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

SUMMARY 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 emboli- zation method. Twenty-one transmural and 18 nontrangmural infarcta of 1 to 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 hours after infarction and showed no evidence of expansion. Of those surviving more than 24 hours, 17 had infarct expansion and 22 did not. In the latter group, four infarcts were transmural and 18 were nontansmural; 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 nontransmura) infarcta 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 signifi- cant inverse relationship (P<0.02) was observed, however, between the extent of expansion and post- infarct 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. Ore Res 49: 80-88, 19S1 PATHOLOGICAL and clinical studies in humans have demonstrated early alterations in left ventric- ular topography in approximately one-third of pa- tients who died as a result of acute myocardial infarction (Hutchins and Bulkley, 1978; Eaton et al., 1979). These topographic alterations, referred to as infarct expansion, are characterized by dilation and thinning of the infarcted zone. Such changes have been observed to appear clinically as early as 3 days after myocardial infarction, and to progress over days to weeks with no evidence to suggest more recent myocardial necrosis or infarct exten- sion. This process appears to be associated with deterioration in cardiac function and increased mor- tality (Eaton et al., 1979), and may be important in the developments of cardiac rupture (Schuster and Bulkley, 1979) and late aneurysm formation. Stud- ies in the human have suggested that certain mor- phological features, including transmural necrosis and infarct size, may be determinants of the devel- opment of expansion.