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Atherosclerosis is the build up of a waxy plaque on the inside of blood vessels. In Greek, athere means gruel, and skleros means hard. Atherosclerosis is often called arteriosclerosis. Arteriosclerosis (from the Greek arteria, meaning artery) is a general term for hardening of the arteries. Arteriosclerosis can occur in several forms, including atherosclerosis.


Atherosclerosis, a progressive process responsible for most heart disease, is a type of arteriosclerosis or hardening of the arteries. An artery is made up of several layers: an inner lining called the endothelium, an elastic membrane that allows the artery to expand and contract, a layer of smooth muscle, and a layer of connective tissue. Arteriosclerosis is a broad term that includes a hardening of the inner and middle layers of the artery. It can be caused by normal aging, by high blood pressure, and by diseases such as diabetes. Atherosclerosis is a type of arteriosclerosis that affects only the inner lining of an artery. It is characterized by plaque deposits that block the flow of blood.
Plaque is made of fatty substances, cholesterol, waste products from the cells, calcium, and fibrin, a stringy material that helps clot blood. The plaque formation process stimulates the cells of the artery wall to produce substances that accumulate in the inner layer. Fat builds up within these cells and around them, and they form connective tissue and calcium. The inner layer of the artery wall thickens, the artery's diameter is reduced, and blood flow and oxygen delivery are decreased. Plaques can rupture or crack open, causing the sudden formation of a blood clot (thrombosis). Atherosclerosis can cause a heart attack if it completely blocks the blood flow in the heart (coronary) arteries. It can cause a stroke if it completely blocks the brain (carotid) arteries. Atherosclerosis can also occur in the arteries of the neck, kidneys, thighs, and arms, causing kidney failure or gangrene and amputation.

Causes and symptoms

Atherosclerosis can begin in the late teens, but it usually takes decades to cause symptoms. Some people experience rapidly progressing atherosclerosis during their thirties, others during their fifties or sixties. Atherosclerosis is complex. Its exact cause is still unknown. It is thought that atherosclerosis is caused by a response to damage to the endothelium from high cholesterol, high blood pressure, and cigarette smoking. A person who has all three of these risk factors is eight times more likely to develop atherosclerosis than is a person who has none. Physical inactivity, diabetes, and obesity are also risk factors for atherosclerosis. High levels of the amino acid homocysteine and abnormal levels of protein-coated fats called lipoproteins also raise the risk of coronary artery disease. These substances are the targets of much current research. The role of triglycerides, another fat that circulates in the blood, in forming atherosclerotic plaques is unclear. High levels of triglycerides are often associated with diabetes, obesity, and low levels of high-density lipoproteins (HDL cholesterol). The more HDL ("good") cholesterol, in the blood, the less likely is coronary artery disease. These risk factors are all modifiable. Non-modifiable risk factors are heredity, sex, and age.
Risk factors that can be changed:
  • Cigarette/tobacco smoke-Smoking increases both the chance of developing atherosclerosis and the chance of dying from coronary heart disease. Second hand smoke may also increase risk.
  • High blood cholesterol-Cholesterol, a soft, waxy substance, comes from foods such as meat, eggs, and other animal products and is produced in the liver. Age, sex, heredity, and diet affect cholesterol. Total blood cholesterol is considered high at levels above 240 mg/dL and borderline at 200-239 mg/dL. High-risk levels of low-density lipoprotein (LDL cholesterol) begin at 130-159 mg/dL.
  • High triglycerides-Most fat in food and in the body takes the form of triglycerides. Blood triglyceride levels above 400 mg/dL have been linked to coronary artery disease in some people. Triglycerides, however, are not nearly as harmful as LDL cholesterol.
  • High blood pressure-Blood pressure of 140 over 90 or higher makes the heart work harder, and over time, both weakens the heart and harms the arteries.
  • Physical inactivity-Lack of exercise increases the risk of atherosclerosis.
  • Diabetes mellitus-The risk of developing atherosclerosis is seriously increased for diabetics and can be lowered by keeping diabetes under control. Most diabetics die from heart attacks caused by atherosclerosis.
  • Obesity-Excess weight increases the strain on the heart and increases the risk of developing atherosclerosis even if no other risk factors are present.
Risk factors that cannot be changed:
  • Heredity-People whose parents have coronary artery disease, atherosclerosis, or stroke at an early
    The progression of atherosclerosis.
    The progression of atherosclerosis.
    (Illustration by Hans & Cassady.)
    age are at increased risk. The high rate of severe hypertension among African-Americans puts them at increased risk.
  • Sex-Before age 60, men are more likely to have heart attacks than women are. After age 60, the risk is equal among men and women.
  • Age-Risk is higher in men who are 45 years of age and older and women who are 55 years of age and older.
Symptoms differ depending upon the location of the atherosclerosis.
  • In the coronary (heart) arteries: Chest pain, heart attack, or sudden death.
  • In the carotid (brain) arteries: Sudden dizziness, weakness, loss of speech, or blindness.
  • In the femoral (leg) arteries: Disease of the blood vessels in the outer parts of the body (peripheral vascular disease) causes cramping and fatigue in the calves when walking.
  • In the renal (kidney) arteries: High blood pressure that is difficult to treat.


