Changes in the 2017 Pediatric Hypertension Clinical Guidelines.

The clinical practice guidelines on diagnosis and management of high blood pressure in children and adolescents have been periodically modified and updated since the original publication in 1977.1 Since the last pediatric blood pressure guideline was published in 2004, known as the Fourth Report,2 the literature on child BP and hypertension has expanded considerably. There has been a recognized need to update the Fourth Report for several years. However, the National Heart, Lung, and Blood Institute (NHLBI) who sponsored previous pediatric BP guidelines announced that NHLBI would no longer sponsor development of new clinical guidelines.3 Subsequently, in 2014 the American Academy of Pediatrics (AAP) agreed to sponsor development of a new pediatric BP clinical practice guideline (CPG). The new CPG for screening and management of high BP in children and adolescents was recently published in Pediatrics.4 This CPG was developed using the rigorous evidence-based approach recommended by the Institute of Medicine in 2011.5 This methodology was consistent with recent NHLBI recommendations on development of CPGs for cardiovascular disease.3 The new pediatric hypertension CPG contains several modifications from the previous guideline to guide clinicians in diagnosis and management of elevated BP and hypertension in children and adolescents. This summary describes those changes made since the 2004 Fourth Report

The Childhood Role in Development of Primary Hypertension.

Primary hypertension is not just an adult disorder. Current US population data on children and adolescents demonstrate a prevalence of elevated blood pressure (BP) and hypertension combined of over 10%. Recent reports from prospective cohort studies describe an association of high BP in childhood with hypertension in young adulthood. Excess adiposity is strongly associated with higher BP in childhood and increases risk for hypertension in adulthood. In addition to overweight/obesity, other exposures that raise the risk for high BP include low birthweight, dietary sodium, and stress. Using intermediate markers of cardiovascular injury, studies on hypertensive children report findings of cardiac hypertrophy, vascular stiffness, and early atherosclerotic changes. Impaired cognitive function has also been demonstrated in hypertensive children. Recent advances in clinical and translational research support the concept that the evolution of primary hypertension begins in childhood

Childhood obesity and blood pressure: back to the future?

The prevalence of childhood hypertension is increasing.1, 2 Studies that apply the 95th percentile definition and repeat measurements on three separate visits, report a pediatric hypertension prevalence of approximately 3.5%3, 4, and among obese children and adolescents the prevalence of both hypertension and prehypertension is even greater. The recently documented increase in hypertension among the young is due largely to the childhood obesity epidemic and possibly other secular changes in lifestyles. These publications and others confirm that hypertension is a prevalent child health condition, especially among overweight and obese children. A consistent positive association between body size and blood pressure level has been observed throughout childhood and adulthood. The report in this issue by Tu et al5 add additional insights on the impact of excess adiposity on blood pressure levels in childhood

Maternal and gestational influences on childhood blood pressure.

Exposures that contribute to a sub-optimal intrauterine environment can have an effect on the developing fetus. Impaired fetal growth that results in low birth weight is an established risk factor for cardio-metabolic disorders later in life. Recent epidemiologic and prospective cohort studies that include the maternal and gestational period have identified maternal and gestational conditions that confer increased risk for subsequent cardio-metabolic disorders in the absence of low birth weight. Maternal pre-conception health status, including chronic obesity and type 2 diabetes, increase risk for childhood obesity and obesity-related higher blood pressure (BP) in child offspring. Maternal gestational exposures, including gestational diabetes, gestational hypertension, and preeclampsia, are associated with higher BP in offspring. Other maternal exposures such as cigarette smoke and air pollution also increase risk for higher BP in child offspring. Recent, but limited, data indicate that assisted reproductive technologies can be associated with hypertension in childhood, despite otherwise normal gestation and healthy newborn. Gestational exposures associated with higher BP in childhood can be related to familial lifestyle factors, genetics, or epigenetic modification of fetal deoxyribonucleic acid (DNA). These factors, or combination of factors, as well as other adverse intrauterine conditions, could induce fetal programing leading to health consequences in later life. Current and developing research will provide additional insights on gestational exposures and fetal adjustments that increase risk for higher BP levels in childhood

The Enigma of Primary Hypertension in Childhood

Beginning in the 1970s, hypertension in children and adolescents has been defined as systolic and/or diastolic blood pressure (BP) that is equal to or greater than the 95th percentile of the normal BP distribution in healthy children. The definition of hypertension in adults is based on longitudinal data that links a BP level with an increased risk for subsequent adverse outcomes related to hypertension including heart failure, kidney failure, stroke, or death. The statistical definition of hypertension continues to be used in childhood because there have been no data that link a BP level in childhood with a heightened risk for adverse outcomes in adulthood. Findings from clinical and epidemiologic research have advanced understanding of high BP in childhood. While hypertension in some children can be secondary to underlying kidney, cardiovascular, or endocrine disorder, it is now known that primary (essential) hypertension can be present in childhood. The prevalence of hypertension in childhood is approximately 2-5% and another 13-18% of children and adolescents have elevated BP and are at heightened risk for developing hypertension. The leading cause of childhood hypertension is primary hypertension, especially in adolescents. For children and adolescents with secondary hypertension, the treatment can focus on managing the underlying cause of hypertension. Less is known about managing primary hypertension in childhood, including diagnosis, evaluation, treatment, and possibilities for prevention. The phenotype of primary hypertension in childhood and recent findings will be discussed

Adolescent and adult African Americans have similar metabolic dyslipidemia.

