Effects of obstructive sleep apnoea on heart rhythm

Abstract

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.

Obstructive sleep apnea, CPAP treatment and bradyarrhythmias: close relationship or simple coincidence? A brief review based on case series

“…Probably structural and electrical remodelling of the cardiac walls due to excessive negative intrathoracic pressure and increased sympathetic activation triggered by apneic events may increase the susceptibility to arrhythmia in SAS patients. Observational studies reported a higher prevalence of bradyarr-hythmia in patients affected by sleep apnea syndrome; preliminary evidence supported the hypothesis that apneic events are associated with bradicardics events [2] .…”

“…Repetitive forced inspiration during OSA with the resulting negative pressure in the chest cavity causes increased transmural gradients across cardiac chambers interfering with autonomic and hemodynamic stability. Infact, these hemodynamic features provoke also left atrial wall strein, increased atrial size with stretch-mediated channels changes and left ventricular hypertrophy and remodeling [2,[6][7][8] .…”

“…During OSA there is an imbalance in gas exchange, thus O 2 level is decrease also to cellular level. Intermittent hypoxia due to repetitive nightly upper airways occlusion increases the oxidative stress [2,7,8] . By molecular point of view myocytes react to this stress condition and lower O 2 level with hypertrophy that creates the global effect of gradual deterioration of left ventricular filling leading to diastolic dysfunction [9] .…”

“…The oscillations between parasympathetic and sympathetic preponderance provoke on the one hand bradycardia and/or pauses (when vagal tone rules, the diving reflex) on the other hand shortening of atrial refractory period, increase in ventricular ectopy burden (when sympathetic nerve activity surges) [2,6] .…”

A 42-Year-Old Female with Well-Controlled Atrial Fibrillation and Mild Obstructive Sleep Apnea

“…3 The intermittent hypoxia, recurrent arousals, sympathetic activation, and intrathoracic pressure swings in patients with OSA are felt to increase their risk of AF. 4 It has been reported that between 21% and 49% of patients with AF have underlying OSA. 5,6 Another study found that patients with AF and severe OSA (AHI > 30 events/h) have a significantly higher chance of not responding to anti-arrhythmic drug therapy as compared to patients with AF and non-severe OSA (AHI ≥ 5 and ≤ 30).…”