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Recent studies suggest that supplemental Ca (SC) increases the risk of cardiovascular events, whereas dietary Ca (DC) decreases the risk of cardiovascular events. Although frequently consumed with meals, it remains unclear whether Ca can mitigate or aggravate the deleterious effects of a high-fat meal on cardiovascular risk factors. This study aimed to evaluate the effects of SC or DC on blood pressure (BP) and microvascular function (MVF) in the postprandial period in obese women challenged with a high-fat meal. In this cross-over controlled trial, sixteen obese women aged 20–50 years were randomly assigned to receive three test meals (2908 kJ (695 kcal); 48 % fat): high DC (HDCM; 547 mg DC), high SC (HSCM; 500 mg SC–calcium carbonate) and low Ca (LCM; 42 mg DC). BP was continuously evaluated from 15 min before to 120 min after meals by digital photoplethysmography. Before and 120 min after meals, participants underwent evaluation of serum Ca and microvascular flow after postocclusive reactive hyperaemia (PORH) by laser speckle contrast imaging. Ionised serum Ca rose significantly only after HSCM. Systolic BP increased after the three meals, whereas diastolic BP increased after LCM and HDCM. Hyperaemia peak, hyperaemia amplitude and AUC evaluated after PORH decreased with LCM. After HDCM, there was a reduction in hyperaemia peak and hyperaemia amplitude, whereas HSCM decreased only hyperaemia peak. However, comparative analyses of the effects of three test meals on serum Ca, BP and MVF revealed no significant meal×time interaction. This study suggests that in obese women SC and DC do not interfere with the effects of a high-fat meal on BP and MVF.

Objectives Obstructive sleep apnea (OSA) is associated with an increased risk of cardiovascular disease (CVD). Several of the proposed mechanisms for the development of CVD in OSA are similar to those proposed for the increased risk of CVD in obesity, so that it is difficult to determine the influence of OSA on these pathogenic mechanisms in obese individuals. The aim of this study was to evaluate the relationship of OSA with endothelial function, oxidative stress, inflammatory biomarkers, metabolic profile, sympathetic nervous system activity, and blood pressure (BP) in obese individuals. Methods This cross-sectional study included 53 obese adults (28 women). Sleep study was performed with WatchPAT 200 (Itamar Medical, Caesarea, Israel) and the diagnosis of OSA was made when apnea-hypopnea index (AHI) ≥5 events/h (n = 33). All participants underwent evaluation of: body adiposity, BP, plasma catecholamines, high sensitivity C-reactive protein (hs-CRP), adiponectin, malondialdehyde, glucose, insulin, lipid profile, and endothelial function (EndoPAT 2000). Results In univariate analysis, participants with OSA compared with those without OSA exhibited higher values of neck circumference, glucose, noradrenaline, and systolic BP. After adjustment for confounders, including adiposity, only glucose and hs-CRP were significantly higher in OSA patients. In correlation analysis, after controlling for confounders, AHI was positively and significantly associated with neck circumference and hs-CRP, while minimum O 2 saturation was associated negatively and significantly with neck circumference, insulin and homeostatic model assessment–insulin resistance (HOMA-IR). Conclusions The present study suggests that in obese individuals OSA is independently associated with inflammation and insulin resistance, but not with BP, plasma catecholamines and endothelial function.

Nutritional intervention for weight loss is one of the treatment options for obstructive sleep apnoea (OSA) in patients with overweight or obesity. However, the effects of moderate energy restriction on OSA severity are not yet known. The present study aimed to evaluate the effects of moderate energy restriction on OSA severity and CVD risk factors in obese patients with OSA. In this 16-week randomised clinical trial, twenty-one obese subjects aged 20–55 years and presenting an apnoea/hypopnoea index (AHI)≥5 events/h were randomised into two groups: the energy restriction group (ERG) and the control group (CG). The ERG was instructed to follow an energy-restricted diet −3347·2 kJ/d (−800 kcal/d) and the CG was advised not to change their food intake. At the beginning and at the end of the study, participants underwent evaluation of the following: OSA (Watch-PAT200®), nutritional parameters, blood pressure, sympathetic activity, inflammatory biomarkers, metabolic profile and endothelial function. The ERG (n11), compared with the CG (n10), had a significantly greater reduction in body weight (Cohen’sd=−1·19;Pd=−0·95;P=0·04) and in plasma concentrations of adrenaline (Cohen’sd=−1·02;P=0·04) as well as a significantly greater increase in minimum O2saturation (Cohen’sd=1·08;P=0·03). Although energy restriction was not associated with significant improvements in CVD risk factors, medium-to-large effect sizes were observed, suggesting that the statistically non-significant difference between groups may be due to the small sample size. This study suggests that in obese patients with OSA, moderate energy restriction is able to reduce the parameters of OSA severity and sympathetic activity.

The aim of this study is to compare spironolactone versus clonidine as the fourth drug in patients with resistant hypertension in a multicenter, randomized trial. Medical therapy adherence was checked by pill counting. Patients with resistant hypertension (no office and ambulatory blood pressure [BP] monitoring control, despite treatment with 3 drugs, including a diuretic, for 12 weeks) were randomized to an additional 12-week treatment with spironolactone (12.5–50 mg QD) or clonidine (0.1–0.3 mg BID). The primary end point was BP control during office (P =1.00). Secondary end point analysis showed similar office BP (33.3% versus 29.3%) and ambulatory BP monitoring (44% versus 46.2%) control for spironolactone and clonidine, respectively. However, spironolactone promoted greater decrease in 24-h systolic and diastolic BP and diastolic daytime ambulatory BP than clonidine. Per-protocol analysis (limited to patients with ≥80% adherence to spironolactone/clonidine treatment) showed similar results regarding the primary end point. In conclusion, clonidine was not superior to spironolactone in true resistant hypertensive patients, but the overall BP control was low (≈21%). Considering easier posology and greater decrease in secondary end points, spironolactone is preferable for the fourth-drug therapy. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT01643434.

Non-fasting hypertriacylglycerolaemia is a risk factor for CVD and the amount of fat in a meal seems to be the main factor influencing postprandial lipaemia. Although several studies suggest that Ca can increase faecal fat excretion, it is not known whether Ca can decrease postprandial TAG. This study aimed to evaluate the influence of dietary Ca (DC) and supplemental Ca (SC) on lipaemia, glucose metabolism, C-reactive protein (CRP) and adiponectin during postprandial period in obese women challenged with a high-fat meal. In this cross-over controlled trial, sixteen obese women aged 20–50 years were randomly assigned to receive three test meals (approximately 2900 kJ; 48 % fat): high DC (547 mg DC), high SC (HSCM; 500 mg SC-calcium carbonate) and low Ca (42 mg DC). Blood samples were collected in the fasting period and at minutes 120 and 240 after meals to evaluate total cholesterol and fractions, TAG, glucose, insulin, high-sensitivity CRP and adiponectin. Serum levels of TAG and insulin increased significantly after all test meals. Only after HSCM total cholesterol did not present a significant increase and LDL-cholesterol had a significant decrease. Postprandial glucose, HDL-cholesterol, CRP and adiponectin did not present significant changes after the three test meals. The comparative analysis of the effects of the three test meals on serum lipids, glucose, insulin, CRP and adiponectin revealed no significant meal-by-time interaction. These results suggest that in obese women challenged with a high-fat meal DC and SC do not interfere with postprandial lipaemia, glucose metabolism, CRP and adiponectin.

Objective The aim of this study was to evaluate high body adiposity and cardiovascular disease (CVD) risk factors prevalence, in renal transplant recipients (RTR), comparing men with women. Methods In this retrospective cross-sectional study, 102 patients (55 men) who were 49 ± 1.2 y and 114.3 ± 9 mo post-transplant (post-tx) were evaluated. Pretransplant (pre-tx) period data and weight gain during the first year post-tx were obtained from patient charts and post-tx data were collected during a routine visit at nephrology clinic. Body mass index (BMI) ≥ 25 kg/m 2 defined overweight and BMI ≥ 30 kg/m 2 defined obesity. Results Pre-tx overweight prevalence was low and similar between men and women (26%), whereas only women showed obesity (11%). Post-tx body weight increased significantly in the entire group, leading to an increase in overweight (to 38% in men and 51% in women) and obesity (to 11% in men and 23% in women) prevalence. Post-tx comparisons between men and women showed that women had higher (women versus men; P 2 ), weight gain during first year post-tx (9.2 ± 1.1 versus 5.5 ± 1 kg), abdominal obesity (57% versus 23%) and diabetes (34% versus 16%) prevalence. The associations between adiposity and CVD risk factors showed that pre-tx overweight increased the risk for diabetes in post-tx; pos-tx high BMI and abdominal obesity increased the risk for metabolic syndrome; abdominal obesity increased the risk for dyslipidemia in women. Conclusions High body adiposity prevalence was high after transplantation and increased the risk for metabolic syndrome, an important CVD risk factor. Women showed higher total body adiposity values, abdominal obesity, and diabetes prevalence than men. Abdominal obesity increased the risk for dyslipidemia in women.

