvement alone

General
– Presentation : HFpEF (restrictive cardiomyopathy)

– U/D : allergic disease, parasitic infection, hypereosinophilic syndrome

– Loeffler endocarditis is term of acute & intermediate phase

– EMF is term of final stage

Prognosis
– Poor, mortality 25% per years in late stage (SCD, arrhythmia, HF)

Diagnosis
Criteria 2 major or 1 major plus 2 minor
Echocardiographic
– LV apex obliteration with apical mural thrombus in absence of underlying RWMA

(Apex maintains inward systolic contractile motion)

– Packing (Apical fibrosis) of the right or Left ventricle apex

– Tethering the AV valve papillary muscles, may be adhesion of valve apparatus to LV

wall: leading to mitral and/or tricuspid regurgitation

– Giant atrial enlargement

– Restrictive filling pattern

– Basal hypercontraction (Merlon sign)

CMR
– LGE : V sign characterized by a 3-layer appearance of myocardium, thickened

fibrotic endocardium and overlying thrombus (ขาว-ดำ-ขาว : fibrous around

thrombus)

Treatment
– Early state : steroid

– Late state : surgical resection (endomyocardiectomy) +/- valve replacement

Pericarditis
Pericarditis

Term
– Acute < 4 weeks

– Incessant 4-12 weeks

– Chronic > 3 months —> consider percardiocentesis

– Incessant : persists for more than 4-6 wks

– Recurrent : relapse after free symptoms at least 4-6 wks

Myocardial involvement is not poor prognosis

Serious complication is tamponade

Grade pericardial effusion

Size in end diastole
– Trivial

– Small (<10 mm)

– Large (> 20 mm)

Diagnosis : 2/4 of criteria (2 clinical & 2 lab)

– Pericardial pain

– Pericardial rub at Lt upper parasternal border

– Found ~ 50% : Independent degree of pericardial effusion

– 3 part of rub : atrial contraction, ventricle contraction, ventricle relaxation

– STE or PR depression

– Pericardial effusion
Etiology
– Infection :

– Viral (parvovirus B19 : myopericarditis)

– Bacteria (most common TB, atypical bacterial)

– Bacterial pericarditis : low glucose (ratio < 0.3 compare with blood), High

neutrophil
– Fungus : rare

– Non-infection

– Autoimmune

– Drug : lupus like, anti-neoplasm

– Neoplasm

– Metabolic : uremia (response with 1-2 wks after dialysis), myoedema

– Trauma

– Peri-infarction pericarditis : self limited, treatment : High dose ASA,

contraindication for ibuprofen.

– Post cardiac injury syndrome : latent peroid weeks to month

– Treat as pericarditis

EKG
– EKG : ไม่มี TWI พร้อมกับ STE ต่างจาก MI
 – EKG : ไม่มี TWI พร้อมกับ STE ต่างจาก MI
Clue ECG in pericarditis
– Sinus tachycardia

– Generalized concave ST elevation (STE II > III)

– PR depression (more spec if > 0.8 mm) : most in inferior lead

– Knuckle sign

– ST segment/Tw height ratio in V6 >= 25% (ใช้แยกจาก early repolarization)

– Spodick's sign

Stage of ECG change in pericarditis

Echo
– RA inversion > 1/3 of cardiac cycle = High intrapericardial pressure

Treatment
– First line : ASA or ibuprofen : 1-2 weeks and then off/tape 50% q 1-2 weeks depend
on symptoms/CRP
– ASA 900 mg q 8 hr in post MI pericarditis or dressler syndrome

– Ibuprofen 600 mg q 8 hr

– Adjunct : colchicine 0.5 mg OD or BID (if BW > 70 —> bid) total 3 month

– If contraindication for ASA, NSAIDs, colchicine : start steroid 0.5 MKD

– Post MI pericarditis : steroid increase heart rupture (not recommend)

– Acute pericarditis : steroid increase risk of recurrence

Specific group
– TB pericarditis : no role NSAIDs

– Role steroid in Non-HIV TB pericarditis

– HIV TB pericarditis : steroid decrease symptom & constriction but increase risk

malignancy

Evaluation
– Response 1 week after treatment

– CRP guide treatment response and length (IIa)

Exercise restriction until resolve at least 3 months

Chronic pericarditis
– In endemic area of TB : clinical setting เข้าได้ สามารถ treatได้เลย ก่อนรอผล biopsy
proven อย่างไรก็ตามสงสัยใน exudative profile

Metastasis pericardial effusion

Recommendation : IIa
– Pericardiotomy in limit pericardiocentesis

– Intrapericardial sclerosing agent/cisplatin

– Radiation
Restrictive cardiomyopathy
Contrictive pericarditis
Cardiac tamponade
RCM & Constrictive pericarditis & Tamponade

Constrictive : deep X, deep Y

– Effect on 2/3 of cardiac cycle : present of deep Y

Restrictive : blunt X, deep Y

Tamponade : deep X, blunt Y
– Effect on all cardiac cycle : blunt Y, No RV diastolic drip-and-plateau

RV infarction
– Acute RV infarction (constrictive physiology) : deep X, deep Y

– Poor RV function (Tamponade physiology) : deep X, blunt Y

– Clinical : Presented with Rt side CHF (HFpEF)

– PE : kussmaul sign (lack of decline/increase in CVP) with Deep Y descend (Not

found deep Y descend in RV infarction)

– Cause of kaussmaulʼs sign : Not found in cardiac tamponade

– RV infarction

– Severe RV failure

– RCM

– Constrictive pericarditis

– Tricuspid stenosis

Physiology of respiratory
Inspiration
– Decrease intrathoracic pressure

– Increase RV filling

– Same RV pressure

– Decrease LV filling

Hemodynamic for CP/RCM

– Diastolic equalization in tamponade & CP, absent in RCM

– Systolic area index : SAI > 1.1 (RV area by LV area in expiration/inspiration)
Constrictive pericarditis : curable diastolic heart failure
– Physiology
– Dissociation of intrathoracic & intracardiac pressure (variation in PCWP to

LVEDP >= 5 mmHg from inspiration to expiration)

– Exaggerated ventricular interdependence

– Physical exam
– Pulsus paradoxus is uncommon

– Pericardial knock ~ 50%

– Clue : Marked right side HF with low BNP/NT-pro-BNP

– Acute : Mx anti-inflammation
 – chronic > 3 months : Mx pericardectomy
– good longitudinal function, Deep X descend

– Imaging support : pericardial thickness > 4 mm, calcified pericardium (chronic

process), normal pericardial thickness =< 2 mm.

Effusive-constrictive pericarditis
– RAP ลดลงน้อยกว่า 50% หรือน้อยกว่า 10 mmHg หลัง pericardiocentesis
Etiology : Idiopathic, TB, radiation, metastasis cancer, Sarcoidosis, amyloid,
hemochromatosis, post-surgery, uremia, drug (procainamide, hydralazine)
Echo
– Septal bounce/shudder (ventricular interdependence), non-specific and can found in

abnormal electrical conduction

– Thickening & bright pericardium

– Medial eʼ > 8 (good longitudinal function)

– Annulus reversus : lat eʼ < med eʼ

– Medial mitral eʼ >= 9 cm/s

– Annulus paradoxus : Low E/eʼ but high PCWP

– IVC plethora & Hepatic vein expiratory diastolic reversal

– Diastolic reversal / diastolic forward flow > 0.79

– In COPD echo mimic constrictive pericarditis

– Increase forward flow velocity of SVC with inspiration > 20 cm/sec in COPD but

in CP not change SVC flow with inspiration

– Increase respiratory variation (can found in tamponade)

– TV inflow after inspiration > 40%
– Delta/Inspiration x100 (ใช้ค่าต่ำเป็นตัวหาร)
– MV inflow (E) after inspiration > 25%
– Delta/Expiration x100 (ใช้ค่าต่ำเป็นตัวหาร)
Management
– Prefer radical pericardiectomy > anterior pericardiectomy
– Symptomatic improvement 80%

– Complication : surgical mortality 10%, post-op low output 20%

RCM : severe diastolic dysfunction
RCM is hemodynamic classification, seek etiology
– Poor longitudinal function, Absence X descend

– Abnormal diastolic function

– No LV dilatation

– Severe biatrial enlarge, wall thickness/normal

– Inability for increase CO with excercise

Etiology
– Primary : idiopathic

– Secondary : Endomyocardium or myocardium

– Infiltrative disease : amyloid, hemochromatosis, sarcoidosis, chloroquine,

oxalosis (calcium oxalate), fredreich ataxia

– Non infiltrative disease : EMF, scleroderma, radiation(valve calcification)

– Storage disease : glycogen storage, Febry, Danon

Echo
– Absence of respiratory variation

– Diastolic hepatic flow reversal with inspiration

Hemodynamic
– Drip & plateau found constrictive pericarditis, restrictive cardiomyopathy, massive

PE, acute RV infarct (not found in tamponade)

Cardiac amyloid : longitudinal strain show cherry ontop (spare apex)
Effusive-constrictive pericarditis
– RAP ลดลงน้อยกว่า 50% หรือน้อยกว่า 10 mmHg หลัง pericardiocentesis

Cardiac tamponade
– Physiology
– Diastolic equalization

– Enhance normal physiology : Exaggerate ventricular interdependence,

Prominent pulsus paradoxus

– Physical exam : no kussmal sign, ewartʼs sign (physical sign of LLL atelectasis from

large pericardial effusion)

– Cardiac tamponade without pulsus paradosus : High RV or LV pressure (e.g. ASD,

AR, chronic LV dysfunction)

– Cardiac tamponade without RV collapsed : High RV pressure (e.g. PHT)

Echo
– Large amount of circumferential pericardial effusion, maximum size ... cm at

posterior part. Swing motion of heart.

– IVC plethora with diastolic hepatic reversal flow during expiration

– M-mode compare MV or AV opening (guide diastolic phase)

– Diastolic RV collapse

– RA inversion > 1/3 of cardiac cycle

– Sign of exaggerated ventricular interdependence : MV/TV inflow variation

 – Respiratory variation of MV/TV inflow (MV > 25%, TV > 40%)
– Reduced eʼ in TDI
CT
– Enlarge SVC (diameter >= thoracic aorta)
– Enlarge IVC (diameter >= twice of abdominal aorta)
– Periportal lymphedema
– Reflux contrast within IVC/Azygos vein
– Enlarge hepatic and renal vein
Cardiac mass
Cardiac mass

Differential cardiac tumor

– Secondary cardiac tumor (30x)

– Primary cardiac tumor

– 75% benign : 50% of benign tumor are myxoma

– Primary malignant cardiac tumor : sarcoma

Description : location, size/attachment, shape, mobility, surface, number

Location
LA myxoma
– Sporadic myxoma : more in middle age women

– Echo : large heterogenous mobile mass with stalk attached to interatrial septum,

obstructing mitral orifice with mean gradient ?, normal MV leaflet

– Carney syndrome (AD): LAMB (Lentigine, Atrial myxoma, Mucocutaneous myxomas,

Blue nervi)
– Mutations in the PRKAR1A gene in chromosome 17

– Ass. Acromegaly, cushing

– Treatment : surgical removal due to risk stroke and obstruction

Papillary fibroelastoma
– Typical valvular : AV > MV > TV > PV

– Echo : multiple papillary frond like appearance at downstream side of valve เหนือ
valve (common is AV valve) ; small, pedunculate by small stalk & high mobile, No
valve destruction
– Management
 – Rt heart location
– Excise only if large

– Consider excision : PFO with Rt to Lt, hemodynamic significant obstruction

– Lt heart location
– Observe in small, non mobile (no stalk)

– Excision : large, >= 1 cm, mobile

Thrombus morphology
– Mural thrombus : 1 surface exposed to blood pool

– Protruding thrombus : > 1 surface exposed to blood pool

– Mobile thrombus : Independent motion

Lamblʼs excrescences
– small non branching at site of valve closure

– No cause of stroke

Lipomatous hypertrophy
– Echo : well demarcated, homogeneous, IAS thickening spare fossa ovals (dumbbell

appearance)

Rhabdomyoma
– Ass. Tuberous sclerosis

– Spontaneous regression in infancy

– Location : Ventricle

Cardiac fibroma
– Large benign tumor 3-10 cm involve ventricle (Free wall, IVS)

– common site at posterolateral myocardial wall

– Presented with PVC/VT/VF/SCD

– Echo : well circumscribed, highly echogenic, solitary tumors, central calcification

– Associated with Gorlin syndrome (multiple nevoid basal cell CA, Odontogenic

keratocysts, bifid rib)

Myocardial lipoma
– Typical asymptomatic

– Symptomatic patient : arrhythmia, valvular dysfunction, ischemia (coronary

compression)
– Echo : broad base immobile, well circumscribed, homogenous pattern without

calcification

Tumor invade IVC

– Renal cell carcinoma
 – HCC
– Pheochromocytoma
– Leiomyosarcoma
– Adrenal carcinoma
– Renal angiomyolipoma

MRI character cardiac mass

– Signal compare with myocardium
Athlete heart
Athlete heart

General
– Competitive athlete: regular competition and systemic training
– Recreational athlete: aim to become stronger

Screening
– History and Physical exam
– Symptom: Angina, DOE, syncope/pre-syncope

– PE: HT, murmur, all extremities pulse, R/O marfan syndrome

– Family Hx: SCD, premature heart disease < 50 years

– EKG

– ESC & Sport committee: endorsed EKG

– AHA: not endorsed for universal EKG screening

– Large false positive rate & cost

My opinion
– Competitive athlete: Hx & family Hx plus PE +/- EKG

– Recreational athlete: Hx & family Hx plus PE + EKG

EKG
– sinus bradycardia > 30 bpm
– 1st AV block or 2nd AV mobitz I
– Incomplete RBBB
– Early repolarization V1-V4
– Isolated LVH by voltage criteria (must : no strain/LAE)
– Ectopic beat < 2000 per day

Echo
– Aerobic training : eccentric hypertrophy with normal diastolic function
– Resistance training : concentric hypertrophy but no RV remodeling
– Low-normal range LVEF but normal-high diastolic function (E >> A)
– LVH regression after stop exercise 3 months
Role EST
– Vigorous/competitive spirt in Male > 40 or Women > 55 plus two risk factor/one
markedly abnormal

Drug
– Diuretic are prohibited in competitive athlete due to mask doping substances

Post MI in athlete
Stop competitive sport 3 months
– Post PCI : limit exercise 2 wks

– Post CABG : limit exercise 4 wks

Bradycardia
Bradycardia

SA nodal exit block

– 1st degree SA block : Canʼt detect from EKG (Delay depolarized atrium)

– 2nd type I : shortening P-P interval

– 2nd type II : Fix P-P interval and pause 2 times of P-P interval

– 3rd SA block : No depolarized atrium (sinus arrest)

Sick sinus syndrome

– Define : Sinus node dysfunction with symptoms, progressive fibrosis of sinus node

tissue
– Persistance atrial standstill : junctional bradycardia (risk thromboembolism)

– Chronotropic incompetence : HR < 80% of age-predicted maximum HR

– Carotid sinus hypersensitivity : sinus pause > 3 sec due to sinus massage

– Reversible cause : OSA (nocturnal bradycardia), infiltrative disease

AV nodal block (Fix P-P interval)

– 1st degree AV block : PR interval > 200 ms (5 mm)

– 2nd Mobitz I

– Intranodal block clue : weckebach, narrow QRS, baseline PR prolong > 300 ms,

escape beat > 50 bpm

– Atypical weckebach : irregular PR prolong, still PR interval is shortest after

dropped beat
– AV node block (narrow QRS, Response to atropine/sympathetic)

– Progressive PR prolong and dropped beat

– PR interval is shortest after dropped beat

– Mostly reversible cause : Drug, ischemia

– 2nd Mobitz II (require pacemaker)

– Below AV block

– Infranodal block clue : short baseline PR (< 160 ms), Presence of BBB, excercise

induced AV block, escape beats < 28 bpm

– Sudden dropped beat

– 3rd AV block DDx vagal AV block

– Prefer vagal AV block if

– Sinus acceleration —> resumption of AV conduction

– Initiation of AVB with PR prolongation or wenckeback

– Prolong PP interval during asystole

– Clinical history suggest vagal tone

Site of AV block
– Effect of vagal tone

– Suppression of AV conduction

– Improved of His-Purkinje conduction

– Effect of exercise (sympathetic stimulation)

– Improved of AV conduction

– Suppression of His-Purkinje conduction

– AV nodal conduction : improved with exercise and atropine, worsening with vagal

maneuver
– Infranodal block : improved with vagal maneuvers
Trifascucular block
– Incomplete = Bifascicular block with PR prolong

– Complete = AV block

Paroxysmal AV block
– Adenosine sensitive AV block (syncope)
– Vagal mediated or vagally triggered AV block (nodal block) : atrial rate < 60 with
progressive PR prolong
– Intrinsic AV block
– Bradycardia-dependent AV block (infra-nodal block) :

– Other name : pause dependent block, phase 4 block, decelerate dependent

block
– Mechanism : slow heart rate —> less negative membrane potential (phase4)

—> hard depolarization in phase 0 เนื่องจากความต่างศักย์ต่ำ

Vagal mediated AV block
– AV block with sinus bradycardia

3rd AB block
– AV block without sinus bradycardia

Tachycardia dependent AV block : phase 2, 3 block

Mimic AV block
– Non conducted PAC
– Concealed junctional ectopy
– AV dissociation
– Echo beats
– Atrial tachyarrhythmias

Pause : > 2 sec

Sinus arrest >= 3 sec
– P wave before pause

– Same PP interval : 2nd AV block

– Non conducted PAC (May be Tw morphology change)

– premature A ต้องมาเร็วกว่าปกติ
– conducted PAC has PR prolong than normal sinus

– No P wave before pause

– Pause = 2xPP interval : 2nd SA exit block Mobitz II

– Pause < 2xPP interval : 2nd SA exit block Mobitz I

Cause of bradycardia
Reversible cause of bradycardia : T-DIE
 – T : Thyroid/HypoThermia
– D : Drug eg. Digoxin, beta-block, CCB

– I : Infarction eg. STEMI

– E : Electrolyte (Hyperkalemia)

The most common inherited conduction disease : SCN5A gene

Physical exam in heart block
– Bradycardia

– Bounding pulse

– JVP : Irregular cannon A wave

Investigation
– Role Echo : LBBB (I), RBBB or fascicular block (IIa)

Specific Tx in bradycardia
– Drug induced bradycardia
– Beta-block : IV glucagon with IV Insulin (IIa)

– CCB : IV calcium plus IV insulin (IIa)

– No used atropine in heart transplant with autonomic reinnervation

– Sinus bradycardia from spinal cord injury or post heart transplant : aminophylline or
theophylline (IIa)
– Inferior wall STEMI with AV block : aminophylline (IIb), dose 250 mg IV bolus
– SSS : oral theophylline (IIb)
– Role Isoproterenol for acute treatment in bradycardia (CPR guideline)
– After failure atropine
– Bradycardia induced TdP
– Acquired LQTS
– Avoid in congenital LQTS due to induced intracellular Calcium overload
– Alternative drug is dopamine, epinephrine
– Dose 2-10 mcq/min IV fusion
Tachyarrhythmia
approach
Tachyarrhythmia approach

Mechanism of arrhythmia
– Automaticity : AT
– Reentry : SVT

– Trigger activity

– EAD : R on T

– DAD : phase 4 after TW from intracelluar calcium overload such as digoxin intoxication,

MI
Aberrancy
– Acceleration dependent block : rate related BBB

– Phase 3 (ashman phenomenon) : long follow with short period

– Phase 4 : bradycardia and spontaneous depolarization of ventricular myocardium

(most is LBBB)

VT vs SVT
Limitation of VT criteria in Na block (flecanide, TCA)
Favor VT
– QRS > 160 ms in LBBB (4 ช่อง), QRS > 140 in RBBB
– North west axis / RBBB with Lt axis / LBBB with Rt axis

Brugada criteria for VT

– All positive/negative concordance

– R to S interval > 100 ms (2.5 small box) : Slow depolarization

– AV dissociation/capture beats/fusion beat.

– Morphology criteria (negative concordance V6 = VT, except RVH)

– LBBB

– Negative V1

–Initial R length > 30-40 ms (~1ช่อง)

– Notch/slurring S wave V5-6

– V6 : qR (Qw = VT) or negative concordance)

– S wave in V5-6 = Scar

– RBBB
– V1 (not rSR = VT)

– V6 : R/S < 1, mono R, mono S or qR, negative concordance

– (not qRs/Rs : V1 กลับหัว = VT)

aVR criteria for VT (Vereckei)
– Initial R (apical VT)

– Initial Q > 40 ms (กว้าง > 1 ช่อง)

– Notch descending QRS
– Vi/Vt : Hight in 40 ms (descending/ascending) ลงช้าขึ้นเร็ว
Lead II criteria
– Initial slow depolarization : Initial QRS to R >= 50 ms —> VT
Arrhythmia
VF : irregular rate, loss of QRS, rate 150 to up 500/min
– initial coarse and then turn fine VF

QTc : prolong > 440 in men (>460 in women), short QTc < 330
Typical atrial flutter : Cavotricuspid isthmus dependent
– Counter clockwise : Negative in inferior lead and Positive in V1

– Clockwise : Positive in inferior lead and negative in V1

Parasystole
– PVC ไม่รบกวน Normal QRS interval และ PVC interval เป็นจำนวนเท่าของมันเอง

Tachycardia
SVT with invisible P wave
– Typical AVNRT

– Junctional tachycardia

– AT with prolong AV block

Reverse wenckeback
– Shortening PR in sinus rhythm with accelerated junctional rhythm

– Cause : Dig intoxication, Beta-agonist, ischemia, myocarditis, post cardiac surgery

Irregular wide complex tachycardia

– AF with WPW (varies of QRS interval)

– AF with preexisting BBB

– Polymorphic VT

Specific approach
Irregular narrow complex tachycardia
– Atrial fibrillation

– Atrial flutter

– MAT

Irregular wide complex tachycardia

– AF with BBB/WFW : fix axis

– Polymorphic VT : alternating axis & amplitude

Regular wide complex tachycardia

– VT

– SVT with BBB (Preexisting BBB or aberrant or preexcitation)

– Paced rhythm

– Acute MI

– Hyperkalemia

– Na channel blocker toxicity

SVT with wide QRS

– SVT with BBB

– SVT with preexcitation

– SVT with abberency (rate dependent BBB)

– Acute MI, Hyperkalemia

AV dissociation
– VT (wide QRS, V > A)

– JET (narrow QRS, V >= A)

– AV block (A > V)

– sinus bradycardia with junction escape

– Isorhythmic AV dissociation (functional block A:V = 1d1)

– SVT with AV dissociation

– AV node reentry/junctional tachycardia with block to atrium

SVT with cycle length alternans

– Double loop reentry

– AVNRT with multiple intra-AV nodal pathway

– Orthodromic AVRT with dual SV nodal pathway

– AVRT with multiple extranodal accessory pathways

– Alternating conduction over dual AV nodal pathways

– Sinus tachycardia/Atrial tachycardia with dual-AV nodal pathways

– AV conduction block (3d2 conduction)

– Extrasystole : bigeminy atrial premature beats

Alternating wide complex & narrow complex tachycardia

– Ipsilateral bypass tract (wide complex slow rate than narrow complex)

– Aberrancy (same cycle length)

– SVT (most is AVNRT) plus VT

Approach reciprocal rhythm (P wave sandwich, QRS-P-QRS)

– True P wave sandwich
 – Reciprocal rhythm (echo beat)
– Negative Pw in inferior lead

– Origin : atrium, AV node/junction, Ventricle

– Pseudo-reciprocal rhythm (escape-capture bigeminy)

– Positive Pw in inferior lead

– Mimickers (mimick escape capture bigeminy)

– AV block

– Reversed reciprocal rhythm

– Block atrial extrasystole

Approach group of beats

f. Varying rate or rhythm of pacemaker cell
– Sinus arrhythmia

– Wandering atrial pacemaker

g. Ectopic impulse or extrasystole : PACs, PJCs, PVCs

h. Dual AV nodal physiology
– Echo beats

– Double fire

i. Block
– SA exist block

– AV block : Mobitz I/II

Intermittent transition from wide to narrow QRS complex

– Change in heart rate

– Peel-back refractoriness

– Rate dependent progressive shortening of bundle branch refractoriness

– Gap phenomena (phase 4 block phenomenon)
– Supernormal conduction (Supernormality)
– Loss of pre-excitation
– PVC ipsilateral to the BBB and equal conduction delay in the both bundle branches
 Ventricular
tachycardia
Ventricular tachycardia (VT)

VT/VF
– Monomorphic VT
– Scar-mediated VT : IHD, Prior MI, Cardiomyopathy

– Idiopathic VT

– Polymorphic VT
– Long QT

– No-long QT : ischemia
Localized VT
Ventricular rhythm
– Define origin below his-bundle
– Ventricular escape rhythm : rate < 50
– AIVR (accelerated idioventricular rhythm) : rate 60-110 at least 3 beats
– AIVR post MI : no increase mortality

– Gradual onset, benign rhythm, enhanced automaticity and increase vagal tone

– เริ่มและจบมักเป็น fusion beat

– Cause : reperfusion, digoxin intoxication, electrolyte abnormal

– Mx : treat U/D if low CO state that require AV synchrony : atropine for drive sinus

rate
– Ventricular Flutter criteria
– Regular, Very fast VT rate of 250-350 bpm seen as large continuous sine Wave

– No identifiable P waves; QRS complexes or T waves fused together

– VF (ventricular fibrillation): Rapid, grossly irregular electrical activity with marked

variability in ekg waveform, ventricular rate usually >300 bpm
– Post VT : Deep TWI in most negative QRS complex during VT (TW memory)

VT : rate > 110

Polymorphic VT (PVT) : multiple venticular foci
– QRS varying amplitude/axis/duration

– Subset : Torsades de Point, Bidirectional VT

– MI เกิด PVT จาก intracellular Ca overload เนื่องจาก cell ไม่สามารถใช้ ATP ขับ Na/K ATPase
ได้ส่งผลให้ Na ใน cell เพิ่มขึ้น ไปแลกกับ Na/Ca exchanger เกิด Intracellular calcium overload
Irregular VT
– frequent capture and fusion beats

– Initial VT
 – On antiarrthythmic drug class I or III
– Polymorphic VT
– Multifocal VT

Torsades de Point (TdP) : PVT in QT prolong

– Mechanism : EADs

– Clue : Pause dependence and then PVC (long-short) —> developed TdP, change of

QRS axis in the same lead

– cause via QT prolong : R on T sequence

– drug, congenital QT prolong, hypokalemia, hypoMg, hypocalcemia

 – Mx : Correct cause, Mg (reduced trigger activity) dose 2 gm IV bolus, Lidocaine,
Isoproterenol (beta agonist), Overdrive pacing
Short-coupled PVC induced TdP (PVC < 300 ms)
– Predominantly affects young patient with syncope and Fm Hx of SCD

– Treatment specific

– Acute treatment : IV verapamil

– Long term : ICD (I) +/- Catheter ablation (IIa)

Bradycardia induced TdP

– Acute management : IV magnesium & temporary pacing
Bidirectional VT : beat to beat alternan (axis shift 180 degree)
– Digoxin intoxication : SVT with block, bidirectional VT

– Increase automaticity : increase intracellular calcium

– Decrease AV conduction : increase vagal effect

– Digoxin Effect : downsloping STD, flat/invert/biphasic T, short QT

– CPVT (familial catecholaminergic PVT)

– Anderson-Tawil syndrome (LQTS 7)

– Arconite posioning

– MI/Myocarditis

Idiopathic VT
– Exclude structural heart by Hx & PE, EKG, Imaging +/- cardiac cath
– Origin 5 site
– Outflow tract VT

– Fascicular VT

– Annulus VT : tricuspid, mitral

– Papillary muscle VT : moderator band, Ant & Post. Papillary muscle

– Epicardium & coronary venous system (must epicardial ablation)

Outflow tract VT
 – Adenosine sensitive VT (RVOT VT)
– Stress or exercise induced VT

– Repetitive monomorphic VT at rest

– Mechanism : cAMP-mediated triggered activity in DAD (Intracellular calcium overload)

– EKG : R wave transition =< V4 lead, if >= V5 lead —> prefer ARVD

– Acute treatment : adenosine

– Prophylaxis treatment : beta-block, Non-DHP Ca2+block, Anti-arrhythmic drug Class IC

– Second line : Ablation if failure medication

– AICD is contraindication in idiopathic VT

Localization Outflow tract VT

– RVOT VT : LBBB with inferior axis, Transition QRS at V3-4 or V2 transition ratio < 0.6

– Anterior vs Posterior (lead I, aVL)

– Anterior sites : Q wave in lead I and aVL (Negative)

– Posterior sites : R wave in lead I (Positive), Early R wave transition (R>S in

V3)
– Intermediate sites : a multi-phasic QRS morphology in lead I

– Septal vs Free wall (inferior lead)

– Septum : Taller, narrower QRS in inferior leads

– Free wall : Broader QRS (>140 ms) and R wave notching in inferior leads,

Later transitional > V4 leads

– LVOT VT

– RBBB with inferior axis (30%)

– LBBB with inferior axis (70%), early transition QRS (V2-3) compare with normal

QRS
– V2 transition ratio > 0.6

– Aortic cusp VT

– EKG similar RVOT VT but not same

– R-wave duration index in V1-2 >= 50% (< 50% in RVOT)

– R/S wave transition in V1-2 >= 30% (< 30% in RVOT)

– Cusp อยู่ posterior และ ไปทางด้านขวามากกว่า RVOT ใน structurally normal heart

ดังนั้น duration และ amplitude ของ R ใน V1 หรือ V2 ควรจะยาวกว่าหากจุดกำเนิดมา
จาก cusp
– Calculation
– R-wave duration index ให้วัด R wave duration ใน V1 หรือ V2 โดยวัดจาก onset
QRS ไปถึงจุดตัด R wave กับ isoelectric line หา ratio เทียบกับ longest QRS
duration จากทั้ง 12 leads เอาค่า ratio ที่มากที่สุดจาก V1 หรือ V2
– R/S wave transition ให้วัด R/S amplitude เอาค่าที่มากที่สุดจาก V1 หรือ V2
Management
– First-line is medication : adenosine, beta-block, Verapamil/diltiazem

– Ablation after failure medication

– RVOT VT : failure medication or decline LV function (I)

– LVOT VT (high risk for ablation) : failure medication include Na blocker (IIa)
Fascicular VT
– Verapamil sensitive VT

– Mechanism : macro-reentry (LAF for antergrade & LPF for retrograde)

– Triad

– Induction with atrial pacing

– RBBB with Lt axis

– No structural heart disease

– Key is short RS interval 60-80 ms, QRS 100-140 ms

– Idiopathic VT (non structural heart)

– Idiopathic fascicular VT : most is RBBB pattern & Lt axis (Post. Fascicular VT)

– Classification

– Post fascicular VT (common) : RBBB + Lt axis + negative in inferior lead

– Ant fascicular VT : RBBB + Rt axis + positive in inferior lead

– Upper septal VT : Normal axis, RBBB

– Mechanism from macro reentry

– Management

– Verapamil is first line treatment, also response to beta-block

– Digoxin induced fascicular VT : Digoxin immune Fab

– Catheter ablation : severe symptoms with fail medication , success rate >= 90%

(expert opinion prefer ablation more than lifelong medication)

Focal Purkinje VT (propanolol sensitive VT)

– Subset in fascicular VT

– Mechanism : enhanced automaticity

– Presentation : exercise or cathecolamine related non-sustained VT

– EKG : relatively narrow QRS

– LBBB in RV distal Purkinje origin

– RBBB in LV distal Purkinje origin

– Treatment : betablock/lidocaine/adenosine, ablation if failure med

Papillary muscle VT
– EKG : RBBB (> 150 ms) with superior axis

– Medication : suggest Anti-arrhythmic drug class I,C

– Ablation is high risk for complication : acute MR

Annulus VT
– Mitral annulus VT : RBBB with persistent in V6 & early R/S transition

– Tricuspid annulus VT : LBBB & Lt axis

Specific approach VT
– LBBB VT with inferior axis
 – From RV to Lt origin : RV scar >> Aortic cusp >> RVOT >> LVOT
– LBBB with late transition (R/S transition in V3-4) & Inferior axis
– Scar-related VT : ARVD, old RV infarction

– Aortic cusp (left or right) VT

VT management
– Monomorphic VT in structural heart
– Acute treatment :

– Cardioversion (I)

– Medication : First line - IV procainamide (IIa), Amiodarone (IIb)

– Ablation for medication failure

– no mortality benefit for ablation VT in ICM

– Polymorphic VT
– Ischemia induced polymorphic VT : First - IV betablock , Second - Lidocaine
PVC
PVC

General
– PVC definition : QRS > 120 ms & TW opposite to QRS
– PVC Ddx PAC with aberrancy, intermittent WPW (short PR follow with QRS)
– Beat after PVC : hypercontraction
– Unifocal or multifocal PVC
– Multiform PVC from single foci, key is same coupling interval, common in digoxin
intoxication.
– PVC : not predict sudden cardiac death in HFrEF

Pathophysiology
– Extrasystole : related with previous QRS complex (fixed coupling interval)
– Reentry (most common)

– Triggered activity

– Supranormal conduction

– Parasystole : จ่ายไฟออกมาไม่เกี่ยวข้องกัน

PVC vs Aberrancy

Term
– VT = PVC x3, sustained VT = 30 sec
– Bigeminy PVC : Sinus = 1V1
– Trigeminy PVC : Sinus = 1V2
– Interpolated PVC แทรกระหว่าง normal sinus โดยไม่ interfere interval sinus และ PR
interval prolong หลัง PVC
Grade PVCs (high grade = high risk VT/VF)
– Grade 1 : occasional PVCs (< 30 beats/hr or 720 beats/day)
– Grade 2 : frequent PVCs (> 30 beats/hr)
– Grade 3 : multiform PVCs
– Grade 4 : repetitive (couplets, salvos : 3-4 PVCs)
– Grade 4A : 2 consecutive beats (couplets)

– Grade 4B : >= 3 comsecutive beats (salvos)

– Grade 5 : R on T PVCs

Causes
– Hypokalemia
– HypoMg
– Digoxin intoxication
– MI : PVC post MI 24-48 hr, suggest observe
– Beta-agonist
– Sympathomimetic/Anxiety

Indication for treatment (long term)

– Must R/O structural heart and treat it
– PCV > 10000 beat or 10-15% in 24 hr (~ LV dysfunction) plus one of following
– High PVC burden : Symptoms

– LV dysfunction

Treatment (long term)

– Treat cause or U/D heart disease
– First line is medication
– First line is BetaBlock

– Other : Verapamil, Diltiazem, amiodarone

– if failure medication —> ablation

SVT
SVT

General
– Polyuria after SVT from ANP
– Loss atrial contraction (15-20% of CO)
– Termination of SVT : Terminate with A —> Exclude AT

AVNRT
– Rate < 250

– Female, Age > 30

AVRT
– Via accessory pathoway

– QRS alternans prefer AVRT > AVNRT

Atrial flutter (A > V)

– Typical flutter (CTA dependence : counter clockwise)
– Positive V1, Negative in II & III (flutter wave in inferior lead)

Atrial tachycardia (A > V)

– Mechanism : focal (เห็น P wave ชัด), macroreentry (ไม่ค่อยเห็น P wave)
– Origin (P wave)
– Crista terminalis (CT) = (-) in V1, (-) in aVR, (+) in I & aVL

– High CT : (+) in inferior lead

– Low CT : (-) in inferior lead

– Tricuspid annulus (TA) & RV free wall

– (-) in V1, (+) in aVR, (-) in inferior lead & Chest lead

– Septal AT Ddx AVNRT/AVRT

 – (+/-) in V1, (-) in inferior lead, (+) in aVR
– Mitral annulus : (+) in V1, (+) in inferior lead, (-) in I & aVL
– Pulmonic vein AT : (+) in V1, increase duration & amplitude (ตัวอ้วนใหญ่)
Localized AT
Inappropriate sinus tachycardia
– resting HR > 100, Average HR > 90 (exclude appropriated response)

Treatment
– First-line: Ivabradine

– Second-line: Beta-block (Metoprolol succinate)

Junctional tachycardia
– Paroxysmal JET : Automaticity มักพบในเด็ก
– Non-paroxysmal JET : Trigger มักพบในผู้ใหญ่ เช่น High sympathetic tone, Post MI,
Digoxin intoxication

Management
– Unstable tachycardia (HR typical >= 150 bpm)
SVT with preexcitation
– Acute treatment :

– First : adenosine, if AF with WFW —> cardioversion

– Second : cardioversion

– Ongoing treatment

– Flecainide or propafenone (IIa)

– Amiodarone (IIb)

– Definited treatment : Ablation

Ablation success rate & complication

 – AVNRT & Typical flutter : 97%
– AVRT 93%
– Overall serious complication ~ 1%

Drug & dose for SVT

Adenosine
– Adenosine :
– Decrease dose : 3 mg IV in via central line (half dose), heart transplant, using
 carbamazepine/dipyridamole
– Increase dose : taking theophylline, significant valvular regurgitation, significant

left to right shunt.

– Regadenosone : specific A1

Effect
- Negative chronotropic effect in SA node
- Negative dromotropic effect in AV node (slow conduction)
- Terminated cAMO mediated trigger activity : Adenosine sensitive AT, RVOT VT
- Shortens atrial action potential : promote artial arrhythmia (AF) via phase III
(increase opening of IK (Ado))
- Antiadrenergic effect : tachycardia
- Sympathetic stumulation : promote PVC
Adenosine receptor
– A1 in SA/AV node : negative chronotropic drug, chest tightness
– A2a : coronary vasodilatation
– A2b : bronchospasm
– A3 : unknown function
Atrial fibrillation
AF : Atrial fibrillation

Mechanism & Clinical forms

– Risk AF : DM, HF, obesity, CAD, HT, Aging, genetic prediposition

– Risk for clinical AF : Old age, Greater BMI, subclinical AF > 1 hr
– Risk stroke : Permanent > persistent > paroxysmal AF > resolved AF
– Atrial flutter : macro-reentry > 2 sq.cm
– Atrial flutter >= 3Q1 suggestive underlying conduction AV disease
– Valvular AF : Prosthesis valve, at least moderate MS, post MV repair

Score predictor
General
– Diagnosis AF duration 30 s at least

– Course AF (Amplitude > 0.5 mm)

– Course AF : Amplitude > 1.0 mm in V1 associated LA hypertrophy or strain

 – Valvular AF : moderate to severe MS, mechanical valve
– BMI > 27 associated with AF
– AF of vagal origin : onset during slow sinus rate during night, early dawn, after eating
– AF of sympathetic origin : onset during acceleration of basic sinus rhythm (physical
exercise, stress)
– CHADS2 score : score 0 risk stroke ~ 2%, Used CHA₂DS₂-VASc score
– Resolved AF rate stroke/mortality still more than non-AF
– AF die from comorbidity, not stroke (Most common cause death is HF)
– No role anti-platelet in AF
– Stroke prevention
– Anti-platelet prevent 20%,

– Anticoagulant prevent upto 60%

– On warfarin, follow-up INR monthly

Classification
– First episode or first-detected AF regardless of symptoms or duration

– Recurrent AF : More than 2 episodes of AF

– Paroxysmal AF : Self terminating episode ≤ 7 days

– Persistent AF : Not self-terminating, duration > 7 days

– Long-standing persistent AF ≥ 1 year

– Permanent (Accepted) AF – Duration > 1 year

AF screening
– Opportunistic screening (ใช้สังเกตุอาการและ EKG strip) in high risk population (age >
65 years)

Investigation
– Echo all case (I, level C) : valve, EF, LA size

– High atrial rate episode : duration > 6 mins and rate > 180 bpm —> w/u AF &

increase risk stroke

– Resting Target HR < 110

– 72 hr holter in ischemic stroke : detect AF 5%, ref AF ESC but AHA stroke suggest at

least 24 hr monitor

Detect atrial high rate episode (AHRE)

– AHRE is term for device detection

– Define AHRE : > 5-6 min & rate > 180 bpm

– Increase risk of stroke but benefit for OAC still controversy,

– consider OAC if AHRE > 24 hr and CHADsVAS >= 2 for men, >= 3 for women

– After detect AHRE —> Seek & Verify AF or not AF

– Apple watch only screening tool : No definite tool for diagnosis AF

Management AF
– Risk modifying factors
Reduced mortality in AF : warfarin, ablation
– CHA2DS2-VASc >= 2 in male or 3 in women : OAC (I)

– CHA2DS2-VASc >= 1 in male or 2 in women : OAC (IIb)

Betablock is not reduced mortality in AF with HFrEF

– Upstream therapy : non pharmacotherapy to prevent AF

– Weight reduction > 10%

– Control HF

Acute treatment
– Drug for control AF (betablock & NDP-CCB IV is rapid onset)

– LVEF < 40% or HF : small dose betablock, option for amiodarone. Add on digoxin

– LVEF > 40% : betablock, diltiazem or verapamil. Add digoxin

– AF during critical illness

– Avoid OAC during critical illness

– Prefer rate control : rate turn to sinus is same before D/C

– OAC before D/C dependence of CHA2Ds2VASc score

Long term treatment

– Rhythm control

– Anti-arrhythmic drug

– No structural heart

– Class IC : Flecainide 200-300 mg, propafenone 450-600 mg

– Class III : dronedarone (contraindication in permanent AF, HF),

sotalol, dofetilide, Amiodarone is the last choice

– Structural heart

– In CAD : dronedarone, sotalol, dofetilide

– In HF : amiodarone, dofetilide

– AF ablation(Catheter/surgical)

– Rate control

– Rate control in AF

– General < 110 bpm

– Symptomatic AF < 80 bpm

– AV nodal blocking drug : betablock, Non-DHP CCBs, Digoxin, Amiodarone

– AV node ablation
Management in atrial flutter
Acute management
– Rhythm control

– Class I : Synchronize cardioversion, Rapid atrial pacing, Oral dofetilide/IV

ibutilide
– Amiodarone is second line

– Rate control

– Class I : IV form of betablock/diltiazem/verapamil (LVEF >= 40%)

– Class IIa : amiodarone

Long term management

– Rhythm control

– 1st line : ablation (AFL ablation ไม่เท่ากับ AF ablation)

– 2nd line : amiodarone, dofetilide, sotalol

– 3rd line : Flecainide or propafenone

– Rate control
– Betablock, diltiazem, verapamil

Drug & dose for control AF

– Amiodarone (IV form concentration 2Q1 or 3Q1)
– Reverse used depenedence : good in bradycardia

– Only rate control in acute atrial flutter

– Rhythm control : Load 300 mg IV in 20 mins and then drip 1200 mg/day (Median

time to convert sinus 4-8 hr)

– Rate control : load 150 mg IV in 10 mins and then drip 600 mg/day

– Monitor : off when QT > 500 ms or QTc increase > 15%

 – Side effect : extracardiac side effect
– Dronnedarone :
– Contraindication in HF, Can used in CAD, LVH

– no extracardiac side effect

– CrCl > 30

– Flecainide (CrCl > 50) : Median time to convert sinus 2 hr

– Used dependence : good in tachycardia

– Contraindication in structural heart disease

– Adminitration with AV nodal blocking drug for prevent A.flutter 1Q1

– Monitor : off when QSR > 25% of baseline

– Propafenone
– Digoxin : 0.25-0.5 mg IV slow push
– Protocol : 0.5 mg IV and then 0.25 mg IV at 2nd & 4th hour

– Beware in CKD, avoid in combine with Dronedarone/Verapamil/quinidine

– Vernakalant : multiple iron channel blocker (Na & K), atrial selective
– Rapid onset : median time to convertion 10 mins

– Dose 3 mg/kg IV drip in 10 mins

– Contraindication : HF NYHA III-IV, Severe AS, Recent ACS < 30 days,

hypotension (SBP < 100), QT > 440

LA occluder
Concept reduced burden of thrombus
– LA occluder in CHADS2 >= 2 (non-valvular AF)

– ASA with warfarin 6 wks (45 days) and echo assess seal of LAA

– If LAA seal : DAPT 6 months and then ASA 325 mg alone

– If LAA not seal : cont warfarin until seal (leak < 5 mm)

– Indication : contraindication for OAC (IIb)

– Undergoing cardiac surgery

– Surgical occlusion or exclusion of LAA (IIb)

AF ablation
– Concept for reduced burden of AF : reduced symptom, no reduce stroke (stroke
depend on risk)
– Pre-op : adequate OAC 3 weeks and cont at least 2 months post ablation

– Post ablation can still AF upto 3 months

– Can continue warfarin or dabigatran during ablation

Population only in symptoms

– Paroxysmal AF with symptomatic with failure med (I, levelA)

– Symptomatic persistent AF (IIb)

– Symptomatic AF with HFrEF (CASTLE-AF)

Outcome : improve QoL/LVEF/long term survival, reduced AF symptom & HF

Procedure : PVI +/- additional line, CFAEs
 – Eliminate trigger or PVI
– Accept AF within 3 months after ablation

Complication
– Death 0.2%

– Stroke 1%

– Temponade 2%

– Esophageal injury 5%

– Atrioesophageal fistula

– onset 2-4 wks

– symptoms : dysphagia, fever, stroke, mediastinitis

– PV stenosis < 1% : Dx by pulmonary vein venogram, Tx : PV stent

– Left phrenic nerve injury 1-2%

Manage OAC in specific condition

– OAC regardless of CHA₂DS₂-VASc score : HCM, ARVD, LV non compaction, specific
adult congenital heart (intracardiac repair, cyanosis, fontan, systemic RV)
Stroke/TIA
– TIA : delay 1 days

– Mild stroke (NIHSS < 8) : delay 3 days

– Moderate stroke (NIHSS 8-15) : delay 6 days, brain imaging evaluation before OAC

– Severe stroke (NIHSS >= 16) : delay 12 days, brain imaging evaluation before OAC

After intracranial hemorrhage

– Delay OAC 4-8 weeks (IIb)

Mitral valve repair and bioprosthetic valve

– On anticoagulant 3 months

PAF with CHADsVAS =< 1 with bleeding from OAC

 – Not recommend OAC
Cardioversion in AF (Medication or electrical cardioversion)
– AF < 48 hr

– After cardioversion

– Low CHA2DS2-VASC score : No OAC

– High CHA2DS2-VASC score (Men >= 2, Women >= 3) : long term OAC

– AF >= 48 hr or unknown duration

– Before cardioversion

– TEE R/O clot before cardioversion

– Anticoagulant 3 wks before cardioversion

– After cardioversion

– Low CHA2DS2-VASC score : OAC 4 wks

– High CHA2DS2-VASC score (Men >= 2, Women >= 3) : long term OAC

Clinical trial
Over all rate & rhythm control in AF

CASTLE-AF
– Population : Symptomatic paroxysmal/persistent AF, EF =< 35% on ICD/CRT-D,

NYHA >= 2
– Intervention : PVI vs medication (rhythm/rate control), run in period 5 wks

– Outcome : decrease death or hospitalization for HF (NNT 6)

 – Criticize : may be false positive from CRT (30% on CRT in AF), no report
anticoagulant treatment
CABANA trial
– Population : Symptomatic paroxysmal/persistent AF, age > 65 or stroke

– HF 15%, CHA2DS2VASc = 3, DM 25%, HT 80%

– Intervention (N total 2204) : Medication rate/rhythm control vs add AF ablation (PVI

base)
– Crossover : Ablation to drug 9%, drug to ablation 27%,

– Ablation arm : repeat ablation 19%, AAD 26.5%

– Medication arm : AAD 88.4%

– Outcome :

– No significant ITT primary endpoint (death, stroke, serious bleeding, cardiac

arrest) but significant per-protocol analysis (delay ablation within 12 months)

– Significant second outcome (mortality or CV hospitalization), AF recurrent
Sudden cardiac
death
Sudden cardiac death (SCD)

– SAD : Define as natural unexpected death within 1 hr of the onset of symptoms

– being well within previous 24 hr

– Most common in young : HCM 30%, coronary anomaly 15%

– Hypoxemia is most common cause non traumatic PEA
– PEA : reversible cause 5H+5T+ (H)Intracranial hemorrhage

– SCD in Athletes : 1.HCM 2.Coronary artery anomalies 3.Myocarditis 4.ARVD

– SCD in age > 35 years : R/O CAD

EKG post arrest

– Non-ST elevation : 58% significant coronary artery disease

SCD approach
Cardiac
– Structural heart disease
– CAD : coronary anomaly

– Myocardial disease : HCM

– Valvular heart esp. mitral valve prolapse (scar at basal-inferolateral)

– Congenital heart

– Mostly presented with PEA : Tamponade, ruptured aorta, Severe PHT/Massive

PE
– Absence of structural heart disease

– Genetic channelopathies

– Brugada syndrome

– Long QT syndrome

– Short QT syndrome

– CPVT

– Early repolarization syndrome

– AF with WPW

– Idiopathic VF

– Commotio cordis

– Metabolic cause : electrolyte imbalance, Drug toxicity

Non-Cardiac : 5H5T
Investigation in SCD, step by step
_. Hx & PE, Blood chemistry, ECG, Holter ECG
`. Echo +/- MRI
a. CAG
b. Provocation : EST (CPVT), Na channel block (Brugada), Adrenaline challenge test
(long QT syndrome, CPVT)
c. EP test, volatage map venticular biopsy
 WPW
& bypass tract
Bypass tract & WPW

General
– EKG of WPW pattern : short PR, delta wave, psuedoinfarct pattern
– Diagnosis WPW syndrome : EKG pattern plus ass. paroxysmal tachycardia
– Conceal bypass : only retrograde, no affect on EKG
– Asymtomatic pre-excitation : abnormal EKG, no history of SVT
– PJRT : slow conduction accessory pathyway, long RP
– Most conceal WPW are located between LV & LA

Type of WPW syndrome

– Type A : V1+, Lt side by pass tract

– Association : HCM

– Type B : V1-, Rt side by pass tract

– Association : Ebstein anomaly

– Type C (rare type) : V1-4 positive delta wave, V5-6 negative delta wave

Inapparent preexcitation
– Absent of delta wave

– PR interval < P delta interval (Most in Lt lateral bypass tract)

Intermitent preexcitation
– Preexcitation alternans : Delta wave alternated with normal QRS

– Concertina preexcitation : cyclic pattern of PR interval and QRS complex —> Pass by

tract with decremental property

Short PR approach
– Enhanced atrioventricular nodal conduction (EAVNC) : tachycardia is common from
sympathetic predominant
– EAVNC (abnormal rapid AV nodal conduction)

– Criteria diagnosis

". AH interval in sinus rhythm (AH-NSR) =< 60 ms

$. Shortest RA pacing cycle length maintaining 1a1 AVN conduction =< 300 ms
(200 bpm)
%. Increase AH interval from AH-NSR (delta AH) =< 100 ms
– Preexcitation syndrome
– LGL

– WPW

– Mahaim-type preexcitation

– Congenital hypoplastic AV node or anatomically small AV node

– Subsidiary pacemaker rhythm
– Atrial ectopic rhythm

– Junctional escape rhythm

– Isorhythmic AV dissociation
 – Normal variant

AV bypass tract
– WPW : Kent bundle

– LGL : James fiber (A-H bundle). short PR without delta wave

– Mahaim fiber : same WPW type B (LBBB) but has decremental property

– Atriofascicular fiber : Atrium to distal RBB

– Nodoventricular fiber : Lower of AVN to IVS or RV

– Nodofascicular fiber : Lower of AVN to BB

– Fasciculoventricular fiber : His bundle or fascicles to RV

Localized bypass tract

– V1 : positive delta wave = Lt side bypass tract
– Ant septal : high risk AV block during ablation
Bad prognosis
– Young age, male
– Ebsteinʼs anomaly
– Multiple bypass tract
– SPERRI < 250 ms (shortest preexcited RR interval) : Induced AF and see shortest RR
interval < 250 ms
– AF

Management
Asymptomatic pre-excitation
– Low risk risk feature

– EKG : intermittent loss of conduction over the AP

– Abrupt loss of pre-excitation during EST

– High risk feature

– Young age

– Pre-excited complex during induced AF rate < 250 ms or 240 bpm (SPERRI :

shortest preexcited RR interval < 250 ms)

– Multiple accessory pathways

– Induced sustained AVRT

– Finding AVRT precipitating preexcited AF

– Accessory pathway antegrade refractory period < 240 ms

– Catheter ablation in specific condition

– Pilot

– High risk arrhythmia : Rapidly conducting pre-excited AF

– Observe (IIa) in low risk

SVT with WPW

– Acute management as SVT

– First-line med is Vagal or adenosine

– Alternative acute medication : Betablock/non-DHPs CCB (IIb)

 – Electrical cardioversion in failure med or unstable hemodynamic
– Long term management

– Ablation (I)

– Medication

– Flecainide or Propafenone in absence of structural heart (IIa)

– Amiodarone-sotalol/Beta-block/non-DHPs CCB (IIb)

AF with WPW
Acute management
– Electrical cardioversion

– Consider IV procainamide, IV Ibutilide or IV flecanide/propafenone

– Avoid AV nodal block agent (III) : digoxin, verapamil, diltiazem, adenosine,

amiodarone IV
– Amiodarone IV : Initial effect AV node block and then block bypass tract (effect

of betablock/calcium block : not found in oral amiodarone)

Long term management
– Ablation bypass tract (I)

– Observe in low risk : intermittent WPW

– Medication

– Flecainide or Propafenone in absence of structural heart (IIa)

