The Role of Thyroid Hormones in Heart Failure

Vale, Catarina; Neves, João Sérgio; Hafe, Madalena von; Borges‐Canha, Marta; Leite‐Moreira, Adelino F.

doi:10.1007/s10557-019-06870-4

Cited by 68 publications

(73 citation statements)

References 104 publications

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“…Euthyroidism was defined when levels of thyroid function tests were within the following reference ranges: FT3 3.1-6.8 pmol/L, FT4 12-22 pmol/L, and TSH 0.27-4.2 μIU/mL. ESS was defined when FT3 and/or FT4 levels were decreased and TSH levels were normal or decreased [13,17,18].…”

Section: Patient Recruitment and Exclusion Criteriamentioning

confidence: 99%

Determinants of deranged thyroid function parameters in children admitted for management of diabetic ketoacidosis/diabetic ketosis

Shao

Guo

et al. 2020

BMC Endocr Disord

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Background: Euthyroid sick syndrome (ESS) frequently arises in children admitted with diabetic ketoacidosis/ diabetic ketosis (DKA/DK). This study evaluates the interplay of various metabolic factors with occurrence of deranged thyroid function tests in children suffering from DKA/DK. Methods: 98 DKA and 96 DK pediatric patients were selected from hospital records. Those on thyroxine replacement, with overt hypothyroidism, or with positive anti-thyroperoxidase (TPO) antibody were excluded. Tests for liver function, renal function, lipid profile, serum osmolarity, thyroid function, c-peptide levels, and glycosylated hemoglobin were done on all patients. Children were divided into euthyroid (n = 88) and ESS groups (n = 106). Results: The ESS group had a higher level of white blood cell count (WBC), plasma glucose (PG), betahydroxybutyric acid (β-HB), triglyceride (TG), anion gap (AG), glycosylated hemoglobin (HbA1c) and a lower level of HCO 3 − , prealbumin (PA), and albumin (ALB) compared with the euthyroid group (P < 0.05). Free T3 (FT3) levels were significantly correlated to β-HB, HCO 3 − , AG, PA, and HbA1c (r = − 0.642, 0.681, − 0.377, 0.581, − 0.309, respectively; P < 0.01). Free T4 (FT4) levels were significantly correlated to β-HB, HCO 3 − , and ALB levels (r = − 0.489, 0.338, 0.529, respectively; P < 0.01). TSH levels were significantly affected by HCO 3 − only (r = − 0.28; P < 0.01). HCO 3 − level was the most important factor deciding euthyroid or ESS on logistic regression analysis (OR = 0.844, P = 0.004, 95%CI = 0.751-0.948). Conclusions: Lower levels of free thyroid hormones and occurrence of ESS were associated with a higher degree of acidosis in children with DKA/DK.

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Section: Patient Recruitment and Exclusion Criteriamentioning

confidence: 99%

Determinants of deranged thyroid function parameters in children admitted for management of diabetic ketoacidosis/diabetic ketosis

Shao

Guo

et al. 2020

BMC Endocr Disord

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“…Accumulating experimental evidence indicates that matrix metalloproteinases play important roles in the pathogenesis and progression of left ventricular dysfunction [19]. Hyroid hormones seem to significantly regulate metalloproteinase expression [20], and to reduce peripheral arterial resistance by acting directly on vascular smooth muscle cells to lower the mean arterial pressure. When this reduction is sensed by the kidney, the renin-angiotensin-aldosterone system is activated to increase renal sodium absorption [21].…”

Section: Discussionmentioning

confidence: 99%

Low tri-iodothyronine syndrome improve the risk prediction of mortality in patients with acute heart failure

