title: Dispersion of repolarization in cardiac resynchronization therapy.
abstract: BACKGROUND
  Proarrhythmic effects of cardiac resynchronization therapy (CRT) as a result of increased transmural dispersion of repolarization (TDR) induced by left ventricular (LV) epicardial pacing in a subset of vulnerable patients have been reported. The possibility of identifying these patients by ECG repolarization indices has been suggested.
  
  
  OBJECTIVE
  The purpose of this study was to test whether repolarization indices on the ECG can be used to measure dispersion of repolarization during pacing.
  
  
  METHODS
  CRT devices of 28 heart failure patients were switched among biventricular, LV, and right ventricular (RV) pacing. ECG indices proposed to measure dispersion of repolarization were calculated. The effects of CRT on repolarization were simulated in ECGSIM, a mathematical model of electrocardiogram genesis. TDR was calculated as the difference in repolarization time between the epicardial and endocardial nodes of the heart model.
  
  
  RESULTS
  
  
  
  METHODS
  The interval from the apex to the end of the T wave was shorter during biventricular pacing (102 +/- 18 ms) and LV pacing (106 +/- 21 ms) than during RV pacing (117 +/- 22 ms, P < or =.005). T-wave amplitude and area were low during biventricular pacing (287 +/- 125 microV and 56 +/- 22 microV.s, respectively, P = .0006 vs RV pacing). T-wave complexity was high during biventricular pacing (0.42 +/- 0.26, P = .004 vs RV pacing). Simulations: Repolarization patterns were highly similar to the preceding depolarization patterns. The repolarization patterns of different pacing modes explained the observed magnitudes of the ECG repolarization indices. Average and local TDR were not different between pacing modes.
  
  
  CONCLUSIONS
  In patients treated with CRT, ECG repolarization indices are related to pacing-induced activation sequences rather than transmural dispersion. TDR during biventricular and LV pacing is not larger than TDR during conventional RV endocardial pacing.
authors.affiliation: Department of Cardiology, Leiden University Medical Center, The Netherlands.
authors.forename: Bart Hooft
authors.initials: BH
authors.lastname: van Huysduynen
authors.forename: Cees A
authors.initials: CA
authors.lastname: Swenne
authors.forename: Jeroen J
authors.initials: JJ
authors.lastname: Bax
authors.forename: Gabe B
authors.initials: GB
authors.lastname: Bleeker
authors.forename: Harmen H M
authors.initials: HH
authors.lastname: Draisma
authors.forename: Lieselot
authors.initials: L
authors.lastname: van Erven
authors.forename: Sander G
authors.initials: SG
authors.lastname: Molhoek
authors.forename: Hedde
authors.initials: H
authors.lastname: van de Vooren
authors.forename: Ernst E
authors.initials: EE
authors.lastname: van der Wall
authors.forename: Martin J
authors.initials: MJ
authors.lastname: Schalij
mesh_terms: D000368:Aged; D018780:Body Surface Potential Mapping; D002304:Cardiac Pacing, Artificial; D003198:Computer Simulation; D004562:Electrocardiography; D005260:Female; D006333:Heart Failure / Q000628:therapy*; D006801:Humans; D008297:Male; D008955:Models, Cardiovascular; D010138:Pacemaker, Artificial; D018754:Ventricular Dysfunction / Q000628:therapy*