Predictors of myocardial fibrosis and loss of epicardial adipose tissue volume in the long-term period after myocardial infarction

Abstract

Aim. To assess the changes of biochemical markers in hospitalization, the relationship with the severity of myocardial fibrosis and the epicardial adipose tissue (EAT) thickness one year after myocardial infarction (MI).Material and methods. A total of 88 patients (65 men and 23 women) with MI were examined. The percentage of cicatricial changes in the myocardium and the EAT thickness were measured using the magnetic resonance imaging (MRI) one year after MI. In the hospitalization (days 1 and 12) and 1 year after MI, the concentrations of N-terminal pro-brain natriuretic peptide (NT-proBNP), stimulating growth factor (ST2), interleukin-33 (IL-33) and type I collagen (COL-1). The data were analyzed using descriptive statistics, correlation and ROC analysis, and logistic regression (Statistica 9.0).Results. One year after MI, cicatricial changes were detected in 68 (77%) patients: 27 people had myocardial fibrosis <5%, 22 patients — 5-15%, and 19 patients >15%. We established that myocardial fibrosis after MI is associated with unfavorable medical history, a complicated course during in-hospital period and higher concentrations of ST2, NT-proBNP, COL-1 compared with patients without myocardial fibrosis. High levels of ST2, NT-proBNP increase the risk of myocardial fibrosis by 1,2 and 1,8 times after hospitalization, respectively. In patients with myocardial fibrosis >15%, IL-33 level was significantly lower in the 1st day of MI. It was found that the EAT thickness increases with fibrosis of 5-15%. An increase in the left (LV) and right ventricular (RV) EAT thickness by 1,33 times and 1,34 times, respectively, increases the risk of myocardial fibrosis (LV EAT thickness, mm (OR 1,33; 95% CI (1,08-1,4), AUC 0,75; RV EAT thickness, mm (OR 1,34; 95% CI (1,15-1,43), AUC 0,79). In patients with myocardial fibrosis >15%, EAT thickness decreases and correlates with NT-proBNP increase in the acute period and a one year after MI.Conclusion. The development of myocardial fibrosis one year after MI is associated with an increase in ST2, NT-proBNP, COL-1, both in the hospitalization and 1 year after MI. The decrease in IL-33 concentration during hospitalization with MI is accompanied by the development of fibrosis >15% of the myocardium.