– Amiodarone-sotalol/Beta-block/non-DHPs CCB (IIb)

 Brugada
syndrome
Brugada syndrome

General
– Prevalence in Thai : Type 1 - 0.41%, Type 2 - 0.86%

– Male > female = 8A1

– AD with incomplete penetrance, Decrease function SCN5A gene : 15% (loss

function Na channel)/CACNA1C (gain function Ca channel)

– Compensate by increase Transient outward K channel (Ito) in phase 1

– Arrhythmic event : SVT 20%, AF 20%,

Diagnosis (only type I)

– ST segment or J wave amplitude >= 2 mm (only type 1 morphology) of one lead V1-

V2 in ICS 2, 3 or 4 with/without provocative drug

– Ddx cocaine overdose (brugada liked ekg and cove type STE in AVR with AV block)

Mechanism
– Decrease inward sodium current

– Decrease calcium current

– Increase outward potassium current

– Phase II reentry

Drug challenge for unmasking brugada

– Indication only of absence of spontaneous type 1, may be type 2 or 3

– Key : Asymptomatic with drug induced type I is low risk : close F/U

– Non type I with Fm Hx of SCD : reassure

– Type I with Fm Hx of SCD : EP study

– Caution during challenge test : infranodal block

– Drug & Dose

– Flecainide 2 mg/kg IV slow push in 10 mins or 400 mg oral single dose

– Ajmaline 1 mg/kg IV slow push in 10 mins (drug of choice)

– Terminate protocol : Dianosis type 1 brugada, ST segment increase >= 2 mm in type

 II, PVC or other arrhythmia, QRS >= 130% of baseline

Type

Presentation
– VF or aborted SCD (more at night)

– Syncope

– Nocturnal agonal respiration

Provocation : Fever, Alcohol, High carbohydrate intake, Drug, Cannabis

Risk for arrhythmic event in asymptomatic
– Fragmented QRS

– Coexist with early repolarization

– Dynamic change in prominent J wave

No associated risk for arrhythmic event

– Positive Fm Hx of brugada syndrome
 – Gene mutation

EPS indication (up to double extrastimuli)

– Only spontaneous asymptomatic brugada type 1 (IIb)

Treatment
– life style modification

– Avoid drug induced, excessive alcohol intake, large meal

– Prompt treatment fever

– Avoid hyperkalemia

– AICD indication therapy

– Aborted cardiac arrest (I)

– Document spontaneous sustained VT (I)

– Spontaneous type 1 with Hx of syncope presume due to Ventricular arrhythmia

(IIa-ESC, I-AHA)
– Drug for electrical storm, recurrent shock or contraindication/refused ICD

– Quinidine (monitor drug level) - Block transient outward K channel

– Tx : prevent electrical storm or treatment

– Dose : Extended release, start 300 mg q 8-12 hr (max 600 mg q 8 hr)

– SE : diarrhea (50%), headache & tinnitus, QT prolong

– Isoproterenol : beta1 agonist

– Tx electrical storm in BrS, SE : palpitation, tachyarrhythmia

 – Dose : 1-2 mcg IV bolus then 2-10 mcq/kg/min
– Ablation at epicardial of RV area; RVOT
– Hx of electrical storm or repeated ICD shock (IIb-ESC)

– Recurrent ICD shocks for polymorphic VT (I-AHA)

Genetic testing
– only for genetic counseling & screening in first degree relatives

Asymptomatic spontaneous brugada type I —> EP study (IIb)

Asymptomatic drug induced brydaga type I —> observe without therapy.
Short QT
syndrome
Short QT syndrome

General
– Common VF > VT (transmural dispersion of repolarization : QT dispersion)

– Mimic brugada syndrome

Genetic mutation
– SQTS1 : gene KCNH2

– SQTS2 : gene KCNQ1

– SQTS3 : gene KCNJ2

Diagnosis
EHRA guideline
– QTc =< 330 (EHRA), QTc =< 340 (ESC)

– QTc =< 360 plus one

– Pathogenic mutation

– Family history of SQTS or sudden death age =< 40

– Survival from VT/VF in absence of heart disease

Management
Drug : quinidine or sotalol
– Indication

– Asymptomatic SQTS with family history of SCD

 – Contraindication for ICD
ICD indication
– survival from cardiac arrest

– Document spontaneous sustained VT

Genetic screening
– considered to facilitate screening of first-degree relatives (IIb)
 Long QT
syndrome
Long QT syndrome

General
– 85% inherited, 15% de novo
– Most common is LQT1 & 2
– Family history is not predictive SCD

Acquired QT prolong
– A : Anorexia nervosa, alcoholism
– B : Bradycardia, Brain (neurologic disease)
– C : CAD, Cardiomyopathy
– D : Drug, Diet (liquid protein)
– E : Electrolyte (HypoCa/K/Mg), Endocrine (hypothyroid), Environment (hypothermia)

Diagnosis : Exclude secondary cause of QTc prolongation

1. QTc ≥480 ms or LQTS risk score > 3
2. confirmed pathogenic LQTS mutation โดยไม่สน QTc
3. QTc ≥460 ms with unexplained syncope
* วัด QTc จาก 12-lead เท่านั้น
* normal QTc ไม่ exclude LQTS
Risk score for LQTS (Revised Schwartz score) > 3 (ESC)

Type of LQTS
LQT1 : activated by exercise
– loss function - reduced K outward (IKs) current (Gene KCNQ1)

– Tx : atenolol > propranolol

LQT2 : activated by sound, pregnancy

– loss function - reduced K outward (IKr) current (Gene KCNH2)

– Tx : nadalol

LQT3 : death at sleep as brugada

– gain function : increase Na inward current (Gene SCN5A)

– Low cardiac event rate but highest risk for dying with an event (20%)

LQT7 (Andersen-Tawil syndrome) : cardiodysrhythmic periodic paralysis

– Triad : dysmorphic physical feature/skeletal anomaly, periodic paralysis, non

sustained VT
– Loss of function - reduced K outward current (KCNJ2 mutation)

– EKG : Prominent U wave, QT prolong is uncommon (16%)

– Low risk cardiac death

LQT8 (Timothy syndrome) :

– gain function - increase L-type Ca2+ current (CACNA1C mutation)

– SCD at early childhood (extremely high risk)

– Ass. AV block, congenital heart, autism, syndactyly/dysmorphic facial, small or

misplaced teeth
Jervel & Lange-Nielsen syndrome
– Homozygous or compound heterozygous mutation KCNQ1 or KCNE1 (Autosomal

recessive)
– ass. with deafness

– High mortality at 40 years (93%)

Romano-ward syndrome
– AD, heterogenous disorder ass. with prolonged QT

– Long QT type 1-6 & 9-13

Memo
RAT : AD, no deafness
– R 1-6 : Romano-ward syndrome

– A 7: Andersen-Tawil syndrome

– T 8: Timothy syndrome

Classification by genotype/phenotype
1. Autosomal dominant (Romano–Ward syndrome) LQT1–6, 9–13
2. Autosomal dominant with extracardiac manifestation
– LQT7 (Andersen–Tawil syndrome), prolonged QT interval + prominent U wave,

polymorphic or bidirectional VT, facial dysmorphisms, hyper-/hypokalaemic

periodic paralysis
– LQT8 (Timothy syndrome) prolonged QT, syndactyly, cardiac malformations,
 autism spectrum disorder และ dysmorphisms
3. Autosomal recessive (Jervell and Lange–Nielsen syndrome) extremely prolonged QT
interval + congenital deafness

Gene
– 90% ของ positive genotype เกิดใน 3 gene คือ KCNQ1, KCNH2 and SCN5A

Provocative test
– Epinephrine test (Low dose adrenaline induced QT prolong)
– Dose 0.1 mcq/kg IV and then 0.1 mcq/kg/min drip for 5 mins and monitor EKG

during drip (beware torsades de point)

– Exercise test (identify LQT1 and LQT2)
– QTc prolongation of 4 minute recovery (QTc >= 445 ms), sense/spec 90%

– QTc > 460 ms at 7 minutes of recovery : predicted long QT type 1 or 2

Risk for SCD

Genetic testing
Patient
– Clinical suspicion for LQTS

– Asymptomatic with QT prolong in absence of other clinical condition

Asymptomatic family members

– genetic testing for family members in index case (class I)

Treatment
Lifestyle modification
– Avoid QT prolong agent/electrolyte abnormal and precipitating cause (strenuous

exercise in LQTS1, Exposure to abrupt loud noises in LQTS2)

Beta-block
– If syncope in long QT : first line is betablock, not ICD

– Indication : LQTS with symptoms (syncope, VT/VF), Asymptomatic with QTc > 470/

pathogenic mutation
– Good response in LQT1, moderate response in LQTS2, poor response i LQTS3.

– Suggest nadalol > propranolol in LQTS2

Flecainide (IIa in AHA, IIb in ESC)

– Add on therapy in LQTS3 with QTc > 500 ms

– Who shortening QTc > 40 ms following acute oral drug test

Lt cardiac sympathetic denervation (sympathetic blockage)

– If limit used/fail/contraindication for betablock
 – ICD contraindication
– Multiple shock with ICD and failure betablock

Indication for ICD

– Survival from SCD
– High risk congenital LQTS :
– Pause-dependent VT

– Bradycardia induced VT

– Recurrent syncope with adequate betablock (IIa)

– Asymptomatic with QTc > 500 with KCNH2/SCN5A mutation (IIb, ESC)

– Persistent symptoms after beta-block plus High risk features (ACC)

– QTc >500 ms

– Genotypes LQT2 and LQT3, Females with genotype LQT2

– Age <40 years of age

– Onset of symptoms at <10 years of age

– Recurrent syncope.
CPVT
CPVT
catecholaminergic polymorphic VT

General
– CPVT1 - RyR2 mutation, AD

– CPVT2 - CASQ2 mutation, AR

– Mechanism of arrhythmia : delay after depolarization (spontaneous leak of calcium)

Clinical presentation at 10-20 years

– exercise induced PVC (severity increase as heart rate increase), exercise induced

polymorphic VT, Bidirectional VT

Diagnosis in normal structural heart

– catecholamine induced bidirectional VT or PVC or VT

– Age < 40 years

– Age > 40 years, must exclude other cause

Treatment
– Avoid competitive sport

– First-line is beta-block

– Add on therapy with Flecainide

ICD indication
– Experience cardiac arrest

– After optimal therapy

– Recurrent syncope

– Polymorphic VT or bidirectional VT

Left cardiac sympathetic denervation

– After optimal medication

– Several ICD shock

– Recurrent symptoms or arrthythmia

 Early
repolarization
syndrome
Early repolarization syndrome

Benign early repolarization syndrome

– Decrease ST segment elevation after tachycardia (Exercise/Isoproterenol)

J wave syndrome
– Brugada syndrome (V1-V3)

– Early repolarization syndrome (except V1-3)

Diagnosis in ERS
– EKG plus symptoms (unexplained VT/VF, arrhythmic syncope)
– End QRS notch or slur

– EKG pattern : J point elevation >= 1 mm in >= 2 contiguous inferior or lateral lead

(exclude V1-3)
– QRS duration < 120

– Physiology : transmural dispersion of repolarisation (local epicardial dispersion of

repolarisation)
Differential diagnosis
Management
– Quinidine add on ICD for secondary prevention of VF
– Isoproterenol for suppressing electrical stroms

– Not suggest genetic testing

ICD indication
Secondary prevention
– Abort sudden cardiac death (I)

– Sustained ventricular arrhythmia

Primary prevention
– Symptomatic patient with syncope in symptomatic family member of ERS (IIb)

– Asymptomatic patient with high risk ECG (high J wave, horizontal/descending ST

segment) with strong family Hx of juvenile SCD (IIb)

Antiarrthythmic
drugs
Anti-arrhythmic drug

Mechanism of tachyarrhythmia
– Automaticity

– Normal automaticity (Pacemaker cell) : warm-up & warm down

– Abnormal automaticity from abnormal cell, precipitating from sympathetic

overactivity : AT, Junctional tachycardia, VT

– Trigger activity : After-depolarization

– EAD (depolarization phase 3) (QT prolong) result Torsade de points, tachycardia,

other arrhythmia
– Cause: hypokalemia, Drug induced QT prolong (anti-arrhythmic class Ia & III

– DAD (depolarization phase 4) (Normal QT) : from intracellular calcium overload

result Bidirectional VT in ischemia/HF, digoxin intoxication, CPVT, Idiopathic

outflow tract VT
– Rx : Amiodarone

– Reentry : Atrial/AV/Ventricular reentry, such as Lt posterior Fascicular VT (Verapamil

sensitive VT)
– Mechanism : substrate - Trigger - Unidirectional block - Excitable gap, central

area of block, Area of slow conduction

– Rx : Increase refectory period or increase tissue conduction

Action potential
pacemaker cell
: resting membrane potential -40 to -70 mV
– Phase 0 : Ca2+ influx

– Phase 3 : K+ efflux

– Phase 4 : Spontaneous depolarization, I(f)-funny current

– Ivabradine (Block I(f)-funny current for treat inappropriate sinus tachycardia (IIa)

Non pacemaker cell

: resting membrane potential -90 mV
– Phase 0 (Depolarization) : Na+ influx, determine conduction velocity

– Phase 1 (Repolarization) : J point —> Transient outward K+ (I to) channel

– Phase 2 (Refractory period) : ST segment —> Ca2+ influx

– Phase 3 (Refractory period) : QT interval —> K efflux

– Phase 4 : I-K1 maintaining the resting potential near -90 mV

 – I-KATP potassium channel is inactivated in response to ischemia or depletion of ATP

Anti-arrhythmic drug
: Class “โซ-เบ-เค-ค่ะ”
Class I : Sodium block (membrane stabilizer), Used dependence block
– IA : Na block++/K block, Prolong repolarization (QT prolong)

– Drug : Proarrhythmic drug (Reentry VT, Torsade)

– Quinidine : block K (I Kr) & Transient outward K channel (I to)

– Rx : Brugada due to block K (Ito)

– Side effect : diarrhea, hemolytic, thrombocytopenia

– Procainamide

– Block bypass tract : Acute Mx in AF with WPW, Stable VT in structural

heart (IIa)
– Side effect : Drug induced lupus

– Disopiramide

– Negative inotropic : Rx AF with HCM

– Anticholinergic drug : Rx vagally medicated paroxysmal AF

– IB : Na block+, shorten repolarization

– Drug : lidocaine, phenytoin, mexiletine

– Lidocaine : Effect on ventricle (no effect on atrium)

– Used in TdP (QT prolong), Digoxin related ventricular tachyarrhythmia,

automatic VT, Second line after amiodarone in ischemia induced VT/VF

– IC : Na block +++, no effect on repolarization, Decrease conduction velocity,

pro-arrhythmic drug : Increase PVCs/VT/VF (reentry)

– Must combine with AV blocking agent in AF/A.flutter

– Off when QRS duration > 25-50%

– Contraindication : structural heart, brugada, SSS, impair AV node function, QRS

> 130
– Drug

– Flecainide : used combine with betablock for prevent atrial flutter 1g1

conductiob
– Propafenone : mild betablock effect (avoid in asthma), used in AF with
 normal heart, can used in renal insufficiency
Class II : Beta block (receptor blockade), no effect on repolarization
Class III : Potassium block (electrophysical properties), prolong repolarization
– Off if QT > 500 ms or QTc increases > 15%

– Reverse used dependence, proarrhythmic drug when bradycardia

– Drug

– Pure K channel blocker (I kr): Sotalol, Ibutilide, dofetilide

– Multiple channel blocker:

– Amiodarone (TdP < 1%),

– Dronedarone (no iodine group, less systemic side effect)

– Sotalol

– Contraindication : HF, CrCl < 40, bronchospasm

– Dofetilide

– Must initial at IPD case

– Drug interactions : HCTZ, Trimethoprim, verapamil, ketoconazole, megestrol

Class IV : Calcium block

– Drug : Verapamil, diltiazem
Beta-block
Metabolite via liver
– C : carvedilol

– P : propranolol

– M : metoprolol

Carvedilol : non selective beta block

Flecanide
– Dose 50, 100 mg tab
– Start 50 mg bid & increase 50 mg every 4 days, max dose 300-400 mg/day (GFR <
35 : max dose 100 mg OD or 50 mg bid)
– Must combine with AV blocking agent in AF/A.flutter
– Off when QRS duration > 25-50%
– Contraindication : structural heart, brugada, SSS, impair AV node function, QRS >
130

Amiodarone
 – Dose : load max 15 mg/min (150 mg in 10 mins)
– Oral (600-800 mg/day) or IV total 10 gm then 100-200 mg/days

– Use together should decrease Warfarin by 1/4 to 1/3, decrease Digitalis by 1/2, Do
not use Simvas > 20 mg/d
– Systemic side effect : Hypo/hyperthyroidism, abnormal LFT, optic neuropathy, sinus
bradycardia, photosensitivity
– Amiodarone toxicity : “PHOTOS”
– “P” : acute or chronic used induced pulmonary fibrosis (1-20%), Prolong QTc

(TdP rare), prolong PR, QRS, Peripheral neuropathy (0.3%)

– “H” : Hepatitis & Cirrhosis (<3%), Hypotension (IV Amiodarone)

– “O” : Ocular toxicities (Cornea Verticillata), Optic neuritis, Photophobia (> 90%)

– “T” : Thyroid dysfunction: Amio contains iodine 37% by weight Hypo (1-22%),

Hyper (<3%)
– “O” Others:

– CNS (3-30%): Ataxia, paresthesia, sleep disturbances, impair memory, and

tremor -> dose dependent; adjust dose

– GI (30%): Nausea, anorexia, constipation -> decrease dose

– Skin: Blue-Grey discoloration (4-9%), photosensitivity (25-75%)

Dronedarone
 – Compare with Amiodarone
– Less systemic side effect

– More recurrent AF

– Contraindication in HF, permanent AF

– Increase mortality in HF with NYHC III-IV (ANDROMEDA study), Permanent AF

(PALLAS study)

Lidocaine
General
– No effect on QTc

– Used dependence : ยิ่ง VT เร็วยิ่ง block ได้ดี

– PK/PD : rapid initial distribution in 5 mins, low potency, fast recovery

Drug used
– Alternative option for VT when failure electrical cardioversion, betablock,

amiodarone
– Stop when VT termination, no drip cont for prevent recurrence

Dose
– Lidocaine for IV form ไม่เหมือนที่ใช้ฉีดยาชา แต่ถ้าจะเอามาใช่ต้องเป็นแบบ preservative
free without adrenaline
– 1%lidocaine = 10 mg per ml
– Dose loading 1-1.5 mg/kg (1%, 5 ml IV) in 3 mins. if not response, repeat next dose
0.5-0.75 mg/kg q 5 mins
– Maintenance : 2%lidocaine 100 ml with 5%DW 250 ml IV rate 10 ml/hr (1 mg/min)
– Decrease dose 50% in advance cirrhosis or liver failure
Side effect : ชารอบปาก, agitation, nystagmus or seizure (must stop drug)
– Management overdose

– EKG same as TCA overdose

– Rx : IV sodium bicarbonate, 10%lipid 1.5 ml/kg bolus with 0.25 ml/kg/min

Calcium channel blocker

– Verapamil
– IV (5 mg/2 ml per amp) : 2.5-5 mg IV q 15-30 min

– Oral sustained release (Isoptin 240 mg, แบ่งครึ่งได้) : 240-480 mg/day. if 480
mg/day, suggest 240 mg bid
– Diltiazem
– IV (5 mg/ml) : 5-10 mg IV q 15-30 mins

– Oral extend PO : 120-360 mg/day

Atropine
– PK : IV rapid onset, half life 2-3 hr
– Dose 0.6 mg IV (Max 3 mg), ET 2-3 times IV dose diluted in 3-5 ml of water
– Increase effect of atropine : post heart transplant, dipyridamole
 – Decrease effect of atropine : theophylline, caffeine
– Beware in glaucoma
– Side effect : anticholinergic symptoms, ataxia

Specific condition
Contraindication in ESRD
– Quinidine, Sotalol, Dofetide

Change pacing threshold

– Increase pacing threshold : Chronic used amiodarone & Flecainide

– Decrease pacing threshold : acute used amiodarone

Congenital heart

Clinical trial
PALLUS study
– Summary : Dronedarone increase mortality in permanent AF
ANDROMEDA
– Summary : Dronedarone increase mortality in severe HF with reduced EF
Basic EP
Basic EP

Regular narrow complex tachycardia

– Invisible P wave (< 70 ms in EP, < 90 ms in EKG)
– Typical AVNRT

– Junctional tachycardia

– AT with prolong AV block

– Short RP
– Orthodromic AVRT

– AT with 1st AV block

– Atypical AVNRT (slow-slow)

– Junctional tachycardia

– Long RP
– AT

– Atypical AVNRT (fast-slow)

– PJRT(persistent junctional reciprocating tachycardia)

– Septal bypass tract, common at left side, tachycardia induced

cardiomyopathy, incessant tachycardia

– Sinus tachycardia

– IART (intraatrial reentry tachycardia) : common in adult congenital heart disease

– Midway P wave
– Sinus tachycardia with first AV block

– Atrial tachycardia with 2P1 AV conduction

– แยกโดย JVP : cannon A, Echo mitral inflow ดู A wave

General
– AVNRT or AVRT : general initiation with ectopic atrial foci
 – PJRT : Possible initiation with sinus rhythm due decremental property of bypass
tract causing atrium recovery and then developed reentry.
– Maintenance of re-entry tachycardia is determined by wave length
– Wave length = Refractory period x conduction velocity

– V > A with narrow QRT

– Septal VT

– Junctional tachycardia

– Positive P wave
– AT

– Atrial flutter

– Sinus tachycardia

– AVNRT
– Typical : early HA in His

– Atypical : early HA in CS

Protocol in EP study
– Baseline measurement
– Sinus node function
– AV & VA conduction
– Arrhythmia induction
– Intervention : Ablation, Device

Read EP tracing
Basic
Surface EKG
– Narrow/wide QRS

– A-V relationship : A rate, V rate

– P wave in inferior lead : positive/negative

– Pacing spike

– Pre-excitation, HV interval

– CS lead (ปลายสาย CS distal = CS1):

– Atrium is large activation

– Ventricular is small activation

Tachycardia
– V:A ratio and relationship

– Long/short/very short RP

– Sequence of A&V conduction

Conduction abnormality
– Prolong A-H, H-V interval

– Intra-His block : split His & prolong > 30 ms (His is spike wave)

– Consequence of A pacing : ดู V
– Extrastimuli : jump & echo beat, arrhythmia induction
 – Incremental pacing : AV block, arrhythmia induction
– Consequence of V pacing : ดู A
– Extrastimuli : arrhythmia induction

– Incremental pacing : V-A block

Normal value
– Rate = 60000/interval (ms)
– Corrected sinus node recovery time (CSNRT) < 525 ms (sinus node function)
– CSNRT = SNRT - basic sinus cycle length

– SNRT : From late AF or late A pacing to first Pw

– Normal SNRT < 1500

– Intraatial conduction time 20-60 ms

– Normal A-H : 60-120 ms
– A-H jump : increase > 50 ms after decrease stimuli by 10 ms

– Normal H-V interval 35-55 ms

– HV interval >= 70 ms : Infra-HIS block

– HV interval > 100 ms (significant AV node disease : pacemaker

– HV >= 70 ms with symptoms : pacemaker

– Negative H-V or H-V interval = 0 : presence of bypass tract (WPW)

– Entrainment (Last RV pacing to first Vs - Tachycardia cycle length) : cut points 115 ms
– > 115 = AVNRT

– < 115 = AVRT

– ถ้า cycle length ต่างกันไม่เกิน 20 ms ถือว่าเท่ากัน

Measurement
– AH in His lead : Shape A to beginning of His

– HV : beginning of His to early V onset (EGM or ECG)

Clue in Tachycardia
– Looked for PVC
– Wobble : cycle length change
– AA predict VV : R/O VT

– VV predict AA : R/O AT, Ventricle origin, AV node dependence

– Prefer AVRT
– Coumel sign

– Narrow QRS with short VA but wide QRS with long VA

– Constant VA interval but vary V-V & A-A interval

– Terminate with narrow QRS during wide QRS tachycardia : AVRT

– Termination with A-H

– Coumel sign : by pass tract same side of bundle branch block : common LBBB
– Prolong cycle length during wide QRS (slow rate) > narrow QRS (fast rate)

– Increase V-A interval during bundle branch block > 30 ms

– Clue : QRS มีทั้งแคบและกว้างในช่วงเวลาเดียวกัน แต่ตัวกว้าง rate ช้ากว่าตัวแคบ

 – Initiation
– Initial AH jump : prefer AVNRT

– Termination
– Termination with A : exclude AT

– Termination with V : not help

– Terminate with narrow QRS during wide QRS tachycardia : AVRT

– Termination with A-H : AVRT

– AV line up & A=V : prefer Typical AVNRT, Ddx Septal AT with prolong PR
– Eccentric atrial activation : exclude AVNRT
– Concentric atrial activation : Atypical AVNRT or Right/septal ORT/AT (แยกโดย
entrainment)
– Very short RP < 50 ms : R/O by pass tract

– Very short/short RP or AV block during tachycardia : exclude AVRT

– Constant AA interval but vary V-A & A-V interval : prefer AT
– AV dissociation
– A > V : AT, Atrial flutter, 2P1 AVNRT, R/O VT

– V > A : VT, JET, AVNRT with upper block

– Cycle length variation > 15% prefer focal AT

Maneuver
– Atrial pacing
– Dual AV nodal pathway (A-H jump) : 20% in normal population but < 1% has

AVNRT
– Increase pre-excitation

– Ventricular pacing
– Retrograde atrial conduction

– Concentric retrograde atrial activation

– AV nodal conduction is common (AVNRT)

– Typical : VA interval < 70 ms

– Atypical : VA interval >= 70 ms

– Septal bypass tract

– Not exclude Lt lateral bypass or slow conduction

– Eccentric retrograde atrial activation

– Presence of bypass tract (AVRT)

– Fastest A activation in High RA : Rt side bypass tract

– Fastest A activation in dCS : Lt side bypass tract

– Fastest A activation in pCS : Septal bypass tract

– Ventricular pacing during tachycardia (pace 10-40 ms faster)

– AT :

– if VA conduction will overdrive suppression AT

– Change atrial activation sequence

– No VA conduction : VA dissociation
 – AV node dependence : AVNRT or ORT
– Capture circuit : A rate follow pacing

– No VA conduction : AV dissociation

– Over fast pacing : terminate tachycardia due to AV block

– Pacing ventricular overdrive pacing

– V-A-A-V = AT

– V-A-V = R/O AT, AV node dependence

– His refractory PVC

– Reset tachycardia by pulling H-H : AVRT

– Delay next atrial depolarization : PJRT

– Terminated SVT without atrial depolarization: AVRT

– Para-hisian pacing : Lower output until QRS wider (not capture His)
– Stim to A interval prolongation : no by pass tract

– Stim to A interval not change : presence of septal by pass tract

Step reading
Tachycardia
– Baseline during sinus rhythm : Pre-excitation

– Tachycardia

– A : V ratio

– VA interval : very short, short, long

– Concentric or eccentric atrial activation

– Concentric : VA interval < 70 ms?

– Spontaneous VA block during tachycardia

– Effect of BBB on tachycardia

– Ipsilateral BBB increase VA conduction in O-AVRT

– Look for clue in tachycardia

– Maneuver

– A pacing : Dual AV node physiology

– V pacing : Response to ventricular pacing

– Entrainment (during tachycardia)

– Step

– Confirm entrainment

– Determine last entrain beat

– VAV (nodal reentry) or VAAV response (AT)

– Post-pacing interval - tachycardia cycle length (Vp conduct A with CL)

– < 115 ms : O-AVRT

– > 115 ms : AVNRT

– Effect on PVC during His refractory period

– Para-hisian pacing
Quiz
Surface EKG : exclude Atrial flutter
AV line-up, A rate 200, V rate 100, earliest A at CS9-10, Block above His
Dx 2P1 AVNRT with A-V block, DDx AT with 2P1 block
Mx : Slow pathway ablation
Narrow complex tachycardia
AV dissociation & A:V = 1P2
Earliest A at high RA
Ddx : Juntional tachycardia, 2P1 AVNRT with upper block, morphology less-liked
fascicular VT

Narrow QRS After His bundle extrasystole and after (long phase recovery)

Infra-Hisian unidirectional AV block with VA conduction

Typical AVNRT
– Earliest A at CS9-10

– Post ventricular overdrive pacing : VAV response (Pseudo VAAV)

– Closed pacing interval - tachycardia cycle length > 115 : prefer AVNRT
Typical AVNRT
– RV pacing : last RV pacing can not advance A

– Late entrainment is A, response V-A-V (Pseudo V-A-A-V)

– Then run SVT with AV line-up

PJRT, Initial with PVC and V-A-V response

Antidromic AVRT (Mahaim fiber)

– Regular WCT, earliest A at CS9-10

– PAC terminate wide complex tachycardia : Dx AV node dependence

– Short HV interval without delta wave

Orthodromic AVRT - Lt lateral bypass tract key, Spontaneous normalized LBBB
aberrancy (Narrow QRS before terminate).
Irregular wide complex tachycardia with varying QRS
Dx : AF with pre-excitation

Fascicular VT : AV dissociation, V > A, Present of H in VT prefer fascicular VT

AVRT : short VA, terminate with A-H

AT : AV line-up but positive PW in lead II,III and non-constant A-V interval

AT : AV line-up, A-A constant but vary V-A & A-V interval
Sinus rhythm with complete AV block without escape rhythm
– RV lead : no QRS complex

Double fire : Dual AV node physiology

– Most likely mechanism of tachycardia : AVNRT

AV node dysfunction (Prolong AV interval) : least like AVNRT

: A pacing, mimic double fire but A to V1 is too short to conduct
AVRT : VV predict AA and constant V-A interval

AVRT with Lt lateral bypass tract

– Earliest A at CS1-2, VV predict AA, Constant VA interval but vary V-V & A-A interval
Prefer Typical AVNRT
– AV line-up

– Mimic AA predict VV but too short to AV conduction, less likely AT

– PVC terminate abberency

PJRT
– Regular narrow complex tachycardia, long RP
 – Terminated with PVC (R/O AT, AVNRT)

His refractory PVC & terminated AVRT

His refractory PVC and advance A -> Present of accessory pathway
Dx : Septal ORT
Para-hisian pacing
– สังเกตุเห็น มี pacing narrow QRS complex & pacing wide QRS complex
– No change cycle length of stim to A : presence of bypass tact
– Earliest A at CS9-10 : Septal bypass tract
– Lt lateral AVRT with AVNRT
Lt lateral bypass tract : Antidromic AVRT (wide QRS) —> PVC —> Orthodromic AVRT
(narrow QRS)

Gap phenomenon
– AH block at S1-S2 at 420 ms then S1-S2 at 379 ms can AV conduction

– โดยปกติ ถ้า S1-S2 at 379 ms จะเกิด AH block เลย

CXR
CXR
 – Right descending PA > 17 mm
– Vascular pruning : rapid tapering pulmonary artery (Severe pulmonary HT or
Eisenmenger)
– RA enlarge : 2.5 cm from paravertibral border
– RV enlarge : lateral CXR > 1/3 of xiphoid to suprasternal notch
– > 1/2 xiphoid to sternal angle

– Widening mediastinum : >= 8 cm or 1/3 of thoracic at level of aortic knob

Position of valve
– CXR PA : horizontal at mid-heart (carina to base of heart), sagittal line at mid-spine,

AV at cross of horizontal & sagittal

– CXR lateral : slope line at apex to carina, horizontal line at mid-heart
Description CXR
– Pulmonary blood flow
– Levocardia/Dextrocardia
– Situs solitus/Situs inversus
– Main PA, Right descending PA
– Left/Right aortic arch & enlargement
– Chamber enlargement

Nearly normal CXR

– Coarctation of aorta
– Calcified pericardium
– MS
– PS
– PHT

Heterotopic cardiac transplantation with Radiosynthetic patch encircles the aortic

anastomosis (median sternotomy approach)
Heterotopic cardiac transplantation (Rt thoracotomy approach)
Absence of pericardium
– CXR : Lt shift and apex upward
– Echo apex at post axillary line, LV & LA distorsion, RV & RA dilatation without PHT
จาก LV ดึงลงมาก
Pectus excavatum

CXR in post MV clip

Cardiac contractility modulation therapy

Total artificial heart

CardioMEMS
– In symptomatic HF with previous hospitalization (IIb)

– Reduced risk recurrent HF

 Basic
Echocardiogram
Basic echo

General
– Interatrial septal aneurysm : bulging 1 cm from interatrial septum plane from TEE
– 2D Parasternal short axis : มองจากขาไปหัว
– Apical 2 chamber : Lt = Inferior, Rt = ant.
– Normal wall motion : thickening > 30%
– Akinesia : thickening < 10%
– LV dilatation : LVEDd index > 30 mm or male > 58 mm, female > 52 mm
– RAP siriraj = 4.8 + (4.6xMinimal IVC diameter in cm)
– LVEDP = Diastolic blood pressure - end diastolic pressure in AR
– PSLX : No papillary muscle = Lt or Non cusp, Posteromedial papillary muscle = Non-
cusp?
Physic & Doppler echo
– Adult echo : 2-4 MHz
– Wavelength ~ Penetration
– Short wavelength : low penetration but high resolution

– Solution (Temporal solution แปลผกผันกับ Spatial solution)

– Temporal solution (frame rate) : increase by reducing sector angle, decrease
 depth
– Require high frame rate in high mobile mass

– Spatial solution (ความสามารถแยกจุดสองจุดออกจากกัน) : Increase frequency —>

(increase axial > lateral solution), change depth ไม่มีผลต่อ spatial solution
– Lateral solution (ความสามารถในการแยกจุดสองแนวซ้ายขวา, depend on beam
width): increase transducer diameter
– Axial solution (ความสามารถแยกจุดสองจุดแนวบนล่าง, depend on spatial pulse
length) : Increase by reduce wave length (increase transmit frequency)
– Harmonic imaging : ส่ง 4 MHz, รับ 2 MHz
– Acoustic output limits : Mechanical index =< 1.9, Thermal index =< 6.0
– PW : Max velocity < 2 m/s, CW : Max velocity 9 m/s
– Compress control : แยกขาวดำ
– Gain control amplification of returning U/S signal
– Measure Doppler : angle =< 20 degree
– Pressure gradient = 4(V2^2-V1^2), assume V1 = 0 if V1 < 1

Aortic root in normal

– Annulus < 2.5

– Sinus < 3.5

– Sinotubular junction < 3.0

– Tubular < 3.0

RV imaging
– Normal RV size < 2/3 LV size in apical 4 chamber
– เทคนิคการจำ 7x -> 35 -> 42 -> 84
RV dilatation :
– Parasternal view : RV end diastolic diameter > 30 mm

– Short axis great : RV end diastolic above aorta 35 mm

– RV focus view

– > 41 mm at base, > 35 mm at mid level, RV longitudinal > 83 mm

– RV EDVs : male 87 ml/m2, female 74 ml/m2

– RV ESVs : male 44 ml/m2, female 36 ml/m2

RV function
– RV FAC (fractional area change) : >= 35%

– RIMP (Right index of myocardial performance)

– RV dysfunction : > 0.43 by PW Doppler or > 0.54 by TDI

– RV GLS : normal > -20 (ยิ่งลบยิ่งดี)

– RV mass = RV myocardial volume from MRI x 1.05

RV diastolic function
– TV E/A ratio

– Impair relaxation : E/A < 0.8

– Pseudonormal filling : E/A = 0.8-2.1, E/eʼ > 6

 – Restrictive filling : E/A > 2.1, DR < 120 ms
RV thickness in diastole : normal 1-5 mm
TAPSE in modified 4 chamber : normal >= 17
TV lateral s velocity : normal >= 9.5
MPI(TDI) >= 0.24
RV inflow view : 1. CS. 2. Eustachian tube. 3. IVC
RV from CMR : lateral RV free wall, diaphragmatic part, Septal part, RV outflow tract

LV imaging
Basal inferior or inferoseptal walls may be hypokinesia in normal heart
LV function
– Normal LVEF : male > 52%, female > 54%
– Fractional shortening : normal > 25%
– MPI (Myocardial performance index) : normal < 0.28
– In mitral regurgitation dP/dT : normal > 1200, severe systolic dysfunction < 400
– Dyskinesia vs Dyssynchrony (In BBB with normal thickness)
Myocardial strain
– Global longitudinal strain (GLS) better reproducibility
– Increase sensitivity ในเคสที่ไม่แน่ใจ
– Normal GLS -20, Impair -15 เป็นต้นไป

3D echo : surgical view

– Lateral axis (red) : ซ้าย-ขวา
– Elevation (green) : หน้า-หลัง
– Depth axis (blue) : บน-ล่าง

Valve
Diastolic function
– 4 phase: Isovolumic relaxation, Early rapid diastolic filling, Diastasis (pressure
equalize of LV/LA) , Atrial contraction
– E/A : E > 1 m/s =S3, A > 1 m/s =S4
– E depend on preload (high preload —> high E)
– DT evaluate at first sloped
– Grade I LV diastolic dysfunction : LAP ~ 10 mmHG & LVEDP ~ 22 mmHg.
 – Pseudonormalization vs normal diastolic function : Valsalva for decrease LV prelead
if psuedonormalization show decrease E/A ratio >= 50%
Value
– Normal E/A 0.8-2, DT 160-240

– Normal TDI : Septal eʼ >= 7 cm/s, Lateral eʼ >= 10 cm/s, E/avg eʼ < 8

– E/med eʼ >15 —> LVEDP > 15 mmHg

– Grade I diastolic dysfunction : DT > 200 ms

Diastolic dysfunction in AF
– E/med eʼ >= 11

– Poor prognosis : DT < 130 ms

– Supportive : E > 1 m/s

Limitation
– Atrial arrhythmia

– MV inflow obstruction : MS

– MR

– CAD, HCM with preserve EF : poorly correlation with hemodynamic

Normal varient
– RA mass : crista terminalis ridge (posterolateral wall of RA near SVC)
– chiari network or Eustachian valve (arises from IVC to lower rim of fossa ovalis)
– RV mass : moderator band
– LV mass : LV band (false tendon)
– AV valve : Lamblʼs excrescences
– Aorta : periaortic-free space
– Epicardial fat (common in AV/interventricular groove)
– Coumadin ridge (warfarin ridge or left lateral ridge) : a band-like embryological
remnant in LA between left superior pulmonary vein and the left atrial appendage
Echo artifact
– Side lobe artifact
– beam width artifact คล้ายๆ side lobe artifact แต่ภาพแนวหน้าหลัง
– Near flied clutter = Ringdown artifect : artifact is trouble when trying to identify
structures that are close to transducer
– Range ambiguity : correct by increase depth
– Refraction : 2 ภาพอยู่ระดับเดียวกัน
– Mirror image : 2 ภาพอยู่ระดับต่างกัน
Aortic arch
Contrast echo
– Prefer Apical 4 chamber view > subcostal 4 chamber view
– Contraindication : significant Rt to Lt shunt or pregnancy

NSS 8 cc + autologous blood 1 cc + air 1 cc or NSS 9 cc + air 1 cc

: เริ่มนับ First beat ตั้งแต่ bubbles fill เต็ม RA
– air bubble < 3 beats : intracardiac shunt

– air bubble > 6 beats : extracardiac shunt

– In normal : no air bubble

– If > 20 bubble —> large shunt

Aneurysm vs Pseudoaneurysm
– Pseudoaneurysm : 2 layer of thrombus & pericardial

– Mx : surgical aneurysmectomy
Key in exam
– Severity and etiology of valve pathology must description
– Global & regional function of LV/RV
TEE
TEE (transesophageal echo)

Absolute Contraindication
– Perforated viscus
– Esophageal stricture/tumor/perforation/laceration/diverticulum
– Active upper GI bleeding

Control probe
5 views
– Deep transgastric view : apex ติด probe, distance 45-50 cm from incisor
– 5 chamber view : 0-20 degree, doppler parallel to AV

– RV inflow view : clockwise and positive angle from 5 chamber view

– 4 chamber view

– Transgastric view : mid LV, distance 40-45 cm from incisor

– Apical short axis view : 0-20 degree, anteflex probe

– Mid papillary short axis : 0-20 degree, anteflex probe

– Basal short axis : 0-20 degree, anteflex probe

– RV basal view : 0-20 degree, clockwise from basal short axis view

– RV inflow view : 90 degree

– 2 chamber view : 90 degree at mid papillary view

– Mid esophageal view : LA ติด probe, deep 30-35 cm

– 5 chamber view : 0-10 degree

– 4 chamber view : 0-10 degree

– Mitral commissural view : 60 degree

– 2 chamber view : 90 degree

– Bicaval view : 90 degree with clockwise rotation (มองจากด้ามจับ)

– LAA view : 90 degree with more counterclockwise rotation
– Rt pulmonary vein view : 90 degree, +/-withdraw and clockwise rotation from
 bicaval view
– Lt pulmonary vein view : 90 degree, +/-withdraw and counterclockwise rotation

from LAA view

– Long axis view : 130 degree (3 chamber view)

– AV short axis view : 30 degree

– Ascending aorta long axis view : withdrawal probe, backward rotation, 90 degree

– Upper esophageal view : short axis great vessel view

– Aortic arch long axis view : 0-10 degree

– Descending thoracic view : Reverse probe

– Descending aorta short axis view : 0-10 degree

– Descending aorta long axis view : 90 degree

Specific valve view

Mid esophageal view
MV
– 0 degree : 4 chamber

– 60 degree : bicommissural view

– 90 : 2 chamber

– 135 : 3 chamber with long axis AV

AV
– 135 degree : Long axis AV

– 45 degree : Short axis AV

LA appendage
– 90 degree : 2 chamber

– ค่อยๆ ปรับ degree จนเห็นครบ LA appendage

ASD
– 90 degree : bicaval view

PV connection
 M-mode
& Doppler
M-mode

M-mode
– Aortic valve : เส้นหนา 2 เส้น (aortic sinus/annulus)
– Mitral valve : muscle ประกบบนล่าง

MV M-mode
EPSS : e point septal separation

MVP : Bileaflet prolapse

Prolapse posterior MV leaflet
– Definition in M mode : systolic bowing of leaflet tips >= 3 mm below C-D line
Color M-mode of MVP : late systolic enhancment
Systolic anterior motion of MV

Fluttering Anterior MV in non severe AR

Atrial flutter 3L1

MS with AF
– Irregular HR, Reduced E-F slope, loss of A-wave, anterior motion of posterior leaflet,

leaflet calcification and diastolic doming. Decrease leaflet separation in diastole.

MS : thickening MV, decrease of EF slope,

AR with MVP

Acute ontop chronic severe AR, LV dilatation, premature mitral closure

– Key severe AR : premature mitral closure (loss a wave)
Acute severe AR
– early MV closure

– Anterior MV leaflet fluttering

Key หลักในการแยก Acute or Chronic severe AR คือ LV dilatation

DCM : increase EPSS & B-bump : found in high LVEDP, PR prolong, LBBB
Left atrial myxoma

Diastolic dysfunction grade II : L wave in high LVEDP

MV m-mode : SAM in HOCM

WPW type-A or pre-excitation syndrome with left lateral accessory pathway
LBBB
– Paradoxical & non-paradoxical LBBB : both found in LBBB
Constrictive pericarditis : septal bounce and 2nd diastolic dripping (ventricular
interdependence), flattening posterior wall
AV M-mode

Low output in LV dysfunction :

Early AV opening in high LVEDP

Acute aortic regurgitation : Mid diastolic aortic valve opening (premature openinng)

Bicuspid aortic valve

: eccentric AV closure

Mid systolic AV closure in HCOM

: Early (mid-systolic) closure of aortic valve most likely due to HOCM
Subaortic stenosis from fibromuscular ridge : fix subaortic obstruction with premature
closure of AV

Subaortic membrane
AV m-mode
LVAD with 1L3 support

Tamponade
Ebsteinʼs anomaly : Right sides are dilated and when LV in systole (right side is in
diastole) and so there must be atrialization of RV at the mitral valve region (delay TV
closure compare with MV)
Paradoxical septal motion

PV M-mode
PHT : Loss of a-notch and systolic notching giving the flying-W sign
Contrast M-mode

The agitated saline appears at RV and after few cycles appears in the LV through the
mitral valve. So, it is extra-cardiac right to left shunt
M-mode contrast echo : The contrast appears first in RV then LV after almost 1 cycle and
the area between mitral leaflets is free of contrast. So, it is right to left shunt at
ventricular level (VSD with Rt to Lt shunt)

M-mode contrast echo : The contrast appears at the same time at both LV and RV, and
fills the mitral valve. So, the shunting is at the atrial level (ASD with Rt to Lt shunt)
CW & PW mode

Color M-mode of functional MR : MR with prominent at early and late systole, mid-
systolic decrease
Diatolic MR

MR with high LV pressure

– MR Vmax 8 m/s

– Diastolic dysfunction grade II

– Can evaluated LV function by dP/dt

dP/dt Isovolumic Phase Index of LV Contractility
Color M-mode : complete heart block with diastolic MR
Chordae rupture with diastolic MR
F wave in isovolumic relaxation time

LV mid cavity obliteration or hyperdynamic ejection fraction

TV prolapse
Valve and subvalve PS
Multiple PAC
Reverse pulsus paradoxus in HCOM

Diastolic reversal flow in pulmonary vein

– In high LA pressure
Systolic reversal flow in pulmonary vein
– Blunt S wave or reverse S wave in high LA pressure or Severe MR
Pulmonic vein stenosis

AR with PVC/PAC

Mild AS with severe AR

Aortic run off : PDA, AR, AV fistula
EST & CPET
EST

General
– Perceived effort of exercise : > 25% of Max cardiac output
– On digoxin แปลผล ST segment ลำบาก เนื่องจาก early change (false positive result)
– Beta-block
– For diagnosis : discontinuation of beta-block

– For risk stratification : may be continue

– HR max (CAD with beta block)= 164-(0.7xAge)

– No role of EST in asymptomatic patient (class III)

– EST in sedentary people with CV risk who plan vigorous physical activity (ESC

IIa, C)

Physiologic change in exercise

– During EST : Increase SBP but same diastolic BP

– Isometric exercise : increase diastolic pressure

– Decrease SVR

– Maximum exercise : increase CO 6 เท่า แต่ increase peak O2 consumption 18 เท่า

– During exercise : Increase HR before SV, Same O2 extraction rate but increase
coronary blood flow
– Old age : same SV, decrease HR and decrease CO
– Athlete : Same CO (Increase SV, Decrease HR), Decrease HR baseline and maximum
HR, Increase O2 consumption

EST : sense/spec 70%, hyperventilation increase sense

– False positive STD, common in inferior lead

Indication
Contradiction
– Severe symptomatic AS

– Uncontrolled arrhythmia

– Decompensated HF

– AMI in 2 day

– Myocarditis/Pericarditis

Aortic aneurysm สามารถ EST ได้แต่ aortic dissection ห้าม EST

Limit interpretation if resting EKG

– LBBB

– Ventricular pacing

– Pre-excitation

– Repolarisation abnormality (LVH, digitalis)

Type of exercise
– Treadmill : High energy consumption & achieve HR

– Bicycle : better tolerated by deconditioned patient

– Arm ergometry : High increase HR & BP but Low rate to achieve target HR

Bruce Protocol : target HR 85% of PMHR, post MI 70% of PMHR or 110/min

– Positive EST : STD 80 ms (60 ms if HR > 130) for J point (horizontal or downslope) >

1 mm for 3 cont. beat at least 2 leads or STE (non-Q lead)

– V5 lead is most common positive

– Upslope STD

– Benign : rapid ST upslope (>= 1.5 mV/sec)

– Equivocal : slow ST upslope

– STE in Q lead : uninterpretation

– Terminate test

– SBP drop > 10 with evidence of ischemia (no evidence of ischemia is relative)

– Sign of poor perfusion

– At least moderate angina

– Sustained VT

– STE > 1 mm (except aVR, aVL, V1)

– STD > 2 mm with suspected ischemia (relative)

– SBP > 250 or DBP > 115 (relative)

– Rate of perceived exertion : 1-20

– Myocardium O2 consumption = PMHR x peak SBP (double product) , normal
25000-40000
– 1 METs = resting metabolic rate (3.5 ml of O2/kg/min)

– Normal > 7 METs

– Functional class
– FC I : > 7 METs

– FC II : 5-6 METs

– FC III : 2-4 METs

– FC IV : 1 METs

– Predicted METs
– In Men : Predicted METs = 18 - (0.15 x age)

– In Women : Predicted METs = 14.7 - (0.13 x age)

– Poor prognosis
– EST induced hypotension (SBP drop > 10)

– Hypotension during recovery phase : low risk CV event

– Poor exercise capacity (< 5 METs)

– Positive EST at low work load (Bruce stage I : 3 mins)

– STD > 2 mm

– STD > 5 leads

– STD > 5 mins of recovery phase

– EST induced STEMI

– STE in aVR ไม่ใช่ high risk feature

– EST induced VT

– Duke treadmill score = exercise time (min) - (5x Max ST change) - (4x angina
index). 0 = none, 1 = non-limiting, 2 = exercise-limiting
– Predict 1 year mortality

– Low risk >= +5 : mortality 0.25%

– Intermediated risk 4 to -10 : : mortality 1.25%

– High risk =< -11 : : mortality 5.25%

– Memo : EST54 (E=exercise time, S=ST change Max, T=Trouble pain)

– Other parameters
– Failure to HR recovery : < 12 bpm after 1st min, < 22 bpm after 2 mins

– SBP recovery : 3 min SBP > 90% of peak exercise or ratio of 3 min SBP/1 min or

ratio of 3 mins/1 min SBP > 1

Predictive variables for prognosis
– Strongest : Functional capacity

– Improved prognosis value > 10 METs

– Intermediate : HR recovery, BP response, Ventricular arrhythmia, Exercise induced

angina
– Abnormal HR response increase mortality

– Weakest : ST depression

Specific condition
– EST induced LBBB
– if induced LBBB at HR > 125, CAD is unlikely

– Incidence of CAD increase when induced LBBB at lower HR

– EST induced RBBB

– Can interpretation ST segment only in inferior lead, V5-6

– EST induced PVC

– Predictive of mortality in symptomatic patient

– EST induced SVT/AF

– Not predictive of Ischemia or CV event

– AIVR post-exercise
– From increase parasympathetic tone, not related with prognosis

– EST for chronotropic incompetence (Sinus node dysfunction)

– Failure to achieve 80% of chronotropic reserve

– Expected HR reserve = 220 - age

– Target HR = baseline HR + 0.8x(Expected HR reserve - baseline HR)

– Chronotropic index = [(HRmax-HRrest)/(220-age-HRrest]

– Normal >= 80%

– On betablock >= 62%

– Chronotropic incompetence (AHA) : Not achieve 80% of PMHR

– EST for determine site of AV block

– e.g. 2l1 AV block (IIa)

– EST for diagnosis CPVT or long QT syndrome

– CPVT : sustained VT or polymorphic VT or > 10 PVCs/min

– LQTS : QTc prolongation >= 50 ms after exercise or adrenaline infusion

 – EST in WPW
– Low risk WPW : abrupt loss of pre-excitation (clear beat to beat)

– Not predict low risk WPW : gradual loss of pre-excitation

– EST in HCM
– 3 Detection : Dynamic LVOT obstruction, CAD, High risk of abnormal BP

response
– Define abnormal BP response : Failure to increase SBP at least 20 mmHg or

fall of > 20 mmHg from peak pressure

– EST in coarctation of aorta
– Hypertensive response : SBP > 230 mmHg

Report
– Protocol name : bruce or modified bruce
– Resting EKG : rhythm, ST-T change, Qw, delta wave, BBB, LVH, QT prolong?
– ระวัง 2l1 AV block in baseline bradycardia
– Stress EKG
– chest pain or dyspnea during exercise

– Horizontal/downslope ST change .... mm at lead..., at ....METs and STD increase

to 2 mm at peak
– ระวัง EST induced hypotension
– ระวัง EST induced WPW/Bundle branch block/PVC
– Recovery EKG
– Chest pain?

– ST change & return to normal within ... mins

– Other finding
– HR recovery at 1 & 3 mins

– SBP recovery at 3 mins

– Arrhythmia during exercise/recovery

– Abnormal BP response

– Interpretations
– Exercise time (mins)

– Termination due to ...

