Amiodarone

Name: Amiodarone

What side effects can this medication cause?

Amiodarone may cause side effects. Tell your doctor if any of these symptoms are severe or do not go away:

  • constipation
  • loss of appetite
  • headache
  • decreased sex drive
  • difficulty falling asleep or staying asleep
  • flushing
  • changes in ability to taste and smell
  • changes in amount of saliva

Some side effects can be serious. If you experience any of the following symptoms, or those listed in the IMPORTANT WARNING section, call your doctor immediately or get emergency medical treatment:

  • rash
  • weight loss or gain
  • restlessness
  • weakness
  • nervousness
  • irritability
  • intolerance to heat or cold
  • thinning hair
  • excessive sweating
  • changes in menstrual cycle
  • swelling in the front of the neck (goiter)
  • swelling of the hands, feet, ankles, or lower legs
  • uncontrollable shaking of a part of the body
  • decreased concentration
  • movements that you cannot control
  • poor coordination or trouble walking
  • numbness or tingling in the hands, legs, and feet
  • muscle weakness

Amiodarone may cause other side effects. Call your doctor if you have any unusual problems while taking this medication.

If you experience a serious side effect, you or your doctor may send a report to the Food and Drug Administration's (FDA) MedWatch Adverse Event Reporting program online (http://www.fda.gov/Safety/MedWatch) or by phone (1-800-332-1088).

What other information should I know?

Do not let anyone else take your medication. Ask your pharmacist any questions you have about refilling your prescription.

It is important for you to keep a written list of all of the prescription and nonprescription (over-the-counter) medicines you are taking, as well as any products such as vitamins, minerals, or other dietary supplements. You should bring this list with you each time you visit a doctor or if you are admitted to a hospital. It is also important information to carry with you in case of emergencies.

Adverse Effects

>10%

Increased liver AST or ALT levels (3-20%; as high as 40-50% in some studies)

Hypotension (16%)

Dizziness (3-40%)

Headache (3-40%)

Malaise (3-40%)

Abnormal gait/ataxia (3-40%)

Fatigue (3-40%)

Impaired memory (3-40%)

Involuntary movement (3-40%)

Sleep disturbances (3-40%)

Photosensitivity (10-75%)

Hypothyroidism (1-22%)

Constipation (10-33%)

Anorexia (10-33%)

1-10%

CHF (3%)

Bradycardia or sinus arrest (3-5%)

AV block (5%)

SA node dysfunction (1-3%)

Hyperthyroidism (3-10%)

Hepatitis and cirrhosis (<3%)

Visual disturbances (2-9%)

Optic neuritis (1%)

Frequency Not Defined

Corneal microdeposits

Demyelinating polyneuropathy

Postmarketing Reports

Hypersensitivity: Anaphylactic/anaphylactoid reaction (including shock), angioedema, urticaria

Pulmonary: Eosinophilic pneumonia, ARDS (in postoperative setting), bronchospasm, possibly fatal respiratory disorders (including distress, failure, arrest, and ARDS), bronchiolitis obliterans organizing pneumonia (possibly fatal), fever, dyspnea, cough, hemoptysis, wheezing, hypoxia, pulmonary infiltrates and/or mass, pulmonary alveolar hemorrhage, pleural effusion, pleuritis

Gastrointestinal: Hepatitis, cholestatic hepatitis, cirrhosis, pancreatitis, dry mouth

Nephrology: Renal impairment, renal insufficiency, acute renal failure

Neurology: Pseudotumor cerebri, parkinsonian symptoms, such as akinesia and bradykinesia (sometimes reversible with discontinuation of therapy)

Endocrine: SIADH, thyroid nodules/thyroid cancer

Dermatology: Toxic epidermal necrolysis (sometimes fatal), erythema multiforme, Stevens-Johnson syndrome, exfoliative dermatitis, drug rash with eosinophilia and systemic symptoms (DRESS), eczema, skin cancer, vasculitis, pruritus, bullous dermatitis

