Amiodarone (Cordarone, Pacerone): A Patient's Guide to Benefits, Risks, Side Effects, and Lab Monitoring

Amiodarone is one of the most powerful medications I prescribe and one of the hardest to manage well. It can hold your heart in a normal rhythm when nothing else has worked. Over months to years it can also damage your thyroid, lungs, liver, eyes, skin, and peripheral nerves, sometimes in ways that don’t fully reverse. You use it safely by knowing what to watch for, following the monitoring schedule without exception, and calling your cardiologist early when something new shows up.

What Amiodarone Is and Why It Works Differently

Amiodarone is an antiarrhythmic. It calms abnormal electrical activity so your heart can hold a normal rhythm. Your heart’s own wiring runs a signal from the top of the right side to the AV node (the relay station between the upper and lower chambers), through the bundle of His and out into the bundle branches, about 60 to 100 times a minute at rest. When that misfires you get an arrhythmia, most often atrial fibrillation (AFib, where the top of the heart quivers instead of beating in a coordinated way) or ventricular tachycardia (where the bottom of the heart fires fast on its own, which is dangerous).

Antiarrhythmics act on the ion channels that let potassium, sodium, and calcium move in and out of heart cells. Most block one Vaughan-Williams class. Amiodarone blocks all four, potassium (class III), sodium (class I), beta-adrenergic receptors (class II), and partially calcium (class IV). That’s why it works when the others fail.

Two features shape everything else. The half-life is extraordinarily long, 15 to 142 days and averaging about 58 days, so loading doses are needed at the start, dose changes take weeks to months to register, and the drug stays in you for months after the last tablet. And it’s fat-soluble, so it accumulates in the liver, lungs, thyroid, skin, and cornea at concentrations 10 to 100 times higher than in your blood. The side effects aren’t random. They land in those organs.

Cordarone and Pacerone are oral tablets, Nexterone is the IV form used in the hospital, and generics are widely available.

When Amiodarone Is the Right Choice

The 2023 American College of Cardiology/American Heart Association/American College of Chest Physicians/Heart Rhythm Society atrial fibrillation guidelines make amiodarone first-line in exactly two settings. Heart failure with reduced ejection fraction, and severe left ventricular hypertrophy meaning a wall thickness above 1.5 cm. Everywhere else, including a structurally normal heart, hypertension without severe thickening, and coronary disease without heart failure, the guideline language is blunt. “Amiodarone is best reserved for patients who do not respond to other recommended antiarrhythmic agents or for whom other antiarrhythmic drugs are contraindicated.”

Your other rhythm-control options for AFib are flecainide or propafenone (class IC drugs, first-line in a structurally normal heart), sotalol (often used in coronary artery disease without heart failure), dofetilide (started in the hospital with specific monitoring), and dronedarone (brand name Multaq, a relative built without the iodine so it causes less thyroid toxicity, with a shorter half-life and an easier side-effect profile, but less effective and contraindicated in NYHA class III-IV heart failure where the PALLAS trial showed harm).

Amiodarone earns its place on effectiveness. The CTAF trial, published in NEJM in 2000, randomized 403 patients who’d had at least one AFib episode in the prior six months. At 16 months, 35 percent of the amiodarone group had recurrent AFib versus 63 percent on propafenone or sotalol. SAFE-T reported a median time to recurrence of 487 days with amiodarone, 74 days with sotalol, and 6 days with placebo. A 2019 Cochrane meta-analysis confirmed it’s the most effective antiarrhythmic for holding sinus rhythm after cardioversion.

In heart failure with reduced ejection fraction (pumping fraction 35 percent or below), most alternatives are off the table. Flecainide and propafenone are contraindicated because of the CAST trial mortality signal, sotalol can worsen heart failure, and dronedarone is contraindicated in NYHA class III-IV. Dofetilide is safe but needs in-hospital initiation, so most centers default to amiodarone. The same reasoning applies when the left ventricular wall is severely thickened above 1.5 cm, which turns up in long-standing hypertension and in hypertrophic cardiomyopathy, where class IC drugs and sotalol carry more arrhythmia risk.

