Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The monoclonal nature of atherosclerotic plaques, as well as their altered cell size, proliferation rate and function have led to the hypothesis that plaque tissue is analogous to benign tumors. To test this hypothesis, we have studied rates of DNA release by histologically-normal human arterial wall tissue and by early atherosclerotic plaques during incubation in a maintenance medium. No DNA was detected in media conditioned by normal arterial tissue after a 24 h incubation period, but plaque tissue (like benign tumors) released 10-100 ng DNA/ml during this period. These data offer additional support for the thesis that atherosclerotic plaques are similar to benign tumors.
Atherosclerosis
PMID:Consideration of atherosclerotic plaques as benign neoplasms. 100 7

Fatty streak was always present in both the thoracic aorta and the abdominal aorta in the youngest subjects studied (aged 10-14 years). Fibrous plaque was present in a small proportion of these young subjects, but a rapid increase in prevalence occurred as early as the fourth decade. Complicated and calcified lesions appeared as early as the age of 20-25 years but a rapid increase in prevalence was seen after age 40 for complicated lesions and after age 50 for calcified lesions. There were differences in the prevalence of severe lesions among the five towns. There was little increase in the extent of atherosclerosis in the thoracic aorta before the age of 40 and in the abdominal aorta before the age of 20. The increase was more rapid after those ages. When atherosclerosis had affected about 50% of the intimal surface of the thoracic aorta and 70% of the intimal surface of the abdominal aorta, the increase slowed down considerably. In contrast to other types of lesion, the extent of fatty streak increased only up to 30 years of age, when it occupied 25-30% of the intimal surface. Then it declined and in the older age groups did not exceed 4-5% in men or women. The extent of fibrous plaque and complicated lesions was at all ages greater in men than in women, while the extent of fatty streak and calcified lesions in older age groups was greater in women. There were marked differences in the extent of atherosclerotic lesions in the five towns.
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PMID:Atherosclerosis of the aorta in five towns. 108 88

Autopsy studies of atherosclerosis of the aorta and the coronary arteries were carried out in 3134 subjects with essential hypertension. A comparison was made with low, average, and high atherosclerosis groups. Essential hypertension was found to accelerate the development of all types of aortic lesion, except fatty streak, as compared with the standardized average atherosclerosis group, and to accelerate the development of fibrous plaque but not complicated and calcified lesions as compared with the high atherosclerosis group. The extent of fibrous plaque in the coronary arteries was greater in the essential hypertension group than in the low and standardized average atherosclerosis groups but did not differ from that in the high atherosclerosis group. The extent of complicated and calcified lesions and the prevalence of coronary stenosis were higher in the high atherosclerosis group than in cases of hypertension. Geographical differences in atherosclerosis among hypertensives in different towns reflected the findings for the whole material. Symptomatic hypertension was found to accelerate aortic atherosclerosis at least to the same extent as essential hypertension. It was conductive to coronary atherosclerosis but not to the same extent as essential hypertension. Coronary stenosis and various manifestations of coronary heart disease were rare in symptomatic hypertension.
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PMID:Atherosclerosis and hypertension. 108 93

The extent of aortic atherosclerosis in subjects with rheumatic heart diseases was similar to that in the standardized average atherosclerosis group of subjects. The extent of coronary atherosclerosis, particularly in men, was similar to that in the low atherosclerosis group. In the aorta, this finding was accounted for by the greater extent of complicated and raised lesions; in the coronary arteries, it was accounted for by the lesser extent of fibrous plaque. Coronary stenosis, fresh myocardial infarction, and large myocardial scar occurred much less frequently in rheumatic subjects than in the high atherosclerosis group. There was no difference in the frequency of stenosis between the rheumatic and low atherosclerosis groups.
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PMID:Atherosclerosis and rheumatic heart disease. 108 96

