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Vol. 13 No. 4 (2026)
International Multidisciplinary Journal for Research & Development

Articles

ARRHYTHMOGENIC EFFECTS OF THYROID HORMONE EXCESS: FROM MOLECULAR MECHANISMS TO CLINICAL OUTCOMES

Published 2026-04-25

  • Xasanova Nargis Qodirovna

Xasanova Nargis Qodirovna
Department of Fundamental Medical Sciences of the Asian International University, Bukhara, Uzbekistan

Abstract

Thyroid hormone excess exerts profound effects on the cardiovascular system, significantly increasing the risk of cardiac arrhythmias. Hyperthyroidism is commonly associated with supraventricular arrhythmias, particularly atrial fibrillation, but may also predispose to ventricular rhythm disturbances. This review aims to provide a comprehensive overview of the arrhythmogenic effects of thyroid hormone excess, focusing on molecular, electrophysiological, and clinical aspects. Thyroid hormones, particularly triiodothyronine (T3), influence cardiac electrophysiology through multiple pathways, including upregulation of β-adrenergic receptors, modulation of ion channel expression, increased Na⁺/K⁺-ATPase activity, and altered intracellular calcium handling. These changes result in shortened action potential duration, increased automaticity, enhanced triggered activity, and facilitation of reentry mechanisms. Clinically, atrial fibrillation remains the most prevalent arrhythmia, associated with a higher risk of thromboembolic complications. Early recognition and appropriate management of thyroid dysfunction significantly reduce arrhythmia burden and improve patient outcomes. Hyperthyroidism should therefore be considered a reversible yet potentially serious cause of cardiac arrhythmias, highlighting the importance of integrating molecular insights into clinical practice for optimal diagnostic and therapeutic strategies.

Keywords

hyperthyroidism, thyroid hormone excess, cardiac arrhythmias, atrial fibrillation, arrhythmogenesis, cardiac electrophysiology, β-adrenergic receptors, ion channel modulation, calcium handling, action potential duration, automaticity, reentry mechanisms, thyrotoxicosis, cardiovascular complications, reversible causes of arrhythmia

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