Triple antiplatelet therapy with cilostazol did not show superiority over dual antiplatelet therapy in reducing adverse cardiovascular outcomes after DES implantation (8.5% vs 9.2%; HR 0.90, p=0.74).
RCT (n=960)
randomized
Sí
Does the addition of cilostazol to dual antiplatelet therapy (aspirin and clopidogrel) reduce the composite of cardiac death, nonfatal myocardial infarction, ischemic stroke, or target lesion revascularization in patients receiving drug-eluting stents?
Adding cilostazol to conventional dual antiplatelet therapy after drug-eluting stent implantation reduces platelet reactivity but does not improve clinical cardiovascular outcomes at 6 months.
Hazard Ratio: 0.9 (95% CI 0.54–1.52)
Tasa de eventos absoluta: 8.5% vs 9.2%
valor p: p=0.74
OBJECTIVES: We aimed to test whether cilostazol has beneficial effects in the real-world patients treated with intracoronary drug-eluting stents (DES). BACKGROUND: The addition of cilostazol on the conventional dual antiplatelet therapy has been reported to reduce platelet reactivity and to improve clinical outcomes after percutaneous coronary intervention in previous studies. METHODS: In a randomized multicenter trial, we enrolled 960 patients who received DES. They were randomized to receive either dual antiplatelet therapy (DAT) (aspirin and clopidogrel) or triple antiplatelet therapy (TAT) (aspirin, clopidogrel, and cilostazol) for 6 months. Primary end point was the composite of cardiac death, nonfatal myocardial infarction, ischemic stroke, or target lesion revascularization (TLR). Secondary end points were P2Y₁₂ reaction unit (PRU) measured with the VerifyNow P2Y12 assay (Accumetrics, San Diego, California) at discharge and at 6 months after the index procedure. All-cause death, stent thrombosis, and each component of the primary end point at 6 months were other secondary end points. Analysis was done on an intention-to-treat basis. RESULTS: At 6 months' follow-up, there was no difference in the primary end point between the 2 groups (8.5% in TAT vs. 9.2% in DAT, p = 0.74). In secondary end point analysis, the TAT group achieved lower PRU levels than the DAT group both at discharge (206.6 ± 90.3 PRU vs. 232.2 ± 80.3 PRU, p < 0.001) and at 6 months (210.7 ± 87.9 PRU vs. 255.7 ± 73.7 PRU, p < 0.001). In the Cox proportional hazards analysis, lesion length (≥28 mm, hazard ratio HR: 2.10, 95% confidence interval CI: 1.25 to 3.52), and PRU level at discharge (every increase in tertile, HR: 1.61, 95% CI: 1.16 to 2.25) were predictors of the primary end point, but not the use of cilostazol (HR: 0.90, 95% CI: 0.54 to 1.52). CONCLUSIONS: Despite the greater reduction of platelet reactivity by addition of cilostazol to conventional DAT, TAT did not show superiority in reducing the composite of adverse cardiovascular outcomes after DES implantation. (The Efficacy of CILostazol ON Ischemic Complications After DES Implantation CILON-T; NCT00776828).
“I think there probably is some antiproliferative effect of cilostazol—a number of studies have suggested this. The meta-analysis shows with some confidence that there's a reduction in TLR, but there's no effect on hard events like MI and death, and then you pay a price in terms of tolerability.”
Suh et al. (Sat,) conducted a rct in Coronary Heart Disease (n=960). Triple antiplatelet therapy (aspirin, clopidogrel, and cilostazol) vs. Dual antiplatelet therapy (aspirin and clopidogrel) was evaluated on Composite of cardiac death, nonfatal myocardial infarction, ischemic stroke, or target lesion revascularization (TLR) (HR 0.90, 95% CI 0.54 to 1.52, p=0.74). Triple antiplatelet therapy with cilostazol did not show superiority over dual antiplatelet therapy in reducing adverse cardiovascular outcomes after DES implantation (8.5% vs 9.2%; HR 0.90, p=0.74).