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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endothelial dysfunction and endothelial cells activation as it was shown in patients with ischemic heart disease play important role in atherosclerosis progression and the development of cardiovascular events. Relationship between E-selectine and functional/ structural changes of the arterial vessels in patients with metabolic syndrome was not explored. We revealed that both activation of the endothelial cells and structural/functional changes of the arterial wall mostly depend on obesity and dislipedemia and in less extent on carbohydrates metabolism disorders.
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PMID:[Possible effect of E-selectine on structure and function of arterial vessels in patients with metabolic syndrome]. 1841 60

High blood pressure, poor glycemic control, obesity, metabolic syndrome, dyslipidemia, smoking and older age are the risk factors for susceptibility to and initiation of CKD. In these conditions, systemic blood pressure can be transmitted to the glomerular capillary network because of impairment of autoregulationary mechanism existing on the afferent arteriole of glomerulus. Glomerular hypertension and endothelial dysfunction are regarded as the common mechanisms underlying in the development of CKD. Albuminuria reflects the dysregulation of glomerular hemodynamics and vascular damage. Low-grade albuminuria (below the current microalbuminuria threshold) is the independent risk factor for the development of CVD. The renin-angiotensin system(RAS), insulin resistance and increased sympathetic nerve activity are implicated in the development of glomerular hypertension and endothelial dysfunction. Endothelial dysfunction could be caused by decrease of BH4 resultant eNOS uncoupling. Endothelial dysfunction could be regarded as the common mechanisms which link CKD and cardiovascular diseases.
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PMID:[Molecular pathogenesis of chronic kidney disease]. 1878 93

Endothelial dysfunction is a major characteristic of the atherosclerotic process and can be used to predict the outcome of cardiovascular disease in humans. Together with obesity and insulin resistance, such dysfunction is common among patients with type 2 diabetes and may explain their poor prognosis in connection with such a disease. Insulin resistance in skeletal muscle, adipose tissue, and the liver, a well-characterized feature of obesity and type 2 diabetes, contributes to the impairment of glucose homeostasis. Furthermore, the myocardial muscle can also be resistant to insulin, which might, at least in part, explain the frequent development of heart failure in individuals suffering from type 2 diabetes. The relationship between insulin resistance and endothelial dysfunction has prompted investigations, which reveal that regular exercise, dietary changes, and/or pharmacological agents can both increase insulin sensitivity and improve endothelial function. Glucagon-like peptide-1, an incretin, lowers blood levels of glucose and offers a promising new approach to the treatment of type 2 diabetes mellitus. Its extensive extra-pancreatic effects, including a favorable influence on cardiovascular parameters, are extremely interesting in this connection. The potential pharmacological effects of glucagon-like peptide-1 and its analogues on the endothelium and the heart are discussed in the present review.
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PMID:The potential beneficial role of glucagon-like peptide-1 in endothelial dysfunction and heart failure associated with insulin resistance. 1879 70

Endothelial dysfunction comprises a number of functional alterations in the vascular endothelium that are associated with diabetes and cardiovascular disease, including changes in vasoregulation, enhanced generation of reactive oxygen intermediates, inflammatory activation, and altered barrier function. Hyperglycemia is a characteristic feature of type 1 and type 2 diabetes and plays a pivotal role in diabetes-associated microvascular complications. Although hyperglycemia also contributes to the occurrence and progression of macrovascular disease (the major cause of death in type 2 diabetes), other factors such as dyslipidemia, hyperinsulinemia, and adipose-tissue-derived factors play a more dominant role. A mutual interaction between these factors and endothelial dysfunction occurs during the progression of the disease. We pay special attention to the possible involvement of endoplasmic reticulum stress (ER stress) and the role of obesity and adipose-derived adipokines as contributors to endothelial dysfunction in type 2 diabetes. The close interaction of adipocytes of perivascular adipose tissue with arteries and arterioles facilitates the exposure of their endothelial cells to adipokines, particularly if inflammation activates the adipose tissue and thus affects vasoregulation and capillary recruitment in skeletal muscle. Hence, an initial dysfunction of endothelial cells underlies metabolic and vascular alterations that contribute to the development of type 2 diabetes.
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PMID:Endothelial dysfunction and diabetes: roles of hyperglycemia, impaired insulin signaling and obesity. 1894 83

