title: Transseptal conduction as an important determinant for cardiac resynchronization therapy, as revealed by extensive electrical mapping in the dyssynchronous canine heart.
abstract: BACKGROUND
  Simple conceptual ideas about cardiac resynchronization therapy assume that biventricular (BiV) pacing results in collision of right and left ventricular (LV) pacing-derived wavefronts. However, this concept is contradicted by the minor reduction in QRS duration usually observed. We investigated the electric mechanisms of cardiac resynchronization therapy by performing detailed electric mapping during extensive pacing protocols in dyssynchronous canine hearts.
  
  
  RESULTS
  Studies were performed in anesthetized dogs with acute left bundle-branch block (LBBB, n=10) and chronic LBBB with tachypacing-induced heart failure (LBBB+HF, n=6). Activation times (AT) were measured using LV endocardial contact and noncontact mapping and epicardial contact mapping. BiV pacing reduced QRS duration by 21±10% in LBBB but only by 5±12% in LBBB+HF hearts. Transseptal impulse conduction was significantly slower in LBBB+HF than in LBBB hearts (67±9 versus 44±16 ms, respectively), and in both groups significantly slower than transmural LV conduction (≈30 ms). In both groups QRS duration and vector and the epicardial AT vector amplitude and angle were significantly different between LV and BiV pacing, whereas the endocardial AT vector was similar. During variation of atrioventricular delay while LV pacing, and ventriculo-ventricular delay while BiV pacing, the optimal hemodynamic effect was achieved when epicardial AT and QRS vectors were minimal and endocardial AT vector indicated LV preexcitation.
  
  
  CONCLUSIONS
  Due to slow transseptal conduction, the LV electric activation sequence is similar in LV and BiV pacing, especially in failing hearts. Optimal hemodynamic cardiac resynchronization therapy response coincides with minimal epicardial asynchrony and QRS vector and LV preexcitation.
authors.affiliation: Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, Limburg, The Netherlands.
authors.forename: Marc
authors.initials: M
authors.lastname: Strik
authors.forename: Caroline J M
authors.initials: CJ
authors.lastname: van Deursen
authors.forename: Lars B
authors.initials: LB
authors.lastname: van Middendorp
authors.forename: Arne
authors.initials: A
authors.lastname: van Hunnik
authors.forename: Marion
authors.initials: M
authors.lastname: Kuiper
authors.forename: Angelo
authors.initials: A
authors.lastname: Auricchio
authors.forename: Frits W
authors.initials: FW
authors.lastname: Prinzen
mesh_terms: D000200:Action Potentials; D000818:Animals; D002037:Bundle-Branch Block / Q000175:diagnosis / Q000503:physiopathology / Q000601:surgery*; D058406:Cardiac Resynchronization Therapy; D004195:Disease Models, Animal; D004285:Dogs; D022062:Electrophysiologic Techniques, Cardiac; D056149:Epicardial Mapping; D005260:Female; D006329:Heart Conduction System / Q000503:physiopathology / Q000601:surgery*; D006333:Heart Failure / Q000175:diagnosis / Q000503:physiopathology / Q000601:surgery*; D006439:Hemodynamics; D008297:Male; D013997:Time Factors; D016277:Ventricular Function, Left; D016278:Ventricular Function, Right
keywords: cardiac resynchronization therapy; electrophysiology; heart failure; left bundle-branch block; pacing