Animal experiments have shown that the administration of calcium antagonists can prevent or slow the progression of atherosclerosis by inhibiting calcium overload and interfering with lipid metabolism and deposition. These encouraging results have prompted clinical trials to evaluate the effects of calcium antagonists (dihydropyridines and diphenylalkylamines) on atherosclerotic plaque formation. In patients with coronary heart disease, several studies have already shown that calcium antagonists can have a positive effect on plaque evolution, while in hypertensive patients no such study has been published to date. The Verapamil in Hypertension Atherosclerosis Study is an ongoing multicentre randomised double-blind parallel group trial comparing the antihypertensive efficacy of verapamil SR 240 mg/day with that of chlorthalidone 25 mg/day in 1464 patients with essential hypertension aged 40 to 65 years. In a randomised subgroup of patients (n = 550), who will be followed up for 3 years, B-mode ultrasonography is being employed to evaluate the effects of the 2 drugs on carotid wall thickness and carotid plaque development. Ultrasonographic evaluations are performed at baseline, after 3 months, and 1, 2 and 3 years after a standardised protocol to determine intimal-medial thickness in 4 segments of the extracranial carotid tree. The most interesting result to date is the high incidence of carotid alterations, with plaques present in 35% and arterial wall thickening in 31.8% of the 311 asymptomatic hypertensive patients processed so far. A preliminary evaluation of the antihypertensive efficacy of the trial medications after 6 months of double-blind treatment indicates a 63.5% response rate to monotherapy and a 7.8% drop-out rate because of drug inefficacy or intolerance.
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PMID:Preliminary clinical experience with calcium antagonists in atherosclerosis. Verapamil in Hypertension Atherosclerosis Study Investigators. 128 76

Atherosclerosis is a complex and multifactorial disease, the endpoint of which is the formation of a calcified plaque. Intermediate events include intimal injury, smooth muscle cell proliferation and migration, macrophage infiltration, lipid accumulation and excess formation of ground substance. To determine whether the newly developed, long-acting calcium antagonist, amlodipine, slows the development of atherosclerotic lesions under experimental conditions, young New Zealand white rabbits were fed on a diet of 2% cholesterol plus 1% peanut oil for up to 12 weeks. Half the rabbits received 1 or 5 mg amlodipine/kg body weight/day. Amlodipine caused a significant and dose-dependent reduction in lesion formation in the thoracic aorta. At the same time thoracic aorta Ca2+ and cholesterol content were maintained at near normal levels, despite the raised plasma cholesterol levels. The protective effect of amlodipine persisted throughout a treatment period of 12 weeks, indicating the absence of tachyphylaxis.
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PMID:The antiatherogenic effects of amlodipine: promise of preclinical data. 128 82

Animal models of atherosclerosis have improved our understanding of the pathogenic mechanisms involved in the formation of the atherosclerotic plaque. However, extrapolation of these data to the clinical situation is difficult. In addition, evaluation of the prevention or regression of atherosclerosis raises methodological problems. Although improved techniques provide a better evaluation of the extension of the plaques and their functional consequences, a number of points remain undecided: when to intervene, in which patients and how to extrapolate the results. A standardisation of the methods of evaluation of the atherosclerotic plaque is essential as is the fact that the benefit observed should be a reduction in cardiovascular complications and not simply the progression or regression of an angiographic lesion.
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PMID:[Methodological problems of prevention/regression trials of atherosclerosis]. 128 94