Objective: Obesity is characterized by chronic subclinical inflammation, which is critical to endothelial dysfunction. Weight loss, induced by lifestyle interventions, is associated with a decline in biomarkers of inflammation and endothelial dysfunction. There is little evidence that high dietary calcium intake may reduce inflammation and improve endothelial function. The purpose of this study was to evaluate the effects of weight loss from a high-calcium energy-reduced diet on biomarkers of inflammation, fibrinolysis, and endothelial function in obese individuals. Methods: In this randomized clinical trial, we analyzed the data from 35 obese adults who lost at least 3% of initial body weight, during a period of 16 wk of energy restriction (� 800 Kcal/d). Individuals were randomized into the following dietary regimens: (1) a high calcium diet (HCD; 1200–1300 mg/d) or (2) a low-calcium diet (LCD

Background Most studies evaluating the conjoint effects of leptin and human soluble leptin receptor (hs-LR) on cardiometabolic risk factors have been conducted in well-characterized ethnic groups. We aimed to assess the associations of leptin and hs-LR with the cardiometabolic risk factors that reflect the components of metabolic syndrome (MetS) in a Brazilian population with varying degrees of adiposity. Methods This is a cross-sectional analysis of adult subjects (n=173, age 45±12 years, 124 women; body mass index [BMI] 35.6±9.5 kg/m2) for association of leptin and its soluble receptor with cardiometabolic risk factors (glucose, BMI, waist circumference, hip circumference, blood pressure, insulin, cholesterol and triglycerides). Plasma hs-LR was measured by ELISA; insulin and leptin were determined by RIA. Metabolic syndrome was defined by NCEP/ATP III. Results Leptin was positively associated with blood pressure, BMI, waist circumference, hip circumference, triglycerides, glucose, insulin and HOMA and inversely correlated with HDL-cholesterol. The hs-LR exhibited inverse relationship with cardiometabolic risk factors (P≤0.006), except for glucose and lipid parameters. Leptin increased, whereas hs-LR decreased, with increasing number of MetS components (P for trend

This aim of this study was to evaluate the association between dietary calcium and variables that include body mass index, abdominal obesity, metabolic profile, and blood pressure levels in renal transplant patients.A cross-sectional study was conducted.Eligible patients were recruited from renal transplant outpatient clinics at Pedro Ernesto University Hospital, Rio de Janeiro, Brazil.A total of 40 men and 34 women aged18 years who had received kidney transplants in the past ≥12 months were included in this study.All patients underwent clinical, dietary, anthropometric, and biochemical evaluation.Participants were classified into the following 2 groups on the basis of their mean dietary calcium intake: group A (600 mg/day) and group B (≥600 mg/day). Patients in group B presented significantly lower levels of waist circumference and waist-to-hip ratio as compared with those in group A (P = .04 and P = .005, respectively), after adjusting for confounding variables such as energy intake, gender, age, physical activity, time since transplantation, and prednisone dose. After controlling for potential confounders, including energy intake and physical activity, subjects in group B had a lower odds ratio for prevalent abdominal obesity as compared with those in group A (odds ratio, 0.17; 95% confidence interval, 0.03 to 0.94; P = .04). Body mass index was significantly lower in patients with higher calcium intake; however, this difference did not reach statistical significance after adjustments for confounding factors. Metabolic profile and blood pressure levels were similar in both groups.The findings of the present study suggest that a higher dietary calcium intake may be associated with lower abdominal adiposity in renal transplant patients.

