THE IN-VITRO EFFECT OF RIDOGREL ON PLATELET-FUNCTION IN NORMOCHOLESTEROLEMIC AND FAMILIAL HYPERCHOLESTEROLEMIC TYPE IIA SUBJECTS

Platelets from familial hypercholesterolaemia type IIa patients are hy perreactive and produce increased amounts of thromboxane A(2). These m odifications of platelet function may play an important role in the oc currence of premature atherosclerosis. One approach to the prevention of the thromboembolic complications of atherosclerosis is the use of a ntiplatelet agents which depress platelet function. Ridogrel, a combin ed thromboxane synthase inhibitor and thromboxane A(2)/prostaglandin e ndoperoxide receptor blocker inhibits platelet aggregation, This study was designed to investigate the in vitro effect of ridogrel on platel et function in normocholesterolaemic and familial hypercholesterolaemi a type IIa subjects, In citrated platelet rich plasma ridogrel signifi cantly inhibited platelet aggregation and thromboxane A(2) production in response to collagen, ADP and arachidonic acid stimulation. In wash ed platelets ridogrel significantly decreased aggregation and serotoni n release, Ridogrel significantly increased cAMP levels in response to thrombin stimulation. In conclusion, ridogrel at low concentrations s ignificantly inhibited the in vitro function of platelets in a dose de pendant manner in both normocholesterolaemic subjects and familial hyp ercholesterolaemia IIa subjects. (C) 1998 Elsevier Science Ltd.