Increased platelet aggregation induced activeiting by anti-glycoprotein IIb/IIIa antibody in patients with acute coronary syndrome

Interaction of glycoprotein (GP) IIb/IIIa with fibrinogen is the final and key reaction in platelet aggregation. In order to evaluate GP IIb-IIIa functional activity in patients with acute coronary syndrome (ACS) we measured platelet aggregation induced by monoclonal antibody CRC54 which is directed against GP IIb/IIIa and is able to stimulate its binding with fibrinogen and subsequent aggregation. Patients with ACS were divided into 3 groups: (1) with Q-wave myocardial infarction (MI), (2) with non Q-wave MI and with unstable angina. Patients with stable angina (SA) and healthy donors formed 2 comparison groups. The level and rate of CRC54-induced aggregation measured both in the absence and in the presence of prostaglandin E-1 (PGE(1)), the inhibitor of platelet activation, in all groups of patients with ACS were greater than or equal to 1.5 times higher than in SA patients and healthy donors. Observed differences in the parameters of CRC54-induced aggregation at least in the presence of PGE(1) could be caused only by increased GP IIb/IIIa fibrinogen binding ability in ACS patients, but not by differences in the level of platelet activation. In all groups of patients with ACS, but not in SA patients and healthy donors, strong correlation (r=-0.5-0.7) was observed between increased parameters of ADP-induced aggregation and aggregation stimulated by CRC54 in the presence of PGE(1). The data obtained indicated that increased of platelet aggregating capacity in ACS might be caused by changes of GP IIb/IIIa functional characteristics and not by enhancement of platelet sensitivity towards physiological agonists including ADP.