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The Antiplatelet Effects of Ticlopidine and Clopidogrel

Peter J. Sharis, MD; Christopher P. Cannon, MD; and Joseph Loscalzo, MD, PhD
[+] Article and Author Information

From Brigham and Women's Hospital, Harvard Medical School, and Boston University School of Medicine, Boston, Massachusetts. For current author addresses, see end of text. Requests for Reprints: Joseph Loscalzo, MD, PhD, Whitaker Cardiovascular Institute, Department of Medicine, Boston University School of Medicine, 88 East Newton Street, Boston, MA 02118-2394; e-mail, jloscalz@bu.edu. Current Author Addresses: Drs. Sharis and Cannon: Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115.


Copyright ©2004 by the American College of Physicians


Ann Intern Med. 1998;129(5):394-405. doi:10.7326/0003-4819-129-5-199809010-00009
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Ticlopidine and clopidogrel achieve antiplatelet effects by inhibiting the binding of adenosine 5′-disphosphate to its platelet receptor. Ticlopidine was first shown to decrease major events compared with placebo or aspirin in patients with stroke or recent transient ischemic attack. Randomized studies in patients undergoing coronary artery stenting have shown that ticlopidine reduces the risk for subacute stent thrombosis compared with warfarin-based regimens. Smaller studies have also shown this drug to have benefit during follow-up in patients with unstable angina, peripheral arterial disease, saphenous vein coronary bypass grafts, and diabetic retinopathy. Clopidogrel was recently approved by the U.S. Food and Drug Administration for the reduction of ischemic events in patients with recent myocardial infarction, stroke, or peripheral arterial disease (incidence, 5.32% per year compared with 5.83% per year for aspirin; P = 0.043) with no added risk for neutropenia. The combination of clopidogrel and aspirin, as well as the utility of clopidogrel in other patient populations and in stenting, requires further study. Ticlopidine and clopidogrel seem to have beneficial effects compared with aspirin (the current standard) in a broad range of patients. These observations highlight the importance of antiplatelet therapy in cardiovascular disease.

Figures

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Figure 1.
Chemical structures of ticlopidine (top) and clopidogrel (bottom).
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Figure 2.
Mechanism of action of ticlopidine and clopidogrel.2

When vascular endothelial cells are damaged, platelets bind to exposed collagen via glycoprotein (GP) Ib/IX receptors complexed to von Willebrand factor. These bound platelets undergo degranulation, releasing adenosine 5′-diphosphate (ADP). The platelets also release numerous other substances, such as thromboxane A , serotonin, and epinephrine, which play a role in the recruitment and aggregation process. The released ADP binds to two types of receptors, a low-affinity type 2 purinergic receptor and a high-affinity purinergic receptor (P2Y1). Ticlopidine and clopidogrel achieve their antiplatelet effect by blocking the binding of ADP to the type 2 purinergic receptor and preventing the activation of the GP IIb/IIIa receptor complex and subsequent platelet aggregation.

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