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Archives of cardiovascular diseases
Sous presse. Epreuves corrigées par l'auteur. Disponible en ligne depuis le vendredi 27 mars 2020
Doi : 10.1016/j.acvd.2020.01.003
Received : 22 July 2019 ;  accepted : 15 January 2020
Obstructive sleep apnoea and cardiovascular consequences: Pathophysiological mechanisms
Syndrome d’apnées obstructives du sommeil et conséquences cardiovasculaire: mécanismes physiopathologiques

Claire Arnaud a, b, Thomas Bochaton c, Jean-Louis Pépin a, b, Elise Belaidi a, b,
a Laboratoire HP2, université Grenoble-Alpes, Grenoble, France 
b INSERM U1042, Grenoble, France 
c Urgences et soins critiques cardiologiques, hôpital cardiologique, hospices civils de Lyon, Bron, France 

Corresponding author at: Université Grenoble Alpes, CHU Grenoble Alpes, HP2, Inserm 38000 Grenoble, France.Université Grenoble Alpes, CHU Grenoble Alpes, HP2, Inserm Grenoble38000France
Graphical abstract

Central illustration: Mechanisms involved in deleterious consequences of obstructive sleep apnoea (OSA). Intermittent hypoxia (IH) leads to sympathetic nervous system overactivity, inflammation, oxidative stress and endoplasmic reticulum stress. Hypoxia-inducible factor-1 (HIF-1) seems to play a major role in OSA and IH consequences. Mitochondrial integrity could also be an interesting target to explain OSA-associated pathologies. Adapted from [61].

The full text of this article is available in PDF format.

Obstructive sleep apnoea syndrome is a growing health concern, affecting nearly one billion people worldwide; it is an independent cardiovascular risk factor, associated with incident obesity, insulin resistance, hypertension, arrhythmias, stroke, coronary artery disease and heart failure. Obstructive sleep apnoea-related cardiovascular and metabolic co-morbidities are a major concern for prognosis and the complexity of obstructive sleep apnoea integrated care. Continuous positive airway pressure, the first-line therapy for the treatment of obstructive sleep apnoea, is highly effective at improving symptoms and quality of life, but has limited effect on co-morbidities. Deciphering the molecular pathways involved in obstructive sleep apnoea metabolic and cardiovascular consequences is a priority to make new pharmacological targets available, in combination with or as an alternative to continuous positive airway pressure. Intermittent hypoxia, a landmark feature of obstructive sleep apnoea, is the key intermediary mechanism underlying metabolic and cardiovascular complications. Experimental settings allowing intermittent hypoxia exposure in cells, rodents and healthy humans have been established to dissect the molecular mechanisms of obstructive sleep apnoea-related co-morbidities. The main objective of this review is to recapitulate the molecular pathways, cells and tissue interactions contributing to the cardiometabolic consequences of intermittent hypoxia. Sympathetic activation, low-grade inflammation, oxidative stress and endoplasmic reticulum stress are triggered by intermittent hypoxia and play a role in cardiometabolic dysfunction. The key role of hypoxia-inducible factor-1 transcription factor will be detailed, as well as the underestimated and less described importance of mitochondrial functional changes in the intermittent hypoxia setting.

The full text of this article is available in PDF format.

Le syndrome d’apnées obstructives du sommeil (SAOS) affecte un milliard de personnes dans le monde. Le SAOS est un facteur de risque indépendant de la survenue d’évènements cardiovasculaires tels que l’hypertension, les troubles du rythme et les pathologies coronariennes. Le SAOS est aussi associé à des troubles du métabolisme tels que l’obésité et l’insulino-résistance. Le traitement de référence du SAOS, la pression positive continue (PPC) est un traitement qui améliore la qualité de vie des patients mais qui a un effet limité sur les comorbidités associées au SAOS. Ainsi, la compréhension des mécanismes à l’origine des conséquences cardiovasculaires et métaboliques du SAOS est un enjeu majeur et ce, afin de proposer de nouvelles cibles thérapeutiques complémentaires ou alternatives à la PPC. Les expériences pré-cliniques ont pour objectifs d’appliquer l’hypoxie intermittente (HI) chez le sujet sain, le rongeur ou encore la cellule afin de décortiquer les mécanismes sous-jacents. À ce jour, les mécanismes induits par l’HI et reconnus comme étant contributeurs des pathologies cardiométaboliques associées au SAOS sont : l’hyper-activation sympathique, l’inflammation de bas grade, le stress oxydant ou encore le stress du réticulum endoplasmique. Dans cette revue, en interaction avec les mécanismes suscités, le rôle central du facteur de transcription induit par l’hypoxie, l’hypoxia inducible factor-1 sera abordé. Par ailleurs, l’altération potentielle structurale et/ou fonctionnelle mitochondriale sera évoquée en tant que nouvelle perspective d’exploration.

The full text of this article is available in PDF format.

Keywords : Obstructive sleep apnoea, Intermittent hypoxia, Cardiovascular consequences, Hypoxia-inducible factor-1

Abbreviations : AHI, CPAP, ER, HIF-1, IH, OSA

Mots clés : Syndrome d’apnées obstructives du sommeil, Hypoxie intermittente, Conséquences cardiovasculaires, Hypoxia-inducible factor-1

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