Triple antiplatelet therapy reduces ischemic events after drug-eluting stent implantation: Drug-Eluting stenting followed by Cilostazol treatment REduces Adverse Serious cardiac Events (DECREASE registry)

Background Cilostazol has reduced restenosis and repeat intervention after drug-eluting stent (DES) implantation. However, there is little data regarding impact of cilostazol on cardiac events after DES implantation. Therefore, we assessed the long-term efficacy and safety of cilostazol in patients undergoing successful DES implantation. Methods The patients (n = 3,099) undergoing successful DES implantation were treated with triple (aspirin, clopidogrel, and cilostazol; triple group, n = 1,443) or dual (aspirin and clopidogrel; dual group, n = 1,656) antiplatelet therapy. We compared adverse outcomes (death, myocardial infarction [MI], or stent thrombosis) at 12 months using the inverse probability of treatment weighted (IPTW) for the entire cohort and propensity score matching. Results After IPTW adjustment, 12-month death (hazard ratio [HR] 0.762, 95% CI 0.401-1.448, P = .4062) was not different between the 2 groups. However, 12-month MI (HR 0.233, 95% CI 0.077-0.703, P = .0097) and stent thrombosis (HR 0.136, 95% CI 0.035-0.521, P = .0036) were significantly lower in triple group with no difference of major bleeding (HR 0.969, 95% CI 0.443-2.119, P = .9372). In the propensity score-matched cohort (965 pairs), 12-month clinical outcomes were similar to those of IPTW adjustment. On extended Cox model, duration of triple antiplatelet therapy was associated with reduction of stent thrombosis (HR 0.056, 95% CI 0.003-0.916, P = .0433) and MI (HR 0.749, 95% CI 0.568-0.988, P = .0408). Conclusions Triple antiplatelet therapy significantly reduced 12-month risks of stent thrombosis and MI after DES implantation compared with dual antiplatelet therapy without increased risk of bleeding complications. The longer duration of triple therapy after DES implantation was associated with the lower risk of stent thrombosis and MI. (Am Heart J 2010;159:284-291.e1.)