Flow of blood from the left ventricle to the left atrium during systole through an incompetent mitral valve.
In developing countries rheumatic disease accounts for the majority of cases of mitral regurgitation, often accompanied by mitral stenosis as a form of mixed mitral disease. In developed countries other causes predominate:
Prolapsing mitral valve.
Myocardial infarction may lead to papillary muscle dysfunction or rupture.
Any disease that causes dilation of the left ventricle, such as dilated cardiomyopathy. Congestive heart failure may also cause mitral regurgitation due to down-ward displacement of the papillary muscle. This leads to a failure of the valve cusps to meet and regurgitation ranging in severity according to the degree of left ventricular enlargement.
Infective endocarditis may cause destruction of the valve cusps.
Idiopathic rupture of chordae tendinae.
In acute mitral regurgitation, retrograde blood flow from the left ventricle into the left atrium causes the left atrial pressure to increase. There is an increase in the pulmonary venous pressure and there may be pulmonary oedema. In longstanding mitral regurgitation there is a gradual enlargement of the left atrium. This allows the increased volume of atrial blood to be compensated for without a rise in the atrial pressure. The left ventricular stroke volume increases due to volume overload and over time this results in left ventricular hypertrophy.
Acute mitral regurgitation (e.g. following rupture of the chordae or papillary muscle dysfunction) presents with acute left-sided heart failure and pulmonary oedema. In most cases mitral regurgitation is chronic and is asymptomatic for many years. Patients may present with palpitations or symptoms of left ventricular failure (dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea). On examination the pulse is normal volume, but may be irregular due to atrial fibrillation. The apex is thrusting and becomes displaced downward and laterally. On auscultation the first heart sound is soft due to incomplete apposition of the valve cusps and there is a pansystolic murmur best heard at the apex radiating to the axilla. There may be a prominent third heart sound due to the sudden rush of blood back into the dilated left ventricle in early diastole.
Patients develop left ventricular failure due to chronic volume overload. Atrial fibrillation is common due to atrial dilation, with an increased risk of thromboembolism. Other complications include pulmonary oedema and infective endocarditis.
The chest X-ray shows cardiomegaly due to left atrial and left ventricular enlargement. Valve calcification may be seen in cases due to rheumatic fever. There may be evidence of pulmonary oedema.
ECG is initially normal, but may show left atrial delay (bifid P waves, p mitrale), left ventricular hypertrophy or atrial fibrillation.
Echocardiography is diagnostic allowing demonstra-tion and quantification of the retrograde blood flow. The clinical effect of the valve lesion is however best assessed by measurement of the left ventricular dimensions (an end systolic dimension of over 5 cm indicates ventricular decompensation).
Mild mitral regurgitation in the absence of symptoms is managed conservatively, more severe disease with evidence of progressive cardiac enlargement is treated surgically. Valve repair is increasingly the operation of choice, but valve replacement may be required for severely diseased valves. Papillary muscle dysfunction and chordal rupture may require emergency valve replacement.
Patients not undergoing surgery may require treatment of any complications such as cardiac failure or atrial fibrillation.
Prophylaxis against infective endocarditis is required.