Heart failure with preserved ejection fraction (HFpEF) accounts for more than half of all heart failure (HF) cases, with its prevalence steadily rising due to population aging, obesity, and the prevalence of metabolic diseases. Obesity, a core risk factor for HFpEF, leads to a distinct clinical phenotype and significantly worsens patient prognosis. Given the limitations of body mass index (BMI) in assessing fat distribution, epicardial adipose tissue (EAT)—a metabolically active fat depot closely adjacent to the myocardium—has emerged as a crucial anatomical and functional bridge linking obesity to HFpEF. Compared to BMI, EAT volume demonstrates a stronger predictive value for diastolic dysfunction and adverse clinical outcomes, highlighting its clinical significance. This review outlines the multifaceted mechanisms through which EAT contributes to HFpEF pathogenesis, including mechanical constraint limiting ventricular diastole, lipid infiltration causing myocardial metabolic disorders, pro-inflammatory factor paracrine secretion inducing fibrosis, microvascular dysfunction, arrhythmogenic effects, and protein modification disorders. Targeting EAT has shown promise in reducing its volume, improving inflammatory status, and enhancing cardiac function. As a pathogenic and therapeutic nexus between obesity and HFpEF, further elucidation of EAT-related mechanisms may facilitate precision diagnosis and intervention for this growing population.

Epicardial adipose tissue (EAT) is implicated in exerting potential proarrhythmic effects. The relationship between EAT and tachyarrhythmias is well documented. However, the connection between EAT and bradyarrhythmias has not been comprehensively explored. This study aimed to investigate the association between EAT and bradyarrhythmias. We retrospectively quantified the volume and density of EAT using chest computed tomography scans from patients with bradyarrhythmias and case-matched controls. Measurements were obtained through manual pericardial contour tracing with a standardized Hounsfield unit threshold of -200 to -50 Hounsfield units. A total of 652 patients were included, comprising 326 patients with bradyarrhythmias (age 74.00 [interquartile range, 64.00-81.00] years, 46.01% female) and 326 matched controls (age 72.50 [interquartile range, 63.00-80.00] years, 46.01% female). Compared with the matched control group, the bradyarrhythmia group had a significantly greater volume (119.13 [interquartile range, 87.30-151.68] cm3 versus 93.00 [interquartile range, 67.87-116.71] cm3, P<0.001) and a lower density of EAT (-92.02±4.00 Hounsfield units versus -90.68±3.73 Hounsfield units, P<0.001). Conditional logistic analysis demonstrated that the volume rather than the density of EAT is a significant influencing factor for bradyarrhythmias. Subgroup analysis indicated a progressive increase in average EAT volume from groups with first-degree to third-degree atrioventricular block. In participants with first-degree atrioventricular block, there was a positive correlation between PR interval and EAT volume (Spearman's correlation coefficient: 0.328, P=0.012). Patients with bradyarrhythmia demonstrated significantly higher EAT volumes compared with matched controls, with a progressive increase observed across advancing grades of AVB. This dose-dependent relationship between EAT burden and conduction system impairment underscores its potential role as a modifiable influencing factor in arrhythmogenesis. Further investigations are warranted to determine whether targeted EAT reduction could mitigate conduction abnormalities. URL: https://www.chictr.org.cn; Unique Identifier: ChiCTR2400088446.

Epicardial adipose tissue measurement is an interesting biomarker for cardiovascular health in a case control study of patients with familial partial type 2 lipodystrophy.

