Abstract:
Introduction
One of the risk factors for atrial fibrillation is obesity. Clinical studies revealed
in this context the important role of the epicardial adipose tissue-a visceral
adipose tissue depot located between the myocardium and the visceral
pericardium, which due to the anatomical proximity to the underlying
myocardium, can contribute to the formation of an arrhythmogenic substrate .
Purpose
To describe the mechanisms through which epicardial adipose tissue is involved
in the pathogenesis of atrial fibrillation.
Material and methods
In order to carry out the literature review, articles published in the last five
years were analyzed, the search in the Pubmed database was performed using
the following keywords: atrial fibrillation, epicardial adipose tissue.
Results
Epicardial adipose tissue secretes a series of bioactive factors called adipokines which act in a
paracrine or vasocrine way meanwhile, it represents a source of reactive oxygen species. Under
certain pathological conditions, such as obesity, epicardial adipose tissue adopts a secretome
dominated by proinflammatory mediators like IL-1β, IL-6 and TNFα, and profibrotic factors such
as activin A-member of TGF-β, as well as matrix metalloproteinases. The lack of an anatomic fascia
between this adipose tissue depot and the myocardium makes possible the fatty infiltration of the
atrial myocardium, which together with the process of fibrosis generates conduction
abnormalities.
Conclusions
Epicardial adipose tissue volume represents one of the risk factors for atrial fibrillation, which suggests the
potential utility of its quantification using imaging techniques. Inflammation, oxidative stress, fibrosis, and
fatty infiltration are through the main pathogenic mechanisms responsible for this association.
