ABSTRACT
Platelet-rich thrombosis following plaque rupture plays a central role in the development of acute
coronary syndromes [1,2]. Exposure of subendothelial matrix leads to platelet adhesion,
predominantly mediated by the interaction between GP Ib=IX receptors and von Willebrand’s factor that is magnified several hundredfold in the presence of high-shear stress [3]. Platelet
adhesion at the site of endothelial injury leads to a release of adenosine diphosphate (ADP) and
calcium-dependent degranulation that subsequently liberates other prothrombotic stimuli.
Furthermore, calcium-mediated phospholipase A2-dependent arachidonic acid formation
provides the substrate for prostaglandin formation. Platelet activation, in turn, is augmented
by a variety of mediators, including serotonin, ADP, thromboxane-A2, collagen, and thrombin-
all potential targets for antiplatelet therapies.
