Clinical effects of oral cilostazol on suppression of platelet function in patients with cerebrovascular disease.

A new antithrombotic drug, cilostazol (6-[4-(1-cyclohexyl-1H-tetrazol-5-yl)butoxy]-3,4-dihydro-2(1H)-qui nolinone OPC-13013), was administered at daily oral doses of 75, 150 and 300 mg for 2 weeks in 15 patients with cerebrovascular disease including cerebral thrombosis, transient ischemic attacks and cerebral arteriosclerosis, and patient response was determined based on the degree of suppression of the platelet function. The antiplatelet-aggregating effect of the drug was determined by measuring the rate of inhibition of platelet aggregation induced by aggregation inducers such as adenosine diphosphate (ADP), collagen and epinephrine. The inhibition rates (percent difference between pre- and post-treatment rates/pre-treatment rate) obtained with the drug at 75 mg/day were 25.5, 36.5 (p less than 0.1) and 10.9% when platelet rich plasma (PRP) was added to ADP, collagen and epinephrine, respectively. The corresponding values at 150 mg/day were 34.2 (p less than 0.1), 50.7 (p less than 0.05) and 48.0% (p less than 0.1), and those at 300 mg/day were 62.1 (p less than 0.01), 71.7 (p less than 0.01) and 48.2% (p less than 0.1), respectively. The inhibitory effect of the drug thus appeared to be dose-related. Adhesiveness was also reduced by the drug, though a bleeding tendency was not indicated, and the reduction was found to be significant at 300 mg/day (p less than 0.05). The drug can, therefore, be considered to be a potent and safe antiplatelet-aggregating agent.