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The thyroid and the heart
R Polikar1, A G Burger, U Scherrer
1Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
Insights
Thyroid hormones directly impact the heart and interact with the sympathetic nervous system, influencing cardiovascular function in hyperthyroid and hypothyroid states. Understanding these mechanisms is key to managing thyroid-related heart conditions.
Area of Science:
- Endocrinology
- Cardiology
- Molecular Biology
Background:
- Thyroid dysfunction, including hyperthyroidism and hypothyroidism, frequently presents with cardiovascular manifestations.
- Thyroid hormones play a critical role in regulating cardiac function and vascular tone.
Purpose of the Study:
- To review the mechanisms by which thyroid hormones affect the cardiovascular system.
- To discuss the pathophysiological consequences of these effects in thyroid disorders.
Main Methods:
- Review of existing literature on thyroid hormone action on the cardiovascular system.
- Analysis of direct and indirect effects of thyroid hormones on myocardial and vascular function.
Main Results:
- Thyroid hormones exert direct effects on the myocardium via nuclear receptors, influencing gene expression and myocardial enzymes.
- Thyroid hormones modulate the sympathetic nervous system, potentially altering adrenergic receptor function and density.
- Hypothyroidism is associated with increased diastolic blood pressure, while hyperthyroidism can lead to left ventricular hypertrophy through direct or workload-related mechanisms.
Conclusions:
- Thyroid hormones have direct chronotropic effects on the heart, independent of the sympathetic nervous system.
- Understanding these complex interactions is crucial for diagnosing and managing cardiovascular complications associated with thyroid disease.
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 associated with increases in diastolic blood pressure that are reversible after hormone substitution and may be mediated in part by sympathetic activation. Moreover, there is increasing evidence that thyroid hormones have direct chronotropic effect on the heart that are independent of the sympathetic nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)