Background Cardiac resynchronization 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, resynchronizaion can instantaneously shorten t-IVT. We sought to determine the acute effect of resynchronization on exercise performance and determine, with pharmacological stress echocardiography, the mechanism underlying this effect.
Methods and Results Twenty two patients with resynchronization 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 resynchronization (atrio-biventricular pacing) in random order. Total-IVT and cardiac output (at rest and peak dobutamine stress) were then measured in each activation mode. Resynchronization acutely increased peak VO2 by 1.6 ± 1.5 ml/kg/min (p<0.001) and shortened peak stress t-IVT by 10 ± 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 resynchronization 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, resynchronization 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 resynchronization-mediated increment in peak VO2.
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