Elevation in serum troponin I predicts the benefit of tirofiban
J L Januzzi1, C U Chae, M S Sabatine
1Cardiology Division, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, Boston, MA 02114, USA.
Insights
Serum troponin I levels identify patients with acute coronary syndromes who benefit from tirofiban therapy. Elevated troponin I significantly reduced death or myocardial infarction rates when treated with tirofiban and heparin.
Area of Science:
- Cardiology
- Biomarkers
- Pharmacology
Background:
- Elevated serum troponins in acute coronary syndromes (ACS) indicate high risk and greater benefit from aggressive antiplatelet/antithrombotic therapies.
- Serum troponin I (TnI) is a marker of cardiac injury.
- The PRISM-PLUS trial investigated treatment strategies for ACS.
Purpose of the Study:
- To determine if serum troponin I levels could predict benefit from GP IIb/IIIa receptor antagonism with tirofiban in ACS patients.
- To assess the efficacy of tirofiban in patients stratified by TnI levels.
Main Methods:
- A subgroup of 55 patients receiving tirofiban/heparin and 55 receiving heparin alone from the PRISM-PLUS trial were analyzed.
- Serial blood samples were collected within 24 hours post-randomization and analyzed for troponin I (TnI) levels.
- Thirty-day event rates for death or myocardial infarction (MI) were compared between treatment groups based on TnI status.
Main Results:
- Among patients with elevated TnI (>0.5 ng/ml), the 30-day death/MI rate decreased from 20.6% (heparin alone) to 3.6% (tirofiban/heparin), an 83% relative risk reduction (p=0.06).
- In TnI-negative patients, 30-day death/MI rates were similar: 9.5% (tirofiban/heparin) vs. 11.1% (heparin alone) (p=NS).
- Baseline characteristics were similar between the two treatment groups.
Conclusions:
- Serum troponins identify ACS patients who benefit from aggressive antiplatelet therapy with tirofiban, irrespective of other high-risk clinical factors like ST segment depression.
- Troponin I serves as a predictive biomarker for treatment response to tirofiban in ACS.
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.
Methods And 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).
Conclusion:
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.
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