INVITED COMMENTARY Towards an animal model of amiodarone-induced thyroid dysfunction

(Correspondence should be addressed to W M Wiersinga) The drug amiodarone, originally introduced in clinical medicine in 1962 for the treatment of angina pectoris, continues to arouse interest among cardiologists and thyroidologists. To the cardiologist amiodarone is one of the most potent antiarrhythmic agents in the manage-ment of cardiac tachyarrhythmias refractory to other treatment modalities. In recent years amiodarone has also been applied succesfully in the treatment of severe congestive heart failure and in the prevention of sudden death in patients with cardiomyopathy. Amiodarone as a class III antiarrhythmic agent prolongs the duration of the action potential in cardiac tissue; it also decreases heart rate and myocardial oxygen consumption. These actions are quite similar to those observed in hypothy