Amiodarone Induced Thyrotoxicosis in the Setting of End Stage Cardiomyopathy

Abstract

Amiodarone is a class III antiarrhythmic agent which has effects of myocardial depolarization and repolarization. Due to its many side effects including thyroid dysfunction, its use is limited to life-threatening arrhythmias. The thyrotoxicosis can be from the iodine content of amiodarone or its direct toxicity on the thyroid gland. Because of the long half-life, causing amiodarone to have effects for months, medical management can be challenging, and thyroidectomy may be indicated. This is a 76-year-old man with a history of systolic heart failure with reduced ejection fraction (15%), on milrinone after cardiac resynchronization therapy, and recurrent ventricular tachycardia on amiodarone. He was admitted after his ICD device fired. During initial admission, his TSH was <0.015mcunit/mL and FT4 was 2.34ng/dL. Due to concern for amiodarone induced thyrotoxicosis (AIT), he was started on methimazole, prednisone, and cholestyramine. FT4 decreased from 2.34ng/dL to 2.23ng/dL and he discharged on methimazole 30mg daily and prednisone 20mg daily with plans to taper. He was seen outpatient with continued improvement in his FT4 to 2.09ng/dL. He was then seen again and found to have a rising FT4 to 2.22ng/dL and his regimen of prednisone was reinitiated at 10mg daily and methimazole increased to 40mg daily. Despite the medication changes, he continued to have an elevation in his FT4 up to 3.00ng/dL at which point he returned to the hospital for further evaluation and was given methimazole 60mg TID, prednisone 20mg daily, and restarted cholestyramine. With his significant cardiovascular risk, aggressive medical management was attempted prior to surgical evaluation. After his thyroid function failed to respond to medical intervention, multidisciplinary discussion was had with patient, family, and physician teams regarding surgical intervention versus continued long-term monitoring. Family elected to pursue surgery. Thyroidectomy was performed by an experienced endocrine surgeon successfully and his FT4 and T3 decreased appropriately requiring him to be initiated on levothyroxine supplementation. AIT can be separated into Type I, in which there is an increase in synthesis of T4 and T3 with amiodarone providing increasing substrate, and Type II in which there is destructive thyroiditis, releasing excess T4 and T3. In the United States, approximately 5% of individuals who are on amiodarone therapy develop hyperthyroidism, majority being Type II. If possible, amiodarone should be discontinued in Type I AIT, but there is no clear evidence for discontinuation in Type II. Medical management includes thionamides for Type I AIT and glucocorticoids for Type II AIT. Patients who are refractory to drug therapy should be treated with thyroidectomy. The advantages of a surgical procedurewith careful cardiovascular monitoring overall outweigh the morbidity and mortality of uncontrolled thyrotoxicosis.