Role of B2-adrenoreceptors Polymorphism in the Development of Cardiovascular Complications in Severe Pneumonia with AH1N1/09 B Influenza in 2019 in Zabaykalsky Territory

The purpose of the study. Th e aim of this study was to study the polymorphism of the ADRB2 gene, as well as the frequency and nature of cardiovascular complications in its presence in patients with severe pneumonia with infl uenza A/H1N1/09. Material and methods. Th e study included 100 patients with pneumonia with infl uenza A/H1N1 / 09 in 2019 in the Trans-Baikal Territory. All patients were treated in the intensive care unit. In patients, the causative agent-infl uenza virus A/H1N1 / 09 was verifi ed by PCR-detection of the pathogen in nasopharyngeal smears or hemagglutination inhibition test (HIT) with an increase in the antibody titer in paired sera. DNA was isolated from peripheral blood leukocytes; fragments were amplifi ed by polymerase reaction and genotyped by short fragment length polymorphism for Gln27Glu and Arg16Gly ADRB2. Results. The patients were divided into 2 groups: Group I (n=41) – patients with cardiovascular complications; group II (n=59) – patients without cardiovascular complications. Th e groups were comparable in gender and age. Among the cardiovascular complications prevailed: arrhythmias (n=13); decompensation of chronic heart failure (n=13); acute myocardial infarction (n=7); pulmonary embolism (n=5); myocarditis/pericarditis (n=3). When studying the ADRB2 polymorphism, it was found that the most unfavorable variant is the homozygous mutation Arg16Gly (Gly/Gly). This mutation was detected in 6 (14.6 %) patients in group I, but was not detected in group II (P=0.003). In the presence of this mutation in patients with severe secondary viral-bacterial pneumonia with infl uenza A/H1N1 / 09, the risk of developing cardiovascular complications increases (HR=2.6; CI 2.06; 3.49). Conclusion. Patients with severe pneumonia during the A/H1N1/09 infl uenza epidemic in 2019 had a high incidence of cardiovascular complications (41 %). The presence of the homozygous Arg16Gly mutation (Gly/Gly) increases the risk of cardiovascular complications by 2.06 times, and the presence of the heterozygous Arg16Gly mutation (Arg/Gly) reduces this risk by 0.5 times