title: Biventricular stimulation improves right and left ventricular function after tetralogy of Fallot repair: acute animal and clinical studies.
abstract: BACKGROUND
  Optimal treatment of right ventricular (RV) dysfunction observed in patients after tetralogy of Fallot (TOF) repair is unclear. Studies of biventricular (BiV) stimulation in patients with congenital heart disease have been retrospective or have included patients with heterogeneous disorders.
  
  
  OBJECTIVE
  The purpose of this study was to determine the effects on cardiac function of stimulating at various cardiac sites in an animal model of RV dysfunction and dyssynchrony and in eight symptomatic adults with repaired TOF.
  
  
  METHODS
  Pulmonary stenosis and regurgitation as well as RV scars were induced in 15 piglets to mimic repaired TOF. The hemodynamic effects of various configurations of RV and BiV stimulation were compared with sinus rhythm (SR) 4 months after surgery. In eight adults with repaired TOF, RV and left ventricular (LV) dP/dt(max) were measured invasively during SR, apical RV stimulation, and BiV stimulation.
  
  
  RESULTS
  At 4 months, RV dilation, dysfunction, and dyssynchrony were present in all piglets. RV stimulation caused a decrease in LV function but no change in RV function. In contrast, BiV stimulation significantly improved LV and RV function (P < .05). Echocardiography and epicardial electrical mapping showed activation consistent with right bundle branch block during SR and marked resynchronization during BiV stimulation. In patients with repaired TOF, BiV stimulation increased significantly RV and LV dP/dt(max) (P < .05).
  
  
  CONCLUSIONS
  In this swine model of RV dysfunction and in adults with repaired TOF, BiV stimulation significantly improved RV and LV function by alleviating electromechanical dyssynchrony.
authors.affiliation: University Hospital of Bordeaux, Bordeaux, France.
authors.forename: Jean-Benoit
authors.initials: JB
authors.lastname: Thambo
authors.forename: Pierre
authors.initials: P
authors.lastname: Dos Santos
authors.forename: Maxime
authors.initials: M
authors.lastname: De Guillebon
authors.forename: Francois
authors.initials: F
authors.lastname: Roubertie
authors.forename: Louis
authors.initials: L
authors.lastname: Labrousse
authors.forename: Frederic
authors.initials: F
authors.lastname: Sacher
authors.forename: Xavier
authors.initials: X
authors.lastname: Iriart
authors.forename: Stephane
authors.initials: S
authors.lastname: Lafitte
authors.forename: Sylvain
authors.initials: S
authors.lastname: Ploux
authors.forename: Pierre
authors.initials: P
authors.lastname: Jais
authors.forename: Xavier
authors.initials: X
authors.lastname: Roques
authors.forename: Michel
authors.initials: M
authors.lastname: Haissaguerre
authors.forename: Philippe
authors.initials: P
authors.lastname: Ritter
authors.forename: Jacques
authors.initials: J
authors.lastname: Clementy
authors.forename: Sanjiv M
authors.initials: SM
authors.lastname: Narayan
authors.forename: Pierre
authors.initials: P
authors.lastname: Bordachar
mesh_terms: D000328:Adult; D000818:Animals; D002304:Cardiac Pacing, Artificial; D004195:Disease Models, Animal; D006801:Humans; D013552:Swine; D013771:Tetralogy of Fallot / Q000503:physiopathology / Q000601:surgery*; D018497:Ventricular Dysfunction, Right / Q000503:physiopathology / Q000628:therapy*; D016277:Ventricular Function, Left; D016278:Ventricular Function, Right