Computer simulations using 14 patient-specific heart models revealed that stellate ganglion modulation—stimulation of key sympathetic nerve clusters—dramatically alters electrical repolarization patterns in hearts damaged by myocardial infarction. The research identified that this autonomic nervous system intervention creates regionally heterogeneous changes that can either increase or decrease arrhythmia vulnerability, with effects detectable through a novel metric called RVI (repolarization vulnerability index) even when conventional testing shows no change. This finding has significant implications for cardiac care, as stellate ganglion modulation is already used clinically to treat life-threatening arrhythmias in post-heart attack patients, yet responses vary widely between individuals. The computational approach offers a potential pathway to predict which patients might benefit most from this intervention, moving beyond the current trial-and-error approach. However, this is a preprint study awaiting peer review, and the findings are based on computer models rather than direct human testing. While the research provides valuable mechanistic insights into how the nervous system influences heart rhythm disorders, clinical validation will be essential to translate these computational predictions into improved patient outcomes.