title: Prognostic implications of elevated troponin in patients with suspected acute coronary syndrome but no critical epicardial coronary disease: a TACTICS-TIMI-18 substudy.
abstract: OBJECTIVE
  The purpose of this study is to determine whether there is clinical significance to elevated troponin I in patients with suspected acute coronary syndromes (ACS) with non-critical angiographic coronary stenosis.
  
  
  BACKGROUND
  Elevation of troponin in patients admitted with ACS symptoms with non-critical coronary artery disease (CAD) may result from coronary atherothrombosis not evident using standard angiography or from other ischemic and non-ischemic causes that may confer increased risk for future events.
  
  
  METHODS
  Patients with ACS enrolled in the Treat Angina With Aggrastat and Determine Cost of Therapy With Invasive or Conservative Strategy-Thrombolysis In Myocardial Infarction (TACTICS-TIMI)-18 were included. Of 2,220 patients enrolled in the trial, 895 were eligible. Patients were divided into four groups according to troponin status on admission and presence of significant angiographic stenosis. Baseline brain natriuretic peptide (BNP) and C-reactive protein (CRP) were obtained on all patients.
  
  
  RESULTS
  The median troponin I levels were 0.71 ng/ml in patients with CAD compared with 0.02 ng/ml in patients without CAD (p <0.0001). Troponin-positive patients with or without angiographic CAD had higher CRP and BNP levels compared with troponin-negative patients (p <0.01 for both). The rates of death or reinfarction at six months were 0% in troponin-negative patients with no CAD, 3.1% in troponin-positive patients with no CAD, 5.8% in troponin-negative patients with CAD, and 8.6% in troponin-positive patients with CAD (p=0.012).
  
  
  CONCLUSIONS
  Elevated troponin in ACS is associated with a higher risk for death or reinfarction, even among patients who do not have significant angiographic CAD. The mechanisms conferring this adverse prognosis merit further study.
authors.affiliation: Section of Cardiology, Baylor College of Medicine, Houston, Texas 77030, USA.
authors.forename: Hisham
authors.initials: H
authors.lastname: Dokainish
authors.forename: Manu
authors.initials: M
authors.lastname: Pillai
authors.forename: Sabina A
authors.initials: SA
authors.lastname: Murphy
authors.forename: Peter M
authors.initials: PM
authors.lastname: DiBattiste
authors.forename: Marc J
authors.initials: MJ
authors.lastname: Schweiger
authors.forename: Amir
authors.initials: A
authors.lastname: Lotfi
authors.forename: David A
authors.initials: DA
authors.lastname: Morrow
authors.forename: Christopher P
authors.initials: CP
authors.lastname: Cannon
authors.forename: Eugene
authors.initials: E
authors.lastname: Braunwald
authors.forename: Nasser
authors.initials: N
authors.lastname: Lakkis
mesh_terms: D000789:Angina, Unstable / Q000097:blood* / Q000401:mortality; D002097:C-Reactive Protein / Q000032:analysis; D023921:Coronary Stenosis / Q000097:blood; D006801:Humans; D009203:Myocardial Infarction / Q000097:blood* / Q000401:mortality; D020097:Natriuretic Peptide, Brain / Q000097:blood; D011379:Prognosis; D016032:Randomized Controlled Trials as Topic; D012189:Retrospective Studies; D016019:Survival Analysis; D013577:Syndrome; D019210:Troponin I / Q000097:blood*
chemical_list: D019210:Troponin I; D020097:Natriuretic Peptide, Brain; D002097:C-Reactive Protein