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The increase in blood pressure (BP) during somatic growth might have direct determinants but also mediating factors. We investigated whether uric acid (UA) and other metabolic factors would mediate the association between body composition components and BP. A cross-sectional study was conducted in 928 children and adolescents (aged 6–18 years), in which body composition and blood biochemistry were evaluated. Structural equation modeling was performed to test the direct and indirect pathways between systolic blood pressure (SBP) and body composition parameters. Muscle mass (MM) showed a strong direct effect on BP, regardless of sex. In girls, a mediating pathway through UA was not significant, but the association between fat mass (FM) and MM with SBP was mediated by the cluster of metabolic factors. In boys, both MM and FM were associated with SBP through a mediating pathway via UA, but not via the cluster of metabolic factors. The association between body composition and BP in children and adolescents has a complex design and also has a sex-specific mediating component. The increase in the UA levels may affect BP levels early in boys. Also, metabolic changes elicited by FM contribute to the increase in BP at an early age in girls. Novelty: MM showed a strong direct effect on BP, regardless of sex. In girls, the association between FM and MM with SBP was mediated by the cluster of metabolic factors. In boys, both MM and FM were associated with SBP through a mediating pathway via UA.

High salt intake has been linked to both obesity and high blood pressure (BP). Part of the variability of BP attributed to salt intake might be BMI-mediated. To investigate whether hypertension would be an effect modifier in the complex network including salt intake, obesity, and BP, we tested the hypothesis that salt intake has direct and BMI-mediated effects on systolic (SBP) and diastolic blood pressure (DBP). Data from 9,028 participants (aged 34-75 years, 53.6% women) were analyzed. A validated formula was used to estimate daily salt intake from the sodium excretion (12 h urine collection). A path model adjusted for covariates was designed in which salt intake has both a direct and a BMI-mediated effect on BP. In normotensives, standardized beta coefficients showed significant direct (Men: 0.058 and 0.052, Women: 0.072 and 0,061, P 0.05) and BMI-mediated (Men: 0.040 and 0.065, Women: 0.038 and 0.067, P 0.05) effect of salt intake on the SBP and DBP, respectively. However, in hypertensive individuals, neither the direct (Men: 0.006 and 0.056, Women: 0.048 and 0.017) nor the indirect effect (Men: -0.044 and 0.014, Women: 0.011 and 0.050) of salt intake on the SBP and DBP were significant. These data suggest that cardiovascular risk stratification should consider the complex interaction between salt intake and weight gain, and their effects on BP of normotensive and hypertensive individuals.

Background: The prevalence of metabolic syndrome (MS) varies according to the different definitions available for clinical practice. The study aimed to estimate and compare the prevalence of MS according to the definitions of the American Heart Association (AHA)/National Heart, Lung, and Blood Institute (NHBI), International Diabetes Federation (IDF), and Joint Interim Statement (JIS) in a sample of climacteric women in Brazil. Methods: A population-based cross-sectional study, using a probabilistic sampling by clusters, involved 874 climacteric women. Clinical and anthropometric variables were acquired while fasting, and MS was defined according to three recommendations. To define the agreement between different definitions on MS, we calculated the sensitivity and specificity for the diagnosis of MS based on AHA/NHBI and IDF in relationship to the JIS definition. Results: The prevalence of MS was 56.9% according to the AHA/NHBI definition, 61.6% by the IDF, and 64.8% by the JIS definition, without statistical significance. When prevalence of MS was stratified by climacteric stages, the ability of the different definitions identifying MS was also similar among groups. It was observed that the MS definition proposed by AHA/NHBI identified 87.4% of MS cases from the total cases diagnosed by JIS, with agreement levels by the Kappa index of 0.835. The IDF detected 95.3% of MS cases compared to the JIS definition and the agreement level was 0.934. Conclusions: The study indicates a high prevalence of MS in climacteric women regardless of the definition used (AHA/NHBI, IDF e JIS). We did not observe significant divergences between definitions.

Blood pressure (BP) is a strong cardiovascular risk factor, predicting cardiovascular mortality in the general population. High salt consumption is a major contributor of increased BP and hypertension. However, there is a controversy on whether BP response to salt intake would be sex-specific. Thus, we aimed to verify the changes in BP according to different salt intake in men and women in a large sample of adults. The present analysis refers to 12 813 participants (from 35 to 64 years) with a validated 12-hour overnight urine collection in which salt intake was estimated. A set of questionnaires, clinical examination, and laboratory tests were carried out during a single visit to one of the six investigation centers involved. Salt intake was 12.9 ± 5.9 g/d in men and 9.3 ± 4.3 g/d in women. BP increases as salt intake increases, regardless of using BP-lowering medication. The slope of increase in BP elicited by salt intake was significantly higher in women than in men. Thus, the increase in BP by salt intake was stepper in women even after controlling for confounders, regardless of using BP-lowering medication or being hypertensive. In conclusion, salt intake is elevated in this large sample of Brazilian adults in which only a few participants are compliant with the recommendation. Also, women have a higher responsiveness of BP according to salt intake than men, and it is not associated with age, BP level, or the use of BP-lowering medication.

BACKGROUND Among several lipid ratios available, the triglyceride/HDL-cholesterol (TG/HDL-C) may detect individuals at risk of cardiometabolic diseases. However, its reference values for different ethnicities are not well established. OBJECTIVE To define sex- and ethnicity-specific reference values for TG/HDL-C ratio in a large sample of healthy multiethnic adults and test its association with cardiometabolic conditions. METHODS An apparently healthy sample (n = 2,472), aged 35–74, free of major cardiovascular risk factors, was used to generate the reference values for the TG/HDL-C. Exclusion criteria were diabetes, elevated blood pressure, obesity, hypercholesterolemia, severe hypertriglyceridemia, and smoking history. Cut-offs based on the reference values were tested in the whole ELSA Brasil study (n = 13,245), stratified by sex and ethnicity, to identify cardiometabolic conditions. RESULTS TG/HDL-C ratio was higher in men than women, and did not change significantly with age, regardless of sex and ethnicity. Also, black individuals showed lower levels of TG/HDL-C as compared to other ethnic groups. ROC curve showed that the cut-off based on the 75th percentile displayed better sensitivities and specificities for men and women, regardless of ethnicity. Also, the sex- and ethnicity-specific cut-offs based on the 75th percentile were significantly associated with all tested cardiometabolic conditions (hypertension, diabetes, obesity, metabolic syndrome, and insulin resistance). Also, we observed that the use of a single sex-specific cut-off (men: 2.6; women: 1.7) could be used for the different ethnicities with good reliability. CONCLUSION The defined TG/HDL-C cut-offs (men: 2.6; women: 1.7) are reliable and showed good clinical applicability to detect cardiometabolic conditions in a multiethnic population.

