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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolic syndrome is a constellation of vascular disease risk factors that includes hyperglycaemia, hypertension, and dyslipidaemia, which are largely mediated by accumulating fat depots, particularly when centrally deposited. Increasing adiposity promotes insulin resistance, low grade inflammation and endothelial dysfunction, which promote the development of atherogenic vascular disease. Increases in percentage body fat result from a number of parameters, including ageing, and changes in lifestyle factors that promote a metabolic imbalance, such as decreasing physical activity and adverse dietary patterns. As Asian populations continue to modernize, levels of physical activity are declining as home and workplace jobs become more automated and sedentary and transportation more readily available. Similarly, dietary changes are introduced, with healthy traditional plant-based diets being replaced by cheaper calorie dense high fat foods. These changes are resulting in rapid increases in the prevalence of obesity throughout Asia, and the subsequent development of the metabolic syndrome. To minimise further development of the obesity pandemic and subsequent vascular disease, innovative population-based preventative lifestyle and therapeutic strategies interventions need to be introduced.
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PMID:The metabolic syndrome and vascular disease in Asia. 1758 42

The complexity of the several pathogenic pathways that cause hypertension and vascular disease and the prolonged interval that appears to predate clinical morbidity have hindered inquiry into the association between GDM and vascular disorders. As a forme fruste of later type 2 diabetes, GDM-affected gravidas are identified as at risk of diabetes-related atherosclerosis, glomerular disruption, and pathogenic retinal angio-genesis. That GDM is evidence for underlying chronic conditions such as dysregulation of innate immune response that, independent of the diabetic state, produces vascular disease is difficult state, produces vascular disease is difficult to assert with the present published literature. Cross-sectional studies of patients with established gestational hypertension or preeclampsia are ambiguous as to the possible pathogenic effect of insulin resistance. Cohort studies initiated in early and mid-pregnancy show evidence that both gestational hypertension and preeclampsia may be more prevalent in gravidas with greater insulin resistance. The association of gestational glucose intolerance with gestational hypertension appears to be independent of obesity and ambient glycemia but explained in part by insulin resistance. Late pregnancy preeclampsia is associated with elevated mid-pregnancy BMI, blood pressure, fasting glucose and insulin, urate, and C-reactive protein, suggestive of metabolic and immune dysregulation. GDM appears to be associated with overexpressed innate immune response, which, in turn, is associated with vascular dysfunction and vascular disease. Among women with GDM, markers of insulin resistance do not appear to correlate with hypertension in short-term cohort studies. However, when non-GDM subjects are compared with subjects with GDM, postpregnancy studies do show an associated with vascular dysfunction and vascular disease. Among women with GDM, markers of insulin resistance do not appear to correlate with hypertension in short-term cohort studies. However, when non-GDM subjects are compared with subjects with GDM, postpregnancy studies do show an association of insulin resistance with both inflammatory dysregulation and vascular dysfunction. Cohort studies that have used population-based pregnancy databases consistently identify a clinically significant association of both gestational hypertension and preeclampsia with later hypertensive disorders. Associations with coronary artery disease or stroke are less consistent, requiring further investigation. Preventing the evolution of diabetes and lipid and immune dysregulation of the metabolic syndrome has become a silent public health issue because of the epidemic of childhood and early adulthood obesity and the opportunity at hand to treat insulin resistance by behavioral and pharmacological interventions. However, limited available literature highlights the need for long-term cohort studies of women with well-characterized metabolic and vascular profiles during pregnancy and decades later. Our present knowledge suggests that screening for GDM provides an opportunity of pregnancy outcome improvement. Limited studies of diabetes prevention in at-risk patient groups suggest that we may have the opportunity to reduce the risk of later diabetes. Additional investigation is required to determine if interventions that prevent or postpone diabetes also delay the onset of vascular disease.
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PMID:Gestational diabetes, pregnancy hypertension, and late vascular disease. 1759 80

