Sonodynamic Therapy Attenuates TLR4/NF-κB Signaling in Epicardial Adipose Tissue of Atrial Fibrillation: Insights from Animal Models, scRNA-seq, and Mendelian Randomization.

BackgroundAlthough an increased epicardial adipose tissue (EAT) volume around the left atrium (LA) is related to the atrial fibrillation (AF) burden, the role of EAT inflammation in AF is unclear. We investigated the association between AF and inflammation of the EAT around the LA. MethodsWe retrospectively identified regions of EAT around the LA and measured the density of these areas using computed tomography (CT). ResultsA total of 32 patients who underwent their first catheter ablation for paroxysmal AF (PAF) were enrolled (mean age 62.5±11.1 years). Patients without a history of AF (n=32), but who underwent cardiac CT and were matched by age, sex, and metabolic risk factors, were enrolled in the control group (62.2±12.1 years). The mean EAT density around the LA was significantly higher in the PAF group than in the control group (−108.1±6.7 vs. −111.6±5.5 Hounsfield units; p=0.02), while the densities of subcutaneous adipose tissue (SAT) in the abdomen and thorax did not differ between the two groups. In a multiple logistic regression analysis, a higher EAT density was significantly associated with the presence of PAF after adjusting for other risk factors (odds ratio: 1.25; 95% confidence interval: 1.08–1.45, p=0.003). ConclusionsThis study supports the hypothesis that inflammation of EAT around the LA, but not SAT, is related to the presence of PAF.

Background The association between epicardial adipose tissue (EAT) and atrial fibrillation (AF) was already described by several authors. In fact, botulinum toxin injection in this tissue reduces new-onset AF after open-heart surgery. Our previous results showed an elevation of adiposity in epicardial stromal vascular cells (SVC), assessed by the higher levels of fatty acid-binding protein 4 (FABP4) in AF patients; and a higher lipid accumulation in these cells after chronic acetylcholine treatment. We wanted to identify the proteins released from EAT SVC in presence/absence of mature adipocytes, that could be exerting a paracrine effect over the myocardium. The identification of these proteins might shed light on possible triggers in epicardial SVC and the mechanisms underlying botulinum toxin benefits on AF. Material and methods Proteomic studies were performed in 32 samples from 8 patients undergoing open-heart surgery (4 with and 4 without AF). Epicardial SVC were isolated by collagenase digestion and cultured in M199 medium. Then, cells were induced or not to adipocyte differentiation. After this intervention, cells were treated or not with acetylcholine (10uM) for 30 min. Conditioned medium was stored until be used. Differential released proteins were identified by nano-high performance liquid chromatography (HPLC) and Triple-Time of flying (TOF) analysis, and quantified by SWATH-Ms proteomics anaylisis. Results The quantitative proteomic approach has identified 111 common proteins in EAT SVC from patients with and without AF. A 79,3% of the genes which encoded the proteins identified were citoplasmic. A 78,4% were classified as components of the cellular exosomes, followed by genes related with centrosome (37,1%), nucleosome (15,5%), lysosomes (40,5%) and nucleolus (37,1%). Acute cholinergic treatment with ACh at 10 uM decreased α-defensin 3 (DEFA3, ID: 59666; p-value = 0,0297) secretion from EAT SVC of AF patients in comparison with EAT SVC from non-AF patients. In the same line, Peptidyl-prolyl cis-trans isomerase A (PPIA, ID: P62937) showed a lower secretion from SVC of AF patients (p=0,0326). After adipogenesis-induction, adipocyte presence modified the protein secretion under ACh treatment: Differences between AF and non-AF patients lied on 2 different proteins: profilin 1 (PFN1, ID: P07737, p-value = 0,0286) and β-enolase (ENO3, ID: P13929, p-value = 0,0414), showing a higher and lower secretion in AF patients regarding non-AF patients, respectively. Conclusions EAT SVC showed a differential protein secretion according adipocyte and AF presence. Although further studies are needed, the proteins differentially secreted in EAT SVC are related to inflammation (DEFA3), structure (PFN1) and glucose metabolism (ENO3), pointing the pathways that could be modified in AF patients. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Plan Estatal de I+D+I 2016-2020 and ISCIII-Subdirecciόn General de Evaluaciόn y Fomento de la Investigaciόn el Fondo Europeo de Desarrollo Regional (FEDER) Figure 1. Common proteins secreted from EAT SVCFigure 2. Differentially secreted proteins in AF

