title: Chronic vagus nerve stimulation improves left ventricular function in a canine model of chronic mitral regurgitation.
abstract: BACKGROUND
  Autonomic dysfunction, characterized by sympathetic activation and vagal withdrawal, contributes to the progression of heart failure (HF). We hypothesized that chronic vagus nerve stimulation (VNS) could prevent left ventricular (LV) remodeling and dysfunction in a canine HF model induced by chronic mitral regurgitation (MR).
  
  
  RESULTS
  After the MR inducing procedure, 12 survived canines were randomly divided into the control (n = 6) and the VNS (n = 6) groups. At month 2, a VNS stimulator system was implanted in all canines. From month 3 to month 6, VNS therapy was applied in the VNS group but not in the control group. At month 6, compared with the control group, the canines in VNS group had significantly higher cardiac output (2.3 ± 0.3 versus 2.9 ± 0.4 L/min, P < 0.05, LV forward stroke volume (20.1 ± 3.7 versus 24.8 ± 3.9 ml, P < 0.05), and end-systolic stiffness constant (2.2 ± 0.3 versus 2.7 ± 0.3, P < 0.05). NT-proBNP and C-reactive protein were decreased significantly in the VNS group. However, no statistical difference was found in LV ejection fraction, LV end-diastolic dimension, LV end-diastolic volume, myocyte cross-sectional area, or collagen volume fraction between two groups.
  
  
  CONCLUSIONS
  Chronic VNS therapy may ameliorate MR-induced LV contractile dysfunction and improve the expression of biomarkers, but has less effect in improving LV chamber remodeling.
authors.affiliation: State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, 100037, People's Republic of China. yuhaiwentt@sina.com.
authors.forename: Haiwen
authors.initials: H
authors.lastname: Yu
authors.affiliation: State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, 100037, People's Republic of China. doctortangmin@hotmail.com.
authors.forename: Min
authors.initials: M
authors.lastname: Tang
authors.affiliation: State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, 100037, People's Republic of China. yujun200721@126.com.
authors.forename: Jun
authors.initials: J
authors.lastname: Yu
authors.affiliation: Cardiac Rhythm Disease Management, Chinese Branch of Medtronic Inc., Shanghai, China. xiaohong.zhou@medtronic.com.
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Zhou
authors.affiliation: Cardiac Rhythm Disease Management, Chinese Branch of Medtronic Inc., Shanghai, China. lepeng.zeng@medtronic.com.
authors.forename: Lepeng
authors.initials: L
authors.lastname: Zeng
authors.affiliation: State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, 100037, People's Republic of China. zsfuwai@vip.163.com.
authors.forename: Shu
authors.initials: S
authors.lastname: Zhang
mesh_terms: D000818:Animals; D002097:C-Reactive Protein / Q000378:metabolism; D003094:Collagen / Q000378:metabolism; D004195:Disease Models, Animal; D004285:Dogs; D005260:Female; D006439:Hemodynamics; D008297:Male; D008944:Mitral Valve Insufficiency / Q000097:blood / Q000503:physiopathology*; D020097:Natriuretic Peptide, Brain / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D010496:Pericardium / Q000473:pathology; D055536:Vagus Nerve Stimulation; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
chemical_list: D010446:Peptide Fragments; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain; D003094:Collagen; D002097:C-Reactive Protein