Studies have shown that lean mass must be an important determinant of blood pressure value in children and adolescents. The absence of adjustment for the collinearity between lean and fat mass (FM), restricted age span, and lack of separate analysis by sex leave a gap in the literature. This study determined direct and indirect effects of the somatic growth indicators linked to the association between age and systolic blood pressure (SBP) in boys and girls. This is a cross-sectional study comprising 1,510 participants (6-18 years). Path analysis was used to test a model in which the association between age and SBP would have a direct and independent component, but also indirect mediating paths through muscle mass (MM), FM, and height. There was no significant association between age and SBP (unstandardized β ± SE) for both girls (0.072 ± 0.236, P = .761) and boys (0.238 ± 0.264, P = .368). Height was not a mediator for the association between age and SBP in both girls (-0.291 ± 0.156, P = .062) and boys (-0.015 ± 0.187, P = .935). Mediating effect of MM was significant for both girls (0.909 ± 0.137, P

Ethnicity is an important determinant of blood pressure levels, being black individuals affected more than any other ethnic group. Arterial stiffening, an independent risk factor for hypertension, is also influenced by ethnicity. However, whether black individuals from different continents would have different patterns of arterial stiffening is still unknown. Thus, the authors aimed to compare pulse wave velocity (PWV) in black subjects living in Angola and Brazil. A total of 677 black individuals from two independent cross-sectional studies conducted in Brazil and Angola were included in this analysis. Carotid-to-femoral PWV was measured following the same protocols for both studies, as well as clinical and anthropometric variables. Adjusted PWV was higher in Brazilian blacks than in Angolans, regardless of sex (men from Brazil: 10.7 ± 1.8 vs men from Angola: 9.9 ± 1.8 m/s, P < .001; women from Brazil: 10.3 ± 1.5 vs women from Angola: 9.2 ± 1.3 m/s, P < .001). Although the cf-PWV was higher in Brazilian blacks, the age-related increase in cf-PWV was higher in Angolan men compared to Brazilians, but not in women. SBP showed the strongest association with cf-PWV, regardless of sex and country. However, age was associated with cf-PWV in all groups, except in Brazilian men. Our results clearly show a difference in PWV between two black populations, and highlight for sex differences in the hemodynamic parameters that might affect blood pressure levels in these populations.

Subendocardial viability ratio (SEVR) is a reliable index of myocardial supply-workload balance. This study sought to investigate whether overweight/obese children and adolescents have altered SEVR and to identify which are the associated factors. This cross-sectional study involved 789 individuals. Central haemodynamic was measured by radial applanation tonometry. Diastolic time was shorter (496 ± 122 vs 537 ± 140 ms, P = .014) and diastolic pressure-time index was lower (2681 ± 412 vs 2814 ± 423 mm Hg seconds, P = .024) in overweight/obese compared with eutrophic girls. SEVR was lower in girls than in boys (1.34 ± 0.39 vs 1.48 ± 0.41, P = .018) but only among overweight/obese. SEVR may be affected by small variations in the temporal determinants of cardiac cycle.

Chronic fructose intake induces major cardiovascular and metabolic disturbances and is associated with the development of hypertension due to changes in vascular function. We hypothesized that high fructose intake for 6 weeks would cause metabolic syndrome and lead to initial vascular dysfunction. Male Wistar rats were assigned to receive fructose (FRU, 10%) or drinking water (CON) for 6 weeks. Systolic blood pressure was evaluated by tail plethysmography. Fasting glucose, insulin and glucose tolerance were measured at the end of the follow-up. Mesenteric vascular bed reactivity was tested before and after pharmacological blockade. Western blot analysis was performed for iNOS, eNOS, Nox2 and COX-2. DHE staining was used for vascular superoxide anion detection. Vessel structure was evaluated by optical and electronic microscopy. Fructose intake did not alter blood pressure, but did increase visceral fat deposition and fasting glucose as well as impair insulin and glucose tolerance. Fructose increased NE-induced vasoconstriction compared with CON, and this difference was abrogated by indomethacin perfusion as well as endothelium removal. ACh-induced relaxation was preserved, and the NO modulation tested after L-NAME perfusion was similar between groups. SNP-induced relaxation was not altered. Inducible NOS was increased; however, there were no changes in eNOS, Nox2 or COX-2 protein expression. Basal or stimulated superoxide anion production was not changed by fructose intake. In conclusion, high fructose intake increased NE-induced vasoconstriction through the endothelial prostanoids even in the presence of a preserved endothelium-mediated relaxation. No major changes in vessel structure were detected.

CNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológico FAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Gerais CAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superior Oral Mucositis (OM) is a common adverse effect of head and neck squamous cell carcinoma (HNSCC) treatment. The purpose of this study was to investigate the significance of early changes in tissue electrical parameters (TEPs) in predicting the development of OM in HNSCC patients receiving radiation therapy (RT). The current study combined two study designs. The first was a case-control study. The control group comprised of RT patients who did not receive head and neck RT, and patients with HNSCC who received RT comprised the case group. In the second part of the study, the case group was included in a parallel cohort. A total of 320 patients were assessed for eligibility, and 135 patients were enrolled. Double blinding was performed, and neither the patients nor the care providers knew the measured parameters. The primary outcome was the detection of between-group changes in local TEPs over the follow-up period. The secondary outcome was the appearance of OM grades II, III, or IV and the predictive value of local TEPs in determining the incidence of OM after RT. The variables, impedance module, resistance, reactance, phase angle, and capacitance, were analyzed by the receiver operator curves (ROC). The case and control groups did not differ in demographic and clinical characteristics. Radiation therapy increased the local impedance module, resistance, reactance, and phase angle and reduced the local tissue capacitance in both groups. Evaluation of TEPs in the first week of RT correlated with the development of OM lesions during cancer therapy. ROC analysis showed that local impedance module and resistance presented higher specificity than did other parameters in predicting OM. In conclusion, local tissue electrical parameters measured at the first RT week can be useful tools to predict oral mucositis.

High salt intake is known to increase blood pressure (BP) and also to be associated with carotid-femoral pulse wave velocity (cf-PWV). However, recent data showed a sex-specific pattern in the salt-induced rise of BP. Thus, we aimed to investigate whether the association between salt intake and arterial stiffness also has a sex-specific pattern. A total of 7755 normotensive participants with a validated 12-h overnight urine collection in which daily salt intake was estimated were included. cf-PWV, as well as clinical and anthropometric parameters, was measured. Salt intake positively correlated with cf-PWV, in which the linear regression was steeper in women than in men (0.0199 ± 0.0045 vs 0.0326 ± 0.0052 m/s per gram of salt, P < .05). cf-PWV increases over the salt quartiles in men and women. However, after adjustment for confounders, the association remained significant only for men. In the path analysis, the direct path (men: 0.048 P < .001, women: 0.029 P = .028) was higher in men while that mediated by SBP (men: 0.020 P < .001, women: 0.034 P < .001) was higher in women. We clearly demonstrated that high salt intake has a direct and independent effect increasing arterial stiffness regardless of sex. Also, the association between salt intake and arterial stiffness is more dependent on BP in normotensive women than it is in normotensive men. These results highlight the need for a sex-specific approach in the evaluation of cardiovascular risk associated with dietary habits.

Background: Stress test is used to detect coronary artery disease (CAD). The QTc interval dispersion (dQTc) is an electrocardiographic index of ventricular repolarization heterogeneity. Some researchers have linked transient myocardial ischemia induced by physical exertion with increased heterogeneity of ventricular repolarization measured by dQTc. Objectives: To study the patterns of dQT in patients with and without chronic obstructive CAD and to define a reliable cutoff point for dQT that could become a diagnostic criterion for myocardial ischemia. Methods: We retrospectively analyzed the electrocardiogram in resting and in exercise of 63 patients submitted to exercise test and cardiac catheterization. We divided the patients into three groups: true negative (VN), true positive (VP) and false positive (FP). VN: patients with coronary lesion lower than 70% and exercise test without myocardial ischemia; VP: individuals with stenosis greater than 70% in coronary arteries and a test suggestive of myocardial ischemia; FP: people with stenosis lower than 70% in the coronary arteries and stress test with ischemia criteria. Values of p < 0.05 were considered statistically significant. Results: Resting dQTc was not different among the three groups. However, for the dispersion of the QTc interval in exercise was, respectively, 47 ± 17 ms, 72 ± 42 ms, and 61 ± 31 ms for VN, VP and FP (p = 0.003). Conclusions: Obstructive chronic coronary disease patients have an increase in dQTc during exercise. Measurement of dQTc may be helpful in the diagnosis of myocardial ischemia in the stress test.

