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Circulation, Vol 76, 68-76, Copyright © 1987 by American Heart Association

ARTICLES

Postinflammatory mitral and aortic valve prolapse: a clinical and pathological study

T Tomaru, Y Uchida, N Mohri, W Mori, A Furuse and K Asano

In this study we reevaluated whether the sole cause of mitral valve prolapse (MVP) and aortic valve prolapse (AVP) is myxomatous degeneration. Forty-two surgical cases of prolapsed valves with mitral and/or aortic regurgitation were reviewed (AVP in nine, MVP in 27, and combined AVP and MVP [CVP] in six). On microscopic examination, myxomatous degeneration was observed in 20 patients, including six with AVP, 13 with MVP, and one with CVP. In the other 22 patients, including three with AVP, 14 with MVP, and five with CVP, microscopic examination revealed fibrosis with vascularization and scattered infiltration of inflammatory round cells caused by postinflammatory changes with or without chronic inflammation. We coined the term "postinflammatory valve prolapse" (PIVP) to describe these valves. Both postinflammatory and myxomatous degeneration were observed in seven patients with floppy mitral valves attributable to PIVP. Rupture of chordae tendineae was present in six patients with myxomatous mitral valve and three with PIVP. Seven patients with PIVP had a history of rheumatic fever. The results suggest that valvular prolapse is produced not only by myxomatous degeneration but also by postinflammatory changes, including those caused by rheumatic fever.

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