Why the study?
Does long-term oral amiodarone treatment alter clinical and chemical variables of thyroid function in patients with symptomatic ventricular tachyarrhythmias?
Does long-term oral amiodarone treatment alter clinical and chemical variables of thyroid function in patients with symptomatic ventricular tachyarrhythmias?
Amiodarone therapy predictably elevates T4 and FT4I levels without necessarily indicating hyperthyroidism, though patients with prior thyroid antibodies or family history are at increased risk for hypothyroidism.
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Amiodarone raises T4 without equating to hyperthyroidism; leaves open refined hypothyroidism risk stratification in arrhythmia patients.
Clinical and chemical variables of thyroid function were studied in 26 patients with symptomatic ventricular tachyarrhythmias before and during long-term oral treatment with amiodarone. The mean (+/-SEM) pretreatment thyroxine (T4) level in the 26 patients was 7.32 +/- 0.33 micrograms/dL, and increased notably to 10.15 +/- 0.47 micrograms/dL by 30 to 120 days after treatment. The free thyroxine index (FT4I) was also notably elevated. Clinical hyperthyroidism or goiter did not develop, but clinical hypothyroidism occurred in four patients during and in one patient after discontinuation of amiodarone treatment. Notable titers of antithyroid antibodies were found in the serum of two of the five and a family history of thyroid disease was present in three of the five hypothyroid patients. An elevation of both the T4 level and the FT4I above the normal range is an expected finding in patients receiving amiodarone and does not by itself indicate hyperthyroidism. Patients with positive antithyroid antibodies or a family history of thyroid disease prior to treatment with amiodarone may be at an increased risk of hypothyroidism developing when treated with this drug.
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Janet A. Amico (1984) studied this question.
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