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arteriosclerosis

arteriosclerosis (ärtĬr´ēōsklərō´sis), general term for a condition characterized by thickening, hardening, and loss of elasticity of the walls of the blood vessels. These changes are frequently accompanied by accumulations inside the vessel walls of lipids, e.g., cholesterol; this condition is frequently referred to as atherosclerosis. Initially lesions are formed on the arterial walls, which results in blistering and the accumulation of low-density cholesterol. This produces higher blood pressure, which facilitates the imbedding of cholesterol and calcium in the vessel walls. The fatty material accumulates calcium and produces hard plaques, thus hardening the walls of the vessels. As the vessel walls thicken, the passageways through the vessels narrow, decreasing the blood supply to the affected region. Constriction of the coronary arteries may affect the heart (see coronary artery disease, heart disease). If the leg vessels are affected, there may be pain with walking and an onset of gangrene. When there is total clotting of a vessel (thrombosis) the result may be a heart attack (if it occurs in the coronary arteries) or stroke (if in cerebral arteries).

Arteriosclerosis risk factors include hypertension, elevated levels of fats in the blood, cigarette smoking, diabetes mellitus, and obesity. Genetic risks are related to the ability of the body to process (uptake and metabolize) low-density lipids that contain cholesterol. Reduction of body cholesterol to normal levels through cholesterol-lowering drugs and a restricted-fat diet is usually prescribed. The latter generally entails substitution of vegetable fats for animal fats, but an exception may be "trans fat," artificially hydrogenated vegetable oils found in margarine and vegetable shortening, which studies have linked to increased risk of coronary disease. Treatment of hypertension, stress management, and cessation of smoking are also important. Increasing consumption of antioxidants and folic acid may be protective. Surgical treatment that bypasses clogged areas or procedures such as angioplasty are sometimes necessary; gene therapy that forces the growth of new blood vessels bypassing an area has also been used. Exercise often can increase utilization of excess low-density lipids. Although the relationship between blood cholesterol levels and arteriosclerosis is not fully understood, the utilization of low-density lipids appears to be a primary indicator of the risk of arteriosclerosis.

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Arteriosclerosis

Arteriosclerosis

The term arteriosclerosis is used to describe several cardiovascular diseases, including those involving the blood vessels. In this instance, the arteries become hardened and blood vessels lose their "elastic" effect. Arteriosclerosis can begin in early childhood.

The primary risk factors for arteriosclerosis include hypertension (high blood pressure ), diabetes mellitus, smoking, and obesity . All of these risk factors are preventable by exercising regularly, smoking cessation, eating at least five servings of fruits and vegetables daily, and through proper stress management.

Two types of arteriosclerosis include Monckeberg's arteriosclerosis, which usually involves restricted movement of the lower extremities, and arteriolar sclerosis, which can lead to decreased vision and peripheral vascular disease. Signs and symptoms of arteriosclerosis include high blood pressure, multiple kidney infections, and poor circulation in the toes and fingers.

see also Atherosclerosis; Cardiovascular Diseases; Heart Disease.

Teresa A. Lyles

Bibliography

Insel, P. M., and Roth, W. T. (2003). "Cardiovascular Disease and Cancer." In Core Concepts in Health, brief 9th edition. New York: McGraw-Hill

Internet Resources

Well-Net/Health Education Associates. "Arteriosclerosis." Available from <http://www.well-net.com/cardiov>

Health with Nutrition. "Arteriosclerosis/Atherosclerosis." Available from <http://www.healingwithnutrition.com>

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arteriosclerosis

arteriosclerosis Blanket term for degenerative diseases of the arteries, in particular atherosclerosis (hardening of the arteries). It is caused by deposits of fatty materials and scar tissue on the artery walls, which narrow the channel and restrict blood flow, causing an increased risk of heart disease, stroke, or gangrene. Evidence suggests that predisposition to the disease is hereditary. Risk factors include cigarette smoking, inactivity, obesity, and a diet rich in animal fats and refined sugar. Treatment is by drugs and, in some cases, surgery to replace a diseased length of artery.

