Sympathetic Innervation Modulates Ventricular Repolarization and Arrhythmia Vulnerability After Myocardial Infarction
Abstract
Abstract Background Sympathetic modulation via the stellate ganglia is increasingly recognized as a contributor to ventricular arrhythmogenesis after myocardial infarction. However, the mechanisms by which autonomic remodeling interacts with chronic infarct substrates to shape arrhythmic vulnerability remain incompletely understood. Objectives To test the hypothesis that left- and right-sided stellate ganglion–mediated SNS modulation differentially reshapes ventricular arrhythmic vulnerability in chronic post-infarcted substrates, and that the RVI detects changes in vulnerability beyond conventional stimulation-based inducibility. Methods Fourteen patient-specific ventricular models with chronic post-infarcted remodeling were reconstructed from imaging data. A total of 336 simulations were performed under different combinations of stellate ganglion modulation, border zone remodeling, and fibroblast density. Arrhythmic vulnerability was quantified using 3D RVI mapping during paced rhythms and compared with conventional stimulation-based inducibility outcomes. Results Stellate ganglion modulation induced marked, regionally heterogeneous changes in repolarization timing, resulting in lower and more negative RVI values in vulnerable regions. More negative RVI values reflect increased propensity for wavefront–waveback interaction and reentry initiation. Across the cohort, stellate modulation consistently decreased RVI min , even when inducibility outcomes remained unchanged. These findings indicate that SNS modulation can create a substrate more permissive to reentry independently of whether ventricular arrhythmia is triggered during programmed stimulation. Conclusions Stellate ganglion–mediated sympathetic modulation dynamically reshapes ventricular arrhythmic vulnerability in chronic post-infarcted substrates. RVI provides a spatially resolved, vulnerability-based metric that complements inducibility testing by revealing autonomic–substrate interactions underlying arrhythmogenesis Condensed Abstract Sympathetic modulation via the stellate ganglia can alter ventricular repolarization and promote arrhythmogenesis after myocardial infarction, yet clinical responses remain heterogeneous. Using 14 patient-specific post-infarction ventricular models, we simulated left- and right-sided stellate modulation across combinations of border zone remodeling and fibrosis (336 simulations). Stellate modulation induced regionally heterogeneous repolarization shortening and reduced RVI values, even when programmed stimulation inducibility remained unchanged. These findings suggest that RVI captures substrate-level vulnerability beyond binary induction testing and may improve mechanistic assessment of autonomic–substrate interactions in chronic infarct substrates.
Authors 8
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Universitat Politècnica de València
Affiliation as printed
Centro de Investigación e Innovación en Bioingeniería, Universitat Politècnica de València, Valencia, Spain
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Universitat Politècnica de València
Affiliation as printed
Centro de Investigación e Innovación en Bioingeniería, Universitat Politècnica de València, Valencia, Spain
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Affiliation as printed
Arrhythmia Department, Heart Institute, Teknon Medical Center, Barcelona, Spain
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Affiliation as printed
Arrhythmia Department, Heart Institute, Teknon Medical Center, Barcelona, Spain
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Affiliation as printed
Arrhythmia Department, Heart Institute, Teknon Medical Center, Barcelona, Spain
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Leiden University Medical Center · Maastricht University Medical Centre · Maastricht University
Affiliation as printed
Department of Experimental Cardiology, Leiden University Medical Center, Leiden, Netherlands
Department of Physiology, Maastricht University Medical Center, Maastricht, The Netherlands
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Universitat Politècnica de València
Affiliation as printed
Centro de Investigación e Innovación en Bioingeniería, Universitat Politècnica de València, Valencia, Spain
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Valencian International University
Affiliation as printed
Valencian International University, Valencia, Spain
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