Epicardial fat and atrial fibrillation: current evidence, potential mechanisms, clinical implications, and future directions

Abstract

Obesity is increasingly recognized as a major modifiable determinant of atrial fibrillation (AF). Although body mass index and other clinical measures are useful indications of general adiposity, much recent interest has focused on epicardial fat, a distinct adipose tissue depot that can be readily assessed using non-invasive imaging techniques. A growing body of data from epidemiological and clinical studies has demonstrated that epicardial fat is consistently associated with the presence, severity, and recurrence of AF across a range of clinical settings. Evidence from basic science and translational studies has also suggested that arrhythmogenic mechanisms may involve adipocyte infiltration, pro-fibrotic, and pro-inflammatory paracrine effects, oxidative stress, and other pathways. Despite these advances, however, significant uncertainty exists and many questions remain unanswered. In this article, we review our present understanding of epicardial fat, including its classification and quantification, existing evidence implicating its role in AF, potential mechanisms, implications for clinicians, and future directions for research.

Associations of Epicardial, Abdominal, and Overall Adiposity With Atrial Fibrillation

“…For primary epicardial fat analyses, we restricted meta-analysis to studies that used either MRI or CT to measure epicardial fat volumes because echocardiography can only measure pericardial separation, not all of which may be adipose tissue, and epicardial fat thickness and area do not necessarily reflect epicardial fat volume. 1 Heterogeneity across studies was quantified using I 2 statistics and was explored using subgroup analyses, sensitivity analyses, and meta-regression techniques. Epicardial fat study characteristics considered as possible sources of heterogeneity included study year, study type, prospective design, study region, imaging modality, measurement method, fat definition, fat location, sample size, publication status, and covariate adjustment.…”

“…[1][2][3][4][5] However, the mechanisms through which obesity causes AF are not fully understood. Previous studies have demonstrated that obesity is associated with diastolic dysfunction, atrial inflammation, myocardial lipidosis, and atrial contractile dysfunction.…”

Association Between Posterior Left Atrial Adipose Tissue Mass and Atrial Fibrillation

“…The stronger association between EAT and the occurrence of AF, in comparison to other markers of overall adiposity, may be explained by several pathophysiological mechanisms. 24 EAT may induce structural and electric remodeling of the LA by fatty infiltration of the LA myocardium causing slow conduction. Mahajan et al 8 recently demonstrated in an animal model that obese sheep had larger LA volumes and pressures, reduced atrial conduction velocity, increased conduction heterogeneity, increased fractionated electrograms, and decreased posterior LA voltage as compared with control nonobese sheep.…”

Obesity Associated Atrial Fibrillation: Epicardial Fat Tissue in Etiopathogenesis

“…Среди данных адипоцитокинов ключевыми медиа-торами развития воспаления и фиброза миокарда предсердий являются активин А, относящийся к семейству трансформирующего фактора роста-b, интерлейкины 6, 8, 1b, фактор некроза опухоли-α, матриксные металлопротеиназы второго и седьмого типа, регулирующие активность межклеточного мат-рикса [29,30]. Кроме того, адипоциты эпикардиаль-ного жира секретируют целый ряд хемотаксических протеинов, в частности, моноцитарный хемотаксиче-ский протеин-1, молекулы межклеточной адгезии, что обуславливает накопление в ЭЖТ моноцитов, трансформирующихся в макрофаги М1-типа, а также других иммунных клеток, участвующих в процессах хронического воспаления [30].…”

“…Кроме того, адипоциты эпикардиаль-ного жира секретируют целый ряд хемотаксических протеинов, в частности, моноцитарный хемотаксиче-ский протеин-1, молекулы межклеточной адгезии, что обуславливает накопление в ЭЖТ моноцитов, трансформирующихся в макрофаги М1-типа, а также других иммунных клеток, участвующих в процессах хронического воспаления [30].…”