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A computer model that represents the connection of a Purkinje fiber to a two-dimensional ventricular muscle tissue is used to study the ionic mechanism responsible for the development of phase 3 early after depolarizations (EADs) in Purkinje fibers, and their propagation to ventricular muscle cells as ectopic beats. The conditions that favor EAD generation (EAD conditions) are only applied to Purkinje cells. The electrical behavior of these cells is described using the DiFrancesco-Noble equations and EAD conditions are simulated multiplying the fast second inward current of the model, iCa.s, by 1.7 (70% iCa,s enhancement) and the delayed K+ current, iK, by 0.3 (70% iK blockade). For these conditions, a single phase 3 EAD developed in the Purkinje fiber propagates to the ventricular muscle tissue generating an ectopic beat. In our simulations, the ionic mechanism underlying phase 3 EAD development is the reactivation of the fast sodium current in Purkinje cells near the Purkinje-ventricular junction. The reactivation of this current is due to greater h-gate values reached as a result of a decrease in the rate of repolarization induced by EAD conditions. The propagation of these phase 3 EADs to the ventricular muscle tissue may trigger some ventricular arrhythmias.