title: Surviving acute myocardial infarction: survivin expression in viable cardiomyocytes after infarction.
abstract: BACKGROUND
  Apoptosis is a key feature in postinfarction remodelling leading to progressive myocyte loss. Both proapoptotic and antiapoptotic factors contribute to the delicate balance between death and survival. The survivin pathway has emerged as essential in the control of apoptosis, although its role in heart disease is unknown.
  
  
  OBJECTIVE
  To evaluate survivin expression after acute myocardial infarction (AMI).
  
  
  METHODS
  Survivin expression was assessed immunohistochemically in the peri-infarct and remote viable myocardium in 17 consecutive patients who died 1-30 weeks after AMI and in four control hearts.
  
  
  RESULTS
  Survivin was expressed by myocytes in the peri-infarct area in eight patients and in the remote region in 13 patients. The rate of survivin expression after AMI was significantly higher in the remote versus peri-infarct regions and compared with control hearts. Its expression was inversely associated with the presence of dilated cardiopathy and of apoptosis, independently from the gross pathology infarct size.
  
  
  CONCLUSIONS
  Survivin myocardial expression after AMI may be associated with the survival of at risk myocardium and may be indicative of more favourable remodelling after AMI. These findings identify a potential new target for the treatment of postinfarction remodelling.
authors.affiliation: Department of Oncology, University Campus Bio-Medico, Rome, 00100 Italy.
authors.forename: D
authors.initials: D
authors.lastname: Santini
authors.forename: A
authors.initials: A
authors.lastname: Abbate
authors.forename: S
authors.initials: S
authors.lastname: Scarpa
authors.forename: F
authors.initials: F
authors.lastname: Vasaturo
authors.forename: G G
authors.initials: GG
authors.lastname: Biondi-Zoccai
authors.forename: R
authors.initials: R
authors.lastname: Bussani
authors.forename: F
authors.initials: F
authors.lastname: De Giorgio
authors.forename: F
authors.initials: F
authors.lastname: Bassan
authors.forename: D
authors.initials: D
authors.lastname: Camilot
authors.forename: M P
authors.initials: MP
authors.lastname: Di Marino
authors.forename: F
authors.initials: F
authors.lastname: Feroce
authors.forename: F
authors.initials: F
authors.lastname: Baldi
authors.forename: F
authors.initials: F
authors.lastname: Silvestri
authors.forename: F
authors.initials: F
authors.lastname: Crea
authors.forename: A
authors.initials: A
authors.lastname: Baldi
mesh_terms: D017209:Apoptosis / Q000502:physiology; D051546:Cyclooxygenase 2; D015853:Cysteine Proteinase Inhibitors / Q000032:analysis*; D004268:DNA-Binding Proteins / Q000032:analysis; D006801:Humans; D051793:Hypoxia-Inducible Factor 1; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D051034:Inhibitor of Apoptosis Proteins; D007527:Isoenzymes / Q000032:analysis; D008565:Membrane Proteins; D008869:Microtubule-Associated Proteins / Q000032:analysis*; D009203:Myocardial Infarction / Q000378:metabolism* / Q000473:pathology; D017202:Myocardial Ischemia / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D009363:Neoplasm Proteins; D009687:Nuclear Proteins / Q000032:analysis; D011451:Prostaglandin-Endoperoxide Synthases / Q000032:analysis; D000077022:Survivin; D014157:Transcription Factors / Q000032:analysis
chemical_list: C107489:BIRC5 protein, human; D015853:Cysteine Proteinase Inhibitors; D004268:DNA-Binding Proteins; C497442:HIF1A protein, human; D051793:Hypoxia-Inducible Factor 1; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D051034:Inhibitor of Apoptosis Proteins; D007527:Isoenzymes; D008565:Membrane Proteins; D008869:Microtubule-Associated Proteins; D009363:Neoplasm Proteins; D009687:Nuclear Proteins; D000077022:Survivin; D014157:Transcription Factors; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases