Prolongation of action potential duration by class III antiarrhythmic agents increases the risk of early afterdepolarization (EAD) developments, which in turn increases the risk of developing ventricular tachycardia (VT) such as torsades de pointes, and/or ventricular fibrillation. Recently, our group has reported that the concave shape (in the localized region) of repolarization potential difference boundary due to EAD clustering occurrence within the tissue may be involved in the triggered activity formation that initiates VT. In the present study, we further investigated how anisotropy of excitation propagation in the ventricle contributes to the triggered activity formation. Simulating excitation propagation in a two-dimensional (2D) ventricular tissue model in which a cardiac rapidly activating delayed rectifier K⁺ channel current (I_Kr) was inhibited by 87% of control by class III antiarrhythmic agents, we examined whether the EAD-induced triggered activity was formed when one side of the 2D tissue was stimulated in the parallel or transverse direction to fiber orientation. By stimulation in the direction parallel to fiber orientation, the EAD-induced triggered activity was formed along the fiber orientation by parallel placing of two EAD clusters of appropriate size at appropriate distances along the fiber orientation. Under the same EAD cluster configuration, even with perpendicular stimulation to the myocardial fiber orientation, triggered activity was formed along the fiber direction. However, triggered activity did not occur when EAD clusters were placed perpendicular to the fiber direction. We concluded that there exists a certain directionality in the triggered activity formation following EAD development. The triggered activity as the initiator of lethal arrhythmias caused by proarrhythmic properties of class III antiarrhythmic agents may exhibit anisotropy-based directionality within the ventricle.