Arrhythmogenic mechanisms in myocarditis are driven by acute inflammation, ion channel alterations, and structural remodeling, requiring individualized therapeutic strategies for arrhythmia management.
Patients with myocarditis
Arrhythmia management strategies
This review summarizes the molecular mechanisms driving arrhythmias in myocarditis and highlights updated, individualized therapeutic strategies.
Myocarditis is an underdiagnosed inflammatory condition ofthe myocardium that may lead to significant complications, including life-threatening ventricular arrhythmias and sudden cardiac death, particularly in young individuals. The arrhythmogenic substrate evolves dynamically across the disease course, driven by acute inflammation, ion channel alterations, immune-mediated cytotoxicity and negative structural remodelling. Persistent myocardial inflammation and fibrosis promote conduction abnormalities, triggered activity and re-entrant circuits, creating a pro-arrhythmic milieu. Despite increasing recognition of its clinical relevance, arrhythmias management in myocarditis remains challenging due to the variability in patient presentation and disease trajectory. This review examines arrhythmogenic mechanisms associated with myocarditis, exploring differential contribution of the above-reported triggers to concurrent electrical instability. Updated therapeutic approaches to managing arrhythmias in myocarditis are discussed, with emphasis on the importance of individualised treatment plans. A deeper understanding of the complex interplay between inflammation and arrhythmias may improve clinical decision-making, and help tailor individualised management strategies for affected patients.
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Curcio et al. (Mon,) conducted a review in Myocarditis and associated arrhythmias. Arrhythmogenic mechanisms in myocarditis are driven by acute inflammation, ion channel alterations, and structural remodeling, requiring individualized therapeutic strategies for arrhythmia management.
synapsesocial.com/papers/6a0ef364a14f152feafa100b — DOI: https://doi.org/10.15420/ecr.2025.52
Antonio Curcio
Electrophysiology
Letizia Rosa Romano
Ospedale Annunziata di Cosenza
Claudia Rocca
University of Calabria
European Cardiology Review
University of Calabria
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