Hematology: Hemolytic anemia, aplastic anemia, pancytopenia, neutropenia, thrombocytopenia, agranulocytosis, granuloma, lupus-like syndrome

Musculoskeletal: Myopathy, muscle weakness, rhabdomyolysis, demyelinating polyneuropathy

Psychiatric: Hallucination, confusional state, disorientation, delirium

Genitourinary: Epididymitis, impotence

Pregnancy & Lactation

Pregnancy: Amiodarone can cause fetal harm when administered to a pregnant woman; fetal exposure may increase potential for adverse experiences including cardiac, thyroid, neurodevelopmental, neurological and growth effects in neonate; inform patient of potential hazard to fetus if amiodarone administered during pregnancy or if patient becomes pregnant while in therapy

Lactation: Amiodarone and one of its major metabolites, DEA, are excreted in human milk, suggesting that breast-feeding could expose the nursing infant to a significant dose of the drug; risk of exposing infant to amiodarone and DEA must be weighed against potential benefit of arrhythmia suppression in the mother; advise mother to discontinue nursing

Pregnancy Categories

A:Generally acceptable. Controlled studies in pregnant women show no evidence of fetal risk.

B:May be acceptable. Either animal studies show no risk but human studies not available or animal studies showed minor risks and human studies done and showed no risk.

C:Use with caution if benefits outweigh risks. Animal studies show risk and human studies not available or neither animal nor human studies done.

D:Use in LIFE-THREATENING emergencies when no safer drug available. Positive evidence of human fetal risk.

X:Do not use in pregnancy. Risks involved outweigh potential benefits. Safer alternatives exist.

NA:Information not available.

Patient Handout

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Uses of Amiodarone

Amiodarone is a prescription medicine used in adults to treat life-threatening heartbeat problems called ventricular arrhythmias, for which other treatment did not work or was not tolerated. 

This medication may be prescribed for other uses. Ask your doctor or pharmacist for more information.

Amiodarone Brand Names

Amiodarone may be found in some form under the following brand names:

  • Cordarone

  • Nexterone

  • Pacerone

Side Effects of Amiodarone

Oral/Injectable:

Call your doctor for medical advice about side effects. You may report side effects to FDA at 1‑800‑FDA-1088.

Amiodarone can cause serious side effects that lead to death including lung damage, liver damage, worse heartbeat problems, and thyroid problems. See "Drug Precautions".

Some other serious side effects of amiodarone include:

  • thyroid problems. Amiodarone can cause thyroid problems, including low thyroid function or overactive thyroid function. Your doctor may arrange regular blood tests to check your thyroid function during treatment with amiodarone. Call your doctor if you have weakness, weight loss or weight gain, heat or cold intolerance, hair thinning, sweating, changes in your menses, swelling of your neck (goiter), nervousness, irritability, restlessness, decreased concentration, depression in the elderly, or tremor.
  • skin problems. Amiodarone can cause your skin to be more sensitive to the sun or to turn a bluish-gray color. In most patients, skin color slowly returns to normal after stopping amiodarone. In some patients, skin color does not return to normal.
  • vision problems that may lead to permanent blindness. You should have regular eye exams before and during treatment with amiodarone. Call your doctor if you have blurred vision, see halos, or your eyes become sensitive to light.
  • nerve problems. Amiodarone can cause a feeling of “pins and needles” or numbness in the hands, legs, or feet, muscle weakness, uncontrolled movements, poor coordination, and trouble walking.

Other side effects of amiodarone include nausea, vomiting, constipation, and loss of appetite.

Call your doctor about any side effect that bothers you.

These are not all the side effects with one amiodarone. For more information, ask your doctor or pharmacist.

