ArticleThyroid : official journal of the American Thyroid Association2017
Myocardial Inactivation of Thyroid Hormones in Patients with Aortic Stenosis.
Article in Thyroid : official journal of the American Thyroid Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Longitudinal Changes in Thyroid Hormones and Serum Albumin Following CABG, AVR, and PCI: An Exploratory Electronic Medical Record Study.Medical sciences (Basel, Switzerland) · 2026Article
- Thyroid hormones and metabolic flexibility: tissue-specific control of energy homeostasis.Frontiers in physiology · 2026Review
- Rethinking strategies for solving thyroid dysfunction at the heart of cardiovascular disease.Molecular medicine (Cambridge, Mass.) · 2025Review
- Metabolic Consequences of Thyroidectomy and Patient-Centered Management.Journal of clinical medicine · 2024Review
- T3 levels and thyroid hormone signaling.Frontiers in endocrinology · 2022Review
- Protective Effects of Thyroid Hormone Deprivation on Progression of Maladaptive Cardiac Hypertrophy and Heart Failure.Frontiers in cardiovascular medicine · 2021Article
- Individualized Therapy for Hypothyroidism: Is T4 Enough for Everyone?The Journal of clinical endocrinology and metabolism · 2020Review
- Paradigms of Dynamic Control of Thyroid Hormone Signaling.Endocrine reviews · 2019Review
- Sex differences in gene expression in response to ischemia in the human left ventricular myocardium.Human molecular genetics · 2019Article
- The Deiodinase Trio and Thyroid Hormone Signaling.Methods in molecular biology (Clifton, N.J.) · 2018Review
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
objectiveThe human heart expresses the type 2 deiodinase (D2) that activates thyroxine (T4) to triiodothyronine (T3). At the same time, the inactivating type 3 deiodinase (D3) has been found in a rat model of right ventricular hypertrophy. It is not known whether the human myocardium metabolizes thyroid hormone. This study examined myocardial thyroid hormone metabolism in patients with aortic valve stenosis (AS) undergoing aortic valve replacement and in patients with coronary artery disease (CAD) undergoing coronary artery bypass grafting surgery.
methodsMyocardial thyroid hormone metabolism was assessed by analyzing the difference in serum thyroid hormone levels between the aortic root (incoming blood) and the coronary sinus (outgoing blood) of patients undergoing cardiac surgery. A total of 23 patients with AS and 35 patients with CAD were included. Patients received a pre-surgical echocardiogram, and pre-, during and post-surgical thyroid hormone serum levels were collected in the myocardial and peripheral circulations.
resultsPatients with AS exhibited the expected left ventricle (LV) hypertrophy (i.e., 20-30% increase in LV posterior wall and interventricular septum thickness and ∼10% increase in AS in LV diastolic diameter). Immediately before cardiopulmonary bypass, blood flowing through the AS myocardium exhibited a 4.6% reduction in T3 and 6.9% increase in rT3 levels, decreasing the serum T3/rT3 ratio by 9.6%. T4 and thyrotropin serum levels remained similar between the aortic root and coronary sinus. In contrast, no myocardial thyroid hormone metabolism was observed in CAD patients. Notably, the AS myocardium lost the ability to inactivate thyroid hormone after cardiopulmonary bypass, possibly due to myocardial stunning.
conclusionsThere is accelerated thyroid hormone inactivation in the AS myocardium, which is likely the result of D3 expression. No evidence to suggest thyroid hormone activation in the myocardium was obtained in the present study.
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