Abstract
Despite the broad array of mechanisms designed to protect the endothelial lining of every blood vessel in the body and maintain the fluid state of blood, injury does occur. Chronic and recurrent damage result in development of lesions characteristic of atherosclerosis. The loss of vascular integrity associated with the pathological process of atherogenesis triggers the haemostatic mechanism. As a result, fibrin and platelets become a part of atherosclerotic lesions and play a role in their progression. Growth of the plaques and destruction of normal endothelium triggers further involvement of platelets leading to occlusion of arteries in the heart and brain, resulting in myocardial infarction and stroke. Understanding the role of platelets in atherosclerosis and limiting its contribution may reduce morbidity and mortality of this dread disease.