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arteriosclerosis

ar·te·ri·o·scle·ro·sis / ärˌti(ə)rēōskləˈrōsis/ • n. Med. the thickening and hardening of the walls of the arteries, occurring typically in old age. DERIVATIVES: ar·te·ri·o·scle·rot·ic / -ˈrätik/ adj.

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arteriosclerosis

arteriosclerosis Thickening and calcification of the arterial walls, leading to loss of elasticity, occurring with ageing and especially in hypertension. See also atheroma; atherosclerosis.

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arteriosclerosis

arteriosclerosis (ar-teer-i-oh-skleer-oh-sis) n. any of several conditions affecting the arteries, especially atherosclerosis.

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Arteriosclerosis

Arteriosclerosis

The cause of atherosclerosis

How plaques form

Diagnosis and treatment

Prevention

Resources

Arteriosclerosis is a common arterial disease that involves areas of plaques forming on the inside of arteries, which restrict, or stop, normal blood flow. The word arteriosclerosis literally means hardening of the arteries. As people age, their blood vessel walls naturally grow a bit stiffer and harder, with less flexibility. A common complication of arteriosclerosis is called atherosclerosis. In this condition, plaques (hardened masses composed of lipids, dead cells, fibrous tissue, and platelets) collect in the arteries. If a plaque grows large enough, it can block the flow of blood through the artery. If this blockage is severe, it can lead to stroke. A stroke occurs when an artery in the brain becomes blocked, depriving an area of the brain of oxygen. Similarly, a heart attack occurs when a blocked coronary artery deprives the heart muscle of oxygen. Damage to either the brain or heart occurs when areas of oxygen-deprived tissue die. A severe complication of atherosclerosis occurs when a piece of the plaque breaks off and migrates through the artery to other sites. This bit of circulating plaque is called an embolism. An embolism causes damage by blocking blood flow at its destination, resulting in oxygen-deprived tissue and tissue death.

Since atherosclerosis causes strokes and heart attacks, it is considered one of the leading causes of illness and death in the United States. Arteriosclerosis has been linked to high blood cholesterol levels, lack of exercise, and smoking. Cholesterol is a substance that is similar to fat and is found in fatty foods. Although a diet low in cholesterol and fat can reduce the risk of atherosclerosis, some people have a genetic predisposition to high cholesterol levels. Even on normal or low fat diets, these individuals still have high cholesterol (hypercholesterolemia), and therefore a high risk of developing atherosclerosis. Researchers are currently working on ways to help people with hypercholesteremia lower their cholesterol levels. For now, lowering cholesterol is achieved through diet and some drug therapies. In the future, it is hoped that a bioengineered gene that makes a cholesterol-neutralizing protein can be implanted into hypercholesteremia patients.

The cause of atherosclerosis

Atherosclerosis means hardening of a paste-like, fatty material. This pasty, fatty material develops within arteries over a period of many years. If the condition is not treated, this material will eventually harden into atherosclerotic plaques.

Although researchers continue to speculate about how and why this fatty material gets into arteries, a consensus has emerged in the last 25 years that points to injury of the artery walls as the underlying cause of atherosclerosis. This injury can be mechanical, such as an artery that has been nicked or cut in some way. Injury can also be in the form of exposure to various agents, such as toxins (including cigarette smoke), viruses, or cholesterol. When the artery wall is injured, it tries to heal itself. The response of the artery cells and the immune system to the injury leads, paradoxically, to the formation of plaques.

How plaques form

Interestingly, all middle-aged and older people have some form of arteriosclerosis. In fact, some experts consider arteriosclerosis part of the normal wear and tear of aging arteries. Most people will not progress beyond arteriosclerosis to atherosclerosis. In some people, however, such as those with hypercholesteremia or people with high-cholesterol diets, hardened plaques form that block the arteries.

Researchers have formed the injury model of atherosclerosis by studying the arteries of people of all ages. In infants, for instance, a fatty streak consisting of lipids and immune cells is present in the innermost layer of arteries. Lipids are molecules found in cholesterol. Even at this young age, the arteries are already responding to injury, most likely the presence of cholesterol.

