Abstract
Aim. To analyze the changes of advanced glycation end products (AGE) and galectin-3, their relationship in patients with chronic heart failure (CHF) and atrial fibrillation (AF), depending on the renal functional and age. Material and methods. 30 patients with CHF II-III FC according to the classification of the New York Heart Association (NYHA) with preserved systolic function were examined (EF >45 %, mean 58.73 [45.38, 88.00] %), mean age 66.86 [46.00, 85.00] years who were on treatment in the Regional Hospital after I.I. Mechnikov. Men accounted for 60 % (18 people), women - 40 % (12 people). All patients were with AF: 17 (56.7 %) - with a permanent form, 13 (43.3 %) - with persistent. The serum creatinine level was determined and the GFR was calculated by CKD-EPI. The level of galectin-3 in the blood was determined by immunofermentive analis using the “Human Galectin-3 Platinum ELISA” kit (GmbH, Austria) on the Stat Fax 2100 (USA) immunofermentive plate analyzer. The fluorescent AGEs in plasma were analysed by quantitative autofluorescence (fluorimeter Hoefer DQ 2000, USA) with fixed spectrum of excitation at 460 nm with 20 % quinine solution as a standard with results expressed with conversion to glycated albumin. Results. AGE (mean 1.579 [0.884, 2.796]) and galectin-3 (mean 8.542 [2.72, 17.73]) levels increased in 83.3 % (25 patients) and 23.3 % (7 patients) respectively. The level of galectin-3 increased with age (by 33.18 %, p<0.05), while the level of AGE did not have significant changes. Levels of AGE and galectin-3 increased with a decrease in GFR (by 18.9 %, p<0.05 and 18.44 %, p<0.05, respectively). The level of AGE and serum creatinine correlated to GFR (r=0.25, p<0.05 and r=-0.22, p<0.05, respectively), while the level of galectin-3 correlated to GFR (r=-0.16, p<0.05). Intake of irbesartan reduced the level of galectin-3 (by 21.66 %) and AGE (by 4.9 %). The level of serum creatinine was decreased (by 4.89 %) and GFR was increased (by 6.3 %) compared with the intake of ACE inhibitors (by 2.9 % and 1.02 %, respectively). Discussion. The results showed changes in AGE with a decrease in GFR in patients with CHF and AF, which makes it possible to consider AGE, as a marker of cardiorenal syndrome and makes it promising to further study it. Galectin-3 showed itself not only as a diagnostic marker, but also as a dynamic (positive effect of using irbesartan). Irbesartan had comparable clinical efficacy with ACE inhibitors in patients with CHF and AF. Conclusions. Among patients with CHF and AF, the level of AGE was increased 83.3 % of patients, galectin-3 - in 23.3 %. Depending on the age, priority was given to galectin-3 (an increase of 33.18 %, p<0.05). The levels of AGE and galectin-3 depends of GFR and were increased (by 18.9 % and 18.44 %, p <0.05 respectively). The use of irbesartan showed a more significant positive effect on the level of galectin-3 and AGE with GFR in the range <60≥30 ml/min/1.73 m2.
Highlights
Chronic cardiovascular diseases (CVD) and chro kidney diseases (KD) are closely interrelated, and they share common risk factors
Materials and methods 30 patients with chronic heart failure (CHF) II-III FC according to the classification of the New York Heart Association (NYHA) with preserved systolic function were examined (EF>45 %, mean 58.73 [45.38, 88.00] %), mean age 66.86 [46.00, 85.00] years who were on treatment in the Regional Hospital a fter I
The results showed that with a decrease in glomerular filtration rate (GFR) there was an increase in the level of both advanced glycation end products (AGE) and galectin-3
Summary
Chronic cardiovascular diseases (CVD) and chro kidney diseases (KD) are closely interrelated, and they share common risk factors. The earliest product of the addition of glucose to the protein is Ne-fructosyl-lysine (PL), with the slow degradation of which various advanced glycation end products (AGE) are formed. Dicarbonyl compounds of endogenous origin, as well as glyoxal, methylglyoxal and 3-deoxyglucosone have an expressed ability to glycate proteins. They are formed by the degradation of glycated proteins, intermediate metabolites of glycolysis and lipid peroxidation. Dicarbonyl compounds directly react with proteins to form AGE [2]. Hydroimidazolones are formed as the final glycation products, which are derivatives of arginine residues modified by glyoxal, methylglyoxal and 3-deoxyglucosone (3-DG), -Nδ- (5-hydro-4-imidazolon-2-yl) ornithine G-H1), Nδ-(5-hydro-5-methyl-4-imidazolon-2-yl)ornithine (MG-H1) and Nδ-(5-hydro-5-(2,3,4-trihydroxybutyl) – 4-imidazolon-2-yl)ornithine and related structural isomers (3DG-H). Other widely studied AGEs are Nδ-carboxymethyl-lysine (CML) and Nδ-carboxyethyl-lysine (CEL), as well as derivatives of cross-linking proteins – pentosidine and glucosezane [2]
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have