Amiodarone

Last updated

Amiodarone
Amiodarone structure.svg
Amiodarone-based-on-hydrochloride-xtal-3D-bs-17.png
Clinical data
Pronunciation /ˌæmiˈoʊdəroʊn/ or /əˈmiːoʊdəˌroʊn/
Trade names Cordarone, Nexterone, Pacerone, others
AHFS/Drugs.com Monograph
MedlinePlus a687009
License data
Pregnancy
category
  • AU:C
Routes of
administration 		By mouth, intravenous, intraosseous
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability 20–55%
Protein binding 96%
Metabolism Liver
Elimination half-life 58 d (range 15–142 d)
Excretion Primarily liver and bile
Identifiers
  • (2-{4-[(2-butyl-1-benzofuran-3-yl)carbonyl]-2,6-diiodophenoxy}ethyl)diethylamine
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard 100.016.157 OOjs UI icon edit-ltr-progressive.svg
Chemical and physical data
Formula C25H29I2NO3
Molar mass 645.320 g·mol−1
3D model (JSmol)
  • CCN(CC)CCOc1c(I)cc(cc1I)C(=O)c2c3ccccc3oc2CCCC
  • InChI=1S/C25H29I2NO3/c1-4-7-11-22-23(18-10-8-9-12-21(18)31-22)24(29)17-15-19(26)25(20(27)16-17)30-14-13-28(5-2)6-3/h8-10,12,15-16H,4-7,11,13-14H2,1-3H3 Yes check.svgY
  • Key:IYIKLHRQXLHMJQ-UHFFFAOYSA-N Yes check.svgY
   (verify)

Amiodarone is an antiarrhythmic medication used to treat and prevent a number of types of cardiac dysrhythmias. [4] This includes ventricular tachycardia, ventricular fibrillation, and wide complex tachycardia, atrial fibrillation, and paroxysmal supraventricular tachycardia. [4] Evidence in cardiac arrest, however, is poor. [5] It can be given by mouth, intravenously, or intraosseously. [4] When used by mouth, it can take a few weeks for effects to begin. [4] [6]

Contents

Common side effects include feeling tired, tremor, nausea, and constipation. [4] As amiodarone can have serious side effects, it is mainly recommended only for significant ventricular arrhythmias. [4] Serious side effects include lung toxicity [7] such as interstitial pneumonitis, liver problems, heart arrhythmias, vision problems, thyroid problems, and death. [4] If taken during pregnancy or breastfeeding it can cause problems in the fetus or the infant. [4] It is a class III antiarrhythmic medication. [4] It works partly by increasing the time before a heart cell can contract again. [4] [6]

Amiodarone was first made in 1961 and came into medical use in 1962 for chest pain believed to be related to the heart. [8] It was pulled from the market in 1967 due to side effects. [9] In 1974 it was found to be useful for arrhythmias and reintroduced. [9] It is on the World Health Organization's List of Essential Medicines. [10] It is available as a generic medication. [4] In 2022, it was the 237th most commonly prescribed medication in the United States, with more than 1 million prescriptions. [11] [12]

Medical uses

Amiodarone has been used both in the treatment of acute life-threatening arrhythmias as well as the long-term suppression of arrhythmias. [13] Amiodarone is commonly used to treat different types of abnormal heart rhythms, such as atrial arrhythmias (supraventricular arrhythmias) and ventricular arrhythmias. [13]

Atrial arrhythmias and supraventricular arrhythmias are terms often used interchangeably to refer to abnormal heart rhythms originating from the upper chambers of the heart, known as the atria. These types of arrhythmias include conditions such as atrial fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia. 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. [14]

Ventricular arrhythmias are abnormal heart rhythms that originate in the ventricles, which are the lower chambers of the heart. These arrhythmias can be potentially life-threatening and may disrupt the heart's ability to pump blood effectively. [14]

Amiodarone can be effective in treating conditions like ventricular fibrillation (a rapid and irregular heartbeat), ventricular tachycardia (fast heartbeat originating from the lower chambers), and cardiac arrest due to shock-resistant ventricular fibrillation. [13]

