Acute myocardial infarction (AMI) is characterized by myocardial cell necrosis,inflammatory response and scar formation. The aim was to reveal whether cardiomyocyte (CMC) apoptosis is present in the infarction zone of the left ventricle compared with postinfarction chronic aneurizm wall.

Subject and methods: Myocardial express necropsies from 24 patients (age range 39–71) who suffered mainly from hypertension (HT) and died from STEMI complicated with Heart Failure (HF) or Cardiogenic Shock were examined. Biopsies from postinfarction aneurism wall from five patients (38–61 y.o), suffering from HT and HF were obtained and their ultrastructure was compared with changes in necropcies from infarction zone.

Results: According to electron microscopic investigation in infarction zones of the left ventricle exept necrotic, hibernated and apoptotic myocytes, as well as apoptotic endothelial and plasmatic cells,macrophages and fibroblasts, with features of pycnosis, nuclear chromatin condensation and cytoplasma vacualization where detected. As the result of prominent interstitial fibrosis, very poor vascularization and moderate matrix edema,CMC usually were dissociated and myocardium loses its synthityal organization. Separately located CMC were hibernated finally resulting in apoptosis. Numerous hibernated and apoptotic CMC were destroyed via secondary necrosis predominantly during short time (three months) after AMI. In aneurism wall 14 years after AMI onset, hibernating and some viable CMC were still present as the result of myocardium neovascularization.

Conclusions: CMC necrosis is the main mechanism of cell death in acute aneurism wall, while apoptosis develops predominantly in subacute periods of AMI. In chronic aneurism wall viable CMC are present, but hibernating and apoptotic CMC prevalent.