title: Ventricular rate control during atrial fibrillation by cardiac parasympathetic nerve stimulation: a transvenous approach.
abstract: OBJECTIVE
  To identify intravascular sites for continuous, stable parasympathetic stimulation (PS) in order to control the ventricular rate during atrial fibrillation (AF).
  
  
  BACKGROUND
  Ventricular rate control during AF in patients with congestive heart failure is a significant clinical problem because many drugs that slow the ventricular rate may depress ventricular function and cause hypotension. Parasympathetic stimulation can exert negative dromotropic effects without significantly affecting the ventricles.
  
  
  METHODS
  In 22 dogs, PS was performed using rectangular stimuli (0.05 ms duration, 20 Hz) delivered through a catheter with an expandable electrode-basket at its end. The catheter was positioned either in the superior vena cava (SVC, n = 6), coronary sinus (CS, n = 10) or right pulmonary artery (RPA, n = 6). The basket was then expanded to obtain long-term catheter stability. Atrial fibrillation was induced and maintained by rapid atrial pacing.
  
  
  RESULTS
  Nonfluoroscopic (SVC) and fluoroscopic (CS/RPA) identification of effective intravascular PS sites was achieved within 3 to 10 min. The ventricular rate slowing effect during AF started and ceased immediately after on-offset of PS, respectively, and could be maintained over 20 h. In the SVC, at least a 50% increase of ventricular rate (R-R) intervals occurred at 22 +/- 11 V (331 +/- 139 ms to 653 +/- 286 ms, p < 0.001), in the CS at 16 +/- 10 V (312 +/- 102 ms vs. 561 +/- 172 ms, p < 0.001) and in the RPA at 18 +/- 7 V (307 +/- 62 ms to 681 +/- 151 ms, p < 0.001). Parasympathetic stimulation did not change ventricular refractory periods.
  
  
  CONCLUSIONS
  Intravascular PS results in a significant ventricular rate slowing during AF in dogs. This may be beneficial in patients with AF and rapid ventricular response since many drugs that decrease atrioventricular conduction have negative inotropic effects which could worsen concomitant congestive heart failure.
authors.affiliation: Department of Internal Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, USA.
authors.forename: P
authors.initials: P
authors.lastname: Schauerte
authors.forename: B J
authors.initials: BJ
authors.lastname: Scherlag
authors.forename: M A
authors.initials: MA
authors.lastname: Scherlag
authors.forename: S
authors.initials: S
authors.lastname: Goli
authors.forename: W M
authors.initials: WM
authors.lastname: Jackman
authors.forename: R
authors.initials: R
authors.lastname: Lazzara
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000175:diagnosis / Q000503:physiopathology*; D001285:Atropine; D002405:Catheterization, Central Venous; D002406:Catheterization, Peripheral; D002572:Cervical Plexus / Q000187:drug effects / Q000601:surgery; D004285:Dogs; D004558:Electric Stimulation; D004562:Electrocardiography; D005726:Ganglia, Parasympathetic / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology*; D006352:Heart Ventricles / Q000294:innervation / Q000503:physiopathology*; D017764:Parasympathectomy; D010276:Parasympatholytics; D010496:Pericardium / Q000294:innervation; D011651:Pulmonary Artery; D014683:Vena Cava, Superior
chemical_list: D010276:Parasympatholytics; D001285:Atropine