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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