Background: Post-infarction arrhythmias are modulated by sympathetic input from the stellate ganglia, with differential effects from the left and right sides. However, the benefit of left-sided or bilateral denervation remains uncertain.
Objective: We investigated how sympathetic stimulation from the left or right stellate ganglia alters reentrant arrhythmia risk in post-infarction hearts. We also evaluated the reentry vulnerability index (RVI) as a predictive marker. RVI is calculated as the difference between local repolarization time and the activation time of adjacent downstream tissue.
Methods: We developed two patient-specific ventricular models based on LGE-MRI, each with distinct infarct locations (anterior and posterior walls). Regional sympathetic stimulation was modeled by increasing IKs conductance, shortening APD in targeted areas. Activation, repolarization, and RVI maps were computed during a pacing protocol and compared to full reentry induction simulations.
Results: RVI mapping identified localized areas with highly negative values, corresponding closely to reentry initiation sites. Notably, reentrant arrhythmias were more frequently induced when sympathetic remodeling overlapped spatially with the infarct region. These findings demonstrate a strong link between regional autonomic input and arrhythmogenic substrate in post-infarction hearts.
Conclusion: RVI is a robust, non-invasive marker of reentrant vulnerability that can anticipate arrhythmogenic regions without requiring full arrhythmia induction. These results underscore the potential of RVI-guided risk stratification and support patient-specific approaches to sympathetic modulation therapy.