MON-345 - Amiodarone-Induced Thyrotoxicosis Presenting as A Rare Case of Ventricular Tachycardia Storm

Background
Amiodarone-induced thyrotoxicosis is an uncommon but serious complication of amiodarone therapy. Distinguishing type I from type II remains difficult in clinical practice. Severe thyrotoxicosis can trigger malignant ventricular arrhythmias. Early diagnosis and targeted management reduce morbidity and mortality.
Case Presentation
A man in his 60s presented with several weeks of fatigue, lower extremity edema, diarrhea, and a 15-pound unintentional weight loss. He has history of atrial fibrillation and ventricular tachycardia with implantable cardioverter-defibrillator placement eight years earlier and failed ablation five years earlier. He had received amiodarone for four years. He denied fever, chills, heat intolerance, diaphoresis, and tremor.
Device interrogation showed five appropriate shocks for sustained ventricular tachycardia. Examination revealed no goiter, thyroid nodules, or ophthalmopathy. Laboratory testing confirmed thyrotoxicosis with TSH 0.01 mIU/L, free T4 6.3 ng/dL, and total T3 214 ng/dL. Thyroid antibodies including TSI, TPO, and TSH receptor antibodies were negative. Thyroid ultrasound showed mildly heterogeneous parenchyma without nodules or increased vascularity.
Treatment began with methimazole 10 mg daily and beta blockade. Amiodarone was continued due to arrhythmia risk. Thyroid hormone levels worsened. Methimazole was stopped and propylthiouracil was started at 200 mg every four hours with metoprolol. Amiodarone was discontinued and replaced with lidocaine and mexiletine. Free T4 increased to 10 ng/dL despite therapy. Cholestyramine was added to enhance hormone clearance.
Free T4 decreased modestly to 9.8 ng/dL. Total T3 later increased to 198 ng/dL, suggesting poor thionamide response and favoring type II disease. Propylthiouracil was tapered. High-dose intravenous hydrocortisone was initiated with continued cholestyramine and beta blockade.
On hospital day six, recurrent ventricular tachycardia occurred. The patient remained stable and was transferred to the cardiac intensive care unit. Catheter ablation was performed successfully. Thyroid function improved gradually with the resolution of ventricular arrhythmias.
Conclusion
This case demonstrates the complexity of amiodarone-induced thyrotoxicosis complicated by ventricular tachycardia. Ultrasound findings, lack of response to thionamides, and steroid responsiveness supported type II disease. Early recognition, accurate subtype identification, and coordinated cardiac and endocrine management are essential to prevent life-threatening arrhythmias.

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