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J Thorac Cardiovasc Surg 1998;115:615-622
© 1998 Mosby, Inc.
SURGERY FOR ACQUIRED HEART DISEASE |
Supported by grant HL 36308 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.
Received for publication July 22, 1997; revisions requested Sept. 11, 1997; revisions received Sept. 19, 1997; accepted for publication Sept. 30, 1997. Address for reprints: L. Henry Edmunds Jr., MD, Department of Surgery, Six Silverstein, Hospital of the University of Pennsylvania, 3400 Spruce St., Philadelphia, PA 19104.
Abstract
Objective: This study tests the hypothesis that neither small nor large myocardial infarctions that include the anterior papillary muscle produce mitral regurgitation in sheep.
Methods: Coronary arterial anatomy to the anterior left ventricle and papillary muscle was determined by dye injection in 41 sheep hearts and by triphenyl tetrazolium chloride in 13. Development of acute or chronic mitral regurgitation and changes in left ventricular dimensions were studied by use of transdiaphragmatic echocardiography in 21 sheep after infarction of 24% and 33% of the anterior left ventricular mass. These data were compared with previous data from large and small posterior left ventricular infarctions.
Results: Ligation of two diagonal arteries infarcts 24% of the left ventricular mass and 82% of the anterior papillary muscle. Ligation of both diagonals and the first circumflex branch infarcts 33% of the left ventricle and all of the anterior papillary muscle. Neither infarction causes mitral regurgitation, although left ventricular cavity dimensions increase significantly at end systole. After the smaller infarction, the left ventricular cavity enlarges 150% over 8 weeks without mitral regurgitation.
Conclusions: In sheep small and large infarctions of the anterior wall that include the anterior papillary muscle do not produce either acute or chronic mitral regurgitation despite left ventricular dilatation. In contrast large posterior infarctions produce immediate mitral regurgitation owing to asymmetric annular dilatation and discoordination of papillary muscle relationships to the valve. After small posterior infarctions that include the posterior papillary muscle, mitral regurgitation develops because of annular and ventricular dilatation during remodeling.
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