Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033377 (prolapse)
 11,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Echocardiographic studies have recently documented high incidence of mitral valve prolapse in cases with papillary muscle dysfunction (PMD). However, any pathologic evidence has not been yet described. To evaluate the incidence and the degree of morphologic prolapse of the mitral valve, we examined 76 cases of mitral regurgitation which were pathologically proved to have PMD among 3,000 consecutive autopsy cases over 60 years of age. The morphologic evidence of "mitral valve prolapse" was defined as overshooting of the mitral leaflet into the left atrium beyond the degree of normal hooding. Papillary muscle dysfunction was classified into three types; Type A due to old myocardial infarction, Type B due to acute myocardial infarction, and Type C induced by other factors such as cardiomyopathies. The following results were obtained: Morphologic "mitral valve prolapse" was found in 19 among the 76 cases (25%) of PMD, but marked "prolapse" was found in only one case. The incidence of morphologic "prolapse" did not show any difference among the types of PMD (cf. Fig. 1). The site of "prolapse" was mainly in the region of posteromedial commissure of the mitral valve. Echocardiographic study of 39 cases with PMD showed mitral valve prolapse in only two cases who belonged to the eight cases having morphologic "mitral valve prolapse". This study suggests that prolapse formation of the mitral valve secondary to PMD can be differentiated morphologically from those following primary myxomatous degeneration of the mitral leaflets as observed in cases with MVP.
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PMID:[A study on prolapse of the mitral valve in autopsy-proved papillary muscle dysfunction]. 653 94

The basic mechanism of ischemic mitral regurgitation (MR) is believed augmented leaflet tethering due to the outward displacement of the papillary muscles by left ventricular (LV) remodeling or dilatation. Annular dilatation and LV dysfunction may not be the central mechanism, but contribute to the development of MR in the presence of augmented tethering. Papillary muscle dysfunction was initially expected to cause leaflet prolapse and MR. However, multiple studies have confirmed that papillary muscle dysfunction per se does not usually cause ischemic MR and recent studies further suggest that papillary muscle dysfunction may occasionally attenuate tethering and MR. Although surgical annuloplasty is usually effective to treat ischemic MR, occasional patients with persistent or recurrent ischemic MR after surgical ring annuloplasty even with advanced downsizing suggest the need for approaches to address tethering. Finally, leaflet tethering in patients with ischemic MR can be heterogeneous, indicating the need for individualized approaches to correct ischemic MR in affected patients.
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PMID:Mechanism of ischemic mitral regurgitation. 1892 93