Atheriosclerosis

Atherosclerosis is a type of arteriosclerosis. It comes from the Greek words athero (meaning gruel or paste) and sclerosis (hardness). It involves deposits of fatty substances, cholesterol, cellular waste products, calcium and fibrin (a clotting material in the blood) in the inner lining of an artery. The build-up that results is called plaque.

[Arteriosclerosis is a general term for the thickening and hardening of arteries. Some hardening of arteries normally occurs when people grow older.]

Plaque may partially or totally block the blood's flow through an artery. Two things that can happen where plaque occurs are

1. bleeding (hemorrhage) into the plaque.
2. formation of a blood clot (thrombus) on the plaque's surface.

If either of these occurs and blocks the entire artery, a heart attack or Stroke may result.

Atherosclerosis affects large and medium-sized arteries. The type of artery and where the plaque develops varies with each person.

Atherosclerosis is a slow, progressive disease that may start in childhood. In some people this disease progresses rapidly in their third decade. In others it doesn't become threatening until they're in their fifties or sixties.

How does atherosclerosis start?

It's a complex process. Exactly how atherosclerosis begins or what causes it isn't known, but some theories have been proposed.

Many scientists think atherosclerosis begins because the innermost layer of the artery becomes damaged. This layer is called the endothelium.

Three of the possible causes of damage to the arterial wall are:

1. elevated levels of cholesterol and triglyceride in the blood,
2. high blood pressure and
3. cigarette smoke. Cigarette smoke greatly aggravates and speeds up the growth of atherosclerosis in the coronary arteries, the aorta and arteries of the legs.

Because of the damage, over time fats, cholesterol, fibrin, platelets, cellular debris and calcium are deposited in the artery wall. These substances may stimulate the cells of the artery wall to produce still other substances that result in further accumulation of cells in the innermost layer of the artery wall where the atherosclerotic lesions form. These cells accumulate and many of them divide. At the same time, fat builds up within these cells and around them. They also form connective tissue.

The innermost layer of the artery becomes markedly thickened by these accumulating cells and surrounding material. If the wall is thickened sufficiently, the diameter of the artery will be reduced and the amount of blood decreased, thus decreasing the oxygen supply. If the oxygen supply to the heart muscle is reduced, a heart attack can occur. If the oxygen supply to the brain is cut off, a stroke can occur. And if the oxygen supply to the extremities occurs, gangrene can result.

Often a blood clot forms and blocks the artery, stopping the flow of blood.

What does the research show?

Scientists are studying other ways in which platelets may play a role in atherosclerosis. For example, they're involved in forming a group of substances called prostaglandins, one of which may damage arteries. They also contain a substance called "platelet growth factor," which can stimulate the growth of smooth muscle cells. These cells are normally present in the artery wall. But their abnormal growth and increase is believed to be one of the earliest events in the atherosclerosis process.

One of the more recent theories suggests that excess lipoproteins in the blood are trapped within the artery wall. When this happens and they accumulate, they become oxidized. That leads to "modified" lipoproteins which are rapidly taken up by smooth muscle cells. This, in turn, leads to the formation of foam cells that lead to the deposition of connective tissue cells and elements.