Emerging cardiometabolic therapies, such as glucagon-like peptide-1 receptor agonists and dual GIP/GLP-1 agonists, have been shown to reduce EAT volume and inflammatory markers, although direct evidence linking these interventions to improved AF outcomes remains limited.<h4>Conclusions</h4>EAT represents a relevant pathophysiological interface between metabolic disease and AF with potential clinical implications. This evidence concerns the gene GLP1R and Other metabolic disease.