Background Fluoine-18-fluorodeoxyglucose-positron emission tomography/computed tomography (FDG-PET/CT) is a useful modality of inflammatory disease. Epicardial adipose tissue (EAT) contains abundant ganglionated plexi, therefore EAT inflammation may cause atrial arrhythmia, such as atrial premature contraction (APC) and atrial fibrillation (AF). Previous studies have shown that inflammatory activity of EAT has relation to the presence of AF. However, it is unknown whether EAT inflammation contributes to the occurrence of AF. Methods Out of 20720 examinees who underwent FDG-PET/CT for screening of cancer in the years 2012–2018, 151 (aged 65.6±12.0 years old, 62 females) had ambulatory electrocardiographic monitoring (Holter ECG) within a year and non-detection of AF. Standardized uptake value (SUV) was measured in fat adjacent to roof of left atrium (ROOF), atrioventricular groove (AV), left main coronary artery (LMT), and right ventricular blood pool (RV). In order to correct for blood pool activity, SUV of ROOF, AV, and LMT were divided by SUV of RV respectively, yielding target-to-background ratio (TBR). As regards to arterial inflammation, measurements were performed with SUV in ascending aorta (A-Ao) and in superior vena cava (SVC) as blood pool. In the same way, SUV of A-Ao was divided by SUV of SVC, yielding TBR. Results According to Holter ECG, APC≥100 beats per day was seen in 60 patients (Group A), but not in the other 91 (Group B). In Group A, TBR of ROOF, AV, and LMT were all significantly higher than Group B (p<0.001, p=0.004, and p=0.008, respectively). During a median follow-up of 179 days, new-onset AF was diagnosed in 7 patients (4 in Group A (6.7%), 3 in Group B (3.3%), p=0.046). There was significant difference in TBR of ROOF between patients with and without new-onset AF (p<0.001), but not in TBR of AV and LMT. In addition, no significant difference was observed in TBR of A-Ao between these two groups. In the Cox proportional hazard analysis, TBR of ROOF was found to be an independent predictor of new-onset AF (odds ratio 40.1, 95% confidence interval 6.05 to 265.9, p<0.001). Conclusions Although EAT inflammation evaluated by SUV is related to frequent APCs, only in fat adjacent to roof of left atrium is associated with and predicts future occurrence of AF. Arterial inflammation measured by SUV has no relation to atrial arrhythmia.

Background Atrial fibrillation (AF) is linked to increased epicardial adipose tissue (EAT) and inflammation, impacting atrial structure and function. Cardiac computed tomography (CCT) enables assessment of EAT volume and the fat attenuation index (FAI), a marker of coronary inflammation. Combined with the Coronary Artery Disease–Reporting and Data System (CAD-RADS) classification, these imaging markers may support risk stratification in AF. Purpose This study aimed to determine whether increased volumes of EAT compartments around the atria are associated with AF. A secondary objective was to explore the relationship between CAD-RADS classification and FAI scores, as assessed using the AI-driven CaRi-Heart® and syngo.via Frontier® platform. Methods This retrospective study included patients with and without AF, presenting with chest pain and a low-to-intermediate likelihood of CAD, all of whom underwent CCT. Volumes of EAT compartments—including total EAT, left atrial EAT (LA-EAT), and biatrial EAT (BA-EAT)—were measured, alongside CAD-RADS classification and FAI values for the three major epicardial coronary arteries. Results The study included 122 participants (mean age: 63.62 ± 7.75 years; 75 males), divided into AF and non-AF groups matched for age, sex, and risk factors. As expected, AF patients had significantly higher EAT volumes (total EAT: 231.8 ± 45.85 vs. 153.2 ± 54.14 mL, p < 0.0001; LA-EAT: 23.55 ± 6.44 vs. 15.54 ± 8.49 mL, p < 0.0001; BA-EAT: 50.24 ± 12.69 vs. 39.84 ± 15.70 mL, p = 0.0002). ROC analysis demonstrated strong diagnostic value for all EAT parameters in detecting AF: total EAT showed the highest performance (AUC = 0.869, 95% CI: 0.79–0.92), followed by LA-EAT (AUC = 0.776, 95% CI: 0.69–0.84) and BA-EAT (AUC = 0.703, 95% CI: 0.61–0.78), all statistically significant (p < 0.0001) with good sensitivity and specificity. AF patients had a higher, though not statistically significant, prevalence of advanced CAD-RADS categories (2–3: 40.5% vs. 31.3%, p = 0.323; 4–5: 33.3% vs. 21.3%, p = 0.189), while CAD-RADS 0–1 was significantly more common in non-AF individuals (47.8% vs. 26.2%, p = 0.032). The total FAI score was higher in the AF group (14.83 ± 10.16 vs. 12.37 ± 7.89, p = 0.0447), though per-vessel differences were not significant. FAI Score Centile analysis revealed a higher inflammatory burden in AF, with more very high percentiles (33.3% vs. 13.8%, p = 0.0172) and fewer minimal values (9.5% vs. 31.3%, p = 0.0073). Conclusions Our results confirm that higher EAT volumes and elevated FAI scores are associated with AF, reflecting increased pericoronary inflammation. Although advanced CAD-RADS categories were more frequent in AF patients, only the lowest category showed a significant difference. These findings highlight the potential of EAT, FAI, and CAD-RADS as non-invasive imaging markers for AF risk assessment.Graphical overview of the study workflow (A) FAI risk and (B) CAD-RADS categories

