ABSTRACT
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 ß-adrenoreceptors (ß-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. AIM: The aim of study was to evaluate the relationship of ß-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 ß1-AR gene, Ser49Gly of ß1-AR gene, Gln27Glu of ß2- AR gene and Ser275 of GNß3 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 ß2-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 ß2-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 ß1-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 ß2-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 ß2-AR gene (OR=1.25, p=0.025), described as an over-dominant model. CONCLUSIONS: The results suggest that congenital genetic alterations in ß-adrenergic pathways may be associated with the development of LT3S in patients with HF and the features of the HF course.