In cases where a patient is experiencing shock-resistant ventricular arrhythmias including stable ventricular tachycardia or unstable ventricular fibrillation, amiodarone may be used. [15] A recent study suggested that another antiarrhythmic, procainamide, may be more effective in stopping ventricular tachycardia – with less side effects and a higher survival rate in patients requiring multiple shocks. [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. [13]

Cardiac arrest

Defibrillation is the treatment of choice for ventricular fibrillation and pulseless ventricular tachycardia resulting in cardiac arrest. While amiodarone has been used in shock-refractory cases, evidence of benefit is poor. [5] Although amiodarone does not appear to improve survival in those who had a cardiac arrest in-hospital, [17] some studies suggested that early administration of amiodarone was associated with better survival and positive outcomes for people who had a cardiac arrest out-of-hospital. [18] [19]

Ventricular tachycardia

Amiodarone may be used in the treatment of ventricular tachycardia in certain instances. [20] Individuals with hemodynamically unstable ventricular tachycardia should not initially receive amiodarone. These individuals should be cardioverted.

Amiodarone can be used in individuals with hemodynamically stable ventricular tachycardia. In these cases, amiodarone can be used regardless of the individual's underlying heart function and the type of ventricular tachycardia; it can be used in individuals with monomorphic ventricular tachycardia, but is contraindicated in individuals with polymorphic ventricular tachycardia as it is associated with a prolonged QT interval which will be made worse with anti-arrhythmic drugs. [21]

Atrial fibrillation

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. While amiodarone is not approved for AF by the US Food and Drug Administration (FDA), it is a commonly prescribed off-label treatment due to the lack of equally effective treatment alternatives. [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. [26] [28] This has been demonstrated in seventeen randomized controlled trials, of which five included a placebo arm. The incidence of severe side effects in this group is low. [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). However, other anti-arrhythmic agents may exert superior rhythm control, rate control and lower mortality rate which may be more favourable than amiodarone in specific cases. [32]

Contraindications

Women who are pregnant or may become pregnant are strongly advised not to take amiodarone. Since amiodarone can be expressed in breast milk, women taking the drug are advised to stop nursing.

It is contraindicated in individuals with sinus nodal bradycardia, atrioventricular block, and second or third-degree heart block who do not have an artificial pacemaker.

Individuals with baseline depressed lung function should be monitored closely if amiodarone therapy is to be initiated.

Formulations of amiodarone that contain benzyl alcohol should not be given to neonates, because the benzyl alcohol may cause the potentially fatal "gasping syndrome". [33]

Amiodarone can worsen the cardiac arrhythmia brought on by digitalis toxicity.

Contraindications of amiodarone also include:

There are no specific guidelines for endurance or high-intensity exercise while taking amiodarone. However, since amiodarone may cause bradycardia and QTc prolongation which can affect exercise capacity and increase the risk of arrhythmias during intense exercise, it would generally be advisable for patients taking this medication to consult their healthcare provider before engaging in high-intensity physical activities such as strenuous endurance exercises. [13]

Side effects

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. [35] [36] Allergic reactions to amiodarone may occur. [35] Most individuals administered amiodarone on a chronic basis will experience at least one side effect. [36] In some people, daily use of amiodarone at 100 mg oral doses can be effective for arrhythmia control with no or minimal side effects. [36]

Some common side effects include:

Amiodarone can potentially cause renal toxicity, but solid studies on whether amiodarone may be toxic to the kidneys are lacking. [43]

Lung

A chest X-ray demonstrating pulmonary fibrosis due to amiodarone. IPF amiodarone.JPG
A chest X-ray demonstrating pulmonary fibrosis due to amiodarone.

Side effects of oral amiodarone at doses of 400 mg or higher include various pulmonary effects. [44] The most serious reaction is interstitial lung disease. Risk factors include high cumulative dose, more than 400 milligrams per day, duration over two months, increased age, and preexisting pulmonary disease. Some individuals were noted to develop pulmonary fibrosis after a week of treatment, while others did not develop it after years of continuous use. [44] Common practice is to avoid the agent if possible in individuals with decreased lung function.

The most specific test of pulmonary toxicity due to amiodarone is a dramatically decreased DLCO noted on pulmonary function testing.

