title: The role of ganglionated plexi in apnea-related atrial fibrillation.
abstract: OBJECTIVE
  This study was conducted to simulate sleep apnea-induced atrial fibrillation (AF) in an experimental model and to determine whether neural ablation will prevent AF.
  
  
  BACKGROUND
  An increasing number of clinical reports have associated sleep apnea and AF, and many possible mechanisms responsible for this relationship have been proposed.
  
  
  METHODS
  Thirty dogs anesthetized with Na-pentobarbital were ventilated by a positive pressure respirator. Protocol 1 (n = 14): After a right thoracotomy, atrial and pulmonary vein programmed pacing at 2x and 4x threshold determined the shortest atrial refractory period. Obstructive apnea was induced by turning off the respirator during end expiration for 2 min. During apnea, programmed pacing was performed with S1-S2 = 5 to 10 ms earlier than the atrial refractory period. Neural activity was monitored from the ganglionated plexi (GP) adjacent to the right pulmonary veins. Protocol 2 (n = 16): Electrical stimulation identified the GP at the right pulmonary artery (RPA). Programmed pacing was again instituted, below atrial refractory period, during 2 min of apnea. After radiofrequency ablation of the RPA GP, continuous programmed pacing was again repeated during 2 min of apnea. In 5 dogs, blood gases were determined at baseline and at 2 min of apnea.
  
  
  RESULTS
  Protocol 1: During apnea, S1-S2 induced AF within 85 +/- 38 s (9 of 10). In 1 case, AF occurred spontaneously at 1 min 36 s of apnea. Recorded GP neural activity progressively increased before AF onset. Systolic but not diastolic blood pressure rose significantly before AF (149 +/- 26 mm Hg to 193 +/- 38 mm Hg, p < 0.05). In 4 dogs, autonomic blockade prevented apnea-induced AF. Protocol 2: AF induced by pacing occurred in 8 of 11 dogs within the 2-min period of apnea, before neural ablation. After ablation, 0 of 6 showed AF during 2 min of apnea (p = 0.009).
  
  
  CONCLUSIONS
  This experimental model of apnea shows a reproducible incidence of AF. After neural ablation of the RPA GP or autonomic blockade, AF inducibility was significantly inhibited.
authors.affiliation: Heart Rhythm Institute, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA.
authors.forename: Muhammad
authors.initials: M
authors.lastname: Ghias
authors.forename: Benjamin J
authors.initials: BJ
authors.lastname: Scherlag
authors.forename: Zhibing
authors.initials: Z
authors.lastname: Lu
authors.forename: Guodong
authors.initials: G
authors.lastname: Niu
authors.forename: Annerie
authors.initials: A
authors.lastname: Moers
authors.forename: Warren M
authors.initials: WM
authors.lastname: Jackman
authors.forename: Ralph
authors.initials: R
authors.lastname: Lazzara
authors.forename: Sunny S
authors.initials: SS
authors.lastname: Po
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001281:Atrial Fibrillation / Q000209:etiology* / Q000517:prevention & control; D001285:Atropine / Q000494:pharmacology; D001341:Autonomic Nervous System / Q000503:physiopathology; D001784:Blood Gas Analysis; D002304:Cardiac Pacing, Artificial; D017115:Catheter Ablation; D004195:Disease Models, Animal; D004285:Dogs; D004558:Electric Stimulation; D022062:Electrophysiologic Techniques, Cardiac; D006325:Heart Atria; D011667:Pulmonary Veins; D020181:Sleep Apnea, Obstructive / Q000150:complications*
chemical_list: D000319:Adrenergic beta-Antagonists; D001285:Atropine