Amiodarone Precautions

Oral/Injectable:

Amiodarone can cause serious side effects that can lead to death including:

  • lung damage
  • liver damage
  • worse heartbeat problems
  • thyroid problems

Call your doctor or get medical help right away if you have any symptoms such as the following:

  • shortness of breath, wheezing, or any other trouble breathing; coughing, chest pain, or spitting up of blood
  • nausea or vomiting; passing brown or dark-colored urine; feel more tired than usual; your skin and whites of your eyes get yellow; or have stomach pain
  • heart pounding, skipping a beat, beating very fast or very slowly; feel light-headed or faint
  • weakness, weight loss or weight gain, heat or cold intolerance, hair thinning, sweating, changes in your menses, swelling of your neck (goiter), nervousness, irritability, restlessness, decreased concentration, depression in the elderly, or tremor.

Because of these possible side effects, amiodarone should only be used in adults with life-threatening heartbeat problems called ventricular arrhythmias, for which other treatments did not work or were not tolerated.

Amiodarone can cause other serious side effects. See "Side Effects". If you get serious side effects during treatment with amiodarone you may need to stop amiodarone, have your dose changed, or get medical treatment. Talk with your doctor before you stop taking amiodarone.

You may still have side effects after stopping amiodarone because the medicine stays in your body months after treatment is stopped.

Tell all your healthcare providers that you take or took amiodarone. This information is very important for other medical treatments or surgeries you may have.

Do not take amiodarone if you:

  • have certain heart conditions (heart block, very slow heart rate, or slow heart rate with dizziness or lightheadedness)
  • have an allergy to amiodarone, iodine, or any of the other ingredients in amiodarone. 

Amiodarone FDA Warning

This medication is intended for use only in patients with the indicated life-threatening arrhythmias because its use is accompanied by substantial toxicity.

Amiodarone has several potentially fatal toxicities, the most important of which is pulmonary toxicity (hypersensitivity pneumonitis or interstitial/alveolar pneumonitis) that has resulted in clinically manifest disease at rates as high as 10 to 17% in some series of patients with ventricular arrhythmias given doses around 400 mg/day, and as abnormal diffusion capacity without symptoms in a much higher percentage of patients. Pulmonary toxicity has been fatal about 10% of the time. Liver injury is common with this medication, but is usually mild and evidenced only by abnormal liver enzymes. Overt liver disease can occur, however, and has been fatal in a few cases. Like other antiarrhythmics, Amiodarone can exacerbate the arrhythmia, e.g., by making the arrhythmia less well tolerated or more difficult to reverse. This has occurred in 2 to 5% of patients in various series, and significant heart block or sinus bradycardia has been seen in 2 to 5%. All of these events should be manageable in the proper clinical setting in most cases. Although the frequency of such proarrhythmic events does not appear greater with amiodarone than with many other agents used in this population, the effects are prolonged when they occur.

Even in patients at high risk of arrhythmic death, in whom the toxicity of amiodarone is an acceptable risk, Amiodarone poses major management problems that could be life-threatening in a population at risk of sudden death, so that every effort should be made to utilize alternative agents first.

The difficulty of using amiodarone effectively and safely itself poses a significant risk to patients. Patients with the indicated arrhythmias must be hospitalized while the loading dose of amiodarone is given, and a response generally requires at least one week, usually two or more. Because absorption and elimination are variable, maintenance-dose selection is difficult, and it is not unusual to require dosage decrease or discontinuation of treatment. In a retrospective survey of 192 patients with ventricular tachyarrhythmias, 84 required dose reduction and 18 required at least temporary discontinuation because of adverse effects, and several series have reported 15 to 20% overall frequencies of discontinuation due to adverse reactions. The time at which a previously controlled life-threatening arrhythmia will recur after discontinuation or dose adjustment is unpredictable, ranging from weeks to months. The patient is obviously at great risk during this time and may need prolonged hospitalization. Attempts to substitute other antiarrhythmic agents when amiodarone must be stopped will be made difficult by the gradually, but unpredictably, changing amiodarone body burden. A similar problem exists when amiodarone is not effective; it still poses the risk of an interaction with whatever subsequent treatment is tried.

