Children with congenital or acquired atrioventricular block are provided with ventricular rate support from a pacing lead that traditionally is positioned at the right ventricular (RV) apex. However, RV apical pacing causes dyssynchronous electrical activation and left ventricular (LV) contraction, resulting in decreased LV function. Chronic RV apical pacing leads to deterioration of LV function and morphology, resulting in cardiac failure in approximately 7% of children. This review describes the pathophysiology of pacing-induced dyssynchronous LV activation and contraction, especially as a result of chronic RV apical pacing. Furthermore, this review provides an overview of the possible alternative pacing sites, such as the RV outflow tract, His-bundle, LV apex, and biventricular pacing.