In teenagers and young adults at high risk for atherosclerosis, layers of macrophages (special white cells that ingest foreign material) and smooth muscle cells overlie the interior wall of arteries. In an attempt to reduce the amount of lipid within the artery, macrophages ingest the lipid. Because under a microscope the lipid within the macrophage appears to be bubbly, or foamy, a macrophage that has ingested lipid is called a foam cell.

As time passes, more and more macrophages ingest more and more lipid, and more foam cells are present within the artery. To rid the artery of the ever increasing load of lipid, foam cells migrate through the artery wall to return the lipid to the liver, spleen, and lymph nodes. As the foam cells penetrate the artery walls, they further injure the artery. This injury attracts platelets, special components of the blood that lead to the formation of blood clots. When one cuts a finger, platelets rush to the site of injury and begin forming a clot to stop the flow of blood. In an artery, platelets also rush to the site of injury and begin the process of clot formation. But instead of helping the situation, the clot further complicates the growing plaque in the artery, which at this point consists of lipid-laden macrophages, lipids, muscle cells, and platelets.

The platelets, in turn, release chemicals called growth factors. Several different growth factors are released by the platelets. One causes the cells in the artery to release proteins and other substances that eventually lead to the formation of a matrix, a collection of tough protein fibers, which further hardens the artery. Another growth factor prompts the development of blood vessels in the plaque. At this stage, the plaque is fully formed. It is large enough to block the flow of blood through the artery. At its center is a pool of lipid and dead artery cells, and it is covered by a cap of connective tissue.

Diagnosis and treatment

Most people are unaware of the atherosclerotic process going on in their arteries. The condition usually goes undiagnosed until a person develops symptoms of blood vessel obstruction, such as the heart pain called angina. Angina is a warning sign that the atherosclerosis may become life-threatening. People with angina take medication and are usually monitored by physicians to make sure the arteries do not become completely blocked. Some angina patients are able to slow or halt the progression of atherosclerosis with proper diet and lifestyle changes, such as quitting smoking.

The atherosclerotic plaques can be visualized by a special x-ray technique. A slim tube called a catheter is inserted through an artery in the leg or other location until it reaches the plaque site. Dye that can be seen on x-rays is shot through the catheter. When an x-ray of the site is taken, the plaque can be clearly seen.

Currently, atherosclerosis in the arteries of the heart is treated with drugs, surgery, or a technique called angioplasty. Like the x-ray technique, angioplasty involves inserting a catheter through an artery. Instead of shooting dye through the catheter, the catheter is used like a plumbers snake (a roto-rooter) to open up the narrowed arteries. Some researchers have used anti-clotting drugs delivered through the catheter to dissolve clots.

Surgery is also used to treat atherosclerotic obstruction of the hearts arteries. Bypass surgery in which a section of an artery in the leg is used to bypass a section of a blocked coronary artery, can allow the heart muscle to again receive adequate oxygen. Because this surgery carries a risk of stroke and other serious complications, angioplasty and drug therapy, in conjunction with diet management, are tried first. If no positive results are found, surgery is performed as a last resort.

One problem with angioplasty is that the solution is often only temporary. The plaques return because angioplasty addresses only the plaques, not the process that leads to their formation. In the future, molecules that target the growth factors released by the platelets may be delivered directly to the plaques through special catheters. This treatment is some years away.

Prevention

Because atherosclerosis may be the result of the arterys response to cholesterol, it makes sense to reduce the intake of cholesterol. Two types of cholesterol are found in foods: cholesterol that contains high density lipoprotein (the HDLs, or good cholesterol) and cholesterol that contains low density lipoprotein (the LDLs, or bad cholesterol). Researchers have found that LDL cholesterol is the culprit in atherosclerosis.

To keep the arteries healthy, individuals should eat no more than 300 milligrams (mg) of cholesterol a day. Cholesterol is found only in animal products; plant foods contain no cholesterol. Since many foods that are high in fat are also high in cholesterol, limiting fat intake can help reduce cholesterol levels. Knowing which foods are high in cholesterol and avoiding these foods (or limiting these foods) can also lower cholesterol. People should have their blood cholesterol

KEY TERMS

Angina Warning pain that signals the progressive worsening of atherosclerosis in heart arteries.

