Repolarization Gradients Alter Post-infarct Ventricular Tachycardia Dynamics in Patient-Specific Computational Heart Models

Abstract

Repolarization heterogeneity contributes to ventricular tachycardia (VT) arrhythmogenesis but the impact of repolarization gradients on post-infarct VT dynamics is not well-characterized. The goal of our study is to assess the effects of repolarization gradients on post-infarct VT dynamics using patient-specific heart models. Baseline models were reconstructed along with the patient-specific scar and infarct border zone from imaging. Models with action potential duration (APD) gradients along apicobasal (AB) and transmural (TM) axes were also reconstructed. Rapid pacing was used to induce VTs. The resultant VT dynamics (inducibility, re-entry pathway, and the exit site) were assessed. Repolarization gradients did not impact VT inducibility but did alter both the reentry pathway and exit site location due to modulations in unidirectional conduction block. Both AB and TM APD gradients alone were also sufficient for inducing these changes in VT dynamics. Lastly, APD gradients revealed multiple distinct morphologies that used similar conducting channels in the patient-specific substrate. These results highlight how the interplay between repolarization gradients and the patient-specific substrate can have consequences on post-infarct VT dynamics.