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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular disease is a major cause of morbidity and mortality in the U.K. and other developed countries. In the U.K., mortality from coronary heart disease has increased progressively over the past 25 years, particularly in males. This paper examines the possible role of trace metals in the development of cardiovascular disease, with particular reference to the effects of cobalt, cadmium and lead in myocardial disease, atherosclerosis and hypertension. It is concluded that cobalt is an unimportant factor in community levels of cardiovascular disease, that cadmium has striking effects on blood pressure in animals and that there is some evidence for an association between environmental lead and high blood pressure.
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PMID:Cardiovascular disease and trace metals. 4 Feb 34

No significant lesions of atherosclerosis or other vascular diseases were found in the aorta and coronary arteries of 34 reindeer and 15 caribou (Rangifer tarandus). Serum lipid, phospholipid, cholesterol and triglyceride levels were similar in caribou and reindeer and did not differ greatly from those reported in other ruminants.
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PMID:An investigation of arterial disease in Alaskan reindeer and Caribou. 4 Nov 8

We have shown that the isoelectric point of thrombin is high and that thrombin is a cation at the pH of blood. On the other hand, prothrombin has a low isoelectric point, being more anionic at the pH of blood. It was also found that thrombin adsorbs readily to surfaces, especially negatively charged surfaces, like behenic acid surfaces at pH 8.2. Furthermore, thrombin adsorbed onto behenic acid was active in the sense that it coagulated fibrinogen. The significance of the electric charge of the thrombin molecule in the mechanism of atherosclerosis is discussed.
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PMID:The isoelectric point of thrombin and its behaviour compared to prothrombin at some solid surfaces. 4 37

The experience of 193 operations on 172 patients with affected renal arteries is described. The causes of failure in the surgery are analyzed. Organ-preserving operations with reconstruction of 189 renal arteries were performed on 136 patients. Primary nephrectomies were performed on 36 patients. During recent 3 years nephrectomies were made in 8% of 70 operations. Postoperative mortality was about 7%, mainly due to atherosclerotic patients. The main causes of uneffective operations are as follows: technical errors in revascularization of the kidney, pyelonephritis and neuroangiosclerosis non-diagnosed preoperatively, progressing lesions of the vessels in atherosclerosis and panarteritis.
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PMID:[Cause of failure in the surgery of renovascular hypertension]. 4 56

The media of arteries is virtually avascular. Thus, oxygen and nutrients must reach the cells of the media by diffusion from the lumen of the vessel and from adventitial vessels. The thickness of the thoracic aorta of man and dog exceeds the effective diffusion distance of oxygen, but nutrition is supplemented by vasa vasorum which enter into the outer layers of the media. Occlusion of vasa vasorum in dogs produces medial necrosis, which indicates that these vessels are essential for the nourishment of the aorta. Recently the microsphere method has been used to provide the first measurements of blood flow through vasa vasorum. There is substantial flow to the outer layers of media of the thoracic aorta in dogs, with virtually no blood flow in the inner layers. The vessels are very responsive to physiological stimuli: they dilate during infusion of adenosine and constrict during stimulation of sympathetic nerves. During acute increases in arterial pressure, blood flow to the media decreases probably from distortion of vasa vasorum. Vasa vasorum may play role in disease states. Insufficient blood flow through vasa vasorum may contribute to medial necrosis of the aorta and to aortic atherosclerosis. A role of vasa vasorum in aortic changes in hypertension and other vascular diseases merits further study.
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PMID:Role of vasa vasorum in nourishment of the aorta. 4 7

The body cholesterol pool increases with decreasing plasma-high-density-lipoprotein (H.D.L.) but is unrelated to the plasma concentrations of total cholesterol and other lipoproteins. This finding supports existing evidence that H.D.L. facilitates the uptake of cholesterol from peripheral tissues and its transport to the liver for catabolism and excretion. Plasma-H.D.L., is reduced in several conditions associated with an increased risk of future ischaemic heart-disease (I.H.D.), namely hypercholesterolaemia, hypertriglyceridaimia, male sex, obesity, and diabetes mellitus, while subjects with existing clinical I.H.D. have lower levels of H.D.L. than healthy subjects within the same community. It is proposed that a reduction of plasma-H.D.L. concentration may accelerate the development of atherosclerosis, and hence I.H.D., by impairing the clearance of cholesterol from the arterial wall.
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PMID:Plasma-high-density-lipoprotein concentration and development of ischaemic heart-disease. 4 38

In six cases an attempt was made to relieve the tension on intracranial aneurysms by temporarily clamping the internal carotid artery in the neck, so as to increase the expansibility of the artery. This approach was based on the concept (or "A principle") that haemorrhage is caused by the aneurysm having to bear the full force of systolic pulse pressure when atherosclerosis prevents this pressure being taken up by the normally expansile arterial wall. Follow-up has been fairly short, but the preliminary findings in four of the six patients are encouraging. More attention must be paid in the future to the significance of atherosclerosis in the onset of bleeding from intracranial aneurysms and the incidence of postoperative problems. The argument that atherosclerosis permits the transmission of the systolic pulse directly to the aneurysm wall requires further investigation. The earlier pathological signs of atherosclerosis must receive greater attention, and post-mortem study of the walls of arteries in immediate juxtaposition to aneurysms with high-powered magnification is required.
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PMID:New approach to management of intracranial aneurysms. 4 79

Cholesterol binds to streptolysin O and related bacterial toxins. In normal serum, only a fraction of the cholesterol attached to lipoprotein is available for binding, probably as a cholesterol-peptide complex formed during catabolic breakdown of the lipoprotein. Cholesterol esterase produced by certain organisms--e.g., Staphylococcus pyogenes and Pseudomonas oeruginosa--augments this fraction both in vitro and in vivo. Endogenous esterase similarly increases the amount of cholesterol-peptide complex, a mechanism which may be activated as a feedback process following binding of toxin to the cholesterol component of the complex. These complexes will thus supply a readily available means of binding bacterial toxins before antibody formation begins; Cholesterol-peptide complexes, either alone or modified by binding to toxin, may function as autoantigens. It is postulated that immune complexes so formed may be involved in atherosclerosis either by directly damaging vessels walls or by cross-reaction of antibody with cell-membrane-bound lipoproteins which equilibrate with plasma-lipoproteins.
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PMID:Functional role of cholesterol in infection and autoimmunity. 4 49

An experimental model of atherosclerosis sheep veins identical to the human disease indicates (i) that ingestion of an atherogenic diet is not a prerequistie in atherosclerosis and (ii) that haemodynamic stress must be the dominant aetiological factor in atherosclerosis. Ultrastructural studies reveal that the early lipid deposition in spontaneous human atherosclerosis and in haemodynamically induced atherosclerosis is related to the trasnformation of extracellular vesicular debris into closely packed membranous profiles with electron-translucent centres. It is postulated that the vesicular dtsintegration of mural cells is due to the same haemodynamic stresses which induce degenerative changes in the vascular connective tissues, and that the lipid accumulation within the vesicular disintegration of mural cells is due to the same haemodynamic stresses which induce degenerative changes in the vascular connective tissues, and that the lipid accumulation within the vesicular debris is a cellular debris which have not undergone resolution or phagocytosis.
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PMID:The role of lipid in the pathogenesis of atherosclerosis. 4 86

Most of the factors that are thought to be involved in atherogenesis can act by producing increased endothelial permeability. They may cause damage in their own separate ways or through their effects on blood-platelets. Several constituents of platelets could produce vascular damage that may result in intimal oedema and subsequent atherosclerosis.
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PMID:Early events in atherogenesis. 4 53


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