Valvular heart disease

M Chadi Alraies, MD Chief Medical Resident Tuesday, August 30, 2011

Valvular heart disease

       

Mitral regurgitation. Mitral stenosis. Aortic stenosis. Aortic regurgitation. Tricuspid regurgitation. Tricuspid stenosis. Pulmonary stenosis Pulmonary regurgitation.
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Jones criteria

Major manifestations
    

Carditis Polyarthritis Chorea Erythema marginatum Subcutaneous nodules

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Minor manifestations


Clinical findings
 

Arthralgia Fever Elevated acute phase reactants (erythrocyte sedimentation rate, C-reactive protein) CProlonged PR interval Positive throat culture for group A beta-hemolytic betastreptococci or positive rapid streptococcal antigen test. antistreptolysin O
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Laboratory findings
 

Evidence of preceding streptococcal infection:

 

MITRAL STENOSIS

Prevalence
  

43% of all VHD in 1960 9% of all VHD in 1985 Rheumatic heart disease still affecting 21 out of 1,000 school-age children in Asia. school2/3 of all patient with rheumatic MS are women.

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Causes
        

Rheumatic fever. Congenital chordal fusion. Congenital papillary muscle malposition. Mitral annular calcification (e.g. ESRD, elderly) Mitral valve repair. Surgical valve replacement. Obstruction by large vegetation. Rheumatoid arthritis. Carcinoid syndrome.
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Pathophysiology


Orifice area <2 cm2:

Diastolic filling of the LV is impaired.  Increased LA pressures.


Orifice area <1 cm2:

LA pressure is > 25 mmHg.  Symptoms of HF  Tachycardia


LV diastolic pressure is usually normal in isolated MS.

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Signs and symptoms

       

Dyspnea Orthopnea PND LL edema Pulmonary edema Mitral facies. Hemoptysis Embolic events: MI, stroke, renal emboli.
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Signs and symptoms

 

Mild MS is asymptomatic at rest and mild exertion. Symptoms triggered by factors that increase blood flow across the mitral valve or shortening of the diastolic period
    

Stress Exercise Infection Pregnancy Atrial fibrillation with RVR

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Physical exam the murmur

       

"Tapping" sensation over area of expected PMI. Accentuated S1 S1 Opening snap. MidMid-diastolic murmur (rumble) low in pitch. S2-OS interval of 70 msec is seen in severe MS. Best heard after exercise, left lateral recumbency. Bell chest piece lightly applied. Pulmonary HTN and RVF occur later in MS.
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ECG
 

Low sensitivity P mitrale:

 

Lead II broad and bifid > 0.12 sec Lead V1 broad and deep negative component of biphasic P V1 wave, longer than 0.04 sec and 1 mm in depth.

 

If pulmonary hypertension is present, tall peaked P waves, right axis deviation, or right ventricular hypertrophy appears. Atrial fib. Atrial flutter.
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CXR

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CXR

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CXR
    

Straight left heart border. Large left atrium. Sharply indenting esophagus. Elevation of left mainstem bronchus. Large right ventricle and pulmonary artery if pulmonary hypertension is present. Calcification occasionally seen in mitral valve.
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2D echocardiogram
 

Estimates the severity of MS Measure the pressure gradient between LA to LV. Define the etiology.

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Treatment
 

BB and CCB for rate control Anticoagulation with warfarin if

Chronic A.fib  Prior embolic events.  Severe MS with LA >5.5 cm on echocardiogram. >5


A.fib recurrence is 20-30% after the first 20-30% episode.

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Surgery


Indications for intervention focus on:

Episode of pulmonary edema,  Decline in exercise capacity,  Evidence for pulmonary hypertension.


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Surgery


Percutaneous mitral balloon valvotomy:



Mitral valve area <1.5 cm2 <1

MVR:


Mitral valve area <1.0 cm2 <1

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Questions?

Mitral regurgitation

Etiology
       

Myxomatous degeneration: MVR, Marfans Mitral annular calcification. Rheumatic heart disease. Congenital malformation. Ruptured papillary muscles and cordae tindinea. Infective endocarditis. Tumors. Functional:


Ischemia, DCM, infiltrative CMP and trauma.

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Prevalence


20% of post Mi patients. 20%

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Sign and symptoms

    

Symptoms typical for the underlying cause. Exercise intolerance. DOE Pulmonary edema and CHF. Triggers for symptoms


Atrial fibrillation, pregnancy and infection.

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Physical exam
 

Forceful, brisk PMI; systolic thrill over PMI. Pansystolic: begins with M1 and ends at or after M1 A2 . Loudest over PMI; transmitted to left axilla, left infrascapular area. After exercise; diaphragm chest piece.

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Tests

ECG
   

Left axis deviation. Left ventricular hypertrophy. P waves broad, tall, or notched in standard leads. Broad negative phase of diphasic P in V1. V1

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CXR

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2D echocardiogram
 

Thickened mitral valve in rheumatic disease. Enlarged left ventricle with above-normal, abovenormal, or decreased function. Regurgitant flow mapped into left atrium.

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Management


Acute MR:
Emergency surgery.  Stabilization with vasodilators (nitroprusside)  Intra-aortic balloon counterpulsation. Intra

Chronic MR:
Afterload reduction: ACEI  Anticoagulation in case of atrial fibrillation.

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When to refer for surgery?

1. 2. 3. 4. 5. 6.

Acute symptomatic MR Severe MR, NYHA II-IV with EF >60%. II>60%. Severe MR, EF 50-60%, ESD 45-50 mm. 50-60%, 45Severe MR, EF 30-50%, ESD 50-55 mm. 30-50%, 50Severe MR, A. Fib with NL EF Severe MR, severe pulmonary HTN, NL EF.