Angioplasty A technique in which a catheter is introduced into an artery narrowed by atherosclerosis in order to widen the artery.

Arteriosclerosis Hardening and thickening of artery walls.

Atherosclerosis Abnormal narrowing of the arteries of the body that generally originates from the buildup of fatty plaque on the artery wall.

Cholesterol A fat-like substance that contains lipids; found in animal products.

Embolism A piece of an arteriosclerotic plaque that breaks off and lodges in a distant artery.

Fatty streak The first stage in atherosclerosis; consists of lipid, macrophages, and immune cells.

Foam cell A macrophage that has ingested lipid.

Hypercholesteremia A genetic condition in which the body accumulates high levels of cholesterol.

Lipid A molecule that is a component of fats and cholesterol.

Macrophages Special white blood cells that ingest foreign substances or materials such as lipids.

Plaque A mass of lipid, fibrous tissue, dead cells, and platelets that collects within the artery; plaques can harden and become so large that they block the flow of blood through the artery.

Platelets Special component of blood that contributes to clot formation.

levels checked periodically, particularly if there is a family history of arteriosclerosis. Those with hypercholesteremia or a history of heart disease may want to try a stricter diet that eliminates all fats and cholesterol. Before embarking on any major dietary change, however, consult a physician.

Arteriosclerosis can be successfully treated but not cured. Recent clinical studies have shown that atherosclerosis can be delayed, stopped, and even reversed by aggressively lowering cholesterol. New diagnostic techniques enable physicians to identify and treat atherosclerosis in its earliest stages. New technologies and surgical procedures have extended the lives of many patients who would otherwise have died.

See also Circulatory system.

Resources

BOOKS

Betteridge, D.J., and J.M. Morrell. Clinicians Guide to Lipids and Coronary heart Disease. London, UK: Oxford University Press, 2003.

Debry, Gerard. Dietary Proteins and Atherosclerosis. Boca Raton, FL: CRC Press, 2004.

Drew, Angela F., ed. Atherosclerosis: Experimental Methods and Protocols. Totowa, NJ: Humana Press, 2001.

Eckardstein, Arnold von, ed. Atherosclerosis: Diet and Drugs. Berlin, Germany: Springer, 2005.

Tonkin, Andrew M., ed. Atherosclerosis and Heart Disease. London, UK: Martin Dunitz, 2003.

PERIODICALS

Warding Off Atherosclerosis. The Lancet v361, i9365 (April 12, 2003).

Kathleen Scogna

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Arteriosclerosis

Arteriosclerosis

Arteriosclerosis literally means "hardening of the arteries." As people age, their blood vessel walls naturally grow a bit stiffer and harder, with less flexibility. A common complication of arteriosclerosis is called atherosclerosis. In this condition, plaques (hardened masses composed of lipids, dead cells, fibrous tissue , and platelets) collect in the arteries . If a plaque grows large enough, it can block the flow of blood through the artery. If this blockage is severe, it can lead to stroke . A stroke occurs when an artery in the brain becomes blocked, depriving an area of the brain of oxygen . Similarly, a heart attack occurs when a blocked coronary artery deprives the heart muscle of oxygen. Damage to either the brain or heart occurs when areas of oxygen-deprived tissue die. A severe complication of atherosclerosis occurs when a piece of the plaque breaks off and migrates through the artery to other sites. This bit of circulating plaque is called an embolism . An embolism causes damage by blocking blood flow at its destination, resulting in oxygen-deprived tissue and tissue death.

Since atherosclerosis causes strokes and heart attacks, it is considered one of the leading causes of illness and death in the United States. Arteriosclerosis has been linked to high blood cholesterol levels, lack of exercise , and smoking. Cholesterol is a substance that is similar to fat and is found in fatty foods. Although a diet low in cholesterol and fat can reduce the risk of atherosclerosis, some people have a genetic predisposition to high cholesterol levels. Even on normal or low fat diets, these individuals still have high cholesterol (hypercholesterolemia), and therefore a high risk of developing atherosclerosis. Researchers are currently working on ways to help people with hypercholesteremia lower their cholesterol levels. For now, lowering cholesterol is achieved through diet and some drug therapies. In the future, it is hoped that a bioengineered gene that makes a cholesterol-neutralizing protein can be implanted into hypercholesteremia patients.


