(CCSP054) SAFETY OF CONTINUING AMIODARONE DOSING IN PATIENTS MANAGED WITH METHIMAZOLE FOR HYPERTHYROIDISM ASSOCIATED WITH THE IODINE LOAD RELEASED FROM AMIODARONE METABOLISM: A CASE SERIES

Background: Amiodarone is a very efficacious anti-arrhythmic drug, favored in patients with coronary artery disease and reduced ejection fracture. However, metabolism of this di-iodinated compound generates a high iodine load, which can result in thyroid dysfunction. In susceptible individuals, particularly patients with sub-clinical thyroid disease or those living in iodine deplete areas, there is a risk of developing “amiodarone induced” thyrotoxicosis (AIT). Our experience suggests a better term is Amiodarone Associated Thyrotoxicosis (AAT), as the drug itself appears to have a much more minor effect on the thyroid than the iodine load it provides. The clinical decision as to whether to continue amiodarone or abort its use in the setting of a hyperthyroid state becomes more complicated in patients suffering clinically important tachyarrhythmias.

METHODS AND RESULTS: We used a retrospective chart review of patients followed in our atrial fibrillation specialty clinic to examine the effect of continuing amiodarone in patients treated with methimazole. Of 185 patients prescribed amiodarone for atrial arrhythmias, and consented the use of their data, 32 patients were found to have documented free T4 values > 29 pmol/L (Upper Limit Normal 25 pmol/L). Individuals who had their amiodarone discontinued or were receiving thyroid supplementation for prior hypothyroidism were excluded from further analysis (9 patients).

The median time from amiodarone exposure to free T4 values > 29 was 30 months with median peak value of 42.6 pmol/L. Of the eligible patients 17 were treated with methimazole 5 mg PO TID (doubled if required). Free T4 resolved to normal limits within 2-7 months. Another 4 asymptomatic patients were monitored clinically and resolved without pharmacological intervention.

Conclusion: Given the prolonged time to clear iodine and amiodarone from the body, and the risk of recurrent arrhythmia if therapy lapses, our clinic has successfully followed the policy of continuing amiodarone dosing to maintain arrhythmia control. This appeared to be universally safe in our population and has not impeded or delayed resolution of the thyroid abnormality. Treatment with methimazole appears to be effective.
Continuing amiodarone therapy avoided anxiety over possible recurrent arrhythmias, diminished tachycardia and sympathetic-induced symptoms, and decreased conversion of T4 to its more active form, T3.
As there was no evidence of thyroid parenchymal toxicity, rather only iodine-induced metabolic derangement, which is not quickly reduced by drug discontinuation, continuation of amiodarone appears to provide clinical benefit.