title: Transient repolarization instability following the initiation of cardiac resynchronization therapy.
abstract: OBJECTIVE
  Cardiac resynchronization therapy (CRT) may cause changes in ventricular repolarization (VR), particularly in the initial phase of treatment. This study investigated the effect of CRT cessation and re-initiation on parameters of VR duration and heterogeneity at different paced heart rates.
  
  
  METHODS
  Cardiac resynchronization therapy was inactivated for 2 weeks in 16 treatment responders to CRT. QT and JT intervals were measured on the surface electrocardiogram at 60, 70, and 80 bpm (randomized order) and vectorcardiography (VCG) was performed with CRT 'on' (day 0), 'off' (day 0, 1, 7, and 14) and after CRT re-initiation (day 14, 15, 16, and 21). On day 0 ('on') and 14 ('off') echocardiography, the 6 min walking distance and brain natriuretic peptide were assessed.
  
  
  RESULTS
  The QT interval at baseline (CRT 'on'), measured at 60, 70, and 80 bpm, was 482 ± 31, 468 ± 37, and 457 ± 39 ms, respectively, and decreased by 5, 5, and 6% during the first week following CRT cessation (all P< 0.05). Immediately after re-initiation on day 14, it increased again by 20 ± 18 (4%; P< 0.05), 34 ± 39 (8%; P< 0.01), and 16 ± 38 ms (4%, ns) followed by a gradual decrease towards previous 'off' levels. Similar changes were observed for the JT interval. Ventricular repolarization duration was significantly shortened by increasing the paced heart rate from 60 to 70 and 80 bpm. Vectorcardiography parameters reflecting VR gradients (ST-vector magnitude, Tarea, and Tavplan) increased significantly (by 31, 45, and 71%) after CRT cessation. A similar but non-significant pattern was observed after CRT re-initiation.
  
  
  CONCLUSIONS
  The increase in repolarization duration and gradients observed after CRT initiation suggests a transient state of VR instability that can be attenuated by programming of higher paced heart rates during the initial phase of treatment.
authors.affiliation: Department of Cardiology, Karolinska University Hospital, Karolinska Institutet, Stockholm S-17176, Sweden. frieder.braunschweig@karolinska.se
authors.forename: Frieder
authors.initials: F
authors.lastname: Braunschweig
authors.forename: Hannes
authors.initials: H
authors.lastname: Pfizenmayer
authors.forename: Aigars
authors.initials: A
authors.lastname: Rubulis
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Schoels
authors.forename: Cecilia
authors.initials: C
authors.lastname: Linde
authors.forename: Lennart
authors.initials: L
authors.lastname: Bergfeldt
mesh_terms: D000368:Aged; D058406:Cardiac Resynchronization Therapy; D004562:Electrocardiography; D006321:Heart / Q000503:physiopathology*; D006329:Heart Conduction System / Q000503:physiopathology; D006333:Heart Failure / Q000503:physiopathology / Q000628:therapy; D006339:Heart Rate / Q000502:physiology; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D016896:Treatment Outcome; D016138:Walking / Q000502:physiology
chemical_list: D020097:Natriuretic Peptide, Brain