Birth weight and its relationship with endothelial function and pattern of endothelium-derived microparticles during childhood: New insight about early vascular damage.

AIMS: To investigate whether a specific endothelium-derived microparticles (EMPs) phenotype could be associated with birth weight and microvascular endothelial function in children. MATERIALS AND METHODS: A total of 95 children aged 6-14 years were recruited. Anthropometric measurements, blood pressure measurement, microvascular endothelial function testing, and biochemical profile analyses were performed. Standardized flow cytometry methods were used to identify and quantify the circulating CD144+, CD31+/annexin V+, and CD62E+ EMPs. KEY FINDINGS: The circulating number of CD31+/annexin V+ EMPs and CD144+ EMP levels were correlated with birth weight, systolic blood pressure, microvascular endothelial function, total cholesterol, and low-density lipoprotein cholesterol (LDL-C) level. In the multivariable logistic regression models, we identified strong evidence of a higher risk of microvascular endothelial dysfunction among children with low birth weight (LBW) and increased levels of both CD31+/annexin V+ EMPs and LDL-C; LBW and elevated LDL-C levels were independent predictors of high circulating numbers of CD31+/annexin V+ and CD144+ > 75th percentile EMPs. SIGNIFICANCE: Our data provide evidence that children with LBW values showed greater numbers of circulating CD31+/annexin V+ and CD144+ EMPs. In addition, LBW and high levels of CD31+/annexin V+ and LDL-C were significant risk factors for the presence of microvascular endothelial dysfunction.

High circulating levels of CD62E+ and CD31+/Annexin V+ endothelium-derived microparticles in children with overweight/obesity: Evidence of early vascular damage.

BACKGROUND: Obesity perturbs endothelium integrity, leading to endothelial activation, which predisposes the release of endothelium-derived microparticles (EMP). We measured the CD31+/annexin V+ and CD62E+ EMP levels to improve our understanding of their contribution to endothelial damage in children with overweight/obesity. SUBJECT AND METHODS: In this cross-sectional study, 107 children with normal weight and 35 children with overweight/obesity were evaluated. Anthropometric measurement, blood pressure, biochemical profile was performed. Standardized flow cytometry methods were used to identify and quantify circulating CD31+/annexin V+ and CD62E+ EMP. RESULTS: Children with overweight/obesity had significantly higher circulating levels of CD31+/annexin V+ (750 [600]) and CD62E+ (1400 [700]) EMP than those with normal weight (P < 0.001 for both). We found that EMP levels were positively correlated with body mass index (BMI), waist circumference, blood pressure, total cholesterol, low-density lipoprotein cholesterol (LDLc), and triglycerides. The multivariable logistic regression model revealed that the risks of having high EMP levels (> 75th percentile) were high in children with both large waist circumference and elevated LDLc level. Receiver operating characteristic (ROC) curves demonstrated that the LDLc levels showed significantly greater discrimination than waist circumference for both CD31+/annexin V+ (P = 0.031) as CD62E+ EMPs (P = 0.041). CONCLUSIONS: Children with overweight/obesity have high circulating CD31+/annexin V+ and CD62E+ EMP levels, which may be an early sign of endothelial apoptosis and inflammatory activation in response to injury. These EMP levels were positively associated with several cardiometabolic risk factors. Our data underscore the negative influence of high-risk metabolic profiles on endothelial integrity in the early stages of childhood obesity.

Low birth weight and its relation to physical fitness parameters in children: Its negative effect on muscle strength and cardiorespiratory endurance.

BACKGROUND: There is increasing evidence that low birth weight has a negative effect on physical fitness, muscle strength, and cardiorespiratory endurance, although the findings are inconsistent. OBJECTIVES: This study aimed to evaluate whether birth weight acts as a prenatal determinant of physical fitness parameters and to determine the role of environmental or biological variables on this effect. METHODS: One hundred and sixty-seven children aged 6-14 years were included in this study. The anthropometric data, physical activity index, standing long jump, flexibility, handgrip strength, and cardiorespiratory fitness were evaluated. RESULTS: A positive correlation was found between birth weight and cardiorespiratory fitness (r = .349; p < .001), right handgrip strength (r = .337; p < .001), and left handgrip strength (r = .320; p < .001), suggesting that children with low birth weight had the worst performance in both cardiorespiratory endurance and grip strength tests. These findings remained significant after adjustment for prematurity, sex, age, physical activity index, and body mass index (BMI). Stepwise multiple regression analyses revealed a significant interaction of high birth weight, older age, and low BMI in predicting better cardiorespiratory endurance (R2  = .308). When handgrip strength was tested as the dependent variable, we found that high birth weight, male sex, and older age emerged as important determinants for both sides. CONCLUSION: Children aged 6-14 years born with a birth weight < 2.5 kg have low handgrip strength and cardiorespiratory fitness, which seems to be mediated partially by influences of both prenatal environment (e.g., birth weight) and biological variables (e.g., age, sex, BMI).