Thyroid

Induced abnormalities in thyroid function are common. [38] [35] In approximately 15-20% of patients, amiodarone treatment results in thyroid dysfunction, either amiodarone-induced hypothyroidism or amiodarone-induced thyrotoxicosis. [45] [46] [34] [20] Both under- and overactivity of the thyroid may occur. [35]

Amiodarone is structurally similar to thyroxine and also contains iodine. Both of these factors contribute to the effects of amiodarone on thyroid function. [20] [45] [47] [48] Amiodarone also causes an anti-thyroid action, via Plummer and Wolff–Chaikoff effects, due its large amount of iodine in its molecule, which causes a particular "cardiac hypothyroidism" with bradycardia and arrhythmia. [49] [50]

Thyroid function should be checked at least every six months. [51]

Eye

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. These deposits typically do not cause any symptoms. About 1 in 10 individuals may complain of a bluish halo. Anterior subcapsular lens deposits are relatively common (50%) in higher doses (greater than 600 mg/day) after 6 months of treatment. Optic neuropathy, nonarteritic anterior ischemic optic neuropathy (N-AION), occurs in 1–2% of people and is not dosage dependent. [55] Bilateral optic disc swelling and mild and reversible visual field defects can also occur.

Loss of eyelashes has been linked to amiodarone use. [56]

Liver

Abnormal liver enzyme results are common in people taking amiodarone. [35] Much rarer are jaundice, hepatomegaly (liver enlargement), and hepatitis (inflammation of the liver). [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. This condition, often referred to as pseudo-alcoholic cirrhosis, presents with similar histopathological features to those observed in patients with alcoholic cirrhosis. [58] [59] However, this extreme adverse event manifestation—pseudo-alcoholic cirrhosis caused by low dose amiodarone—is very rare. [36]

Skin

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. The discoloration will slowly improve upon cessation of the medication, however, the skin color may not return completely. [60]

Pregnancy and breastfeeding

Use during pregnancy may result in a number of problems in the infant including thyroid problems, heart problems, neurological problems, and preterm birth. [61] Use during breastfeeding is generally not recommended though one dose may be okay. [61]

Other

Long-term use of amiodarone has been associated with peripheral neuropathies. [62]

Amiodarone is sometimes responsible for epididymitis. Amiodarone accumulates in the head of the organ and can cause unilateral or bilateral inflammation. It tends to resolve if amiodarone is stopped. [63]

Some cases of gynecomastia have been reported in men on amiodarone. [64]

A retrospective cohort study found an increased risk of digestive, liver, head and neck and liver cancers amongst male patients exposed to amiodarone versus female participants in the same study and the general population. [65] This study also identified that the Standardized Incidence Ratio of cancer occurrence increased significantly in males aged 20-59 and >80 years old who were exposed to a higher dose of Amiodarone in comparison to those exposed to a lower dose. This suggests that there is a dose-effect relationship. [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. Amiodarone and its effect on cancer is still a topic that requires more robust research.

Drug-drug interactions

The pharmacokinetics of numerous drugs, including many that are commonly administered to individuals with heart disease, are affected by amiodarone. [66] [67] [68]

Amiodarone has particularly important interactions with the following drugs:

Amiodarone inhibits the action of the cytochrome P450 isozyme family; such inhibition reduces the clearance of many drugs, including the following: [68] [74] [75]

In 2015, Gilead Sciences warned healthcare providers about people who began taking the hepatitis C drugs ledipasvir/sofosbuvir or sofosbuvir along with amiodarone, who developed abnormally slow heartbeats or died of cardiac arrest. [76]

Metabolism

Amiodarone is extensively metabolized in the liver by CYP3A4, a member of the cytochrome P450 superfamily of enzymes, therefore, amiodarone and can affect the metabolism of numerous other drugs that depend on cytochrome P450, such as digoxin, phenytoin, warfarin, etc. [26] [77] [78] [46]

The major metabolite of amiodarone is desethylamiodarone (DEA), which also has antiarrhythmic properties. [26]

The metabolism of amiodarone is inhibited by grapefruit, leading to elevated serum levels of 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. This interaction is dose-dependent with simvastatin doses exceeding 20 mg. This drug combination, especially with higher doses of simvastatin, should be avoided. [80]

Amiodarone is extensively metabolized in the liver. The primary metabolic pathway of amiodarone is by cytochrome P450 (CYP) enzymes, particularly CYP3A4 and CYP2C8. [73] [46] [68] [81] [82] The metabolism of amiodaron can be characterized by two phases: [83]

