Comparative left ventricular function following atrial, septal, and apical single chamber heart pacing in the young.
Ventricular pacing, typically initiated from a RV apical electrode, inherently causes abnormal biventricular activation, decrease LV function, and causes histopathological changes. Since pacing initiated in childhood can be expected to have a more protracted course compared with the adult, the consequences of this alteration in LV hemodynamics gain added significance among the young pacemaker recipient. The purpose of this study was to evaluate the potential of improving paced LV function by a septal electrode implant site. Acute alterations in cardiac index, LV pressure, and contraction indices, including dP/dt, Vmax, and Vpm, were compared among 22 patients (median age 10 years) with normal cardiac anatomy during intracardiac electrophysiological studies. LV hemodynamics were measured during intrinsic rhythms and following 15 minutes of atrial, RV apical, and septal pacing at an appropriate exercise rate for age of 150 ppm. Results showed a significant decrease in LV dP/dt, Vmax, and Vpm, and increase in LV end-diastolic pressure only with apical pacing. Septal pacing, in spite of loss of any atrial contribution to ventricular filling, maintained comparable indices with intrinsic and atrial paced rhythms. This study demonstrates that normalized LV function is maintained by septal and deteriorates with apical pacing acutely among young, nonischemic hearts. Continued evaluation of appropriate pacing electrode designs to permit septal implant is needed to ensure optimal chronically paced LV function.
Karpawich
P P
PP
Section of Pediatric Cardiology, Children's Hospital of Michigan, Wayne State University, School of Medicine, Detroit 48201, USA.
Mital
S
S
D000293:Adolescent; D000328:Adult; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D004567:Electrodes, Implanted; D004594:Electrophysiology; D005260:Female; D006439:Hemodynamics; D006801:Humans; D007223:Infant; D008297:Male; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*