title: Biventricular pacing reduces the induction of monomorphic ventricular tachycardia: a potential mechanism for arrhythmia suppression.
abstract: OBJECTIVE
  The aim of the present study was to evaluate in a prospective randomized fashion the electrophysiologic effects of acute biventricular (BV) pacing. We hypothesized that (1) the local coupling interval in the left ventricle in response to right-sided ventricular premature beats is prolonged when BV pacing is applied during the drive train compared with right ventricular (RV) pacing, and (2) BV programmed electrical stimulation (PES) decreases the induction of ventricular arrhythmias compared with standard RV-PES, regardless of the presence of intraventricular conduction delay.
  
  
  BACKGROUND
  Previous studies have suggested that BV pacing might decrease the frequency of ventricular arrhythmias; however, the mechanism of arrhythmia suppression remains unclear.
  
  
  METHODS
  Eighteen patients with coronary artery disease were randomized to RV-PES or BV-PES with a repeat study using the other pacing mode. The RV effective refractory periods were measured during RV-PES and BV-PES. In addition, the local LV S(1)-S(2) coupling interval was measured at 600/450 ms and 400/350 ms during RV-PES and BV-PES.
  
  
  RESULTS
  BV-PES had no effect on RV effective refractory periods. On the other hand, the local LV S(1)-S(2) coupling intervals increased significantly during BV-PES compared with RV-PES (P < .0001). Ventricular tachycardia was induced in six patients using RV-PES but in only one patient with BV-PES (RR = 83%, P = .01). No difference was observed in the induction of ventricular fibrillation.
  
  
  CONCLUSIONS
  BV-PES significantly reduced the induction of ventricular tachycardia compared to RV-PES, with no significant effect on ventricular fibrillation induction. Our findings may help explain the reduced incidence of ventricular arrhythmias noted with chronic BV pacing.
authors.affiliation: University of Texas Southwestern Medical Center, Dallas, Texas; Dallas VA Medical Center, Dallas, Texas, USA.
authors.forename: Robert C
authors.initials: RC
authors.lastname: Kowal
authors.forename: Stephen L
authors.initials: SL
authors.lastname: Wasmund
authors.forename: Michael L
authors.initials: ML
authors.lastname: Smith
authors.forename: Niraj
authors.initials: N
authors.lastname: Sharma
authors.forename: George N
authors.initials: GN
authors.lastname: Carayannopoulos
authors.forename: Brian
authors.initials: B
authors.lastname: Le
authors.forename: John
authors.initials: J
authors.lastname: Cogan
authors.forename: Ali M
authors.initials: AM
authors.lastname: Kizilbash
authors.forename: Jose A
authors.initials: JA
authors.lastname: Joglar
authors.forename: Mohamed H
authors.initials: MH
authors.lastname: Hamdan
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D018592:Cross-Over Studies; D004562:Electrocardiography; D006329:Heart Conduction System / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D008875:Middle Aged; D011446:Prospective Studies; D011930:Reaction Time / Q000502:physiology; D017180:Tachycardia, Ventricular / Q000503:physiopathology / Q000517:prevention & control*