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Atherosclerosis - The fatal plug in your arteries

Almost every one of us has heard of, and known friends and relatives who have suffered from, angina, a heart attack, ischemic heart disease or a coronary. All of these conditions are due to disease of the coronary arteries that supply the muscle of the heart itself with blood, oxygen and nutrients so that it can work normally.

Atherosclerosis literally means "hardening of the arteries". It is a disease that causes thickening and stiffness of the wall of the artery, leading to serious consequences. In fact, OVER ONE HALF of ALL deaths in the US are a direct or indirect result of atherosclerosis, making it the single largest "killer disease" of them all. The basic abnormality in this condition is the formation of a "plaque" which is a thickened area on the inner lining of the blood vessel. This plaque or "atheroma" (derived from the Greek word for 'gruel') is composed of a porridge-like accumulation of fats and their compounds within a fibrous coat. 

Atherosclerosis affects medium and large sized arteries in the body. It most frequently affects the aorta (the largest blood vessel in the body), the coronary arteries, the cerebral arteries (which supply the brain) and sometimes arteries in the legs and abdomen. The involvement of the arteries is usually located at bifurcations - places where the artery branches into two. 

How is an atheroma formed ?

While the exact answer is not known, there are some parts of the puzzle that have been unravelled. According to the most popular theory - called the "Reaction to Injury hypothesis" - atherosclerosis is initiated by injury to the inner lining of the artery. The artery is lined by a single layer of cells called "endothelium", which may be damaged by a variety of insults including high blood pressure, increased concentration of fats in blood, toxins in cigarette smoke and many other factors. When the endothelium is damaged, it becomes leaky. Fats in the blood can seep through this leaky layer, and irritate the artery wall. Special types of blood cells called platelets and monocytes stick to these areas of injury and release chemical substances.

In response to this irritation by chemicals and fats, the muscle cells in the wall of the arteries move towards the inner lining, and begin to divide and increase in number. They also produce other substances which collect in the inner lining. The monocytes, in addition, imbibe fats from the blood and swell up in size. The result is the formation of an atheromatous plaque in the inner lining of the artery.

Why is an atheromatous plaque dangerous ?

An atheroma initially forms in the inner lining of the artery - a layer called the tunica intima. Over a period of time, it grows and begins to encroach upon the lumen or cavity of the artery. It thus makes the artery narrow. Since the volume of blood flow across a tube like an artery depends closely on the cross-sectional area of the tube, this narrowing causes a decrease in blood flow in the diseased artery. As a consequence, the part of the body supplied by that artery gets less blood and oxygen and nutrients than usual. For example, if a coronary artery is affected, the heart muscle gets less nourishment, and cannot perform it's work normally. 

On the other hand, if the plaque grows outwards away from the cavity of the artery, it weakens the wall of the artery by destroying the muscle layer in it. As a result, the artery wall cannot withstand the high pressure inside it, and it starts to dilate and become thin and stretched out - a condition called "aneurysm". This is dangerous because beyond a certain limit, the aneurysm will rupture due to the high pressure inside it.

And then there are complications of the plaque itself !

A long standing plaque will begin to deposit calcium within it, and this makes the artery extremely stiff and hard. Ulceration is a dangerous complication. The inner wall of an artery is normally very smooth and allows blood to flow without any friction in a stream-lined manner. When a plaque forms, it roughens the inner surface causing turbulence in blood flow. After some time, the lining of fibrous tissue over the plaque may be eroded by this turbulent flow, and the inner core of the plaque is exposed to the blood stream. When blood is exposed to this fatty core, it is stimulated to clot or harden, and this may cause the blood vessel to suddenly become totally blocked (thrombosis). When this happens in a coronary artery, there is a sudden decrease in blood flow to heart muscle which causes a heart attack (myocardial infarction).

What are the risk factors for atherosclerosis ?

While no one is quite sure why exactly some people develop atheromas at a very young age while others don't, there are some well defined risk factors that predispose to atheroma. Some of these factors are "permanent" - that is, they cannot be modified - and include age, gender and a history of atheroma in families. Older persons and males are at high risk, as are those whose family members suffer from atherosclerotic complications. In addition, there are some factors that can be modified by lifestyle changes, and include smoking, diabetes, high blood pressure and high serum cholesterol levels. Some "weak factors" that are less closely associated with atherosclerosis include lack of exercise, stress, obesity and a high carbohydrate diet. 

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