Objectives This study compared serum cystatin C (CysC) with conventional biomarkers of renal function in terms of their ability to predict illness severity in patients in a mixed intensive care unit (ICU). The present study also tested the hypothesis that increased CysC could predict illness severity in different clinical conditions in adult patients admitted to the ICU. Design and methods The performance of serum creatinine, urea and CysC, as well as the Glomerular Filtration Rate (GFR) estimates (Cockcroft–Gault/MDRD/Larsson and CKD-EPI Equations) in predicting illness severity was compared in 60 critically ill patients. Adult patients admitted to the hospital were screened for eligibility in this prospective and observational study. The mean patient age was 52 ± 19 years. The average APACHE II score was 9.5 ± 6 for the entire sample. The patients were assigned to two different degrees of severity, and the internally derived cut off value was an APACHE II score Results Both serum CysC and urea showed significant correlations with APACHE II, even after controlling for age. Urea and CysC levels, as well as the GFR estimated by the method of Larsson and Cockcroft–Gault, remained significantly increased in patients in the APACHEII ≥ 10 group. The ROC curve analyses indicated that both urea and CysC levels have high sensitivity and specificity in the prediction of illness severity using the APACHE II as a gold standard prognostic stratification system. Furthermore, CysC was more accurate than the Larsson, CKD-EPI CysC, CKD-EPI Cr-CysC, Cockcroft–Gault and CKD-EPI Cr CFR estimation methods compared with the MDRD method. Additionally, CysC was a good predictor in both young and old patients, whereas urea was not predictive of illness severity. Conclusions Our findings suggest that CysC and GFR estimates (Larsson or CKD-EPI CysC methods) are good predictors of illness severity in adult patients hospitalized in a mixed ICU.

It is known that dietary habits have a strong influence on body metabolism. In the last decades, the dietary habits have changed worldwide, and the consumption of fructose, especially in sugar-sweetened beverages, increased significantly. In this perspective, the present review aimed to summarize the effects of fructose on different cardiometabolic conditions. Clinical, experimental, and epidemiological studies evidenced that fructose can exert several deleterious effects when its consumption is above the recommended amounts. The increased fructose consumption decreases satiety, favoring a positive energy balance, increases adipogenesis, leading to visceral fat accumulation, induces ectopic fat accumulation, especially in the skeletal muscle and liver, leading to insulin resistance, inflammation, and lipid metabolism impairment, increases arterial blood pressure and causes vascular damage. Therefore, increased fructose consumption is linked to the development of alarming cardiometabolic conditions, such as obesity, insulin resistance, type 2 diabetes, non-alcoholic fatty liver disease, and cardiovascular diseases, through several different mechanisms. Further clinical and experimental studies are still necessary to elucidate additional signaling pathways and mechanisms by which fructose is involved in all the mentioned cardiometabolic disorders. Also, the reported findings raise the need for the creation of public health policies aimed to prevent diet-associated cardiometabolic disorders, thus improving the population quality of life.

African–Americans present higher prevalence of left ventricular hypertrophy (LVH) when compared with white populations. However, there is a lack of information about the prevalence and determinants of LVH in black individuals living in Africa. A cross-sectional study was performed with a non-probabilistic sample comprised of 609 University workers from Angola/Africa, describing the prevalence of LVH and the determinants of left ventricular mass. Echocardiographic measurements were performed and left ventricular mass was indexed to body surface area. Systolic and diastolic blood pressures were measured, along with anthropometric and clinical variables. Chamber diameter and wall thickness were higher in men compared to women. Additionally, LVM was higher in men (114.2 ± 36 vs 98.4 ± 31.9, P

Background Aging declines essential physiological functions, and the vascular system is strongly affected by artery stiffening. We intended to define the age- and sex-specific reference values for carotid-to-femoral pulse wave velocity (cf-PWV) in a sample free of major risk factors. Methods and results The ELSA-Brasil study enrolled 15,105 participants aged 35–74years. The healthy sample was achieved by excluding diabetics, those over the optimal and normal blood pressure levels, body mass index ≤18.5 or ≥25kg/m 2 , current and former smokers, and those with self-report of previous cardiovascular disease. After exclusions, the sample consisted of 2158 healthy adults (1412 women). Although cf-PWV predictors were similar between sex (age, mean arterial pressure (MAP) and heart rate), cf-PWV was higher in men (8.74±1.15 vs. 8.31±1.13m/s; adjusted for age and MAP, P n =15,105) increased by twice the age-related slope of cf-PWV growth, regardless of sex (0.0919±0.182 vs. 0.0504±0.153m/s per year for men, 0.0960±0.173 vs. 0.0606±0.139m/s per year for women). Conclusions cf-PWV is different between men and women and even in an optimal and normal range of MAP and free of other classical risk factors for arterial stiffness, reference values for cf-PWV should take into account MAP levels. Also, the presence of major risk factors in the general population doubles the age-related rise in cf-PWV.

Carotid‐femoral pulse wave velocity (PWV) has been used as the gold standard method to estimate arterial stiffness. However, its use in clinical practice is still limited because reference values for specific groups, such as black children, remain unknown. The authors aimed to investigate predictors and to propose preliminary reference values of PWV in this population. Prepubertal schoolchildren (N=157; mean age, 9.36±1.41 year) from Luanda (Angola) with normal blood pressure values and without obesity were included. Mean PWV was 5.73±0.68 m/s, with no difference between the sexes. Univariate regression analysis showed a significant (P

High salt intake is related to an increase in blood pressure and development of hypertension. However, currently, there are no national representative data in Brazil using the gold standard method of 24-h urine collection to measure sodium consumption. This study aimed to determine salt intake based on 24-h urine collection in a sample of 272 adults of both genders and to correlate it with blood pressure levels. We used a rigorous protocol to assure an empty bladder prior to initiating urine collection. We excluded subjects with a urine volume

The dietary–sodium restriction is a standard approach following an acute myocardial infarction (MI). We examined the hypothesis in which the use of a high or low–sodium diet would worsen post–infarction left ventricular remodeling in rats and facilitate the development of heart failure. Left coronary artery ligation or sham–operated (SO) was produced in male Wistar rats (250–290 g). After surgery, animals were assigned to one of the three diets: standard amount of sodium (0.3% NaCl, SO and MI groups), a high–sodium diet (0.6% NaCl, SO–High and MI–High groups), or a low–sodium diet (0.03% NaCl, SO–Low and MI–Low groups). Diets were provided for 8 weeks post–surgery. Mortality rate was elevated in high–salt group (MI–Low, 21.4%; MI, 35.3%; MI–High, 47.6%). Contractility parameter was seen to be impaired in MI–Low animals (3195 ± 211 mm Hg/s) compared with MI (3751 ± 200 mm Hg/s). Low–salt diet did not prevent myocardial collagen deposition (MI–Low, 5.2 ± 0.5%; MI, 5.0 ± 0.4%) nor myocyte hypertrophy (MI–Low, 608 ± 41μ 2 ; MI, 712 ± 53 μm 2 ) in left ventricle after MI. High–salt intake increases collagen volume fraction (SO, 3.3 ± 0.4%; SO–High, 4.7 ± 0.4%) in animals sham, but no major changes after MI. Our results show that ventricular remodeling was not altered by immediate introduction of low sodium after MI, and it may be a safe strategy as a therapeutic intervention to avoid volume retention. However, high sodium can be harmful, accelerating the post–infaction ventricular remodeling.

