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06/10/2023
Valvular Heart Disease

AKLOG A.(MD)
Cardiac Physiology
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06/10/2023
Systole AV/PV – opens
S1-S2 MV/TV – closes

Diastole AV/PV – closes

S2-S1 MV/TV – opens
Cardiac Physiology
3

06/10/2023
Regurg/ Insuff – leaking (backflow) of blood across a closed valve
Stenosis – Obstruction of (forward) flow across an opened valve

Systole AV/PV – opens-------Aortic Stenosis

S1-S2 MV/TV – closes------Mitral Regurg

Diastole AV/PV – closes------Aortic Regurg

S2-S1 MV/TV – opens-------Mitral Stenosis
 4
Mitral Stenosis

06/10/2023
 Causes:
Rheumatic
 almost all cases in adults

50% of pts who have ARC don’t remember it.

Mitral Annular Calcification- massive (rare)
Congenital – rare
SLE, RA
infective endocarditis with large vegetations
cor triatriatum
left atrial myxoma
 5

06/10/2023
 Predominant MS occurs in ~ 40% of all patients
with RHD (90% of pts with RHD have mitral valve
involvement)
 2/3 of MS- women
 Pathology
 Commissural fusion, leading to bowing or doming in diastole
 Thickening of leaflet tips, remainder of leaflet with variable thickening
 Subvalvular aparatus typically affected: fusion, shortening, fibrosis,
calcification of chordae
 These all changes lead to narrowing at the apex of the funnel-shaped valve
-------"fish-mouth“ valve
Pathophysiology

06/10/2023
Cardiac hemodynamic
 Primary hemodynamic consequence of MS is a pressure gradient
between the LA and LV in diastole

 The elevated LA pressure is reflected backward, causing an increase

in pulmonary venous, capillary, and arterial pressures and resistance
leading to poor pulmonary complaince and exertional dyspnoea

 In patients with moderate MS, the CO is normal or almost so at rest

but rises subnormally during exertion

 In patients with severe MS, the CO is subnormal at rest and may fail
to rise or may even decline during activity
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06/10/2023
 Pulmonary hypertension results from:

1) passive backward transmission of the elevated LA pressure;

2) pulmonary arteriolar constriction, which presumably is triggered by LA

and pulmonary venous hypertension (reactive pulmonary hypertension)

3) interstitial edema in the walls of the small pulmonary vessels;

4) organic obliterative changes in the pulmonary vascular bed.

Pathophysiology: LV and RV function
8

06/10/2023
 LV function is usually normal
 Decreased LVEF in about 1/3 of MS patients:
Rheumatic carditis
Chronic volume overloading
Concomitant CAD
Septal hypertrophy in patients with PHT

 RV function is normal in absence of pulmonary hypertension.

Symptoms 9

06/10/2023
 Fatigue  Afib
 Palpitations  Systemic embolism
 Cough
 Pulmonary infection
 Right sided failure
 SOB
 Left sided failure
 Hepatic Congestion
 Orthopnea  Edema
 PND  Worsened by conditions that  cardiac
output.
 Hemoptysis-
 Exertion,fever, anemia,
tachycardia, Afib,
intercourse, pregnancy,
thyrotoxicosis
Physical examination/Signs 10

06/10/2023
Mitral faces :-malar flush with pinched Auscultation:
and blue facies  Loud S1- as loud as S2 in aortic area
Palpation:  opening snap(OS)
 Small volume pulse  A2 to OS interval inversely
 Tapping apex-palpable S1 proportional to severity
 RV lift  Diastolic rumble: length proportional
to severity
 Palpable S2
 In severe MS with low flow- S1, OS
& rumble may be inaudible
 11

Mitral Stenosis: Physical Exam

06/10/2023
 First heart sound (S1) is accentuated and snapping
 Opening snap (OS) after aortic valve closure
 Low pitch diastolic rumble at the apex
 Pre-systolic accentuation (esp. if in sinus rhythm)
 12
DDX diastolic murmur at apex

