Čulić V. Cardiovascular mechanisms of thyroid hormones and heart failure: Current knowledge and perspectives. World J Cardiol 2024; 16(5): 226-230 [PMID: 38817644 DOI: 10.4330/wjc.v16.i5.226]
Corresponding Author of This Article
Viktor Čulić, MD, PhD, Full Professor, Senior Scientist, Department of Cardiology and Angiology, University Hospital Centre Split, University of Split School of Medicine, Šoltanska 2, Split 21000, Croatia. viktor.culic@st.t-com.hr
Research Domain of This Article
Cardiac & Cardiovascular Systems
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Cardiol. May 26, 2024; 16(5): 226-230 Published online May 26, 2024. doi: 10.4330/wjc.v16.i5.226
Cardiovascular mechanisms of thyroid hormones and heart failure: Current knowledge and perspectives
Viktor Čulić
Viktor Čulić, Department of Cardiology and Angiology, University Hospital Centre Split, University of Split School of Medicine, Split 21000, Croatia
Author contributions: Čulić V wrote this editorial, consulted and analysed literature, and created tables.
Conflict-of-interest statement: Prof. Čulić has nothing to disclose.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Viktor Čulić, MD, PhD, Full Professor, Senior Scientist, Department of Cardiology and Angiology, University Hospital Centre Split, University of Split School of Medicine, Šoltanska 2, Split 21000, Croatia. viktor.culic@st.t-com.hr
Received: December 24, 2023 Revised: April 12, 2024 Accepted: April 18, 2024 Published online: May 26, 2024 Processing time: 150 Days and 17.7 Hours
Abstract
A multiple hormonal imbalance that accompanies heart failure (HF) may have a significant impact on the clinical course in such patients. The non-thyroidal illness syndrome (NTIS), also referred to as euthyroid sick syndrome or low triiodothyronine syndrome, can be found in about 30% of patients with HF. NTIS represents a systemic adaptation to chronic illness that is associated with increased cardiac and overall mortality in patients with HF. While conclusions on thyroid-stimulating hormone, free triiodothyronine, total and free thyroxine are currently unresolved, serum total triiodothyronine levels and the ratio of free triiodothyronine to free thyroxine seem to provide the best correlates to the echocardiographic, laboratory and clinical parameters of disease severity. HF patients with either hyper- or hypothyroidism should be treated according to the appropriate guidelines, but the therapeutic approach to NTIS, with or without HF, is still a matter of debate. Possible treatment options include better individual titration of levothyroxine therapy, combined triiodothyronine plus thyroxine therapy and natural measures to increase triiodothyronine. Future research should further examine the cellular and tissue mechanisms of NTIS as well as new therapeutic avenues in patients with HF.
Core Tip: The non-thyroidal illness syndrome, also referred to as euthyroid sick syndrome or low triiodothyronine syndrome, can be found in about 30% of patients with heart failure (HF). Serum total triiodothyronine levels and the ratio of free triiodothyronine to free thyroxine seem to correlate the best with the echocardiographic, laboratory and clinical parameters of the severity of HF. Future research should further explore cellular and tissue mechanisms of this syndrome as well as possible therapeutic options in patients with HF.
