Thyroid Research and Practice

: 2015  |  Volume : 12  |  Issue : 1  |  Page : 26--28

Ventricular tachycardia and thyrotoxicosis

Mahadeb Yovan, Toofany Reaz 
 Department of Endocrinology, Saint Luc University Clinics, Hippocrate Avenue, Brussels, Belgium

Correspondence Address:
Dr. Mahadeb Yovan
Hippocrate Avenue, 10,1200 Brussels


Hyperthyroidism is a commonly encountered endocrine disease that can be associated with a wide array of symptoms. Among the latter, rythmological manifestations are relatively frequent and comprise mainly supraventricular tachycardia (atrial fibrillation, flutter, sinus tachycardia, and atrial tachycardia). However, very few ventricular dysrhythmias have been described in literature. We report here the case of a woman in her late fifties who presented hemodynamically well-tolerated ventricular tachycardia in a context of thyrotoxicosis due to iodine overload.

How to cite this article:
Yovan M, Reaz T. Ventricular tachycardia and thyrotoxicosis.Thyroid Res Pract 2015;12:26-28

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Yovan M, Reaz T. Ventricular tachycardia and thyrotoxicosis. Thyroid Res Pract [serial online] 2015 [cited 2021 Oct 26 ];12:26-28
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Ventricular tachycardia (VT) is potentially a lethal cardiac arrhythmia. Etiologies are diverse: It can arise as a consequence of ischemic or structural heart disease or electrolyte deficiencies (hypokalemia, hypocalcemia, hypomagnesemia). It is usually triggered by certain factors namely sympathomimetic agents (amphetamines or cocaine), drugs that prolong the QT complex, rheumatologic disorders (systemic lupus erythematosus and rheumatoid arthritis), digitalis toxicity, and inherited cardiac channelopathies like the Brugada syndrome. [1] Certain triggering factors are however quite rare, as depicted by the case presented below.

 Case Report

The present case concerns a 57-year-old woman. The medical history of the patient includes coeliac disease and former tuberculosis infection but no known cardiac disease. Sustained VT (about 90 complexes) had been diagnosed in Holter monitoring in another hospital a month ago and the patient had been treated with Bisoprolol 2.5 mg once daily. The patient had undergone coronary computed tomography (CT) scan 3 days before in the same hospital and the latter had excluded coronary lesions. A blood test performed by the family doctor had pointed out thyrotoxicosis, which was why she was first addressed to the endocrine department of our hospital. She was then addressed via the endocrinologist to our cardiac department for palpitations and well-tolerated hypotension. An electrocardiogram (ECG) done in consultation showed broad complex tachycardia of 150/min with atrioventricular dissociation and right QRS complex axis deviation [Figure 1]. VT was diagnosed and the patient was admitted to the intensive care unit. Hyperthyroidism due to Iodine overload was confirmed on the basis of the following measures: Thyroid-stimulating hormone (TSH)<0.001 mU/l (normal range: 0.2-4); thyroxine (T 4 ): 13.1 μg/dl (normal range: 4.8-11.9); triiodothyronine (T 3 ): 185 μg/dl (normal range:45-182);and urinary Iodine concentration: 1610 μg/dl (normal range: 6-20). Thyroid-stimulating immunoglobulins were not found.{Figure 1}

Ultrasonography showed a multinodular goiter with one paraisthmic nodule of less than a centimeter. The Iodine isotope scanning showed diffuse hyperacidity in the thyroid gland.


The patient was treated by Propylthiouracil (3×20 mg/day) for the hyperthyroid state. VT was managed using intravenous beta-blockers and Vaughan-Williams Class Ic antiarrhythmics. As beta-blocker, metoprolol was chosen with a switch towards Bisoprolol after 2 days. Flecainide was used as antiarrhythmic after ischemic disease had been ruled out by the coronarography. Paroxystic episodes of VT were observed during the first week following admission to the intensive care unit, the frequency of such episodes receding progressively. No more episodes of VT were observed after this period and the patient was discharged with oral bisoprolol and Flecainide treatment.


There are few known cases of VT associated with hyperthyroidism. Three cases are reported in literature. The first is that of a 34-year-old woman without any cardiac history who presented cardiac arrest after VT, which was the initial sign of thyrotoxicosis. [2] The second case is that of a 4-year-old boy admitted because of febrile convulsions. Monomorphic VT was noted and responded to antithyroid treatment after antiarrhythmic drugs were deemed ineffective. [3] The third case is that of a patient with thyroid storm who developed VT during a knee operation. [4]

Thyroid hormone mediates the expression of both structural and regulatory genes in the cardiac myocyte. The main thyroid hormone produced by the thyroid gland is T 4 but the latter is five times less active than T 3 . The cardiac cellular actions of thyroid hormone are mediated by the binding of T 3 to nuclear receptors. The heart relies mainly on serum T 3 because no significant myocyte intracellular deiodinase activity takes place, and it appears that T 3 , and not T 4 , is transported into the myocyte. [5] The subsequent binding of the T 3 -receptor complexes to DNA regulates the expression of genes, specifically those regulating calcium cycling which, in turn, controls cardiac myocyte contraction.

One of the most important thyroid hormone-responsive cardiac genes includes sarcoplasmic reticulum Ca 2+ -ATPase and its inhibitor phospholamban, which regulate the uptake of calcium into the sarcoplasmic reticulum during diastole. [6] Thyroid hormones also regulate transcription of contractility proteins like the fast myosin with higher ATPase activity, and in the slow myosin, the ion channels sodium potassium ATPase and the sodium/calcium exchanger, which together coordinate the electrochemical responses of the myocardium. [7]

Thyroid hormone affects the action potential duration and repolarization currents in cardiac myocytes. [8] Cardiac-pacemaker activity resides in specialized myocytes found in the sinoatrial node that generate an action potential without an input signal. The pacemaker-related genes and activated cyclic nucleotide-gated channels 2 and 4 are transcriptionally regulated by thyroid hormone. [9] Stimulation of adrenergic receptors causes an increase in the intracellular second messenger, CAMP, which in turn accelerates diastolic depolarization and increases heart rate. Despite these well-characterized mechanisms, it is not clear how hyperthyroidism predisposes to atrial fibrillation and other potential arrhythmias like VT. It has been suggested that hyperthyroidism resembles a hyperadrenergic state; however, no evidence suggests that thyroid hormone excess enhances the sensitivity of the heart to adrenergic stimulation. In hyperthyroidism, serum levels of catecholamines remain low or normal. [10]

Several components of the cardiac myocyte β-adrenergic system are regulated by thyroid hormone, such as the β1 -adrenergic receptor and adenylate cyclase. [7] This explains why treatment of hyperthyroidism with adrenergic blockade improves many, if not all, of the cardiovascular signs and symptoms associated with hyperthyroidism.


Hyperthyroidism is mostly associated with supraventricular arrhythmias, whose management rarely calls for emergency. However, as illustrated by this case report, VT can also be induced by this endocrinological disorder. The underlying mechanism is not clear. Management of hyperthyroidism calls for iodine organification blockers and perchlorate in case of iodine overload. Beta-receptor agonists are used for to manage tachycardia and class Ic antiarrhythmics may be used if cardiac ischemic disease is absent. There is no consensus concerning this pharmacological management, the association of ventricular arrhythmias and hyperthyroidism being very rare. However, this case illustrates that hyperthyroidism should be investigated in case of VT.

Declaration of interest

The authors do not declare any conflict of interest.


This work did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.


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