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The plaques begin naturally as a fatty streak in the arteries of children and adolescents. New channels for blood flow are cut through the edges of the plaque in a process called neovascularization. The atherosclerotic plaques generally continue to enlarge through reorganization and further accumulation of lipids when they are available, resulting in a hardened and clogged artery.

Occlusive plaques are known as lesions and they may rupture, ulcerate, or erode the inner arterial surface; hemorrhage; thrombose; or cause an aneurysmal dilation by weakening the arterial wall. When occurring in the coronary arteries, those supplying the heart, it can result in heart attacks, chest pain (angina pectoris), sudden cardiac death perhaps from plaque rupture or vasospasm, and chronic ischemic heart disease with chronic heart failure.

Other Forms of Arteriosclerosis

Another form of arteriosclerosis that occurs due to deposits in the arteries is Monckeberg medial calcific sclerosis. This is a disorder characterized by calcium deposits in the muscular arteries of persons over 50 years of age.

The third form of arteriolosclerosis consists of two variants that occur in the small arteries and arterioles, hyaline arteriosclerosis and hyperplastic arteriosclerosis. These disorders may induce downstream ischemic injury, which is a reduction in the oxygen that gets to the tissue and results in cell death, and are most often associated with hypertension and diabetes.

Hyperplastic arteriolosclerosis is an "onion-skinning" of the artery seen in severe hypertension, with the inner diameter, lumen, being obliterated. In malignant hypertension, the arteriole may undergo necrosis. Hyaline arteriolosclerosis is caused by leakage of blood plasma components across the endothelium, and is seen in the elderly and in nephrosclerosis.

References:

Kum ar, Cotran, Robbins. Robbin's Basic Pathology, 7th edition (medical school text)

MayoClinic.com

Learn more about this author, Alicia M Prater PhD.
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