Songyun Wang1, Xiaoya Zhou1, Bing Huang1, Zhuo Wang1, Liping Zhou1, Mingxian Chen2, Lilei Yu3, Hong Jiang4. 1. Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei, China. 2. Department of Cardiology, the Second Xiangya Hospital of Central South University, Changsha, Hunan, China. 3. Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei, China,. Electronic address: whuyulilei@163.com. 4. Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei, China,. Electronic address: whujianghong@163.com.
Abstract
BACKGROUND: Previous study has shown that spinal cord stimulation (SCS) may suppress atrial fibrillation (AF) inducibility, but the mechanism for this is elusive. OBJECTIVE: The purpose of this study was to determine whether SCS could inhibit AF inducibility by suppressing autonomic remodeling in a canine model of rapid atrial pacing (RAP)-induced AF. METHODS: Eighteen canines were randomly divided into an RAP group (n = 9) and an RAP+SCS group (n = 9). Effective refractory period (ERP), window of vulnerability (WOV), AF inducibility, autonomic neural function, and activity from the anterior right ganglionated plexus (ARGP) and left stellate ganglion (LSG) were measured at baseline, at 3 hours of RAP, and at 6 hours of RAP. Then, ARGP and LSG were excised for Western blot and messenger RNA analysis. In another 4 dogs (control group, which received sham RAP and sham SCS), tissues were also excised for analysis. RESULTS: In the RAP group, RAP resulted in (1) a significant decrease in ERP and an increase in ERP dispersion, ΣWOV, and AF inducibility and (2) activation of ARGP and LSG versus baseline. In the RAP+SCS group, however, these changes were significantly attenuated by SCS. Compared with the control group, c-fos and nerve growth factor (NGF) were significantly up-regulated and small conductance calcium-activated potassium channel type 2 (SK2) was significantly down-regulated in the RAP group. In the RAP+SCS group, however, c-fos, NGF, and SK2 remained at a normal level compared with the control group. CONCLUSION: SCS may suppress RAP-induced AF by inhibiting autonomic remodeling, and the underlying mechanism of the salutary effect of SCS might contribute to modulation of the expression of c-fos, NGF, and SK2.
BACKGROUND: Previous study has shown that spinal cord stimulation (SCS) may suppress atrial fibrillation (AF) inducibility, but the mechanism for this is elusive. OBJECTIVE: The purpose of this study was to determine whether SCS could inhibit AF inducibility by suppressing autonomic remodeling in a canine model of rapid atrial pacing (RAP)-induced AF. METHODS: Eighteen canines were randomly divided into an RAP group (n = 9) and an RAP+SCS group (n = 9). Effective refractory period (ERP), window of vulnerability (WOV), AF inducibility, autonomic neural function, and activity from the anterior right ganglionated plexus (ARGP) and left stellate ganglion (LSG) were measured at baseline, at 3 hours of RAP, and at 6 hours of RAP. Then, ARGP and LSG were excised for Western blot and messenger RNA analysis. In another 4 dogs (control group, which received sham RAP and sham SCS), tissues were also excised for analysis. RESULTS: In the RAP group, RAP resulted in (1) a significant decrease in ERP and an increase in ERP dispersion, ΣWOV, and AF inducibility and (2) activation of ARGP and LSG versus baseline. In the RAP+SCS group, however, these changes were significantly attenuated by SCS. Compared with the control group, c-fos and nerve growth factor (NGF) were significantly up-regulated and small conductance calcium-activated potassium channel type 2 (SK2) was significantly down-regulated in the RAP group. In the RAP+SCS group, however, c-fos, NGF, and SK2 remained at a normal level compared with the control group. CONCLUSION: SCS may suppress RAP-induced AF by inhibiting autonomic remodeling, and the underlying mechanism of the salutary effect of SCS might contribute to modulation of the expression of c-fos, NGF, and SK2.
Authors: Peter Hanna; Eric Buch; Stavros Stavrakis; Christian Meyer; John D Tompkins; Jeffrey L Ardell; Kalyanam Shivkumar Journal: Cardiovasc Res Date: 2021-06-16 Impact factor: 10.787