Physicians may be able to make a diagnosis of atherosclerosis during a physical exam by means of a stethoscope and gentle probing of the arteries with the hand (palpation). More definite tests are electrocardiography, echocardiography or ultrasonography of the arteries (for example, the carotids), radionuclide scans, and angiography.
An electrocardiogram shows the heart's activity. Electrodes covered with conducting jelly are placed on the patient's body. They send impulses of the heart to a recorder. The test takes about 10 minutes and is performed in a physician's office. Exercise electrocardiography (stress test) is conducted while the patient exercises on a treadmill or a stationary bike. It is performed in a physician's office or an exercise laboratory and takes 15-30 minutes.
Echocardiography, cardiac ultrasound, uses sound waves to create an image of the heart's chambers and valves. A technician applies gel to a hand-held transducer, presses it against the patient's chest, and images are displayed on a monitor. This technique cannot evaluate the coronary arteries directly. They are too small and are in motion with the heart. Severe coronary artery disease, however, may cause abnormal heart motion that is detected by echocardiography. Performed in a cardiology outpatient diagnostic laboratory, the test takes 30-60 minutes. Ultrasonography is also used to assess arteries of the neck and thighs.
Radionuclide angiography and thallium (or sestamibi) scanning enable physicians to see the blood flow through the coronary arteries and the heart chambers. Radioactive material is injected into the bloodstream. A device that uses gamma rays to produce an image of the radioactive material (gamma camera) records pictures of the heart. Radionuclide angiography is usually performed in a hospital's nuclear medicine department and takes 30-60 minutes. Thallium scanning is usually done after an exercise stress test or after injection of a vasodilator, a drug to enlarge the blood vessels, like dipyridamole (Persantine). Thallium is injected, and the scan is done then and again four hours (and possibly 24 hours) later. Thallium scanning is usually performed in a hospital's nuclear medicine department. Each scan takes 30-60 minutes.
Coronary angiography is the most accurate diagnostic method and the only one that requires entering the body (invasive procedure). A cardiologist inserts a catheter equipped with a viewing device into a blood vessel in the leg or arm and guides it into the heart. The patient has been given a contrast dye that makes the heart visible to x rays. Motion pictures are taken of the contrast dye flowing though the arteries. Plaques and blockages, if present, are well defined. The patient is awake but has been given a sedative. Coronary angiography is performed in a cardiac catheterization laboratory and takes from 30 minutes to two hours.


Treatment includes lifestyle changes, lipid-lowering drugs, percutaneous transluminal coronary angioplasty, and coronary artery bypass surgery. Atherosclerosis requires lifelong care.
Patients who have less severe atherosclerosis may achieve adequate control through lifestyle changes and drug therapy. Many of the lifestyle changes that prevent disease progression-a low-fat, low-cholesterol diet, losing weight (if necessary), exercise, controlling blood pressure, and not smoking-also help prevent the disease.

