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

This consensus document has been drawn up following the round-table conference 'Cholesterol Consensus: a Trans-Atlantic Perspective', Amsterdam, 31 October and 1 November 1991. Its recommendations are as follows. Elevated plasma cholesterol level should be viewed as one of a number of important risk factors that contribute to the high incidence of coronary heart disease in industrialized societies. Control of lipid abnormalities forms an essential part of an overall preventive strategy of risk factor reduction. Both population and individual strategies are required. To reduce the mean plasma cholesterol levels of populations, a multidisciplinary approach is needed, involving the health-care professions, government, food manufacturers and distributors, community and consumer organizations, and the media. While it is desirable for all individuals to know their plasma cholesterol level, universal screening is recommended only where resources for treatment and follow-up are sufficient to cope with the case load detected. As an interim measure, screening should be focused on individuals at special risk. The recommendations of the European Atherosclerosis Society and the U.S. National Cholesterol Education Program should be followed with regard to thresholds for treatment by dietary counselling and pharmacological methods, and targets for cholesterol reduction. These recommendations should be periodically reviewed as new research data becomes available. A number of key areas for research are listed.
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PMID:Cholesterol consensus: a trans-Atlantic perspective. Amsterdam, The Netherlands, 31-October-1 November 1991. 145 42

The aim of this study was to evaluate the prevalence of arterial hypertension and other risk factors in patients suffering from peripheral arterial disease (PAD) in two clinical samples (1.: 102 patients with PAD 69 M, 33 F, studied in our angiology laboratory, matched for sex and age with 102 healthy volunteers; 2.: 184 hospitalized patients, 80 M, 104 F, mean age 57.2 +/- 10.8, with PAD) and in two epidemiological cohorts (1.: Trabia Study, 835 subjects; 2.: Casteldaccia Study, 723 subjects). All patients were subjected to a full clinical and laboratory examination, including the determination of the ankle/arm pressure ratio (Winsor index, positive for PAD when lower than 0.95). In the first clinical study we observed a significantly (p < 0.01) greater prevalence of arterial hypertension (51.9 vs 9.8%), hypercholesterolemia (48.2 vs 21.6%), hypertriglyceridemia (53.7 vs 26.1%), smoking habit (64.3 vs 44.2%), and hyperglycemia (26 vs 7,9%) in PAD patients than in controls. In the second clinical study considering separately the patients under and over 65 years, all risk factors resulted to be more prevalent in younger people than in the aged, except for diabetes and hypertension. In our epidemiological experience, the prevalence of PAD increases with aging, above all in males. In the Trabia Study the risk factors, more associated with PAD, were hypercholesterolemia, smoking and obesity (41.18%) in males and hypertension and hypercholesterolemia (33.3%) and obesity (25%) in females. In the Casteldaccia Study the most important risk factors were smoking (64.28%), hypercholesterolemia (42.86%) and hypertriglyceridemia (35.71%) in males, and obesity (60%), hypercholesterolemia (30%) and diabetes (20%) in females. Cholesterol levels and smoking were significantly higher in PAD patients than in the general population, whereas hypertriglyceridemia and glycemia were not. Arterial hypertension was significantly associated with PAD in the Trabia but not in the Casteldaccia Study. Obesity was significantly associated to PAD in females in both studies. In the Casteldaccia Study, lower HDL-cholesterol levels were observed in PAD patients, above all in males, whereas significantly greater Apo-B values and lower Apo-A1 levels (in males) were shown. The different levels of associated risk factors and their prevalence in PAD patients confirm the multifactorial pathogenesis of atherosclerosis. The exact role of each risk factor in the genesis of PAD is difficult to be evaluated due to the complex biological and statistical interrelationships among different risk factors. However, the management of associated risk factors may favourably influence the risk profile in each patient suffering from PAD.
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PMID:Prevalence of risk factors in patients with peripheral arterial disease. A clinical and epidemiological evaluation. 146 Mar 57

An elevated plasma LDL concentration is a major risk factor for the development of atherosclerosis and coronary heart disease. The concentration of LDL in plasma is determined, to a large extent, by events in the liver, since this organ is the source of LDL (via VLDL) and is the major site of LDL catabolism. LDL uptake by the liver is mediated largely by receptor-dependent mechanisms and fully 80 to 90% of whole body receptor-dependent LDL catabolism occurs in the liver. The rate of receptor-dependent LDL uptake by the liver is influenced by dietary and genetic factors. Cholesterol and fatty acids are the major dietary factors that alter receptor-dependent LDL uptake by the liver and appear to do so by regulating LDL receptor gene transcription. Regulation of LDL receptor gene transcription by sterols is mediated by sterol regulatory elements within the LDL receptor promoter, but how the nucleus actually senses cellular cholesterol levels and how dietary fatty acids might influence this process remain to be elucidated. Genetic factors may affect the basal rate of receptor-dependent LDL transport or the sensitivity of the LDL receptor pathway to regulation by dietary lipids. An understanding of how dietary lipids regulate hepatic LDL transport and plasma LDL levels, and identification of the major genetic factors that determine responsiveness to dietary lipids is crucial to the development of safe and effective dietary guidelines and to the selection of individuals most likely to benefit from diet modification.
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PMID:Hepatic clearance of plasma low density lipoproteins. 146 22

