(Circulation. 1996;94:866-868.)
© 1996 American Heart Association, Inc.
Articles |
Inhibitors of Platelet Glycoprotein IIb/IIIa Receptors
Will They Be Useful When Given Chronically?
St Luke's Episcopal Hospital/Texas Heart Institute, Houston.
Correspondence to James T. Willerson, MD, St Luke's Episcopal Hospital/Texas Heart Institute, 6720 Bertner Ave, Room B524 (MC1-267), Houston, TX 77030-2697.
Key Words: Editorials • glycoproteins • receptors • platelets
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Introduction |
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Inhibitors of the platelet glycoprotein IIb/IIIa (GP IIb/IIIa) receptors prevent platelet aggregation in response to a wide variety of agonists of platelet aggregation, reducing the likelihood of thrombus development at sites of vascular injury.1 2 3 4 A monoclonal antibody (7E3, Coller antibody, or ReoPro) given to high-risk patients undergoing coronary artery angioplasty, including those with unstable angina, recent myocardial infarction, and complicated coronary artery stenoses, reduced the risk of myocardial infarction and the need for a second interventional procedure in the initial 30 days after the procedure and reduced the need for a second interventional procedure in the following 6 months.5 6 This same antibody also reduced the risk of development of myocardial infarction and continuing rest angina in patients with unstable angina.4 Synthetic peptide inhibitors of GP IIb/IIIa receptors have been modestly protective to date,7 and it is not clear whether their less marked protective effect than ReoPro has been the result of less-than-optimal dosing or because ReoPro blocks fibronectin receptors in addition to its GP IIb/IIIa receptor inhibition. In this issue of Circulation, Theroux et al8 demonstrate that a nonpeptide inhibitor of GP IIb/IIIa receptors reduces the risk of continuing unstable angina, death, and nonfatal myocardial infarction and the need for interventional procedures in patients with unstable angina, and Kereiakes et al9 describe an altered dose-effectiveness of an oral GP IIb/IIIa inhibitor when given after ReoPro.
Protection by inhibition of GP IIb/IIIa receptors should be anticipated from a knowledge of the pathophysiology of conversion from stable to unstable angina and myocardial
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