Key terms

Arteriosclerosis — Hardening of the arteries. It includes atherosclerosis, but the two terms are often used synonymously.
Cholesterol — A fat-like substance that is made by the human body and eaten in animal products. Cholesterol is used to form cell membranes and process hormones and vitamin D. High cholesterol levels contribute to the development of atherosclerosis.
HDL Cholesterol — About one-third or one-fourth of all cholesterol is high-density lipoprotein cholesterol. High levels of HDL, nicknamed "good" cholesterol, decrease the risk of atherosclerosis.
LDL Cholesterol — Low-density lipoprotein cholesterol is the primary cholesterol molecule. High levels of LDL, nicknamed "bad" cholesterol, increase the risk of atherosclerosis
Plaque — A deposit of fatty and other substances that accumulates in the lining of the artery wall.
Triglyceride — A fat that comes from food or is made from other energy sources in the body. Elevated triglyceride levels contribute to the development of atherosclerosis.
Most of the drugs prescribed for atherosclerosis seek to lower cholesterol. Many popular lipid-lowering drugs can reduce LDL-cholesterol by an average of 25-30% when combined with a low-fat, low-cholesterol diet. Lipid-lowering drugs include bile acid resins, "statins" (drugs that effect HMG-CoA reductase, an enzyme that controls the processing of cholesterol), niacin, and fibric acid derivatives such as gemfibrozil (Lobid). Aspirin helps prevent thrombosis and a variety of other medications can be used to treat the effects of atherosclerosis.
Percutaneous transluminal coronary angioplasty and bypass surgery are invasive procedures that improve blood flow in the coronary arteries. Percutaneous transluminal coronary angioplasty (coronary angioplasty) is a non-surgical procedure in which a catheter tipped with a balloon is threaded from a blood vessel in the thigh into the blocked artery. The balloon is inflated, compresses the plaque to enlarge the blood vessel, and opens the blocked artery. Coronary angioplasty is performed by a cardiologist in a hospital and generally requires a hospital stay of one or two days. It is successful about 90% of the time, but for one-third of patients the artery narrows again within six months. It can be repeated and a "stent" may be placed in the artery to help keep it open (see below).
In coronary artery bypass surgery (bypass surgery), a detour is built around the blockage with a healthy vein or artery, which then supplies oxygen-rich blood to the heart. It is major surgery appropriate for patients with blockages in two or three major coronary arteries or severely narrowed left main coronary arteries, and for those who have not responded to other treatments. It is performed in a hospital under general anesthesia and uses a heart-lung machine. About 70% of patients experience full relief; about 20% partial relief.
Three other semi-experimental surgical procedures may be used to treat atherosclerosis. In atherectomy, a cardiologist shaves off and removes strips of plaque from the blocked artery. In laser angioplasty, a catheter with a laser tip is inserted to burn or break down the plaque. A metal coil called a stent may be permanently implanted to keep a blocked artery open.

Alternative treatment

Alternative therapies that focus on diet and lifestyle can help prevent, retard, or reverse atherosclerosis. Herbal therapies that may be helpful include: hawthorn (Crataegus laevigata), notoginseng root (Panax notoginseng), garlic (Allium sativum), ginger (Zingiber officinale), hot red or chili peppers, yarrow (Achillea millefolium), and alfalfa (Medicago sativum). Relaxation techniques including yoga, meditation, guided imagery, biofeedback, and counseling and other "talking" therapies may also be useful to prevent or slow the progress of the disease. Dietary modifications focus on eating foods that are low in fats (especially saturated fats), cholesterol, sugar, and animal proteins and high in fiber and antioxidants (found in fresh fruits and vegetables). Liberal use of onions and garlic is recommended, as is eating raw and cooked fish, especially cold-water fish like salmon. Smoking, alcohol, and stimulants like coffee should be avoided. Chelation therapy, which uses anticoagulant drugs and nutrients to dissolve plaque and flush it through the kidneys, is controversial. Long-term remedies can be prescribed by specialists in ayurvedic medicine, which combines diet, herbal remedies, relaxation and exercise, and homeopathy, which treats a disease with small doses of a drug that causes the symptoms of the disease.


Atherosclerosis can be successfully treated but not cured. Recent clinical studies have shown that atherosclerosis can be delayed, stopped, and even reversed by aggressively lowering LDL 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. Research continues.


