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Activation of platelets is central to the pathophysiology of unstable angina. We studied whether inhibition of the final common pathway for platelet aggregation with tirofiban, a nonpeptide glycoprotein IIb/IIIa receptor antagonist, would improve clinical outcome in this condition.

In a double-blind study, we randomly assigned 3232 patients who were already receiving aspirin to additional treatment with intravenous tirofiban or heparin for 48 hours. The primary end point was a composite of death, myocardial infarction, or refractory ischemia at 48 hours.

The incidence of the composite end point was 32 percent lower at 48 hours in the group that received tirofiban (3.8 percent, vs. 5.6 percent with heparin; risk ratio, 0.67; 95 percent confidence interval, 0.48 to 0.92; P=0.01). Percutaneous revascularization was performed in 1.9 percent of the patients during the first 48 hours. At 30 days, the …