Obesity is the major risk factor for the development of hypertension. This association accentuates the risk of cardiovascular disease, as it is frequently accompanied by the components of the metabolic syndrome. This randomised open parallel study evaluated the chronic effects of moxonidine--a selective imidazoline receptor agonist--on blood pressure, plasma catecholamines, leptin, insulin and components of the metabolic syndrome in obese hypertensives. Amlodipine was used as the control drug. Our results showed that moxonidine and amlodipine significantly reduced blood pressure when measured using the oscillometric method and 24-hour blood pressure monitoring. Moxonidine therapy decreased systolic blood pressure from 160.4 +/- 2.4 to 142.1 +/- 3.3 mmHg (p < 0.005) and diastolic blood pressure from 102.4 +/- 1.3 to 89.7 +/- 1.6 mmHg (p < 0.005) after 24 weeks of treatment. Moxonidine administration reduced the supine arterial plasma levels of adrenaline from 63.2 +/- 6.6 to 49.0 +/- 6.7 pg/ml (p < 0.005), the supine arterial plasma levels of noradrenaline from 187.9 +/- 10.7 to 149.7 +/- 13.2 pg/ml (p < 0.01) and the orthostatic venous plasma levels of noradrenaline from 258.6 +/- 25.0 to 190.3 +/- 16.4 pg/ml (p = 0.03). Those variables were not changed by amlodipine. The plasma levels of leptin and insulin 120 min after a glucose load decreased after moxonidine administration from 27.2 +/- 3.5 to 22.6 +/- 2.9 pg/ml (p < 0.05) and from 139.7 +/- 31.2 to 76.0 +/- 15.2 U/ml (p < 0.05), respectively. Amlodipine, however, did not modify those variables. This study showed a comparable reduction in blood pressure with both antihypertensive drugs. Moxonidine decreased sympathetic nervous activity, improved insulin resistance and reduced the plasma levels of leptin.

Insulin resistance is frequently associated with obesity-related hypertension. Leptin resistance and increased plasma leptin levels are frequent companions in this association. To examine whether in obesity hypertension with insulin resistance, plus hyperleptinemia, the sodium content of erythrocyte (Naie) reflects a positive sodium balance related to the physiological loss of leptin in sodium reabsorption, we studied a group of obese hypertensive patients, and a group of lean normotensive subjects. In obese hypertensives, fasting glucose, insulin and the insulin resistance index were higher as compared to the lean individuals (107.0 ± 4.1 mg/dl, 10.2 ± 1.4 pU/ml and 2.94 ± 0.52, respectively, vs 98.7 ± 4.1 mg/dl, 7.22 ± 1.33 U/ml, and 1.79 ± 0.16, respectively, p < 0.002). Both the leptin/BMI 2 index as well as the Naie were significantly higher in the obese hypertensive group as compared to control group (1.9± 0.21 vs 1.25 ± 0.27, respectively p < 0.01, and 12.5 ± 0.51 vs 10.7 ± 0.5 mEq/ml/cell, respectively p < 0.05). In obese hypertensives the leptin/BMI 2 index was significantly associated with DBP (r= = 0.41, p < 0.04), MBP (r= 0.44, p < 0.03), Naie (r = 0.41, p < 0.05) and age (r = 0.43, p = 0.03). We conclude that in obese hypertensive patients Naie is increased reflecting a state of positive sodium balance. In these patients, the elevated circulating leptin concentrations were one of the main regulators of the content of sodium in erythrocytes.

