In this review the roles of platelets and the Gp IIb/IIIa receptor in arterial thromboembolism are described in detail, and it is explained why blocking this receptor could be a rational strategy in certain conditions. The pharmacology and clinical efficacy of GP IIb/IIIa recepor antagonists are discussed. Thrombus formation can be summarised in six steps: vascular injury or rupture of an atherosclerotic plaque, initial adhesion to the vessel wall, activation of platelets, stabile adhesion, aggregation and fibrin formaton. The activation of the GP IIb/IIIa receptor on the platelet surface is the final common pathway in platelet activation, and is essential to thrombus formation. The receptor requires both vWF and fibrinogen as ligands for thrombus formation in arteries. Three GP IIb/IIIa receptor antagonists are lisenced to clinical use; abciximab, eptifibatide and tirofiban. Abciximab is a fab fragment of an antibody, eptifibatide is a cyclic heptapeptide based on snake venom, and tirofiban is a non-peptide tyrosin derivate. The latter two bind to the ligand binding pocket on GP IIb/IIa, the binding site of abciximab is unknown. In PCI, GP IIb/IIIa recptor antagonists are shown to reduce the risk of death and myocardial infarction after 30 days and six months, with a moderatly increased risk of major bleeding. In acute coronary syndromes, these agents are less efficacious and further research should be preformed to see who might benefit most from the agents. Trilas with oral GP IIb/IIIa recptor antagonists have been diappointing, as they have been assosiated with increased mortality.