Abstract 15092: Human Epicardial Adipose Tissue is a Source of Inflammatory Mediators in Aortic Stenosis
INTRODUCTION: It is widely established that epicardial adipose tissue (EAT) influences key pathogenic mechanisms of coronary atherogenesis through secretion of several inflammatory mediators. Recent studies have demonstrated that pathophysiology of aortic valve stenosis (AS) is characterized by early atherosclerosis and inflammation.
HYPOTHESIS: In the present study we aimed to evaluate the amount of EAT and its secretory profile in human AS.
METHODS: We measured EAT thickness by echocardiography in 70 pts with isolated, severe AS, 54 pts with isolated, severe coronary artery disease (CAD), 37 pts with both AS and CAD, and 23 controls matched for age, gender, BMI and cardiovascular risk factors. During cardiac surgery, EAT and subcutaneous adipose tissue (SC) were collected from pts with isolated AS and CAD. The secretome of EAT and SC was analyzed by human cytokine 27-plex immunoassay.
RESULTS: Compared to controls, EAT thickness was significantly and similarly increased in pts with isolated AS and isolated CAD (p<0.05). In pts with coexistent AS and CAD, EAT thickness was significantly greater than the other 3 groups (p<0.05). Overall, EAT of AS and CAD pts showed a more marked inflammatory profile than SC. In particular, in AS pts, of 27 measured factors (including cytokines, chemokines, growth factors, and angiogenic mediators), 17 showed significant greater levels in EAT with respect to SC (p<0,05) (Fig A). In CAD pts, EAT secreted significant greater levels of 7 inflammatory mediators with respect to SC (p<0,05). Of note, in AS pts, there was a close relationship between EAT thickness and levels of secreted inflammatory mediators (p<0,05) (Fig B).
CONCLUSIONS: This represents the first demonstration of increased EAT thickness in pts with severe AS. In AS pts, EAT inflammatory secretory profile is exalted with respect to SC and shows a close relationship with the amount of EAT. Overall, these preliminary data suggest a potential role for EAT in the pathogenesis of AS.
Author Disclosures: V. Parisi: None. P. Formisano: None. V. D’Esposito: None. F. Passaretti: None. M. Ambrosio: None. D. Liguoro: None. A. Caruso: None. G. Grimaldi: None. T. Lonobile: None. F. Baldascini: None. A. Bevilacqua: None. G. Ferro: None. G. Rengo: None. N. Ferrara: None. D. Leosco: None.
- © 2014 by American Heart Association, Inc.