A healthy lifestyle-eating right, regular exercise, maintaining a healthy weight, not smoking, and controlling hypertension-can reduce the risk of developing atherosclerosis, help keep the disease from progressing, and sometimes cause it to regress.
  • Eat right-A healthy diet reduces excess levels of LDL cholesterol and triglycerides. It includes a variety of foods that are low in fat and cholesterol and high in fiber; plenty of fruits and vegetables; and limited sodium. Fat should comprise no more than 30%, and saturated fat no more than 8-10%, of total daily calories according to the American Heart Association. Cholesterol should be limited to about 300 milligrams per day and sodium to about 2,400 milligrams. The "Food Guide" Pyramid developed by the U.S. Departments of Agriculture and Health and Human Services provides daily guidelines: 6-11 servings of bread, cereal, rice, and pasta; 3-5 servings of vegetables; 2-4 servings of fruit; 2-3 servings of milk, yogurt, and cheese; and 2-3 servings of meat, poultry, fish, dry beans, eggs, and nuts. Fats, oils, and sweets should be used sparingly. Mono-unsaturated oils, like olive and rapeseed (Canola) are good alternatives to use for cooking.
  • Exercise regularly-Aerobic exercise can lower blood pressure, help control weight, and increase HDL ("good") cholesterol. It may keep the blood vessels more flexible. Moderate to intense aerobic exercise lasting about 30 minutes (or three 10-minute exercise periods) four or more times per week is recommended, according to the Centers for Disease Control and Prevention and the American College of Sports Medicine. Aerobic exercise includes walking, jogging, and cycling, active gardening, climbing stairs, or brisk housework. A physician should be consulted before exercise if a person has atherosclerosis or is at increased risk for it.
  • Maintain a desirable body weight-Losing weight can help reduce total and LDL cholesterol, reduce triglycerides, and boost HDL cholesterol. It may also reduce blood pressure. Eating right and exercising are two key components in maintaining a desirable body weight.
  • Do not smoke or use tobacco-Smoking has many adverse effects on the heart but quitting can repair damage. Ex-smokers face the same risk of heart disease as non-smokers within five to 10 years of quitting. Smoking is the worst thing a person can do to their heart and lungs.
  • Seek treatment for hypertension-High blood pressure can be controlled through lifestyle changesreducing sodium and fat, exercising, managing stress, quitting smoking, and drinking alcohol in moderation-and medication. Drugs that provide effective treatment are: diuretics, beta-blockers, sympathetic nerve inhibitors, vasodilators, angiotensin converting enzyme inhibitors, and calcium antagonists. Hypertension usually has no symptoms so it must be checked to be known. Like cholesterol, hypertension is called a "silent killer."



Morgan, Peggy. "What Your Heart Wishes You Knew About Cholesterol." Prevention (September 1997): 96.


American Heart Association. 7320 Greenville Ave. Dallas, TX 75231. (214) 373-6300.
National Heart, Lung and Blood Institute. PO Box 30105, Bethesda, MD 20824-0105. (301) 251-1222.
Texas Heart Institute. Heart Information Service. PO Box 20345, Houston, TX 77225-0345.


a common form of arteriosclerosis in which deposits of yellowing plaques (atheromas) containing cholesterol, other lipoid material, and lipophages are formed within the intima of large and medium-sized arteries.
 Cross-section of artery showing progressive narrowing of diameter due to atherosclerosis and plaque formation.
adj., adj atherosclerot´ic.

ƒThe word atherosclerosis comes from the Greek, athere, meaning “soft, fatty, gruel-like,” and scler- meaning “hard.” These terms are descriptive of the material deposited on the inner lining (tunica intima) of an artery and of the state of the arterial muscle walls once they have been affected by the disease.

In a normal artery the endothelial lining is tightly packed with cells that allow for the smooth passage of blood and act as a protective covering against harmful substances circulating in the bloodstream. The endothelial lining is surrounded by a sheath of muscle cells. In the earliest stage of atherosclerosis fatty streaks form along the intima. The lesions are widely scattered at first, but as the disease progresses they become more numerous and can eventually cover the entire intimal surface of an artery. Later, atheromas of newly formed muscle cells filled with cholesterol build up and protrude into the lumen of the vessel. These deposits cause the inner wall to become roughened and also cause the muscle wall to be rigid and inelastic. Narrowing of the lumen and hardening of the muscle wall decrease the rate at which blood can flow through the vessel and may lead to ischemia of the tissues served by the vessel and the development of clots within the vessel itself. The process also damages and deforms the muscle wall to the extent that it becomes weakened and may develop an aneurysm.

The eventual outcome of the atherosclerotic process in large arteries can be stroke syndrome, or occlusion of one or more of the coronary arteries and myocardial infarction.
Etiology. The exact cause of atherosclerosis is not yet known; it is most likely a combination of factors rather than just one. Heredity seems to play some role; men in certain families have been found to be more susceptible than the average. The fact that women seldom are affected by the disease before menopause suggests that the female sex hormones are associated with prevention of the disease. Atherosclerosis is accelerated by hypertension, probably because of the added stress on the linings of the large blood vessels. Persons suffering from disorders of metabolism, particularly diabetes mellitus, are especially susceptible and tend to develop atherosclerosis earlier in life than persons who do not have these disorders. Another major factor is hyperlipidemia, particularly high serum cholesterol, which is closely associated with the development of coronary heart disease (see heart).


