Molecular and Genetic Medicine

Atrial Fibrillation (AF) is the most common persistent arrhythmia with adverse clinical outcomes. AF ectopic firing and re-entry depends on several mechanisms: (1) ion channel dysfunction; (2) Ca²⁺-handling abnormalities; (3) structural remodelling; (4) autonomic neural dysregulation. The oxidized CAMKII enzyme pathway establishes a connexion between redox imbalance and the electrical and functional cardiomyocyte properties altered in AF patients. Postoperative atrial fibrillation (PoAF) is the most common complication after cardiac surgery and a subtype of AF, associated with increased time spent in the intensive care unit (ICU), in-hospital stay, stroke incidence and 30-day and long-term mortality. Recent studies have implicated oxidative stress in AF pathophysiology including mechanisms such as an imbalance in reactive oxygen species (ROS) production, decreased endothelial nitric oxide synthase (eNOS) activity and nitric oxide unavailability. Indeed, NADPH oxidase enzymes (NOX) are largely responsible for this imbalance, which is supported by the beneficial effect of statins in early atrium electrical remodelling. Epicardial adipose tissue has a direct contact with the myocardium, located between the myocardium and visceral pericardium, and it has been established a clinical relationship between EAT and the development of AF. In this review, we explore pathophysiological mechanisms of AF and POAF, as well as its implications for management.