Introduction: Weight loss is one of the treatment options for obstructive sleep apnea (OSA) in patients with excess body adiposity. However, the effects of moderate energy restriction on OSA are not known. Objective: To evaluate the effects of moderate energy restriction on severity of OSA, blood pressure (BP), sympathetic activity, oxidative stress, inflammation, body adiposity, metabolic profile and endothelial function in obese patients with OSA. Methods: A 16-week randomized clinical trial, involving 21 obese subjects aged 20-55y with apnea/hipopnea index (AHI) ≥ 5 events/h. Subjects were randomized in 2 groups: 11 in energy restriction group (ERG) and 10 in control group (CG). ERG was instructed to follow an energy-restricted diet (-800 kcal/day) and CG was advised not to change food intake. At the beginning and at the end of the study, participants underwent evaluation of: OSA with Watch- PAT200® including the determination of OSA severity parameters, body adiposity, BP, plasma catecholamines, c-reactive protein (CRP), adiponectin, malondialdehyde, metabolism of glucose, lipid profile and endothelial function (Endo PAT 2000®). Results: ERG, compared to CG, presented significantly greater reduction in body weight (-5.6±1.8 vs. 0.4±1.2kg, p4% (-33.7±15.6 vs. 1.8±7.9, p=0.04); plasma adrenaline (-12.7±3.0 vs. -1.3±3.9pg/mL, p=0.04); and significantly greater increase in minimum O2 saturation (4.6±1.6 vs. -0.6±1.4%, p=0.03). ERG showed greater decrease, however without statistical significance, in systolic BP (-4.2±1.9 vs. 2.3±1.4mmHg, p=0.05), insulin (-5.1±1.9 vs. -0.7±1.3μU/mL, p=0.07) and HOMA-IR (-1.2±0.5 vs. -0.08±0.3, p=0.09). During the study period, changes in body adiposity presented significant correlation with changes in parameters of OSA severity, BP, insulin, HOMA-IR, norepinephrine and adiponectin. Changes in parameters of OSA severity presented significant association with changes in CRP. Conclusions: This study suggests that in obese patients with OSA moderate energy restriction is able to reduce body adiposity, parameters of OSA severity and sympathetic nervous system activity.

Fifteen patients with uncomplicated mild to moderate primary hypertension (7 males, 8 females, age range 36-65 years) were submitted to a double blind randomized crossover study, receiving MgO 3 times a day at a daily dose of 1.0 g (600 mg/day of magnesium) and placebo for a period of 6 weeks. This was to test the effects of oral magnesium supplementation on blood pressure and sodium, potassium, calcium and magnesium intraerythrocyte concentrations. Concomitantly, plasma renin activity and serum aldosterone was also measured. Oral magnesium reduced significantly the systolic (delta = -7.6 mmHg, P0.05); diastolic (delta = -3.8 mmHg, P0.01) and mean blood pressure (delta = -5.9 mmHg, P0.01). After magnesium supplementation intraerythrocyte sodium concentration was reduced (delta = -0.55 mEq/l per cell, P0.01) and intraerythrocyte magnesium concentration was increased (delta = 1.20 mg/dl per cell, P0.01). The diminution of the blood pressure correlated positively with the reduction in intraerythrocyte sodium (r = 0.66, P0.01) after magnesium. However, our results have shown that the blood pressure response to oral magnesium was not homogeneous. Forty percent of our patients had their blood pressure effectively controlled (more than 10 mmHg reduction in mean blood pressure), being the hypotensive effect more evident in patients with recent hypertension and in those where the reduction in intraerythrocyte sodium was significantly greater than in the non-responder individuals. Intraerythrocyte potassium and calcium, serum aldosterone, plasma renin activity and urinary sodium excretion were maintained unchanged after magnesium supplementation. These data showed that oral magnesium supplementation may reduce the blood pressure, which can be partially explained by the decrease in intracellular sodium and augment in intracellular magnesium.

Objective To test whether long-term antihypertensive treatment with metoprolol succinate (a β1-adrenoceptor blocker) or olmesartan medoxomil (an angiotensin II AT1-receptor blocker) reverses microvascular dysfunction in hypertensive patients. Methods This study included 44 hypertensive outpatients and 20 age and sex-matched healthy controls. We used skin capillaroscopy to measure capillary density and recruitment at rest and during PORH. Endothelium-dependent vasodilation of skin microcirculation was evaluated with a LDPM system in combination with ACh iontophoresis, PORH, and LTH. Results Pretreatment capillary density in hypertensive patients was significantly reduced compared with controls (71.3 ± 1.5 vs. 80.6 ± 1.8 cap/mm2; p

