Abstract
One of the major causes of morbidity and mortality in the developed world is atherosclerosis. Recent research has suggested that the interaction of platelets with the endothelium is important in both the progression of atherosclerosis and the development of the acute complications of the disease. Both of these cells secrete various signalling molecules and express adhesion molecules, which can influence the development of pathological states. Certainly, there may be a vicious cycle in which platelet activation promotes atherosclerosis; a process involving inflammation and the activation of many other cell types (for example, leukocytes and smooth muscle cells), which causes further platelet activation. Therefore, intense effort has been made to develop therapeutic agents that can modulate the function of these cells, with the ultimate aim to retard (or even reverse) the progression of atheroma growth.