Mitral valve prolapse (MVP) is an abnormality with a prevalence of about 6% in the female polulation and a lower prevalence in males. Among the several causes is a group now called idiopathic familial MVP. Autosomal dominant inheritance is apparent in several recorded pedigrees. Several extracardiac abnormalities have been noted. Complications are thought to include an increased risk of arrhythmia, endocarditis and mitral regurgitation. Although the high MVP prevalence and low population frequency of these complications are inconsistent with a high risk of complications in everyone with MVP, reports of patients with a high rate of complications in MVP may reflect the effects of a specific gene. In the practice of medicine it is apparent that only a small fraction of patients develop clinically important complications. We suspect that familial MVP may be etiologically heterogeneous and that high risk of complications may be restricted to patients with MVP due to only some of those etiologies. Families may show difference associated abnormalities that reflect etiologic heterogeneity and indicate that in individuals with certain abnormalities a particular prognosis is likely. These hypotheses will be tested by the study of large extended families of probands with MVP to determine inheritance patterns, associated abnormalities and complications in relatives of probands using medical history, physical examination, electrocardiography, 24 hour taped electrocardiogram, and echocardiography. Glycosaminoglycans(GAG) will be studied in urine and cultured fibroblasts. Linkage of MVP to the loci of 25 markers will be tested. This study may also show that the MVP in different families can be distinguished by mode of inheritance, by associated cardiac or extracardiac abnormalities and complications, or by differences in genetic linkage to other genetic markers, or abnormalities in urine or cellular GAG. This study will seek also to identify clinical and genetic features of MVP with a high risk for complications.