In 2003, Gurbel et al. (1) observed that the response of platelets to the P2Y12 inhibitor clopidogrel was nonuniform and suggested that patients who have persistently high ex vivo platelet reactivity while receiving clopidogrel might be prone to stent thrombosis and myocardial infarction. This hypothesis has subsequently been confirmed, most notably in the ADAPT-DES (Assessment of Dual Antiplatelet Therapy With Drug-Eluting Stents) study (2), although randomized clinical trials have thus far failed to demonstrate a clinical benefit for strategies that are based on such findings (3–5). The utility of platelet function testing may be diminished in patients treated with the newer P2Y12 antagonists prasugrel and ticagrelor; however, the fact remains that most patients, even among the highest risk strata, are still discharged on clopidogrel, and platelet function testing is not commonly performed (6). As the mechanical and device-related aspects of stent implantation continue to improve, the proportional contribution of the pharmacological response to platelet-inhibiting drugs increases. These considerations become particularly important in an era of high consumer expectations and public reporting of percutaneous coronary intervention (PCI) outcomes.
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