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( Mitral valve prolapse)
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. In its nonclassic form, MVP carries a low risk of complications. In severe cases of classic MVP, complications include mitral regurgitation, infective endocarditis, and — in rare circumstances — cardiac arrest, usually resulting in sudden death. The mitral valve, so named because of its resemblance to a bishop's miter, is the heart valve that prevents the backflow of blood from the left ventricle into the left atrium. It is composed of two leaflets (one anterior, one posterior) that close when the left ventricle contracts.[1] 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 often causes rupture, and is commonly found in the chordae tendineae attached to the posterior leaflet. Advanced lesions&_160;—&_160;also commonly involving the posterior leaflet&_160;—&_160;lead to leaflet folding, inversion, and displacement toward the left atrium. The term mitral valve prolapse was coined by J. Michael Criley in 1966 and gained acceptance over the other descriptor of "billowing" of the mitral valve, as described by JB Barlow.[2]
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