Robust evidence demonstrating the ability of drug-eluting stent (DES) technology to reduce restenosis in comparison to bare metal stents (BMS) has led to widespread DES uptake. Balanced against this significant clinical benefit, however, is concern about the incidence of stent thrombosis (ST) in DES patients. Observational and randomised trial data suggest that there is a cumulative incidence of ST in DES patients of between 0.5%–1% per year [1, 2], correlating in some series with a similar rate of death and myocardial infarction .
There are well established procedural risk factors for ST such as stent under-deployment , length of stented segment , and idiosyncratic factors including a form of hypersensitivity . However, the inappropriate termination of aspirin and clopidogrel therapy appears to be particularly hazardous . In DES patients there is therefore an important reliance for some (as yet undetermined) period of time on dual antiplatelet therapy [8, 9], possibly as a result delayed stent endothelialisation . This requirement for ongoing dual antiplatelet therapy, together with evidence of considerable biological variability in the response of individuals to antiplatelet therapies, particularly clopidogrel [11, 12], and association between poor response and adverse cardiovascular outcome [13, 14] has raised the important question: can poor responses to these agents render some individuals at risk of DES ST? There is now growing evidence from laboratory based assays that variability in the response to antiplatelet agents, particularly clopidogrel, can contribute to ST in DES patients [15–21].
Typically, clopidogrel is given in standard doses to patients receiving DES, despite both experimental and clinical data demonstrating important biological variation in response. However, clinical detection of reduced responsiveness to clopidogrel and/or aspirin has been hampered both by a lack of point-of-care assays and by an appropriate definition of what constitutes "resistance" .
The purpose of this study was to test the hypothesis that platelet reactivity whilst on aspirin and clopidogrel, assessed using two near patient assays, a novel modification of Thrombelastograph® (TEG) PlateletMapping™  and Accumetrics VerifyNow™, would be significantly greater in a consecutive group of patients who survived DES ST than in matched DES controls.