Epicardial adipose tissue (EAT) is often associated with atrial fibrosis, and both can provide the substrate for atrial fibrillation (AF). However, most AF patients have no evidence of left atrial (LA) fibrosis based on bipolar voltage mapping. We determined whether EAT differs in AF patients without LA fibrosis compared to matched controls without AF. Patients undergoing cardiac CT before first-time AF catheter ablation were prospectively enrolled. LA bipolar voltage mapping was performed, and patients were divided into -LVZ (LA low voltage zones < 5% of LA surface area; no fibrosis) and +LVZ (LA low voltage zones ≥ 5%; fibrosis). A control group without AF was matched to -LVZ patients. EAT was quantified on CT using standard signal thresholding to quantify total and regional volumes. AF patients were followed for 1-year postablation to assess atrial arrhythmia (AA) recurrence. -LVZ (n = 50) had higher total EAT volumes than matched controls (n = 48) (79 [58-109] vs. 51 [37-73] cm³, p < 0.001), higher LA EAT (9 [6.3-12] vs. 4.2 [2.9-5.8] cm³, p < 0.001), higher posterior LA EAT (9.7 [6.4-12] vs. 5.9 [2.8-7.2] cm³, p < 0.001) and higher right atrial EAT (7.3 [5.1-9.9] vs. 4.8 [3.2-6.5] cm³, p < 0.001). These differences remained even after correcting EAT for BMI and LA volumes. There were no significant differences in EAT volumes between -LVZ and +LVZ (n = 25). There was no significant association between EAT and AF recurrence postablation. EAT volume is greater in AF patients without evidence of LA fibrosis compared to matched controls without AF. These findings support an association of EAT with AF pathogenesis even in the absence of LA fibrosis.

Background/Objectives: Atrial fibrillation (AF) is associated with increased epicardial adipose tissue (EAT), atrial dilation, and coronary inflammation, though causality remains unclear. Cardiac computed tomography (CCT) allows for precise quantification of EAT volume and the left atrial volume index (LAVI), along with the calculation of the fat attenuation index (FAI), indicating coronary inflammation. Combined with the Coronary Artery Disease-Reporting and Data System (CAD-RADS), these imaging markers may improve AF risk stratification. This study evaluates the association between peri-atrial EAT volumes, LAVI, CAD-RADS, and FAI scores in AF patients using advanced AI platforms. Methods: This retrospective study analyzed 122 patients presenting with angina-type pain and a low-to-intermediate likelihood of CAD, who underwent CCT. Patients were divided into two groups based on rhythm status: 42 with AF and 80 without AF. Total EAT, left atrial (LA-EAT), and bi-atrial EAT (BA-EAT) volumes were assessed, along with LAV, CAD-RADS classification, and FAI scores measured using CaRi-Heart® and syngo.via Frontier®. Results: AF patients exhibited significantly higher EAT volumes (total EAT: 231.8 ± 45.85 vs. 153.2 ± 54.14 mL, p < 0.0001; LA-EAT: 23.55 ± 6.44 vs. 15.54 ± 8.49 mL, p < 0.0001; BA-EAT: 50.24 ± 12.69 vs. 39.84 ± 15.70 mL, p = 0.0002) and elevated LAVI values (57.7 ± 11.44 vs. 45.9 ± 12.58 mL/m2, p < 0.0001). ROC analyses confirmed strong diagnostic performance of total EAT (AUC = 0.869), LA-EAT (AUC = 0.776), BA-EAT (AUC = 0.703), and the LAVI (AUC = 0.756). Higher CAD-RADS categories (2–5) were more frequent in AF, although significant differences were observed only in the lowest category (0–1; 26.2% AF vs. 47.8% non-AF, p = 0.032). Total FAI scores were also higher in AF patients (14.83 ± 10.16 vs. 12.37 ± 7.89, p = 0.044). Conclusions: Increased EAT volumes, an elevated LAVI, and higher FAI scores are significantly associated with AF, suggesting a combined structural and inflammatory substrate. EAT, the LAVI, the FAI, and CAD-RADS collectively represent valuable non-invasive imaging biomarkers for early AF risk assessment.

