Abstract

The systematization of literature data on the associations of β-adrenoreceptors (β-AR) genes polymorphisms with the course of heart failure (HF) and with the development of low triiodothyronine syndrome (LT3S), and the results of our own study were presented. The study of associations of β-AR system genes polymorphisms with the clinical outcome of HF and the effectiveness of β-adrenoblockers (β-AB) has been continued. It has been demonstrated that carrier state of the A allele of the Ser49Gly (c.145A > G) polymorphism of the b1-AR gene leads to a decrease in the risk of combined end point. At the same time, the carrier state of the G allele of the Gln27Glu (c.79C> G) polymorphism of the b2-AR gene increases the risk of combined end point. Administration of bisoprolol at a dose of > 5 mg leads to a reduction of the risk of the combined endpoint, provided the G/A genotype of the Ser49Gly (c.145A > G) polymorphism of the β1-AR gene is present. The use of bisoprolol at this dose also reduces the risk of re-hospitalisation and combined endpoint, provided the homozygous genotype (C/C) of the Gln27Glu (c.79C > G) polymorphism of the β2-AR gene is present. The probability of the low triiodothyronine syndrome increases with the homozygous G/G genotype of the Gln27Glu polymorphism of the β2-AR gene and in the presence of the C/T polymorphism of the Serβ75 GNβ3 gene. The genotype C/G of the Gln27Glu polymorphism of the β2-AR gene is associated with a decreased risk of LT3S.

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