title: Elevation in serum troponin I predicts the benefit of tirofiban.
abstract: BACKGROUND
  Elevations in serum troponins among patients with acute coronary syndromes have been shown to identify those patients who are at high risk for poor outcome and who accrue larger relative benefits from aggressive antiplatelet and antithrombotic therapies. We studied a group of patients from the PRISM-PLUS trial to explore whether simply using serum troponin I, a serum marker of cardiac injury, could predict benefit of GP IIb/IIIa receptor antagonism with tirofiban.
  
  
  RESULTS
  For this study, the subjects consisted of 55 patients receiving the combination therapy of tirofiban/heparin, and 55 receiving heparin alone. The baseline characteristics were similar between the two treatment groups. Serial blood samples were obtained over the first 24-hour period following randomization to study drug, and were analyzed for troponin I (TnI) levels. Among those patients with elevated serum TnI (>0.5 ng/ml), the 30-day event rate for death or myocardial infarction (MI) was reduced from 20.6% among the heparin only group to 3.6% for those treated with the combination of tirofiban/heparin, an absolute risk reduction of 17% and relative risk reduction of 83% (p=0.06). Among the TnI negative patients, the rates of death/MI at 30 days were 9.5% and 11.1% among the combination and heparin treated groups respectively (p=NS).
  
  
  CONCLUSIONS
  Irrespective of high-risk clinical factors, including ST segment depression, these data support the hypothesis that serum troponins identify those who benefit from aggressive antiplatelet therapy with tirofiban.
authors.affiliation: Cardiology Division, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, Boston, MA 02114, USA.
authors.forename: J L
authors.initials: JL
authors.lastname: Januzzi
authors.forename: C U
authors.initials: CU
authors.lastname: Chae
authors.forename: M S
authors.initials: MS
authors.lastname: Sabatine
authors.forename: I K
authors.initials: IK
authors.lastname: Jang
mesh_terms: D000208:Acute Disease; D000368:Aged; D015415:Biomarkers / Q000097:blood; D003327:Coronary Disease / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy*; D004359:Drug Therapy, Combination; D005260:Female; D006493:Heparin / Q000008:administration & dosage; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000209:etiology / Q000517:prevention & control; D017202:Myocardial Ischemia / Q000097:blood / Q000209:etiology / Q000517:prevention & control; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors; D011446:Prospective Studies; D012307:Risk Factors; D015996:Survival Rate; D000077466:Tirofiban; D019210:Troponin I / Q000097:blood*; D014443:Tyrosine / Q000008:administration & dosage* / Q000031:analogs & derivatives*
chemical_list: D015415:Biomarkers; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D019210:Troponin I; D014443:Tyrosine; D006493:Heparin; D000077466:Tirofiban