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Is the myocardium source or target of non-thyroidal illness syndrome? Observations on local thyroid hormone metabolism in chronic heart failure and controls.

Poster Created on 30 May 2016

Authors

Johannes W Dietrich, Axel Kloppe, Leif I. Bösche, Apostolos Chatzitomaris, Harald H. Klein, Andreas Mügge, Assem Aweimer

Abstract

Background
The relation between thyroid homeostasis and myocardial function is governed by complex interactions. Recently published data suggest a U-shaped relationship between serum levels of FT3 and the risk of atrial fibrillation. In addition, heart failure (HF) can result from both hypo- and hyperthyroidism. In this study, we examined the intracardiac thyroid hormone metabolism in patients with and without systolic HF.

Methods
This study covered 11 patients with HF (LV-EF<35% and NYHA II/III) undergoing implantation of a CRT (cardiac resynchronization therapy) device, and a control group of six age- and sex-matched subjects without HF (LV-EF>55%) planned for electrophysiological testing. Exclusion criteria were thyroid disease or exposition to iodinated radiocontrast agents within three months before investigation. In all patients, blood samples were obtained simultaneously from various compartments (peripheral-venous, peripheral-arterial, right atrium, coronary sinus). Concentrations of TSH, FT3, FT4 and BNP were determined in all samples. Total deiodination capacity (SPINA-GD) was calculated from measured values for FT3 and FT4.

Results
While TSH levels were unchanged, FT3 concentrations and SPINA-GD were significantly reduced and concentrations of FT4 and BNP were increased in peripheral venous samples of patients with HF. Similarly, FT3 was reduced in right atrial samples, and SPINA-GD was decreased in the coronary sinus of patients suffering from HF. BNP concentrations were increased in all compartments in patients with HF, but highest in samples from coronary sinus (table). Results of Student’s t test were confirmed with a linear mixed effects model.

Conclusions
In the HF group samples from peripheral veins reflected a slight, but classical pattern of non-thyroidal illness syndrome (NTIS or TACITUS). A similar constellation was observable in samples from right atrium and coronary sinus. The results suggest that deiodinases are downregulated in myocardial tissue of patients with HF. Therefore, peripheral organs and the heart, but not the lung may contribute to the constellation of NTIS. This spatial diversity in the pathogenesis of NTIS may be promotive for cardiac complications, including atrial fibrillation, in critical illness.

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