Progression of Atherosclerosis

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An artery is tough on the outside and smooth on the inside; it actually has three layers: an outer tissue layer, an elastic muscular middle that is very strong, and an inner layer of endothelial cells. The endothelium is very smooth so that blood can flow easily through the lumen (hollow vascular channel through which blood flows) with no obstacles in its path.

Interestingly, the process whereby we develop atherosclerosis begins while we are babies. Autopsy studies have shown that early vascular changes associated with atherosclerosis begin in infancy, and obvious fatty streaks are evident in the major arteries by early childhood. These changes occur in 50 percent of children between the ages of ten and fourteen years of age.

In time, these fatty streaks continue to grow, eventually collecting fatty debris, overgrown smooth muscle cells, and connective tissue within the wall of the blood vessel. These streaks and fibrous plaques form mainly at arterial stress areas, such as where an artery branches, or where a large vessel sharply curves. Although these fibrous plaques are plainly visible by the time we reach our twenties, blood flow is not significantly impaired until 60-70 percent of the lumen is obstructed.

While we still do not completely understand why debris begins to collect in blood vessels, we do know quite a bit about the ensuing inflammatory process. The central event in atherosclerosis appears to be an interruption of the normal function of endothelial cells lining blood vessels. More than just a protective covering, this layer is a very active player in blood vessel reaction and function. Numerous metabolic events take place within these cells every moment of the day.

In brief, the endothelium's job is to make sure blood flows smoothly, and when more blood is needed to an area, endothelial cells signal the underlying smooth muscle cells to contract or dilate as needed. Under normal conditions, the endothelium also controls blood viscosity (sluggishness), preventing it from coagulating within the lumen.

Once the lining of an artery is injured, cholesterol can enter the blood vessel wall where it is easily oxidized. Cholesterol is a waxy substance essential for functions throughout the body: it is used in cells for membrane repair, steroid synthesis, and other functions. Cell membranes contain a significant amount of this fatty substance, and the brain is especially rich in cholesterol. Like other fats, it cannot dissolve in blood, and must be transported to and from cells by special carriers called lipoproteins. However, oxidized cholesterol is very irritating, triggering an inflammatory response involving numerous chemicals and immune cells.

When this occurs, the wall of the blood vessel can attract specialized white blood cells called macrophages. Normally these cells slide right over the lining of the blood vessel, but when endothelial cells are not working properly, these immune cells can attach to the endothelium, enter, and interact with the oxidized cholesterol. A series of complex events is then triggered leading to a localized, intense inflammatory reaction. More white blood cells are drawn to the area of macrophage attachment, reacting as they would to a virus or other foreign body.

When infections occur, white blood cells flow to the site of an invasion and attempt to kill the invader by spraying it with a barrage of destructive free radicals. The same series of immunological events occurs along the lining of our blood vessels. Blood flowing past areas of intense inflammation causes LDL-cholesterol to enter the wall of the blood vessel. Another type of fatty molecule called HDL, or high-density lipoprotein, also carries cholesterol, but in general, it is removing cholesterol that has accumulated in the blood as a result of cell breakdown.

When LDL cholesterol enters the site of a macrophage attack, it too comes under attack by free radicals, and is oxidized, magnifying inflammation in the blood-vessel wall. In an effort to contain this irritation, the macrophages gobble up the oxidized LDL cholesterol and soon look like cells filled with foam—hence the apt designation, foam cell. As more oxidized cholesterol accumulates, the inflammatory reaction becomes more intense.

FIGURE 9.1 Cross-section of an artery showing the changes caused by atherosclerosis.

The oxidized cholesterol has induced an inflammatory response that produced a build-up of calcified fibrous tissue, partially obstructing the lumen.

FIGURE 9.1 Cross-section of an artery showing the changes caused by atherosclerosis.

The oxidized cholesterol has induced an inflammatory response that produced a build-up of calcified fibrous tissue, partially obstructing the lumen.




In an effort to contain the fire, the body attempts to wall off the inflamed area with scar tissue. The smooth muscle cells under the endothelium react by overgrowing, further aggravating the problem. The inflammation soon grows from a small fatty streak to a thick, crusty overgrowth that protrudes into the lumen. We call this thickened crud a plaque. In time, calcium can enter the plaque, further weakening the wall of the blood vessel.

Not infrequently, an ulcer crater forms in the center of the plaque. This can trigger clotting of the blood that is flowing by, resulting in either a sudden occlusion of the vessel, as occurs in a stroke or heart attack, or the clot can break free and travel to a smaller artery further down the line, causing an embolism. Sometimes a shower of emboli produce numerous smaller blood vessel occlusions. If this occurs in the carotid artery in the neck, this torrent of clots can enter the tiny arteries of the eye, resulting in a loss of vision on the side of the arterial plaque.

The ultimate cause of a heart attack or stroke is the development of unstable plaques, which either have roofs that rupture, spilling toxic fats into the blood vessel, or that are stripped of their endothelial lining. Both events cause blood clots to develop at the site. The crud itself rarely totally blocks off the artery.

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