title: Autonomic Remodeling: How Atrial Fibrillation Begets Atrial Fibrillation in the First 24 Hours.
abstract: BACKGROUND
  The mechanism(s) of how atrial fibrillation (AF) sustains itself in the first 24 hours is not well understood.
  
  
  OBJECTIVE
  We sought to investigate the role of autonomic remodeling in the first 24 hours of AF simulated by rapid atrial pacing (RAP).
  
  
  METHODS
  Forty-eight rabbits were divided into 6 groups. One group (n = 8) was euthanized after baseline recordings. Another group (n = 8) did not receive RAP during the 24-hour period to serve as controls. In the other 4 groups, rabbits were euthanized after RAP for 4, 8, 12, or 24 hours (n = 8 for each). Before and after designated hours of RAP, atrial effective refractory period, heart rate variability, and left vagal and sympathetic nerve activity (VNA and SNA, respectively) were determined. The right and left atrial tissues were obtained for immunocytochemical analysis for growth-associated protein 43 (GAP43), tyrosine hydroxylase (TH), and choline acetyltransferase (ChAT).
  
  
  RESULTS
  RAP resulted in progressively shortened atrial effective refractory period and slower heart rate. In the first 12 hours of RAP, both SNA and VNA progressively increased. Then, VNA remained stably elevated but SNA began to attenuate. The high-frequency component and low-frequency/high-frequency ratio of heart rate variability followed the trend of VNA and SNA, respectively. The density of GAP43-positive, ChAT-positive, and TH-positive neural elements in the right and left atria was progressively higher with RAP.
  
  
  CONCLUSIONS
  AF resulted in progressive autonomic remodeling, manifesting as nerve sprouting, sympathetic and vagal hyperinnervation. Autonomic remodeling may play an important role in sustaining AF in the first 24 hours.
authors.affiliation: *Cardiovascular Center, First Affiliated Hospital of Xinjiang Medical University, Urumqi, China; †Heart Rhythm Institute, University of Oklahoma Health Sciences Center, Oklahoma City, OK; and ‡Department of Cardiovascular Diseases, The 6th People's Hospital, Shanghai Jiaotong University, Shanghai, China.
authors.forename: Ling
authors.initials: L
authors.lastname: Zhang
authors.forename: Sunny S
authors.initials: SS
authors.lastname: Po
authors.forename: Huan
authors.initials: H
authors.lastname: Wang
authors.forename: Benjamin J
authors.initials: BJ
authors.lastname: Scherlag
authors.forename: Hongliang
authors.initials: H
authors.lastname: Li
authors.forename: Juan
authors.initials: J
authors.lastname: Sun
authors.forename: Yanmei
authors.initials: Y
authors.lastname: Lu
authors.forename: Yitong
authors.initials: Y
authors.lastname: Ma
authors.forename: Yuemei
authors.initials: Y
authors.lastname: Hou
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial; D004195:Disease Models, Animal; D022062:Electrophysiologic Techniques, Cardiac; D006325:Heart Atria / Q000294:innervation*; D006329:Heart Conduction System / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology; D008297:Male; D011817:Rabbits; D012032:Refractory Period, Electrophysiological / Q000502:physiology; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D013997:Time Factors; D014630:Vagus Nerve / Q000503:physiopathology*; D055536:Vagus Nerve Stimulation