Rare Case of Amiodarone-Induced Thyrotoxicosis Triggering Life-Threatening VT Storm: ENDO 2026
USA: A rare and life-threatening case of amiodarone-induced thyrotoxicosis (AIT) presenting as a ventricular tachycardia (VT) storm was highlighted at ENDO 2026, highlighting the importance of prompt diagnosis and multidisciplinary management in patients receiving long-term amiodarone therapy.
The case was presented by Sarah Mohamed, Rochester General Hospital, New York, NY, United States.
Amiodarone, a widely used antiarrhythmic medication, is known to cause thyroid dysfunction because of its high iodine content and direct effects on the thyroid gland. Although AIT is an uncommon complication, severe thyrotoxicosis can precipitate serious cardiovascular events, including malignant ventricular arrhythmias.
The patient, a man in his 60s, sought medical attention after experiencing several weeks of fatigue, leg swelling, diarrhea, and an unintended weight loss of approximately 15 pounds. His medical history included atrial fibrillation and ventricular tachycardia, for which he had undergone implantable cardioverter-defibrillator (ICD) placement eight years earlier and an unsuccessful catheter ablation five years before presentation. He had been receiving amiodarone therapy for four years.
Interrogation of his ICD revealed five appropriate shocks delivered for sustained ventricular tachycardia. Despite significant thyrotoxicosis, he did not report classic hyperthyroid symptoms such as heat intolerance, excessive sweating, tremors, fever, or chills.
Laboratory investigations confirmed marked thyrotoxicosis, with a suppressed thyroid-stimulating hormone level of 0.01 mIU/L, elevated free thyroxine (T4) of 6.3 ng/dL, and total triiodothyronine (T3) of 214 ng/dL. Testing for thyroid autoantibodies was negative. Thyroid ultrasound demonstrated mildly heterogeneous thyroid tissue without nodules or increased blood flow, findings that did not strongly support autoimmune hyperthyroidism.
Initial treatment included methimazole and beta-blocker therapy, while amiodarone was continued because of ongoing arrhythmia concerns. However, thyroid hormone levels continued to rise. Clinicians subsequently switched treatment to high-dose propylthiouracil and metoprolol, while replacing amiodarone with lidocaine and mexiletine. Despite these measures, free T4 levels increased further, reaching 10 ng/dL.
To improve hormone clearance, cholestyramine was added. Although thyroid hormone levels showed slight improvement, persistent elevation of T3 and poor response to antithyroid medications suggested type II AIT, a destructive thyroiditis caused by amiodarone-related thyroid injury rather than excess hormone production.
Based on this evolving clinical picture, propylthiouracil was tapered and high-dose intravenous hydrocortisone was initiated. The patient's thyroid function gradually improved following corticosteroid therapy, further supporting the diagnosis of type II AIT.
On the sixth day of hospitalization, the patient developed recurrent ventricular tachycardia and was transferred to the cardiac intensive care unit. He subsequently underwent successful catheter ablation, after which both his thyroid status and arrhythmia burden improved.
According to the authors, the case highlights the diagnostic challenges associated with amiodarone-induced thyrotoxicosis and emphasizes the importance of distinguishing between AIT subtypes. They noted that early recognition, accurate classification of the disorder, and close collaboration between endocrinology and cardiology teams are critical to preventing potentially fatal arrhythmic complications.
Reference:
MON-345 - Amiodarone-Induced Thyrotoxicosis Presenting as A Rare Case of Ventricular Tachycardia Storm.
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