With the growing prevalence of obesity and impaired glycemic control, and the correlation between these conditions and an elevated predisposition for the development of vascular disease, research emphases are increasingly being targeted to the mechanistic bases and functional outcomes of these relationships. Given this, the current issue of Microcirculation, presents a series of reviews that summarize knowledge on an array of topics relevant to obesity, insulin resistance, and vascular dysfunction. The first chapters discuss altered patterns of blood flow regulation, vascular reactivity, microvascular density, and vascular wall mechanics. The second grouping details alterations to coronary, renal, and hepatic circulations and the implications of these effects for organ function. Additionally, one article presents knowledge and outlines future research directions for the study of endothelial permeability and barrier function within insulin resistance. The last group of articles discusses the effects of inflammation with obesity and insulin resistance on vascular function, and also details the role of perivascular adipose tissue in contributing to vascular dysfunction. The final review extends this general topic to the effects of the metabolic syndrome on microvascular dysfunction, wherein obesity and impaired glycemic control are contributing elements to a larger constellation of systemic pathologies. The authors hope that this Special Topics Issue will be informative for its readers and will provide a basis for future investigation into microvasculopathy in obesity and insulin-resistance.
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PMID:Vascular dysfunction in obesity and insulin resistance. 1761

The metabolic syndrome (MetS) is a distinctive phenotype associated with an increased risk of vascular disease. Carotid plaque is a surrogate marker of subclinical atherosclerosis and a powerful predictor of vascular outcomes. The relationship between the MetS and subclinical atherosclerosis in multiethnic populations has not been well characterized. The authors have evaluated the association of the MetS with subclinical atherosclerosis among 1895 community residents from the Northern Manhattan Study (mean age, 68.0+/-9.7 years; 59% women; 25% black; 22% white; 51% Hispanic). The prevalence of the MetS was 41% (35% in men, 45% in women), and 57% of subjects had carotid plaque. In a multivariate-adjusted logistic regression model, the MetS was a significant predictor of plaque presence (odds ratio, 1.36; 95% confidence interval, 1.10-1.67). Additionally, the number of MetS components was significantly associated with plaque prevalence. Further studies are needed to understand the role of the MetS in the progression from subclinical to clinical atherosclerotic disease.
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PMID:The metabolic syndrome and subclinical carotid atherosclerosis: the Northern Manhattan Study. 1768 55

There is increasing acknowledgment of the public health burden of metabolic syndrome. The metabolic syndrome is defined as emerging cardiovascular risk factors, or atherosclerosis, that are related to underlying insulin resistance. One of the adipokines, adiponectin, has antiatherogenic effects and augments the metabolic effects of insulin. To reduce mortality from cardiovascular disease, it is important to understand the pathophysiological properties of adiponectin and receptors in atherosclerotic regions. Recently, T-cadherin, which has been recognized as a unique cadherin molecule, has been characterized as a novel adiponectin receptor on vascular endothelial cells and smooth muscle. Notably, T-cadherin (also known as CDH13, cadherin 13, and H-cadherin) is abundantly expressed in injured vascular endothelial and smooth muscle cells in atherosclerotic regions. In the present review, we describe recent progress in research on adiponectin receptors, with emphasis on the unique vascular adiponectin receptor, T-cadherin, and its role in vascular disease.
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PMID:Adiponectin receptors, with special focus on the role of the third receptor, T-cadherin, in vascular disease. 1787 43

Insulin resistance is a major contributor to macro- and microvascular complications, particularly in the presence of the metabolic syndrome, and is also associated with polycystic ovary syndrome. Impaired nitric oxide metabolism and endothelial function are important components of the vascular disease. Increasing the bioavailability of arginine, the precursor of nitric oxide, thus potentially offers protection against end-stage disease. We have recently demonstrated that dietary supplementation with a novel silicate inositol arginine complex reduces vasculopathy and glomerular sclerosis in the insulin-resistant JCR:LA-cp rat. The objective of this study was to address the absorption of, and the underlying metabolic alterations caused by, the arginine silicate inositol complex and arginine HCl (as a reference agent) in obese insulin-resistant male and female JCR:LA-cp rats. Male and female rats were treated with the preparations at 1.0 mg/(kg d) (expressed as arginine HCl) from 8 to 12 and 12 to 18 weeks of age, respectively. Obese female, but not male, rats treated with the arginine silicate inositol complex showed a reduced rate of weight gain without concomitant reduction in food intake. Plasma silicon levels were raised very significantly in arginine silicate-treated rats, consistent with significant absorption of the complex. In male rats, arginine levels were elevated by treatment with arginine silicate only; and female rats responded to both preparations. Plasma concentrations of oxides of nitrogen in rats treated with the silicate complex showed a dimorphism, decreasing in male and increasing in female rats. Fasting insulin levels were elevated in male rats treated with the arginine silicate complex, whereas fasting and postprandial insulin levels were decreased in female rats. Furthermore, female, but not male, rats treated with either of the arginine preparations showed significant reductions in cholesterol, triglyceride, and phospholipid concentrations. We conclude that the arginine silicate inositol complex is absorbed efficiently, raising plasma arginine levels, and is more biologically effective than the free amino acid hydrochloride. This has different beneficial metabolic effects in both sexes of an animal model of insulin resistance and cardiovascular disease, consistent with reduction in end-stage disease.
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PMID:Metabolic effects of a novel silicate inositol complex of the nitric oxide precursor arginine in the obese insulin-resistant JCR:LA-cp rat. 1788 39

