Thyroid hormone and the cardiovascular system

doi:10.1016/0002-9343(90)90531-H

The American Journal of Medicine

Volume 88, Issue 6, June 1990, Pages 631-637

https://doi.org/10.1016/0002-9343(90)90531-H Get rights and content

Abstract

To understand the pathophysiology of thyroid heart disease, it is necessary to recognize that thyroid hormone has effects on both the peripheral circulation and the myocardium. One of the earliest responses to thyroid hormone administration is a decline in systemic vascular resistance and an increase in cardiac output and cardiac contractility. In many ways, this response is similar to the curdiovascular response to exercise and is associated with increased left ventricular work. The majority of cardiac adaptations to changes in thyroid function are physiologic; however, certain patients do demonstrate clinical evidence of cardiac disease. Atrial arrhythmias, limitations in exercise tolerance, and congestive heart failure are reported to occur as a result of hyperthyroidism and are more common in older patients. Thyroid hormone also plays an important role in the regulation of blood pressure. Diastolic hypertension is a common accompaniment of hypothyroidism. By understanding the mechanisms by which thyroid hormone affects both the peripheral circulation as well as the myocardium, it is possible to predict the clinical response to the treatment of various thyroid disease states.

References (64)

E Morkin et al.
Biochemical and physiologic effects of thyroid hormone on cardiac performance
Prog Cardiovasc Dis
(1983)
GS Levey
Catecholamine sensitivity, thyroid hormone and the heart
Am J Med
(1971)
RC Smallridge et al.
Rest and exercise left ventricular ejection fraction before and after therapy in young adults with hyperthyroidism and hypothyroidism
Am J Cardiol
(1987)
JV Nixon et al.
Alterations in left ventricular mass and performance in patients treated effectively for thyrotoxicosis
Am J Med
(1979)
MJ Friedman et al.
Left ventricular systolic and diastolic function in hyperthyroidism
Am Heart J
(1982)
J Suko
Alterations of Ca²⁺-uptake and Ca²⁺-activated ATPase of cardiac sarcoplasmic reticulum in hyper- and hypothyroidism
Biochem Biophys Acta
(1971)
JFY Hoh et al.
Electrophoretic analysis of multiple forms of cardiac myosin: effect of hypophysectomy and thyroxine replacement
J Mol Cell Cardiol
(1978)
K Schwartz et al.
Myosin isoenzyme distribution correlates with speed of myocardial contraction
J Mol Cell Cardiol
(1981)
D Rohrer et al.
Thyroid hormone markedly increases the mRNA coding for sarcoplasmic reticulum Ca²⁺-ATPase in the rate heart
J Biol Chem
(1988)
T Feldman et al.
Myocardial mechanics in hyperthyroidism: importance of left ventricular loading conditions, heart rate and contractile state
J Am Coll Cardiol
(1986)

FR Keating et al.

Treatment of heart disease associated with myxedema

GS Levey et al.

Catecholamine-thyroid hormone interactions and the cardiovascular manifestations of hyperthyroidism

Am J Med

(1990)

CH Parry

Collections from the unpublished papers of the late Caleb Hilliel Parry

Dis Heart

(1825)

RJ Graves

Newly observed affection of the thyroid gland in females

Lond Med Surg J

(1835)

I Klein et al.

New perspectives on thyroid hormone, catecholamines and the heart

Am J Med

(1981)

LJ Degroot

Thyroid and the heart

Mayo Clin Proc

(1972)

I Klein et al.

Unusual manifestations of hypothyroidism

Arch Intern Med

(1984)

W Grossman et al.

The enhanced myocardial contractility of thyrotoxicosis

Ann Intern Med

(1971)

JC Forfar et al.

Hyperthyroid heart disease

Clin Endocrinol Metab

(1985)

AM Ginsberg

The historical development of the present conception of cardiac conditions in exophthalmic goiter

Ann Intern Med

(1931)

E Goetsch

Adrenaline hypersensitiveness in clinical states of hyperthyroidism

NY State J Med

(1918)

WB Likoff et al.

Thyrotoxicosis as the sole cause of heart failure

Am J Med Sci

(1943)

G Sandler et al.

The nature and prognosis of heart disease in thyrotoxicosis

Q J Med

(1959)

JS Graettinger et al.

A correlation of clinical and hemodynamic studies in patients with hypothyroidism

J Clin Invest

(1957)

M Amidi et al.

Effect of the thyroid state on myocardial contractility and ventricular ejection rate in man

Circulation

(1968)

WF Crowley et al.

Non-invasive evaluation of cardiac function in hypothyroidism

N Engl J Med

(1977)

I Klein

Thyroid hormone and high blood pressure

L Lansberg

Catecholamines and hyperthyroidism

Clin Endocrinol Metab

(1977)

JH Oppenheimer

Thyroid hormone action at the cellular level

Science

(1979)

HH Samuels et al.

Thyroid hormone action in cell culture: demonstration of nuclear receptors in intact cells and isolated nuclei

JH Oppenheimer et al.

Advances in our understanding of thyroid hormone at the cellular level

Endocr Rev

(1987)

J Kapitola et al.

