Mitral valve insufficiency (regurgitation) is the condition characterized by backflow of the blood from the left ventricle to the left atrium during systole, due to mitral valve prolapse, rheumatic or ischemic heart disease, infective endocarditis, cardiomyopathy or mitral apparatus calcification. Depending primarily on the onset of the disease, acute or chronic, mitral valve insufficiency leads to various clinical pictures.
Patients may be asymptomatic or may have manifestations like fatigue caused by reduced cardiac output, tachypnea or dyspnea, orthopnea, paroxysmal nocturnal dyspnea and hemoptysis due to pulmonary hypertension . When atrial fibrillation due to left atrium dilatation occurs, most patients experience palpitations. In children, failure to thrive is an important hallmark of almost all serious heart conditions.
When mitral regurgitation happens abruptly, being caused by an acute accident like chordal or papillary muscle rupture due to myocardial infarction, compensatory mechanisms do not have time to install and symptoms are dramatic, as patients present with pulmonary edema or cardiogenic shock. In chronic severe mitral regurgitation, patients slowly progress to congestive heart failure and pulmonary edema .
A clinical examination reveals a left atrial lift caused by the left atrium filling with blood during systole. The first heart sound is normal or diminished, while the second heart sound is split into early stages of the disease because the aortic valve closes early. The splitting interval diminishes as pulmonary hypertension starts . A third sound caused by increased ventricular filling may also appear, while the pulmonary component of the second heart sound is accentuated if pulmonary hypertension has begun. Mitral valve prolapse is accompanied by an ejection systolic click.
The murmur caused by mitral regurgitation is best heard at the apex and radiates towards the axilla and subscapular area. It is usually pansystolic, but may also be presystolic in acute settings or telesystolic in mitral valve prolapse or papillary muscle dysfunction. The intensity decreases as the left ventricle dysfunction advances .
Peripheral pulse is sharp but has a small volume; atrial fibrillation presents late in the course of the disease and the characteristic pulse abnormality is noted. The dilated left atrium may compress the left main bronchus, leading to wheezing and, rarely, lung atelectasis and hyperinflation.
The postero-anterior radiography may show a normal aspect of the heart or enlarged left atrium and left atrial appendage; if mitral regurgitation begins abruptly, the X-ray shows signs of pulmonary edema with normal sized left atrium. The pulmonary edema might be more prominent in the right upper lobe . Cardiomegaly is present in chronic regurgitations.
Echocardiography is the most valuable tool in assessing mitral regurgitation. Two-dimensional (2D) echocardiography is useful in measuring heart dimensions and characterizing the mitral apparatus while trying to identify the cause of the disease and associated abnormalities. Color flow echocardiography describes the direction of the flow . Quantitative and semi-quantitative measurement methods should be used in evaluating disease severity .
Spectral Doppler (pulse and continuous) is useful in calculating the severity of the regurgitation (by measuring parameters such as vena contracta, proximal isovelocity surface area, and regurgitant fraction) and evaluating a possible concomitant mitral stenosis . If doubt about severity persists, stress echocardiography and exercise testing should be performed .
Transesophageal echocardiography and heart catheterization are indicated in cases where heart anatomy is uncertain , whereas cardiac magnetic resonance imaging (MRI) is more accurate in determining ventricular function and size. Catheterization is also useful in grading the regurgitation .
Brain natriuretic peptide has prognostic value in severe mitral regurgitation and can be used in risk stratification .