Mitral Valve Prolapse

Heart mitral prolapse

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as explained in Wikipedia

Mitral valve prolapse (MVP) is a valvular heart disease characterized by the displacement of an abnormally thickened mitral valve leaflet into the left atrium during systole.

The diagnosis of MVP depends upon echocardiography, which uses ultrasound to visualize the mitral valve. Early studies estimated a prevalence of 38% among healthy teenagers; with improved echocardiographic techniques and clear diagnostic criteria, the true prevalence of MVP is estimated at 2-3% of the population.

It is is the heart valve that prevents the backflow of blood from the left ventricle into the left atrium of the heart. It is composed of two leaflets, one anterior and one posterior, that close when the left ventricle contracts. Each leaflet is composed of three layers of tissue: the atrialis, fibrosa, and spongiosa. Patients with classic mitral valve prolapse have excess connective tissue that thickens the spongiosa and separates collagen bundles in the fibrosa. This is due to an excess of dermatan sulfate, a glycosaminoglycan. This weakens the leaflets and adjacent tissue, resulting in increased leaflet area and elongation of the chordae tendineae. Elongation of the chordae tendineae often causes rupture, commonly to the chordae attached to the posterior leaflet. Advanced lesions—also commonly involving the posterior leaflet—lead to leaflet folding, inversion, and displacement toward the left atrium.

Prolapse occurs when the mitral valve leaflets are displaced more than 2 mm above the mitral annulus high points. The condition can be further divided into classic and nonclassic subtypes based on the thickness of the mitral valve leaflets: up to 5 mm is considered nonclassic, while anything beyond 5 mm is considered classic MVP.

Classical prolapse may be subdivided into symmetric and asymmetric, referring to the point at which leaflet tips join the mitral annulus. In symmetric coaptation, leaflet tips meet at a common point on the annulus. Asymmetric coaptation is marked by one leaflet displaced toward the atrium with respect to the other. Patients with asymmetric prolapse are susceptible to severe deterioration of the mitral valve, with the possible rupture of the chordae tendineae and the development of a flail leaflet.

Echocardiography is the most useful method of diagnosing a prolapsed mitral valve. Two- and three-dimensional echocardiography are particularly valuable as they allow visualization of the mitral leaflets relative to the mitral annulus. This allows measurement of the leaflet thickness and their displacement relative to the annulus. Thickening of the mitral leaflets >5 mm and leaflet displacement >2 mm indicates classic mitral valve prolapse.

MVP may occur with greater frequency in individuals with Ehlers-Danlos Syndrome, Marfan syndrome or polycystic kidney disease. Other risk factors include Graves’ disease. and chest wall deformities such as Pectus Excavatum.

Signs and symptoms

Some patients with MVP experience heart palpitations, atrial fibrillation, or syncope, though the prevalence of these symptoms does not differ significantly from the general population. Between 11 and 15% of patients experience moderate chest pain and shortness of breath. These symptoms are most likely not caused directly by the prolapsing mitral valve, but rather by the mitral regurgitation that often results from prolapse. In addition, the American Heart Association has linked anxiety and panic attack disorders to mitral valve prolapse. A correlation has been reported between bipolar disorder and mitral valve prolapse.

For unknown reasons, MVP patients tend to have a low body mass index (BMI) and are typically leaner than individuals without MVP.


Upon auscultation of an individual with mitral valve prolapse, a mid-systolic click, followed by a late systolic murmur heard best at the apex is common.

In contrast to most other heart murmurs, the murmur of mitral valve prolapse is accentuated by standing and valsalva maneuver (earlier systolic click and longer murmur) and diminished with squatting (later systolic click and shorter murmur). The only other heart murmur that follows this pattern is the murmur of hypertrophic cardiomyopathy. A MVP murmur can be distinguished from a hypertrophic cardiomyopathy murmur by 1) the presence of a mid-systolic click which is virtually diagnostic of MVP, and 2) the fact that hand grip maneuver intensifies the murmur of MVP and diminishes the murmur of hypertrophic cardiomyopathy.

Both valsalva maneuver and standing decrease venous return to the heart thereby decreasing left ventricular diastolic filling and causing more laxity on the chordae tendineae. This allows the mitral valve to prolapse earlier in systole, leading to an earlier systolic click and a longer murmur. Hand grip maneuver increases total peripheral resistance and therefore increases back pressure on the mitral valve resulting in a more intense murmur without changing the timing of the systolic click.

The MVP complications mitral regurgitation and congestive heart failure may, in turn, cause arrhythmias and atrial fibrillation that may progress and lead to sudden death. However, there is no evidence that a prolapsed valve itself contributes to such arrythmias.

Generally, MVP is a benign disorder. However, MVP patients with a murmur, not just an isolated click, have a general mortality rate that is increased by 15-20%. The major predictors of mortality are the severity of mitral regurgitation and the ejection fraction.


Most patients need only reassurance. Those with mitral valve prolapse and symptoms of dysautonomia (palpitations, chest pain) may often benefit from beta-blockers (e.g., propranolol). Patients with prior stroke and/or atrial fibrillation may require blood thinners, such as aspirin or warfarin. However, although beta blockers are commonly prescribed, they may be of limited benefit. Unless otherwise contraindicated, many people with MVPS benefit from non-drug interventions, such as increased fluid and sodium intake, avoiding adrenalin-like substances found in many over-the-counter medications, avoiding caffeine, and getting regular cardiovascular exercise.

Mitral valve prolapse associated with severe mitral regurgitation can be treated with repair or surgical replacement of the mitral valve. Repair of the mitral valve is always preferable to replacement and should be performed by surgeons that are skilled in the procedure. Current ACC/AHA guidelines suggest that early repair of mitral valve, performed in centers of surgical excellence, should be considered even in patients without symptoms of heart failure. Symptomatic patients, those with evidence of diminished left ventricular function or left ventricular dilatation need urgent attention.

Treatment with magnesium supplements may help reduce symptoms of MVP


4 thoughts on “Mitral Valve Prolapse

  1. Ashley,
    There is a group of cardiologists on WordPress putting together a heart blog to inform and educate people about the current cardiovascular issues facing many patients today. I noticed that you have an interest in MVP. We have been fortunate enough to get a well-published and international expert on MVP and mitral regurgitation to contribute a series of posts for the blog. We hope that the blog will help you and any others that may have questions about their health. Thanks!


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