Chained occurrences of early afterdepolarizations may create a directional triggered activity to initiate reentrant ventricular tachyarrhythmias.

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It has been believed that polymorphic ventricular tachycardia (VT) such as torsades de pointes (TdP) seen in patients with long QT syndromes is triggered by creating early afterdepolarization (EAD)-mediated triggered activity (TA). Although the mechanisms creating the TA have been studied intensively, characteristics of the arrhythmogenic (torsadogenic) substrates that link EAD developments to TA formation are still not well understood. Computer simulations of excitation propagation in a homogenous two-dimensional ventricular tissue with an anisotropic conduction property were performed to characterize torsadogenic substrates that potentially form TA. We examined how the configuration of islands (clusters) of myocytes with synchronously chained occurrence of EADs within the tissue, each EAD cluster size and stimulation from different directions impact the TA creation. The presence of EAD clusters within the tissue created local regions of cardiomyocytes maintained at a depolarized membrane potential above 0 mV due to the chained occurrence of EADs. When the local area contained a concave surface border, the TA was created depending on its curvature. We found that the distance of EAD clusters was a critical factor for the development of EAD-mediated TA and polymorphic VT in long QT syndromes, that there existed a region of the distance favorable for the development of TA and VT, and that the TA was always created along the myocardial fiber orientation regardless of stimulating directions. The chained occurrences of EADs may create a directional TA. Our findings provide deeper understandings of the cardiac arrhythmogenic substrates for preventing and treating arrhythmias.