Endothelial Dysfunction in Children With Obstructive Sleep Apnea Is Associated With Elevated Lipoprotein-Associated Phospholipase A2 Plasma Activity Levels.
Obstructive sleep apnea (OSA) is a highly prevalent condition, especially in obese children, and has been associated with increased risk for endothelial dysfunction and dislipidemia, which are precursors of atherosclerosis. Lipoprotein-associated phospholipase A2 (Lp-PLA2) is recognized as an independent risk factor for cardiovascular risk and atheromatous plaque activity. We hypothesized that Lp-PLA2 levels would be elevated in children with OSA, particularly among obese children who also manifest evidence of endothelial dysfunction.



One hundred sixty children (mean age 7.1±2.3 years), either nonobese with (n=40) and without OSA (n=40) or obese with (n=40) and without OSA (n=40) underwent overnight polysomnographic and postocclusive reperfusion evaluation and a fasting blood draw the morning after the sleep study. In addition to lipid profile, Lp-PLA2 plasma activity was assessed using a commercial kit. Obese children and OSA children had significantly elevated plasma Lp-PLA2 activity levels compared to controls. Furthermore, when both obesity and OSA were concurrently present or when endothelial function was present, Lp-PLA2 activity was higher. Treatment of OSA by adenotonsillectomy resulted in reductions of Lp-PLA2 activity (n=37;P<0.001).



Lp-PLA2 plasma activity is increased in pediatric OSA and obesity, particularly when endothelial dysfunction is present, and exhibits decreases on OSA treatment. The short-term and long-term significance of these findings in relation to cardiovascular risk remain undefined.
Section of Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Biological Sciences Division, The University of Chicago, IL lgozal@peds.bsd.uchicago.edu.
Leila
L
Kheirandish-Gozal
Section of Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Biological Sciences Division, The University of Chicago, IL.
Mona F
MF
Philby
Section of Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Biological Sciences Division, The University of Chicago, IL.
Zhuanghong
Z
Qiao
Section of Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Biological Sciences Division, The University of Chicago, IL.
Abdelnaby
A
Khalyfa
Section of Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Biological Sciences Division, The University of Chicago, IL.
David
D
Gozal
D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase / Q000097:blood*; D050197:Atherosclerosis / Q000201:enzymology* / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D015992:Body Mass Index; D002648:Child; D002675:Child, Preschool; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D007087:Illinois / Q000453:epidemiology; D008297:Male; D009765:Obesity / Q000150:complications / Q000201:enzymology / Q000503:physiopathology; D017286:Polysomnography; D015995:Prevalence; D018570:Risk Assessment / Q000379:methods*; D012307:Risk Factors; D020181:Sleep Apnea, Obstructive / Q000201:enzymology / Q000453:epidemiology / Q000503:physiopathology*; D014664:Vasodilation
D015415:Biomarkers; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; C526684:PLA2G7 protein, human
atherosclerosis; cholesterol; endothelial dysfunction; sleep apnea