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The thyroid and the heart.
Abstract
Cardiovascular manifestations are a frequent finding in hyperthyroid and hypothyroid states. In this review, potential mechanisms by which thyroid hormones may exert their cardiovascular effects and pathophysiological consequences of such effects are briefly discussed. Two major concepts have emerged about how thyroid hormones exert their cardiovascular effects. First, there is increasing evidence that thyroid hormones exert direct effects on the myocardium, which are mediated by stimulation of specific nuclear receptors, which in turn leads to specific mRNAs production. Furthermore, there is some evidence that thyroid hormones may also activate extranuclear sites and may directly alter plasma membrane function. Second, thyroid hormones interact with the sympathetic nervous system by altering responsiveness to sympathetic stimulation presumably by modulating adrenergic receptor function and/or density. Pathophysiological consequences of such direct and indirect thyroid hormone effects include increased myocardial contractility and relaxation that may be related to stimulation by T3 of specific myocardial enzymes. However, when left ventricular hypertrophy occurs in association with hyperthyroidism, it may be related to either direct thyroid hormone-induced stimulation of myocardial protein synthesis or to thyrotoxicosis-induced increases in cardiac work load. Although hyperthyroidism generally has little or no effect on mean arterial blood pressure, hypothyroidism is often as…
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“in the hyperthyroid state the increase in renin release secondary to the hormone-dependent decrease in systemic vascular resistance may stimulate the angiotensin-aldosterone axis and consequently sodium reabsorption (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23).”
From The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans (2002) · cites this paper as [15]
In the citing paper
“Sympatho-adrenal stimulation could thus contribute to sustain BP levels during acute hypothyroidism as a possible mechanism counteracting the decrease in myocardial inotropism and cardiac output (4,14,15).”
From The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans (2002) · cites this paper as [15]
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Metadata
- Authors
- Polikar, R., Burger, A. G., Scherrer, U., & Nicod, P.
- Affiliations
- Centre Hospitalier Universitaire Vaudois (CH)
- ORCID
- Burger, A G
- Venue
- Circulation
- Published
- 1993-05
- Volume
- 87
- Issue
- 5
- Pages
- 1435-1441
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2069934475
- Cited by
- 475
- References
- 0
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 8 · 2023: 7 · 2022: 13 · 2021: 14 · 2020: 10 · 2019: 6 · 2018: 14 · 2017: 10 · 2016: 14 · 2015: 14 · 2014: 15 · 2013: 11 · 2012: 13
- FWCI
- 9.04
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- IRIS (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Keywords
- thyroid hormones, hyperthyroidism, hypothyroidism, cardiovascular effects, myocardium, nuclear receptors, sympathetic nervous system, adrenergic receptors, left ventricular hypertrophy, thyrotoxicosis, blood pressure, chronotropic effect, cardiac contractility
- MeSH terms
- Animals, Cardiovascular Diseases, Humans, Thyroid Diseases
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