Atherosclerosis is characterised by intimal lesions called atheromas that protrude into vessel lumens. An atheromatous plaque consists of a raised lesion with a soft, yellow core of lipid (mainly cholesterol and cholesterol esters) covered by a white fibrous cap. In addition to mechanically obstructing blood flow, atherosclerotic plaques can rupture, leading to catastrophic vessel thrombosis; plaques also weaken the underlying media and thereby lead to aneurysm formation.
Key steps of pathogenesis:
Endothelial injury, which causes increased vascular permeability, leukocyte adhesion, and thrombosis
Accumulation of lipoproteins (mainly LDL and its oxidized forms) in the vessel wall
Monocyte adhesion to the endothelium, followed by migration into the intima and transformation into macrophages and foam cells
Factor release from activated platelets, macrophages, and vascular wall cells, inducing smooth muscle cell recruitment, either from the media or from circulating precursors
Smooth muscle cell proliferation
Lipid accumulation both extracellularly and within cells (macrophages and smooth muscle cells)