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ORIGINAL ARTICLE

Arterial alterations in severely obese children with obstructive sleep apnoea

, , , , &
Pages 230-236 | Received 19 Nov 2008, Accepted 10 Sep 2009, Published online: 09 Mar 2010
 

Abstract

Background. Obstructive sleep apnoea (OSA) in obese adults is associated with cardiovascular disease independently of obesity. Vascular alterations exist in children with obesity and may constitute the first stage in the development of adulthood cardiovascular disease. Objective. To investigate the relationship between OSA and early arterial alterations in obese children. Design. Cross-sectional study of a prospective cohort. Patients. A total of 51 children with severe obesity managed at a teaching hospital outpatient clinic. Measurements. Polysomnography was performed. We measured the intima-media thickness and incremental elastic modulus (Einc) to assess the mechanical characteristics of the common carotid artery. Arterial endothelial function was evaluated by measuring flow-mediated dilation and glyceryl trinitrate-mediated dilation (GTNMD) of the brachial artery. Results. A total of 24 (47%) children had a desaturation index (DI) >10/h and 7 (14%) had a respiratory event index >10/h. DI >10/h was associated with significantly higher values of Einc (4.0 ± 0.5 vs. 2.4 ± 0.4 mm Hg−1·103, p=0.003) and GTNMD (18.0±1.1 vs. 14.1 ± 1.0 %, p=0.02) after adjustment for age, sex, body mass index, fasting insulin, and leptin. In the univariate analysis, GTNMD correlated positively with DI (r=0.14, p=0.02) after adjustment for age, sex, fasting insulin and leptin. By multivariate analysis with BMI as an additional independent variable, both GTNMD and Einc correlated significantly with DI (β=0.4, p=0.02 and β=0.27, p=0.04, respectively). Conclusions. OSA in children is associated with arterial alterations independently from obesity. The increased vasodilation in response to glyceryl trinitrate reflects pre-existing vasoconstriction probably induced by intermittent hypoxia. OSA should be detected early in children with severe obesity.

Acknowledgements

We thank Yves Lebouc and his staff (Endocrinology Laboratory, Armand-Trousseau Teaching Hospital, Paris, France) for performing the plasma glucose, insulin, and leptin assays.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

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