8225 Amiodarone-Induced Thyrotoxicosis; Unusual Outcome for a Relatively Common Problem

Abstract Disclosure: A. Abobaker: None. A. Naji: None. F. Ansari: None. M. Mushref: None. Background: Amiodarone-Induced Thyrotoxicosis (AIT) affect a significant proportion of patients taking Amiodarone. AIT manifests in different types and can be challenging to treat. Herein, we present a case of Amiodarone-induced thyrotoxicosis complicating ventricular tachycardia (VT) in a patient with prior history of non-ischemic dilated cardiomyopathy (DCM) requiring plasmapheresis and total thyroidectomy. Clinical case: A 38-year-old male with history of non-ischemic DCM, VT status post multiple endocardial ablations, ICD placement, and maintenance medical treatment with amiodarone and mexiletine, who was admitted to hospital on account of symptomatic episodes of ventricular tachycardia. Initial laboratory work showed significant hyperthyroidism; TSH 0.03 µIU/ml (n 0-3-5.6 µIU/ml), free T4 4.06 ng/dl (n 0-6-1-6 ng/dl) and free T3 5.1 pg/ml (n 2.5-3.9 pg/ml). Thyroid ultrasound showed moderate thyromegaly without thyroid nodules. Amiodarone was stopped, and he was started on methimazole and prednisone for a presumed mixed type AIT. During the hospital course, he developed multiple episodes of VT requiring multiple shocks by ICD. He was subsequently treated with sotalol and discharged after he was stable with improvement in his thyroid function. Consequently, he was re-admitted several times with VTs and worsening thyroid hormones level. Endocrinology team was consulted, who initially treated the patient with increasing dose of both methimazole, glucocorticoids and cholestyramine. However, due to lack of clinical response and the complicated cardiovascular presentation, total thyroidectomy after achievement of euthyroid-state was recommended. To expedite the process, the patient received plasmapheresis for 7 days with significant improvement of thyroid hormones level, and he successfully underwent total thyroidectomy. His hospital course after thyroidectomy was complicated by the development of refractory VT necessitating endocardial ablation. He was then discharged on antiarrhythmics and levothyroxine. Despite normal thyroid function after surgery, the patient was re-admitted after 15 months with VT storm and eventually underwent heart transplant surgery. Conclusion: Amiodarone-induced thyrotoxicosis, especially when unresponsive to medical treatment, poses a critical challenge, particularly in patients with arrhythmias complicating cardiomyopathy. In our case, the patient necessitated plasmapheresis followed by total thyroidectomy due to the failure of medical interventions. This approach should be considered in patients who require prompt attainment of euthyroid state. Presentation: 6/3/2024