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Relationships between the activity of neurohormonal systems and intracardiac hemodynamics in patients with heart failure: focus on galectin-3

В. И. Подзолков, N. A. Dragomiretsksya, A. V. Kazadaeva, Yu. G. Beliaev, А. В. Толмачева

2022Russian Journal of Cardiology27 citationsDOIOpen Access PDF

Abstract

The introduction of novel biomarkers necessitates their detailed study in patients with different heart failure (HF) phenotypes as part of a personalized approach to assessing the disease severity and predicting outcomes. Aim . To assessthe activity of following neurohormonal systems: N-terminal probrain natriuretic peptide (NT-proBNP) and galectin-3 in HF with preserved, mildly reduced and reduced ejection fraction (EF). Material and methods . In 69 patients with NYHA class II-IV HF, along with a general clinical examination, the level of NT-proBNP and serum galectin-3 was determined by enzyme immunoassay. Results . Patients included in the study were divided into 3 groups: preserved EF (HFpEF) — 23 patients, mildly reduced EF (HFmrEF) — 26 patients, and reduced EF (HFrEF) — 20 patients. In patients with HF, the level of galectin-3 did not directly depend on EF, but was associated with NT-proBNP level as follows: there was a tendency to increase the concentration of galectin-3 in the tertile groups of NT-proBNP. Correlation analysis revealed significant feedback (r=-0,41, p<0,05) between galectin-3 and left ventricular EF only in patients with preserved systolic function. In the same group of HFpEF patients, the maximum values of serum galectin-3 indices were noted, reaching 10,5 [6,5; 14,5] ng/ml. Conclusion . Analysis of neurohormonal activity demonstrated a unidirectional increase in NT-proBNP and galectin-3 in patients with HF, regardless of left ventricular EF, while the maximum values of galetin-3 were observed in patients with HFpEF.

Topics & Concepts

MedicineGalectin-3Internal medicineHeart failureEjection fractionCardiologyNatriuretic peptideIntracardiac injectionGalectins and Cancer BiologyPeptidase Inhibition and AnalysisSignaling Pathways in Disease