One of the more recent theories suggests that excess lipoproteins, LDL, in the blood are trapped within the artery wall. When this happens and they accumulate, they become oxidized. This, in turn, leads to the formation of foam cells that lead to the deposition of connective tissue cells and elements. LDL contains specific functional groups which allow it to be recognised by most cells in the body and remain soluble in blood plasma. Therefore LDL readily passes through the endothelium, contributing to the development of plaques, atheromas.
Plaque formation begins as fatty streaks on the inner arterial wall.
Over time the fat deposits accumulate and grow, narrowing the lumen of the artery. Subsequent damage to the endothelial wall causes blood platelets to adhere and contributes to blood clot formation. Surrounding smooth muscle tissue also proliferates to form larger plaques. Hardening of the arterial wall is due to various depositions within the plaque including lipids, cholesterol crystals, and calcium salts. These depositions make the arteries bone-like rigid tubes.