The cause of atherosclerosis

Atherosclerosis means "hardening of a paste-like, fatty material." This pasty, fatty material develops within arteries over a period of many years. If the condition is not treated, this material will eventually harden into atherosclerotic plaques.

Although researchers continue to speculate about how and why this fatty material gets into arteries, a consensus




has emerged in the last 20 years that points to injury of the artery walls as the underlying cause of atherosclerosis. This injury can be mechanical, such as an artery that has been nicked or cut in some way. Injury can also be in the form of exposure to various agents, such as toxins (including cigarette smoke ), viruses, or cholesterol. When the artery wall is injured, it tries to heal itself. The response of the artery cells and the immune system to the injury leads, paradoxically, to the formation of plaques.


How plaques form

Interestingly, all middle-aged and older people have some form of arteriosclerosis. In fact, some experts consider arteriosclerosis part of the normal wear and tear of aging arteries. Most people will not progress beyond arteriosclerosis to atherosclerosis. In some people, however, such as those with hypercholesteremia or people with high-cholesterol diets, hardened plaques form that block the arteries.

Researchers have formed the injury model of atherosclerosis by studying the arteries of people of all ages. In infants, for instance, a "fatty streak" consisting of lipids and immune cells is present in the innermost layer of arteries. Lipids are molecules found in cholesterol. Even at this young age, the arteries are already responding to injury, most likely the presence of cholesterol.

In teenagers and young adults at high risk for atherosclerosis, layers of macrophages (special white cells that ingest foreign material) and smooth muscle cells overlie the interior wall of arteries. In an attempt to reduce the amount of lipid within the artery, macrophages ingest the lipid. Because under a microscope the lipid within the macrophage appears to be "bubbly," or foamy, a macrophage that has ingested lipid is called a foam cell .

As time passes, more and more macrophages ingest more and more lipid, and more foam cells are present within the artery. To rid the artery of the ever increasing load of lipid, foam cells migrate through the artery wall to return the lipid to the liver, spleen, and lymph nodes. As the foam cells penetrate the artery walls, they further injure the artery. This injury attracts platelets, special components of the blood that lead to the formation of blood clots. When you cut your finger, platelets rush to the site of injury and begin forming a clot to stop the flow of blood. In an artery, platelets also rush to the site of injury and begin the process of clot formation. But instead of helping the situation, the clot further complicates the growing plaque in the artery, which at this point consists of lipid-laden macrophages, lipids, muscle cells, and platelets.

The platelets, in turn, release chemicals called growth factors. Several different growth factors are released by the platelets. One causes the cells in the artery to release proteins and other substances that eventually lead to the formation of a matrix, a collection of tough protein fibers, that further hardens the artery. Another growth factor prompts the development of blood vessels in the plaque. At this stage, the plaque is fully formed. It is large enough to block the flow of blood through the artery. At its center is a pool of lipid and dead artery cells, and it is covered by a cap of connective tissue .


Diagnosis and treatment

Most people are unaware of the atherosclerotic process going on in their arteries. The condition usually goes undiagnosed until a person develops symptoms of blood vessel obstruction, such as the heart pain called angina. Angina is a warning sign that the atherosclerosis may become life-threatening. People with angina take medication and are usually monitored by physicians to make sure the arteries do not become completely blocked. Some angina patients are able to slow or halt the progression of atherosclerosis with proper diet and lifestyle changes, such as quitting smoking.

The atherosclerotic plaques can be visualized by a special x-ray technique. A slim tube called a catheter is inserted through an artery in the leg or other location until it reaches the plaque site. Dye that can be seen on x rays is shot through the catheter. When an x ray of the site is taken, the plaque can be clearly seen.

Currently, atherosclerosis in the arteries of the heart is treated with drugs, surgery , or a technique called angioplasty. Like the x-ray technique, angioplasty involves inserting a catheter through an artery. Instead of shooting dye through the catheter, the catheter is used as a "roto rooter" to open up the narrowed arteries. Some researchers have used anti-clotting drugs delivered through the catheter to dissolve clots.