Drugs That Ameliorate Epicardial Adipose Tissue Inflammation May Have Discordant Effects in Heart Failure With a Preserved Ejection Fraction as Compared With a Reduced Ejection Fraction

Background Epicardial adipose tissue (EAT) contributes to atrial myopathy and atrial fibrillation (AF) through adipokines release, endothelial dysfunction, atrial remodeling and fibrosis. Recently, it was shown that sodium-glucose co-transporter 2 inhibitors (SGLT2i) reduced AF incidence, EAT volume, and inflammation, while glucagon-like peptide-1 receptor agonists (GLP-1Ra) improved heart failure symptoms and reduced left atrial volume. Purpose This study assessed the expression of inflammatory markers, SGLT2 and GLP-1R in human EAT from AF and non-AF patients, examined the effect of EAT-derived mediators on atrial endothelial cells (AEC), and determined the effect of SGLT2i and GLP-1Ra. Methods EAT and subcutaneous AT (SAT) from 80 cardiac surgery patients were analyzed. Conditioned media (CM) from tissues were added to AECs for 24 h. Adipo-cytokines release, mRNA and protein expression levels, ROS and NO formation, platelet and monocyte adhesion and thrombin generation were determined. Results EAT showed M1 macrophage infiltration, and elevated markers of inflammation (IL-1β, IL-6, TNF-α), endothelial activation, fibrosis, thrombosis and oxidative stress, along with SGLT2 and GLP-1R compared to SAT. Oxidative stress in EAT was reduced by inhibitors of NADPH oxidases, NO synthase, AT1R, empagliflozin (SGLT2i), semaglutide (GLP-Ra), with strongest inhibition by a mixture of IL-1ß, IL-6 and TNF-aneutralizing antibodies and combination of empagliflozin plus semaglutide at low concentration (10 nM). In EAT, SGLT2 and GLP-1R were observed in adipocytes and infiltrated macrophages, while SGLT2 colocalized with microvascular endothelial cells. EAT-CM had higher levels of ICAM-1, VCAM-1, pro-inflammatory cytokines, and leptin and lower adiponectin than SAT-CM. Empagliflozin and semaglutide treatment of EAT reduced the release of pro-inflammatory mediators and increased that of adiponectin, with the strongest effect observed with their combination. Cytokines, leptin, SGLT2, GLP-1R, and ROS in EAT were elevated in AF patients compared to non-AF patients. Exposure of AECs to EAT-CM impaired NO formation, induced ROS, pro-thrombotic and pro-adhesive responses, NF-κB activation, and upregulated p53, TGF-β, and SGLT2. Empagliflozin and semaglutide inhibited these effects via the AT1R/NADPH oxidases/SGLT2 and GLP-1R/cAMP/PKA pathways, respectively in a synergistic manner. Conclusions EAT showed increased expression of pro-inflammatory mediators, SGLT2 and GLP-1R compared to SAT. This effect was more pronounced in AF patients. EAT-derived mediators promoted NO/ROS imbalance, pro-inflammatory, pro-adhesive, pro-thrombotic, and pro-fibrotic responses in AECs. Empagliflozin plus semaglutide synergically reduced in situ expression and release of EAT-derived inflammatory mediators. Thus, the combination of SGLT2i plus GLP-1Ra appears as an interesting strategy to reduce the deleterious impact of EAT on the atrium and, hence, atrial myopathy.

