Obesity and Central Blood Pressure in Children and Adolescents

Obese children more often than not, become obese adolescents and eventually obese adults. Obesity in adulthood is associated with a raft of related disorders and of particular relevance to this commentary, an increased risk of developing cardiovascular disease, and longitudinal studies suggest that childhood obesity increases the risk for adult morbidity and mortality irrespective of the current adult body mass index (BMI).1 Concomitant with the ever-increasing rate of obesity in children and adolescents, is the awareness that the obesity-related disorders historically only identified in adults, are now increasingly common in obese children and in particular, obese adolescents. Moreover, severe obesity defined as 120% of the 95th BMI percentile,2 the fastest growing subcategory of obesity in children and adolescents, is associated with a more severe cardiometabolic risk factor profile that includes dyslipidemia, hypertension, type 2 diabetes, vascular dysfunction, and increased left ventricular mass.3 Early childhood marks the beginning of natural age-related changes to arterial wall properties, and obese children have a higher risk of blood vessel damage and cardiovascular disease compared with their normal weight peers.4 Obese children exhibit increased intima-media thickness and stiffness of the carotid artery,5,6 and increased pulse wave velocity.7 Evidence suggests that central blood pressure (BP) is more strongly related to surrogate measures of cardiovascular risk including carotid intima-media thickness and left ventricular mass than brachial BP in adults.8–10 However, the effect of severe obesity during adolescence on central BP remained to be elucidated, and this was the question posed by Harbin et al.11 in their research published in this issue of the Journal. The role of severe obesity and sex on central BP was determined in 348 children and adolescents aged 8–18 years, across a range of BMI values. Obesity status was determined by BMI percentiles and stratified into three categories: normal weight (≥5th to <85th BMI percentile), overweight/obese (≥85th to <95th BMI percentiles, ≥100% to <120% of the 95th BMI percentiles), and severe obesity (≥120% of the 95th BMI percentile, or absolute BMI >35 kg/m2). Anthropometric measurements were recorded, body composition was measured using dual X-ray absorptiometry, and pubertal maturity determined using the Tanner stage. Seated brachial systolic (SBP) and diastolic blood pressure (DBP) were measured via an automated sphygmomanometer, and following 15 minutes of supine rest, radial and carotid arterial waveforms were recorded via applanation tonometry using SphygmoCor MM3 software (AtCor Medical, Sydney, Australia). No significant sex differences were identified for radial-aortic and carotid-aortic SBP and DBP. The authors attribute this contrast with previously published data demonstrating that males had higher brachial SBP and central aortic pressure compared with females, to different methodology and a younger cohort. Youth with severe obesity had significantly higher radial-aortic and carotid-aortic SBP compared with overweight/obese and normal weight youth, which adds to previous findings of elevated brachial BP in obese adults, adolescents, and children.12–14 Furthermore, this study extends similar findings of elevated central BP in obese adults to a pediatric population with severe obesity.12 Interestingly BMI, which does not distinguish between fat and lean mass, nor total-body percent fat mass and visceral adipose tissue, was a significant predictor of radial-aortic and carotid-aortic SBP and DBP. Central adiposity has long been linked to hypertension in adults, with the finding that cardiovascular and metabolic complications of obesity were more common in patients with the upper body obesity phenotype.15 Harbin et al. posit that their findings may be a consequence of the relatively short period of exposure to excess adiposity, the ability to physiologically compensate for increased adiposity, and/or may result from the effect of height on BP. In adults, arterial tonometry has been shown to provide a simple and noninvasive estimation of central aortic BP from the radial and carotid artery pulse waveform.16–18 However, there is scant data from children and adolescents. The SphygmoCor system utilizes a mathematical method which identifies the upper limb arterial system as a relationship between input (aortic pressure wave) and output (peripheral pressure wave) signals of the system in the frequency domain. A generalized aortic-radial pressure transfer function based on invasively acquired data from an adult population calculates a central aortic pressure waveform that is used to determine estimates of central BP. SphygmoCor has been extensively validated in adults with studies identifying acceptable estimation accuracy for central systolic BP and central pulse pressure.19 However, children are not just small adults and considering the differences not only in size, but also in vascular tree morphology, heart rate and mean BP, it could be postulated that a more accurate estimation of central BP could be made from a generalized transfer function derived from a pediatric populations rather than that derived from an adult population. Indeed, this has been shown to be the case in a study of 8- and 14-year-olds, whereby age-specific transfer functions more accurately predicted central systolic pressure measured at the carotid artery in children than did an existing adult transfer function.20 Central systolic BP was underestimated in both age groups, using the adult transfer function. In 8-year-old children the adult transfer function underestimated central BP by 3.7 (2.2) mm Hg (mean (standard deviation)) and by 6.8 (6.0) mm Hg in 14-year-olds. However, in the context of the Harbin et al.11 study, if the central BP was derived from a pediatric transfer function instead of the adult transfer function utilized by SphygmoCor, would this represent a clinically relevant difference? In a clinical setting, for healthy children who do not exhibit elevated BP, whether their central BP is slightly underestimated will probably not matter. However, for severely obese children and adolescents who exhibit markedly elevated BP even at this early age, underestimation of central BP may mask the impact of elevated central BP on cardiac and blood vessel morphology. However, this is a moot point as currently there is not a well-validated normal reference range for central BP in children and adolescents, which brings the clinical utility of measuring central BP in this population into doubt. Nonetheless, as evidence suggests that central BP reflects the hemodynamic load on target organs more accurately than brachial BP and is more strongly associated with preclinical organ damage, focused research investigating the risk for cardiovascular disease in relation to elevated central BP in discrete populations, such as the obese children and adolescents in the Harbin et al. study, is instrumental in further elucidating the prognostic value of central BP with regard to mitigating disease progression. Dr Walter has no conflict of interest to disclose.