Arteriosclerosis characterized by irregularly distributed lipid deposits in the intima of large and medium-sized arteries, causing narrowing of arterial lumens and proceeding eventually to fibrosis and calcification. Lesions are usually focal and progress slowly and intermittently. Limitation of blood flow accounts for most clinical manifestations, which vary with the distribution and severity of lesions. In lower animals, atherosclerosis of swine and fowl closely resemble human atherosclerosis.
Synonym(s): nodular sclerosis
[G. athērē, gruel, + sclerosis]

Atherosclerosis, the most common form of arteriosclerosis, is a complex process that begins with the appearance of cholesterol-laden macrophages (foam cells) in the intima of an artery. Current theories view atherosclerosis as an inflammatory rather than a degenerative process. It is more likely to begin at areas of vascular turbulence, and biochemical mediators of inflammation are increasingly recognized as markers of atherosclerosis. Smooth muscle cells respond to the presence of lipid by proliferating, under the influence of platelet factors. Circulating monocytes and lymphocytes adhere to the intimal surface and penetrate the endothelium to mediate a local inflammatory process. A plaque forms at the site consisting of fibroblasts, leukocytes, and further deposition of lipid. In time, the plaque becomes fibrotic and may calcify. Expansion of an atherosclerotic plaque leads to gradually increasing obstruction of the artery and ischemia of tissues supplied by it. Ulceration, thrombosis, or embolization of a plaque, or intimal hemorrhage and dissection, can cause more acute and severe impairment of blood flow, with the risk of infarction. These are the principal mechanisms of coronary artery disease (arteriosclerotic heart disease with or without heart failure, angina pectoris, myocardial infarction), peripheral vascular disease (particularly occlusive disease of a lower limb causing intermittent claudication or gangrene), and stroke (cerebral infarction due to occlusion of carotid or intracranial arteries). Independent risk factors for atherosclerosis are male sex, advancing age, the postmenopausal state, a family history of atherosclerosis, cigarette smoking, hypertension, diabetes mellitus, elevated plasma LDL cholesterol, elevated plasma homocysteine, overweight, and a sedentary life style. Mounting evidence suggests that a history of infection with Chlamydia pneumoniae and elevation of plasma levels of triglycerides, fasting insulin, fibrinogen, C-reactive protein, amyloid A, interleukin-6, and lipoprotein Lp(a) are also independent risk factors. The diagnosis of atherosclerosis is usually based on history and physical examination and confirmed by angiography, Doppler ultrasonography, and other imaging techniques. Treatment is largely mechanical: balloon stretching, laser ablation, or surgical removal of plaques, and various bypass and grafting procedures. The prevention of atherosclerosis is a major objective of modern medicine. Preventive measures include regular vigorous exercise, a diet low in fat and cholesterol, maintenance of a healthful weight, avoidance of tobacco, and use of pharmacologic agents as indicated for control of hypertension, diabetes mellitus, and elevated cholesterol.


/ath·ero·scle·ro·sis/ (-sklĕ-ro´sis) a form of arteriosclerosis in which atheromas containing cholesterol, lipoid material, and lipophages are formed within the intima and inner media of large and medium-sized arteries.atherosclerot·ic


A form of arteriosclerosis characterized by the presence of lesions (called plaques) on the innermost layer of the walls of large and medium-sized arteries. The plaques contain lipids, collagen, inflammatory cells, and other substances and can impede blood flow or rupture, leading to serious problems such as heart attack or stroke.

ath′er·o·scle·rot′ic (-rŏt′ĭk) adj.
ath′er·o·scle·rot′i·cal·ly adv.


