Fig. 1.

Atherosclerotic plaque formation. (A) Lipoprotein retention to the vascular wall and disturbed flow activate the expression of adhesion molecules (vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1)) on endothelium with subsequent monocyte recruitment to the vessel wall. Monocytes differentiate to macrophages, take up oxidised low density lipoprotein (oxLDL), form foam cells and a pro-inflammatory reaction is activated. Vascular modifications result in SMC migration to the subendothelial space. (B) A stable plaque is formed of a lipid core and the accumulation of necrotic cells as foam cells undergo apoptosis and necrosis. SMC secrete macromolecules like collagen, elastin, fibronectin and extracellular matrix facilitating fibrous cap formation. (C) Thin fibrous cap results in a vulnerable plaque prone to rupture and secondary complications like thrombus formation. Macrophage proteolytic activity with matrix metalloproteinases (MMPs) being the main proteolytic enzymes has been associated with plaque rupture.