title: Instantaneous effects of resynchronisation therapy on exercise performance in heart failure patients: the mechanistic role and predictive power of total isovolumic time.
abstract: BACKGROUND
  Cardiac resynchronisation therapy improves peak oxygen uptake (peak VO(2)) 3-9 months after device implantation. In chronic heart failure, total isovolumic time (t-IVT) is a major determinant of peak VO(2) and of cardiac output at peak dobutamine stress. In selected patients, resynchronisation can instantaneously shorten t-IVT. We sought to determine the acute effect of resynchronisation on exercise performance and determine, with pharmacological stress echocardiography, the mechanism underlying this effect.
  
  
  RESULTS
  Twenty-two patients with resynchronisation were studied within 3 months after device implantation. On a single study day, sequential cardiopulmonary exercise tests were performed during native activation (left bundle branch block) and resynchronisation (atrio-biventricular pacing) in random order. Total-IVT and cardiac output (at rest and peak dobutamine stress) were then measured in each activation mode. Resynchronisation acutely increased peak VO(2) by 1.6 (SD 1.5) ml/kg/min (p<0.001) and shortened peak stress t-IVT by 10 (SD 7) s/min (p<0.001), with the effects in individual patients showing a correlation (r = -0.46, p<0.05). Amongst all measurements during native activation, the best predictor of gain in peak VO(2) from resynchronisation was peak stress t-IVT (r = 0.71, p<0.001) with every increment of 5 s/min of peak stress t-IVT during native activation predicting an 8% gain in peak VO(2). No conventional measures during native activation at rest or on stress (including QRS duration, Tei index, tissue Doppler intraventricular delay, and resting t-IVT) added significant additional information.
  
  
  CONCLUSIONS
  In eligible patients, resynchronisation can acutely augment peak VO(2), possibly through a mechanism of t-IVT shortening. Under native activation, long t-IVT during peak stress is the single best predictor of acute resynchronisation-mediated increment in peak VO(2).
authors.affiliation: National Heart and Lung Institute, Imperial College, London, UK. t.salukhe@imperial.ac.uk
authors.forename: T V
authors.initials: TV
authors.lastname: Salukhe
authors.forename: K
authors.initials: K
authors.lastname: Dimopoulos
authors.forename: R
authors.initials: R
authors.lastname: Sutton
authors.forename: P
authors.initials: P
authors.lastname: Poole-Wilson
authors.forename: M Y
authors.initials: MY
authors.lastname: Henein
authors.forename: M
authors.initials: M
authors.lastname: Morgan
authors.forename: J R
authors.initials: JR
authors.lastname: Clague
authors.forename: D P
authors.initials: DP
authors.lastname: Francis
mesh_terms: D000368:Aged; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D002306:Cardiac Volume / Q000502:physiology*; D025401:Echocardiography, Stress / Q000379:methods; D005080:Exercise Test / Q000379:methods; D017079:Exercise Tolerance; D005260:Female; D006333:Heart Failure / Q000628:therapy*; D006801:Humans; D008297:Male; D010101:Oxygen Consumption / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology