Expansion of acute myocardial infarction: its relationship to infarct morphology in a canine model.

Abstract

Regional dilation (expansion) of newly infarcted myocardium has been associated with increased mortality. To study this entity further and to define the relationship of expansion to infarct morphology, infarcts were created in 44 open-chest dogs by a coronary ligation and coronary embolization method. Transmural (21) and 18 nontransmural infarcts of 1-11 days of age were studied. Infarct expansion was quantified by comparison of lengths of infarct and noninfarct containing segments of transversely sliced hearts. Five dogs died less than 6 h after infarction and showed no evidence of expansion. Of those surviving more than 24 h, 17 had infarct expansion and 22 did not. In the latter group, 4 infarcts were transmural and 18 were nontransmural; in the former, all 17 infarcts with expansion were transmural. Infarct thinning for the 17 infarcts with expansion was significantly greater than that observed in the nontransmural infarcts, or the nonexpanded transmural infarcts (P < 0.001). Of the 21 transmural infarcts, the largest infarct without expansion was 10.8%, and the smallest infarct with expansion was 11.3% of left ventricular weight. Among infarcts with expansion, there was a poor correlation between the extent of expansion and infarct size (r = 0.19). A significant inverse relationship (P < 0.02) was observed between the extent of expansion and postinfarct survival for the transmural infarcts. Although infarct expansion occurred only in transmural infarcts exceeding a critical but relatively small threshold of injury, the absence of a further relationship between transmural infarct size and extent of expansion suggests that other anatomic, metabolic or hemodynamic factors affect the development of acute infarct expansion.