Nonrheumatic subvalvular mitral regurgitation presents with characteristic clinical and hemodynamic findings, including sudden dyspnea, sinus rhythm, and a high V wave on catheterization, often without clear predisposing factors.
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May aid recognition of nonrheumatic subvalvular MR; leaves open prospective validation in larger cohorts.
Thirty-three patients are reported with nonrheumatic mitral regurgitation due to rupture or stretching of the chordae tendinaeae or papillary muscles. Nineteen (58%) had no definite predisposing etiological factors (average age 59 years). Six (19%) had a previous myocardial infarction. It is proposed that rupture or stretching of the chordae resulted from degenerative or ischemic changes in the chordae and/or papillary muscles. Six young patients had ruptured chordae from other causes. Two patients had myocardial infarction resulting in rupture of the posteromedial papillary muscle. Characteristic clinical findings included progressive dyspnea of sudden onset, sinus rhythm, systolic thrill, accentuated pulmonary valve closure sound, third heart sound, and widely propagated pansystolic murmur. The electrocardiogram frequently showed inferolateral ischemic changes. Plain chest radiographs usually showed a normal-sized heart and left atrium in patients in sinus rhythm. At cardiac catheterization a characteristic high V wave in the pulmonary artery wedge pressure was seen in 88% of patients. The left ventricular end-diastolic pressure was highest in the six postinfarct patients in whom the ejection fraction was significantly low.
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Caves et al. (1973) studied this question.
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