Epicardial adipose tissue (EAT) regulates lipid metabolism and immune cell recruitment in coronary arteries. Increased EAT contributes to coronary artery disease (CAD), but exercise prevents CAD. We hypothesized that exercise, irrespective of CAD presence, would produce EAT with increased M2 macrophages and upregulation of anti-inflammatory cytokine transcripts. Female Yucatan pigs (n = 7) were sedentary or exercised, and the left circumflex coronary artery was occluded or remained nonoccluded (2 × 2 design). Bulk and single-nuclei transcriptomic sequencing performed on EAT identified immune, endothelial, smooth muscle, adipocytes, adipocyte progenitor cells (APSCs), and neuronal cells, with adipocytes and APSCs predominant. Nonoccluded (N) sedentary (Sed) EAT had the most M1 macrophages and CD8+ T cells. Sed EAT had the most cells expressing tumor necrosis factor (TNF) superfamily genes. Exercise (Ex) upregulated peroxisome proliferator-activated receptor (PPAR) γ (G) expression and enriched PPAR signaling, which suppresses activation, in macrophages and T cells, particularly in occluded (O) Ex EAT. By contrast, N_Ex EAT had few CD8+ T cells with low PPARG expression. Adipocytes and immune cells in O_Sed EAT had the most communication via growth factors and adhesion molecules. Exercise mitigates EAT inflammation via modulation of immune cell subpopulations, decreased TNF superfamily, and increased PPARG gene expression, and decreased communication between adipocytes and immune cells. However, the effect of exercise on the EAT immune environment is modulated by coronary artery occlusion status. Future studies of the impact of exercise and coronary artery occlusion on EAT would benefit from using a progressive nutritionally induced model of CAD.NEW & NOTEWORTHY A sedentary lifestyle increases the number of inflammatory M1 macrophages and CD8+ T cells, their expression of tumor necrosis factor genes, and the number of communications between these immune cells and adipocytes in epicardial adipose tissue (EAT). The expression of peroxisome proliferator receptor and genes in control of cell activation in macrophages and T cells in nonoccluded and occluded EAT increases in response to exercise.

Hepatic and pericardial fat in coronary computed tomography angiography and its association with coronary artery disease.

Introduction: Epicardial adipose tissue (EAT), a fat depot between the myocardium and pericardium, produces pro-inflammatory adipokines, contributing to inflammation, insulin resistance, and endothelial dysfunction. EAT has been recognized as an independent risk factor for cardiovascular diseases, including atrial fibrillation (AFib) and acute ischemic stroke (AIS). This study explores the association between EAT and AIS risk, with a focus on populations with cardiovascular comorbidities. Material and Methods: This meta-analysis adhered to MOOSE and PRISMA guidelines. A comprehensive search of PubMed, SCOPUS, and Embase databases was conducted, targeting studies evaluating the association between EAT and AIS. Inclusion criteria encompassed RCTs, cohort, case–control, and cross-sectional studies. Quality assessment was performed using appropriate tools, and statistical analysis involved pooled odds ratios (ORs) with 95% confidence intervals (CIs) using a binary random-effects model. Results: The search identified 711 studies, eight of which met the inclusion criteria, yielding 7412 participants. Analysis revealed that increased EAT thickness significantly correlated with higher odds of AIS (aOR: 3.60 [2.26–5.74], I2 = 74.24%). Sensitivity analysis confirmed the robustness of these findings despite publication bias. Higher epicardial adipose volume was also associated with an increased AIS risk (aOR: 1.17 [1.03–1.34], I2 = 49.54%). Conclusions: Increased EAT thickness and volume are associated with a higher risk of AIS in populations with cardiovascular comorbidities, including AFib. EAT’s pro-inflammatory and pro-thrombotic properties may contribute to stroke pathophysiology. These findings highlight the potential utility of EAT measurement in stroke risk stratification and support further research to integrate EAT assessment into clinical practice.

Epicardial adipose tissue (EAT) is a metabolically active visceral fat depot located between the myocardium and the visceral pericardium, exerting direct paracrine and vasocrine effects on the heart and coronary vessels. Under physiological conditions, EAT supports myocardial energy metabolism and thermoregulation through fatty acid supply and adaptive metabolic flexibility. In cardiometabolic disorders such as obesity, type 2 diabetes, and heart failure, EAT undergoes pathological remodelling characterized by increased thickness, adipocyte hypertrophy, immune cell infiltration, and secretion of pro-inflammatory and fibrotic mediators. These alterations contribute to myocardial fibrosis, stiffness, and coronary atherosclerosis, particularly in heart failure with preserved ejection fraction. Pharmacological modulation of EAT has therefore emerged as a promising therapeutic approach in cardiovascular prevention. Agents such as statins, peroxisome proliferator-activated receptor gamma agonists, adenosine monophosphate-activated protein kinase activators, glucagon-like peptide-1 receptor agonists, and sodium-glucose cotransporter 2 inhibitors exert both systemic and depot-specific effects. They reduce EAT thickness, suppress inflammatory signalling, enhance insulin sensitivity, and promote adipocyte browning and oxidative metabolism. Among these, sodium-glucose cotransporter 2 inhibitors and glucagon-like peptide-1 receptor agonists show the most consistent effects in shifting EAT towards a less inflammatory and more metabolically active phenotype. The goal of this review is to provide an overview of current pharmacological interventions that influence EAT and to summarize how much is known about their molecular mechanisms from in vitro and in vivo studies. The target audience includes cardiovascular researchers and clinicians seeking to better understand how metabolic and antidiabetic therapies modulate cardiac fat biology and function.

