Platelets are small, anucleate blood elements of critical importance in
cardiovascular disease. The ability of platelets to activate and aggregate to form
blood clots in response to endothelial injury, such as plaque
rupture, is well established. These cells are therefore important contributors to ischaemia in
atherothrombosis, and antiplatelet
therapy is effective for this reason. However, growing evidence suggests that platelets are also important
mediators of inflammation and play a central role in
atherogenesis itself. Interactions between activated platelets, leukocytes and endothelial cells trigger autocrine and paracrine activation signals, resulting in leukocyte recruitment at and into the vascular wall. Direct physical interaction may contribute also, through platelet adhesion molecules assisting localization of monocytes to the site of
atherogenesis and platelet granule release contributing to the chronic inflammatory milieu which leads to foam cell development and accelerated
atherogenesis. Recent studies have shown that antiplatelet
therapy in animal models of accelerated
atherogenesis can lead to decreased plaque size and improve plaque stability. This review examines the complexity of platelet function and the nature of interactions between activated platelets, leukocytes and endothelial cells. We focus on the growing body of evidence that platelets play a critical role in
atherogenesis and contribute to progression of
atherosclerosis.