Of the many causes of mitral valve regurgitation, rheumatic heart disease (50%) and the prolapsing mitral valve are the most common. Any disease that causes dilatation of the left ventricle may cause mild mitral regurgitation, e.g.:
• Aortic valve disease
• Acute rheumatic fever
• Hypertensive heart disease
• Ischaemic heart disease
IN HYPERTROPHIC CARDIOMYOPATHY, left ventricular contraction is disorganized and mitral regurgitation
MYOCARDIAL INFARCTION OR INFECTIVE ENDOCARDITIS- Mitral regurgitation may follow these conditions.
CONNECTIVE TISSUE DISORDERS such as systemic lupus erythematosus-mitral regurgitation may occur. COLLAGEN ABNORMALITIES such as Marfan’s syndrome and Ehlers-Danlos syndrome may be associated with mitral regurgitation.
DEGENERATION OF THE VALVE CUSPS OR MITRAL ANNULAR CALCIFICATION may result in regurgitation.
RUPTURE OF THE CHORDAE TENDINEAE (due to myocardial infarction or trauma) and infective endocarditis may cause very sudden mitral regurgitation.
Regurgitation into the left atrium produces left atrial dilatation but little increase in left atrial pressure if the regurgitation is long-standing as the regurgitant flow is accommodated by the large left atrium. With acute mitral regurgitation the normal compliance of the left atrium does not allow much dilatation and the left atrial pressure rises. Thus, in acute mitral regurgitation the left atrial v wave is greatly increased and pulmonary venous pressure rises to produce pulmonary oedema. Since a proportion of the stroke volume is regurgitated, the stroke volume increases to maintain the forward cardiac output and the left ventricle therefore enlarges.
Mitral regurgitation can be present for many years and the cardiac dimensions may be greatly increased before any symptoms occur. The increased stroke volume may be sensed as a ‘palpitation’. Dyspnoea and orthopnoea may develop owing to pulmonary venous hypertension occurring as a direct result of the mitral regurgitation and secondarily to left ventricular failure. Fatigue and lethargy develop because of the reduced cardiac output. In the late stages of the disease the symptoms of right heart failure also occur and eventually lead to congestive cardiac failure. Cardiac cachexia may develop. Thromboembolism is less common than in mitral stenosis, but subacute infective endocarditis is much more common.
The physical signs of uncomplicated mitral regurgitation are:
A LATERALLY DISPLACED, THRUSTING, DIFFUSE APEX BEAT AND A SYSTOLIC THRILL.
A SOFT FIRST HEART SOUND occurs because of the incomplete apposition of the valve cusps and their partial closure by the time ventricular systole begins.
A PAN-SYSTOLIC MURMUR due to regurgitation occurring throughout the whole of systole, which is loudest at the apex but radiates widely over the precordium and in to the axilla.
A PROMINENT THIRD HEART SOUND occurs because of the sudden rush of blood back into the dilated left ventricle in early diastole. Sometimes a short mid-diastolic flow murmur may follow the third heart sound. The signs related to atrial fibrillation, pulmonary hypertension, and left and right heart failure may develop later in the disease. The onset of atrial fibrillation has a much less dramatic effect on symptoms than in mitral stenosis.
The chest X-ray may show left atrial and left ventricular enlargement. There is an increase in the CTR, and valve
calcification may be seen.
The ECG shows the features of left atrial delay (bifid P waves) and left ventricular hypertrophy as manifest by tall R waves in the left lateral leads, e.g. leads I, AVL and V6, and deep S waves in the right-sided precordial leads, e.g. leads VI and V2• (SVI plus RVs or RV6 >35 mm indicates left ventricular hypertrophy.) Left ventricular hypertrophy occurs in about 50% of patients with mitral regurgitation. Atrial fibrillation may be present.
The echocardiogram shows a dilated left atrium and left ventricle. There may be specific features of chordal or papillary muscle rupture. CW Doppler can determine the velocity of the regurgitant jet.
This demonstrates a prominent left atrial systolic pressure wave, and when contrast is injected into the left ventricle it may be seen regurgitating into an enlarged left atrium during systole.
Mild mitral regurgitation in the absence of symptoms can be managed conservatively following the patient with serial echocardiograms. Prophylaxis against endocarditis is required (see p. 10). Any evidence of progressive cardiac enlargement generally warrants early surgical intervention by either mitral valve repair or replacement. The advantages of surgical intervention are diminished in more advanced disease. In patients who are not considered appropriate for surgical intervention, or in whom surgery will be considered at a later date, management usually involves treatment with ACE inhibitors, diuretics and possibly anticoagulants. Sudden torrential mitral regurgitation,
as seen with chordal or papillary muscle rupture or infective endocarditis, may necessitate emergency mitral valve replacement.
Prolapsing (billowing) mitral valve
This is also known as Barlow’s syndrome or floppy mitral valve. It is due to excessively large mitral valve leaflets, an enlarged mitral annulus, abnormally long chordae or disordered papillary muscle contraction. Histology may demonstrate myxomatous degeneration of the mitral valve leaflets. It is more commonly seen in young women than in men or older women and it has a familial incidence. Its cause is usually unknown but it may be due to Marfan’s syndrome, thyrotoxicosis, rheumatic or ischaemic heart disease. It also occurs in association with atrial septal defect and as part of hypertrophic cardiomyopathy. Mild mitral valve prolapse is so common that it should be regarded as a normal variant.
During ventricular systole, a mitral valve leaflet (most commonly the posterior leaflet) prolapses into the left atrium. This may result in abnormal ventricular contraction, papillary muscle strain and some mitral regurgitation. Usually the syndrome is not haemodynamically serious. Thromboembolism may occur.
Atypical chest pain is the most common symptom. Usually the pain is left submammary and stabbing in quality. Sometimes it is substernal, aching and severe. Rarely it is similar to typical angina pectoris. Palpitations may be experienced because of the abnormal ventricular contraction or because of the atrial and ventricular arrhythmias that are commonly associated with mitral valve prolapse.
The most common sign is a mid-systolic click, which is produced by the sudden prolapse of the valve and the tensing of the chordae tendineae that occurs during systole. This may be followed by a late systolic murmur due to some regurgitation. Sometimes, pan-systolic mitral regurgitation occurs. The signs typically fade quickly but return later.
The chest X-ray is usually normal unless significant mitral regurgitation is present.
The ECG is often abnormal with inverted or biphasic T waves in the inferior leads (leads II, III and AVF) and in the left lateral precordial leads (leads Vs and V6). The ST segment may also be slightly depressed in these leads.
The diagnosis is confirme on M-mode echocardiography, which typically shows posterior movement of one or both mitral valve cusps into the left atrium during systole. Cardiac catheterization Contrast angiograms performed during cardiac catheterization reveal the systolic prolapse of the mitral valve into the left atrium, and mitral regurgitation, if present, is seen. This investigation is not normally required.
Usually, f3-blockade is effective for the treatment of the atypical chest pain and palpitations. Sometimes more specific antiarrhythmic drug treatment is necessary. When a prolapsing mitral valve is associated with significant mitral regurgitation and atrial fibrillation, anticoagulation is advised to prevent thromboembolism. Very occasionally, mitral valve replacement may be necessary for severe regurgitation, although many surgeons prefer to repair rather than replace such valves. Prophylaxis against endocarditis is advised if there is significant mitral valve regurgitation.