atherosclerosis(redirected from Atherosclerotic plaques)
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Causes and symptoms
- 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.
- Heredity-People whose parents have coronary artery disease, atherosclerosis, or stroke at an early 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.
- 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.
- 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."
The 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.
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.
atherosclerosisA 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.
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.
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.
Balloon angioplasty (PCTA), stenting, CABG; plaque scraping or “grinding” largely abandoned due to poor outcomes.