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January 11, 1979New England Journal of Medicine551 citations

Regional Cardiac Dilatation after Acute Myocardial Infarction

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LELeland W. EatonEaton (Taiwan)JWJames L. WeissUniversity of Southern CaliforniaBBBernadine H. BulkleyCardiac Imaging

Key Points

  • This research aims to investigate early topographic changes in the heart after acute myocardial infarction.
  • Studied 28 patients during the first two weeks post-infarction using serial two-dimensional echocardiography.
  • Calculated regional end-diastolic segment lengths and wall thicknesses for left ventricular walls.
  • Compared changes in infarcted versus non-infarcted regions.
  • Eight patients exhibited infarct expansion with 25% overall left ventricular dilatation compared to 5% in others.
  • No significant differences in peak creatine kinase levels or Killip classification observed between groups.
  • Higher eight-week mortality observed in those with regional expansion (50% vs 0%, P<0.004).

Abstract

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 less than 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 less than 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.

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Cite This Study

Eaton et al. (1979) studied this question.

synapsesocial.com/papers/69e143ecbdb497f747a1a171https://doi.org/10.1056/nejm197901113000202
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