Key result
Amiodarone antiarrhythmic response is linked to greater T4 monodeiodination inhibition and elevated TSH.
Why the study?
The effects of chronic amiodarone treatment on thyroid and cardiac function parameters in patients with refractory ventricular arrhythmias were not fully understood.
Observational (n=50)
Amiodarone responders show more thyroid inhibition; this association leaves open whether TSH monitoring could predict efficacy in refractory arrhythmias.
The effects of chronic amiodarone treatment on several thyroid and cardiac function parameters were studied in 50 euthyroid patients with refractory ventricular arrhythmias, divided in responders and nonresponders according to their sensitivity to the antiarrhythmic action of the drug. No differences in the severity of cardiac disease and blood amiodarone concentrations were found in the two groups. Amiodarone induced a significant inhibition of peripheral T4 monodeiodination, more pronounced in responders compared to nonresponders. On the contrary, only in responsive patients, elevated basal and TRH-stimulated TSH levels were observed (despite serum T3 levels were not different from those in nonresponders) and the indirect indices of cardiac performance, particularly the systolic time intervals, fell in a range usually observed in the hypothyroid states. These findings suggest that amiodarone, besides the well-known inhibition of T4 to T3 conversion, also induces a partial resistance to the thyroid hormones, which is probably involved in the therapeutical effectiveness of the drug.
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Beck‐Peccoz et al. (1986) conducted an observational in Refractory ventricular arrhythmias (n=50). Chronic amiodarone treatment vs. Nonresponders vs Responders was evaluated on Thyroid and cardiac function parameters (peripheral T4 monodeiodination, TSH levels, and systolic time intervals). Chronic amiodarone treatment in 50 patients induced greater inhibition of T4 monodeiodination and elevated TSH levels in antiarrhythmic responders compared to nonresponders.
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