Low triiodothyronine syndrome and selenium deficiency - undervalued players in advanced heart failure? A single center pilot study

Abstract

Background 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). 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. Methods The 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. Results The 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). Conclusions Low 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.

Combined use of low T3 syndrome and NT-proBNP as predictors for death in patients with acute decompensated heart failure

“…LT3S is an important phenotype among HF patients with thyroid disorders. In our study, 28.3 % of euthyroid patients hospitalized with acute decompensated HF presented with LT3S, which was similar to the report of 15.3–53.5 % by previous studies [ 3 – 6 , 8 ]. The mechanisms underlying this disorder may be attributable to multiple factors including decreased T4 transportation into tissues [ 9 ], impaired T4 to T3 conversion result from diminished activity of phenolic ring deiodinase (type I and type II deiodinase) [ 10 – 12 ], increased inactivation of T4 and T3 associated with increasing activity of tyrosil ring deiodinase (type III deiodinase) [ 10 , 13 ] and impairment of TRH metabolism [ 13 , 14 ].…”

“…The involvement of T3 in comorbidities of patients with decompensated HF might represent a potential advantage for prognostic value over established biomarkers such as natriuretic peptides, which have been validated to be important markers for left ventricular dysfunction. Although previous published reports have demonstrating that low T3 was associated with worse outcomes in patients with acute HF during hospitalization [ 4 ] and long term follow-up [ 4 – 6 , 8 , 21 ], data about the combination of LT3S and NT-proBNP as risk predictors was limited. A study by Chuang et al showed that total T3 remained as predictor of prognosis for mortality beyond clinical risk factor and NT-proBNP, while free T3 was not predictive in univariate analysis in 106 critically ill patients with acute HF [ 21 ].…”

Thyroid Dysfunction and Dysmetabolic Syndrome: The Need for Enhanced Thyrovigilance Strategies

“…Renin release is decreased, and salt sensitivity is increased; therefore, the blood volume is increased [ 16 ]. In severe heart failure patients, euthyroid sick syndrome or low T3 syndrome with normal TSH and T4 levels is common and is associated with poorer outcomes [ 21 ]. Atherosclerosis develops in hypothyroidism due to hyperlipidemia, hypercoagulability of blood, endothelial dysfunction, increased arterial stiffness, and hypertension [ 16 ].…”

The Effect of Beta-Blockers on a Course of Chronic Heart Failure in Patients With a Low Triiodothyronine Syndrome

“…The occurrence of LT 3 S in HF patients may reach 30% [3]. The LT 3 S is associated with impaired peripheral conversion of inactive T 4 to active T 3 by deiodinases by increasing proinflammatory potential, hypoxia [4][5][6][7][8]. The LT 3 S that accompanies HF can lead to a number of disorders, including the reduction of systolic heart function, the development of arrhythmias, increased vasoconstriction [1,[9][10][11].…”