Troponin Levels Identify CAD Patients Likely to Benefit from Tirofiban: Results from the PRISM-Troponin Study, A substudy of the Platelet Receptor Inhibition in Ischemic Syndrome Management Study - PRISM-Troponin

May 01, 2003
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Date Presented:
01/01/1999
Date Published:
01/01/1999
Date Updated:
05/01/2003
Original Posted Date:
05/01/2003
References

Description:

The goal of the substudy was to assess the efficacy of early troponin measurements as a criterion for selecting patients most likely to respond to glycoprotein IIb/IIIa inhibitor therapy.

Hypothesis:

To assess the efficacy of early troponin measurements as a criterion for selecting patients most likely to respond to glycoprotein IIb/IIIa inhibitor therapy.

Study Design

Study Design:

Patients Enrolled: 2240

Patient Populations:

Patients with CAD enrolled in the PRISM trial with chest pain in the preceding 24 hours.

Primary Endpoints:

Death, MI, or recurrent ischemia after 48 hour infusion and at 7 days and 30 days

Drug/Procedures Used:

Baseline levels of troponin I and troponin T were measured. All patients treated with aspirin and randomly assigned to treatment with tirofiban or heparin.

Principal Findings:

Approximately 70% of patients at normal levels of troponin at baseline; in these patients, the efficacy of tirofiban was equivalent to heparin. Approximately 29% of patients at elevated levels of troponin at baseline; in these patients, the combined endpoint of death plus MI at 30 days was 2.5% in the tirofiban group versus 17% in the heparin group. In addition, the need for revascularization was also doubled in the heparin group.

Interpretation:

The data from this substudy indicate that troponin I and troponin T are reliable markers of elevated risk in patients with acute coronary syndromes and could be used to identify patients who are likely to benefit from treatment with tirofiban.

Writer's Note: This is an important substudy of PRISM. Troponin values are easily and quickly measured and seem to identify patients whose risk/benefit ratio is altered by the presence of a (+) troponin.

References:

Lancet. 1999 Nov 20;354(9192):1757-62. ESC 1999, Clinical Trials, presented by CW Hamm, Bad Nauheim, Germany

Keywords: Acute Coronary Syndrome, Platelet Aggregation Inhibitors, Troponin I, Heparin, Troponin T, Fibrinolytic Agents, Tyrosine, Platelet Glycoprotein GPIIb-IIIa Complex


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