Coronary Artery Disease

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Information on Coronary Artery Disease

Coronary artery disease (CAD) accounts for over 600,000 deaths per year and for almost a third of all deaths occurring between the ages of 35 and 65. Since the coronary arteries supply blood to the heart, CAD may be understood as a "supply and demand" problem. When the blood flows through the coronary arteries to heart muscle falls below critical levels, or when demands on the heart increase beyond the available flow, the heart muscle cells do not get enough oxygen to do their job of pumping. This "decreased flow in relation to demand" may cause warning symptoms that range from chest pain to abnormalities of heart rhythm; sometimes the first, and last, warning symptoms of decreased blood flow is a massive and fatal heart attack. Often, reversible symptoms precede the permanent damage of a heart attack. These reversible changes are usually due to ischemia, a temporarily decreased blood supply usually due to obstructed blood flow. The characteristic response of any muscle to inadequate blood supply is pain; when the heart muscle is so deprived, the resulting pain is known as angina. When the blood flow falls to a critical level in relation to a given demand, the muscle tissue affected may be permanently and irreversibly damaged or "killed"; this event is known as an infarction of the muscle tissue, and in the case of the heart as a myocardial infarction or heart attack. The term coronary thrombosis or simply coronary is often used to describe this irreversible event because a blood clot, or thrombosis, in one or more coronary arteries is usually the cause of the blocked blood flow that leads to infarction.

In short, coronary artery disease is a continuum of disease that ranges from insignificant symptoms to an infarction large enough to cause death. And in recent years, scientists have discovered a great deal about atherosclerosis, the underlying process which causes progressive narrowing of the coronary arteries.

In a normal artery, blood is strictly confined to the lumen (the central channel through which blood flows) by a smooth lining of flattened cells which are tightly joined to each other. When kept in good repair, this lining, called the endothelium, permits blood to flow without sludging or clotting. Surrounding the lining is a relatively thin sheath of muscle cells.

The earliest change in atherosclerosis is believed to be the formation of fatty streaks along the inner lining of the artery. These streaks are largely composed of cholesterol that is deposited in and around muscle cells next to the lining. At a later stage, plaques begin to form and protrude into the channel. These plaques are made up of an overgrowth of newly formed muscle cells that become engorged with cholesterol. As plaques spread and thicken, they eventually make the artery wall so rigid that it can no longer dilate or contract in response to changing needs for blood. Also, the inner wall becomes roughened, and blood may begin to clot in reaction to the irregular surface. The eventual result is a narrowed artery.

What makes the artery's muscle cells start to overgrow? Answering this question has been extremely difficult because the earliest stages of atherosclerosis are hard to observe in animals and virtually impossible to study in people. But a consensus is emerging that some kind of damage to the endothelial lining cells of the artery is the first event. For example, a frequent cause of such damage may simply be wear and tear by excessively rapid or turbulent flow of blood in a particular area; thus high blood pressure may lead to atherosclerosis in part by increasing stress on the linings of major blood vessels.

Once the lining cells are damaged, blood penetrates into the arterial wall, which normally is shielded from direct exposure to the bloodstream. When this happen, at least two constituents of blood appear to harm the muscle cells in the wall, namely; platelets and low-density lipoprotein cholesterol (LDL-cholesterol).

Platelets are cell fragments that circulate in the bloodstream. They are, in effect, little bags of chemicals that initiate the clotting of blood. Platelets ordinarily do not stick to each other or to blood vessel walls, but when the endothelium is damaged, they gather in the area of injury. Once there, they stick to the injured surface and begin to release their chemicals, among them thromboxane, which stimulate other platelets to aggregate in the same neighborhood. Some very recent research indicates that while producing thromboxane, platelets manufacture a by-product which combines with LDL-cholesterol and changes its chemical nature in ways that make it very damaging to the artery's muscle cells.

LDL-cholesterol is a term for cholesterol attached to a complex protein (low-density lipoprotein). When LDL is modified by the platelet by-product, the resulting protein-cholesterol complex is chemically altered so that the muscle cells take it up very avidly. Unfortunately, once the cells have ingested cholesterol, they can dispose of it only very slowly. Consequently, cholesterol accumulates and the cell begins to bloat with accumulated fat. The more LDL-cholesterol there is in the blood, the more rapidly this process takes place.

At the same time that the platelets are releasing the substance that modifies LD-cholesterol, they also seem to release a factor that stimulates the muscle cells to proliferate. Thus, when part of an artery's lining is damaged, the underlying muscle cells are exposed to two abnormal influences: one stimulus to increase their numbers and another stimulus to gorge themselves on cholesterol. The result is a plaque, which now deforms the arterial wall and thus, presumably, creates additional turbulence in the flow of blood and even further damage to the artery's lining.

The above is but one model, rather neat in explaining many features of atherosclerosis. The story is undoubtedly more complex. But even though we do not yet know the exact chemistry of atherosclerosis, we can attempt to modify its progression by eliminating risk factors that have been shown by long-term studies to be associated with CAD. The list of possible risk factors is long, with new suggestions added every year, but the following summarizes the most important information as it now stands:

(a) Almost all experts agree that cigarette smoking, high blood pressure, and elevated cholesterol levels are the "big three" risk factors. And even though there is no final proof that reducing or eliminating these risk factors will decrease the incidence of heart attacks, most experts anticipate that conclusive evidence will eventually emerge. In fact, many believe that attention to these risk factors by large numbers of people (particularly males) accounts for the recent reversal of heart attack death rates.

(b) The "big news" of recent years has been the rediscovery of the apparently protective role of HDL (high-density lipoprotein), one of the five major fractions of cholesterol-containing lipid in the blood. This has been so convincingly established in the minds of some experts that they are recommending the measurement of HDL along with, or even in place of, the total cholesterol concentration. As a practical matter, strenuous exercise and a decreased intake of saturated fats seem to correlate with an increase in this protective cholesterol fraction. Much remains to be learned about HDL, but there seems to be little doubt that, unlike other cholesterol fractions, more is better.

 

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