Antiaggregatory, physiological and clinical effects of ticlopidine in subjects with peripheral atherosclerosis.

Twelve patients with varying degrees of peripheral atherosclerotic disease were given an antiaggregatory drug, ticlopidine [5-(6-chlorobenzyl)-4,5,6,7-tetrahydrothieno-(3,2-C)-pyridine HCl] in a single blind trial for one or four months and the effects on platelet aggregation, blood coagulation, marcro- and micro-circulation and walking distance were studied. Two patients were excluded; one because of nausea attributable to the drug, one because of lack of co-operation. No statistically significant changes in circulation parameters or walking distance were noted. No changes were observed in APT-time, thrombine- and Reptilase-clotting time, platelet counts, concentrations of fibrinogen and fibrinopeptide A in plasma or serum antithrombin activity. The mean concentration of fibrinopeptide A was slightly increased in all patients. ADP-induced aggregation was inhibited in all patients. Aggregation induced by arachidonic acid was partially inhibited but not abolished in all patients. Prostaglandin G2-induced aggregation was not altered by ticlopidine but collagen-induced aggregation was inhibited. Ticlopidine, in contrast to acetyl-salicylic acid, inhibits the primary aggregation but also seems to interfere with the release action. Treatment of larger patient groups for longer periods are necessary to determine the clinical usefulness of ticlopidine.