[Pathophysiology of carotid stenosis].

Carotid stenosis is an important cause of atherothrombotic cerebral infarction. Moreover, it reflects the severity of systemic atherosclerosis and is a useful predictor of cardiovascular events. Atherosclerotic changes often develop at the site of carotid bifurcation, where shear stress can easily induce endothelial cell damage. The extent of this damage depends on various risk factors such as hypertension, dyslipidemia, and diabetes mellitus. Endothelial cell dysfunction induces the accumulation of inflammatory cells, migration and proliferation of smooth muscle cells, and release of various cytokines and chemokines, which cause carotid plaques and stenosis. Carotid plaques consist of a lipid core with infiltration inflammatory cells covered with a fibrous cap. Cerebral infarction occurs as a result of rupture and thrombus formation on the surface of the carotid plaque by thromboembolic and hemodynamic mechanisms. Rupture-prone carotid plaques are called vulnerable or unstable plaques. The characteristics of vulnerable plaques are active inflammation, with extensive macrophage accumulation, a thin cap with a large lipid core, endothelial denudation with superficial platelet aggregation, fissures, and severe stenosis. To assess the risk of cardiovascular events, it is important to identify vulnerable plaques by imaging techniques and novel assays such as the high-sensitivity C-reactive protein assay. In patients at a high risk of developing cerebral infarction, carotid endoarterectomy or stenting with the best medical treatment is useful in reducing cerebrovascular events.