title: Prognostic significance of elevated troponin I after percutaneous coronary intervention.
abstract: OBJECTIVE
  We sought to assess the incidence and clinical significance of elevated cardiac troponin I (cTnI) after percutaneous coronary intervention (PCI).
  
  
  BACKGROUND
  Elevated creatine kinase-MB (CK-MB) is prognostically important after PCI, but the prognostic significance of elevated cTnI after PCI is uncertain.
  
  
  METHODS
  In a prospective substudy of the Sibrafiban Versus Aspirin to Yield Maximum Protection From Ischemic Heart Events Post-acute Coronary Syndromes (SYMPHONY) trials, which randomized patients with acute coronary syndromes (ACS) to receive aspirin or sibrafiban, we measured cTnI (positive, > or =1.5 ng/ml) and CK-MB (positive, > or =7 ng/ml) in 481 patients with PCI. Samples were collected immediately before and at 0, 8 and 16 h after PCI and analyzed by a core laboratory. The primary end point was the Kaplan-Meier estimate of death, myocardial infarction or severe, recurrent ischemia at 90 days.
  
  
  RESULTS
  Overall, 230 patients (48%) had elevated cTnI after PCI. Such patients underwent PCI sooner and were more likely to have coronary stenting. Elevated cTnI was associated with nonsignificantly higher risks of the primary end point (11.5% vs. 8.7%; p = 0.15) and of death (1.8% vs. 0.4%; p = 0.4) and a significantly higher risk of death or infarction (10.6% vs. 4.2%; p = 0.005). This pattern was more pronounced for patients who became positive only after PCI: primary end point, 20.7% vs. 10.1% for patients who remained negative after PCI (p = 0.05); death, 5.2% vs. 0% (p = 0.02); death or infarction, 18.1% vs. 4.1% (p = 0.007).
  
  
  CONCLUSIONS
  Elevated cTnI, often observed after PCI in patients with ACS, is associated with worse 90-day clinical outcomes. This marker, therefore, is a useful prognostic indicator in such patients.
authors.affiliation: Division of Cardiology, St. Michael's Hospital, 30 Bond Street, Toronto, Ontario, Canada M5B-1W8. cantorw@smh.toronto.on.ca.
authors.forename: Warren J
authors.initials: WJ
authors.lastname: Cantor
authors.forename: L Kristin
authors.initials: LK
authors.lastname: Newby
authors.forename: Robert H
authors.initials: RH
authors.lastname: Christenson
authors.forename: Robert H
authors.initials: RH
authors.lastname: Tuttle
authors.forename: Vic
authors.initials: V
authors.lastname: Hasselblad
authors.forename: Paul W
authors.initials: PW
authors.lastname: Armstrong
authors.forename: David J
authors.initials: DJ
authors.lastname: Moliterno
authors.forename: Robert M
authors.initials: RM
authors.lastname: Califf
authors.forename: Eric J
authors.initials: EJ
authors.lastname: Topol
authors.forename: E Magnus
authors.initials: EM
authors.lastname: Ohman
mesh_terms: D000789:Angina, Unstable / Q000097:blood* / Q000188:drug therapy / Q000628:therapy; D015906:Angioplasty, Balloon, Coronary; D001241:Aspirin / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form; D018572:Disease-Free Survival; D005260:Female; D006331:Heart Diseases / Q000401:mortality; D006801:Humans; D007527:Isoenzymes / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy / Q000628:therapy; D010091:Oximes / Q000627:therapeutic use; D010880:Piperidines / Q000627:therapeutic use; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011379:Prognosis; D011446:Prospective Studies; D012680:Sensitivity and Specificity; D015607:Stents; D019210:Troponin I / Q000097:blood*
chemical_list: D015415:Biomarkers; D007527:Isoenzymes; D010091:Oximes; D010880:Piperidines; D010975:Platelet Aggregation Inhibitors; D019210:Troponin I; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form; D001241:Aspirin; C100917:sibrafiban