Penile erection is a neurovascular process controlled by numerous tightly regulated events, and occurs in response to the activation of pro-erectile autonomic pathways. It is dependent on an adequate inflow of blood to the erectile tissue through both endothelium-dependent vasodilatation and corporal smooth muscle relaxation. Pathologic alteration in the endothelium of penile vasculature and/or erectile tissue and/or impairment of neurovascular processes can result in erectile dysfunction (ED). Both cardiovascular disease (CVD) and ED have been linked to endothelial dysfunction. Endothelial dysfunction is a vascular condition resulting in a diminished vasodilatory response to pharmacologic and physiologic stressors. Endothelial dysfunction may be a pathophysiologic mechanism underlying both ED and CVD, forming a unifying link between these two conditions. Furthermore, in the general population and in men with diabetes or obesity, ED may be a valuable early marker for serious subclinical CVD, coronary artery disease and atherosclerosis.
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PMID:New horizons in erectile and endothelial dysfunction research and therapies. 1900 15

Rheumatoid arthritis (RA) is associated with an increased risk of cardiovascular disease. Traditional cardiovascular risk factors (including male sex, family history for cardiovascular disease, age, dyslipidaemia, arterial hypertension, diabetes mellitus, smoking and obesity) do not adequately account for the extent of cardiovascular disease in RA. The pathogenesis of accelerated atherosclerosis in RA is not clear. Increasing evidence suggests a key role of inflammation in the onset and progression of atherosclerosis. Endothelial dysfunction represents the earliest manifestation of atherosclerosis. Hypertension prevalence in patients with RA is higher than that in the general population, It is attributable risk to the development of future cardiovascular events. Despite its serious complications, control of hypertension is far from adequate in the general population and even more so in rheumatoid arthritis patients.
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PMID:[Cardiovascular disorders in rheumatoid arthritis]. 1902 75

Cardiovascular disease is by far the most common complication of type 2 diabetes and also the most serious one. Suffering from type 2 diabetes mellitus not only dramatically increases the risk of cardiovascular disease but is also associated with poor survival, both acutely and in the long term after a myocardial infarction. In fact, total mortality from coronary artery disease in subjects with type 2 diabetes mellitus, without a previous myocardial infarction, is as high as that of non-diabetic individuals with a previous infarction. Intense research efforts have thus been directed towards exploring the reasons for why particularly type 2 diabetic patients have such a poor prognosis suffering from cardiovascular disease. Obesity-related type 2 diabetes ("diabesity"), including the metabolic syndrome, is rapidly rising in prevalence. About 80% of all type 2 diabetes co-exists with insulin resistance. Endothelial dysfunction is a ubiquitous abnormality in insulin-resistant states that might contribute to premature atherosclerosis in a multifactorial and complex way. Low grade inflammation may play a role in development insulin resistance and type 2 diabetes and it has been proposed that atherosclerosis is basically an inflammatory disease. Thus, the pathophysiology of insulin resistance, the metabolic syndrome, and atherosclerosis may share inflammatory basis as a common denominator. Also, insulin resistance is not confined to skeletal muscle, adipose tissue and the liver, but also to the endothelium. Insulin resistance and endothelial dysfunction co-exist, where chronic inflammation may be a crucial factor. Accordingly, the possibility that physical activity or pharmacological agents that increase insulin sensitivity also improve endothelial function, or vice versa, has been investigated. Many different alterations in life style and drugs that improve endothelial function are known to lower the risk of contracting diabetes. In this review, the pharmacological treatment available against type 2 diabetes mellitus is discussed with particular emphasis on its impact on the endothelium.
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PMID:Hypoglycemic pharmacological treatment of type 2 diabetes: targeting the endothelium. 1903 7