– Achieve METs, % of PMHR, Double product (Max HR x peak SBP)

– Duke treadmill score (DTS)

– Positive EST at recovery phase, ... METs, FC ..., High risk features
Cardiopulmonary exercise testing : CPET

– VO2 = CO x (A - V)O2 difference

– VO2 = O2 consumption

– AT = VO2 at RER > 1.0

– Anaerobic threshold

– RER = VCO2/VO2
– Respiratory exchange ratio

– Normal cardiac reserve : increase 50-70% of resting

Interpretation
". Maximal exercise : RER > 1.05 (ต้องเกินถึงแปลผลได้)
$. Peak oxygen consumption
– Peak VO2 =< 14 ml/kg/min (no betablock)

– Peak VO2 =< 12 ml/kg/min (on betablock)

– Peak VO2 =< 50% of age predicted if age < 50 or female

%. Right heart cath : shock with CI < 2

Stress imaging
Stress Imaging (CMR, Echo, nuclear)

General
– Normal myocardial : ใช้ energy from fatty acid, ถ้า ischemia จะเริ่มมาใช้ glucose แทน
– Beta-block or non-dihydropyridine CCB มีผลในช่วง stress
– Most specific stress imaging : vasodilator stress echo
– Most sensitive stress imaging : Vasodilator stress MRI/SPECT

Imaging technique for viability

Stress imaging : wall motion or perfusion

– Exercise test prefer more than pharmacologic test due to physiologic

– Limit in LBBB, if LBBB suggest pharmacologic test

– Pharmacologic test

– Dobutamine : contraction reserve

– Contraindication : NSTEMI/Ua < 24 hr, STEMI < 7 day, recent active

arrhythmia, severe symptomatic AS, BP > 220/120, recent pulmonary

embolism, active myocarditis/pericarditis
 – Contraindication for atropine : acute angle glucoma
– Adenosine : perfusion reserve

– Contraindication : risk for bronchospasm, bradycardia or 2nd/3rd heart

block
– Assess epicardial CAD and microvascular dysfunction

Stress echo : exercise test or pharmacologic test

– High negative predictive value

– Negative Stress echo = low risk, not mean no CAD

– Functional assessment, not anatomy assessment

– may be normal function in known stenosis

– highest spec for diagnosis CAD

– Exercise stress

– Treadmill : high workload

– Supine bicycle : low workload but good imaging

– Pharmacologic stress : Max dobutamine 40 mcq/kg/min, low dose is 20 mcq/kg/min

for viability test

– Low flow low gradient AS : Max dobutamine 20 mcq/kg/min

– 4 phase of Imaging acquire (within 1 min)

– Base, low, high, peak

– Base, low, peak, recovery

– End point : severe angina/dyspnea, severe STD, arrhythmia, High BP, Hypotension

(SBP < 10), Target HR

– Diastolic wall < 6 mm assume no viability

Response after stress in CAD

– Biphasic response is spec for viability

– Volume response in end systolic volume after stress

– Normal response decrease volume 25-30%

– Abnormal response : failure to decrease volume

– Look for intracavitary obstruction

– Hypotension during DSE : no correlate with prognosis

Phase of response
– EST : resting, peak, recovery

Concept
– Response to any phase of dobutamine : viable/normal without ischemia (eg.

Myocarditis)
– Biphasic response or decrease function : ischemia or hibernation

– Initial poor contraction

– Infarct : non response to any dose dobutamine

– Stun : no infarct/no ischemia, response to low/high dose inotrop

– Hibernation : biphasic response

– Positive stress echo

– High spec : LV dilatation > New worsening MR > New RWMA

– High spec : LV dilatation > New worsening MR > New RWMA
– High false positive (High sense) : Akinesia —> Dyskinesia, lack of hyperkinesia
Example
– Resting : good LVEF, normal wall motion

– Low dose : Increase LVEF

– Peak dose : enlargement of LV cavity, RWMA at ..., No intracavity obstruction

– Finding : Increase LVESV response to stress, impaired LV systolic function with

stress, maximum HR (> 85% of PMHR), ...METs.

– Interpretation : Positive DSE for inducible ischemia with biphasic response,

Infarction/Ischemia at LAD territory

Stress echo in VHD

– Indication : asymptomatic moderate-severe VHD, severity not matching with

symptoms
– Suggestion perform in : AS or MS > AR or MR

Asymptomatic moderate/severe AS
– Donʼt perform in asymtomatic very severe AS (mean gradient > 55mmHg)

– Positive test : hypotension or lack of rise > 20mmHg in systemic blood pressure or

ST abnormalities.
SPECT myocardial perfusion imaging (MPI) : gramma radiation
ข้อดี : ทำเร็ว, ESRD ทำได้, arrhythmia ทำได้, Device ทำได้
– Exercise test > Pharmacologic test

– LBBB prefer vasodilator test

– Vasodilator : adenosine, dipyridamole, regadenoson

Contraindication for adenosine : at least 2nd AV block, asthma

 หยุด caffeine 12 hr
– Tracers : Technetium-sestamibi & tetrofosmi (high energy : best imaging) >
thallium-201 (better for viability)
– Normal สีส้ม, perfusion defect สีม่วง
– Lung/heart ratio > 0.5 = pulmonary edema
– Viability : delayed enhance 3-4 hr จากสีม่วงเป็นส้ม
– Low cost but high radiation, ทำได้ใน ESRD
– Rest nuclear imaging : ดู viability
– Reduced sensitivity in LM or TVD

– Risk for TVD or LM : TID (>1.2), decrease SBP, Increase RV tracer uptake

Artifact
– Breast attenuation mimics ant. wall infarct

– Diaphragmatic attenuation mimics inferior wall infarct

PET MPI : positron radiation

– better accuracy but limit availability & cost

– FDG (fluorodeoxyglucose) for test viability : uptake = viable

– Concept normal myocardial used fatty acid metabolism, If ischemia will change

to glucose metabolism
Standard projection in MPI

Interpretation
– Size of defect defect

– Small < 10% of LV (1 segment)

– Medium 10-20% of LV (2-3 segments)

– Large > 20% of LV (at least 4 segments)

– Summed stress score (SSS) > 8 (moderate ischemia) correlated with sudden cardiac

death
– Summed difference score (ischemia) = Summed stress score - Summed rest score

Reading
– Rest & stress EF, TID

– Area of complete/partial reversible & fix defect (include segment 17)

– Extra-cardiac uptake, artifact

– Interpretation : coronary territory and extent of abnormal

Example
– Myocardial ischemia/infarction at LAD territory

– Rest & stress EF, TID

– Heart-Lung ratio

– Mx : Revascularization in High risk

Cardiac MRI ~ 45 mins

– Risk nephrogenic systemic fibrosis : low risk in CKD, risk 2.5-5% in ESRD
– Contraindication : aortic graft (zenith stent graft), MRI non-compatible device
(Specific condition management), Unknown source of cerebral aneurysm clip
– Device : conventional lead abandon, recent lead implantation < 6 weeks
 – Dose gadolinium
– Single dose 1 ml/kg (standard dose)

– Half dose for perfusion (dose 0.5 ml/kg)

– Viability : dose (1 ml/kg)

– Adenosine 4-6 mins

– Assess : function, perfusion, viability
– ประเมิน infarct size after ACS 7 days (stable size)
– Only pharmacologic test : stress —> rest
– Adequate vasodilator

–hemodynamic responese or splenic switch off ม้ามดำ

Adenosine 140 mcq/kg/min over 3-4 mins
Side effect : bronchospasm, chest tightness via adenosine A1 receptor
Dobutamine in contra for adenosine
Max 40 mcq/kg/min +/- atropine 0.3-0.6 mg (target HR)
– Tracer : gadolinium ไปใน interstitium, จะไม่เข้า cell ถ้า membrance ปกติ จะเข้าใน cell
เมื่อ acute infart or fibrosis
– less sensitivity in multivessel disease, limit in GFR < 30

Interpretation (signal intensity : hyper/iso/hypo)

– Myocardial dysfunction

– Stunning : normal perfusion

– Hibernate : perfusion defect in stress

– Infarct = scar

– Calcium สีดำ
– Step
– Black blood (T1): anatomy

– CINE - bright blood (CINE STEADY-STATE free precession :SSFP): function

 – CINE - bright blood (CINE STEADY-STATE free precession :SSFP): function
(global and regional function) & anatomy, bright regurgitation jet = severe
regurgitation
– Coronary artery (T2 fat suppression : suppress epicardial fat): black pericardium,
ดูได้แค่ ostial & proximal lesion, lipomatous hyperthrophy
– Perfusion : ischemia(submural or transmural)
– Early enhancement (T1-weighted Fast Spin Echo): ดู hyperemia in myocarditis
(เลือดดำ, myocardium ขาว), abnormal >= 4
– Delay enhancement (ภาพนิ่ง, น้ำเทา, scar ขาว) : scar (transmural or submural),
May false positive in acute MI
– Concept : scar increase volume of distribution and delayed wash-in & wash-

out
– เจอขาวดำขาว ก็ scar ดำ คือ core infarct or hemorrhage
– thrombus : ดำ
– Enhance in pericarditis

– T2-weighted image (black blood, gray myocardium) : myocardial edema (water

in cell) —> increase signal intensity
– Long TI study (white blood, gray myocardium) : thrombus (black), Myocardium
(gray)
– Velocity-encoded technique : ดู flow
– T2* for detect iron load

– Clinical important iron loading < 20 ms

– Severe cardiac iron loading < 10 ms

– Transmural scar > 50%, subendocardardial scar < 50%

– Ischemic beyond scar : นับเป็น segment ถ้า transmural ischemia and submural scar ก็
ไม่ถือว่ามี ischemic beyond scar
– Key ในข้อสอบ อย่าลืมดู MVO (resolve 4-6 wks), RV infarction, Myocardial edema,
Thrombus, Pericarditis
Scar pattern
– HCM : RV insertion scar or patch infiltration
– Myocarditis
– Increase myocardial signal intensity in T2-weighted (Myocardial edema)

– Increase global myocardial early gadolinium in T1-weight (Hyperemia)

– Late gadolinium enhancement (mid wall scar) finding 40%

– Eosinophilic myocarditis : scar pattern involved subendocardial

– Amyloid scar pattern : found 80%
– ICM scar pattern : found 100%
MRI : prefer in evaluated Rt side valve, useful for quantify reguritation, LV volume/
function
Limitation MRI
– AS : underestimate velocity by MRI if Vmax > 4 m/s
– Estimation regurgitation by eyeball is pitfalls

Reading CMR for ischemia

– Aorta (R/O dissection) and PA size (R/O thrombus)
– Pericardial & pleural effusion, extracardiac mass, lung infiltration
– Global & regional LV function & RV function
– LV/RV thickness, LA/RA dilatation, IAS thickness

– Thrombus at LV/LA and RV/RA

– Perfusion defect at ...
– Myocardial scar pattern : LV, RV, Atrium and MVO
– Pericardial effusion and enhancement in late gadolinium
– Dx : Positive CME with ischemic beyond scar at LAD territory
 Syncope
& Tilt table test
Syncope and Tilt table test

Syncope
– Syncope = TLOC due to cerebral hypoperfusion
– TLOC = transient (< 5 mins), unresponsive (no response to speech/touch/pain),
unaware (loss of memory) and uncontrolled (fall, abnormal movement)
– Sudden cessation of cerebral blood flow 6-8 sec

– Systolic BP 50-60 mmHg at heart level = 30-45 mmHg at brain in upright

position
– Myoclonus must < 10 sec, irregular in amplitude, asynchronous, asymmetrical

– Neurogenic cause : vertebrobasilar TIA, Epileptic seizure

Syncope vs Seizure
 – Orthostatic reflex syncope
– Postpradial hypotension : SBP drop >= 20 mmHg in supine/sitting within 2

hr after meal
– Carotid sinus syndrome : require spontaneous symptoms + Positive CCS

– Carotid sinus massage : positive test if pause > 3 sec, bradycardia or

hypotension (SBP drop > 50 mmHg), risk stroke/TIA 0.25%

– Caution but not contraindication : previous TIA/stroke, carotid stenosis

– Carotid sinus hypersensitivity : positive carotid sinus massage without

spontaneous symptoms
– Cardiac syncope : no prodrome, supine position
– Structural : excertional syncope in severe AS/HOCM, cardiomyopathy,

obstructive cause (tamponade, myxoma, PE)

– Arrhythmia (syncope in supine) : VT/VF, family HX of SCD, Sinus pause

– Define : asystole >= 3 sec, VT, SVT > 160 bpm for > 32 beats

– No prodrome or prodrome < 5 sec

– Tachyarrhythmia : SVT, VT, VF

– Brandyarrhythmia : Sinus node, AV node

Suggestive clinical features : type of syncope
Indication for carotid sinus massage
– Age > 40 years with syncope of unknown origin compatible with reflex mechanism

Carotid sinus massage

– risk stroke 0.24%, careful in prior stroke/TIA or known carotid stenosis

– ใช้สามนิ้วนวดขึ้น/ลงทั้งซ้ายและขวาในท่านอนและนั่ง ครั้งละ 10 sec

Indication for EST
Must exclude abnormal EKG & structural heart
– Syncope during exercise

– Exercise induced AV block

– Benign tachyarrhythmias (Outflow tract VT, Fascicular VT)

– Malignant ventricular tachyarrthymias (long QT syndrome type I, CPVT)

– Atypical vasovagal syncope

Tilt table test

– No class I indication in syncope
– To evaluation of syncope : History & PE & EKG
– if absence of cardiac cause, good prognosis

– Reproduction of reflex syncope

– Vasodepressor, mixed syncope and orthostatic syncope : benign nature

– Mx : avoidance of trigger, increase fluid intake, physical counter-

pressure maneuvers (handgrip, arm-tensing, leg-crossing, tilt training.

– Indication : สรุปทำในกรณีไม่แน่ใจ
– Considered in patients with suspected reflex syncope, orthostatic hypotension,

postural orthostatic tachycardia syndrome, or psychogenic pseudosyncope (IIa)

– Recurrent syncope that suspected reflex syncope

– ใช้แยกจาก orthostatic hypotension, falls, jerking, epilepsy

 – ใช้แยกจาก orthostatic hypotension, falls, jerking, epilepsy
– Single unexplained syncope in high risk setting

– Not recommend to assess treatment (III)

Positive rate tilt table test

– Vasovagal syncope ~ 3/4

– Cardiac syncope ~ 1/2

– Protocol : tilting to 70 degree

– Unmedicated phase 20 mins

– Medication phase 20 mins : 300-400 mcq SL NTG

– Additional Standing phase 20 mins

– Positive test : loss of consciousness/po stural tone + hypotension/bradycardia

– Orthostatic hypotension : fall SBP >= 20 (30 in supine HT) or DBP >= 10 mmHg
or SBP < 90 with symptoms
– All type reflex syncope : BP drop and follow with HR drop in all case
– HR < 40 more than 10 sec : cardioinhibitory

– SBP < 60 mmHg with HR drop < 10% : vasodepressor

Table for Ddx type of reflex syncope & orthostatic syncope
– Orthostatic hypotension

– Initial OH < 30 sec : Young asthenic (ผอมสูง), old, drug induced

– Classic OH
– Delay OH (neurogenic OH), onset 3-30 mins : Old, autonomic failure, drug
induced
– Key แยกจาก reflex syncope ตรงที่ HR ต้องเร็วขึ้น
– POTS : HR > 30 bpm or HR > 120 bpm within 10 mins after standing, symptoms

syncope is rare
– Vasodepressor type : common in age > 60
– Cardioinhibitory or Mix type : common in age =< 60
Adenosine sensitive syncope
– Low adenosine level —> sensitive to adenosine

– Presented with syncope without prodrome : asystolic pause (paroxysmal AV block)

– Test : Adenosine 5-triphosphate (ATP) test, ATP 20 mg and then asystole > 6 sec or

AV block >= 10 sec —> pacemaker

– Treatment : Try theophylline (block adenosine receptor) +/- pacemaker

Treatment
Vasovagal syncope
Drug for vagovagal syncope (after failure salt/fluid intake & maneuvers & recurrent)
– Midodrine (IIa) : alpha agonist (vasocontrictor)

– Fludrocortisone, SSRI, orthostatic training, DDD pacemaker (all is IIb)

– Fludocortisone (0.1 mg), start 0.1 mg/day and increase 0.2 mg/day in 14 days

– SSRI (Fluoxetine) in vasovagal syncope with anxiety sensitivity

– Betablock in vasovagal syncope

– ESC is class III

– AHA is class IIb in age >= 42

Maneuvers (only in long prodrome)

– Arm tensing

– Leg crossing

– Squating

– Tile training (home): ยืนห่างจากกำแพงแล้วหลังพิงกำแพง, start 2-5 min upto 30min bid
Orthostatic hypotension
– First step

– Adequate hydration/salt

– Acute water ingestion (> 240-480 ml in 5 mins) : gastric distention

increasing sympathetic activity

– Reduce vasoactive drug (not stop)

Advice : โรคไม่อันตราย แต่ระวังศีรษะกระแทกพื้น แนะนำกินน้ำ 2-3 L per days และกินเกลือ

10 gm per day ถ้ามีอาการให้นั่งหรือนอน และทำ counter maneuver ถ้ายังมีอาการค่อย
พิจารณายา
– Second step (if symptoms persist)
– Drug (IIa) : Midodrine (alpha agonist), Fludrocortisone

– Mechanical treatment (IIa) : Counter-pressure maneuvers, Compression

garments, Head-up tilt sleeping (> 10 degree)

 – Drug specific in orthostatic hypotension
– Droxidopa in neurogenic OH due to Parkinson disease (IIa)

– Pyridostigmine in refractory neurogenic OH (IIb)

– Octretide in refractory neurogenic or postprandial OH (IIb)

Indication for pacing

– Carotid sinus syndrome : cardioinhibitory or mixed (IIa)

– Recurrent vasovagal syncope & age > 40 & pause 3 s with symptoms or 6 s (AHA

IIb, ESC IIa)

Expected 2 year syncope recurrence rate without cardiac pacing
– Hypotension

– Suspected bradycardia : > 25% recurrent rate

– Established bradycardia : 2-25% recurrent rate

– No hypotension

– Established bradycardia : =< 5% recurrent rate

Indication for implantable loop recorder (IRL) ใส่กรณีไม่แน่ใจ

– High risk and unexplained syncope after comprehensive evaluation (I)

– Early evaluation in recurrent syncope (I)

: Type of loop recorder - External 2-4 weeks - Implantable 1-3 years

Holter monitoring
Holter monitoring

Concept

General
– Palpitation symptoms :

– 1st time Holter diagnosis rate 16%

– 2 times Holter diagnosis rate rate 25%

– Lead V1 & V5 is same as 12 lead EKG

– non of definitions based on axis are true in Holter

– Holter detect only QRS complex

Type of monitoring
– Holter monitoring
– Enough symptoms to detect within 24-72 hr (2 days)

– External patch recorder (patient activated or auto trigger) : only one lead
– Record duration 2-14 days (2 weeks)
 – External loop recorder (patient activated or auto trigger)
– Symptoms likely to recurrent within =< 4 weeks

– Event monitoring
– Capacitating symptoms within 2-6 wks

– Implantable loop recorder : suggest in infrequent symptoms > 30 days, duration 2-3
years, invasive and high cost

Scan mode
– Page : View ECG one page at a time

– Quickscan : Scaning mode เครื่องหยุดเวลาที่สงสัย

– Retro : analyses with no operator intervnetion มักจะพลาดในกลุ่ม arrthythmia ที่ rate
เปลี่ยนเล็กน้อย
– SI : superimposes (overlays) individual beats with addditional beast to form an image
and stops at each pre-set Auto Stop.

Default role
– กรณี AF สามารถปรับ duration for diagnosis ได้ สามารถใช้ exclude PAC ที่มาบ่อยๆได้
– Supraventricular beat จาก holter รวม PAC & escaped beats
– Late : relative pause (good with high heart rate)
– Drop : absolute pause (good with low heart rate)

Quantitative measurment
– Sporadic

– Rare (1-4 extrasystolies/hr, < 100/days)

– Frequent (4-40 ext rasystolies/hr, 100-10000/days)

– Numerous (40-140 extrasystolies/hr, 100-10000/days)

– Very numerous (> 400 extrasystolies/hr, > 10000/days)

Differential
Differential SVT
– Sinus tachycardia : gradual onset & termination

– AVNRT : start with PAC and PR prolongation

Differential pause
– Sinus pause or SA exit block

– AV block

– Post premature compensatory pause

Description
– PVC : number, morphology, daily variation

Basic reading
– Basic rhythm : sinus rhythm/AF/pace rhythm (ApVs, AsVp)
 – A & V rate
– QRS complex : narrow or wide QRS (BBB, Delta wave)

– Premature beats (PAC, PVC, PJC)

– Premature wide QRS : PVC, intermittent WPW, PAC with abberrency

– Tachyarrhythmia (AT, A flutter, AF, SVT, VT)

– Timing, Rate, Initiation & Termination

– Bradyarrhythmia (AV block, SSS : SA exit block)

– Timing, rate (A & V rate), regular/irregular, Pause (AF off set pause, pause during

AF)
– ST change, QT interval
– Other finding
– Diagnosis
– Managment

Example

Quiz
Artifact
Case vasovagal syncope (mix type) on DDD (rate 40-120), drop rate 40 bpm, drop size
10 bpm and window 25 sec, Intervention 70 bpm
– A-lead undersening

– Crosstalk with ventricular safety pacing

– Pseudofusion of V-pacing

Management
– check A-lead (R/O A-lead ตกลง Ventricle) and adjust sensing A-lead
– Prolong PVARP for crosstalk
– Prolong AV delay for correct pseudofusion of V-pacing
AVNRT : Start with PAC conduct to slow pathway and retrograde to fast pathway (AV
node reentry). Terminate with P wave exclude AT

AF with intermittent complete heart block

Baseline sinus rhythm with frequent PAC
PAC initiated AF with upper rate behavior pacemaker rate (DDD) and then change to
non-tracking mode (AF)

S-AICD : AF with asthman phenomenon —> ATP —> defibrillation —> convert to sinus
rhythm
Stable coronary
artery disease
Stable CAD

SCAD : stable remain at least 60 days

General
– Pathogenesis of Atherosclerosis : Immunologic mechanism or lipoprotein

mediation
– Typical atherosclerosis : eccentric lesion, lipid deposition, focal distribution

– Graft arteriosclerosis : concentric lesion, no lipid core, diffuse distribution

– Multi-vessel disease : at least 2 vessel disease

Non obstructive CAD

: define by angiogram, stenosis >= 20% but < 70% (LM < 50%)
: define by CTA, stenosis 1-49%
Non apparent CAD : stenosis < 20% from angiogram

Symptoms by CCS & NYHC

Ischemic cascade
– Ischemia - diastole - systole - ekg - angina
Associated other vascular disease

CAD may with/without IHD

Echo ทุกคน
W. Suitable of revascularization : comorbidity & QoL
Y. LVEF < 50%
– Typical angina : CAG

– Atypical angina : stress imaging

Z. Pretest probability
– Men ไม่มีทาง PTP < 15%
– Women ไม่มีทางที่ PTP > 85%
– Men > 70 + typical angina = Yes SCAD

– Women < 60 + non angina = No SCAD

– Women < 50 + atypical angina = No SCAD

ESC : CAD consortium basic

ACC : The diamond forrester
 – Low PTP < 15% : no further test
– Intermediate PTP

– Intermediate low 15-65% : EST

– Intermediate high 65-85% : stress imaging

– High PTP > 85% = Stable CAD : risk stratification

High risk noninvasive test : EF < 35%, perfusion abnormal >= 10% (>= 2/16), High risk
EST, stress induced LV dysfunction/dilatation, Stress induced RWMA >= 3 segment, High
CAC score > 400, CCTA showed TVD or LM
Overall treatment
Goal : prevent death/MI (ASA, statin, ACEI/ARB), improved QoL (Beta-block)
First-line drug for symptom : Short-acting nitrate plus beta-block or CCB
Drug and dose
– CCB (DHP or Non-DHP)
– Verapamil

– Oral sustained release (Isoptin 240 mg, แบ่งครึ่งได้) : 240-480 mg/day. if 480
mg/day, suggest 240 mg bid
– Diltiazem HCL (Herbesser 100, 200 mg) : start 100 mg OD (max 400 mg/day)
แบ่งครึ่งไม่ได้
– Nondihydropyridine CCB : not recommend combine with beta-block

– Ivabradine (Coralan 5 mg) : start 2.5 mg bid, Adjust q 2 wks (Max 7.5 mg bid)
– Side effect : Visual disturbances, Headache/Dizziness,

– Beware : severe renal dusfunction, age > 75, not used with verapamil/

diltiazem
– Monolin SR (20, 60 mg)
– 20 mg bid (immediated release)

– 60 mg OD (Extended release), Max 240 mg OD

– Inhibition of fatty acid oxidation (to glucose oxidation) : not suggest combine in same
group of action
– Ranolazine (375, 500, 750 mg) : start 375 mg bid, adjust q 2-4 wks (Max 750

mg bid)
– Side effect : QT prolong, Dizziness, Constipation, neusea

– Contraindication : cirrhosis

– Trimetazidine (35 mg modifed release) : Fix dose 35 mg bid

– Side effect : GI dicomfort, movement disorder, neusea, headache

– Contraindication : movement disorder, GFR < 30

– Allopurinol for anti-ischemic effect 600 mg per days

Intervention & mortality
Reduction of mortality
– 40% in smoking cessation (most cost effectiveness & powerful)

– 25% in statin/beta-block/ACEI

– 15% in ASA

Anti-thrombosis drug
– SCAD : Prasugrel or ticagrelor may consider in high risk elective PCI (Hx of stent
thrombosis, LM stent), (IIb,C)
Management
– Influenza vaccine (I,B)
– Beta-block for symptoms & mortality benefit
– CCB (DHP or Non-DHP)

Stress Imaging in ICM for evaluated viability (IIb, ESC)

Time for revascularization

– High risk (CCS III, LM/TVD/pLAD, LV dysfunction) : within 2 weeks
– Other risk : within 6 weeks

Revascularization
Significant CAD : LM >= 50%, Non-LM >= 70%, FFR =< 0.8, iFR =< 0.89
– Mortality risk < 0.5%

– Goal is complete revascularization

– Revascularization for mortality benefit

– LM

– Proximal LAD

– LV dysfunction with DVD/TVD

– Large area of ischemia (>10%) or FFR < 0.75

– Single remaining vessel

– For symptomatic relief : CCS III-IV

Improved survival after revascularization compare with medication

 – LM (Prefer CABG > PCI)
– PCI when anatomy is suitable, SYNTAX < 33, High STS >= 5%

– TVD : prefer CABG > PCI

– PCI when TVD in non-DM with SYNTAX =< 22

– Proximal LAD with SVD/DVD : CABG = PCI

– LV dysfunction (EF < 35%) :

– TVD : CABG

– SVD or DVD : PCI > CABG

– Ischemia mediated VT : CABG = PCI

– Area of ischemia >= 10%

SVD or DVD (without pLAD) : Prefer PCI > CABG

PCI vs CABG
– Evaluated Clinical condition & Coronary anatomy
– Overall operative mortality for CABG 4%
– CABG (Class I) All in most, EF 35% (I) except : One/Two vessel without pLAD (IIb,
ESC)
– PCI (ESC)
– Class I : All one/two vesse disease, LM/TVD in non-DM with SYNTAX =< 22

– Class IIa : LM with SYNTAX 23-32, EF =< 35%

– Class IIb : TVD in DM with SYNTAX =< 22

– Class III : LM with SYNTAX >= 33, TVD in DM with SYNTAX > 22
Indication : LV aneurysmectomy during CABG
– NYHA class III-IV

– Large LV aneurysm

– Large thrombus formation

– Aneurysm is origin of arrhythmia

Vulnerable plaque
Reassessment
– New or recurrent symptoms (I)
– Asymptomatic : Reassess for prognosis after expiration of valid period of test (IIb)
– Non-invasive imaging surveillance in high risk patients 6 months after

revascularization (IIb)
– Re-looked CAG at 3-12 months after high risk PCI (unprotected LM). (IIb)

– EST at least 2 years after last test (IIb)

– Routine non-invasive imaging stress test may consider 1 year after PCI and 5

years after CABG (IIb)

SCAD trial
CABG vs Medication
: CASS : EF > 35%, CCS I-II
: STICH : EF < 35%,
Exclude LM , CCS III-IV
: improved HF
= No all mortality benefit at 5 year (benefit offset by surgical death)
but 10 years decrease mortality in STICH trial

PCI vs medication
: COURAGE
exclude EF < 30%, severe ischemia
: FAME2 (FFR)
= No all mortality benefit, Improvement symptom, Decrease urgent revascularization

PCI vs CABG
: BARI (multiple CAD)
POBA vs CABG
= No all mortality benefit, trend in DM. Decrease revasculaization in CABG
: SYNTAX (multiple CAD or LM),
Score =< 22, 22-33, >= 33
LM >= 33 : CABG,TVD > 22 : CABG
: FREEDOM : (DM with multiple CAD, Exclude LM) : Decrease mortality & MI (not depend
on SYNTAX)
: EXCEL (Everolimus stent): (only LM, Exclude SYNTAX > 33) : non inferior for MACE

Summary
: PCI vs Medication : Decrease revascularization and symptoms
: CABG > PCI : DM, Complex CAD

ORBITA trial
– Population : SCAD with SVD, exclude CTO, LM

– Most CCS II-III, 90% normal LVEF

– Intervention : PCI vs sham intervention

– Outcome : no improved exercise time at 6 weeks

LEADERS FREE trial

– Population : High risk bleeding undergo PCI

– STEMI 5%, NSTEMI/UA 35%, SCAD 60%

– Bleeding risk >= 15%

– Intervention : DCS vs BMS

– DCS (BioFreedom stent) : A polymer-free and carrier-free drug-coated stent

(umirolimus)
– Outcome : Decrease primary outcome (Death, MI, stent thrombosis) : RRR 27%,

driving by MI
COMPASS
– Population : High risk SCAD (65 up or < 65 with 2 risk) or PAD

– Exclude : hemorrhagic stroke, ischemia stroke within 1 month, Need DAPT or

OAC
– Intervention 3 arms : ASA 100 mg vs Rivaroxaban 5 mg bid vs Rivaroxaban 2.5 mg

bid with ASA 100 mg

– Outcome : 3MACE decrease (best in ASA with rivaroxaban) NNT 76, Increase major

bleeding but same fatal bleeding

NSTEMI/UA
NSTEMI/UA

General
NSTEMI
– การให้ trombolytic ทำให้เกิด plaque bleeding turn to STEMI ได้
ACS with normal EKG 5%
MI = Trop-T rise/fall + evidence of ischemia (clinical, EKG, Echo, CMR, CAG, patho)
Myocardial injury = Trop-T > 99 percentile
– Acute : Rise/Fall Trop-T

– Without evidence of ischemia eg. HF, myocarditis

– Chronic : stable (variation =< 20%) in CKD or structural heart

– Recurrent MI : > 28 days after MI

– Reinfarction : =< 28 days after MI

Universal definition of MI
– Myocardial injury (Troponin > 99% of UNL)
– Acute : Troponin change > 20%

– Chronic : Troponin change <= 20%

– Sign of acute ischemia

– Symptom of myocardial ischemia

– Ischemia from EKG (ST/T change, New pathologic Qw)

– Imaging evidence (wall motion, viability)

– Coronary thrombus or autopsy

– Subtype
– Type 1 : Plaque rupture or autopsy coronary thrombus

– Type 3 : cardiac death with symptoms suggestive of MI (Ischemia by EKG, VF,

Troponin)
– Type 4A : Post PCI, compatible with MI definition plus troponin > 5 times of URL

in patient with normal baseline

– Type 4B : stent thrombosis same as type 1

– Type 4C : Restenosis

– Type 5 : Post CABG, compatible with MI definition (EKG define only new Qw)

plus troponin > 10 times of URL in patient with normal baseline

Symptoms
– Pain : pressure, squeezing, burning sensation
– Radiation : left or right arm/Rt shoulder (LR 2.5), both arm (LR 7.1)
– N/V (LR 1.9)
– Diaphoresis (LR 2.0)

Timing for Troponin

Chest pain
– Low probability for ACS

– Pain > 6 hr with initial negative troponin

– Pain < 6 hr without rising/falling troponin (Interval 3 hr)

– 1 hr algorithm for R/O ACS

– Pain > 3 hr and initial troponin < 5 ng/dL

– Pain < 3 hr and initial troponin < 12 ng/dl

 – Delta change troponin 0-1 hr < 3 ng/dL

Definition of unstable angina

– Angina or equivalent at rest or minimal exertion, lasting > 10 mins

– Severe and new onset (within prior 4-6 wks)

– Crescendo pattern
Braunwald classification for UA

Symptoms
– Pain : pressure, squeezing, burning sensation

– Radiation : left or right arm/Rt shoulder (LR 2.5), both arm (LR 7.1)

– N/V (LR 1.9)

– Diaphoresis (LR 2.0)

EKG : STD >= 0.5 mm in >=2 cont lead. (STD from J0-J80 msec below isoelectric
segment)

Wellens syndrome
– Clinical : recent history of angina with present free pain

– Type A : Biphasic, with initial positivity & terminal negativity (25% of cases)

– Type B : Deeply and symmetrically inverted (75% of cases)

Pseudo-wellens syndrome
– Hypokalemia (U wave)

– LVH

– Early repolarization

Grace risk score 2.0

– Estimates mortality at 6 months
 – Grace > 140 (High risk) : PCI within 24 hr
– Grace 110-140 (Intermediate risk) : PCI < 72 hr

– Score calculation : Age, HR, SBP, Cr, ST change, Abnormal cardiac enzyme, Killip
class, Cardiac arrest?
TIMI risk
– Estimates composite of Death/MI/Urgent revascularization at 14 days
– TIMI 0-1 (low risk) : non invasive test
– Score calculation
– Age >= 65

– >= CAD risk (DM, HT, DLP, Current smoker, Family of CAD)

– ASA within 7 days

– Severe angina >= 2 episode in 24 hr

– ST change >= 0.5 mm

– Positive cardiac marker

– Know coronary stenosis > 50%

Risk criteria & Timing for invasive strategy

– Very high risk < 2 hr (immediate invasive)

– : Intermittent STE, acute HF

– High risk < 24 hr (early invasive)

– : TropT rise/fall, GRACE > 140, Dynamic change EKG

– Intermediate-risk < 72 hr (invasive)

– : LV dysfunction or CHF

– Low risk : non invasive or invasive test

– Low risk grace =< 109 with non DM and GFR > 60 and good EF, no previous

revascularization

Anticoagulant
– On fondaparinux undergoing PCI : 70-85 IU/kg of UFH single bolus (50-60 IU/kg in
concomitant with GPIIb/IIa inhibitors
– On warfarin : wait for INR < 2.5 start LMWH or haparin
– UFH : Initial bolus of 60 units/kg (maximum: 4,000 units) then 12 units/kg/hour
 (maximum: 1,000 units/hour) as continuous infusion.
– Target aPTT of 1.5 to 2 times control (approximately 50 to 70 seconds)

– On enoxaparin and go on PCI

– At least 2 dose & Last dose enoxaparin < 8 hr : no add heparin

– Received only one dose or Last dose enoxaparin 8-12 hr : add enoxaparin 0.3

mg/kg IV or half dose heparin

– Last dose enoxaparin > 12 hr : full dose heparin or Enoxaparin 0.5 mg/kg IV

Specific group
– Sign of acute cocaine or methamphetamine intoxication with NSTEMI
– Treatment : Benzodiazepines, avoid beta-block
STEMI
STEMI

Term
– Metalloroteinases are associated with expansion and remodeling of ventricular after
MI
– Infarct expansion : after infarct เกิด LV dilatation
– Infarct extension : necrosis tissue progression ในแนวลึกและกว้าง

General
– STEMI : 15% spontaneous reperfusion
– Transient STEMI : re-infarction 5%
– Same outcome : immediate PCI vs Delayed PCI (in 24-48 hr)

– Cause of coronary thrombosis

– Plaque rupture 60-70% : interruption of a thin fibrous cap overlying a lipid rich

core.
– Plaque erosion (+thrombosis ontop), risk factor : Female, DM, smoking

– Pathogenesis : absent or disrupted endothelium overlying a plaque that is

characterized by greater proliferation of smooth muscle and by the

presence of abundant proteoglycans.
– Calcified nodule : female, old age, calcification

– Recurrent ~ 4% per year

– Keep HCT >= 25% or Hb >= 7 (IIb)
Pitfall EKG in STEMI
– Posterior wall STEMI

– Lateral wall STEMI

– Hyperacute T

Mortality rate without reperfusion

– Inferior wall : 8%

– Anterior wall : 16%

– Acquire BBB : 24%

EKG evolution in STEMI

– Not found short QT in STEMI EKG

ESC
– chest pain, must EKG within 10 mins
– Time zero at Dx STEMI, time to PCI = time to wire cross lesion
– Strategy : If PCI available within 120 min -> Primary PCI, if not -> thrombolytic
– Quality

– Walk in at PCI center : PCI within 60 mins

– Walk in at non PCI center : PCI within 90 mins

– Onset chest pain 12-48 hr

– On going symptoms (angina, unstable V/S, life threatening arrhythmia) -> PCI

(Ic)
– No symptoms -> PCI (IIa)

– Onset > 48 hr, PCI is harm

– Cardiogenic shock : routine revascularization of non-IRA lesion is harm (III)
– Re-perfusion stregedy decrease post MI pericarditis
Fibrinolytic
– Prefer fibrin specific agent : Tenecteplase (TNK), alteplase, reteplase
– Compare with SK : no anaphylaxis, same ICH but less major bleeding, less death

– Effective SK ~ 50% reperfusion, ICH < 1%

– Fibrinolytic : decrease mortality absolute risk 2%, relative risk 20%

– STEMI onset after 12 hr : no role fibrinolytic

– Post SK follow with fondaparinux after 24 hr

– Post reperfusion with TNK follow with stat enoxaparin IV and then sc

Dose fibrinolytic
– Streptokinase dose 1.5 mU IV drip in 1 hr with 10% loading

– Lowest intracranial hemorrhage

– Regimen Accelerate regimen 1.5 mU in 20 min vs standard regimen 1.5 U in 60

min : Accelerate regimen higher rate reperfusion 75% vs 50%

– Complication if hypotension Ddx : anaphylaxis (may be add methyprednisolone

100-200 mg before SK), acute bleeding, SK induced hypotension (activate

plasmin & bradykinin —> vasodilate)
– Tenecteplase (TNK)

– Most fibrin specific

– Half dose in age >= 75 years

– Single IV bolus base on weight (Dose = BW/2)

– < 60 kg : 30 mg

– 60-69 kg : 35 mg

– 70-79 kg : 40

– 80-89 kg : 45 mg

– > 90 kg : 50 mg

– Alteplase (tPA)

– Shortest half-life

– 15 mg IV bolus and then 0.75 mg/kg (max 50 mg) IV drip in 30 mins and then 0.5

mg/kg (max 35) IV drip in 60 mins

– Reteplase (rPA)

– 10 unit IV bolus and 10 unit IV bolus next 30 mins

Contraindication for fibrinolytic

– Not recommend in pregnancy

– Not recommend SK in recent SK within 6 months

Management life threatening bleeding after thrombolysis
No specific treatment
– 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

– Heparin neutralization dose : 1-1.5 mg per 100 USP units of heparin (max 50 mg)

– Platelets transfusion

Antiplatelet
For thrombolytic drug
– Dose Clopidogrel with thrombolytic drug

– If age >= 75 : clopidogrel only 75 mg stat

– If age < 75 : clopidogrel load 300 mg

– Recuse PCI without loading dose (age >= 75)

– Time =< 24 hr : Clopidogrel 300 mg loading

– Time > 24 hr

– Clopidogrel 600 mg loading (I)

– Prasugrel 60 mg loading (IIa)

– > 24 hr after fibrin-specific agent

 – > 48 hr after non-fibrin-specific agent
– No other P2Y12 with thrombolytic drug

For PCI
– Aspirin : loading 150–300 mg chewed or 75–250 mg intravenous (not already on an

aspirin maintenance dose).

– Ticagrelor (90 mg) : 2 tab loading and then 1 tab po bid pc

– Contraindication in Hx of hemorrhagic stroke

– Clopidogrel (75 mg, 300 mg) : 600 mg loading and then 75 mg po OD pc

– New loading Clopidogrel before PCI in previous Clopidogrel used (IIb)

– Prasugrel (10 mg) : loading 60 mg and then 10 mg PO OD pc (maintenance 5 mg in

BW < 60 kg)
– Contraindication : Hx of any stroke/TIA, pathologic bleeding, BW < 60, Age >=

75
– Cangrelor (IV P2Y12i) : used in P2Y12i naive undergoing PCI.

– Dose : Bolus of 30 mg/kg i.v. followed by 4 mg/kg/min infusion for at least 2 h or

duration of procedure, whichever is longer.

Glycoprotein IIb/IIIa antagonists : used only for bail-out. (IIa)
– Abciximab (Low specific but High affinity to receptor) : Bolus of 0.25 mg/kg i.v. and

0.125 mcg/kg/min infusion (maximum 10 mcg/min) for 12 h.

– Eptifibatide (High specific but low affinity to receptor) : Double bolus of 180 mcg/kg

i.v. (given at a 10 min interval) followed by an infusion of 2.0 lg/kg/min for up to 18 h.

(Not recommend GFR < 30)
– Tirofiban : Bolus of 25 lg/kg over 3 min i.v., followed by an infusion of 0.15 mcg/kg/

min for up to 18 h.

PCI
– STEMI within 12-48 hr
– Symptomatic : Primary PCI (I, level C)

– Asymptomatic : Primary PCI (IIa, level B)

– Defer stent in High thrombus

– Complete revascularization during admission : stage PCI 48 hr after culprit lesion

Anticoagulant
Primary PCI
– Routine used UFH in all case (Ic) : mostly dose 70 IU/kg

– Dose 70-100 IU/kg without GP IIb/IIIa inhibitor planned

– Dose 50-70 IU/kg with GP IIb/IIIa inhibitor

– Enoxparin IV (IIa) : dose 0.5 mg/kg

– Bivalirudin (IIa) : direct thrombin inhibitor, used in case of heparin induced

thrombocytopenia
– Dose : 0.75 mg/kg i.v. bolus followed by i.v. infusion of 1.75 mg/kg/h for up to 4 h

– Fondaparinux is harm
After fibrinolytic
Post fibrin specific agent
– Age < 75 : enoxaparin 30 mg IV bolus and then 1 mg/kg (max 100mg) sc q 12 hr, Max

8 days
– Age >= 75 : No enoxaparin IV bolus, 0.75 mg/kg sc (max 75 mg) for first 2 dose.

– eGFR < 30 : enoxaparin 1 mg/kg sc q 24 hr

Post SK follow fondaparinux next 24 hr

– fondaparinux 2.5 mg IV bolus and then 2.5 mg sc OD, max 8 days

UFH : 60 IU IV bolus (Max 4000 IU) and then drip 12 IU/kg/hr (Max 1000 IU)
– Target aPTT 50-70 s or 1.5-2.0 times

Other drug
– Morphine for HF and dyspnea (IIb)
– PPI in only high risk GI bleeding
– Beta-block (add during hospitalization) : EF < 40% (I), Preserve EF (IIa)
– IV beta block in SBP > 120 (IIa)

– Avoid beta-block post STEMI (Increase risk cardiogenic shock): SBP < 120, HR >

110 or < 60
– High intensity statin in all case (LDL < 70 or decrease 50%)
– ACEI (add as soon as possible)
– Reduced EF, DM, Anterior wall infarct (I)

– Routine used (IIa)

– MRA add after BB & ACEI in EF < 40% without renal failure or hypokalemia

Investigation
– CTA in STEMI (III, level C)

Hospital discharge
– early D/C 48-72 hr in low risk patient (Age < 70, EF > 45%, One or two vessel,
successful PCI and no persistence arrhythmias)

MINOCA (Myocardial infarction with non-obstructive coronary arteries)

STEMI setting : MI in non atherosclerosis epicardial coronary
– Diagnosis consist of 3 criteria

– Universal AMI criteria

– Non obstructive epicardial coronary artery (< 50%)

– No clinically overt specific cause

– MINOCA : myocarditis, coronary spasm, coronary emboli, microvascular dysfunction,

Takotsubo, PE
Coronary microvascular dysfunction
SCAD setting
– Symptoms & objective evidence of myocardial ischemia with absence of obstructive

CAD plus evidence of impaired coronary microvascular function

– Evidence of impaired coronary microvascular function

– Impaired coronary flow reserve (<2.5)

– Ischemic ECG changes but no epicardial spasm during acetylcholine testing

– Abnormal coronary microvascular resistance indices, eg, index of

microcirculatory resistance >25.

– Coronary slow flow phenomenon: TIMI frame count >25

Complication
Rupture free wall
– Incident 2.5-5%, mortality 15%

– Acute < 48 hr, Late >= 48 hr (common within 2 weeks)

– Echo in concealed ruptured free wall : disrupt LV free wall with pericardial wall-off
 and color Doppler flow thought ruptured site +/- forming pseudoaneurysm,
coagulum at pericardium with RA/RV collapsed along cardiac cycle.
Aneurysm
– Pseudoaneurysm

– Narrow base

– Wall composed of thrombus & pericardium

– High risk rupture

– True aneurysm

– Wide base

– Wall composed of myocardium

– Low risk rupture

Papillary muscle rupture

: common is posteromedial PM due to single blood supply
– Posterior-medial PM : supplied by PDA

– Anterior-lateral PM : supplied by DG and LCx

Syndrome
Kounis syndrome (Allergic angina/MI)
– Type I : vasospasm

– Type II : culprit lesion with pre-existing CAD

– Type III : coronary thrombosis (eosinophils and mast cell)

Clinical trial
ISIS-2
– Population : STEMI

– Intervention : Placebo vs ASA vs SK vs ASA plus SK

– Outcome of mortality

– Placebo : 13%

– ASA = SK : 10.5%

– ASA plus SK : 8%

COMMIT trial
– Population : STEMI without PCI

– Intervention : Placebo vs Clopidogrel

– Outcome : Decrease mortality, RRR 7%

CULPRIT-SHOCK
– Population : STEMI with cardiogenic shock

– Intervention : Culprit lesion only VS immediate multivessel PCI

– Include CTO lesion

– Follow

– Outcome : Culprit lesion only decrease mortality, renal failure

Criticize : prefer culprit lesion only in non-DM, non-anterior wall STEMI

TREAT trial
– Population : STEMI with fibrinolytic

– Age 18-75, no anticoagulation

– Open label, non inferior trial

– Fibrinolytic : TNK, Alteplase, Reteplase, streptokinase only 5%

– Intervention : ticagrelor vs clopidogrel

– Ticagrelor 180 mg load and 90 mg bid (load delay 11 hr after fibrinolytic

with clopidogrel)
– Clopidogrel 300 mg load and then 75 mg OD

– Follow : total N 3800

– Outcome

– 1st : Same TIMI bleeding at 30 days

– Same all death

– Criticize

– population anterior wall 1/3 but all death only 2.6% (น้อยกว่าความเป็นจริง)
– This is switching P2Y12 inhibitor trial from 48 to 12 hr
Antiplatelet
Antiplatelet therapy

Third step of platelet cascade

!. Adhesion
#. Activation : ASA & P2Y12i
$. Aggregation : GP IIb/IIa inhibitor, Vorapaxar
 – ASA = Warfarin but warfarin increase bleeding
– DAPT superior to warfarin + ASA

General
 – Vorapaxar (oral form) : Protease activated receptor (PAR-1) antagonist, inhibit
platelet aggregation.
– Contraindication : Hx of cerebrovascular event

Platelet resistance
– ASA : ASP > 25 U

– Clopidogrel : ADP > 50 I

ASA
– In ACS : Decrease death, RRR 19% (same as thrombolyic)

– Low dose ASA : block COX1

– High dose ASA : block COX1 & 2

Clopidogrel via CYP2C19 หลีกเลี่ยงการใช้คู่กับยาที่ inhibit CYP2C19

– PPI : pantoprazole inhibit CYP2C19 น้อยสุด หลีกเลี่ยง omeprazole or esomeprazole
– Add on clopidogrel in NSTEMI (MACE, RRR 18%)
– High on-treatment platelet reactivity (Clopidogrel resistance) : loss of function
CYP2C19*2 allele

Secondary prophylaxis (CAPRIE trial)

– ASA = Clopidogrel in MI, stroke (ischemic event), ASA trend to more bleeding

– Prefer Clopidogrel in PAD (decrease ischemic event)

Prasugrel (Effient)
– Indication : before invasive strategy (Known anatomy & plan PCI) or STEMI
 – Contraindication : Prior any stroke/TIA, age > 75, BW < 60 kg, moderate to severe
liver disease
– Compare with clopidogrel (decrease MACE, RRR 18%)

Ticagrelor
– Contraindication : previous hemorrhagic stroke & ICH, moderate to severe liver

disease, OAC
– Compare with clopidogrel (decrease MACE, RRR 16%)

– In high ischaemic-risk patients : ticagrelor 60 mg twice a day on top of aspirin for

longer than 12 months may be considered for up to 3 years. (IIb)

Switch anti-platelet
Acute setting
– low to high potent : loading

– High to low/potent : loading after 24 hr

Chronic setting
– Reversible (Ticagrelor) to non-reversible anti-platelet : loading after 24 hr

– Non-reversible to reversible anti-platelet : normal dose after 24 hr

Duration of DAPT
Score
– Precise-DAPT : Used to decision short/long DAPT after PCI for predict bleeding
event
– DAPT score : Used to decision extended DAPT beyond 1 years for predict bleeding &
ischemic event
Anti-thrombotic agent

Clinical trial
 Anomalous
coronary origin
Anomalous coronary artery

Approach
– Normal origin
– Anomalous coronary ostium : Slit-like/fish-mouth-shaped orifice, acute angle

takeoff, hypoplasia of the proximal coronary artery

– Coronary course : intramural course, interarterial course

– Anomalous origin

High risk anatomy

– Intramural course

– Fish-mouth-shaped orifice

– Acute angle

– Inter-arterial course

– Proximal narrow & elliptic vessel shape

General
– ALCAPA/ARCAPA : Key is abnormal flow in myocardium (enlarge perforator branch)
– Coronary AV fistula (No abnormal flow in myocardium)
– Coronary aneurysm
– Dilated coronary ostium (flow in diastolic phase)
– Anomalous coronary artery : cause of SCD in patient < 35 years
– Separate origin พบเยอะสุดใน anomalous coronary origin

Dilated coronary sinus

– PHT : No coronary artery dilatation

– PAPVR

– Persistent of left SVC

 – Unroofed CS
– Coronary AV fistula : coronary artery dilatation
– ALCAPA : coronary artery dilatation with intramural artery dilatation

ALCAPA
– Anomalous left coronary artery from pulmonary artery
– Other name : Bland-White-Garland syndrome (BWG)

– CAG is gold standard

– LM from pulmonary artery (Venous blood)

– Blood supple to Lt system from RCA, bronchial artery

– RCA dilatation : normal native coronary dilation & collateral vessel (key :

intramyocardial vessel dilatation)

– Presentation : MI, Arrhythmia

– PE : cont. murmur with diastolic accentuation at LUPSB (same as coronary AV

fistula)
– Echo : Large coronary arising from Rt cusp, Turbulent diastolic flow within

interventricular septum and RV apex, Take off vessel from posteromedial of PA

with abnormal color flow to PA, LV dysfunction and MR
– Treatment : surgical all case

– Takeuchi procedure (aortopulmonary window & intrapulmonary tunnel to LM)

– Reimplantation of anomalous coronary

– CABG with ligation ALCAPA

– Follow up : Echo and non invasive stress test q 3-5 years

ARCAPA
– Rare

– Treatment : surgery in symptomatic, LV dysfunction, Ischemia

ACAOS
– Anomalous of Coronary artery arising from opposite sinus

– Malignant subtype : coronary vessel อยู่ระหว่าง aorta & pulmonary artery

– Surgery

– LM/LAD from Rt cusp

– RCA from Lt cusp with evidence of ischemia or high risk anatomy (intramural

course, fish-mouth-shaped orifice, acute angle)

– Benign : LCx from Rt cusp (common is posterior courses)
Angiographic view
Coronary AV fistula
– Common RCA to Rt side heart (Rt ventricle/Atrium, coronary sinus, pulmonary
vasculature)
- Coronary-cameral fistula (coronary to chamber of heart)
– Presentation : Angina, CHF, PHT, Cont. murmur with diastolic accentuation
– Echo : dilatated coronary artery (>3mm), Chamber enlarge, Flow via shunt
– Physiology
– To systemic vein or RA : mimic ASD

– To PA : mimic PDA

– To RA : volume load mimic MR

– To LV : mimic AR

– Treatment
– Small fistula : follow up

– Catheter based coil closure/Surgical closure

– Surgery in large lumen/multiple communication/tortuous/aneurysm

– Transcatheter closure : must suitable anatomy, less invasive

– Follow up echo q 3-5 years

Kawasaki disease with coronary involvement

– Risk for accelerated atherosclerosis, aneurysm
Treatment for prevent coronary thrombosis
– Acute phase : High dose ASA (3-5 mg/kg/day) for 4-6 wks

– Chronic phase (aneurysm can regress)

– Small aneurysm (diameter =< 4 mm) : Low dose ASA

– Large aneurysm (diameter >= 8 mm) : OAC > DAPT

Coronary ectasia (>1.5 เท่า ของ normal)

Absent LM (split LCx & LAD from Lt cusp)

Single coronary artery

Congenital ostial stenosis

Coronary crossing : benign

Coronary spasm
Coronary spam

General
– Vasospastic angina, referred to as Prinzmetal or variant angina.
– Low rate sudden death

– Manifested as rest angina associated with ST-segment elevation

– Ddx vasospastic angina when ST-segment elevation : STEMI, takotsubo

syndrome, early repolarization.

– Pathogenesis: imbalance of vagal and sympathetic tone in triggering coronary
spasm
– MI in vasospastic angina : usually due to concurrent obstructive CAD disease.

