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  1. Pyvovar S, Rudyk Y, Lozyk T, Galchinskaya V, Chenchik T
    PMID: 31215885
    The study was aimed at investigation of the effect of the "low triiodothyronin syndrome" (LT3S) on the course of heart failure (HF) developed on the background of post-infarction cardiosclerosis. The biennial study included 157 patients with HF (with a myocardial infarction on the background of coronary heart disease). During hospitalization, a standardized assessment was carried out, hemodynamic parameters, clinical and biochemical blood tests, levels of thyroid hormones (thyroid stimulating hormone (TSH), free T3f and T4f, reverse T3r) were determined. Statistical analysis has shown that for the diagnosis of LT3S in patients with HF on the background of post-infarction cardiosclerosis, it is advisable to use serum T3f level, ≤2.07 pmol/l. The frequency of LT3S in patients with HF during hospitalization is 17.8%. Patients with LT3S are younger, have larger left ventricular size, lower ejection fraction, a high relative risk of re-hospitalization within 2 years due to decompensation of HF (2.224 [1.363-3.630]). A regression model of the re-hospitalization of patients with HF has been described, which included: weight, thyroxine and triiodothyronine concentrations, non-toxic goiter, growth, total cholesterol levels and LDL cholesterol, blood granulocyte content. It is shown that the risk of re-hospitalization of patients with HF due to decompensation of the disease increases when the equation of this model exceeds ≥1,321 (sensitivity - 93.78% and specificity - 40.45%, p=0.0001).
  2. Pyvovar S, Rudyk I, Isayeva G, Lozyk T, Galchinskaya V, Bondar T
    PMID: 31804204
    The work was aimed at studying the relationship between the efficiency of bisoprolol and the polymorphism of β1- and β2-adrenergic receptors (β-AR) genes in patients with heart failure. The two-year study included 251 patients with heart failure (with myocardial infarction on the background of coronary heart disease). During hospitalization, a standardized examination and prescription of therapy was carried out, including β-adrenergic blocking agent (β1-AB) - bisoprolol. Afterward, 61 (24.4%) patients stopped taking β1-AB (bisoprolol) as a result of intolerance or violation of compliance; 190 patients took bisoprolol for 2 years. The frequency of rehospitalization (RH) due to decompensation of heart failure (HF) (or intravenous injection of loop diuretics), mortality, and the development of a composite endpoint (CE) for 2 years was taken into account. The control group consisted of 55 healthy individuals. Genotyping was performed using 3 polymorphisms (Gly389Arg of the β1-АR gene, Ser49Gly of the β1-АR gene, Gln27Glu of the β2-АR gene) using the polymerase chain reaction. Genetic and epidemiological analysis was carried out using the SNPStats program. The use of bisoprolol with HF reduces the risk of re-hospitalization (odds ratio (OR)=0.519 (0.278-0.967); p=0.037) and CE (OR=0.494 (0.271-0.900); p=0.030) for 2 years of treatment. Treatment of patients with bisoprolol in a dose of >5 mg leads to a decrease in the risk of CE with G/A polymorphism Ser49Gly (c.145A> G) of the β1-AR gene (OR=0.18 (0.04-0.84), with p=0.014). The use of this drug at this dose also leads to a decrease in the frequency of RH and CE with the homozygous genotype C (C/C) of the Gln27Glu polymorphism (c.79C>G) of the β2-AR gene (OR=0.09 (0.02-0.46), at p=0.018 and OR=0.14 (0.04-0.58), at p=0.006, respectively).
  3. Antonova I, Gridnyev O, Galchinskaya V
    Wiad Lek, 2022;75(11 pt 2):2779-2784.
    PMID: 36591768 DOI: 10.36740/WLek202211211
    OBJECTIVE: The aim: The aim of the present study was to establish a link between polymorphic variants of the microsomal epoxide hydrolase gene and the severity of COPD in patients with COPD and coronary heart disease.

    PATIENTS AND METHODS: Materials and methods: The study included 128 patients with COPD and IHD, who were divided into two groups: group 1 included 72 patients with in¬frequent exacerbations of COPD (0-1 per year) and group 2 included 56 patients with frequent exacerbations of COPD (exacerbation of COPD ≥2 per year). The control groups consisted of 15 smokers without COPD and IHD, 11 practically healthy non-smokers and 11 patients with IHD who do not smoke. All patients underwent DNA isolation and purification, followed by determination of the Tyr113His polymorphism of the EPHX1 microsomal epoxide hydrolase gene (rs1051740).

    RESULTS: Results: There was a significant association of the carriage of the CC genotype of the EPHX1 gene in patients with COPD and IHD (RO = 21.326 [95.0% CI 4.217-107.846], p <0.001) with a more severe course of COPD compared with the TT genotype of the EPHX1 gene.

    CONCLUSION: Conclusions: Patients with COPD and coronary heart disease who were carriers of a homozygous variant СС of the EPHX1 gene have a reliable association with a more severe course of COPD with frequent exacerbations (higher class according to GOLD classification and more severe symptoms of COPD according to the СAT questionnaire).

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