CELLULAR-RESPONSE OF THE EVOLVING MYOCARDIAL-INFARCTION AFTER THERAPEUTIC CORONARY-ARTERY REPERFUSION

This study describes the cellular response of the evolving myocardial infarction in humans after early coronary artery reperfusion by one or more of the following therapies: streptokinase, percutaneous transluminal coronary angioplasty, tissue plasminogen activator, and/or coronary artery bypass graft surgery. Postmortem histologic changes were compared in two groups (n = 43 pairs) of human hearts with acute myocardial infarction matched for clinical age and left ventricular location of the infarct. The treatment group received one or more of the forms of reperfusion therapy. The control group received conventional therapy. The treatment group was judged to have an older histologic age infarct, P < 0.002, compared with documented clinical age. For example, infarcts that were clinically 4 days old or less were judged histologically to be 1 day older. The treatment group had a higher Cellular Response Index, P < 0.017; more hemorrhage within the infarct, P < 0.001; a greater extent of selective myocardial cell necrosis, and a lesser extent of coagulation necrosis, P < 0.05; more patchy, nontransmural distribution of necrosis, P < 0.04; and a more florid cellular response, specifically more macrophages, P < 0.034, and reactive stromal cells, P < 0.05. In infarcts less than 3 days old clinically, the treatment group had hemorrhage and a cellular response which were wide-spread throughout the lesion, P < 0.05, n = 18 pairs. In infarcts 3 to 4 days old clinically, the treatment group had a florid cellular response due to more macrophages, P < 0.05, n = 9 pairs. In infarcts 5 to 10 days old, the treatment group had more macrophages, P < 0.01; and more phagocytosis, P < 0.003. In infarcts 10 to 40 days old clinically, the treatment group had scar formation that was patchy, P < 0.05. In conclusion, this study demonstrates that early therapeutic coronary artery reperfusion after an acute myocardial infarction alters the pattern of injury and the cellular response to the evolving myocardial infarction so that the classical criteria for infarcts need to be modified. © 1991.