Mitral Valve Prolapse (MVP) is usually a variant of normal occurring in about 4% 
of the population. Complications are relatively uncommon, but false associations 
due to ascertainment bias have had a potential for iatrogenic harm. Adverse 
outcomes which do occur in a subset of MVP subjects are considered here in 
relation to the contributions of genes, gender and geometry. There are definite 
associations between MVP and several dominantly inherited connective tissue 
abnormalities; it occurs in 85% of adults with Marfan syndrome. All these 
contribute to a very small proportion of the MVP population. A larger less 
easily characterised group with dominant inheritance and some features of a 
connective tissue disorder awaits DNA studies for identification. For most MVP 
subjects our data define significant family aggregation consistent with 
polygenic inheritance; the likelihood of a first degree relative having MVP is 
about two and a half times the population average. There is a higher prevalence 
in young women than in men-5% versus 3%; this has also been demonstrated for 
floppy mitral valve (MV) at autopsy. MVP complications of chordal rupture, 
severe mitral regurgitation and infective endocarditis are, however, two to 
three times more common in men, are age related and evident after the age of 50 
years. Higher blood pressure in men may contribute to this in accordance with a 
response-to-injury hypothesis to explain progressive valve changes. Leaflet, 
annulus and left ventricular size differences and septal changes are geometric 
variants with a potential for increasing tension-related valve injury.(ABSTRACT 
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