Vasospasm may trigger thrombus formation

– Clinical presentation : chest pain generally lasts 5 to 15 minutes
– Exercise does not usually provoke an episode of spasm

– Vasospastic angina alone : Prognosis is good in patients receiving medical therapy

Risk factors and triggers

– Smoking : major risk factor for vasospastic angina
– Hypertension and hypercholesterolemia
– Allergic vasospastic angina (Kounis syndrome)
– Hyperventilation
– Cocaine, Cannabinoids
– Drug : Propranolol, Oral sumatriptan, 5-Fluorouracil, acetylcholine

Diagnosis
Investigation
– Role stress test : screen for significant fixed coronary artery disease
– Role CAG : transient ischemic ST-segment changes, severe fixed obstruction needs
to be excluded.

Provocative test
Indication : angina without document EKG change (common STEMI)
– intra-coronary ergonovine incremental dose up to 60 ucq

– intra-coronary acetylcholine incremental dose up to 200 mcq

Treatment
– CCB : diltiazem, amlodipine, nifedipine
– Long acting nitrate.
– Avoid : non selective beta-block, low dose ASA (used with caution)
– Statins : effective in preventing coronary spasm and may exert their benefits via
 endothelial nitric oxide or direct effects on the vascular smooth muscle.
– Lifestyle modification : smoking cessation, avoid triggers for vasospastic angina.
CAG & PCI
CAG & PCI

Indication for CAG

– Suspect CAD

– SCAD : high risk

– Control angiogram 3-12 months in high risk PCI : unprotected LM

– NSTEMI/UA : all case except low risk

– STEMI : all case

– HF : suspected CAD

– Arrhythmia (VT/VF) : intermediate prob for CAD by age and symptom

– Pre-op evaluation

– Valvular surgery

– Male > 40 or female post menopause

– Risk CAD >= 1 or suspect CAD

– MR related ischemia

– Pre-op as non operative patient

No absolute contraindication : if benefit > risk go CAG

JL (Judkin)
– size = length during primary & secondary curve

– Femoral : female 3.5, male 4

– Radial : JL 3.5, JR 4

AL (Amplatz) : for high takeoff coronary

Multipurpose : for SVG graft
Guide catheter มี internal lumen ใหญ่กว่า
Sheath size
– size depend on internal lumen but external diameter is plus 2 Fr size

Diagnostic catheter
– size depend on external lumen

Catheter size : 6 F = outer diameter 2 mm

– 1 F = 1/3 mm

Manifold = trifold 3 อันต่อกัน

INT accept before cath
– INR < 2.2 : radial approach

– INR < 1.8 : Femoral approach

Contrast : < 4 ml/kg or volume < 3.7 x GFR

– High (1400-180p mosm) : เลิกใช้แล้ว
– Low (500-850 mosm) : Iopromide (ultravist), loversol (Optiray)

– Iso (290 mosm) : Iodixanol (Visipaque)

– Risk CIN : Iso = low (ESC)

IV hydration (expected contrast volume > 100 ml)

 – 1 ml/kg/hr - 12 hr before and 24 hr after procedure
– 0.5 ml/kg/hr - 12 hr before and 24 hr after procedure in EF =< 35% or NYHA >= 3

Metformin before PCI

– Check renal function before PCI

– Can hold or cont. MFM

– If hold : hold 48 hr before PCI & restart 48 hr later

– If cont : check renal function after PCI, hold MFM when renal deterioration

Radiation
– Fluoroscopy time =< 60 mins
– Air Kerma-Area Product (Pka) = Dose x Area of irradiated field
– > 500 Gy.cm2 : notify patient & doctor

– Radiation > 5 Gray —> delay next radiation 60 days

– < 2 Gray : good

– > 15 Gray : dermal necrosis

– High radiation expose : lateral view fluoroscopy, High magnification (ขยายภาพ), high
frame rate (normal 7.5 FPS), collimation (ส่องแสงระยะทางไกล)
– Occupation dose limit (per year), steep angulation
– Whole body (badge inside lead) & Len : 20 mSV/year

– Skin & Extremities : 500 mSV/year

Definition
– CTO : TIMI 0 duration 3 months
– Functional CTO : TIMI 0-1

– Correct when symptoms (antegrade procedure)

– 99% antegrade flow but no contrast column (subtotal occlusion)

– 95% antegrade flow with contrast column
– Lesion length : นับตั้งแต่เริ่มตีบ 50% จนถึงเริ่มหายตีบ 50%
– Focal lesion < 10 mm (Type A lesion)

– Tubular lesion 10-20 mm (Type B lesion)

– Diffuse lesion >= 20 mm (ไม่เท่ากับ diffuse disease), Type C lesion

– Tortuosity (lesion หักมุม 90 องศา)
– Mild : 1 หักมุม
– Moderate : 2 หักมุม
– Severe : 3 หักมุม (Type C lesion)
– Angulation
– < 45 degree : mild

– 45-60 degree : moderate

– > 60 degree : severe (type C lesion)

– Stenosis > 90% : symptom at rest

– Stenosis >= 70% : symptom with stress
 – TVD in Lt dominant : LAD + pLCX and dLCx
– Ramus intermedius : within 5 mm from LM, supply as OM or DG

Myocardial blush grade

Pitfall
Puncture site : ห้ามใช้ skin crease เป็น land mark
– skin puncture site : 1 inch below inguinal ligament

– Arterial puncture site : lower-medial of head femor

– Arterial puncture site : common femoral artery (เหนือ bifurcation ใต้ inferior
epigastric artery)
– Common femoral a. แตกเป็น superficial and deep (profunda femoralis)
Pressure damp : ไม่ควรฉีด contrast
– สาเหตุ : tip cath at vessel wall, ostial disease, deep engage, engage to side branch,
small vessel
Wire นำ catheter เสมอ, wire ติดห้าม force
Aspirate sheath ก่อนใส่ wire เสมอ ป้องกัน clot emboli

Anatomy
– RCA - Conus branch : 1st branch (to anterior) supplies RVOT

– SA node artery (to posterior): 2nd branch - RV branch - Acute marginal

branch
– LAD - DG : lateral wall

Part of vessel
– Mid RCA : 1st main RV branch to acute marginal branch

– Or marginal branch separate between proximal/distal

– Mid LAD : first septal branch to last large DG or DG2

– Mid LCx : 1st to 2nd OM

CINE
– View เรียกตามตำแหน่งตัวรับภาพ หรือ ทิศทางลำแสงที่ยิง
– AP view จะเห็น cath ขนานกับ spine
– แยก RAO/LAO ดูจาก spine/cath ตรง descending aorta ว่าอยู่ด้านไหนของคนไข้
– Cranial view เห็น diapharm
– LAD : distal at apex, septal branch, วิ่งออกจาก spine

Left system : 6 view,

cranial ดู LAD, caudal ดู LCx
Cranial for see distal part
Caudal for see proximal part
RAO 30 degree, LAO 60 degree
– RAO caudal (LCx at mid and down): ดู LM, LCx, OM
– RAO(PA) cranial (LCx at mid and upward) : ดู LAD & DG, limit ostial-DG,
– LAO cranial (LAD at mid and down) : ดู Lt dominant, bifurcation (LAD-DG)
– LAO caudal (LAD at mid and up) : ดู LM and bifurcation, proximal-mid LCx
– AP caudal

Left main
– Ostial : LAO cranial, AP cranial

– Bifurcation : LAO caudal, AP caudal

Right system : 3 view

Cranial for see distal part
Caudal for see proximal part
– LAO cranial: ดู RPD,RPL, รูป C
– RAO : ดู mid RCA, รูป L
– AP cranial : distal RCA and bifurcation (PDA-PL)
Coplanar view in TAVI
Physiologic flow reserve
– Concept : flow reserve (after hyperremia : resistance is constant) = Assume pressure
proximal/distal
– Resistant depend on microvascular

– Same stenosis : infarct may be no significant decrease flow reserve but in

ischemia may be significant decrease flow

– used in lesion 50-90% stenosis

– Normal reference at tip of cath & tip pressure below 2-3 cm after lesion

– false high FFR in Culprit artery

– Acute MI (microvascular obstruction)

– Small perfusion territory

– Myocardial infarction scar

– Little viable tissue

– Small vessel

– Abundant collaterals

FFR, measure after hyperemic agent : adenosine : dose 40–>80–>120 mcq IC

– FFR =< 0.8 : Treat, FFR =< 0.5 : Total occlusion

iFR (Instant wave-Free Ratio) : measure in diastolic period of Pd/P-aorta (75% of distal
diastole), no require hyperemic agent
– iFR =< 0.89 : Treat
IVUS (intravascular ultrasound)
– Cut off limit 3.5 or 4.0 mm2 for major epicardial artery

– Cut off limit 6.0 mm2 for LM

– Post stent : LM 8.0 mm2, LM-bifurcation 7 mm2, pLAD 6 mm2, pLCX 5 mm2

– IVUS guide therapy : decrease MACE & Stent thrombosis

OCT (optical coherence tomography)

– superior resolution < 10 micrometer

– 10 times resolution of IVUS

– Optical fiber 74 mm imaging acquire in under 3 sec

– OCT provide treatment precision : stent size, placement, expansion, apposition

– Assess : fibrous cap, vulnerable plaque, calcium, edge dissection, mechanism of ISR
High risk PCI & ischemic event
Coronary arterial stent
POBA
– Compare with stent : same mortality and MI but reduced target vessel
 revascularization
– Drug-coated balloons : treatment of in-stent restenosis (I)
Stent
– BMS : cobalt chromium, stainless steel, platinum chromium
– DES : Paclitaxel, Everolimus, Sirolimus, Zotarolimus
– DCS (drug coating stent) : polymer-free and carrier free drug-coated stent, ชื่อยี่ห้อ
biofreedom ใช้ DAPT only 1 months
BMS : Prefer in large vessel, DAPT compliance, No more used in future
– 20-30% restenosis within 6-9 months

DES : All DES are superior to BMS in terms of the rates of target lesion revascularization.
– First generation : Sirolimus- and paclitaxel-eluting stents

– Second generation : Everolimus- and zotarolimus-eluting stents (EES and ZES)

– Resolute zotarolimus-eluting stents (R-ZES) = Everolimus-eluting stent (EES) =

Ridaforolimus-eluting stent (RES) > Endeavor zotarolimus-eluting stents (E-ZES)

for lowering the rate of target vessel revascularization.
– Third generation : biodegradable polymers, polymer-free stents, and biodegradable

stents on the basis of poly-L-lactide (PLLA) or magnesium

– DCS (BioFreedom : umirulimus) : On DAPT 1 months, Less revascularization,

Same MI/Death
Heparin & ACT during PCI
– Heparin 70-100 U/kg
– Optimal ACT level q 30 mins
– Hemochron device : ACT 300-350

– Hemotec system (ศิริราช ไม่รู้ใช้ยี่ห้ออะไร) : ACT 250-300

– On Glycoprotein IIb/IIIa : ACT 200-250

Pre-treatment
– Elective CAG, Clopidogrel pre-treatment or administration in cath lab (IIb) : not
reduced MACE
Complication
– No reflow : coronary dissection, distal emboli, high clot burden, vascular spasm,
shock
– Mx spasm : Adenosine, verapamil, nitropusside. NTG dilate only epicardial artery

– Slow coronary blood flow

– Coronary dissection

– Spasm

– High burden thrombus

– Microvascular obstruction

– High LVEDP

– Pseudoaneurysm : Mx U/S guide compression, Sx when > 2 cm

– Blue toe syndrome (atherosclerotic microemboli)
– Clinical : bilateral lower extremity pain, livedo reticularis, purpuric and

ecchymotic lesions in lower extremites

– Definite : skin biopsy (cholesterol crystal in vessel)

– No specific treatment and general treatment (statin)

– Radial hematoma grading

– ISR
Stent thrombosis : Definition ACS with angiographic (thrombus in stent or 5 mm
proximal/distal to stent with/without occlusion) or pathologic confirm
– Probable : unexplianed death within 30 days or Target vessel MI without

angiographic confirm
– Possible : unexplianed death after 30 days

Minimize stent thrombosis

– Stent : Lower stent thrombosis rate, Appropriated vessel sizing, High pressure stent

deployment and post-dilatation

– Avoid : Edge dissection, Inadequate inflow/outflow, two stents in bifurcation

– Used more potent P2Y12 (DAPT) amd continue without interruption

– Case scenario

– Acute : PCI technique

 – Subacute : Clopidogrel resistance
– Late : stop anti-platelet
– Very late : atherosclerosis risk

Smooth tapering lumen in angiogram

– Coronary spasm

– Coronary dissection

– External mass compressed coronary

Spontaneous Coronary dissection (common is LAD)
– Common in woman age 40 years, postpartum, cocaine, EDS, FMD, hormone therapy,

connective tissue disease, vasculitis, amphetamine

– Think of ACS in young without CV risk, Coronary ambiguous or tortuosity (symmetry

sign)
– Types of SCAD

– Type I: intimal tear, classic radiolucent flap.

– Type II: no intimal rupture (IVUS/OCT show intramural hematoma)

– Prefer conservative Tx (spontaneous arterial healing), high complication with PCI

– Revascularization if unstable hemodynamic or high risk anatomy (LM, ostial LAD)

– Medication as ACS

Iatrogenic coronary dissection

Management
– Not extend beyond ostial : stent

– Extend beyond ostial to aorta

– < 4 cm : stent

– >= 4 cm : surgery

Coronary perforation
– Type I : extra-luminal without extravasation
– Type II : Pericardial/Myocardial blush without contrast jet extravasation
 – Mx type I & II : ballon inflation 3-5 mins (Max 8 ATM)
– Type III : Extravasation > 1 mm perforation
– Mx as type I & II and call for surgery

– Type IV : perforation into anatomy cavity

– Mx as type III, if extravasation into low pressure chamber —> no intervention

– Type V : distal perforation

– Mx : Inflate balloon distally proximal to site of perforation (Max 8 ATM)

– If failure : 1.Thrombin. 2.Microcoil. 3.Fat embolism. 4.Clotted autologous

blood. 5.Mircoparticles
– Prepare for pericardiocentesis

LV gram
Myocardial bridge
– IVUS : half-moon sign
– Treatment in present of ischemia : BB or CCB
– Fail medication : Myotomy procedure

– Deep > 5 mm is not suitable for myotomy, consider CABG

Blood supply in conduction system

White vs Red thrombus
– White thrombus : Platelets are predominantly involved in thrombosis

– Red thrombi : Rich in fibrin and trapped erythrocytes

CAG Reading
– View
– Catheter type & position : aorta, LV, engage.
– Access site : femoral, radial

– Pre-contrast : pericardial effusion/calcification, calcification of coronary/valve/aorta

– Contrast phase :
– Ostial LM

– Dissection

– Stenosis lesion of native vessel & vein graft

– TIMI & Blush flow

– Bridging myocardial

– Aneurysmal change

– Other
– LV gram : Takotsubo cardiomyopathy, VSR, VSD, MR, Septal/apical HCM, LV

aneurysm with thrombus

– Aortogram : Ascending aortic aneurysm, AR, Ruptured sinus of Valsava
– RV gram : ARVD, PS
PCI technique

Term
– Post stent inflation : หลัง inflate stent, used other balloon to dilatation

Technique
– Radial vs Femoral access : radial access decease major bleeding 40%
– Deploy stent : must fully deflated and wait up to 30 sec before removed balloon

Bifurcation lesion

Bifurcation technique
– Definition : side branch >= 1.5 mm & stenosis >= 50%

– Prefer one stent > two stent technique

– Prefer only one stent in main branch

– Provisional side branch-stent by TAP technique

– Indication : dissection, residual stenosis > 75%, TIMI < 2

– Distal LM : prefer double-kiss crush (DK)

Contraindication of Rotablator Rotalink
– Guide-wire not pass

– Last remaining vessel

– Saphenous vein grafts

– Thrombus prior treatment

– Significant dissection

CTO
Indication PCI in CTO :
– Angina resistant to medication or with large area of ischemia in territory of occluded

vessel (IIa)
 Cather ฉีดขวามันจะงอน้อยกว่า
ซ้ายมันจะมีงอ 2 ที่

RAO = overidding aorta

Left PA seen VSD

Main PA supravalve PS RAO seen VSD LAO seen VSD

TOF

Dissection

CAD

Spasm
Double LAD
Collateral

Stent thrombosis

ACS
ASD
SVC seen ASD

Coronary perforation

ASD
Coronary ectasia

LM dissect
With device closure PDA coil lateral view
PDA AP view
PDA

CTO Angiogram

Dcrv

CoA
RCA collateral to
left main to PA
Double LAD
Alcapa

LAD ไม่เห็นไม่มั่นใจ

Rca anatomy

BT shunt
LAO

Aneurysm LM from right cusp

ACAOS

Righ from left

Calcified VSR
LVต้องแยกกับperiacrdium

Myocardium
Lcx from righ cusp

HCM

Constrictive
morphologic
Transeptal type
Eye-sign

Anterior dot sign -

interarterial
Dot sign
-right
Retroaortic
Prosthesis valve Coronary AV fistula

Bileaflet
tk

Perforation
Hemodynamic
Hemodynamic

Indication for Swan-Gagz catheter

No mortality benefit, no routine used
– Short term Mx in acute cardiogenic shock

– Evaluation for heart transplant or Mechanical circulatory support

– Uncertainty hemodynamic status

– Refractory/recurrent heart failure

– Facilitate weaning from inotrope

Pulmonary artery catheter : tip at lower half of lung
– IJV to RA : < 15 cm
– RA to RV : < 15 cm

– RV to PA : < 15 cm

– PA to PCWP : < 15 cm

Contraindication
– severe coagulopathy or thrombocytopenia

– TV or PV prosthesis

– Pacemaker lead

– LBBB

Normal PCWP < 12 mmHg, SVR 800-1200 dyne.sec.cm, CI 2.5-4

Mean PCWP < PA diastolic pressure ~ 1-3 mmHg
– Severe MR (Mean PCWP > PA diastolic pressure)

– PHT (Mean PCWP < PA diastolic pressure at least 3 mmHg)

โดยทั่วๆไป PCWP ~ LVEDP except MS/MR, high PEEP, temponade

– Measure PCWP : เริ่ม QRS or ค่ากลางของ a wave กับ x wave (C wave)
– LV dysfunction : PCWP วัดจาก peak a wave ~ LVEDP
Location of tip catheter at zone 3 of lung for true wedge, if zone 2 can measure PA
 – Damp : loss energy
– Overdamped waveform : loss of energy (กราฟเตี้ยลงหรือราบ)
– Underdamped wave form : ring artifact, overshoot

– Every increment in PEEP 5 mmHg : Increase PCWP 2-3 mmHg

Interpretation by monitor
Fick method
: Direct Fick or Indiect Fick (assume O2 consumption)
 – If no shunt : pulmonary blood flow = systemic blood flow
– Cardiac output = O2 consumption/arterioveneous O2 gradient
– High CO : low arterioveneous O2 gradient

– Low CO : high arterioveneous O2 gradient

– O2 consumption
– Separate calculation

– Machine measurement

– Estimation 3.5 cc/kg/min in healthy person

Summary Assume Fick formula

– limit in high output state
: CO = (3.5 x BW)/[13.4 x Hb x (Arterial O2 sat - PA O2 sat)]
or (125xBSA)/[13.4 x Hb x (Arterial O2 sat - PA O2 sat)]
SVR (normal range 800-1200 dyn.s/cm5)
– R = V/I = (MAP - RAP)/CO (wood unit)

– Wood unit x 80 = dyn.s/cm5

PVR (normal < 3 wood unit)

– PVRi = PVR x BSA (ไม่ใช่หาร)
– R = V/I = (mPAP - PCWP)/CO (wood unit)

Venous blood
– Mix venous oxygen sat from pulmonary artery (SvO2)
– Central venous O2 sat (ScvO2) from IVC and SVC
– SvO2 > ScvO2 (ส่วนใหญ่ ScvO2 from SVC)
– In normal : IVC O2 sat > SVC O2 sat เนื่องจาก blood flow ผ่านไตเยอะ แต่ไม่ค่อยได้ใช้
ไม่ใช่จากสมองใช้ O2 เยอะ
– If low cardiac output —> decrease O2 Delivery

– —> tissue extract more O2 per beat —> low SvO2

– If severe multiorgan failure/cyanide poisoning

– —> cell canʼt extract O2 —> high SvO2

Thermodilution
– CO แปรผกผันกับ AUC
– Limit in low output state, AF, TR/PR

Underestimate
– In severe TR or PR, CO may be underestimation

– In severe AR, CO may be underestimation

Overestimate
– Limitation in low CO : result may be overestimation

– In severe MR, CO may be overestimation (Lt side output)

– Shunt Lt to Rt, Rt to Lt —> over estimated cardiac output

– AUC น้อยกว่าความเป็นจริง
Fluid challenge test
Predict fluid responsiveness (ไม่เท่ากับ hypovolumia)
– Fluid responsiveness : increase CO 15% by thermodilution after colloid 500 ml in 15

mins
– Fluid challenge in LV dysfunction : crystalloid > 200 ml/15-30mins

– Best is passive leg raising test and evaluate CO by thermodilution method, cut-off

10% for intubation, 12% for spontaneous breaths

– Limit : high abdominal pressure (ascites), severe hypovolumia

– Method : นั่ง 45 องศา 60 s แล้วนอนยกขา 45 องศากับลำตัว

Cut-off in positive pressure ventilation
– Stroke volume variation (SVV) by software monitoring, cut-off 13%

– PPV (PPmax-PPmin)/[(PPmax+PPmin)/2]*100, cut-off 11% for TV >= 7 mL/kg and 8%

for TV < 7 ml/kg

– IVC variation (IVCmax-IVCmin)/[(IVCmax-IVCmin)/2]*100 : measure 1 cm from

hepatic vein, cut-off 15%

Spontaneously breathing
– Collapsibility index of IVC [(IVCmax-IVCmin)/IVCmax]*100, cut-off > 40%

Qp/Qs
~ ScvO2 = 75%
Simplify Qp/Qs : flow แปรผกผันกับ O2sat
= [Sat arterial O2 - Sat mix venous O2]/[Sat pulmonary vein O2 - Sat pulmonary vein O2]
– Mix venous sat = (3xSat SVC O2 + Sat IVC O2)/4

Valve area by Hakki formula (limit in tachycardia)

 = CO/square root peak to peak gradient (if HR > 100, AVA should devided by 1.35)
Gorlin equation : Valve flow / (44.5 x Square root of mean gradient)
Valve flow = CO / (Systolic ejection period per beat x HR)
Valve area (Gorlin equation) = CO/(Systolic ejection period per beat x HR x 44.5 x
Square root of mean gradient)
MVA = mitral valve flow / (38 x square root mean gradient)
MVA = 220/PHT
Qp/Qs by Echo
– ASD : (SV RVOT)/(SV LVOT)

– VSD : (SV RVOT)/(SV LVOT)

– PDA : (SV LVOT)/(SV RVOT)

– Qp/Qs by cath ใน shunt ทุกระดับคิดแบบทั่วไป คือ ใช้ก่อนและหลัง shunt (ไม่เหมือน echo)

Oxygen step up
O2 step up : if Qp/Qs > 1.3
– 7-5-5-7% : (SVC/IVC to RA) - (RA to RV) - (RV to PA) - (SCV to PA)

– SVC/IVC to RA : ASD, PAPVR, VSD with TR, Ruptured sinus of valsava to RA,

coronary AV fistula to RA, Gerbode defect

CVP wave form
PCWP vs CVP wave
– PCWP: prominent V wave

– CVP: prominent A wave

– LA vs PCWP : wave from V wave delay compare with LA

EKG guide wave form

– A wave follow P wave 80 ms

– A wave at R wave (EKG)

– V wave at T wave (EKG)

End diastole of myocardium = peak R

LVEDP = C wave
– A : atrium contraction

– Large A wave :

– Increase resistant to RA: TS, tricuspid atresia, RA myxoma

– Decrease RV compliance : PHT, PS, Acute PE, RV infartion

– Cannon A wave : AV dissociation

– Absent A wave : AF

– C : tricuspid bulging, early systole

– X : RV pulling TV

– Prominent X descent : temponade, Constrictive pericarditis, RV overload (ASD)

 – Blunted X descent : RCM
– V : atrial filling, ventricle contraction
– Giant V wave (> 10 mmHg of LAP)

– Rt side (CVP) : TR, ASD

– Lt side (PCWP) : MR, MS, VSD, LV failure

– Y : Opening TV, early ventricular filling (atrial emptying)

– Rapid Y descent : constrictive pericarditis, RCM

– Blunted Y descent : Tamponade, TS, atrial myxoma

Hemodynamic in valvular heart
Pressure
– Wave (ห้ามจำ pattern) : Arterial, Atrial, Ventricle
– Peak in systole or diastole (EKG correlation)

– CVP/PCWP : peak A wave in diastole, peak V wave in systole

– Artery : downward slope in diastolic phase, presented dicrotic notch, high diastolic
pressure compare with LV
– LV: early diastolic near zero and upward slop
AS
 – Approach Gradient LV-Ao
– Fix obstruction : subvalve, valve, supravalve

– Dynamic LVOT obstruction : HCOM

– Mean gradient AS : doppler = cath

– Peak gradient : doppler = peak instantaneous in cath
– Peak to peak gradient in cath < peak gradient in cath
– Carabelloʼs sign (AVA < 0.6 cm2) in severe AS
– : Ao pressure increase 5 mmHg หลังเอา cath ออกจาก aortic valve
– Post PVC : increase pulse pressure & increase gradient, increase SBP
– Arterial wave form : delay upstroke Ao preesure (รูปสามเหลี่ยมด้านเท่า) +/- Pulsus
alternan (LV dysfunction)

HCOM
– Systolic pressure LV > LVOT but Systolic LVOT = Ao
– Brockenbrough-braunwald-morrow sign : decrease BP and pulse pressure +
increase gradient after PVC (increase contraction)
– Ao pressure : spike and dome (ลดลง) but subvalve AS (No spike and dome)
– Arterial wave form : Early peaking
– Pattern of HCOM hemodynamic
– Post PVC

– Effect RV pacing

– Effect Atrial click

– Valsalva maneuver
PS
– significant peak-peak gradient >= 60 mmHg
– subvalve PS Ddx double chamber RV
Severe PR
– PA graph คล้าย RV เลย

PS after percutaneous balloon valvuloplasty, developed severe PR

AR
– Ao diastolic pressure ~ LVEDP
– Wide pulse pressure (40-60 mmHg)
– Rapid increase LV pressure during diastole (อ่าน LV lowest pressure ด้วย), LVEDP >>
PCWP
– Slope = pressure half time
– Severe AR : key is wide pulse pressure
– Decompensated AR : Rapid increase LV pressure during diastole and equalize LVEDP
and Diastolic BP
– Acute severe AR : diastolic premature MV closure, Premature AV opening
– Chronic severe AR : wide pulse pressure, bisferien pulse, high LVEDP
MR
– Giant V wave (V > 3 times of PCWP or > 40 mmHg or peak - PCWP > 10)
– Acute severe MR : large V wave in PA (Cameback PA tracing) with rapid Y descent,
pseudo-constriction
MS
– gradient across MS, PCWP > LVEDP
– Mean gradient PCWP & LVEDP overestimate Mean gradient LA & LVEDD

– PCWP : High PCWP and increase mean/LVEDP gradient between PCWP &

LVEDP with Giant V wave.

– ความต่างพื้นที่ใต้กราฟช่วง diastole คือ mean gradient

– MS S/P PBMV and developed severe MR and hypotension (decrease pulse pressure)
RV infarct
– CVP/PCWP ratio >= 0.67 (2/3)

Constrictive pericarditis
– Key is LV/RV interdependence

– square root sign or deep Y descend

– RV-LV Discordance in inspiration (Increase RV but decrease LV pressure)

– Diastolic equalization (LVEDP - RVEDP < 5 mmHg)

– Ddx : Restrictive cardiomyopathy, temponade, severe TR, decompensated Lt

side HF, RV infarction, Acute MR

– RV systolic pressure < 50
Restrictive cardiomyopathy
– square root sign or deep Y descend

– RV-LV concordance in inspiration

Constrictive : deep X, deep Y : W shape with high pressure

Restrictive : blunt X, deep Y
Tamponade : deep X, blunt Y : squa
PDA : pullback catheter from Ao to PA
PDA with PHT with aortic stenosis : pullback from LV to Ao —> Ao to PDA to PA —> PA to
RV
Shock on IABP
– Hypotension & low pulse pressure

– Ao diastolic peak, ไม่ใช่ systolic peak

– IABP 2r1, Diastolic augmentation (Peak arterial wave form at diastole), Systole unload
(Decrease systole pressure after augmentation beat)
Presure-volume
Loop
Pressure volume loop

AS
– Decrease SV & Lt shift (increase LVESV but same LVSDV) : บีบน้อย
– increase LV pressure
MS
– Decrease volume (preload & SV) & Rt shift (decrease LVEDV but same LVESV) : เติม
น้อย
– Same LV pressure
– Decrease LV wall stress (afterload)
AR
– Increase volume & Lt shift
– Short isovolumic relaxation
– Not true isovolumic relaxation (blood backward to LV)
MR
– Increase volume & Lt shift
– Short isovolumic contraction
– Not true isovolumic contraction (flow cont. back to LA)
RV failure
– normal RV function is trapezoidal shape

– Volume shift to the right and decrese contraction with increase pressure

LV PV loop
– ชื่อ slope : Ea (elastane of arterial) = afterload or LV wall tension
– ชื่อ slope : Emax (End systolic elastane) or ชื่อเส้น ESPVR (End-systolic pressure-
volume = contraction, Preload = LV end diastolic volume
– EDPVR (End-diastolic pressure-volume relationship) : if slop increase = diastolic
dysfunction
– Slope = compliance (diastolic function or lusitrophy)

– Acute MI : decrease contractility (Decrease SV), same preload & afterload

– Cardiogenic shock : decrease contractility, increase preload
– IABP : Decrease afterload, same contractility, same preload
– LVAD : Same afterload, same contractility (Loss of isovolumic periods), reduced
preload (LV unloading)
– ECMO : Increase afterload, same contractility, reduced preload
– Impella : decrease LV volume, decrease LV wall stress/afterload, same contraction
CRT : PV loop shift to the left, increase contractility

Post MV clip
Post TAVI

Cardiac tamponade
= PV loop คล้าย MS but decrease pressure

ASD
: PV loop same as MS but decrease of LV systolic pressure
VSD
PDA
: Increase SV, Decrease after load & LV systolic pressure
– Mimic MR but normal isovolumic contraction

TOF
– Specific pattern recognition PV loop in TOF
Temporary pacing
Temporary pacing

General
– Post MI : AV block, spontaneous recovery in 2-7 days, only 9% require permanent
pacing

Indication
– Symptomatic bradycardia
– non-response to medication

– Severe bradycardia

– Torsade de point : PVC with R on T or QT prolong : set pacing rate 90-110

Contraindication
– High risk ventricular arrhythmia : hypothermia, digoxin intoxication

Internal temporary pacing

Device
– Cardiac pacing catheter : balloon tipped flexible
– In severe TR : prefer rigid pacing catheter and under fluoroscope/echo guide

– J-shape pacing catheter for right atrial pacing : insert antero-medially for tip in

RA appendage
– Pulse generator
Procedure temporary pacing
First technique
– Connect pacing catheter with pulse generator, set rate 80-120 or 2 times above HR,

output 1.5-2.0 mA
– Insert pacing catheter and monitor sensing indicator

– Show sensing when tip in RV

– When tip catheter in RV : deflate balloon and set output 5 mA

– ปรับจนได้ ventricular capture

Second technique
– Assess site : RT IJV or Rt subclavian > femoral due to risk DVT/PE

– Connect pacing catheter with alligator clip and V1 monitoring

– Balloon after tip catheter พ้นจาก introducer sheath (10 cm)

– RA : negative large Pw and negative small QRS

– RV : positive Pw and large QRS

– When tip catheter in RV : deflate balloon

– Insert tip catheter to RV apex (show STE)
– CXR ตัวสายโก่งขึ้นเล็กน้อยที่บริเวณ tricuspid annulus
– Connect with pulse generator
Complication
– lead induced RV perforate
– Cardiac arrhythmia
– Pneumothorax
– Hiccups due to diaphragmatic stimulation
– Infection
– Venous thrombosis
Setting pacing parameters
 – Asynchronous pacing mode (VOO) : above intrinsic rate 10-20 bpm
– Set output : Initial output 5-10 mA
– Normal RV apex pacing threshold 0.5-1.0 mA, high if > 1.5 mA

– Pacing output at least 3 times above pacing threshold

– DDx increase theshold : lead malposition, lead ทะลุ RV apex, problem in endo/
myocardium such as electrolyte, anti-arrhythmic drug, MI, myocarditis
– Set sensing
– Set synchronous/demand mode (VVI)

– Set pacing rate below intrinsic rate 10 bpm

– Increase sensing until not detect QRS (sensing threshold)

– Set sensing 1/3-1/2 of sensing threshold

– Default sensitivity : 1 mV (R 2.5 mV)

– Set require HR and lock control

External pacing
Method
– place pads in AP position (black on anterior chest, red on posterior chest), sternum-

apex position
– set pacemaker to demand

– turn pacing rate to > 30bpm above patients intrinsic rhythm

– set mA to 70 (normal 50-100 mA)

– start pacing and increase mA until pacing rate captured on monitor

– if pacing rate not captured at a current of 120-130mA -> resite electrodes and

repeat the above.

– once pacing captured, set current at 10% above threshold
Device indication
Device indication

– Pacing-induced cardiomyopathy : LVEF ≤45%, dyskinesia during RV pacing and

absence of other known causes of cardiomyopathy
– EF drop >= 10% and V pacing >= 20-40% (most is single ventricular pacing)

CRT
– EKG : positive QRS in V1
– Good responder : female, LBBB, DCM

– Response at 6 months

– Avoid apical LV pacing

– Improved hemodynamic & QoL, reduced mortality

Indication
: EF < 35% with optimal med plus
– Sinus rhythm with NYHA II-IV

– LBBB

– QRS >= 130 (I)

– Non-LBBB

– QRS >= 150 (IIa)

– QRS 130-149 (IIb)

– AF with NYHA III-IV

– QRS >= 130 (IIa)

Contraindication : QRS < 130 increase mortality

Physiologic ventricular activation (CRT, His bundle pacing)
– EF 35-50% with AV block that predict pacing >= 40%

– CRT (IIa)

– His bundle pacing (IIb)

– Upgrade to CRT from PM or ICD (I, B)

– HF with LVEF < 35%

– Plus high percentage V pacing (>= 40%)

– Plus NYHA III-IV with optimal medication

ICD
– Key for tachycardia (VT/VF)
– ICD = Pacemaker + shock
–Concept program : shock เมื่อไม่แน่ใจเสมอ
– Shock from coil to pulse generator (pulse generator must in Lt side)

Indication
1)CHF with optimal medical treatment
– ICM

– Primary prevention : symptomatic HF FC II-III & EF < 35% despite optimal med

for 3 months or at least 40 days after MI (I), EP study induced ventricular

arrhythmia (I)
– NYHA class I with ICM EF =< 30%
 – NYHA class IV who candidates for LVAD/heart-transplantation (IIa)
– Wearable ICD : within 40 days after MI or 90 days after revascularization
(IIb) —> Then reassess LVEF
– EF =< 40% with non-sustained VT and induced sustained VT on EP study (I)

– Secondary prevention (No reversible cause, life expect > 1 year, No NYHA IV)
– SCA survivor

– No role ICD in VF/polymorphic VT ass. transient ischemia or acute MI

=< 48 hr with complete revascularization

– Sustained spontaneous monomorphic VT

– Cardiac syncope

– EF =< 35% (I)

– EF > 35% with EP study inducible ventricular arrhythmia (IIa)

– DCM
– Primary prevention :

– EF =< 35%, FC II-III despite >= 3 months of optimal therapy (Ia)

– Add ICD decrease SCD & trend decrease over all mortality

– But presented of CRT, add on CRT-D : neutral over all mortality

– NICM with lamin A/C mutation plus 2 risk factor (NSVT, EF < 45%, male,

nonmissense mutation)
– EF =< 35% despite optimal medication, FC I (IIb)

– Neuromuscular disorder
 – Emery-Dreifuss and limb-girdle type IB with progressive cardiac
involvment
– Myotonic dystrophy type I with PPM indication

– Secondary prevention
– SCA survivor

– Sustained spontaneous VT

– Suspected arrhythmogenic syncope (IIa)

– EP study or Not (IIa)

2)VT/VF
No role of ICD in VF/polymorphic VT with transient ischemia or acute MI <48 hr (with
complete revascularization)
– Survival from SCD

– Spontaneous sustained VT in structural heart disease

– VT that severe enought eg. Syncope

3)High risk for SCD from VT/VF

Contraindication
– Complete reversible cause

– VT/VF storm (Recurrent VT/VF >= 2 episodes or >= 3 appropriate ICD therapies

during 24 hr or shock-refractory VT/VF)

– Good meaning of life < 1 years

– CHF, NYHC IV

Subcutaneous ICD : shock 80 J only

– Pro : Less invasive procedure, low systemic infection, less myocardial damage

– Con : No ATP mode, No pacing But can to biV pacing

Indication
– Inadequate vascular access or high risk for infection plus

– whom pacing for bradycardia or VT termination or as part of CRT

Pacemaker
– Key for treatment bradycardia (for symptom or prognosis)
– SSS : prefer DDD > AAI
– Benefit DDD over AAI : reduced pacemaker syndrome, incidence AF/stroke,

improved exercise capacity

– Role EP study in suspected SSS (IIb)
Indication (No revesible cause)
– Any symptomatic bradycardia (define long pause > 3 sec : eg. SA node disease with

symptoms
– Symptomatic second degree AV block mobitz I

– Symptomatic first degree AV block (PR must > 300 ms)

– Any high risk asymptomatic bradycardia

– SA/AV block with long pause > 6 sec

– AF with long pause 5 sec

– High grade/Complete AV block (Acquire)

– AV block mobitz II or infranodal block mobitz I

– Determine level of the block and guide permanent pacing : Role EPS/

carotid sinus massage/pharmacological challenge (atropine,

isoproterenol, procainamide), IIb
– Mobitz I with neuromuscular disease ass. progressive conduction disorder

(I)
– Bundle branch block with symptoms

– EF > 35%

– Unexplained syncope + EP study (HV>= 70 ms, 2nd or 3rd his-perkinje

block) —> PPM (Ia)

– Unexplained syncope —> EP study (IIa) or Empirical PPM (IIb)

– EF =< 35% : consider ICD/CRT-D

– Alternate bundle branch block

– Offending drugs eg. tachy-bradycardia syndrome

– High risk disease with rapid progression of AV block (regardless of symptoms)

– Specific condition

– Carotid sinus syndrome (cardio-inhibitory type) and recurrent unpredictable

syncope (I, B)
– Some vasovagal syncope

– Some LQTs

– Epilepsy ass. With severe symptomatic bradycardia (ictal bradycardia) where

ineffective anti-epileptic drug

Additional ICD after PPM (Indication for ICD for primary prevention)
– Neuromuscular disease (Kearns-Sayre syndrome, myotonic dystrophy type1, limb-

girdle type 1B, Emery Dreifuss muscular dystrophies) plus

– Asymptomatic second/third AV block or HV interval of > 70 ms (I)

– Infiltrative cardiomyopathy (amyloid, sarcoid) plus

– Mobitz II AV block/third AV block (IIa)

– Lamin A/C gene, limb-girdle, Emery Dreifuss muscular dystrophies

– PR interval > 240 ms and LBBB (IIa)

– Myotonic dystrophy type I plus one of following (IIb)

– PR > 240 ms

– QRS > 120

 – Fascicular block
– Anderson-Febry disease plus QRS > 110 ms (IIb)
Pacing mode
– Permanent AF with complete heart block : VVI
– Other : DDD

SND & AV block in specific condition

– AV or TV surgery : wait 3-5 days
– MV surgery, CABG or AF surgery : wait 5-7 days
– Surgical myectomy or alcohol septal ablation for HCM : wait 2-7 days
 – AV block in Acute MI : wait at least 72 hr
– Post op AV block in adult congenital heart : wait at least 72 hr
– Post TAVR
– AV block with Symptom or hemodynamic instability : PPM

– Persistent BBB : Careful surveillance (IIa)

– Persistent LBBB : new LBBB occurs 10% after TAVI and resolve in 50% at 6-12

months
– PPM (IIb)

– Consider PPM

– LBBB with wide QRS complex >= 160 ms

– EP study in LBBB 130-160 ms with PR prolong, LBBB > 160 ms

– HV > 65 ms predictive for high grade AV block

Congenital complete heart block

– Etiology : Anti-Ro/La from mother via placenta
– Common AV nodal block > Infranodal block

Indication for pacing

– Symptoms (I)

– Asymptomatic plus risk feature (I)

– Wide QRS escape

– Mean daytime HR < 50 bpm

– Complex ventricular ectopy

– Ventricular dysfunction

– Asymptomatic without risk feature (IIa)

His bundle pacing

 – Better ventricular resynchronization and greater improved hemodynamic parameters
than BiV pacing
– RV pacing (Interventricular & Intraventricular dyssynchrony) : increase AF & HF

Hospitalization
– His bundle pacing (compare RV pacing)
– Benefit : decrease death, HF or upgrade to a biventricular pacing

– Reversal bundle branch block by His bundle pacing

– Risk : Need more battery/changing device, Long operation

– Limitation : Technical challenging (low success rate 50-90%), High pacing

threshold
– Selective vs Non-selective his bundle pacing
– Selective : S-V interval = H-V interval, Pacing morphology is identical to intrinsic

QRS complex
– Non-selective : Pseudo-delta wave (fusion of captured neighboring ventricular

myocardium and his bundle)

LV septal pacing (LBBB pacing)

– New method : lead stability than His bundle pacing

Cardiac contraction modulator (CCM)

– Concept for reverse LV modeling and improved LVEF without increase O2
consumption
– Improved NYHF & Peak V2, reduced HF hospitalization

– 3 pacing lead : one RA and two RV septum lead

– Biphasic electrical signal to RV septum during absolute myocardial refractory

period (High voltage & long duration)

– FC III-IVa plus LVEF 25-45% with non LBBB

EP study guide AICD

– ICM with EF =< 40% plus
– Early post MI 40 days or 90 days post revascularization (I)

– ICM with non-sustained VT (I)

– DCM with suspected arrthymogenic syncope (IIa)

– Sarcoid with syncope or extensive scar (IIa)
– Asymptomatic ARVC, EPS for risk stratification (IIb)
– Asymptomatic spontaneous brugada syndrome type I (IIb)
– Post TOF repair with suspected arrhythmic syncope plus
– Ventricular dysfunction or hypertrophy (IIa)

– Adult congenital heart with frequent ventricular arrhythmia plus high risk feature
– High risk feature 9 ข้อ (IIa)
– Prior palliative systemic to pulmonary shunt

– Unexplained syncope
 – QRS duration >= 180
– Decrease LVEF or diastolic dysfunction

– Dilated RV

– Severe PR/PS

– Frequent PVC

– Atrial tachycardia

– Elevated BNP

– No role EP study : HCM, LQTS, SQTS, CPVT, early repolarization syndrome

Pace maker syndrome

- Loss AV synchrony (VVI, AAI with PR prolong)
- Loss interventricular synchrony (DDD mode with high V pacing)

Clinical trial
AICD trial
Secondary prevention (Ischemic or Non ischemic)
- AVID : Medication (cordarone) vs AICD --> Decrease mortality
- CIDS : Medication vs AICD --> Decrease mortality in first 3 years
- CASH (Sudden death) : No mortality benefit in 10 years
Meta-analysis : Decrease mortality, Decrease arrhytmic death

Primary prevention
- MADIT (Post MI, EF < 35%, Hx of non sustain VT or inducibel VT ) : Cordarone vs AICD
--> Decease morality
- MUSTT (Post MI, EF < 40%, EP study guide) : Cordarone vs AICD --> Decease morality
- MADIT II (Post MI 4 weeks, EF < 30%) --> Decease morality
- SCD-HeFT (DCM/ICM EF < 35%, FC II/III) --> Decease morality
- DANISH (DCM EF < 35%, FC II-III) ---> no benefit mortality, subgroup age < 55, may be
benefit
Pacing mode
& ICD
Pacing mode & ICD

Pacemaker coding
– Pace
– Sense
– Response to sense : O=none, T=trigger, I=inhibited
– Rate adaptive response
– Multiple site pacing

Pacemaker problem
– Patient

– Lead

– Pacemaker

Normal value
– Impedance lead 200-2000 ohms

– Battery changing if Impedance > 3000 ohm or Voltage < 2.5 V

– Threshold A & V pacing : < 1.5 Voltage at 0.4 ms

– Set pacing >= 2 times of threshold (A safety margin 1.5 V, V safety margin 2.0 V)

– A sense > 2 mV

– V sense > 5 mV

Term
– BOL : beginning of life

– EOL : end of life, EOS : end of survice

– ERI/T : elective replacement indication/time ~ 3 months longevity

– Far-field sensing : intrinsic activity is sensed in wrong chamber

– Crosstalk : specific term V-sense สัญญาณ A-pace

General
– Unnecessary A pacing : increase risk AF

– Unnecessary V pacing : increase risk LV dysfunction

– AV uncoupling (AV synchrony): increase risk AF

Identify ventricular pacing

Wide QRS
– RV pacing : Left axis, Negative V1 and Positive aVL

– Positive V1 : Posterior mid to lower RV septum pacing

– LV pacing : Right axis, Positive V1 and Negative aVL

– LV septal pacing : Left axis, Positive V1 and aVL

Narrow QRS
– BiV pacing : Northwest axis, Positive V1 and Negative aVL
 – His bundle pacing : Normal axis

Pacing EKG
_. Pacing mode
`. Appropriated rate
 – Slow rate
– Failure to capture

– Failure to pace = oversensing until prove otherwise,

– Functional undersensing

– True undersensing : Intrinsic or extrinsic (myopotentials, EMI)

– Hyteresis

– Fast rate

– Normal response

– Atrial arrhythmia

– PMT

– Normal rate

b. Failure to capture (Pw or QRS not follow every spike)

– Normal pacing threshold : battery depletion, functional noncapture (PVC,

psuedofusion)
– Increase pacing theshold

– Normal impedance : lead dislodge/perporation, exit block, electro-

myocardium interface (metabolic, drug, MI)

– Decrease impedance : insulation break (insulation cut by suture,

degradation of insulation)
– subclavian crush syndrome : insulation break or lead fracture

– Increase impedance : lead fracture, loose screw

c. Failure to pace (ไม่มี spike ในตำแหน่งที่ควรมี)

– Oversensing something

– Intrinsic cardiac signals : Cross-talk, Pw/Tw

– Extrinsic cardiac signals : Non cardiac activity, EMI (Electromagnetic

interfere)
– No output (Pacemaker/circuit interruption)

– Ddx battery depletion, circuit failure, coil fracture, loose screw

d. Failure to sense : undersensing (ไม่ควรมี spike แต่มี)

– Undersense—>Overpace, Oversense—>Underpace

– Ddx lead dislodge, poor lead position, lead insulation failure, magnet application,

EMI (electromagnetic interference), battery depletion

– Automatic mode switch not activated in AF with DDD mode —> Mx : Increase

sensing A wave in AF
e. Pacing mimic malfunction
Pacing mode
– Rate = 60000/RR interval (msec)
– Blanking : ไม่รับรู้
– Refractory : รับรู้ แต่ไม่ตอบสนอง
– Single chamber : AV dissociation
– Dual chamber : P synchronous
– A-A timing

– V-V timing

– A-V timing & V-A timing : กรณี PVC มาจะดู V-A timing ใน next beat
– P synchronous
– Yes : dual chamber pacemaker —> A tracing : DDD

– No : single chamber pacemaker —> V sensing : VVI

– DDI = non-tracking P sensing, In P sense follow by non tracking P (Ap follow with Vp
by fix interval but As follow by Vp at lower normal limit)
– DDD = in P sense follow by fix AV interval
– Sensed AV interval < Paced AV interval (20-30 sec)

– DVI = fix VA interval

– VDD = Same as DDD but no A pacing
– DOO = ignored intrinsic P and R wave (Fix VA and VA interval)
– Mode switch from P tracking to non tracking in rapid atrial rhythm (DDD to DDI/VVI)
– Dynamic AV delay : high HR follow with short AV delay
– blanking period : prevent oversensing
– Total atrial refractory period (TARP) = sense AV interval + Post ventricular atrial
refractory period (PVARP)
– PVARP in A-lead : prevent sense retrograde Pw
– Ventricular refractory period (VRP) in V-lead : prevent Tw oversensing
– Maximum tracking rate setting : Depend on TARP
AV delay programing
Key is minimized RV pacing
– Aim RV pacing < 40% and AV delay =< 250-300 msec
 – Consider upgrading to CRT or His bundle pacing : RV pacing > 40% with maximal AV
delay (250-300 msec) and LVEF =< 50%
– Avoid minimized RV pacing in LV dysfunction with PR interval > 230 ms (Increase
death & HF)

Pacing mimic malfunction

Wenckebach behavior vs 271 block
– Upper rate behavior (Only in dual chamber)

– 1n1 conduction (normal) : A rate =< Max tracking rate (MTR)

– Wenckebach behavior (Reverse), Fix RR interval and shortening AA

– TARP > A rate > MTR

– Mx increase MTR, must shortening PVARP ถ้าไม่ปรับ shortening PVARP จะ

เกิด 2n1 block —> increase risk PMT
– 2n1 block : TARP < A rate

– Mx : shortening TARP (short PVARP/AVI, program rate adaptive AV (RA-AV)

– Normal setting : Upper tracking rate < TARP rate, ถ้า UTR > TARP rate จะเกิด 2n1 ก่อน
wenckebach behavior
V pacing rate = Upper rate limit
– Sinus tachycardia with synchronous V pacing

– PMT (no Pw in EKG)

– Sensor-induced tachycardia (in Rate adaptive response)

Mimic malfunction
– Ventricular oversensing

– MVP (managed ventricular pacing mode, Medtronic), promote intrinsic

ventricular rhythm (AAI <—> DDD) : A sense not follow with V and next A sense
will follow with V safety pacing ถ้ามีแบบนี้อีกครั้งจะเปลี่ยนจาก AAI to DDD
– AV search hysteresis (Boston)

– Ventricular undersensing
– Ventricular sense response (VSR)

– Ventricular safety pacing in V sensing period (avoid Cross talk from A-pacing :

avoid loss Vp) : Fix 110 ms after A-pacing

– Crosstalk (V-sense สัญญาณจาก A-pace)
– Management : Using bipolar, Decrease A output, decrease V sense,

prolong PAVB, program VSP on

– MVP

Only dual chamber pacemaker : upper rate behavior, PMT, mode switch, crosstalk
ICD mode
– Detection : rate and duration (12-16 beats)
– Discrimination VT/VF : rate, morphology, abrupt onset, stability (regular/irregular,

cut-point 40 ms)
– EGM :
– Nearfield

– Farfield (resemble surface EKG)

– ATP : faster than detectable 10-20% for 0.5-3 sec or 81% of tachycardia cycle
 length, total 8-10 beats
– BURST : consistently electrical pulse

– RAMP : accelerate electrical pulse

– Shock : Max 15-35 J (Threshold shock + 10 J)

Test Shock after AICD implantation
– Indication : subcutaneous ICD implantation, right-pectoral transvenous ICD
implantation/changes.
– Contraindication : documented nonchronic cardiac thrombus, AF without adequate
anticoagulation, critical aortic stenosis, unstable CAD, recent stroke or TIA,
haemodynamic instability, morbidities associated with poor outcomes.
ICD programming
– Dual chamber vs Single chamber AICD
– No decrease number of inappropriate shocks

– MADIT-RIT trial : Single zone program (200 BPM) reduced inappropriate therapies
and improved survival compare with conventional zone program (VT 170 bpm, VF
200 bpm)

CRT
– Need Bi-V pacing > 95%
– Maximal V-V pacing interval 80 ms

– Inadequate LV pacing : lead problem, Rapid atrial arrhythmia, frequent PVC

Device problem
– Atrial high rate
– Atrial tachycardia

– Far-field ventricular signal

– PMT (Pacemaker Mediated Tachycardia) : Rate at MTR with retrograde Pw

– Initiation/Termination with PVC

– Mx : Disruption VA conduction - Extend PVARP, Carotid sinus massgae,

Verapamil/betablock, Uncoupling of VA synchrony, ปิดเครื่อง

– Control PVC, Find loss A capture?/A undersensing?

