INFARCT SIZE AND LOCATION DETERMINE DEVELOPMENT OF MITRAL REGURGITATION IN THE SHEEP MODEL

Objective: This study tests the hypothesis that neither small nor larg e myocardial infarctions that include the anterior papillary muscle pr oduce mitral regurgitation in sheep. Methods: Coronary arterial anatom y to the anterior left ventricle and papillary muscle was determined b y dye injection in 41 sheep hearts and by triphenyl tetrazolium chlori de in 13. Development of acute or chronic mitral regurgitation and cha nges in left ventricular dimensions were studied by use of transdiaphr agmatic echocardiography in 21 sheep after infarction of 24% and 33% o f the anterior left ventricular mass, These data were compared with pr evious data from large and small posterior left ventricular infarction s. Results: Ligation of two diagonal arteries infarcts 24% of the left ventricular mass and 82% of the anterior papillary muscle. Ligation o f both diagonals and the first circum-flex branch infarcts 33% of the left ventricle and all of the anterior papillary muscle. Neither infar ction causes mitral regurgitation, although left ventricular cavity di mensions increase significantly at end systole. After the smaller infa rction, the left ventricular cavity enlarges 150% over 8 weeks without mitral regurgitation. Conclusions: In sheep small and large infarctio ns 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 produc e immediate mitral regurgitation owing to asymmetric annular dilatatio n 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 ventricu lar dilatation during remodeling.