Search Results (160)

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. Full article

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. Full article

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. Full article

Background: Epicardial adipose tissue (EAT) is a visceral fat depot surrounding the myocardium. It contributes to coronary artery disease (CAD) through local inflammation, while its metabolic activity, including the expression of uncoupling protein-1 (UCP-1) and incretin receptors (GLP-1R, GIPR), may exert protective effects. The relationship between EAT immunohistochemical features and imaging-derived volume remains unclear. Methods: We prospectively studied 50 patients undergoing cardiac surgery: 25 with CAD undergoing coronary artery bypass grafting and 25 without CAD undergoing valve replacement. EAT samples were immunohistochemically stained for CD3, CD68, MPO, UCP-1, GLP-1R, and GIPR. Preoperative CT was used to quantify EAT volume. Results: Patients with CAD more frequently had higher CD3 immunopositivity compared to the control group (84.0 vs. 58.3%, p = 0.047), with no difference in MPO and CD68 immunoexpression. UCP-1 expression was elevated in CAD patients (p = 0.004), whereas GLP-1R and GIPR immunopositivity were similar. EAT volume did not differ between CAD and non-CAD patients (102.87 cm³ vs. 99.38 cm³, p = 0.964) but correlated modestly with BMI (r_s = 0.325, p = 0.021). UCP-1 and GLP-1R immunopositivity, as well as larger LVEDD (left ventricular end-diastolic diameter), were positively associated with greater EAT volume. Conclusions: EAT in CAD exhibits increased T-cell infiltration and elevated UCP-1 expression, indicating an inflammatory yet metabolically active profile. Larger EAT volume was associated with UCP-1 and GLP-1R expression, underscoring the immunometabolic role of EAT in CAD. Full article

Background/Objectives: The causes and mechanisms underlying the development of leptin resistance (LR) in patients with cardiovascular disease (CVD) remain unknown. Investigating the characteristics of adipose tissue in patients with CVD is a relevant scientific problem that may help to uncover the missing links in the pathogenesis of LR. This study aimed to evaluate systemic and local markers of LR in patients with different forms of CVD, and to determine the prevalence and tissue-specific expression patterns that contribute to LR. Methods: The study included 108 patients with myocardial infarction (MI), 96 patients with chronic coronary heart disease (CHD), and 96 patients with acquired heart disease (AHD). On day 1 of admission to the hospital, leptin and leptin receptor concentrations and the serum-free leptin index (FLI) were measured. Leptin resistance (LR) was defined as a leptin level of >6.45 ng/mL and FLI of >25. In chronic CHD and AHD patients, LEP, LEPR1, LEPR2, LEPR2/2, LEPR3, LEPR3/2, and LEPR4 expression as well as leptin and soluble leptin receptor secretion were assessed in subcutaneous (SAT), epicardial (EAT), and perivascular (PVAT) adipose tissue. Results: MI and chronic CHD patients are characterized by elevated leptin levels and high FLI values in the blood serum, which indicates a high prevalence of LR, in contrast to AHD patients. In chronic CHD, the LR level was highest in EAT and moderate in SAT. Reduced leptin sensitivity in EAT is underlied by decreased expression of LEPR1, LEPR2, LEPR2/2, LEPR3, LEPR3/2, and LEPR4, and increased leptin production by epicardial adipocytes, which contributes to enhancement of leptin resistance at the systemic level. Conclusions: A high LR rate was detected in patients with MI and chronic CHD. The identified changes in EAT lead to the development of leptin resistance in chronic CHD patients. Full article

Background: Immune dysregulation has emerged as a central mechanism in atrial fibrillation (AF), with accumulating evidence implicating T-cell subsets, cellular senescence, checkpoint dysfunction, and inflammatory signaling. Although individual studies have provided important insights, a comprehensive synthesis across histological, mechanistic, prognostic, and genetic domains has been lacking. Methods: We systematically reviewed 16 studies published between 2009 and 2025, encompassing histological investigations, translational and mechanistic analyses, interventional cohorts, prognostic studies, and Mendelian randomization. Data on immune cell subsets, cytokines, signaling pathways, and clinical outcomes were extracted. Risk of bias was assessed using ROBINS-I and RoB 2, while certainty of evidence was graded using the GRADE framework. Results: Histological studies consistently demonstrated infiltration of atrial tissue by T lymphocytes and macrophages, with greater intensity in persistent and permanent AF, causally linked to atrial dilatation and fibrosis. Epicardial adipose tissue emerged as a key reservoir of tissue-resident memory T cells that promote IL-17- and IFN-γ-mediated fibroinflammatory remodeling. Mechanistic analyses highlighted CD8⁺PAR1⁺ cytotoxic T cells, PD-1/PD-L1 checkpoint disruption, and adipose–myocardial crosstalk as pivotal drivers of AF. Prognostic studies indicated that immune biomarkers provide incremental predictive value beyond conventional risk scores, while genetic evidence supported a causal role for immune dysregulation in AF susceptibility and progression. Conclusions: Across multiple levels of evidence, immune dysregulation is a primary determinant of AF development, progression, and outcomes. Integration of immune biomarkers into clinical practice may enhance risk stratification and inform the design of immune-targeted therapies for atrial fibrillation. Full article

