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

We investigated the familial aggregation of the metabolic syndrome in Korean families with adolescents. In a cross-sectional observational study, the body mass index, waist circumference, blood pressure, fasting glucose, serum triglyceride, HDL-cholesterol, total cholesterol and fasting insulin concentrations, and homeostasis model assessment (HOMA) score, were examined in each individual in 132 Korean nuclear families. Most variables of the metabolic syndrome in offspring were significantly correlated with those of parents. Compared with sons, daughters had more significant difference for the metabolic parameters according to clustering of risk factors of their parents. Especially, daughters showed higher correlations with their parents for waist circumference, with their mothers for fasting glucose and HDL-cholesterol, and with their fathers for fasting insulin than sons. Compared with children whose parents did not have the metabolic syndrome, the odds ratios in children with at least one parent with the metabolic syndrome were 4.1 (1.6-10.6) for overweight, 3.6 (1.3-10.2) for abdominal obesity, 5.0 (2.0-12.3) for high triglycerides, and 4.8 (1.1-21.0) for the metabolic syndrome. We also observed significant correlations in variables of the metabolic syndrome between siblings and between spouses. In Korean families with adolescents, there is a familial aggregation of the metabolic syndrome, with daughters resembling their parents more than sons. These findings may have significant implications for clinical interventions directed at adolescents at high risk for the metabolic syndrome.
Atherosclerosis 2006 May
PMID:Familial aggregation of the metabolic syndrome in Korean families with adolescents. 1612 14

Increasing evidence has shown that atherogenesis is not only caused by hypercholesterolemia. Several risk factors including abdominal obesity, dyslipidemia, hyperglycemia, bacterial and viral infection, hyperhomocysteinemia have been identified recently, all mediated through inflammation, which can lead to atherosclerosis. Several events have also been identified to be involved in the overall inflammation reaction in the blood vessel which include endothelium dysfunction, expression of adhesion molecules, recruitment of leukocytes to the injured endothelium, migration of monocytes to the arterial intima, and transformation of monocytes to macrophages. In order to facilitate the assessment of early risk for atherogenesis we have made an effort in this review to identify soluble markers that will allow the detection of these risk factors and the identification of associated inflammation events. Since early risks for atherogenesis are largely preventable with dietary modification and lifestyle changes, capable of detecting early risks by monitoring soluble risk markers is conceivably important for asymptomatic individuals to avoid serious or fatal consequences of atherosclerosis. These soluble markers should also be useful for monitoring the effectiveness of intervention and for the identification of therapeutic targets.
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PMID:Linking inflammation and atherogenesis: Soluble markers identified for the detection of risk factors and for early risk assessment. 1634 70

The metabolic syndrome, which is very common in the general population, is defined by the clustering of several classic cardiovascular risk factors, such as type 2 diabetes, hypertension, high triglycerides and low high-density lipoprotein cholesterol (HDL). Central obesity and insulin resistance, which are the two underlying disorders of the syndrome, are further risk factors for cardiovascular disease. Moreover, a panel of novel (non-traditional) risk factors are ancillary features of the metabolic syndrome. They include biomarkers of chronic mild inflammation (e.g. C-reactive protein, CRP), increased oxidant stress (e.g. oxidized low density lipoprotein, LDL), thrombophilia (e.g. plasminogen activator inhibitor-1, PAI-1) and endothelial dysfunction (e.g. E-selectin). Therefore, subjects with the metabolic syndrome are potentially at high risk of developing atherosclerosis and clinical cardiovascular events.In recent years several longitudinal studies have confirmed that subjects with the metabolic syndrome present with atherosclerosis and suffer from myocardial infarction and stroke at rates higher than subjects without the syndrome. The risk of cardiovascular disease (CVD) is particularly high in women with the syndrome and in subjects with pre-existing diabetes, CVD and/or high CRP. However, an increased risk is already present in subjects with a cluster of multiple mild abnormalities. The risk related to the metabolic syndrome is definitely higher when subjects affected are compared to subjects free of any metabolic abnormality.
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PMID:The metabolic syndrome and cardiovascular disease. 1644 90