Epicardial adipose tissue (EAT), the visceral fat of the heart, is highly inflammatory fat depot with pro-inflammatory transcriptome and proteosome. EAT contributes to the development and progression of coronary artery disease (CAD) and atrial fibrillation (AF) through multifactorial inflammatory pathways. However, the paradigm linking EAT inflammation and cardiovascular risk was recently reevaluated. EAT inflammation may be also necessary process for adipose tissue remodeling and expansion to accommodate excess lipids. EAT inflammation may be also considered an adaptive response of adipose tissue to the effects of glucagon-like peptide-1 receptor (GLP-1Rs) and glucose-dependent insulinotropic polypeptide (GIP) analogs. The presence of GLP-1 (GLP-1R) and GIP receptors (GIP-R) suggest direct interaction of these agents with EAT. EAT GLP-1R and GIP-R activation can induce a beneficial balance between increased adipogenesis and reduced ectopic fat accumulation. Cardiovascular effects of liraglutide, semaglutide and tirzepatide can be mediated by EAT inflammation.

Heart failure (HF) is a major cardiovascular complication in people with type 2 diabetes (T2D), where heart failure with preserved ejection fraction (HFpEF) is the most common presentation. Despite its high prevalence, HF in T2D often remains undiagnosed during its early stages due to nonspecific symptoms and the limitations of conventional diagnostic tools. Epicardial adipose tissue (EAT), a visceral fat depot surrounding the myocardium, has emerged as a mechanistic and clinically relevant contributor to myocardial dysfunction. In T2D, EAT expansion fosters a pro-inflammatory, fibrotic, and metabolically adverse milieu that may directly promote the onset and progression of HF. This perspective synthesizes current translational evidence on the role of EAT in the pathogenesis of HF among individuals with T2D. We highlight diagnostic challenges related to imaging-based quantification and the limited sensitivity of natriuretic peptide-based screening, while emphasizing the potential relevance of emerging biomarkers such as GDF-15, Galectin-3, sST2, LDL particle size, GGT, and soluble low-density lipoprotein receptor-related protein 1 (sLRP1) to enhance early detection and risk stratification. Additionally, therapeutic approaches—including lifestyle modification, SGLT2 inhibitors, and GLP-1 receptor agonists—are considered for their potential to modulate EAT volume and reduce cardiovascular risk. Advancing knowledge on EAT biology and its circulating biomarkers holds promise to refine HF risk stratification and support translational efforts toward precision cardiometabolic care.

Obesity remains a dominant risk factor for cardiovascular disease, yet its classification continues to rely heavily on body mass index (BMI)—a metric that fails to capture individual variability in fat distribution, metabolic health, and cardiometabolic risk. This narrative review analyzes 35 articles published between 2018 and 2025 to explore the limitations of BMI and outlines emerging strategies for obesity redefinition through a precision medicine lens. Drawing from recent advances in imaging, metabolomics, and genomic profiling, we highlight alternative metrics such as visceral adipose tissue (VAT), epicardial adipose tissue (EAT), waist-to-hip ratio (WHR), and multi-omic phenotyping that provide superior predictive value for cardiovascular outcomes. The review synthesizes data on metabolically healthy and unhealthy phenotypes, emphasizes the pathophysiological role of EAT in heart failure and arrhythmogenesis, and discusses the cardioprotective effects of pharmacologic agents such as glucagon-like peptide-1 (GLP-1) receptor agonists. Clinical implications include improved risk stratification, earlier disease detection, and individualized therapeutic targeting. Despite current barriers to widespread implementation—such as imaging cost, access to omics, and lack of guideline integration—this paradigm shift holds promise for refining cardiovascular prevention strategies. Redefining obesity using biologically informed, phenotype-based models is indispensable for aligning clinical practice with the complexities of modern cardiometabolic disease.

Abstract Background The role of pericoronary adipose tissue (PCAT) inflammation in coronary collateral circulation (CCC) development remains unclear. This study compared PCAT characteristics in chronic total occlusion (CTO) patients with good versus poor collaterals. Methods Twenty left anterior descending CTO patients were stratified into poor (P-CCC, n=8) and good collateral (G-CCC, n=12) groups per Rentrop classification. CT-derived fat attenuation index (FAI), epicardial adipose tissue (EAT) volume, and histologic markers (macrophage polarization, microvascular density) were analyzed. Results Compared to the P-CCC group, the G-CCC group exhibited significantly lower FAI (−93.6±7.2 vs. −70.8±2.4 HU, p&amp;lt;0.05) but higher EAT volume (8491.3 [7951.6–13060.0] vs. 3452.8 [1741.7–6425.4] mm³, p&amp;lt;0.05). Histologically, relative to P-CCC PCAT, G-CCC PCAT showed increased M2 macrophage density (14.47±2.87 vs. 3.47±1.63, p&amp;lt;0.05), a higher M2/M1 ratio (4.40±2.17 vs. 0.95±0.61, p&amp;lt;0.05), and greater microvascular density (4.69±1.11 vs. 2.21±0.50, p&amp;lt;0.05). Conclusion PCAT inflammation is associated with enhanced collateral vessel formation. These findings highlight PCAT's potential as a therapeutic target for collateral promotion, warranting further investigation into its molecular mechanisms.

Abstract Emerging evidence suggests that epicardial adipose tissue (EAT) contributes to the pathophysiology of obesity‐related heart failure. However, the relationship between EAT and subclinical cardiac dysfunction in obese individuals without cardiac symptoms or known cardiac disease remains largely unknown. This study enrolled 87 asymptomatic obese adults and 30 healthy nonobese controls in the prospective multicenter study (EARLY‐MYO‐OBESITY, NCT05277779), and explored the association between EAT and subclinical cardiac dysfunction by assessing EAT volume, cardiac morphology, function, and tissue characteristics through cardiac magnetic resonance (CMR). Compared to controls, obese participants exhibited elevated EAT volume alongside systolic and diastolic dysfunction, manifested by significant reductions in left ventricular global longitudinal peak systolic strain (LVGLS) and early diastolic longitudinal strain rate (e'SR). Linear regression revealed that EAT volume was independently associated with decreased LVGLS (unstandardized β coefficient −0.118, p &lt; .001) and e'SR (unstandardized β coefficient −0.008, p &lt; .001). After multivariable adjustment, EAT volume remained independently associated with LVGLS (unstandardized β coefficient −0.092, p &lt; .001) and e'SR (unstandardized β coefficient −0.006, p = .002). Furthermore, EAT volume independently predicted cardiac dysfunction defined by LVGLS &lt; 15% (odds ratio 1.095, p &lt; .001) and e'SR &lt; 0.57 s −1 (odds ratio 1.064, p &lt; .001). This study establishes that increased EAT volume is independently associated with subclinical cardiac dysfunction in asymptomatic obese individuals. Despite similar left ventricular ejection fraction, obese individuals with elevated EAT volume exhibit more pronounced impairment in both systolic and diastolic function, which may represent a distinct pathophysiological feature in heart failure progression.

BackgroundPatients with coronary heart disease on long-term lipid-lowering agents typically maintain relatively low lipid levels. However, an elevated systemic inflammatory state represents another major risk factor for poor prognosis in these individuals. This study aims to investigate the relationship between systemic inflammation and adverse outcomes in patients with chronic coronary syndrome(CCS), as well as its synergistic interaction with epicardial adipose tissue (EAT).MethodsThis is a double-center retrospective cohort study. From March 2017 to September 2023, We retrospectively included 278 patients with CCS from two medical institutions in China, all of whom had been receiving long-term statin therapy. Participants underwent cardiovascular magnetic resonance (CMR) imaging and blood testing. Systemic inflammatory response index (SIRI) were derived, and CMR parameters, including EAT volume, were measured. Cox regression analysis was used to evaluate the association between each variable and major adverse cardiovascular events (MACEs). Mediation analysis was applied to assess the interrelationships among systemic inflammatory markers, indexed EAT volume, and CMR parameters.ResultsBoth the SIRI and indexed EAT volume were independently associated with MACEs. Combining SIRI and indexed EAT volume significantly improved the predictive capacity for MACEs. EAT volume partially mediated the relationship between SIRI and MACEs, and similarly, SIRI partially mediated the association between EAT volume and MACEs. Additionally, we observed analogous interrelationships among SIRI, indexed EAT volume, and extracellular volume (ECV).ConclusionIn patients with CCS on long-term statin therapy, elevated SIRI and increased EAT volume represent more important risk factors than lipid levels. SIRI and EAT volume interact with each other and collectively contribute to a poor prognosis in these patients.

