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.
Highlights
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
We showed that epicardial adipose tissue (EAT)-derived and circulating secreted frizzled-related protein 4 (SFRP4) expression levels are increased in patients with coronary artery disease (CAD) and in epicardial adipocytes of CAD patients, the concentrations of leptin, tumor necrosis factor-α, and IL-1, were higher, while the levels of adiponectin, IL-10, and FGF-β were lower than those in subcutaneous adipocytes [23, 24]
An increase in EAT thickness was closely related to the development of cardiac fibrosis at 1-year post-myocardial infarction (MI)
Summary
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. 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. Its visceral component, is central to the initiation of many pathophysiological processes, including cardiac fibrosis development [1]. The involvement of VAT in inflammatory responses renders it a key player in cardiac fibrosis development. EAT seems to play an important role in the inflammatory process within the atherosclerotic plaque which contributes to progression of coronary artery disease [7, 8]
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