Pacing-induced electromechanical ventricular dyssynchrony does not acutely influence right ventricular function and global hemodynamics in children with normal hearts.
BACKGROUND
Right ventricular (RV) pacing may be detrimental to ventricular function. However, the acute effects of electromechanical dyssynchrony on RV function are not well characterized in children. We studied acute effects of electromechanical dyssynchrony, induced by RV apical and RV outflow pacing, in children with normal hearts, evaluating electromechanical synchrony, hemodynamic response, and RV function.


METHODS
Seventeen children (mean +/- SD, 12 +/- 4 years) with normal cardiac structure/function were paced after accessory pathway ablation, at baseline (AOO), and with AV pacing (DOO) from the RV apex and RV outflow. QRS duration was determined from surface ECG. Intra- and interventricular mechanical dyssynchrony and regional ventricular function were determined using tissue Doppler imaging. Global RV systolic and diastolic functions were assessed by RV dP/dT(max) and RV dP/dT(neg) using pressure-tipped transducers. Regional RV function was assessed by tissue Doppler imaging. Cardiac index (CI) and blood pressures were measured.


RESULTS
RV apical and outflow pacing induced significant electromechanical dyssynchrony manifested by lengthening of the QRS duration, increased LV intraventricular delay (49 +/- 34 ms, 53 +/- 43 ms, respectively, P < 0.001), and increased interventricular delay (60 +/- 29 ms, 55 +/- 37 ms, P < 0.0001) versus AOO pacing. However, there was no change in blood pressure, CI, RV dp/dT(max), RV dP/dT(neg), or regional tissue Doppler velocities, indicating preserved hemodynamics and preserved global and regional RV systolic and diastolic function.


CONCLUSIONS
In children with normal cardiac function and structure, pacing-induced electromechanical dyssynchrony did not acutely affect RV systolic and diastolic function and did not acutely alter global hemodynamics. Therefore, electromechanical dyssynchrony may only be an important therapeutic target in the setting of decreased RV function.
Friedberg
Mark K
MK
Division of Pediatric Cardiology, Department of Pediatrics, Stanford University, Stanford, California 94304, USA.
Dubin
Anne M
AM
Van Hare
George F
GF
McDaniel
George M
GM
Niksch
Alisa
A
Rosenthal
David N
DN
D000293:Adolescent; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D002675:Child, Preschool; D003326:Coronary Circulation; D005260:Female; D006801:Humans; D008297:Male; D009200:Myocardial Contraction; D012016:Reference Values; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*; D055815:Young Adult