For ventricular tachycardia and ventricular fibrillation, fast rhythms from the bottom of the heart that can cause sudden cardiac arrest, amiodarone is used acutely in the hospital (usually IV Nexterone) to break or suppress sustained VT or during cardiac arrest resuscitation, and chronically in patients with an implantable defibrillator (ICD, the device that watches for dangerous rhythms and shocks them) who are getting too many shocks. SCD-HeFT, the largest heart failure trial, showed no survival benefit versus placebo and suggested possible harm in NYHA class III heart failure. So an ICD plus medical therapy is the foundation, and amiodarone gets added to suppress symptoms rather than as a mortality drug.

How Amiodarone Is Dosed

Dosing runs in two phases. Loading builds tissue stores, maintenance holds the rhythm.

For atrial fibrillation, loading is typically 600 to 800 mg per day for 1 to 4 weeks, then 100 to 200 mg per day for maintenance. Some patients take the loading dose all at once in the morning, others split it (300 mg twice daily) to cut down on stomach upset. For ventricular arrhythmias the load is more aggressive, 800 to 1,600 mg per day for 1 to 3 weeks with a total cumulative load around 10 grams, then 200 to 400 mg per day. The lowest effective maintenance dose is what you want, since side effects track with cumulative exposure. Follow your schedule exactly. Loading is what gets the drug to a level where it can control the rhythm at all.

IV amiodarone in the hospital, for sustained ventricular tachycardia, for atrial fibrillation with a rapid rate that’s destabilizing you, or during cardiac arrest resuscitation, is usually a 150 mg bolus over 10 minutes, then an infusion at 1 mg per minute for 6 hours, then 0.5 mg per minute for the rest of the 24-hour period, then a switch to oral.

Miss a dose and take it as soon as you remember that same day. If you’re close to the next scheduled dose, skip the missed one and take the next at the regular time. Don’t double up. With a half-life this long, one missed dose barely moves your blood level. Miss several days and call your cardiologist before restarting, because the team may want to repeat part of the loading.

Your First Weeks on Amiodarone

Most people feel no dramatic change in the first few days while the drug loads into tissue. Keep taking your other heart medications, the anticoagulant and beta-blocker included, and start the sun protection routine on day one rather than later.

Early complaints are usually mild. Nausea or stomach upset responds to taking the dose with food, and some patients do better shifting it to dinner. Mild fatigue is common, since amiodarone has beta-blocker-like effects that slow the heart rate, and if you’re already on a beta-blocker the combination can leave you sluggish. Tell your cardiologist, because the beta-blocker dose sometimes needs to come down. Lightheadedness on standing comes from the combined blood pressure effect. Stand up slowly, drink enough water, and call if it persists.

By the end of the first month your rhythm should be steadier. If you had AFib you may have converted on your own or with an electrical cardioversion, and if you were getting ICD shocks they should be less frequent. Most cardiologists see you back at 1 month, with the first formal labs (TSH, liver enzymes, EKG) drawn at 3 to 6 months from the start.

Thyroid Effects

The thyroid is the organ amiodarone affects most often. Rates run 2 to 24 percent depending on regional iodine status, and a 2025 Icelandic nationwide cohort study found a five-year cumulative incidence of any thyroid dysfunction of 38.5 percent. The cause is the iodine load. Each 200 mg tablet holds about 75 mg of organic iodine, roughly 10 percent released daily, against a recommended daily intake of 150 micrograms. That excess combines with direct toxic effects on thyroid cells.

Hypothyroidism affects 5 to 22 percent, more often women with underlying autoimmune thyroid disease and people in iodine-sufficient regions like the US, with median onset about 6 months. Watch for fatigue, weight gain, cold intolerance, constipation, dry skin, brain fog, a slow heart rate, and low mood. Management is straightforward. You usually stay on amiodarone, start levothyroxine, and titrate to a normal TSH.

Hyperthyroidism affects 2 to 12 percent, runs higher in iodine-deficient areas, and shows up later, median onset around 24 months. Watch for unintended weight loss, heat intolerance, tremor, anxiety, palpitations, diarrhea, and worsening of the arrhythmia that brought you here. Amiodarone-induced thyrotoxicosis comes in two forms. Type 1 is iodine-driven, in patients with pre-existing nodular goiter or latent Graves’ disease, treated with thionamide drugs such as methimazole that block hormone synthesis. Type 2 is a destructive thyroiditis from direct drug toxicity in an otherwise normal gland, treated with corticosteroids. They overlap often enough that telling them apart takes endocrinology input and usually a thyroid ultrasound with Doppler flow studies. Type 2 usually means stopping the drug. Type 1 is a judgment call weighed against how badly you need amiodarone.