Vitamins K2 and D3 may improve cardiovascular health by modulating inflammation and vascular calcification. Inflammation contributes to atherosclerosis and can be assessed through imaging and systemic biomarkers. This study investigated whether vitamin K2 and D3 supplementation reduces inflammation in epicardial adipose tissue (EAT), including pericoronary adipose tissue (PCAT), and systemic inflammation in elderly men at cardiovascular risk. In the Aortic Valve DECalcification (AVADEC) trial, 388 men aged 65-74 received daily vitamin K2 (720μg) and D3 (25μg) or placebo for 24 months. EAT inflammation was assessed using non-contrast CT [EAT volume and attenuation] and contrast-enhanced CT [PCAT attenuation]. Systemic inflammation was evaluated via hs-CRP, IL-6, TNF-α, Fetuin-A, and osteopontin (OPN). Dephosphorylated uncarboxylated matrix Gla protein (dp-ucMGP), the inactive form of MGP, served as a proxy for vitamin K2 status. After 24 months, EAT volume increased in the placebo group (Δ5.66cm3,95% CI 1.35; 9.98) and non-significantly in the vitamin group (Δ3.44cm3, 95% CI -0.44; 7.33), with an intergroup difference of -2.22cm3 (95% CI -8.01; 3.57). EAT attenuation declined similarly (intergroup difference: 0.32 HU, 95% CI -0.23; 0.87). PCAT attenuation remained unchanged. No significant changes were seen in systemic markers, though OPN increased modestly in the vitamin group (Δ25.72pg/mL, 95% CI 2.40; 49.05). dp-ucMGP decreased significantly with supplementation (intergroup difference: 255.31pmol/L, 95% CI -289.56; -221.05). Despite reduction in dp-ucMGP, high-dose vitamin K2 and D3 supplementation did not affect EAT, PCAT or systemic inflammation over 24 months. Alternative strategies may be needed to target inflammatory pathways in cardiovascular disease prevention.

ObjectiveAdipose tissue is recognized as a crucial regulator of atrial fibrillation (AF). However, the effect of epicardial adipose tissue (EAT) on the pathophysiology of AF might be different from that of other adipose tissues. The purpose of this study was to explore the distribution features of different adipose tissues in AF patients and their relationships with left atrial (LA) remodeling and function.MethodsA total of 205 participants (including 112 AF and 93 non-AF patients) were recruited. Color doppler ultrasound was used to measure the thickness of subcutaneous, extraperitoneal, and intra-abdominal adipose tissue. Cardiac CT scan was performed to measure the mean thickness of EAT surrounding the whole heart (total-EAT) and specific regions, including left atrium (LA-EAT), left ventricle, right ventricle, interventricular groove, and atrioventricular groove. LA anatomical remodeling and function were measured by echocardiography, while electrical remodeling was evaluated by P-wave duration and dispersion using Electrocardiography (obtained after cardioversion or ablation in AF patients). Relationship between the thickness of different adipose tissues and LA remodeling and function was analyzed.ResultsThe thickness of subcutaneous, extraperitoneal, and intra-abdominal adipose tissue was similar between AF and non-AF patients, and had no or only weak association with LA remodeling and dysfunction. However, compared to non-AF participants, total-EAT thickness significantly increased in both paroxysmal and persistent AF patients (non-AF vs. paroxysmal AF vs. persistent AF: 6.31 ± 0.63 mm vs. 6.76 ± 0.79 mm vs. 7.01 ± 1.18 mm, P < 0.001), which was positively correlated with the LA size and P-wave duration and dispersion, and negatively correlated with LA ejection fraction and peak strain rate. More interestingly, EAT thickness in AF patients did not increase uniformly in different regions of the heart. Compared to EAT surrounding the other regions, LA-EAT was found to accumulate more greatly, and had a closer relationship to LA remodeling and dysfunction. Multivariate logistic regression analysis also showed that LA-EAT was significantly correlated with the presence of AF (OR = 4.781; 95% CI 2.589–8.831, P < 0.001).ConclusionRather than other adipose tissues, accumulation and redistribution of EAT, especially surrounding the LA, is associated with LA remodeling and dysfunction in AF patients.

