Abstract
Epicardial adipose tissue (EAT) is associated with the incidence, perpetuation, and recurrence of atrial fibrillation (AF), with elusive underlying mechanisms. We analyzed adipokine expression in samples from 20 patients with sinus rhythm (SR) and 16 with AF. Quantitative real-time PCR showed that connective tissue growth factor (cTGF) expression was significantly higher in EAT than in subcutaneous adipose tissue (SAT) or paracardial adipose tissue (PAT) from patients with AF, and in EAT from patients with SR (P < 0.001). Galectin-3 expression was significantly higher in EAT than in SAT or PAT (P < 0.001), with no significant differences between patients with AF and SR (P > 0.05). Leptin and vaspin expression were lower in EAT than in PAT (P < 0.001). Trichrome staining showed that the fibrosis was much more severe in patients with AF than SR (P < 0.001). We found a linear relationship between cTGF mRNA expression level and collagen volume fraction (y = 1.471x + 27.330, P < 0.001), and logistic regression showed that cTGF level was an independent risk factor for AF (OR 2.369, P = 0.027). In conclusion, highly expressed in EAT, cTGF is associated with atrial fibrosis, and can be an important risk factor for AF.
Highlights
Structural remodeling is a key process in the development and perpetuation of atrial fibrillation (AF), which is manifested by fibrosis[6]
There was no significant differences between sinus rhythm (SR) patients and AF patients in demographical data including age (P = 0.741), sex (P = 0.821), Body Mass Index (BMI) (P = 0.631), or smoking status (P = 0.936)
Previous work has suggested that Epicardial adipose tissue (EAT) plays a key role in atrial remodeling by infiltrating into the myocardium[22] and secreting Activin A, predisposing the tissue to atrial fibrosis[7]
Summary
Structural remodeling is a key process in the development and perpetuation of AF, which is manifested by fibrosis[6]. A study demonstrated that EAT could induce atrial fibrosis via secretion of Activin A, which contributed to the development of AF7. It was supposed in this study that some adipokines expressed in EAT could facilitate the process of atrial remodeling. We screened previous reports to find potential adipokines that could be expressed in adipose tissue and associated with fibrosis. Previous research studied the link between mRNA level of chemerin[16] or omentin-117 in EAT and coronary atherosclerosis, which demonstrated the feasibility and reliability of mRNA quantification. This study compared the expression of cTGF, gal-3, leptin and vaspin www.nature.com/scientificreports/. The quantitative relationship between adipokine expressions, atrial fibrosis and AF was analyzed
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