Abstract

Background. Individual genetic features can influence to formation of structural and functional changes in organs during EH and encourage the search for biological markers of the state of the myocardium and conclusions about their diagnostic effectiveness.
 Aim: to improve the early diagnosis of changes in the structure and function of the myocardium and the formation of prerequisites for chronic heart failure (CHF) in women with EH carriers of various polymorphic variants of the LGALS-3 gene (rs2274273), based on galectin-3 plasma level.
 Materials and methods.  180 postmenopausal women, average age 57,34±0,45, residents of the Podillya region of Ukraine were examined. The main group included 113 women with EH, of which 62 people had EH II, 51 people - EH with CHF C stage according to the ESH 2023 classification. The control group included 67 women without signs of cardiovascular pathology. In addition to the general clinical examination, the research used the enzyme immunoassay method to determine the level of galectin-3 in blood plasma, genotyping of the LGALS3 gene (rs2274273) by means of polymerase chain reaction, and ultrasound of the heart. The statistical processing of the obtained results was carried out using the package of statistical programs SPSS, STATISTICA v. 10.0. Using the MedCalc Software Ltd. Odds ratio calculator (https://www.medcalc.org/calc/odds_ratio.php) the conformity of the frequency distribution of genotypes in the studied population to the Hardy-Weinberg equilibrium was checked and calculated the odds ratio (OR) of the development of left ventricular myocardial hypertrophy (LVH) and CHF on the background of EH. The threshold levels of galectin-3 in blood plasma for the diagnosis of LVH and CHF were calculated using the ROC analysis method.
 Results. During study the frequency distribution of genotype variants of the galectin-3 gene (rs2274273) among women residents of the Podillya region of Ukraine, it was found that both in people without cardiovascular pathology and in patients with EH II and EH III, the GA genotype predominates, although there is a significant difference between the frequency of occurrence genotypes GA and GG are not noted (p>0.05). The AA genotype variant is significantly less frequent than both the GA and GG genotypes (p<0.01). The frequency distribution of genotype variants corresponds to the Hardy-Weinberg equilibrium. Moreover, the ratio between genotypes in patients of different stages of EH does not reliably differ from that in the control group. However, in EH complicated by CHF among patients with LVEF < 50% A allele carriers significantly predominate compared to GG homozygotes (79.31%, n=23 vs. 20.69%, n=6). In patients with EH, it was found that the concentration of galectin-3 in blood plasma in carriers of the A allele is significantly higher than in carriers of the GG genotype: EH without CHF - 16.82±0.54 ng/ml vs. 12.82±0.54 ng/ml (p<0.01); EH with CHF – 35.70±1.53 ng/ml vs. 25.39±1.38 ng/ml (p<0.001). The threshold levels of galectin-3 plasma concentrations, which indicate the presence of LVH and CHF, are significantly higher in carriers of the A allele than in carriers of the GG genotype.
 Conclusion. The carriers of the A allele of the LGALS3 gene (rs2274273) have a greater chance of developing CHF with a LVEF < 50% (OR 4.60; 95% CI 1.35 - 15.73 z statistic 2.43 p<0.01 χ2=6 .28; p=0.0122) and correspondingly higher levels of galectin-3 in blood plasma compared to carriers of the GG genotype.

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