title: Effect of renal sympathetic denervation on the inducibility of atrial fibrillation during rapid atrial pacing.
abstract: BACKGROUND
  Atrial fibrillation (AF) is associated with activity of renin-angiotensin-aldosterone system (RAAS). Reduction in renal noradrenaline spillover could be achieved after renal sympathetic denervation (RSD). The relationship between RSD and AF is unknown.
  
  
  OBJECTIVE
  The objective of the study was to investigate the inducibility of AF during atrial rapid pacing after RSD.
  
  
  METHODS
  Thirteen dogs were used for the study as follows: control group (seven dogs) and RSD group (six dogs). In the control group, dogs were subjected to atrial pacing at 800 beats/min for 7 h, and atrial effective refractory period (AERP) was measured every hour in the status of non-pacing. Subsequently, pacing was stopped and the burst pacing (500 bpm) was repeated to induce AF three times. In the RSD group, after each renal artery ablation, the procedure of pacing and electrophysiological measurement was exactly same as in the control group. Blood was collected before and after pacing to measure the levels of renin, angiotensin II and aldosterone.
  
  
  RESULTS
  There was a persistent decrease in AERP in both groups. However, 7 h after cessation of pacing, the induced number of times and duration of AF were higher in the control group than that in the RSD group (1.0 ± 1.26 vs 3.14 ± 2.54, P = 0.03; 16.5 ± 25.1 vs 86.6 ± 116.4, P = 0.02). The plasma aldosterone concentration increased significantly 7 h after rapid pacing in control group (renin, 119.8 ± 31.1 vs 185.3 ± 103.5 pg/ml, P < 0.01; aldosterone, 288.2 ± 43.1 vs 369.6 ± 109.8 pg/ml, P = 0.01). The levels of renin and aldosterone showed a decreasing trend in RSD group, but this did not attain statistical significance.
  
  
  CONCLUSIONS
  Episodes of AF could be decreased by renal sympathetic denervation during short-time rapid atrial pacing. This effect might have relationship with decreased activity of RAAS.
authors.affiliation: Cardiovascular Research Institute of Wuhan University, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang, Wuhan City, 430060, People's Republic of China.
authors.forename: Qingyan
authors.initials: Q
authors.lastname: Zhao
authors.forename: Shengbo
authors.initials: S
authors.lastname: Yu
authors.forename: Minghui
authors.initials: M
authors.lastname: Zou
authors.forename: Zixuan
authors.initials: Z
authors.lastname: Dai
authors.forename: Xule
authors.initials: X
authors.lastname: Wang
authors.forename: Jinping
authors.initials: J
authors.lastname: Xiao
authors.forename: Congxin
authors.initials: C
authors.lastname: Huang
mesh_terms: D000450:Aldosterone / Q000097:blood; D000704:Analysis of Variance; D000792:Angiography; D000804:Angiotensin II / Q000097:blood; D000818:Animals; D001281:Atrial Fibrillation / Q000503:physiopathology* / Q000517:prevention & control*; D002304:Cardiac Pacing, Artificial; D004195:Disease Models, Animal; D004285:Dogs; D004797:Enzyme-Linked Immunosorbent Assay; D006325:Heart Atria / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology*; D007668:Kidney / Q000294:innervation*; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System; D013562:Sympathectomy / Q000379:methods*
chemical_list: D000804:Angiotensin II; D000450:Aldosterone; D012083:Renin