Objective. We studied, as a physiological benchmark, acute effects of right ventricular (RV) apical, RV outflow, and left ventricular (LV) pacing in children with normal cardiac function on LV and RV function and ventricular-ventricular interactions. Design. The design of the study was a prospective, acute intervention. Setting. The study was conducted in a tertiary care electrophysiology laboratory. Population and Methods. Seven children (mean ± SD, 12 ± 4 years) were paced after accessory pathway ablation, at baseline (AOO), and with atrioventricular pacing (DOO) from the RV apex, RV outflow, and left ventricle. Outcome Measures. Right ventricular dP/dTmax and RV dP/dTneg (high-fidelity transducer-tipped catheters, Millar Instruments, Houston, TX, USA), cardiac index (Fick), blood pressure, and QRS duration were measured at each pacing condition. Intra- and interventricular mechanical dyssynchrony, systolic- and diastolic peak tissue velocities, and isovolumic acceleration were recorded by tissue Doppler imaging at the lateral mitral, septal, and tricuspid annuli at each condition. Results at each pacing condition were compared by repeated-measures analysis of variance. Results. Pacing prolonged QRS duration, causing electrical dyssynchrony (86 ± 19 ms [baseline], 141 ± 44 ms [RV apex], 121 ± 18 ms [RV outflow], and 136 ± 34 ms [LV], P < .01). Right ventricular outflow pacing caused LV intraventricular delay (63 ± 52 vs. 12 ± 7 ms, P < .05). Right ventricular apical pacing caused interventricular delay (61 ± 29 vs. 25 ± 18 ms, P < .05). There were no significant changes in blood pressure, cardiac index, RV dp/dTmax, RV dP/dTneg, regional tissue velocities, or isovolumic acceleration during any of the pacing conditions, indicating preserved ventricular function and hemodynamics. No important ventricular-ventricular interactions were seen. Conclusions. In children with normal cardiac anatomy and function, single-site RV apical, RV outflow, and LV pacing induce electromechanical dyssynchrony without significantly changing ventricular function or hemodynamics, or adversely affecting ventricular-ventricular interactions.
- Ventricular function
- Ventricular-ventricular interactions