title: Atrial fibrillation electrical remodelling via ablation of the epicardial neural networks and suprathreshold stimulation of vagosympathetic nerve.
abstract: BACKGROUND
  Numerous studies have shown that the cardiac autonomic nervous system (CANS) is involved in the occurrence and persistence of atrial fibrillation (AF). The CANS is commonly considered to consist of the extrinsic and intrinsic autonomic nerves. The influence of exogenous and endogenous nerve stimulation plexus ablation on pulmonary vein sleeves and atrial myocardium provides important information in understanding the occurrence and persistence of AF. Vagosympathetic nerve stimulation and epicardial neural networks are important participants in atrial electrical remodelling (AER). Elucidation of the changes in the electrophysiological indicators of the atrial and pulmonary veins caused by epicardial neural network ablation and autonomic nerve stimulation may provide a theoretical basis for the clinical treatment of AF.
  
  
  METHODS
  A total of 13 beagle dogs were randomly divided into 2 groups: the control group (n=6), which was treated with a simple rapid atrial pacing (RAP) for 6 h, and the experimental group (n=7), which was treated with RAP+vagus nerve stimulation (VNS) for 6 h. Both groups were treated with epicardial ganglia plexus (GP) ablation after 6 h. We measured the monophasic action potential (MAP), various parts of the effective refractory period (ERP), and AF induction rate before and after pacing or ablation.
  
  
  RESULTS
  With the extension of the pacing time, the atrial MAP and ERP of the 2 groups shortened and returned to normal after ablation plexus. After GP ablation, the atrial AF-induced rate did not decrease significantly compared with that of the pulmonary vein.
  
  
  CONCLUSIONS
  Vagus nerve threshold stimulation exacerbated the deterioration of electrical remodelling, whereas the epicardial neural network ablation blocked or reversed the AER.
authors.affiliation: Department of Cardiology, First Affiliated Hospital, Xinjiang Medical University, Urumqi, Xinjiang, China (mainland).
authors.forename: Yanmei
authors.initials: Y
authors.lastname: Lu
authors.affiliation: Department of Cardiology, First Affiliated Hospital, Xinjiang Medical University, Urumqi, Xinjiang, China (mainland).
authors.forename: Juan
authors.initials: J
authors.lastname: Sun
authors.affiliation: Department of Cardiology, First Affiliated Hospital, Xinjiang Medical University, Urumqi, Xinjiang, China (mainland).
authors.forename: Xianhui
authors.initials: X
authors.lastname: Zhou
authors.affiliation: Department of Cardiology, First Affiliated Hospital, Xinjiang Medical University, Urumqi, Xinjiang, China (mainland).
authors.forename: Qinquan
authors.initials: Q
authors.lastname: Sun
authors.affiliation: Department of Cardiology, First Affiliated Hospital, Xinjiang Medical University, Urumqi, Xinjiang, China (mainland).
authors.forename: Shuai
authors.initials: S
authors.lastname: Sun
authors.affiliation: Department of Cardiology, First Affiliated Hospital, Xinjiang Medical University, Urumqi, Xinjiang, China (mainland).
authors.forename: Baopeng
authors.initials: B
authors.lastname: Tang
mesh_terms: D000200:Action Potentials; D000818:Animals; D001281:Atrial Fibrillation / Q000503:physiopathology*; D064752:Atrial Remodeling; D017115:Catheter Ablation / Q000379:methods; D004195:Disease Models, Animal; D004285:Dogs; D004594:Electrophysiology; D005260:Female; D008297:Male; D009415:Nerve Net; D010496:Pericardium / Q000378:metabolism; D011667:Pulmonary Veins / Q000473:pathology / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology*; D014630:Vagus Nerve / Q000502:physiology*; D055536:Vagus Nerve Stimulation