How does atherosclerosis begin?

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How does atherosclerosis begin?

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Dr. Michael DeBakey of the Baylor University states that no one knows precisely

how atherosclerosis begins or what triggers the process. Most Americans, members

of Western society, and to a varying extent members of other developed societies

have some degree of atherosclerosis by the time they reach adulthood.

 

In fact, autopsies performed on young American soldiers (in their twenties)

killed in the Korean War revealed some degree of atherosclerosis in their

arteries. By contrast, death due to atherosclerosis is uncommon in less

developed societies.

 

Dr. DeBakey states that the symptoms which signal atherosclerosis are related to

a number of factors, including the site where the artery is narrowing, how much

narrowing there is, and how fast it is developing.

 

If the artery's passage is being filled in over a period of time, causing only

minor slowing of the circulation, the body, by a remarkably adaptive mechanism,

develops alternative channels of blood flow around the obstructed site. These

channels, or new blood vessels, are called collateral vessels and can shunt

blood around the obstructed area so it reaches the vital organs and tissues.

 

Atherosclerosis was once thought to be a degenerative disorder, one in which the

body's parts simply wore out. However, this is not true.

 

Heart attacks now represent one of the major causes of death in men under age 40

in the United States. Further more, when you look at the arteries under a

microscope, you find that the changes which occur in the wall of the artery

initially are characterized by a growth of new cells, not by degeneration.

(Degeneration may occur later, however, after the wall of the blood vessel has

been severely damaged.)

 

Most researchers of atherosclerosis believe that something causes the protective

lining of the innermost layer of the artery (the endothelium) to be damaged,

thereby allowing toxic substances from the bloodstream to enter the artery wall.

These substances then build up, eventually causing the artery to narrow and be

blocked. The precise cause and nature of the original injury to the arterial

lining is not known.

 

One of the potential sources of damage to the arterial wall lining is a high

level of cholesterol and triglycerides in the blood.

 

These fats are transported in the blood by complex, spherical vehicles called

lipoproteins.

 

These fats have been proved dangerous in animal studies.

 

Another potential source of damage is high blood pressure . This phenomenon may

be explained by comparing the circulation in the human body to fluid in a pipe:

If fluid is forced through a pipe at a high pressure over a period of time,

there will be a greater degree of strain on the system of pipes (and on the

pump) than if the liquid flowed through at a low pressure.

 

A third possible cause of injury to the arterial wall lining is cigarette

smoking. The smoker breathes in carbon monoxide with the cigarette smoke, which

displaces some of the oxygen that should be carried in the blood.

 

This, then, could result in the lining of the arteries some distance from the

heart being deprived of oxygen as there would not be enough oxygen left in the

bloodstream to feed these distant arteries.

 

In addition, the nicotine contained in cigarette smoke can directly damage the

heart and blood vessels.

 

And, as if these were not enough reasons not to smoke, some individuals are

sensitive to tobacco smoke and have what appears to be an allergic reaction.

 

The " invisible " damage that results, revealed only years later, is believed to

be due to the formation of substances in the blood, called " immune complexes, "

that are provoked into existence by the tobacco smoke.

 

These substances are then deposited onto the artery wall, subsequently causing

injury to the cells that make up the wall's lining.

 

Once these cells are injured, they become dislodged from the artery wall,

exposing the tissue underneath.

 

This tissue, called collagen, now has direct contact with the bloodstream.

 

Collagen has a propensity for attracting and collecting certain cells from the

blood, called platelets. Platelets are intimately involved in the formation of

blood clots, and under normal circumstances we need them to help us stop

bleeding when we are cut or wounded.

 

However, when platelets, which are sticky cells, collect in great numbers at a

site where they are not wanted in an artery-they may lead to the formation of a

clot that blocks the artery and stops the normal flow of blood.

 

A blood clot in this way can cause a heart attack or stroke.

 

Other ways in which platelets may play a role in atherosclerosis are being

explored. For example, it is known that platelets are involved in the formation

of substances called prostaglandins, one of which may cause damage to the

arteries.

 

Platelets also contain a substance called " platelet growth factor " which can

stimulate the growth of smooth-muscle cells.

 

Although smooth muscle cells are normally present in the artery wall, their

growth and proliferation is believed to be one of the earliest events in the

development of atherosclerosis.

 

The significance of platelet growth factor substance in the development of

atherosclerosis in humans remains to be established, but much research is going

on in this field.

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