BACKGROUND: The assessment of chronic subclinical inflammation caused by coronary atherosclerosis (CA) is more accurate when using local biomarkers such as T-regulatory (Treg) lymphocytes from epicardial (EAT) and thymic adipose tissue (TAT). However, their use is limited by high invasiveness, necessitating alternative methods for evaluating Treg parameters. One of such methods is multi-spiral computed tomography coronary angiography (MSCT)-based assessment of EAT parameters. AIM: To investigate the relationship between properties of FoxP3+ Treg in peripheral blood (PB), epicardial, thymic, and subcutaneous adipose tissue and CT-based radiological characteristics of EAT in high cardiovascular risk patients with (HCVR) varying severity of CA. METHODS: The study included 20 HCVR patients, stratified by CA severity with Gensini Score (GS): severe (GS26,5; n=13) and moderate CA group (GS≤26,5; n=7). Level of nuclear translocation of FoxP3 (LNTF) and relative content (RC) of CD4+CD25hiFoxP3+ and CD4+CD25loFoxP3+ Treg were quantified by imaging flow cytometry in EAT, TAT, SAT and PB. EAT volume and density were measured using MSCT. RESULTS: The moderate CA group showed significantly lower RC of CD4+CD25hiFoxP3+ Treg lymphocytes in TAT compared to severe CA (6,12 (3,77; 12,00) vs. 13,5 (7,48; 17,4) %, p=0,046). In severe CA group, inverse correlations were found: between EAT density and LNTF in CD4+CD25hiFoxP3+ Tregs in TAT (rs=-0,63; p=0,021) and LNTF in CD4+CD25loFoxP3+ Tregs in SAT (rs =-0,58; p=0,036). Notably, reversed correlations were observed between level of nuclear translocation of FoxP3 in CD4+CD25hiFoxP3+ Tregs EAT and EAT density for groups with varying severity of atherosclerosis ((GS≤26,5; rs=0,79; p=0,035) vs. (GS26,5; rs=-0,71; p=0,006)). In PB of severe CA group correlation was found between RC of CD4+CD25loFoxP3+ Tregs and EAT volume (rs=-0,60; p=0,006). CONCLUSION: Patients with severe CA demonstrate multiple inverse correlations between CT density characteristics of EAT and LNTF across all fat depots. These findings suggest an exhaustion of the immunosuppressive potential of Treg during CA progression, while also indicating the potential MSCT utility for indirect assessment of the immunosuppressive potential of this cell population.

Cardiovascular disease (CVD) is a leading cause of mortality in systemic sclerosis (SSc). Early risk identification is crucial for improving prognosis. The aim of this study was to develop a clinical prediction model for assessing cardiovascular disease risk in SSc patients via integrating clinical and imaging data. We retrospectively analyzed the occurrence of CVD among 245 SSc patients and 245 controls. SSc patients were stratified by CVD event. Independent predictors of CVD risk were identified using Cox regression analysis in SSc patients. Receiver operator characteristic (ROC) curves assessed the model's predictive performance. Kaplan-Meier (KM) curves evaluated the association of these factors with event-free survival. SSc patients exhibited significantly higher CVD events than controls. Significant differences were observed between SSc patients with and without events regarding age, sex, disease duration, modified Rodnan skin score (mRSS), erythrocyte sedimentation rate (ESR), anti-Scl-70 antibody (ATA), anti-U3 RNP, pulmonary arterial hypertension (PAH), interstitial lung disease (ILD), coronary artery calcium score (CACS) and epicardial adipose tissue (EFV). Cox regression identified CACS, mRSS, EFV, and ATA as independent predictors of increased CVD risk. The combined model (CACS, EFV, mRSS, ATA) achieved an area under the curve (AUC) of 0.910, showing high accuracy for predicting CVD events in SSc. KM analysis confirmed significantly reduced event-free survival in patients with high CACS, high mRSS, ATA positivity, or high EFV (all P < 0.05). CACS, mRSS, EFV, and ATA are independent risk factors for CVD events in SSc patients. A model combining these factors effectively predicts CVD incidence in this population. Key Points • CACS, mRSS, EFV, and ATA were identified as independent predictors of cardiovascular events. • The combination of CACS, EFV, mRSS, and ATA yielded a high AUC of 0.910, demonstrating strong predictive capability with high specificity and sensitivity for cardiovascular events in SSc individuals.

