AIM: 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 β2-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 β-adrenergic pathways may be associated with the development of LT3S in patients with HF and the features of the HF course.
PATIENTS AND METHODS: Materials and methods: 354 patients with HF on a background of post-infarction cardiosclerosis were included in the 2-yeared follow-up study. LT3 S was diagnosed at 89 (25.1%) patients. The levels of thyroid-stimulating hormone, free T3f and T4f, and reversible T3 were determined. The echocardioscopy was performed.
RESULTS: Results: Patients with HF in combination with LT3 S have a heavier functional class by NYHA, greater dilatation of the left heart cavities, less myocardial contractility, a higher frequency of atrial fibrillation and re-hospitalization. The use of β-ABs in patients with HF without LT3 S leads to a likely decrease in hospitalization frequency, while in patients with LT3 S it has an opposite effect. The frequency of rehospitalization increases with an excess of β-ABs dose > 5 mg (equivalent to bisoprolol). At these patients a decrease in serum T3 level and negative dynamics of parameters of intracardiac hemodynamics are observed.
CONCLUSION: Conclusions: The use of β-ABs in patients with LT3 S leads to an increase in re-hospitalization at a dose over 5.0 mg (equivalent to bisoprolol). In these patients there is a decrease in serum T3, an increase in T4 level; and the ejection fraction decrease; and heart cavities size increase.