Atrial Fibrillation in Acute Obstructive Sleep Apnea: Autonomic Nervous Mechanism and Modulation

Abstract

BackgroundThe mechanisms of atrial fibrillation (AF) induced by obstructive sleep apnea (OSA) are not completely understood. This study investigated the roles of the intrinsic and extrinsic cardiac autonomic nervous system in OSA‐induced AF and provided noninvasive autonomic nervous modulation for the suppression of OSA‐induced AF by using low‐level transcutaneous electrical stimulation (LL‐TS) of the auricular branch of the vagus nerve at the tragus.Methods and ResultsEighteen dogs received tracheostomy under general anesthesia and were randomly divided into 3 groups: the OSA group (OSA was simulated via clamping of the endotracheal tube at end expiration for 1.5 minutes every 10 minutes, n=6), the LL‐TS + OSA group (simulated OSA plus LL‐TS, at 80% of the slowing sinus rate, n=6), and the control group (sham surgery without stimulation, n=6). The effective refractory period was significantly shortened after 1 hour of simulated OSA, and the window of vulnerability and plasma norepinephrine levels were both markedly increased in the OSA group. OSA dramatically increased the neural function and activity of the intrinsic and extrinsic cardiac autonomic nervous system, including the superior left ganglionated plexus, the left stellate ganglion, and the left renal sympathetic nerve. OSA also significantly upregulated the expression levels of c‐fos and nerve growth factor in the superior left ganglionated plexus and the left stellate ganglion. However, LL‐TS markedly improved these parameters.ConclusionsThese findings suggest that the intrinsic and extrinsic cardiac autonomic nervous system plays crucial roles in the acute stage of OSA‐induced AF. Noninvasive LL‐TS suppressed shortening of atrial refractoriness and autonomic remodeling, which prevented OSA‐induced AF.

Serum N-Acetylneuraminic Acid Is Associated with Atrial Fibrillation and Left Atrial Enlargement

“…Many studies have been performed in regard to the mechanism and therapeutic strategies of AF. Multiple factors, including advancing age, male sex, obesity, heart failure, obstructive sleep apnea, anxiety, systemic arterial hypertension, and biomarkers such as N-terminal pro-Btype natriuretic peptide (NT-proBNP), have been identified as factors correlated with AF development [12][13][14][15]. Our study showed that the level of plasma Neu5Ac was significantly higher in the AF group than in the control group, indicating that Neu5Ac was significantly correlated with AF.…”

Connexin 43 reduces susceptibility to sympathetic atrial fibrillation

“…At present, the exact mechanism underlying the initiation, maintenance and recurrence of atrial fibrillation is unclear. Although previous studies have demonstrated that remodeling and regeneration of the sympathetic nervous system are associated with the occurrence and maintenance of atrial fibrillation (23)(24)(25), there is a lack of detailed information. In order to better understand the underlying mechanism.…”

Low-Level Vagus Nerve Stimulation Reverses Obstructive Sleep Apnea-Related Atrial Fibrillation by Ameliorating Sympathetic Hyperactivity and Atrial Myocyte Injury

“…Previous studies have shown that low-level vago-sympathetic trunk stimulation (LLVS) at voltages that do not slow the sinus rate or AV conduction, could decrease AF inducibility and AF duration, and prolonged ERP induced by acute OSA on a rabbit model ( Gao et al, 2015 ), but no changes have yet been manifested in the structural remodeling of the left atrium (LA). Yu et al (2017) demonstrated that noninvasive low-level transcutaneous electrical stimulation could prevent the incidence of AF in a 1-h OSA dog model. They also recorded neural activity from the superior left ganglionated plexus (SLGP), the left stellate ganglion (LSG), and the left renal sympathetic nerve (RSN), as well as changes in fast neuron markers in SLGP and LSG, but the nerve distribution in LA has not yet been investigated.…”