In the quarter century since it was recognized that Although the development of auscultatory,‘, z 4, 5 midsystolic clicks and late systolic murmurs were of angiographic,“, 7 echocardiographic, 8-12 and pathologmitral valve origin,‘, 2 a considerable body of infor- ic13, 14 methods of recognizing MVP has facilitated mation has accumulated about the condition that is clinical diagnosis and investigation of this condition, now generally known as mitral valve prolapse the resultant multiplicity of diagnostic methods and (MVP). 3 The central feature of MVP is posterior criteria has alrio engendered confusion. The frequent and superior systolic displacement of the mitral discordances between the presence or absence of leaflets in relation to the mitral am&s, due to MVP by different techniques~* 5 has raised the possistructural enlargement or abnormal distensibility of bility that patients identified by different methods the mitral valve. MVP occurs most often in a may not have the same condition. 16 Particular conprimary or “idiopathic form”-commonly associ- cern exists about whether MVP diagnosed either by ated with alterations of body habitus and blood auscultatory or laboratory methods or by the prespressure and evidence of heritibility-or as a sec-e. nce of the symptom complex known commonly as ondary feature of several connective tissue diseases, the “mitral prolapse. syndrome” 15**‘, I* accurately whereas the same abnormal motion pattern may be identifies anatomic MVP as documented by anaproduced without intrinsic valvular abnormality by tomic, pathology or MVP that is clinically “pathologconditions that alter left ventricular size or geome- ic” because of a significant risk of important complitry. cations.‘9