We investigated the relationship between the clustering of risk factors for metabolic syndrome and the plasma C-reactive protein (CRP) concentration as measured by high-sensitive CRP assay. Body mass index, waist circumference, triglycerides (TGs), high-density lipoprotein cholesterol, fasting glucose, systolic and diastolic blood pressures, insulin, and CRP were measured in 1046 Korean adults (560 males; age, 18-64 years) in 2003 to 2004. There were statistically significant positive correlations for log CRP with body mass index, waist circumference, log TG, log insulin, and log homeostasis model assessment in both sexes after adjusting for age and smoking status. High-density lipoprotein cholesterol showed a significant negative correlation with log CRP in both sexes. For both sexes, the mean level of log CRP increased with increasing number of risk factors of metabolic syndrome (P for trend <.01 for males and <.001 for females). Stepwise multivariate linear regression analysis showed that waist circumference contributed the largest portion of the variance in CRP levels in both sexes. Log homeostasis model assessment and log TG were independently associated with log CRP levels only in females. These results indicate that CRP, a marker of inflammation that underlies atherosclerosis, is associated with the clustering of each metabolic syndrome risk factor and, furthermore, that abdominal obesity is the strongest predictor of CRP level in the Korean adult population.
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PMID:Association of C-reactive protein with the metabolic risk factors among young and middle-aged Koreans. 1704 62

Metabolic syndrome, indicated by insulin resistance/hyperinsulinemia, obesity, central obesity, atherogenic dyslipidemia, and hypertension, contributes to atherosclerotic cardiovascular disease. However, it is controversial whether the indicators of metabolic syndrome are related to subclinical atherosclerosis collectively or individually. Whether there is any gender-based difference in the mechanisms of metabolic syndrome-induced atherosclerosis progression is also unknown. Two models were compared in this study. Model 1 assumes that a latent factor, metabolic syndrome per se, impacts subclinical atherosclerosis (collective effects model); Model 2 assumes the effect of the syndrome is mediated through its indicators (individual effects model). Data were obtained from the Los Angeles Atherosclerosis Study. The cohort consists of 573 adults (age, 40-60 years) who were asymptomatic for cardiovascular disease. Subclinical atherosclerosis was assessed by measuring common carotid artery intima-media thickness (CCA-IMT) using B-mode ultrasound. Three examinations were completed at 1.5-year intervals from 1995-1999. The analyses were performed with SAS 8.2 and AMOS 4.0. The results showed that atherogenic effects of metabolic syndrome were mediated through its indicators; there were gender-based differences in the mechanisms of metabolic syndrome-induced atherosclerosis. Central obesity was significantly associated with the baseline IMT for men only, whereas triglycerides were significantly associated with the progression of IMT for women only. Systolic blood pressure was significantly associated with the baseline and progression for both men and women. However, fasting insulin was not found to be significantly associated with the baseline and progression of IMT in the multivariate model, although it was significantly associated with other components of metabolic syndrome.
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PMID:Metabolic syndrome and progression of atherosclerosis among middle-aged US adults. 1650 91

People of South Asian origin constitute a large, visible minority in Canada and are known to be at heightened risk for premature coronary artery disease. Conventional risk factors clearly confer risk in South Asians but do not adequately explain their excess risk compared with other populations. Rates of smoking, hypertension and levels of low density lipoprotein-cholesterol tend to be similar or lower in South Asians, although diabetes is more prevalent. Recent studies have suggested that the metabolic syndrome and abdominal obesity may play a causative role in both the prevalence of diabetes and the premature atherosclerosis noted in South Asians. It is possible that genetically susceptible individuals develop abdominal obesity and insulin resistance when exposed to a toxic environment of reduced energy expenditure and increased caloric consumption. This pattern is increasingly noted in parallel with urbanization, suggesting that the increased cardiovascular risk in South Asians may be preventable through lifestyle interventions and the judicious use of medicines to attain optimal levels of blood pressure, lipids and glucose.
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PMID:Is South Asian ethnicity an independent cardiovascular risk factor? 1652 Aug 47

High blood pressure is often associated with various metabolic abnormalities, including abdominal obesity, dyslipidemia, elevated plasma glucose, and insulin resistance, which are the main features of the metabolic syndrome. The metabolic syndrome is extremely common worldwide. This high prevalence is of considerable concern because several studies suggest that the metabolic syndrome carries an increased risk for cardiovascular events. Several lines of evidence seem to indicate that the metabolic syndrome is associated with an increased prevalence of preclinical cardiovascular and renal changes, such as left ventricular hypertrophy, microalbuminuria, impaired aortic elasticity, and early carotid atherosclerosis, most of which are recognized as significant independent predictors of adverse cardiovascular outcomes. It is conceivable that these data may partly explain the high rates of cardiovascular morbidity and mortality that are observed in patients with the metabolic syndrome.
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PMID:The metabolic syndrome and its relationship to hypertensive target organ damage. 1652 97

