title: Increased sympathetic activity after atrioventricular junction ablation in patients with chronic atrial fibrillation.
abstract: OBJECTIVE
  The aim of this study was to determine the changes in sympathetic nerve activity (SNA) after atrioventricular junction (AVJ) ablation in patients with chronic atrial fibrillation (AF).
  
  
  BACKGROUND
  Polymorphic ventricular tachycardia (PMVT) has been reported after AVJ ablation in patients paced at a rate of < or =70 beats/min. We hypothesized that AVJ ablation results in sympathetic neural changes that favor the occurrence of PMVT and that pacing at 90 beats/min attenuates these changes.
  
  
  METHODS
  Sympathetic nerve activity, 90% monophasic cardiac action potential duration (APD90), right ventricular effective refractory period (ERP) and blood pressure measurements were obtained in 10 patients undergoing AVJ ablation. Sympathetic nerve activity was analyzed at baseline and during and after successful AVJ ablation for at least 10 min. Data were also collected after ablation at pacing rates of 60 and 90 beats/min. The APD90 and ERP were measured before and after AV block during pacing at 120 beats/min.
  
  
  RESULTS
  Sympathetic nerve activity increased to 134 +/- 16% of the pre-ablation baseline value (p < 0.01) after successful AVJ ablation plus pacing at 60 beats/min and decreased to 74 +/- 8% of baseline (p < 0.05) with subsequent pacing at 90 beats/min. Both APD90 and ERP increased significantly.
  
  
  CONCLUSIONS
  1) Ablation of the AVJ followed by pacing at 60 beats/min is associated with an increase in SNA. 2) Pacing at 90 beats/min decreases SNA to or below the pre-ablation baseline value. 3) Cardiac APD and ERP increase after AVJ ablation. The increase in SNA, along with the prolongation in APD, may play a role in the pathogenesis of ventricular arrhythmias that occur after AVJ ablation.
authors.affiliation: University of Texas Southwestern, Medical Center and Dallas Veterans Affairs Medical Center, USA. Hamdan@ryburn.swmed.edu
authors.forename: M H
authors.initials: MH
authors.lastname: Hamdan
authors.forename: R L
authors.initials: RL
authors.lastname: Page
authors.forename: C J
authors.initials: CJ
authors.lastname: Sheehan
authors.forename: J D
authors.initials: JD
authors.lastname: Zagrodzky
authors.forename: S L
authors.initials: SL
authors.lastname: Wasmund
authors.forename: K
authors.initials: K
authors.lastname: Ramaswamy
authors.forename: J A
authors.initials: JA
authors.lastname: Joglar
authors.forename: M L
authors.initials: ML
authors.lastname: Smith
mesh_terms: D000200:Action Potentials; D000328:Adult; D000368:Aged; D001281:Atrial Fibrillation / Q000503:physiopathology* / Q000601:surgery; D001794:Blood Pressure; D002036:Bundle of His / Q000503:physiopathology / Q000601:surgery*; D002037:Bundle-Branch Block / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D006328:Cardiac Catheterization; D017115:Catheter Ablation / Q000009:adverse effects*; D002908:Chronic Disease; D017147:Defibrillators, Implantable; D004554:Electric Countershock; D004594:Electrophysiology / Q000379:methods; D006339:Heart Rate; D006352:Heart Ventricles / Q000294:innervation* / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D011184:Postoperative Period; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D017180:Tachycardia, Ventricular / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy