CoChat
Sign Up
Cited by 476Thyroid Disorders and TreatmentsCardiac electrophysiology and arrhythmiasCardiovascular Function and Risk Factors

The thyroid and the heart.

Polikar, R, Burger, A G, Scherrer, U, Nicod, P·1993·Circulation
DOI 10.1161/01.cir.87.5.1435
Open this paper in CoChat — free account

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…

Integrity signals

Registry

Crossref · 10.1161/01.cir.87.5.1435

Cites

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • In the hyperthyroid state, an increase in renin release secondary to the hormone-dependent decrease in systemic vascular resistance may stimulate the angiotensin-aldosterone axis and sodium reabsorption.

    “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]

  • Sympatho-adrenal stimulation could contribute to sustain BP levels during acute hypothyroidism as a possible mechanism counteracting the decrease in myocardial inotropism and cardiac output.

    “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]

Cites

Still being checked.

Cited by

Sorted by citations

Related

Authors
Polikar, R., Burger, A. G., Scherrer, U., & Nicod, P.
Affiliations
Centre Hospitalier Universitaire Vaudois (CH)
ORCID
Burger, A G
Venue
Circulation
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
1993-05
Volume
87
Issue
5
Pages
1435-1441
ISSN
  • 0009-7322 (ISSN-L)
  • 1524-4539
DOI
10.1161/01.cir.87.5.1435
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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review