Background Black people have a higher risk of developing hypertension and presenting higher vascular stiffening. Our aim was to investigate whether the association between race and aortic stiffness could be explained by differences in the primary risk factors. Methods and Results We analyzed data from 11 472 adults (mean age, 51.9±8.9; 53.8% female) self‐reported as white (n=6173), brown (n=3364), or black (n=1935). Their carotid‐to‐femoral pulse wave velocity (cf‐PWV) as well as clinical and anthropometric parameters were measured. cf‐PWV was higher in blacks than in whites or browns (men: white, 9.63±1.81; brown, 9.63±1.88; black, 9.98±1.99; women: white, 8.84±1.64; brown, 9.02±1.68; black, 9.34±1.91; P P >0.05). The association between race and arterial stiffness was significant for brown and black women in the highest cf‐PWV quartile, even after controlling for covariates. There were no differences in the age‐related increase in cf‐PWV among the racial groups after adjustment, confirming the strong effect of age and mean arterial pressure on cf‐PWV revealed by the multiple linear regression. Conclusions Racial differences in cf‐PWV were mainly attributed to differences in mean arterial pressure and age, although they cannot fully explain the association between race and cf‐PWV in women in the highest cf‐PWV values. This suggests that therapeutic approaches to overcome the effects of aging on the vascular system should focus on blood pressure control, especially in the black population.

Summary Non-invasive assessment of central arterial pulse wave augmentation has been proved to be useful in predicting cardiovascular adverse events. Previous studies have shown that prepubescent girls had greater central augmentation pressure compared with height-matched boys. This study sought to investigate which factors contribute to the body height-independent sexual differences in central arterial wave reflection observed in childhood. This cross-sectional study involved 819 children and adolescents (6-18 years of age) of both sexes. Phenotypes of central haemodynamic were obtained by radial applanation tonometry. Heart rate corrected augmentation index (Aix@75) was greater in girls compared with boys (2.9 ± 10.7 vs. -1.7 ± 12.9%, p

It has been suggested that the increase in heart rate (HR) at the onset of exercise is caused by vagal withdrawal. In fact, endurance runners show a lower HR in maximum aerobic tests. However, it is still unknown whether endurance runners have a lower HR at 4 s after the onset of exercise (4th-sec-HR). We sought to measure the HR at the onset of the 4 s exercise test (4-sET), clarifying its relationship to heart rate variability (HRV), spectral indices, and cardiac vagal index (CVI) in endurance runners (ER) and healthy untrained controls (CON). HR at 4th-sec-HR, CVI, and percent HR increase during exercise were analyzed in the 4-sET. High frequency spectrum (HF-nu), low frequency spectrum (LF-nu), and low frequency/high frequency band ratio (LF/HF) were analyzed from the HRV. ER showed a significantly higher HF, and both a lower LF and LF/HF ratio compared with the CON. ER presented a significantly lower 4th-sec-HR, although neither CVI nor HR increases during exercise were statistically different from the CON. In conclusion, ER presented a lower 4th-sec-HR secondary to increased vagal influence over the sinus node. CVI seems to be too weak to use for discriminating individuals with respect to the magnitude of HR vagal control.

Myocardial infarction (MI) is a major risk for ventricular arrhythmia. Pause-triggered ventricular arrhythmia can be caused by increased myofilament Ca binding due to sarcomeric mutations or Ca-sensitizing compounds. Myofilament Ca sensitivity is also increased after MI. Here we hypothesize that MI increases risk for pause-triggered ventricular arrhythmias, which can be prevented by myofilament Ca-desensitization and contractile uncoupling. To test this hypothesis, we generated a murine chronic MI model using male B6SJLF1/J mice (n=40) that underwent permanent ligation of the left anterior descending coronary artery. 4 weeks post MI, cardiac structure, function and myofilament Ca sensitivity were evaluated. Pause-dependent arrhythmia susceptibility was quantified in isolated hearts with pacing trains of increasing frequency, followed by a pause and an extra stimulus. Coronary ligation resulted in a mean infarct size of 39.6±5.7%LV and fractional shortening on echocardiography was reduced by 40% compared to non-infarcted controls. Myofilament Ca sensitivity was significantly increased in post MI hearts (pCa50: Control=5.66±0.03; MI=5.84±0.05; p

OBJECTIVES: The present study was performed to investigate 1) whether aerobic exercise training prior to myocardial infarction would prevent cardiac dysfunction and structural deterioration and 2) whether the potential cardiac benefits of aerobic exercise training would be associated with preserved morphological and contractile properties of cardiomyocytes in post-infarct remodeled myocardium. METHODS: Male Wistar rats underwent an aerobic exercise training protocol for eight weeks. The rats were then assigned to sham surgery (SHAM), sedentary lifestyle and myocardial infarction or exercise training and myocardial infarction groups and were evaluated 15 days after the surgery. Left ventricular tissue was analyzed histologically, and the contractile function of isolated myocytes was measured. Student's t-test was used to analyze infarct size and ventricular wall thickness, and the other parameters were analyzed by the Kruskal-Wallis test followed by Dunn's test or a one-way analysis of variance followed by Tukey's test (p

Hyperuricemia is associated with cardiovascular disease and its prevalence is unknown in black Africans. This study reports hyperuricemia distribution and its association with cardiovascular risk factors in a selected Angolan population. A cross-sectional study in 585 black Africans was performed. Hyperuricemia was defined as uric acid >7.0 mg/dL in men or >5.7 mg/dL in women. Overall prevalence was 25%. Hyperuricemia was associated with hypertension (odds ratio [OR], 2.20; confidence interval [CI], 95% 1.41-3.47), high waist circumference (OR, 1.67; CI, 95% 1.05-2.65), and metabolic syndrome (OR, 1.66; CI, 95% 1.07-2.57). Compared to those with uric acid levels in the first quartile, individuals in the fourth quartile showed higher body mass index, waist circumference, systolic blood pressure, and plasma levels of creatinine and triglycerides. Hypertension, high waist circumference, and metabolic syndrome were the major cardiovascular risk factors associated with hyperuricemia.

BACKGROUND Obesity has been described as a predictor of cardiovascular mortality, and some studies have reported an association with obesity and increased aortic stiffness. Other studies have not identified obesity to be an independent risk factor. Therefore, the purpose of our study was to determine the association between aortic stiffness and obesity in the Brazilian population. METHODS A cross-sectional study recruited 1,662 individuals aged 25-64 years from the population of Vitoria, Brazil following the guidelines of the MONICA-WHO Project. Anthropometric, clinical, and hemodynamic measurements and analyses of aortic stiffness (using carotid-femoral pulse wave velocity

A high salt diet is a known risk factor for cardiovascular diseases that leads to cardiac hypertrophy and creates a substrate for arrhythmias and sudden death. However, acute arrhythmogenesis after infarction has not been studied. Male Wistar rats (21 days) received drinking water (MI) or 1% NaCl solution (MI-Salt-C) for 4 weeks. Water was given to another group for 4 weeks, and on the day before surgery, animals received a 1% NaCl solution (MI-Salt-A). Non-invasive systolic blood pressure (SBP) was obtained before surgery. Myocardial infarction (MI) was produced by permanent occlusion of the left coronary artery. Electrocardiogram was monitored during the first 30 min post-occlusion to evaluate arrhythmias. Although SBP was not altered by salt intake (SHAM: 114±2, MI: 112±2, MI-Salt-C: 115±2, MI-Salt-A: 116±4 mm Hg), ventricular hypertrophy was observed in the animals receiving chronic salt diet (SHAM: 0.22±0.008, MI: 0.23±0.007, MI-Salt-C: 0.28±0.01; MI-Salt-A: 0.23±0.01 g/cm; P0.05). Ventricular premature beats increased in both salt-loaded groups compared to MI group (MI: 805±81, MI-Salt-C: 1145±98; MI-Salt-A: 1023±77; P0.05). Atrioventricular blockade was only observed in animals subjected to high salt intake (MI-Salt-C: 38.9%; MI-Salt-A: 42.1%). High salt intake was associated with increased post-infarct arrhythmias; however, this effect was unrelated to ventricular hypertrophy.