06/10/2023
 MS
 significant MR
 severe AR (Austin Flint murmur).
 TS
 Atrial septal defect
 Left atrial myxoma
 Mitral Stenosis: Natural History 13

06/10/2023
 Time to clinical presentation varies
 From a few years in countries with a high prevalence of rheumatic fever to 20 years
in countries where rheumatic fever is rare
 20-40 year latency from rheumatic fever to symptom onset.
 Additional 10 years before disabling symptoms
 Progressive, lifelong disease,
 Usually slow & stable in the early years.
 Progressive acceleration in the later years
 14
Mitral Stenosis: Complications

06/10/2023
 Atrialdysrrhythmias
 Systemic embolization (10-25%)
Risk of embolization is related to, age, presence of atrial
fibrillation, previous embolic events
 Congestive heart failure
 Pulmonary infarcts (result of severe CHF)
 Hemoptysis
Massive: 20 to ruptured bronchial veins (pulm HTN)
Streaking/pink froth: pulmonary edema, or infection
 Endocarditis
 Pulmonary infections
Investigations 15

06/10/2023
 Chest x-ray-
 Straightening of the upper left border of the cardiac silhouette,
 Prominence of the main pulmonary arteries,
 Pulmonary congestion
 Barium swallow
 EKG
 LAE

 RVH

 Premature contractions
 Atrial flutter and/or fibrillation
  freq. in pts with mod-severe MS for several years
 80% of pts with MS &~ are in AF
Investigations… 16

06/10/2023
 Role of Echocardiography
 Diagnosis of Mitral Stenosis
 Assessment of hemodynamic severity
mean gradient, MVA, pulmonary artery
pressure
 Assessment of right ventricular size and function.
 Assessment of valve morphology to determine suitability for
percutaneous mitral balloon valvuloplasty
 Dx and assessment of concomitant valvular lesions
 Reevaluation of patients with known MS with changing symptoms
or signs.
 F/U of asymptomatic patients with mod-severe MS
Mitral Stenosis:Therapy 17

06/10/2023
 Medical
 Penicillin prophylaxis for rheumatic MS
 Diuretics for HF
 Digitalis/Beta blockers/CCB: Rate control in A Fib
 Anticoagulation: In A Fib
 Endocarditis prophylaxis

 Balloon valvuloplasty for patients with MV score of < 8

 Effective long term improvement
 Surgical
 Mitral commissurotomy
 Mitral Valve Replacement
 Mechanical
 Bioprosthetic
Mitral regurgitation 18

06/10/2023
 MR may result from an abnormality or disease process that
affects any one or more of the five functional components
of the MV apparatus (leaflets, annulus, chordae tendineae,
papillary muscles, and subjacent myocardium)

 Can be acute or chronic

 Can be primary or secondary/functional
Mitral Regurgitation:Etiology 19

06/10/2023
 Valvular-leaflets  Annulus
 Myxomatous MV Disease  Calcification, IE (abcess)
 Rheumatic  LV dilatation & functional
regurgitation
 Endocarditis
 Congenital-clefts
 Papillary Muscles
 CAD (Ischemia, Infarction,
 Chordae Rupture)
 Fused/inflammatory  HCM
 Torn/trauma  Infiltrative disorders
 Degenerative  Trauma
 IE
Etiology
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Pathophysiology
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 In acute severe MR
• The regurgitant volume is delivered into a normal-sized LA
having normal or reduced compliance=> LA pressures rise
markedly for any increase in LA volume. => elevated
pulmonary venous pressures => pulmonary edema
• LV systolic function may be normal, hyperdynamic, or
reduced.