Inhibition of the early circulatory effects of triiodothyronine in rats by propranolol

Physiol Bohemoslov

(1981)

Cited by (351)

Hypertension in thyroid disease and primary hyperparathyroidism
2022, Endocrine Hypertension: From Basic Science to Clinical Practice
Thyroid hormones activate nuclear receptors to alter the transcription of a range of major cardiac proteins, thus affecting numerous cardiac functions. Overt hyperthyroidism decreases systolic vascular resistance, increases cardiac contractility and heart rate, and is associated with systemic and pulmonary hypertension, especially systolic hypertension. Overt hypothyroidism has the opposite effect to increase systemic vascular resistance, decrease cardiac contractility, and increase diastolic blood pressure. Impairment of renal perfusion in hypothyroidism may also contribute to the hypertensive effect of hypothyroidism. Treatment improves systemic and pulmonary hypertension. The effects of both subclinical hyperthyroidism and subclinical hypothyroidism are less uniform. Primary hyperparathyroidism is associated with hypertension. Hypercalcemia increases vascular contractility, impairs vasodilatation, and increases systemic vascular resistance, but the elevation of parathyroid hormone level may also have a direct effect. The cardiovascular benefit of treatment of hyperparathyroidism is more inconsistent.
Clinical manifestation and images of a patient having cardiovascular involvement in myxoedema coma
2021, Medical Journal Armed Forces India
Myxoedema coma is an endocrine emergency characterised by diminished sensorium associated with features of severe hypothyroidism. The disease carries a high mortality of 30%–60 %. The cardiac manifestation of the disease consists of bradycardia, hypotension, pericardial effusion and certain echocardiographic changes such as heart block and features of hypothermia. Here, we report a case of myxoedema coma with characteristic cardiac manifestations. These manifestations revert promptly on starting treatment, and achieving a eumetabolic status as was demonstrated in this patient.
Ubiquitin proteasome system (UPS) activation in the cardiac hypertrophy of hyperthyroidism
2019, Molecular and Cellular Endocrinology
Ubiquitin proteasome system (UPS) is the main proteolytic pathway in eukaryotic cells. Changes in proteasome expression and activity have been associated to cardiovascular diseases as cardiac hypertrophy. Considering that cardiac hypertrophy is commonly associated to hyperthyroidism condition, the present study aimed to investigate the contribution of UPS in cardiac hypertrophy induced by thyroid hormones. Hyperthyroidism was induced in male Wistar rats by intraperitoneal injections of triiodothyronine (T3; 7  μg/100 g of body weight) for 7 days and confirmed by raised levels of total T3 and decreased levels of total T4. In addition, systolic blood pressure and heart rate were significantly increased in hyperthyroid group. Cardiac hypertrophy was confirmed in hyperthyroid group by increased heart weight/tibia length ratio and by increased α-MHC/β-MHC relative expression. Both catalytic (20SPT) and regulatory subunits (19SPT) of the constitutive proteasome were upregulated in hyperthyroid hearts. In addition, the transcripts that encode immunoproteasome subunits were also elevated. Furthermore, ATP-dependent chymotrypsin-like activity (26SPT) was significantly increased in hyperthyroid group. Despite the upregulation and activation of UPS in hyperthyroid hearts, the content of polyubiquitinated proteins was unaltered in relation to control. Together, these results evidence the activation of cardiac proteasome by thyroid hormones, which possibly contribute to the maintenance of protein quality control and regulation of cardiac hypertrophy in response to thyroid hormones.
Acute Exercise Promptly Normalizes Myocardial Myosin Heavy-Chain Isoform mRNA Composition in Diabetic Rats: Implications for Diabetic Cardiomyopathy
2023, Medicina (Lithuania)
Heart failure in a cat due to hypertrophic cardiomyopathy phenotype caused by chronic uncontrolled hyperthyroidism
2023, Acta Veterinaria Hungarica
Thyroid hormone disorder and the heart: The role of cardiolipin in calcium handling
2023, Experimental Physiology

View all citing articles on Scopus

^☆: This study was presented in part at the 64th Annual Meeting of the American Thyroid Association, San Francisco, California, and was supported in part by the National Institutes of Health, Bethesda, Maryland, Grant #HL-41304.

View full text

Thyroid hormone and the cardiovascular system☆

Abstract

Prog Cardiovasc Dis

Am J Med

Am J Cardiol

Am J Med

Am Heart J

Biochem Biophys Acta

J Mol Cell Cardiol

J Mol Cell Cardiol

J Biol Chem

J Am Coll Cardiol

Am J Med

Collections from the unpublished papers of the late Caleb Hilliel Parry

Dis Heart

Newly observed affection of the thyroid gland in females

Lond Med Surg J

New perspectives on thyroid hormone, catecholamines and the heart

Am J Med

Thyroid and the heart

Mayo Clin Proc

Unusual manifestations of hypothyroidism

Arch Intern Med

The enhanced myocardial contractility of thyrotoxicosis

Ann Intern Med

Hyperthyroid heart disease

Clin Endocrinol Metab

The historical development of the present conception of cardiac conditions in exophthalmic goiter

Ann Intern Med

Adrenaline hypersensitiveness in clinical states of hyperthyroidism

NY State J Med

Thyrotoxicosis as the sole cause of heart failure

Am J Med Sci

The nature and prognosis of heart disease in thyrotoxicosis

Q J Med

A correlation of clinical and hemodynamic studies in patients with hypothyroidism

J Clin Invest

Effect of the thyroid state on myocardial contractility and ventricular ejection rate in man

Circulation

Non-invasive evaluation of cardiac function in hypothyroidism

N Engl J Med

Thyroid hormone and high blood pressure

Catecholamines and hyperthyroidism

Clin Endocrinol Metab

Thyroid hormone action at the cellular level

Science

Thyroid hormone action in cell culture: demonstration of nuclear receptors in intact cells and isolated nuclei

Advances in our understanding of thyroid hormone at the cellular level

Endocr Rev

Inhibition of the early circulatory effects of triiodothyronine in rats by propranolol

Physiol Bohemoslov