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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study was to cross-sectionally analyze, in a group of essential hypertension patients without diabetes mellitus, the influence of the metabolic syndrome (MS) on the stroke volume index to pulse pressure (SVi/PP) ratio, a measure of total arterial compliance. A total of 528 essential hypertension patients, aged 18 to 72 years, free from cardiovascular and renal disease (41% of whom had MS) were enrolled. All participants underwent routine blood chemistry, echocardiographic examination, and 3 blood pressure measurements at the end of echocardiographic examination. When compared with participants who did not have MS, hypertensive patients with MS exhibited lower SVi/PP ratio (0.65+/-0.22 vs 0.73+/-0.21 mm Hg; P=.0003). The independent association of MS with SVi/PP ratio (beta=0.10; P=.02) was confirmed in a multivariate regression model including age, sex, and other potential confounders as covariates. The authors' finding may help to explain the enhanced cardiovascular risk associated with MS.
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PMID:Impact of the metabolic syndrome on total arterial compliance in essential hypertension patients. 1768 62

Limited evidence is available about the relationship between ambulatory heart rate (HR) and target organ damage (TOD) in uncomplicated hypertension. We sought to investigate the association between ambulatory HR and subclinical cardiac, vascular and renal markers of TOD in never-treated essential hypertensives. A total of 580 subjects with recently diagnosed (<or= 1 year) grade 1 and 2 hypertension, categorized by tertiles of HR levels, assessed by two 24-h ambulatory blood pressure monitoring at 1- to 4-week interval, sex and the presence or absence of TOD were considered for this analysis. All subjects also underwent laboratory and ultrasonographic investigations searching for microalbuminuria (MA), left ventricular hypertrophy (LVH) and carotid atherosclerosis (carotid thickening/plaque). In the whole population, as well as in both genders, LVH, carotid atherosclerosis and MA prevalence rates did not significantly increase with 48-h HR tertiles. When patients were categorized according to the presence or absence of TOD (that is, LVH, carotid atherosclerosis or MA) no significant intergroup differences in 48-h HR were found. Furthermore, average 48-h HR was similar in patients without organ involvement as in those with one, two or three TOD signs. Finally, in a multivariate analysis age, 48-h systolic blood pressure and metabolic syndrome assessed by ATP III criteria, but not HR were independently associated with TOD. Our findings showing that 48-h ambulatory HR is not associated with markers of TOD do not support the view that a faster HR may have an additive value in predicting organ damage in the early phases of essential hypertension.
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PMID:Ambulatory heart rate and target organ damage in never-treated essential hypertensives. 1782 95

We examined oxidative stress and metabolic characteristics of the spontaneously hypertensive hyperlipidemic rat (SHHR) when it was fed a high-fat diet and sucrose solution (HFDS) after N(G)-nitro-L-arginine methyl ester ingestion to develop a rat model of metabolic syndrome. This study was carried out to assess the effects of pioglitazone on levels of lipid peroxide (LPO), Cu,Zn superoxide dismutase (Cu,Zn-SOD), catalase (CAT), glutathione peroxidase (GPx), and non-esterified fatty acids (NEFA) in the plasma and liver tissue in HFDS-SHHR compared with Sprague-Dawley rats (SD). In the HFDS-treated groups, levels of LPO, CAT, GPx, and NEFA were elevated and levels of Cu,Zn-SOD were reduced in the plasma and liver tissue, with a marked accumulation of visceral fat. The changes induced by HFDS feeding were severe in the SHHR model that had essential hypertension and hyperlipidemia, when compared with SD that did not have these essential risk factors. Subcutaneous injection of 10 mg/kg per day of pioglitazone for 2 months significantly restored levels of LPO, CAT, GPx, Cu,Zn-SOD, and NEFA in the HFDS-SHHR group, and visceral fat accumulation was reduced. These results suggest that HFDS-SHHR is a suitable model of metabolic syndrome and that pioglitazone treatment can improve oxidative dysregulation in this rat model.
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PMID:Effects of pioglitazone on increases in visceral fat accumulation and oxidative stress in spontaneously hypertensive hyperlipidemic rats fed a high-fat diet and sucrose solution. 1791 67

