2017 HRS/EHRA/ECAS/APHRS/SOLAECE expert consensus statement on catheter and surgical ablation of atrial fibrillation: executive summary.

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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