INTRODUCTION

Atherosclerosis is a systemic inflammatory disease characterized by the accumulation of monocytes/macrophages and lymphocytes in the intima of large arteries. Rupture or erosion of the advanced lesion initiates platelet activation and aggregation (the atherothrombotic process) on the surface of the disrupted atherosclerotic plaque.

Several risk factors (including diabetes, hypercholesterolemia, hypertension, and smoking) have been implicated in the initiation and progression of atherosclerosis. Although these risk factors are systemic in nature, atherosclerotic plaques are not randomly distributed but occur with preference to specific locations in the arterial tree. Atherothrombotic lesions colocalize with regions of low shear stress throughout the arterial tree, such as the aortic arch, the carotid artery, the coronary arteries, the infrarenal aorta, and the femoral artery. Consequently, athero-thrombotic clinical manifestations include coronary artery disease (CAD), cerebrovascular disease, and peripheral artery disease (PAD), all of which are potentially life-threatening. The demonstrated beneficial role of antiplatelet drugs in reducing the incidence of nonfatal myocardial infarction (MI), nonfatal stroke, and vascular death in many large clinical trials has demonstrated the major role of platelets in the thrombotic complications of atherosclerosis in the coronary, peripheral, and cerebral vascular systems.

PLATELETS IN CORONARY ARTERY DISEASE

Endothelial dysfunction

Coronary atherosclerosis is the primary cause of heart disease in industrialized nations.