Abstract
The pericardial space, which contains pericardial fluid (PF), maintains homeostatic conditions that facilitates optimal heart function. The loss of PF during surgery perturbs the equilibrium of this environment, contributing to postsurgical complications, including postoperative pericardial adhesion formation (PPAF) and postoperative atrial fibrillation (POAF), both of which involve immune-mediated pathways. We have yet to fully understand the exact pathophysiology of these adverse events. This study aimed to establish the immune profile of human PF, determine whether specific markers can drive inflammatory processes, such as fibrosis, and elucidate the underlying mechanisms that can result in such phenomena.
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