Abstract

BackgroundThe function of deiodinases – selenoproteins converting thyroid hormones may be disturbed by oxidative stress accompanying heart failure. Selenium (Se) may be used by glutathione peroxidase, leading to a lack of deiodinase and triiodothyronine (T3). The aim of the study was the evaluation of the prevalence and clinical significance of low T3 syndrome in heart failure and the assessment of the association of low fT3 and Se deficiency.MethodsThe study group consisted of 59 consecutive patients hospitalized due to decompensated HFrEF NYHA III or IV. Exclusion criteria were: thyroid dysfunction, severe systemic disease, treatment with amiodarone, steroids or propranolol. Group A included 9 patients with low free T3 (fT3) concentration below 3.1 pmol/L. Group B consisted of the remaining 50 patients with normal fT3 levels.ResultsThe prevalence of low T3 syndrome was 15.3%. The prevalence of Se deficiency was 74.6%. We demonstrated correlations between fT3 and main clinical variables (i.e. NT-proBNP, LVEF, hsCRP), but we did not find correlation between fT3 and the Se level. Kaplan-Meier survival analysis showed lower survival probability in patients with low fT3 (p < 0.001).ConclusionsLow T3 syndrome is frequently found in patients with HFrEF and is associated with a poor outcome. We did not identify any significant correlation between Se and fT3 level.

Highlights

  • The function of deiodinases – selenoproteins converting thyroid hormones may be disturbed by oxidative stress accompanying heart failure

  • We found no differences between the low free T3 (fT3) group and normal fT3 group in parameters analyzed during 24-h ECG monitoring: max

  • Our results show that low fT3 concentration is frequently found in severe heart failure (HF) patients (15.3%)

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Summary

Introduction

The function of deiodinases – selenoproteins converting thyroid hormones may be disturbed by oxidative stress accompanying heart failure. Selenium (Se) may be used by glutathione peroxidase, leading to a lack of deiodinase and triiodothyronine (T3). It has been proven that either hyperthyroidism or hypothyroidism has a harmful influence on the cardiovascular system and can lead to heart failure (HF) [1]. There is a hypothesis that the function of deiodinases may be disturbed by oxidative stress and selenium (Se) deficiency accompanying HF. Heart failure may lead to an imbalance between pro-oxidant and anti-oxidant. Fraczek-Jucha et al BMC Cardiovascular Disorders (2019) 19:105 enzymes leading to an excess of reactive oxidant species (ROS).

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