Lung Toxicity

This is the one I worry about most, because when it’s bad it can be fatal. Reported incidence is 1 to 2 percent, though some series show rates up to 17 percent in higher-risk populations, and mortality of severe amiodarone-induced lung disease approaches 10 percent of those affected. Risk climbs with advanced age, pre-existing lung disease (COPD, pulmonary fibrosis, asthma), a ventricular arrhythmia as the indication since those patients run higher doses, higher cumulative dose, recent cardiothoracic surgery, and high inspired oxygen exposure.

The usual picture builds over weeks to months. A new cough, often dry. Shortness of breath with exertion that keeps getting worse. Sometimes a low-grade fever, sometimes pleuritic chest discomfort. Acute presentations within days do happen, especially after recent surgery with high inspired oxygen.

Keep your threshold for calling low. Call your cardiologist about any new persistent cough lasting more than 1 to 2 weeks, new shortness of breath with exertion that’s worse than your baseline, any unexplained fever above 100.4 F (38 C), or new chest discomfort. The workup starts with a chest X-ray, moves to a high-resolution CT scan of the chest if the X-ray is suggestive, and includes pulmonary function tests with DLCO (diffusing capacity for carbon monoxide) to measure how well your lungs transfer oxygen. Treatment is stopping the drug, which takes months to wash out, plus corticosteroids in moderate to severe cases.

Liver Effects

Liver enzyme elevations (AST and ALT) show up in 15 to 30 percent of users. True hepatitis or cirrhosis is rare, under 3 percent, or about 0.6 percent annually. The FDA label carries a boxed warning for potentially fatal hepatotoxicity and says to stop the drug if transaminases exceed three times the upper limit of normal, or double in a patient whose baseline was already elevated. Mild rises are common and usually don’t require stopping. Persistent or worsening rises deserve a look for other causes, including alcohol, viral hepatitis, a statin effect, or fatty liver disease, plus closer follow-up. Yellowing of the skin or eyes, dark urine, or right-sided abdominal pain means call.

Eye Effects

Tiny golden-brown deposits in the cornea, the clear layer at the front of the eye, develop in over 90 percent of long-term users. An ophthalmologist finds them on slit-lamp examination. They rarely cause symptoms and almost never require stopping the drug.

Optic neuropathy is the one to respect. Inflammation of the optic nerve happens in less than 1 to 2 percent of patients and can cause permanent vision loss. A critical review of 296 reported cases found a mean of 9 months from starting amiodarone to visual loss, range 1 to 84 months. About 44 percent came on insidiously and nearly one-third were asymptomatic when discovered. After the drug was stopped, 58 percent improved, 21 percent stayed unchanged, and 21 percent worsened. About 20 percent ended up meeting criteria for legal blindness.

So any new visual change, blurring, halos around lights, a gap in your visual field, anything you notice that wasn’t there before, means an urgent ophthalmology visit. Not in a few weeks. That same week or the next day.

Skin Effects and Sun Protection

Photosensitivity, meaning you burn from light exposure that wouldn’t normally burn you, affects 10 to 75 percent of users depending on the series, showing up as a red rash on the face, arms, or other exposed skin, sometimes painful, sometimes itchy. A blue-gray discoloration, usually on the nose, cheeks, and forehead, develops in 4 to 9 percent, more often in fair-skinned people with heavy cumulative sun exposure. It comes from amiodarone deposits in the skin combined with sun-induced changes, and it does reverse after stopping the drug, but reversal takes months to years and some patients keep a persistent pigmentation.

Treat sun protection as part of the medication. For patients whose outdoor exposure runs year-round, I’m strict about it. Daily broad-spectrum sunscreen at SPF 30 or higher on all exposed skin, applied 15 to 30 minutes before you go outside. Use physical blockers (zinc oxide or titanium dioxide) or a product combining physical and chemical UV filters, since chemical-only sunscreens work less well here. Reapply every 2 hours outdoors, and after sweating or swimming. Broad-brimmed hat, long sleeves and pants during peak hours from 10 am to 4 pm, UV-protective sunglasses. Skip tanning beds, watch the sun through car and house windows, and be careful at altitude when you’re skiing or hiking, where UV exposure is higher. Prevention beats treatment by a wide margin.

