Whether there is a link between the antiarrhythmic efficacy of
amiodarone and its blocking effect on the peripheral conversion of tetraiodothyronine (T4) to
triiodothyronine (T3) is uncertain. If such a link exists, oral intake of T3 during
amiodarone treatment could reverse, at least partially, the antiarrhythmic efficacy of
amiodarone. To assess the safety of oral intake of T3 during
amiodarone treatment and gain further insight into the relation between the antiarrhythmic action of
amiodarone and its metabolic effect on T4, 7 patients (aged 32 to 62 years) with multiple
ventricular premature complexes (VPCs) but no underlying
heart disease were studied. Antiarrhythmic treatment was indicated for symptomatic relief only. Each patient underwent a 48-hour ambulatory electrocardiographic recording, electrocardiography and thyroid function tests, including plasma T4, T3, reverse T3 (rT3), free T4, free T3 and
thyroid-stimulating hormone without treatment (baseline) after 1 month of
amiodarone therapy and after a second month of
amiodarone therapy with increasing doses of oral T3 (up to 75 micrograms/day). Treatment with
amiodarone resulted in a decrease in plasma T3 and free T3, an increase in plasma rT3, a marked diminution in the frequency of VPCs and a prolongation of the corrected QT interval (QTc). During treatment with
amiodarone and T3, plasma T3 and free T3 increased and plasma T4, free T4 and rT3 levels decreased; the frequency of VPCs remained low despite shortening of the QTc to values not different from baseline. Thus, in patients with frequent VPCs and no underlying
heart disease, oral intake of T3 during
amiodarone treatment is safe and does not abolish the antiarrhythmic efficacy of
amiodarone, despite a shortening of the QTc.(ABSTRACT TRUNCATED AT 250 WORDS)