Epicardial adipose tissue (EAT), a visceral adipose tissue depot directly in contact with the heart, has been linked to an increased risk of atrial fibrillation. Despite the recognition of its significance, the exact mechanisms behind EAT arrhythmogenicity are yet to be fully understood. This thesis provides a comprehensive understanding of the relationship between EAT and arrhythmias. In Chapter 2, we summarize electrocardiographic evidence showing that EAT accumulation is associated with cardiac conduction slowing and describe potential structural and paracrine mechanisms of EAT arrhythmogenicity. In Chapter 3, we explore the effects of EAT secretome on conduction and arrhythmogenesis. In Chapter 4, we characterize the microRNA content of EAT-derived extracellular vesicles and assess its consequences on conduction. Chapter 5 explores the consequences of a reduction in ciliated fibroblasts on cardiac conduction. A reduction in ciliated fibroblasts has been observed in atrial fibrillation patients compared to healthy individuals, and this reduction could be linked to fibrosis and conduction impairment. In Chapter 6, we look into extracellular electrogram analysis and validate some parameters using an in silico model of neonatal rat ventricular myocytes on multielectrode arrays (Chapter 6). The last chapter of this thesis (Chapter 7) provides an overall discussion of the chapters above, and a critical appraisal of the data in the context of the current literature.