title: Effects of pulmonary vein ablation on regional atrial vagal innervation and vulnerability to atrial fibrillation in dogs.
abstract: BACKGROUND
  Pulmonary vein (PV) isolation has proven to be an effective therapy for atrial fibrillation (AF). However, clinical evidence suggests that suppression of AF after PV isolation could not be fully attributed to the interruption of electrical conduction in and out of the PVs. Furthermore, little is known regarding the effects of ablation around the PVs on the atrial electrophysiological properties. We aimed to study the changes in atrial response to vagal stimulation (VS) after PV ablation (PVA).
  
  
  METHODS
  We studied 11 adult mongrel dogs under general anesthesia. Bilateral cervical sympathovagal trunks were decentralized. Propranolol was given to block sympathetic effects. Multipolar catheters were placed into right atrial appendage (RAA), distal and proximal coronary sinus (CSD, CSP), and left atrial free wall (LAFW). PVA was performed via trans-septal approach. Atrial effective refractory period (AERP) and vulnerability window (VW) of AF were measured with and without VS before and after ablation to isolate the PVs.
  
  
  RESULTS
  After ablation, AERP shortening in response to VS significantly decreased in the left atrium (43.64 +/- 21.57 vs 11.82 +/- 9.82 msec, P < 0.001 at LAFW; 50.91 +/- 26.25 vs 11.82 +/- 14.01 msec, P < 0.001 at CSP; 50 +/- 31.94 vs 17.27 +/- 20.54 msec, P < 0.005 at CSD), while the response to VS did not change significantly at RAA (58.18 +/- 28.22 vs 50.91 +/- 22.12 msec, P = 0.245). After ablation, atrial fibrillation VW during VS narrowed (20.63 +/- 11.48 vs 5.63 +/- 8.63 msec, P < 0.03 at LAFW; 26.25 +/- 12.46 vs 5.00 +/- 9.64 msec, P = 0.001 at CSP; 28.75 +/- 18.47 vs 6.88 +/- 7.53 msec, P < 0.02 at CSD, and 33.75 +/- 24.5 vs 16.25 +/- 9.91 msec, P = 0.03 at RAA).
  
  
  CONCLUSIONS
  Ablation around the PV ostia diminishes left atrial response to VS and decreases the atrial VW. The attenuated vagal response after ablation may contribute to the suppression of AF.
authors.affiliation: Texas Heart Institute/St. Luke's Episcopal Hospital, Houston, Texas 77030, USA.
authors.forename: Mehdi
authors.initials: M
authors.lastname: Razavi
authors.forename: Shulong
authors.initials: S
authors.lastname: Zhang
authors.forename: Donghui
authors.initials: D
authors.lastname: Yang
authors.forename: Robert A
authors.initials: RA
authors.lastname: Sanders
authors.forename: Biswajit
authors.initials: B
authors.lastname: Kar
authors.forename: Scott
authors.initials: S
authors.lastname: Delapasse
authors.forename: Tomohiko
authors.initials: T
authors.lastname: Ai
authors.forename: Wendel
authors.initials: W
authors.lastname: Moreira
authors.forename: Bari
authors.initials: B
authors.lastname: Olivier
authors.forename: Dirar S
authors.initials: DS
authors.lastname: Khoury
authors.forename: Jie
authors.initials: J
authors.lastname: Cheng
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000517:prevention & control*; D017115:Catheter Ablation / Q000379:methods*; D004285:Dogs; D005260:Female; D006325:Heart Atria / Q000294:innervation* / Q000503:physiopathology; D008297:Male; D011667:Pulmonary Veins / Q000601:surgery*; D012032:Refractory Period, Electrophysiological; D014630:Vagus Nerve / Q000502:physiology*