Imbalance between the circulating endothelium-derived apoptotic microparticles and the endothelial colony-forming units of progenitor cells in patients undergoing diagnostic coronary angiography.

PURPOSE: The involvement of the circulating endothelium-derived microparticles (EMPs) and the endothelial progenitor cells (EPCs) has been shown in the pathogenesis of coronary artery disease (CAD). The current study aimed to explore whether the Friesinger index is associated with the levels of the apoptotic CD144+/CD31+/annexin V+ â€‹EMPs and the number of endothelial colony-forming units of progenitor cells in patients undergoing coronary angiography. PATIENTS AND METHODS: Fifty-seven patients with a median age of 62 years (range: 48-84 years) were enrolled. Quantification of the apoptotic CD144+/CD31+/annexin V+ EMPs was performed by flow cytometry. The number of endothelial colony-forming units defined by CFU-Hill was assessed by cell culture. RESULTS: There was a positive correlation between the Friesinger index and the circulating levels of the apoptotic CD144+/CD31+/annexin V+ EMPs (rho=0.817, p<0.001), whereas a negative correlation was found with the number of CFU-Hill (rho â€‹= â€‹- 0.649, p<0.001). Multivariable logistic analysis showed that the risk of having moderate/severe CAD was five times greater among male patients (OR:5.32; 95% CI: 1.19 - 16.33; p=0.038) and almost one and a half times higher among those with a higher level of apoptotic CD144+/CD31+/annexin V+ EMPs (OR:1.74; 95% CI: 1.23 - 2.28; p=0.001). Finally, the circulating levels of apoptotic EMPs labelled for CD144+/CD31+/annexin V+ presented a good discrimination of moderate/severe CAD, with an AUC of 0.85 (95% CI â€‹= â€‹0.74 - 0.96; p< 0.001). CONCLUSIONS: Moderate or severe CAD is associated with increased levels of apoptotic EMPs and reduced EPC colony-forming capacity, increasing the occurrence of endothelial injuries.

Emerging evidence for the opposite role of circulating irisin levels and brown adipose tissue activity measured by infrared thermography in anthropometric and metabolic profile during childhood.

Irisin is an adipomyokine that increases browning of adipose tissue and thermogenesis, thereby protecting against obesity and insulin resistance. However, the correlation between irisin, brown adipose tissue (BAT), and childhood obesity, as well as its association with an increased risk of developing metabolic diseases, has not been completely elucidated. This study aimed to investigate the association between irisin levels and BAT activity measured by infrared thermography among children and verify their correlation with anthropometric and metabolic parameters. This study included 42 children with normal weight and 18 overweight/obese children. Anthropometric data, irisin levels, lipid and glucose profile were evaluated. The percentage of the thermally active portion of the supraclavicular area (%AreaSCR) before and after a cold stimulus was measured by infrared thermography, and the differences between the percentages of thermally active (Δ%AreaSCR) was calculated as an index of BAT activation. The results were correlated with anthropometric and metabolic parameters. Circulating irisin levels was positive correlated with age (rho=0.327, P= 0.011), body mass index (BMI) (rho=0.707, P<0.001), waist circumference (rho=0.624, P<0.001), total cholesterol (rho=0.361, P=0.044), triglycerides (rho=0.419, P=0.001), and low-density lipoprotein cholesterol (LDLc) (rho=0.381, P= 0.003). Active BAT was negatively correlated with BMI, waist circumference, triglycerides, LDLc and irisin levels. We observed that normal weight children increased significantly the Δ% AreaSCR as compared to overweight/obese children. In conclusion, circulating irisin levels and BAT activity appear to have opposing roles, since normal weight children had greater BAT activity and lower circulating levels of irisin.

Polymorphism of the bradykinin type 2 receptor gene modulates blood pressure profile and microvascular function in prepubescent children.

