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

An analysis of the surgical treatment of acute arterial trombosis of the extremities in 86 patients is presented. The causes of thrombosis were mainly obliterating atherosclerosis, artery trauma and postembolic occlusion. Best results of reconstructive operations were obtained in patients with postembolic occlusion of the arteries and their posttraumatic trombosis, worst results - in obliterating atherosclerosis. Thrombendarterectomy and autovenous shunts and prostheses were found to be the mos effective reconstructive operations.
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PMID:[Results of the surgical treatment of acute thrombosis of the major arteries of the limbs]. 649 25

Electron beam computed tomography (EBCT) is a cross-sectional imaging method with high temporal and spatial resolution. So far, it has mainly been applied for the detection of coronary artery calcifications which permit the very sensitive detection of coronary atherosclerosis even in the very early stages. However, after intravenous injection of a contrast agent, EBCT also permits the direct visualization of the coronary artery lumen. For these investigations, a volume data set is acquired that consists of 40 axial cross-sections of the heart (3 mm slice thickness). To evaluate the coronary arteries as to the presence of stenoses and occlusions, various forms of post-processing, including shaded surface display, maximum intensity projection, and multiplanar reconstruction, are applied. The sensitivities and specificities for the detection of coronary artery stenoses and occlusions are about 90%. Best results are obtained for coronary artery bypass grafts, the left main coronary artery, and the left anterior descending coronary artery, while reduced image quality impairs the results for the right coronary artery and the left circumflex coronary artery.
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PMID:Noninvasive coronary angiography by contrast-enhanced electron beam computed tomography. 959 14

The purpose of this study was to determine the effects of oral estrogen replacement therapy with conjugated equine estrogens (CEE), alone or in combination with continuous medroxyprogesterone acetate (MPA), on lumbar spine bone mineral content (BMC) and density (BMD) and on serum chemistries in ovariectomized cynomolgus monkeys when therapy is initiated following a 2 year hypoestrogenic period. Study design was done in the form of a randomized, placebo-controlled, nonhuman primate paraclinical trial. Monkeys were subjects in an experiment designed to study the effects of a lipid-lowering diet combined with hormone replacement therapy on atherosclerosis. Initially, they were ovariectomized and fed a high-fat diet for 24 months. They were then were allocated to three treatment groups by stratified randomization and were fed a diet containing reduced dietary fat for an additional 28 months. Treatment groups consisted of: (1) an untreated group (ovx, n = 24); (2) a CEE-treated group (CEE, n = 19); and (3) a CEE plus continuous MPA group (CEE + MPA, n = 20). Lumbar spine BMC and BMD values were measured by dual-energy x-ray absorptiometry at baseline and 4, 10, 16, 22, and 28 months of treatment. Serum chemistries were relevant to bone metabolism at 22 and 28 months. Rates of gain in BMC and BMD were greater (p < 0.05) in hormone-supplemented animals (groups 2 and 3) than in untreated ovx animals during the first 16 months of treatment, resulting in increased BMC and BMD measurements in these groups. Serum markers of bone metabolism were significantly lower (p < 0.05) in the hormone-treated groups (groups 2 and 3) compared with ovx animals after 22 and 28 months of treatment, indicating reductions in bone turnover rate. Oral estrogen replacement with CEE at doses similar to those taken by women leads to significantly increased BMC and BMD in monkeys, even when therapy is begun 2 years after ovariectomy. Most of the increase occurred during the first 16 months of treatment. The addition of MPA to the CEE regimen provided no additional benefit.
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PMID:Effects on bone of oral hormone replacement therapy initiated 2 years after ovariectomy in young adult monkeys. 976 48

The risk of coronary heart disease and atherosclerosis is increased in both Type 2 and Type I diabetes mellitus. The dyslipidaemia of Type 2 diabetes consists of hypertriglyceridaemia and low levels of high-density lipoprotein (HDL) cholesterol. In Type I diabetes, hypertriglyceridaemia is also present, but when glycaemic control is good, HDL cholesterol levels may be normal or even increased. In both types of diabetes, nephropathy is associated with an exacerbation of hypertriglyceridaemia, a decline in HDL cholesterol level and an increase in serum cholesterol. In the absence of nephropathy, serum cholesterol levels are typically similar to those of the background non-diabetic population. The risk of coronary heart disease (CHD) associated with serum cholesterol is, however, considerably higher in diabetics than in non-diabetic people, and is much less in diabetic populations living in countries where the average cholesterol level is low, even when hypertension is present. Currently, the strongest evidence that lipid-lowering drug therapy will decrease the risk of CHD, particularly in secondary prevention, comes from trials of statins that lower cholesterol. There is growing experimental and observational evidence that hypertriglyceridaemia, because of its effects on cholesteryl ester transfer, leading to the formation of a small low-density lipoprotein susceptible to oxidation, compounds the risk of serum cholesterol in diabetes. Both fibrates and statins can decrease this cholesteryl ester transfer. Further studies of fibrates with clinical end-points should clarify their role in the prevention of CHD. In the meantime, statins should be part of routine diabetic clinical practice, fibrates having a more limited role when hypertriglyceridaemia is extreme.
Baillieres Best Pract Res Clin Endocrinol Metab 1999 Jul
PMID:Diabetic dyslipidaemia. 1076 66