– Crosstalk issues
– Mx : On Ventricular safety pacing, Decrease A output/Bipolar, Decrease V sense,

Extend post AV blanking

– CRT : Pacing =< 93% (abnormal)
– Capture ? : check output and lead position

– Control frequent PVCs or atrial tachycardia

– Drug induced threshold change

– Drug induced increase threshold : Flecanide, chronic Amiodarone used

– Drug induced decrease threshold : acute Amiodarone used decrease threshold,

sotalol

– Artifact
– EMI : All channel & High rate (50 Hz)

– Lead fracture : single EGM channel & High amplitude (High impedance &

threshold)
– Myopotential : High rate (crescendo/decrescendo amplitude)

– Diaphragmatic myopotential : observe in V channel

– Pectoral myopotential : observe in any unipolar sensing lead (may be

produced by provocative maneuver)

 – Loose screw

Troubleshooting
– PMT —> PVARP
– Atrial oversensing of ventricular spike —> PVAB (post ventricular atrial blanking)
– Ventricular oversensing of atrial spike —> PAVB + VSP (post atrial ventricular
blanking + ventricular safety pacing)

Normal function DDD pacemaker

– Mimic AAI & loss A sensing but show fusion beat (not AAI)

Rate drop response

PMT terminate by autoprolong PVARP

DDD, Non capture A pacing, retrograde V-A conduction

– Check A lead & increase A pacing output

Irregular Vp from Pw oversensing

Output failure/Oversense something

Loss A capture & Ventricular oversensing of atrial stimuli (cross-talk)

PMT & after magnet apply : Loss A capture & A undersening with Ventricular oversensing
of atrial stimuli (cross-talk)
– Mx : Check A lead

Atrial & ventricular lead switch, DDD mode in complete heart block
Undersening
– VOO mode : on magnets or noise reversion feature

– Functional ventricular undersening

– Undersensing A wave with ventricular safety pacing
 – VVI with V undersensing

Mode switch
CRT & sinus rate above upper limit

Tacograms
VT —> ATP —> spontaneous termination
Under-treatment VT
Mx : add VT zone detect interval 400 ms due to syncope during episode

Tam tract sign from Tacogram

– Double count T wave

Regular narrow complex tachycardia with AV line-up

– Post over drive pacing : VAV response

– Dx : typical AVNRT
Cardiac device
Programing
Cardiac device programing

CIED : cardiac implantable electronic devices

Check device
P : Patient data
L : lead impedance
S : sensing, Decrease backup pacing until show intrinsic rate
T : threshold (Pulse amplitude, Pulse width), Increase pacing above intrinsic rate แล้วกด
test ค้างจน loss capture
O : observation (record event)

Before surgery
Key
– Pacemaker dependence?
– No intrinsic rate after back-up rate < 30 bpm or require 40-60% pacing

– Type of surgery : bipolar (stop bleeding), Unipolar (cutting)

– Stand by magnet (Found in Siriraj CCU)

EMI (electromanetic interference)

– Sx site < 15 cm from generator or lead above umbilicus
– Monopolar > bipolar
– Long burst of electrocautery (> 5-10 sec)
Magnet response
Pacemaker mode : asynchronous mode & suspend rate response
– Medtronic : DOO/VOO 85 bpm

– If ERI (Elective replacement indicator) : VOO 65 bpm

– Boston : DOO/VOO 100 bpm

– If ERI : DOO/VOO 85 bpm

– St. Jude : DOO/VOO 98 or 100 bpm

– If ERI : VOO < 85 bpm or 86.3 bpm

ICD mode : deactivate ICD, still ATP & pacing แนะนำปิด shock mode ทุกเคส
- Set VOO/DOO and turn off ICD
Apply external pad defibrillator
– Apply anterior-posterior
– Anterior pad > 8-10 cm from device
– After external defibrillation : recheck pacemaker due to cardioversion can cause
power-on-reset (revert to VVI mode)

Adjust device for MRI

– Concept device in MRI : Increase impedance, EMI : over-sensing
– แนะนำทำใน center ที่มี cardio และมีเครื่อง check ตลอดเวลา
Check compatible for MRI
– >= 6 weeks after device implant
 – Safe MRI < 3 Tesla
– ดูบัตร MRI compatible
– Lead compatible

Check MRI contraindication

– lead abandon

– Increase threshold lead/device (should not exceed 2.0 voltage at 0.4 ms)

– Non pectoral region device (abdominal device)

Programing device
– DOO/AOO/VOO

– Increase output & pulse width (set A & V output : 5 voltage at 1.0 ms)

– In CRT-D : off defibrillation mode, set to RV pacing (DOO, set 5 voltage at 1.0 ms)

– Set high output RV pacing over LV pacing due to lower rate diaphragmatic

stimuli

Type of device
Lead & device MRI compatible
ICD therapy
– Key : Minimizing unnecessary shock, Minimizing inappropriate shock
– Classification of ICD therapy
– Appropriate therapy

– Inappropriate therapy

– Avoidable

– Phantom : รู้สึกไปเอง
– Undersensing VT/VF
– Programming error : High cut-off rate, Therapy inhibited by discreminator

– System failure : lead failure, Battery/capacitor failure

– Cause of inappropriate shock : AF with RVR, Tw oversensing, lead fracture,

insulation breakage, EMI
– ICD programming
– Slow VT : set VT zone 10/min below clinical VT
Mechanical
support
Percutaneous mechanical support

Algorithm for select percutaneous MCS

– Circulatory support

– Ventricular support

VT/VF storm : induced RV failure

– Mechanical support of choice : ECMO

– Biventricular failure : no role LV impella or tandem heart

Comparison of percutaneous MCS
IABP
IABP

– Tip at proximal part descending

– Distal to Lt subclavial artery 1-2 cm : just below carina (T4-5)

– Ballon ยาว 10 cm ภายในเป็น gas helium

– above L1-2 (celiac a : T12-L1, renal artery : L1-2)

– Hight : < 162 = 34 cc, > 162 = 40 cc

Concept : increase O2 supply & decrease O2 demand

– Diastolic augmentation : Increase coronary blood flow

– Systolic unload : Decrease SVR

– Result : Increase MAP, decrease SBP 20%, increase DBP 30%,

– increase CO 20%, decrease PCWP 20%

Indication : no decrease mortality

– STEMI with cardiogenic shock (AHA : I)

– refractory cardiogenic shock (ESC : IIb)

Contraindication
– At least moderate AR

– AAA

– Severe bilateral PAD

Complication
– limb ischemia

– Systemic emboli : stroke, bowel ischemia

– Aortic rupture

– Infection

Monitor
– Anticoagulant : PTT 50-70 s

– Consider : more than 24 hr, frequency < 1^1

– ไม่ควร stand by IABP เกิน 30 mins

– Pulse

Control IABP : decrease SBP and increase DBP

– EKG trigger : Limit in AF but still recommend first in AF, arrhythmia, pacing

– inflate at peak T wave (dicrotic notch : aortic valve close)

– diastolic augment

– deflate at initial R wave

– early deflate เป็น 2 หยัก

– Delay deflate : no shape deep V (no diastolic augmentation)

– Pressure trigger : Limit in poor heart pumping, work during CPR

– Trigger change pressure 40 mmHg

– Pacemaker trigger
 – Asynchronous pump (internal trigger) : in CPR

Time error
– Early inflation : increase afterload (ischemia), induced AR (harm)

– Late inflation : suboptimal augment DBP & coronary blood flow (no induced

ischemia)
– Early deflation : suboptimal afterload reduction, potential retrograde coronary blood

flow (ischemia)
– Late deflation : increase afterload (ischemia)
ECMO
ECMO

General
– ECMO is circulatory support (not ventricular support)

Indication for ECMO

VA-ECMO (SAVE score ประเมิน survival)
– ECPR : after conventional CPR > 10 mins

– withness cardiac arrest

– No flow less than 5 mins and effective CPR

– Bridge to recovery/decision/transplant/bridge/destination therapy

VV-ECMO
– In Severe ARDS < 7 days plus predicted mortality > 50%, Murray score >= 3, RESP

score risk class IV or more

Contraindication
– Age > 75

– Aortic disease : aortic dissection, severe AR, unrepaired coartation

– Irreversible or end stage organ + not candidates for LVAD or transplant

– contraindication for anticoaggulant (can used heparin free ECMO in specific circuit)

Price ECMO
– Base system 1-2 ล้านบาท
– Each pump set 80000 บาท

Survival rate
VA-ECMO
– High survival rate in fulminant myocarditis (70%)

– Low survival rate in CPR (30%)

VV-ECMO
– ARDS survival rate 70%

Size and position

– Cannula size for conduct flow ~ 80% of CO

– VV-ECMO : Flow 50-80% of CO or 50-80 ml/kg/min

– Fem-IJ : femoral vein drainage (2 cm below diapharm) and return internal jugular

vein in RA
– Fem-fem : femoral vein drainage (2 cm below diapharm) and femoral vein return

in RA
– Pediatric (Veno-venous double lumen VV-ECMO) via IJV

– VA-ECMO

– Peripheral VA-ECMO (Prefer percutaneous > open technique) : Femoral vein

drainage in RA and femoral artery return in external iliac artery (ควรใส่ขาคนละ

ข้าง) +/- distal limb perfusion cannula for prevent limb ischemia
 – Central VA-ECMO with LV venting : Venous drainage from RA appendage and
arterial return to ascending aorta +/- LV venting via LV apex
– Pediatric : Cervical VA-ECMO

Setting & Monitor

– Set heat exchanger 37 degree (Adjust in theraputic hypothermia)
– Transmembrane gradient : normal < 50 mmHg
– Pre-pump : -50 to -100 mmHg

– Pre-membrane : 100-350 mmHg

– Post-membrane : 100-300 mmHg

– Heparin bolus 50-100 U/kg and then 20-50 U/kg/hr

– Target ACT 180-220, Platelet > 80000

– Target aPTT 60-80 sec

– Tartet Anti-Xa 0.3-0.7 IU/ml

– Gas exchange
– Sweep gas flow : adjust q 10-20 mins, Keep CO2 35-45, premembrane O2 >=

75%, O2sat > 90% in cardiogenic shock (O2sat > 85% in ARDS)
– Ventilator : TV 4-6 cc/kg, Peak IP < 20-25, PEEP at least 10 in ARDS

– Ventilator : keep ETCO2 20-30

– Keep MAP 65-90 mmHg

– Keep Hct > 28%

CRRT with ECMO

– Independent CRRT access : problem in access site
– Hemofiltration filter in ECMO system :
– Inlet of hemofilter connect to post ECMO pump and Outlet of hemofilter connect

to ECMO circult
– Inlet & outlet of hemofilter connect to pre-ECMO pump

Problem & Complication

– Harlequine syndrome : Found only in peripheral VA-ECMO with defect lung gas
exchange
– Diagnosis : Diffence SpO2 of Rt arm < Lt arm or Leg plus significant instrinsic

output and coexisting pulmonary dysfunction

– Mx : Adjust ventilator, Increase ECMO flow, Decrease inotrope, VAV-ECMO (Add

return cannula to pulmonary circulation), change to central VA-ECMO

– Loss of circuit flow : low blood volume, tamponade, Tension pneumothorax, circuit
clot/obstruction
– Desaturation in VV-ECMO : R/O recirculation
– Pulmonary edema in VA-ECMO
– Mx : Increase inotropic drug, Increase flow ECMO to decrease blood to lung ,

Atrial septostomy, LV venting

 – Limb ischemia & stroke up to 25%
– Clot in circuit up to 20%
– Infection up to 40%

Weaning ECMO
VA-ECMO : VA-ECMO > 2 wks (Increase mortality) consider change to LVAD
– Ready to weaning

– Myocardium recovery

– ECMO flow < 2-3 L/min

– Pulsatile arterial wave > 24 hr

– MAP > 60 without high dose inotrope (Inotrope score < 10)

– Echo parameter

– EF > 20%

– AV VTI > 10 cm

– Lat MV sʼ > 6 cm/sec

Protocol weaning
– Decrease flow 0.5 L/min q 5 mins, not less than 1.5 L/min without low CO syndrome

VV-ECMO
– Ready to weaning

– Pulmonary gas exchange > 50-80% of total gas exchange

– Improved respiratory machenism

– Improved CXR

– Protocol weaning

– Decrease sweep gas

– Decrease ECMO flow until 30% of CO

Drug in ECMO
- No dose adjust : Ceftriaxone, Tazocin, Meropenam, Vancomycin, Amikacin, Oseltamivir,
Morphine
- Require increase dose : midazolam, fentanyl
LVAD
LVAD

General
– 1 year survival 70-80%

– Risk : Infection 20%, RV failure 10%, Stroke 10%, GI Bleeding 5%

– LVAD, used in only dilated heart

– Measure BP by doppler pressure : MAP 70

– ทำแผลสายที่ท้องทุกวัน
– Setting LVAD only speed
– ใส่ LVAD : defibrillation ได้
– ใส่ LVAD ก็ treat HF ตามปกติ

Indication
– Bridge to transplant

– Destination therapy (not a transplant candidate)

– EF =< 25% and Peak VO2 < 14 (or 50% age/sex predicted) plus one of following

– HF hospitalization without precipitation >= 3 times in 12 months

– HYNA class IIIb-IV despite optimal med for at least 45 days

– Dependence on

– Inotropic dependence for > 14 days

– Dependence on IABP for 7 days

– Progressive end-organ dysfunction (poor perfusion) & refractory HF

– Bridge to recovery, decision, intervention

Indication (ESC 2016) for LVAD

Contraindication for LVAD

– Contraindication for anticoagulation/antiplatelet

– Mechanical valve

– Severe RV failure

– HCM or Restrictive cardiomyopathy

– Irreversible other organ : cirrhosis, ESRD

– Lack of care giver

 – Limit survival < 24 months
Donʼt CPR in LVAD

Type of LVAD
– Short term

– CentriMag : ~ 2 weeks, Price of base system 3.5 ล้าน & echo pump set 300000
บาท
– Long term
– Heart ware (No in Thailand)

– Heart Mate

– Heartmate III less pump thrombosis than heartmate II (both are cont. flow

but Heartmate III is pseudopulsatile)

– Heartmate III price : base system 2.5 ล้าน & each pump 6 ล้านบาท

INTERMACS (NYHA III-IV) : severity of CHF 7 level

– Level 1 : critical cardiogenic shock, die in hours

– Mx : Balloon pump, ECMO, short term LVAD

– Level 2 : progressive decline despite inotropic support

– Level 3 : inotropic dependence

– INTERMACS 2-3 : appropriate for long term LVADs or transplant

– Level 4-5 : resting symptoms

– Level 6-7 : NYHA III

– INTERMACS 4-7 : LVADs not improved survival

– : LVAD, improved QoL (increase 6MWT) but risk complication

Evaluated RV before LVAD

– RV stroke work index = (mPAP-RAP)/SV index, risk for RV failure < 0.3 mmHg.liter/

m2
– Predicts RV failure after MI < 1: pulmonary artery pulsatility index (PAPi) = (sPAP-

dPAP)/RAP
Echo in LVAD
– ตามหา inflow and out flow cannula : cont. flow

Complication
– All stroke 10% in 6 months

– Bleeding esp. GI bleeding in cont flow via small bowel AVM (angiodysplasia) & wVF

deficiency
– Treatment : Danazol, octreotide, Thalidomide (Antiangiogenic properties)

– Infection 10% esp. drive-line infection

– RV failure 30% due to IVS shift, TR, previous RV dysfunction, increase PVR

– Ventricular arrhythmia 20%

– Pump thrombosis 10% in heartmate II (dark urine, increase power)

– Aortic insufficiency

– Hemolysis 1%
Heart transplant
Heart transplantation

Surgical technique
– Orthotopic heart transplantation : เอา heart เดิมออก ใส่ heart ใหม่เข้าไป
– Biatrial anastomosis : risk for sinus node dysfunction

– Bicavial anastomosis (vessel to vessel) : ผ่าตัดยากกว่า

– Heterotopic heart transplantation

Denervation transplant heart

– No angina

– Higher resting HR

– Orthostatic hypotension

– No response to carotid massage

– Reliance on circulating E and NE (excercise)

– Increase beta receptor : increase sense to E and NE (drug)

Survival : median survival 12 years

– 1 year : 90% —> 5 year : 70% —> 10 year : 50%

– Heart & lung transplant : 1 year : 70% —> 5 year : 30%

Indication : without liver and renal failure

– Pumping failure

– Refractory cardiogenic shock requiring device

– Inotrope dependence

– NYHA III-IV with max medication and CRT

– Congenital heart

– Cardiopulmonary exercise

– On beta block : Vo2 max < 12 ml/kg/min

– No beta block : Vo2 max < 14 ml/kg/min (4 METs)

– Ventricular arrhythmia : failure med/ablation

– Refractory angina : failure to revascularization or medication

Contraindication
– Age > 65

– irreversible other organ

– Systemic disease, life expect < 2 years

– Active infection

– Psych illness

– Active substance abuse

– GFR < 30

– PVR > 6 wood unit or 3 wood unit after vasodilator

– Must r/o left heart disease or treat increase LVEDP (volume overload)

– Support : PA systolic pressure < 50

– Severe COPD (FEV1 < 1)

– Obesity BMI > 35
– PRA (panel reactive antibody > 10%) : risk rejection
– Active smoking within 6 months
Screening : recipient
– PRA < 10% ( MFI class < 1500)

– Anti-HIV, HBsAg, HBc IgG,Anti-HCV, VCV/HSV IgG, CMV, EBV IgG

– Cancer screening

– Vaccination : influenza vaccine yearly, pneumococcal vaccine q 5 years

– Free cancer more than 5 years

– Full vascular access screening : PAD screening

Donor : ควรมีผล Echo, CAG ถ้าอายุเยอะ

Endomyocardial biopsy : tissue 4 ชิ้น เนื่องจาก rejection เป็น spot disease

– 12 times in first year

– q 1 week in first month

– q 2 weeks in second month

– q 4 weeks in 3rd-6th month

 –q 12 weeks after 6th month
– q 6 month at 2nd year

– yearly after 2nd year

CAG
– Yearly CAG in first 3-5 years

Immunosuppressive agent
Induction
– Thymoglobulin

– Basiliximab

– ATGAM

– OKT3

Maintenance
– Calcineurin inhibitor (CNI) : Cyclosporin, Tacrolimus

– Side effect : nephrotoxicity, hyperglycemia, hypertension, hyperlipidemia,

hyperK, HypoMg, HypoNa, tremor, neuropathy

– Anti-proliferative : MMF, AZA, Mycophenolic acid (MPA)

– Side effect of MMF/MPA : N/V, diarrhea, BM suppression (leukopenia)

– Steroid

– mTOR inhibitor : Silorimus, Everloimus

Cardiac allograft rejection

– Most complication within 30 days after transplant
– Hyperacute via preexisting antibody : vascular occlusion
– Acute cellular rejection (3 grade) : via T cell lymphocyte, เกิดใน 6 เดือนแรก
– 1R rejection : ปรับ oral drug
– 2R-3R : serious

– Antibody-mediated rejection : chronic

– Risk : female, history of pregnancy, elevated PRAs

– Coronary vasculopathy : intima hyperplasia

– No chest pain due to post heart transplant : denervated nerve

– Tx : statin plus everolimus

Other complication
– SSS : resolved in 2-4 wks, consider pacing for unexplained syncope
– PV stenosis : No LA enlarge but High PCWP and normal LVEDP

– Atrial arrhythmia : R/O rejection

– Ventricular arrhythmia : R/O CAV/rejection

– Cause of death in heart transplant

– 0-30 day : graft failure (not graft rejection)

– 1-12 months : infection

– > 5-10 years : malignancy

– Most common malignancy : skin cancer

– Malignancy leading cause of death : Lung cancer and lymphoma

– Most common comorbidity

– Short term (< 1 year) : DM from steroid

– Long term (> 5 years) : cardiac allograft vasculopathy

Coronary vasculopathy : CAV

Post cardiac transplantation
– Incidence 10% per year, common after 5 years

– Pathogenesis

– Diffuse fibroproliferative & smooth muscle proliferative

– Circumferential intimal thickening

– Intramyocardial & epicardial involve

– Less collateral vessel

– Endothelial lymphocyte

– Subendocardial T-cell (Atherosclerosis : T-cell in edge of plaque)

– Risk factor

– Immune : rejection, HLA antibody (Tx : mToRi (sirolimus, everolimus), MMF)

– Non immune : CMV infection, metabolic disease, ischemic reperfusion/organ

preservation injury, donor brain death

– Presentation : MI without angina, HFrEF/HFpEF, arrhythmia, SCD

– Workup : CAG with IVUS

 –if Dx CAV : first 5 years : CAG with IVUS yearly, > 5 years : non invasive imaging
– Management
– ASA

– Statin for anti-inflammation

– CCB & ACEI : improved microvascular function & delay CAV

– CMV prophylaxis/treatment

Quiz
– Drug has no effect : digoxin, atropine
– Immunosuppressive drug increase risk neoplasm in long term
– No side effect of hepatic dysfunction in long term
Primary prevention
Primary prevention

Risk of mortality

Normal waist circumference (รอบเอว)

– Male =< 90 cm (AHA: 40 inches or 102 cm)

– Female =< 80 cm (AHA: 35 inches or 88 cm)

Normal BMI 18.5-23 kg/m2

BMI : increase 5 kg/m2
– 30% increase all cause mortality

– 40% increase CV mortality

– 120% increase DM related mortality

Term
– Primodial prevention : ป้องกันก่อนเกิด risk factor
– Key is health behavior : stop smoking, Physical activity & Diet, Decrease BW,

Environment pollution
– Screening
– Opportunistic screening: no predefined strategy but is done when the

opportunity arises.
– Systematic screening: part of a screening programme or in targeted

subpopulations (ie subjects with FHx of premature CVD or familial

hyperlipidaemia
Screening
– Age >= 20 years : ASCVD risk assessment every 5 years
– Check lipid after age > 20 years

– Check BP after >= 18 years

Diet
– Key concept : Healthy diet & maintain weight
– Recommend C:P:F = 45-65 : 10-20 : 20-35 (55a15a30)
– Sat fat < 10% of TC, PUFA ~ 10% of TC, MUFA ~ 10% of TC

– Cooking oil : high smoking point, high PUFA & MUFA

– DASH diet (I, A) : prevent HT & lower BP
–เน้นผักและธัญญพืช
– Mediterranean diet (IIa, A) : improve QoL & life expectancy
– Good fat diet (total fat 41%, sat fat 9%) with restrict calories (plant base, lean

meat)
– Low-fat diet (IIa, B) : improve QoL & life expectancy
– Low-carbohydrate diet (IIb, A) : short term greater weight loss
Healthy diet (ESC)
– 5 : < 5 gm of salt per day (1 ช้อนชา)
– 4 : 40 gm fibre from wholegrain per day
– 3 : 3 serving of fruit & vegetable, 30 gm of nuts per days
– 2 : 2 times of fish per week
– 1 : < 10% of total energy of sat fatty acid, 1-2 drink of alcohol per day
– Avoid sugar-sweetened soft drink
กินผักมีเม็ด กินเผ็ดไม่เมา เพลาหวานมันเค็ม มุมมั่นกเนผักกินปลา
– กินผัก : กินผักและผลไม้
– มีเม็ด : wholegrain
– กินเผ็ดได้
– ไม่เมา : less alcohol
– เพลาหวานมันเค็มเค็ม : ลดหวาน มัน เค็ม
Dietary fat
– Cholesterol

– Triglyceride

– Saturated fatty acid : ไขมันสัตว์และไขมันจากกะทิ มะพร้าว เนย

– increase LDL & atherosclerotic, recommend < 7-10% of total calories

– Unsaturated fatty acid : ไขมันจากพืช

– Trans-unsaturated fatty acid or partial hydrogenated (ไม่ดี) : ข้อมูลโภชนาการ
ระบุ 0 gm (< 0.5 gm),
– Transaturation fat (donut, bakery, margarine): increase Cholesterol, LDL

CHD & SCD, decrease HDL

– Recommend trans-fat < 1% of total calories

– MUFA (1 พันธะคู่): mono-bond unsaturation fat.

– PUFA (หลายพันธะคู่) : Decrease atherosclerotic PUFA > MUFA
– Omega-3 : EPA, DHA

– Omega-6
Salt
– Normal salt consume 9-12 gm per days
– Salt restriction 2-3 gm per days
– เกลือ 1 ช้อนชา = 5 gm of salt
– Salt 5 gm = Na 2 gm

ASA for primary prevention

– Statin era : No net benefit in ASA for primary prevention
– Non-statin era (previous era) : trend to decrease non-fatal MI
Low dose ASA (75-162 mg)
Indication : Low-dose aspirin (75-100 mg orally daily)
AHA 2019, IIb
– Age 40 to 70 years plus

– Higher ASCVD risk plus

– Not at increased bleeding risk.

JACC 2018
– 10-year CHD risk is > 10% & Coronary calcium score > 1 (หนึ่ง)

Asymptomatic DM
– Non invasive screening for CAD : no benefit for CV death but decrease CV events

Risk modifier CV disease

– Socioeconomic

– BMI and central obesity

 – Family history of CV disease, male < 55 years, female < 65 years
– Carotid artery screening plaque (IIb)
– Carotid ultrasound IMT (III, level A)

– CT coronary calcium (IIb)

– ABI (IIb)

Alcohol drinking
– 1 Drink = 10-14 gm of alcohol
– Calculate gm of alcohol = % alcohol x cc x 0.789(ความถ่วงจำเพาะ)
– Limit drink per day : men =< 3 drinks, women =< 1.5 drinks

Obesity
– Abdominal obesity related CV/mortality > BMI

Smoking cessation
Five-AS
– Ask : ถามยังสูบบุหรี่ไหม
– Advice : เลิกบุหรี่และแนะนำ CV benefit
– Assess : ติดบุหรี่แต่ไหน (nicotine dependence)
– Assist :
– Non-pharmacotherapy : กำหนดวันเวลาและโอกาสที่จะหยุดชัดเจนและปรับพฤติกรรมไป
ทำอย่างอื่น
– Pharmacotherapy in moderate to high nicotine dependence
– First line : Varenicline or combination

– Varenicline : avoid in psychiatric disease

– Nicotine : avoid in MI

– Bupropion : avoid in seizure

– Arrange : นัดหมายมาติดตามผล
Drug
Clinical trial
ASCEND trial
– Population (N=15480) : DM without previous MACE

– Insulin used 25%, HbA1C ~ 7, Duration of DM 7 years

– Intervention : ASA 100 mg vs placebo

– Outcome (7 years) : MACE prevent NNT 91 vs Major bleeding NNH 112 (Driven by GI

bleeding)
Criticise : more benefit in 5 years-Vascular risk score >= 10%
ARRIVE trial (negative study)
– Population : Moderate CV risk (Estimated 10-years major CV risk 10-20%), exclude

DM
– Observe ASCVD event 8.5%, High drop-out rate

– 43% on statin

– Intervention : RCT, ASA 100 mg vs Placebo

– Outcome : Composite of CV death/MI/Stroke/UA/TIA : No significant. Increase GI

bleeding

ASPREE
– Population : Age > 70, No CAD

– Intervention : RCT, ASA 100 mg vs Placebo

– Outcome (N 19100) : Primary end point (mortality, dementia, disability) : no

significant. Increase death/bleeding (driving by cancer related death). Same CV

event
DM
DM

: DM - life years loss 6 year

DM with CVD - life years loss 12 years
– Diabetes-specific Risk Enhancers = CVD equivalent

– DM type II ≥10 years or DM type I ≥ 20 years

– DM with target organ damage

– Albuminuria ≥30 mcg albumin/mg creatinine

– eGFR <60 ml/min/1.73 m 2

– Retinopathy or Neuropathy

– ABI <0.9

– Every 1% increase HbA1C ass. increase CV event 10-15%

– Every 1% HbA1C reduction ass. 37% reduction in microvascular complication

– Early onset DM < 45 years

– ASA for primary prophylaxis in DM with ASCVD risk > 10%

– HbA1C ที่เพิ่มขึ้น related with heart failure แต่การลด HbA1C ด้วยยาส่วนใหญ่ไม่ได้ลด HF

HbA1C 6.0 = FBS 126 mg%

– Every increase HbA1C 1% = Increase FBS ~ 30%

Initial treatment
– Initial HbA1C > 9% start combine drug

– Target HbA1C : young 6.5-7%, elderly with healthy 7-7.5%

– Not achieved goal HbA1C in 3 months : start triple therapy

– Consider initiate basal insulin with HbA1C > 10

Clinical trial in DM (FDA)
– Non-inferior trial for CV outcome benefit : cut point 0-1.3

– Superior trial for CV outcome benefit: cut point < 1.0

Control DM
– Decrease microvascular outcome : renal, eye

– Early and control without hypoglycemia for 10 years : decrease CV outcome

Drug + life style modification

– 1st line : MFM

– 2nd line drug with CV benefit

– SGLT2 inhibitor : empagliflozin (Jardiance), Canagliflozin

– GLP-1 agonist : Liraglutide SC injection (Victoza or Saxenda), Semaglutide

Drug type
– Insulin provider : insulin, SU
– Insulin sensitizer : MFM, TZD
– Insulin enhancer : GLP-1 agonist, DPP-4 inhibitor
– no combination GLP1A with DPP4i

– Glucose excreter : SGLT-2 inhibitor

Drug choosen
h. First line : Metformin +lifestyle modification
– If A1c > 1.5 % above Target : early combination

i. Second line drug

– Established ASCVD : add GLP1RA or SGLT2I (if HbA1C is at goal, consider switch to

one of these agent)

– SGLT2I: Empagliflozin, Canagliflozin

– GLP1RA: Liraglutide, Semaglutide

– HF special concern or CKD : prefer SGLT2I

– CKD : consider SGLT2I > GLP1RA (decrease CKD progressions)

– Minimize weight gain or promote weight loss : GLP1RA (semaglutide> liraglutide>

dulaglutide> exenatide> lixisenatide) or SGLT2I

– Minimize hypoglycemia : DPP4i or GLP1RA or SGLT2I or TZD

– Cost is a major issue : SU or TZD (Last generation SU is less hypoglycemia)

– No ASCVD or CKD : ตัวไหนก็ได้

– Consider GLP1RA as first line injection before basal insulin

Drug profile
MFM
 – No weight gain, no hypoglycemia
– Short term decrease microvascular complication

– 10 years decrease MI & death

– MFM XR, less GI side effect

– Not recommend start in GFR < 45, discontinue when GFR < 30

TZD
– less hypoglycemia, increase HF

– Decrease death in recent stroke

– Avoid combine with insulin due to risk fluid retention

– Contraindication : symptomatic HF (FC III/IV), avoid combine with insulin (increase

HF)
– ไม่ได้เพิ่ม Death จาก heart failure
SU
– General
– esp. glibenclamide (ischemic preconditioning by block K ATP channel)

– Glibenclamide : high risk for hypoglycemia, not recommend age > 60

– Glimipiride (dose 1, 2, 4 mg, Max 6 mg/day) : start 1 mg OD at morning with meal

– Glibenclamide (5 mg tab, Max 10 mg bid) : start 2.5 mg at morning with meal OD

Insulin
– weight gain & hypoglycemia

– Avoid combine with SU

SGLT2 inhibitor
: Secondary prevention : Decrease MACE via non glycemic effect (via hemodynamic HF)
and renal progression
: Primary prevention : Decrease only HF hospitalization & renal progressions
: Decrease glucose absorption at proximal tubule (70-80 gm/day)
– Empagliflozin (Jardiance 10 & 25 mg) : start dose 10 mg OD morning with/without

food
– Not recommend in GFR < 45

– Effect on hemodynamic & metabolic effect : Decrease Hb1AC ~ 0.7 (depend on

baseline HbA1C), Decrease BW ~ 2 kg, Decrease CV death & HF, Decrease

proteinuria (afferent constriction), Decrease BP 5 mmHg, Decrease uric, No
hypoglycemia.
– Side effect : UTI, euglycemia DKA (volume depletion, *hypoK)

– Canagliflozin

– General

– Increase risk for amputation, bone fracture

– Dapagliflozin (forxiga 5, only 10 mg in Thai) : start 5 mg OD (max 10 mg/day)

– Suggest GFR >= 60, Approved GFR >= 45

GLP-1 receptor agonist

– General

– Decrease 3-MACE, RRR 22% (effect decrease atherosclerosis), decrease BW

 – Increase insulin, decrease glucagon, effect on post-prandial glucose
– Contraindication : ESRD, MEN2, Familial Hx of medullary thyroid cancer, caution
in pancreatitis
– Discontinue DPP4i before start GLP-1RA
– Liraglutide (Victoza or Saxenda : 18 mg/3ml) : Saxenda ไม่น่าใช้
– Decrease MACE driving by CV death, Decrease albuminuria

– Dose initial 0.6 mg SC OD step q week (max 1.8 mg in Victoza or 3 mg in

Saxenda), Not recommend in GFR < 30

– Side effect : Decrease appetile, N/V & diarrhea, Hypoglycemia(Saxenda)

– Semaglutide (SUSTAIN-6 trial) : decrease MACE driving by decrease stroke

DDP4 inhibitor (-gliptin) :

– General

– Neutral CV outcome & weight

– Decrease destroy GLP1, effect on post-prandial glucose

– Saxagliptin & Alogliptin may increase HF

– Risk for acute pancreatitis

– Sitagliptin (Januvia : 25, 50 & 100 mg) : fix dose 100 mg PO OD

– GFR 30-50 : dose 50 mg OD, GFR < 30 & ESRD : dose 25 mg OD

– Alogliptin (Dose 6.25, 12.5, 25 mg) : start 25 mg PO OD
– GFR 30-60 : dose 12.5 mg OD

– GFR < 30 or ESRD : dose 6.25 mg OD

– Oseni (Alogliptin 25 mg with TZD 15 or 30 mg)

– Linaglitin (Tradjenta) (Dose 5 mg) : start fix dose 5 mg

– Potent and selective DDP4

– Main excrete via liver, no renal adjust

Insulin
Clinical trial
Over all clinical trial
ACCORD
– Population : DM patient

– Baseline BP 139/76

– Intervention : SBP < 140 vs < 120 mmHg

– Data : BP 133 vs 119 mmHg

– Follow 8 years, Total N 4700

– Outcome : same MACE, Decrease stroke (NNT for 5 years = 89)

Leader trial
– Population : DM type 2 with HbA1C >= 7%

– Plus Age >= 50 with Cv disease or Age >= 60 with CV risk

– Intervention : liraglutide vs placebo

– Follow up : 4.5 years

– Outcome : Decrease MACE (CV death, MI, stroke) esp. CV death & all death

– HbA1C 0.5-1%,

EMPA-REG
Non inferior trial : NI margin 1.3
– population : DM with establish CVD 99%, baseline HbA1C 8, Hx of HF 10%

– Intervention : add on emplaglifozin

– Outcome : 3MACE superiority (RRR 14%), driven by CV death, Decrease HF

hospitalization (Decrease 1/3)

CANVAS
Non inferior trial : NI margin 1.3
– population : DM with CV risk, establish CVD 65%.

– baseline HbA1C 8, Hx of CHF 10%

– Exclude : complex CAD (SYNTAX score > 32), EF < 20%, bicuspid, severe AR

– Intervention : add on canagliflozin

– Outcome : 3MACE superiority (RRR 14%), no sig. in subgroup, Decrease HF

hospitalization (decrease 1/3)

DECLARE-TIMI 58
– Population (N 17160) : DM with HbA1C > 6.5 with GFR >= 60 plus

– Established CVD (40%)

– Risk factor (DLP, HT, smoking) (60%)

– Intervention : Dapagliflozin 10 mg vs Placebo

– Outcome (mean F/U 4.2 years) : co-primary efficacy

– Non-inferior for MACE

– Superior for HF hospitalization/CV death

– Decrease renal composite

Dyslipidemia
Dyslipidemia

General
– Clinical ASCVD (ไม่เท่ากับ ASCVD risk score)
– consists of MI (ACS or SCAD or coronary revascularization), stroke/TIA,

symptomatic PAD, aortic aneurysm, all of atherosclerotic origin

– Family history of premature ASCVD (males <55, females <65)
– LDL > 190 : look for Tuberous xanthoma, xanthelasma
– LDL < 70, suggest direct LDL measurement
– Abnormal LDL > 130
– TG > 175, increase ASCVD risk
– Acceptable lower LDL = 35
– Lipid should be re-evaluated 4-6 weeks after ACS

Secondary dyslipidemia
Metabolic syndrome
– Central obesity in Asians : Men >= 90 cm, women >= 80 cm
Concept
– Secondary prevention : Target LDL < 70 with high intensity statin
– Primary prevention : Target LDL < 100
 – DM & age > 40, High LDL > 190, CVD risk >= 5-10%, GFR < 60
– Subclinical atherosclerosis : Target LDL < 130
– Coronary artery calcium score

AHA 2013 : 4 major statin benefit

- ASCVD (CAD, PAD include ABI < 0.85, Stroke) & age >= 21 : High intensity statin (if age
> 75, moderate intensity)
Target LDL decrease >= 50%, May LDL < 70/Non HDL < 100
- LDL >= 190 : High intensity statin
Target LDL decrease >= 50%, May LDL < 100/Non HDL < 130
- Age 40-75 with LDL 70-189
- DM : Target LDL decrease >= 50%, May LDL < 100/Non HDL < 130
- High intensity statin in 10 years ASCVD risk >= 7.5%
- Moderate intensity statin in 10 years ASCVD risk >= 7.5%
- 10 years ASCVD risk >= 7.5% : moderate intensity statin
- Target LDL decrease 30-50%, May LDL < 100/Non HDL < 130
AHA 2018
– 10-year ASCVD risk score
– < 5% = low risk

– 5-7.5% = Borderline risk

– 7.5-20% = intermediate risk

– >= 20% = High risk

Primary prevention
– Young age group

– 0-19 years: life style, except familial hypercholesterolemia

– 20-39 years: prefer statin in LDL-C >= 160 plus strong family Hx of ASCVD

– Persistent LDL > 190 (after life style modification) regardless of ASCVD risk

– High intensity statin & target LDL < 100

– DM (age >= 40): give statin in all DM if LDL > 70

– Simple DM: moderate intensity station (decrease LDL 30-50%)

– DM with high risk in age 50-70: high intensity statin: decrease LDL > 50%

– High risk DM = DM with complication

– DM II >= 10 years

– DM I >= 20 years

– Albuminuria >= 30 mcg of albumin/mg creatinine

– eGFR < 60

– Retinopathy, Neuropathy

– ABI < 0.9

– Age 40-75 years with LDL > 70

– ASCVD risk >= 7.5-19.9% with risk enhancing factor +/- CAC : moderate

intensity statin
– Risk enhancing factor: Fm Hx premature ASCVD, LDL > 160, CKD, metabolic
 syndrome, rheumatoid arthritis, Psoriasis, Ankylosis spondylitis, HIV, women
specific condition
– Coronary calcium score (CAC)

– CAC = 0 : no statin

– CAC = 1-99, especially after age 55 : moderate intensity statin

– CAC = 100+ and/or ≥75 th percentile : moderate intensity statin

– ASCVD risk >= 20%: high intensity statin

– Age >= 75 years with LDL 70-189

– Moderate intensity statin (IIb), avoid statin if CAC = 0

Secondary prevention
– Very high risk group: multiple CV event (MI, stroke, symptomatic PAD) or 1 CV event

plus multiple high risk condition

– Multiple high risk condition: aged >= 65, DM, HT, CKD, HF, smoking, prior CABG/

PCI, persistent LDL-C >= 100

– Target Max statin & LDL-C < 70

– Non-very high risk group: high or moderate statin & target LDL decrease > 50%
Hypertriglyceridemia
– Secondary cause : DM, Chronic liver, CKD, nephrotic syndrome, hypothyroid
 – Fasting TG >= 500 and ASCVD risk >= 7.5 % : start statin
– Life style modification : very low fat diet, avoid refined carbohydrates, avoid alcohol,
consumption of omega-3
– If persistently elevated TG : fibrate therapy for prevent acute pancreatitis

ESC 2016
Very high risk (Target LDL < 70)
– CVD

– DM with TOD or risk factor (HT, DLP, smoking)

– CKD (GFR < 30)

– 10 years CVD >= 10%

High risk (Target LDL < 100)

– Family DLP. Severe HT

– DM without TOF

– CKD, GFR 30-59

 – 10 years risk >= 5-10%
Low to moderate risk (Target LDL < 115)
Target
– Very high risk
– High intensity statin

– If LDL still > 70, add Ezetimibe

– No very high risk

– Age < 75 : high intensity statin

– If LDL still > 70, add Ezetimibe

– Age >= 75 : moderate intensity statin

AACE 2017
Extreme risk : Target LDL < 55
- Progressive ASCVD (UA after LDL < 70)
- ASCVD with DM/CKD (GFR < 60)/Familial hypercholesterolemia
- Premature ASCVD (male < 55, Female < 65)

Thai guideline 2016

Intensity of statin
- High intensity (decrease LDL >= 50%) : Atorvastatin 40, Rosuvastatin 20
- Moderate intensity (decrease LDL 30-50%) : Atorvastatin 10-20, Rosuvastatin 10,
Simvastatin 20-40, Pravastatin 40-80

Treatment
– First line : statin (Maximum tolerated dose), Rule of 6% LDL reduction (double dose
statin)
– Second line : ezetimibe 10 mg OD (specific population: ASCVD, Initial LDL > 190),

PCSK9i.
– BAS or nicotinia acid (without clinical ASCVD)

Target : 1. LDL. 2. Non-HDL (> LDL 30)

Specific population
– CKD (GFR < 60), ref KDIGO 2013 : Atorvastatin 20, simvastatin 40, Rosuvastatin 10,
Pravastatin 40
– Pregnancy : Statin class X, BAS class B, Fibrate and niacin class C

Monitoring
– Adjust Rx 8-12 weeks, if reach target F/U q 12 months

– LFT and CPK at baseline

– F/U LFT 8-12 weeks after start/increase statin

Complication of treatment
- Liver enzyme (ALT) : can use in chronic stable liver disease
- Elevate < 3xULN --> Cont Rx and recheck 4-6 weeks
- Elevate > 3xULN --> Stop/Reduce dose and recheck 4-6 weeks
- Baseline CK > 4xULN --> Do not start.
- Elevated CK during F/U. No routine F/U CK
- < 4xULN
- No symptom --> Cont
- Symptom --> Stop 2-4 weeks --> Same/Another statin (Usual dose)
- 4-10xULN
- No symptom --> Cont
- Symptom --> Stop 6 weeks --> Another statin (low dose & High efficacy)
- > 10xULN --> Stop 6 weeks
– Rhabdomyolysis (CK >10xULN + renal injury)
Interaction (Max dose statin)
– Max simvastatin 20 mg : Amiodarone, Amlodipine, Ranolazine
– Max simvastatin 10 mg : Diltizem, Dronedarine, Verapamil
– Avoid simvastatin or Max Atorvastatin 10 mg : Cyclosporin, Protease inhibitor
– Gemfibrosil : Avoid Simvastatin/Pravastatin, acceptable Atorvastatin
– Pravastatin (high safety) no interaction due to non cypt pathway, except gemfibrosil.

Drug and dose

Statin (กินก่อนนอนลด LDL ได้ดีกว่ากินตอนเช้า แต่ adherence แย่กว่า)
– Atorvastatin : max dose 80 mg
 – Rosuvastatin : max dose 20 mg
– Simvastatin

Intensity of statin

Ezetimibe 10 mg OD : Add on simvastatin/Atorvastatin

– NNT 50 MACE outcome in 7 years, decrease LDL 20%

– Inhibit cholesterol transport protein (Nieman Pick C1-like1 protein)

– Vytolin (Ezetimibe 10 plus simvastatin 10/20/40)

PCSK9i
– Protein Convertase Subtilisin/Kexin type 9 inhibitor : action decrease degrade LDL

receptor
– Used when LDL >= 70 after statin plus ezetimibe
Fibrate
– Indication : Triglyceride > 500-1000 mg/dL

– Avoid combine with statin : increase risk rhabdomyolysis 5.5 times via

gluconidation pathway (increase statin level)

– Fenofibrate (50, 150) : initial 50 mg OD (max 150 mg)

– GFR must >= 45

Cholestyramine
– Decrease GI absorb of LDL but More GI side effect (ทานห่างจากมื้ออาหาร 4 hr)
– Dose 4 gm/packet : initial 4 gm PO q 12-24 hr, increase dose monthly (Max 12 gm q

12 hr)
Niacin (Nicotinic acid) : no decrease CV event
Scoring system
Syndrome
Familial hypercholesterolemia
– Loss of function mutation in LDL receptor gene (decrease LDL clearance)

– Autosomal dominant (severity depend on heterozygote/hemozygote): LDLR,

ApoB, PCSK9
– Autosomal recessive (Disease only in homozygoye): LDLRAP1

– Level of untreat LDL-C

– Heterozygous FH : LDL 200-400, Increase CVD 20 times

– Homozygous FH : LDL > 400

– Physical exam : Corneal arcus in young age, tendon xantgomas

– Diagnosis criteria : Heterozygous FH (used Dutch lipid clinical network)

Tangier disease
– familial disease defect in ABCA1

– Clinical : Low HDL, premature atherosclerosis, orange discolored tonsils

Homozygous familial hypercholesterolemia
– Gene : low density lipoprotein receptor (LDLR)

– Sign : cutaneous planar xanthomas

Lipid clinical trial

FOURIER
– Population : age > 40 with establish ASCVD (stable CAD) or major risk factor,

baseline LDL 92
– Intervention : SC evolocumab q 2 wks fix dose (LDL 80 vs 30)

– Outcome : decreae 5MACE & 3MACE, driving by MI/stroke/coronary

revascularization (follow 26 months).

 – Side effect : injection site rejection
ODYSSEY Outcome
– Population : Age > 18, ACS (STEMI 39%, NSTEMI 48%)

– Intervention : Alirocumab SC q 2 wks vs placebo, treat to target LDL < 70

– Outcome : decrease 4 MACE (Death, MI, stroke, UA), follow 48 months

Criticize : benefit in baseline LDL > 100, decrease new onset DM

SPIRE-1 & SPIRE-2 : bococizumab

– Early terminate trial due to developed antibody and decrease response LDL

– Outcome

– SPINE-1 : Same MACE

– SPINE-2 (high CV disease) : decrease MACE

REDUCE-IT
– Population : Receive statin & TG 135-499 mg/dl plus

– Age >= 45 with establish CV disease (70%)

– Age >= 50 with DM plus risk factor (30%)

– Intervention : Icosapent ethyl 4 gm/day (Pure EPA (Omega-3) : eicosapentaenoic

acid) vs Placebo)
– Intervention : Decease TG 18%, Increase LDL 3%

– Placebo : Decrease TG 2.2%, Increase LDL 10%

– Outcome (N 8179, median F/U 5 years) : Decrease 4-MACE (death/MI/stroke/

coronary revascularization), RRR 26%

– Adverse event : AF, Bleeding, Constipation/Diarrhea, Edema

CETP inhibitor
: cholesterol ester transfer protein
 – ILLUMINATE : negative trial, increase death via increase HT (RAS system)
– dal-OUTCOMES : negative trial

– ACCELERATE : negative trial

REVEAL : positive trial

– Population : establish ASCVD

– Intervention : Anacetrapib vs placebo

– Outcome : Decrease 3MACE drive via MI, Increase HDL, Decrease LDL.