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Questions?

Aortic stenosis

Etiology
    

Bicuspid valve. Degenerative Congenital Rheumatic Infective endocarditis.

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Prevalence
  

25% of patients over age 65 years and 25% 35% of those over age 70 years 35% The most common surgical valve lesion in developed countries, and many patients are elderly.

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Risk factors
  

Hypertension, Hypercholesterolemia, and Smoking

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Signs and symptoms



Cardiac output is maintained until the stenosis is severe (with a valve area < 0.8 cm2). cm2
LV failure,  Angina pectoris.  Syncope exertional and a late finding.


all occur with exertion. exertion.

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Physical exam


  

Powerful, heaving PMI to left and slightly below MCL. Small and slowly rising carotid pulse. A2 normal, soft, or absent. Paradoxic splitting of S2 if A2 is audible. S2 A2

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Physical exam
 

Prominent S4. S4 Midsystolic: begins after M1, ends before A2, M1 A2 reaches maximum intensity in mid systole. Right second ICS parasternally or at apex, heard in carotids and occasionally in upper interscapular area. Patient resting, leaning forward, breath held in full expiration.
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Tests

ECG
   

Left axis deviation. Left ventricular hypertrophy. LBBB Repolarization changes.

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CXR
  

Concentric left ventricular hypertrophy. Prominent ascending aorta, small knob. Calcified valve.

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2D echocardiogram
   

Poststenotic dilation of the aorta, Restricted opening of the aortic leaflets, Bicuspid aortic valve in about 30%. 30%. Increased transvalvular flow velocity

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Management


Medical management
No vasodilators.  Indicated in asymptomatic patients only with preserved LV function.


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Surgery, when?


Symptomatic:
Improve survival in preserved and depressed LVF  Depressed LV function.


Prophylactic AVR:
Patients going for CABG with severe AS  Patients going for other valvular surgery with moderate AS.


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Questions?

Aortic regurgitation

Etiology
1. 2. 3. 4. 5. 6. 7. 8.

Bicuspid aortic valve. HTN Rheumatic Congenital Aneurysm of the sinus of Valsalva. Infective endocarditis. Post aortic stenosis repair. Osteogenesis imperfecta.
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Pathophysiology
 

Increased preload and afterload to the LV. The response to these effects is to hypertrophy by laying sarcomeres end to end. end. Increasing the LV chamber size greater than the wall thickness (eccentric hypertrophy). The amount of hypertrophy is substantial and greater than that seen in aortic stenosis or mitral regurgitation.
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Signs and symptoms



LV failure is a late event and may be sudden in onset. Exertional dyspnea and fatigue are the most frequent symptoms. Angina pectoris.

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Physical exam
   

wide arterial pulse pressure. waterwater-hammer pulse or Corrigan's pulse. Quincke's pulses (subungual capillary pulsations) Duroziez's sign (to and fro murmur over a partially compressed peripheral artery, commonly the femoral) Musset's sign (head bob with each pulse).

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The apical impulse is

prominent,  laterally displaced,  usually hyperdynamic, and  may be sustained.


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The murmur


Aortic diastolic murmur is usually high-pitched highand decrescendo. A mid or late diastolic low-pitched mitral lowmurmur (Austin Flint murmur) may be heard. Patient leaning forward, breath held in expiration.

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Tests

ECG
 

Left axis deviation. Left ventricular hypertrophy.

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Management


Acute aortic regurgitation

Treatment of the underlying infection.  Surgical management.


Chronic regurgitation
vasodilators, such as hydralazine, nifedipine, and ACE inhibitors, can reduce the severity of regurgitation.  prescribe ACE inhibitors whenever the LV diastolic size is increased > 5.0 cm.


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Surgery, when?


LV dysfunction EF is < 55% or if the LV end55% endsystolic dimension is > 5.0 cm. aortic root diameters of > 5.0 cm in Marfan or > 5.5 cm in non-Marfan patients. nonsurgical risk is higher than in aortic stenosis patients with a similar EF.

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Questions?

Tricuspid regurgitation

Etiology
1.
1. 2. 3. 4. 5. 6.

RV geometry abnormality:
Pulmonary hypertension Severe pulmonic regurgitation. LVF RV infarction. Cor pulmonale. Mitral stenosis.

2.
1. 2. 3. 4. 5.

Anatomic issues with the valve itself:

Infective endocarditis. Ebstein's anomaly Marfans syndrome Carcinoid syndrome TV prolapse.
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Signs and symptoms



RV failure
hepatomegaly,  edema, and  ascites


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Physical exam
 

  

Cyanosis may be present. Occasionally systolic thrill at lower left sternal edge. Systolic pulsation of liver. Blowing, coarse, or musical murmur. Murmur usually becomes louder during inspiration.

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Management


 

Elimination of the cause of the tricuspid regurgitation. Intravenous diuretics should initially be used. Torsemide is better absorbed.

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Surgery, when?
   

Symptoms and annular dilatation. Endocarditis. Ebsteins anomaly. Bioprosthetic valve, and not a mechanical valve, is used.

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DD of systolic murmur

Intervention

HOCM

Aortic Stenosis

Mitral Regurgitation

Mitral Prolapse

Valsalva
or

Increased Increased Decreased Decreased Increased Markedly increased Markedly increased

Decreased Increased Decreased Increased Increased Increased Increased

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Standing Handgrip or squatting Supine position with legs elevated Exercise Amyl nitrite

Decreased or same Decreased Increased

Inc or dec Increased Decreased

No change Decreased Decreased Decreased Decreased Increased Increased Increased

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IsoProterenol

References
1. 2.

CMDT 2007 ACC/AHA 2006 Guidelines for the management of patient with valvular heart disease.

THANK YOU
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