Amiodarone - Clinical Pharmacology

Electrophysiology/Mechanisms of Action:

In animals, Amiodarone is effective in the prevention or suppression of experimentally induced arrhythmias. The antiarrhythmic effect of Amiodarone may be due to at least two major properties:

1. a prolongation of the myocardial cell-action potential duration and refractory period and 2. non-competitive antagonism of α- and β-adrenoceptors.

Amiodarone prolongs the duration of the action potential of all cardiac fibers while causing minimal reduction of dV/dt (maximal upstroke velocity of the action potential). The refractory period is prolonged in all cardiac tissues. Amiodarone increases the cardiac refractory period without influencing resting membrane potential, except in automatic cells where the slope of the prepotential is reduced, generally reducing automaticity. These electrophysiologic effects are reflected in a decreased sinus rate of 15 to 20%, increased PR and QT intervals of about 10%, the development of U-waves, and changes in T-wave contour. These changes should not require discontinuation of Amiodarone as they are evidence of its pharmacological action, although Amiodarone can cause marked sinus bradycardia or sinus arrest and heart block. On rare occasions, QT prolongation has been associated with worsening of arrhythmia (see WARNINGS).

Hemodynamics:

In animal studies and after intravenous administration in man, Amiodarone relaxes vascular smooth muscle, reduces peripheral vascular resistance (afterload), and slightly increases cardiac index. After oral dosing, however, Amiodarone produces no significant change in left ventricular ejection fraction (LVEF), even in patients with depressed LVEF. After acute intravenous dosing in man, Amiodarone may have a mild negative inotropic effect.

Pharmacokinetics:

Following oral administration in man, Amiodarone is slowly and variably absorbed. The bioavailability of Amiodarone is approximately 50%, but has varied between 35 and 65% in various studies. Maximum plasma concentrations are attained 3 to 7 hours after a single dose. Despite this, the onset of action may occur in 2 to 3 days, but more commonly takes 1 to 3 weeks, even with loading doses. Plasma concentrations with chronic dosing at 100 to 600 mg/day are approximately dose proportional, with a mean 0.5 mg/L increase for each 100 mg/day. These means, however, include considerable individual variability. Food increases the rate and extent of absorption of Amiodarone. The effects of food upon the bioavailability of Amiodarone have been studied in 30 healthy subjects who received a single 600 mg dose immediately after consuming a high-fat meal and following an overnight fast. The area under the plasma concentration-time curve (AUC) and the peak plasma concentration (Cmax) of Amiodarone increased by 2.3 (range 1.7 to 3.6) and 3.8 (range 2.7 to 4.4) times, respectively, in the presence of food. Food also increased the rate of absorption of Amiodarone, decreasing the time to peak plasma concentration (Tmax) by 37%. The mean AUC and mean Cmax of the major metabolite of Amiodarone, desethylAmiodarone (DEA) increased by 55% (range 58 to 101%) and 32% (range 4 to 84%), respectively, but there was no change in the Tmax in the presence of food.

Amiodarone has a very large but variable volume of distribution, averaging about 60 L/kg, because of extensive accumulation in various sites, especially adipose tissue and highly perfused organs, such as the liver, lung, and spleen. One major metabolite of Amiodarone, DEA, has been identified in man; it accumulates to an even greater extent in almost all tissues. No data are available on the activity of DEA in humans, but in animals, it has significant electrophysiologic and antiarrhythmic effects generally similar to Amiodarone itself. DEA's precise role and contribution to the antiarrhythmic activity of oral Amiodarone are not certain. The development of maximal ventricular Class III effects after oral Amiodarone administration in humans correlates more closely with DEA accumulation over time than with Amiodarone accumulation.