The remarkable extent to which interactions between the plasma lipoproteins, inflammatory factors and the haemostatic system contribute to the response to injury and growth of the plaque in atherosclerosis is being increasingly documented. High plasma concentrations of very-low density (VLDL) and low-density lipoproteins (LDL), together with oxidatively modified LDL and lipoprotein (a), can induce responses in vascular endothelial cells, smooth muscle cells, monocytes/macrophages, platelets, neutrophils and humoral factors that are in a variety of ways both procoagulant and antifibrinolytic. Plasma high-density lipoproteins appear to promote anticoagulant mechanisms. Post-prandial lipaemia is associated with transient changes in factor VII which may be indicative of temporary hypercoagulability. The cellular and humoral effects of LDL and VLDL on the haemostatic system appear to be largely reversible, which may help to explain the prompt improvement in the atherothrombotic state gained by correction of hyperlipidaemia.
Baillieres Best Pract Res Clin Haematol 1999 Sep
PMID:Lipoproteins and the haemostatic system in atherothrombotic disorders. 1085 85

Recent years have seen the expansion of information linking raised plasma levels of individual clotting factors and evidence of disturbances of fibrinolytic activity with the risk of thrombotic manifestations of arterial disease, both in community-based, apparently healthy populations and in patients with known atherosclerosis. Some of these prothrombotic changes in the haemostatic system may result partly from underlying chronic inflammation or acute infection and may, in turn, contribute substantially to the thrombotic risk which accompanies these underlying processes. The importance of the coagulation system in the pathogenesis of arterial thrombosis is further illustrated by the benefit in the Thrombosis Prevention Trial of low-intensity, dose-adjusted warfarin in the primary prevention of ischaemic heart disease. Clinical trials of bezafibrate, which is being used for its fibrinogen-lowering as well as lipid-modifying properties, are in progress.
Baillieres Best Pract Res Clin Haematol 1999 Sep
PMID:Haemostatic function, arterial disease and the prevention of arterial thrombosis. 1085 86

Anabolic steroids are synthetic derivatives of testosterone modified to enhance the anabolic rather than the androgenic actions of the hormone. The anabolic effects are considered to be those promoting protein synthesis, muscle growth and crythopoiesis. There are numerous side-effects to anabolic steroids, including hypertension and atherosclerosis, blood clotting, jaundice, hepatic carcinoma, tendon damage, psychiatric and behavioural effects and, in males, reduced fertility and gynaccomastia. Anabolic steroids were added to the International Olympic Committee's list of banned substances in 1975. The majority of 'evidence' concerning the efficacy of anabolic steroids as performance enhancing agents is anecdotal. In the main, experimental investigations have been poorly designed scientifically, clinically and statistically. The percentage of positive test results from IOC accredited laboratories has remained consistently low. However, athletes take their steroids during training and out-of-competition testing is not conducted in all countries, although international co-operation is now under consideration. Despite the lack of conclusive evidence, steroids users will continue to hold the view that their effects are efficacious and they are therefore unlikely to be persuaded to curtail their use.
Baillieres Best Pract Res Clin Endocrinol Metab 2000 Mar
PMID:Anabolic steroids. 1093 10

Familial hypercholesterolaemia is characterized by elevated serum cholesterol, tendon xanthomas, xanthelasmas, arcus corneae and premature atherosclerosis. Rheumatological manifestations include acute episodes of polyarthritis and tendinitis. Patients who are homozygous for familial hypercholesterolaemia have cardiovascular and rheumatological manifestations more frequently and at an earlier age than patients who are heterozygous.
Baillieres Best Pract Res Clin Rheumatol 2000 Sep
PMID:Rheumatic manifestations of hyperlipidaemia. 1098 88

Chronic splanchnic ischaemia is a relatively unusual clinical entity consisting of pain and/or weight loss and caused by chronic splanchnic disease (i.e. stenosis and/or occlusion of the coeliac and superior mesenteric artery). The occlusive disease is usually caused by atherosclerosis and is in itself not rare in older individuals. Extensive collateral circulation can develop between the three splanchnic arteries and may compensate for the decreased splanchnic perfusion over time. The pathophysiology of chronic splanchnic ischaemia has still not been completely elucidated.A reliable diagnosis of chronic splanchnic ischaemia, based on a proven causal relationship between the occlusive disease and the symptoms, can be very difficult. Traditionally, tests for evaluating the haemodynamic consequences of the vascular stenoses were not available. Important improvements in establishing a more reliable diagnosis have been achieved with duplex ultrasound and magnetic resonance evaluation of the splanchnic circulation. Tonometry is another promising functional test that may prove useful not only for gaining greater insight into the pathophysiology of chronic splanchnic ischaemia but also for the clinical evaluation of this syndrome. The natural history of chronic splanchnic disease suggests that progressive disease may result in acute mesenteric ischaemia. Surgical reconstruction of the coeliac and/or the superior mesenteric artery is the therapeutic standard with excellent short and long-term results. Satisfactory early results using angioplasty with or without stent suggest that this type of intervention may relieve symptoms in selected patients with a higher surgical risk.
Best Pract Res Clin Gastroenterol 2001 Feb
PMID:Chronic splanchnic ischaemia. 1135 3

Systemic lupus erythematosus (SLE) is a connective tissue disease characterized by the formation of autoantibodies and immune complexes. The heart and lungs are among the organ systems commonly affected in SLE. Pericarditis, premature coronary atherosclerosis, pleuritis and pulmonary infections are the most prevalent cardiopulmonary manifestations. Other rare associations include myocarditis, coronary arteritis, acute lupus pneumonitis/pulmonary haemorrhage, acute reversible hypoxaemia and 'shrinking lung' syndrome. Current imaging modalities may provide earlier detection of subclinical disease, which may aid in preventing these potentially fatal complications. The response to treatment varies, depending on the presentation of disease. In this chapter we address the frequency, diagnosis and monitoring, and treatment regimens of cardiac and pulmonary involvement in patients with SLE.
Best Pract Res Clin Rheumatol 2002 Apr
PMID:How to manage patients with cardiopulmonary disease? 1204 50


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