title: Elevated troponin I level on admission is associated with adverse outcome of primary angioplasty in acute myocardial infarction.
abstract: BACKGROUND
  In patients with acute myocardial infarction (AMI) undergoing thrombolytic therapy, an elevated troponin level on admission is associated with a lower reperfusion rate and a complicated clinical course. Whether an elevated troponin level on admission similarly predicts an adverse outcome in patients undergoing primary angioplasty is currently unknown and was investigated in the present study.
  
  
  RESULTS
  Cardiac troponin I (cTnI) was determined on admission in 110 consecutive patients with AMI associated with ST-segment elevation or left bundle branch block who underwent primary angioplasty. Fifty-four patients (49%) had an elevated cTnI (>/=0.4 ng/mL) on admission. In patients with elevated cTnI, primary angioplasty was less likely to achieve TIMI 3 flow (as classified by the Thrombolysis in Myocardial Infarction trial) in univariate (76% versus 96%, P:=0.03) or in multivariate (odds ratio 0.1, 95% CI 0.02 to 0.54) analysis. Patients with elevated cTnI were more likely to develop congestive heart failure (23% versus 9%, P:<0.05) and death, heart failure, or shock (30% versus 9%, P:=0.006). Elevated cTnI remained a significant predictor of the composite end point after controlling for other clinical data that were available early in the course, including time to presentation and angiographic results (relative risk 5.2, 95% CI 1.03 to 26.3). During a follow-up of 426+/-50 days, elevated admission cTnI was a predictor of cardiac mortality (11% versus 0%, P:=0.012), adverse cardiac events (cardiac mortality or nonfatal reinfarction; 19% versus 5.4%, P:=0.04), and adverse cardiac events plus target vessel revascularization (32% versus 14%, P:=0.054).
  
  
  CONCLUSIONS
  In patients with ST-segment elevation AMI, an elevated cTnI on admission is associated with an increased risk of primary angioplasty failure and a more complicated clinical course.
authors.affiliation: Division of Cardiology, Cedars-Sinai Medical Center/UCLA School of Medicine, Los Angeles, CA 90048-1865, USA.
authors.forename: S
authors.initials: S
authors.lastname: Matetzky
authors.forename: T
authors.initials: T
authors.lastname: Sharir
authors.forename: M
authors.initials: M
authors.lastname: Domingo
authors.forename: M
authors.initials: M
authors.lastname: Noc
authors.forename: K Y
authors.initials: KY
authors.lastname: Chyu
authors.forename: S
authors.initials: S
authors.lastname: Kaul
authors.forename: N
authors.initials: N
authors.lastname: Eigler
authors.forename: P K
authors.initials: PK
authors.lastname: Shah
authors.forename: B
authors.initials: B
authors.lastname: Cercek
mesh_terms: D000208:Acute Disease; D000368:Aged; D017130:Angioplasty; D015415:Biomarkers; D017023:Coronary Angiography; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D009203:Myocardial Infarction / Q000097:blood / Q000175:diagnosis / Q000601:surgery*; D011379:Prognosis; D012307:Risk Factors; D019210:Troponin I / Q000097:blood*
chemical_list: D015415:Biomarkers; D019210:Troponin I