Circulation, Vol 65, 1446-1450, Copyright © 1982 by American Heart Association
JS Hochman and BH Bulkley
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.
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