title: Renal sympathetic denervation suppresses ventricular substrate remodelling in a canine high-rate pacing model.
abstract: OBJECTIVE
  This study sought to assess whether renal sympathetic denervation (RSD) could suppress ventricular substrate remodelling and attenuate heart failure (HF) progression.
  
  
  RESULTS
  Nineteen dogs were randomised into three groups - seven sham-operated controls, six with right ventricular pacing to induce HF, and six with RSD followed eight weeks later by pacing induction of HF. Haemodynamic variables were monitored at baseline and after HF. Levels of ventricular interstitial fibrosis, BNP, Ang II, aldosterone and TGF-β were measured. All the dogs in the HF and HF﹢RSD groups showed increased left and right ventricular diastolic dimensions, but the dogs in the HF﹢RSD group had a higher left ventricular ejection fraction (LVEF) than the HF dogs (0.42±0.05 vs. 0.35±0.04, p<0.01). Compared with the dogs with HF alone, the HF+RSD dogs had lower left ventricular end-diastolic pressure (LVEDP) (3.3±1.6 vs. 25±3.7 mmHg, p<0.01) and less fibrous tissue. The levels of BNP, Ang II, aldosterone and TGF-β expression in ventricular tissue were higher in the HF dogs than in the sham-operated and HF﹢RSD dogs.
  
  
  CONCLUSIONS
  RSD suppressed ventricular substrate remodelling induced by long-term rapid ventricular pacing.
authors.affiliation: Cardiovascular Research Institute of Wuhan University, Renmin Hospital of Wuhan University, Wuhan City, China.
authors.forename: Zixuan
authors.initials: Z
authors.lastname: Dai
authors.forename: Shengbo
authors.initials: S
authors.lastname: Yu
authors.forename: Qingyan
authors.initials: Q
authors.lastname: Zhao
authors.forename: Yanyan
authors.initials: Y
authors.lastname: Meng
authors.forename: Huang
authors.initials: H
authors.lastname: He
authors.forename: Yanhong
authors.initials: Y
authors.lastname: Tang
authors.forename: Xi
authors.initials: X
authors.lastname: Wang
authors.forename: Jinping
authors.initials: J
authors.lastname: Xiao
authors.forename: Xule
authors.initials: X
authors.lastname: Wang
authors.forename: Congxin
authors.initials: C
authors.lastname: Huang
mesh_terms: D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000097:blood / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D002304:Cardiac Pacing, Artificial; D017115:Catheter Ablation; D004195:Disease Models, Animal; D018450:Disease Progression; D004285:Dogs; D005260:Female; D005355:Fibrosis; D006333:Heart Failure / Q000097:blood / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D007668:Kidney / Q000294:innervation*; D008297:Male; D020097:Natriuretic Peptide, Brain / Q000097:blood; D013562:Sympathectomy / Q000379:methods*; D013997:Time Factors; D016212:Transforming Growth Factor beta / Q000097:blood; D016277:Ventricular Function, Left; D017725:Ventricular Pressure; D020257:Ventricular Remodeling
chemical_list: D016212:Transforming Growth Factor beta; D000804:Angiotensin II; D020097:Natriuretic Peptide, Brain; D000450:Aldosterone