Amiodarone has an exceptionally long half-life due to a combination of several factors: [13]

Excretion

Excretion is primarily via the liver and the bile duct with almost no elimination via the kidney and it is not dialyzable. [1] Elimination half-life average of 58 days (ranging from 25 to 100 days [Remington: The Science and Practice of Pharmacy 21st edition]) for amiodarone and 36 days for the active metabolite, desethylamiodarone (DEA). [1] There is 10-50% transfer of amiodarone and DEA in the placenta as well as a presence in breast milk. [1] Accumulation of amiodarone and DEA occurs in adipose tissue and highly perfused organs (i.e. liver, lungs), [1] therefore, if an individual was taking amiodarone on a chronic basis if it is stopped it will remain in the system for weeks to months. [1]

Whereas amiodarone is primarily eliminated from the body through hepatic metabolism and biliary excretion, a very small portion of amiodarone and its metabolites are excreted unchanged in urine or feces. [73] [46]

The liver plays a significant role in the elimination of amiodarone. After being extensively metabolized by cytochrome P450 enzymes, particularly CYP3A4 and CYP2C8, amiodarone is transported into bile via multidrug-resistant protein 2 (MRP2) transporter. Bile containing amiodarone and its metabolites is then released into the gastrointestinal tract.[ 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. [13]

Pharmacology

Amiodarone is categorized as a class III antiarrhythmic agent, and prolongs phase 3 of the cardiac action potential, the repolarization phase where there is normally decreased calcium permeability and increased potassium permeability. It has numerous other effects, however, including actions that are similar to those of antiarrhythmic classes Ia, II, and IV.[ medical citation needed ]

Amiodarone is a blocker of voltage gated potassium (KCNH2) and voltage gated calcium channels (CACNA2D2). [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. It is suggested that amiodarone may also exacerbate the phenotype associated with Long QT-3 syndrome causing mutations such as ∆KPQ. This effect is due to a combination of blocking the peak sodium current, but also contributing to an increased persistent sodium current. [90]

Amiodarone chemically resembles thyroxine (thyroid hormone), and its binding to the nuclear thyroid receptor might contribute to some of its pharmacologic and toxic actions. [91] The mechanisms of action of amiodarone include blocking potassium ion channels (prolonging repolarization), blocking sodium ion channels, and antagonizing alpha- and beta-adrenergic receptors. [13] The action of amiodarone can be characterized by the following effects: [13]

History

The original observation that amiodarone's progenitor molecule, khellin, had cardioactive properties, was made by the Russian physiologist Gleb von Anrep while working in Cairo in 1946. [92] Khellin is obtained from a plant extract of Khella or Ammi visnaga , a common plant in north Africa. Anrep noticed that one of his technicians had been cured of anginal symptoms after taking khellin, then used for various, non-cardiac ailments. This led to efforts by European pharmaceutical industries to isolate an active compound.[ 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. It became popular in Europe as a treatment for angina pectoris. [93] [94] [95]

As a doctoral candidate at Oxford University, Bramah Singh determined that amiodarone and sotalol had antiarrhythmic properties and belonged to a new class of antiarrhythmic agents (what would become the class III antiarrhythmic agents). [96] Today the mechanisms of action of amiodarone and sotalol have been investigated in more detail. Both drugs have been demonstrated to prolong the duration of the action potential, prolonging the refractory period, by interacting among other cellular functions with K+ channels. [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. [97] [98]

The US Food and Drug Administration (FDA) was reluctant to officially approve the use of amiodarone since initial reports had shown an increased incidence of serious pulmonary side effects of the drug. In the mid-1980s, the European pharmaceutical companies began putting pressure on the FDA to approve amiodarone by threatening to cut the supply to American physicians if it was not approved. In December 1985, amiodarone was approved by the FDA for the treatment of arrhythmias. [2] [99]

Name

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. This is partially supported by dronedarone which is noniodinated benzofuran derivative of amiodarone, where the arylmethanone is conserved.[ citation needed ]

Dosing

Amiodarone is available in oral and intravenous formulations.

