title: Delayed trans-septal activation results in comparable hemodynamic effect of left ventricular and biventricular endocardial pacing: insights from electroanatomical mapping.
abstract: BACKGROUND
  We sought to compare left ventricular (LVepi) and biventricular epicardial pacing (BIVepi) with LV (LVendo) and BIV endocardial pacing (BIVendo) in patients with chronic heart failure with an emphasis on the underlying electrophysiological mechanisms and hemodynamic effects.
  
  
  RESULTS
  Ten patients with chronically implanted cardiac resynchronization devices underwent temporary LVendo and BIVendo pacing with an LV endocardial roving catheter. A pressure wire and noncontact mapping array were placed to the LV cavity to measure LVdP/dtmax and perform electroanatomical mapping. At the optimal endocardial position, the acute hemodynamic response (AHR) was superior to epicardial stimulation, the AHR to BIVendo pacing and LVendo pacing being comparable (21±15% versus 22±17%; P=NS). During intrinsic conduction, QRS duration was 185±30 ms, endocardial LV total activation time 92±27 ms, and trans-septal activation time 60±21 ms. With LVendo pacing, QRS duration (187±29 ms; P=NS) and endocardial LV total activation time (91±23 ms; P=NS) were comparable with intrinsic conduction. There was no significant difference in endocardial LV total activation time between LVendo and BIVendo pacing (91±23 versus 85±15 ms; P=NS). Assessment of isochronal maps identified slow trans-septal conduction with both LVendo and BIVendo pacing resulting in activation of almost the entire LV endocardium prior to septal breakout, thereby limiting any possible fusion with either pacing mode.
  
  
  CONCLUSIONS
  The equivalent AHR to LVendo and BIVendo pacing may be explained by prolonged trans-septal conduction limiting fusion of electrical wavefronts. The optimal AHR was associated with predominantly LV pre-excitation and depolarization. Our results suggest that LV pacing alone may offer a viable endocardial stimulation strategy to achieve cardiac resynchronization.
authors.affiliation: Division of Imaging Sciences and Biomedical Engineering, King's College, London, United Kingdom.
authors.forename: Manav
authors.initials: M
authors.lastname: Sohal
authors.forename: Anoop
authors.initials: A
authors.lastname: Shetty
authors.forename: Steven
authors.initials: S
authors.lastname: Niederer
authors.forename: Zhong
authors.initials: Z
authors.lastname: Chen
authors.forename: Tom
authors.initials: T
authors.lastname: Jackson
authors.forename: Eva
authors.initials: E
authors.lastname: Sammut
authors.forename: Julian
authors.initials: J
authors.lastname: Bostock
authors.forename: Reza
authors.initials: R
authors.lastname: Razavi
authors.forename: Frits
authors.initials: F
authors.lastname: Prinzen
authors.forename: C Aldo
authors.initials: CA
authors.lastname: Rinaldi
mesh_terms: D018780:Body Surface Potential Mapping / Q000379:methods*; D058406:Cardiac Resynchronization Therapy / Q000379:methods*; D004699:Endocardium / Q000503:physiopathology*; D005260:Female; D005500:Follow-Up Studies; D006329:Heart Conduction System / Q000503:physiopathology*; D006333:Heart Failure / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy*; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D019028:Magnetic Resonance Imaging, Cine; D008297:Male; D008875:Middle Aged; D016896:Treatment Outcome; D016277:Ventricular Function, Left / Q000502:physiology
keywords: bundle-branch block; cardiac resynchronization therapy; heart failure