Recent studies have suggested that dietary Ca may have beneficial effects on adiposity, insulin resistance, dyslipidaemia and blood pressure (BP). One potential mechanism underlying these benefits involves modifications in intracellular Ca concentration ([Ca2+]i). The present study aimed to evaluate the associations of dietary Ca with adiposity, erythrocyte [Ca2+]i, metabolic profile, BP, inflammatory state and endothelial function in healthy pre-menopausal women. In the present cross-sectional study, seventy-six women aged 18–50 years were submitted to the evaluation of dietary intake, anthropometric parameters, body composition, erythrocyte [Ca2+]i, biochemical variables, endothelial function and BP. A FFQ was used to assess usual dietary intake. Endothelial function was evaluated by serum concentrations of adhesion molecules and by the peripheral arterial tonometry (PAT) method, using Endo-PAT 2000®. Participants were allocated into two groups according to Ca intake: low-Ca group (LCG;n32; n44; ≥ 600 mg/d). Women in the LCG compared with those in the HCG exhibited, after adjustments for potential confounders, higher values of BMI, waist circumference, waist:height ratio, percentage of body fat, insulin, homeostasis model assessment of insulin resistance, leptin, diastolic and mean BP; and lower levels of HDL-cholesterol, adiponectin and vascular cell adhesion molecule 1. Endothelial function assessed by PAT and [Ca2+]iwas similar in both groups. Subjects in the HCG had lower OR for prevalent overweight, obesity, abdominal obesity, insulin resistance, HDL-cholesterol 120 mmHg. The findings of the present study suggest that high Ca intake is inversely associated with some cardiovascular risk factors.

Despite the availability of nonpharmacological approaches and pharmacological therapies for hypertension, blood pressure control rates are disappointing all over the world [1]. Among several considerations, hypertension is usually associated with metabolic disorders, especially obesity, diabetes, and dyslipidemia, which may contribute to a greater difficulty of lowering blood pressure. In fact, the significant association between systemic hypertension and other cardiometabolic risk factors is well recognized, such as an elevated body mass index, waist circumference, fasting glucose, triglycerides, and a reduced HDL cholesterol, even not reaching criteria for diagnosis of metabolic syndrome. Individually, each one of these metabolic disorders is associated with adverse cardiovascular outcomes. This special issue presents some papers related to these cardiometabolic risk factors and their involvement mainly in prognosis and treatment of hypertensive patients. Firstly, a very low diastolic blood pressure, with a threshold value of 70 mmHg, was associated with increased all-cause mortality. It has been discussed that blood pressure level is the most important factor in cardiovascular risk evaluation even in hypertensive subjects with important metabolic disorders. The linear relationship between blood pressure and cardiovascular mortality starting from 115/75 mmHg is well known [2]. Nevertheless, cardiovascular events have also been observed after insistent lowering of blood pressure, at least in patients with coronary artery disease [3]. Sleep disorders have been increasingly studied in recent years. Obstructive sleep apnea is related to cardiovascular disease and metabolic dysfunction, but sleep duration is a parameter not commonly considered in this association. Indeed, short sleep duration has been previously associated with an increased likelihood for hypertension [4]. In a paper of this collection, interactions of deficient sleep with race/ethnicity were noted even after adjusting to metabolic factors such as body mass index and diabetes. This was an interesting finding considering that insulin resistance exacerbated by renin angiotensin system (RAS) activation might be a mechanism involved in the link between sleep disorders and metabolic syndrome. The causal relationship of RAS and oxidative stress with vascular inflammation was documented in this special issue in a study with an experimental model of metabolic syndrome. In this protocol, a RAS inhibitor and an antioxidant agent were able to attenuate metabolic factors and systolic blood pressure in spontaneously hypertensive rats submitted to fructose administration. The interaction between hypertension and diabetes seems to be the principal concern to the cardiovascular system. The mechanisms that may increase cardiovascular risk in diabetic hypertensive patients are not completely understood. Oxidative stress and low-grade inflammation resulting in endothelial dysfunction as the first process of atherosclerosis were reviewed in this special issue. These factors may be also relevant in patients with longer duration of type 1 diabetes. In another paper, a cross-sectional study carried out in 20 Brazilian cities demonstrated that less than one quarter of treated type 1 diabetic patients achieved the target values for systolic and diastolic blood pressure. These data indicate that a more aggressive approach of this population is extremely necessary also in developing countries. Nutritional factors involved in the treatment of hypertensive subjects are also discussed in this special issue. Many dietary components, especially sodium, potassium, calcium, and magnesium, are reviewed based on the available evidence. Restriction of daily sodium intake is recommended in several guidelines about hypertension. However, low salt intake has resulted in cardiovascular mortality in some particular groups of patients including diabetic subjects [5]. Potassium, calcium, and magnesium supplementations are not indicated as a usual practice for hypertensive subjects, but natural source of these micronutrients is the mainstay of the Dietary Approaches to Stop Hypertension (DASH) plan. Also, as a nonpharmacological approach, two original papers in this collection demonstrated the beneficial effects of dark chocolate consumption on endothelial function in specific populations: stage 1 hypertensive subjects with excess body weight and younger hypertensive individuals with low cardiovascular risk who already present endothelial dysfunction. It has been reported that these favorable outcomes are associated with reasonably high amount of polyphenol in dark chocolate. Lastly, in a study that enrolled patients with uncontrolled hypertension and criteria for metabolic syndrome, moxonidine therapy resulted in blood pressure reduction and improvement of blood pressure control rates, especially in younger individuals. The pharmacological treatment of hypertension in the context of metabolic syndrome presents many challenges in the daily clinical practice due to several mechanisms involved in this medical condition including the sympathetic nervous system (SNS) hyperactivation. Thus, moxonidine, a selective agonist at the imidazoline receptor subtype 1 which determines a decrease in SNS activity, may be beneficial in this circumstance. Undoubtedly, hypertension is very commonly associated with other metabolic chronic conditions. In fact, more than 80% of hypertensive patients present one or more concomitant metabolic risk factors. This clinical condition has a growing global prevalence, clearly related to the modern lifestyles characterized by lack of physical activity resulting in overweight or obesity. Hopefully, we believe that this special issue can help to better understand the interaction between raised blood pressure levels and cardiometabolic factors, pointing out the involvement of insulin resistance and RAS/SNS activation as linking factors and also discussing some therapeutic options for this population. Mario Fritsch Neves Agostino Virdis Antonio Felipe Sanjuliani Eduardo Vera Tibirica

