Atherosclerosis - The fatal plug in
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
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