Amiodarone is metabolized to DEA by the cytochrome P450 (CYP) enzyme group, specifically CYP3A and CYP2C8. The CYP3A isoenzyme is present in both the liver and intestines. In vitro, Amiodarone and DEA, exhibit a potential to inhibit CYP2C9, CYP2C19, CYP2D6, CYP3A, CYP2A6, CYP2B6 and CYP2C8. Amiodarone and DEA have also a potential to inhibit some transporters such as P- glycoprotein and organic cation transporter (OCT2).

Amiodarone is eliminated primarily by hepatic metabolism and biliary excretion and there is negligible excretion of Amiodarone or DEA in urine. Neither Amiodarone nor DEA is dialyzable.

In clinical studies of 2 to 7 days, clearance of Amiodarone after intravenous administration in patients with VT and VF ranged between 220 and 440 mL/hr/kg. Age, sex, renal disease, and hepatic disease (cirrhosis) do not have marked effects on the disposition of Amiodarone or DEA. Renal impairment does not influence the pharmacokinetics of Amiodarone. After a single dose of intravenous Amiodarone in cirrhotic patients, significantly lower Cmax and average concentration values are seen for DEA, but mean Amiodarone levels are unchanged. Normal subjects over 65 years of age show lower clearances (about 100 mL/hr/kg) than younger subjects (about 150 mL/hr/kg) and an increase in t½ from about 20 to 47 days. In patients with severe left ventricular dysfunction, the pharmacokinetics of Amiodarone are not significantly altered but the terminal disposition t½ of DEA is prolonged. Although no dosage adjustment for patients with renal, hepatic, or cardiac abnormalities has been defined during chronic treatment with Amiodarone, close clinical monitoring is prudent for elderly patients and those with severe left ventricular dysfunction.

Following single dose administration in 12 healthy subjects, Amiodarone exhibited multi-compartmental pharmacokinetics with a mean apparent plasma terminal elimination half-life of 58 days (range 15 to 142 days) for Amiodarone and 36 days (range 14 to 75 days) for the active metabolite (DEA). In patients, following discontinuation of chronic oral therapy, Amiodarone has been shown to have a biphasic elimination with an initial one-half reduction of plasma levels after 2.5 to 10 days. A much slower terminal plasma-elimination phase shows a half-life of the parent compound ranging from 26 to 107 days, with a mean of approximately 53 days and most patients in the 40- to 55-day range. In the absence of a loading-dose period, steady-state plasma concentrations, at constant oral dosing, would therefore be reached between 130 and 535 days, with an average of 265 days. For the metabolite, the mean plasma-elimination half-life was approximately 61 days. These data probably reflect an initial elimination of drug from well-perfused tissue (the 2.5- to 10-day half-life phase), followed by a terminal phase representing extremely slow elimination from poorly perfused tissue compartments such as fat.

The considerable intersubject variation in both phases of elimination, as well as uncertainty as to what compartment is critical to drug effect, requires attention to individual responses once arrhythmia control is achieved with loading doses because the correct maintenance dose is determined, in part, by the elimination rates. Daily maintenance doses of Amiodarone should be based on individual patient requirements (see DOSAGE AND ADMINISTRATION).

Amiodarone and its metabolite have a limited transplacental transfer of approximately 10 to 50%. The parent drug and its metabolite have been detected in breast milk.

Amiodarone is highly protein-bound (approximately 96%).

Although electrophysiologic effects, such as prolongation of QTc, can be seen within hours after a parenteral dose of Amiodarone, effects on abnormal rhythms are not seen before 2 to 3 days and usually require 1 to 3 weeks, even when a loading dose is used. There may be a continued increase in effect for longer periods still. There is evidence that the time to effect is shorter when a loading-dose regimen is used.

Consistent with the slow rate of elimination, antiarrhythmic effects persist for weeks or months after Amiodarone is discontinued, but the time of recurrence is variable and unpredictable. In general, when the drug is resumed after recurrence of the arrhythmia, control is established relatively rapidly compared to the initial response, presumably because tissue stores were not wholly depleted at the time of recurrence.

