2016 Volume 54Annual Issue 28AM-Abstract Pages S277
Recent experimental studies have shown that alterations in subcellular Na channel expression might be involved in Brugada syndrome (BrS). We present with a theoretical model of phase-2 reentry (P2R), which has considered to trigger lethal arrhythmias in BrS. We conducted computer simulations of AP propagation in a myofiber model, where myocytes were electrically coupled with both gap junctional mechanism and electric field mechanism, which is an interference effect between membrane potentials in the intercalated discs, and investigated relations between the spatial and subcellular expressions of Na channels and P2R. No proarrhythmic changes in the AP propagation were observed in the myofiber with the spatial heterogeneity of Na channels. However, the alteration in Na channel expression at the subcellular level as well as the spatially-heterogeneous Na channel expression could induce P2R. Alterations in Na channel expression within myocytes might be responsible for the triggering of lethal arrhythmias in BrS.
