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Cardiovascular effects of hyperthyroidism

Author
Irwin Klein, MD
Section Editor
Douglas S Ross, MD
Deputy Editor
Jean E Mulder, MD

INTRODUCTION

Thyroid hormone has important effects on cardiac muscle, the peripheral circulation, and the sympathetic nervous system that alter cardiovascular hemodynamics in a predictable way in patients with hyperthyroidism. The main changes are [1]:

Increases in heart rate, cardiac contractility, systolic and mean pulmonary artery pressure, cardiac output, diastolic relaxation, and myocardial oxygen consumption

Reductions in systemic vascular resistance and diastolic pressure

The major cardiovascular manifestations of hyperthyroidism will be reviewed here. Other symptoms associated with this disorder are discussed separately. (See "Overview of the clinical manifestations of hyperthyroidism in adults".)

PATHOPHYSIOLOGY

The cellular actions of thyroid hormone are mediated by the binding of triiodothyronine (T3) to nuclear receptors. It is T3 and not thyroxine (T4) that is transported into the cardiac myocyte. The subsequent binding of the T3-receptor complexes to DNA regulates the expression of genes, specifically those regulating calcium cycling in the cardiac myocyte [1,2]. T3 may also have non-nuclear actions through mechanisms not yet fully understood [3].

           

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Literature review current through: Nov 2016. | This topic last updated: Fri Jul 17 00:00:00 GMT 2015.
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