The reduction in cardiovascular mortality and morbidity observed over the last decade may be considered to be largely the result of the prevention of lipid disorders. The beneficial effects of diet and increased consumption of unsaturated fatty acids on ischaemic heart disease is a generally accepted concept. The low death rate from coronary artery disease amongst Greenland eskimos who eat a lot of fish has been confirmed by epidemiological studies of other large fish eating populations like the Japanese. The results reported by Bang and Dyerberg have been confirmed by the Zutphen study undertaken by Kromhout in the Netherlands. Fish oil act by the intermediary of the omega-3 fatty acids. Fish oil is rich in high unsaturated omega-3 fatty acids, the most important one being eicosapentaenoic (EPA) and docosahexaenoic acids (DHA). On the basis of epidemiological studies and clinical and experimental observations, it would appear that the consumption of marine polyunsaturated fatty acids has at least a preventive effect on phenomena of atherosclerosis and thrombosis. Their efficacy on the regression or stabilisation of the atheromatous plaque has not been demonstrated. The sites of action are multiple: decreased platelet aggregation; inhibition of thromboxane A2 production; reduction of triglyceride and VLDL concentration; improved blood rheology; action on the endothelium and proliferation of the intimal cells, vascular tone and vasomotricity. The importance of cardiovascular mortality and the hopes raised by clinical and epidemiological trials justify the pursuit of complementary studies on the efficacy and modes of action of marine polyunsaturated omega-3 fatty acids.
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PMID:[Atheroma and fish oils]. 128

The infrarenal abdominal aorta is a common site for clinically significant atherosclerosis. As has been shown in other susceptible locations, vessel geometry, flow division rates, and pulsatility may result in hemodynamic conditions which influence the preferential localization of disease in the abdominal aorta segment. Pulsatile flow visualization was performed in a glass model of the aorta constructed from measurements of angiograms and cadaver aortas. Flow rates and pulsatile waveforms were varied to reflect typical physiological conditions. Under normal resting conditions, the flow patterns in the infrarenal aorta were more complex than those in the suprarenal location. Time varying vortex patterns appeared at the level of the renal arteries and propagated through the infrarenal aorta into the common iliac arteries. A region of oscillating velocity direction extended from the renal arteries to the aortic bifurcation along the posterior wall. Dye became trapped along the posterior wall, requiring several cardiac cycles for clearance. In contrast, there was rapid clearance of the dye in the anterior aorta. Under postprandial conditions, the flow patterns in the aorta were basically unchanged. Simulated exercise conditions created laminar hemodynamic features very different from the resting conditions, including a decrease in dye residence time. This study reveals significant time-dependent variations in the hemodynamics of the abdominal aorta under differing physiologic conditions. Hemodynamic factors such as low wall shear stress, oscillating shear direction, and high particle residence time may be related to the clinically seen preferential plaque localization in the infrarenal aorta.
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PMID:Pulsatile flow visualization in the abdominal aorta under differing physiologic conditions: implications for increased susceptibility to atherosclerosis. 129 93

Since the seventies, and in particular the eighties of this century, findings on pathogenetic mechanisms of ischaemic heart disease are expanding markedly and are becoming more accurate. This makes it possible to know and understand better factors which influence the genesis and development of myocardial ischaemia including the most serious clinical forms (unstable angina pectoris, acute myocardial infarction and sudden cardiac death). Diminution of the cardiac flow and/or increased oxygen demands of the heart muscle are not the only determinants of myocardial ischaemia which is influenced markedly also by neurohumoral, metabolic, prothrombotic (proaggregation and procoagulation) factors as well as antithrombotic and haemodynamic factors. Acute coronary syndromes have as a rule, in particular in patients with out severe atherosclerotic stenosis of the coronary arteries, a common pathophysiological mechanism of fissuration of the atherosclerotic plaque followed by different grades of dynamic coronary occlusion depending on vasoconstriction--spasm of the coronary arteries and thrombus formation. The coronary arteries, usually affected with atherosclerosis, may be due to the comprehensive action of various factors temporarily, intermittently or permanently occluded. In case of the development of acute coronary syndromes thrombosis plays a key role. Better knowledge of pathogenetic mechanism of IHD markedly changes views on treatment and management of patients with IHD in particular patients with acute coronary syndromes. The authors emphasize strategies focused (also preventively) on preventing progression of the disease with the aim to improve survival and the short-term and long-term prognosis.
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PMID:[Pathogenesis of myocardial ischemia and acute coronary syndromes]. 129 43


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