atherosclerosis

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atherosclerosis

(ăth'ərōsklərō`sĭs): see arteriosclerosisarteriosclerosis
, 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.
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.

Atherosclerosis

 

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.

REFERENCES

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.

L. A. MIASNIKOV

atherosclerosis

[‚ath·ə·rō‚sklə′rō·səs]
(medicine)
Deposition of lipid with proliferation of fibrous connective tissue cells in the inner walls of the arteries.

atherosclerosis

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
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Comparison of atherogenic index and lipid profiles in candidates for coronary artery bypass graft surgery versus normal people.
There is a statistically significant (p = 0.041) increase in the Atherogenic Coefficient (AC) of the male rat [40.39% increase].
Atherogenic index of plasma [log(triglycerides/HDL-cholesterol)]: theoretical and practical implications.
This indicate that the increased levels of non-fasting triglycerides may indicate the presence of increased levels of atherogenic remnant lipoproteins.
Considering the (total-cholesterol--HDL-cholesterol): HDL-cholesterol ratio, the atherogenic index was elevated in diabetic rats (DM) (Table 3) due to the dyslipidemia that is characteristic of this pathology.
Comstock et al., "Cytomegalovirus infection, lipoprotein(a), and hypercoagulability: An atherogenic link?" Arteriosclerosis, Thrombosis, and Vascular Biology, vol.
Ejezie et al., "Atherogenic index of plasma as useful predictor of cardiovascular risk among postmenopausal women in Enugu, Nigeria," African Health Sciences, vol.
Abbreviations AIP: Atherogenic index of plasma T2DM: Type 2 diabetes mellitus CVD: Cardiovascular disease LDL-C: Low-density lipoprotein cholesterol HDL-C: High-density lipoprotein cholesterol TC: Total cholesterol TG: Triglyceride UA: Uric acid eGFR: Estimated glomerular filtration rate FBG: Fasting blood glucose PPBG: Postprandial blood glucose FINS: Fasting insulin BUN: Blood urea nitrogen BMI: Body mass index GPO: Glycerol-3-phosphate oxidase HbA1c: Hemoglobin A1c SCr: Serum creatinine DR: Diabetic retinopathy DN: Diabetic nephropathy DPN: Diabetic peripheral neuropathy CDS: China Diabetes Society SBP: Systolic blood pressure DBP: Diastolic blood pressure EPA: Eicosapentaenoic acid.
(22) The authors concluded that "Bergamot extract supplementation significantly lowered plasma lipids (TCTG, and LDL-C) and improved the lipoprotein profile by decreasing atherogenic small, dense LDL particles".
Table 2--Lipid profile (%), atherogenic and thrombogenic indexes and omega 6: omega 3 ratio of adipose tissue and Longissimus dorsi muscle from pigs fed with different net energy levels.
As depicted in the above table the mean values of TC/ HDL are increasing with severity of COPD, which indicates the atherogenic risk.
In the present study, we sought to extend these observations by examining risk when nonHDLc is discordant with apo B or LDLp--to determine if CHD risk is more closely related to total atherogenic lipoprotein particle cholesterol (nonHDLc) or rather to atherogenic particle number (apo B or LDLp).