PT  - JOURNAL ARTICLE
AU  - T V Salukhe
AU  - K Dimopoulos
AU  - R Sutton
AU  - P Poole-Wilson
AU  - M Y Henein
AU  - M Morgan
AU  - J R Clague
AU  - D P Francis
TI  - Instantaneous effects of resynchronisation therapy on exercise performance in heart failure patients: the mechanistic role and predictive power of total isovolumic time
AID  - 10.1136/hrt.2006.099218
DP  - 2008 Jan 01
TA  - Heart
PG  - 59--64
VI  - 94
IP  - 1
4099  - http://heart.bmj.com/content/94/1/59.short
4100  - http://heart.bmj.com/content/94/1/59.full
SO  - Heart2008 Jan 01; 94
AB  - 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.