OBJECTIVE -Visceral obesity is shown to be a predictor of morbidity and mortality. We evaluated the association of measurements of generalized adiposity and visceral fat area (VFA), with abnormalities of metabolic syndrome (MS).RESEARCH DESIGN AND METHODS -Seventy-six women (47.9 Ϯ 9.2 years) with BMI of 38.7 Ϯ 5.4 kg/m 2 underwent anthropometric measurements, laboratory procedures, bioeletrical impedance, and abdominal computed tomography (CT) scan. Diagnosis of MS was based on the presence of abdominal obesity and at least two of the following components: hypertension, dyslipidemia, and glucose intolerance and/or hyperinsulinemia.RESULTS -BMI was correlated with both components of adipose tissue-subcutaneous (r ϭ 0.66, P Ͻ 0.01) and VFA (r ϭ 0.33, P Ͻ 0.02)-and leptin levels (r ϭ 0.38, P Ͻ 0.01). In contrast, VFA was correlated with 2-h glucose and insulin levels (r ϭ 0.32 and 0.35, P Ͻ 0.05, respectively), triglyceride, HDL cholesterol, and uric acid (r ϭ 0.33, -0.34 and 0.24, P Ͻ 0.05, respectively). Subjects with high VFA, matched for BMI, showed greater plasma glucose area under the curve (621 Ϯ 127 vs. 558 Ϯ 129 mg ⅐ h Ϫ1 ⅐ dl Ϫ1 , P Ͻ 0.05), 2-h insulin (804 Ϯ 599 vs. 579 Ϯ 347 pmol/l, P Ͻ 0.05), and uric acid levels (0.33 Ϯ 0.07 vs. 0.26 Ϯ 0.06 mmol/l, P Ͻ 0.05) than subjects with low VFA. In logistic regression analysis, waist circumference, VFA, and 2-h insulin were identified as independent predictors of MS. Receiver operating characteristic curve analysis pointed out the values of 104 cm for waist circumference (58.1% specificity, 84.1% sensitivity), 158.5 cm 2 for VFA (78.1% specificity, 52.3% sensitivity), and 559.8 pmol/l for 2-h insulin (71.9% specificity, 69.8% sensitivity); the presence of at least two of the three variables resulted in a degree of concordance of 76%.CONCLUSIONS -While BMI was unable to differentiate between obese people and those at higher risk for MS, abdominal fat was shown to be associated with its metabolic abnormalities. The usefulness of abdominal fat in the identification of high-risk subjects may be improved when combined with 2-h insulin determination. Diabetes Care 26:1725-1730, 2003O besity is considered a major public health problem due to its increasing prevalence and high morbidity and mortality, mainly attributed to abnormalities included in the spectrum of the metabolic syndrome (MS) (1-3). Particularly, upper-body obesity has been shown to be an important predictor of cardiovascular disease (4). The search for markers able to identify subjects at high risk to develop MS is motivated by the potential benefits of early interventions.The simplicity of BMI assessment has made this widely used to classify subjects' risk of morbidity and mortality (1,5). However, BMI is not accurate to quantify body fat excess or the distribution of fatness. Recent studies have reported populations with low prevalence of obesity but high incidence of typical disturbances of MS (6,7), thereby raising the question of whether BMI plays a role in the identification of patients at high ...

Objective - Effects of Sibutramine on the Treatment of Obesity in Patients with Arterial Hypertension Artigo OriginalThe prevalence of obesity and its associated morbidities has increased in several countries worldwide, including Brazil 1,2 . The increase in body mass index has proved to be a determinant factor for elevation of blood pressure, both for obese and nonobese children and adults 3,4 . In addition, the presence of obesity is related to a 2.5 higher risk of arterial hypertension, mainly in patients with central body fat distribution 5 . Several hypotheses exist for the pathophysiology of arterial hypertension in this obese population. The first and more accepted hypothesis proposes that hyperinsulinemia secondary to insulin resistance existing in these patients leads to greater sympathetic activity and to renal sodium retention, which would account for the increase in pressure levels [6][7][8] . The second hypothesis associates the arterial hypertension existing in these patients with the mechanical compression of renal parenchyma by visceral fat. This leads to hyperactivation of the renin-angiotensinaldosterone system (RAAS), higher sodium reabsorption, and a subsequent elevation in blood pressure by a mechanism independent from insulinemia 9,10 .Even though we have not reached a consensus about the causes of arterial hypertension in the obese, several clinical studies confirm the importance of weight loss to better control blood pressure levels 11,12 .The great challenge has been to find effective clinical treatments, which do not impair blood pressure control, to induce weight loss in hypertensive patients. Of the several treatments available for weight control, we can count on appetite suppressing drugs, which comprise a generic class of drugs derived from amphetamines that act through adrenergic receptors, and, therefore, may aggravate hypertension. More recently, other options include orlistat that inhibits gastrointestinal fat absorption, and sibutramine, an appetite suppressant that blocks serotonin, dopamine, and noradrenaline reuptake 13 .The use of sibutramine is associated with an increase in satiety scores and a lack of decline in 24-hour energy

