Transcriptomic and Proteomic Analysis of the Epicardial Adipose Tissue

The study of epicardial adipose tissue (EAT) has been limited by its accessibility due to its proximity to the heart. Moreover, many common animal models do not have EAT, leaving its functional role underestimated and poorly elucidated. Recent advances in medicine and science have allowed for better studies that provide a more comprehensive understanding of its physiological role. One way to dissect its function is the study of its gene expression. In this chapter, we summarize transcriptomic and proteomic analyses which show that EAT expresses a unique set of genes setting it apart from other adipose tissues in the body. This distinctive set of genes modulates a feedback mechanism that has direct interaction with the myocardium. The EAT shares its blood supply with the coronary arteries and innervation with the cardiac muscle, provides physical protection, and regulates energetic metabolites needed by the myocardium. Transcriptomic and proteomic studies show that it is a local source of adipokines with paracrine influence on the myocardium due to the intimate microcirculation shared by both tissues. These analyses also show that it has a role in the immune and endocrine systems affecting the rest of the body. Furthermore, regulation of EAT gene expression is not monolithic and can be affected by multiple factors such as sex, age, underling disease, medication, etc. Gene expression studies can therefore provide great insight into the function of EAT and its role in health and disease

Expert consensus document: Defining the major health modifiers causing atrial fibrillation: a roadmap to underpin personalized prevention and treatment

Despite remarkable advances in antiarrhythmic drugs, ablation procedures, and stroke-prevention strategies, atrial fibrillation (AF) remains an important cause of death and disability in middle-aged and elderly individuals. Unstructured management of patients with AF sharply contrasts with our detailed, although incomplete, knowledge of the mechanisms that cause AF and its complications. Altered calcium homeostasis, atrial fibrosis and ageing, ion-channel dysfunction, autonomic imbalance, fat-cell infiltration, and oxidative stress, in addition to a susceptible genetic background, contribute to the promotion, maintenance, and progression of AF. However, clinical management of patients with AF is currently guided by stroke risk parameters, AF pattern, and symptoms. In response to this apparent disconnect between the known pathophysiology of AF and clinical management, we propose a roadmap to develop a set of clinical markers that reflect the major causes of AF in patients. Thereby, the insights into the mechanisms causing AF will be transformed into a format that can underpin future personalized strategies to prevent and treat AF, ultimately informing better patient care

Atrial Fibrillation and Epicardial Adipose Tissue

Atrial fibrillation (AF) is associated with increased cardiovascular morbidity and mortality with projections that it will affect 8–12 million people in the United States by 2050. Obesity has been identified as an important independent risk factor for AF, with weight loss leading to decreased AF burden and improved arrhythmia free survival. The precise mechanisms by which obesity contributes to AF remain poorly understood. However, it has recently been speculated that epicardial adipose tissue (EAT) may be a key mediator between obesity and AF. EAT is a visceral fat depot with anatomic contiguity to the myocardium. Under physiological conditions, EAT plays an important protective role via mechanical, metabolic, and thermogenic functions. However, under pathophysiological conditions, it may contribute to development of AF through various mechanisms including fatty infiltration, fibrosis, inflammation, oxidative stress, atrial remodelling, and genetic factors. EAT has been shown in multiple studies to be a risk factor for development of AF and predictor of recurrence after catheter ablation. The mechanisms directly linking EAT to the pathogenesis of AF also are uncertain. Multiple pharmacologic options have been proposed to target EAT; however, the efficacy of targeted reduction in EAT requires further investigation