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Amiodarone was initially developed in the early 1960s as a treatment for angina pectoris, since it produces coronary vasodilation and decreases cardiac oxygen demand. However, its pronounced antiarrhythmic effects redirected its use and amiodarone has become a widely used class III anti-arrhythmic drug. Compared to other antiarrhythmic drugs, it is more effective in treating both supraventricular and ventricular arrhythmias.1 It has few negative inotropic effects. The use of amiodarone is, however, limited by the relative frequent occurrence of serious and potentially life threatening side effects. Because of these side effects, generally it is not the drug of first choice in the treatment of arrhythmias.
Pharmacology of amiodarone
Amiodarone is an iodine-rich drug with strong structural similarities to the thyroid hormones (figure 1).2 After oral intake, absorption is limited (30–50%). When absorbed, it is metabolised in the liver to produce the active metabolite desethyl-amiodarone. Due to its lipophilic nature, it has strong tissue affinity and a large volume of distribution. In chronic users, high concentrations are found in fatty tissue, liver and lung and somewhat lower concentrations in kidney, heart, skeletal muscle, thyroid gland and brain. The distribution to these tissues is relatively slow, requiring high initial loading doses. Due to the relatively slow distribution, a steady state of tissue concentrations is reached only after 2 months. The relation between serum concentrations and clinical effect is not very clear. Serum concentrations >2.5 mg/l are associated with an increased risk of toxicity. The elimination half-life after oral long term treatment is 50–60 days. Each molecule of amiodarone contains two iodine atoms, approximately 37% of iodine by weight. The most commonly used oral dose of 200 mg per day results in an iodine uptake of 70 mg per day. About 10% (7 mg) is released in the body as iodine, which is an overwhelming amount compared to the normal …