 In chronic MR
 LV “unloads” itself into left atrium
Chronic left atrial overload
 22
Pathophysiology…

06/10/2023
 Chronic overload on left ventricle  heart failure
 Volume of regurgitant flow determined by:
Ventriculo-atrial gradient
Diastolic time
Size of the regurgitant orifice
 LVE → annulus dilation → increased MR
 Backflow → LAE, Afib, Pulmonary HTN
 SinceEF rises in severe MR in the presence of
normal LV function, even a modest reduction in this
parameter (<60%) reflects significant dysfunction.
 Natural History 23

06/10/2023
 Chronic MR (variable course)

 Chronic MR may be protected from pulmonary

congestion by dilated, highly compliant left atrium

 Acute MR usually with fulminant pulmonary edema

MR Symptoms 24

06/10/2023
 Similar to MS
 Dyspnea, Orthopnea, PND
 Fatigue
 Pulmonary HTN, right sided failure
 Hemoptysis
 Systemic embolization in A Fib
 Recognizing Chronic MR 25

06/10/2023
 Pulse:  Murmer-Fixed MR:
 brisk, low volume  Pansystolic
 Apex:  Loudest apex to axilla
 Hyperdynamic  Murmer-Dynamic
 Laterally displaced MR(MVP)
 Palpable S3 +/- thrill  Mid systolic
 Late parasternal lift 2 to  +/- click
LA filling   upright
 S 1 soft or normal
 S 3 / flow rumble if severe
 S 2 wide split (early A2) unless
LBBB
Assessing Severity of Chronic MR
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06/10/2023
Measure the Impact on the LV:
 Apical displacement and size
 Palpable S3
 Longer/louder MR murmer (chronic MR)
 S3 intensity/ length of diastolic flow rumble
 Wider split S2 (earlier A2) unless HPT narrows the split
 Recognizing Mitral Regurgitation
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06/10/2023
 ECG:  CXR:

 LA enlargement  LV
 Afib   LA
 LVH (50% pts.  pulmonary
With severe MR) vascularity
 RVH
 Combined
hypertrophy
MR Echocardiography 28

06/10/2023
 Baseline evaluation to identify etiology, quantify
severity of MR
 Assess and quantify LV function and dimensions
 Annual or semi-annual surveillance of LV
function, estimated EF and LVESD in
asymptomatic severe MR
 To establish cardiac status after change in
symptoms
 Baseline study post MVR or repair
Treatment MR
29

 Depends on cause, type, severity

06/10/2023
 Medical
 Vasodilators

For acute MR - to reduce the regurgitant fraction and increase

forward flow,
For chronic ,isolated severe MR use if there is systemic HTN
 Diuretics for treatment of congestion( HF)
 Anticoagulation for atrial fib
 Penicillin – for rheumatic fever recurrence prophylaxiss
 ??SBE Prophylaxis – prevent endocarditis
 Avoid isometric forms of exercise in severe MR
Treatment MR…
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 Surgical (repair or replacement of the valve )

06/10/2023
 Acute severe MR- repair of valve
 Indications for MV surgical treatment of chronic MR
depends on symptom, LVEDV, and EF
 Surgery is indicated in severe MR

 Symptomatic
 Asymptomatic severe MR
 Progressive LV dysfunction(LVEF < 60% and/or
ESLV > 40 mm)
 Recent-onset AF and pulmonary hypertension(PA
pressure 50 mmHg at rest or 60 mmHg with
exercise.)
 Aortic Stenosis
31

 Etiology

06/10/2023
 Bicuspid Valve
Usually
asymptomatic until > 30 yrs
Associated aortic coarctation (40%)
Becomes stenotic later in life
 Unicuspid Valve
Generally repaired in early childhood
 Subvalvular (membrane or ridge)

 Degenerative (“senile”)
 Calcification of leaflets and commisures(=30% of persons >65 years exhibit aortic valve
sclerosis, 2% exhibit frank stenosis)
 Chronic inflammatory process?
 Rheumatic AS: is almost always associated with involvement of the mitral valve and with
AR
 Fibrosis and calcification of commisures
 Degeneration of prosthetic valves (especially bioprosthetic)
 AS 32

Left ventricular out flow obstruction can be caused by

06/10/2023

 Valvular aortic stenosis- most common cause-
Approximately 80% of adult patients with symptomatic
valvular AS are male

 Supravalvular aortic stenosis- majority of patients (60 to 75

percent) have an hourglass deformity, consisting of a discrete
constriction of a thickened ascending aorta at the superior aspect
of the sinuses of Valsalva

 Subvalvular aortic stenosis- include a thin membrane (the most

common lesion), thick fibromuscular ridge, diffuse tunnel-like
obstruction, abnormal MV attachments, and occasionally,
accessory endocardial cushion tissue
 Pathophysiology
33

 Normal aortic valves area is 3.0-4.0 cm2.

