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Published on: December 11, 2017
Acute effects of single-site pacing from the left and right ventricle on ventricular function and
Mark K Friedberg1, Anne M Dubin, George F Van Hare
1Department of Pediatrics, Division of Pediatric Cardiology, Stanford University, Stanford, Calif, USA.
Insights
In children with normal heart function, pacing from the right ventricle (RV) apex, RV outflow, or left ventricle (LV) causes electrical dyssynchrony but does not significantly impact heart function or hemodynamics.
Area of Science:
- Pediatric Cardiology
- Electrophysiology
- Cardiac Physiology
Background:
- Pacing in children can affect cardiac function and ventricular interactions.
- Understanding the acute effects of different pacing sites is crucial for managing pediatric patients.
Purpose of the Study:
- To evaluate the acute effects of right ventricular (RV) apical, RV outflow, and left ventricular (LV) pacing on LV and RV function and ventricular-ventricular interactions in children with normal cardiac function.
Main Methods:
- Prospective, acute intervention study in a tertiary care electrophysiology laboratory.
- Seven children (12 +/- 4 years) underwent pacing at baseline, RV apex, RV outflow, and LV.
- Measurements included cardiac function (dP/dTmax, cardiac index), hemodynamics (blood pressure), QRS duration, and mechanical dyssynchrony via tissue Doppler imaging.
Main Results:
- Pacing significantly prolonged QRS duration, indicating electrical dyssynchrony.
- RV outflow pacing induced LV intraventricular delay, and RV apical pacing caused interventricular delay.
- No significant changes were observed in cardiac index, blood pressure, or ventricular contractility/relaxation parameters.
Conclusions:
- Single-site RV apical, RV outflow, and LV pacing in children with normal cardiac anatomy and function induce electromechanical dyssynchrony.
- These pacing strategies do not significantly alter ventricular function, hemodynamics, or adversely affect ventricular-ventricular interactions.
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/dT(max) and RV dP/dT(neg) (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/dT(max), RV dP/dT(neg), 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.
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