Available evidence clearly indicates a rapid progression in the prevalence of obesity worldwide. As a consequence, there has also been a marked increase in the prevalence of type 2 diabetes all over the world and this chronic metabolic disease is now considered as a coronary heart disease risk equivalent. However, even in the absence of the hyperglycaemic state which characterizes type 2 diabetic patients, non diabetic individuals with a specific form of obesity, named abdominal obesity, often show clustering metabolic abnormalities which include high triglyceride levels, increased apolipoprotein B, small dense low dendity lipoproteins and decreased high density lipoproteins-cholesterol levels, a hyperinsulinemic-insulin resistant state, alterations in coagulation factors as well as an inflammatory profile. This agglomeration of abnormalities has been referred to as the metabolic syndrome which can be identified by the presence of three of the five following variables: abdominal obesity, elevated triglyceride concentrations, low HDL-cholesterol levels, increased blood pressure and elevated fasting glucose. Post-mortem analyses of coronary arteries have indicated that obesity (associated with a high accumulation of abdominal fat measured at autopsy) was predictive of earlier and greater extent of large vessels atherosclerosis as well as increase of coronary fatty streaks. Metabolic syndrome linked to abdominal obesity is also predictive of recurrent coronary events both in post-myocardial infarction patients and among coronary artery disease men who underwent a revascularization procedures. It is suggested that until the epidemic progression of obesity is stopped and obesity prevented or at least properly managed, cardiologists will be confronted to an evolving contribution of risk factors where smoking, hypercholesterolemia and hypertension may be relatively less prevalent but at the expense of a much greater contribution of abdominal obesity and related features of the metabolic syndrome.
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PMID:[Impact of obesity in contemporary cardiology]. 1659 98

Recent studies suggest that adipose tissue hormones ("adipokines") are involved in the pathogenesis of various complications of obesity, including hyperlipidemia, diabetes mellitus, arterial hypertension, atherosclerosis, and heart failure. Apelin and visfatin are two recently described adipokines, although they are also synthesized outside adipose tissue. Apelin exists in at least three forms, consisting of 13, 17, or 36 amino acids, all originating from a common 77-amino-acid precursor. In the cardiovascular system, apelin elicits endothelium-dependent, nitric oxide-mediated vasorelaxation and reduces arterial blood pressure. In addition, apelin demonstrates potent and long-lasting positive inotropic activity which is preserved even in injured myocardium and is not accompanied by myocardial hypertrophy. Apelin synthesis in adipocytes is stimulated by insulin, and plasma apelin level markedly increases in obesity associated with insulin resistance and hyperinsulinemia. In addition to regulating cardiovascular function, apelin inhibits water intake and vasopressin production. Visfatin, previously recognized as a pre-B cell colony-enhancing factor (PBEF), is abundantly expressed in visceral adipose tissue and is upregulated in some, but not all, animal models of obesity. Preliminary studies suggest that plasma visfatin concentration is also increased in humans with abdominal obesity and/or type 2 diabetes mellitus. Visfatin binds to the insulin receptor at a site distinct from insulin and exerts hypoglycemic effect by reducing glucose release from hepatocytes and stimulating glucose utilization in peripheral tissues. Thus, apelin and visfatin are unique among adipose tissue hormones in that they are upregulated in the obese state and both exert primarily beneficial effects.
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PMID:Apelin and visfatin: unique "beneficial" adipokines upregulated in obesity? 1694 Sep 39

Diabetes mellitus (DM) is considered a major public health problem in both developed and developing countries due to its chronic complications, at the macro or microcirculation, with great impact on mortality and morbidity in all patients. The disease is considered the end of a pathophysiologic process involving peripheral and hepatic insulin resistance and reduced insulin secretion that have been started years before the clinical diagnosis. Metabolic syndrome (MS) is a disorder that results from the increasing prevalence of obesity worldwide. DM is frequently associated with clinical and laboratory features of MS, like abdominal obesity, hypertension, dyslipidemia and microalbuminuria that are also risk factors for cardiovascular disease. Populational studies have demonstrated increasing prevalence of all the features of MS from pre-diabetes to clinical DM resulting in a great risk of cardiovascular disease. The prevalence of MS in DM type 2 is estimated to be >80%. Glitazones are PPAR-gamma agonists that improve insulin sensitivity. These drugs induce the transcription of genes related to glucose and lipid metabolism, and expression of inflammatory and endothelial proteins associated with atherosclerosis process resulting in an improvement in endothelial function. However several questions need to be clarified regarding the glitazones, in special those associated with their adverse effects such as weight gain, edema and heart failure.
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PMID:[Glitazones and the metabolic syndrome: mechanism of action, pathophysiology and therapeutic indications]. 1676 93


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