Background: Despite advances in ablation strategies, a substantial proportion of patients with atrial fibrillation (AF) experience arrhythmia recurrence, highlighting the need for improved preprocedural risk stratification. One of the emerging factors associated with arrhythmogenic remodeling is epicardial adipose tissue (EAT), particularly in the proximity of the left atrium (LA), due to its metabolic and inflammatory activity. Methods: This study investigated whether preprocedural assessment of EAT parameters on computed tomography (CT), including volume, mean attenuation, and attenuation dispersion, could predict AF recurrence following ablation. Seventy patients with AF underwent either pulsed field or cryoballoon ablation and were followed for 18 months. Results: Recurrence of AF occurred in 26 (37.1%) patients. Both higher LA-EAT attenuation (OR 1.09; 95% CI: 1.02–1.17) and greater total-EAT volume (OR 2.41; 95% CI: 1.16–4.99) were independently associated with arrhythmia recurrence. Subgroup analysis revealed that LA-EAT volume was highly predictive of recurrence in patients with persistent AF (AUC = 0.91), whereas LA-EAT attenuation demonstrated greater prognostic value in those with paroxysmal AF (AUC = 0.80). Conclusions: These findings suggest that quantitative evaluation of EAT using routine cardiac CT may enhance risk stratification before ablation. Full article

Diabetes mellitus (DM) has emerged as a significant issue for both individual patients and global health. Elevated blood glucose levels lead to complications affecting the cardiovascular system. Due to this fact and the growing population of patients with DM, it is crucial to broaden the knowledge concerning DM pathogenesis, allowing for the prevention and alleviation of organ-specific complications. Nowadays, pharmacological and non-pharmacological approaches are implicated in DM management. Epicardial adipose tissue (EAT) was indicated to modulate the impact of diabetes mellitus on the heart. Emerging evidence indicates that antidiabetic drugs can significantly influence EAT, often independently of their glucose-lowering effects, suggesting additional cardiometabolic benefits. However, not all drug classes, and even agents within the same class, exhibit identical effects on EAT, highlighting that some therapies may be preferred over others for cardiovascular benefit. Lifestyle interventions, commonly recommended to patients with DM, might also target epicardial fat. This article extensively reviews the impact of current DM treatment on EAT and depicts potential mechanisms. It also aims to identify gaps in knowledge and potential future directions. Insights from this work may guide future research and therapeutic strategies aimed at reducing cardiovascular risk in patients with DM. Full article

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are widely used in the management of type 2 diabetes and obesity due to their metabolic benefits. Beyond weight loss and glycemic control, emerging evidence suggests they may also exert cardioprotective effects. In the context of heart failure (HF), particularly HF with preserved ejection fraction (HFpEF), GLP-1RAs have been associated with improvement in symptoms, physical capacity, biomarkers, and structural cardiac remodeling. These benefits appear to be independent of weight loss, suggesting additional mechanisms including anti-inflammatory effects, improved myocardial metabolism or modulation of epicardial adipose tissue. However, current data largely come from non-HF dedicated trials, with limited standardization of the HF phenotype. Results are overall inconsistent and may suggest potential harm in some cases, particularly in HF with reduced ejection fraction (HFrEF). This review aims to summarize the current evidence on the role of GLP-1RAs in heart failure, explore possible underlying mechanisms and highlight key gaps in knowledge. Full article

Epicardial adipose tissue (EAT), the visceral fat layer next to the myocardium, has become an important focus in heart failure with preserved ejection fraction (HFpEF). When enlarged and inflamed, EAT increases pericardial restraint, releases fibroinflammatory mediators, and disrupts myocardial energetics, thereby reproducing the high-pressure, exercise-intolerant HFpEF phenotype regardless of body mass index. Modern echocardiography, cardiac CT, and MRI, enhanced by artificial intelligence texture analytics, now enable precise depot-specific quantification, making EAT a measurable therapeutic target. Early interventional studies suggest that caloric restriction, bariatric surgery, SGLT2 inhibitors, GLP-1 receptor agonists, statins, PCSK9 antibodies, and colchicine can reduce EAT volume or alter its inflammatory profile, with concurrent improvements in haemodynamics and biomarkers. However, definitive outcome trials are still pending. Priority directions include standardising imaging cut-offs, mapping EAT immune–metabolic niches, and testing combined metabolic–inflammatory regimens to translate EAT modulation into precision therapy for HFpEF. This review aims to synthesise current mechanistic, diagnostic, and therapeutic insights on EAT in HFpEF and outline future research priorities. Full article