This study was undertaken to compare the antihypertensive efficacy of zofenopril 30 mg + hydrochlorothiazide 12.5 mg fixed combination versus zofenopril alone in patients with essential hypertension with and without the metabolic syndrome, according to National Cholesterol Education Program-Adult Treatment Panel III criteria. After a 4-wk placebo washout period, 463 patients with mild to moderate essential hypertension (diastolic blood pressure [DBP] 95-115 mm Hg) aged 18 to 75 y were randomly assigned 2:1:1 to treatment with zofenopril+hydrochlorothiazide, zofenopril, or hydrochlorothiazide for 12 wk in an international, multicenter, double-blind, parallel-group study. DBP and systolic blood pressure changes with treatment were calculated. The first 12 wk of treatment were followed by a 24-wk open-label period during which only safety was assessed. Reported here is a subanalysis of the main study results, performed in patients with and without metabolic syndrome, limited to a zofenopril+hydrochlorothiazide versus zofenopril comparison. The antihypertensive effect of zofenopril+hydrochlorothiazide or zofenopril was similar in patients with (77%) and without metabolic syndrome. In patients with and without metabolic syndrome, however, DBP and systolic blood pressure reductions were significantly greater with zofenopril+hydrochlorothiazide (with metabolic syndrome: 14+/-8/21+/-14 mm Hg; without metabolic syndrome: 15+/-7/23+/-14 mm Hg) than with zofenopril alone (with metabolic syndrome: 10+/-9/11+/-15; without metabolic syndrome: 12+/-10/14+/-18 mm Hg). The safety of the 2 treatments was similar in patients with and without metabolic syndrome. The fixed combination of zofenopril+hydrochlorothiazide improved the efficacy of zofenopril alone. This effect was particularly evident in patients with metabolic syndrome, in whom blood pressure control is more difficult to achieve and who are at greater risk for cardiovascular events.
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PMID:Antihypertensive efficacy of zofenopril plus hydrochlorothiazide fixed combination for treatment in metabolic syndrome. 1802 26

Though it has long been recognised that there is a hereditary component to the obstructive sleep apnoea/hypopnoea syndrome (OSAHS), identifying its genetic basis remains elusive. Hypertension and metabolic syndrome, like OSAHS, are polygenic disorders, physiologically complex and the product of highly organised, hierarchical systems within the body. Elucidating their genetic basis is difficult when they are considered in isolation but even more difficult if their interrelationships with each other are brought into play. Not least of the problems is the lack of adequate and consistent phenotyping, which has hampered genetic dissection of these diseases; in addition, sleep-disordered breathing has not been factored into most studies dealing with essential hypertension or metabolic syndrome. Genome-wide scans have yielded inconsistent results in all three disorders under discussion and candidate gene studies of possible regulatory molecules require more rigorous replication. One approach would be to use 'intermediate' phenotypes and dense mapping of candidate genes for identifying genotype-phenotype correlations. This review focuses on genetic factors, which may be responsible for the expression of cardiovascular disease and metabolic syndrome in the context of OSAHS.
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PMID:Genetic aspects of hypertension and metabolic disease in the obstructive sleep apnoea-hypopnoea syndrome. 1820 63

Obesity is the main intermediate phenotype of primary hypertension (PH), and increased fat mass is directly related to target organ damage (TOD) and metabolic syndrome (MS). The aim of the study was to assess the sensitivity and specificity of body mass index (BMI), percentile-based, definitions of obesity [BMI > 95th percentile (pc)], and overweight (BMI > 85th pc), and BMI thresholds for cardiovascular (cv) complications (BMIcv) described by Katzmarzyk et al. (Pediatrics 114:198-205, 2004) in predicting risk of TOD and MS in 122 adolescents with PH. Our results indicated that the prevalence of left ventricular hypertrophy (LVH) and carotid intima-media thickness (cIMT) above 2 standard deviations (SDS) was the same, irrespective of the criteria used. BMIcv was more sensitive as a marker of LVH than were the cut-off values of the 85th pc and 95th pc of BMI (87.5%, 75%, 62.5%, respectively; P < 0.0001). BMIcv thresholds and cut-off values of the 85th pc of BMI were of the same sensitivity in predicting the presence of MS (95.8% and 95.8%, respectively) and were more sensitive than the cut-off values of the BMI 95th pc (87.5%; P = 0.02). Metabolic abnormalities, including insulin resistance, were more marked in patients with greater BMI, irrespective of cut-off value. However, only when a stratification system using the 85th pc of BMI was used, were the differences significant for a homoeostasis model assessment for insulin resistance (HOMA-IR) and for serum concentrations of high-density lipoprotein (HDL)-cholesterol, triglycerides and adiponectin. We concluded that BMIcv is more sensitive for diagnosing the presence of LVH and that the cut-off value of the 85th pc of BMI is more sensitive for predicting presence of MS in children with PH.
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PMID:Different BMI cardiovascular risk thresholds as markers of organ damage and metabolic syndrome in primary hypertension. 1825 58

