Epicardial adipose tissue (EAT) is a fat deposit surrounding the heart and located under the visceral layer of the pericardium. Due to its unique features, the contribution of EAT to the pathogenesis of cardiovascular and metabolic disorders is extensively studied. Especially, EAT can be associated with the onset and development of coronary artery disease, myocardial infarction and post-infarct heart failure which all are significant problems for public health. In this article, we focus on the mechanisms of how EAT impacts acute coronary syndromes. Particular emphasis was placed on the role of inflammation and adipokines secreted by EAT. Moreover, we present how EAT affects the remodeling of the heart following myocardial infarction. We further review the role of EAT as a source of stem cells for cardiac regeneration. In addition, we describe the imaging assessment of EAT, its prognostic value, and its correlation with the clinical characteristics of patients.
Heart failure (HF) is a complex syndrome characterized by impaired cardiac function. Two common subtypes of HF include heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF). In this study, we aimed to evaluate and compare the plasma levels of 3-nitrotyrosine (3-NT)—as a marker of nitrosative/oxidative stress and myeloperoxidase (MPO)—as an indicator of inflammation between HFpEF and HFrEF. Twenty-seven patients diagnosed with HFpEF and twenty-two with HFrEF were enrolled in this study. Additionally, forty-one patients were recruited for the control group. An echocardiographic assessment was conducted, followed by the collection of blood samples from all participants. Subsequently, the levels of 3-NT and MPO were quantified using the ELISA method. Comprehensive clinical characteristics and medical histories were obtained. Circulating levels of 3-NT were significantly higher in the HFpEF patients than in the control and the HFrEF groups. Nitrosative/oxidative stress is significantly intensified in HFpEF but not in HFrEF.
Background: Epicardial adipose tissue (EAT) may contribute to the pathogenesis of atrial fibrillation (AF). The attenuation of EAT assessed by means of computed tomography (CT) may reflect the severity of local tissue inflammation. This study aimed to systematically analyze the relationship between the attenuation of EAT surrounding the left atrium (LA-EAT) and AF recurrence after catheter ablation (CA). Methods: Five databases were searched up to April 10, 2025. Original studies involving adult patients with paroxysmal or persistent AF undergoing CA were included if they provided quantitative measurements of LA-EAT attenuation on cardiac CT before ablation. Results: A total of seven retrospective observational studies with 2440 patients were included in the analysis. The percentage of male participants ranged from 60.9% to 73.0%, and the mean or median age of patients varied from 57.5 to 68.2 years. The mean body mass index across studies ranged from 24.0 to 32.4 kg/m2. A pooled analysis of all included trials demonstrated that the mean LA-EAT attenuation in the AF recurrence group was −78.97 ± 15.34 HU, which was less negative compared to the non-recurrence group (−81.37 ± 15.46 HU; mean difference [MD] = 2.22; 95% confidence interval [CI]: 0.84 to 3.61; p = 0.002). Conclusions: LA-EAT attenuation is significantly more positive in patients experiencing AF recurrence compared to those without recurrence following CA procedures.
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.
Background/Objectives: Atrial fibrillation (AF) is a significant contributor to ischemic stroke; however, existing thromboembolic risk scores exhibit only moderate predictive accuracy. Lipoprotein(a) (Lp(a)), a genetically determined lipoprotein characterized by proatherogenic and prothrombotic properties, may play a role in cardioembolic events in AF. Nonetheless, its clinical relevance in this context remains ambiguous. The goal of this systematic review and meta-analysis was to look at the differences in circulating Lp(a) levels between AF patients who had an ischemic stroke and those who did not, as well as to see if Lp(a) could help figure out who is at risk of thromboembolic events. Methods: A thorough search was performed in PubMed/MEDLINE, Embase, Scopus, Web of Science, and CENTRAL until September 2025, in accordance with PRISMA 2020 and Cochrane Handbook guidelines. Eligible studies encompassed adults with AF and accessible data on Lp(a) concentrations, contrasting individuals with and without ischemic stroke. Results: Five observational studies involving 20,678 atrial fibrillation patients (3104 with ischemic stroke) were incorporated. The pooled analysis revealed markedly elevated Lp(a) concentrations in stroke patients relative to non-stroke controls (MD = 2.42 mg/dL; 95% CI 0.68–4.16; p = 0.007). Conclusions: While Lp(a) testing is not presently endorsed in AF guidelines, our results indicate a possible correlation with ischemic stroke risk. Nonetheless, these findings must be regarded with caution owing to significant heterogeneity, the predominance of Chinese cohorts, and the exceedingly low certainty of evidence as per GRADE assessment. Additional extensive, multi-ethnic, and rigorously designed prospective studies are necessary to ascertain whether Lp(a) constitutes an independent risk factor for ischemic stroke in atrial fibrillation.
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.