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Mitral valve prolapse: causes, symptoms, diagnosis, treatment
Last reviewed: 05.07.2025
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Mitral valve prolapse is a prolapse of the mitral valve leaflets into the left atrium during systole. The most common cause is idiopathic myxomatous degeneration. Mitral valve prolapse is usually benign, but complications include mitral regurgitation, endocarditis, valve rupture, and possible thromboembolism.
Mitral valve prolapse is usually asymptomatic, although some patients experience chest pain, dyspnea, and manifestations of sympathicotonia (eg, palpitations, dizziness, presyncope, migraines, anxiety). Symptoms include a clear midsystolic click followed by a systolic murmur in the presence of regurgitation. Diagnosis is by physical examination and echocardiography. Prognosis is good. No specific treatment is required unless mitral regurgitation is present, although beta-blockers may be effective in patients with signs of sympathicotonia.
Mitral valve prolapse is a common condition. The prevalence is 1-5% in healthy individuals. Women and men are affected equally often. Mitral valve prolapse usually develops following the adolescent growth spurt.
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What causes mitral valve prolapse?
Mitral valve prolapse is most often caused by myxomatous degeneration of the mitral valve and chordae tendineae. The degeneration is usually idiopathic, although it may be inherited in an autosomal dominant or (occasionally) X-linked recessive manner. Myxomatous degeneration may also occur in connective tissue dysplasia (eg, Marfan or Ehlers-Danlos syndrome, adult polycystic kidney disease, osteogenesis imperfecta, pseudoxanthoma elasticum, systemic lupus erythematosus, polyarteritis nodosa) and muscular dystrophies. Mitral valve prolapse is often found in patients with Graves' disease, hypomastia, von Willebrand syndrome, sickle cell anemia, and rheumatic heart disease. Myxomatous degeneration may also affect the aortic or tricuspid valve, resulting in prolapse; tricuspid regurgitation is rare.
Normal (ie, nonmyxomatous) mitral valve leaflets may prolapse if there is papillary muscle dysfunction or the mitral annulus is dilated (eg, in dilated cardiomyopathy) or narrowed (eg, in hypertrophic cardiomyopathy or atrial septal defect). Transient mitral valve prolapse may occur when there is marked volume depletion, such as with severe dehydration or during pregnancy (when the woman is lying down and the pregnant uterus compresses the inferior vena cava, reducing venous return).
Mitral regurgitation (MR) is the most common complication of mitral valve prolapse. MR may be acute (due to ruptured chordae tendineae or stretched mitral valve leaflets) or chronic. Complications of chronic MR include heart failure and atrial fibrillation with thromboembolism. It is unclear whether MR leads to stroke independently of MR or AF. In addition, MR increases the risk of infective endocarditis, as do thickened, enlarged mitral valve leaflets.
Symptoms of Mitral Valve Prolapse
Most often, mitral valve prolapse is asymptomatic. Occasionally occurring vague symptoms (e.g., chest pain, dyspnea, palpitations, dizziness, near-syncope, migraine, anxiety) are considered to be related to poorly differentiated disorders in adrenergic impulse transmission and sensitivity, rather than to mitral valve pathology. In approximately one third of patients, emotional stress provokes palpitations, which may be signs of benign arrhythmias (atrial extrasystoles, paroxysmal atrial tachycardia, ventricular extrasystoles, complex ventricular ectopia).
Some patients present with mitral regurgitation, less commonly with endocarditis (fever, weight loss, thromboembolic complications) or stroke. Sudden death occurs in less than 1% of cases, most often due to rupture of the chordae tendineae and mobile mitral valve leaflets. Death due to fatal arrhythmia is rare.
Typically, mitral valve prolapse does not cause any visible cardiac symptoms. Isolated mitral valve prolapse produces a pronounced mid-systolic click, heard best with a stethoscope with the diaphragm to the left of the apex when the patient is in the left lateral decubitus position. In mitral valve prolapse with mitral regurgitation, the click is accompanied by a late systolic mitral regurgitation murmur. The click becomes audible or moves closer to the first heart sound (S1) and becomes louder with maneuvers that decrease the size of the left ventricle (LV) (eg, squatting, standing, Valsalva maneuver). The same maneuvers produce or increase and prolong the mitral regurgitation murmur. This is because the decrease in left ventricular size causes the papillary muscles and chordae tendineae to close more centrally below the valve, causing a more rapid and pronounced prolapse with earlier significant regurgitation. Conversely, squatting and isometric handgrip result in a decrease in the S-click and a shorter mitral regurgitation murmur. The systolic click may be confused with the click of congenital aortic stenosis; the latter differs in its occurrence at very early systole and its absence of change with body position or changes in left ventricular volume. Other findings include a systolic thrill, presumably caused by vibration of the valve leaflets; these symptoms are usually transient and may vary with different respiratory phases. An early diastolic opening sound, caused by return of the prolapsed valve to its normal position, is rarely heard.
Other physical findings associated with mitral valve prolapse but not of diagnostic value include hypomastia, pectus excavatum, straight back syndrome, and small anteroposterior chest diameter.
Diagnosis of mitral valve prolapse
The presumptive diagnosis is made clinically and confirmed by two-dimensional echocardiography. A holosystolic displacement of 3 mm or a late systolic displacement of > 2 mm allows the diagnosis to be made in 95% of patients with mitral valve prolapse; this figure is slightly higher if echocardiography is performed with the patient standing. Thickened large mitral valve leaflets and a displacement of 5 mm are thought to indicate more extensive myxomatous degeneration and a higher risk of endocarditis and mitral regurgitation.
Holter monitoring and 12-lead ECG may be useful in identifying and documenting arrhythmias in patients with palpitations.
What do need to examine?
How to examine?
Prognosis and treatment of mitral valve prolapse
Mitral valve prolapse is usually benign, but severe myxomatous degeneration of the valve may lead to mitral regurgitation. In patients with severe mitral regurgitation, the incidence of left ventricular and left atrial enlargement, arrhythmias (eg, atrial fibrillation), infective endocarditis, stroke, need for valve replacement, and death is approximately 2% to 4% per year.
Mitral valve prolapse usually does not require treatment. Beta-blockers can be prescribed to reduce the manifestations of sympathicotonia (eg, palpitations, migraines, dizziness) and the risk of dangerous tachycardia, although there are no data confirming these effects. Atenolol 25-50 mg once a day or propranolol 20-40 mg twice a day are usually prescribed. Additional treatment may be needed for atrial fibrillation.
Treatment of mitral regurgitation depends on the severity and associated changes in the atrium and LV.
Antibiotic prophylaxis of endocarditis is recommended before risky procedures only in the presence of mitral regurgitation or thickened, enlarged valves. Anticoagulants to prevent thromboembolism are recommended only for patients with atrial fibrillation who have had a previous transient ischemic attack or stroke.