Intrinsic myocyte dysfunction and tyrosine kinase pathway activation underlie the impaired wall thickening of adjacent regions during postinfarct left ventricular remodeling

Guido Melillo, João A C Lima, Robert M. Judd, Pascal J. Goldschmidt-Clermont, Howard S. Silverman

Research output: Contribution to journalArticle


Left ventricular remodeling after infarction is accompanied by dysfunction of regions adjacent to the infarct. We hypothesized that myocyte contractile abnormalities and elongation greater than in remote regions underlie adjacent-region dysfunction in the remodeled ventricle. The activation of the tyrosine kinase pathway, which mediates in vitro hypertrophy by stretch and/or angiotensin, was also assessed in myocytes separately isolated from adjacent and remote regions. Methods and Results. ECG-gated magnetic resonance imaging short-axis images were acquired 2 weeks after coronary ligation in rats. After the rats were killed, myocytes were isolated from animals with large (n=7) and small (n=7) infarcts and from 4 sham-operated controls. Regional wall thickening was correlated with local myocyte function and morphology. Cytochemistry for tyrosine-phosphorylated proteins was performed in myocytes from the same regions. Remodeled ventricles were dilated relative to controls by 93.7%, and wall thickening in adjacent regions was less than in remote regions (27.8 ± 6.11% versus 54.0 ± 10.1%, P

Original languageEnglish
Pages (from-to)1447-1458
Number of pages12
Issue number7
Publication statusPublished - Apr 1 1996



  • heart failure
  • magnetic resonance imaging
  • myocardial infarction
  • remodeling
  • tyrosine kinase

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

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