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Biomarkers of fibrosis, renal dysfunction and inflammation, their correlations in patients with chronic heart failure of ischemic etiology

Medvedeva E. A.
Federal State Budgetary Institution «Federal Almazov North-West Medical Research Center» of the Ministry of Health of the Russian Federation, Akkuratova 2, St. Petersburg 197341

Keywords: heart failure, renal dysfunction, fibrosis, inflammation, galectin-3, ST-2

DOI: 10.18087/rhfj.2017.2.2302

Background. The biomarker strategy of managing patients with CHF in the aspects of diagnosis, prediction and evaluation of the treatment efficacy has been extensively studied in the recent decades. At the same time, interrelations of cardiac fibrotic processes with other pathogenetically and predictively important markers associated with inflammation, myocardial stress, and renal dysfunction remain understudied. Aim. To evaluate concentrations of biomarkers for fibrosis, renal dysfunction, and inflammation and their correlations in CHF patients with EF ≥40 % after MI. Materials and methods. The study included 103 patients with CHF after MI who had a history of primary transcutaneous coronary intervention (TCI), with preserved or intermediate ejection fraction (EF >40 %) and NTproBNP >125 pg / ml. The reference group consisted of 51 patients who had had MI without signs of CHF and had NT-pro BNP <125 pg / ml. A general clinical examination and EchoCG were performed for all patients. The immunoenzyme method was used to measure galectin 3 and ST-2 as fibrosis markers; as parameters of renal dysfunction, concentration of cystatin C was measured and glomerular filtration rate (GFR) was calculated using the CKD-EPI formula. Endogenous inflammation was evaluated by hsCRP concentration. Results. In the main group (group 1), the median (quartiles 1 and 3) concentration of NT-proBNP was 445.23 (245.39–896.93) pg/ml vs. 67.16 (40.17–86.61) pg / ml in the reference group. Plasma levels of ST-2 did not significantly differ between patients with CHF (40.70; 33.45–49.27 ng/ml) and reference group patients without CHF (39.21; 32.64–46.38 ng/ml) (р>0.05) and were higher than the margin level of 35 ng / ml. In group 1, the plasma level of cystatin C was 987.67 (854.68–1161.19) ng / ml and GFR was 58.5 ml / min / 1.73 m2 (44.0–79) and did not significantly differ from the reference group. In patients with CHF, strong negative correlations were found for galectin 3 and GFR (r1= –0.49; p<0.01) and positive correlations were found for galectin 3 and cystatin C (r1=0.62, p<0.01); the correlation of ST-2 and cystatin C was not significant (r1=0.21; p>0.05). Also, significant correlations were found for ST-2 and NT-proBNP in patients with CHF (r1=0.36; р<0.01) and for galectin 3 with NT-proBNP (r1=0.38) and galectin 3 with hsCRP (r1=0.56; р<0.01); no significant correlations were observed in the reference group. Conclusion. In patients with CHF after MI, plasma concentrations of ST-2 and galectin 3 correlated with NTproBNP concentrations. Levels of galectin 3 correlated with renal dysfunction and the marker of endogenous inflammation.
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Medvedeva E. A. Biomarkers of fibrosis, renal dysfunction and inflammation, its correlations in patients with chronic heart failure of ischemic etiology. Russian Heart Failure Journal. 2017;18 (2):83–86

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