CoChat
Sign Up
Cited by 245Thyroid Disorders and TreatmentsCardiovascular Function and Risk FactorsCardiac electrophysiology and arrhythmias

The DOI matches its Crossref record; 77 of the 77 references it cites were found in a registry or an index.

Effects of Thyroid Hormone on Cardiac Function - The Relative Importance of Heart Rate, Loading Conditions, and Myocardial Contractility in the Regulation of Cardiac Performance in Human Hyperthyroidism

Biondi, Bernadette, Palmieri, Emiliano A., Lombardi, Gaetano, Fazio, Serafino·2002·The Journal of Clinical Endocrinology & Metabolism
DOI 10.1210/jcem.87.3.8302
Open this paper in CoChat — free account

Abstract

The cardiovascular manifestations of thyroid hormone excess, including tachycardia, a widened pulse pressure, a brisk carotid and peripheral arterial pulsation, a hyperkinetic cardiac apex, and loud first heart sound have long been recognized and are a cornerstone for clinical diagnosis (1–9). A number of studies in the past decades have provided critical insights into the mechanisms that are responsible for the hyperdynamic cardiocirculatory state in overt hyperthyroid patients, suggesting that it probably results from the combined effects of thyroid hormone on certain molecular pathways on the heart and vasculature, at both the genomic and nongenomic level (10). Despite these advances, it is not yet clear whether, in spontaneous human hyperthyroidism, the high cardiac output state (11–24) is sustained prevalently by changes in peripheral hemodynamics (vascular hypothesis), or by changes in myocardial contractility (myocardial hypothesis) (19, 21). This issue has major clinical and pathophysiological implications. In fact, although peripheral and myocardial mechanisms are not mutually exclusive, the major contribution of one of the two mechanisms may have important consequences with regard to the “economy” of the cardiovascular system, given the notion that increased cardiac performance due to inotropic stimulation is less efficient than that due to modulation of the loading status. Accordingly, here we review research on the effects of spontaneous human hyperthyroidism on heart rate, preload, afterload, and myocardial contractility in an attempt to establish how these factors interact with each other and to what extent they contribute to increasing cardiac performance at rest. Heart rate is an important mechanism for the regulation of cardiac output. Apart from determining the rate of cardiac ejection, it affects both systolic and diastolic function. An accelerated heart rate increases the minute stroke work at any given level of cardiac preload—a finding consistent with improved myocardial contractility (force-frequency relation) (25). A high heart rate also increases the rate of myocardial relaxation, thus improving early cardiac filling (lusitropic effect) (25). However, acceleration of the frequency of cardiac contraction does not increase cardiac performance if preload is not augmented or, at least, maintained constant. Pacing-induced increase in contraction frequency generally reduces preload and stroke volume, so that cardiac output remains constant (26, 27). On the other hand, an increased heart rate reduces diastolic filling time and, thus, leads to greater dependence on atrial systole. This explains the important pathophysiologic impact of atrial fibrillation on cardiac performance. Interestingly, heart rate may also affect peripheral hemodynamics. Studies of atrially paced normal subjects have demonstrated that an increase in the frequency of cardiac contraction reduces the “dynamic” compliance of the arterial tree and augments arterial pressure (28–30). This effect probably results from altered timing of the reflected pressure wave from the peripheral arterial tree consequent to the reduction in absolute duration of systole. That is, as systolic time lessens because of increased heart rate, the reflected pressure wave returning from the peripheral arterial tree would be added to and so enhance the forward pressure wave, thereby increasing blood pressure (Fig. 1). Potential effect of the increase in heart rate on arterial pressure in hyperthyroid patients. Potential effect of the increase in heart rate on arterial pressure in hyperthyroid patients. Thyroid hormone has a consistent positive chronotropic effect, and resting sinus tachycardia is the most common cardiovascular sign of human hyperthyroidism (31). The increase in heart rate does not remain constant during 24 h; rather, circadian variation is preserved and is even more pronounced than in normal subjects (32). An increased incidence of atrial fibrillation has also been consistently reported in patients with overt hyperthyroidism (1, 10). The increase in chronotropism and batmotropism in hyperthyroid patients is probably caused by unbalanced sympatho-vagal tone due to a relative rather than an absolute adrenergic overdrive (33). This interpretation is strengthened by the observation that both catecholamine metabolism and adrenergic cardiovascular responsiveness do not differ substantially from normal in patients with hyperthyroidism (34–41). On the other hand, the close correlation between thyroid hormone level and night heart rate in hyperthyroid patients, which is least influenced by sympathetic tone, suggests that thyroid hormone may directly affect sino-atrial node firing (32, 42). Preload is the hemodynamic force exerted on the ventricular wall during filling and, thus, corresponds to ventricular end-diastolic wall stress or tension sensu strictu. It contributes greatly to the determination of ventricular end-diastolic volume and m

Overview

Integrity signals

Registry

Crossref · 10.1210/jcem.87.3.8302

Cites

77 of 77 references verified0 citation errors · 0 not checkable

Statistics

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

Verification

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?

Citations

Cites

Cited by

Sorted by citations

See all 245

Related

See all

Metadata

Authors
Biondi, B., Palmieri, E. A., Lombardi, G., & Fazio, S.
Affiliations
Federico II University Hospital (IT)
Corresponding author
Biondi, Bernadette
ORCID
Biondi, Bernadette
Venue
The Journal of Clinical Endocrinology & Metabolism
Publisher
The Endocrine Society
Published
2002-03
Volume
87
Issue
3
Pages
968-974
ISSN
  • 0021-972X (ISSN-L)
  • 1945-7197
DOI
10.1210/jcem.87.3.8302
OpenAlex
W1978801392
Cited by
245
References
76
Citations by year
2026: 2 · 2025: 8 · 2024: 8 · 2023: 10 · 2022: 6 · 2021: 12 · 2020: 10 · 2019: 19 · 2018: 13 · 2017: 12 · 2016: 7 · 2015: 16 · 2014: 10 · 2013: 11 · 2012: 10
FWCI
4.94
Type
journal article
Language
en
Open access
closed
Locations
  • The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
Keywords
hyperthyroidism, thyroid hormones, cardiac function, heart rate, preload, afterload, cardiac contractility, cardiac output, force-frequency relationship, lusitropic effect, diastolic function, atrial contraction, tachycardia, pulse pressure, stroke volume
MeSH terms
Heart, Heart Rate, Humans, Hyperthyroidism, Myocardial Contraction, Thyroid Hormones

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