Obese patients with type 2 diabetes and impaired glucose tolerance are at increased risk of development of cardiovascular diseases. Endothelial dysfunction may be a reason for development of atherosclerosis and cardiovascular diseases. Lifestyle modification, increased physical activity, weight reduction, energy restricted diet and good glycaemia control can be useful for the endothelial function improvement and may decrease the risk of cardiovascular diseases. The aim of this study was to evaluate the effects of basal insulin analog and metformin on glycaemia control and weight as risk factors of endothelial dysfunction. Total of 15 patients (9 male and 6 female) with type 2 diabetes were studied. The patients were monitored over six months period. Glycated hemoglobin (HbA1c), fasting plasma glucose (FPG), postprandial plasma glucose (PPG), and body mass index (BMI) were observed. Mean age of the subjects was 53,4 +/- 6,27 years. Mean diabetes duration was 3,71 +/- 1,89 years. At the end of the study mean body mass index decreased from 27,5 +/- 1,45 kg/m2 to 25,7 +/-1,22 kg/m2. In this study we included diabetic patients with fasting glycaemia over 7 mmol/dm3, postmeal glycaemia over 7,8 mmol/dm3 and glycated hemoglobin over 7%. Prior to the study, the patients were treated with premix insulin divided in two daily doses and metformin after the lunch, which did not result in sufficient regulation of glycaemia. We started treatment with one daily insulin basal analog and three daily doses of metformin and monitored the above mentioned parameters. We advised patients to change their lifestyle, to practice energy restricted diet and to increase their daily physical activity. Insulin doses were titrated separately for each patient (0,7-1 IU/kg). Weight reduction was recorded after the study. Mean fasting glycaemia decreased from 8,6+/-0,49 mmol/dm3 to 7,04+/-0,19 mmol/dm3 (p < 0,05). Mean postmeal glycaemia decreased from 9,74 +/- 0,79 mmol/dm3 to 7,6 +/- 0,43 mmol/dm3 (p<0,05). Mean HbA1c decreased from 8,80 +/- 0,59 % to 7,11 +/- 0,22 % (p<0,05). Treatment with one daily doses of basal insulin analog and three daily doses of metformin with lifestyle modification and weight reduction, in obese patients with type 2 diabetes can be useful for the endothelial function improvement and may decrease the risk of cardiovascular diseases.
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PMID:Effects of basal insulin analog and metformin on glycaemia control and weight as risk factors for endothelial dysfunction. 1912

Endothelial dysfunction may link obesity to cardiovascular disease (CVD). We tested the hypothesis that visceral abdominal tissue (VAT) as compared with subcutaneous adipose tissue (SAT) is more related to endothelium-dependent vasodilation. Among Framingham Offspring and Third Generation cohorts (n = 3,020, mean age 50 years, 47% women), we used multivariable linear regression adjusted for CVD and its risk factors to relate computed tomography (CT)-assessed VAT and SAT, BMI, and waist circumference (WC), with brachial artery measures. In multivariable-adjusted models, BMI, WC, VAT, and SAT were positively related to baseline artery diameter and baseline mean flow velocity (all P < 0.001), but not hyperemic mean flow velocity. In multivariable-adjusted models, BMI (P = 0.002), WC (P = 0.001), and VAT (P = 0.01), but not SAT (P = 0.24) were inversely associated with percentage of flow-mediated dilation (FMD%). However, there was little incremental increase in the proportion of variability explained by VAT (R(2) = 0.266) as compared to SAT (R(2) = 0.265), above and beyond traditional risk factors. VAT, but not SAT was associated with FMD% after adjusting for clinical covariates. Nevertheless, the differential association with VAT as compared to SAT was minimal.
Obesity (Silver Spring) 2009 Nov
PMID:Visceral and subcutaneous adiposity and brachial artery vasodilator function. 1928 19

Endothelial dysfunction and increased intima-media thickness (IMT) have been found in obese patients. Both regional fat distribution and liver steatosis may influence these markers of subclinical atherosclerosis. We sought to determine the interrelationships of endothelial function, carotid IMT, visceral and subcutaneous adipose tissue accumulation, and liver steatosis in severely obese subjects. In 64 severely obese patients (BMI 42.3 +/- 4.3 kg/m(2)), we determined (i) endothelial function as flow-mediated dilation (FMD) of the brachial artery, (ii) carotid IMT, (iii) visceral fat diameter, and (iv) degree of liver steatosis using ultrasound. FMD was associated inversely with visceral fat diameter and degree of steatosis (r = -0.577, P < 0.0001 and r = -0.523, P < 0.0001, respectively). Carotid IMT correlated with visceral fat mass (r = 0.343, P = 0.007) but not with liver steatosis. After adjustment for conventional cardiovascular risk factors, FMD was predicted independently by the visceral fat diameter, age, and sex (r(2) = 0.48, P < 0.0001), but not by the degree of liver steatosis or plasma adiponectin levels. In contrast, age and sex were the only predictors of IMT (r(2) = 0.33, P < 0.001). In obese patients, visceral fat diameter is a major determinant of endothelial dysfunction, independent of traditional risk factors or the degree of liver steatosis and plasma adiponectin. Measurement of visceral fat diameter by ultrasound is a novel and simple method to identify subjects with an increased risk for atherosclerosis within an obese population.
Obesity (Silver Spring) 2009 Sep
PMID:Influence of visceral obesity and liver fat on vascular structure and function in obese subjects. 1932 43


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