We are grateful to Dr. Roger Jelliffe for his interest in the results of our study published in The American Journal of Cardiology .

With regard to the sponsor of the study, we confirm that this study was sponsored by the investigators, as were the previous studies from our center on the topic of residual platelet reactivity on antiplatelet treatment, but the REsponsiveness to CLOpidogrel and StEnt Thrombosis (RECLOSE) trial that was supported by an unrestricted grant from the Italian Ministry of Health.

These studies by our group have shown that poor responsiveness to clopidogrel is a strong independent predictor of cardiac death and stent thrombosis in patients receiving drug-eluting stent, including patients treated for unprotected left main disease. In this high-risk subset of patients, high residual platelet reactivity after 600-mg clopidogrel was the only predictor of cardiac death and stent thrombosis. According to the results of these studies, we performed routine in vitro tests to assess residual platelet reactivity on antiplatelet treatment before percutaneous coronary intervention to guide patient care. In our institution since April 2010, all patients undergoing unprotected left main disease percutaneous coronary intervention were treated with prasugrel, whatever the responsiveness to clopidogrel. Prasugrel provides a faster and deeper platelet aggregation inhibition compared with clopidogrel, while the proportion of nonresponder patients is negligible. We would outline that our study included only patients who were responders to clopidogrel loading. Nevertheless, the deeper platelet aggregation inhibition achieved with prasugrel was associated with an 80% reduction of the composite of cardiac death and myocardial infarction at 1 year without increase in major bleeding.

We agree that pharmacokinetic data would have strengthened our conclusions, but these data were not available. Again, it would be good to avoid the “one-size-fits-all” approach to antiplatelet therapy, but a true individualized therapy also using genomics or the models suggested is very far from reality, considering the variations in each individual patient of platelet aggregation induced by many variables (surgery, bleeding, physical activity, acute coronary syndrome, and others,) or spontaneously over time.