Previous reports reveal that +9/-9 polymorphism of the bradykinin B2 receptor (BDKRB2) is suggestive of cardiometabolic diseases. The aim of this study was to examine the impact of BDKRB2 + 9/-9 polymorphism genotypes on the blood pressure parameters and microvascular function in prepubescent children. We screened for BDKRB2 + 9/-9 polymorphism in the DNA of 145 children (86 boys and 59 girls), and its association with body composition, blood pressure levels, biochemical parameters, and endothelial function was determined. No significant association of the BDKRB2 genotypes with gender (P=0.377), race (P=0.949) or family history of cardiovascular disease (CVD) (P=0.858) was observed. Moreover, we did not identify any interaction between BDKRB2 genotypes with a phenotype of obesity (P=0.144). Children carrying the +9/+9 genotype exhibited a significant linear trend with higher levels of systolic blood pressure and pulse pressure (P<0.001). Moreover, the presence of +9 allele resulted in a decrease of reactive hyperemia index, showing a decreasing linear trend from -9/-9 to +9/+9, wherein this parameter of endothelial function was the lowest in the +9/+9 children, intermediate in the +9/-9 children, and the highest in the -9/-9 children (P<0.001). There was a significant inverse correlation between reactive hyperemia index and systolic blood pressure (r= - 0.348, P< 0.001) and pulse pressure (r= - 0.399, P< 0.001). Our findings indicate that the +9/+9 BDKRB2 genotype was associated with high blood pressure and microvascular dysfunction in prepubescent Brazilian children.

Is low birth weight an additional risk factor for hypertension in paediatric patients after kidney transplantation?

Hypertension (HTN) remains a common complication after kidney transplantation among paediatric patients. Although low birth weight (LBW) has been implicated as an important risk factor for cardiovascular diseases, its effect on transplantation patients has not yet been addressed. It is essential to determine whether children with LBW who undergo transplantation are more likely to develop post-transplantation HTN. For this study, the medical records of 96 kidney recipients were retrospectively examined. A total of 83 patients fulfilled the inclusion criteria. Overall, post-transplantation HTN was observed in 54% of the recipients. Multivariate logistic regression revealed that time from transplantation >14 months (odds ratio (OR) 3.6; 95% confidence interval (CI) 1.31-10.06; P = 0.013), current CKD (OR 2.6; 95% CI 1.01-7.20; P = 0.045), presence of LBW (OR 3.6; 95% CI 1.04-12.32; P = 0.044) and current overweight/obesity (OR 3.7; 95% CI 1.02-13.91; P = 0.047) were associated with post-transplantation HTN. In conclusion, our data provide evidence for the first time that LBW is a significant predictive factor in the development of post-transplantation HTN. This finding has important clinical implications as it serves to alert clinicians about this additional risk factor in paediatric patients undergoing kidney transplant.

Detrimental Impact of Low Birth Weight on Circulating Number and Functional Capacity of Endothelial Progenitor Cells in Healthy Children: Role of Angiogenic Factors.

OBJECTIVE: To provide a comprehensive assessment of the relationship of birth weight with both endothelial progenitor cell function and angiogenic factors in children. STUDY DESIGN: Anthropometric measures, biochemical profile, endothelial progenitor cell number, endothelial progenitor cell colony-forming units, vascular endothelial growth factor-A, and nitric oxide plasma levels of 58 children aged 7-11 years were determined. RESULTS: A positive correlation was observed between birth weight and circulating endothelial progenitor cell number (r= 0.461; P= .001), endothelial progenitor cell colony-forming units (r= 0.512; P < .001), vascular endothelial growth factor-A (r= 0.407; P= .002), and nitric oxide (r= 0.547; P < .001) levels, whereas the adjustment for prematurity, family history of cardiovascular disease, and systolic blood pressure levels did not modify these associations. CONCLUSION: Low birth weight was associated with a decrease in the circulating/functional capacity of endothelial progenitor cells among healthy children, independent of traditional cardiovascular risk factors. This detrimental impact was accompanied by lower circulating levels of angiogenic factors.

Beneficial Impact of Moderate to Vigorous Physical Activity Program on Circulating Number and Functional Capacity of Endothelial Progenitor Cells in Children: The Crucial Role of Nitric Oxide and VEGF-A.

