Valvular Heart Diseases

Valvular Heart Diseases

Assistant Prof.Dr Ghazi F. Haji
Interventional cardiology
Baghdad College of Medicine

Valvular Heart Disease

• Left sided valve lesions:
– Aortic: stenosis / regurgitation
– Mitral: stenosis / regurgitation

• Right sided valve lesions:

– Tricuspid: stenosis / regurgitation
– Pulmonary: stenosis / regurgitation

• Prosthetic heart valves

Aortic stenosis
Aetiology

• Aortic stenosis may be congenital or acquired.

• Congenital malformations may be tricuspid, bicuspid or more rarely unicuspid / quadricuspid

• Acquired causes include the following:

- Degenerative disease
- Rheumatic disease
- Calcific e.g. end-stage renal failure, Paget’s disease
- Miscellaneous e.g. rheumatoid involvement

Symptoms

• Exertional dyspnoea or fatigue
• Angina
• Syncope
Physical findings
• Slow rising pulse
• Reduced systolic and pulse pressure
• Systolic thrill over the aortic area
• Ejection systolic, crescendo-decrescendo murmur
• Soft or inaudible second heart sound
• ECG: LVH, AV node conduction defects


Echocardiography

• Thickened valves with reduced motion, sometimes calcified

• When stenosis is severe, the peak gradient across the aortic valve is usually > 60mmHg.

Medical therapy

• Conservative treatment should be offered for mild to moderate aortic stenosis and to asymptomatic patients with severe aortic stenosis as follows:

- Advise to report symptoms

- Avoid vigorous exercise
- Antibiotic prophylaxis for endocarditis
- Regular follow-up ± echocardiography

Surgical/ Interventional therapy

• Aortic valve replacement should be offered to the following:
- Symptomatic pts with severe AS
- Pts with severe AS undergoing CABG surgery
- Pts with moderate AS undergoing CABG surgery
- Asymptomatic pts with severe AS and LV dysfunction


• Balloon valvuloplasty: bridge to surgery in haemodynamically unstable patients, or palliation for patients with serious comorbid conditions

• Transcatheter aortic valve replacement

Aortic regurgitation
Aetiology

• Either due to primary disease of the aortic valve or wall of the aortic root or both.

• Causes of primary aortic valve disease include:
- Congenital eg. bicuspid aortic valve
- Acquired: rheumatic valve disease, infective endocarditis, trauma, connective tissue disease.

• Causes of primary aortic root disease include:

- Degenerative, cystic medial necrosis (eg. Marfan’s), aortic dissection, syphilis, connective tissue disease, hypertension.

Clinical history

• Chronic severe AR
Dyspnoea is the principal symptom
Syncope is rare and angina is less frequent than in
aortic stenosis.


• Acute severe AR
LV decompensation occurs readily with fatigue,
severe dyspnoea and hypotension.

Physical findings

• Collapsing pulse

• Wide pulse pressure

• Peripheral signs- De Musset’s, Corrigan’s, Quinke’s, Muller’s, Duroziez’s

• Hyperdynamic apex beat

• Early blowing diastolic murmur

ECG: Left axis deviation, LV hypertrophy.

• CXR: Cardiomegaly, aortic calcification, aortic root dilatation

Echocardiography

Management

• Medical treatment

- Diuretics, digoxin, salt restriction
- Vasodilators
- Endocarditis prophylaxis

• Without surgery, death usually occurs within 4 years of developing angina and within 2 years after onset of heart failure.

surgical therapy

• Severe acute AR requires prompt surgical intervention.

• Chronic severe AR

- Symptomatic patients with normal LV function
- Symptomatic patients with LV dysfunction or dilatation
- Asymptomatic patients with LV dysfunction or dilatation (EF<50% or end-systolic diameter > 55mm)


• Aortic valve and root replacement- if aortic root diameter is ≥ 50mm.

Mitral stenosis

Aetiology

• Rheumatic

• Congenital

• Carcinoid, SLE, rheumatoid arthritis, mucopolysaccharidoses.

• Left atrial myxoma, ball-valve thrombus, infective endocarditis with large vegetation and cor triatriatum.

Rheumatic mitral stenosis

• Fusion of the valves, commisures and chordae

• Symptoms usuually occur in the 3rd or 4th decade, but mild MS in the aged is becoming more common.

• 25% of patients have pure mitral stenosis and two-thirds are female.

