Scar-related ventricular tachycardia (VT) is sustained by reentrant circuits within the infarcted myocardium and remains a major clinical challenge. While patient-specific computational models are widely used to investigate VT mechanisms, the effectiveness of different pacing strategies for inducing clinically relevant VT has yet to be fully characterized.
In this study, VT inducibility was investigated using five patient-specific ventricular models reconstructed from clinical imaging data. Non-infarcted myocardium was modeled using a human ventricular cell model, while infarct regions incorporated non-conductive scar tissue and gray zone regions characterized by reduced conduction velocity. Two pacing strategies were evaluated. In the baseline strategy, programmed stimulation with up to four extrastimuli (S1–S4) was applied at six left ventricular sites adjacent to the infarcted region (selected based on the American Heart Association segmentation), as well as at two right ventricular sites located at the outflow tract and apex. In the proposed strategy, pacing was performed exclusively in the right ventricle—specifically at five sites in the right ventricular outflow tract (RVOT) and three sites at the right ventricular apex—using programmed stimulation with up to five extrastimuli (S1–S5).
Both strategies successfully induced sustained scar-related VT. Notably, the proposed RV-based strategy achieved a higher inducibility rate compared to the baseline approach (67.5% [27/40] vs. 47.5% [19/40]). Furthermore, the proposed strategy induced more reentrant episodes (28 vs. 21) while yielding an identical number of clinically relevant VT morphologies (12 in both strategies).
These findings demonstrate that a simplified RV-based pacing strategy is sufficient to effectively probe arrhythmogenic substrates in patient-specific models.