HOPE-3
: concept statin benefit dependent on risk, not baseline LDL
– Population : Intermediated CV risk

– Women >= 60, Men >= 55

– Additional risk : Increase wrist to hip circumference ratio, smoking, dysglycemia,

mild renal dysfunction, low HDL, Fx Hx of CHD

– Exclude : CVD

– Baseline LDL 127

– Intervention : Rosuvastatin 10 mg vs Placebo +/- Candesartan 16 mg/day plus HCTZ

12.5 mg
– Decrease LDL 40 (intervention) vs 30 (placebo)

– Outcome : same MACE (NNT 91)

CLEAR
– Population : LDL > 70 with max statin

– Intervention : bampedoic vs placebo

– Bampedoic : inhibitor of ATP citrate lyase

– Outcome : reduce LDL, no adverse effect

Anti-inflammation
CANTOS
– Population : previous MI and hsCRP >=2 mg/L

– Intervention (RCT) : placebo vs canakinumab (monoclonal Ab targeting IL-1beta)

– Effective dose 150 mg SC q 3 months

– Follow 48 months (4 years)

– Outcome : Decrease MACE, increase fatal infection, same all mortality, decrease

cancer mortality
Hypertension
Hypertension

Mechanism of HTN
– Sympathetic tone: Beta-block

– Renin-angiotensin system: ACEI/ARB

– Salt-water: Diuretic

BP measurement : 2 ข้างต่างกันใช้ค่าสูง, no caffeine > 30 mins, rest

– Cuff at heart level, arm/back support, feet flat on floor

– Record 3 times BP, 1-2 mins apart, additional measurement if first two reading differ

> 10 mmHg (average last 2 BP reading)

New definition : BP >= 130/80 obtained on >= 2 occasion

Increase BP +20/10 : double death from stroke, heart, vascular disease
– Decrease SBP 10 mmHg : Decrease stroke 1/4, CHF 1/4, CAD 1/8, Mortality 1/8

J curve of MACE found in High CV risk population (SBP < 120-130)

– Low SBP < 120 : Increase stroke

– Low SBP < 130 : Increase AKI

– Low DBP : Increase MI

Resistance HT : uncontrol BP with at least 3 BP-lowering medication

– One of these should be a diuretic

– All agent dose (> 50% of maximum dose)

– Treatment : add spironolactone

Treatment should be individualized on Biological age, not chronological age

Office BP measurement
– Seated 5 mins (back and arm support), BP measure 1-2 min apart total 3 times
 – In AF ใช้เครื่องวัดแบบปรอท
HM BP
– วัดเช้าหลังตื่นนอนปัสสาวะ และตอนเย็นก่อนกินยา โดยเลือกวัดติดกันทุกวันเป็นเวลา 7 วันใน
ทุกเดือน
White coat HT : office BP 130/80-160/100 and daytime ABPM or HBP < 130/80
24 hr ABPM in Masked HT

In target BP 140/90
Home BP : SBP/DBP -5 mmHg
24 hr ABPM : SBP/DBP -10 mmHg (target BP in AHA & ESC)
– Daytime - 5 mmHg (same home BP)

– Night time -20 mmHg

– Nocturnal hypertension (AHA: BP >= 110/65, ESC >= 120/70): : autonomic failure
Screening secondary HTN (AHA 2017)
– Onset < 30 or diastolic HT >= 65

– HypoK

– Disproportionate TOD

– Abrupt onset/accelerated/malignant/exacerbrate HT

– Drug resistant HT

Most common secondary HT

– Age < 18 : Renal parenchyma disease, Coarctation of Ao

– Age 19-40 : Renal parenchyma disease, Fibromuscular dysplasia (women)

– Age 40-65 : Primary aldosteronism, OSA, cushingʼs syndrome

– Age > 65 : Atherosclerotic renovascular disease, renal parenchymal disease

Systemic approach secondary HT

Blood pressure variability

: Define BP variable >15 mmHg, Increase mortality
– CCB decrease blood pressure variability

Cause
– Drug adherence

– Autonomic dysfunction : DM

– Sympathetic excess : tachycardia

– Obesity

– OSA

– Vascular stiffness in old age

AHA 2017
Diagnosis
– Normal BP < 120/80

– F/U yearly

– Elevated BP >= 120/80

– Lifestyle modification and reassess in 3-6 months

– HT stage I >= 130/80

– ASCVD or 10 years risk < 10%

– Lifestyle modification and reassess in 3-6 months

– ASCVD or 10 years risk >= 10%

– Anti-HT x1 and reassess in 1 month

– HT stage II >= 140/90 (include ischemic stroke)

 – Anti-HT x1
– Anti-HT x2 in HT stage II and BP above 20/10 from target

Threshold for start anti-HTN

– High risk (ASCVD >= 10%) : BP 130/80

– Equivalent : Clinical CVD, HF (HFrEF & HFpEF), DM, CKD (Stage 3 or 1,2 plus

albuminuria >= 300), Post-KT, Elderly > 65 with healthy, stroke, symptomatic
PAD
– Low or intermediated risk or stroke : BP 140/90

Target BP 130/90 in all groups

Lab test : Basic lab + UA + TFT + check DM/lipid

– Optional : echo, uric, urine albumin
Non pharmacologic
– Weight reduction/Excercise

– Reduced alcohol

– DASH diet/Potassium supplement/Sodium reduction

Target BP & Pharmacologic treatment (AHA)

– First line : HCTZ, CCBs, ACEI/ARB

– If BP > 20/10 of target start dual drug

 – In IHD : target 130/80, suggest betablock in first 3 years (not suggest atenolol due to
less reduction CV event)
– HF, CKD, DM, PAD, 65up : target 130/80
– Previous stroke : start drug >= 140/90 but target BP < 130/80
– CKD with albuminuria > 300 mg/day : first line ACEI
– Chronic AR : avoid beta-block & non-DHP
– Thoracic aortic disease : betablock
– Pregnancy : methyldopa, nifedipine, labetalol
– AF : ARB for prevent recurrent AF

Resistant HT
Definition
– AHA : BP > 130/80 with 3 anti-HT (CCB, ACEI/ARB, diuretic) at maximally tolerated

dose
– ESC : BP > 140/90 with 3 anti-HT (CCB, ACEI/ARB, diuretic, BB) at maximally

tolerated dose
Step approach
– Exclude pseudoresistance: ไม่กินยา, white coat HT
– Assess secondary HT: drug (NSIADs, contraceptive, sympathomimetic), alcohol
– Assess TOD: ตา, หัวใจ, ไต, เท้า
Mx
– add spironolactone 25-50 mg in GFR > 45 & K < 4.5,
– then beta-block if HR > 70
Intervention
– Renal artery stenosis

– Atherosclerotic renal artery stenosis : medication

 – Non atherosclerotic renal artery stenosis with fail medication : renal angioplasty
+/- stent, IIb, levelC

ESC 2018
HT define SBP >= 140 or DBP >=90
– High normal : SBP 130-139 or DBP 85-89

Screening BP after >= 18 years (Age > 50 years : more frequent screening)
– Optimal BP (< 120/80) : repeat BP every 5 years

– Normal BP (120-129/80-84) : repeat BP every 3 years

– High normal BP (130-139/85-89) : repeat BP at least annually (consider w/u masked

HT with ABPM/HBPM)

Target organ damage

Asymptomatic
– Atrial stiffness : Pulse pressure >= 60 mmHg, Carotid-femoral PWV > 10 m/s

– LVH by EKG/Echo

– GFR < 60 or Microalbuminuria > 30 mg/24hr

– ABI < 0.9

– Advance retinopathy : hemorrhage or exudates, papilloedema

Established CV/Renal disease : CVA, CAD, PAD, HF include HFpEF, atheromatous plaque
on imaging, AF

White coat hypertension

– Treatment in patient with TOD or high CV risk (IIb,C)

Treatment
Main: Life style modification in BP >= 130/85, Aim BP control in 3 months
– High normal BP >= 130/85, start Anti-HT in very high risk (esp. CAD)

– Grade 1 : BP >= 140/90

– Immediate start Anti-HT in High risk (CVD, Renal disease, DM)

– Except age > 80, start treatment SBP >= 160/90

– Grade 2 or 3 (>= 160/100) : Immediated start Anti-HT

Target BP
– SBP (should not < 120/70)

– Age < 65 : keep < 130 (120-129) mmHg

– Age >= 65 : keep < 140 (130-139) mmHg

– DBP 70-80 mmHg

Drug
– Prefer single pill combination

– Used mono-therapy

– Grade I HT (SBP < 150) with low risk patient

– High normal BP (SBP < 140) with very-high/high risk

– Frail or older patient (Age > 80)
Thai guideline 2019

Compare target BP
– Concept treatment to BP 120/80
Drug
Thiazide-like diuretic
– Chlorthalidone (25 mg) : start 12.5 mg/day, Max 50 mg/day

– Benefit more than HCTZ : potency, long half life, restore night-time dipping,

metabolic effect
ACEI
– If angioedema from ACEI, wait 6 weeks before change to ARB

ARB
– Prevent recurrence AF (IIa)

– Azilsartan (40, 80mg OD) : edarbi

– Edarbyclor (Azilsartan 40 mg + chlorthalidone 12.5 mg)

– Valsartan (80, 160) : initial 40 mg OD or bid, Max 320 mg/day

Calcium blocker
– L type calcium channel block (dilate afferent arteriole of glomerulus)

– Localization : Cardiac & smooth muscle (DHPs, non-DHP)

– T type calcium channel block (dilate efferent arteriole of glomerulus)

– Localization : SA/AV node, Perkinje cells, Neuron (Verapamil, Diltizaem)

Lercanidipine (10, 20 mg) : initial 10 mg, Max 20 mg

– Leg edema ~ 1%

Manidipine (10, 20 mg) : initial 10 mg, Max 20 mg (แบ่งได้)

Beta-block
– Labetalol (100 mg tab) : start 100 mg q 12 hr (max 400 mg q 12 hr)

Alpha-2 adrenergic receptor agonist

– Methyldopa (250, 500 mg) : start 250 mg q 8-12 hr, increase q 2 days (Max 3 gm/

day)

Clinical trial
SPRINT
– Population : Age >= 50, SBP 130-180

– Additional CVD risk (High risk) : Clinical CVD, CKD (GFR < 60), Framingham 10-

year CVD risk >=15%, Age >= 75

– Exclude : stroke, DM

– Data : BP 136 vs 121 mmHg, Avg 1.8 vs 3 drug of anti-HT

– Intervention : SBP < 120 vs SBP < 140

– Measure : rest 5 mins in quiet room, Automate avg 3 times of BP

– Official BP more than SPRINT trial 10 mmHg

– Follow : mean 3.26 years

– Outcome : NNT 61 (Total MI/Stroke/HF/CA death) : prominent in CV death & HF (may

be from cardioprotective effect of drug more than decrease BP)

– Adverse effect : Hypotension, Abnormal electrolyte, AKI

HOPE-3
– Population : Intermediated CV risk

– Women >= 60, Men >= 55

– Additional risk : Increase wrist to hip circumference ratio, smoking, dysglycemia,

mild renal dysfunction, low HDL, Fx Hx of CHD

– Exclude : CVD

– Intervention : Candesartan 16 mg/day plus HCTZ 12.5 mg vs Placebo

– Data : 134 vs 128 mmHg

– Follow 7 years, Total N 12000

– Outcome : same MACE

ACCOMPLISH
– Population : HT with high CV risk

– Intervention : Benazepril plus (amlodipine vs HCTZ)

– Follow N 11500

– Outcome :

– DM show J curve of MACE when BP < 120

– Non DM show no J curve

SYMPLICITY HTN-3 trial

– Population : Resistant HTN (cause from vascular stiffness)

– Intervention : renal denervation vs sham control

– Simple catheter at main

– Outcome : no effect on BP
SPYRAL HTN-ON MED trial
– Population : Uncontrol HT with stable 1-3 drug (SBP 150-180)

– Average drug 2.2 ตัว

– Donʼt require drug adjustment

– Intervention : renal denervation vs sham control

– Spiral catheter at main & branch

– Outcome : positive 24 hr Home BP at 6 month (decrease BP 9/6)

Hypertensive
emergency
Hypertensive emergency

Definition BP > 180/120 with target organ damage

Treatment goal : MAP decrease 25% in 1 hr and to 160/100 in 2-6 hr, Normal in 24-48 hr
Except 3 condition can decrease to normal BP stat : Aortic dissection, severe
preeclampsia/eclampsia, pheochromocytoma crisis

Specific condition
Aortic Dissection : Beta-block, nitroprusside. Avoid direct vasodilator
– target SBP < 120 and HR < 60 in 1 hr

– Drug : beta-block, Nicardipine, Nitroprusside

ACS
– Immediately reduced SBP < 140 mmHg

– Drug : NTG, Beta-block

Acute heart failure

– Immediately reduced SBP < 140 mmHg
– Drug : NTG, Nitroprusside

Stroke : nicardipine
Ischemia stroke
– Non candidates for reperfusion : < 220/120

– Candidates for reperfusion : before Rx < 185/110, during/after Rx < 180/105

– Drug : Nicardipine, beta-block

Spontaneous ICH : goal SBP 150-220

– ESC reference

– Initial SBP < 220 mmHg : observe, Immediate BP lowering (III)

– Initial SBP > 220 mmHg : BP lowering to target SBP < 180 mmHg

– AHA (within 6 hr)

– Keep SBP 150-220 mmHg

– Drug : Nicardipine, Beta-block

Hypertensive encephalopathy : nicardipine
Eclampsia/preeclampsia
– Drug : MgSO4 then : 1. Hydralazine 2.Labetolol 3.Nicardipine

– Immediately reduced BP target : SBP < 160 & DBP < 105 (ESC)

– Reduced SBP < 140 within 1 hr (AHA)

Hypertension associated Pheochromocytoma : avoid beta-block

– Reduced SBP < 140 within 1 hr (AHA)

– Drug of choice : phentolamine

Elective major surgery

– If BP >= 180/110, defer surgery
Nitroprusside 50 mg with 5%DW 500 ml (1a10) Start 10 ml/hr adjust q 2 mins
– Not effect on microcirculation

– Max dose 1a5 rate 150 ml/hr

– Cyanide toxicity or methemoglobinemia if dose > 10 mcg/kg/min โดยระวังในโรค

ตับ (ตับเปลี่ยน cyanide to thiocyanade และขับออกทางไต) —> sodium
thiosulfate ป้องกันได้
– Nitroprusside more effect arterial vasodilator than NTG (more venodilator)
– Avoid in acute myocardial ischemia, renal insufficiancy
– Toxicity
– Cyanide intoxication : metabolic acidosis from lactic acidosis

– Thiocyanate toxicity : hyperreflexia, seizure, altered mentation

Nitroglycerine 1a5 IV rate 3 ml/hr, Max 60 ml/hr, rate > 15 ml/hr (arterial vasodilator)
 – NTG : venodilatation—> decrease preload, atherosclerotic coronary vasodilatation ,
arterial vasodilator(>50 mcq/min)
– ระวัง reflex tachycardia, headache, low preload condition

Nicardipine 1a5 IV rate 5-75 ml/hr

– side effect : negative inotropic and angina

– Safe in renal failure

Labetalol : non selective beta blocker & alpha block. (25 mg/5 mL)
– Diluted with NSS/D5W : 1 mg/ml

– 20 mg IV in 2 mins then 40-80 mg IV q 10 mins (Max 300 mg) or drip 1-2 mg/min

(total max 300 mg/day)

– Example case BW 60 kg. Labetalol (1a1) 20 ml IV in 2 mins then 60-120 ml/hr

Esmolol : ultra-short selective beta-1 blocker

– Amp 2.5 gm/10 ml, Diluted with NSS/D5W 2500 mg/250 ml (10a1)

– Initial bolus 0.5-1 mg/kg IV over 30 sec then 0.05-0.3 mg/kg/min (Adjust q 4 mins)

– Example case BW 60 kg. Esmolol (10a1) : 3-6 ml IV bolus and then IV rate 20-120 ml/

hr

Phentolamine (non selective alpha block)

– treat in catecholamine induced HT (pheochromocytoma, amphetamine overdose)
Aortic disease
Aortic disease

General
Aortic root - ascending - arch - descending - diaphragm - abdominal aorta
Widening mediastinum : >= 8 cm or 1/3 of thoracic at level of aortic knob
True aneurysm = diameter 1.5x of normal (all layer)
– Size

– Ascending aorta >= 5 cm

– Descending aorta >= 4 cm

– Abdominal aorta >= 3 cm

– Type : fusiform, Saccular, dissecting aneurysm

Abnormal size aorta : male > female ~ 0.4 cm

– Annulus part (2.5) : male 2.9, female 2.5.

– Sinus part (3.5) : male 3.7, female 3.3

– Sinotubular (3) : male 3.2, female 2.9

– Proximal ascending (3) : male 3.4, female 3.1

Grade
– Mild >= 3.5 cm

– Moderate >= 4 cm

– Severe >= 5 cm
Annual growth rate
– Ascending aorta 1 mm per year

– Descending aorta 3 mm per year

Ascending part พบ aneurysm บ่อยสุด เนื่องจากรับ pressure เยอะ

Risk of Aneurysm rupture
– < 5 cm แตก 4% within 1 year
– >= 8 cm แตก 80% within 1 year
Intramural hematoma : Rupture of vasa vasorum in tunica media
Interrupted aortic arch : 80% ass. 22q11 deletion
Right side aortic arch : TOF, Pulmonary atresia, Tuncus arteriosus

Symptoms & sign

– Pain 90%

– Back pain : 40% in type A, 70% in type B

– Pulse deficit 30%

– AR murmur in Ao dissection type A ~ 50%

Echo modality
– Extension of flap
– True lumen : systolic expansion, diastolic collapse, systolic jet away from lumen

– False lumen : diatolic expansion, thrombus formation

– Mechanism and severity of AR

– Assess coronary involvement

– Pericardial & pleural effusion

Echo finding : example

– Ascending aortic dilatation ... cm. Effacement of aortic root?

– Intimal flap at proximal ascending aorta to descending thoracic and abdominal aorta

+/- thrombus/SEC in false lumen

– Prolapse/flail of AV leaflet with severe AR

– Minimal pericardial effusion +/- sign of cardiac tamponade

 – Dx :Marfan syndrome with Dissecting aortic aneurysm involved ascending aorta to
abdominal aorta (Standford type A) with acute ontop chronic severe AR

Aortic CT finding
Indiction for intervention in TAA
e. Symtomatic (ไม่ขึ้นกับขนาด) : pain, emboli, fistula
f. Asymtomatic
– PAU (common in descending), mycotic, intramural hematoma with TAA (ดูใน
noncontrast CT)
– 60 mm in descending aorta and not suit for TEVAR
– >= 55 mm In normal or bicuspid aortic
– 50 mm with risk in bicuspid AV : family Hx of dissection, HT, coarctation, incease
diameter > 3 mm/year.
 – 4.5 cm with AV surgery
– 2.5 cm/BSA in turner syndrome with aortic root/ascending aorta
Marfan or marfanoid ระบุเฉพาะ ascending aorta และ prefer surgery > TEVAR
– >= 50 mm

– 45 mm with risk : family Hx of dissection, increase size > 3 mm/year, HT, severe AR/

MR, desire pregnancy, TGFBR1 or 2 (anti-proliferative) include loeys-dietz

syndrome (LDS)
– LDS is AD (hypertelorism: ตาห่าง, bifid uvula/cleft palate, arterial tortuosity) :
early intervention ascending aortic diameter >= 45 mm

Indication for intervention in AAA : prefer life expect > 2 years

> 45 mm : screening yearly
e. Symtomatic : pain, emboli, fistula
f. Asymtomatic
– 5.5 cm in male, prefer 5 cm in female

– Growth exceeds 10 mm/year

AAA prefer EVAR > open surgery (ขึ้นกับ anatomy fit for EVAR? or fit for surgery)
EVAR ต้องมี neck length ~ 10 mm
Chimney ต้องให้ DAPT 3-6 months and then ASA
TEVAR ให้ ASA alone
# Screening ultrasound AAA, level1A
– Male 65-75 years who have ever smoking

50% of bicuspid aortic valve มี root or ascending dilatation (fibrillin-1 def)

10% of Bicuspid aortic มี coartation of aorta
50% of coartation of aorta มี. Bicuspid aortic valve
Bicuspid aortic valve ให้ screening first degree relatives
Artery of adamkiewicz : branch of aorta level T9-12 supple spinal cord
– R-L fusion : dilatation root & tubular

– R-N fusion : dilatation tubular & arch

– Genetic in young age : root dilation

Grade of atherosclerosis (aortic plaque)
—> ASA treatment (IIa, C)
– Grade 1 or normal : < 2 mm

– Grade 2 : Intimal thickness > 2 mm

– Grade 3 : atheroma protruding < 5 mm

– > 4 mm increase risk stroke

– Grade 4 : atheroma protruding >= 5 mm

– Grade 5 : >= 2 mm plus mobile or ulcer

Summary indication for intervention in aortic aneurysm

Aortic dissection (must has flap) : acute < 14 days, chronic > 90 days
– Type A : ascending or A+B.

– Back pain 40%, Coronary involvement 10% (RCA > LM)

– Mortality 1% per hr in first 24 hr

– Type B : descending.

– Back pain 70%

Work up in stable
– ใน setting low prob ส่ง D-dimer for R/O & prognosis + TEE + CXR
– ใน setting high prob ส่ง TTE ถ้าไม่ชัดค่อย CT
Work up in unstable อะไรก็ได้ขอให้ได้คำตอบและเร็วสุด

Treatment aortic dissection or Intramural hematoma

– Pain control

– Beta-block, goal SBP < 120, HR < 60 : esmolol or labetolol, alternative verapmil,

diltizem. If HR < 60 : nitroprusside or nicardipine

– Avoid CCB in marfan syndrome —> increase risk aortic expansion

Type B
– Uncomplicated type B: medication —> TEVAR

– Complicated type B (renal fail, visceral ischemia, rupture): TEVAR > surgery

– Prefer Sx > TEVAR in connective tissue disease, except previous cardiac surgery

Asymtomatic PAU
 – diameter > 20 mm or neck > 10 mm —> early intervention

Follow up imaging, if not require intervention

– First at initial, next 6 months and then yearly

Exercise
– Root > 4.5 cm : avoid competitive sport

– Avoid isometric exercise

Family screening
Bicuspid aortic valve or Thoracic aortic aneurysm
– Screening first degree relatives (IIb)

Syndrome
Marfan syndrome
– Autosomal dominant, 30% de novo mutations.

– PE : High arch palate, tall sature, thrumb & wrist sign, MVP, AR

– Only aortic root (size of sinus of valsava)

– Effacement of this junction suggests annuloaortic ectasia and often is seen in

patients with Marfan syndrome

Loeys-Dietz syndrome
– No lens subluxation
PAD
PAD
– PAD : risk for CV death 25-30% within 5 years
– MRA is imaging of choice in PAD (Coartation, PAD, renal artery stenosis)
– May-Thurner syndrome : Left common iliac vein compression against lumbar
vertebrae by Right common iliac artery
– Cause : young age Lt DVT

– Management : stent at left common iliac vein

– Hypothenar Hammer Syndrome : repettitive blunt truama over hypothemar eminence

—> thrombosis or aneurysm at ulnar artery leading digital emboli/ischemia/gangrene
Renal artery stenosis
General
– Define stenosis >= 60%

Concept
– Single renal artery stenosis

– Activate RAS system but opposite normal renal function is diuresis

 – Mx : ACEI/ARB
– Bilateral renal artery stenosis
– Activate RAS system —> volume overload

– Mx : Renal artery intervention

– Single renal artery stenosis ไม่เท่ากับ Single normal kidney

Syndrome of renovascular disease
– Asymptomatic

– Renovascular HT

– Accelerated CV disease : CHF, Stroke, Secondary aldosteronism

– Ischemic nephropathy

Clinical situation for suspicious renal artery stenosis

– Onset HT < 30 years

– Severe HT > 55 years with CKD/HF

– Abdominal bruit

– Rapid/Worsening/Resistant HT

– Hypertensive crisis

– AKI after RAAS blocker

– Unexplained atrophic kidney

– Flash pulmonary edema

Investigation
– First-line : DUS

– If stenosis >= 60% : CTA in GFR > 60, MRA in GFR > 30

– Second-line : CTA, MRA

– Hemodynamic impact : systolic pressure gradient > 20 mmHg or resting pressure

ratio distal to stenosis < 0.9

– Gold standard : DSA (Digital subtraction angiography)

Medication for single renal artery stenosis

– ACEI/ARB (I,B)

– CCB or Beta-block (I,C)

Indication for revascularization

– Hemodynamic significant RAS

– Recurrent/unexplained/Flash HF

– Accelerated/Resistant/Malignant HT

– No routine revascularization in secondary to atherosclerosis

– Preserve only in renal artery stenosis related recurrent HF/Flash pulmonary

edema or acute oligo-anuric renal failure (bilateral RAS without renal atrophy)
– FMD : balloon angioplasty > stent
Carotid stenosis
General
– Carotid stenosis = stenosis >= 50%

– Symptomatic carotid stenosis (must onset stroke within 6 months)

Investigation
– First-line : Duplex ultrasound

– Further investigation : CTA or MRA (extent & severity of extracranial carotid stenosis)

Role revascularization
– Symptomatic stenosis 50-99%

– Prefer CEA than carotid artery stent

– Timing revascularization: preferably within 14 days of symptoms onset

– Asymptomatic stenosis 60-99% with increase risk stroke plus life expectancy >

5 years
– Prefer CEA (IIa) than Carotid stent (IIb)
CEA : accept procedure risk death/stroke
– Asymptomatic : < 3%

– Symptomatic : < 6%

Treatment
– Anti-platelet

– Single anti-platelet (ASA or clopidogrel)

– Carotid surgery (I)

– Asymptomatic (IIa)

– DAPT (ASA plus clopidogrel) for 1 months and then single antiplatelet in carotid

stent
– Concomitant with AF : OAC monotherapy except within 1 months post carotid

stent (OAC plus single antiplatelet)

– Carotid stent

– Specific condition that prefer carotid stent more than CEA

– Age > 80 years

– Clinically significant comorbidity : cardiac disease, severe pulmonary

disease
– Contralateral internal carotid artery occlusion

– Contralateral recurrent laryngeal nerve palsy

– Previous radical neck surgery or radiotherapy

– Recurrent stenosis after CEA.

– Used emboli protection device (IIa, C)

Plan CABG setting

Carotid duplex ultrasound in pre-op CABG
– Hx of TIA/Stroke < 6 months (I,B)

– Hx of TIA/Stroke >= 6 months plus (IIb,B)

– Age >= 70, multivessel CAD, concomitant PAD, carotid bruit

Scheduled for CABG, Role carotid revascularization (Prefer CEA)
– Recent TIA/stroke within 6 months plus

– Carotid stenosis 50-99% (IIa)

– Asymptomatic carotid stenosis 70-99% plus one of following (IIb)

– Contralateral occlusion

– Bilateral carotid stenosis 70-99%

– Increase risk of ipsilateral stroke

– Contralateral TIA/stroke

– Ipsilateral silent infarction on cerebral imaging

– Intraplaque haemorrhage or lipid-rich necrotic core on MRA

– U/S imaging : stenosis progression (>20%), spontaneous embolization on

transcranial Doppler, impaired cerebral vascular reserve, large plaques,

echolucent plaques, or increased juxta-luminal hypoechogenic area
No role screening in urgent CABG without recent stroke/TIA

Lower extremity arterial disease (LEAD)

General
– Claudication : relieved by rest within 10 mins

Diagnosis
– ABI indication (Sense 80%, Spec 90%)
 – Suspected LEAD : Bruit, Symptom/claudication, Non-healing wound > 2 wks
– Risk for LEAD : CAD, PAD, AAA, CKD, HF

– Asymptomatic : age > 65, age < 65 with high CV risk, age > 50 with family Hx of

LEAD
– ABI interpretation
– Normal ABI 0.9-1.4

– ABI =< 0.9 : Dx LEAD

– ABI > 1.4 : perform Toe-brachial index (abnormal =< 0.7) ใช้เครื่องวัด sat at
Toe, Doppler waveform analysis, pulse volume recording
– Symptomatic PAD : ABI < 0.8

– Chronic limb ischemia : ABI =< 0.7

– Rest pain : ABI < 0.5

– Exercise treadmill ABI test : exertional leg symptoms but resting ABI > 0.9

Investigation
– Duplex ultrasound : first-line for confirm diagnosis

– Duplex ultrasound screening AAA (IIa)

– MRA/CTA : Imaging guide intervention

Screening comorbidity
– HF screening :TEE or natriuretic peptides (IIa)

Treatment
– Supervise exercise & smoking cessation

– Anti-platelet (ASA or Clopidogrel) for symptomatic patient only

– Symptomatic PAD

– Cilostazol : only for release symptoms

– Asymptomatic PAD : class III in ESC, IIa in AHA

– Statin in all patient : improved walking distance

– CCB (e.g. verapamil) : improved walking distance

– Revascularization for relief symptoms/improved walking distance/QoL : medication is

first-line for improved symptoms

– Isolated crural lesion (below popliteal artery) : medication only

– Femoro-popliteal artery

– Stenosis/occlusive lesion < 25 cm : endovascular repair with stent

– Occlusive Lesion >= 25 cm : prefer open surgery

– Aortoiliac lesion

– Isolated iliac lesion (lesion < 5 cm, not extend to common femoral artery) :

endovascular repair with stent

– Other lesion : Open surgery or hybrid

– After endovascular repair : DAPT 1 month then single anti-platelet

limb ischemia
Chronic limb ischemia
– Other term : critical limb ischemia
– Chronic >= 2 weeks & Clinical pattern with threatened limb viability (ischemic rest
pain, non-healing wound, gangrene)
– ABI should be =< 0.7
– Role revascularization in infra-popliteal lesion
– Surgical bypass using great saphenous vein (I)

– Endovascular repair (IIa)

– Wound healing therapy (IIb) : Intermittent pneumatic compression, hyperbaric

oxygen
Acute limb ischemia
– Symptoms < 2 weeks

Clinical stage
Management
– Heparin & analgesic

– Urgent revascularization

– Catheter-base thrombolysis is effective (I, A)

– Mechanical thrombectomy (IIa)

Evaluated cause of acute limb ischemia

– Cause of thrombosis or embolization : Echo or addition rhythm monitoring for detect

AF
Subclavian artery stenosis
– Define : stenosis >= 50%
– Etiology : Takayasu arteritis, Fibromuscular dysplasia

Indication for revascularization

– Symptomatic : stent or Sx

– Asymptomatic

– Proximal stenosis with undergo CABG and used ipsilateral LIMA (risk for

coronary steal syndrome)

– Ipsilateral arteriovenous fistula for dialysis (IIa)

AV fistula
– After groin puncture post cath : incidence 1%
– Can conservative treatment if no groin hematoma (spontaneously closure 50% in
one year)

Mesenteric ischemia
Acute mesenteric ischemia
– Investigation : CTA (I), D-dimer (IIa)

– Treatment :

– First-line is endovascular revascularization in acute thrombotic occlusion

– Open surgery is optional

Chronic mesenteric ischemia

– Investigation : First-line is Duplex ultrasound

– Treatment :

– Revascularization (I)

– No delay revascularization in order to improved nutrition (III)

Takayasuʼs arteritis
– Diagnosis from ACR criteria 3/6 criteria
– Physical exam : Apical heaving (LVH due to HT), unequal of peripheral pulse, absent
Rt/Lt radial pulse, Arterial bruit at carotid/subclavicular/brachial/abdominal.
– Lab : ESR, CRP
– Treatment : Prednisolone 1 MKD and gradually reduced as symptoms and
inflammatory process
– Refractory : AZA, MMF
Coarctation of aorta
Coartation of aorta

Type
– Congenital

– Preductal

– Postductal

– Juxtaductal

– Acquire associate with Atherosclerotic disease

Spectrum
– Coartation

– Aortic arch hypoplasia

– Interrupted aortic arch

General
– Hemodynamic significant :

– Peak to peak gradient > 20 mmHg by cath or Mean gradient > 20 mmHg by

echo
– Upper extremity/lower extremity gradient > 10 mmHg

– Gradient 10-20 mmHg plus

– LV dysfunction or AR

– Significant collateral by CT/MRA

– Must looked for bicuspid AV, shone, turner syndrome, VSD

– Echo aortic arch : delay upstroke of systolic flow & continuous diastolic forward flow

(saw tooth appearance), increase distance between Lt common carotid artery and Lt
subclavian artery
– Complication :

– rupture cerebral aneurysm ~ 10% : screening intracranial aneurysm (IIb, B)

 – HT

Physical exam
– SEM at left inter-scapular region, radio-femoral delay, higher BP in arms > legs

CXR
– Figure of 3 sign

– Rib notching

– Found in other conductions : SVC obstruction, neurofibromatosis

Echo
– Suprasternal view : narrowing coarctation distal to left subclavian artery with post

stenosis dilatation. Turbulent flow with persistent diastolic forward flow cross
coarctaion of aorta, mean gradient ... mmHg.
– Doppler in descending aorta : delay upstroke and persistent diastolic forward flow

(sawtooth appearance)

Indication for intervention : prefer stent > surgery

– upper limb hypertension or LVH with upper > lower limb BP 20 mmHg, level1C

– > 50% narrow relative to Ao at diapharm level (IIa, C)

Indication for intervention (20 mmHg)

: HT plus significant coarctation
Non invasive finding (I)
– Non invasive pressure between upper & lower > 20 mmHg (regardless of symptoms)

– > 10 mmHg plus either LV dysfunction or AR

– Mean doppler systolic gradient > 20 mmHg

– > 10 mmHg plus either LV dysfunction or AR

– Pathologic BP response during exercise (SBP > 230)

 – Significant LVH
Imaging finding (IIa)
– HT with narrow >= 50%, regardless of pressure gradient

Intervention (prefer stent > only balloon)

– Peak to peak gradient >= 20 mmHg

– Peak to peak gradient < 20 mmHg (> 10 mmHg) with significant collateral flow

Intervention vs surgery correction

– Depend on heart team
– Prefer intervention : recurrent, discrete coarctation

– ASA 6 months & endocarditis precaution

– Prefer surgery : long segment stenosis

– Surgical type
Follow up
– Post repair/intervention : follow up every 2 years for look for complication restenosis
or aneurysm formation (prefer CMR)

Syndrome
Turner syndrome : 30% aortic dilatation
– women with TS ; risk for aortic dissection 100 เท่า
– แนะนำ TTE q 3-5 years in low risk, thoracic MRI q 3-5 years in moderate risk,
thoracic MRI q 1-2 years in high risk
Cardioembolism
Cardioembolism

7 clinical indicating cardioembolism

– Abrupt onset stroke

– High NIH >= 10 in age >= 70 years

– Varies arteries distributions

– Other sign of systemic thromboembolism

– Infarct involved cortex, subcortical, large lenticulostriate

– Hyperdense MCA. MCA sign excluding ICA stenosis

– Repid recanalization

High embolic potential

– Thrombi : AF, MI, cardiomyopathy, Mechanical valve

– Vegetation : IE

– Tumors : Myxoma, fibroelastoma

 – Aortic atheroma

Cryptogenic stroke
– Absence of overt source of stroke

– Embolic stroke of undetermined source

– Non-lacunar brain infarct without proximal arterial stenosis or cardioembolic source

Role of Echo
– Routine echo is not recommend (III) : no cost effectiveness

– Low yield (2%) of echo on no history of cardiac disease, normal exam, ECG and CXR

– TTE with off axis (LA appendage), Agitated NSS bubble, 3D, PFO, TEE

– If TTE negative for cardio-embolism

– TEE : add on cardiac mass only 3%, add on aorta atherosclerosis 50%

Monitor EKG 72 hr in high risk embolic case for AF detection (I)

– if still suspected AF : long term monitoring (IIa,B)

Diagram for Ischemic stroke

Role of PFO closure

– PFO found in normal population 1/3
– Atrial septal aneurysm with PFO or Large PFO (>= 4 mm) increase risk stroke

– PFO cause paradoxical emboli

– PFO closure : Increase LA pressure —> may be increase AF

– Procedure risk 6-10% : transfusion, tamponade, urgency sx

 – PFO with desaturation without PHT : consider closure

Duration of VKA
– LV thrombus : VKA INR 2-3 at least 3 months

Syndromic disease
Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)
– AD, major disease-associated genes : ENG, ACVRL1, SMAD4

– Clinical manifestations : epistaxis, gastrointestinal bleeding (IDA), mucocutaneous

telangiectasia. AVMs in pulmonary, hepatic and cerebral circulations.

– Consensus criteria : Definite = 3/4 criteria, Suspected 2/4 criteria

– Spontaneous and recurrent epistaxis

– Multiple mucocutaneous telangiectasia at characteristic sites

– Visceral involvement (eg, gastrointestinal telangiectasia; pulmonary, cerebral, or

hepatic arteriovenous malformations [AVMs])

– A first-degree relative with HHT

Clinical trial
PFO closure device in cryptogenic stroke
Pulmonary
embolism
Pulmonary embolism

Hemodynamic in PE

Normal RV function : governed by 4 part

– Systemic venous return

– RV afterload (PA load)

– Pericardial compliance

– Contraction of RV free wall & IVS

General
– Acute PE with hypotension : SBP < 90 or SBP drop >= 40 for 15 min, exclude
hypovolemia, arrhythmia
– U/S DVT positive 30-50% in PE.

Clinical prediction rule

– Very low probability (< 1.8%) : no further investigation
– PERC score = 0

– Low probability (< 15%) : Sent D-dimer (only ELISA), if negative exclude.
– Cutoff : 500 ng/ml (age < 50), Age x10 (age >=50)

– False low D-dimer : Too early, Too late (more than 3 days), underfilled collection

tube
 – Investigation in pregnancy
– Low probability : D-dimer

– Non-low probability : 1. Leg ultrasound 2.VQ-Spec 3.CT-PA

CXR
– Hampton hump sign : sign of lung infarction
– Westermarkʼs sign : represents a focus of oligemia (hypovolemia) (leading to
collapse of vessel) seen distal to PE
– Pallas sign : enlarge Right descending pulmonary artery

Echo
– McCornellʼs sign (RV free wall akinesia with sparing RV apex) in severe PHT or
massive PE, Not found in RV infarction
 – IVC plethora : IVC > 21 mm plus
– Collapsed < 20% with quiet respiration

– Collapsed < 50% with sniff

– RV > LV basal diameter

– LV eccentricity index > 1.1
– PA systolic pressure > 50 mmHg (combine previous PHT)

CTA
CT for all case : no decrease mortality
– Filling defect

– RV > LV basal diameter

Investigation
Suspected PE with hypotension
– Suitable for CTA —> go CTA

– Not suitable CTA (condition is critical) : Echo for RV overload or dysfunction

Suspected PE without hypotension

– Low clinical probability : D-dimer, if positive —> CTA, if negative R/O

– Not recommend D-dimer in high clinical probability

– High clinical probability : CTA

Absolute role echo in PE in critical condition

Prognosis
High early mortality risk
– Shock with RV dysfunction from CT/Echo (Echo : RV dysfunction/dilatation, End

diastolic RV/LV ratio >= 1.0)

– Support : sPESI >= 1, Biomarkers : Elevate Troponin/NT-proBNP > 600/BNP >

100
Intermediated risk (sPESI >= 1, PESI III-IV)
– Intermediated-high (both positive) : RV dysfunction & positive biomarker
 – Intermediated-low (one positive) : RV dysfunction or positive biomarker
Low risk (sPESI = 0, PESI I-II)
Simplified PESI (pulmonary embolism severity index) : 6 point
– Age > 80

– Cancer

– Chronic HF or Chronic lung disease

– PR >= 110 bpm

– SBP < 100 mmHg

– Arterial O2 sat < 90%

(30 days mortality : 0 point = 1%, >= 1 point = 10%)

Treatment
PE with shock (high risk)
– IV Heparin (UHF) in case of high suspected PE with hypotension

– Following with thrombolysis after confirm imaging (thrombolysis during

anticoagulant is only relative contraindication)

– Time : Best outcome within 48 hr but still useful in symptomatic patient up-to 14

days
– If contraindication or failure thrombolysis : surgical embolectomy or percutaneous

catheter-directed treatment
Intermediated-high risk
 – Anticoagulant : if heparin target PTT ratio 1.5-2
– Admit intensive care unit.
– : If hemodynamic decompensation
– Non-high risk bleeding : systemic thrombolysis

– High risk bleeding : surgical embolectomy or percutaneous catheter-directed

treatment
– Role thrombolytic without hypotension (ESC III,B): neutral mortality in 7 days,
improved hemodynamic, increase stroke rate

Dose anticoagulant & fibrinolysis

– tPA (alteplase) : 100 mg IV over two hours.
– Streptokinase : 250,000 units IV over 30 minutes then 100,000 units/hour for 24
hours.
– Urokinase : 4400 units/kg IV over 10 minutes then 4400 units/kg per hour for 12
hours
– TNK (tenecteplase) : prefer in PE-related cardiac arrest
<60 kg: 30 mg
≥60 to <70 kg: 35 mg
≥70 to <80 kg: 40 mg
≥80 to <90 kg: 45 mg
≥90 kg: 50 mg
Role catheter-directed thrombolysis (CDT)
Surgical pulmonary embolectomy is first line (I,C), CDT is second line (IIa,C)
– Contraindication to systemic thrombolysis

– Failed thrombolysis

Dose thrombolysis in CDT (1/5 of systemic thrombolysis)

– rt-PA bolus 4-6 mg then infusion 1 mg/hr (24 mg/day) or 20 mg in 15 hr

– Can cont. heparin 400 unit/hr

CTEPH
– Dx after 3 month post acute PE
Investigation

IVC filter
– site : below renal vein
Indication
– Contraindication for anticoagulant

– Recurrent acute PE despite therapeutic anticoagulant

Prevention of VTE in hospital

 – compression stocking : limit in PAD
– Intermittent pneumatic compression
– Contraindication : PAD, DVT, CHF

Dose NOAC in DVT-VTE/PE

– Class I,level B in all NOAC
– A1R3, no require heparin
– Other require LMWH 5 days

Duration of anticoagulant for VTE/PE

– Provoked by surgery or transient risk factor : 3 months
– Unprovoked VTE/PE : extended anticoagulant

Clinical trial
PEITHO trial : RCT
– Population : intermediated risk PE

– Intervention : TNK plus UFH vs UFH

– Outcome : Reduced composite of death and hemodynamic compromise at 7 days

(2.6% vs 5.6%) but increase major bleeding (8.3% vs 1.4%)

Pulmonary HTN
Pulmonary hypertension (PHT)

– Normal mean PA 14 +/- 3 mmHg

– Eccentricity index (septal shift overtime) : normal = 1, abnormal > 1.8 (Diastolic LV,
inner chamber length/width)
– Delta pressure = Flow x Resistance
– Echo : PW/Mid systolic notching
– RVH : RVdD >= 5 mm
– Pulmonic valve AT (RVOT) < 105 ms
– PVR/SVR
– Normal =< 0.25

– Severe PHT > 0.75

– Inoperable > 1

– Prevalence of PHT
– Lt side heart 2/3

– Miscellaneous 1/5

– Lung disease 1/5

– PAH 2-3%

– CTEPH 2-3%

Type
– Pre capillary PH : type I, III, IV, V
– Type I : structural lumen narrow & functional vasoconstriction 20%

– Type III : prefer FEV1 < 60% predicted (COPD), FVC < 70% predicted (IPF)

– Post capillary PH : type II, V

New classification
Step investigation
ESC
`. Echo
a. สงสัยอะไรส่งตามที่ส่งสัย เช่น สงสัยทาง chest : PFT/CLCO, HRCT
b. V/Q scan
c. Left heart cath : confirm PAHT
CXR
– PHT : RPD, male >= 17 mm, female >= 15 mm

Prognosis
– Predict poor prognosis : PVR increase follow as progression of disease, CO drop &
RAP high in late
– Good predictor prognosis after treatment : Functional class & NT-proBNP
– PAP not predict prognosis
– Good prognosis in PHT related congenital heart (Eisenmenger : prognosis ~ 20

years)
– Poor prognosis in PHT related AIDs and portopulmonary HTN
– High risk : RA area in 4 chamber > 26 cm2 or pericardial effusion, RAP > 14 mmHg,
Cardiac index < 2.0
Genetic
– BMPR2
Drug associated PHT
RVSP
– RVSP =< 36 mmHg, TR vel =< 2.8 m/s : exclude PHT
– RVSP 36-51, TR vel 2.8-3.4 m/s plus 2 different categories

– RVSP > 51 mmHg, TR vel > 3.4 m/s : confirm PHT

Echo evaluated PHT

– mPAP = TVI of TR + RAP
– mPAP by systolic-diastolic

– mPAP by abbas = SPAP + RAP

– mPAP by Mahan = 90 - (0.62 x Acceleration time of PA flow by PW)

Role echo screening in asymptomatic patient (I)

– systemic sclerosis
 – BMPR2 mutation carrier
– first degree relatives with HPAH
– Portopulmonary hypertension for liver transplant
PVR by siriraj Echo
– TRvel/RVOT VTI
– < 0.175 : no PHT

– 0.175-0.275 : ref PVR (abbas) low

– >= 0.275 : ref PVR (abbas) high

Estimate PVR = 10(TR vel/RVOT VTI) + 0.16

Pulmonary venoocclusive disease

– Anatomy : post capillary
– Hemodynamic : Pre-capillary, PCWP < 15 and mPAP > 25 mmHg
– Clinical suspicious in venodilator and developed HF

Vasodilator testing for closure or heart transplantation

Modified Barst criteria
– PVRi < 6 wood unit and PVR/SVR < 0.3

– PVRi 6-9 wood unit and PVR/SVR 0.3-0.5

– Require vasoreactivity test (match all)

– Decrease PVRi 20% —> Final PVRi < 6 wood unit

– Decrease PVR:SVR 20% —> Final PVR:SVR < 0.3

Closure in congenital heart with PHT (ESC)

 – Define PHT in congenital heart : PVRi >= 4
Recommend for correction of congenital heart disease with Lt to Rt shunt
– PVRi < 4 (PVR < 2.3 WU) : correct (IIa)

– PVRi > 8 (PVR > 4.6 WU) : not correct (IIa)

– PVRi 4-8 WU : controversy

Vasodilator test for PAHT (arterial)

– 10-15% positive vasoreactivity test and 50% stop responding within 1 year
Indication for 3 setting
– idiopathic PAHT

– Drug induced PAHT

– Familial primary PAHT

Contraindication in FC IV
Positive response
– Decrease in mPAP >= 10 mmHg and less than 40 mmHg without decrease CO

Dose :
– Inhale nitric oxide 10-20 PPM (part per million) for 10 mins

– IV epoprostenol

– IV adenosine

Criteria for exercise-PH

– mPAP > 30 mmHg & total PVR > 3
– Cause of exercise-PH : Unmasked PVD, Exercise-induced rise in LA pressure.

Fluid loading test

– To unmask PHT from Lt side heart with borderline PAWP
– Selection : PCWP 13-15 mmHg with HFpEF
– Intervention : fluid load 500 ml in 5 mins
– Interpretation : PCWP > 18 mmHg is abnormal after fluid load

Goal of therapy
 – Clinical : FC I-II, no syncope, 6-min walk > 440
– Echo/MRI : RA area < 18cm2, no pericardial effusion
– Lab : BNP < 50, NT-pro BNP < 300
– CPET : peak Vo2 > 15 and VE/VCO2 sloped < 36
– Hemodynamic : Normalized RV function (RAP < 8, CI > 2.5, SVO2 > 65%)

Role of anticoagulation
– 3 groups : IPAH, HPAH, PAH due to anorexigens (IIb)

Specific treatment
FC II-III : All oral drug
– FC II : not used IV epoprostenol.

– If used combine : ERA + PDE-5i

– Initial combine : Ambrisentan plus tadalafil (I,B)

– Sequential combine (I,B) : Sildenafil + Macitentan, Bosentan + Riociguat, ERA/

PDE-5i + Selexipag
– FC III : initial combination Ambrisentan plus tadalafil (I,B), other drug combine IIa or

IIb
FC IV : combine with IV epoprostenol (I, A), other drug is IIb

Drug for PHT

– Mechanism is vasodilatation & antiproliferation
– Drug Reduced morbid & mortality : Epoprostenol, Macitentan, Selexipag
– High dose CCB in WHO-FC I-III (IPAH, HPAH and DPAH with response to
vasodilator test)
– CCB is contraindication for eisenmenger

– Consider combine in High risk group

– Class I recommend for drug combination in FC II-III : Ambrisentran + Tadalafil
– Class I recommendation in FC IV : Epoprostenol IV
– Riociquat : recommend in FC II-III

Endothelin receptor antagonist

: Teratogenic effect
– Bosentan (dual ET-A & B receptor antagonist) : drug with choice for congenital

heart with eisenmenger; Other ERAs, PDE-5i, prostanoid (IIa)

– Dose : 62.5 mg PO bid x4 weeks and then 125 mg bid

– Side effect : Hepatotoxicity

– Ambrisentan (selective ET-A receptor antagonist)

– Dose : 5 or 10 mg OD

– Side effect : peripheral edema, hemolytic anemia

– Macitentan (non-selective ET-A & AT-B receptor antagonist) : dose 10 mg PO OD

– Dose : 10 mg PO OD
 – Side effect : anemia, cold-like symptoms
Nitric oxide pathway (via cGMP)
– ห้ามให้คู่กันใน pathway เดียวกัน
– Phosphodiesterase-5 inhibitors

– Sildenafil : 20 mg tab, start 0.5 tab tid

– Side effect : headache, flushing, epitaxis, negative inotropic effect

– Tadalafil

– sCG stimulator

– Riociquat : initial 0.5 mg PO tid (max 2.5 mg tid)

– Inhaled NO

Prostacyclin pathway
– Prostacyclin analogues

– Iloprost (IV, oral, aerosol) : inhalation 2.5-5 mcq/inhalation for 6-9 times/day

(Max 45 mcq/day)
– Side effect : flushing & jaw pain

– Beroprost

– Epoprostenol

– Terprostinil

– Prostacyclin receptor agonist

– Selexipag

CCB :
– Amlodipine : upto 20 mg/day

– Nifedipine : 120-240 mg/day, start 30 mg (SR) bid.

– Diltiazem (prefer in tachycardia) : 240-720 mg/day, start 60 mg tid

ไม่มี verapamil
Treatment effect
– PAHT : Decrease PVR but still same mPAP
– PHT from Lt side heart : Decrease mPAP

Atrial septostomy as bridge to transplant

– Avoid in baseline RAP > 20 mmHg, O2sat < 85%RA, High LVEDP
– Physiologic change
– Decompress Rt heart chambers

– Increase LV preload

– Increase CO

Lung or heart lung Transplantation

– PHT FC II : survival 5 years
– PHT FC III : survival 2.5 years

– Lung transplantation : survival 4 years

Indication
– Only NYHA FC III-IV on max medication

– 6MWT < 350

– CI < 2 L/min

– RAP > 15 mmHg

– Failing IV epoprostenol

Ballon pulmonary angioplasty

– Concept for destroy web/constriction part, not destroy clot
– Repeat intervention 6-7 times in 2-3 years
– Decrease PA pressure 20-30%

Acute fluid management in PHT

– Acute RV failure : fluid load
– Acute ontop chronic RV failure
– Reverse bernheim effect —> diuretic

– No Reverse bernheim effect —> fluid challenge

Clinical trial
SERAPHIN
– Population: PAHT

– Intervention : macitentan vs placebo

– Outcome : improved primary composite outcome (of death, atrial septostomy, lung

transplantation, initiation of prostanoids or worsening PAHT)

BREATHE-1
– Population : PAHT

– Intervention : bosentan vs placebo

 – Outcome : improved 6MWT, WHO classification and hemodynamic
GRIPHON
– Population : PAHT

– Intervention : Selexipag vs placebo

– Outcome : decrease composite of death and complication related to PHT

Approach to
cardiology
Approach in cardiology

Key : History ans physical exam

– ถามประวัติเคยทราบโรคหัวใจหรือเคยตรวจหัวใจหรือไม่ ได้ยาอะไร ได้ตรวจเพิ่มเติมอะไรบ้าง
– General appearance (หน้าตาจำเพาะ, ตัวยาว), ดูเขียว, เหลือง, clubbing, ดูลิ้น(cyanosis,
macroglossia), ดูตา (ptosis), skin lesion & Sx scar
– V/S (HR, RR, BP, BT) plus O2sat

Set problem list depend on history (not physical exam)

Etiology approach
– Congenital-Infect-inflam-trauma-tumor-drug-toxic-metabolic-endocrinopathy-

infiltrative-arrhythmia

Cyanosis
– Young onset

– Increase pulmonary blood flow : TGA, Truncus arteriosus, TAPVR

– Decrease pulmonary blood flow : TOF, PS/PA, Tricuspid atresia, Ebsteinʼs

anomaly
– Adult onset

– Loud P2 : Eisenmenger syndrome

– Normal P2 : Pink TOF, Ebsteinʼs anomaly, ASD/VSD plus (Peferential TR,

CTEPHT, Prominent eustachian valve)

Acute chest discomfort/pain

– Cardiovascular

– ACS (see ACS approach below)

– Pericarditis

– Aortic dissection

– Chest : Pneumothorax, Pleuritis, PHT (RV ischemia), PE

– GI

– Musculoskeleton

ACS (acute coronary syndrome)

– Atherosclerosis

– Premature : Abnormal lipid

– Late atherosclerosis

– Non atherosclerosis

– Aortic dissection to coronary ostial

– Anomalous coronary in origin

– Coronary spasm

– Vasculitis

– Spontaneous coronary dissection

 – Emboli
– MINOCA approach

Angina on exertion
– Coronary cause

– Atherosclerosis

– Non atherosclerosis

– Anomalous coronary

– Coronary dissection

– Coronary vasculitis

– External compression

– Mass

– Aneurysm

– Coronary course

– Microvascular obstruction

– Non-coronary cause

– Aortic stenosis

– HCM/HOCM

– Severe PHT (RV ischemia)

Transient loss of consciousness

– Syncope

– Reflex

– Othrostatic

– Cardiac syncope

– Structral heart

– Non-structural heart

– PE

– Seizure

– Ddx Sudden cardiac death

Palpitation
– Arrthythmia (Bradycardia, tachycardia, extrasystole)

– Structural or Non-structural heart

– Psychiatric cause

– Drug : Alcohol, Caffeine

– Metabolic & Endocrine : Hypoglycemia, Hyperthyroid, Anemia, Pheochromocytoma

Prolong fever
– Infection

– Systemic infection

– Deep

– Rheumatologic disease

– Hematologic disease

Ischemic stroke
– Atherosclerosis

– Emboli

– Cardioembolic : AF, IE, LA/LV thrombus, Myxoma, Fibroelastoma

– Arterial to arterial emboli

– Shunt : cardio shunt, extracardiac shunt

– Vasculitis : dissection, takayasu arteritis

Edema
– Localized edema

– Generalized edema : หัวใจ, ตับ, ไต

Dyspnea
– Acute : acute HF (Left & Right side), PE, Airway disease, Pneumonitis, Metabolic

disease (acidosis), surgical cardiac tamponade, pneumothorax

– Progressive (not chronic)

– Heart

– Lung

– Metabolic disease : Hypo/hyperthyroid, Adrenal insufficiency, Hyperglycemia

(Ketone acidosis)
– Deconditioning

Heart failure
Acute HF (exclude non cardiogenic pulmonary edem)
– Rt side : Tamponade, Acute PE, RV infarct

– Lt side :

– Accelerated HT : RAS, pheochromocytoma, Drug withdrawal (clonidine), thyroid

strom
– ACS

– Acute myocarditis

– Acute valvular regurgitation

– Acute obstruction : myxoma, prosthesis valve thrombosis

– Tachybradyarrhythmia

Progressive Lt side HF
– Preload : volume overload

– Contractility
 – Endocardial disease
– Valvular disease

– Acute : volume load (regurgitation), Dynamic LVOT obstruction

– Chronic

– Pressure load : linear progression of symptom

– Volume load : acute decompensation

– Inflow/outflow obstruction : myxoma, cor triatriatum

– Myocardial disease

– HFrEF : approach cardiomyopathy, L-TGA

– HFpEF : restrictive cardiomyopathy (EMF, Amyloid, HOCM), HCM,

hypertensive heart, high output HF

– Afterload : High BP, Fix obstruction after aortic valve

Rt side HF
– Approach Rt side HF

– High output HF : AV fistula (ประวัติ trauma)

Right side heart failure

Approach 1
– Pulmonary hypertension

– Approach PHT 5 types

– Type 1 Increase pulmonary blood flow : ASD, VSD, PDA, Pre-TV shunt or

extracardiac shunt
– Type 3

– Type 4

– Non pulmonary hypertension

– Pericardial disease : CP, Mass compression

– Myocardial disease : RCM, ARVD, Ebstein abnormality, Infiltrative disease,

ICM/DCM
– Endocardial disease

– Pulmonic valve disease : PS, PR

– Tricuspid valve disease : TS (carcinoid), primary TR

– Inflow/outflow obstruction : Rt atrium myxoma, cor-triatriatum dexter

Approach 2
– Pressure load

– Volume load

– Myocardial disease
Huge cardiomegaly
– ICM/DCM
– Multivalvular heart disease
– Massive pericardial effusion

Approach : no murmur in short case

– MS/Cor triatriatum
– Constrictive pericarditis
– Ebstein anomaly
– Dextrocardia
– Coarctation of aorta
– Takayasu arteritis

Abnormal distribution of peripheral pulses

– Delay radio-femoral pulse : CoA, Takayasuʼs arteritis
– Absent radial pulse : subclavian steel syndrome, Classic BT shunt, CABG with radial
graft
– Asymmetrical pulse : takayasuʼs arteritis, PAD

QRS axis change

 – VT
– WPW
– Pericardial effusion
– Intermittent/abberent BBB, if narrow = fascicular block

Normal CXR
– Constrictive pericarditis
– Coarctation of aorta

Cardiac mass
– Anatomical variant
– Implanted device
– Thrombus
– Vegetation
– Tumor : Primary or metastasis
– Artifact

Coronary dilatation
– High RA pressure
Increase flow
– ALCAPA/ARCAPA

– Coronary AV fistula

Normal flow
– Coronary atherosclerosis (diffuse)

– Arteritis : Takayasu, Kawasaki (multifocal)

Apical thickness
– Apical HOCM
– EMF
– Apical thrombus
– LV non compaction

Differential cyanosis : red hand & blue toe

– PDA with reverse shunt

– PDA plus Severe coarctation or interrupted aortic arch

Pulsus paradoxus
Reverse pulsus paradoxus
– HCOM

– Isorhythmic AV dissociation

– Intermittent positive pressure ventilator

Unilateral pulmonary edema

– MR with jet to pulmonary vein

– Pulmonary vein obstruction

– PE and compensate flow to other pulmonary artery

Physical exam
Physical exam

Key in short/long case

– Pale, Cyanosis, Jaundice

– Surgical scar

– Hepatosplenomegaly

– eg. Diagnosis severe rheumatic MS with PHT with AF

JVP
Normal JVP < 3 cm above sternal angle in 45 degree (RAP = 8 cmH2O = 6 mmHg)
– sternal angle above mid RA 5 cm in 45 degree

– measure CVP at mid chest wall & ICS4

– In upright position : JVP above clavicle (RAP > 10 cmH2O)

Hepatojugular reflux : Increase JVP >= 4 cm with >= 10 sec abdominal pressure
– อย่าลืมตรวจ Kussmaulʼs sign ทุกครั้ง

JVP wave form

– A : atrium contraction

– Regular canon A wave : PHT, TS, Decrease RV compliance,

– Irregular canon A wave : complete heart block

– C : tricuspid bulging, early systole

– X : atrial relaxation

– V : atrial filling, ventricle contraction

– Giant V wave : TR, ASD

– Y : Opening TV, early ventricular filling

Y wave is deep more X wave

In normal JVP : A wave is more prominent more than V wave

Pulse

– Lower extremity pulse : posterior tibial artery (dorsalis pedis is absent in some
patient)
Normal SBP both arm ต่างกันไม่เกิน 10 mmHg
– if > 15 mmHg & chest pain R/O dissection Ddx atheromatous disease

Normal SBP at lower extremity > upper extremity 10-20 mmHg

– Bezold-Jarisch reflex : low preload —> increase contraction & HR —> oversensing

carotid sinus baroreceptors —> bradycardia & hypopnea

– Cheyne-stroke respiration : low cardiac output

– Sustained heaving : sustained to S2 or 2/3 of cardiac cycle

– Kussmaulʼs sign : not found in tamponade

– RV failure, RCM, Constrictive pericarditis, Tricuspid stenosis

– Carvallo sign : Increase intensity when inspiration in TR, PS but in severe RV

dusfunction will negative carvallo sign, Decrease pulmonic ejection click

Pulsus
Pulsus alternan
– Common regular pulse, More readily detect in distal artery and standing

– Condition : severe LV dysfunction, cardiac arrhythmia, sign of poor tissue perfusion

Pseudo-pulsus alternans
– Difference from pseudo-electrical alternans (EKG sign : alternation in axis or

amplitude because alter conduction)

– Condition : Atrial flutter or post block —> high amplitude of next beat

Pulsus bigeminus
– Mimic pseudo-pulsus alternans

– Condition : pulse in bigeminy PVC/PAC

Pulsus paradoxus
– Condition : cardiac tamponade, restrictive cardiomyopathy, effusive constrictive

pericarditis, massive PE, Severe airway disease, Tension pneumothorax

– Cardiac tamponade without pulsus paradosus (e.g. ASD, AR, chronic LV dysfunction)

– Cardiac tamponade without RV collapsed : High RV pressure (e.g. PHT)

Reverse pulsus paradoxus

– Inspiratory rising in arterial pressure

– Condition : HCOM, Intermittent PPV, AV dissociation

Pulsus interuptus : case MV prosthesis obstruction

Pulsus tardus (Pulsus parvus et tardus)
– Delay upstroke and systolic peak

– Pulsus parvus : low amplitude pulse

– Condition : aortic stenosis

Pulsus magnus (Pulsus celer et magnus)

– High amplitude pulse

– Condition : Aortic regurgitation

Artery
– Rate & rhythm

– Amplitude

– Contour : bisferiens pulse (pulsus celer et magnus)

– Severe AR : high volume in second peak

– HCOM : less volume in second peak

– IABP : second peak in diastole

– Dicrotic pulse : second peak in diastolic > 50% of pulse pressure

– Found in cardiac tamponade, severe heart failure, hypovolemic shock

– BP

– Arterial thrill & bruit

Radial artery test
– Barbeau test: oximeter to provide a reading of the oxygen saturation before,

immediately after, and two minutes after radial artery occlusion.

