In the last few years it became obvious that platelets are involved in the development of atherosclerotic diseases. This involvement of platelets has been taken into account in the "response to injury" hypothesis of atherosclerosis. The hypothesis is based on the assumption that atherosclerotic lesions result from endothelial injury, followed by the interaction of vessel wall constituents with lipoproteins, macrophages, and platelets. In the first part of this review, general aspects of platelet activation are summarized and the pathways of platelet aggregation as well as their involvement in blood coagulation are discussed. The second part of this paper describes the influence of cholesterol, lipoproteins, and apolipoproteins upon the activation and metabolic behavior of platelets. Physiological and pathophysiological processes particularly occurring in different types of hyperlipoproteinemias and atherosclerotic disorders are discussed in this context.