Efficacy of Cilostazol in reducing restenosis in patients undergoing contemporary stent based PCI: a meta-analysis of randomised controlled trials

Abstract

Aims: Cilostazol has been associated with reduction in restenosis in patients undergoing coronary and peripheral arterial angioplasty. Our objective was to evaluate the impact of cilostazol on restenosis in patients undergoing contemporary PCI with bare metal (BMS) or drug eluting stents (DES) and treated with aspirin and thienopyridine. Methods and results: Ten randomised trials (n=2,809 patients) comparing triple antiplatelet therapy (aspirin, thienopyridine and cilostazol) with standard dual antiplatelet therapy were included. Summary risk ratios for restenosis, late loss, target lesion revascularisation (TLR) and target vessel revascularisation (TVR) were calculated using fixed-effects models. Cilostazol was associated with a significant reduction in late loss in BMS (mean difference 0.24 mm, 95% CI 0.15-0.33, p<0.001) and DES groups (mean difference 0.12 mm, 95% CI 0.07-0.18, p<0.001). Cilostazol therapy was associated with a significant reduction in angiographic restenosis (Odds ratio [OR] 0.52, 95% CI 0.41-0.66, p<0.001) with consistent benefits in patients treated with BMS (OR 0.49, 95% CI 0.35-0.70, p<0.001) or DES (OR 0.54, 95% CI 0.38-0.76, p=0.001). Addition of cilostazol to dual antiplatelet therapy was associated with a significant reduction in TLR (OR 0.38, 95% CI 0.25-0.58, p<0.001), with no difference in subacute stent thrombosis (OR 1.91, 95% CI 0.33-11.08, p=0.47), or major bleeding (OR 0.87, 95% CI 0.44-1.74, P=0.69) but with an increased risk of skin rash (OR 3.67, 95% CI 1.86-7.24, p<0.001). Conclusions: Cilostazol in addition to dual antiplatelet therapy is associated with a reduction in angiographic restenosis in patients undergoing stent based PCI. This inexpensive drug may be particularly beneficial in patients who are at high risk of restenosis and it should undergo further evaluation in large, definitive randomised controlled trials.