Pharmacodynamics:

There is no well-established relationship of plasma concentration to effectiveness, but it does appear that concentrations much below 1 mg/L are often ineffective and that levels above 2.5 mg/L are generally not needed. Within individuals dose reductions and ensuing decreased plasma concentrations can result in loss of arrhythmia control. Plasma-concentration measurements can be used to identify patients whose levels are unusually low, and who might benefit from a dose increase, or unusually high, and who might have dosage reduction in the hope of minimizing side effects. Some observations have suggested a plasma concentration, dose, or dose/duration relationship for side effects such as pulmonary fibrosis, liver-enzyme elevations, corneal deposits and facial pigmentation, peripheral neuropathy, gastrointestinal and central nervous system effects.

Monitoring Effectiveness:

Predicting the effectiveness of any antiarrhythmic agent in long-term prevention of recurrent ventricular tachycardia and ventricular fibrillation is difficult and controversial, with highly qualified investigators recommending use of ambulatory monitoring, programmed electrical stimulation with various stimulation regimens, or a combination of these, to assess response. There is no present consensus on many aspects of how best to assess effectiveness, but there is a reasonable consensus on some aspects:

1. If a patient with a history of cardiac arrest does not manifest a hemodynamically unstable arrhythmia during electrocardiographic monitoring prior to treatment, assessment of the effectiveness of Amiodarone requires some provocative approach, either exercise or programmed electrical stimulation (PES). 2. Whether provocation is also needed in patients who do manifest their life-threatening arrhythmia spontaneously is not settled, but there are reasons to consider PES or other provocation in such patients. In the fraction of patients whose PES-inducible arrhythmia can be made noninducible by Amiodarone (a fraction that has varied widely in various series from less than 10% to almost 40%, perhaps due to different stimulation criteria), the prognosis has been almost uniformly excellent, with very low recurrence (ventricular tachycardia or sudden death) rates. More controversial is the meaning of continued inducibility. There has been an impression that continued inducibility in Amiodarone patients may not foretell a poor prognosis but, in fact, many observers have found greater recurrence rates in patients who remain inducible than in those who do not. A number of criteria have been proposed, however, for identifying patients who remain inducible but who seem likely nonetheless to do well on Amiodarone. These criteria include increased difficulty of induction (more stimuli or more rapid stimuli), which has been reported to predict a lower rate of recurrence, and ability to tolerate the induced ventricular tachycardia without severe symptoms, a finding that has been reported to correlate with better survival but not with lower recurrence rates. While these criteria require confirmation and further study in general, easier inducibility or poorer tolerance of the induced arrhythmia should suggest consideration of a need to revise treatment.

Several predictors of success not based on PES have also been suggested, including complete elimination of all nonsustained ventricular tachycardia on ambulatory monitoring and very low premature ventricular-beat rates (less than 1 VPB/1,000 normal beats).

While these issues remain unsettled for Amiodarone, as for other agents, the prescriber of Amiodarone should have access to (direct or through referral), and familiarity with, the full range of evaluatory procedures used in the care of patients with life-threatening arrhythmias.

It is difficult to describe the effectiveness rates of Amiodarone, as these depend on the specific arrhythmia treated, the success criteria used, the underlying cardiac disease of the patient, the number of drugs tried before resorting to Amiodarone, the duration of follow-up, the dose of Amiodarone, the use of additional antiarrhythmic agents, and many other factors. As Amiodarone has been studied principally in patients with refractory life-threatening ventricular arrhythmias, in whom drug therapy must be selected on the basis of response and cannot be assigned arbitrarily, randomized comparisons with other agents or placebo have not been possible. Reports of series of treated patients with a history of cardiac arrest and mean follow-up of one year or more have given mortality (due to arrhythmia) rates that were highly variable, ranging from less than 5% to over 30%, with most series in the range of 10 to 15%. Overall arrhythmia-recurrence rates (fatal and nonfatal) also were highly variable (and, as noted above, depended on response to PES and other measures), and depend on whether patients who do not seem to respond initially are included. In most cases, considering only patients who seemed to respond well enough to be placed on long-term treatment, recurrence rates have ranged from 20 to 40% in series with a mean follow-up of a year or more.

