Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive liver disease linked to type 2 diabetes (T2D), obesity, and dyslipidaemia, which are all parts of the metabolic syndrome. In 2024, for non-cirrhotic MASH with mild to advanced fibrosis, resmetirom, a selective thyroid hormone receptor-β agonist, became the first FDA-approved treatment for this condition. By increasing β-oxidation and lipid metabolism, it minimises systemic thyroid or cardiac effects while reducing hepatic fat, inflammation, and fibrosis. Resmetirom is being developed for use in combination with lifestyle interventions, such as diet and exercise, to maximize patient benefit. Nevertheless, the lack of congruence between clinical trial populations and real-world payer criteria underscores access obstacles that necessitate policy reform. The successful delivery of screening programs depends on the education of providers from various disciplines and the establishment of uniform screening standards. Future studies should investigate the clinical application of resmetirom in combination with agents that may provide additional benefits, such as GLP-1 receptor agonists, SGLT2 inhibitors, and statins. These results are significant in light of recent long-term safety monitoring of these agents, particularly regarding the thyroid axis. Ensuring equitable uptake will be crucial, as it involves defining fair access through payer endpoints, conducting cost-effectiveness analysis, and considering patient-reported outcomes. Resmetirom represents a breakthrough in MASH management, offering potential metabolic benefits in conjunction with comprehensive clinical and lifestyle approaches.

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.