Background. Hypertension and excess body weight are important risk factors for endothelial dysfunction. Recent evidence suggests that high-polyphenol dark chocolate improves endothelial function and lowers blood pressure. This study aimed to evaluate the association of chocolate 70% cocoa intake with metabolic profile, oxidative stress, inflammation, blood pressure, and endothelial function in stage 1 hypertensives with excess body weight.Methods. Intervention clinical trial includes 22 stage 1 hypertensives without previous antihypertensive treatment, aged 18 to 60 years and presents a body mass index between 25.0 and 34.9 kg/m2. All participants were instructed to consume 50 g of chocolate 70% cocoa/day (2135 mg polyphenols) for 4 weeks. Endothelial function was evaluated by peripheral artery tonometry using Endo-PAT 2000 (Itamar Medical).Results. Twenty participants (10 men) completed the study. Comparison of pre-post intervention revealed that (1) there were no significant changes in anthropometric parameters, percentage body fat, glucose metabolism, lipid profile, biomarkers of inflammation, adhesion molecules, oxidized LDL, and blood pressure; (2) the assessment of endothelial function through the reactive hyperemia index showed a significant increase: 1.94 ± 0.18 to 2.22 ± 0.08,P=0.01.Conclusion.In individuals with stage 1 hypertension and excess body weight, high-polyphenol dark chocolate improves endothelial function.

Dietary intervention is an important approach in the prevention of cardiovascular disease. Over the last decade, some studies have suggested that a calcium-rich diet could help to control body weight, with anti-obesity effects. The potential mechanism underlying the impact of calcium on body fat has been investigated, but it is not fully understood. Recent evidence has also suggested that a calcium-rich diet could have beneficial effects on other cardiovascular risk factors, such as insulin resistance, dyslipidemia, hypertension and inflammatory states. In a series of studies, it was observed that a high intake of milk and/or dairy products (the main sources of dietary calcium) is associated with a reduction in the relative risk of cardiovascular disease. However, a few studies suggest that supplemental calcium (mainly calcium carbonate or citrate) may be associated with an increased risk of cardiovascular events. This review will discuss the available evidence regarding the relationship between calcium intake (dietary and supplemental) and different cardiovascular risk factors and/or events.