Package/Label Display Panel

Amiodarone Hydrochloride Tablets

200 mg

100 Tablets

Amiodarone HYDROCHLORIDE 
Amiodarone hydrochloride tablet
Product Information
Product Type HUMAN PRESCRIPTION DRUG LABEL Item Code (Source) NDC:0904-6556(NDC:68382-227)
Route of Administration ORAL DEA Schedule     
Active Ingredient/Active Moiety
Ingredient Name Basis of Strength Strength
Amiodarone HYDROCHLORIDE (Amiodarone) Amiodarone HYDROCHLORIDE 200 mg
Inactive Ingredients
Ingredient Name Strength
LACTOSE MONOHYDRATE  
MAGNESIUM STEARATE  
SILICON DIOXIDE  
SODIUM STARCH GLYCOLATE TYPE A POTATO  
POVIDONE, UNSPECIFIED  
STARCH, CORN  
Product Characteristics
Color WHITE (WHITE TO OFF- WHITE) Score 2 pieces
Shape ROUND (ROUND) Size 10mm
Flavor Imprint Code ZE;65
Contains     
Packaging
# Item Code Package Description
1 NDC:0904-6556-61 100 BLISTER PACK in 1 CARTON
1 1 TABLET in 1 BLISTER PACK
Marketing Information
Marketing Category Application Number or Monograph Citation Marketing Start Date Marketing End Date
ANDA ANDA079029 08/10/2009
Labeler - Major Pharmaceuticals (191427277)
Registrant - Major Pharmaceuticals (191427277)
Revised: 09/2017   Major Pharmaceuticals

Dosing Geriatric

Refer to adult dosing. No specific guidelines available. Dose selection should be cautious, at low end of dosage range, and titration should be slower to evaluate response. Although not supported by clinical evidence, a maintenance dose of 100 mg daily is commonly used especially for the elderly or patients with low body mass (Zimetbaum 2007).

What is amiodarone?

Amiodarone affects the rhythm of your heartbeats.

Amiodarone is used to help keep the heart beating normally in people with life-threatening heart rhythm disorders of the ventricles (the lower chambers of the heart that allow blood to flow out of the heart). Amiodarone is used to treat ventricular tachycardia or ventricular fibrillation.

Amiodarone is for use only in treating life-threatening heart rhythm disorders.

Amiodarone may also be used for purposes not listed in this medication guide.

What other drugs will affect amiodarone?

Amiodarone takes a long time to completely clear from your body. Drug interactions are possible for up to several months after you stop using amiodarone. Talk to your doctor before taking any medication during this time. Keep track of how long it has been since your last dose of amiodarone.

Many drugs can interact with amiodarone. Not all possible interactions are listed here. Tell your doctor about all your current medicines and any you start or stop using, especially:

  • an antibiotic or antifungal medicine;

  • an antidepressant;

  • anti-malaria medicine;

  • antiviral medicine to treat hepatitis, HIV, or AIDS;

  • asthma inhalers;

  • a blood thinner;

  • cancer medicines;

  • a diuretic or "water pill";

  • heart or blood pressure medication;

  • medicine to prevent vomiting;

  • medicine to treat mental illness; or

  • "statin" cholesterol medicine (Lipitor, Zocor, Vytorin, and others).

This list is not complete and many other drugs can interact with amiodarone. This includes prescription and over-the-counter medicines, vitamins, and herbal products. Give a list of all your medicines to any healthcare provider who treats you.

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