Epicardial adipose tissue (EAT) is linked to both Atrial fibrillation (AF) and metabolic syndrome (MetS). Whether EAT inflammation relates to AF type, recurrence after ablation, or MetS, is incompletely known, likewise if it can be measured by CT angiography. To establish the link between (1) atrial EAT inflammatory composition and AF type, AF recurrence, and metabolic comorbidities. (2) EAT inflammation and EAT-volume or density. Patients undergoing thoracoscopic ablation for advanced AF (that is, usually persistent, with enlarged left atria and previous failed ablations) with a cardiac CT-scan before and 6months after surgery were enrolled. CT-EAT atrial volume and attenuation (density), were used for analyses. Patients' left atrial appendages (LAA + EAT) were excised during ablation and stained for adipocytes and different inflammatory cells. Among the 134 included patients, 113 had a LAA available for (immuno)histo-chemistry. Patients with persistent versus paroxysmal AF had more EAT neutrophils: 155[257] versus 63[106] cells/mm2, (p = 0.003), and less anti-inflammatory CD163 + macrophages: 126[134] versus 224[179], (p = 0.03). The AUC curve for differentiating persistent from paroxysmal AF through neutrophil-count was 0.75 (p value < 0.001, CI 0.63-0.87). EAT neutrophil-count related to CT-EAT-attenuation (multivariable analysis: expB 1.01, CI 1.00-1.02, (p = 0.04)). CT-EAT-attenuation distinguished persistent from paroxysmal AF: - 73.0 ± 4.6 versus - 75.3 ± 5.3HU, (p = 0.03). Patients with versus without recurrence had similar inflammatory cell counts, but larger adipocytes, multivariable analysis: ExpB 1.002, CI 1.00-1.003, (p = 0.02). Hypertensive and diabetic patients also had an increased adipocyte size. Patients with persistent versus paroxysmal AF exhibited increased EAT neutrophils, which is reflected by CT-EAT-attenuation. Those with AF recurrence, hypertension and diabetes had adipocyte hypertrophy which may imply a common mechanism underlying these conditions.

Prevalent atrial fibrillation (AF) in patients with hypertrophic cardiomyopathy (HCM) represents an important issue with regard to stroke events caused by embolization and is associated with high mortality. Increased epicardial adipose tissue (EAT), which shows high metabolic activity, can locally influence the activity of the autonomic ganglia, enhancing autonomic dysregulation and increasing the likelihood of AF. We tested the hypothesis that EAT is associated with prevalent AF in HCM patients. Sixty-two patients with idiopathic HCM diagnosed on the basis of ultrasound cardiography findings and histopathological evaluation of myocardium obtained by right ventricular biopsy underwent cardiac magnetic resonance imaging to estimate the extent of EAT. EAT area was significantly higher in the group with AF episodes than in the group without. An increased incidence of AF was found to be significantly related to an increase in EAT, and this association persisted after adjustment for body mass index, sex, and age. Time domain measures of heart rate variability measured by Holter electrocardiography, standard deviation of normal to normal, and standard deviation of the average of normal to normal were negatively related to EAT area. EAT was positively correlated with intraventricular septal thickness and cystatin C level and negatively correlated with the 24-hour creatinine clearance rate. Increased EAT area in HCM patients is significantly related to the presence of AF, which is associated with changes in baseline autonomic nervous tone, left ventricular mass, and chronic kidney disease.

Dietary patterns influence epicardial adipose tissue fatty acid composition and inflammatory gene expression in the Ossabaw pig

IntroductionSystemic markers of inflammation strongly correlate with an increased risk of atrial fibrillation (AF). However, the local immune drivers of this increased AF risk remain poorly defined. Recently, a wealth...

Epicardial adipose tissue (EAT) is an active endocrine organ that is closely associated with occurrence of atrial fibrillation (AF). However, the role of EAT in the development of postoperative AF (POAF) remains unclear. We aimed to investigate the association between EAT profile and POAF occurrence in patients who underwent cardiovascular surgery. We obtained EAT samples from 53 patients to evaluate gene expression, histological changes, mitochondrial oxidative phosphorylation (OXPHOS) capacity in the EAT, and protein secretion in EAT-conditioned medium. EAT volume was measured using computed tomography scan. Eighteen patients (34%) experienced POAF within 7 days after surgery. Although no significant difference was observed in EAT profile between patients with and without POAF, logistic regression analysis identified that the mRNA expression levels of tumor necrosis factor-alpha (TNF-α) were positively correlated and adipocyte size in the EAT was inversely correlated with onset of POAF, respectively. Mitochondrial OXPHOS capacity in the EAT was not associated with POAF occurrence; however, it showed an inverse correlation with adipocyte size and a positive correlation with adiponectin secretion. In conclusion, changes in the secretory profile and adipocyte morphology of the EAT, which represent qualitative aspects of the adipose tissue, were present before the onset of AF.