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

Figures

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  Figure 1. Study protocol (A) and changes in blood gases between the control group and the OSA group (n=6) (B). *P<0.05 vs the control group. BS indicates baseline; ERP, effective refractory period; LL‐TS, low‐level transcutaneous electrical stimulation; LSG, left stellate ganglion; OSA, obstructive sleep apnea; RSN, renal sympathetic nerve; ΣWOV, cumulative window of vulnerability; SLGP, superior left ganglionated plexus.

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  Figure 2. Changes in ERP and ΣWOV among the control, OSA, and LL‐TS + OSA groups (n=6). A, ERP at baseline. (B) ERP at 1 hour. (C) ΣWOV in the 3 groups. *P<0.05 vs the control group; # P<0.05 vs the OSA group. BS indicates baseline; ERP, effective refractory period; LA, left atrium; LAA, left atrial appendage; LIPV, left inferior pulmonary vein; LL‐TS, low‐level transcutaneous electrical stimulation; LSPV, left superior pulmonary vein; OSA, obstructive sleep apnea; RA, right atrium; RAA, right atrial appendage; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein; ΣWOV, cumulative window of vulnerability.

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  Figure 3. Changes in BP and norepinephrine plasma levels in the OSA (A), control (B), and LL‐TS + OSA (C) groups (n=6). *P<0.05 vs the control group; # P<0.05 vs the OSA group. BP indicates blood pressure; BS, baseline; LL‐TS, low‐level transcutaneous electrical stimulation; OSA, obstructive sleep apnea.

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  Figure 4. Autonomic neural function changes in the control, OSA, and LL‐TS + OSA groups. A, The anatomical position of the SLGP and representative example of sinus rate–slowing response to SLGP stimulation. (B) Sinus rate–slowing response to the high‐frequency stimulation of the SLGP across groups (n=6). (C) The anatomical position of the LSG and representative illustration of systolic BP–increasing response to LSG stimulation. (D) systolic BP–increasing response to the high‐frequency stimulation of the LSG in the 3 groups (n=6). *P<0.05 vs the baseline, **P<0.01 vs the baseline. BP indicates blood pressure; BS, baseline; LAA, left atrial appendage; LL‐TS, low‐level transcutaneous electrical stimulation; LOM, ligament of Marshall; LSG, left stellate ganglion; LSPV, left superior pulmonary vein; LV, left ventricle; OSA, obstructive sleep apnea; PA, pulmonary artery; SLGP, superior left ganglionated plexus.

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  Figure 5. Autonomic neural activity changes in the control, OSA, and LL‐TS + OSA groups. A, C, and E, Representative examples of the neural recordings from the SLGP, LSG and left RSN in different groups at baseline and 1 hour. B, D, and F, Quantitative analysis of autonomic neural activity in the SLGP, LSG, and left RSN (n=6). *P<0.05 vs the control group; # P<0.05 vs the OSA group. BS indicates baseline; LL‐TS, low‐level transcutaneous electrical stimulation; LSG, left stellate ganglion; OSA, obstructive sleep apnea; SLGP, superior left ganglionated plexus; RSN, renal sympathetic nerve.

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  Figure 6. The expressions levels of c‐fos and NGF in the control, OSA, and LL‐TS + OSA groups. A and B, Representative examples and relative protein expression levels of c‐fos and NGF in SLGP and LSG in the 3 groups (n=6). C and D, Representative photos and quantitative analyses of c‐fos‐immunoreactive and NGF‐immunoreactive neurons in LSG (n=6). *P<0.05 vs the control group; # P<0.05 vs the OSA group. DAPI indicates 4′,6‐diamidino‐2‐phenylindole; LL‐TS, low‐level transcutaneous electrical stimulation; LSG, left stellate ganglion; NGF, nerve growth factor; OSA, obstructive sleep apnea; SLGP, superior left ganglionated plexus; TH, tyrosine hydroxylase.

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  Figure 7. Schematic diagram illustrating how OSA initiates AF and the potential mechanism underlying the antiarrhythmic effect of LL‐TS. OSA increases afferent signaling to the central nervous system, which integrates this information and leads to hyperactivity of the intrinsic and extrinsic cardiac autonomic nervous system, which increases the nerve activity of GP, LSG and RSN. Increased GP, LSG and RSN neural activities contribute to the initiation and maintenance of AF. However, LL‐TS decreases input to the central nervous system and down‐regulates the nerve activities of GP, LSG and RSN, which suppresses OSA‐induced AF. AF indicates atrial fibrillation; GP, ganglionated plexus; LL‐TS, low‐level transcutaneous electrical stimulation; LSG, left stellate ganglion; OSA, obstructive sleep apnea; RSN, renal sympathetic nerve.