PURPOSE: Endothelial progenitor cells (EPCs) appear to interact with physical training. This study aimed to provide a comprehensive assessment of the relationship of moderate to vigorous physical activity (MVPA) with both angiogenic factors and EPC function in healthy children. METHODS: Forty children (22 boys and 18 girls) aged 7 to 11 years participated in a 10-week MVPA program (duration: 45 min; intensity: 75%-85% of heart rate reserve; frequency: 4 sessions/wk). The anthropometric data, biochemical profile, EPCs number, EPCs colony-forming units, and vascular endothelial growth factor-A (VEGF-A) and nitric oxide (NO) plasma levels were evaluated before and after the MVPA program. RESULTS: After a 10-week MVPA program, a significant increase was detected in circulating/functional capacity of EPCs, NO, and VEGF-A levels, associated with improvement of waist circumference and estimated maximum rate of oxygen consumption (VO2max). A strong positive correlation was found between delta of EPCs number and variation of both NO level (r = .677, P < .001) and VEGF-A level (r = .588, P < .001). Furthermore, a significant correlation between NO level variation and delta of VEGF-A level was observed (r = .708, P < .001). CONCLUSION: Our findings suggest that lifestyle intervention implemented by MVPA program can contribute meaningfully to improve circulating/functional capacity of EPCs in healthy children, possibly due to the increase of plasma NO and VEGF-A levels.

Implication of galanin gene rs948854 polymorphism in depressive symptoms in adolescents.

Genetic, social, and environmental conditions contribute to the development of depression, but the pathophysiological mechanisms are still unclear. Data accumulated in recent years provide significant evidence for a direct role of galanin (GAL). This study aimed to investigate the relation between SNPs in the galaninergic system and depressive symptoms in adolescents. A total of112 adolescents aged 10-18years participated in this study. The Children Depression Inventory (CDI) was used to evaluate depressive symptoms. The effects of rs948854 and rs4432027 SNPs, both located within the promoter region of the GAL gene, rs11665337 in the GALR1 receptor, and rs8836 in the GALR2 receptor on depressive symptoms were examined. The results indicated that 30.4% of the participants had depression. We found that girls were significantly more likely to be depressive than boys. Furthermore, rs948854 minor (G) allele was associated with depressive symptoms. Adolescents carrying the GG and AG genotype for the A/G (rs948854) SNP showed higher CDI scores than those carrying homozygous AA. The binomial logistic regression analysis revealed that adolescents carrying the GG genotype at SNP rs948854 had a higher likelihood of being depressive than adolescents carrying the AA or AG genotypes (P=0.033). Moreover, individuals whose mothers had a positive history for depression and who were sedentary were more likely to display depressive symptoms (P=0.013 and P=0.032, respectively). In conclusion, the SNP rs948854 in the GAL gene seems to be involved in the modulation of depressive state, especially in individuals with GG genotype.

Cardiac Autonomic Dysfunction in Offspring of Hypertensive Parents During Exercise.

Offspring of hypertensive parents present autonomic dysfunction at rest and during physiological maneuvers. However, the cardiac autonomic modulation during exercise remains unknown. This study tested whether the cardiac autonomic modulation would be reduced in offspring of hypertensive parents during exercise. Fourteen offspring of hypertensive and 14 offspring of normotensive individuals were evaluated. The groups were matched by age (24.5±1.0 vs. 26.6±1.5 years; p=0.25) and BMI (22.8±0.6 vs. 24.2±1.0 kg/m2; p=0.30). Blood pressure and heart rate were assessed simultaneously during 3 min at baseline followed by 3-min isometric handgrip at 30% of maximal voluntary contraction. Cardiac autonomic modulation was evaluated using heart rate variability. Primary variables were subjected to two-way ANOVA (group vs. time). P value<0.05 was considered statistically significant. Blood pressure and heart rate were similar between groups during exercise protocol. In contrast, offspring of hypertensive subjects showed a reduction of SDNN (Basal=34.8±3.5 vs. 45.2±3.7 ms; Exercise=30.8±3.3 vs. 41.5±3.9 ms; p group=0.01), RMSSD (Basal=37.1±3.7 vs. 52.0±6.0 ms; Exercise=28.6±3.4 vs. 41.9±5.3 ms; p group=0.02) and pNN50 (Basal=15.7±4.0 vs. 29.5±5.5%; Exercise=7.7±2.4 vs. 18.0±4.3%; p group=0.03) during the exercise protocol in comparison with offspring of normotensive parents. We concluded that normotensive offspring of hypertensive parents exhibit impaired cardiac autonomic modulation during exercise.