06/10/2023
 Obstruction to LV outflow produces a systolic pressure
gradient between the LV and aorta
 Significantgradient usually doesn’t occur until valve area
has ’d from ~ 3.0 cm2 to < 2.0 cm2
 Symptoms “usually” not seen until the valve area is < 1 cm2
 Progression ~ 0.1 cm2/year
 This leads to concentric hypertrophy of the LV maintaining
normal CO for many years; however, excessive hypertrophy
becomes maladaptive, and LV function declines
Aortic Stenosis: Symptoms
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06/10/2023
 May be a long asymptomatic period
 Symptomatic
 Usually have severe AS with AVA of 1 cm2 or less
 Cardinal Symptoms
 Chest pain (angina)
Reduced coronary flow reserve
Increased demand-high afterload
 Syncope/Dizziness (exertional pre-syncope)
Fixed cardiac output
Vasodepressor response
 Dyspnea on exertion & rest
 Impaired exercise tolerance
 Other signs of LV failure
 Diastolic & systolic dysfunction
 Aortic Stenosis: Physical Findings35

06/10/2023
 Pulse, and BP are normal until late in the course of the
disease
 Pulsus Parvus et Tardus (The peripheral arterial pulse rises
slowly to a delayed sustained peak)
 Narrow pulse pressure
 LV impulse is usually displaced laterally. A double apical
impulse(Sustained Bifid LV impulse)
 carotid systolic thrill
 Paradoxical spliting of the second heart sound
 S3 (with left ventricular failure)
 S4 (with left ventricular hypertrophy)
 Aortic Stenosis: Physical Findings
36

• systolic crescendo-decrescendo, loudest at the base of the heart),

06/10/2023
may radiate to the carotids
• May sometimes be transmitted to the apex, be confused with
murmur of MR (Gallavardin effect)
Natural History of Aortic Stenosis

37
 Angina -5 yr survival

06/10/2023
 Syncope -3 yr survival
 Congestive Heart Failure -1-2 yr survival
 Investigations 38

06/10/2023
 ECG- LV hypertrophy, ST-T changes (LV  Echocardiogram
strain pattern)  Etiology
 Chest x-ray-  Valve gradient and area
 LV hypertrophy causes only rounding of  LVH
the apex,
 Systolic LV function
 advanced disease may show LV dilatation,
pulmonary congestion, LA, PA and RV  Diastolic LV function
enlargement  LA size
 Concomitant regional wall motion
abnormalities
 Coarctation associated with bicuspid
AV
Treatment

39

 Medical

06/10/2023
 Avoid strenuous exercise in severe AS
 Avoid dehydration and hypovolemia
 Penicillin prophylaxis for rheumatic AS
 Diuretics for LHF/RHF
 Digitalis/Beta blockers/CCB: Rate control in A Fib
 Anticoagulation: In A Fib
 ???Endocarditis prophylaxis
 Vasodilator - may be unwise(SO AVOID) in pts with severe AS

 Since there is a risk that this will reduce aortic pressure and
coronary perfusion without an equivalent reduction in the left
ventricular afterload
 Surgical- valve replacement based on indications
 Aortic regurgitation 40

06/10/2023
• Caused by primary valve disease or by primary aortic root disease.
Pathophysiology… 41

06/10/2023
Pathphysiology
Increased total stroke volume
Increased LVEDV
Increased LV pre and after load
Finally adaptive measures fail
LV function declines
SV and EF decline
 Pathophysiology… 42

06/10/2023
 Acute AR: nl LV poorly tolerates sudden increase
LVEDV  massive increase LVEDP leading to pulm
edema, hypotension +/- cardiogenic shock