BACKGROUND: African Americans (AAs) have lower triglyceride (TG) and higher high-density lipoprotein cholesterol (HDL-C) than other ethnic groups; yet, they also have higher risk for developing diabetes mellitus despite the strong relationship of dyslipidemia with insulin resistance. No studies directly compare adolescents and adults with regard to relationships among dyslipidemia, high-sensitivity C-reactive protein (hs-CRP), and insulin resistance. Here, we compare AA adolescents to adults with regard to the relationships of adiposity-related lipid risk markers (TG-to-HDL ratio and non-HDL-C) with body mass index (BMI), waist circumference (WC), homeostasis model of insulin resistance (HOMA), and hs-CRP. METHODS: Two cohorts of healthy AA were recruited from the same urban community. Participants in each cohort were stratified by TG-to-HDL ratio (based on adult tertiles) and non-HDL-C levels. BMI, WC, HOMA, and hs-CRP were compared in adolescents and adults in the low-, middle-, and high-lipid strata. RESULTS: Prevalence of TG-to-HDL ratio greater than 2.028 (high group) was 16% (44 of 283) in adolescents and 33% (161 of 484) in adults; prevalence of non-HDL-C above 145 and 160, respectively, was 8% (22 of 283) in adolescents and 12% (60 of 484) in adults. Values of hs-CRP were lower, and HOMA values were higher in adolescents (both P \u3c .01). As both TG-to-HDL ratio and non-HDL-C strata increased, BMI, WC, HOMA, and hs-CRP increased in both adolescents and adults. In the high TG-to-HDL ratio and non-HDL-C groups, BMI and WC were similar in adolescents vs adults (BMI, 34 kg/m(2) vs 32 kg/m(2); WC, 101 cm vs 101 cm). After adjusting for non-HDL-C and other covariates, a 2-fold increase in TG-to-HDL ratio was associated with increases of 10.4% in hs-CRP (95% CI, 1.1%-20.5%) and 24.2% in HOMA (95% CI, 16.4%-32.6%). Non-HDL-C was not significant in models having TG-to-HDL ratio. CONCLUSION: The elevated TG-to-HDL ratio is associated with similar inflammation and metabolic risk relationships in adolescent and adult AAs

Relationship of adipokines with insulin sensitivity in African Americans.

INTRODUCTION: Cytokines produced by adipose tissue, including adiponectin, have been associated with metabolic abnormalities. The purpose of this study was to examine the relationship of insulin sensitivity measured by euglycemic hyperinsulinemic insulin clamp with plasma adiponectin and other adipokines in young adult African Americans. METHODS: Participants were healthy African Americans. Anthropometric measures, blood pressure, an oral glucose tolerance test and an euglycemic hyperinsulinemic insulin clamp were performed. Insulin sensitivity measurements were adjusted for percentage of fat mass. Plasma concentrations of adiponectin, plasminogen activator inhibitor-1 (PAI-1) and interleukin-6 (IL-6) were assayed on plasma from fasting blood samples. Pearson correlation coefficients and multiple regression models were fitted to assess the association between glucose sensitivity and cytokines. RESULTS: In univariate analysis, there were statistically significant correlations of plasma adiponectin level (r = 0.19, P = 0.004), PAI-1 (r = -0.19, P = 0.020) and IL-6 (r = -0.24, P \u3c 0.001) with measures of insulin sensitivity after adjustment for both fat mass and insulin clamp concentration. In multivariate analysis, adiponectin [geometric mean ratios (GMR) 1.15, P = 0.007], PAI-1 (GMR 0.998, P = 0.021) and body mass index (GMR 0.95, P \u3c 0.001) were each independently associated with insulin sensitivity. For IL-6, there was no significant association with insulin sensitivity independent of obesity. CONCLUSION: These data show a significant and independent positive correlation of adiponectin with insulin sensitivity. The relationship of IL-6 with insulin sensitivity seems to be dependent on adiposity

Associations of cardiac structure with obesity, blood pressure, inflammation, and insulin resistance in African-American adolescents.

To determine if obesity, blood pressure (BP), markers of inflammation, and insulin resistance are associated with cardiac structure in African-American adolescents, a cross-sectional study was performed on a cohort oversampled for high BP and obesity. Measurements included the following: anthropometrics, BP, homeostasis model assessment (HOMA) to assess insulin resistance, high-sensitivity C-reactive protein, and plasma adipokines (adiponectin, interleukin-6, plasminogen activator inhibitor-1). Echocardiogram measurements were left-ventricular mass index (LVMI) (g/m(2.7)), LV relative wall thickness (LVRWT), left-atrial diameter index [LADI (mm/m)], and LV diastolic time intervals. LADI (r (2) = 0.25) was associated with body mass index (BMI) systolic BP (SBP) and female sex. LVMI (r (2) = 0.35) variation was associated with BMI SBP, heart rate, age, and male sex. LVRWT (r (2) = 0.05) was associated with HOMA. Tissue diastolic intervals were not associated with any risk factor. Inflammatory markers and adipokines were associated with BMI but were not independently associated with any echocardiographic measures. In African-American adolescents, BMI and SBP, but not inflammatory markers or adipokines, are important correlates of LA size and LVM