**7. Mechanisms of arrhythmias**

Two theories suggest that an abnormal repolarization (local re-excitation by phase 2 reentry in the epicardium) or a defect of the depolarization (disturbances in depolarization of RVOT can cause conduction delay) may be responsible of phenotype and VF in BrS [40–43]. However, in BrS the arrhythmias are usually polymorphic VT or VF, and these cannot be supported by macro-reentry mechanisms. VF depends of a firing focus initiated by early or delayed afterdepolarization or a micro-re-entry [44]. Surviving cells surrounded by fibrosis has demonstrated to be responsible of slow conduction and reentry in inhomogeneous scars [45]. The residual electrical activity within scar was reported as delayed or isolated EGMs, late potentials or diastolic EGMs and their elimination during sinus rhythm was effective to prevent VT/VF [45]. In peripheral zone of substrate when a sufficient degree of cell damage was reached such as we found with TEM and resting potentials are reduced the polymorphic VT/VF may occur. This event could be originated through a firing focus or by multiple wavelets from a reentrant microcircuit, and would explain the "diastolic electrical activity" observed in our patients.

In addition, we found pre-systolic potentials as was previously reported by Haissaguerre et al. [15]. As show **Figure 8**, the Purkinje fibers in RVOT could be involved in the origin of pre-systolic potentials and in genesis of early-onset PVCs that can trigger VT or VF, by spontaneous depolarization or micro-reentry circuit in the Purkinje network [30].