Objectives: To evaluate the acute effects of colony-stimulating factor (G-CSF) on ventricular arrhythmias after coronary occlusion in rats. Materials and Methods: Male Wistar rats (10 weeks) received G-CSF (100 μg.kg-1) or vehicle. Thirty minutes later, animals were infarcted by coronary occlusion under artificial respiration. Electrocardiogram was monitored for 30 min to evaluate ventricular arrhythmias. Results: G-CSF treatment reduced the number of premature ventricular beats and the number and duration of ventricular tachycardia. The incidence of ventricular fibrillation was significantly reduced by G-CSF (MI-Cont: 11.2 ± 2.4 vs. MI-GCSF: 5.4 ± 1 events; P < 0.05). However, total duration of ventricular fibrillation was not altered (MI-Cont: 84 ± 16 vs. MI-GCSF: 76 ± 13 sec). Conclusions: Acute administration of G-CSF before coronary ligature in rats reduces the incidence of ventricular premature beats and ventricular tachycardia, suggesting a possible direct electrophysiological effect of this cytokine independently of its genomic effects. However, the data suggest that G-CSF treatment may affect the spontaneous recovery from ventricular fibrillation. Acute G-CSF administration acts directly on cardiac electrophysiology, different from chronic treatment.

G-CSF is a critical regulator of hematopoietic cell proliferation, differentiation and survival. It has been reported that G-CSF attenuates renal injury during acute ischemia-reperfusion. In this study we evaluated the effects of G-CSF on the renal and cardiovascular systems of 2K1C hypertensive mice.Male C57BL/6 mice were subjected to left renal artery clipping (2K1C) or sham operation and were then administered G-CSF (100 μg/kg/day) or vehicle for 14 days.Arterial pressure was higher in 2K1C + vehicle animals than in 2K1C + G-CSF (150±5 vs. 129±2 mmHg, p0.01, n=8). Plasma angiotensin I, II and 1-7 concentrations were significantly increased in 2K1C + Vehicle when compared to the normotensive Sham group. G-CSF prevented the increase of these vasoactive peptides. The clipped kidney/contralateral kidney weight ratio showed a less atrophy of the ischemic kidney in the treated group (0.50±0.02 vs. 0.66±0.01, p0.05). The infarction area in the clipped kidney was completely prevented in 7 out of 8 2K1C + G-CSF mice. Administration of G-CSF protected the clipped kidney from apoptosis.Our data indicate that G-CSF prevents kidney infarction and markedly attenuates the increases in plasma angiotensin levels and hypertension in 2K1C mice, reinforcing the protective effect of G-CSF on kidney ischemia.

Coronary artery disease is the leading cause of death in the developed world and in developing countries. Acute mortality from acute myocardial infarction (MI) has decreased in the last decades. However, the incidence of heart failure (HF) in patients with healed infarcted areas is increasing. Therefore, HF prevention is a major challenge to the health system in order to reduce healthcare costs and to provide a better quality of life. Animal models of ischemia and infarction have been essential in providing precise information regarding cardiac remodeling. Several of these changes are maladaptive, and they progressively lead to ventricular dilatation and predispose to the development of arrhythmias, HF and death. These events depend on cell death due to necrosis and apoptosis and on activation of the inflammatory response soon after MI. Systemic and local neurohumoral activation has also been associated with maladaptive cardiac remodeling, predisposing to HF. In this review, we provide a timely description of the cardiovascular alterations that occur after MI at the cellular, neurohumoral and electrical level and discuss the repercussions of these alterations on electrical, mechanical and structural dysfunction of the heart. We also identify several areas where insufficient knowledge limits the adoption of better strategies to prevent HF development in chronically infarcted individuals.

The aim of the present study was to evaluate the effect of low-dose spironolactone initiated during the early stages of hypertension development and to assess the effects of chronic pressure overload on ventricular remodeling in rats. Male spontaneously hypertensive rats (SHRs) (4 weeks) were randomized to receive daily spironolactone (20 mg/kg) or vehicle (mineral oil) from 4 weeks to 8 months of age. Systolic blood pressure was measured non-invasively by tail-cuff pletysmography at baseline, 4 and 8 months. Hemodynamic assessment was performed at the end of treatment by arterial and ventricular catheterization. An in situ left ventricular pressure-volume curve was created to evaluate dilatation and wall stiffness. Systolic blood pressure at 1 month of age was higher in SHRs than in the Wistar group; it increased throughout the follow-up period and remained elevated with treatment (Wistar: 136 ± 2, SHR: 197 ± 6.8, SHR-Spiro: 207 ± 7.1 mmHg; p0.05). Spironolactone reduced cardiac hypertrophy (Wistar: 1.25 ± 0.03 SHR: 1.00 ± 0.03, SHR-Spiro: 0.86 ± 0.02 g; p0.05) and left ventricular mass normalized to body weight (Wistar: 2.51 ± 0.06, SHR: 2.70 ± 0.08, 2.53 ± 0.07 mg/g; p0.05). Moreover, the left ventricular wall stiffness that was higher in SHRs was partially reduced by spironolactone treatment (Wistar: 0.370 ± 0.032; SHR: 0.825 ± 0.058; SHR-Spiro: 0.650 ± 0.023 mmHg/ml; p0.05). Our results show that long-term spironolactone treatment initiated at the early stage of hypertension development reduces left ventricular hypertrophy and wall stiffness in SHRs.

OBJECTIVE: To evaluate the effect of spironolactone on ventricular stiffness in spontaneously hypertensive adult rats subjected to high salt intake. INTRODUCTION: High salt intake leads to cardiac hypertrophy, collagen accumulation and diastolic dysfunction. These effects are partially mediated by cardiac activation of the renin-angiotensin-aldosterone system. METHODS: Male spontaneously hypertensive rats (SHRs, 32 weeks) received drinking water (SHR), a 1% NaCl solution (SHR-Salt), or a 1% NaCl solution with a daily subcutaneous injection of spironolactone (80 mg.kg-1) (SHR-Salt-S). Age-matched normotensive Wistar rats were used as a control. Eight weeks later, the animals were anesthetized and catheterized to evaluate left ventricular and arterial blood pressure. After cardiac arrest, a double-lumen catheter was inserted into the left ventricle through the aorta to obtain in situ left ventricular pressure-volume curves. RESULTS: The blood pressures of all the SHR groups were similar to each other but were different from the normotensive controls (Wistar = 109±2; SHR = 118±2; SHR-Salt = 117±2; SHR-Salt-S = 116±2 mmHg; P

Our aim was to evaluate the effects of granulocyte colony-stimulating factor (G-CSF) on early cardiac arrhythmias after myocardial infarction (MI) and the impact on survival. Male Wistar rats received repeated doses of 50 μg/kg G-CSF (MI-GCSF group) or vehicle (MI group) at 7, 3, and 1 days before surgery. MI was induced by permanent occlusion of left coronary artery. The electrocardiogram was obtained before occlusion and then for 30 minutes after surgery. Events and duration of ventricular arrhythmias were analyzed. The levels of connexin43 (Cx43) were measured by Western blot immediately before MI production. Survival was significantly increased in MI-GCSF pretreated group (74% versus 52.9% MI, P < 0.05). G-CSF pretreatment also significantly reduced the ventricular premature beats when compared with the untreated-MI group (201 ± 47 versus 679 ± 117, P < 0.05). The number and the duration of ventricular tachycardia were smaller in the MI-G-CSF group, as well as the number of ventricular fibrillation episodes (10% versus 69% in MI, P < 0.05). Cx43 levels were significantly increased by G-CSF treatment (1.27 ± 0.13 versus 0.86 ± 0.11; P < 0.05). The MI size 24 hours after occlusion was reduced by G-CSF pretreatment (36 ± 3% versus 44 ± 2% of left ventricle in MI group; P < 0.05). The increase of Cx43 expression in the heart may explain the reduced incidence in ventricular arrhythmias in the early phases after coronary artery occlusion in rats, thus increasing survival after MI.

