RETN and atrial fibrillation: Two potential mechanisms can be proposed for this association: firstly,the actions of proinflammatory cytokines and adipo-fibrokines released from EAT,such as activin A, adiponectin, and resistin, which can induce fibrotic changes onthe atrial myocardium[2,4,11]; and secondly, adipocyte infiltration on the atrialmyocardium, which can cause blockage of local conduction and promote themicro-reentry circuit; and potential modulations of the autonomic nervous system bythe ganglionic plexus within the EAT, which may influence the occurrence of AF.