Mitral valve prolapse

background

The mitral valve lies between the heart's left atrium and the left ventricle. It has two flaps (leaflets) that open and close like a pair of swinging doors. When the heart beats, the left ventricle pumps blood out to the body and the leaflets swing shut. This keeps the blood in the ventricle from going back into the left atrium. If the mitral leaflets are too floppy, big, thin, or have the wrong shape, they may not shut properly. This condition, called mitral valve prolapse (MVP), allows blood to leak back (regurgitate) into the left atrium.
MVP is a common heart valve defect. It was first described in the 1960s as a heart murmur during the late systolic (contracting) phase of the heartbeat, accompanied by prolapse (improper positioning) of one or both mitral valve leaflets. In the mid-1980s, a study using two-dimensional echocardiography suggested that MVP occurs in nearly 40% of teenage girls. However, due to increased understanding of normal heart valve structure, the definition of MVP was revised to distinguish what is true MVP vs. normal valve structure. According to the Framingham Heart Study, MVP affects between two and three percent of the U.S. population. It remains unclear how many cases are hereditary vs. idiopathic (arising suddenly from an unknown cause). Nonetheless, it is the most common cause of non-ischemic (does not stop blood flow) mitral regurgitation.
Usually, MVP is a genetic (inherited) condition that does not cause health problems. Most patients with MVP require no invasive treatment. However, rare but serious complications may occur, which include severe mitral regurgitation, infectious endocarditis (inflammation of the heart's inner lining), heart attack, stroke, or sudden cardiac death. Echocardiography, which is used to diagnose MVP, may also identify patients at high risk for complications. When necessary, treatment generally involves surgery to physically correct mitral valve defects.

Related Terms

American College of Cardiology/American Heart Association (ACC/AHA) Task Force, annula, annuloplasty, asymmetric mitral valve prolapse, atrial fibrillation, Calcineurin, cerebrovascular events, classic mitral valve prolapse, collagen, connective tissue disorders, dominant cutis laxa, echocardiography, Ehlers-Danlos syndrome, elastin, ErbB3, fibroblast growth factor (FGF), fibroelastic deficiency, filamin A, flail mitral valve prolapse, floppy mitral valve, Framingham Heart Study, heart attack, heart murmur, hypertrophic cardiomyopathy, infectious endocarditis, late systolic murmur, leaflet resection, leaflet thickening, left atrial enlargement, left ventricular dilatation, Marfan syndrome, mitral annulus, mitral regurgitation, mitral valve leaflets, mitral valve prolapse (MVP),MMVP1, MMVP2, myxomatous degeneration, NFAT, non-classic mitral valve prolapse, non-flail mitral valve prolapse, osteogenesis imperfecta, pseudoxanthoma elasticum, severe mitral regurgitation, Sox9, stroke, sudden cardiac death, symmetric mitral valve prolapse, three-dimensional echocardiography, transesophageal echocardiography, transforming growth factor beta (TGF-beta), two-dimensional echocardiography, Wnt/beta-catenin, X-linked valvular dystrophy.

types of the disease

True mitral valve prolapse: Mitral valve prolapse (MVP) was first described in the 1960s as a heart murmur during the late systolic (contracting) phase of the heartbeat, accompanied by prolapse (improper positioning) of one or both mitral valve leaflets. Prolapse of the mitral valve was determined by comparing its position relative to the mitral annulus, a structure that surrounds the mitral valve. MVP was diagnosed based on the assumption that a normal mitral annulus is flat (planar). It was later determined that the annulus is not planar, but rather shaped like a saddle. Because normal heart anatomy was not clearly understood until the late 1980s, many healthy individuals were initially misdiagnosed with MVP. In fact, in the mid 1980s, nearly 40% of teenage girls were diagnosed with MVP using a two-dimensional echocardiography. After normal mitral anatomy was determined using three-dimensional echocardiography, true MVP was defined as mitral leaflet prolapse of at least two millimeters in the long-axis view of the mitral valve. According to the Framingham Heart Study, MVP affects between two and three percent of the U.S. population, less than previously suggested.
Classic vs. non-classic mitral valve prolapse: Prolapse of at least five millimeters, accompanied by leaflet thickening, is defined as classic MVP. Classic MVP is associated with a higher risk of complications (such as infectious endocarditis, sudden cardiac death, heart attack, stroke, or severe mitral regurgitation).
If there is little to no thickening of the mitral leaflets, non-classic MVP is diagnosed. Non-classic MVP and prolapse of less than two millimeters are not significantly associated with the complications of classic MVP, and thus are thought to be normal variants of mitral valve structure.
Symmetric vs. asymmetric mitral valve prolapse: In classic MVP, the point where the mitral leaflets join may be even (symmetric) or uneven (asymmetric). Asymmetric MVP is more likely to result in mitral regurgitation rendering the patient more prone to deterioration of the mitral valve, and thus is more severe than symmetric MVP.
Flail vs. non-flail mitral valve prolapse: In asymmetric MVP, the structure of the mitral flaps may worsen and result in a flail leaflet, in which the tip of the mitral flap turns upward. Flail leaflets are more likely to result in mitral regurgitation, and thus are more severe than non-flail asymmetric leaflets.
Myxomatous vs. non-myxomatous mitral valve prolapse: MVP generally results from a process called myxomatous degeneration, in which the connective tissues form abnormally. This causes the mitral leaflets to enlarge and thicken. However, leaflet thickening does not occur in all cases of MVP. If the connective tissues are not sufficiently elastic (a trait called fibroelastic deficiency), the prolapsed leaflets may be thin. Another form of non-myxomatous MVP is associated with hypertrophic cardiomyopathy, in which prolapse results from elongation (but not necessarily thickening) of the mitral leaflets.