Key result
Lower adiponectin and higher hsCRP and C-peptide predict pronounced EAT adipocyte hypertrophy with 82% accuracy.
Why the study?
Data on factors determining the severity of epicardial adipose tissue adipocyte hypertrophy in patients with coronary atherosclerosis are lacking in the literature.
Cross-Sectional (n=42)
Decreased adiponectin and increased hsCRP and C-peptide levels are strongly correlated with epicardial adipocyte hypertrophy in patients with CAD undergoing CABG.
May support noninvasive epicardial fat assessment in CAD; hypothesis-generating, requires prospective validation before clinical use.
The changes of epicardial adipose tissue’s (EAT) morphofunctional characteristics represent an important factor of cardiometabolic impairments development. However, factor data determining the severity of EAT adipocytes’ hypertrophy in patients with coronary atherosclerosis are absent in literature. Aim: To compare the size of the EAT adipocyte and the percentage of hypertrophied adipocytes with the parameters of glucose/insulin metabolism, blood lipid transport function, adipokines’ profile and serum levels of high sensitive C-reactive protein (hsCRP) in patients with chronic coronary artery disease (CAD) undergoing coronary artery bypass grafting (CABG); to establish statistically significant determinants of a pronou ced degree of EAT adipocytes’ hypertrophy. Material and Methods. The study included 42 patients (m/f 28/14) aged 53–72 y.o. with CAD, who underwent CABG. The material for the study was EAT adipocytes obtained by the enzymatic method from intraoperative explants. The basal blood levels of glycemia, insulinemia, C-peptide, blood lipid transport function, adipokines and hsCRP were determined. The median indicators of the size of EAT adipocytes and the proportion of EAT adipocytes over 100 μm were 87.32 μm and 14.64%, respectively. The total sample of patients was divided into two groups: gr. 1 with an average size of EAT adipocytes less than or equal to 87.32 μm and gr. 2 with an average size of EAT adipocytes more than 87.32 μm. Gr. 2 had higher body mass index, waist and hip circumferences, triglycerides, hsCRP, and lower adiponectin levels, while the median proportion of hypertrophied adipocytes was three times higher than in group 1. A model of multiple logistic regression was constructed, according to which statistically significant determinants of the pronounced EAT adipocytes’ hypertrophy are represented by the decreased level of adiponectin, and increased concentrations of hsCRP and C-peptide, which reflects the biosynthesis and secretion of insulin. The predictive accuracy of the model was 82%, sensitivity 85%, specificity 79%, AUC = 0.89. Conclusion. Our results indicate a close correlation between the development of EAT adipocytes hypertrophy, impaired production of adiponectin, insulin, and inflammation processes. Concentrations of adiponectin, hsCRP, and basal C-peptide in the blood are biomarkers that accurately determine the presence of EAT adipocyte hypertrophy.
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Koshelskaya et al. (2023) conducted a cross-sectional in Chronic coronary artery disease (CAD) (n=42). Pronounced EAT adipocytes' hypertrophy (> 87.32 μm) vs. EAT adipocytes ≤ 87.32 μm was evaluated on Statistically significant determinants of pronounced EAT adipocytes' hypertrophy. Decreased adiponectin and increased hsCRP and C-peptide accurately predicted pronounced epicardial adipose tissue adipocyte hypertrophy (AUC = 0.89, accuracy 82%).
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