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Assessing Endothelial Vasodilator Function with the Endo-PAT 2000
Published on: October 15, 2010
Endothelial dysfunction in children without hypertension: potential contributions of obesity and obstructive sleep
Rakesh Bhattacharjee1, Jinkwan Kim2, Wadha H Alotaibi3
1Division of Pediatric Pulmonary Medicine, Department of Pediatrics, Pritzker School of Medicine, Comer Children's Hospital, The University of Chicago, Chicago, IL; Division of Pediatric Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Comer Children's Hospital, The University of Chicago, Chicago, IL; Division of Pediatric Sleep Medicine, University of Louisville School of Medicine, Louisville, KY.
Insights
Obesity and obstructive sleep apnea (OSA) in children independently increase endothelial dysfunction risk. Their combined presence significantly elevates this risk, with myeloid-related protein 8/14 (MRP8/14) potentially indicating inflammation.
Area of Science:
- Pediatric Cardiology
- Sleep Medicine
- Vascular Biology
Background:
- Endothelial dysfunction is linked to childhood obesity and obstructive sleep apnea (OSA).
- The interaction between OSA and obesity in pediatric endothelial dysfunction is not well understood.
Purpose of the Study:
- To investigate the combined effects of obesity and OSA on endothelial function in children.
- To explore the association between myeloid-related protein 8/14 (MRP8/14) and endothelial dysfunction in this population.
Main Methods:
- Recruited prepubertal, nonhypertensive children.
- Assessed endothelial function via modified hyperemic test and measured serum MRP8/14 levels.
- Diagnosed OSA using overnight polysomnography and categorized children as obese (OB) or nonobese (NOB).
Main Results:
- Children with both OSA and obesity showed the highest prevalence of endothelial dysfunction (62.5%).
- Endothelial dysfunction was also observed in obese children without OSA (38.7%) and nonobese children with OSA (20.0%).
- No endothelial dysfunction was found in nonobese children without OSA (0.0%).
- Endothelial dysfunction severity correlated with elevated MRP8/14 levels (r = 0.343, P < .001).
Conclusions:
- Obesity and OSA are independent risk factors for endothelial dysfunction in children.
- The concurrent presence of obesity and OSA significantly amplifies the risk of endothelial dysfunction.
- MRP8/14 may serve as a biomarker for inflammation-related endothelial dysfunction in children.
Background:
Endothelial dysfunction can develop in the context of both obesity and obstructive sleep apnea (OSA) in children. However, the potential interactions between OSA and obesity have not been defined.
Methods:
Children who were prepubertal and nonhypertensive 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, and blood was drawn for assessment of myeloid-related protein 8/14 (MRP8/14) levels using a commercial enzyme-linked immunosorbent assay. Overnight polysomnography defined the presence of OSA or absence of OSA (NOSA) in subjects investigated for sleep-disordered breathing. Anthropometric measurements were performed to assign subjects to obese (OB) and nonobese (NOB) categories.
Results:
Fifty-four children with OSA who were obese and nonobese (mean age, 7.90 ± 0.26 years; mean BMI z-score, 1.70 ± 0.3; obstructive apnea-hypopnea index [OAHI], 7.36 ± 1.09) were compared with 54 children without OSA who were obese and nonobese (mean age, 8.26 ± 0.24 years; mean BMI z-score, 1.41 ± 0.18; OAHI, 0.86 ± 0.07). Of those subjects, 62.5% of the OB-OSA category, 38.7% of the OB-NOSA category, and 20.0% of the NOB-OSA category had evidence of endothelial dysfunction, compared with 0.0% of the NOB-NOSA category (P < .01). The degree of endothelial dysfunction in all groups was associated with circulating MRP8/14 levels (r = 0.343, P < .001).
Conclusions:
Both obesity and OSA can independently increase the risk for endothelial dysfunction, and the concurrent presence of both markedly increases such risk. Although the mechanisms underlying endothelial dysfunction remain unclear, a potential role for MRP8/14 as an inflammatory biomarker of endothelial dysfunction is suggested.
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