• Lutembacher’s syndrome- associated with an atrial septal defect


Pathophysiology

• Normal mitral valve area = 4-6cm2.

• A mitral valve area ≤ 1cm2 equates to severe mitral stenosis.

• Symptoms usually develop when mitral valve area ≤ 2.5cm2

• Symptoms in mild mitral stenosis usually precipitated by exercise, emotional stress, infection, pregnancy or fast atrial fibrillation.

Natural history

• Long latent period of 20 to 40 years

• Once significant limiting symptoms occur, 10-year survival rate is 5-15%.

• With severe pulmonary hypertension, mean survival falls to
< 3 years.

• Mortality from untreated mitral stenosis is due to progressive heart failure (60-70%), systemic embolism (20-30%) and pulmonary embolism (10%).


Clinical features

• Dyspnoea

• Haemoptysis may also occur
• Angina
• Embolic events

Physical findings

• Mitral facies
• Tapping apex beat
• Right ventricular heave, loud P2
• Loud first heart sound.
• Opening snap.
• Rumbling, mid-diastolic murmur with presystolic accentuation in sinus rhythm.

echo evaluation

• Assessment of valve morphology: degree of leaflet thickness, mobility and calcification and extent of subvalvular fusion.
• Estimation of left atrial size.
• Doppler echo: estimation of mitral valve area, transvalvular gradient and PA pressure.


edical treatment

• The asymptomatic patient with mild mitral stenosis should be managed medically. Medical therapy includes:
- Avoidance of unusual physical stress.
- Salt restriction.
- Diuretics if needed.
- Control of heart rate – β-blocker or digoxin.
- Anticoagulation for AF or prior embolic event.
- Annual follow-up.
- Echocardiography if deterioration in clinical condition.

Management of symptomatic mitral stenosis

• Patients with symptoms should undergo clinical re-evaluation with echocardiography.

• NYHA class II symptoms and mild mitral stenosis may be managed medically.

• NYHA class II symptoms and at least moderate stenosis (MVA≤1.5cm2 or mean gradient ≥5mmHg) may be considered for balloon valvuloplasty.

• NYHA class III or IV symptoms and severe mitral stenosis should be considered for balloon valvuloplasty or surgery.


Mitral valve replacement

• Severe mitral stenosis and contraindications to surgical commisurotomy or balloon valvuloplasty:

- Restenosis following surgical commisurotomy or balloon valvuloplasty

- Significant mitral regurgitation

- Extensive calcification of the subvalvular apparatus.

• Operative mortality ranges from 3-8% in most centres.

Mitral Regurgitation

Chronic MR Acute MR Mitral valve prolapse
Aetiology

Mitral regurgitation may be caused by abnormalities of the valve leaflets, chordae tendinae, papillary muscles or mitral annulus:

• Valve leaflets

- myxomatous degeneration
- rheumatic heart disease
- infective endocarditis
• Chordae tendinae
- congenital, infective endocarditis, trauma, rheumatic fever, myxomatous
• Papillary muscles
- myocardial ischaemia, congenital abnormalities, infiltrative disease
• Mitral annulus
- dilatation eg. ischaemic or dilated cardiomyopathy
- calcification due to degeneration, hypertension, diabetes,
chronic renal failure


Clinical features

• Symptoms usually occur with LV decompensation: dyspnoea and fatigue.

• Physical findings include:
- Pulse: sharp upstroke
- Apex: displaced, hyperdynamic
- Pansystolic murmur

Natural history

• The natural history of chronic MR depends on the volume of regurgitation, the state of the myocardium and the underlying cause.
• Preoperative LV end-systolic diameter is a useful predictor of postoperative survival in chronic MR.
• The preoperative LV end-systolic diameter should be < 45mm to ensure normal postoperative LV function.

Medical treatment

• Symptomatic patients may benefit from the following drug therapy whilst awaiting surgery:
• Vasodilator therapy
• Diuretics
• Digoxin / Beta-blockers in presence of atrial fibrillation.
• Endocarditis prophylaxis


Surgical treatment

• Symptoms or left ventricular end systolic diameter ≥45mm.

• Mitral valve repair or replacement.

• Mitral valve repair better preserves LV function and avoids the need for chronic anticoagulation.

