Abstract
Carotid artery atherosclerosis is an important etiology of carotid artery stenosis
and subsequent cerebrovascular events. Carotid atherosclerosis follows a pattern that
begins with endothelial dysfunction, marked by impaired nitric oxide-mediated vasodilation
and increased endothelial permeability, and is followed by intimal low-density lipoprotein
(LDL) accumulation. Retained oxidized LDL results in a pro-inflammatory environment
that results in inflammatory cell inflammation and foam cell formation, the basis
of the fatty streak. Migrating medial vascular smooth muscle cells, which undergo
phenotypic switching, lead to plaque growth and fibrous cap formation. The unique
geometry of the carotid bifurcation contributes to the complex local hemodynamic environment
and predisposes the carotid bifurcation to endothelial dysfunction. In later stages
of atherosclerosis, higher wall shear stress erodes the fibrous cap and increases
the risk of plaque rupture. Several parameters of carotid bifurcation geometry, including
the bifurcation angle and relative diameters of the internal and common carotid arteries,
also contribute to disturbed flow and atherosclerotic plaque development.
Keywords
carotid stenosis - atherosclerosis - pathophysiology - hemodynamics
