To assess the early topographic changes after acute transmural myocardial infarction, we studied 28 patients during the first two weeks after infarction by serial two-dimensional echocardiography. Regional end-diastolic segment lengths and wall thicknesses for anterior and posterior left ventricular walls were calculated. Eight patients showed infarct expansion, with disproportionate dilatation and transmural thinning in the infarcted zone, that was significantly different (P<0.005) from changes in non-infarcted regions. This regional expansion led to an overall left ventricular dilatation in these eight patients of 25 per cent compared to 5 per cent in the 20 patients without infarct expansion. Although the eight patients with regional expansion did not have significantly higher peak creatine kinase or Killip classification, they had a significantly greater eight-week mortality (four of eight versus none of 20, P<0.004). Thus, regional cardiac dilatation may be an early, lethal consequence of transmural infarcts, and appears to be an important mechanism of acute cardiac dilatation after myocardial infarction. (N Engl J Med 300:57–62, 1979) STUDIES directed at preservation of ischemic myocardium have focused almost exclusively on limiting tissue necrosis. Animal studies suggest that this approach will benefit only the group of patients in whom intervention is instituted within hours of the onset of the ischemic event.1,2 Relatively little attention has been paid to the potentially preventable early topographic changes that may occur within the already infarcted zone of myocardium, especially in the larger transmural infarcts. Post-mortem studies in patients dying at this hospital within 30 days after acute myocardial infarction have shown that 72 per cent of the hearts have some thinning and dilatation.
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