SUN-340 - Beyond Atrial Fibrillation: Ventricular Tachycardia as A Rare Manifestation of Thyroid Storm

Introduction: Thyroid storm is the most severe form of thyrotoxicosis, marked by acute multiorgan dysfunction and mortality rates between 3.6% and 17%. Cardiovascular (CV) complications are the most clinically significant, including congestive heart failure, cardiogenic shock, and supraventricular tachyarrhythmias, most frequently atrial fibrillation (Afib). Although Afib is a common manifestation of severe thyrotoxicosis, ventricular tachyarrhythmias are rare and usually occur in patients with underlying structural or ischemic heart disease. Their occurrence without structural cardiac pathology is extremely uncommon. This report describes a case of monomorphic ventricular tachycardia (VT) in a patient with Graves’ disease who had recently discontinued methimazole and had no prior cardiac history.
Case Summary: A 50-year-old man with Graves’ disease presented to the emergency department with palpitations and dyspnea after exertion. He had discontinued methimazole six months prior and reported a viral illness two weeks prior to symptom onset. On arrival, he was tachycardic to the 230s; ECG demonstrated monomorphic VT. He received lidocaine bolus and infusion with conversion to underlying Afib. Thyroid studies revealed undetectable thyroid stimulating hormone and free T4 >7 ng/dL, with a Burch-Wartofsky score of 55, consistent with thyroid storm. The patient was admitted to the coronary care unit and treated with propylthiouracil, SSKI, prednisone, propranolol, and cholestyramine. Evaluation for alternative VT etiologies included cardiac magnetic resonance imaging and stress myocardial perfusion imaging, all of which were negative; coronary angiography was deferred due to iodine exposure risk. No recurrent VT occurred during hospitalization, and the patient was discharged with a wearable defibrillator.

Discussion: The increased risk of arrhythmias and adverse CV events is significantly elevated due to thyroid storm. The most frequently observed arrhythmias are supraventricular, whereas ventricular arrhythmias are infrequently found except in those with pre-existing intrinsic cardiac disease. This case highlights that severe thyrotoxicosis alone may be sufficient to precipitate malignant ventricular arrhythmias, as demonstrated by monomorphic VT in this patient with Graves’ disease and no evidence of structural heart disease. The mechanism, however, remains unclear, but it is thought to be due to excess thyroid hormone, which has been shown to shorten the cardiac action potential duration and the refractory period, thereby increasing myocardial excitability. Another potential substrate for ventricular arrhythmias is myocarditis. Prompt Initiation of antithyroid therapy, is the first step in controlling heart rate and stabilizing arrhythmias while the patient achieves euthyroid status.

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