title: Infarct-related artery occlusion, tissue markers of ischaemia, and increased apoptosis in the peri-infarct viable myocardium.
abstract: OBJECTIVE
  Unfavourable cardiac remodelling often complicates acute myocardial infarction (AMI) as a result of increased cardiomyocyte apoptosis. It is currently unclear whether ongoing or recurrent ischaemia is an independent determinant for increased apoptosis in peri-infarct viable myocardium.
  
  
  RESULTS
  In order to assess the link between infarct-related artery (IRA) occlusion, ischaemia, and apoptosis, 30 subjects dying 7-120 days after AMI (16 with IRA occlusion and 14 with patent IRA) and five control subjects were selected at autopsy. Cardiomyocytes were defined as apoptotic if co-expressing TUNEL and activated caspase-3. Expression of both hypoxia-inducible factor-1 and cyclo-oxygenase-2 was assessed in the peri-infarct myocardium and considered as tissue markers of ischaemia. Evidence of ischaemia was significantly more frequent in cases with IRA occlusion (53%) than in cases with patent IRA (15%) or control hearts (0%, P=0.026). The finding of IRA occlusion and markers of ischaemia identified cases with higher apoptotic rates (ARs) in the peri-infarct viable myocardium [12.2% (8.2-14.0), P<0.001 vs. others], whereas IRA occlusion without ischaemia was associated with lower AR, not significantly different from patent IRA [3.0% (1.0-7.9) vs. 2.2% (1.0-5.8), respectively, P=0.42]
  
  
  CONCLUSIONS
  Ischaemia in the peri-infarct viable myocardium is present in over 50% of subjects dying late after AMI with IRA occlusion, and it is associated with increased apoptosis. Relief of ischaemia after AMI may prove of benefit in preventing apoptosis and its consequences.
authors: Department of Medicine, Virginia Commonwealth University MCV Campus, Richmond, VA, USA. abbatea@yahoo.com
authors: Antonio
authors: A
authors: Abbate
authors: Rossana
authors: R
authors: Bussani
authors: Giuseppe G L
authors: GG
authors: Biondi-Zoccai
authors: Daniele
authors: D
authors: Santini
authors: Alessandro
authors: A
authors: Petrolini
authors: Fabio
authors: F
authors: De Giorgio
authors: Fortunata
authors: F
authors: Vasaturo
authors: Susanna
authors: S
authors: Scarpa
authors: Anna
authors: A
authors: Severino
authors: Giovanna
authors: G
authors: Liuzzo
authors: Antonio Maria
authors: AM
authors: Leone
authors: Feliciano
authors: F
authors: Baldi
authors: Gianfranco
authors: G
authors: Sinagra
authors: Furio
authors: F
authors: Silvestri
authors: George W
authors: GW
authors: Vetrovec
authors: Filippo
authors: F
authors: Crea
authors: Luigi M
authors: LM
authors: Biasucci
authors: Alfonso
authors: A
authors: Baldi
mesh_terms: D000199:Actins / Q000378:metabolism; D000368:Aged; D000369:Aged, 80 and over; D017209:Apoptosis / Q000502:physiology*; D001344:Autopsy; D015415:Biomarkers / Q000378:metabolism; D016022:Case-Control Studies; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism; D023921:Coronary Stenosis / Q000378:metabolism / Q000473:pathology*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology; D017202:Myocardial Ischemia / Q000378:metabolism / Q000473:pathology*; D032383:Myocytes, Cardiac / Q000473:pathology*; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D000199:Actins; D015415:Biomarkers; C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases