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

Generalised obesity is a major risk factor for cardiovascular disease, diabetes, hypertension and premature death, but abdominal or central obesity is even more closely related to these. Diabetes causes accelerated atherosclerosis and this results in peripheral vascular and ischaemic heart disease and stroke, major causes of death in diabetics in the Caribbean. Diabetics who have abdominal obesity are therefore at increased risk for these events. 485 patients attending the Diabetes Referral Clinic at the University Hospital of the West Indies, Jamaica, were evaluated for abdominal obesity based on the ratio between their waist and hip measurements. There was an increase in the numbers of diabetics with increasing age. Abdominal obesity was significantly more prevalent among females (90%) than among males (34.9%) (mean 2 = 142; p < 0.0001), and massive obesity was detected in 31.1% of females. However, the prevalence of abdominal obesity among males and females was not significantly age-related. Given the high prevalence of obesity in this clinic population, more precise studies of abdominal obesity associated morbidity in diabetics should be undertaken.
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PMID:The age-prevalence profile of abdominal obesity among patients in a diabetes referral clinic in Jamaica. 936 94

Truncal obesity judged by increased waist-hip ratio (WHR) is an important risk factor for atherosclerosis. One of the mechanisms postulated by which truncal obesity increases coronary risk is high blood pressure (BP). Studies of correlation of WHR with systolic and diastolic BP have shown conflicting results. A study on 443 persons (250 males, 193 females) for WHR measurement during a comprehensive cardiovascular survey in an urban population of Rajasthan was undertaken. The mean WHR in males was 0.90 +/- 0.07 and in females 0.87 +/- 0.08. The median value was 0.91 in males and 0.88 in females. Correlational analysis of WHR with anthropometric and clinical parameters showed that in males there was a positive relationship of WHR with weight (r = 0.11), body mass index (r = 0.13) and systolic (r = 0.11) and diastolic BP (r = 0.11) but not with age and height. In females no significant relationship was seen with these variables. When classified according to the US Fifth Joint National Committee (JNC-V) recommendations for diagnosis of truncal obesity (WHR males > 0.95, females > 0.85) it was seen in 42 (17%) males and 131 (68%) females. Sub-analysis of these two groups showed that mean values of systolic and diastolic BP were not significantly different in truncally obese subjects. However, stratified analysis after classifying WHR in four groups (WHR < 0.85, 0.85-0.89, 0.90-0.95 and > 0.95) showed that in males there was a significantly rising trend of weight, body mass index, systolic and diastolic BP with increasing WHR. WHR of > or = 0.85 was associated with higher systolic and diastolic BP.
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PMID:Waist-hip ratio and blood pressure correlation in an urban Indian population. 942 39

Several lines of evidence have demonstrated that increased plasma cholesterol plays a primary role in the etiology of atherosclerosis and ischemic heart disease (IHD). Our ability to manage IHD adequately based on plasma cholesterol or low density lipoprotein (LDL) cholesterol concentrations is challenged, however, by evidence suggesting that a significant proportion of individuals with IHD or who will eventually develop IHD have desirable cholesterol concentrations. These observations have generated much interest in the scientific community, with the resultant identification of new metabolic risk factors that may help, in the future, to improve our ability to reduce the risk of IHD adequately. This review presents evidence that hypertriglyceridemia, particularly when associated with reduced high density lipoprotein (HDL) cholesterol concentrations and abdominal or visceral obesity, is a highly atherogenic phenotype, one that requires aggressive risk reduction management. Hypertriglyceridemia is frequently associated with elevated plasma apolipoprotein B concentrations, with states of hyperinsulinemia or insulin resistance and with small, dense LDL particles, which may all contribute to increase the risk of IHD further. This evidence suggests that a therapeutic strategy based on the assessment of plasma triglyceride concentrations, along with HDL cholesterol levels and abdominal obesity, may be a cost effective approach to assessing the high atherogenic risk of visceral obesity and insulin resistance. We can no longer afford to focus our attention exclusively on the detection and management of elevated LDL cholesterol concentrations, and need to adopt comprehensive risk reduction strategies in order to lower the incidence of IHD.
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PMID:Atherosclerosis prevention for the next decade: risk assessment beyond low density lipoprotein cholesterol. 967 70

The metabolic syndrome consists of a cluster of metabolic disorders, many of which promote the development of atherosclerosis and increase the risk of cardiovascular disease events. Insulin resistance may lie at the heart of the metabolic syndrome. Elevated serum triglycerides commonly associate with insulin resistance and represent a valuable clinical marker of the metabolic syndrome. Abdominal obesity is a clinical marker for insulin resistance. The metabolic syndrome manifests 4 categories of abnormality: atherogenic dyslipidemia (elevated triglycerides, increased small low-density lipoproteins, and decreased high-density lipoproteins), increased blood pressure, elevated plasma glucose, and a prothrombotic state. Various therapeutic approaches for the patient with the metabolic syndrome should be implemented to decrease the risk of cardiovascular disease events. These interventions include decreasing obesity, increasing physical activity, and managing dyslipidemia; the latter may require the use of pharmacotherapy with cholesterol-lowering and triglyceride-lowering drugs.
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PMID:Hypertriglyceridemia, insulin resistance, and the metabolic syndrome. 1035 72

The association of several risk factors, obesity, dyslipoproteinemia, hepatic steatosis, insulin resistance and hypertension with Type 2 (non-insulin-dependent) diabetes mellitus and myocardial infarction has long been known and has been termed the "metabolic syndrome". In 1988 Reaven introduced syndrome X as the link between insulin resistance and hypertension. It has been suggested that a critical factor in the association between obesity, Type 2 diabetes and cardiovascular morbidity is the mass of intraabdominal fat. Striking similarities exist between the metabolic syndrome and untreated growth hormone (GH) deficiency in adults. The central findings in both these syndromes are abdominal/visceral obesity and insulin resistance. Other features common to both conditions are premature atherosclerosis and increased mortality from cardiovascular diseases. These similarities indicate that undetectable and low levels of GH may be of importance in the metabolic aberrations observed in both these conditions. Recent investigations have found that abdominal/visceral distribution of adipose tissue is associated with endocrine disturbances including increased activity of the hypothalamic-pituitary-adrenal axis and a blunted secretion of GH and sex steroids. Theoretically, these endocrine perturbations can be a consequence of obesity, but the endocrine aberrations may have causal effects. We studied moderately obese, middle-aged men with a preponderance of abdominal body fat. As a group, they had slight to moderate metabolic changes known to be associated with abdominal/visceral obesity. Nine months of GH treatment reduced their total body fat and resulted in a specific and a marked decrease in both abdominal subcutaneous and visceral adipose tissue. Moreover, insulin sensitivity improved and serum concentrations of total cholesterol and triglyceride decreased. Diastolic blood pressure also decreased. The finding that GH replacement in men with abdominal obesity can diminish the negative metabolic consequences of visceral obesity suggests that low levels of this hormone are of importance for the metabolic aberrations associated with visceral/abdominal obesity.
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PMID:Growth hormone and the metabolic syndrome. 1044 70

Of the major risk factors of coronary heart disease dyslipoproteinemia, obesity, hypertension, and diabetes are nutrition related and can be considered of metabolic origin. Dyslipoproteinemia affects 2/3 of the adult population. The risk of coronary heart disease can be decreased 2-5 fold by lowering hypercholesterinemia; atherosclerosis in the coronaries may regress and total mortality may decrease. Atherogenic dyslipidemia (i.e. hypertriglyceridaemia, low HDL cholesterol levels, elevated concentrations of small dense LDL) increases the risk as part of the metabolic syndrome. Obesity is already highly prevalent, and it is affecting ever growing proportions of the adult population. Abdominal obesity furthermore predisposes patients to complications. No effective therapy is available for obesity. 3/4 of hypertensive patients are obese and more than half of them have insulin resistance. By decreasing blood pressure, the risk of stroke decreases by about 40%, that of coronary heart disease by 14-30%. Slimming cures are the most important non-pharmacological way of treating hypertension. 5% of the population has diabetes mellitus, and a further 5% has impaired glucose tolerance. Type 2 diabetes predisposes patients to macrovascular complications. The risk of coronary heart disease can be decreased by controlling diabetes by e.g. metformin.
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PMID:[Major nutrition-related risk factors of ischemic heart disease: dyslipoproteinemia, obesity, hypertension, glucose intolerance]. 1044 32

Patients with Cushing's disease (CD) mainly die because of cardiovascular accidents. The aim of this study was to evaluate whether patients with CD still have increased cardiovascular risk and suffer from premature atherosclerosis once cured. Fifteen patients cured from CD for a long term period (5 yr), 30 sex-and age-matched controls, and 30 body mass index (BMI)-matched controls were included in this study. BMI; waist to hip ratio (WHR); systolic (SBP) and diastolic (DBP) blood pressures; serum total, low density lipoprotein (LDL), and high density lipoprotein (HDL) cholesterol; serum triglycerides, fibrinogen, and lipoprotein(a) levels; prothrombin time; activated partial thromboplastine time; and basal and glucose load-stimulated insulin and glucose levels were measured in patients and controls. By echo-Doppler ultrasonography, the intima media thickness (IMT), systolic and diastolic media-media distances, blood systolic (SPV) and diastolic (DPV) peak velocity, systolic (SLD) and diastolic (DLD) lumen diameter, and distensibility coefficient (DC) were measured at both common carotid arteries where the presence, size, and location of atherosclerotic plaques were also evaluated. Compared with a sex- and age-matched control population, CD patients had BMI (P < 0.001), WHR (P < 0.001), SBP (P < 0.005), DBP (P < 0.05), fasting glucose (P < 0.001) and insulin (P < 0.05), glucose load-stimulated glucose and insulin levels (P < 0.05), total cholesterol (P < 0.05), LDL cholesterol (P < 0.01), fibrinogen (P < 0.01), and lipoprotein(a) (P < 0.05) levels higher and HDL cholesterol levels (P < 0.05) lower than controls. At ultrasonography, in the patients, IMT (P < 0.05), SPV (P < 0.05) and DPV (P < 0.001) were significantly increased whereas SLD (P < 0.001), DLD (P < 0.001), and DC (P < 0.05) were significantly decreased compared to controls. In addition, CD patients had higher WHR (P < 0.05), DBP (P < 0.05), glucose load-stimulated glucose and insulin levels (P < 0.05), and fibrinogen levels (P < 0.01) and lower HDL cholesterol (P < 0.05) levels than BMI-matched controls. At ultrasonography, increased common carotid arteries IMT (P < 0.05) and DPV (P < 0.05) and decreased DLD (P < 0.05) and DC (P < 0.05) were measured in patients compared to those in BMI-matched controls. Atherosclerotic plaques were found in 26.7% of patients, in none of the sex- and age-matched controls, and in 3.3% of the BMI-matched controls. In CD patients, a significant correlation was found between both WHR and fasting serum insulin levels and DBP (r = 0.52 and r = 0.55; P < 0.05), triglycerides levels (r = 0.56 and r = 0.77; P < 0.05), and IMT (r = 0.64 and r = 0.56; P < 0.05). Right (r = -0.70; P < 0.005) and left (r = -0.65; P < 0.01) DC were inversely correlated to the duration of CD in the patient group. At the multiple regression analysis, WHR was the best predictor of fasting insulin levels (beta = 0.77; P < 0.05), and vice versa, fasting insulin level was the best predictor of WHR (beta = 1.20; P < 0.05). In conclusion, patients cured from CD for a long term period have a high prevalence of atherosclerosis and maintain increased several cardiovascular risk factors of the active disease, probably due to a residual abdominal obesity and/or insulin resistance syndrome.
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PMID:Persistence of increased cardiovascular risk in patients with Cushing's disease after five years of successful cure. 1044 57

Central obesity is increasingly recognized as a risk factor for atherosclerosis and type 2 diabetes mellitus. Here we present a hypothesis that may explain the excess atherosclerosis, endothelial dysfunction and progressive beta-cell failure. Central obesity is associated with increased cytosolic triglyceride stores in non-adipose tissues such as muscles, liver and pancreatic beta-cells. A high cytosolic triglyceride content is accompanied by elevated concentrations of cytosolic long-chain acyl-CoA esters, the metabolically active form of fatty acids. These esters inhibit mitochondrial adenine nucleotide translocators, resulting in an intramitochondrial ADP deficiency. In vitro, such ADP deficiency is a potent stimulator of mitochondrial oxygen free radical production, and we assume that this mechanism is also active in vivo. The decline of organ function with normal ageing is thought to be due, at least partly, to a continuous low-grade mitochondrial oxygen free radical production. In tissues containing increased cytosolic triglyceride stores this process will be accelerated. Tissues with a high-energy demand or poor free radical scavenging capacity, such as pancreatic beta-cells, are likely to be more susceptible to this process. This is how we explain their gradual dysfunctioning in central obesity. Likewise we propose that the enhanced production of oxygen free radicals in endothelial cells, or vascular smooth muscle cells, leads to the increased subendothelial oxidation of LDL and atherosclerosis, as well as to the endothelial dysfunction and microalbuminuria.
Atherosclerosis 2000 Jan
PMID:Cytosolic triglycerides and oxidative stress in central obesity: the missing link between excessive atherosclerosis, endothelial dysfunction, and beta-cell failure? 1058 Jan 66

