Epicardial Adipose Tissue and Postoperative Atrial Fibrillation

Abstract

BackgroundAtrial fibrillation (AF) often occurs after cardiac surgery and is associated with increased risk of stroke and mortality. Prior studies support the important role of inflammation in the pathogenesis of postoperative atrial fibrillation (POAF). It is known that an increased volume and a pro-inflammatory phenotype of epicardial adipose tissue (EAT) are both associated with AF onset in non surgical context. In the present study, we aim to evaluate whether also POAF occurrence may be triggered by an increased production of inflammatory mediators from EAT.MethodsThe study population was composed of 105 patients, with no history of paroxysmal or permanent AF, undergoing elective cardiac surgery. After clinical evaluation, all patients performed an echocardiographic study including the measurement of EAT thickness. Serum samples and EAT biopsies were collected before surgery. Levels of 10 inflammatory cytokines were measured in serum and EAT conditioned media. After surgery, cardiac rhythm was monitored for 7 days.ResultsForty-four patients (41.3%) developed POAF. As regard to cardiovascular therapy, only statin use was significantly lower in POAF patients (65.1% vs. 84.7%; p-0.032). Levels of Monocyte Chemoattractant Protein-1 (MCP-1), in both serum and EAT, were significantly higher in POAF patients (130.1 pg/ml vs. 68.7 pg/ml; p = <0.001; 322.4 pg/ml vs. 153.4 pg/ml; p = 0.028 respectively). EAT levels of IL-6 were significantly increased in POAF patients compared to those in sinus rhythm (SR) (126.3 pg/ml vs. 23 pg/ml; p = <0.005).ConclusionHigher EAT levels of IL-6 and MCP-1 are significantly associated with the occurrence of POAF. Statin therapy seems to play a role in preventing POAF. These results might pave the way for a targeted use of these drugs in the perioperative period.

Radiomics signature of epicardial adipose tissue for predicting postoperative atrial fibrillation after pulmonary endarterectomy

“…In pathological contexts, EAT switches from an anti-inflammatory phenotype to a pro-inflammatory phenotype, mediated in part by the release of fatty acids and pro-inflammatory adipokines, including interleukin-1b, interleukin-6, activin-A, and tumor necrosis factor-alpha ( 33 ). These pro-inflammatory cytokines have been reported to be associated with POAF after cardiac surgery ( 15 , 16 ). To a certain extent, the EAT volume and radiodensity reflect its pathological status.…”

“…Epicardial adipose tissue (EAT) is a special visceral adipose tissue located between the myocardium and the visceral pericardium ( 14 ). It produces numerous pro-inflammatory cytokines which can promote the development of POAF ( 15 , 16 ). Quantitative analysis of EAT can be performed by cardiac computed tomography (CT).…”

The association between epicardial adipose tissue thickness and left atrial phasic function in patients with non-valvular atrial fibrillation

“…Similarly, there are no fascial boundaries between the atrium and the ventricles, thus, multiple adipose cytokines secreted by EAT around the left ventricle can reach the atrium and affect atrial fibrosis [7]. A variety of inflammatory mediators secreted by EAT are also closely related to the occurrence of AF [8]. In addition, EAT is rich in autonomic ganglion plexus, and the excitation of sympathetic and parasympathetic nerves can increase intracellular calcium concentration and shorten action potential duration, thus promoting the occurrence and development of AF [9].…”

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

“…IL-1β stimulates activin A expression ( Arai et al, 2011 ) that has been reported to be produced by epicardial adipose tissue (EAT) of patients evolving POAF after cardiac surgery ( de Kretser et al, 2012 ; Wang et al, 2019 ). We recently reported an increased inflammatory status of EAT also in POAF ( Petraglia et al, 2022 ). However, further evidence is required to confirm all these hypothetic mechanisms in order to clarify the role of EAT in cardiovascular disease and AF.…”