Dataset related to the article "Epicardial Adipose Tissue-Derived IL-1β Triggers Postoperative Atrial Fibrillation"

This record contains raw data related to the article "Epicardial Adipose Tissue-Derived IL-1β Triggers Postoperative Atrial Fibrillation" <strong>Background and aims:</strong> 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)-1β, atrial remodeling, and POAF in a population of coronary artery disease (CAD) patients. <strong>Methods:</strong> We collected EAT and atrial biopsies from 40 CAD patients undergoing cardiac surgery. Serum samples and EAT-conditioned media were screened for IL-1β and IL-1ra. Atrial fibrosis was evaluated at histology. The potential role of NLRP3 inflammasome activation in promoting fibrosis was explored <em>in vitro</em> by exposing human atrial fibroblasts to IL-1β and IL-18. <strong>Results:</strong> 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-1β and IL-1ra levels between POAF and no-POAF patients. EAT-mediated IL-1β secretion and expression were significantly higher in the POAF group compared to the no-POAF group. The <em>in vitro</em> study showed that both IL-1β and IL-18 increase fibroblasts' proliferation and collagen production. Moreover, the stimulated cells perpetuated inflammation and fibrosis by producing IL-1β and transforming growth factor (TGF)-β. <strong>Conclusion:</strong> EAT could exert a relevant role both in POAF occurrence and in atrial fibrotic remodeling.本数据集收录与论文《心外膜脂肪组织来源的IL-1β诱发术后心房颤动》（Epicardial Adipose Tissue-Derived IL-1β Triggers Postoperative Atrial Fibrillation）相关的原始数据。 **背景与研究目的**：术后心房颤动（Post-operative atrial fibrillation, POAF）指术后即刻新发的心房颤动，与不良心血管事件风险升高及永久性心房颤动风险增加密切相关。目前术后心房颤动的发病机制尚未完全阐明，而心外膜脂肪组织（epicardial adipose tissue, EAT）炎症可能是其潜在的强效诱发因素。本研究旨在探讨冠状动脉疾病（coronary artery disease, CAD）患者群体中，心外膜脂肪组织分泌的白细胞介素（interleukin, IL）-1β、心房重构与术后心房颤动之间的关联。 **方法**：我们从40例行心脏手术的冠状动脉疾病患者中采集心外膜脂肪组织与心房活检标本。对血清样本及心外膜脂肪组织条件培养基中的IL-1β与IL-1ra水平进行检测。通过组织病理学方法评估心房纤维化程度。通过将人心房成纤维细胞暴露于IL-1β与IL-18中，在体外（in vitro）探究NLRP3炎症小体（NLRP3 inflammasome）活化促进纤维化的潜在作用。 **结果**：本研究中40%的患者发生了术后心房颤动。伴与不伴术后心房颤动的患者在临床及超声心动图参数（包括左心房容积与心外膜脂肪组织厚度）上均无显著差异。术后心房颤动与组织病理学检测的心房纤维化程度无显著关联。术后心房颤动组与非术后心房颤动组患者的血清IL-1β及IL-1ra水平无显著统计学差异。相较非术后心房颤动组，术后心房颤动组患者的心外膜脂肪组织IL-1β分泌水平及表达量均显著升高。体外实验结果显示，IL-1β与IL-18均可促进成纤维细胞增殖与胶原合成。此外，受刺激的成纤维细胞可通过分泌IL-1β与转化生长因子（transforming growth factor, TGF）-β进一步加剧炎症反应与纤维化进程。 **结论**：心外膜脂肪组织可能在术后心房颤动的发生及心房纤维化重构中发挥重要作用。