– The response can be categorized into 1 of 4 types : type D +/- type C response

should not undergo transradial catheterization of that wrist.

PMI (may be from RV apex)
– Found ~ 50% (long case ตรวจไม่ได้บอกตรวจไม่ได้)
– location, size, contour of PMI & RV, thrill

– Beware dextrocardia

PMI contour
– Tap PMI in MS

– Slap PMI in volume load

– Heave PMI in pressure load

Apical impulse (apex only)

– Double and sustained apical impluse = HCM

– Diffuse apical impulse : LV dilatation, systolic dysfunction

– Tapping apex (palpable S1) : MS

– Sustained apex : LVH

Heaving
– Sustained heaving (> 2/3 systole-hangs out to S2) : pressure load
– Non-sustained heaving (hyperdynamic) : volume load
– RV heave at parasternal ICS 3-4
– Physiologic RV heaving (non-sustained) : Thin chest wall, straight back syndrome

Sequence heart sound

: S1-EjectionClick-MidSystolicClick-lateSystolicClick-S2-OS-PericardialKnock-Tumor
plop-S3-SummationGallop-S4
Diastolic extra-sounds : OS, Pericardial knocks, tumor plop, S3, S4
Systolic dysfunction
: diffused apex, s3 (low pitch):Gr 3-4 diastolic dysfunction, regurgitation
Diastolic dysfunction
: sustain apex, s4 (grade 1 diastolic dysfunction)
S1 intensity
– Loud S1 ต้องความรู้สึกเปรียบเทียบกับ S1คนอื่น ไม่สามารถใช้เปรียบเทียบแบบ Loud P2 ได้
– Increase S1: short PR, hyperkinetic state, MS, LA myxoma (ตีบMS-บางThin chest
wall-เร็วTachycardia-สั้นShort PR)
– Decrease/soft S1 : prolong PR, low CO, severe calcified MS, LBBB, premature

closure of MS, Prolapse/flail mitral leaflet, severe AR (premature closure MV)

S2 intensity
Increase S2
– Increase A2 : HTN, Dilated aorta

– Increase P2 : Pulmonary HTN

Decrease S2
– Decrease A2 : AS

– Decrease P2 : PS

Single S2
– Absent A1 : Severe AS

– Absent P2 : PS, COPD, obesity, RVOT obstruction

– A2-P2 occur together : aging (decrease inspiratory delay P2)

S3
– Physiologic sound before 40 years, may be disappear with standing

– Normal in third trimester

– Found in High output/LV dysfunction

– Right side S3 at left sternal border (increase with inspiration)

Opening snap
– High pitch at apex

– May not OS in non-mobile MS or MR is present

– OS is same timing as tumor plop (tumor plop may be a little bit delay)

Pericardial Friction Rub.

– best heard with leaning forward at LLSB

– Pleural rub : 1-2 component low pitch sound at lateral chest during inspiration/

expiration
– Not correlate well with volume of pericardial effusion

– Pleural rub : accentuated during inspiration

3 phases
 – (1) atrial systole
– (2) ventricular systole
– (3) rapid ventricular filling during early diastole.
S4
– Pathologic sound (atrial gallop), low pitch
– Heard best in left lateral decubitus at apex during expiration

– Not heard in AF

Split heart sound

– Split S2 : high pitch at LUPSB

– Split S1 : high pitch at apex

– S3 : low pitch at apex

– S4 : low pitch at apex

Physiologic split S2
– Delay PV closure : Increase RV volume

– Early AV closure : Decrease LV volume

Persistent splitting (wide spilt S2)

– Late PV closure : severe TS, ASD, RBBB, Ebstein anomaly, severe PS

– Early AV closure : left side preexcitation

Fixed splitting S2
– 70% in hemodynamic significant secundum ASD, PS, sinus venosus ASD, VSD with

Lt to Rt (early A2 closure)
Paradoxical splitting
– A2 delay : LBBB, RV pacing, severe AS, LV dysfunction, HCM, dilated aorta

– P2 early : Rt side preexcitation

Murmur
Position : Parasternal area or sternal border (ไม่ใช้คำว่า Parasternal border)
Innocent murmur
– Short mid-systolic murmur at LLSB or apex

– Pulmonic ejection murmur : early to mid systolic crescendo-decrescendo at

pulmonic area
Systolic murmur
– Ejection systolic murmur: begin after S1

– Regurgitation systolic murmur : begin with S1

Continuous murmur
– Benign : venous hum (Rt supraclavicular area), mammary souffle (late pregnancy or

lactation)
– Pathologic : Exclude to-and-fro murmur : AS/AR

– Systolic accentuation : PDA (loudest at 2nd left ICS +/- sign PHT), Coarctation of

aortic (auscultation in mid-back from collateral vessel)

– Diastolic accentuation :

– Ruptured sinus of valsava (active precordium, thrill, loudest at RUSB)

 –ALCAPA/RACAPA
– Coronary AV fistula (Loudest at LLSB)

To-and fro murmur

– AS with AR

– VSD with AR

– MR with AR

– MS with ASD

Thrill
– LLPSB : small VSD (no PMI shift)
– LUPSB : PS, small outlet VSD
– RUPSB : AS

Valve click
– Mechanical valve
– Tilting disk

– Aortic valve : click at S2

– Mitral valve : click at S1

– Ball & Cage

– Aortic valve : click at S1

– Mitral valve : click at S2 with SEM (valve obstruct LVOT)

 – Bioprostesis mitral valve : SEM (valve obstruct LVOT)
– Vascular click
– Increase pressure : AV click in HT, PV click in PHT

– Dilatation of vessel : Ascending Aortic aneurysm, PHT, PA dilatation

– Valvular Click :
– PS or Bicuspid AS ejection click

– Click at Maximum valve opening (follow S1)

– Pulmonic ejection click : Decrease intensity during inspiration

– MV mid systolic click : MVP

– Supravalvular AS : no ejection click, radiate to Rt carotid > Lt carotid

Dynamic auscultation
– Must evaluated in long case with normal cardiac exam
Valsava maneurver in MR vs TR :
– Increase TR murmur : release phase in first 5 beats
 – Increase MR murmur : release phase after 5 beats
Dynamic auscultation : HCOM = MVP
– MVP : ยืนเบ่ง early+ดัง, นั่งกำ delay+เบา
Squatting
– Initial : Increase venous return

– Decrease intensity in HCM, Increase intensity in AS

– Static phase : increase SVR

– Decrease intensity in HCM & AS

Carotid sinus massage
– True is carotid sinus pressure at internal carotid at angle of mandible

– Time 5 sec, try both side

Valsalva maneuver : 4 phase

– Initial pressure rise : expiratory force blood into LA—> rising SV, increase SBP

– Reduced venous return and compensation : decrease CO & tachycardia

 – Pressure release : slight fall in SV due to decrease LA return, decrease SBP
– Return cardiac output

Memo HR & BP in valsalva (phase I-IV)

– BP : ขึ้น-ลง-ลง-ขึ้น
– HR : คง-ขึ้น-คง-ลง
Valsava response in situation
A : normal response
B : LV dysfunction without elevate LVEDP, absence overshooting in phase 4
C : Elevate LVEDP (valvasa square wave sign, Absence overshooting in phase 4 with
little change in BP during phase 2

Specific name of heart murmur

– Carey Coombs murmur : Mid diastolic murmur in rheumatic fever
– Austin Flint murmur : mid- late diastolic murmur in AR.
– Gallavadin sign : musical components of the systolic murmur heard at apex of aortic
stenosis
– Graham- Steel murmur : high pitched, diastolic in pulmonary regurgitation.
– Rytands murmur : mid diastolic atypical murmur in Complete heart block.
– Docks murmur : continuous diastolic murmur with early and late accentuation in LAD
artery stenosis.
– Mill wheel murmur : due to air in RV cavity following cardiac catheterization.
– Stills murmur : inferior aspect of  lower left sternal border, systolic ejection sound,
 vibratory/musical quality in subaortic stenosis, small VSD
– Cole-Cecil murmur : diastolic murmur in AR, prominent at Lt axilla
– Cabot-Locke murmur : diastolic murmur in severe anemia in LUPSB due to flow in LM
coronary
– Mean-Lerman scratch : Systolic murmur at sternum from pericardial-pleural friction
rub in hyperthyroid
– Cooing Dove murmur or seagull murmur : aortic stenosis or aortic regurgitation
Peripheral
– Grade of leg edema

– Pigmented purpuric dermatosis (sign of chronic venous congestion)

EKG
EKG

Lead EKG
– lead I, aVL : high lateral lead
– Lead V5-6 : low lateral lead

Lewis lead for detect Pw electrogram

Conduction
– Sinus node : crescent-shape 1-2 cm in long and 0.5 cm wide at junction of SVC with
RA
– PR interval : conduction from AV node to purkinje fiber
– Lt ventricular conduction system
– Anterior fascicular block

– Posterior fascicular block

– Left septal fiber : นำกระแสไฟฟ้าจาก posterior to anterior septal

Axis
– Normal axis -30 to +90 degree
– North-west axis or AVR + : Dextrocardia, VT
– QRS alternan
– Pericardial effusion

– Alternate block

– Intermittent WPW

– Other origin : PVC

– Tachycardia

Limb lead reversal

In normal : Lead aVF+ve เสมอ
– LA-RA : aVR & aVL reverse, lead I invert

– LA-LL : negative Pw in lead III

– RA-LL : aVR+ve, Lead I, II, III, aVF-ve

– RA-RL : flat lead II

– LA-RL : flat lead III

– Bilateral arm-leg reversal (LA-LL, RA-RL) : flat lead I

Term
– T wave invertion : deep >= 1 box
– Sinus bradycardia < 60
– Extreme sinus bradycardia < 40

– Sinus tachycardia > 100

– Sinus arrhythmia : > 120 ms or 10% variation in PP interval
– Junctional rhythm : QRS < 120, rate 40-60/min
– AIVR rate 60-120 bpm
– Ventricular rate 20-40/min
– Atrial tachycardia 150-250 bpm
– Atrial flutter rate ~ 300 bpm (250-350 bpm)
– AF rate > 350 bpm
– Sinus pause >= 2 sec, Sinus arrest >= 3 sec
– Junctional rhythm (originate around AV node, QRS < 120 ms)
– Junctional bradycardia < 40 bpm

– Junctional escape 40-60 bpm

– Accelerated junctional rhythm 60-120 bpm

– Junctional tachycardia > 100 bpm

– Normal QRS 70-100 ms, > 120 ms (3 small box) = wide QRS at least 1 lead
– Compensatory pause
– Full/Complete compensatory pause : control previous interval P wave : found in

PVC
– Incomplete compensatory pause : found in PAC

– Ventriculophasic sinus arrhythmia in AV block : PP interval enclosing a QRS complex

is shorter than a PP interval not enclosing a QRS

The Mechanism 
PseudoNormal EKG
– Abnormal QT
– Pulmonary embolism

Chamber enlarge
RAE : Pw in lead II >= 2.5 mm, Positive Pw V1 >= 1.5 mm
LAE : PW in lead II > 120 ms, Deep negative Pw in V1
RVH
– Rt axis deviation

– Dominant R wave in V1 (> 7mm tall or R/S ratio > 1).

– Dominant S wave in V5 or V6 (> 7mm deep or R/S ratio < 1).

– Support : RAE, RV strain

RVH 3 type
● RVH type A : pressure load in PS, MS

– R > S in V1 with RAD

– ST segment depression + TWI in V1-2

● RVH type B : volume load such as ASD

– RBBB like + RAD

● RVH type C : COPD with corpulmonale
 – Low voltage + poor R progression
– No tall R in V1
– RAD + RAE
– Deep S in V1-3 (mimic ant wall MI)
LVH
– Sokolow-Lyon: S in V1 + R in V5/6 >= 35 mm, R in aVL >= 11 mm
– Cornell: R in aVL + S in V3 >= 28 mm in men or >= 20 mm in women
– If LAFB : S in III + Max (R+S) in any lead >= 30 mm in men or >= 28 mm in

women
– R in aVL >= 11 mm
– Katz-Wachtel phenomenon (biventricular hypertrophy) : QRS amplitude in V2-5 >=
50
– LVH/Enlarge :
– LV dilatation : Q wave V5-6, normal ST segment

– LV hypertrophy : strain pattern V5-6 + invert T wave

– Volume vs Pressure load LVH

– Pressure load : LVH with strain

– Volume load : LVH with upright TW

P wave
– Atrial conduction system
– Internodal bundle : Anterior, Middle (Wenkebachʼs bundle), Posterior (Thorelʼs

bundle)
– Interatrial bundle (beckmannʼs bundle) : connect RA-LA

– Wandering pacemaker : natural cardiac pacemaker site shifts between SA node

(normal varian) : least 3 morphologies of Pw, Irregular PP interval with constant PR
interval, Rate < 100 (If rate > 100 = MAT)
– Low atrial rhythm (CS rhythm) : Negative Pw in inferior lead and positive Pw in AVR
– Pw negative in V2 : ติด lead สูงไป, low atrial rhythm
– Himalayan P-waves > 5 mm
– Sinus : postive Pw in I, II lead and negative Pw in aVR
– DDx positive Pw in AVR : Rt & Lt arm lead reversal, Dextrocardia, Non sinus Pw

– Retrograde P or low atrial rhythm : negative Pw in inferior lead

– Biphasic P wave in inferior lead
– Bachmannʼs bundle block

– Anisotropic and slow conduction in atrium

– Tw plus Pw

– AT can not identify atrial enlarge

PR segment
– Atrial conduction (Pw) - AV node - His bundle - purkinje
– PR can not depress > 0.8 mm
 – Atrial repolarization until 60-80 ms after QRS (2-3 times longer than Pw) : mimic ST
depression (upsloped pattern)
PR depression differential
– Pericarditis

– Normal varian

– Atrial infarction : rare due to thin wall and dual blood supply (thebesian veins)

Q wave
– No pathologic Qw
– Septal Q wave in left-side lead (I, aVL, V5-6)

– Not seen in V1-3

– Qw predict site of infarct, not deep of infarction

Pathologic Qw : wide 1 mm (40 ms), deep 2 mm or 25% of QRS

– V2-3 : any deep, wide 0.5 small box

– Other lead : deep 1 small box, wide 0.75 small box (two contiguous lead)

QRS complex
– Normal QRS highest in V4-5
– High QRS from myocardial thickness or myocardial delay conduction
– Ventricular activation time : จากเริ่ม QRS to peak R wave (ไฟฟ้าวิ่งจาก endo to
epicardial)
– Low voltage : QRS =< 5 mm in limb lead or =< 10 mm in chest lead

– Cause : obesity, copd, pericardial effusion, severe hypothyroid, subcutaneous

emphysema, ICM, infiltrative disease (amyloid)

– Poor R wave progression : R wave height ≤ 3 mm in V3 and R in V1 < R in V2 < R in

V3
– Cause : Prior anteroseptal MI/DCM, Right Ventricular Hypertrophy (usually seen

in COPD), LBBB/LAFB, WPW type B, Misplace to higher position, Clockwise

cardiac rotation
Classification of IVCD
– Specific IVCD : RBBB, LBBB, Fascicular block

– Associated with CAD, HT, Cardiomyopathy

– Non-specific IVCD : Diffuse or multi-fascicular delay, Masquerade BBB (Combine

BBB block), Drug intoxication (Na block), Hyperkalemia, Hypoxemia/Acidosis

Fascicular & BBB
– Anterior fascicular (Anterior-superior region)

– Posterior fascicular (Postero-inferior region)

– Septal fascicular (Central & apical region)

– Narrow QRS, Rw in V1 >= 5 mm or V2 >= 15 mm (Deep S < 5 mm in V1-2)

– No Qw in V5-6

– Rw crescendo in V1-3 and decrease from V5-6

– LBBB
 –V1 : small r but deep S
– V5-6 : notch R wave, Secondary TWI, no Q/S wave

– RBBB (no negative concordance)

– V1 : rsRʼ with TWI V1-3

– V5-6 : R > S wave

– Masquerading BBB : bilateral BBB delay (ผสม RBBB & LBBB)

– Type I (Standard type) : precordial lead V1-V6 = RBBB and limb lead = LBBB

– Type II (Precordial type) : Precordial lead V4-V6 = LBBB and lead V1-V3 = RBBB

– rSr' or rSRʼ in V1-V2

– Benign Patterns: narrow -r' of fast inscription

– Higher placement of leads V1, V2

– Normal variant, with late activation of the posterobasal LV

– Incomplete RBBB

– Athletes: 35-50% due to physiologic RV enlargement

– Pectus Excavatum, due to change of heart location in chest

– Pathological Patterns: wider-R' often taller then -r, with slower ascent/descent.

– Type 2 Brugada pattern

– RV enlargement, hypertrophy from a variety of pathologies

– Arrhythmogenic RV cardiomyopathy (ARVC)

– WPW syndrome

– Hyperkalemia

– Na + channel blockers (class I AADs, TCAs)

Fragmented QRS
– Not typical BBB & QRS < 120 ms

– Prefer scar (prior MI)

T wave inversion
– TWI > 1 mm in two cont. positive lead
– Normal TW highest in V4-5
– If TW highest in V2-3 : beware MI

– TWI in lead III is a normal variant.

– Pathological TWI is symmetrical and deep (>3mm)
• Normal finding in children (up to 13 years)
• Persistent juvenile T wave pattern
• Myocardial ischaemia/infarction
• Bundle branch block
 – RBBB with secondary TWI not more than V3
• Ventricular hypertrophy
• Pulmonary embolism
• Hypertrophic cardiomyopathy
• Takotsubo cardiomyopathy
– QRS and TW must positive in AVR (origin from apex)

• Raised intracranial pressure

ST deviation
– STE from epicardial early repolarization or endocardial delay depolarization
 – Convex : Typical STEMI
– Concave : Typical pericarditis

ST elevate : at least two contiguous lead

– V2-3

– Women : 1.5 small box

– Men

– >= 40 years : 2 small box

– < 40 years : 2.5 small box

– Other lead : 1 small box

Posterior wall STEMI (Inferiobasal wall) : STE 0.5 small box in V7-9, STD 0.5 small box
in V1-3
– Men < 40 years : STE 1 small box

LM occlusion : STE in aVR > V1

RV infartion : most is ischemia, most recover after reperfusion
– STE in V1

– STE in V1 & STD in V2

– STE in V3-4R : >= 0.5 small box

– Age < 30 years >= 1 small box.

PPV 100%, NPV 80%

ST depression : 0.5 small box at least two contiguous lead

– NSTEMI

– Digoxin effect

– Strain from LVH

– Bundle branch block

– Hypercalcemia

ST elevation
– STEMI, spasm (convex), key look for reciprocal change
 – Pericarditis (saddleback : concave), key : multiple lead STE, no reciprocal change, no
evolution of Qw
– LV aneurysm : ต้องมี Q wave, STE > 2 wks, T wave hight/QRS hight ratio < 0.36
– Brugada
– Early repolarization : upslope
– LBBB
– Takotsubo cadiomyopathy
– Hyperkalemia

Inferior wall STEMI

– Proximal RCA : RV infarction

– Mid RCA : No RV infarction

– Distal RCA : isolated posterior wall STEMI

Anterior wall STEMI

– STEMI V1-2 : lesion above septal perforator

– STEMI I, aVL : lesion above DG1

De-winter EKG = proximal LAD occlusion

– short ST segment (< 3 box) following peak T wave, may be STE in AVR, 50% wrap

around LAD

STEMI with LBBB

– Cabrera's sign : notching at 40 milliseconds in the upslope of the S wave in lead V3

and V4
– Chapmanʼs sign : notch in the upslope of the R wave in lead I, aVL or V6

– Modified Sgarbossa Criteria:

• ≥ 1 lead with ≥1 mm of concordant ST elevation

 • ≥ 1 lead of V1-V3 with ≥ 1 mm of concordant ST depression
• ≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive discordant STE
(≥ 25% of the depth of the preceding S-wave.)
– Original Sgarbossa Criteria : >= 3 point, spec 90%

– Discordant STE > 5 mm, specific in RV pacing

DANAMI : STEMI
– A : no Q, no TWI = acute

– B : Qw, no TWI = poor prognosis

– C : Qw, TWI = reperfusion with infartion

 – D : no Q, TWI = reperfusion without infartion

EKG evolution in STEMI

Pitfall ECG in ACS
– Diffuse STD & AVR elevation
– Acute LM : unstable hemodynamic

– support STE in aVR >= 2 small box, STE in aVR > V1

– Chronic LM or TVD : stable hemodynamic

– Acquire RBBB
– Plus LAFB & STE in V4 : pLAD STEMI

– Plus S1Q3T3 + clinical sat drop + lung clear : Acute massive PE

– LV aneurysm (Persistent STE in chest lead)

– Normal ST in I, aVL : chronic lesion

– STD in I, aVL : acute ontop chronic

– Hyperacute T : Ddx hyperkalemia or Ant wall STEMI

– Echo : LV function & wall motion

– Waiting for lab K

QT interval
Measurement (no U wave)
– Measure longest QT (usually V2-3) in ACC

–ถ้ามี 2 notch แต่ไม่เตะ baseline ให้นับ notch หลัง

– Measure at same lead and best show of end Tw by eyeball and Tangent method

– Limit interpretation in QRS prolong

– QT = QT - (QRS duration - 120 ms)

– JTc = QTc - QRS duration

– In AF : average QTc (Fridericia) in longest & shortest RR

Method
– Bazettʼs formula: QTc = QT / √ RR (sec) in lead II (limit only HR 60-100)
 – Fridericia formula: QTc = QT/RR^1/3 in fast heart rate
– Eyeballing method (only HR 60-100) : QTc prolong is QT reaches beyond halfway

– Tachycardia : QT < 50% of RR interval = short QT

– Automated digital machine : often longer than other measurement

QTc prolonged (ACC)

– QTc >= 450 ms in men

– QTc >= 460 ms in women

– QTc > 500 : risk of torsades de pointes

QTc is abnormally short if < 390ms

Congenital long QT >= 480, start beta-block QT >= 470
Congenital short QT =< 330
U wave
Abnormalities of the U wave
– Prominent U waves : >1-2mm or 25% of height of the Tw

– Inverted U waves

Etiology
– Severe hypokalaemia

– Digoxin

– Bradycardia

Electrolyte
Hyperkalemia : suppress SA/AV node & conduct pathway
– Tall peak T, small/absence P, wide QRS, bradycardia

– Prolong PR, STE

Hypokalemia : re-entry arrhythmias

– flat T, U wave, long QT

Hypercalcemia : block conduction pathway

– flat T & P but short QT, J point elevate

Hypocalcemia : decrease myocardium contraction

– QT prolong, TW change

Hypomagnesemia : irregular contraction & arrhythmia

– tall T, STD, QT prolong, TdP
Hypermagnesemia : delay conduction
– PR prolong, wide QRS, bradycardia

Na channel blocking toxicity (TCA/Flecanide overdose)

– Rt axis deviation, positive in AVR (R wave > 3 mm, R/S ratio > 0.7), sinus tachycardia,

IVCD

Specific EKG
– EKG in DCM : Goldbergerʼs triad
Statistics
Stat

General
– P-value : ความน่าจะเป็นที่สองกลุ่มจะแตกต่างกันโดยความบังเอิญ
– Statistical significance is determined by acceptable threshold of false rejection the
null
– Cross comparison vs Head to head comparison
– % Attributive risk (excess risk) = (Incidence in expose - incidence in un-expose)/
Incidence in expose
– Odds ratio in case control studies : assesses effect based on the disease
– Relative risk in cohort : assesses effect based on exposure
– 95% confidential interval = mean +/- [1.96xSD/(√N)]
– SD = standard deviation, N = จำนวนประชากรใน study

Error in statistic
– Systematic error : effect on validity
– Cause : selection bias, information bias, instrumental bias, interviewer bias,

confounding
– Random error : effect on precise (confident interval) —> correct by increase sample
size
Hypothesis testing
– Null hypothesis (H0) : ตั้งให้ตรงข้ามกับสิ่งที่เราต้องการพิสูจน์
– Type I error (alpha) < 5% (false positive) No benefit from treatment but study show
benefit (ฟลุก)
– e.g. significant in subgroup analysis

– Type II (beta) : less power, less event, benefit from treatment but study show no
benefit (ตาไม่ถึง)
– e.g. insignificant in subgroup analysis due to small population

– Power = 1-beta, ความสามารถของ study ที่บอกว่า study มี benefit แล้วมี benefit จริงๆ
– Increase power by increase N
Research design
– Cohort study (Factors —> Diseases)
– Prospective cohort study

– Retrospective cohort study

– Cross-sectional study (snap shot) : เป็นการศึกษา ณ จุดเวลาหรือช่วงเวลาใดเวลาหน่ึง

ทำการเก็บข้อมูลเพียงคร้ังเดียวไม่มีการติดตามผลไปข้างหน้าหรือย้อนกลับไปในอดีต
– Advantage : know burden of disease

– Disadvantage :

– ไม่สามารถบอก incidence ได้

– ไม่สามารถสรุปได้ว่าโรคและปัจจัยเสี่ยง อะไรเกิดก่อนหลัง (limit search causes of
outcomes)
– Case control studies (Disease —> Factors)
– Advantages : Rare disease, Several exposures, Long latency, Rapidity, Low cost,

Small sample size, No ethical problem, Efficient, Cost-effective for rare

outcomes
– Disadvantages : recall bias & selection bias
– Nested case-control study : เหมือน case-control ทั่วไปแต่ศึกษา cohort หนึ่งๆโดย
ติดตามไปจนมีการเกิดโรคแล้วย้อนกลับมาดู exposure ในอดีต แล้วเลือกกลุ่ม control ขึ้นมา
(ลด recall bias)
– Historical control
– Time period effect : treatment change —> prognosis change

– Cohort effect : charecter of subject difference

– Experimental study
– Cross over trial (randomization)

– ต้องมี wash-out period เพื่อป้องกัน carry over effect

– Quasi-experimental study : high selection & confounding bias
– อาสาสมัครเข้ากลุ่มโดยไม่ได้ใช้
– วิธีการสุ่ม เนื่องจากข้อจากัดต่างๆ เช่น ปัญหาจริยธรรม ปัญหาเรื่องการจัดการ เช่น ใน
การทดลองโดยการผ่าตัดสองวิธีที่ต่างกัน
– PROBE (prospective open-label single blinded endpoint)
– Outcome ที่วัดต้องชัดเจน (hard endpoint)
– ข้อดี/เสีย : pragmatic test (ผลการรักษาเหมือนในโลกความเป็นจริง คือ รู้ว่าได้ยา
อะไร)
– PCT (Pragmatic clinical trial) : used real world data and propensity score
matching
– Highlight : goal for improved practice, flexible protocol, more representative,

useful in clinical practice

Term and model
– Nocebo effect : กินยาหลอกไม่ปวด แต่พอรู้ว่าเป็น statin ปวดทันที
– Placebo effect : กินยาหลอกแล้วดีขึ้น
– Such as ORBITA trial : PCI no effect on symptoms

– Association (correlation) : positive/negative correlation โดยความสัมพันธ์นั้นอาจเป็นจริง

หรือไม่ก็ได้
– ความสัมพันธ์ที่ไม่เป็นจริง (Artifactual correlation): สาเหตุอาจเกิดจากความบังเอิญ,
อิทธิพลขององค์ประกอบอื่นที่ไม่ได้ควบคุม, bias, ผิดพลาดของสมมุติฐาน
– ความสัมพันธ์ที่อาจเป็นจริง :
– องค์ประกอบนั้นเป็นสาเหตุให้เกิดโรค
– โรคเป็นสาเหตุให้เกิดองค์ประกอบนั้น
–องค์ประกอบที่สามทำให้เกิดเหตุการณ์ทั้งสองอย่างพร้อมกัน
– Causation (causal association) : change in one variable produced a change in
another variable
– Hawthorne effect : the alteration of behavior by the subjects of a study due to their
awareness of being observed
– Rosenthal effect : ผู้ทำวิจัยรู้ hypothesis แล้วเกิด bias ในการเก็บข้อมูล
– Regression to the mean : การวัดข้อมูลใดซ้ำๆในคนไข้คนเดียวกัน ค่าจะเข้าใกล้ mean
– Joint frailty model : total number of events/patient-years of follow-up
– Random effect survival model which allows for unobserved heterogeneity or for

statistical dependence between observed survival data

– Propensity score matching (cohort study)
– Limitation : match only record data, unmeasured confounding, interpretation

is less intuitive (ไม่ตรงไปตรงมา)

– Risk study : Hill criteria for prove risk factor, not risk marker
Confounder
– คุณสมบัติของ Confounder
– Prognostic factor

– Unequal distribution among groups

– Confounding by indication
– Confounding factor : ต้องไม่มีผลต่อ exposure
– Effect modifier : factor นั้นมีผลต่อ exposure
– Eliminating effect of confounder
– Design phase : randomization, matching

– Analysis phase

– Stratified analysis : Mantel-Haenszel method

– Multiple regression : Linear, Logistic, Poisson, Cox

– Propensity score method

– Instrumental variable analysis

Bias
– Verification bias (workup bias) : diagnostic test result influence whether patient
undergo confirmation by standard test (บางเคสไม่ได้ทำ standard เคสทุกคน) :
Decrease sense, Increase specificity
– Spectrum bias : severity ของโรคในแต่ละกลุ่มที่ทำ test เท่ากัน
 – Real world data : Confounding bias, Misclassification bias
– Immortal time bias :
– Such as SGLT2Inhibitor : คนที่ได้ยาถูก select ให้รอดมาแล้วกว่าจะมาได้ยา พอเทียบ
กับกลุ่มไม่ได้ยาจึงตายน้อยกว่า

Statistical test
# Categorical data
– 2 groups

– Unmatched groups : Chi square test (large samples) or Fisherʼs test (small

samples)
– Matched groups : McNemarʼs test

– 3 groups or more

– Unmatched groups : Chi square test

– Matched groups : Cochrane Q

# Continuous data
– 2 groups

– Normal distribution (parametric)

– Unpaired 2 groups : Independent T-test

– Paired 2 groups : Pairs T-test

– Non-normal distribution (non-parametric)

 –Unpaired 2 groups : Man-Whitney U test
– Paired 2 groups : Wilcoxon test

– 3 group or more

– Normal distribution (parametric)

– Unmatched groups : One-way ANOVA

– Matched groups : Repeated measures ANOVA

– Non-normal distribution (non-parametric)

– Unmatched groups : Kruskal-Wallis test

– Matched groups : Friedman test

General for statistic test

– T tests are used to determine whether the mean of two independent groups are

equal.
– Continuous data 3 or more group : ANNOVA

– Categorical data : Fisherʼs exact or Chi-square test (approximate) กี่กลุ่มก็ได้

– Time-to-event : Log rank (surival analysis)
Diagnostic test
– Focus on test : discriminate disease patient
– Sense/Spec : depend on severity of disease, non-depend on pretest probability

– Likelihood ratio

– Odd ratio

– ROC curve

– Focus on diagnosis : disease probability

– PPV/NPV

– Likelihood ratio : ดีกว่า sense/spec ตรงที่สามารถแบ่ง test result เป็นหลายกลุ่มได้

เช่น มาก ปานกลาง น้อย ไม่ใช่แค่ Positive or Negative
– LR+ = Sense/(1-Spec)

– LR+ = [A/(A+C)]/[B/(B+D)] : Prob test+ve in disease group/Prob test+ve

in non-disease group
– LR- = (1-Sense)/Spec

– Prob test-ve in disease group/Prob test-ve in non-disease group

– ROC curve : AUC 0.5-1, AUC 0.5 = bad test, AUC 1 = perfect test
– แกน Y = sense
– แกน X = 1-Spec
– Calculate post-test probability
– If Estimated pre-test probability 20% & test LR+ 6.0 —> calculated pretest odd =

Pr/(1-Pr)=0.2/(1-0.2)=0.25
– Post test odds = pre-test odds x LR = 0.25x6.0 = 1.5

– Post-test probability = odds/(1+odds) = 1.5/(1+1.5) = 60%

– Magnitude of treatment effect : not only stat significant
– Absolute risk reduction

– NNT

– Relative risk (risk ratio) = [a/(a+b)]/[c/(c+d)] = Incidence rate in exposed Gr/

incidence rate in unexposed Gr

– Relative risk reduction = [a/(a+b)]-[c/(c+d)]

– Odd ratio (case control study) = ad/bc (อัตราต่อรอง)

– ในข้อมูลเดียวกัน odd ratio จะมีค่าห่างจาก 1 มากกว่า ralative risk เสมอ
– Odd ~ RR in small volume of a << c and b << d
– Hazard ratio (คือ risk/odd ratio เฉลี่ย overtime) : คำนวนโดย Cox regression model
– Probability that an individual at time t has an event at that time. eg. Event-

free survival analysis

– Limit : depend on number at risk, measure time to first event (not repetitive

events)
– Relative Hazard ratio : 1-HR
Analysis
– Survival analysis
– Only in binary outcome(Yes or No)

– Estimate survival curve by Kaplan-Meier method (บอกความแตกต่างเป็นตัวเลข)

– Log rank test ในการคำนวน P significant ระหว่างสอง survival curve
– Sensitivity analysis : คำนวน worst case scenario ในผู้ป่วยที่ loss follow-up
Subgroup analysis
– null hypothesis : no difference in two group

– P value for interaction (ควร > 0.1)

– No significant (P > 0.1) : แปลว่าข้อมูลสามารถนำไปใช้กับประชากรกลุ่มใดก็ได้
– P < 0.1 : โอกาสเกิดจากความบังเอินน้อยกว่า 10% แต่ต้อง study เพิ่มเพื่อดูในประชากร
กลุ่มนี้
– Stat significant in subgroup = 0.05/number of subgroup in pre-specified subgroup
and must significant in main analysis
Analysis of agreement of 2 methods (ในตัวแปลเดียวกัน)
– Categorical

– 2 categories : Cohenʼs Keppa, McNemarʼs test

– > 2 categories : Weighted kappa

– Numerical : Paired T-test, Bland & Altman diagram, Intraclass correlation coefficienty

Pearson correlation : Quantify association between two parametric viariables

– ดูการวัดค่าของ test 2 test ว่ามีความสัมพันธ์กันไหม เป็นไปในทิศทางใด
– Values range from -1 to +1
– -1 : negative correlation

– 0 : no correlation

– +1 : positive corrrelation
Clinical important effect & non inferiority trial
– Failure to prove superiority ไม่เท่ากับ claim non-infeiority
– Concept of non-inferiority trial : new treatment can be slightly inferior to standard
treatment, but magnitude of inferiority must be clinical unimportant
– P value for non inferiority : one-tail test (< 0.025)

– At least 50% of minimal treatment effect should be preserved

– Non-inferiority must analysis both intention to treat & per-protocol but

Superiority trial : analysis only intention to treat

– Choice of analysis
– Intention to treat analysis (ITT) : analysed in the groups to which they were

randomized, regardless of whether they received intervention (analysis ตามขาที่

ถูก random)
– Advantage : preserved randomization (Decrease bias)

– Disadvantages : Analysis may underestimated adverse effect

– Per protocol analysis : known as an "on-treatment" represents a "best-case

scenario" to reveal the effect of the drug being studied.(ถ้าถูก random ขาไหนแล้ว
ไม่ได้ treat แบบขานั้น ก็ตัดทิ้งไปเลยไม่เอามาคิด)
– As-treated analysis : comparing with the treatment regimen that they received. It
does not consider which treatment they were assigned for the treatment.
 (Analysis ตามที่ได้รับการรักษา)

Clinical trial in DM (FDA)

– Non-inferior trial for CV outcome benefit : cut point 0-1.3

– Trial for CV outcome benefit : cut point 1.3-1.8 ต้องมี post approval study
– If < 1.8 : No FDA approve

– Superior trial for CV outcome benefit: cut point < 1.0

Clinical appraisal trial
General
– Research question

– Internal validity

– Result

– External validity & generalizability

Assess : B-A-O-N-I-II
B : Bias
– Allocation bias : แบ่งกลุ่มไม่เท่ากัน (P valve for heterogenity)
– Ascertainment bias : bind ไม่หมด เช่น trial intervention
A : Analysis, ITT (ดูDrop-out/Cross-over ต้องไม่เกิน 20%)
O : Outcome
N : Number (event rate เข้าได้กับ real world?)
I : type I error ดูว่า allocation เท่ากันไหม
II : type II error ดู power & event rate พอไหม
Assessment of validity
– Patient random?

– Concealed of randomization (ไม่รู้ว่าโดน random อยู่กลุ่มไหนก่อนเข้า study)

– Similar prognosis in two study group
– Study blinded (ไม่รู้ว่าโดน random อยู่กลุ่มไหนหลังเข้า study) : blinded patient/Blind
placebo/Clinician/Data collector/Adjudicator of outcome/Data analysts
– Follow-up complete
– Intention to treat analysis
– Early termination
: Truncated RCT
– Stopping randomized trials early for benefit
 – Likely to valid result
– Preplanned formal stopping role

– Few interim analyses using a stringent P valve (P value < 0.001)

– Large number of outcome events before termination (at least 200-300

events)
– Not too good to be truth

Meta-analysis appraisal
– Concept
– Fixed-effect model : no heterogeneity between study (ค่าจริงมีแค่ค่าเดียว)
– Apply only in all study are functionally identical

– Random-effect model : between-study variation (แต่ละ study มีค่าจริงของตัวเอง)

– More realistic & conservative

– Study selection & end point

– Kappa agreement for selected paper from two expert : accept >= 0.7

– Publication bias
– Eggerʼs test must no stat significant = no publication bias

– Heterogeneity
– Cochranʼs Q test (depend on high study numbers)

– Q test < 0.1 : heterogeneity

– l^2 index (I square) : not depend on study numbers, True heterogeneity accounts

for % of total variation of effect estimates among included studies.

– I^2 > 50% : high heterogeneity

– I^2 < 20% : low heterogeneity

– Random-effect model for high heterogeneity

– Fix effect model is ideal

Issues in Reading Meta-analysis
– Selection of trials / search strategy

– Complete or not complete? : database selection, language restriction,

unpublished data
– GIGO (garbage in, garbage out) : remove unwanted results, include wanted

result
– Publication and reporting biases

– Publication bias (negative trial โอกาสได้รับตีพิมพ์น้อยกว่า): assess by funnel plot

– Reporting bias : no report & publish in negative trial (negative trial ไม่ส่งเรื่องให้ตี
พิมพ์)
– Robust statistic
– results are concordance in all sensitivity analyses

– use both fixed and random effect models

What to do when heterogeneity detected?
– Recheck studies characteristic

– Do not combine at all, just do systematic review

– Remove article(s) : high risk of bias

– Grouping into sub-categories (pre-specified)

– Individual patient data analysis

– Random effect model แทน fix effect model

– Meta-regression (effect of years and duration of study)
Key investigation
Key investigation

EST
– Protocol name : bruce or modified bruce
– Resting EKG : rhythm, ST-T change, Qw, delta wave, BBB, LVH, QT prolong?
– ระวัง 2I1 AV block in baseline bradycardia
– Stress EKG
– chest pain or dyspnea during exercise

– Horizontal/downslope ST change .... mm at lead..., at ....mins (...METs) and STD

increase to 2 mm at peak
– ระวัง EST induced hypotension
– ระวัง EST induced WPW/Bundle branch block/PVC
– Recovery EKG
– Chest pain?

– ST change & return to normal within ... mins

– Other finding
– HR recovery at 1 & 3 mins

– SBP recovery at 3 mins

– Arrhythmia during exercise/recovery

– Abnormal BP response

– Interpretations
– Exercise time (mins)

– Termination due to ...

– Achieve METs, % of PMHR, Double product (Max HR x peak SBP)

– Duke treadmill score (DTS)

– Positive EST at recovery phase, ... METs, FC ..., High risk features

Stress echo
– Resting : good LVEF, normal wall motion
– Low dose : Increase LVEF
– Peak dose : enlargement of LV cavity, RWMA at ..., No intracavity obstruction
– Finding : Increase LVESV response to stress, impaired LV systolic function with
stress, maximum HR (> 85% of PMHR), ...METs.
– Interpretation : Positive DSE for inducible ischemia with biphasic response,
Infarction/Ischemia at LAD territory

SPECT myocardial perfusion imaging

– Rest & stress EF, TID
– Area of complete/partial reversible & fix defect (include segment 17)

– Extra-cardiac uptake, artifact

– Interpretation : coronary territory and extent of abnormal

Example
 – Myocardial ischemia/infarction at LAD territory
– Rest & stress EF, TID
– Heart-Lung ratio
– Mx : Revascularization in High risk

CMR
Reading CMR for ischemia
– Aorta (R/O dissection) and PA size (R/O thrombus)

– Pericardial & pleural effusion, extracardiac mass, lung infiltration

– Global & regional LV function & RV function

– LV/RV thickness, LA/RA dilatation, IAS thickness

– Thrombus at LV/LA and RV/RA

– Perfusion defect at ...

– Myocardial scar pattern : LV, RV, Atrium and MVO

– Pericardial effusion and enhancement in late gadolinium

– Dx : Positive CME with ischemic beyond scar at LAD territory

CTA
– Aortic size & R/O dissection
– PA size and branch : R/O thrombus
– Pericardial and pleural effusion
– Valve and prothesis valve. eg. Bicuspid AV, sternal wire.
– Chamber dilatation
– Extracardia : lung mass, hilar mass
– Coronary
– Coronary origin

– Anomalous origin R/O interarterial type, ALCAPA

– Normal origin R/O AV fistula

– Calcified coronary

– Coronary stenosis

– Dilatation/Aneurysm coronary : saccular, fusiform

– Coronary dominant

Angiogram
– View
– Catheter type & position : aorta, LV, engage.
– Access site : femoral, radial

– Pre-contrast : pericardial effusion/calcification, calcification of coronary/valve/aorta

– Contrast phase :
– Ostial LM

– Dissection

– Stenosis lesion of native vessel & vein graft

 –TIMI & Blush flow
– Bridging myocardial

– Aneurysmal change

– Other
– LV gram : Takotsubo cardiomyopathy, VSR, VSD, MR, Septal/apical HCM, LV

aneurysm with thrombus

– Aortogram : Ascending aortic aneurysm, AR, Ruptured sinus of Valsava

– RV gram : ARVD, PS

Holter
– Basic rhythm : sinus rhythm/AF/pace rhythm (ApVs, AsVp)
– A & V rate

– QRS complex : narrow or wide QRS (BBB, Delta wave)

– Premature beats (PAC, PVC, PJC)

– Premature wide QRS : PVC, intermittent WPW, PAC with abberrency

– Tachyarrhythmia (AT, A flutter, AF, SVT, VT)

– Timing, Symptom, Rate, Initiation & Termination

– Bradyarrhythmia (AV block, SSS : SA exit block)

– Timing, Symptoms, rate (A & V rate), regular/irregular, Pause (AF off set pause,

pause during AF)

– ST change, QT interval
– Other finding
– Diagnosis
– Managment

##Echo##
Prothesis valve
– Position & type of Prosthesis valve : MV or AV, Bileaflet/Tilting disc/Cage-ball
– Rocking motion of prosthesis valve, severe paravalvular leakage with eccentric jet
regurgitation.
– Combine with infective endocarditis : abscess, pseudoaneurysm, vegetation

– Dx : Prothesis valve dehiscence with infective endocarditis

– Limited opening and closure of prosthesis valve leaflet with forward turbulent flow
across prosthesis valve (mean gradient ...mmHg) with severe eccentric jet
regurgitation.
– Combine with thrombus or pannus

– Dx : Prothesis valve thrombosis

IE
– Vegetation : oscillating mass, irregular round shape, size ... mm attach to anterior
mitral valve leaflet
– Abscess : heterogeneous perivalvular echo density size ... mm
– Pseudoaneurysm : pulsatile perivalvular echo free space with color Doppler flow
 detected at ....
Rupture sinus of Valsava
– Filamentous structure protruding from Rt sinus of valsava into RVOT (Windsock
appearance). Color & Doppler showed continuous flow across Rt sinus of valsava
into RV outflow tact
– Drop out of interventricular septum size ... at 10 oʼclock compatible with
perimembranous VSD with Lt to Rt shunt
Ruptured papillary muscle
– Common is posterior medial papillary muscle
– Severe MR due to Flail posterior mitral leaflet. Homogeneous hypermobile mass
attach to cordae tendinae of posterior MV and protruding into LV. Presented/
absence of posterior/anterior papillary muscle
– Good LVEF with inferior wall akinesia
– Dx : Inferior wall MI with Severe MR due to partial ruptured of posteromedial papillary
muscle.
Rheumatic MS
– Calcified MV leaflet and Limited MV excursion with diastolic doming (hockey-stick
appearance)
– PSAX : MV showed commissural fusion MV (fish-mouth appearance)
– Wilkinʼs score
– Mean gradient across MV and Pressure half time
– Severe LAE with SEC/thrombus
– PHT, Enlarged RV & RV function
Parachute mitral valve
– Eccentric opening of MV orifice, thickened and restricted MV leaflet/chordae,
Unbalanced cordal attachment, Cordal tendinaes converge to single papillary muscle
(usually posteriormedial), Variable-sized anterolateral papillary muscle.
Cor Triatriatum
– Echo : thin membrane separate LA into two chamber, connect between opening of
LA appendage to opening upper part of fossa ovalis
Bicuspid AV
– PSAX : systolic doming +/- diatolic prolapse, eccentric AV closure
– SAX : Two cusp & commissures with Raphe (right & left fusion), oval opening
Aortic dissection
– Ascending aortic aneurysm size ... cm with effacement of aortic root.
– Intimal flap at proximal ascending aorta to descending thoracic and abdominal aorta
+/- thrombus/SEC in false lumen
– Prolapse/flail of AV leaflet with severe AR
– Minimal pericardial effusion +/- sign of cardiac tamponade
– Dx : Marfan syndrome with Dissecting aortic aneurysm involved ascending aorta to
abdominal aorta (Standford type A) with acute ontop chronic severe AR
Myxoma
 – Large heterogenous mobile mass with stalk attached to interatrial septum,
obstructing mitral orifice (mean gradient ... mmHg), normal MV leaflet.
Papillary fibroelastoma
– Multiple papillary frond like appearance at downstream side of valve (common is AV
valve) ; small, pedunculate by small stalk & high mobile, **no valve destruction**
Lipomatous hypertrophy
– Well demarcated, homogeneous, IAS thickening spare fossa ovals (dumbbell
appearance)
ASD
– Secundum ASD : IAS drop-out size ... mm with left to right shunt, CS dilatation, +/-
MVP, no LA enlarge until age > 40.
– Primum ASD : lowest part of IAS drop-out, LA enlarge, TV-MV continuation (AV valve
at same level), Groove neck deformity +/- anterior mitral valve cleft with MR.
– Sinus venosus ASD with PAPVR : TEE showed abnormal pulmonary vein connection,
PAPVR : fuse SVC with RUPV (tear drop sign : RUPV-SVC/Ao)
– Coronary sinus ASD with persistent Lt SVC : confirm by contrast echo injection at Lt
arm : first visualized in CS and then RA
– PW across ASD
PDA
– Measure defect size (significant > 6 mm) and gradient across PDA, PHT
– Turbulent high velocity from descending Ao to left PA with Lt to Rt flow
– Cont flow with systolic accentuation
– Look for PA endarteritis (vegetation at PA)
VSD
– IVS drop out size... at ...Oʼclock, compatible with perimembranous VSD with left to
right shunt, +/- prolapsed Rt/non-cusp of AV leaflet
– Dx restrictive perimembranous VSD with Lt to Rt shunt and moderate AR due to AV
leaflet prolapse
TOF
– TOF : non-restrictive VSD with bidirectional shunt, overriding aorta (Ddx DORV),
Right side aortic arch, subvalve PS, small PA, RV thickness, preserved aortic-mitral
continuity. Ass. ASD
– Post TOF repair : increase echogenicity at IVS near AV (patch VSD)
Truncus arteriosus
– both ventricles connected to common arterial trunk via single tri-leaflet truncal valve
and PA arises from common arterial trunk, non restricted VSD beneath truncus with
bidirectional shunt. Moderate truncal valve regurgitation
L-TGA
– Parallel of great vessel in PSLA
– TGA : Short axis showed Ao is anterior and mPA is posterior.
– Ao is left side : L-loop

– L-TGA: Ventricular inversion (Atrioventricular discordance &

 Ventriculoarterial discordance), Morphologic LA connect to systemic RV,
apical displacement of left side TV with moderate/severe TR
– Ao is right side : D-loop
Ebsteinʼs anomaly
– Apical displacement > 8 mm/m2 of septal & post leaflets
– Fenestration, Redundant, Elongated, Sail like with Tethering (FREST) of ant. leaflet
– Abnormal chordal attachment
– Atrialization of RV
– Poor coaptation of TV : moderate to severe TR
– RV function
– Small PA
– Ass. Anomalies : ASD/PFO
Coarctation of aorta
– Suprasternal view : narrowing coarctation distal to left subclavian artery with post
stenosis dilatation. Turbulent flow with persistent diastolic forward flow cross
coarctaion of aorta, mean gradient ... mmHg.
– Doppler in descending aorta : delay upstroke and persistent diastolic forward flow
(sawtooth appearance)
VSR
– Serpiginous septal tear, irregular border, disrupted interventricular septum with thin
wall myocardium at apical septum/basal-inferoseptum, compatible with VSR with Lt
to Rt shunt (peak PG ... Hg)
– LV function and regional function
Concealed ruptured free wall
– Disrupted LV free wall with pericardial wall-off and color Doppler flow thought
ruptured site +/- forming pseudoaneurysm, coagulum at pericardium with RA/RV
collapsed along cardiac cycle.
HOCM
– Septal type HCM : concentric LVH with asymmetrical septal hypertrophy, small LV
cavity, SAM with posterior eccentric jet leading to mild/moderate MR, LVOT
obstruction with peak gradient ... mmHg, LA dilatation.
– Apical type HCM : concentric LVH with spade shape of LV, apical pseudo aneurysm
+/- thrombus, LV dilatation
– CW : Dragger shape +/- diastolic forward flow from high apical LV chamber pressure
in diastole
– PW : Lobster claw found in mid LV obstruction, apical HCM with aneurysm
– Reverse pulsus paradoxus
EMF
– LV apex obliteration with apical mural thrombus in absence of underlying RWMA
(Apex maintains inward systolic contractile motion)
– Packing (Apical fibrosis) of the right or Left ventricle apex

– Tethering the AV valve papillary muscles, may be adhesion of valve apparatus to LV

 wall: leading to mitral and/or tricuspid regurgitation
– Giant atrial enlargement
– Restrictive filling pattern
– Basal hypercontraction (Merlon sign)
Constrictive pericarditis
– Septal bounce/shudder (ventricular interdependence), non-specific and can found in
abnormal electrical conduction
– Thickening & bright pericardium
– Medial eʼ > 8 (good longitudinal function)
– Annulus reversus : lat eʼ < med eʼ
– Medial mitral eʼ >= 9 cm/s

– Annulus paradoxus : Low E/eʼ but high PCWP

– IVC plethora & Hepatic vein expiratory diastolic reversal
– Diastolic reversal / diastolic forward flow > 0.79

– Post radiation : Thickening & calcified mitral-aortic intervalvular fibrosa (aorto-mitral

curtain), MAC, calcification proximal RCA and LM, Calcified ascending aorta
– Dx : Radiation heart disease with constrictive pericarditis
Cardiac tamponade
– Large amount of circumferential pericardial effusion, maximum size ... cm at
posterior part. Swing motion of heart.
– IVC plethora with diastolic hepatic reversal flow during expiration
– M-mode compare MV or AV opening (guide diastolic phase)
– Diastolic RV collapse

