Eptifibatide, a
cyclic peptide, is a highly specific, intravenously administered
glycoprotein (
GP) IIb/IIIa receptor antagonist. By preventing
fibrinogen binding to the
GP IIb/IIIa receptor,
eptifibatide inhibits platelet aggregation and prevents
thrombus formation. Clinically, the
drug is used as an adjunct to
heparin and
aspirin. The PURSUIT trial, conducted in >10,000 patients with
unstable angina or non-Q-wave
myocardial infarction (MI), showed that
eptifibatide (180 microg/kg bolus then 2 microg/kg/min infusion for < or =72 hours) reduces the 30-day risk of death or nonfatal MI, with this benefit apparent at 96 hours. The absolute reduction in this end-point of 1.5% persisted at 6 months. The
drug is effective in patients undergoing
percutaneous coronary intervention (PCI), and, as shown in the North American subgroup, in patients in whom medical management is appropriate.
Eptifibatide is also beneficial in patients undergoing PCI, whether or not they have
unstable angina or non-Q-wave MI. In a dosage of 135 microg/kg then 0.5 microg/kg/min for 24 hours,
eptifibatide reduced the 30-day risk of a combined end-point (death, nonfatal MI and urgent or emergency coronary interventions) by 2.5% (absolute reduction) in patients undergoing PCI in the IMPACT-II trial, when measured by per-protocol (patients treated), but not intent-to-treat, analysis. The
drug also decreased the incidence of abrupt vessel closure and ischaemic cardiovascular complications in the first 24 hours (the period of greatest risk).
Bleeding episodes are the most common adverse event associated with
eptifibatide therapy. Although the incidence of major
bleeding is increased with
eptifibatide, most
bleeding episodes are minor and occur at the vascular access site. The
drug is not associated with an excess of intracranial bleeds,
stroke or
thrombocytopenia, does not appear to increase
bleeding risk in patients undergoing
coronary artery bypass graft (CABG), and does not cause antibody formation. Limited data suggest that
eptifibatide may improve coronary flow when combined with
alteplase in patients with acute Q-wave MI, but the possibility of increased
bleeding with
eptifibatide plus thrombolytics should be borne in mind.
CONCLUSIONS: Intravenous
eptifibatide, when combined with
aspirin and
heparin, reduces the 30-day risk of ischaemic events in patients with
unstable angina and non-Q-wave MI and decreases ischaemic cardiovascular complications at the time of greatest risk in patients undergoing PCI. With its acceptable tolerability profile
eptifibatide is a suitable option as a short term adjunct in these clinical settings. Whether
eptifibatide in combination with fibrolysis may improve outcome in patients with acute Q-wave MI has yet to be determined.