Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy - PURSUIT
Eptifibatide for death/MI/revascularization in acute coronary syndromes.
Inhibition of platelet aggregation with eptifibatide would have reduced the frequency of adverse outcomes in patients with acute coronary syndromes who did not have persistent ST-segment elevation.
Patients Screened: Not given
Patients Enrolled: 10,948
Mean Follow Up: 6 months
Mean Patient Age: 64
Symptoms of ischemic chest pain at rest, lasting 10 minutes or longer, within the previous 24 hours
Transient ST-segment elevation of more than 0.5mm, transient or persistent ST-segment depression of more than 0.5mm, T-wave inversion of more than 1 mm within 12 hours before or after chest pain, or a serum concentration of creatine kinase MB isoenzyme (CK-MB) above the upper limit of normal.
Persistent ST-segment elevation of more than 1 mm
Active bleeding or a history of bleeding diathesis
Gastrointestinal or genitourinary bleeding within 30 days
Systolic blood pressure above 200 mm Hg or diastolic blood pressure above 110 mm Hg
Major surgery within the previous 6 weeks
Nonhemorrhagic stroke within the previous 30 days
Any history of hemorrhagic stroke
Planned administration of a platelet glycoprotein IIb/IIIa receptor inhibitor or thrombolytic agent
Thrombolytic therapy within the previous 24 hours.
Composite of death from any cause or nonfatal myocardial infarction at 30 days.
Mortality from all causes within 30 days
First or recurrent myocardial infarction within 30 days
Composite death or nonfatal myocardial infarction at 96 hours and 7 days
Measures of the safety and efficacy of treatment in patients undergoing percutaneous revascularization.
Eptifibatide (bolus 180 mcg/kg, followed by infusion of 1.3 mcg/kg/min); Eptifibatide (bolus dose of 180 mcg/kg followed by infusion of 2.0 mcg/kg/min); or a bolus and infusion of placebo.
A total of 10,948 patients were randomized: 1487 patients to the low-dose eptifibatide group, 4722 to the high-dose eptifibatide group, and 4739 to the placebo group.
Eptifibatide was associated with a significant reduction in the incidence of death or myocardial infarction at 96 hours, 7 days, and 30 days. A 1.5% absolute reduction in the frequency of the composite end point was reached by 4 days and maintained for 30 days.
On the basis of the frequency of nonfatal infarction as determined by the investigators at the study sites, eptifibatide had a consistent and highly significant benefit at all time points; at 30 days, the incidence of the composite end point was 8.1 percent in the eptifibatide group, as compared with 10.0 percent in the placebo group (P=0.001).
Bleeding was more common among patients treated with eptifibatide than among those receiving placebo, and there were more red-cell transfusions among the patients treated with eptifibatide (11.6 percent vs. 9.2 percent; relative risk, 1.3; 95 percent confidence interval, 1.1 to 1.4).
Strokes occurred with similar frequency in the two groups (0.7 percent in the eptifibatide group and 0.8 percent in the placebo group, P=0.41).
Eptifibatide, a synthetic cyclic heptapeptide, is a selective inhibitor of the platelet glycoprotein IIb/IIIa receptor. Inhibition of platelet aggregation with eptifibatide reduced the incidence of the composite end point of death or nonfatal myocardial infarction in patients with acute coronary syndromes who did not have persistent ST-segment elevation. In PURSUIT, the apparently moderate absolute reduction of 1.5 percent in the incidence of death or nonfatal myocardial infarction was achieved in a real-life setting and in a broad population of patients. PURSUIT represents the largest study of glycoprotein IIb/IIIa inhibition to date, and is consistent with the overall reduction of death and myocardial infarction observed with this class of compounds.
1. N Engl J Med 1998;339:436-43. Final results
Clinical Topics: Acute Coronary Syndromes
Keywords: Risk, Myocardial Infarction, Infarction, Isoenzymes, Acute Coronary Syndrome, Stroke, Creatine Kinase, Platelet Aggregation Inhibitors, Peptides, Research Personnel, Confidence Intervals, Platelet Glycoprotein GPIIb-IIIa Complex
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