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Circulation. 2002;106:379-385
doi: 10.1161/01.CIR.0000019581.22812.B2
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(Circulation. 2002;106:379.)
© 2002 American Heart Association, Inc.


Current Perspective

Platelet Glycoprotein IIb/IIIa Inhibitors

Recognition of a Two-Edged Sword?

Martin J. Quinn, MD, PhD; Edward F. Plow, PhD; Eric J. Topol, MD

From the Departments of Cardiovascular Medicine and Molecular Cardiology, The Cleveland Clinic Foundation, Cleveland, Ohio.

Correspondence to Eric J. Topol, MD, Department of Cardiovascular Medicine, Desk F 25, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195. E-mail topole@ccf.org


Key Words: thrombosis • platelets • glycoproteins


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 


*    Introduction
 
Glycoprotein (GP) IIb/IIIa antagonists are potent inhibitors of platelet aggregation that provide marked protection from ischemic events in patients undergoing percutaneous coronary intervention (PCI).1,2 Abciximab, the prototypic GP IIb/IIIa inhibitor, has been studied in >8000 patients undergoing elective or high-risk PCI.2,3,4 In these patients, it produces a consistent 35% to 56% reduction in ischemic end points at 30 days, with a significant 22% reduction in the risk of death, as shown in a combined analysis of long-term (3-year minimum) follow-up of the Evaluation of 7E3 for the Prevention of Ischemic Complications (EPIC), Evaluation in PTCA to Improve Long-term Outcome with abciximab GP IIb/IIIa blockade (EPILOG), and Evaluation of Platelet IIb/IIIa Inhibitor for Stenting (EPISTENT) trials.5 Similar results, albeit of a smaller magnitude, have been seen with the small-molecule antagonists tirofiban and eptifibatide, with a 16% to 35% reduction in ischemic events in patients undergoing PCI.1,6 Attempts to expand the therapeutic indication of GP IIb/IIIa antagonists to other conditions associated with platelet-mediated thrombosis, however, have been less fruitful than expected. Instead of reducing major ischemic events, long-term oral GP IIb/IIIa inhibitor therapy7 has uniformly increased the fatality rate. Furthermore, the overall efficacy of a number of the intravenous antagonists in non–ST-segment elevation acute coronary syndromes (ACS), or in combination with thrombolysis in ST-segment elevation myocardial infarction (MI), has been less than anticipated.8 Of particular concern is the fact that there has been a paradoxical increase in adverse events in 2 of the trials of intravenous therapy in ACS.9,10 Platelets are known . . . [Full Text of this Article]




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