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Border-zone (BZ) tissue, representing viable yet re-modelled myocardium surrounding infarct scars, has been strongly correlated with arrhythmogenic risk post-myocardial infarction. How the electrophysiological re-modelling in BZ tissue facilitates arrhythmogenesis, particularly of a focal origin, is currently unknown. In this study, we used computational models of human ventricular tissue to quantify spatial changes in action potential duration (APD) and effective refractory period (ERP) in the presence of electrophysiological BZ remodelling. Reductions in sodium channel conductivity to 35% increased ERP by > 30 ms relative to healthy tissue in absence of significant changes in APD due to a decrease in tissue excitability. When combined with re-modelling of re-polarising potassium currents, larger changes in ERP of > 60 ms occurred, due to concurrent increases in APD. Spatial plots of ERP along interfaces between healthy and BZ regions showed high spatial ERP gradients. Such heterogeneity may facilitate unidirectional block of nearby focal ectopic beats, providing an important focal arrhythmogenenic substrate.

Modulation of Effective Refractory Period at the Infarct Border:Zone Provides a Mechanism for Focal Arrhythmogenesis