Background The growing epidemic of metabolic syndrome has been related to the increased use of fructose by the food industry. In fact, the use of fructose as an ingredient has increased in sweetened beverages, such as sodas and juices. We thus hypothesized that fructose intake by hypertensive rats would have a worse prognosis in developing metabolic disorder and non-alcoholic fatty liver disease. Methods Male Wistar and SHR rats aged 6 weeks were given water or fructose (10%) for 6 weeks. Blood glucose was measured every two weeks, and insulin and glucose sensitivity tests were assessed at the end of the follow-up. Systolic blood pressure was measure by plethysmography. Lean mass and abdominal fat mass were collected and weighed. Liver tissue was analyzed to determine interstitial fat deposition and fibrosis. Results Fasting glucose increased in animals that underwent a high fructose intake, independent of blood pressure levels. Also, insulin resistance was observed in normotensive and mostly in hypertensive rats after fructose intake. Fructose intake caused a 2.5-fold increase in triglycerides levels in both groups. Fructose intake did not change lean mass. However, we found that fructose intake significantly increased abdominal fat mass deposition in normotensive but not in hypertensive rats. Nevertheless, chronic fructose intake only increased fat deposition and fibrosis in the liver in hypertensive rats. Conclusions We demonstrated that, in normotensive and hypertensive rats, fructose intake increased triglycerides and abdominal fat deposition, and caused insulin resistance. However, hypertensive rats that underwent fructose intake also developed interstitial fat deposition and fibrosis in liver.

Fructose acutely interferes with cardiovascular function in humans and in animals, but the mechanisms remain unclear. Thus, we tested whether fructose can affect endothelial function without the interference of its metabolic effect by exposing the rat aorta to a high fructose concentration and then evaluate the vascular responses to vasoactive agents. We observed that fructose exposure causes overactivation of NADPH oxidase, which enhances superoxide anion production and increases NO degradation. Additionally, the enhanced vasoconstrictor action of hydrogen peroxide might exacerbate contractile responses. This vasoactive imbalance might be the key role by which fructose induces vascular dysfunction.

Scientists worldwide have disseminated the idea that increased dietary salt increases blood pressure. Currently, salt intake in the general population is ten times higher than that consumed in the past and at least two times higher than the current recommendation. Indeed, a salt-rich diet increases cardiovascular morbidity and mortality. For a long time, however, the deleterious effects associated with high salt consumption were only related to the effect of salt on blood pressure. Currently, several other effects have been reported. In some cases, the deleterious effects of high salt consumption are independently associated with other common risk factors. In this article, we gather data on the effects of increased salt intake on the cardiovascular system, from infancy to adulthood, to describe the route by which increased salt intake leads to cardiovascular diseases. We have reviewed the cellular and molecular mechanisms through which a high intake of salt acts on the cardiovascular system to lead to the progressive failure of a healthy heart.

BACKGROUND: Left atrial volume index (LAVI) increase has been associated to left ventricle (LV) diastolic dysfunction (DD), a marker of cardiovascular events (atrial fibrillation, stroke, heart failure, death). OBJECTIVE: To evaluate the relationship between LAVI and diferente grades od DD in Brazilian patients submitted to echocardiogram, studying LAVI increase determinants in this sample. METHODS: We have selected 500 outpatients submitted to echocardiography, after excluding arrhythmia, valvar or congenital cardiopathy, permanent pacemaker or inadequate ecocardiographic window. LAVI was obtained according to Simpson's method. DD was classified according to current guidelines. The clinical and echocardiographic variables were submitted to linear regression multivariate analysis. RESULTS: Mean age was 52 ± 15 years old, 53% were male, 55% had arterial hypertension, 9% had coronary artery disease, 8% were diabetic, 24% were obese, 47% had LV hypertrophy. The mean ejection fraction of the left ventricle was 69.6 ± 7,2%. The prevalence of DD in this sample was 33.8% (grade I: 66%, grade II: 29% e grade III: 5%). LAVI increased progressively according to DD grade: 21 ± 4 mL/m2 (absent), 26 ± 7 mL/m2 (grade I), 33 ± 5 mL/m2 (grade II), 50 ± 5 mL/m2 (grade III) (p < 0,001). In this sample, LAVI increase independent predictors were age, left ventricular mass, relative wall thickness, LV ejection fraction and E/e' ratio. CONCLUSION: DD contributes to left atrial remodeling. LAVI increases as an expression of DD severity and is independently associated to age, left ventricle hypertrophy, systolic dysfunction and increased LV filling pressures.

According to hypertension guidelines, the recommended electrocardiographic (ECG) diagnostic criteria for left ventricular hypertrophy (LVH) are the Sokolow–Lyon and Cornel voltage criteria, both with general acceptance by primary care physicians. However, it was recently reported that the R-wave voltage in lead aVL (RaVL) was as good as other more complicated and time-consuming ECG criteria to detect LVH in hypertensive patients. Therefore, our aim was to investigate if the ability of the RaVL to identify echocardiographic left ventricular hypertrophy (ECHO-LVH) could be translated to the general population, a more realistic assessment of its utility in a nonreferral setting. 682 participants (43.5 % males), aged between 27 and 72 years from the urban population of Vitoria, ES, Brazil, were enrolled. We investigated the association of ECHO-LVH (LV mass >51 g/Ht2.7) with several ECG voltage measurements: Sokolow–Lyon and Cornel criteria, S-wave voltage in lead V3 (SV3) and RaVL. The RaVL showed the best positive correlation with LV mass indexed to Ht2.7, superior to both Cornell and Sokolow–Lyon criteria and was not influenced by gender. Analysis of the ROC curves showed that the RaVL depicted a significant superior performance in relation to all the other measurements in the ability to detect ECHO-LVH. SV3 was not correlated with LV mass. Thus, it seems that most of Cornell’s performance depends on its simplified version, that is, RaVL. We have shown that the simple and single assessment of RaVL presented a greater diagnostic ability in detecting ECHO-LVH in the general population, signaling its value mainly as a screening tool.

The effect of a salt-based diet on the coronary responsiveness in aged hypertensive rats (SHR) still is unclear. We investigated the effects of high salt intake on the relaxation properties of coronary arteries of aged SHRs. Male SHR (32 week-old) received drinking water (SHR) or 1% NaCl solution (SHR-Salt) for 8 weeks. Isolated coronary segments were subjected to concentration–response curves to acetylcholine (ACh) in the presence or absence of L-NAME (100 μM), enalaprilate (10 μM), losartan (10 μM), and spironolactone (100 μM). Salt intake did not increase blood pressure in old SHRs, but caused ventricular hypertrophy. The endothelium-dependent relaxation in SHRs was lower than in Wistar rats. However, salt intake did not add further impairment. Both enalaprilate and losartan reduced the vasodilator response in coronary arteries from Wistar, but did not affect SHR-salt rats. Conversely, losartan attenuated the impaired ACh relaxation observed in SHR. Spironolactone reduced the relaxation induced by ACh in coronary arteries from Wistar rats but not in SHR. The renin–angiotensin–aldosterone system participates in the impaired coronary relaxation in aged SHR, but does not partake in this deleterious effect under increased salt intake, indicating that age could differentiate the effects of high sodium intake in coronary arteries of SHR.

