Endothelial dysfunction in obese non-hypertensive children without evidence of sleep disordered breathing

Abstract

BackgroundEndothelial dysfunction is a complication of both obesity and obstructive sleep apnea syndrome (OSAS), the latter being highly prevalent among obese children. It is unknown whether obesity causes endothelial dysfunction in children in the absence of OSAS. This study examines endothelial function in obese and non-obese children without OSAS.MethodsPre-pubertal non-hypertensive children were recruited. Endothelial function was assessed in a morning fasted state, using a modified hyperemic test involving cuff-induced occlusion of the radial and ulnar arteries. The absence of OSAS was confirmed by overnight polysomnography. Anthropometry was also performed.Results55 obese children (mean age 8.6 ± 1.4 years, mean BMI z-score: 2.3 ± 0.3) were compared to 50 non-obese children (mean age 8.0 ± 1.6 years, mean BMI z-score 0.3 ± 0.9). Significant delays to peak capillary reperfusion after occlusion release occurred in obese compared to non-obese children (45.3 ± 21.9 sec vs. 31.5 ± 14.1 sec, p < 0.01), but no differences in the magnitude of hyperemia emerged. Time to peak reperfusion and percentage of body fat were positively correlated (r = 0.365, p < 0.01).ConclusionsOur findings confirm that endothelial dysfunction occurs early in life in obese children, even in the absence of OSAS. Thus, mechanisms underlying endothelial dysfunction in pediatric obesity are operational in the absence of sleep-disordered breathing.

Impact of Adenotonsillectomy on Insulin Resistance and Lipoprotein Profile in Nonobese and Obese Children

“…25 Sleep architecture, respiratory events, and arousals were scored using standard pediatric criteria. 26 Apneas were defined as $ 90% airflow decrement lasting at least two breaths, and hypopneas were defined as > 50% decrement in nasal airflow accompanied by a 3% desaturation and/or an EEG arousal.…”

Endothelial Dysfunction in Children Without Hypertension

“…11,12 We have recently shown that obesity in children is associated with an increased risk for the development of endothelial dysfunction prior to the onset of hypertension. 13 Indeed, using a modifi ed hyperemic test after cuffinduced occlusion of the radial and ulnar arteries, we demonstrated that signifi cant delays occur in the vascular reperfusion kinetics among children who were obese and nonhypertensive and who did not suffer from either diabetes or obstructive sleep apnea (OSA). 13 The exclusion of OSA 13 is particularly relevant, considering that obesity markedly increases the risk for sleep-disordered breathing.…”

“…13 Indeed, using a modifi ed hyperemic test after cuffinduced occlusion of the radial and ulnar arteries, we demonstrated that signifi cant delays occur in the vascular reperfusion kinetics among children who were obese and nonhypertensive and who did not suffer from either diabetes or obstructive sleep apnea (OSA). 13 The exclusion of OSA 13 is particularly relevant, considering that obesity markedly increases the risk for sleep-disordered breathing. [14][15][16] OSA is a highly prevalent condition in children, in which intermittent occlusion of the upper airway during sleep leads to recurrent oxyhemoglobin desaturations, elevated CO 2 levels, sleep fragmentation, and reduced sleep effi ciency.…”

“…13 Central, obstructive, and mixed apneic events were counted. Obstructive apnea was defi ned as the absence of airfl ow with continued chest wall and abdominal movement for a duration of Ն 2 breaths .…”

Endothelial Dysfunction in Children With Obstructive Sleep Apnea Is Associated With Epigenetic Changes in the eNOS Gene

“…5 Furthermore, the concurrent presence of obesity and OSA magnifi ed the severity of endothelial dysfunction, thereby reinforcing the assumption that both conditions will impose incremental, long-term cardiovascular risk. [6][7][8] However,…”