Human endothelial cells (EA.hy 926 line) were enriched with cholesterol using cationized low density lipoprotein (LDL). Cholesterol-loaded cells interacted with native apolipoprotein (apo) E-free high density lipoprotein3 (HDL)3 as well as with dimethyl suberimidate-modified HDL3 (DMS-HDL3). At 4 degrees C both HDL preparations showed a saturable high affinity binding with a KD of 31 and 50 micrograms of protein/ml and a Bmax of 226 and 436 ng/mg cell protein for native HDL3 and DMS-HDL3 particles, respectively. Competition of binding of 5 micrograms apo E-free 125I-labelled HDL3/ml by unlabelled DMS-HDL3 and tetranitromethane-treated HDL3 (TNM-HDL3) was very poor, whereas unlabelled native HDL3 competed very effectively with 125I-labelled HDL3 binding. Thus, both types of modified HDL did not compete for the high affinity binding sites for native HDL. Unlabelled native HDL3 and unlabelled DMS-HDL3 both competed for the binding of 125I-labelled DMS-HDL3 very effectively. These experiments indicate that there are two distinct high affinity binding sites for HDL on cationized LDL-loaded EA.hy 926 cells: one specific HDL binding site, which only binds native HDL, and a second binding site for both native HDL and DMS-HDL. The modified HDL fractions were used to study the relation between HDL binding and HDL-mediated efflux. Efflux of cell cholesterol was measured as the increase of cholesterol mass in the medium after 24 h of incubation with 0.2 mg native HDL3/ml, or the same amount of modified HDL3. DMS-HDL3-mediated efflux was identical to efflux mediated by native HDL3. TNM-HDL3 also induced efflux of cell cholesterol; however, efflux induced by TNM-HDL3 was only 45-50% of the amount obtained with native HDL3. So both DMS- and TNM-modified HDL3 induced efflux of cholesterol, although these particles do not bind to the specific high affinity sites for native HDL. These results do not indicate a link between binding of HDL to specific receptors for native HDL and HDL-mediated efflux of cholesterol from loaded endothelial cells.
Atherosclerosis 1992 Dec
PMID:Binding of modified high density lipoproteins to endothelial cells: relation with cellular cholesterol efflux? 146 59

The prevalence of abnormal lipid and lipoprotein values was determined in 125 consecutive patients with lower-extremity arteriosclerosis obliterans, and the lipid and lipoprotein abnormalities in these patients were characterized. Only 13% of the patients had normal lipid/lipoprotein profiles. Forty-eight percent of patients had low levels of high-density lipoprotein cholesterol. High-density lipoprotein cholesterol values were lower in patients with concomitant coronary heart disease compared with those without heart disease. High-density lipoprotein cholesterol values were inversely related to weight, to triglyceride values, and to diabetes mellitus. Twenty-eight percent of patients had "desirable" total cholesterol levels (< 200 mg/dL), and 32% had low-density lipoprotein cholesterol values less than 130 mg/dL. Following National Cholesterol Education Program guidelines may be misleading in patients with documented lower-extremity atherosclerosis; therefore, complete lipid/lipoprotein profiles should be performed in these patients.
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PMID:Lipid and lipoprotein abnormalities in lower-extremity arteriosclerosis obliterans. 146 32

The Cholesterol Lowering Atherosclerosis Study, a randomized angiographic clinical trial, demonstrated the beneficial effect of niacin/colestipol plus diet therapy on coronary atherosclerosis. Outcome was determined by panel-based estimates (viewed in both still and cine modes) of percent stenosis severity and change in native artery and bypass graft lesions. Computer-based quantitative coronary angiography (QCA) was also used to measure lesion and bypass graft stenosis severity and change in individual frames closely matched in orientation, opacification, and cardiac phase. Both methods jointly evaluated 350 nonoccluded lesions. The correlation between QCA and panel estimates of lesion size was 0.70 (p less than 0.0001) and for change in lesion size was 0.28 (p = 0.002). Agreement between the two methods in classifying lesion changes (i.e., regression, unchanged, or progression) occurred for 60% (210 of 350) of the lesions kappa +/- SEM = 0.20 +/- 0.05, p less than 0.001). The panel identified 442 nonoccluded lesions for which QCA stenosis measurements could not be obtained. Lesions not measurable by QCA included those with stenosis greater than 85% that could not be reliably edge tracked, segments with diffuse or ecstatic disease that had no reliable reference diameter, and segments for which matched frames could not be located. Seventy-nine lesions, the majority between 21% and 40% stenosis, were identified and measured by QCA but were not identified by the panel. This comparison study demonstrates the need to consider available angiographic measurement methods in relation to the goals of their use.
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PMID:Comparison of computer- and human-derived coronary angiographic end-point measures for controlled therapy trials. 154 94

