Long-term efficacy of high-dose tirofiban versus double-bolus eptifibatide in patients undergoing percutaneous coronary intervention

Background There is no head-to-head comparison between tirofiban versus eptifibatide in patients undergoing percutaneous coronary intervention (PCI) when added to standard antiaggregating drugs (AAD) to prevent ischemic events within 1 year. Methods We compared real-world patients undergoing PCI who were on oral single AAD and were block randomized to receive, immediately preintervention, high-dose tirofiban (n = 519) or double-bolus eptifibatide (n = 147) and a second oral antiplatelet agent. The incidence of composite ischemic events within 1 year, including death, acute myocardial infarction, angina, stent thrombosis or repeat PCI or coronary bypass surgery (primary end-point) was modelled by forced Cox's regression. Results There were overall 65 composite ischemic events: 47 (9.1%) in the tirofiban group and 18 (12.2%) in the eptifibatide group (univariate log-rank test: P = 0.22). On the basis of 21 potential covariates fitted simultaneously, multivariable adjusted hazard ratios showed that age [hazard ratio 1.03, 95% confidence interval (Cl) 1.01-1.07, P = 0.01], chronic renal failure (hazard ratio 3.21, 95% Cl 1.02-10.10, P = 0.05), pre-PCI values of creatine kinase-myocardial band (CK-MB) (hazard ratio 1.002, 95% Cl 1.0002-1.0054, P = 0.04), intra-aortic balloon pump (hazard ratio 5.88, 95% CI 12.33-14.85, P = 0.0002) and the presence of eptifibatide (hazard ratio 1.85, 95% Cl 1.04-3.29, P = 0.04) were significant risk factors whereas thrombolysis by tenecteplase (hazard ratio 0.19, 95% CI 0.05-0.69, P = 0.01) was a significant protector. Interestingly, eptifibatide versus tirofiban efficacy was explained based on pre-PCI values of CK-MB. Conclusion Head-to-head comparison between eptifibatide and tirofiban in patients undergoing PCI while on double AAD showed that eptifibatide had a lower efficacy on the incidence of composite ischemic events within 1 year, which might be explained by a reduced action on CK-MB pre-PCI. J Cardiovasc Med 12:29-36 (C) 2010 Italian Federation of Cardiology.