They are collectively referred to as supraventricular or atrial arrhythmias because they occur above (supra) the ventricles in the electrical conduction system of the heart.

[16] However, due to a small sample size and lack of statistical significance, more evidence is required, and amiodarone remains the drug of choice in ventricular arrhythmias.

[15][16] Amiodarone is also commonly used as the first-line therapy for patients who receive shocks from implantable cardioverter defibrillators caused by ventricular arrhythmias.

Combining amiodarone with beta-blockers has been shown to reduce the likelihood of experiencing inappropriate shocks from implantable cardioverter defibrillators.

[21] Individuals who have undergone open heart surgery are at an increased risk of developing atrial fibrillation (or AF) in the first few days post-procedure.

[13][22][23] In the ARCH trial, intravenous amiodarone (2 g administered over 2 d) has been shown to reduce the incidence of atrial fibrillation after open heart surgery when compared to placebo.

[24][25] However, clinical studies have failed to demonstrate long-term efficacy and have shown potentially fatal side effects such as pulmonary toxicities.

[26][27] So-called 'acute onset atrial fibrillation', defined by the North American Society of Pacing and Electrophysiology (NASPE) in 2003, responds well to short-duration treatment with amiodarone.

[29][30][31] Amiodarone is an effective, antiarrhythmic-of-choice in achieving cardioversion to sinus rhythm in critical care populations with new onset atrial fibrillation (NOAF).

[13] At oral doses of 400 mg per day or higher, amiodarone can have serious, varied side effects, including toxicity to the thyroid gland,[34] liver, lung, and retinal functions, requiring clinical surveillance and regular laboratory testing.

Risk factors include high cumulative dose, more than 400 milligrams per day, duration over two months, increased age, and preexisting pulmonary disease.

[51] Corneal micro-deposits (cornea verticillata,[54] also called vortex or whorl keratopathy) are almost universally present (over 90%) in individuals taking amiodarone longer than 6 months, especially doses greater than 400 mg/day.

Anterior subcapsular lens deposits are relatively common (50%) in higher doses (greater than 600 mg/day) after 6 months of treatment.

[57] In clinical observations, it has been noted that the administration of amiodarone, even at lower therapeutic doses, has been associated with the development of a condition mimicking alcoholic cirrhosis.

[36] Long-term administration of amiodarone (usually more than eighteen months) is associated with a light-sensitive blue-grey discoloration of the skin, sometimes called ceruloderma; such patients should avoid exposure to the sun and use sunscreen that protects against ultraviolet-A and -B.

[65] These results should be interpreted with caution due to limitations of the study design and care should be taken prior to altering current clinical and prescribing practices.

The pharmacokinetics of numerous drugs, including many that are commonly administered to individuals with heart disease, are affected by amiodarone.

[79] On 8 August 2008, the US Food and Drug Administration (FDA) issued a warning of the risk of rhabdomyolysis, which can lead to kidney failure or death, when simvastatin is used with amiodarone.

[medical citation needed] Some of these compounds can be reabsorbed back into systemic circulation through enterohepatic recirculation, where they may undergo additional rounds of metabolism before eventually being excreted again into bile.

[medical citation needed] Because renal excretion contributes only minimally to the elimination of amiodarone, dose adjustment based on kidney function is generally not necessary.

This is because most patients with normal renal function can adequately clear the drug through hepatic metabolism and biliary elimination pathways.

[87] Amiodarone slows the conduction rate and prolongs the refractory period of the SA and AV nodes.

[88] It also prolongs the refractory periods of the ventricles, bundles of His, and the Purkinje fibers without exhibiting any effects on the conduction rate.

[88] Amiodarone has been shown to prolong the myocardial cell action potential duration and refractory period and is a non-competitive β-adrenergic inhibitor.

[89] It also shows beta blocker-like and calcium channel blocker-like actions on the SA and AV nodes, increases the refractory period via sodium- and potassium-channel effects, and slows intra-cardiac conduction of the cardiac action potential, via sodium-channel effects.

[citation needed] Amiodarone was initially developed in 1961 at the Labaz company, Belgium, by chemists Tondeur and Binon, who were working on preparations derived from khellin.

[95] Based on Singh's work, the Argentinian physician Mauricio Rosenbaum began using amiodarone to treat his patients who have supraventricular and ventricular arrhythmias, with impressive results.

Based on papers written by Rosenbaum developing Singh's theories, physicians in the United States began prescribing amiodarone to their patients with potentially life-threatening arrhythmias in the late 1970s.

[2][99] Amiodarone may be an acronym[citation needed] for its IUPAC name (2-butyl-1-benzofuran-3-yl)-[4-[2-(diethylamino)ethoxy]-3,5-diiodophenyl]methanone,[100] where ar is a placeholder for phenyl.

In India, amiodarone is marketed (produced by Cipla Pharmaceutical) under the brand name Tachyra.