Abstract

Abstract The problem of cardiovascular comorbidity becomes particularly relevant in the context of a pandemic, since it is known that cardiovascular diseases (especially arterial hypertension – AH and coronary heart disease – CHD) significantly increase the frequency of hospitalizations and fatal outcomes in patients with COVID-19. From these positions, it is fundamentally important to identify a group of individuals with a high prognostic probability of developing combined cardiovascular pathology in the cohort of patients with hypertension. There is a hypothesis about the genetic relationship between different diseases, which helps to identify their common genetic variants, which in turn makes it possible to determine new loci of susceptibility for each of the comorbid conditions. Recent data indicate the feasibility of developing this problem from the standpoint of genetic polymorphism. Material and methods The work is based on the results of a comprehensive examination of 100 patients with AH. A molecular genetic study to determine the main variants of gene polymorphism was performed on a DT 96 amplifier manufactured by DNA Technology (Russia). The method for determining the variants of gene polymorphism was a polymerase chain reaction with real-time detection of the results. Results All patients included in the study were divided into 2 groups: patients with AH without CHD – 62% (62 people) and patients with AH with CHD – 38% (38 people). The relationships of polymorphism of 9 main variants of genes involved in the pathogenesis of isolated AH and in combination with CHD were studied. When analyzing the frequency of the studied genes in patients with hypertension with and without CHD, statistically significant differences were obtained for the NOS3 T-786C polymorphic gene, which was significantly more common in comorbid patients. Patients with a combination of AH and CHD are characterized by the presence of the CC genotype and the C allele of the VOS3 gene (p=0.040 and p=0.035), while the TT genotype of the T-786C polymorphic marker of the NOS3 gene is characteristic of patients with isolated AH. It should be noted that the carrier of the “mutant” allele C of the T-786C polymorphism of the NO3S gene, according to our calculated statistical data, increases the risk of CHD in patients with hypertension by 5 times (OR=5.242, p=0.035). Conclusion The study of the genetic aspects of comorbidity is theoretically important for understanding the mechanisms of its formation. From a practical point of view, it is valuable to use modern genetic approaches for early detection of a prognostically unfavorable category of AH patients with a high risk of comorbid pathology developing. Funding Acknowledgement Type of funding sources: None.

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