In this study, we assessed the impact of COVID-19 on the course of HFmrEF by determining the biomarkers furin and NT-proBNP, questionnaires (EQ-5D-5L), and cardiac ultrasound. A comprehensive examination of 72 patients with HFmrEF (main group) and 18 apparently healthy individuals (control group). The main group was divided into two subgroups depending on the history of coronavirus disease. All patients gave their consent to participate in the study. In the group of patients with a history of coronavirus infection compared to the patients without a COVID-19 history were established: significantly higher concentrations of NT-proBNP (1002.79±215.94 pg/ml and 405.37±99.06 pg/ml, respectively, p-value 0.01), uric acid (429.08±27.01 mmol/l vs. 354.44±28.75 mmol/l, p-value 0.04) and a lower furin to NT-proBNP ratio (0.87± 0.26 and 1.38 ± 1.16, p-value 0.045) in blood serum; using the EQ-5D-5L questionnaire, a significant deterioration of quality of life indicators (64.21±3.04 points vs. 72.81±1.82 points by VAS, p-value 0.02); higher indicators of LVMMi (157.39±6.14 g/m2 and 138.68±6.02 g/m2, p-value 0.03), LA dimensions (43.74±0.95 mm and 41.12±0.85 mm, p-value 0.04) and RA dimensions (40.76±1.23 mm and 37.75±0.85 mm, p-value 0.04). Coronavirus infection in patients with HFmrEF leads to disorders of intracardiac hemodynamics and persistent negative structural changes of the heart. The ratio of furin to NT-proBNP serum levels can be used to determine the impact of the HF syndrome itself on the patients' subjective assessment of their quality of life.
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).
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).