 Chronic AR: LV overload  LV dilatation, eccentric

hypertrophy, insidious prog to CHF (decades,
typically)
Pathophysiology… 43

06/10/2023
 In advanced stages there may be considerable
elevation of the LA, PA wedge, PA, and RV
pressures and lowering of the forward CO at
rest
 Myocardial ischemia may occur in patients
with AR because myocardial oxygen
requirements are elevated by LV dilatation,
hypertrophy, and elevated LV systolic tension
 Eccentric Hypertrophy
 44
Symptoms

06/10/2023
 Approximately ¾ of patients with predominant valvular
AR are men;
 women predominate among patients with primary
valvular AR who have associated rheumatic mitral valve
disease.
 Patients may remain asymptomatic for decades
 Patients may complain of pounding and uncomfortable
sense of heart beat, palpitation
 Dyspnea, orthopnea, PND
 Chest pain.
 Nocturnal angina >> exertional angina
 ( diastolic aortic pressure and increased LVEDP thus 
coronary artery diastolic flow)
 Peripheral Signs of Severe AR 45

 Quincke’s sign: capillary pulsation

06/10/2023
 Corrigan’s sign: water hammer pulse
 De Musset’s sign: systolic head bobbing
 Mueller’s sign: systolic pulsation of uvula
 Durosier’s sign: femoral retrograde bruits
 Traube’s sign: pistol shot femorals
 Widened pulse pressure
 Systolic – diastolic = pulse pressure
 Peripheral Signs of Severe 46

AR…

06/10/2023
Becker's sign — Visible pulsations of the retinal arteries and
pupils.
Mayne's sign — More than a 15 mmHg decrease in diastolic
blood pressure with arm elevation from the value obtained
with the arm in the standard position.
Rosenbach's sign — Systolic pulsations of the liver.
Gerhard's sign — Systolic pulsations of the spleen.
Hill’s sign: BP Lower extremity >BP Upper extremity by
> 20 mm Hg - mild AR
> 40 mm Hg – mod AR
> 60 mm Hg – severe AR
 Central Signs of Severe AR 47

06/10/2023
 Apex:  Aortic diastolic murmur
 Enlarged High pitched, blowing,
 Displaced decrescendo ,diastolic
 Hyper-dynamic murmur at LSB
 Palpable S3 Best heard at end-
 Austin-Flint murmur- a soft, expiration & leaning
low-pitched, rumbling mid- forward
diastolic murmur at the apex length correlates with
(produced by the diastolic
severity (chronic AR)
displacement of the anterior
leaflet of the mitral valve by
the AR stream )
 Assessing Severity of AR 48

06/10/2023
 Assess severity by impact on peripheral signs and LV
  peripheral signs =  severity
  LV =  severity
 S3
 Austin -Flint
 LVH
 Radiological cardiomegaly
Natural history 49

06/10/2023
Asymptomatic %/Y
 Normal LV function (~good prognosis)
 Progression to symptoms or LV dysfunction <6
 Progression to asymptomatic LV dysfunction < 3.5
 75% 5-year survival
 Sudden death < 0.2
 Abnormal LV function
 Progression to cardiac symptoms 25
 Symptomatic (Poor prognosis)
 Mortality > 10
 50
Laboratory

06/10/2023
 ECG- signs of LV hyperthrophy with strain
 Echocardiography
 Chest X-ray
Treatment of AR 51

06/10/2023
 Medical
 Afterload reduction: ACEI, nifedipine, hydralazine
 Use BB cautiously, if at all, given prolonged diastole and
therefore  regurg volume
 Surgical
 AVR – 4% mortality alone, 6.8% with CABG
 LV dysfunction often irreversible, despite AVR
Treatment of AR… 52

06/10/2023
 Acute AR- surgery is required urgently
 Chronic AR- avoid isometric exercise
 Treat hypertension with vasodilators
 Surgical treatment –valve replacement
53

06/10/2023
Thank u