Circulation. 1998;97:312-314
(Circulation. 1998;97:312-314.)
© 1998 American Heart Association, Inc.
Oral Platelet Glycoprotein IIb/IIIa Receptor Antagonists: The Present Challenge Is Safety
David A. Vorchheimer, MD;
; Valentin Fuster, MD, PhD
From the Cardiovascular Institute, Mount Sinai Medical Center, New York,
NY.
Correspondence to Valentin Fuster, MD, PhD, Director, Cardiovascular Institute, Mount Sinai Medical Center, 1 Gustave Levy Place, Box 1030, New York, NY 10029-6574. E-mail Valentin—Fuster@SMTPLINK.MSSM.edu
Key Words: Editorials • glycoproteins • platelets • platelet aggregation inhibitors • drugs
An indisputable body
of angiographic,1 2
angioscopic,3
pathological,4 and
biochemical5 evidence supports the role of
thrombus in the pathogenesis of acute myocardial infarction, unstable
angina, and percutaneous coronary
intervention.6 Compelling data from large-scale
trials and analyses have established the role of platelet
inhibitors in reducing coronary events in patients
with the acute coronary syndromes and in maintaining patency of
vascular grafts in the long term.7 8 Persistent
reports of high clinical event rates in the modern era of acute
coronary syndromes despite aggressive medical therapy have
spurred the development of more effective antiplatelet agents.
Despite its efficacy, aspirin is a relatively weak antiplatelet
agent, inhibiting only thromboxane
A2–mediated platelet aggregation. The final
common pathway of platelet aggregation involves activation of the
platelet glycoprotein IIb/IIIa (GP IIb/IIIa) receptor
to allow fibrinogen binding.9 Studies involving a
number of intravenous inhibitors of GP IIb/IIIa
receptors have demonstrated efficacy in reducing ischemic
complications after percutaneous
angioplasty10 11 12 and in the acute
coronary syndromes.13 14 15 16
In patients who have survived an episode of unstable angina or
myocardial infarction, activation of the hemostatic system may persist
for several months after the acute event.5
Studies with GP IIb/IIIa
inhibitors12 16 and with specific
antithrombins17 have demonstrated efficacy of
these agents during the short-term period coinciding with
intravenous administration, with subsequent decay in
clinical benefit after cessation of parenteral treatment so that no
demonstrable clinical benefit is evident at late (1 month) follow-up.
Hence, there exists a compelling rationale for long-term
antiplatelet treatment, including GP IIb/IIIa inhibition. More than
one dozen oral . . . [Full Text of this Article]
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