Abstract
Purpose. To study the influence of polymorphisms of arterial hypertension genes and their various combinations on individual risk factors of sudden cardiac death.
 Materials and methods. 319 young people from 18 to 24 years of age who are entering military service by conscription were examined. The survey identified 69 individuals with signs of increased risk of sudden cardiac death after being examined for secondary risk factors of sudden cardiac death and taken a blood test to determine the polymorphisms of the genes AGT 521 CT, GNB3 825 CT, CYP11B2 344 CT, NOS3 786 TC.
 Results. The greatest influence on the severity of secondary risk factors was exerted by the following variants of a combination of gene polymorphisms: AGT 521 CT and NOS3 786 TC in the individuals with a heterozygous risk variant, both genes showed a significant increase in the duration of the corrected QT interval, heart rate, and a decrease in heart rate variability. AGT 521 CT and CYP11B2 344 CT homozygous risk variant of the CYP11B2 344 CT and the heterozygous risk variant AGT 521 CT is associated with a longer duration of the corrected QT interval, and the heterozygous risk variant for both genes is associated with higher heart rate values. AGT 521 CT and GNB3 825 CT combination of a homozygous risk variant of the gene GNB3 825 CT and the heterozygous variant of the gene AGT 521 CT is associated with the greatest effect on a heart rate.
 Conclusions. The presence of a homozygous risk variant of the gene NOS3 786 TC, a heterozygous risk variant of the gene GNB3 825 CT is prognostically unfavorable for its effect on the severity of secondary risk factors for sudden cardiac death. The combination of the heterozygous variant AGT 521 CT with a heterozygous variant of NOS3 786 TC and a homozygous risk variant by the gene CYP11B2 344 CT and the heterozygous risk variant AGT 521 CT are also the most unfavorable in terms of its effect on secondary risk factors for sudden cardiac death. Secondary risk factors of sudden cardiac death are influenced by both individual polymorphisms of genes of arterial hypertension, and their various combinations.
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