Purpose This study aimed to investigate the effects of telerehabilitation-based core stabilization exercise training on epicardial adipose tissue (EAT), functional exercise capacity, mobility, and balance in individuals with hypertension. Method Forty-eight individuals with hypertension were randomly divided into two groups: exercise and control. All participants underwent a core stabilization endurance test (bridge test) and core muscle strength assessment using a pressure biofeedback unit, the six-minute walk test (6MWT) for functional exercise capacity, and the Timed Up and Go (TUG) test for functional mobility and balance before and after the intervention. EAT was measured with echocardiography. The exercise group underwent telerehabilitation and performed core stabilization exercise synchronously 3 days a week for 8 weeks. The control group received periodic reminders about general physical activity recommendations throughout the study period. Results After the exercise intervention, 6MWT distance (F = 41.476, p < 0.001, η2=0.474), 6MWT% distance (F = 37.805, p < 0.001, η2=0.451), and TUG test score (F = 36.236, p < 0.001, η2=0.441) were improved significantly in the exercise group compared to the control group. EAT thickness (F = 9.435, p = 0.004, η2=0.170) was significantly lower in the exercise group compared to the control group. Conclusion Telerehabilitation-based core stabilization exercise intervention reduces EAT and increases functional exercise capacity and mobility/balance in individuals with hypertension. ClinicalTrials.gov Identifier: NCT06083376.

The incidence and progression of atrial fibrillation (AF), the most common type of cardiac arrhythmia, correlate with atrial fibrosis. An increased epicardial adipose tissue (EAT) volume is associated with increased atrial fibrosis. Although the presence and severity of atrial fibrosis have been evaluated through various invasive and noninvasive methods, reports examining the association between EAT volume (EATV) and the left atrial (LA) stiffness index through echocardiography or LA compliance as determined by LA pressure are lacking. Therefore, we investigated the relationship between EAT and the LA stiffness index and directly measured LA pressure in patients undergoing AF ablation. We retrospectively examined 165 patients who underwent catheter ablation for AF between December 2022 and March 2025. The EATV was measured using contrast-enhanced computed tomography. The LA stiffness index was calculated as the ratio of the early mitral inflow velocity to the early annular tissue velocity. LA pulse pressure was assessed as the difference between peak and nadir LA pressure. A weak correlation was observed between the LA-EATV index (LA-EATVI) and the LA stiffness index. No significant correlation was observed between the LA-EATVI and LA pulse pressure. Our study showed a weak correlation between the LA-EATVI and the LA stiffness index, but not with LA pulse pressure in patients with AF. Changes in the LA owing to EAT may need to be evaluated quantitatively and qualitatively.

