The platelet is a mediator of various thrombotic, endothelial and inflammatory processes, and, as such, is pivotal in the initiation and progression of atherosclerosis. Medical therapies targeting pathways involved in platelet aggregation and activation are fundamental in our treatment of unstable and treated atherosclerotic disease; they include established and developmental drugs aimed at inhibiting thromboxane A₂ (TxA₂), the platelet adenosine diphosphate (ADP) and glycoprotein IIb/IIIa receptors, thrombin, collagen, and von Willebrand factor.^w1 Antiplatelet agents are a mainstay of the treatment of patients with acute coronary syndromes (ACS) because they have been shown to reduce the risk of death, myocardial infarction (MI), and urgent revascularisation. Some patients, however, experience adverse cardiac events, such as coronary stent thrombosis, despite treatment with single or dual antiplatelet therapy. Whether such patients are resistant to the effects of these agents, or experience cardiac events for other reasons, has been the subject of debate. The evidence for “aspirin resistance” as a clinical entity, however, is weak, and it has not been conclusively demonstrated to cause ischaemic events. With other agents, by contrast, it is possible to identify a subset of patients with low response or non-response whose risk for ischaemic events is elevated and for whom dosage adjustment or other measures may be helpful. This article aims to present concisely various aspects of antiplatelet therapy non-response and potential ways to overcome it.

PRIMARY AND SECONDARY PREVENTION OF VASCULAR EVENTS BY ASPIRIN AND CLOPIDOGREL

The role of antiplatelet therapy in the secondary prevention of vascular events was confirmed by the Antithrombotic Trialists’ Collaboration Group meta-analysis. Around 140 000 high risk patients for vascular events due to pre-existing disease or a recent vascular event from 195 trials were included, and the pooled analysis of the general antiplatelet class, with all agents combined, yielded a significant 2.5% absolute reduction in the number of major vascular events (non-fatal MI …