Fig. 4.

Overview of the pathogenesis of atherosclerosis. Accumulation of LDLs in the blood leads to LDLs being transported into the endothelium, where they become oxidised. Infiltrating monocytes become activated and differentiate into macrophages and begin to ingest oxidised-LDLs to become foam cells. Over time, foam cells conglomerate to form fatty streaks. Simultaneously, due to inflammation and stimulant factors, VSMCs begin to proliferate and migrate into the intima and form a cap around the fatty streak. Endothelial cells overlying the growing plaque become calcified, with reduced elasticity. Over time this cap restricts blood flow due to a luminal constriction. If the plaque ruptures, a thrombus forms and obstructs the lumen completely, or partially. This can lead to ischaemia downstream leading to an ischaemic attack in the brain, or rupture to cause a haemorrhagic stroke.

Adapted from [107]