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Observational Study
. 2015 Jul;39(7):1086-93.
doi: 10.1038/ijo.2015.67. Epub 2015 May 18.

Interrelationships between obesity, obstructive sleep apnea syndrome and cardiovascular risk in obese adolescents

D Koren  1 , J A Chirinos  2 , L E L Katz  3 , E R Mohler  4 , P R Gallagher  5 , G F Mitchell  6 , C L Marcus  7
Affiliations
Observational Study

Interrelationships between obesity, obstructive sleep apnea syndrome and cardiovascular risk in obese adolescents

D Koren et al. Int J Obes (Lond). 2015 Jul.

Abstract

Background/objectives: Obstructive sleep apnea syndrome (OSAS) may be a cardiovascular disease (CVD) risk factor independently of obesity in adults. Pediatric studies have associated OSAS with endothelial dysfunction, but few studies have examined relationships between OSAS and macrovascular sequelae. Our objective was to examine OSAS's independent contribution to macrovascular CVD risk measures in obese adolescents.

Subjects/methods: This cross-sectional observational study was conducted at Children's Hospital of Philadelphia Clinical Research and Academic Sleep Centers, and University of Pennsylvania Vascular Research Unit. Thirty-one obese non-diabetic adolescents underwent anthropometric measurements, overnight polysomnography, fasting laboratory draw and cardiovascular imaging. Cardiovascular outcome measures included maximal carotid intima-media thickness (cIMTmax), a measure of carotid structural changes, and carotid-femoral pulse wave velocity (CFPWV), an aortic stiffness measure whose relationship vis-à-vis OSAS in children has not been previously examined. Carotid diameter and augmentation index (AIx, measuring central pressure augmentation from wave reflections) were assessed. Potential confounding variables examined included blood pressure, lipoproteins, high-sensitivity C-reactive protein, insulin and glucose.

Results: The apnea hypopnea index, a primary OSAS measure, was not associated with cIMTmax, carotid diameter, CFPWV or AIx. body mass index (BMI) associated positively with cIMTmax (r=0.52, P=0.006) and CFPWV (r=0.45, P=0.01). Mean asleep end-tidal CO2 was negatively associated with carotid diameter (r=-0.63, P<0.0005). Insulin levels were negatively associated with AIx (r=-0.53, P=0.02).

Conclusions: OSAS did not predict carotid structural changes or arterial stiffness independently of BMI in obese adolescents. Higher insulin levels associated with lower central pressure wave augmentation. Finally, long-term hypercapnia may predispose to carotid narrowing.

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Conflict of interest statement

Conflict of Interest:

L.E. Levitt Katz provides consultation services to Janssen pharmaceuticals and to Takeda Pharmaceuticals. C.L. Marcus has research support from Ventus and Philips Respironics in the form of loaned equipment only for investigator-initiated studies, not relevant to the current manuscript. Dr. Mitchell is owner of Cardiovascular Engineering, Inc., a company that develops and manufactures devices to measure vascular stiffness, serves as a consultant to and receives honoraria from Novartis, Merck and Enopace, and is funded by research grants HL094898, DK082447, HL107385 and HL104184 from the National Institutes of Health. The remaining authors reported no relevant conflicts of interest.

Figures

Figure 1
Figure 1. Relationship between carotid artery diameter and end-tidal CO2
Association between common carotid artery diameter and mean end-tidal carbon dioxide.
Figure 2
Figure 2. Relationship between obesity and pulse wave velocity
Association between degree of obesity and carotid-femoral pulse wave velocity. BMI=body mass index.
See this image and copyright information in PMC

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