Objective To study the effect of bivalirudin plus loading dose of cilostazol-based triple-antiplatelet therapy strategy in patients undergoing percutaneous coronary intervention (PCI). noted in the characteristics of the culprit vessels or the use of drug-eluting stents between two groups (Table 2). Prior to PCI, the mean TIMI flow grade and TMPG were almost comparative between the two groups. Following PCI, the TMPG III in the cilostazol group was significantly higher than that in the control group, as shown in Table 3 (P<0.05). Table 2 Angiographic findings Table 3 TIMI flow grade and TMPG during PCI Clinical results As exhibited in Table 4, the left ventricular ejection fraction did not significantly differ between the two groups before and at 30 days after PCI (both P<0.05). The MACE rate in the cilostazol group was significantly lower than that in the control group at 30 days after PCI (P<0.05). However, the CP-724714 rates of cardiac death, nonfatal reinfarction, target vessel revascularization, new congestive heart failure, and subacute stent thrombosis did not significantly differ between two groups. Table 4 The 30-day MACE and complications after PCI Thrombocytopenia and bleeding complications The rates of minor or major bleeding or thrombocytopenia did not significantly differ between the two groups (Table 4, P>0.05). Discussion Previous studies of antithrombotic strategy in patient CP-724714 who underwent PCI focused mostly on bivalirudin or triple-antiplatelet therapy after PCI. The ISAR-REACT 3 trial had shown that although bivalirudin failed to offer a net clinical benefit as compared with unfractionated heparin, it significantly decreased the incidence of major bleeding for patients with stable/unstable angina undergoing PCI after pretreatment with clopidogrel.9 In the ACUITY trial, patients with a moderate or high risk of acute coronary syndromes and receiving invasive therapy using glycoprotein IIb/IIIa inhibitors were enrolled, and it was exhibited that bivalirudin was correlated with the incidence of bleeding and ischemia resembling those treated with heparin.10 In the HORIZONS-AMI trial,1 the risk of acute stent thrombosis was increased within 24 hours in patients who were diagnosed with ST-segment elevation myocardial infarction and underwent PCI. The early elevation in stent thrombosis with bivalirudin alone possibly results from platelet activation caused by adenosine diphosphate prior to maximal thienopyridine blockade of the P2Y12 receptor CP-724714 or by the activity of residual thrombin following the suspended use of bivalirudin. Adequate platelet inhibition probably leads to the reduced risk of ischemic clinical events. Cilostazol is usually a potent type III phosphodiesterase inhibitor which was already well-known for its various benefits, such as antiplatelet and antithrombotic IKK-gamma (phospho-Ser376) antibody effects, vasodilating properties, reductions in clopidogrel resistance, and other pleiotropic actions.11C13 Cilostazol has been proven to suppress ADP-induced platelet aggregation, collagen, arachidonic acid, and epinephrine.14 Based on the studies above, combined administration of cilostazol, clopidogrel, and aspirin known as triple-antiplatelet therapy had been recommended. A previous study demonstrated that this incidences of death, myocardial infarction, target lesion revascularization, or stent thrombosis after stenting were reduced by approximately 50% using triple-antiplatelet therapy compared with those by dual-antiplatelet therapy.15 Recent clinical trials found that triple-antiplatelet therapy exerts a more potent inhibition upon ADP-induced platelet aggregation compared CP-724714 with dual-antiplatelet therapy.16,17 Previous studies exhibited that triple-antiplatelet therapy decreased the risk of long-term cardiac and cerebral events after PCI for patients with acute coronary syndromes, especially those with high-risk profiles.18 But a.