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Heart failure and cardiomyopathy
Instantaneous effects of resynchronisation therapy on exercise performance in heart failure patients: the mechanistic role and predictive power of total isovolumic time
  1. T V Salukhe1,2,
  2. K Dimopoulos1,2,
  3. R Sutton1,2,
  4. P Poole-Wilson1,2,
  5. M Y Henein1,2,
  6. M Morgan2,
  7. J R Clague2,
  8. D P Francis3
  1. 1
    National Heart and Lung Institute, Imperial College, London, UK
  2. 2
    Royal Brompton Hospital, London, UK
  3. 3
    International Centre for Circulatory Health, St. Mary’s Hospital, London, UK
  1. Dr T V Salukhe, National Heart Lung Institute, Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK; t.salukhe{at}


Background: Cardiac resynchronisation therapy improves peak oxygen uptake (peak VO2) 3–9 months after device implantation. In chronic heart failure, total isovolumic time (t-IVT) is a major determinant of peak VO2 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.

Methods and 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 VO2 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 VO2 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 VO2. 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 VO2, 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 VO2.

  • resynchronisation
  • exercise performance
  • stress echocardiography
  • total isovolumic time

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  • Competing interests: None.

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