title: Troponin concentrations for stratification of patients with acute coronary syndromes in relation to therapeutic efficacy of tirofiban. PRISM Study Investigators. Platelet Receptor Inhibition in Ischemic Syndrome Management.
abstract: BACKGROUND
  A major challenge for physicians is to identify patients with acute coronary syndromes who may benefit from treatment with glycoprotein-IIb/IIIa-receptor antagonists. We investigated whether troponin concentrations can be used to stratify patients for benefit from treatment with tirofiban.
  
  
  METHODS
  We enrolled 2222 patients of the Platelet Receptor Inhibition in Ischemic Syndrome Management study with coronary artery disease and who had had chest pain in the previous 24 h. All patients received aspirin and were randomly assigned treatment with tirofiban or heparin. We took baseline measurements of troponin I and troponin T. We recorded death, myocardial infarction, or recurrent ischaemia after 48 h infusion treatment and at 7 days and 30 days.
  
  
  RESULTS
  629 (28.3%) patients had troponin I concentrations higher than the diagnostic threshold of 1.0 microg/L and 644 (29.0%) troponin T concentrations higher than 0.1 microg/L. 30-day event rates (death, myocardial infarction) were 13.0% for troponin-I-positive patients compared with 4.9% for troponin-I-negative patients (p<0.0001), and 13.7% compared wth 3.5% for troponin T (p<0.001). At 30 days, in troponin-I-positive patients, tirofiban had lowered the risk of death (adjusted hazard ratio 0.25 [95% CI 0.09-0.68], p=0.004) and myocardial infarction (0.37 [0.16-0.84], p=0.01). This benefit was seen in medically managed patients (0.30 [0.10-0.84], p=0.004) and those undergoing revascularisation (0.37 [0.15-0.93] p=0.02) after 48 h infusion treatment. By contrast, no treatment effect was seen for troponin-I-negative patients. Similar benefits were seen for troponin-T-positive patients.
  
  
  CONCLUSIONS
  Troponin I and troponin T reliably identified high-risk patients with acute coronary syndromes, managed medically and by revascularisation, who would benefit from tirofiban.
authors.affiliation: Department of Cardiovascular Medicine, Stanford University Medical School, CA, USA.
authors.forename: C
authors.initials: C
authors.lastname: Heeschen
authors.forename: C W
authors.initials: CW
authors.lastname: Hamm
authors.forename: B
authors.initials: B
authors.lastname: Goldmann
authors.forename: A
authors.initials: A
authors.lastname: Deu
authors.forename: L
authors.initials: L
authors.lastname: Langenbrink
authors.forename: H D
authors.initials: HD
authors.lastname: White
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D003327:Coronary Disease / Q000097:blood / Q000188:drug therapy*; D003402:Creatine Kinase / Q000097:blood / Q000187:drug effects; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006493:Heparin / Q000627:therapeutic use*; D006801:Humans; D007262:Infusions, Intravenous; D007527:Isoenzymes; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000401:mortality; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D012307:Risk Factors; D000077466:Tirofiban; D019210:Troponin I / Q000097:blood*; D020107:Troponin T / Q000097:blood*; D014443:Tyrosine / Q000031:analogs & derivatives* / Q000627:therapeutic use
chemical_list: D015415:Biomarkers; D005343:Fibrinolytic Agents; D007527:Isoenzymes; D010975:Platelet Aggregation Inhibitors; D019210:Troponin I; D020107:Troponin T; D014443:Tyrosine; D006493:Heparin; D003402:Creatine Kinase; D000077466:Tirofiban