Etymology: Gk, athere, meal, sklerosis, hardening
a common disorder characterized by yellowish plaques of cholesterol, other lipids, and cellular debris in the inner layers of the walls of arteries. Atherosclerosis may be induced by injury to the arterial endothelium, proliferation of smooth muscle in vessel walls, or accumulation of lipids in hyperlipidemia. It usually occurs with aging and is often associated with tobacco use, obesity, high homocysteine levels from eating red meat, hypertension, elevated low-density lipoprotein and depressed high-density lipoprotein levels, and diabetes mellitus. The condition begins as a fatty streak and gradually builds to a fibrous plaque or atheromatous lesion. The vessel walls become thick, fibrotic, and calcified, and the lumen narrows, resulting in reduced blood flow to organs normally supplied by the artery. The plaque eventually creates a risk for thrombosis and is one of the major causes of coronary heart disease, angina pectoris, myocardial infarction, and other cardiac disorders. Plaque rupture is usually provoked by activation of the sympathetic nervous system, such as sudden awakening, heavy physical exertion, or anger. Antilipemic agents do not reverse atherosclerosis. Segments of arteries obstructed or severely damaged by atheromatous lesions may be replaced by patch grafts or bypassed, as in coronary bypass surgery; the lesion may be removed from the vessel via endarterectomy; or obstructed arteries may be opened by balloon angioplasty or by the insertion of stents. A diet low in cholesterol, calories, and saturated fats, together with avoidance of smoking, stress, and a sedentary lifestyle, may help prevent the disorder. See also arteriosclerosis. atherosclerotic, adj.
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Pathogenesis of atherosclerosis


A common type of arteriosclerosis found in medium and larger arteries in which raised areas in the tunica intima are formed from smooth muscle cells, cholesterol and other lipids. Atherosclerosis is characterised by the progressive narrowing and hardening of arteries due to intramural deposition of LDL and calcium secondary to exposure of smooth muscle to lipid, resulting in platelet-induced smooth muscle proliferation and increased risk of future stroke and myocardial infarction.
Clinical findings
Pain in the tissues supplied by atherosclerotically narrowed arteries.
Angiography and Doppler ultrasonography studies.
“Hard” risk factors
Hypertension > 160/95 mm Hg, increased LDL-C (total cholesterol > 265 mg/dl), smoking > 1 pack/day, diabetes.

“Soft” risk factors
Male, family history of atherosclerosis, obesity, increased apoB, increased apoC-III, increased total cholesterol, increased triglycerides, decreased HDL-C, markedly increased homocysteine (a highly reactive amino acid toxic to vascular endothelium and which may potentiate the auto-oxidation of LDL-C, promoting thrombosis).

Complications in lesions
Aneurysms (dissecting and fusiform of arterial wall subjacent to atheroma), bleeding into plaque, calcification, thrombosis.
Medical management
Lifestyle changes: exercise, vegetarian diet (fish better than meat and eggs), 1–2 alcoholic drinks/day (red wine may be best), possibly biofeedback modalities (e.g., yoga), cholesterol-lowering drugs-statins.
Surgical management
Balloon angioplasty (PCTA), stenting, CABG; plaque scraping or “grinding” largely abandoned due to poor outcomes.


Hardening of the arteries Heart disease A common type of arteriosclerosis found in medium and larger arteries in which raised areas in the tunica intima are formed from smooth muscle cells, cholesterol, and other lipids; the progressive narrowing and hardening of arteries due to intramural deposition of LDL, and calcium, 2º to exposure of smooth muscle to lipid, resulting in platelet-induced smooth muscle proliferation, and ↑ risk of future stroke and MI Clinical Atherosclerosis is symptomatic when the narrowing of an artery ↓ the blood flow to a particular tissue enough to cause pain in the tissues supplied by that artery Diagnosis Clinically significant atherosclerosis is identified by angiography and Doppler ultrasonography studies factors HTN 'Hard' risk factors HTN > 160/95 mm Hg, ↑ LDL-C–total cholesterol > 265 mg/dL, smoking > 1 pack/day, DM 'Soft' risk factors ♂, family Hx of ASHD, obesity, ↑ apoB, ↑ apoC-III, ↑ total cholesterol, ↑ TGs, ↓ HDL-C, ↑↑↑ homocysteine, a highly reactive amino acid, which is toxic to vascular endothelium and may potentiate the autooxidation of LDL-C, promoting thrombosis Complications in lesions Aneurysms–dissecting and fusiform of arterial wall subjacent to atheroma, bleeding into plaque, calcification, thrombosis Medical management Lifestyle changes–eg, exercise, vegetarian diet, fish better than meat and eggs, 1-2 alcoholic drinks/day–red wine may be best, possibly biofeedback modalities–eg, yoga, Cholesterol-lowering drugs—statins Surgical management Balloon angioplasty–PCTA, plaque scraping or 'grinding'—largely abandoned due to poor outcomes, stenting, CABG. See Atherosclerotic plaque.