Granulocyte colony-stimulating factor (G-CSF) has been used in some animal models and humans with well-established cardiovascular diseases. However, its effects in the initial stage of progressive non-ischemic heart failure are unknown.Wistar rats (260-300 g) were divided into three groups: control (without any intervention), ISO (150 mg/kg isoproterenol hydrochloride sc, once a day for two consecutive days), and ISO-GCSF (50 μg/kg/d G-CSF for 7 days beginning 24 h after the last administration of ISO). Echocardiography was performed at baseline and after 30 days of follow-up. Subsequently, animals were anesthetized for hemodynamic analysis. The left ventricle was removed for analysis of interstitial collagen deposition and cardiomyocyte hypertrophy.Isoproterenol led to left ventricular dilation (control, 7.7 ± 0.14 mm; ISO, 8.7 ± 0.16 mm; ISO-GCSF 7.8 ± 0.09 mm; p0.05), myocardial fibrosis (control, 2.0 ± 0.18%; ISO, 9.1 ± 0.81%; ISO-GCSF 5.9 ± 0.58%; p0.05) and cardiomyocyte hypertrophy (control, 303 ± 10 μm(2); ISO, 356 ± 18 μm(2); ISO-GCSF 338 ± 11 μm(2); p0.05). However, G-CSF partially prevented collagen deposition and left ventricular enlargement, with a slight effect on hypertrophy. Characterizing a compensated stage of disease, hemodynamic analysis did not change.G-CSF administered for 7 days was effective in preventing the onset of ventricular remodeling induced by high-dose isoproterenol with decreased collagen deposition and chamber preservation.

The main purpose of this study was to investigate the effects of short-term L-NAME treatment on the contractile function of left ventricle (LV) myocytes and the expression of proteins related to Ca2+ homeostasis. Data from Wistar rats treated with L-NAME (L group, n = 20; 0.7 g/L in drinking water; 7 days) were compared with results from untreated controls (C group, n = 20). Cardiomyocytes from the L group showed increased (p < 0.05) fractional shortening (23%) and maximum rate of shortening (20%) compared with the C group. LV from the L group also showed increased (p < 0.05) expression of the ryanodine receptor 2 and Na+/Ca2+ exchanger proteins (76% and 83%, respectively; p < 0.05). However, the L and C groups showed similar in vivo hemodynamic parameters of cardiac function. In conclusion, short-term NOS inhibition determines an increased expression of Ca2+ regulatory proteins, which contributes to improving cardiomyocyte contractile function, preserving left ventricular function.

We evaluated the use of body weight (BW) loss soon after acute myocardial infarction (MI) in rats as a marker of acute heart failure (HF).Female Wistar rats (200-240 g) were submitted either to sham operation or to coronary artery occlusion. In individual cages, daily BW and food and water intake were measured. Seven days later, cardiac function was evaluated by left ventricular catheterization. HF was defined by a left ventricular end-diastolic pressure greater than the upper limit of the 95% confidence interval. MI group was then divided into those that developed HF (n = 27; MI-HF) and those that did not (n = 47; MI).The MI-HF group experienced increased BW loss (sham: 4.2 ± 0.6% MI: 0.4 ± 0.8%, MI-HF: -4.9 ± 1.2%; p0.05) and reduced water and food intake compared with other groups. HF animals showed greater lung weight (sham: 1.460 ± 0.076 g, MI: 1.748 ± 0.086 g, MI-HF: 2.033 ± 0.13 g; p0.05). Infarct area was significantly different between the groups (MI: 35.9 ± 0.9%, MI-HF: 39.7 ± 1.3%; p0.05). ROC curve showed that BW loss over 7 days has 100% sensitivity and 72.3% specificity for identifying acute HF. Moreover, excluding the effect of infarct area on these results, a sample of animals with the same infarct area displayed similar morphometric and hemodynamic patterns as the entire sample. Multivariate linear regression analysis confirmed that BW loss is a HF marker independent of infarct area.BW is an easy and reliable noninvasive method to detect HF early after MI in rats.

Granulocyte colony-stimulating factor (G-CSF) reduces myocardial injury and improves cardiac function after myocardial infarction (MI). We investigated the early alterations provided by G-CSF and the chronic repercussions in infarcted rats.Male Wistar rats (200-250g) received vehicle (MI) or G-CSF (MI-GCSF) (50 μg/kg, sc) at 7, 3 and 1 days before MI surgery. Afterwards MI was produced and infarct size was measured 1 and 15 days after surgery. Expression of anti- and proapoptotic proteins was evaluated immediately before surgery. 24 hours after surgery, apoptotic nuclei were evaluated. Two weeks after MI, left ventricular (LV) function was evaluated, followed by in situ LV diastolic pressure-volume evaluation.Infarct size was decreased by 1 day pre-treatment before occlusion (36±2.8 vs. 44±2.1% in MI; P0.05) and remained reduced at 15 days after infarction (28±2.2 vs. 36±1.4% in MI; P0.05). G-CSF pretreatment increased Bcl-2 and Bcl-xL protein expression, but did not alter Bax in LV. Apoptotic nuclei were reduced by treatment (Sham: 0.46±0.42, MI: 15.5±2.43, MI-GCSF: 5.34±3.34%; P0.05). Fifteen days after MI, cardiac function remained preserved in G-CSF pretreated rats. The LV dilation was reduced in MI-G-CSF group as compared to MI rats, being closely associated with infarct size.The early beneficial effects of G-CSF were essentials to preserve cardiac function at a chronic stage of myocardial infarction.

Nitric oxide (NO) modulates the expression of the chaperone Hsp72 in the heart, and exercise stimulates both NO production and myocardial Hsp72 expression. The main purpose of the study was to investigate whether NO interferes with an exercise-induced myocardial Hsp72 expression.Male Wistar rats (70-100 days) were divided into control (C, n=12), L-NAME-treated (L, n=12), exercise (E, n=13) and exercise plus L-NAME-treated (EL, n=20) groups. L-NAME was given in drinking water (700 mg·L(-1)) and the exercise was performed on a treadmill (15-25 m·min(-1), 40-60 min.day(-1)) for seven days. Left ventricle (LV) protein Hsp content, NOS and phosphorylated-NOS (p-NOS) isoforms were measured using Western blotting. The activity of NOS was assayed in LV homogenates by the conversion of [(3)H]L-arginine to [(3)H]L-citrulline.Hsp72 content was increased significantly (223%; p0.05) in the E group compared to the C group, but exercise alone did not alter the NOS content, p-NOS isoforms or NOS activity. Contrary to our expectation, L-NAME enhanced (p0.05) the exercise-induced Hsp72 content (EL vs. C, L and E groups = 1019%, 548% and 457%, respectively). Although the EL group had increased stimulatory p-eNOS(Ser1177) (over 200%) and decreased inhibitory p-nNOS(Ser852) (ñ50%) compared to both the E and L groups (p0.05), NOS activity was similar in all groups.Our results suggest that exercise-induced cardiac Hsp72 expression does not depend on NO. Conversely, the in vivo L-NAME treatment enhances exercise-induced Hsp72 production. This effect may be due to an increase in cardiac stress.

