Our understanding of the pathophysiology of acute coronary syndromes (ACS)
has now been substantiated by many studies showing that atherothrombosis pl
ays a predominant role. This article reviews the molecular interactions in
thrombosis that may serve as therapeutic targets for more effective managem
ent of these syndromes. In particular, the discovery of the fact that the g
lycoprotein (GP) IIb-IIIa receptor plays a central and common role in plate
let-mediated thrombosis has focused the therapeutic efforts. Blockade of th
is receptor has emerged as a new and potent strategy for inhibition of plat
elet aggregation and thus of clot formation. A number of trials have now co
rroborated the need for such antithrombotic drugs in the management of pati
ents with non-ST-segment elevation ACS.