Expansion of acute myocardial infarction: an experimental study.

Abstract

Expansion (regional dilatation and thinning) of acutely infarcted myocardium in man has been shown to correlate with overall cardiac dilatation and rupture. We studied gross and histopathologic features and the time course of expansion in rats. Infarcts were produced in 84 rats by ligation of the left coronary artery and studied at 1, 2, 3, 4, 5 and 7 days. All hearts were prepared by potassium diastolic arrest, gel distention and fixation. Expansion was graded 0 to 4+ : 1+, mild thinning of infarcted wall; 2+, mild thinning and dilatation; 3+, moderate thinning and dilatation; and 4+, marked thinning and dilatation. There were 80 transmural infarcts, and 66% showed expansion; 36 of 80 (45%) were graded 1-2+ and 17 of 80 (21%) 3-4+. None of the four exclusively nontransmural infarcts showed expansion. Expansion was present in 61% of transmural infarcts at 1-2 days, in 65% at 3-4 days and in 80% at 5-7 days. The percentage of rats with severe (3-4+) expansion increased markedly over this period, from 0% at 1-2 days to 23% at 3-4 days to 65% at 5-7 days. Histopathologic infarct evolution was roughly twice as rapid as that of humans; 5-7 day-old infarcts showed well-developed granulation tissue. Thus, expansion can be produced in an animal model. A critical infarct size of 17% appeared necessary for significant (greater than 1+) expansion, and the degree of expansion correlated with infarct size. Although this phenomenon begins early after infarction, its extent progresses over days, making interventions to interrupt its development feasible.