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Hashimoto's thyroiditis and congenital long QT syndrome: a dangerous addition causing torsades-case report
Ramesh Acharya1, Vaishnavi Sabesan1, Deepti Pandit1
1Texas Tech University Health Science Center El Paso, Paul L. Foster School of Medicine, The Hospitals of Providence-Transmountain, 2000 B Transmountain Road, El Paso, TX 79911, USA.
Background:
Hypothyroidism leads to a prolonged QT interval due to modulation of the potassium channel by low circulating T3, leading to a disproportionate lengthening of the action potential. Patients with long QT syndromes (LQTS) have an increased risk of symptomatic ventricular arrhythmias and sudden cardiac death (SCD).
Case Summary:
A 40-year-old female with a previous history of congenital LQTS, Type 1 diabetes mellitus, anaemia, and untreated hypothyroidism was brought to the hospital with an abrupt onset of palpitations and disorientation following multiple (>30) automated implantable cardioverter-defibrillator shocks with no identifiable triggers. Emergency medical services telemetry monitoring en route to the hospital revealed torsades de pointes (TdP), following which she received 4 g of magnesium sulfate intravenously and reverted to sinus rhythm. Electrocardiogram revealed sinus rhythm with a prolonged QTc of 515 ms. The laboratory testing revealed high TSH with low T4. The myxoedema coma score was markedly elevated at 40, indicating severe hypothyroidism. The thyroid peroxidase antibody was >600 IU/mL, indicating Hashimoto's thyroiditis. Echocardiography showed left ventricular ejection fraction of 55%-60% with no wall motion abnormalities. We treated the patient with intravenous hydrocortisone, levothyroxine, and liothyronine. After the treatment, she had no further episodes of torsades, and QTc improved to her baseline of 479 ms.
Discussion:
Hypothyroidism is linked to electrocardiographic abnormalities such as sinus bradycardia, QT interval prolongation, malignant ventricular arrhythmias such as ventricular premature beat, ventricular tachycardia, TdP, and ventricular fibrillation. Assessment of thyroid function is of high value in QT prolongation syndromes to avoid SCD incidence. Thyroid hormone influences ventricular inhomogeneity, and L-thyroxine replacement treatment may minimize malignant ventricular arrhythmia and sudden cardiac death in patients with primary hypothyroidism. Our case highlights the importance of urgent electrolyte replacement and levothyroxine therapy to avoid the risk of ventricular arrhythmias.
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