Antonio Berruezo

Myocarditis is an important and frequently underrecognized cause of atrioventricular conduction disease and ventricular arrhythmias and may also be associated with atrial arrhythmias and sinus node dysfunction. Arrhythmic risk evolves over time as a result of the interplay between myocardial inflammation, fibrosis, and genetic predisposition. Despite its clinical relevance, guidance for the diagnosis, treatment, and follow-up of arrhythmias in myocarditis has remained limited. This consensus statement provides a structured framework for the management of arrhythmias in myocarditis and inflammatory cardiomyopathy (Infl-CMP), integrating disease phase and genetic background into clinical decision-making. It offers practical guidance across the disease spectrum, including diagnostic evaluation, therapeutic strategies, and longitudinal follow-up. The document was jointly developed by the European Heart Rhythm Association of the European Society of Cardiology (ESC) in collaboration with the Heart Failure Association of the ESC, the ESC Working Group on Myocardial & Pericardial Diseases, and the European Association of Preventive Cardiology of the ESC, together with the Heart Rhythm Society, the Asia Pacific Heart Rhythm Society, and the Latin American Heart Rhythm Society. Consensus advice is organized using a phase-aware framework distinguishing hot, hot-to-cold, and cold phases, with clinical consensus statements graded according to opinion-, observational-, or randomized trial-based evidence and supported by formal author voting. Arrhythmia management is stratified by disease phase. During active inflammation, antiarrhythmic therapy is combined with aetiology-targeted treatment or immunosuppression when indicated. In later stages, substrate-based strategies include pharmacological therapy, device implantation, or ablation. Emphasis is placed on hot-to-cold transition as an arrhythmogenic window and on risk stratification.

Myocarditis is an important and frequently underrecognized cause of atrioventricular conduction disease and ventricular arrhythmias and may also be associated with atrial arrhythmias and sinus node dysfunction. Arrhythmic risk evolves over time as a result of the interplay between myocardial inflammation, fibrosis, and genetic predisposition. Despite its clinical relevance, guidance for the diagnosis, treatment, and follow-up of arrhythmias in myocarditis has remained limited. This consensus statement provides a structured framework for the management of arrhythmias in myocarditis and inflammatory cardiomyopathy (Infl-CMP), integrating disease phase and genetic background into clinical decision-making. It offers practical guidance across the disease spectrum, including diagnostic evaluation, therapeutic strategies, and longitudinal follow-up. The document was jointly developed by the European Heart Rhythm Association of the European Society of Cardiology (ESC) in collaboration with the Heart Failure Association of the ESC, the ESC Working Group on Myocardial & Pericardial Diseases, and the European Association of Preventive Cardiology of the ESC, together with the Heart Rhythm Society, the Asia Pacific Heart Rhythm Society, and the Latin American Heart Rhythm Society. Consensus advice is organized using a phase-aware framework distinguishing hot, hot-to-cold, and cold phases, with clinical consensus statements graded according to opinion-, observational-, or randomized trial-based evidence and supported by formal author voting. Arrhythmia management is stratified by disease phase. During active inflammation, antiarrhythmic therapy is combined with aetiology-targeted treatment or immunosuppression when indicated. In later stages, substrate-based strategies include pharmacological therapy, device implantation, or ablation. Emphasis is placed on hot-to-cold transition as an arrhythmogenic window and on risk stratification.

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 postinfarcted 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 RVImin, 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