Arterial thrombosis is the acute complication that develops on the chronic lesions of atherosclerosis and causes heart attack and stroke, today the most common causes of mortality in developed countries. Platelets, with fibrin, are prominent components of the thrombi (clots) that occlude arteries, but may also participate in the development and progression of the atherosclerotic plaque. Thus, platelets are central to the process of atherothrombosis, a term that describes the combination of acute and chronic events in arterial disease. The normal function of platelets, however, is to arrest bleeding from wounds, which requires adhesion to altered vascular surfaces and rapid cellular activation with the ensuing accumulation of additional platelets and fibrin into a growing thrombus. Progress in understanding the mechanisms of platelet adhesion, activation and aggregation may improve the ability to prevent thrombosis and, possibly, the progression of atherosclerosis.Platelets are anucleated blood cells that originate from the cytoplasm of megakaryocytes in the bone marrow and circulate to 'survey' the integrity of the vascular system, where they discriminate between normal endothelial cell lining and areas with lesions (Fig. ). In physiological conditions, this function contributes to hemostasis, the process that arrests hemorrhage after tissue trauma, but in diseased arteries it may lead to thrombotic occlusion of the vessel lumen with obstruction of blood flow and subsequent tissue damage. Platelets seem to be less relevant in the pathogenesis of venous thromboembolism; that topic is not addressed here. Maintaining a balance between blood fluidity and rapid thrombus formation in response to injury is a key attribute of endothelial cells; to that end, they control vascular tone and synthesize inhibitors as well as activators of platelet function and blood clotting 1,2 (Fig. ). The main trigger for the formation of a hemostatic thrombus after traumatic vascular injury is the loss of the endothelial cell barrier between extracellular matrix components and flowing blood. The response of platelets to this event develops in three successive but closely integrated phases that involve adhesion, activation and aggregation (Table ).