Pathogenesis of ischemic mitral insufficiency

M. R. Llaneras, M. L. Nance, J. T. Streicher, P. L. Linden, S. W. Downing, J. A.C. Lima, R. Deac, L. H. Edmunds, A. F. Carpentier, R. W. Frater, J. H. Oury

Research output: Contribution to journalArticlepeer-review

Abstract

We developed a new animal model of ischemic mitral insufficiency in sheep and used it to test the hypothesis that the combination of posterior papillary muscle infarction and left ventricular dilatation was required to produce mitral regurgitation after acute inferior myocardial infarction of moderate size. In 12 sheep, ligation of the first two circumflex marginal coronary arteries infarcted 23 % of the left ventricular mass, increased left ventricular cavitary area from 13.2 ± 1.2 cm2 to 20.0 ± 2.7 cm2 by 8 weeks and did not produce ischemic mitral regurgitation. In 13 sheep, ligation of the second and third circumflex marginal arteries infarcted 21 % of the left ventricular mass and, in 11 of these sheep, the posterior papillary muscular mass as well. When the papillary muscle was included, this infarction produced progressively severe mitral regurgitation over 8 weeks, as left ventricular cavitary area increased from 12.5 ± 2.6 cm2 to 22.8 ± 3.8 cm2. We conclude that neither posterior papillary muscle infarction nor left ventricular dilatation alone produces ischemic mitral regurgitation after moderate-sized inferior wall infarction, but that the combination does.

Original languageEnglish (US)
Pages (from-to)439-443
Number of pages5
JournalJournal of Thoracic and Cardiovascular Surgery
Volume105
Issue number3
DOIs
StatePublished - 1993
Externally publishedYes

ASJC Scopus subject areas

  • Surgery
  • Pulmonary and Respiratory Medicine
  • Cardiology and Cardiovascular Medicine

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