Submitted by Edna Reis (ednareis@bc.ufes.br) on 2011-04-20T13:43:25Z No. of bitstreams: 2 v32n2a05.pdf: 627827 bytes, checksum: dff2dabc30806b23053f63b3f6d32608 (MD5) license_rdf: 21504 bytes, checksum: cfe16b28a928230b24b965de15e8a5ff (MD5) Approved for entry into archive by Patricia Barros(patricia.barros@ufes.br) on 2011-10-10T20:10:33Z (GMT) No. of bitstreams: 2 license_rdf: 21504 bytes, checksum: cfe16b28a928230b24b965de15e8a5ff (MD5) v32n2a05.pdf: 627827 bytes, checksum: dff2dabc30806b23053f63b3f6d32608 (MD5) Made available in DSpace on 2011-10-10T20:10:33Z (GMT). No. of bitstreams: 2 license_rdf: 21504 bytes, checksum: cfe16b28a928230b24b965de15e8a5ff (MD5) v32n2a05.pdf: 627827 bytes, checksum: dff2dabc30806b23053f63b3f6d32608 (MD5) Previous issue date: 2010-04 Introdução: A concentração da creatinina no plasma é usada para avaliar a função renal, mas a depuração da creatinina plasmática (DCP) constitui método mais sensível para essa finalidade. Objetivo: Correlacionar a DCP em coleta urinária de 12 horas noturna com a de 24 horas. Métodos: Noventa e cinco voluntários (34-64 anos) coletaram urina durante 24 horas em dois frascos: diurno (das 7h às 19h) e noturno (das 19h às 7h do dia seguinte). A coleta de sangue se deu em jejum para medidas bioquímicas. A correlação entre as variáveis foi feita pelo teste Pearson (r) e a concordância de medidas, pelo teste de Bland-Altman. Resultados: Urinas de quatro indivíduos foram recusadas por erro de coleta. Na amostra final (n = 91; 42 homens), havia 23 hipertensos e cinco diabéticos. A DCP (mL/min/1,73 m2) foi menor no período noturno em mulheres (77,8 ± 22,7 versus 88,4 ± 23,6; p < 0,05) e similar em homens (91,2 ± 22,9 versus 97,3 ± 30,9; p > 0,05). As correlações entre a DCP na urina de 12 horas noturna ou diurna e a de 24 horas foram fortes (r = 0,85 e 0,83, respectivamente). Em 85 e 83 dos 91 indivíduos, a medida da DCP noturna e diurna, respectivamente, foi concordante com a de 24 horas. Conclusão: A urina de 12 horas, sobretudo quando coletada à noite, fornece valores de DCP similares àqueles obtidos em coleta de 24 horas. Como essa coleta é mais fácil de ser feita em pacientes ambulatoriais à noite, esse período deveria ser preferido para a medida da filtração glomerular. ABSTRACT Introduction: Creatinine concentration in plasma has been used to evaluate renal function. However, the endogenous creatinine clearance (CrCl) is more sensitive to this goal. Objective: Correlate the CrCl calculated from urinary collects of 12 h and 24 h. Methods: Ninety five volunteers (34-64 y) collected the urine for 24 h into two bottles: night, from 7 am to 7 pm and day, from 6 am to 7 pm. A fasting blood sample was used to measure plasma creatinine. Correlation between variables was determined by Pearson method (r) and the agreement between night and 24 h CrCl was determined by the Bland-Altman plot. Results: Urines of 4 individuals were discarded because of collect errors. In the final sample (n = 91; 42 males), hypertension was found in 23 and diabetic in 5. The CrCl (mL/min/1.73 m2) was slightly lower in females in the night (77.8 ± 22.7 versus 88.4 ± 23.6; p < 0.05) and similar in males (91.2 ± 22.9 versus 97.3 ± 30.9; p > 0.05). Strong correlations were observed between the CrCl calculated from the night and day urines and the 24 h (r = 0.85 and 0.83; respectively). Agreement between the CrCl calculated from night or day urine and the 24 h urine was observed, respectively, to 85 and 83 individuals. Conclusion: The 12 h urine, mainly obtained at night, gives CrCl values similar to those obtained in the 24 h collect. Since urine collect is easier to outpatients at night, this period should be chosen in the clinical evaluation of the glomerular filtration rate.

Top of pageAbstract Left ventricular hypertrophy is an important predictor of cardiovascular risk and sudden death. This study explored the ability of four obesity indexes (body mass index, waist circumference, waist–hip ratio and waist–stature ratio) to identify left ventricular hypertrophy. A sample of the general population (n=682; 43.5% men) was surveyed to assess cardiovascular risk factors. Biochemical, anthropometric and blood pressure values were obtained in a clinic visit according to standard methods. Left ventricular mass was obtained from transthoracic echocardiogram. Left ventricular hypertrophy was defined using population-specific cutoff values for left ventricular mass indexed to height2.7. The waist–stature ratio showed the strongest positive association with left ventricular mass. This correlation was stronger in women, even after controlling for age and systolic blood pressure. By multivariate analysis, the main predictors of left ventricular hypertrophy were waist–stature ratio (23%), systolic blood pressure (9%) and age (2%) in men, and waist–stature ratio (40%), age (6%) and systolic blood pressure (2%) in women. Receiver-operating characteristic curves showed the optimal cutoff values of the different anthropometric indexes associated with left ventricular hypertrophy. The waist–stature ratio was a significantly better predictor than the other indexes (except for the waist–hip ratio), independent of gender. It is noteworthy that a waist–stature ratio cutoff of 0.56 showed the highest combined sensitivity and specificity to detect left ventricular hypertrophy. Abdominal obesity identified by waist–stature ratio instead of overall obesity identified by body mass index is the simplest and best obesity index for assessing the risk of left ventricular hypertrophy, is a better predictor in women and has an optimal cutoff ratio of 0.56. Keywords: abdominal adiposity, body mass index, left ventricular hypertrophy

Angiotensin-converting enzyme inhibitors reduce blood pressure and attenuate cardiac and vascular remodeling in hypertension. However, the kinetics of remodeling after discontinuation of the long-term use of these drugs are unknown. Our objective was to investigate the temporal changes occurring in blood pressure and vascular structure of spontaneously hypertensive rats (SHR). Captopril treatment was started in the pre-hypertensive state. Rats (4 weeks) were assigned to three groups: SHR-Cap (N = 51) treated with captopril (1 g/L) in drinking water from the 4th to the 14th week; SHR-C (N = 48) untreated SHR; Wistar (N = 47) control rats. Subgroups of animals were studied at 2, 4, and 8 weeks after discontinuation of captopril. Direct blood pressure was recorded in freely moving animals after femoral artery catheterism. The animals were then killed to determine left ventricular hypertrophy (LVH) and the aorta fixed at the same pressure measured in vivo. Captopril prevented hypertension (105 + or - 3 vs 136 + or - 5 mmHg), LVH (2.17 + or - 0.05 vs 2.97 + or - 0.14 mg/g body weight) and the increase in cross-sectional area to luminal area ratio of the aorta (0.21 + or - 0.01 vs 0.26 + or - 0.02 microm(2)) (SHR-Cap vs SHR-C). However, these parameters increased progressively after discontinuation of captopril (22nd week: 141 + or - 2 mmHg, 2.50 + or - 0.06 mg/g, 0.27 + or - 0.02 microm(2)). Prevention of the development of hypertension in SHR by using captopril during the prehypertensive period prevents the development of cardiac and vascular remodeling. Recovery of these processes follows the kinetic of hypertension development after discontinuation of captopril.

The objective of this study was to investigate the association between sodium intake and metabolic syndrome (MS) in individuals free from the confounding effects of increased blood pressure (BP). In all, a total of 1655 individuals (45.8% men) who participated in the MONICA-WHO/Vitoria Project, mean age 45+/-11 years were investigated. According to NCEP-ATP lll criteria, MS prevalence was 32.9 and 85% of these individuals had BP >130/85 mm Hg. Thus, high BP represents the main MS risk factor. Twelve-hour nocturnal urine (1900 to 0700 hours) was used to measure urinary sodium and potassium excretion. Sodium excretion was associated with BP. From the optimal BP level up to stage lll hypertension, the mean (median) sodium excretion increased from 99 (89) to 128 (134) mEq and from 81 (69) to 112 (103) mEq in men and women, respectively (P