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 circulating levels of the major adrenal steroids, corticosterone (Cmpd. B), deoxycorticosterone (DOC), and aldosterone were compared in male and female, arteriosclerotic, breeder and non-arteriosclerotic virgin, Sprague--Dawley rats under resting conditions, i.e., quiescence, and after exposure to a mild stress, i.e., movement from one room to another just prior to autopsy. Under resting conditions, the arteriosclerotic animals had significantly greater circulating levels of Cmpd. B, DOC and aldosterone than the non-arteriosclerotic animals. Both the arteriosclerotic and non-arteriosclerotic animals were able to respond adequately to the mild stress stimulus. However, the female breeder rats which manifest the most severe aortic sclerosis, showed the greatest increase in Cmpd. B and aldosterone in response to the mild stress. Although no statistically significant differences could be found between female breeders with grossly visible aortic sclerosis of clear, minimal, moderate, or severe degree, it was apparent that adrenal steroid responsiveness becomes progressively compromised with increasing severity of arteriosclerosis, e.g., unusually high or low levels of Cmpd. B and aldosterone under both quiescent and mild stress conditions. It is suggested that there may be some connection between abnormal hypothalamic-pituitary-adrenal-gonadal function in repeatedly-bred and the pathogenesis of their naturally-occurring ateriosclerosis.
Atherosclerosis
PMID:Aldosterone, deoxycorticosterone and corticosterone differences between arteriosclerotic breeder vs nonarteriosclerotic virgin rats. 94 89

A sub-strain of male and female spontaneously hypertensive rats (SHR) capable of having massively obese or non-obese offspring were bred repeatedly or were maintained as virgin controls. When the male and female breeders had sired or given birth to 5 litters of young, they were autopsied along with their 10-month-old celibate brothers and sisters. Virgin and breeder SHR developed high blood pressure (250 +/- 10 mm Hg). Breeder rats were significantly heavier than their virgin cohorts; pituitary and adrenal glands, hearts, and kidneys were significantly enlarged while thymi were severely involuted in breeder vs virgin SHR. The hyperlipidemia, fatty liver, hyperglycemia, and islet hyperplasia, characteristic of virgin SHR, were greatly exacerbated in breeder SHR. Blood levels of corticosterone, deoxycorticosterone, and aldosterone were greatly elevated in breeder vs virgin SHR. Although breeder rats of genetically normotensive strains develop aortic sclerosis, none of the breeder SHR developed aortic sclerosis. Instead, intimal fibrinohyalin lesions appeared confined to the testes and ovaries. It is suggested that the anatomical appearance or resistance of the arterial wall to the development of lesions is genetically mediated but this genetic programming may be modified by metabolic and hormonal factors with particular emphasis on the participation of adrenocorticoids.
Atherosclerosis
PMID:Hyperlipidemia, hyperglycemia and hypertension in repeatedly bred parents of the obese spontaneously hypertensive rat (obese/SHR) unaccompanied by arteriosclerosis. 674 80

Wall thickening and intimal changes obtained by enhanced CT are early findings of aortic sclerosis. These findings are often detected in the lower abdominal aorta and middle thoracic descending aorta of normal subjects over 30 years of age, as predictors of atherosclerosis. Arterial calcification is a useful sign for evaluating atherosclerosis, especially, in the coronary arteries. The sensitivity and specificity of CT-detected coronary calcification in coronary stenosis by CAG were 76% and 80%, respectively, in our study. In the patients with atherosclerosis, MRI demonstrates wall thickening, intimal projection and narrowing of the lumen in the aorta and large arteries. MRA can be applied to more peripheral arteries, particularly, in the head and extremities, and will be available for screening of atherosclerotic disease in the near future.
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PMID:[Evaluation of arterial sclerosis by CT, MR imaging and MR angiography]. 841 68

Cardiovascular motality is high in patients with chronic renal failure treated with dialysis, and secondary hyperparathyroidism may promote atherosclerogenesis. Recent studies have revealed advanced atherosclerosis in hemodialysis patients by using high-resolution B-mode ultrasonography. Multiple regression analyses indicated that hyperphosphatemia and hyperparathyroidism were associated with increased intima-media thickness (IMT) of the carotid and femoral arteries in hemodialysis patients, respectively. Hypocalcemia and hyperparathyroidism independently and adversely affect the lipoprotein profile by suppressing hepatic triglyceride lipase (HTGL), a lipid-regulating enzyme playing important roles in the metabolism of intermediate density lipoprotein (IDL) and high density lipoprotein (HDL). Plasma IDL is raised markedly, and HDL is lowered in uremia. These lipoprotein changes are closely associated with increased aortic pulse wave velocity (PWV), an index of aortic sclerosis. These findings support the hypothesis that deranged calcium-phosphate homeostasis and secondary hyperparathyroidism promote atherosclerosis in uremia, at least partly by affecting lipoprotein metabolism. Adequate dialysis and efforts to normalize calcium, phosphate and PTH would be beneficial in preventing not only bone disease, but atherosclerosis as well.
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PMID:Atherosclerosis in uremia: possible roles of hyperparathyroidism and intermediate density lipoprotein accumulation. 935 Jun 91

