The mechanism of action of amiodarone is based on blockade of voltage-gated potassium channels in the cells of the heart muscles. As a result, amiodarone has the ability to prolong the action potential of the heart and thus break certain arrhythmias. In addition to its effect on potassium channels, amiodarone also has properties of a sodium and calcium channel blocker, as well as an alpha and beta blocker, and an inhibitory effect on muscarinic receptors. Thus, amiodarone can theoretically be assigned to all four classes of antiarrhythmic agents.
Amiodarone is 96% bound to plasma proteins. Degradation occurs via the liver and is catalyzed by the CYP3A4 and CYP2C8 enzymes. The plasma half-life for amiodarone is extremely long, averaging 9-100 days. In some cases, times of 200 days have been measured. Excretion is mainly via feces and to a small extent via urine.
Drugs that interact with (inhibit or induce) the enzyme CYP3A4 may interact, sometimes dangerously. Especially with CYP3A4 inhibiting agents, increased and sometimes toxic plasma levels of amiodarone may occur. Life-threatening effects may be the consequence.