Thyroid disorders, both hyperthyroidism and hypothyroidism, have been known to cause many cardiovascular effects. There are lot of studies on the arrhythmogenic potential of thyroid hormones and it was postulated to be due to decrease in the action potentials of atrial and ventricular cardiomyocytes, thereby decreasing the refractoriness of the cardiomyocytes and maintaining multiple re-entrant circuits (1-5). Hypothyroidism is generally associated with sinus bradycardia, prolonged PR interval, low amplitude P-wave and QRS complexes, altered ST segment and flat or inverted T waves. The low amplitude waves are most commonly seen in hypothyroid patients with pericardial effusion. There have been case reports of long QT interval and ventricular tachycardia of torsade de pointes in hypothyroidism and their reversibility occurred with the restoration of the euthyroid state⁶.Diligent literature search showed paucity of cases of Paroxysmal Supraventricular Tachycardia (PSVT) in hypothyroidism⁷.

A 22 year female presented with complaints of sudden onset palpitations and dyspnoea associated with diaphoresis for two hours before admission. There was no history of hypertension, coronary artery disease, hypothyroidism or diabetes mellitus. She was a non smoker, non alcoholic and not a habitual drinker of tea or coffee. Her blood pressure at the time of presentation was 112/64 mmHg and pulse rate was 200 / min. Rest of her systemic examination was normal. 

Biochemical profile at the time of presentation is as follows: serum thyroid stimulating hormone (Thyroid Stimulating Hormone)- 44.3μU/mL, frees T3 (FT3)-(2.3 pg/ml), free T4 (FT4)-0.3 ng/mL and anti Thyroid Peroxidase antibodies was positive. Electrocardiogram (ECG) of patient showed features of PSVT (Figure 1). Initially carotid massage was applied but in view of persistent tachyarrhythmia, IV Adenosine 12 mg was given. Repeat ECG showed normal rhythm.

Laboratory analysis showed just a slightly increase of cholesterol level, with no electrolyte disturbances. Structural heart disease and systemic vasculitis were investigated and excluded. Thyroxin replacement therapy was started first 25 μg/day, then 50 μg/day. Clinical signs improved substantially and no other episode of PSVT was noted. Subsequent echocardiography revealed normal study. 

Cardiovascular manifestation is seen in both hypothyroidism and hyperthyroidism. Thyroid abnormalities produce changes in blood pressure, cardiac contractibility, myocardial oxygen consumption, cardiac output and systemic vascular resistance^8,9.Clinical features like palpitations, exercise intolerance, exertional dyspnoea, systolic hypertension, angina, atrial fibrillation, peripheral Edema, and congestive heart failure are commonly described in hyperthyroidism. These manifestations are diametrically opposite to those described in hypothyroidism. In hypothyroidism, features like fatigue, cold intolerance, bradycardia, diastolic hypertension, pericardial effusion and narrow pulse pressure are common features. 

ECG abnormalities seen in hypothyroidism generally are prolonged conduction, low voltage complexes, sinus bradycardia, atrio-ventricular or bundle branch blocks and rarely, long QT interval & ventricular tachycardia of “torsade de pointes”⁶.The pathogenesis of long QT and the subsequent polymorphic VT of “torsade de pointes” in hypothyroidism could give us clues regarding the pathogenesis of PSVT in hypothyroidism. The depolarisation phase of the cardiac action potential (phase 1) is caused by rapid influx of Na+ and Ca++ ions. Since the peak density of the slow inward current is lower in hypothyroidism, which potentially causes single or repetitive depolarisation in phase 2 and 3 of the cardiac action potential, resulting in Early After-depolarisations (EADs). These EADs appear as pathologic U waves on a surface ECG, and, when they reach a threshold, may trigger tachyarrhythmia’s. These are relatively common in the deep endocardial region and mid-myocardial layer (composed of M cells) of the ventricle because they have less rapid delayed rectifier potassium currents¹⁰.A similar mechanism acting at the supraventricular level could possibly have led to the PSVT in our patient. Other possible mechanisms postulated for the development of arrhythmias are alteration of myocyte-specific gene expression, myofibril swelling, endothelial dysfunction, interstitial Edema, arterial stiffness, premature atherosclerosis. It is also seen that disturbances of the sympathetic-vagal tone with a relative increase in sympathetic tone and autoimmunity may predispose to tachyarrhythmia⁷.The possibility of thyroxine replacement therapy causing the tachyarrhythmia also has to be considered. A study done on this shows that thyroxine replacement therapy increased the frequency of atrial premature complexes in patients with baseline arrhythmias but did not cause new-onset supraventricular or ventricular tachyarrhythmias¹¹.

Our patient did not develop any further tachyarrhythmic episodes after becoming euthyroid by increasing the dose; it is safe to assume that PSVT was caused by hypothyroidism, rather than thyroxine replacement therapy. This casereport emphasizes the fact that tachyarrhythmia can also be manifestation of hypothyroidis

ECG : electrocardiography 

PSVT : Paroxysmal Supraventricular Tachycardia 

TSH : Thyroid stimulating hormone 

TPO : Thyroid peroxidase 

EAD : Early after-depolarisation

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