Nerves and the QT Interval

Distal sensorimotor neuropathy, meaning numbness, tingling, or weakness in the hands or feet, develops in 5 to 10 percent of long-term users. It’s usually slowly progressive and may not fully reverse after the drug is stopped. Any new numbness, tingling, weakness, or balance problem should prompt a call to your cardiologist. The workup runs through neurology, sometimes nerve conduction studies, and a decision about dose reduction or stopping.

Amiodarone prolongs the QT interval on your EKG, the time between when the ventricles fire and when they recover. With most QT-prolonging drugs that raises the risk of a dangerous rhythm called torsades de pointes. Amiodarone is the odd exception, with torsades under 1 percent on oral therapy and under 2 percent with IV, because its multichannel blocking prevents the electrical instability that triggers torsades. You still need baseline and annual EKG monitoring, and caution about combining it with other QT-prolonging drugs.

Drug Interactions

Amiodarone inhibits several liver enzymes other drugs depend on for clearance (CYP3A4, CYP2C9, CYP2D6, CYP1A2) plus P-glycoprotein, so drugs cleared by those pathways build up.

Warfarin (Coumadin) is the big one. Add amiodarone and the INR roughly doubles within 3 to 4 days, so the standard move is to cut the warfarin dose by one-third to one-half right away and recheck the INR within a week. If warfarin is added to amiodarone, the starting dose is lower than usual. Make sure both prescribers know about both drugs. The direct oral anticoagulants (apixaban, rivaroxaban, edoxaban, dabigatran) are far less affected. Edoxaban may need dose adjustment; apixaban and rivaroxaban usually continue at standard doses with normal attention to bleeding signs.

Digoxin levels rise, so the dose gets cut by 50 percent or stopped, with a level check 1 to 2 weeks later. Simvastatin and lovastatin carry a higher risk of statin-induced muscle injury (rhabdomyolysis) with amiodarone, and the FDA caps simvastatin at 20 mg per day and lovastatin at 40 mg per day in patients taking it. Rosuvastatin, atorvastatin, and pravastatin interact far less and run at standard doses. I often reach for pravastatin in amiodarone patients who need a statin.

Sofosbuvir-containing hepatitis C regimens have caused symptomatic bradycardia (a dangerously slow heart rate) severe enough to require a pacemaker, so that combination is avoided and your hepatologist will pick a sofosbuvir-free regimen. Beta-blockers and the non-dihydropyridine calcium channel blockers (verapamil, diltiazem) add to amiodarone’s heart-slowing effect, useful for rate control but capable of causing bradycardia or AV block, so doses get adjusted. Avoid other QT-prolonging drugs where you can, including azole antifungals, fluoroquinolone antibiotics, some antipsychotics (haloperidol, ziprasidone), some antiemetics (ondansetron, domperidone), and methadone. If one is necessary, the QT gets watched more closely.

Carry a written medication list or keep one on your phone, and show it to every new prescriber. Ask your pharmacist to flag any new prescription that might interact.

The Monitoring Schedule

This is the part that makes the drug usable, and the 2023 ACC/AHA/ACCP/HRS guidelines lay it out.

Before you start, you need TSH (plus free T4 if the TSH is abnormal), AST and ALT, a complete blood count, a basic metabolic panel for kidney function and electrolytes, an EKG, and a chest X-ray. Some centers add pulmonary function tests with DLCO, though the 2023 guidelines call the value of routine PFTs uncertain. Get an ophthalmologic baseline if one is available.

At 3 to 6 months, TSH, AST and ALT, an EKG, and a clinic visit to go over new symptoms. Every 6 months after that, TSH plus AST and ALT. Annually, an EKG, a skin exam by your primary care doctor or dermatologist, and a neurological exam by your primary care doctor or cardiologist. As needed, a chest X-ray whenever new respiratory symptoms develop, a high-resolution chest CT if the X-ray is suggestive, ophthalmology for any visual change, endocrinology for an abnormal thyroid panel, hepatology for persistent liver enzyme elevation, and neurology for new neurological symptoms.

Get the blood drawn before your visit rather than at it, so results are in hand when you talk. Don’t skip visits because you feel fine, and call to move labs earlier if any of the symptoms below turn up. Catching these problems before they cause symptoms is the entire point.

