Postoperative Atrial Fibrillation After CABG: Inflammatory Mechanisms, Predictive Factors, and Emerging Interventions

Postoperative atrial fibrillation (POAF) is the most common arrhythmia following coronary artery bypass grafting (CABG) and is associated with increased morbidity, mortality, and reduced long-term survival. Inflammation plays a central role in POAF pathogenesis, with interleukin-6 (IL-6) acting as a key mediator of postoperative inflammatory signaling. The multifactorial pathophysiology of POAF involves atrial structural remodeling, autonomic imbalance, and electrophysiological alterations. Elevated IL-6 levels contribute to atrial fibrosis and remodeling, creating a vulnerable substrate that promotes atrial fibrillation initiation and maintenance. Atrial fibrosis represents a critical mechanistic link between inflammation and POAF development, suggesting shared proarrhythmic pathways with other forms of atrial fibrillation. Established clinical predictors of POAF include advanced age, end-stage renal disease, hypertension, obesity, and left atrial enlargement. Emerging preventive strategies, such as partial cardiac autonomic denervation, posterior pericardiotomy, and calcium chloride injection into atrial ganglionated plexi, have demonstrated significant reductions in POAF incidence without additional procedural risk. Pharmacological approaches, including prophylactic corticosteroids, may further reduce POAF rates in selected patients. Clinically, POAF is associated with increased risk of stroke, prolonged hospitalization, heart failure exacerbation, and higher short- and long-term mortality, underscoring the importance of improved risk stratification and effective preventive strategies following CABG.