Inflammation-Driven Arrhythmias: Bridging Immunology and Electrophysiology

Cardiac arrhythmias, including atrial fibrillation, ventricular tachycardia, and sudden cardiac death, remain a leading cause of morbidity and mortality worldwide. While traditional models of arrhythmogenesis have focused on structural remodeling and ion channel dysfunction, emerging evidence highlights the pivotal role of immune-inflammatory processes in shaping arrhythmic substrates. This review synthesizes current knowledge on the immunobiology of the heart and the mechanisms by which cytokine signaling, inflammasome activation, and immune cell-cardiomyocyte interactions promote electrical instability. Clinical data from myocarditis, autoimmune cardiomyopathies, postmyocardial infarction, and systemic inflammatory diseases provide strong evidence linking inflammation with arrhythmic outcomes. We also evaluate diagnostic strategies-including biomarkers, advanced imaging modalities, electrocardiographic phenotypes, and endomyocardial biopsy-that enable the identification of inflammatory substrates, while discussing the safety challenges of ablation, device therapy, and immunomodulation in this context. Emerging technologies such as artificial intelligence, molecular imaging, and multiomics approaches are advancing risk stratification and paving the way for precision therapies. Despite persistent gaps in specificity, standardization, and trial evidence, integrating immunology with electrophysiology offers a transformative framework for predicting, preventing, and managing inflammation-driven arrhythmias. This convergence may ultimately yield novel therapeutic targets and improve outcomes in high-risk patient populations.