Daily Life on Amiodarone

Exercise isn’t restricted, though the drug’s beta-blocker-like effect lowers your maximum heart rate, so expect a small drop in peak performance over the first few months if you train hard. Travel is fine. Bring enough medication for the trip plus a few extra days, keep it in your carry-on in the original prescription container, carry a printed medication list with your prescriber’s contact information, and hold the sun protection routine, especially at altitude. Being off by a few hours across time zones is harmless with this half-life. No special diet is required, though go easy on alcohol, which can worsen the liver effects and isn’t good for any arrhythmia patient. On warfarin and amiodarone together, keep vitamin K intake from leafy greens consistent as you would on warfarin alone.

Pregnancy is treated as a contraindication. Amiodarone crosses the placenta and accumulates in fetal tissues including the fetal thyroid, and the risk of neonatal hypothyroidism and developmental effects is substantial. Women of reproductive age on amiodarone need reliable contraception. Any pregnancy on amiodarone requires immediate consultation with maternal-fetal medicine to weigh the maternal indication against the fetal risk. If you’re planning a pregnancy, talk to your cardiologist well in advance, since switching to a different antiarrhythmic ideally allows several months of washout first.

Amiodarone is generally continued through surgery and procedures. Anesthesia teams know that high inspired oxygen during general anesthesia has been linked to rare cases of acute pulmonary toxicity, and they minimize it when they safely can. If you’re also on warfarin, the holding plan is the same as for warfarin alone, since amiodarone doesn’t change bleeding risk on its own. Tell every proceduralist you’re on it, including your dentist, dermatologist, podiatrist, and the GI doctor doing your colonoscopy. The medication card earns its keep here.

When to Call and When to Go to the ER

Call your cardiologist within 1 to 2 days for a new persistent cough, worsening shortness of breath, or chest discomfort (lung); any new vision change such as blurring, halos, or field loss (eyes); yellowing of skin or eyes, dark urine, or right-sided or severe abdominal pain (liver); new numbness, tingling, or severe muscle weakness (nerves); a new rash, blue-gray discoloration, or severe photosensitivity (skin); unexplained rapid weight change, heat or cold intolerance, or new fatigue or mood change (thyroid); any concern about a new medication interaction; or missed doses for more than 3 days. Each can be the first sign of an organ toxicity that’s much easier to manage caught early.

Go to the ER or call 911 for severe shortness of breath at rest, chest pain that’s severe or doesn’t resolve, fainting or near-fainting, severe lightheadedness or near-collapse, a heart rate over 150 or under 40 with symptoms, sudden severe weakness or numbness on one side of the body, or a sudden severe headache, difficulty speaking, or vision loss.

Stopping Amiodarone

Amiodarone gets stopped for a serious side effect (pulmonary toxicity, severe hepatotoxicity, optic neuropathy, unmanageable thyroid dysfunction, or progressive peripheral neuropathy), because the arrhythmia genuinely resolved (less common than patients hope), because an alternative opened up such as a successful catheter ablation or a transition to dofetilide, for pregnancy or planned pregnancy, or because the goal of care shifted to comfort in end-stage illness.

The washout is long. The drug effect persists for weeks to months after your last dose, and thyroid, liver, or other side effects can continue in that window, so monitoring continues for at least 6 months after stopping. A new antiarrhythmic started during washout has to be chosen carefully and dosed conservatively, because amiodarone is still active.

The arrhythmia often returns eventually, especially with structural heart disease, and your cardiologist should have a plan ready (rate control, electrical cardioversion, restarting an antiarrhythmic, or a catheter ablation referral). Side effects usually improve after stopping but may not fully reverse. Skin discoloration can take months to years to fade, peripheral neuropathy can persist, and pulmonary fibrosis from severe lung toxicity may not reverse at all. Permanent damage is concentrated in patients who kept taking the drug through warning signs that got missed because monitoring lapsed. The earlier a side effect is caught and the drug stopped, the better your chance of full recovery.

Frequently Asked Questions About Amiodarone

Why is amiodarone considered both highly effective and highly toxic?

Amiodarone is highly effective because it blocks all four classes of cardiac ion channels (potassium, sodium, calcium, and beta-adrenergic receptors). That multichannel activity is why it works when other antiarrhythmics fail. The toxicity comes from a different feature: amiodarone is fat-soluble and accumulates in tissues with high lipid content (liver, lung, thyroid, skin, cornea) over time, where it produces organ-specific damage. The two features are linked, the same pharmacology that makes amiodarone effective also drives the side effects.

Can amiodarone cause permanent damage?

