There is a strong correlation between the level of plasma low-density lipoprotein (LDL) and death by cardiovascular disease (CVD). As a main carrier of cholesterol, a high low-density lipoprotein concentration stimulates atherogenesis by its capacity to become oxidized and to become endocytosed by macrophages in the vessel wall forming cholesterol-rich plaques that are sites for arterial occlusion. New evidence points at a second role of low-density lipoprotein in increasing cardiovascular disease-risk. Contact with low-density lipoprotein induces platelet hypersensitivity to agonists that initiate platelet functions thereby enhancing adhesion, aggregation and secretion of granule contents. The signalling pathways that mediate the priming of platelets by native and oxidized low-density lipoprotein have now been characterized.