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Valvular Heart Disease

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

       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



       Exertional dyspnoea or fatigue
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


       Thickened valves with reduced motion, sometimes calcified
       Grading of stenosis severity is as follows:
      -     Normal valve area = 3-4cm2
      -     Mild stenosis = 1.5-3cm2
      -     Moderate stenosis = 1.0-1.5cm2
      -     Severe stenosis 1.0cm2
       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 valve replacement

      In the absence of LV dysfunction, operative risk is

      Indicators of higher mortality are NYHA class, LV dysfunction, age, concomitant coronary artery disease, and aortic regurgitation.

      Valve replacement usually results in reduced LV volumes, improved LV performance and regression of LV hypertrophy.

Transcatheter Aortic Valve (TAVI)
       Novel alternative therapy
       Performed via femoral, subclavian or transapical approaches
       Currently reserved for high risk, symptomatic severe degenerative aortic stenosis

Aortic regurgitation

       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.

Pathophysiology of aortic regurgitation

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

       Colour flow
      - width of the jet at its origin
      - extent into the LV
      - Rate of decline of aortic reguritant flow
      - Diastolic flow reversal into the descending aorta


       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



       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


       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

       Haemoptysis may also occur
       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.

Medical 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 (MVA1.5cm2 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


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
       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

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
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  
        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

         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.


       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.


Satheesh Nair

Manchester Heart Centre


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