Peripheral Vascular Resistance Impairment during Isometric Physical Exercise in Normotensive Offspring of Hypertensive Parents / Prejuízo da Resistência Vascular Periférica durante o Exercício Físico Isométrico em Indivíduos Normotensos Filhos de Hipertensos

Abstract Background: A family history of hypertension is associated with vascular and autonomic abnormalities, as well as an impaired neurohemodynamic response to exercise. Objective: To test the hypothesis that normotensive individuals with a family history of hypertension present an impaired peripheral vascular resistance response to exercise. Methods: The study included 37 normotensive volunteers of both sexes who were sedentary, eutrophic, and nonsmokers, comprising 23 with (FH+; 24 ± 3 years) and 14 without (FH-; 27 ± 5 years) a family history of hypertension. Blood pressure, heart rate (DIXTAL®), forearm blood flow (Hokanson®), and peripheral vascular resistance were simultaneously measured for 3 minutes during rest and, subsequently, for 3 minutes during an isometric exercise at 30% of maximal voluntary contraction (Jamar®). Results: At rest, the FH+ and FH- groups present similar mean blood pressure (83 ± 7 versus 83 ± 5 mmHg, p = 0.96), heart rate (69 ± 8 bpm versus 66 ± 7 bpm, p = 0.18), forearm blood flow (3 ± 1 mL/min/100 mL versus 2.7 ± 1 mL/min/100 mL, p = 0.16), and peripheral vascular resistance (30 ± 9 units versus 34±9 units, p = 0.21), respectively. Both groups showed a significant and similar increase in mean blood pressure (∆ = 15 ± 7 mmHg versus 14 ± 7 mmHg, p = 0.86), heart rate (∆ = 12 ± 8 bpm versus 13 ± 7 bpm, p = 0.86), and forearm blood flow (∆ = 0.8 ± 1.2 mL/min/100 mL versus 1.4 ± 1.1 mL/min/100 mL, p = 0.25), respectively, during exercise. However, individuals in the FH+ group showed no reduction in peripheral vascular resistance during exercise, which was observed in the FH- group (∆ = -0.4 ± 8.6 units versus -7.2 ± 6.3 units, p = 0.03). Conclusion: Normotensive individuals with a family history of hypertension present an impaired peripheral vascular resistance response to exercise.

Resumo Fundamento: O histórico familiar para hipertensão arterial está relacionado a anormalidades vasculares e autonômicas, bem como disfunções no comportamento neuro-hemodinâmico durante o exercício físico. Objetivo: Testar a hipótese de que indivíduos normotensos com histórico familiar de hipertensão arterial apresentam resposta prejudicada da resistência vascular periférica durante o exercício físico. Métodos: Foram avaliados 37 normotensos de ambos os sexos, sedentários, eutróficos e não tabagistas, sendo 23 com histórico familiar positivo (HF+, 24 ± 3 anos) e 14 com histórico familiar negativo (HF-, 27 ± 5 anos) para hipertensão arterial. Foram identificados pressão arterial, frequência cardíaca (DIXTAL®), fluxo sanguíneo muscular do antebraço e resistência vascular periférica local (Hokanson®) por 3 minutos durante o repouso e, em seguida, 3 minutos durante exercício isométrico de preensão palmar a 30% da contração voluntária máxima (Jamar®). Resultados: Em repouso, os grupos HF+ e HF- apresentaram valores semelhantes de pressão arterial média (83 ± 7 mmHg versus 83 ± 5 mmHg, p = 0,96), frequência cardíaca (69 ± 8 bpm versus 66 ± 7 bpm, p = 0,18), fluxo sanguíneo muscular (3 ± 1 mL/min/199 mL versus 2,7 ± 1 mL/min/100 mL, p = 0,16) e resistência vascular periférica (30 ± 9 unidades versus 34 ± 9 unidades, p = 0,21), respectivamente. Durante o exercício, HF+ e HF- mostraram aumento significativo e semelhante da pressão arterial média (∆ = 15 ± 7 mmHg versus 14 ± 7 mmHg, p = 0,86), frequência cardíaca (∆ = 12 ± 8 bpm versus 13 ± 7 bpm, p = 0,86) e fluxo sanguíneo muscular (∆ = 0,8 ± 1,2 mL/min/100 mL versus 1,4 ± 1,1 mL/min/100 mL, p = 0,25), respectivamente. Entretanto, no grupo HF+ não houve redução significativa da resistência vascular periférica durante o exercício, fato que ocorreu no grupo HF- (∆ = -0,4 ± 8,6 unidades versus -7,2 ± 6,3 unidades, p = 0,03). Conclusão: Indivíduos normotensos com histórico familiar de hipertensão arterial apresentam resposta prejudicada da resistência vascular periférica durante o exercício físico.

