title: Apoptosis in recent myocardial infarction.
abstract: OBJECTIVE
  Apoptosis is considered a common pathological feature in acute myocardial infarction (MI) and heart failure; however its role in the later phases post MI has not been characterized. The goal of our study was to investigate by pathological examination human hearts at 20 to 30 days post MI and identify signs of ongoing cell apoptosis.
  
  
  METHODS
  Two hearts were collected at autopsy from patients who died 20 to 30 days from the onset of MI (Cases 1 and 2). Gross anatomy and light microscopy examination of the hearts was performed to define the infarcted area and the infarct-related artery. The in situ end-labeling of DNA fragmentation (TUNEL) was performed to identify apoptotic cells and the apoptotic rate (AR) was calculated.
  
  
  RESULTS
  There were no signs of acute necrosis in any of the specimens examined. A high number of myocardiocyte were positive at TUNEL examination in specimens obtained at sites of infarction, mean AR = 44%, but not in specimens derived from the same patients at regions remote from the MI, AR = 0.
  
  
  CONCLUSIONS
  High grade apoptosis is present at sites of infarction and not in regions remote from the infarcted area in the later phases post MI. These data support persistent myocardiocyte loss and identify a possible explanation of progressive left ventricular dysfunction in the subacute phases of MI.
authors: Dipartimento di Scienze Cardiovascolari, Università Campus Bio-Medico, Roma, Italia.
authors: A
authors: A
authors: Abbate
authors: R
authors: R
authors: Melfi
authors: G
authors: G
authors: Patti
authors: F
authors: F
authors: Baldi
authors: A
authors: A
authors: D'Ambrosio
authors: A
authors: A
authors: Manzoli
authors: A
authors: A
authors: Baldi
authors: G
authors: G
authors: Di Sciascio
mesh_terms: D000368:Aged; D017209:Apoptosis; D001344:Autopsy; D006801:Humans; D020287:In Situ Nick-End Labeling; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000473:pathology / Q000503:physiopathology