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.