INTRODUCTION:Cardiac resynchronization therapy (CRT) improves hemodynamic function, as well as reduces hospitalizations and mortality among patients with systolic dysfunction, QRS prolongation, and heart failure. The magnitude of the hemodynamic response is associated with improved outcomes, so optimization of this parameter is a goal of therapy. The purpose of this study was to evaluate the effect of left ventricular (LV) electrical delay, as assessed by the QLV interval, on the acute hemodynamic response to CRT. METHODS AND RESULTS: This study included 31 patients undergoing biventricular ICD placement. At implant, invasive LV dP/dt was measured by a micromanometer catheter during biventricular (BV) or LV only pacing. Both atrial sensing (AS) and atrial pacing (AP) modes were evaluated at 5 different AV delays, tested in randomized order. The QLV interval was measured at the LV pacing site. Compared with intrinsic rhythm, CRT increased LV dP/dtmax by 9.5 ± 8.8% with BV pacing and 10.0 ± 9.2% with LV pacing (P = 0.38) during AS. With AP, CRT increased LV dP/dtmax by 16.0 ± 10.8% and 15.3 ± 11.1%, respectively (P = 0.47). QLV was strongly correlated with the hemodynamic response in all pacing configurations. Multivariate analysis showed that with BV pacing QLV was an independent predictor of the hemodynamic response with a 1.7% increase in %LV dP/dt for every 10 milliseconds prolongation of QLV. CONCLUSIONS: LV electrical delay is a strong predictor of the acute hemodynamic response to CRT. This relationship is independent of pacing mode.
RCT Entities:
INTRODUCTION: Cardiac resynchronization therapy (CRT) improves hemodynamic function, as well as reduces hospitalizations and mortality among patients with systolic dysfunction, QRS prolongation, and heart failure. The magnitude of the hemodynamic response is associated with improved outcomes, so optimization of this parameter is a goal of therapy. The purpose of this study was to evaluate the effect of left ventricular (LV) electrical delay, as assessed by the QLV interval, on the acute hemodynamic response to CRT. METHODS AND RESULTS: This study included 31 patients undergoing biventricular ICD placement. At implant, invasive LV dP/dt was measured by a micromanometer catheter during biventricular (BV) or LV only pacing. Both atrial sensing (AS) and atrial pacing (AP) modes were evaluated at 5 different AV delays, tested in randomized order. The QLV interval was measured at the LV pacing site. Compared with intrinsic rhythm, CRT increased LV dP/dtmax by 9.5 ± 8.8% with BV pacing and 10.0 ± 9.2% with LV pacing (P = 0.38) during AS. With AP, CRT increased LV dP/dtmax by 16.0 ± 10.8% and 15.3 ± 11.1%, respectively (P = 0.47). QLV was strongly correlated with the hemodynamic response in all pacing configurations. Multivariate analysis showed that with BV pacing QLV was an independent predictor of the hemodynamic response with a 1.7% increase in %LV dP/dt for every 10 milliseconds prolongation of QLV. CONCLUSIONS: LV electrical delay is a strong predictor of the acute hemodynamic response to CRT. This relationship is independent of pacing mode.