Abstract
Background: The mechanisms for the vein of Marshall (VOM) mediated atrial fibrillation (AF) are not completely understood. We sought to evaluate the contribution of the intrinsic cardiac autonomic nervous system in VOM mediated AF.Method: Seven mongrel dogs were administered propranolol and continuously exposed to left superior ganglionated plexi (LSGP) stimulation, LSGP + low-level VOM stimulation, LSGP + atropine administration, LSGP + VOM filling with ethanol separately. The effective refractory period (ERP) and window of vulnerability (WOV) at the left superior pulmonary vein (LSPV), left inferior pulmonary vein (LIPV) and left atrial appendage (LAA) were measured.Result: LSGP stimulation significantly shortens the ERP and prolonged the ERP dispersion and WOV in LSPV, LIPV, and LAA. Interestingly, low-level VOM stimulation, atropine administration, or VOM filling with ethanol were able to attenuate the effects of LSGP in all sites.Conclusion: VOM as an inter-communication pathway of ganglionated plexis plays an important role in the development of vagal-related AF.
Highlights
The concept of vagal atrial fibrillation (AF) was first put forward by Coumel, who suggested that the autonomic nervous system plays a pathophysiological role in a subset of patients with AF [1, 2]
The window of vulnerability (WOV) at left superior pulmonary vein (LSPV), left inferior pulmonary vein (LIPV), and left atrial appendage (LAA) was significantly prolonged after left superior ganglionated plexi (LSGP) stimulation from 1.4±3.8 ms, 0 ms, to 4.3 ± 5.4 ms in the baseline state to 50 ± 8.2 ms, 41.4 ± 12.2 ms, and 54.3 ± 11.3 ms, respectively
LSGP + Low-Level vein of Marshall (VOM) Stimulation Attenuates the Effects of LSGP
Summary
The mechanisms for the vein of Marshall (VOM) mediated atrial fibrillation (AF) are not completely understood. We sought to evaluate the contribution of the intrinsic cardiac autonomic nervous system in VOM mediated AF. Method: Seven mongrel dogs were administered propranolol and continuously exposed to left superior ganglionated plexi (LSGP) stimulation, LSGP + low-level VOM stimulation, LSGP + atropine administration, LSGP + VOM filling with ethanol separately. The effective refractory period (ERP) and window of vulnerability (WOV) at the left superior pulmonary vein (LSPV), left inferior pulmonary vein (LIPV) and left atrial appendage (LAA) were measured
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