– RA inversion > 1/3 of cardiac cycle

– Sign of exaggerated ventricular interdependence : MV/TV inflow variation

– Respiratory variation of MV/TV inflow (MV > 25%, TV > 40%)

– Reduced eʼ in TDI
Cardiac amyloid
– Biatrial enlargement, Increase LV/RV wall thickness (not used hyperthrophy),
Granular sparking appearance of myocardium (Non harmonic imaging), Thickness of
valve/interatrial septum (> 6 mm), pericardial effusion, diastolic dysfunction,
pericardial effusion, Decrease GLS and apical sparing pattern (Cherry on top)
LVNC
– Prominent trabeculation and deep recess of LV (usually apical & lateral LV),
Intertrabecular space filled by direct blood flow (color Doppler flow at intertrabecular
space)
– non-compact/compact part, Mostly LV dysfunction
– Echo : 2/1 (short axis view in end systole or end diastole)

– CMT : 2.3/1 (long axis view in end diastole), at least 4 segment or trabeculated

mass > 20% of global LV mass

ARVD
– Reduced RV function, Aneurysm/dyskinesia/akinesia of RV free wall, RV apex
 dilatation, prominent RV trabeculation
Takotsubo cardiomyopathy
– Basal hyperkinesia with apical LV ballooning +/- LVOT obstruction, Reduced LV
function with RWMA
ALCAPA
– Large coronary arising from Rt cusp, Turbulent diastolic flow within
interventricular septum and RV apex, Take off vessel from posteromedial of PA
with abnormal color flow to PA, LV dysfunction and MR
Pre-op evaluation
Pre-op surgery

Step approach pre-op

!. Emergency surgery : no required pre-op
– Urgency surgery : pre-op only unstable cardiac condition

– Semi-urgent surgery (Sx in cancer) : Assessment obstructive cardiac cause,

PHT, unstable cardiac condition

$. Active/unstable cardiac condition?
%. Low risk surgery : go on surgery
&. METs > 4 : go on surgery
'. Clinical risk factor >= 2
Surgical risk
https://riskcalculator.facs.org/RiskCalculator/PatientInfo.jsp (ref AHA)

– At least 4 METs : climb two flights of stairs or walk up a hill or run short distance
 – 10 METs : strenuous sport : swimming
– Carotid endarterectomy is intermediate risk Sx
– Evaluated risk peri-op MI and CV death
– Peri-op EKG monitoring in all case
– Anesthetic technique
– GA : Reduce sympathetic tone : decrease venous return, vasodilatation —> may

decrease organ perfusion (If MAP < 60 duration > 30 min : increase risk MI,
stroke, death)
– Spinal block : decrease cardiac sympathetic drive : reduced myocardial

contractility, HR, change in cardiac loading condition (Aortic stenosis)

– Defer surgery in BP > 180/110 in elective surgery

Unstable cardiac condition

– Unstable angina
– Acute HF
– Significant cardiac arrhythmias
– Symptomatic valvular heart disease
– Recent MI within 30 days and residual myocardial ischemia

Clinical risk factor (5 item)

– IHD
– HF

– Stroke or TIA

– CKD (Cr > 2 or GFR < 60)

– DM require insulin

Elevated risk in RCRI >= 2

Pre-op investigation
EKG (Pre-op) in intermediate or high risk surgery
Echo (Pre-op)
- Low-intermediate surgery : no routine (III), prefer in suspected AS/MS/HF
- High risk surgery (IIb)
- documented LV dysfunction/VHD with last echo > 1 year
Pre-op CAG : Stable CAD with CCS III-IV (I), Carotid endarterectomy (IIb)
Pre-op stress imaging :
- High risk Sx + METs < 4 + at least 3 risk factor (I level C)
- Intermediate risk Sx + Med < 4 + at least 1 risk factor (IIb C)

Indication for CAG pre-op valve surgery (if CAG stenosis > 50% —> CABG, IIa)
– Male > 40 or Female postmenopause

– Ischemic MR or LV dysfunction
 – Hx of CVD or at least one risk
CT coronary in low prob CAD or high risk CAG, IIa
ถ้ามี symptomatic AF ไปผ่า valve แนะนำ surgical ablation ด้วย, IIa

Cause of peri-operative CV event

– Catecholamine surges

– Prothrombotic environment

– Blood loss/volume shift

– Coronary plaque destabilization

– Fix coronary disease (stress testing predict)

Pre-op medication
Beta block : on strong data for initiation, cont if previous used
- If start between 2-30 days before surgery : HR 60-70, SBP > 100
Statin (Initiation pre-op) in vascular surgery (ESC IIb, AHA IIa) : at least 2 wks before Sx
ACEI/ARB : Cont during non cardiac surgery, if initiation at least 1 wk before Sx
– ESC suggest transient discontiation

– Withholding 24 hr before non-cardiac surgery (Canadian Guideline)

ASA (I) : at least 4 wks after BMS/DCS, at least 3-12 months after DES
P2Y12 inhibitor (IIa) : at least 4 wks after BMS/DCS, at least 3-12 months after DES

Flow chart
MI after non-cardiac surgery (MINS) : define Trop-T > 30 ng/L
Patient condition
– Asymptomatic post CABG in 6 years : no require CAG pre-op (I)
– Post PCI
– Asymptomatic recent balloon angioplasty : delay surgery 2 wks

– Asymptomatic recent BMS/DCS : delay surgery 1-3 months

– Asymptomatic recent DES : delay surgery 6-12 months

– Discontinue P2Y12i for surgery in 3-6 months since DES implantation (IIb)

– Recent MI : delay surgery 30 days and W/U residual myocardial ischemia

– Post ACS without PCI
– Discontinue P2Y12i after 1 months but cont. ASA

– Discontinue after 1 month

– Non high ischemia risk (IIa)

– High ischemic risk : post ACS (IIb)

– Discontinue after 6 months (I, levelB)

– Stable CAD : evaluated risk before surgery such as EST or Stress imaging
– Heart failure : delay Sx at least 3 months in high-intermediate Sx
– Valvular heart disease
– Asymptomatic severe AS
 – Low to intermediate risk Sx : go on Sx
– High risk Sx : correct AS before Sx

– Significant MS (MVA < 1.5)

– Asymptomatic and SPA < 50 : go on surgery

– Symptomatic or SPA > 50

– Low-intermediate risk Sx : controversy

– High risk Sx : correct MS before Sx

– Tachyarrhythmia : Cont oral anti arrhythmic drug & monitor EKG perioperative Sx
– Bradyarrhythmia : indication as pace maker guideline
– PAD : assess IHD if >= 3 risk factor and consider pre-op stress test (IIa)
– PAH
– Intermediate to high risk Sx —> refer to center

– PAH specific treatment before surgery

– COPD : stop smoking > 2 months before Sx

– Congenital heart with Eisenmenger : avoid sudden drop in SVR (sat drop and
induced arrhythmia), maintain hydration, IE prophylaxis, IV filter, DVT/PE prophylaxis
– Prevent post-op AF : beta-block, amiodarone. (Statin no benefit)

Interruption anticoagulant
– Almost surgery require interrupt anticoagulant (warfarin 5 days)
– Stop LMWH 24 hr before Sx

– If INR > 2, stop LMWH

– Bridge (start 24-72 hr)

– CHADS2 >= 5 or CHADSVASc >= 7

– Prior embolic

– Valvular AF < 6 months

– Non valvular AF < 3 months

– No bridge
– CHADS2 =< 2 without prior embolic

– Major bleeding or ICH < 3 months

– Platelet abnormal include ASA

– High INR

– Previous bleeding with bridging or similar procedure

Protocol bridging anticoagulant from BRIDGE trial (Depend on CHADS2)
Adjust UFH (heparin) : keep PTT ratio 1.5-2

Interruption anti-platelet
– P2Y12 inhibitor interrupt 6 month after ACS or PCI : Class I, level
– No P2Y12 inhibitor interrupt within 1 month after ACS or PCI : Class III

Surgical risk
– Low bleeding surgical risk : cont. DAPT

– Moderate bleeding surgical risk : Cont. ASA

 – High bleeding surgical risk (vascular reconstruction, complex visceral procedure,
neurosurgery, Tranbronchial operation) : discussion
12 months after ACS or PCI
– Low bleeding surgical risk : cont ASA

– Moderate bleeding surgical risk : consider interrupt ASA

Procedure bleeding risk
Clinical trial
CARP trial : RCT
– Pre-op coronary revascularization before elective vascular surgery, No improve long

term mortality
NOAC
NOAC

NOACs
– AF with Post bioprosthesis AVR

– 3 เดือนแรก warfarin
– หลัง 3 เดือน NOAC ได้, IIa

– NOAC is Harm in mechanical valve : dabigatran (RE-ALIGN)

– Increase risk thrombotic in first 3 months after Sx + All increase bleeding

– เพราะ warfarin inhibit contact factor จาก contract valve ซึ่ง dabigatran ไม่มี
Indication & contraindication

Score for predicted TTR (SAMe-TT2R2)

– Score 0-2 : prefer warfarin

– Score >=3 : prefer NOAC

NOAC : Efficacy and safety
Overview NOAC/DOAC
– Reduced mortality 10%

– Reduced ICH & hemorrhagic stroke 50%

– Increase GI bleeding 25%

– Low dose NOAC (D110,E30) : increase ischemic stroke

Dabigatran (Thrombin inhibitor) : bid dose, RELY trial

– D110 : Thrombotic event - non inferior to warfarin, less bleeding

– D150 : Thrombotic event - superior to warfarin,

– Same over all bleeding but GI bleeding more than warfarin

– Metabolism : เด่นขับทางไต ไม่ผ่านตับ

– Do not NG feeding

Rivaroxaban (Xa inhibitor) : OD dose, high CHADS2 at least 3, ROCKET AF trial

– Thrombotic event : non inferior to warfarin

– Same over all bleeding, increase GI bleeding but less Intracranial bleeding

Apixaban (Xa inhibitor) : bid dose, decrease mortality, ARISTOTLE trial

– Thrombotic event : superior to warfarin
 – Less bleeding and less major GI bleeding
– Decrease death

Edoxaban (Xa inhibitor) : OD dose, decrease mortality, ENGAGE AF trial

– Thrombotic event : non inferior to warfarin

– Less bleeding

– Endoxaban 30 mg

– increase ischemic stroke but decrease GI bleeding

– Decrease death (30 mg)

NOAC in specific condition

– High risk GI bleeding : apixaban (5) or dabigatran (110)
– CKD with GFR < 50 : less recommend dabigatran
– Age > 75 : apixaban (5 or 2.5 adjust)
 – Prefer used only Cirrhosis child A

NOAC/VKA in post PCI

Concept : Prefer dual anti-thrombotic > triple anti-thrombotic drug, if triple anti-
thrombotic —> prefer short duration
– Rivaroxaban: prefer 15 mg > 20 mg OD (ref: Pioneer-AF)

– Dabigatran: prefer 150 mg bid > 110 mg bid (ref: Redual-PCI)

Duration of triple therapy : 4-6 weeks (AHA AF 2019)

– If triple therapy : recommend only clopidogrel

– If Dual therapy : recommend clopidogrel or ticagrelor

HASBLED score
– H: hypertension (SBP > 160)

– Abnormal kidney or LFT (Cr > 2.6, Bilirubin > 2, Liver enzyme > 3 เท่า)
– S: Stroke
– B: Bleeding tendency
 – L: labile INR (< 60%)
– E: Elderly (Age > 65)
– D: Drug (NSAIDs, Anti-platelet) or Alcohol

Adjusted dose NOAC

Depend on cockcroft & gault
– not recommend : dabrigatran in GFR < 30, other NOAC in GFR < 15

– ESRD : Apixaban 5 mg bid (IIb)

– R15 : GFR 15-50

– D110 : GFR 30-50

– Prefer initial D110 in age > 80 or high bleeding risk

– D75 (US) : GFR 15–30 or GFR 30-50 with dronedarone/ketoconazole

– E30 : GFR 15-50 or Dose reduction criteria (BW ≤ 60 kg, potent P-Gp inhibitor)

– A2.5 : GFR 15-30 or 2/3 criteria (age ≥ 80, BW ≤ 60 kg, Cr ≥ 1.5)

Pharmacology in NOAC
– NOAC ที่มี food effect สูงที่สุดและ Bioavailability สูงที่สุด (>80%) คือ Rivaroxaban
– Renal clearance เยอะที่สุดคือ Dabigatran (85%) น้อยที่สุดคือ Apixaban (25%)
– All NOAC is substrate ของ P-glycoprotein แต่มีแค่ 2 ตัวที่ metabolized ผ่าน cytochrome
P450 enzyme CYP3A4 คือ Apixaban กับ Rivaroxaban
– ยาร่วมที่เป็น strong P-glycoprotein inhibitor จะเพิ่มฤทธิ์ของ NOAC ทุกตัว ได้แก่ยา
Amiodarone, Dronaderone, Ciclosporin, Tacrolimus, Verapamil, Clarithromycin,
Quinidine, Itraconazole Ketoconazole, Posaconazole, Voriconazole และ Anit-HIV drug
ที่เป็น Protease Inhibitor (Ritonavir Telaprevir)
– ยาร่วมที่เป็น P-glycoprotein และ CYP3A4 inducer จะให้ผลลดฤทธิ์ของ NOAC ได้แก่ยา
Carbamazepine, Phenobarbital Phenytoin, Primidone, Rifampicin, St Johnʼs Wort

NOAC & drug interaction

: dranedarone, rifampicin, PI, -azole, phenytoin, verapamil, keppra, +/- amiodarone,
immunosuppressive drug, TKI
: reduced dose in clarithromycin/erythromycin (Moderate P-go competition & strong
CYP3A4 inhibitor)
: Contraindication : Imatinib, Crizotinib, Cyclosporin, Tacrolimus
: metabolized via cytochrome P450 enzyme CYP3A4 : Apixaban & Rivaroxaban
: Less drug interaction : Edoxaban
Reduced dose
– Verapamil : Dabigatran

– Tacrolimus : Apixaban

– Dronedarone, claritromycin, Ketoconazole/Itraconazole : Edoxaban

Specific NOAC in specific drug
Same dose
– Verapamil/Diltiazem/Amiodarone/Fluconazole : Rivaroxaban

– Rifampin : Edoxaban

– Ticagrelor : Dabigratran

No interaction with NOAC

– Digoxin, Azithromycin

My opinion
– Concern drug interaction : prefer Endoxaban

– Concern renal function : prefer Apixaban

– Concern bleeding : prefer Dabigratran (reversal agent)

Switch
– VKA to NOAC (memo : READ)
– INR < 3.0 can start rivaroxaban

– INR < 2.5 can start edoxaban

– INR < 2 start all NOAC (apixaban, dabigatran)

– NOAC to VKA : off NOAC after INR near therapeutic level (half dose for edoxaban)
– NOAC switch LMWH : สวมรอยเลย
– UFH to NOAC : หลังหยุด heparin 4 hr เริ่ม NOAC
Dosing error
– ลืมกินยา
– BID drug :

– Within 6 hr กินทันทีและdose ถัดไปตามปกติ

– After 6 hr รอกิน dose ถัดไป
– OD drug
– Within 12 hr : กินทันทีและdose ถัดไปตามปกติ
– After 12 hr : รอกิน dose ถัดไป
– ไม่แน่ใจว่าลืมกินหรือกินยาไปแล้ว (practice รอกินมื้อถัดไป)
– BID drug : รอกิน dose ถัดไป
– OD drug
– Within 12 hr (depend on CHAD-VAS)

– if CHA2DS2-VAS >= 3 : กินยาทันทีและ dose ถัดไปตามปกติ

– if CHA2DS2-VAS =< 2 : รอกิน dose ถัดไป
– After 12 hr รอกิน dose ถัดไป
Pre-op NOAC
Procedure risk bleeding
– Minor bleeding risk : cataract/glaucoma Sx, endoscope without Bx, superficial Sx,

Dental extraction 1-3 teeth

– Low bleeding risk

– High bleeding risk

Lab monitoring
– General : LFT before start NOAC and then yearly
– Dabigatran : level correlation TT > PTT
– Rivaroxaban & Edoxaban : level correlation PT
Clinical used PT/PTT in NOAC
– Excludes clinical relevant bleeding
– Dabigatran : normal aPTT/TT

– On-therapy or above levels (Checking compliance) : normal PT/PTT not exclude

– Dabigatran : prolong aPTT

– Apixaban/Rivaroxaban/Endoxaban : prolong PT

Reversal agent
– Dabigratran
– Idarucizumab 5 gm IV (life threatening/major bleeding/Urgency surgery) or 4F-

PPC or aPCC 50 U/kg

– If no reversal agent : acute H/D

– If normal PTT or TT : exclude clinically relevant bleeding

– NOAC (Xa inhibitor) : 4F-PPC or aPCC 50 U/kg

– Andexanet alfa (FXa inhibitor reversal agent) : infusion in 2 hr

– Recommend for Rivaroxaban and Apixaban in life threatening bleeding

– Ciraparantag (Aripazine) : Universal reversal agent

Warfarin overdose
– Warfarin metabolism via cytochrome p450 enzyme CYP2C9 and VKORC1

– High INR without bleeding

– INR < 5 : observe

– INR 5-9 : no routine used oral Vit K, if used dose 1-2.5 mg PO

– INR > 9 : oral Vit K 2.5-5 mg PO

– Non major bleeding : Vit K 2-5 mg oral/IV

 – Major bleeding : Vit K 5-10 mg IV

Clinical trial
PIONEER AF
– Population : non valvular AF (score 3) with coronary stent (ACS 50%, STEMI 10%)

– Exclude : Prior stroke/TIA, GI bleeding, Hb < 10

– Intervention

– Clopidogrel plus Rivaroxaban 15 mg OD (GFR < 50, Rivaroxaban 10 mg)

– DAPT (1,6,12 months) plus Rivaroxaban 5 mg bid

– Standard Tx : DAPT (1,6,12 months) plus warfarin

– Follow 12 month : N total 2000

– Outcome : less bleeding than standard treatment, same MACE (secondary endpoint)

RE-DUAL PCI
– Population : Non valvular AF (score 3) with coronary stent (ACS 50%, STEMI 10%),

include previous bleeding > 1 months

– Intervention :

– Dabigatran 150 bid + Clopidogrel

– Dabigatran 110 bid + Clopidogrel

– Standard Tx : Warfarin + DAPT (BMS 1 months, DES 3 months of ASA)

– Follow 12 months

– Outcome : Less bleeding in standard Tx, Same MACE (secondary endpoint)

AUGUSTUS trial (ออล-กู๊ส-ตูส)

– Population : AF plus ACS or Post PCI

– Plan P2Y12i and Follow up 6 months

– Mean CHA2DS2VASc 3.9, mean HAS-BLED 2.9

 – ACS 60% (No PCI 24%), SCAD 40%
– Intervention : On Clopidogrel with2x2 (Placebo vs ASA, Warfarin vs Apixaban)

– Outcome :

– Bleeding : NOAC plus clopidogrel is less than triple antithrombotic therapy

(warfarin plus DAPT), NNT 9

– Death/hospitalization : NOAC plus clopidogrel is less than triple antithrombotic

therapy (warfarin plus DAPT), NNT 18

Summary
– Triple warfarin : lowest all cause death and ischemic event

– Triple NOAC & Dual NOAC : same death & ischemic event

– Dual NOAC : lowest death and hospitalization

– Dual warfarin : Highest death and ischemic event

Pregnancy &
Heart disease
Pregnancy with heart disease

WHO classification of maternal CV risk

– Class I : no risk
– Small/Repaired : mild PS, PDA, MVP

– Atrial or Ventricle ectopic beats

– Class II : small increase risk

– Unoperated ASD/VSD

– Repaired TOF

– Most arrhythmias : SVT

– Asymptomatic Ebsteinʼs anomaly

– Class II-III
– Mild LV dysfunction, HCM, tissue valve heart, Repair CoA

– Class III : Significant increase risk, need intensive specialist

– Mechanical valve

– Systemic RV

– Fontan circulation

– Unrepaired cyanotic heart disease, Other complex congenital heart

– Ao dilatation 40-45 mm in Marfan, Ao dilatation 45-50 mm in bicuspid AV

– Class IV : Extremely high risk, termination should be discussed (contraindication for

pregnancy)
– PAHT any cause

– Symptomatic LV dysfunction (EF < 30% or NYHA III-IV)

– Previous peripartum cardiomyopathy with any residual impairment

– Severe MS, Severe symptomatic AS

– Bicuspid AV with Ao dilatation > 50 mm, Marfan with Ao dilatation > 45 mm or >

40 mm with Family Hx of dissection/SCD

– Native severe CoA

– Add on in ESC 2018

– Vascular Ehlers-Danlos : risk uterine rupture

– Systemic RV with moderate/severe decrease function

– Fontan with any complication

mWHO class I-II : manage local hospital

Predictor poor maternal CV event

– Prior cardiac event
– HYHA III-IV
 – Moderate-severe obstruction/regurgitation (any valve)
– LV/RV dysfunction (EF<40%, TAPSE < 16)
– PAHT
– Cardiac medication before pregnancy
– Cyanosis (O2sat < 90%), repair or un-repair
– NT-proBNP > 128 at GA 20 wks
– Mechanical valve
– History of smoking
Predictor of neonatal event
– HYHA III-IV
– Maternal Lt side obstruction
– Cyanosis (O2sat < 90%)
– Cardiac medication before pregnancy
– Mechanical valve
– During pregnancy
– Used OAC

– Maternal cardiac event

– Decline cardiac output

– Smoking

– Abnormal uteroplacental flow

Physiologic in pregnancy
– Increase CO, SV, HR (significant after 2nd trimester), return to normal at months
post labor
– Increase intravascular volume 40%

– Decrease SVR (better in AR but worse in AS) and PVR

– Decrease SVR (if cyanotic heart : increase Rt to Lt —> Desaturation)

– Same BP

– Uterine contraction : 300-500 blood into circulation

Labor
– Increase O2 consumption

– Increase baseline CO and BP during uterine contrcation

Post-partum
– Increase blood shift from placenta

– Increase preload and cardiac output

Structural heart disease

– 3rd trimester

– Increase CO, SV, LV mass, E/eʼ

– Decrease LVEF
Normal EKG change in pregnancy
– Increase ventricular rate
– Left axis deviation
– PAC & PVC
 – Prominent Qw in inferior lead
– Flat Tw or TWI in lead III, V1-3

Before pregnancy management

– Contraindication for pregnancy
– WHO class IV, O2 sat < 85%, Hx of dissection type B

– Bicuspid AV with Ao > 50 mm, Marfan/LoeyDietz with Ao > 45 mm (Ao > 40 cm

increase risk), Turner with aortic size index > 25 mm/m2, All vascular Ehlers-Danlos
– Severe AS should intervention before pregnancy if
– 3 condition : Symptoms, EF < 50%, Symptoms during excercise

– PS (peak gradient > 64) : pre-pregnancy ballon valvulotomy

– If pregnancy and asymptomatic : go on pregnancy

– Severe MS (MVA < 1.5 cm2) : pre-pregnancy intervention in MVA < 1.0 cm2 (I,C),
MVA < 1.5 cm2 (Ia)
– Symptomatic Ebsteinʼs anomaly (HF or cyanosis)
– Severe PR with dilatation of RV : Pre-pregnancy bioprosthesis valve replacement
– Severe AR/MR : pre-pregnancy intervention in 3 condition (symptoms, impaired LV
function, LV dilatation)
– On warfarin : switch to UFH (prefer UFH than LMWH) : 6-12 weeks before
pregnancy
– Post ACS without residual ischemia/LV dysfunction : delay pregnancy 12 months
Antepartum/Peripartum management
– General advice in heart disease
– Low salt, rest in lateral postion

– Avoid vasovagal syncope (ลดเบ่ง, ท้องผูก)

– O support all case in cyanotic heart
– Ascending Ao dilatation : Repeat echo q 4-12 wks during pregnancy & 6 months
post-partum, if limited Echo —> MRI
– Beta-block in Marfan/Heritable thoracic aortic disease

– Celiprolol in Ehlers-Danlos

– Severe MS (MVA < 1.5 cm2) with symptom (NYHA III/IV) or SPA > 50 mmHg after
medication
– PBMC after GA 20 wk and medication : selective B1 block, diuretic

– Beta1-blocker

– Mechanical prosthesis and anticoagulant

– Cont warfarin if < 5 mg/day

– If warfarin > 5 mg, can used in 2nd or 3rd trimester

– Admit to bridge warfarin/LMWH at GA 36 wks (UFH, Keep aPTT >=2x)

– Must monitor In LMWH: Target Anti-Xa level 46 hr post dose and then

weekly (4-6 hr post dose)

– Mitral valve or Rt side valves : Target anti-Xa level 1.0-1.2 U/mL

– Aortic valve : Target anti-Xa level 0.8-1.2 U/mL

– LMWH should replaced by UFH at least 36 hr before plan delivery

– ACS (STEMI/NSTEMI) : invasive management, advice risk fetus damage

– Delay labor 2 weeks post ACS

– Massive PE : Thrombolytic drug is relative contraindication

– Used only in life threatening condition : SK, Altepase

– Tachyarrhythmia : avoid cordarone

– SVT

– Acute Mx

– First line : vagal manoeuver or adenosine

– Second line : IV metoprolol or propranolol

– Long term : digoxin, metoprolol/propranolol (beware in 1st trimester)

– 2nd line : soltalol, flecaide

– 3rd line : Verapamil, propafenone, procainamide

– Unstable VT : cardioversion is safe

– Bradyarrhythmia
– SSS or reflex bradycardia : try Lt lateral decubitus

– AV block : temporary pacing or permanent pace after GA 8 wks

– Hypertension :
– BP >= 170/110 is emergency, admit

– BP > 150/95 : start drug

– BP > 140/90 : non pharmacologic Tx (Low salt, Ca 1 gm/day)

– Consider drug in gestational HT, pre-existing HT with superimpose

gestational HT, HT with symptoms/subclinical organ damage

– Goal target BP in pregnancy with HT < 140/90 in all situation

– Moderate-High risk pre-eclampsia : ASA 100-150 mg/day from GA 12 to 36-37

wks (ESC I,A)

 – High risk of pre-eclampsia: HT during a previous pregnancy, CKD,
autoimmune disease (SLE or APS), DM type 1/2, chronic HT.
– Moderate risk of pre-eclampsia (at least 2 risk factors): first pregnancy age

>= 40 years or interval of > 10 years, BMI of >= 35 kg/m 2 at first visit, family
history of pre-eclampsia, multiple pregnancy.
– Calcium supplement 1.5-2 g/day in low calcium diet for prevention pre-

eclampsia
– Drug in severe HT : 1st is methydopa, labetalol, nifedipine. 2nd is hydralazine.

3rd is nitroprusside (risk fetal cyanide toxicity), NTG

– VTE on LMWH (base on BW) : no require monitoring
– Cardiac surgery : best period GA 24-37 wks (1st trimester : high risk fetal abnormaly,
3rd trimester : high risk preterm labor)
– Acute heart failure
– Induction lung maturation at GA > 23 wks + 5 days

– HF therapy : lasix, hydralazine/nitrate, betablock

– Vaginal delivery with peridural analgesia

– Cardiomyopathy (peripartum cardiomyopathy)

– Bromocriptine accompanied by OAC (stop lactation during bromocriptine)

– HCM
– Betablock in LVOT obstruction

– Cardioversion in persistant AF (IIa,C)

– Congenital heart disease

– Fetal echo in GA 18-22 weeks

– AF with pre-excitation : rhythm control during pregnancy

Mode of delivery
– Vaginal delivery is first : Regurgitation valve, HCOM, arrhythmia, Ascending aorta <
40 mm
– Induction in all at GA 40 wks

– Cesarean section (admit at GA 34-36 wks) : Hx of Ao dissection, Ascending aorta

> 45 mm or marfan aortic diameter 40-45 mm, Severe AS, Severe MS with FC III-IV,
Preterm while on oral anticoagulant (should stop > 2 wks), Eisenmenger syndrome
or severe PHT, severe HF, unstable arrthythmia
– Prefer epidural > GA

– Spinal block decrease sympathetic tone (decrease SVR)

– caution in CO sensitive reduction in preload and PHT with shunt

(Cyanosis)
– GA used selective inhalation agents

Post-partum
– Immediate increase CO 60-80% after delivery, resolved in 6-12 wks
– VTE prophylaxis
 – High risk (1/3 of following : Recurrent VTE > 1, Unprovoked VTE/estrogen
related, Hx of VTE plus thrombophilia or Fm Hx) : LMWH 6 wks + compression
stocking
– Intermediated risk : LMWH at least 7 days + compression stocking

Drug in pregnancy and breast feeding

Data : www.safefetus.com
– Pregnancy category classification : not recommend in ESC

– ส่วนใหญ่ category C ส่วนใหญ่ให้ได้

Betablock (prefer used selective beta-block)
– Non-selective beta-block associated with IUGR & hypoglycemia

– Category C

– Propranolol : safe in breast feeding

– Metoprolol : concentrated in milk

– Bisoprolol

– Category D

– Atenolol : transfer to milk

– Carvedilol (2nd, 3rd trimester), report C in AHA, ไม่ให้ใน breast feeding

Furosemide (C) : excrete in milk (caution)
Spironolactone (C), excreated in milk (discontinue)
Anti-platelet
– ASA (B), breast feeding only low dose ASA

– Clopidogrel (C), not recommend for breast feeding

Drug for PAH

– Category B : Sildenafil, epoprosternol, Treprostinil, tadalafil

– Category X : Bosentan and amrisentan

Anti-lipid
– Statin (X) and contraindication for breast feeding

– Stop statin 1-2 months before pregnancy

– Gemfibrozil (C)

– Fenofibrate (C)

– Niacin (A)
Anti-HT
– ACEI/ARB (D)

– HCTZ (B) : excrete in milk (caution)

Anti-arrhythmic drug
– Sotalol (B)

– Adenosine (C)

– Digoxin (C) : ให้ได้

– Flecanide/Propafenone (C) : recommend in WPW (I, C)

– Verapamil/Diltiazem (C) : prefer verapamil

– Amiodarone (D)

– Pricainamide (C)

Warfarin : Can breast feeding

Heparin & adenosine : no excrete via breast feeding

Investigation in pregnancy
– CMR without gadolinium

Contraception
– Estrogen containing contraceptives are harmful in high thromboembolic risk
(Cyanosis, Fontan physiology, mechanical valve, prior thrombotic event, PAH)
 Infective
endocarditis
Infective endocarditis

Term
– Acute : < 2 wks
– Subacute : >=2 wks to months
– Prosthetic valve IE : early < 1 year, late >= 1 year

Duke criteria
– Pathogen in absence of primary foci
– not include S.epidermidis in major criteria

– Single blood or IgG Ab > 800 for Coxiella burnetii

– Echo criteria : vegetation, abscess, new dehiscence/regurgitation

– No minor echo criteria : No fistula, aneurysm or perforate in criteria

– In ESC criteria include minor into major criteria

– Predisposition (minor criteria)

– IVDU

– Previous IE

– Heart : prosthetic heart, significant regurgitation or turbulent flow

– Invasive procedure within 60 days

– Immunologic phenomenon
– Osler node (septic emboli or vasculitis) : acute painful erythema at finger tips

– Rothʼs spot

– Embolic phenomenon
– Janeway (microabscess/septic emboli in S.aureus) at thenar/hypothenar

– subacute painless hemorrhagic macule

– Conjunctival hemorrhage

– Sphincter hemorrhage

– Mycotic aneurysm
General
– Remittent fever : ไข้ฟันปลา ไม่เตะ baseline
– Leukopenia in IE ass. Splenomegaly
– S.aureus bacteremia ass. IE ~ 1/4
 – Non bacterial thrombotic endocarditis : ก้อนๆไม่ค่อยสะบัด
– SLE with APS : mural mass, เด่น MV
– Malignancy : marantic endocarditis

– S.gallolyticus (bovis) : seek GI tumor

– HACEK : large and friable vegetation
– Prosthetic valve dysfunction : must r/o IE
– Risk for IE : include invasive procedure with in 60 days, pacemaker & ICD
– AV block in IE : พบใน AV > MV, 88% sense for abscess
– Medical treatment in S.aureus prosthetic valve is 50% mortality
– Prothesis valve IE is highest mortality
– Native valve IE with IVDU is lowest mortality
– Involve TV > MV, common pathogen : S.aureus, Embolism 70-80%,

– S.aureus bacteremia ass. IE 25-30%

Pathogen
– Native valve IE : common pathogen is S.viridian

– Prosthesis valve IE

– Early first year : S.aureus

– After 1 year : S.epidermidis

– Risk of prosthesis valve IE : orotracheal intubation and self expandable valve

– Uncommon pathogen

– Salmonella : HIV

– Listeria monocytogenes : Genitourinary tract infection

– Bartonella : alcoholic cirrhosis, homeless

Emboli
– Renal manifestation in IE is renal infarction
– IE with 1 st emboli : not predict recurrent emboli
– Risk emboli : size > 10 mm. MV (ant. MV leaflet), S.aureus, Candida, HACEK,
perivavular abscess
– Emboli : most common within 2 wks
Large emboli or distal emboli : fungus is common
– Mechanical valve IE with cerebral emboli : stop anticoagulant 2 wks
– Hemorrhagic stroke or Major ischemic stroke : delay surgery upto 4 weeks
– Mycotic aneurysm : viridan

Echo
– TEE more sensitive than TTE but same spec
– TEE sense 70%
– Prosthetic valve IE : TTE sense < 50%
– Vegetation < 4 mm, TTE is limited
– Vegetation like :
 – Papilllary endothelioma, papillary fibroelastoma
– Flail leaflet
– Myxomatous MV
– Thrombi
– Echo follow ตรงตำแหน่งที่ jet กระแทกด้วยดู IE
– Vegetation : oscillating mass, irregular round shape, size ... mm attach to anterior
mitral valve leaflet
– Abscess from echo : heterogeneous perivalvular echo density
– Pseudoaneurysm : pulsatile perivalvular echo free space with color Doppler flow
at ....
– Rocking motion ขยับเกิน 15 องศา

Echo finding : example

– Diffuse nodular thickening of AV leaflet with small oscillating mass size 0.5 cm attach

to ....
– Severe AR due to perforate of both AV leaflet with two eccentric AR jet

– Pseudoaneurysm of AV size ... cm beneath posterior aortic annulus

– Thickening of periaortic structure

Antibiotic
Empirical antibiotic
: Indication for acute severely illness
– Native valve : Ampicillin & Cloxacillin (12 gm/day) + Gentamycin (3 mg/kg/day)

– Penicillin allergy : Vancomycin plus gentamicin

– Prosthesis valve (< 12 months post Sx) : Vancomycin + Gentamicin + Rifampin

Timing for surgery

– Uncontrol infection : Abscess, false aneurysm, fistula, enlarge vegetation, PVE with
staph or non-HACEK gram negative, Fungi or resistance organism, persistent
infection (persistent bacteremia > 5-7 days)
Optimal time for IE with cerebral complication
– ICH : delay at least 4 weeks (IIa)

– Early surgical without delay if only TIA, no coma

Role mitral valve repair in IE
– Early surgical within 1-2 wk after antibiotic

– Surgical before annular extension

– Mitral repair with autologous pericardium

IE prophylaxis
– Prosthetic valve include TAVI

– Valve repair or annuloplasty

– Cardiac transplantation with valvulopathy

– Unrepair cyanotic heart or repaired with residual regurgitation or shunt. eg Post TOF

repair with residual PR

Antibiotic 30-60 mins before procedure
– Amoxycillin 2 gm oral

– Clindamycin 600 mg oral

– Azithromycin 500 mg oral

CIED infection
– Local pocket infection : ABx 10-14 days
– Local infection: early or late

– CIED infection (lead infection): with systemic symptoms ~ 3/4

– Device infection
– Removal of all hardware (lead & generator)

– Duration of antibiotic 2-6 weeks after CIED removal

– Negative vegetation on TEE : 2 wks

– Lead vegetation : 2-4 wks

– Plus valve vegetation : 4-6 wks as IE

– Time for re-implant permanent device

– Consider epicardial lead

– Wait at lead 6 week if possible or at least 72 hr after negative culture

– In valve vegetation: implant after 2 weeks from first negative H/C

– Duration of antibiotic : start after device removal

Clinical trial
Partial Oral VS IV Antibiotic Treatment of Endocarditis (POET)
– Population (Non-inferior trial) : Stable left side IE  (N=400)

– Streptococcus 50%, E.faecalis 23%, S.aureus 20%, Prosthetic valve 26%

– Exclude : reduced GI uptake or BMI >40

– Intervention : Oral vs IV antibiotic

– Previous treatment with IV antibiotic at least 10 days

– Outcome at 6 months : Same composite of all-cause mortality, unplanned cardiac

surgery, embolic events, relapse of bacteremia

CPR
CPR

Hypoxic arrest (จมน้ำ) : A-B-C

Cardiac arrest & Hypoxic arrest from FB : C-A-B
– Cardioversion in any stable, prevent R on T

– Defibrillation in unstable or CPR

– CPR after defibrillator stat except good consciousness

Biphasic
– narrow regular (suspected SVT) 50 - 100J Biphasic

– narrow irregular (suspected AF) 120 - 200J Biphasic

– wide regular (suspected VT) 100J Biphasic * 200J Monophasic

– Torsade de point : defibrillation

Titrate dose, max 200J Biphasic (*360J Monophasic)

OHCA (out of hospital cardiac arrest)

Basic life support
Screen safety first
– Check response แตะไหล
– Call for help (team, AED, ambulant car)
– Check pulse 5-10 sec (adult : carotid artery, infant < 1 years : brachial artery)
– BLS
– Unconsciousness : CAB

– Consciousness : ABC

– AED
– First : เปิดเครื่อง
– Second : adhesive pad
IHCR (In-hospital cardiac arrest)
– 1st chain : surveillant for detection high risk patient

OHCA
– 1st chain : recognition and activation emergency system
Chest compression (defibrillation is first)
– Position : lower half of sternum

– rate 100-120 /min

– Deep 5 cm, ห้ามกดลึกกว่า 6 cm (1/3 of chest wall)

– rate 100-120 /min
– Full recoil
– Interrupt chest compression < 10 sec
– Quality CPR : PetCO2 >10, DBP from A-line > 20 mmHg
– In pregnancy GA > 20 wks, CPR เหมือนปกติ แต่ทำ manual left uterine displacement
ด้วย
– If not ROSC in 4 mins : emergency C/S

Respiratory support
– If no tube 30_2, rescuers breathing > 1 s per beat

– Change person when 5 cycle or 2 mins

– If intubation, ambu-bag q 6 sec (volume 500-600 ml : half of ambu-bag)

Respirator care
– Normal ventilation : end tidal CO2 30-40 mmHg

– End tidal CO2 < 10 mmHg : less-likely to ROSC

Airway arrest
– เห็น FB obstruction ไม่ใช้มือล้วงเพราะอาจดันลงไป ใช้ด้ามช้อนงัดขึ้นมา
 – เห็น FB obstruction ไม่ใช้มือล้วงเพราะอาจดันลงไป ใช้ด้ามช้อนงัดขึ้นมา
– ยังรู้สึกตัวและเขียว (only complete airway obstruction, Donʼt do in partial airway
obstruction)
– Age < 1 ปี : back-blow (inter-scapular)/chest thrust
– Age > 1 ปี : abdominal thrust (ก้มตัวมากๆ กำมือขวา ด้านหัวแม่โป้งติด epigastrium)
– ไม่รู้สึกตัว
– 1st :Chest compression

– 2nd :airway เอา FB ออก

Drug
– Adrenaline 1 mg IV q 3-5 mins

– In VT/VF arrest : start adrenaline after second shock

– Amiodarone :

– Refractory VT/VF (after 3rd shock)

– 1st dose 300 mg IV

– 2nd dose 150 mg IV

– Stable arrhythmia

– 150 mg IV drip in 10 min and then 1 mg/min in first 6 hr

– Lidocaine

– Refractory VT/VF (after 3rd shock)

– 1st dose 1.0-1.5 mg/kg IV/IO

– 2nd dose 0.5-0.75 mg/kg IV/IO

– Summary : 1% lidocaine 5-10 ml IV in first dose & half at second dose

– Outcome : Same survival to hospital D/C but less survival to hospital

admission compare with amiodarone (ALIVE trial)

– MgSO4 1-2 gm with NSS 10-20 ml in Torsade de point

– 10%Calcium gluconate 15-30 ml in suspected hyperkalemia (contraindication in

digoxin intoxication)
– Atropine 0.6 mg IV (Max 3 mg)

– Dopamine 2-20 mcg/kg/min

– Adrenaline 2-10 mcg/min

– Drug in endotracheal tube : dose 2-2.5 times in adrenaline, lidocaine, naloxone

Unstable sign
Bradycardia < 50 bpm
Tachycardia > 150 bpm
– Hypotension

– Sign of shock
 – Chest pain
– Alternation of consciousness
– Heart failure

Reversible cause
– 5H : hypovolumia, hypoxemia, hydrogen ion (acidosis), hypo/hyperK, hypothermia
– 5T : Tension pneumothorax, cardiac Tamponade, Toxin, pulmonary thrombosis (PE),

coronary Thrombosis (MI)

– Bradycardia : hypoxemia, ACS, hyperkalemia, metabolic acidosis, increase

intracranial pressure
– Pregnancy : addition bleeding, drugs, embolic, fever, hypertension, anesthetic

complication/accident
Emergency CAG
– STEMI

– Electrical/hemodynamically unstable and cardiovascular is suspected

ROSC
– Stable at least 20 mins

– End tidal CO2 > 40 mmHg

Prognosis
– end tidal CO2 < 10 mmHg after CPR > 20 mins —> decide for stop CPR

Survival rate

CPR in newborn-infant-childhood
– เกิน 8 ปี and secondary sex characteristics (F : breast bud, M : auxiliary hair ใช้ adult
CPR
Infant
– Chest compression :

– Two thumb encircling hands : กรณี 2 คน, higher effective CPR

– Two finger hand : กรณีคนเดียว, อีกมือใช้ hold airway
– Below nipple line
– Deep 1/3 of AP diameter
– หมดสติต่อหน้า (cardiac cause) : ตามทีมก่อนแล้วค่อย CPR
– หมดสติไม่มีใครเห็น (respiratory arrest) : CPR ก่อนแล้วค่อยตามทีม
– BLS
– ช่วยคนเดียว (30_2)
– ช่วย 2 คน (15_2)
– Breathing
– Pediatric : ambu-bag 3-5 sec
Role of coronary intervention

Clinical trial
COACT trial
Patient: Out-of -hospital cardiac arrest without STEMI and shockable rhythm
– Acute unstable coronary lesions less than 20% of total trial, sign of ischemia from

EKG 65%
– Exclude unstable hemodynamic/ventricular arrhythmia

Intervention (RCT, N 552): Immediate CAG vs delay CAG

Outcome: No significant primary end point (survival at 90 days)
Comment : No CAG benefit due to selected right patients and misleading understand due
to right timing of CAG
Cardiac surgery
Cardiac surgery

– Must identified PFO with before bypass cardiac surgery due to increase risk air
emboli
– Aortic cross clamp time should < 120 mins
– Echo post op 4 wks

Specific concomitant comorbidity

– Screening PAD (ABI measurement) if CABG requiring saphenous vein

– PAD : prefer radial graft and sparing saphenous vein

– Screening carotid stenosis (Carotid artery duplex ultrasound) : recent stroke/TIA

within 6 months

Increase post-op sternal wound infection

– DM

– Obesity

– COPD

– Prolong time of surgery

– Both LIMA & RIMA

– Thoracic radiation

CT of ascending aorta evaluated before CABG

– Age > 70

– Sign of extensive generalized atherosclerosis

Techniques of CABG
– On-pump CABG (arrest heart & using cardiopulmonary bypass)

– Most widely used technique

– Off-pump coronary artery bypass (OPCAB)

– Newer technique : lower complication rate in good hand surgery

– Prefer in significant atherosclerotic aortic disease

Graft patency : Ideal coronary artery for bypass > 1-1.5 mm

– LIMA : 1 year = 95%, 5 years = 90%, 10 years = 90%

– RIMA & radial : 1 year = 95%, 5 years = 90%, 10 years = 70%

– Radial artery : prone to severe spasm

– SVG : 1 year = 80%, 5 years = 70%, 10 years = 50%

LIMA alway be used to LAD unless

– Emergency operation & hemodynamic decompensation

– Hx of chest wall radiation or radical mastectomy

– Proximal Lt subclavian artery stenosis

Used bilateral IMA : less recurrent angina but high rate sternal infection
Prefer radial artery > vein graft
 – Radial artery should not be used if positive Allen test or calcific degenerative radial
artery.
Rt gastroepiploic artery (jump to PD) : infrequently used due to
– Artery is fragile

– Small diameter

– Vessel twisting

– Increase operative time (need laparotomy)

Aortic surgery
– David procedure : valve sparing aortic root replacement

– Bentall procedure : composite graft replacement of aortic valve, aortic root and

ascending aorta, with re-implantation of the coronary arteries into the graft.
– complication : coronary site implatation
 Cardiac
Rehabilitation
Cardiac rehabilitation

General
– Start rehabilitation after clinical stabilization

Component of cardiac rehabilitation

– Medical evaluation

– Prescribed exercise

– CV risk factor modification

– Education & counseling

Goal of cardiac rehabilitation

– Improved QoL & Functional capacity

– Minimize chance of recurrence

– Decrease morbidity & mortality (previous era)

– Control coronary risk factor

No reduced HF hospitalization

Contraindication
– Active medical problem

– Severe symptomatic valvular heart

– Serious arrhythmia

– Acute endocarditis/pericarditis

– BP > 180/110 mmHg or Sinus tachycardia > 120 bpm

– Disease that might worsen by exercise

Rehabilitation program
– Phase I : Inpatient, Early start without harm
– Goal : prevent effects of immobilization/deconditioning

– HR during exercise (upper limit only 120 bpm)

– Post-MI : not more than 20 bpm over resting

– Post-CABG : not more than 30 bpm over resting

– Duration : start 5-10 mins upto 20-30 mins, 2-4 times/day

– Terget for 5 METs (ประกอบกิจวัตรประจำวันได้) or 70% of Max HR

– Respiratory training (incentive spirometer, threshold inspiratory trainer) :

improved inspiratory muscle weakness

– Calisthenic exercise
 – Phase 1.5 : Transition care, home care or pre-training at home
– Phase II : outpatient program (rehab center), need supervision
– Start 2-4 weeks post MI, 4-6 weeks post heart surgery

– Moderate aerobic exercise intensity : 3-6 METs, able to talk but not sing, Borg

scale 12-13 (Range 6-20), 40-60% VO2max

– Phase III : lifelong at home/community facility, no need supervision

ECG monitoring during exercise

: monitor for first 6-12 session
– Survival SCD

– History of serious arrhythmia

– EF < 30%

– Abnormal hemodynamic response during exercise

– Severe CAD
 – Patient with ICD

Exercise program
: Warm-up & Cool-down
– Type of exercise : aerobic, resistive, flexibility, balance

– Suggest start with aerobic in cardiac rehab

– Intensity of exercise

– Light (METs < 3, Heart rate reserve < 40%) : ร้องเพลงได้

– Moderate (METs 3-6, Heart rate reserve 40-60%, 50-70% maximum HR) : พอพูด
ได้
– Vigorous (METs > 6, Heart rate reserve 60-70%) : พูดลำบาก
– Duration of exercise : start slow & go slow.
– In METs < 3 : short period 5-10 mins and frequent

Sexual intercourse = 3-5 METs

– Post MI/Post PCI : delay 1 wks

– Post CABG : delay 6-8 wks

– Not recommend in ischemia symptoms at rest, HF NYHC III-IV

Exercise
Primary prevention
– No upper limit of exercise

– Recommend

– At least 150 mins per week for moderate aerobic physical activity

– Or At least 75 mins per week for vigorous physical activity

Secondary prevention
– J-curve benefit of exercise

– Start exercise : at least 2 weeks after complete revascularization or stable HF for 3

months.
– Not recommend in ischemia symptoms at rest

– Recommend : aerobic exercise, moderate intensity 30-60 min/day, 5-7 days/week

– 60-70% of MPHR (Borg scale 12-14) : เหนื่อยแบบพอพูดเป็นประโยคสั้นๆ

Suitable for Resistance training
: general start after aerobic training 2-4 weeks
– Restrict exercise

– Post PCI 2 weeks

– Post MI 4 weeks

– Post CABG 8 weeks

– Post pericarditis 12 weeks (3 months)

– Post myocarditis 24 weeks (6 months)

– METs >= 5

– BP < 160/100

– LVEF >= 35%

– No active cardiac condition

Resistance exercise
– ยกน้ำหนัก 50% of 1-RM (Repetition maximum: น้ำหนักมากสุดที่ยกครั้งเดียวแล้วหมดแรง)
– ให้ยกน้ำหนักช่วงหายใจออก โดยยกน้ำหนักแล้วนับเลขจำนวนครั้ง (eg. Bicep flexion -
exhale)
Recommendation in healthy adults of all ages
– At least 150 minutes a week of moderate intensity

– 2 km in 30 mins (Walk 4 km/hr)

– At least 75 minutes a week of vigorous intensity aerobic physical activity

Counseling after ICD

– จำกัดยกแขนไม่เกินระดับไหล 2 สัปดาห์
– หลีกเลี่ยงยกของหนักข้างใส่เครื่อง 2-4 สัปดาห์
– Training HR threshold : at least 10 bpm below program VT/VF zone
– No competitive exercise within 6 months after ICD implantation
Driving
Recommend delay
– Post PCI : 2 weeks

– Post MI : 4 weeks

– Post CABG : 8-12 weeks

– Post ICD implantation : ไม่แนะนำขับรถสาธารณะ

– Syncope
– 3 months restriction : VT/VF syncope

– Post ICD for secondary prevention

– Appropriated ICD shock

– Out flow tract VT S/P ablation

– 1 months restriction

– Post ICD for primary prevention

– SVT with medication

– Reflex syncope

– 1 weeks restriction

– S/P PPM

– SVT S/P ablation

– No recommend driving

– VT/VF without ICD

– Untreated SVT

– Untreated syncope

– If > 6 times per years in Vasovagal syncope

Example
Male 55 years, Taxi driver, TVD (refused CABG), EF 30%, admit due to HF and plan D/C
– ไม่แนะนำขับรถสาธารณะ
– พิจารณา Suitable anatomy for PCI
– แนะนำ ICD for primary prevention (after 90 days post revascularization)
Rehabilitation
– Phase I : เดินขยับตัวยืนแขนขาข้าวเตียง 10-20 นาที 3 รอบต่อวัน (max HR 120)
– Phase II : จำเป็นต้องเข้า rehab program & need supervision 10 ครั้ง
– Light to moderate physical activity : ทำกิจวัตรประจำวันได้
– Moderate physical activity (70% Max HR) พอพูดได้เป็นประโยค
– Phase III :
– Moderate physical activity : เดินวิ่งช้าพอพูดเป็นประโยคได้
– Vigorous physical activity only in complete revascularization & stable HF more
than 3 months
ถ้าออกกำลังกายแล้วมีอาการเจ็บหน้าอก ต้องหยุดออกและรีบมาพบแพทย์
Therapeutic
hypothermia
Therapeutic hypothermia

General
– Hypothermia concept : ischemia-reperfusion brain injury
– Abort programmed cell death pathways by reduced release amino acids and free

radicals.
– Decrease cerebral metabolic rate

– VT/VF : reduced mortality 25% and improved neurologic outcome

– Post arrest maintain oxygen sat >= 94%

Indication
ROSC and failure to meaningfully response to verbal command
– VT/VF arrest (class I, B)

– Non shockable rhythm arrest (I, C)

Contraindication
– Intracerebral hemorrhage
– Severe Hemorrhage
– Severe sepsis
– Refractory hypotension
– Major surgery within 14 days

Method
4 stage of hypothermia : Initiation, maintenance, rewarming, return to normothermia
– Goal temperature 32-36 C for at least 24 hr (33C vs 36C is same mortality &

neurologic outcome)
– Method to induced and maintenance hypothermia

– Ice bag, Cooling blankets : simple & effective but difficult to titrate to target

temp
– Temperature-regulated surface and endovascular device : easy temp control

– Hemodynamic

– Initial phase : hypertension (vasocontriction), cold diuresis

– During hypothermia : bradycardia, QT prolong, Hyperglycemia (DTX q 1 hr until

stable), hypoglycemia, HypoKalemia, Infection (pneumonia), coaggulopathy

– Rewarming

– Keep O2sat 94-96%, CVP 10-12 mmHg

– Initial Glucose and q 1 hr during initiation, Electrolyte q 4 hr

– Rewarm 0.25C q 1 hr (12-16 hr to rewarm) and keep normothermia for 48 hr (avoid

hyperthermia)
– Beware : hyperkalemia, hypotension, hypoglycemia

– Assess neurologic outcome at 72 hr

Complication
– Shivering : common during temp 32-34C
– Mx : Mg sulfate 4 g IV bolus for increase shivering threshold or Anesthetics or

Cisatracurium 0.15 mg/kg IV q 10 mins

Protocol
Poor neurologic outcome
– Evaluated neuro outcome 72 hr after normal temperature