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Symptomatic obstructive sleep apnoea (OSA) has been proven to be a risk factor for hypertension and vascular dysfunction, and has been proposed to be causally related with cardiac arrhythmias and sudden cardiac death. Searches of bibliographical databases revealed that several mechanisms seem to underpin the association between OSA and cardiac arrhythmias: intermittent hypoxia associated with autonomic nervous system activation and increased oxidative stress, which may lead to cardiac cellular damage and alteration in myocardial excitability; recurrent arousals, resulting in sympathetic activation and coronary vasoconstriction; and increased negative intrathoracic pressure which may mechanically stretch the myocardial walls and, thus, promote acute changes in myocardial excitability as well as structural remodelling of the myocardium. Findings from cross-sectional studies suggest a high prevalence of cardiac arrhythmias in patients with OSA and a high prevalence of OSA in those with cardiac arrhythmias. Preliminary evidence from uncontrolled interventional studies suggests that treatment of OSA may prevent cardiac arrhythmias. In conclusion, there is preliminary evidence that OSA is associated with the development of cardiac arrhythmias. Data from randomised controlled studies are needed to definitively clarify the role of OSA in arrhythmogenesis.

Original publication

DOI

10.1183/09031936.00128412

Type

Journal article

Journal

Eur Respir J

Publication Date

06/2013

Volume

41

Pages

1439 - 1451

Keywords

Atrial fibrillation, autonomic nervous system, cardiac arrhythmias, hypoxaemia, sleep disordered breathing, sudden cardiac death, Arrhythmias, Cardiac, Cross-Sectional Studies, Death, Sudden, Cardiac, Heart, Humans, Hypertension, Hypoxia, Myocardium, Observational Studies as Topic, Oxidative Stress, Prevalence, Risk Factors, Sleep Apnea, Obstructive