Autoimmunity and Biological Therapies in Cardiac Arrhythmias

Abstract

Autoimmune (AI) diseases have a notable rise globally, affecting up to 9.4% of the global population. Cardiac involvement is not unusual in AI diseases, leading to arrhythmias through many pathophysiological mechanisms like myocardial inflammation, fibrosis, and autoantibodies targeting critical cardiac structures, leading to cardiac rhythm disorders. This review focuses on the role of autoantibodies in arrhythmias in diseases like sarcoidosis, lupus, rheumatoid arthritis, scleroderma, and others, highlighting new findings about autoantibodies against critical structural myocardial components. On the other hand, the review describes the AI association with conditions such as sinus bradycardia, atrioventricular blocks, inappropriate sinus tachycardia, atrial fibrillation, ventricular tachycardia, and sudden cardiac death, describing those processes. Emerging biomarkers indicative of inflammation, fibrosis, and autoimmunity that can predict arrhythmia risk are examined. The review also explores the field of managing cardiac arrhythmias with alternative cell therapy approaches that target gene substrate as a promising way to transfer, silence, and edit cellular disorders associated with arrhythmia generation that may help treat these conditions in the future.