Obstructive sleep apnea and endothelial function in school-aged nonobese children: effect of adenotonsillectomy.
BACKGROUND
Obstructive sleep apnea (OSA) in children is associated with cardiovascular morbidity such as systemic and pulmonary hypertension. However, it remains unclear whether endothelial dysfunction occurs in pediatric OSA and whether it is reversible on effective treatment of OSA.


RESULTS
Consecutive nonobese children (aged 6 to 11 years) who were diagnosed with OSA after overnight polysomnography and control children matched on the basis of age, gender, ethnicity, and body mass index underwent blood draw the next morning for soluble CD40 ligand, asymmetric dimethylarginine (ADMA), and nitrotyrosine levels, as well as 2 iterations of 60-second cuff-occlusion tests for assessment of endothelial function. These tests were repeated 4 to 6 months after adenotonsillectomy. OSA children showed blunted reperfusion kinetics after release of occlusion, which completely normalized in 20 of 26 patients after adenotonsillectomy. All 6 children in whom no improvements occurred had a strong family history of cardiovascular disease (versus 2 of the remaining 20 patients; P<0.04). Plasma nitrotyrosine and ADMA levels were similar in OSA and control children; however, soluble CD40 ligand levels were higher in OSA children and were reduced after treatment, particularly in those with normalized hyperemic responses.


CONCLUSIONS
Postocclusive hyperemia is consistently blunted in children with OSA, and such altered endothelial function is reversible 4 to 6 months after treatment, particularly if a family history of cardiovascular disease is not present. Although no evidence for either nitric oxide-dependent oxidative/nitrosative stress or for the increased presence of the circulating nitric oxide synthase inhibitor ADMA was found in children with OSA, soluble CD40 ligand levels were increased in OSA and reflected the changes in endothelial function after treatment.
Gozal
David
D
Kosair Children's Hospital Research Institute, University of Louisville School of Medicine, 570 S Preston St, Suite 204, Louisville, KY 40202, USA. david.gozal@louisville.edu
Kheirandish-Gozal
Leila
L
Serpero
Laura D
LD
Sans Capdevila
Oscar
O
Dayyat
Ehab
E
D000233:Adenoidectomy; D001120:Arginine / Q000031:analogs & derivatives / Q000097:blood; D001835:Body Weight; D023201:CD40 Ligand / Q000097:blood; D002648:Child; D004730:Endothelium, Vascular / Q000502:physiology*; D005260:Female; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology; D000860:Hypoxia / Q000276:immunology / Q000503:physiopathology / Q000601:surgery; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D017286:Polysomnography; D020181:Sleep Apnea, Obstructive / Q000276:immunology / Q000503:physiopathology* / Q000601:surgery*; D014068:Tonsillectomy; D014443:Tyrosine / Q000031:analogs & derivatives / Q000097:blood; D014657:Vasculitis / Q000503:physiopathology*
D023201:CD40 Ligand; D009569:Nitric Oxide; C002744:3-nitrotyrosine; D014443:Tyrosine; C018524:N,N-dimethylarginine; D001120:Arginine