Orally, it is available under the brand names Pacerone (produced by Upsher-Smith Laboratories, Inc.) and Cordarone (produced by Wyeth-Ayerst Laboratories). [1] [2] It is also available under the brand name Aratac (produced by Alphapharm Pty Ltd) in Australia and New Zealand, and further in Australia under the brands Cardinorm and Rithmik as well as a number of generic brands. Also Arycor in South Africa (Produced by Winthrop Pharmaceuticals.). In South America, it is known as Atlansil and is produced by Roemmers.

In India, amiodarone is marketed (produced by Cipla Pharmaceutical) under the brand name Tachyra. It is also available in intravenous ampules and vials.

The dose of amiodarone administered is tailored to the individual and the dysrhythmia that is being treated. When administered orally, the bioavailability of amiodarone is quite variable. Absorption ranges from 22 to 95%, with better absorption when it is given with food. [26]

Related Research Articles

<span class="mw-page-title-main">Cardioversion</span> Conversion of a cardiac arrhythmia to a normal rhythm using an electrical shock or medications

Cardioversion is a medical procedure by which an abnormally fast heart rate (tachycardia) or other cardiac arrhythmia is converted to a normal rhythm using electricity or drugs.

<span class="mw-page-title-main">Antiarrhythmic agent</span> Heart rhythm medication

Antiarrhythmic agents, also known as cardiac dysrhythmia medications, are a class of drugs that are used to suppress abnormally fast rhythms (tachycardias), such as atrial fibrillation, supraventricular tachycardia and ventricular tachycardia.

<span class="mw-page-title-main">Dofetilide</span> Antiarrhythmic medication

Dofetilide is a class III antiarrhythmic agent. It is marketed under the trade name Tikosyn by Pfizer, and is available in the United States in capsules containing 125, 250, and 500 μg of dofetilide. It is not available in Europe or Australia.

<span class="mw-page-title-main">Quinidine</span> Antiarrythmic medication

Quinidine is a class IA antiarrhythmic agent used to treat heart rhythm disturbances. It is a diastereomer of antimalarial agent quinine, originally derived from the bark of the cinchona tree. The drug causes increased action potential duration, as well as a prolonged QT interval. As of 2019, its IV formulation is no longer being manufactured for use in the United States.

<span class="mw-page-title-main">Flecainide</span> Antiarrhythmic medication

Flecainide is a medication used to prevent and treat abnormally fast heart rates. This includes ventricular and supraventricular tachycardias. Its use is only recommended in those with dangerous arrhythmias or when significant symptoms cannot be managed with other treatments. Its use does not decrease a person's risk of death. It is taken by mouth or injection into a vein.

<span class="mw-page-title-main">Sotalol</span> Medication

Sotalol, sold under the brand name Betapace among others, is a medication used to treat and prevent abnormal heart rhythms. Evidence does not support a decreased risk of death with long term use. It is taken by mouth or given by injection into a vein.

<span class="mw-page-title-main">Catheter ablation</span> Removal or termination of an electrical pathway from parts of the heart

Catheter ablation is a procedure that uses radio-frequency energy or other sources to terminate or modify a faulty electrical pathway from sections of the heart of those who are prone to developing cardiac arrhythmias such as atrial fibrillation, atrial flutter and Wolff-Parkinson-White syndrome. If not controlled, such arrhythmias increase the risk of ventricular fibrillation and sudden cardiac arrest. The ablation procedure can be classified by energy source: radiofrequency ablation and cryoablation.

Proarrhythmia is a new or more frequent occurrence of pre-existing arrhythmias, paradoxically precipitated by antiarrhythmic therapy, which means it is a side effect associated with the administration of some existing antiarrhythmic drugs, as well as drugs for other indications. In other words, it is a tendency of antiarrhythmic drugs to facilitate emergence of new arrhythmias.

<span class="mw-page-title-main">Azimilide</span> Chemical compound

Azimilide is a class ΙΙΙ antiarrhythmic drug. The agents from this heterogeneous group have an effect on the repolarization, they prolong the duration of the action potential and the refractory period. Also they slow down the spontaneous discharge frequency of automatic pacemakers by depressing the slope of diastolic depolarization. They shift the threshold towards zero or hyperpolarize the membrane potential. Although each agent has its own properties and will have thus a different function.