To assess the impact of the National Cholesterol Education Program (NCEP) guidelines, the 7,347 primary care members of the Florida Medical Association received a confidential mailed questionnaire. A follow-up survey polling 5% of the nonresponders validated the initial observations. Of the 1,909 analyzed returns, 96% of the physicians' responses indicated that they believed cholesterol is an important factor in preventing atherosclerosis. However, responses to other questions were far less uniform. For example, 92% of general internists (n = 495) reported being aware of the NCEP guidelines versus 98% of cardiologists (n = 212) (p less than .01) and only 78.7% of OB/GYN specialists (n = 218) (p less than .0001). While 88.2% of general internists responded that the guidelines were relevant in treating their patients, 80.2% of OB/GYN physicians answered likewise (p less than .03). Moreover, only 54% of OB/GYN specialists reported routinely measuring serum cholesterol in their patients compared to 96.7% of general internists (p less than .0001). Most Florida primary care physicians are aware of the NCEP guidelines; however, the impact varies widely among practitioners.
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PMID:Florida's response to the Physician's National Cholesterol Education Program. 155 93

We report a case of cholesterol crystal embolization associated with secretory diarrhea, megacolon and acalculous cholecystitis. Cholesterol emboli were found within the submucosal arterioles of the small and large bowel as well as in the gallbladder wall. Cholesterol crystal embolization is an often unrecognized disease, occurring in elderly patients with severe atherosclerosis. Cholesterol emboli may induce misleading gastrointestinal manifestations with both hemorrhagic and ischemic lesions. Though an uncommon symptom in this setting, secretory diarrhea did not seem to be fortuitous and could have been also a consequence of cholesterol crystal embolization.
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PMID:[Embolisms of cholesterol crystals and their digestive manifestations]. 155 37

Hypoalphalipoproteinemia (plasma HDL-cholesterol concentration at or below 35 mg/dl as reported in the National Cholesterol Education Program Guidelines) is a well known risk factor for premature coronary artery disease (CAD). In hypertriglyceridemic patients, hypoalphalipoproteinemia is commonly believed to be linked to the derangement of triglyceride metabolism. In this study the occurrence of primary hypoalphalipoproteinemia has been investigated in a cohort of hypertriglyceridemic patients whose plasma triglyceride concentration had been normalized either through diet or diet plus drug treatment. Following the initial visit, 115 hypertriglyceridemic patients received dietary advice and returned for the second visit four months later. Diet reduced plasma triglycerides in all the patients. HDL-cholesterol increased in 76 patients whereas in the others, it remained unchanged or even decreased. Plasma triglyceride concentration was normalized (less than 200 mg/dl) in 54 patients by diet alone, but among these 11 remained hypoalphalipoproteinemics. Patients in whom, despite dietary restrictions, triglycerides exceeded 200 mg/dl, were considered for pharmacological treatment with Bezafibrate (300 mg t.i.d.) for 4 months. Thirty-nine concluded the study. Treatment significantly decreased plasma triglyceride concentration in all the subjects. Normalization was achieved in 32 patients. Four of them, however, remained hypoalphalipoproteinemic. These results indicate that a subgroup of hypertriglyceridemic patients remained hypoalphalipoproteinemic even after normalization of triglyceride levels. In these patients hypertriglyceridemia and hypoalphalipoproteinemia may occur as expression of two distinct primary metabolic defects.
Atherosclerosis 1992 Jan
PMID:Relationship of triglycerides and HDL cholesterol in hypertriglyceridemia. 157 23

A spontaneous high density lipoprotein (HDL) deficiency syndrome in chickens associated with a Z-linked (sex-linked) mutation has been reported (F. Poernama et al, J Lipid Res 1990;31:955-963). The mutant, called WHAM (Wisconsin hypo-alpha mutant), has a 70-90% reduction in plasma HDL cholesterol and apolipoprotein A-I (apo A-I) concentrations. In the present study, the effect of the HDL deficiency on diet-induced or spontaneous atherosclerosis was assessed. Control chickens maintained on a high-cholesterol diet for 28 weeks experienced a 2.4-fold rise in the plasma very low density lipoprotein cholesterol concentration, while the same diet induced a 3.7-fold rise in the low density lipoprotein cholesterol concentration in WHAM chickens. The high-cholesterol diet did not elevate the plasma HDL cholesterol or apo A-I concentrations in either group. Both the aortic area of involvement and the width of lesions were quantified by gross and microscopic examination, respectively. Cholesterol feeding produced a significant increase in the area of the aorta with atherosclerotic lesions in both control and mutant chickens. The HDL deficiency in WHAM chickens did not correlate with a higher lesion area or increased lesion thickness. To assess the effect of HDL deficiency on spontaneous atherosclerosis, a separate group of control and WHAM chickens was maintained on a low-fat, cholesterol-free diet for 3 years. At the end of the 3-year period, the area and thickness of the spontaneous aortic lesions in control and WHAM chickens were not significantly different. Spontaneous HDL deficiency in chickens is therefore not associated with increased susceptibility to atherosclerosis.
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PMID:High density lipoprotein deficiency syndrome in chickens is not associated with an increased susceptibility to atherosclerosis. 157 21


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