Abstract
Obstructive sleep apnoea (OSA) is a major health concern worldwide and adversely affects multiple organs and systems. OSA is associated with obesity in >60% of cases and is independently linked with the development of numerous comorbidities including hypertension, arrhythmia, stroke, coronary heart disease and metabolic dysfunction. The complex interaction between these conditions has a significant impact on patient care and mortality. The pathophysiology of cardiometabolic complications in OSA is still incompletely understood; however, the particular form of intermittent hypoxia (IH) observed in OSA, with repetitive short cycles of desaturation and re-oxygenation, probably plays a pivotal role. There is fast growing evidence that IH mediates some of its detrimental effects through adipose tissue inflammation and dysfunction. This article aims to summarise the effects of IH on adipose tissue in experimental models in a comprehensive way. Data from well-designed controlled trials are also reported with the final goal of proposing new avenues for improving phenotyping and personalised care in OSA.
Abstract
Fast growing evidence strongly suggests that cardiovascular and metabolic alterations induced by intermittent hypoxia in OSA are mediated through adipose tissue inflammation and dysfunction. bit.ly/2W929Pe
Footnotes
Number 3 in the Series “Sleep Disordered Breathing” Edited by Renata Riha and Maria Bonsignore
Provenance: Submitted article, peer reviewed.
Previous articles in this series: No. 1: Masa JF, Pepin J-L, Borel J-C, et al. Obesity hypoventilation syndrome. Eur Respir Rev 2019; 28: 180097. No. 2: Bruyneel M. Telemedicine in the diagnosis and treatment of sleep apnoea. Eur Respir Rev 2019; 28: 180093.
Conflict of interest: S. Ryan has nothing to disclose.
Conflict of interest: C. Arnaud has nothing to disclose.
Conflict of interest: S.F. Fitzpatrick has nothing to disclose.
Conflict of interest: J. Gaucher has nothing to disclose.
Conflict of interest: R. Tamisier has nothing to disclose.
Conflict of interest: J-L. Pépin reports grants and research funds from Air Liquide Foundation, grants and personal fees from Agiradom, AstraZeneca, Philips and Resmed, grants from Fisher and Paykel and Mutualia, grants from Vitalaire, and personal fees from Boehringer Ingelheim, Jazz Pharmaceuticals, Night Balance and Sefam, outside the submitted work.
Support statement: Funding was received from the Agence Nationale de la Recherche (ANR-12-TECS-0010 and ANR-15-IDEX-02) and the Agir pour les Maladies Chroniques. Funding information for this article has been deposited with the Crossref Funder Registry.
- Received January 18, 2019.
- Accepted May 9, 2019.
- Copyright ©ERS 2019.
This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0.