The metabolic syndrome in hypertension: European society of hypertension position statement

University of Valencia and CIBER 06/03 Physiopathology of Obesity and Nutrition, Institute of Health Carlos III, Madrid, Spain.
Journal of Hypertension (Impact Factor: 4.22). 11/2008; 26(10):1891-900. DOI: 10.1097/HJH.0b013e328302ca38
Source: PubMed

ABSTRACT The metabolic syndrome considerably increases the risk of cardiovascular and renal events in hypertension. It has been associated with a wide range of classical and new cardiovascular risk factors as well as with early signs of subclinical cardiovascular and renal damage. Obesity and insulin resistance, beside a constellation of independent factors, which include molecules of hepatic, vascular, and immunologic origin with proinflammatory properties, have been implicated in the pathogenesis. The close relationships among the different components of the syndrome and their associated disturbances make it difficult to understand what the underlying causes and consequences are. At each of these key points, insulin resistance and obesity/proinflammatory molecules, interaction of demographics, lifestyle, genetic factors, and environmental fetal programming results in the final phenotype. High prevalence of end-organ damage and poor prognosis has been demonstrated in a large number of cross-sectional and a few number of prospective studies. The objective of treatment is both to reduce the high risk of a cardiovascular or a renal event and to prevent the much greater chance that metabolic syndrome patients have to develop type 2 diabetes or hypertension. Treatment consists in the opposition to the underlying mechanisms of the metabolic syndrome, adopting lifestyle interventions that effectively reduce visceral obesity with or without the use of drugs that oppose the development of insulin resistance or body weight gain. Treatment of the individual components of the syndrome is also necessary. Concerning blood pressure control, it should be based on lifestyle changes, diet, and physical exercise, which allows for weight reduction and improves muscular blood flow. When antihypertensive drugs are necessary, angiotensin-converting enzyme inhibitors, angiotensin II-AT1 receptor blockers, or even calcium channel blockers are preferable over diuretics and classical beta-blockers in monotherapy, if no compelling indications are present for its use. If a combination of drugs is required, low-dose diuretics can be used. A combination of thiazide diuretics and beta-blockers should be avoided.

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    ABSTRACT: For many years, it has been recognized that hypertension tends to cluster with various anthropometric and metabolic abnormalities including abdominal obesity, elevated triglycerides, reduced high-density lipoprotein cholesterol, glucose intolerance, insulin resistance and hyperuricemia. This constellation of various conditions has been transformed from a pathophysiological concept to a clinical entity, which has been defined metabolic syndrome (MetS). The consequences of the MetS have been difficult to assess without commonly accepted criteria to diagnose it. For this reason, on 2009 the International Diabetes Federation, the American Heart Association and other scientific organizations proposed a unified MetS definition. The incidence of the MetS has been increasing worldwide in parallel with an increase in overweight and obesity. The epidemic proportion reached by the MetS represents a major public health challenge, because several lines of evidence showed that the MetS, even without type 2 diabetes, confers an increased risk of cardiovascular morbidity and mortality in different populations including also hypertensive patients. It is likely that the enhanced cardiovascular risk associated with MetS in patients with high blood pressure may be largely mediated through an increased prevalence of preclinical cardiovascular and renal changes, such as left ventricular hypertrophy, early carotid atherosclerosis, impaired aortic elasticity, hypertensive retinopathy and microalbuminuria. Indeed, many reports support this notion, showing that hypertensive patients with MetS exhibit, more often than those without it, these early signs of end organ damage, most of which are recognized as significant independent predictors of adverse cardiovascular outcomes.
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    ABSTRACT: There is a neglected epidemic of both obesity and metabolic syndrome in industrialized and unindustrialized countries all over the globe. Both conditions are associated with a high incidence of other serious pathologies, such as cardiovascular and renal diseases. In this article, we review the potential underlying mechanisms by which obesity and metabolic syndrome promote hypertension, including changes in cardiovascular-renal physiology induced by leptin, the sympathetic nervous system, the renin-angiotensin-aldosterone system, insulin resistance, free fatty acids, natriuretic peptides, and proinflammatory cytokines. We also discuss the potential underlying mechanisms by which obesity promotes other cardiovascular and renal conditions, as well as available nonpharmacologic and pharmacologic approaches for treating obesity-induced hypertension. The findings presented herein suggest that adipocytes may be a key regulator of cardiovascular and renal function.
    Current Hypertension Reports 02/2015; 17(2):520. DOI:10.1007/s11906-014-0520-2 · 3.90 Impact Factor
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    ABSTRACT: Purpose We investigated the association between metabolic syndrome (MS), its components and the presence of subclinical organ damage in hypertensive perimenopausal women. Patients/methods 152 women with newly diagnosed, untreated arterial hypertension (mean age 51.0 ± 3.5 years) were included in the study. In all subjects anthropometrical measurements, 24-hr blood pressure monitoring, echocardiographic examination, and carotid ultrasound were performed. Carotid-femoral pulse wave velocity (PWV) was measured to obtain data on vascular compliance. As the index of early kidney damage both glomerular filtration rate was calculated and albumin/creatinine ratio in the urine sample was measured. A fasting blood sample was taken to measure glucose and lipid concentration. Results MS was found in 41% of patients. Patients with MS exhibited elevated left ventricular mass index (LVMI 84.7 vs. 78.8 g/m2.7, p = 0.03), higher intima-media thickness (IMT 0.67 vs. 0.62 mm, p = 0.003), greater prevalence of LV hypertrophy (30% vs. 13%, p = 0.01), and carotid plaques (24% vs. 15%, p = 0.01). The multivariate regression analysis revealed that components of MS (systolic blood pressure and waist circumference) are stronger predictors of LVM than MS itself. The relationship between MS and LVMI lost its significance when BMI was included in the model, and remained significant for IMT. Conclusion In hypertensive perimenopausal women components of MS are stronger predictors of subclinical organ damage than MS itself. Left ventricular mass and hypertrophy are more strongly correlated with increasing body weight than with the presence of MS. MS, independently of BMI, influences the level of subclinical atherosclerosis in the study group.
    Advances in Medical Sciences 09/2014; DOI:10.1016/j.advms.2013.12.002 · 0.96 Impact Factor

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