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atherosclerosis (ăthˌərōsklərōˈsĭs): see arteriosclerosis.
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The following article is from The Great Soviet Encyclopedia (1979). It might be outdated or ideologically biased.



a chronic disease characterized by a thickening and loss of elasticity of the arterial walls and constriction of their lumina, followed by disruption of the blood supply of organs. It usually affects the entire arterial system, although in an uneven manner.

Atherosclerosis was once identified with arteriosclerosis. This identification was made as part of a concept which combined essentially different diseases—hence the incorrectness of the identification. Elderly people are the most frequent victims of atherosclerosis. The external manifestations of the disease are usually preceded by an asymptomatic period of many years’ duration. Atherosclerotic changes occur to some degree in many young people. Males suffer from atherosclerosis three to five times as often as females. A hereditary predisposition and individual characteristics of the organism are factors in the development of the disease. Diabetes mellitus, obesity, podagra, cholelithiasis, and other conditions also help to promote it. A diet rich in animal fats is a significant predisposing factor, but not a primary cause, of atherosclerosis. Other significant causal factors are physical inactivity, mental and emotional stress that traumatizes the nervous system, a strenuous tempo of life, noise, and certain working conditions.

Atherosclerosis develops as a result of a disturbance of the metabolism of lipides (fatlike substances), especially cholesterol, and changes in the structure and function of the vascular wall and the coagulative and anticoagulative systems. A disturbance of cholesterol metabolism increases blood cholesterol, which eventually becomes an important (though not essential) link in the development of the disease. In atherosclerosis there is apparently not only a decrease in the degree of utilization and excretion of excess food cholesterol but also an increased synthesis of it in the body. Metabolic disturbances are connected with disorders of the regulatory nervous and endocrine systems.

Atherosclerosis is characterized by the formation in the vascular wall of atherosclerotic plaques, more or less solid coatings of the innermost layer of the artery. At first the albuminous substance of this layer swells; then it becomes more permeable and cholesterol penetrates into the vascular wall. The accumulation of cholesterol in the arterial walls causes secondary changes in the vessels manifested by a proliferation of connective tissue. The atherosclerotic plaques then undergo several changes. They may break down to form a gruel-like substance (hence the name atherosclerosis), they may have calcium deposited in them (calcinosis), or a semitransparent homogeneous substance may be produced (hyaline). The process is progressive. The lumina of the vessels become narrow. Because of the circular arrangement of the plaques the vessels lose their capacity to dilate, and this in turn impairs the regulation of the blood supply to organs during strenuous work. Uneven-nesses within the vessels promote the formation of clots and thrombi, which aggravate the circulatory disorder to the point where circulation ceases entirely. The development of thrombi is also aided by a decrease in the intensity of the anticoagulation processes. Some investigators ascribe the development of atherosclerosis to the impairment of blood clotting and the accumulation of thrombotic masses in the vascular walls, followed by adiposis, loss of cholesterol, and connective tissue reaction.

If atherosclerotic changes are dominant in the blood vessels of the heart, brain, kidneys, or lower extremities, disturbances which determine the clinical picture of the disease will arise in the organ that suffers from an inadequate blood supply. Atherosclerosis of the cardiac vessels is manifested by coronary insufficiency or myocardial infarction. Cerebral atherosclerosis may result in the impairment of mental activity or, if pronounced, in paralysis of one kind or another. Atherosclerosis of the renal arteries is usually manifested by persistent hypertension. Atherosclerosis of blood vessels in the legs may cause intermittent claudication, ulcers, gangrene, and so forth.

Treatment and prevention. The treatment and prevention of atherosclerosis is aimed at regulating general and cholesterol metabolism. Efforts to normalize working and living conditions are of value—the observance of proper work and rest regimens, exercise, and so forth. The diet should not be rich, especially in animal fats and carbohydrates. It should include foods containing vitamins and vegetable oils. Physicians prescribe certain vitamins, hormones, and drugs that inhibit the synthesis of cholesterol and promote its excretion, as well as drugs that prevent clotting (anticoagulants) and dilate the blood vessels. Treatment must be strictly individualized and supervised by a physician.


Il’inskii, B. V. Ateroskleroz. Leningrad, 1960.
Miasnikov, A. L. Gipertonicheskaia bolezn’ i ateroskleroz. Moscow, 1965.
Glezer, G. A., and L. A. Miasnikov. Preduprezhdenie ateroskleroza. Moscow, 1966.


The Great Soviet Encyclopedia, 3rd Edition (1970-1979). © 2010 The Gale Group, Inc. All rights reserved.


Deposition of lipid with proliferation of fibrous connective tissue cells in the inner walls of the arteries.
McGraw-Hill Dictionary of Scientific & Technical Terms, 6E, Copyright © 2003 by The McGraw-Hill Companies, Inc.


a degenerative disease of the arteries characterized by patchy thickening of the inner lining of the arterial walls, caused by deposits of fatty material; a form of arteriosclerosis
Collins Discovery Encyclopedia, 1st edition © HarperCollins Publishers 2005
References in periodicals archive ?
pylori infection may change the level of serum lipid profile and increase the risk factors of atherogenesis [11].
Mirzaei, "Antiatherosclerotic effects of vitamins D and E in suppression of atherogenesis," Journal of cellular physiology, vol.
LDL-TG and small VLDLTG are responsible for the acceleration of atherogenesis. It becomes one of the possible explanations for atherogenesis acceleration in patients with chronic HCV infection and advanced liver fibrosis, albeit further research on the association between altered lipoprotein metabolism and accelerated atherogenesis in chronic HCV patients is needed [48].
Reiss, "Methotrexate in atherogenesis and cholesterol metabolism," Cholesterol, vol.
Abdul'yanov et al., "Manganese as a potential marker of atherogenesis," Doklady Biochemistry and Biophysics, vol.
In consideration of the variety of cells that participate in atherogenesis, the large number of cytokines that is expressed by each of them and the pleiotropic activity of each cytokine; it is almost impossible to describe minutely all interactions taking place during atherogenesis [23].
Further investigations are needed to examine the protective function of miR-106b-5p against atherogenesis in vivo .
Current understanding of cellular and molecular mechanisms of atherogenesis is based on the classical lipid theory of atherosclerosis, postulating that the most important event in the disease development is the accumulation of extracellular and intracellular lipids in the arterial intima (Schonfelder 1969; Konstantinov et al.
(51-53) Therefore, colchicine therapy may be responsible for less aggressive course of atherogenesis in most studies on FMF.
Because previous studies have identified cleaved caspase-3 in both human [28] and mouse [29] atherosclerotic plaques, where it colocalizes with dead macrophages and lipid-rich plaque components [30], we aimed to investigate the impact of caspase-3 deletion on atherogenesis by crossbreeding caspase-3 knockout ([Casp3.sup.-/-]) mice with ApoE knockout ([ApoE.sup.-/-]) mice.
New findings that the avenanthramides (AVE) contained in oats may reduce the risk of atherogenesis (plaque formation in the arteries) further confirm them as a so-called 'superfood.' As with all foods, moderation is still key.