A decisao terapeutica deve ser baseada no risco cardiovascular considerando-se a presenca de fatores de risco, lesao em orgao-alvo e/ou doenca cardiovascular estabelecida, e nao apenas no nivel da PA. ABORDAGEM PARA NIVEIS DE PA ENTRE 130-139/85-89 mmHg A justificativa para intervencoes em pessoas com esses niveis de PA baseia-se no fato de que metade do onus atribuivel ocorre para pressoes sistolicas entre 130 e 150 mmHg, isto e, incluindo o comportamento limitrofe de PA1 (Grau B). Uma importante consideracao a [...]

Recent evidence has suggested obesity as an independent risk factor for chronic kidney disease. However, the temporal relation between body mass index (BMI) and early renal dysfunction is unknown. This study aimed at evaluating whether longitudinal variations in BMI would reflect on changes in estimated glomerular filtration rate (GFR) in hypertensive individuals with excess body weight.This was a cross-sectional, longitudinal study.Of the 218 participants who attended the first examination, 150 were available for paired final analyses. At the end of follow-up, GFR decreased by 1.024 mL/min for each 1-kg/m(2) increment in BMI (P0.03). When BMI was analyzed in quartiles, a positive graded relation with GFR changes was observed in quartiles 1 and 2 (individuals who maintained or lost weight), and a negative relation in quartiles 3 and 4 (individuals who gained weight, P=0.05). A significant difference was observed between the smallest and highest BMI quartiles (P=0.01). At the end of follow-up, the 76 participants (51%) who gained weight (+4.6+/-0.4 kg) showed a reduction in GFR (-2.99+/-1.99 mL/min) of borderline significance (P=0.06) and a significant increase in fasting plasma glucose and triacylglycerol levels. Conversely, the 74 participants who maintained or lost weight showed no significant change in GFR and in fasting plasma glucose and triacylglycerol levels, although their blood pressure decreased significantly.Our study showed a significant temporal association between changes in BMI and GFR in overweight and obese hypertensive patients.

Among the main etiologies of secondary arterial hypertension figure out the tumorous affections of adrenal gland, located on cortex - primary aldosteronism (Conn’s syndrome) and Cushing’s syndrome - or at glandular medulla - pheocromocytoma. Although these tumors are at most benign the surgical resection is needed in order to eliminate the disturbances provided by them and to limit the mass growth, being curative in about 80-90% of the cases. In this paper some particularities above surgical treatment of these diseases will be focused emphasizing the pre-operative prepare of the patients and the currently preconized approach.

Arterial hypertension (AH) is a highly prevalent disease, and is a major cardiovascular (CV) risk factor1; therefore, achieving blood pressure (BP) control goals as soon as possible is paramount to reduce that risk2. That means that approximately 70% of hypertensive individuals will need antihypertensive drug combination3, and up to 30% of hypertensive individuals are estimated to use four or more drugs to achieve BP control4. Thus, drug combination is currently described as an important strategy to manage AH, providing effective and safe BP reduction. Drug choice is based on effective BP reduction and CV outcomes. Despite the existence of a significant number of drugs to treat AH, their control rates are still very low, contributing to the high CV morbidity and mortality rates observed in Brazil and worldwide1,2. According to the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) and the Hypertension Optimal Treatment (HOT) Study, only 26% and 33% of the patients, respectively, could control their BP with monotherapy, while in the Losartan Intervention for Endpoints Reduction (LIFE) Study, 90% of the patients needed combined therapy for that purpose3 . Drug combination is mainly aimed at increasing antihypertensive efficacy, with fewer adverse events. It is worth noting the importance of considering therapy adherence. The pathophysiology of AH involves multiple factors and mechanisms, making its control difficult when only one drug is used, because counterregulatory mechanisms that attenuate the antihypertensive effect of the drug can occur. The association of drugs with different mechanisms of action has a greater impact on BP reduction as long as there is pharmacokinetic compatibility and no disparity of effects and properties3-5. Thus, the choice of the drugs to be combined should contemplate two aspects: synergism of the mechanisms of action and opposition to counterregulatory mechanisms triggered after the beginning of therapy with a certain drug. The desired antihypertensive efficacy is more likely to be achieved by using lower doses of the drugs involved. Thus, fewer adverse events are observed, with no loss of antihypertensive drug potency3-5. Another important aspect is that drugs should be preferably combined in a single galenic presentation, facilitating their administration, and assuring lower cost, with a consequent improvement in treatment adherence2,6.