Thrombotic complications of vascular disease constitute the leading cause of morbidity and mortality in much of the developed world. Current drug therapies available to treat the thrombotic component of arterial and venous vascular complications remain limited. Novel safe and effective treatment strategies to reduce formation of occlusive thrombosis will likely have a major impact on reducing the economic burden of vascular disease on the healthcare system. Enhancing endogenous fibrinolysis by targeting plasminogen activator inhibitor-1 (PAI-1), the primary inhibitor of circulating plasminogen activators, has been shown to be effective in markedly attenuating the formation of arterial and venous occlusive thrombosis in animal models. In addition, animal and human studies of PAI-1 deficiency indicate that spontaneous bleeding complications associated with even complete PAI-1 deficiency would be rare. Patients most likely to benefit from PAI-1 inhibition would be those at high risk for vascular events where PAI-1 is elevated, such as is observed in obesity, diabetes and the metabolic syndrome. Since obesity and metabolic syndrome are now epidemic, and will likely have a major adverse impact on vascular thrombotic events, it may be time to test the clinical effectiveness of PAI-1 inhibition in a patient population at high risk for vascular thrombosis.
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PMID:Plasminogen activator inhibitor-1 in vascular thrombosis. 1789 48

Aging disorders pose an increasing challenge for the public health care systems in Europe. An important approach to cope with this task is the identification of relevant novel disease genes and the control of risk factors using new technological capabilities. A key element in this process is the availability of well classified, large enough patient cohorts and the establishment of quality-controlled central banks for DNA, serum, plasma, and cells/tissues/RNA/proteins together with the development of an IT based infrastructure to provide samples and data required for biomedical studies. The Danubian Biobank initiative connects universities, associated teaching hospitals and endpoint-related rehabilitation clinics along the Danube river and in neighbouring regions. The scientific network focuses on diabetes-related endpoints, vascular disease (e.g. myocardial infarction, stroke, arterial thrombosis, kidney failure), metabolic disease (e.g. obesity, diabetes, metabolic syndrome), and neurodegenerative disorders (e.g. dementia syndromes, Parkinsonism). Task forces are set up for the relevant topics of the biobank project including patient recruitment, sample and data management, public health, epidemiology and genetics, enabling technologies, and research strategies. The project aims to select the most relevant and promising scientific targets utilizing the core competences developed in the individual partner institutions. For this purpose a series of dedicated workshops and conferences are organized as well as joint research grant proposals are submitted.
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PMID:[The Danubian Biobank Initiative: synchronizing the biobanking activities of the Danube universities]. 1793 6

A cluster of risk factors associated with obesity defines the metabolic syndrome and identifies cardiometabolic risk. Accumulation of fat in the visceral depot is a more reliable predictor of cardiovascular disease than is total body mass or body mass index. The recent discovery of the endocannabinoid-CB1 receptor system and its impact on the regulation of energy metabolism represents a significant advance that will help target visceral fat and its metabolic implications. As a highly active endocrine organ, visceral fat secretes many bioactive molecules, known as adipokines. Dysregulation of these adipokines contributes to the pathogenesis of the obesity-associated metabolic syndrome, resulting in insulin resistance, type 2 diabetes, hypertension, hyperlipidemia, and vascular disease. Even modest weight reduction leads to reduced cardiometabolic risk by affecting the individual components comprising the metabolic syndrome.
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PMID:The progression of cardiovascular risk to cardiovascular disease. 1793 92

The metabolic syndrome (MS) is the combination of factors which, when occurring in an individual, can result in an increased risk of diabetes mellitus (DM) and of episodes of vascular disease. We present a systematic review of the diagnostic criteria, pathology, prevalence and risk of vascular disease (including stroke) associated with the MS and, if the patients have already suffered cerebral ischemia and have the MS and/or DM, the appropriate therapies from which they could benefit.
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PMID:The metabolic syndrome and cerebrovascular disease: suspicion and evidence. 1797 40


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