Abstract

Autoimmune diseases substantially increase the risk of atrial and ventricular arrhythmias and sudden cardiac death through shared immune-mediated mechanisms. Pro-inflammatory cytokines, autoantibodies, and progressive myocardial fibrosis disrupt ion channel function, impair conduction, and create re-entrant substrates. Across systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and systemic sclerosis (SSc), these pathways manifest as atrial fibrillation, ventricular arrhythmias, conduction disease, and heightened arrhythmic mortality. Anti Ro/SSA antibodies, in particular, contribute to QT prolongation and atrioventricular (AV) block, while cytokines such as TNF α, IL 1β, and IL 6 remodel electrophysiological properties and promote fibrosis. Advanced cardiac imaging, especially cardiac magnetic resonance (CMR), detects inflammation and fibrosis even when ejection fraction is preserved, enabling earlier intervention. Management requires a dual approach: standard arrhythmia therapies alongside aggressive control of systemic inflammation with disease-specific immunosuppression. Despite growing evidence, major gaps remain, including the absence of randomized trials targeting immune-driven arrhythmias and the need for integrated risk models incorporating inflammatory biomarkers.

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