Journal
EUROPEAN HEART JOURNAL
Volume 36, Issue 13, Pages 795-805APublisher
OXFORD UNIV PRESS
DOI: 10.1093/eurheartj/eht099
Keywords
Myocardial fibrosis; Epicardial adipose tissue; Atrial fibrillation; Atrial fibrosis; Activin A
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Funding
- Fondation de France
- Fondacoeur Association
- Assistance Publique-Hopitaux de Paris (APHP)
- European Commission (Collaborative Project ADAPT) [HEALTH-F2-2008-201100]
- Assistance Publique-Hopitaux de Marseille (Programme Hospitalier de Recherche Clinique)
- National Agency of Research (Adipofib)
- Fondation de La Recherche Medicale
- Fondation Leducq 'Structural Alterations in the Myocardium and the Substrate for Cardiac Fibrillation'
- European Union (EUTRAF)
- French National Agency through the national program 'Investissements d'avenir' [ANR-10-IAHU-05]
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Aims Recent studies have reported a relationship between the abundance of epicardial adipose tissue (EAT) and the risk of cardiovascular diseases including atrial fibrillation (AF). However, the underlying mechanisms are unknown. The aim of this study was to examine the effects of the secretome of human EAT on the histological properties of the myocardium. Methods and results Samples of EAT and subcutaneous adipose (SAT), obtained from 39 patients undergoing coronary bypass surgery, were analysed and tested in an organo-culture model of rat atria to evaluate the fibrotic properties of human fat depots. The EAT secretome induced global fibrosis (interstitial and peripheral) of rat atria in organo-culture conditions. Activin A was highly expressed in EAT compared with SAT and promoted atrial fibrosis, an effect blocked using neutralizing antibody. In addition, Activin A levels were enhanced in patients with low left-ventricular function. In sections of human atrial and ventricular myocardium, adipose and myocardial tissues were in close contact, together with fibrosis. Conclusion This study provides the first evidence that the secretome from EAT promotes myocardial fibrosis through the secretion of adipo-fibrokines such as Activin A.
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