Cardiac and pericardial inflammatory changes and post-cardiac surgery atrial fibrillation

Postoperative atrial fibrillation (POAF) is one of the most common complications after cardiac surgery with an estimated incidence of up to 20-55 % of patients. POAF is associated with higher morbidity, prolonged hospital stays, and increased healthcare costs. The underlying mechanism of POAF is multifactorial, with evolving evidence supporting the central role of atrial muscle fibrosis and localized intrapericardial inflammation in the pathogenesis of this condition. In patients with atrial fibrillation, it was found that fibrosis of the atrial muscle can lead to the disruption of the structural and electrical properties, thus promoting the process of arrhythmogenesis. Perioperative stressors, such as tissue trauma and oxidative stress, can further exacerbate the development of inflammation and atrial fibrosis. Key intrapericardial inflammatory markers, including interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), were found to be significantly elevated in patients undergoing cardiac surgery. These cytokines accumulate in the pericardial space, triggering a localized inflammatory cascade, that can promote adverse atrial remodeling. The interaction between pre-existing fibrotic changes in the atrial muscle and the inflammatory environment induced by perioperative stressors plays a crucial role in the pathogenesis of POAF. By targeting these inflammatory pathways within the pericardial cavity, future therapeutic strategies can potentially reduce the incidence of POAF thus improving patient outcomes. The aim of this review is to consolidate the current evidence on the local inflammatory changes that occur at the cardiac and pericardial compartments and their role in the development of POAF.