Clopidogrel: How good is it and how does it work?

Abstract

Until recently, long-term antiplatelet therapy for the treatment and prevention of the complications of atherothrombotic disease was limited to aspirin. Although an incredibly cost-effective therapy, in placebo-controlled clinical trials approximately 75% of patients at risk continue to experience thrombotic events despite chronic aspirin therapy. The availability of the thienopyridines, in particular clopidogrel, represents an important addition to the physician's armamentarium. A number of clinical trials have confirmed the efficacy of the combination of clopidogrel and aspirin therapy compared with aspirin alone, with multiple other important large-scale clinical trials currently ongoing. The exact mechanism of this benefit is still being elucidated but is clearly related to the inhibition of the many consequences of platelet activation--vascular inflammation, endothelial dysfunction, and localized angiogenesis/mitogenesis--and not just aggregation.

Bleeding tendency in dual antiplatelet therapy with aspirin/clopidogrel: rescue of the template bleeding time in a single-center prospective study

“…The exact mechanism of benefit has not yet been elucidated but is clearly related not just to inhibition of platelet aggregation (IPA) but also to modification of the many consequences of the platelet activation-endothelial relationships [2]. The current gold standard for testing platelet function is light transmission platelet aggregometry (LTA), which is used to categorize patients receiving ASA and/or CLOP therapy as responders or nonresponders.…”

Uneventful Removal of an Epidural Catheter Guided by Impedance Aggregometry in a Patient With Recent Coronary Stenting and Treated With Clopidogrel and Acetylsalicylic Acid

“…Clopidogrel is a potent noncompetitive inhibitor of ADP-induced platelet aggregation, inhibiting the binding of ADP to platelet membrane receptors. 15 ADP binding is necessary for activation of the glycoprotein IIb/IIIa receptor, which is the binding site for fibrinogen. Accordingly, platelet activation by ADP is diminished in patients receiving effective doses of clopidogrel.…”

Case report: An unusual complication of clopidogrel

“…The exact mechanism of the development of hallucinations with Clopidogrel is not clear. It acts on the ADP receptors on the platelet membrane, and by inhibiting this, causes platelet inhibition [5]. Its main metabolite (formed in the liver) is pharmacologically inactive.…”