Aortic sclerosis is a calcific disease of the aortic valvular leaflets defined as focal leaflet thickening without significant obstruction to left ventricular outflow. Several clinical factors are associated with calcific aortic valve disease, including male sex, smoking, hypertension, age, hypercholesterolemia, and diabetes. Histologic and biochemical studies suggest similarities between the mechanisms involved in the development of aortic sclerosis and atherosclerosis, suggesting these two diseases may share common pathophysiologic mechanisms. In a recent prospective trial, the presence of aortic sclerosis was associated with an approximately 50% increase in cardiovascular mortality and myocardial infarction, even after correction for age, gender, known coronary artery disease, and clinical factors associated with a aortic sclerosis.
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PMID:Aortic valve sclerosis as a marker of active atherosclerosis. 1182 33

Aortic stenosis is a progressive disease of aging with serious complications. A common disease of the elderly, it may inexorably progress to stenosis. Recent retrospective studies have correlated risk factors commonly associated with coronary and vascular atherosclerosis with an accelerated rate of aortic valve stenosis. Although hydroxymethyl glutaryl co-enzyme A reductase inhibitor (statin) treatment therapy has been shown to delay the rate of progression of valvular aortic stenosis, the salutary mechanism of the statin may be cholesterol-lowering and/or anti-inflammatory. Further prospective studies are warranted to investigate the mechanism and medical therapy of aortic sclerosis and stenosis.
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PMID:Calcific aortic stenosis: new pathophysiologic insights and possible new medical therapy. 1258 51

Calcified "degenerative" aortic stenosis is currently the most common valvulopathy in industrialised countries. In the course of the last decade, experimental studies have allowed a better understanding of the physiopathology of this vavlulopathy. The latest development is the evidence for the initiation and progression of this disease, similar to those described for atherosclerosis. Lipid disturbances, in particular hypercholesterolaemia, constitute an important factor in the initiation of valvular lesions, but also in aortic orifice calcification. Certain preliminary clinical studies are in favour of the significance of statins for slowing the progression of aortic stenosis. This potential beneficial effect requires confirmation by randomised prospective studies and raises hopes for medical therapy in order to avoid the evolution of ordinary aortic sclerosis into tight calcified aortic stenosis.
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PMID:[New concepts on the physiopathology and therapy of aortic stenosis]. 1518 76

Cardiologists long assumed that aortic valve sclerosis/stenosis is a wear-and-tear, degenerative process; recent studies suggested that lipoproteins can play a key role in the development of both sclerosis/stenosis in the aortic valve. Thus, sclerosis/stenosis cannot be considered as a simple degenerative process, but on the contrary it is complex and involves multiple pathogenetic mechanisms. Experimental, clinical and epidemiological data support the link between aortic valvulopathy and atherosclerosis: both are caused by inflammation, lipid deposition, and accumulation of extracellular bone matrix protein. In non-randomized clinical studies, hydroxy-methylglutaryl-coenzyme A reductase inhibitors minimized the progression of aortic valvulopathy. The major pharmacological effect, supposed to underlie the inferred (but still unproven) impact of statins on aortic sclerosis/stenosis is plasma cholesterol reduction. Lately, retrospective clinical studies supported this hypothesis and suggested a key role for statins in delaying the progression of aortic valvulopathy. However, the potential favorable effects of statins require confirmation. Prospective trials in Canada and Europe are now ongoing (ASTRONOMER--Aortic Stenosis Progression Observation Measuring Effects of Rosuvastatin; SEAS--Simvastatin and the Ezetimibe in Aortic Stenosis) and will address the use of cholesterol-lowering drugs in reducing the progression of aortic valve stenosis and in improving clinical outcomes.
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PMID:[Can we prevent the progression of aortic valve sclerosis and stenosis? The need for a prospective, randomized trial]. 1608 23

Aortic valve disease includes a wide spectrum of conditions, from leaflets thickening to hemodynamically significant aortic stenosis and is one of the most important causes of morbidity and mortality worldwide. Studies performed during the last years bring consistent evidence that these lesions of the aortic valves share remarkable similarities with atherosclerotic lesions. They also reveal new risk factors for its development, which are superposed in fact with the major risk factors for atherosclerosis. Moreover, large prospective studies reported an increased risk for cardiovascular events and for total and cardiovascular mortality in patients with aortic sclerosis. Hence, recent papers also propose therapeutic targets, using statins for delaying the progression of the disease.
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PMID:New insights into the pathogenesis and prognosis of aortic sclerosis. 1636 36

Aortic valve stenosis (AVS), including a range of disorder severities, from mild leaflet thickening without valve obstruction, 'aortic sclerosis', to severe calcific aortic stenosis, is a progressive, active process of valve modification, mediating by chronic inflammation (similar to atherosclerosis for cardiovascular risk factors) and biological features. AVS is the expression of early tissue damage due to endothelial damage and oxidative, inflammatory processes, and appears as a surrogate marker for cardiovascular events associated with coronary artery disease (CAD). AVS progression correlates with coronary artery risk factors, such as hypertension, age and cholesterol, and a quantitative evaluation of valve and coronary calcium score comprises a useful marker for cardiovascular prognosis. The low concordance of AVS with CAD appears to be due to other genetic or metabolic factors more specific for calcification processes. Moreover, both pathologies appear to be included within atherosclerotic disease and may be the object of the same clinical therapy and prevention.
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PMID:Aortic valve stenosis and coronary artery disease: pathophysiological and clinical links. 1816 8


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