he ischemic mitral regurgitation (MR) is known as a clinically important prognostic factor of acute myocardial infarction, and it is important to understand the mechanism of ischemic MR for successful treatment of ischemic MR. However, the mechanism of ischemic MR has not been known clearly. The purposes of this study were to evaluate the role of papillary muscle ischemia and LV dysfunction in the development of ischemic MR and to relate structural and functional changes of LV with severity of ischemic MR.

Left thoracotomy was performed in ten mongrel dogs. In group 1 (n=5), first and second obtuse marginal (OM) branches were ligated, and in group 2 (n=5), second and third OM branches were ligated. Epicardial echocardiography was performed at baseline, during infusion of esmolol, and during ligation of OM branches to measure end diastolic and end systolic area, fractional area shortening of LV, incomplete leaflet closure distance and area of mitral valve, and jet area of MR. Myocardial contrast echocardiography was performed to evaluate perfusion of papillary muscle and to measure risk area during ligation of OM branches.

1) Zligation of OM branches, but the significant MR developed in only one dog during esmolol infusion (p=NS), and in four dogs during ligation of OM branches (p<0.05). 2)Ischemia of papillary muscle was provoked in none of group 1, but four of five dogs in group 2 (p<0.05). Ischemic MR developed in all four dogs with provocation of papillary muscle ischemia, but in none of six dogs with maintained perfusion of papillary muscle (p=0.005). 3)Only incomplete leaflet closure area was significantly related with the severity of ischemic MR (r=0.71, p<0.05).

Ischemia of papillary muscle is the important etiologic factor in development of ischemic MR in acute posterior myocardial infarction. It will be useful to assess and restore the perfusion of papillary muscles for the treatment of ischemic MR.