ABSTRACT
Vascular inflammation, coronary constriction, and thrombus formation are central to
all acute coronary syndromes (ACSs). Adhesion and aggregation of activated platelets,
initially described during thrombosis, now appear pivotal to all three processes.
Several platelet adhesion receptors participate but the integrin glycoprotein (GP)
IIb/IIIa occupies a critical role. GPIIb/IIIa antagonists used as an adjunct to percutaneous
coronary intervention show clear benefit. However in the setting of ACS results have
been disappointing. Indeed, trials of oral GPIIb/IIIa antagonists in patients with
ACS were associated with increased mortality. Difficulties with drug dosing and variable
pharmacodynamics may contribute to suboptimal receptor occupancy, incomplete inhibition
of platelet aggregation, paradoxical partial agonist activity, and proinflammatory
effects. Moreover, variable responses of patients to GPIIb/IIIa antagonists may reflect
population heterogeneity.
KEYWORDS
Glycoprotein IIb/IIIa antagonist - thrombosis - inflammation - partial agonist