Opposite relations of epicardial adipose tissue to left atrial size in paroxysmal and permanent atrial fibrillation

Abstract

Objectives:Atrial fibrillation has been associated with obesity in epidemiological studies. Epicardial adipose tissue is an ectopic fat depot in the proximity of atria, with endocrine and inflammatory properties that is implicated in the pathophysiology of atrial fibrillation. Inflammation also has a role in atrial arrhythmogenesis. The aim of this study was to investigate the potential relations of epicardial adipose tissue to left atrial size and to adiponectin and the pro-inflammatory mediators, high-sensitivity C-reactive protein, and interleukin-6 in paroxysmal and permanent atrial fibrillation.Methods:This was a cross-sectional study of 103 atrial fibrillation patients, divided into two subgroups of paroxysmal and permanent atrial fibrillation, and 81 controls, in sinus rhythm. Echocardiography was used for estimation of epicardial adipose tissue and left atrial size and high-sensitivity C-reactive protein, interleukin-6 and adiponectin were measured in all subjects.Results:Atrial fibrillation patients had significantly larger epicardial adipose tissue compared with controls (0.43 ± 0.17 vs 0.34 ± 0.17 cm, p = 0.002). Atrial fibrillation presence was independently related to epicardial adipose tissue thickness (b = 0.09, p = 0.002). Opposite associations of epicardial adipose tissue with left atrial volume existed in atrial fibrillation subgroups; in the paroxysmal subgroup, epicardial adipose tissue was directly related to left atrial volume (R = 0.3, p = 0.03), but in the permanent one the relation was inverse (R = −0.7, p < 0.0001). Adiponectin, high-sensitivity C-reactive protein and interleukin-6 were elevated in both atrial fibrillation groups. Only interleukin-6 was related to epicardial adipose tissue size.Conclusion:Opposite associations of epicardial adipose tissue with left atrial size in paroxysmal and permanent Atrial fibrillation and elevated inflammatory markers, suggest a role of epicardial adipose tissue and inflammation in the fibrotic and remodeling process.

Do most patients with obesity or type 2 diabetes, and atrial fibrillation, also have undiagnosed heart failure? A critical conceptual framework for understanding mechanisms and improving diagnosis and treatment

“…If the dysfunctional epicardial adipose tissue is adjacent to the LV, the result is an impairment of LV distensibility, leading to HFpEF . However, if the afflicted epicardial fat surrounds the left atrium (LA), electroanatomical fragmentation and structural remodelling of the LA lead to an atrial myopathy . Importantly, in contrast to the myopathic process in the LV, atrial myopathy has an easily discerned biomarker (i.e.…”

“…Importantly, in contrast to the myopathic process in the LV, atrial myopathy has an easily discerned biomarker (i.e. the finding of AF on a surface electrocardiogram) . Therefore, AF may represent the first indication of a dysmetabolism‐related inflammatory myopathy that causes HFpEF.…”

“…The available evidence supports this pathophysiological framework. Epicardial adipose tissue is increased in patients with HFpEF and in those with AF, and is particularly prominent when HFpEF and AF coexist, particularly if patients have evidence of systemic inflammation or are at risk of adverse outcomes . Coronary microvascular dysfunction is exceptionally common in HFpEF and, when present, is associated with a two‐fold increase in the prevalence of AF .…”

“…the finding of AF on a surface electrocardiogram). [20][21][22][23] Therefore, AF may represent the first indication of a dysmetabolism-related inflammatory myopathy that causes HFpEF.…”

“…Epicardial adipose tissue is increased in patients with HFpEF and in those with AF, 17,[22][23][24][25][26][27][28] and is particularly prominent when HFpEF and AF coexist, 24 particularly if patients have evidence of systemic inflammation or are at risk of adverse outcomes. 21,27 Coronary microvascular dysfunction is exceptionally common in HFpEF and, when present, is associated with a two-fold increase in the prevalence of AF. 29,30 Cardiac magnetic resonance imaging (MRI) reveals meaningful myocardial fibrosis (in the LA and LV) in both patients with HFpEF 31-36 and those with AF.…”