Adolescents with youth-onset type 2 diabetes (YO-T2D) have an increased risk for cardiometabolic complications. The impact of vertical sleeve gastrectomy (VSG) on fat distribution and cardiac morphology/function in YO-T2D is unknown. To evaluate changes in body composition, abdominal and cardiac fat depots, and cardiometabolic health in adolescents with YO-T2D undergoing VSG. Anthropometrics, labs and imaging were used to assess participants pre-surgery and 3-12 months post-surgery. MRI quantified pericardial (PAT), epicardial (EAT), subcutaneous (SAT) and visceral adipose tissue (VAT), hepatic fat fraction (HFF) and cardiac morphology/function. Mixed-effects models assessed longitudinal changes. By 12 months, weight decreased from 134.3 ± 5.1 to 103.3 ± 5.2 kg, VAT 1943 ± 148 to 1248 ± 150 cm3, HFF 23.2% ± 2.3% to 5.3% ± 2.3% and PAT and EAT by 27% and 33% (all p < 0.01). Homeostatic model assessment of insulin resistance (HOMA-IR) improved (7.8 ± 1.2 to 1.7 ± 1.2 [p < 0.01]). BMI, SAT, resting heart rate (RHR), left ventricular (LV) mass and cardiac output (CO) also decreased (all p < 0.05). VAT decreases correlated with decreases in HFF (r = 0.70, p = 0.01), HOMA-IR (r = 0.60, p = 0.04) and CO (r = 0.70, p = 0.03). HFF decreases correlated with decreases in BMI (r = 0.70, p = 0.03), HOMA-IR (r = 0.90, p < 0.001), RHR (r = 0.90, p = 0.002), CO (r = 0.80, p = 0.007) and LV mass (r = 0.70, p = 0.02). VSG reduces ectopic and regional fat and improves associated insulin sensitivity and cardiac health in adolescents with YO-T2D.

Epicardial adipose tissue (EAT) exhibits brown-like features, including the expression of uncoupling protein 1 (UCP1). EAT interacts dynamically with cardiac cells to modulate local cardiac tissue physiology and metabolic function. No studies have evaluated the impact of UCP1 inhibition on oxidative phosphorylation (OXPHOS) in fresh EAT explants. This study aimed to determine the unique bioenergetic characteristics of fresh EAT explants by comparing it to subcutaneous adipose tissue (SAT). Furthermore, the key impact of UCP1 inhibition on EAT respiration and how this process is influenced by the presence of type 2 diabetes mellitus (DM) or coronary artery disease (CAD), was also evaluated. EAT and SAT biopsies were collected from 205 (151 male and 51 female) study participants, undergoing cardiac surgery. Participants were stratified according to the presence/absence of DM or CAD. Markers of mitochondrial content and bioenergetics were evaluated. EAT demonstrated a higher bioenergetic activity compared to SAT, in both nicotinamide adenine dinucleotide (NADH)-linked and fatty acid oxidation (FAO)-linked OXPHOS. Importantly, UCP1 inhibition with guanosine 5'-diphosphate (GDP), flattens the differences between the tissues in the NADH-linked OXPHOS; in contrast these differences were potentiated in the FAO-linked OXPHOS. Minor differences in mitochondrial content and respiration were observed when subjects were stratified according to either DM or CAD. This study emphasizes the important bioenergetic differences between EAT and SAT, which are crucial in the context of the local cardiomyocyte metabolism, as well as the impact of UCP1 inhibition in EAT. A deeper understanding of the unique characteristics of EAT and its metabolic micro-environment may provide valuable insights into the cardiovascular disease pathologies.

Epicardial adipose tissue (EAT), an active endocrine and paracrine organ, contributes to cardiovascular pathogenesis. While cardiac magnetic resonance (CMR) is the reference standard for quantifying EAT volume (EATV), its clinical utility is limited. Non-contrast chest CT (NCCT), widely used in radiology, offers a potential alternative. Although coronary CT angiography (CCTA) improves EAT-myocardial border delineation, its use is restricted by contrast allergy risks and increased radiation exposure. This study investigates the feasibility of NCCT for EATV assessment compared to CMR. We enrolled 120 non-ischemic heart disease patients undergoing both NCCT and CMR during a single hospitalization. EATV was measured using CMR-based volumetric analysis and NCCT-based grayscale threshold segmentation. EAT thickness was quantified at six anatomical sites (left/right atrioventricular grooves, anterior/posterior/superior interventricular grooves, and right ventricular free wall) on both modalities. Statistical analysis compared volume and thickness measurements. EATV derived from NCCT threshold segmentation showed no significant difference compared to CMR volumetry (P> 0.05). Similarly, EAT thickness measurements across all six sites demonstrated no significant differences between NCCT and CMR (all P> 0.05). NCCT-based grayscale threshold segmentation provides EATV measurements comparable to the CMR reference standard. This validates NCCT as a rapid, cost-effective, and clinically feasible alternative for accurate EAT quantification.