- Case Report
- Open Access
Primary hypothyroidism presenting with Torsades de pointes type tachycardia: a case report
© Shojaie and Eshraghian; licensee BioMed Central Ltd. 2008
- Received: 22 September 2008
- Accepted: 06 November 2008
- Published: 06 November 2008
Hypothyroidism can manifest with cardiac abnormalities, often consisting of a combination of morphologic and functional changes. Low voltage, sinus bradycardia, and slowed conduction are usually found on electrocardiography.
There are few reports of occurrence of torsades de pointes as the first presentation of long QT syndrome in the course of hypothyroidism.
In present report we briefly describe a 50-years-old woman with severe hypothyroidism who presented with presyncope, prolongation of the QT interval, and polymorphic ventricular tachycardia (torsades de pointes).
Our patient responded well to treatment with levothyroxine and QT intervals normalized and ventricular tachycardia was abolished two months after levothyroxine therapy.
- Ventricular Tachycardia
- Thyroid Stimulate Hormone
- Right Bundle Branch Block
- Primary Hypothyroidism
Hypothyroidism has various cardiovascular manifestations including impaired diastolic function, reduced contractility and infrequently pericardial effusion and heart failure. Electrocardiographic (ECG) changes in hypothyroidism are bradycardia, right bundle branch block (RBBB), flat or inverted T wave, QRS prolongation, QT prolongation and infrequently ventricular arrhythmia, torsadess de pointes. We describe a patient with severe hypothyroidism who presented with presyncope and polymorphic ventricular tachycardia (torsadess de pointes) and treated with levothyroxine.
Hypothyroidism results from reduced secretion of both T3 and T4, occurring in most cases as a consequence of destruction of the thyroid gland itself, usually by an inflammatory process. In some cases, it is secondary to decreased secretion of TSH, due to either pituitary or hypothalamic disease . It is well known that an excess or deficit of thyroid hormones effect the cardiovascular system. The electrocardiographic changes in hypothyroidism include sinus bradycardia, low voltage QRS complexes and prolongation of QT interval. The P wave amplitude is usually very low and complete or incomplete right bundle branch block has been observed in patients with hypothyroidism. Cold intolerance, dryness of skin, weakness, constipation, hoarseness, shortness of breath, impairment of memory, menstrual dysfunction and even heart failure are common sign and symptoms of hypothyroidism. Cardiovascular manifestations of hypothyroidism include significant bradycardia, cardiac dilatation, weak arterial pulses, hypotension, distant heart sound, nonpitting facial and peripheral edema and evidence of congestive heart failure such as ascitis, orthopnea and paroxysmal dyspnea .
The physiological chronotropic response and normal tension of the heart muscle in diastolic phase depend on the proper expression of tri-iodothyronine in the heart cells and its stimulating influence on Na+-K+ ATPase and Ca2+ ATPase in endoplasmic reticulum. Normal heart contractility is also related to proper tri-iodothyronine-stimulated transcription of the myosin heavy-chain alpha gene and inhibition of the heavy-chain beta gene. Moreover, proper tri iodothyronine expression in the cardiac muscle affects the number of b-adrenergic receptors and their sensitivity to catecholamines.
Profound hypothyroidism and decreased expression of tri-iodothyronine in the heart cells may cause a worsening of cardiac contractility, a decreasing heart rate and a slowing down of the conduction of electrical stimuli in the heart muscle. This may be the reason for bradycardia and elongation of the QT interval and, in consequence, life-threatening arrhythmias may occur, for example torsades de pointes-type tachycardia.
The upper limit for duration of the normal QT interval corrected for heart rate (Q Tc) is often given as 0.44 sec. The term torsades pointes refer to a ventricular tachycardia characterized by QRS complexes of changing amplitude that appear twist around the isoelectric line. This term is usually used to describe a syndrome characterized by prolonged ventricular repolarization with QT intervals usully exceeding 500 msec .
There are few published reports of occurrence of torsades de pointes as the first presentation of long QT syndrome in the course of hypothyroidism. Hanslik et al. described a woman with myxoedema coma who initially presented a bizarre ECG with excessively prolonged QT intervals as predominant feature .
Kukala et al reported a 78 year-old woman with primary hypothyroidism and atrial fibrillation treated with sotalol, complicated with cardiac arrest due to ventricular fibrillation (VF) and torsades de pointes . Chojnowski et al reported a 51-years-old woman with Hashimoto disease and hypothyroidism with repeated torsade de piontes tachycardia and cardiogenic sock in the course of her disease . In two above mentioned cases the patients were known cases of hypothyroidism and torsades de piontes; although is not frequent, was occurred in the course of their diseases.
However, occurrence of torsades de pointes as the first manifestation of hypothyroidism is very rare. In 2006 Schenck et al. described a patient with severe hypothyroidism who presented with presyncope, prolongation of the QT interval, and polymorphic ventricular tachycardia (torsades de pointes) . In 1983 Fredlund and Olsson reported two patients with long QT interval, ventricular tachycardias of torsades de pointes type and repeated ventricular fibrillation episodes, who also turned out to have significant hypothyroidism . As expected, our patient responded well to treatment with levothyroxine and QT intervals normalized and ventricular tachycardia was abolished two months after levothyroxine therapy.
Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
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