Peripheral Vascular Resistance Impairment during Isometric Physical Exercise in Normotensive Offspring of Hypertensive Parents.

BACKGROUND:: A family history of hypertension is associated with vascular and autonomic abnormalities, as well as an impaired neurohemodynamic response to exercise. OBJECTIVE:: To test the hypothesis that normotensive individuals with a family history of hypertension present an impaired peripheral vascular resistance response to exercise. METHODS:: The study included 37 normotensive volunteers of both sexes who were sedentary, eutrophic, and nonsmokers, comprising 23 with (FH+; 24 ± 3 years) and 14 without (FH-; 27 ± 5 years) a family history of hypertension. Blood pressure, heart rate (DIXTAL®), forearm blood flow (Hokanson®), and peripheral vascular resistance were simultaneously measured for 3 minutes during rest and, subsequently, for 3 minutes during an isometric exercise at 30% of maximal voluntary contraction (Jamar®). RESULTS:: At rest, the FH+ and FH- groups present similar mean blood pressure (83 ± 7 versus 83 ± 5 mmHg, p = 0.96), heart rate (69 ± 8 bpm versus 66 ± 7 bpm, p = 0.18), forearm blood flow (3 ± 1 mL/min/100 mL versus 2.7 ± 1 mL/min/100 mL, p = 0.16), and peripheral vascular resistance (30 ± 9 units versus 34±9 units, p = 0.21), respectively. Both groups showed a significant and similar increase in mean blood pressure (∆ = 15 ± 7 mmHg versus 14 ± 7 mmHg, p = 0.86), heart rate (∆ = 12 ± 8 bpm versus 13 ± 7 bpm, p = 0.86), and forearm blood flow (∆ = 0.8 ± 1.2 mL/min/100 mL versus 1.4 ± 1.1 mL/min/100 mL, p = 0.25), respectively, during exercise. However, individuals in the FH+ group showed no reduction in peripheral vascular resistance during exercise, which was observed in the FH- group (∆ = -0.4 ± 8.6 units versus -7.2 ± 6.3 units, p = 0.03). CONCLUSION:: Normotensive individuals with a family history of hypertension present an impaired peripheral vascular resistance response to exercise. FUNDAMENTO:: O histórico familiar para hipertensão arterial está relacionado a anormalidades vasculares e autonômicas, bem como disfunções no comportamento neuro-hemodinâmico durante o exercício físico. OBJETIVO:: Testar a hipótese de que indivíduos normotensos com histórico familiar de hipertensão arterial apresentam resposta prejudicada da resistência vascular periférica durante o exercício físico. MÉTODOS:: Foram avaliados 37 normotensos de ambos os sexos, sedentários, eutróficos e não tabagistas, sendo 23 com histórico familiar positivo (HF+, 24 ± 3 anos) e 14 com histórico familiar negativo (HF-, 27 ± 5 anos) para hipertensão arterial. Foram identificados pressão arterial, frequência cardíaca (DIXTAL®), fluxo sanguíneo muscular do antebraço e resistência vascular periférica local (Hokanson®) por 3 minutos durante o repouso e, em seguida, 3 minutos durante exercício isométrico de preensão palmar a 30% da contração voluntária máxima (Jamar®). RESULTADOS:: Em repouso, os grupos HF+ e HF- apresentaram valores semelhantes de pressão arterial média (83 ± 7 mmHg versus 83 ± 5 mmHg, p = 0,96), frequência cardíaca (69 ± 8 bpm versus 66 ± 7 bpm, p = 0,18), fluxo sanguíneo muscular (3 ± 1 mL/min/199 mL versus 2,7 ± 1 mL/min/100 mL, p = 0,16) e resistência vascular periférica (30 ± 9 unidades versus 34 ± 9 unidades, p = 0,21), respectivamente. Durante o exercício, HF+ e HF- mostraram aumento significativo e semelhante da pressão arterial média (∆ = 15 ± 7 mmHg versus 14 ± 7 mmHg, p = 0,86), frequência cardíaca (∆ = 12 ± 8 bpm versus 13 ± 7 bpm, p = 0,86) e fluxo sanguíneo muscular (∆ = 0,8 ± 1,2 mL/min/100 mL versus 1,4 ± 1,1 mL/min/100 mL, p = 0,25), respectivamente. Entretanto, no grupo HF+ não houve redução significativa da resistência vascular periférica durante o exercício, fato que ocorreu no grupo HF- (∆ = -0,4 ± 8,6 unidades versus -7,2 ± 6,3 unidades, p = 0,03). CONCLUSÃO:: Indivíduos normotensos com histórico familiar de hipertensão arterial apresentam resposta prejudicada da resistência vascular periférica durante o exercício físico.

