No role for triple antiplatelet therapy?

Studies have shown that adjunctive cilostazol to dual ntiplatelet therapy in patients undergoing percutaneous oronary intervention (PCI) may decrease late restenosis nd enhance inhibition of adenosine diphosphate (ADP)nduced platelet aggregation, providing a rationale for triple ntiplatelet therapy (3–5). The appealing hypothesis that riple antiplatelet therapy may provide more profound latelet aggregation inhibition and, at the same time, less yperplastic vessel wall response to stent implantation was xamined in this issue of the Journal by the CILON-T Influence of CILostazol-based triple antiplatelet therapy N ischemic complication after drug-eluting stenT imlantation) trial investigators in a large cohort of all-comer atients receiving coronary drug-eluting stents (DES) who ere randomized to dual or triple antiplatelet therapy (6). The primary end point of the study, based on the dual ffect of cilostazol, was a composite of acute atherothromotic events and late ischemic events (death, myocardial nfarction, stroke, and target vessel revascularization). The econdary end point focused on platelet aggregation inhibiion as assessed by VerifyNow P2Y12 assay (Accumetrics, an Diego, California) at discharge and at 6 months. There was no difference between groups in the rate of the rimary end point (8.5% in the triple antiplatelet therapy nd 9.2% in the dual antiplatelet therapy), and as expected, arget vessel revascularization was the most frequent event f the primary end point (6.6% and 7.2%, respectively). hus, in patients receiving DES, cilostazol had no effect on he risk of clinically driven target vessel revascularization