Studies performed during the last decade indicate that adipose tissue is not only a site of triglyceride storage but also an active endocrine organ which secretes many biologically active mediators referred to as "adipokines". In contrast to many adipokines which are overproduced in obese individuals and exert deleterious effects on insulin sensitivity, lipoprotein metabolism and cardiovascular system, such as leptin, tumor necrosis factor-alpha, plasminogen activator inhibitor-1, resistin, etc., adiponectin seems to be a unique adipokine which is produced in lower amounts in obese than in lean subjects and possesses predominantly beneficial activities, i.e. increases insulin sensitivity, stimulates fatty acid oxidation, inhibits inflammatory reaction and induces endothelium-dependent nitric oxide-mediated vasorelaxation. Adiponectin binds two receptors, AdipoR1 and AdipoR2. Adiponectin knockout mice exhibit various manifestations of the metabolic syndrome such as insulin resistance, glucose intolerance, hyperlipidemia, impaired endothelium-dependent vasorelaxation and hypertension, as well as augmented neointima formation after vascular injury. Clinical studies indicate that plasma adiponectin concentration is lower in patients with essential hypertension and ischemic heart disease. Raising endogenous adiponectin level or increasing the sensitivity to this hormone may be a promising therapeutic strategy for patients with metabolic and cardiovascular diseases. Among currently used drugs, thiazolidinediones (peroxisome proliferator activated receptor gamma agonists) are most effective in elevating adiponectin level.
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PMID:Adiponectin and its role in cardiovascular diseases. 1833 52

The field of primary aldosteronism (PA) and aldosterone-related hypertension has undergone rapid evolution. From a relatively rare curiosity PA has become a common problem particularly in selected hypertensive populations. Patients with PA and aldosterone-related hypertension appear to be at higher cardiovascular and renal risk than comparable patients with essential hypertension probably due to the pleiotropic effects of aldosterone. Aldosterone is also linked to metabolic syndrome and diabetes. The aldosterone-to-renin ratio (ARR) has allowed the widespread screening for PA, but the exact cut-off values may vary in different population groups. All patients with hypertension and hypokalaemia, and young patients with hypertension, hypertension with an incidental adrenal mass, and severe or resistant hypertension should be screened. The use of the ARR to screen all hypertensives for PA is controversial as the test lacks specificity and many patients with false-positive tests will undergo complex and expensive testing to confirm the diagnosis. The fludrocortisone suppression test, the saline infusion test or 24-hour aldosterone excretion may be used to confirm PA in patients with a positive ARR. Adrenal venous sampling is the most reliable test to detect the presence of an aldosterone-producing adenoma, but spiral CT scan or adrenocortical scintigraphy may be useful in centres without facilities for adrenal venous sampling. Spironolactone is emerging as an important antihypertensive agent in patients with resistant hypertension and aldosterone-related hypertension. The ARR may be a useful guide to drug selection in hypertensives patients, but further research is needed to make more definitive recommendations.
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PMID:Primary aldosteronism and aldosterone-associated hypertension. 1858 13

Several studies documented an association between metabolic syndrome (MetS) and left ventricular (LV) hypertrophy. However, only in a few of these studies the impact of MetS on left ventricular mass (LVM) was separately analysed by gender, with conflicting results. The aim of our study was to verify, in a wide sample of essential hypertensive patients, the influence of gender, if any, on the relationship between MetS and LVM. We enrolled 475 non-diabetic subjects (mean age: 46 +/- 11 years), with mild-to-moderate essential hypertension, of whom 40% had MetS, defined on the basis of Adult Treatment Panel III (ATPIII) criteria. All the patients underwent a 24-h ambulatory blood pressure monitoring and an echocardiogram. LVM indexed for height (2.7) (LVMH (2.7)) was significantly (P < 0.001) higher in women with MetS (n=83) than in those without it (n=97; 54+/-17 vs 42+/-11 g m(-2.7)). An equally significant difference in LVMH (2.7) was documented also in male gender between the two groups with (n=105) and without MetS (n=190; 51+/-14 vs 43+/-11 g m(-2.7); P < 0.001). The relationship between MetS and LVMH (2.7) remained statistically significant (P < 0.001) in both sexes, in multiple regression analyses, even after adjustment for potential confounding factors. Our results seem to suggest that the relationship between MetS and LVM is not significantly affected by gender, being LVM increased in both hypertensive women and men with MetS.
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PMID:Relationships between metabolic syndrome and left ventricular mass in hypertensive patients: does sex matter? 1914 6

Important mechanism of pathogenesis of hypertension in obesity is renin-aldosterone system in adipose tissue. Adrenal cells can be also stimulated to aldosterone secretion by local adrenal fat cells and also by other factors from fat tissue (lipids, endocrine disruptors). Local system renin-aldosteron is active also in other tissues and organs in obesity related hypertension. Feed back is closed by recently investigated fact that aldosteron hypersecretion can cause metabolic syndrome. Between systemic approach to obesity a new phenomenon of organ obesity is coming - adipokines from local fat cells can influence organ and tissue function e.g. in essential hypertension.
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PMID:[System renin-aldosterone in fat tissue and other organ and tissues]. 1863 Jun 37


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