title: Left ventricular epicardial electrograms show divergent changes in action potential duration in responders and nonresponders to cardiac resynchronization therapy.
abstract: BACKGROUND
  A consistent feature of electrophysiological remodeling in heart failure is ventricular action potential duration (APD) prolongation. However, the effect of reverse remodeling on APD during cardiac resynchronization therapy (CRT) has not been determined in these patients. We hypothesized (1) that CRT may alter APD and (2) that the effect of CRT on APD may be different in patients who exhibit a good hemodynamic response to CRT compared with those with a poor response.
  
  
  RESULTS
  Left ventricular (LV) activation recovery intervals, as a surrogate for APD, were measured from the LV epicardium in 13 patients at day 0, 6 weeks, and 6 months after CRT implant. Responders to CRT were defined as those demonstrating a ≥15% reduction in LV end-systolic volume at 6 months. The responder group had a significant reduction in LV activation recovery interval (mean, -13±12 ms; median, -16 ms; interquartile range, -2 to -19 ms) during right ventricular pacing at 6 months (P<0.05). Conversely, the nonresponders showed a significant increase in activation recovery interval (mean, +22 ms±16; median, 17 ms; interquartile range, 8 to 35 ms; P<0.05). One patient in each group was on amiodarone.
  
  
  CONCLUSIONS
  In patients with heart failure, LV epicardial APD (activation recovery interval) altered during CRT. The effect on APD was opposite in patients showing a good hemodynamic response compared with nonresponders. The findings may provide an explanation for the persistent high incidence of arrhythmias in some patients with CRT and the additional mortality benefit observed in responders of CRT.
authors.affiliation: Kings College London, London, United Kingdom. zhong.chen@kcl.ac.uk
authors.forename: Zhong
authors.initials: Z
authors.lastname: Chen
authors.forename: Ben
authors.initials: B
authors.lastname: Hanson
authors.forename: Manav
authors.initials: M
authors.lastname: Sohal
authors.forename: Eva
authors.initials: E
authors.lastname: Sammut
authors.forename: Nick
authors.initials: N
authors.lastname: Child
authors.forename: Anoop
authors.initials: A
authors.lastname: Shetty
authors.forename: Ryan
authors.initials: R
authors.lastname: Boucher
authors.forename: Julian
authors.initials: J
authors.lastname: Bostock
authors.forename: Jaswinder
authors.initials: J
authors.lastname: Gill
authors.forename: Gerald
authors.initials: G
authors.lastname: Carr-White
authors.forename: C Aldo
authors.initials: CA
authors.lastname: Rinaldi
authors.forename: Peter
authors.initials: P
authors.lastname: Taggart
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000368:Aged; D001145:Arrhythmias, Cardiac / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D058406:Cardiac Resynchronization Therapy / Q000379:methods*; D004452:Echocardiography; D022062:Electrophysiologic Techniques, Cardiac / Q000379:methods*; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology*; D006801:Humans; D008297:Male; D013318:Stroke Volume / Q000502:physiology; D016896:Treatment Outcome; D020257:Ventricular Remodeling