Prognostic potential of cardiac structural and functional parameters and N-terminal propeptide of type III procollagen in predicting cardiac fibrosis one year after myocardial infarction with preserved left ventricular ejection fraction.

The aim of the study were to evaluate the prognostic potential of serum level of N-terminal propeptide procollagen type III (PIIINP) and heart parameters for predicting heart cardiac fibrosis 1 year after ST-segment elevation myocardial infarction (STEMI) with preserved left ventricular ejection fraction (LVEF). 68 patients with STEMI and preserved LVEF with acute heart failure of the I-III degree according to the Killip classification were examined. Echocardiography was performed and PIIINP levels were measured on days 1 and 12, as well as 1 year after STEMI. A year after STEMI, was performed contrast magnetic resonance imaging and patients were assigned into four groups depending on the severity of cardiac fibrosis: cardiac fibrosis 0% (n=49, 57% of 86 patients); ≤5% (n=18, 20.9%); 6-15% (n=10, 11.6%); ≥16% (n=9, 10.5%). Direct correlations between the severity of cardiac fibrosis, PIIINP level and indicators of diastolic function were established. The risk of cardiac fibrosis increases at the level of PIIINP ≥381.4 ng / ml on the 12th day after STEMI with preserved LVEF (p=0.048). Thus, measuring the level of PIIINP in the inpatient period can allow timely identification of patients with a high risk of cardiac fibrosis 1 year after STEMI with preserved LVEF.

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

The aim of this study was to determine the relationship between the thickness of epicardial adipose tissue (EAT) and perivascular adipose tissue (PVAT) and the adipokine-cytokine profile of patients with coronary heart disease, which can be of significant importance for predicting the course of cardiovascular disease (CVD). Eighty-four patients with CVD were assessed and divided into two groups based on the presence of visceral obesity (VO). In patients with VO, the thickness of the epicardial deposits of the left and right ventricles were 1.75 and 1.43 times greater, respectively, than in patients without VO. For patients with VO, the prevalence of the volume of the left anterior descending artery was 10% higher, and the middle third of the envelope artery was 28% higher, when compared to patients without VO. When evaluating inflammatory status, it was established that the concentration of tumor necrosis factor-α, interleukin (IL)-1ß, and leptin in the blood serum of patients with VO exceeded the values of patients without VO. The level of anti-inflammatory IL-10 was 2-times lower in patients with VO. The findings of this study show that increased EAT and PVAT are independent risk factors of CVD, as well as a possible model for the assessment of drug effectiveness for CVD.

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

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.

Association of inflammatory markers and poor outcome in diabetic patients presenting with ST segment elevation myocardial infarction.

OBJECTIVE: Carbohydrate metabolism disorders (CMD) significantly impact the development and progression of all forms of ischemic heart disease, and inflammation is regarded as a general pathogenetic link between CMD and ischemic heart disease. METHODS: A total of 601 patients with ST segment elevation myocardial infarction (MI) (STEMI), admitted within 24 hours from the onset of symptoms during 1 year, were included in this registry study. The blood levels of inflammation markers were measured at days 10-14 with further follow up at 1 year. RESULTS: The analysis of acute-phase percutaneous coronary intervention impact on the 1-year outcomes showed that endovascular revascularization significantly improved the 1-year prognosis of STEMI patients both with and without CMD. The analysis of inflammation markers showed significantly higher levels of interleukin (IL)-6 and sCD40L in MI patients with diabetes mellitus, and impaired glucose tolerance. Additionally, the patients with impaired glucose tolerance had significantly higher IL-12 levels. In the diabetic MI patients, the odds ratio of a poor 1-year outcome was high for patients with a high Killip classification of acute heart failure upon admission. CONCLUSION: Persistent inflammation in STEMI patients with CMD undergoing percutaneous coronary intervention might be responsible for vascular complications within 1 year after MI. Comorbid diabetes mellitus or impaired glucose tolerance can amplify the significance of the inflammatory response for the development of adverse 1-year outcomes.