Effects of ADP-receptor antagonism beyond traditional inhibition of platelet aggregation.

Atherothrombosis, or thrombus formation, at the site of a disrupted atherosclerotic plaque is the common pathophysiology related to myocardial infarction, ischaemic stroke and peripheral arterial disease. A growing body of evidence demonstrates an important role for vascular inflammation in the pathophysiology of atherosclerosis/atherothrombosis and the importance of the platelet as a mediator of inflammation. Clopidogrel is an ADP receptor antagonist that is superior to acetylsalicylic acid (ASA) for the prevention of ischaemic stroke, myocardial infarction and vascular death in patients with symptomatic atherosclerosis. The use of clopidogrel as well as ASA provides sustained, incremental benefit in patients with coronary manifestations of atherothrombosis. Recent evidence indicates that clopidogrel reduces markers of vascular inflammation across the cerebrovascular, coronary and peripheral circulations. These effects are not observed after treatment with ASA alone. Further studies have revealed that clopidogrel may have potential anticoagulant effects and may inhibit arterial vasoconstriction. These broader effects may contribute to the protective benefits of clopidogrel and should be considered when evaluating antiplatelet agents and optimising antiplatelet regimens.