Amiodarone-induced thyroid diseases: what the cardiologist needs to know

Amiodarone is one of the most commonly used antiarrhythmic drugs worldwide, with an associated incidence of thyroid dysfunction reported in approximately 15-20% of patients. In amiodarone-induced hypothyroidism, thyroid hormone replacement is necessary alongside continuing amiodarone therapy. Among the dysfunctions, amiodarone-induced thyrotoxicosis (AIT) presents both diagnostic and therapeutic challenges, requiring collaborative work and continuous consultation between the treating cardiologist and endocrinologist. The decision to either discontinue or continue amiodarone must be individualized in every case. According to the current guidelines of the European Thyroid Association (ETA) and the American Thyroid Association (ATA), type 1 AIT is treated with antithyroid drugs, while type 2 AIT is managed with steroids. Additionally, non-selective beta-blockers, primarily propranolol, play an important role in treating both types of AIT by not only reducing symptoms of sympathetic overactivity but also at higher doses inhibiting peripheral conversion of thyroid hormones, aiding faster achievement of euthyroidism. In rare, severe thyrotoxic crises, plasmapheresis or emergency thyroidectomy may become necessary alongside immediate discontinuation of amiodarone. After an episode of AIT, before restarting amiodarone—due to the high risk of relapse—definitive treatment of hyperthyroidism with radioactive iodine therapy or surgical thyroid removal is recommended.