In essential hypertensive patients, considered to be insulin-resistant, a blunted decline in nocturnal blood pressure is associated with increased adrenergic tone and left ventricular mass. Since insulin stimulates the sympathetic system, we tested whether insulin resistance and insulinemia influence left ventricular mass and the 24-hour blood pressure profile. We studied 29 nonobese hypertensive patients with office diastolic pressure between 95 and 110 mm Hg and normal oral glucose tolerance test after a 4-month washout period. They were then assigned to M-mode echocardiographic evaluation and 24-hour ambulatory blood pressure monitoring. The glucose and insulin responses to a 75-g oral glucose load were compared with those obtained in 16 weight-matched normotensive control subjects. During the oral glucose tolerance test the hypertensive patients compared with control subjects presented higher levels of glucose at 60 minutes (138.7 +/- 30.3 versus 108.7 +/- 35.7 mg/dL; P < .05) and 90 minutes (114.0 +/- 23.8 versus 94.8 +/- 31.1 mg/dL; P < .05) and insulin at 60 minutes (287.1 +/- 259.4 versus 142.1 +/- 83.9 pmol/L; P < .05). However, peak insulin levels after glucose load did not correlate with ambulatory blood pressure values or left ventricular mass index. Left ventricular mass index showed significant correlation with mean sleeping systolic pressure (rs = 56, P < .05) and diurnal systolic pressure (rs = .37, P < .05) but not with mean diurnal or sleeping diastolic pressures. In conclusion, our results indicate that in nonobese hypertensive patients, insulin resistance does not have any influence on the 24-hour blood pressure profile or on left ventricular mass index.(ABSTRACT TRUNCATED AT 250 WORDS)

BackgroundHypertensive patients with reduced blood pressure fall (BPF) at night are at higher risk of cardiovascular events (CVE).MethodsWe evaluated in hypertensive diabetic patients, if a reduced nocturnal BPF can precedes the development of diabetic nephropathy (DN). We followed 70 patients with normal urinary albumin excretion (UAE) for two years. We performed 24-hours ambulatory BP monitoring in baseline and at the end of the study.ResultsFourteen (20%) patients (GI) developed DN (N = 11) and/or CVE (n = 4). Compared to the remaining 56 patients (GII) in baseline, GI had similar diurnal systolic (SBP) and diastolic BP (DBP), but higher nocturnal SBP (138 ± 15 vs 129 ± 16 mmHg; p < 0.05) and DBP (83 ± 12 vs 75 ± 11 mmHg; p < 0,05). Basal nocturnal SBP correlated with occurrence of DN and CVE (R = 0.26; P < 0.05) and with UAE at the end of the study (r = 0.3; p < 0.05). Basal BPF (%) correlated with final UAE (r = -0.31; p < 0.05). In patients who developed DN, reductions occurred in nocturnal systolic BPF (12 ± 5 vs 3 ± 6%, p < 0,01) and diastolic BPF (15 ± 8 vs 4 ± 10%, p < 0,01) while no changes were observed in diurnal SBP (153 ± 17 vs 156 ± 16 mmHg, NS) and DBP (91 ± 9 vs 90 ± 7 mmHg, NS). Patients with final UAE < 20 μg/min, had no changes in nocturnal and diurnal BP.ConclusionsOur results suggests that elevations in nocturnal BP precedes DN and increases the risk to develop CVE in hypertensive patients with T2DM.

Reductions in both the insulin levels and the resistance index reinforced metformin capacity to improve peripheral sensitivity. Moreover, such benefits were not accompanied by any hypotensive effects. Since leptin levels were affected neither by metformin per se nor by the induced insulinaemia reduction, our data support the role of body weight as the major determinant of circulating leptin levels.

Sibutramine therapy induced greater body weight loss than placebo in hypertensive obese patients. This was associated with WHR reduction, decreases in VF and insulin resistance. The maintenance of leptin levels during sibutramine therapy may be important to avoid weight recovery, although this finding must be confirmed by other prospective studies.

Purpose -To evaluate left ventricular mass (LVM) index in hypertensive and normotensive obese individuals. Methods -Echocardiographic evaluation of hypertensive individuals is based on preestablished guidelines for detecting left ventricular hypertrophy, determined in relation to populations of normotensive individuals. In turn, the definition of normal left ventricular mass implies its correction by influencing physiological factors. Thus, sex, body habitus, and possibly age are of importance in this correction.The best index of left ventricular mass is that obtained using the physiological scale of weight and height variables, regarding both men and women.Therefore, the ideal index would be lean body mass 1 , but this method is not practical and has not been used. Thus, indexing ventricular mass by body surface area (BSA) is preferred 2 . However, such an index leads to underestimation of left ventricular hypertrophy in obese individuals (with a greater BSA), because its regards obesity as a continuous physiological variable that would determine increases in left ventricular mass also on a physiological scale 3 . To correct this, use of mass by height, whose limits are within the physiological range and thus maintain a normal and not a pathological relation to ventricular mass, has been proposed as an index [4][5][6] . More recent studies 7-11 further suggest that left ventricular mass index should be determined by height or even height raised to a power of 2, 2.7, or 2.13, because no first order relation has been demonstrated between height and left ventricular mass.In this sense, some selection criteria have been established that have been used for the correction of mass by these proposed indexers (men -126/143g/m; 49.2g/m 2.7 ; women -105/102g/m; 46.7g/m 2.7 )4,11 . Such criteria, up to the present, have preferentially been used in larger population studies 11,[13][14][15][16] with the purpose of detecting the impact of the different indexes used on the prevalence of

Em sintonia com a tendência científica mundial e a orientação da Associação Médica Brasileira, as IV Diretrizes Brasileiras de Hipertensão fundamentam suas orientações segundo Graus de Recomendação baseados em níveis de evidência dos estudos clínicos de referência:Grau A -grandes ensaios clínicos aleatorizados e metanálises. Grau B -estudos clínicos e observacionais bem desenhados. Grau C -relatos e séries de casos. Grau D -publicações baseadas em consensos e opiniões de especialistas.