Statin therapy modulates thickness and inflammatory profile of human epicardial adipose tissue.
Adipose Tissue
/ diagnostic imaging
Aged
Aortic Valve
/ pathology
Aortic Valve Stenosis
/ complications
Atorvastatin
/ therapeutic use
Biopsy
Calcinosis
/ complications
Coronary Artery Disease
/ diagnosis
Cytokines
/ metabolism
Echocardiography
Female
Follow-Up Studies
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors
/ therapeutic use
Inflammation
/ diagnosis
Male
Pericardium
/ diagnostic imaging
Retrospective Studies
Aortic stenosis
Epicardial adipose tissue
Inflammation
Statin
Journal
International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291
Informations de publication
Date de publication:
01 Jan 2019
01 Jan 2019
Historique:
received:
14
05
2018
revised:
12
06
2018
accepted:
27
06
2018
entrez:
21
11
2018
pubmed:
21
11
2018
medline:
20
7
2019
Statut:
ppublish
Résumé
Epicardial adipose tissue (EAT) thickness and pro-inflammatory status has been shown to be associated with several cardiac diseases, including aortic stenosis (AS). Thus, cardiac visceral fat could represent a potential new target for drugs. In the present study we evaluate the effect of statin therapy on EAT accumulation and inflammation. Echocardiographic EAT thickness was assessed in 193 AS patients taking (n.87) and not taking (n.106) statins, undergoing cardiac surgery. To explore the association between statin therapy and EAT inflammation, EAT biopsies were obtained for cytokines immunoassay determination in EAT secretomes. An in vitro study was also conducted and the modulation of EAT and subcutaneous adipose tissue (SCAT) secretomes by atorvastatin was assessed in paired biopsies. Statin therapy was significantly associated with lower EAT thickness (p < 0.0001) and with lower levels of EAT-secreted inflammatory mediators (p < 0.0001). Of note, there was a significant correlation between EAT thickness and its pro-inflammatory status. In vitro, atorvastatin showed a direct anti-inflammatory effect on EAT which was significantly higher compared to the SCAT response to statin incubation (p < 0.0001). The present study indicates a robust association between statin therapy and reduced EAT accumulation in patients with AS. The present data also suggest a direct relationship between EAT thickness and its inflammatory status, both modulated by statin therapy. The in vitro results support the hypothesis of a direct action of statins on EAT secretory profile. Overall our data suggest EAT as a potential new therapeutic target for statin therapy.
Sections du résumé
BACKGROUND
BACKGROUND
Epicardial adipose tissue (EAT) thickness and pro-inflammatory status has been shown to be associated with several cardiac diseases, including aortic stenosis (AS). Thus, cardiac visceral fat could represent a potential new target for drugs. In the present study we evaluate the effect of statin therapy on EAT accumulation and inflammation.
METHODS
METHODS
Echocardiographic EAT thickness was assessed in 193 AS patients taking (n.87) and not taking (n.106) statins, undergoing cardiac surgery. To explore the association between statin therapy and EAT inflammation, EAT biopsies were obtained for cytokines immunoassay determination in EAT secretomes. An in vitro study was also conducted and the modulation of EAT and subcutaneous adipose tissue (SCAT) secretomes by atorvastatin was assessed in paired biopsies.
RESULTS
RESULTS
Statin therapy was significantly associated with lower EAT thickness (p < 0.0001) and with lower levels of EAT-secreted inflammatory mediators (p < 0.0001). Of note, there was a significant correlation between EAT thickness and its pro-inflammatory status. In vitro, atorvastatin showed a direct anti-inflammatory effect on EAT which was significantly higher compared to the SCAT response to statin incubation (p < 0.0001).
CONCLUSIONS
CONCLUSIONS
The present study indicates a robust association between statin therapy and reduced EAT accumulation in patients with AS. The present data also suggest a direct relationship between EAT thickness and its inflammatory status, both modulated by statin therapy. The in vitro results support the hypothesis of a direct action of statins on EAT secretory profile. Overall our data suggest EAT as a potential new therapeutic target for statin therapy.
Identifiants
pubmed: 30454723
pii: S0167-5273(18)33054-7
doi: 10.1016/j.ijcard.2018.06.106
pii:
doi:
Substances chimiques
Cytokines
0
Hydroxymethylglutaryl-CoA Reductase Inhibitors
0
Atorvastatin
A0JWA85V8F
Types de publication
Journal Article
Multicenter Study
Langues
eng
Sous-ensembles de citation
IM
Pagination
326-330Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2018 Elsevier B.V. All rights reserved.