مرکز منطقه ای اطلاع رساني علوم و فناوري

Abstract :

Atherosclerosis and its complications are the leading cause of death both in our country and the world. Atheroma plaques are the typical lesion of atherosclerosis and affect intimal layers of medium and large arteries. Endothelial dysfunction plays a major role in the initiation of atherosclerosis. Endothelial dysfunction is a common point in risk factors of atherosclerosis. Inflammatory cells begin to accumulate in intima by the effect of cytokines and chemokines secreted with passage of LDL (low-density lipoprotein) through endothelium. Foam cells are formed as a result of phagocytosis of LDL by macrophages and seen as yellow streaks under the intima. Those lesions are first lesions of atherosclerosis and do not cause stenosis and termed as fatty streaks. The necrotic lipid core is formed by apoptosis of foam cells. Extracellular connective tissue (capsule) synthesis begins around the lipid core by proliferation of smooth muscle cells that migrate to intima. Fibrous plaque is a lesion with a fibrous capsule around the lipid core and narrows the lumen. Unstable plaque is formed by proliferation of inflammatory cells and thinning of capsule through enlargement of lipid core. Tear of plaque capsule and contact of plaque content with blood results in formation of a complicated lesion in which thrombus and fibrin bind on plaque. Atherosclerosis is a chronic inflammatory disease in which endothelial dysfunction, dyslipidemia and inflammatory cells play a central role and triggered by many risk factors.