Yes, in a minority of patients. Pulmonary fibrosis, optic neuropathy with permanent vision loss, persistent skin discoloration, and progressive peripheral neuropathy can outlast drug discontinuation. The risk of permanent damage is highest in patients who continue the drug despite warning signs that get missed because monitoring lapsed. Following the monitoring schedule catches problems early when reversal is much more likely.

How long does amiodarone stay in my system after I stop?

Months. The half-life is 15 to 142 days, averaging about 58. After discontinuation, the pharmacologic effect (both beneficial and toxic) persists for weeks to months as the drug clears from tissue stores. The monitoring schedule should continue for at least 6 months after stopping if you’ve had any side effects from the drug.

What’s the difference between amiodarone and dronedarone?

Dronedarone (brand name Multaq) is a related drug designed to retain some of amiodarone’s effectiveness while reducing iodine-related thyroid toxicity (dronedarone has the iodine moiety removed). It has a shorter half-life and a more manageable toxicity profile, but it’s less effective for AFib maintenance and is contraindicated in NYHA III-IV heart failure (the PALLAS trial showed harm). Amiodarone remains the more effective and more broadly applicable of the two.

Will I have to be on amiodarone forever?

Maybe. For atrial fibrillation, some patients can come off amiodarone if catheter ablation is successful or if the arrhythmia goes into prolonged remission. For ventricular arrhythmias and HFrEF, amiodarone is often a long-term commitment. The decision is individualized and gets revisited periodically.

References

1. Joglar, Jose A., Mina K. Chung, Anastasia L. Armbruster, et al. “2023 ACC/AHA/ACCP/HRS Guideline for the Diagnosis and Management of Atrial Fibrillation.” Journal of the American College of Cardiology 83, no. 1 (2024): 109-279.

2. Roy, Denis, Mario Talajic, Paul Dorian, et al. “Amiodarone to Prevent Recurrence of Atrial Fibrillation (CTAF).” New England Journal of Medicine 342, no. 13 (2000): 913-920.

3. Singh, Bramah N., Steven N. Singh, Domenic J. Reda, et al. “Amiodarone Versus Sotalol for Atrial Fibrillation (SAFE-T).” New England Journal of Medicine 352, no. 18 (2005): 1861-1872.

4. Valembois, Lucie, Etienne Audureau, Akiko Takeda, et al. “Antiarrhythmics for Maintaining Sinus Rhythm After Cardioversion of Atrial Fibrillation.” Cochrane Database of Systematic Reviews (2019): CD005049.

5. Bardy, Gust H., Kerry L. Lee, Daniel B. Mark, et al. “Amiodarone or an Implantable Cardioverter-Defibrillator for Congestive Heart Failure (SCD-HeFT).” New England Journal of Medicine 352, no. 3 (2005): 225-237.

6. Al-Khatib, Sana M., William G. Stevenson, Michael J. Ackerman, et al. “2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias.” Journal of the American College of Cardiology 72, no. 14 (2018): e91-e220.

7. Tsaban, Gal, Dan Ostrovsky, Hilmi Alnsasra, et al. “Amiodarone and Pulmonary Toxicity in Atrial Fibrillation: A Nationwide Israeli Study.” European Heart Journal (2024).

8. Guðjónsson, Páll, Ari J. Jóhannesson, Eydís Eyþórsson, and Kristín Andersen. “Amiodarone Induced Thyroid Dysfunction: A High Cumulative Incidence in a Nationwide Cohort Study in Iceland.” Journal of Internal Medicine (2025).

9. Passman, Rod S., Charles L. Bennett, James M. Purpura, et al. “Amiodarone-Associated Optic Neuropathy: A Critical Review.” American Journal of Medicine 125, no. 5 (2012): 447.e7-447.e16.

10. Vassallo, Peter, and Richard G. Trohman. “Prescribing Amiodarone: An Evidence-Based Review of Clinical Indications.” JAMA 298, no. 11 (2007): 1312-1322.

11. Tisdale, James E., Mina K. Chung, Kathleen B. Campbell, et al. “Drug-Induced Arrhythmias: A Scientific Statement From the American Heart Association.” Circulation 142, no. 15 (2020): e214-e233.

12. Hohnloser, Stefan H., Harry J. G. M. Crijns, Martin van Eickels, et al. “Effect of Dronedarone on Cardiovascular Events in Atrial Fibrillation (ATHENA).” New England Journal of Medicine 360, no. 7 (2009): 668-678.