Atherosclerosis is a disease characterised by the formation of fibrofatty plaques (atheromas) in large and medium-sized arteries. These plaques accumulate in the lumen of these arteries, narrowing them and impeding blood flow. The reduced blood flow results in ischemia due to lack of oxygen transport, thus resulting in severe damage and necrosis in organs.
Pathogenesis of Atherosclerosis
The Response to Injury Hypothesis
FATTY STREAK→ MATURE ATHEROSCLEROTIC LESION
-
Chronic inflammation (slow, long-term inflammation that is persistent) induced by an injury to the endothelial lining of the artery results in endothelial dysfunction. Endothelial dysfunction leads to the constriction of blood vessels, instead of the dilation.
-
This exacerbates the development of fatty plaques, as it recruits platelets and monocytes to the site of injury.
-
Growth factors and cytokines are released, resulting in the migration of smooth muscle cells and fibroblasts into the endothelium lining. This results in the production and accumulation of collagen.
-
Cholesterol from the blood and lipids are engulfed by macrophages, inducing the formation of the atherosclerotic lesion.
-
This produces a raised plaque composed of fibrous and fatty elements that causes stenosis of the vessel lumen. This plaque can eventually break into smaller pieces and get released in the bloodstream, causing other severe blockages.
