Increase epicardial fat thickness predictors in stable coronary artery disease patients with borderline coronary artery stenosis

Aim. To identify increase epicardial fat thickness (EAT) predictors in stable coronary artery disease (CAD) patients with borderline coronary arteries stenosis. Material and methods. 201 stable CAD pts with borderline CA stenosis participated at the study. Patients underwent a physical examination, clinical and biochemical blood tests, assessment of systemic inflammation markers and atherosclerotic plaque stability, genetic markers, instrumental studies (ECG, ultrasound of the heart, neck vessels, coronary angiography, determination of instrumental markers of stiffness, cognitive functions and the presence of early vascular aging syndrome (EVAS) were assessed. Statistical calculations were performed in the RStudio program. Multivariate regression models were built using the forward and backward step methods of minimizing the Akaike information criterion (AIC). ROC analysis methods for risk formulas of multivariate models the best risk threshold based on the sum of sensitivity and specificity was calculated, and 95% CI was estimated. Results . The 1st group consisted of pts with phenotype stable CAD without diabetes mellitus (DM) and obesity (71 (35.3%) patients), the 2st group consisted of pts with phenotype stable CAD and type 2 DM (51 (25.4%) patients), the 3st group consisted of pts with phenotype stable CAD and metabolically unhealthy obesity phenotype (MUOF) (79 (39.3%) patients). In patients with stable coronary artery disease without DM and MUOF, the most significant predictor of increased EAT was the age of hypertension manifestation younger than 44.5 years (56 [11.58; 388.56], p < 0.001). The multivariate logistic regression model included following factors increased the odds of increased EAT in patients with stable CAD and DM: age at onset of hypertension younger than 44 years (59.92 [7.34; 1792.85], p = 0.002), fasting blood glucose level > 8.3 mmol/l (33.4 [3.92; 998.67], p = 0.007), and TNF-alpha level > 0.42 pg/ml (11.46 [1.17; 315.34], p = 0.069). In the group of patients with phenotype of CAD with MUOF, it was found that an increase of anti-inflammatory IL-10 level reduced the chances of an increase in EAT (p = 0.101), as well as taking the main groups of drugs affecting CAD prognosis during preceding year (p = 0.020). At the same time, the presence of more than 22.5 points on the MMSE scale increased the chances of an increase in EAT (p = 0.043). Conclusion. Predictors of an increase EAT varied depending on the clinical phenotype of CAD and mainly consisted of indicators characteristic of EVAS, namely, the early hypertension debut and systemic inflammation markers activated our data once again indicate a close relationship between increase EAT, as an important predictor of the development of CVD in general, and CAD in particular, and EVAS, which is one of the fundamental factors in CVD development in young people.