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Endothelial Dysfunction in Children With Obstructive Sleep Apnea Is Associated With Elevated Lipoprotein-Associated
Leila Kheirandish-Gozal1, Mona F Philby2, Zhuanghong Qiao2
1Section of Sleep Medicine, Department of Pediatrics, Pritzker School of Medicine, Biological Sciences Division, The University of Chicago, IL lgozal@peds.bsd.uchicago.edu.
Insights
Lipoprotein-associated phospholipase A2 (Lp-PLA2) levels are elevated in children with obstructive sleep apnea (OSA) and obesity, indicating increased cardiovascular risk. Treatment for OSA reduced these levels.
Area of Science:
- Pediatric Cardiology
- Sleep Medicine
- Biomarkers
Background:
- Obstructive sleep apnea (OSA) is common in obese children, increasing atherosclerosis risk.
- Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a cardiovascular risk marker.
- Endothelial dysfunction and dyslipidemia are precursors to atherosclerosis.
Purpose of the Study:
- To investigate Lp-PLA2 levels in children with OSA, particularly obese children with endothelial dysfunction.
- To assess the impact of obesity and OSA on Lp-PLA2 activity.
- To evaluate Lp-PLA2 changes after OSA treatment.
Main Methods:
- 160 children (nonobese/obese, with/without OSA) underwent polysomnography and blood tests.
- Lp-PLA2 plasma activity and lipid profiles were measured.
- Endothelial function was assessed via postocclusive reperfusion.
Main Results:
- Elevated Lp-PLA2 activity was observed in obese and OSA children compared to controls.
- Concurrent obesity and OSA, or presence of endothelial dysfunction, further increased Lp-PLA2.
- Adenotonsillectomy for OSA led to significant Lp-PLA2 reduction.
Conclusions:
- Pediatric OSA and obesity increase Lp-PLA2 activity, especially with endothelial dysfunction.
- Lp-PLA2 levels decrease after OSA treatment.
- The long-term cardiovascular implications require further study.
Background:
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.
Methods And Results:
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).
Conclusions:
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.
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