title: Inflammation abnormalities and inducibility of atrial fibrillation after epicardial ganglionated plexi ablation.
abstract: BACKGROUND
  Epicardial ganglionated plexi (GP) ablation can prevent atrial fibrillation inducibility. However, the long-term effects of GP ablation on atrial fibrillation have not been elucidated.
  
  
  METHODS
  Thirteen adult dogs of either sex, weighing 13-17kg, were randomly assigned to a sham-operated group (n=6) or a GP ablation group (n=7). After right thoracotomy, the atrial effective refractory period (AERP) was measured and atrial fibrillation was induced by right atrial rapid burst pacing. Atrial fibrillation and AERP were remeasured after anterior right and inferior right GP ablation in the GP ablation group. The animals were allowed to recover for 8 weeks, after which atrial fibrillation and AERP were measured again. Concentrations of C-reactive protein, tumour necrosis factor-alpha (TNF-α) and interleukin-6 were measured in the blood and atrial tissues.
  
  
  RESULTS
  After 8 weeks, atrial fibrillation was induced in all animals in the GP ablation group. AERP and dispersion of AERP (dAERP; maximum AERP minus minimum AERP) were increased after GP ablation but AERP recovered after 8 weeks. There were no significant differences in the concentrations of C-reactive protein, TNF-α or interleukin-6 in venous blood between the two groups and the concentration of C-reactive protein in the atrium did not change before and after GP ablation. However, the concentrations of TNF-α and interleukin-6 in the atrium increased significantly 8 weeks after GP ablation (P<0.05).
  
  
  CONCLUSIONS
  Increased concentrations of TNF-α and interleukin-6 in the atrium after GP ablation provide a new causative factor in terms of atrial fibrillation vulnerability.
authors.affiliation: Cardiovascular Research Institute of Wuhan University, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan City 430060, PR China.
authors.forename: Qingyan
authors.initials: Q
authors.lastname: Zhao
authors.forename: Shudi
authors.initials: S
authors.lastname: Zhang
authors.forename: He
authors.initials: H
authors.lastname: Huang
authors.forename: Yuguo
authors.initials: Y
authors.lastname: Zhang
authors.forename: Hongping
authors.initials: H
authors.lastname: Deng
authors.forename: Shengbo
authors.initials: S
authors.lastname: Yu
authors.forename: Congxin
authors.initials: C
authors.lastname: Huang
mesh_terms: D055011:Ablation Techniques / Q000009:adverse effects*; D000818:Animals; D001281:Atrial Fibrillation / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology; D017763:Autonomic Denervation / Q000009:adverse effects*; D002097:C-Reactive Protein / Q000378:metabolism; D002304:Cardiac Pacing, Artificial; D004195:Disease Models, Animal; D004285:Dogs; D022062:Electrophysiologic Techniques, Cardiac; D005260:Female; D005725:Ganglia, Autonomic / Q000503:physiopathology / Q000601:surgery*; D006325:Heart Atria / Q000276:immunology / Q000503:physiopathology; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D010496:Pericardium / Q000294:innervation*; D012032:Refractory Period, Electrophysiological; D012307:Risk Factors; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D015854:Up-Regulation
chemical_list: D018836:Inflammation Mediators; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein