Postoperative atrial fibrillation following coronary artery bypass grafting surgery: role of IL-6 from structural to electrical remodeling

Abstract

Postoperative atrial fibrillation (POAF) is a common complication of coronary artery bypass grafting (CABG) surgery, and contributes significantly to morbidity, mortality, and rising healthcare costs. Although the underlying mechanisms for POAF are not completely understood, surgery-related inflammation, often in the presence of pre-existing factors, renders the atria susceptible to the induction and persistence of POAF. Notably, interleukin-6 (IL-6), a primary cytokine of the inflammatory cascade, has been identified as one of the principal molecular components of POAF pathogenesis. Atrial fibrosis may also be a key mechanistic link by which inflammation contributes to POAF. Recently, it has been shown that atrial fibrosis, in combination with the presence of an electrophysiological substrate capable of maintaining atrial fibrillation (AF), also promotes arrhythmia, suggesting that POAF shares proarrhythmic mechanisms with other types of AF. In this review, the impact of inflammation and the particular role of IL-6, on the structural and electrical changes that promote to the development of POAF is summarized.