Zhang

Liao

Cheang

et al. 2019

Preprint

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Background Clinical studies have suggested that low tri-iodothyronine (T3) syndrome negatively affects the clinical outcomes of patients with acute heart failure (AHF). The aim of this prospective cohort study was to evaluate the effect of low T3 syndrome in terms of prognosis and risk predictive potential in AHF.Methods Low T3 syndrome was defined by a low free T3 level (<3.1 pmol/L) accompanied by a normal thyroid-stimulating hormone level. The association between the free T3 level and mortality and the incremental risk prediction were estimated in adjusted models.Results In total, 312 patients with AHF for whom detailed thyroid hormone profiles were available were prospectively enrolled. Seventy-two patients exhibited low T3 syndrome. Over a median follow-up period of 35 months, 121 cumulative deaths occurred. Cardiovascular death was observed in 94 patients. After extensive adjustment for confounders, the low T3 syndrome associated hazard ratio (95% conﬁdence interval) was 1.74 (1.16-2.61, P =0.007) for all-cause mortality and 1.90 (1.21-2.98, P =0.005) for cardiovascular mortality. The regression splines suggested a negative linear relationship between the free T3 level and mortality risk. Considering reclassification, adding low T3 syndrome to the fully adjusted model improved the risk prediction for all-cause mortality (Integrated discrimination improvement [IDI] 2.0%, P = 0.030; net reclassification improvement [NRI] 8.9%, P = 0.232) and cardiovascular mortality (IDI = 2.5%, P = 0.030; NRI 21.3%, P = 0.013).Conclusions Low T3 syndrome reclassified risk prediction for mortality beyond traditional risk factors.

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“…In spite of their wide effects on metabolism, the use of THs for therapeutic purposes remains controversial because, as mentioned, these hormones may induce other non-metabolic effects. In more detail, like hyperthyroidism, treatment with exogenous THs can induce thyrotoxicosis, a condition characterized by a variety of adverse symptoms, such weight loss, osteoporosis, atrial fibrillation, embolic events, and increased risk of heart failure [33,34,181].…”

Section: The 35-diodothyronine (35-t2) As a Hormonementioning

confidence: 99%

“…Given their action on metabolism, it seemed, in the past, that they could be used as pharmacological agents for the treatment of obesity. However, this approach could be not applied, due to adverse side effects on many organs and systems and, in particular, on the cardiovascular system and the heart's rhythm [33,34]. Yet, in recent years, it has been found that some metabolites of thyroid hormones, and especially 3,5-diiodo-L-thyronine (3,5-T2), are endowed with interesting metabolic activities that may be of clinical interest as possible therapeutic options in the treatment of overeating disorders [20].…”

Section: Introductionmentioning

confidence: 99%

Genomic and Non-Genomic Mechanisms of Action of Thyroid Hormones and Their Catabolite 3,5-Diiodo-L-Thyronine in Mammals

Giammanco

Schiera

Liegro

2020

IJMS

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Since the realization that the cellular homologs of a gene found in the retrovirus that contributes to erythroblastosis in birds (v-erbA), i.e. the proto-oncogene c-erbA encodes the nuclear receptors for thyroid hormones (THs), most of the interest for THs focalized on their ability to control gene transcription. It was found, indeed, that, by regulating gene expression in many tissues, these hormones could mediate critical events both in development and in adult organisms. Among their effects, much attention was given to their ability to increase energy expenditure, and they were early proposed as anti-obesity drugs. However, their clinical use has been strongly challenged by the concomitant onset of toxic effects, especially on the heart. Notably, it has been clearly demonstrated that, besides their direct action on transcription (genomic effects), THs also have non-genomic effects, mediated by cell membrane and/or mitochondrial binding sites, and sometimes triggered by their endogenous catabolites. Among these latter molecules, 3,5-diiodo-L-thyronine (3,5-T2) has been attracting increasing interest because some of its metabolic effects are similar to those induced by T3, but it seems to be safer. The main target of 3,5-T2 appears to be the mitochondria, and it has been hypothesized that, by acting mainly on mitochondrial function and oxidative stress, 3,5-T2 might prevent and revert tissue damages and hepatic steatosis induced by a hyper-lipid diet, while concomitantly reducing the circulating levels of low density lipoproteins (LDL) and triglycerides. Besides a summary concerning general metabolism of THs, as well as their genomic and non-genomic effects, herein we will discuss resistance to THs and the possible mechanisms of action of 3,5-T2, also in relation to its possible clinical use as a drug.

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The Role of Thyroid Hormones in Heart Failure

Cited by 68 publications

References 104 publications

Determinants of deranged thyroid function parameters in children admitted for management of diabetic ketoacidosis/diabetic ketosis

Determinants of deranged thyroid function parameters in children admitted for management of diabetic ketoacidosis/diabetic ketosis

Low tri-iodothyronine syndrome improve the risk prediction of mortality in patients with acute heart failure

Genomic and Non-Genomic Mechanisms of Action of Thyroid Hormones and Their Catabolite 3,5-Diiodo-L-Thyronine in Mammals

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