Birth Weight and Its Relationship with the Cardiac Autonomic Balance in Healthy Children.

Several studies indicate that the fetal environment plays a significant role in the development of cardiometabolic disease later in life. However, a few studies present conflicting data about the correlation between birth weight and the impairment of cardiac autonomic modulation. The purpose of the present study was to provide further knowledge to elucidate this contradictory relationship. One hundred children aged 5 and 14 years had anthropometric parameters, body composition and blood pressure levels determined. Heart rate variability (HRV) was evaluated by heart rate monitoring, including measurements of both the time and frequency domains. The results showed inverse correlation between the HRV parameters with BMI (RMSSD: P = 0.047; PNN50: P = 0.021; HF: P = 0.041), systolic (RMSSD: P = 0.023; PNN50: P = 0.032) and diastolic (PNN50: P = 0.030) blood pressure levels. On the other hand, there were consistent positive correlations between the HRV parameters and birth weight (RMSSD: P = 0.001; PNN50: P = 0.001; HF: P = 0.002). To determine the effect of birth weight on HRV parameters, we perform multivariate linear regression analysis adjusted for potentially confounding factors (prematurity, gender, age, BMI, physical activity index and SBP levels). These findings were preserved even after adjusting for these confounders. Our results suggested that impaired cardiac autonomic modulation characterized by a reduction in the parasympathetic activity occurs in children with low birth weight. One possible interpretation for these data is that a vagal withdrawal, rather than a sympathetic overactivity, could precede the development of hypertension and other cardiometabolic diseases in children with low birth weight. However, long-term studies should be performed to investigate this possibility.

Serum Endocan Levels Associated with Hypertension and Loss of Renal Function in Pediatric Patients after Two Years from Renal Transplant.

Endocan is an important biomarker of inflammation and endothelial dysfunction that increases in association with several chronic diseases. Few published data have described the role of endocan in pediatric renal transplant (RT) patients. We evaluated the endocan concentrations in 62 children who underwent renal transplantation and assessed their relationships with the patients' blood pressure and loss of renal function. The endocan levels were significantly elevated in the pediatric RT patients who had hypertension and a loss of renal function. We determined positive correlations between the endocan concentrations and the hemodynamic variables (systolic blood pressure: r = 0.416; P = 0.001; pulse pressure: r = 0.412; P = 0.003). The endocan levels were inversely correlated with the estimated glomerular filtration rate (r = -0.388; P = 0.003). An endocan cutoff concentration of 7.0 ng/mL identified pediatric RT patients who had hypertension and a loss of renal function with 100% sensitivity and 75% specificity. In conclusion, the endocan concentrations were significantly elevated in pediatric RT patients who had both hypertension and a loss of renal function. The correlations between the endocan levels and the hemodynamic variables and the markers of renal function strengthen the hypothesis that it is an important marker of cardiorenal risk.

[Cardiac autonomic modulation in healthy subjects with a family history of chronic kidney disease].

INTRODUCTION: The positive family history of chronic kidney disease (FH+) is a risk factor for the appearance and development of this disease. Thus, it is important to assess traits that may be related to familial predisposition to chronic kidney disease. OBJECTIVE: To evaluate the autonomic modulation by heart rate variability in individuals with FH+. METHODS: We studied 9 health subjects with FH+ and 22 health subjects with negative family history for chronic kidney disease (FH-) matched for age (27 ± 6 vs. 26 ± 4 anos; p = 0.39, respectively). Heart rate was measured continuously by the Polar S810i® for 10 minutes of rest in the supine position. The heart rate variability was evaluated by the time domain, mean of NN intervals (MNN), standard deviation of the NN intervals (SDNN), root mean squared differences of successive NN intervals (RMSSD) and percentage of NN intervals with a difference of duration greater than 50 ms (pNN50) and the fields of low frequency (LF), high frequency (HF) and ratio low/ high (LF/HF). Laboratory biochemical tests were performed after fasting for 12 hours. Results are expressed as mean ± standard deviation, adopting as significant p < 0.05. RESULTS: The groups FH+ and FH-were similar in serum creatinine (p = 0.98), estimated glomerular filtration rate (p = 0.49) and heart rate (p = 0.68). The groups FH+ and FH- showed no significant differences in relation to indices of heart rate variability MNN; SDNN; RMSSD; pNN50; Total power; LF; HF and LF/HF ration, respectively. CONCLUSION: These findings suggest that the cardiac autonomic modulation is preserved in health subjects with HF+.

