Inflammatory pathways in atrial fibrillation: mechanisms and novel therapeutic targets

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, and inflammation has been suggested as a predisposing factor for AF. Systemic inflammatory disorders (including autoimmune disorder, diabetes mellitus, and obesity) or local inflammation of the heart or pericardium are linked to AF. Inflammation is known to trigger various signalling pathways and to directly influence proinflammatory cytokines, in turn promoting structural and electrical changes in the atria, increasing the susceptibility to AF. Inflammation induces oxidative stress and an imbalance in the autonomic nervous system, and enhances atrial or pulmonary vein arrhythmogenesis by modulating electrophysiological characteristics and fibrogenesis. This review explores the complex pathophysiological processes linking inflammation to AF and identifies potential novel therapeutic targets.