Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2018 Mar 16;17(1):40.
doi: 10.1186/s12933-018-0679-y.

Relationships between epicardial adipose tissue thickness and adipo-fibrokine indicator profiles post-myocardial infarction

Olga Gruzdeva  1   2 , Evgenya Uchasova  3 , Yulia Dyleva  1 , Daria Borodkina  4 , Olga Akbasheva  5 , Ekaterina Belik  1 , Viktoria Karetnikova  1   2 , Natalia Brel  1 , Alexander Kokov  1 , Vasiliy Kashtalap  1 , Olga Barbarash  1
Affiliations

Relationships between epicardial adipose tissue thickness and adipo-fibrokine indicator profiles post-myocardial infarction

Olga Gruzdeva et al. Cardiovasc Diabetol. .

Abstract

Background: Determination of the impact of visceral obesity and epicardial adipose tissue thickness on stimulating growth factor levels during hospitalization for myocardial infarction is of potential importance for predicting outcomes and assessing the development of cardiofibrotic changes associated with maladaptive myocardial remodeling. In this study, we aimed to investigate the relationships between epicardial adipose tissue thickness, adipokine profiles, and the stimulating growth factor 2/interleukin-33 signaling system during hospitalization for myocardial infarction, and with the cardiac fibrosis extent 1-year post-MI in patients with visceral obesity.

Methods: Eighty-eight patients with myocardial infarction were grouped based on their visceral obesity. Serum leptin, adiponectin, stimulating growth factor 2, and interleukin-33 levels were measured on days 1 and 12 and at 1 year. The epicardial adipose tissue widths and the cardiac fibrosis areas were measured on day 12 and at 1 year.

Results: Visceral obesity was associated with epicardial adipose tissue thickness increases, adipokine imbalances, elevated leptin levels, and lower adiponectin levels during early hospitalization, and cardiac fibrosis development. Patients without visceral obesity had higher interleukin-33 and stimulating growth factor 2 levels during early hospitalization and lower cardiac fibrosis rates. Epicardial adipose tissue thickness was positively associated with cardiac fibrosis prevalence and interleukin-33 levels and negatively associated with stimulating growth factor 2 levels. The cardiac fibrosis extent was negatively associated with interleukin-33 levels and positively associated with stimulating growth factor 2 levels.

Conclusions: Increases in epicardial adipose tissue thickness are associated with cardiac fibrosis development 1-year post-myocardial infarction and are higher in patients with visceral obesity. The metabolic activity of the epicardial adipose tissue is associated with elevated interleukin-33 and reduced stimulating growth factor 2 levels.

Keywords: Adiponectin; Cardiac fibrosis; Epicardial adipose tissue; Interleukin-33; Stimulating growth factor 2; Visceral obesity.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Epicardial fat (red arrows) on the MRI of the heart on a short axis
Fig. 2
Fig. 2
Myocardial fibrosis (white arrows) on T1-weighted images late enhancement. Short axis of the left ventricle of the heart
Fig. 3
Fig. 3
Levels of adipokines in patients with myocardial infarctions according to the presence of visceral obesity. OB-R soluble leptin receptor, FLI free leptin index, MI myocardial infarction. The data presented are the medians and the 25th and 75th quartiles. ap < 0.05 compared with the control group, bp < 0.05 for the levels measured on days 1 and 12 post-MI; cp < 0.05 for the levels measured on day 1 and at 1-year post-MI; dp < 0.05 for the levels measured on day 12 and at 1-year post-MI; ep < 0.05 for comparisons between the study groups
Fig. 4
Fig. 4
Correlations between the adipokines and the stimulating growth factor 2/interleukin-33 and the degree of cardiac fibrosis in patients without visceral obesity. sOB-R soluble leptin receptor, ST stimulating growth factor, IL interleukin, MI myocardial infarction, r correlation coefficient
Fig. 5
Fig. 5
Correlations between the adipokines and the stimulating growth factor 2/interleukin-33 and the degree of cardiac fibrosis in patients with visceral obesity
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Fuster JJ, Ouchi N, Gokce N, Walsh K. Obesity-induced changes in adipose tissue microenvironment and their impact on cardiovascular disease. Circ Res. 2016;118:1786–1807. doi: 10.1161/CIRCRESAHA.115.306885. - DOI - PMC - PubMed
    1. Ma Y, Iyer RP, Jung M, Czubryt MP, Lindsey ML. Cardiac fibroblast activation post-myocardial infarction: current knowledge gaps. Trends Pharmacol Sci. 2017;38:448–458. doi: 10.1016/j.tips.2017.03.001. - DOI - PMC - PubMed
    1. Wu Y, Zhang A, Hamilton DJ, Deng T. Epicardial fat in the maintenance of cardiovascular health methodist debakey. Cardiovasc J. 2017;13:20–24. - PMC - PubMed
    1. Ciccone MM, Cortese F, Gesualdo M, Riccardi R, Di Nunzio D, Moncelli M. Novel cardiac bio-marker: ST2: a review. Molecules. 2013;18:15314–15328. doi: 10.3390/molecules181215314. - DOI - PMC - PubMed
    1. Venteclef N, Guglielmi V, Balse E, Gaborit B, Cotillard A, Atassi F, et al. Human epicardial adipose tissue induces fibrosis of the atrial myocardium through the secretion of adipo-fibrokines. Eur Heart J. 2015;36:795–805. doi: 10.1093/eurheartj/eht099. - DOI - PubMed

Publication types

MeSH terms