Obesity is strongly associated with an increased risk of heart failure. Recent studies indicate that epicardial adipose tissue plays a critical role in the development of obesity-related cardiomyopathy. This distinct visceral fat depot, located between the myocardium and the visceral pericardium, is involved in direct cross-talk with the adjacent myocardium, influencing both its structural integrity and electrophysiological function. This review aims to provide an up-to-date overview of the morphological, metabolic, immunological, and functional alterations of this adipose compartment in the context of obesity, and to explore its contribution to the pathogenesis of heart failure. Moreover, the article synthesizes current evidence on the potential cardioprotective effects of emerging anti-obesity pharmacotherapies—particularly GLP-1 and dual GLP-1/GIP receptor agonists—on metabolic pathways associated with epicardial fat that are implicated in obesity-induced cardiomyopathy. Further clinical trials are required to clarify the impact of these therapies on the course and prognosis of heart failure, as well as on the epidemiology and societal burden of the disease. Full article

Adipose tissue enlargement in obesity leads to hypoxia, which may promote premature aging. This study aimed to understand the hypoxic response in 3D cultures of SGBS cells, a model for brown-like adipose tissue expressing uncoupling protein 1 (UCP1). Single-nucleus RNA sequencing of SGBS organoids revealed a heterogeneous composition and sub-population-specific responses to hypoxia. The analysis identified a cluster of transcriptional repression, indicating dying cells, and implied a role of ferroptosis in this model. Further experiments with SGBS cells and white adipose tissue-derived stem/progenitor cells showed that Acyl-CoA synthetase long-chain family member 4 (ACSL4), a key enzyme in ferroptosis, is expressed only in the presence of browning factors. Hypoxia downregulated ACSL4 protein in SGBS organoids but induced an inflammaging phenotype. Analysis of brown-like epicardial adipose tissue from cardiac surgery patients revealed a significant positive correlation of ACSL4 mRNA with UCP1 and hypoxia-inducible pro-inflammatory markers, while ACSL4 protein appeared to be inversely correlated. In conclusion, this study demonstrates that adipocytes’ capability to undergo ACSL4-mediated ferroptosis is linked to brown-like adipogenesis, suggesting an opportunity to modulate ferroptotic signaling in adipose tissue. The dual role of hypoxia by inhibiting ACSL4 but promoting inflammaging indicates a relationship between ferroptosis and aging that warrants further investigation. Full article

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. Full article

Background: While epicardial adipose tissue (EAT) is a known predictor of adverse cardiovascular outcomes, lipomatous hypertrophy of the interatrial septum (LHIS) is composed of metabolically active fat such as brown adipose tissue, which may exert a different effect. This study investigates the coronary atherosclerosis profile in patients with LHIS using CTA, compared with a propensity score-matched control group. Methods: A total of 142 patients were included (n = 71 with LHIS and n = 71 controls) and propensity score-matched for age, gender, BMI, and the major CV risk factors (matching level, <0.05). CTA imaging parameters included HRP, coronary stenosis severity (CADRADS), and CAC score. Results: The mean age was 60.9 years +/− 10.6, there were nine (6.3%) women, and the mean BMI is 28.04 kg/m² +/− 4.99. HRP prevalence was significantly lower in LHIS patients vs. controls (21.1% vs. 40.8%; p < 0.011), while CAC (p = 0.827) and CADRADS (p = 0.329) were not different, and there was no difference in the obstructive disease rate. There was no difference in lipid panels (cholesterol, LDL, HDL, TG) and statin intake rate. Conclusions: HRP prevalence is lower in patients with LHIS than controls, while coronary stenosis severity and CAC score are not different. Clinical relevance: LHIS may serve as imaging biomarker for reversed CV risk. Full article

The most frequently used laboratory animals for studies on adipose tissue properties and obesity are rodents. However, there are significant differences in the types of visceral fat depots between rodents and humans, including fat depots in the heart area. The large human fat depot of greatest interest in cardiac research is the epicardial adipose tissue (EAT). Its properties are widely investigated, because the EAT lies directly on the heart’s surface and can easily affect myocardial physiology. The major fat depot in rodents‘ chest—pericardial fat—is located on the ventral surface of the parietal lamina of the pericardium and is often incorrectly referred to as the EAT. Further confusion arises from reports claiming that rodents are entirely devoid of the EAT. We decided to verify adipose tissues in the heart area of 16 male Sprague Dawley rats under physiological conditions and in obesity. The animals in the NFD group (n = 8) were fed with a standard diet while these in the HFD group (n = 8) were fed with a high-fat diet (31% fat) starting from 4 weeks after birth. When the animals reached 12 weeks, the presence of fat deposits was verified. Additionally, their blood was collected to characterize carbohydrate and lipid metabolism changes, adipokine profile alterations, and their systemic inflammation status. The obesogenic diet caused significant disturbances in their carbohydrate and lipid metabolism, as well as hyperleptinemia. A high-fat diet primarily promoted the accumulation of pericardial fat, which was absent in the NFD rats and observed in 6 out of the 8 HFD animals. In both groups, adipocytes were also found directly on the hearts’ surfaces (EAT), albeit in very small numbers and limited to the atrioventricular groove on the dorsal side of the hearts. These adipocytes were dispersed among the vessels, making quantitative assessment and separation difficult, however, macroscopic evaluation revealed no noticeable differences in its extent. In conclusion, although rats are not entirely devoid of the EAT, their suitability for studying the properties of the EAT appears to be considerably limited. Full article