Acute mitral regurgitation

Aetiology

Important causes of acute mitral regurgitation include:

• Infective endocarditis
• Ischaemic dysfunction or rupture of papillary muscle.
• Malfunction of prosthetic valve.

Chronic versus Acute MR

Finding Chronic MR Acute MR

Symptoms subtle onset obvious

Appearance normal/mildly severely ill
dyspnoeic
Tachycardia not striking always present
Apex beat displaced not displaced
Systolic thrill common a bsent
Murmur harsh pansystolic soft or absent early systolic component
ECG-LVH usually present absent
CXR severe cardiomegaly normal heart size


Acute mitral regurgitation
Medical therapy
The following therapies may be beneficial in reducing the severity of MR
- Vasodilator therapy
- Inotropic therapy
- Intra-aortic balloon counterpulsation

Surgical therapy

• Indicated in patients with acute severe MR and heart
failure.
• Higher mortality rates than for elective chronic MR

Mitral valve prolapse

General features

• 2-6% of the general population

• Twice as common in women.
• Due to myxomatous proliferation of the mitral valve.
• Primary condition, or secondary finding in connective tissue
diseases e.g. Marfan’s syndrome.
• Vast majority asymptomatic.
• Palpitations, dizziness, syncope, or chest discomfort.
• Mid-systolic click, late systolic murmur


Echocardiographic criteria

• M-mode criterion: ³ 2mm posterior displacement of one or both

leaflets.

• 2-D echo findings: Systolic displacement of one or both leaflets

within the left atrium in the parasternal long-axis view; leaflet
thickening, redundancy, chordal elongation and annular dilatation.

Natural history

• Benign prognosis in most patients

• Complications may occur in patients with a systolic murmur,

thickened leaflets, an increased LV or LA size, especially in men
> 45 years old

• Complications include progressive mitral regurgitation, infective

endocarditis, cerebral emboli, arrhythmias and rarely sudden death.

Management

• Asymptomatic patients without MR or arrhythmias have an excellent prognosis – follow-up every 3-5 years.

• Patients with a long systolic murmur may show progression of MR and should be reviewed annually.

• Severe MR requires surgery, often mitral valve repair.

Tricuspid stenosis
Almost always rheumatic

• The low cardiac output state causes fatigue; abdominal discomfort may occur due to hepatomegaly and ascites.

• The diastolic murmur of tricuspid stenosis is augmented by inspiration.

• Medical management includes salt restriction and diuretics.

• Surgical treatment in patients with a valve area <2.0cm2 and a mean pressure gradient >5mmHg.

Tricuspid regurgitation

Most common cause is annular dilatation due to RV failure of any cause

• Symptoms and signs result from a reduced cardiac output, ascites, painful congestive hepatomegaly and oedema.


• The pansystolic murmur of TR is usually loudest at the left sternal edge and augmented by deep inspiration.

• Severe functional TR may be treated by annuloplasty or valve replacement. Severe TR due to intrinsic tricuspid valve disease requires valve replacement.

Pulmonary stenosis

• Most commonly due to congenital malformation

• Survival into adulthood is the rule, infective endocarditis is a risk and right ventricular failure is the most common cause of death.

• Carcinoid plaques may lead to constriction of the pulmonary valve ring.

Pulmonary regurgitation
• Most common cause is ring dilatation due to pulmonary hypertension, or dilatation of the pulmonary artery secondary to a connective tissue disorder.

• May be present and well-tolerated for many years

• The clinical manifestations of the primary disease tend to overshadow the pulmonary regurgitation.

Physical examination

– right ventricular heave
– high-pitched, blowing, early diastolic decrescendo murmur
• left sternal edge
• augmented by deep inspiration.


• Pulmonary regurgitation is seldom severe enough to require specific treatment. Surgery may be required because of intractable RV failure.

Prosthetic valves

Prosthetic valves may be divided into 2 broad categories:

Mechanical valves

• Very good durability.
• Require long-term anticoagulation.
• May cause mild haemolysis.

Bioprosthetic (tissue) valves

• Porcine variety most commonly used.
• Limited durability.
• Anticoagulation for first 3 months only.

Mechanical versus tissue valves

• No difference in survival, haemodynamics or in probability of
developing endocarditis, valve thrombosis or systemic embolism.

• Valve-related failure is much more common with tissue valves.

• Anticoagulant-related bleeding occurs with mechanical valves.

• Elderly patients tend to receive tissue valves.

Thank you