• It 's the lesion found in the narrowed coronary arteries of nearly all people who have angina, and is the most important underlying cause of heart attacks.
• It is also the abnormality found in the neck arteries of those who suffer some kinds of stroke (ischemic and embolic stroke).
• It's the abnormality found in the aorta, femoral arteries or smaller leg arteries of people who suffer with the leg & foot gangrene that comes about in smokers (and diabetics and other people who lose the pulse points in their legs because of peripheral vascular disease).

Even worse, some people with severe atherosclerosis have every one of the above problems and spend long periods of their lives more or less disabled by them. Since this pathologic lesion is so widespread in causing serious disease, its biology has been studied extensively. Much more is known now than was understood fifty years ago - but a simple and foolproof way of reversing the damage that atherosclerosis does to arteries is not known.

• Atherosclerosis affects the walls of the artery.
• It is a progressive process that becomes increasingly worse over time. At first the changes are slight and cannot be called either abnormal or a disease. These first signs of fat being laid down in artery walls happen to everyone.
• Initially, there are "fibrofatty" plaques that sit on the inner lining of the artery. These begin as isolated patches of cells containing lipid (fat) and these spots coalesce into streaks of fatty material that are visible in the lining of the artery (the intima, that's the name of the lining). These fatty streaks are not raised enough to project into the opening of the artery, and are not considered disease. (All children over age 10 have some fatty streaks in the largest artery- the aorta. Not all fatty streaks progress.)
• (After age 20
• An atheroma is sometimes called an "intermediate lesion"
• The wall of the artery
• When the surface of the lining is defective then clotting begins inside the bloodstream. This is the end-stage lesion and it always carries with it the liklihood that a clot will form. When a clot forms, it can quickly plug blood flow in the entire vessel. If it forms and is not large enough to plug the vessel, it can reduce the blood flow enough to starve the tissues that the artery supplies - but allow it to survive. If that tissue is muscle, whether heart or leg, there is pain if the muscle is excercised because. Once it forms, no matter what its size, there is a chance that some or all of it will break off from the inside surface of the lining and go spinning down the bloodstream where it will lodge in a smaller artery.
• A clot stuck to the defective wall where it was formed is called a thrombus. The broken-off clot that has travelled (or is travelling) in the blood stream is called an embolus.
• The bouts of damage that each can cause are called "thrombotic events" and "embolic events". An example of a thrombotic event is a heart attack. Another, less severe, example is a period where angina worsens. An example of an embolic event is a stroke.

• Kumar: Robbins and Cotran: Pathologic Basis of Disease, 7th ed.Copyright © 2005 Saunders, An Imprint of Elsevier
• Gleissner CA. Leitinger N. Ley K. Effects of native and modified low-density lipoproteins on monocyte recruitment in atherosclerosis. [Review] [117 refs] [Journal Article. Research Support, N.I.H., Extramural. Research Support, Non-U.S. Gov't. Review] Hypertension. 50(2):276-83, 2007 Aug. (Through a complex cascade of interactions between adhesion molecules and chemotactic factors, monocytes enter the subendothelial space, where they develop into macrophages, foam cells, and dendritic cells under the influence of cytokines, growth factors, and lipoproteins.6–8 Foam cells eventually undergo secondary necrosis and form the lipid core of advanced atherosclerotic plaques. When exposed by rupture or erosion, it triggers acute thrombotic events leading to myocardial infarction and strokes.)