Inflammation and arrhythmogenesis: a narrative review of the complex relationship

Abstract

Abstract Background A biological mechanism called inflammation is necessary for reacting to damaging stimuli, but it can also, ironically, play a role in the formation of arrhythmias, or the group of disorders known as arrhythmogenesis. This review delves into the intricate relationship that exists between localized and systemic inflammation and the electrophysiological changes that result in abnormal heart rhythms. Main body Through oxidative stress, autonomic dysfunction, electrolyte imbalances, and coagulation activation, systemic inflammation may impact arrhythmogenicity. Similar to neuropathic alterations, direct cellular damage, and structural remodeling, localized heart inflammation also predisposes to arrhythmias. Studies demonstrating the impact of cytokines on ion channel expression and function, along with clinical associations between inflammatory indicators and arrhythmia incidence, offer the molecular insights. Immune cells like macrophages that alter cardiac conduction are involved in the interaction between inflammation and electrophysiology, which further complicates the situation. Clinical ramifications include the use of anti-inflammatory drugs to treat arrhythmic episodes and the possible adjustment of arrhythmia treatment based on inflammatory condition. Even yet, further thorough study is necessary to fully understand the efficacy of these medicines. Conclusions Arrhythmogenesis and inflammation are inherently linked by a number of mechanisms that change the electrical characteristics of the heart. Arrhythmia treatment and prevention may benefit from therapeutic approaches that reduce inflammatory processes. The difficulties that still exist in applying this information to clinical settings highlight the necessity of continuing studies to better comprehend the subtleties of inflammation-induced electrical alterations. Progress in identifying biomarkers of inflammation and developing tailored therapies will be crucial in enhancing the prognosis of individuals suffering from arrhythmogenic disorders that are aggravated by inflammation.