A Freeze on Tailored Antiplatelet Therapy?

It is widely known that there is interindividual variation in the response to aspirin and clopidogrel, drugs that represent 2 major classes of antiplatelet therapies in use today. Variation in response can be defined clinically (ie, not all patients who are exposed to the drug are protected from platelet-mediated thrombotic events such as myocardial infarction). Response can also be defined pharmacodynamically in the laboratory by using ex vivo measures of platelet inhibition such as the VerifyNow platform, a whole-blood, point-of-care test. A rich history of epidemiological and genetic data demonstrates an association between the variability in laboratory responses and clinical outcomes among patients receiving antiplatelet therapy. To test the hypothesis that measures of ex vivo platelet function are truly risk factors and not merely risk markers, the Double Randomization of a Monitoring Adjusted Antiplatelet Treatment Versus a Common Antiplatelet Treatment for DES Implantation, and a Interruption Versus Continuation of Double Antiplatelet Therapy, One Year After Stenting (ARCTIC) study randomly assigned patients undergoing percutaneous coronary intervention (PCI) to a strategy of platelet function testing and subsequent adjustment of antiplatelet therapy versus usual care. The primary results from ARCTIC failed to demonstrate a benefit from incorporating platelet function test results into the management of antiplatelet therapies in this population.1 In a secondary analysis published in this issue of Circulation ,2 the ARCTIC investigators assessed the extent to which outcomes differed after hospital discharge by performing a landmark analysis. Similar to the previously reported primary findings, a strategy of platelet function test–driven treatment changes did not affect clinical outcomes from the time …