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

Abstract

BackgroundDetermination 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.MethodsEighty-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.ResultsVisceral 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.ConclusionsIncreases 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.

Epicardial fat tissue in patients with diabetes mellitus: a systematic review and meta-analysis

“…Previous studies have suggested that measurements of EFT are a substitute for visceral fat [8,9] EFT can secrete inflammatory factors, such as TNF-alpha, IL-6, adipocytokines, and leptin, via paracrine or endocrine activities [9,10] to locally regulate the myocardium and coronary artery function and regulate lipid and energy homeostasis in vivo. EFT has the ability to release and uptake free fatty acids and to affect low glucose utilization, which plays an important role in metabolic syndrome and coronary artery disease [11][12][13][14][15][16]. EFT can be measured by echocardiography, cardiac magnetic resonance imaging, and computed tomography (CT) [17].…”

Relationship between epicardial and perivascular fatty tissue and adipokine-cytokine level in coronary artery disease patients

“…PVAT and EAT have the same embryological origin, and the increase in the size of either fat store is associated with the calcification of the coronary arteries [18,19], as well as the development of CAD [20]. Some researchers believe that an increase in the thickness of epicardial fat reflects the presence of visceral obesity in the body and serves as a prognostic marker of coronary heart disease and its associated complications [21]. The results obtained in this study show that EAT thickness is directly dependent on the value of the PVAT; this concurs with the results of previous studies [22,23].…”

Epicardial adipose tissue: pathophysiology and role in the development of cardiovascular diseases

“…Так, в ЭЖТ значительно более выраженная ýкспрессия IL-26, IL-1β, MCP-21, TNF-α и резистина по сравнению с подкожной жировой тканью [22]. Увеличение толщины ЭЖТ тесно связано с повышенным сердечно-сосудистым риском и уменьшением выделения адипокинов из ЭЖТ [23,24]. При наличии сердечно-сосудистых факторов риска, таких как ожирение, жировая ткань характеризуется повышенной инфильтрацией макрофагов, лимфоцитов и тучных клеток.…”