The objective of the present study was to determine whether the intima-media thickness (IMT) is independently related with obesity, and central fat accumulation in healthy subjects. Common carotid artery IMT, parameters of body fat accumulation and distribution (body mass index, waist circumference, waist-to-hip ratio), blood pressure levels, and circulating fasting insulin, glucose, and lipid (cholesterol, HDL-cholesterol, triglycerides, LDL-cholesterol) levels were determined in a population of non-diabetic normal weight and obese subjects. Smoking habits (packs-years) were also taken into account. 239 healthy subjects (143 women and 96 men), with age ranging between 18 and 45 years, were enrolled into the study. They were divided indo two groups according to the body mass index (BMI), obese (132 subjects, 77 woman and 55 men, with BMI greater than 27.0) and controls (107 subjects: 66 women and 41 men, with BMI lower than 27.0). Common carotid artery intima-media thickness was measured by B-mode ultrasound imaging. Fasting plasma metabolic parameters (glucose and lipids) and insulin levels were determined by enzymatic and radioimmunological assays, respectively. Insulin sensitivity was estimated by insulin tolerance test (ITT) and the rate constant for plasma glucose disappearance (KITT) during the 3- to 15-min period following the regular insulin injection was taken as a measure of in vivo insulin action. Obese patients showed higher IMT than controls, and IMT was significantly associated with BMI in the whole population (r = 0.316, p < 0.001). Age (r = 0.327, p < 0.001), KITT (r = -0.201, p < 0.01), fasting blood glucose (r = 0.187, p < 0.01), LDL-chol (r = 0.201, p < 0.01), smoking (r = 0.147, p < 0.05), MBP levels (r = 0.154, p < 0.05), cholesterol (r = 0.152, p < 0.05) and HDL-chol (r = -0.159, p < 0.05) were also significantly associated with IMT. Age (r = 0.330, p < 0.05), BMI (r = 0.299, p < 0.01), waist (r = 0.312, p < 0.001), WHR (r = 0.266, p < 0.001) and KITT (r = -0.259, p < 0.01) were the parameters most strongly correlated with IMT in women, and age (r = 0.324, p < 0.001), BMI (r = 0.338, p < 0.001) waist (r = 0.325, p < 0.001) and LDL-chol (r = 0.283, p < 0.01) where the parameters most strongly correlated with IMT in men. When a stepwise multiple regression analysis was performed for the whole population, only age (p < 0.001) and BMI (p < 0.001) maintained a significant positive relationship with IMT. When a stepwise multiple regression analysis was performed separately for men and women, BMI or waist circumference or WHR were alternatively entered into the model; interestingly, only age, BMI and waist were still significantly correlated with IMT, whereas WHR did not maintain a significant correlation with IMT. In conclusion, BMI and waist circumference, but not WHR, are strongly and independently associated with the IMT of common carotid artery. These results suggests that central fat accumulation may accelerate the development of earlier clinically silent stages of atherosclerosis, thus possibly explaining the higher prevalence of cardiovascular diseases in patients with abdominal obesity.
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PMID:Microcirculatory damage of common carotid artery wall in obese and non obese subjects. 1071 72

Decreased serum levels of high-density lipoprotein cholesterol (HDL-C) are a well-known risk factor for coronary heart disease (CHD) in the general population and have been suggested as one of the best predictor of CHD after renal transplantation. However, very heterogeneous HDL-C levels have been reported in renal transplant recipients. In this patient population, serum HDL-C levels are determined by complex interactions between hormonal, environmental (such as a high amount of abdominal adipose tissue), and genetic factors and drugs (particularly glucocorticoids). We, therefore, evaluated the effects of the cholesteryl ester transfer protein (CETP) gene TaqIB polymorphism as well as of abdominal obesity on HDL-C levels in 78 male renal transplant recipients who were receiving azathioprine and/or ciclosporin A in combination with prednisone as immunosuppression. The patients were classified into genotypic groups according to the presence or absence of the restriction site (B1 allele or B2 allele, respectively). The distribution of CETP genotypes was similar to that previously described in the general population. Overall, HDL-C levels were 19 and 26% higher in B1B2 and B2B2 patients as compared with B1B1 homozygotes (p < 0.05), even after control for other lipid measurements. Patients with abdominal obesity (waist girth >/=93 cm) showed reduced HDL-C levels as compared with lean (waist girth <93 cm) patients (1.20 +/- 0.28 vs. 1.42 +/- 0.41 mmol/l, respectively, p < 0.01). Moreover, the HDL-C levels were markedly affected by the CETP TaqIB polymorphism in lean patients (+28 and +41% in B1B2 and B2B2 as compared with B1B1 patients, p < 0.05), but no significant difference was observed among obese patients. Significantly lower total cholesterol:HDL-C ratios were obtained in lean B2B2 homozygotes, suggesting that these patients could be less susceptible to atherosclerosis than lean B1B1 homozygotes. In addition, patients with the B1B1 genotype had more documented CHD as compared with patients carrying at least one B2 allele, supporting the protective effect of the B2 allele against CHD. In conclusion, considerable variation in HDL-C levels appears to be explained by the CETP TaqIB gene polymorphism in male renal transplant recipients, but this potential protective gene effect appears strongly reduced by concomitant abdominal obesity.
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PMID:HDL cholesterol and TaqIB cholesteryl ester transfer protein gene polymorphism in renal transplant recipients. 1075 10


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