Modulação autonômica cardíaca em indivíduos saudáveis com histórico familiar de doença renal crônica / Cardiac autonomic modulation in healthy subjects with a family history of chronic kidney disease

INTRODUÇÃO: O histórico familiar positivo para a doença renal crônica (HF+) é um fator de risco para o surgimento e desenvolvimento dessa doença. Desta forma, é importante avaliar traços que possam estar correlacionados à predisposição familiar para a doença renal crônica. OBJETIVO: Avaliar a modulação autonômica, pela variabilidade da frequência cardíaca, de indivíduos com HF+. MÉTODOS: Foram avaliados nove indivíduos saudáveis com HF+ e 22 indivíduos saudáveis com histórico familiar negativo para doença renal crônica (Grupo HF-), pareados por idade (27 ± 6 vs. 26 ± 4 anos; p = 0,39, respectivamente). A frequência cardíaca foi medida continuamente pelo cardiofrequencímetro Polar S810i® durante 10 minutos de repouso na posição supina. A Variabilidade da Frequência Cardíaca (VFC) foi avaliada pelos índices do domínio do tempo, média dos intervalos RR (MNN), desvio padrão dos intervalos RR (SDNN), raiz média quadrática das diferenças de intervalos RR sucessivos (RMSSD) e percentual de intervalos RR com diferença de duração maior que 50 ms (pNN50), e pelos domínios de baixa frequência (BF), alta frequência (AF) e razão baixa/alta (BF/AF). Os exames laboratoriais foram realizados após jejum de 12 horas. Os resultados são expressos como média ± desvio padrão, adotando como significativo p < 0,05. RESULTADOS: Os grupos HF+ e HFforam semelhantes em relação à estimativa da taxa de filtração glomerular (p = 0,49) e frequência cardíaca (p = 0,68). Os grupos HF+ e HF- não apresentaram diferenças significativas em relação aos índices da variabilidade da frequência cardíaca MNN; SDNN, RMSSD, pNN50, Potência total; BF; AF u.n e razão BF/AF. CONCLUSÃO: A modulação autonômica cardíaca está preservada em indivíduos saudáveis com HF+.

INTRODUCTION: The positive family history of chronic kidney disease (FH+) is a risk factor for the appearance and development of this disease. Thus, it is important to assess traits that may be related to familial predisposition to chronic kidney disease. OBJECTIVE: To evaluate the autonomic modulation by heart rate variability in individuals with FH+. METHODS: We studied 9 health subjects with FH+ and 22 health subjects with negative family history for chronic kidney disease (FH-) matched for age (27 ± 6 vs. 26 ± 4 anos; p = 0.39, respectively). Heart rate was measured continuously by the Polar S810i® for 10 minutes of rest in the supine position. The heart rate variability was evaluated by the time domain, mean of NN intervals (MNN), standard deviation of the NN intervals (SDNN), root mean squared differences of successive NN intervals (RMSSD) and percentage of NN intervals with a difference of duration greater than 50 ms (pNN50) and the fields of low frequency (LF), high frequency (HF) and ratio low/ high (LF/HF). Laboratory biochemical tests were performed after fasting for 12 hours. Results are expressed as mean ± standard deviation, adopting as significant p < 0.05. RESULTS: The groups FH+ and FH-were similar in serum creatinine (p = 0.98), estimated glomerular filtration rate (p = 0.49) and heart rate (p = 0.68). The groups FH+ and FH- showed no significant differences in relation to indices of heart rate variability MNN; SDNN; RMSSD; pNN50; Total power; LF; HF and LF/HF ration, respectively. CONCLUSION: These findings suggest that the cardiac autonomic modulation is preserved in health subjects with HF+.