Surgery is also used to treat atherosclerotic obstruction of he heart's arteries. Bypass surgery in which a section of an artery in the leg is used to "bypass" a section of a blocked coronary artery, can allow the heart muscle to again receive adequate oxygen. Because this surgery carries a risk of stroke and other serious complications, angioplasty and drug therapy, in conjunction with diet management, are tried first. If no positive results are found, surgery is performed as a last resort.

One problem with angioplasty is that the solution is often only temporary. The plaques return because angioplasty addresses only the plaques, not the process that leads to their formation. In the future, molecules that target the growth factors released by the platelets may be delivered directly to the plaques through special catheters . This treatment is some years away.


Prevention

Because atherosclerosis may be the result of the artery's response to cholesterol, it makes sense to reduce the intake of cholesterol. Two types of cholesterol are found in foods: cholesterol that contains high density lipoprotein (the HDLs) and cholesterol that contains low density lipoprotein (the LDLs). Researchers have found that LDL cholesterol is the culprit in atherosclerosis.

To keep the arteries healthy, individuals should eat no more than 300 mg of cholesterol a day. Cholesterol is found only in animal products; plant foods contain no cholesterol. Since many foods that are high in fat are also high in cholesterol, limiting fat intake can help reduce cholesterol levels. Knowing which foods are high in cholesterol and avoiding these foods (or limiting these foods) can also lower cholesterol. People should have their blood cholesterol levels checked periodically, particularly if there is a family history of arteriosclerosis. Those with hypercholesteremia or a history of heart disease may want to try a stricter diet that eliminates all fats and cholesterol. Before embarking on any major dietary change, however, consult your physician.

See also Circulatory system.


Resources

books

Acierno, Louis J. The History of Cardiology. New York: Parthenon Publishing Group, 1994.

Filer, Lloyd J. Jr., Ronald M. Lauer, and Russell L. Leupker, eds. Prevention of Atherosclerosis and Hypertension Beginning in Youth. Philadelphia: Lea and Febiger, 1994.

Fuster, Valentin, ed. Progression-Regression of Atherogenesis: Molecular, Cellular, and Clinical Bases. Dallas: American Heart Association, 1992.

Yeagle, Philip. Understanding Your Cholesterol. San Diego: Academic Press, 1991.


periodicals

Ross, Russell. "The Pathenogenesis of Atherosclerosis: A Perspective for the 1990s." Nature 362 (April 29, 1993): 801+.

Tunis, Sean R., et al. "The Use of Angioplasty, Bypass Surgery, and Amputation in the Treatment of Peripheral Vascular Diseases." New England Journal of Medicine 325, no. 8 (August 22, 1991): 556.

"Warding Off Artherosclerosis." The Lancet v361, i9365 (April 12, 2003).


Kathleen Scogna

KEY TERMS

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Angina

—Warning pain that signals the progressive worsening of atherosclerosis in heart arteries.

Angioplasty

—A technique in which a catheter is introduced into an artery narrowed by atherosclerosis in order to widen the artery.

Arteriosclerosis

—Hardening and thickening of artery walls.

Atherosclerosis

—Abnormal narrowing of the arteries of the body that generally originates from the buildup of fatty plaque on the artery wall.

Cholesterol

—A fat-like substance that contains lipids; found in animal products.

Embolism

—A piece of an arteriosclerotic plaque that breaks off and lodges in a distant artery.

Fatty streak

—The first stage in atherosclerosis; consists of lipid, macrophages, and immune cells.

Foam cell

—A macrophage that has ingested lipid.

Hypercholesteremia

—A genetic condition in which the body accumulates high levels of cholesterol.

Lipid

—A molecule that is a component of fats and cholesterol.

Macrophages

—Special white blood cells that ingest foreign substances or materials such as lipids.

Plaque

—A mass of lipid, fibrous tissue, dead cells, and platelets that collects within the artery; plaques can harden and become so large that they block the flow of blood through the artery.

Platelets

—Special component of blood that contributes to clot formation.

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