Inflammatory cytokines and cardiac arrhythmias: from pathogenesis to potential therapies

Abstract

Cardiac arrhythmias, including atrial fibrillation and ventricular arrhythmias, are significant contributors to cardiovascular morbidity and mortality. Recent research has highlighted the critical role of inflammation in the pathogenesis of these arrhythmias, with inflammatory cytokines acting as key mediators. Cytokines such as interleukin-1, interleukin-6, tumor necrosis factor-alpha, and interleukin-17 are involved in promoting myocardial fibrosis, ion channel dysfunction, and autonomic dysregulation, which contribute to arrhythmic events. This review explores the relationship between inflammatory cytokines and cardiac arrhythmias, focusing on their molecular mechanisms, impact on heart tissue remodeling, and the role they play in arrhythmogenesis. Cytokine-induced inflammation leads to electrical and structural changes in the myocardium, which predispose the heart to arrhythmias. Elevated levels of pro-inflammatory cytokines can cause fibrosis, alter ion channel activity, and impair the normal conduction of electrical impulses. Additionally, cytokines enhance autonomic dysfunction, further increasing the risk of arrhythmia development. These findings underscore the significance of inflammation in the onset and progression of cardiac arrhythmias, particularly in conditions such as heart failure and atrial fibrillation, where persistent inflammation is prevalent.

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