Background and aims: Post-operative atrial fibrillation (POAF), defined as new-onset AF in the immediate period after surgery, is associated with poor adverse cardiovascular events and a higher risk of permanent AF. Mechanisms leading to POAF are not completely understood and epicardial adipose tissue (EAT) inflammation could be a potent trigger. Here, we aim at exploring the link between EAT-secreted interleukin (IL)-1 beta, atrial remodeling, and POAF in a population of coronary artery disease (CAD) patients.Methods: We collected EAT and atrial biopsies from 40 CAD patients undergoing cardiac surgery. Serum samples and EAT-conditioned media were screened for IL-1 beta and IL-1ra. Atrial fibrosis was evaluated at histology. The potential role of NLRP3 inflammasome activation in promoting fibrosis was explored in vitro by exposing human atrial fibroblasts to IL-1 beta and IL-18.Results: 40% of patients developed POAF. Patients with and without POAF were homogeneous for clinical and echocardiographic parameters, including left atrial volume and EAT thickness. POAF was not associated with atrial fibrosis at histology. No significant difference was observed in serum IL-1 beta and IL-1ra levels between POAF and no-POAF patients. EAT-mediated IL-1 beta secretion and expression were significantly higher in the POAF group compared to the no-POAF group. The in vitro study showed that both IL-1 beta and IL-18 increase fibroblasts' proliferation and collagen production. Moreover, the stimulated cells perpetuated inflammation and fibrosis by producing IL-1 beta and transforming growth factor (TGF)-beta.Conclusion: EAT could exert a relevant role both in POAF occurrence and in atrial fibrotic remodeling.

Epicardial Adipose Tissue-Derived IL-1β Triggers Postoperative Atrial Fibrillation / S. Cabaro, M. Conte, D. Moschetta, L. Petraglia, V. Valerio, S. Romano, M.F. Di Tolla, P. Campana, G. Comentale, E. Pilato, V. D’Esposito, A. Di Mauro, M. Cantile, P. Poggio, V. Parisi, D. Leosco, P. Formisano. - In: FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY. - ISSN 2296-634X. - 10:(2022 May 05), pp. 893729.1-893729.9. [10.3389/fcell.2022.893729]

Epicardial Adipose Tissue-Derived IL-1β Triggers Postoperative Atrial Fibrillation

D. Moschetta;P. Poggio
;
2022

Abstract

Background and aims: Post-operative atrial fibrillation (POAF), defined as new-onset AF in the immediate period after surgery, is associated with poor adverse cardiovascular events and a higher risk of permanent AF. Mechanisms leading to POAF are not completely understood and epicardial adipose tissue (EAT) inflammation could be a potent trigger. Here, we aim at exploring the link between EAT-secreted interleukin (IL)-1 beta, atrial remodeling, and POAF in a population of coronary artery disease (CAD) patients.Methods: We collected EAT and atrial biopsies from 40 CAD patients undergoing cardiac surgery. Serum samples and EAT-conditioned media were screened for IL-1 beta and IL-1ra. Atrial fibrosis was evaluated at histology. The potential role of NLRP3 inflammasome activation in promoting fibrosis was explored in vitro by exposing human atrial fibroblasts to IL-1 beta and IL-18.Results: 40% of patients developed POAF. Patients with and without POAF were homogeneous for clinical and echocardiographic parameters, including left atrial volume and EAT thickness. POAF was not associated with atrial fibrosis at histology. No significant difference was observed in serum IL-1 beta and IL-1ra levels between POAF and no-POAF patients. EAT-mediated IL-1 beta secretion and expression were significantly higher in the POAF group compared to the no-POAF group. The in vitro study showed that both IL-1 beta and IL-18 increase fibroblasts' proliferation and collagen production. Moreover, the stimulated cells perpetuated inflammation and fibrosis by producing IL-1 beta and transforming growth factor (TGF)-beta.Conclusion: EAT could exert a relevant role both in POAF occurrence and in atrial fibrotic remodeling.
atrial fibrillation; cardiac remodeling; cytokines; epicardial adipose tissue; fibrosis; inflammation;
Settore MED/50 - Scienze Tecniche Mediche Applicate
5-mag-2022
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/1029791
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