Introduction
Activated platelets play a pivotal role in the pathophysiology of acute coronary syndromes, and dual antiplatelet therapy with both aspirin and clopidogrel has become one of the cornerstones of their treatment.1 Similarly, dual antiplatelet therapy is mandated following percutaneous coronary intervention (PCI) with stent insertion to prevent stent thrombosis.2
Recently, there has been considerable interest in the phenomenon of inter-patient variability of clopidogrel response (sometimes termed ‘clopidogrel resistance’)3 and, to a lesser degree, the variability of aspirin response. This has led to interest in tailoring the dos
