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Pol. Merkur. Lek (Pol. Med. J.), 2019, XLVII/281: 170-176 Maximize

Pol. Merkur. Lek (Pol. Med. J.), 2019, XLVII/281: 170-176

Title: The association of polymorphisms of β-adrenergic receptors genes with the low triiodothyronine syndrome in patients with a heart failure 

Authors: Pyvovar SM, Rudyk IS, Kopytsya MP, Lozyk TV, Galchinskaya VY, Bondar TM. 

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The association of polymorphisms of β-adrenergic receptors genes with the low triio
dothyronine syndrome in patients with a heart failure

Pyvovar SM, Rudyk IS, Kopytsya MP, Lozyk TV, Galchinskaya VY, Bondar TM.

Government Institution L.T. Malaya Therapy National Institute of the National Academy of Medical Sciences of Ukraine, Kharkiv, Ukraine

The course of heart failure (HF) and its progression is associated with comorbidities, genetic factors and a dynamics of a number of biomarkers. The low triiodothyronine syndrome (LT3S) is observed in some patients with HF. Extremely little data are available in the literature regarding the effect of  β-adrenoreceptors (β-AR) genes polymorphisms on the development of LT3S and many contradictory results about their association with HF course. This encourages new research in this area.
The aim of study
was to evaluate the relationship of β-adrenergic receptors gene polymorphisms with low triiodothyronine syndrome in patients with a heart failure.
Materials and methods
. 354 patients with HF on a background of postinfarction cardiosclerosis were included to the study. At 89 (25.1%) patients LT3S was diagnosed. The course of HF was studied for 2 years. Mean levels of thyroid stimulating hormone (TSH), free T3f and T4f were evaluated. Genotyping of 4 single nucleotide polymorphisms (Gly389Arg of β1-AR gene, Ser49Gly of β1-AR gene, Gln27Glu of β2- AR gene and Ser275 of GNβ3 gene) was performed by polymerase chain reaction. Genetic and epidemiological analysis was performed using the SNPStats program.
Results
. The risk of LT3S in patients with HF increases with homozygous G/G variant of Gln27Glu polymorphism of the β2-AR gene (OR=2.21, p=0.037), described as a recessive model of inheritance. There was a tendency to increase the risk of LT3S development in the presence of the genotype C/T of the Ser275 polymorphism of the GNb3 gene (OR=1.75, p=0.054), described as an over-dominant model. The genotype C/G of the Gln27Glu polymorphism of the β2-AR gene was associated with a decreased risk of LT3S development (OR=0.54, p=0.037), described as over-dominant model. Patients with HF carriers the A allele (A/GA/A) of the Ser49Gly polymorphism of the β1-AR gene have a lower risk of repeated hospitalization due to HF decompensation (OR=0.50, p=0.032), described as a dominant model. There was a tendency to increase the risk of re-hospitalization in the G-allele (C/GG/ G) variant of the Gln27Glu polymorphism of the 2-AR gene (OR=1.68, p=0.057), described as a dominant heredity model. At patients with HF in combination with LT3S the risk of re-hospitalization increases at C/G variant of the Gln27Glu polymorphism of β2-AR gene (OR=1.25, p=0.025), described as an over-dominant model.
Conclusions
. The results suggest that congenital genetic alterations in -adrenergic pathways may be associated with the development of LT3S in patients with HF and the features of the HF course.

Key words: low triiodothyronine syndrome, β1-adrenoreceptors, β2- adrenoreceptors, G-protein, heart failure, single-nucleotide polymorphisms, risk

Pol Med J, 2019; XLVII (281); 170–176