Arteriosclerosis characterized by irregularly distributed lipid deposits in the intima of large and medium arteries; such deposits provoke fibrosis and calcification. Atherosclerosis is set in motion when cells lining the arteries are damaged as a result of high blood pressure, smoking, toxic substances in the environment, and other agents. Plaques develop when low-density lipoproteins accumulate at the site of arterial damage and platelets act to form a fibrous cap over this fatty core. Deposits impede or eventually shut off blood flow.
[G. athērē, gruel, + sclerosis]


A degenerative disease of arteries in which fatty plaques of ATHEROMA develop on the inner lining of arteries so that the normal flow of blood is impeded. The cause of atherosclerosis is not clearly understood but it is related to diet, especially one high in saturated fats and to the resulting concentration of low density LIPOPROTEINS in the blood. Interaction of antibodies with heat-shock protein 60 leading to endothelial damage seems to be a probable mechanism. Smoking is a major risk factor for the disease. High blood pressure (HYPERTENSION) is also damaging to arteries and encourages atherosclerosis. This, in turn, encourages hypertension. Atherosclerosis affects most of the arteries in the body but is especially dangerous when it narrows the CORONARY ARTERIES that supply the heart muscle with blood, or the CAROTID and VERTEBRAL arteries and their branches, that supply the brain. Coronary narrowing causes ANGINA PECTORIS and heart attacks and narrowing of the brain arteries causes STROKE and DEMENTIA. Atherosclerosis may also interfere with the blood supply to the limbs and often causes GANGRENE. It is the major cause of death in the Western world and is responsible for more deaths than any other single condition. Worldwide, many more women die from heart attacks and strokes than from breast cancer.


the 'hardening of the arteries' that occurs to a variable extent with ageing. The main cause is atherosclerosis, when deposits known as atheromatous plaques are formed, mainly of cholesterol, in the walls of arteries and cause narrowing of the lumen, e.g. in the coronary arteries (leading to angina or thrombosis), in the cerebral arteries (leading to stroke or senile dementia) or in arteries in the legs (causing ischaemic pain when walking). See also claudication.


irregular fibrolipid deposits within endothelium of large and medium-sized arteries (especially coronary, cerebral and limb arteries at points of bifurcation), causing arterial stenosis, reduced and turbulent blood flow and increased intra-arterial shear stress; strongly associated with diabetes mellitus, hypertension, high-fat/low-fibre diets, cigarettes, obesity, sedentary and high-stress lifestyle (see type A behaviour pattern)

atherosclerosis (aˈ·thrō·skl·rōˑ·sis),

n degenerative disease characterized by plaques of cholesterol and lipids in the arterial walls, leading to thickening of arteries and ultimately to coronary heart disease, angina, and other cardiac diseases.
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A form of arteriosclerosis in which fatty deposits occur in the middle coat of large and medium-sized arteries, as for example the central retinal artery. The deposits or plaques, which form at the site of arterial damage (due to high blood pressure, smoking, etc.), consist initially of lipid deposits and later of fibrous tissue and insoluble calcium salts. The deposits lead to a reduction and often a blockage of the blood flow resulting in angina, stroke or heart attack. Atherosclerosis occurs usually in elderly people. See arteriosclerosis; atheroma.


Arteriosclerosis characterized by irregularly distributed lipid deposits in the intima of large and medium-sized arteries, causing narrowing of arterial lumens and proceeding eventually to fibrosis and calcification.
[G. athērē, gruel, + sclerosis]

atherosclerosis (ath´ərōsklərō´sis),

n a degenerative disease principally affecting the aorta and its major branches, the coronary artery, and the larger cerebral arteries. The arterial changes include narrowing of the lumen of the vessels; weakening of the arterioles, leading to rupture; an increased tendency toward development of atheromatous plaques; and thrombi. Atherosclerosis is a common cause of myocardial infarctions and cerebrovascular accident.


a common form of arteriosclerosis in humans in which deposits of yellowing plaques (atheromas) containing cholesterol, other lipoid material, and lipophages are formed within the intima of large and medium-sized arteries. It is a common finding in cetaceans and sirenians and also in aoudads.