Tachycardia-induced cardiomyopathy (TIC) is a disease where prolonged tachycardia or arrhythmia causes an impairment of the myocardium, which can result in heart failure. People with TIC may have symptoms associated with heart failure and/or symptoms related to the tachycardia or arrhythmia. Though atrial fibrillation is the most common cause of TIC, several tachycardias and arrhythmias have been associated with the disease.

<span class="mw-page-title-main">Acecainide</span> Antiarrythmic drug

Acecainide is an antiarrhythmic drug. Chemically, it is the N-acetylated metabolite of procainamide. It is a Class III antiarrhythmic agent, whereas procainamide is a Class Ia antiarrhythmic drug. It is only partially as active as procainamide; when checking levels, both must be included in the final calculation.

<span class="mw-page-title-main">Ibutilide</span> Chemical compound

Ibutilide is a Class III antiarrhythmic agent that is indicated for acute cardioconversion of atrial fibrillation and atrial flutter of a recent onset to sinus rhythm. It exerts its antiarrhythmic effect by induction of slow inward sodium current, which prolongs action potential and refractory period of myocardial cells. Because of its Class III antiarrhythmic activity, there should not be concomitant administration of Class Ia and Class III agents.

<span class="mw-page-title-main">Lorcainide</span> Antiarrythmic agent

Lorcainide is a Class 1c antiarrhythmic agent that is used to help restore normal heart rhythm and conduction in patients with premature ventricular contractions, ventricular tachycardiac and Wolff–Parkinson–White syndrome. Lorcainide was developed by Janssen Pharmaceutica (Belgium) in 1968 under the commercial name Remivox and is designated by code numbers R-15889 or Ro 13-1042/001. It has a half-life of 8.9 +- 2.3 hrs which may be prolonged to 66 hrs in people with cardiac disease.

<span class="mw-page-title-main">Dronedarone</span> Medication

Dronedarone, sold under the brand name Multaq, is a class III antiarrhythmic medication developed by Sanofi-Aventis. It was approved by the US Food and Drug Administration (FDA) in July 2009. Besides being indicated in arrhythmias, it was recommended as an alternative to amiodarone for the treatment of atrial fibrillation and atrial flutter in people whose hearts have either returned to normal rhythm or who undergo drug therapy or electric shock treatment i.e. direct current cardioversion (DCCV) to maintain normal rhythm. It is a class III antiarrhythmic drug. The FDA label includes a claim for reducing hospitalization, but not for reducing mortality, as a reduction in mortality was not demonstrated in the clinical development program. A trial of the drug in heart failure was stopped as an interim analysis showed a possible increase in heart failure deaths, in people with moderate to severe congestive heart failure.

<span class="mw-page-title-main">Pilsicainide</span> Chemical compound

Pilsicainide (INN) is an antiarrhythmic agent. It is marketed in Japan as サンリズム (Sunrythm). It was developed by Suntory Holdings Limited and first released in 1991. The JAN applies to the hydrochloride salt, pilsicainide hydrochloride.

<span class="mw-page-title-main">Landiolol</span> Chemical compound

Landiolol, sold under the brand name Onoact among others, is a medication used for the treatment of tachycardia, atrial fibrillation, and atrial flutter. It is a beta-adrenergic blocker; an ultra short-acting, β1-superselective intravenous adrenergic antagonist, which decreases the heart rate effectively with less negative effect on blood pressure or myocardial contractility. In comparison to other beta blockers, landiolol has the shortest elimination half-life, ultra-rapid onset of effect, and predictable effectiveness with inactive metabolites. The pure S-enantiomer structure of landiolol is believed to develop less hypotensive side effects in comparison to other β-blockers. This has a positive impact on the treatment of patients when reduction of heart rate without decrease in arterial blood pressure is desired. It is used as landiolol hydrochloride.

<span class="mw-page-title-main">Junctional ectopic tachycardia</span> Irregular heartbeat due to abnormal conduction from the atrioventricular nerve

Junctional ectopic tachycardia (JET) is a rare syndrome of the heart that manifests in patients recovering from heart surgery. It is characterized by cardiac arrhythmia, or irregular beating of the heart, caused by abnormal conduction from or through the atrioventricular node. In newborns and infants up to 6 weeks old, the disease may also be referred to as His bundle tachycardia or congenital JET.

<span class="mw-page-title-main">Arrhythmia</span> Group of medical conditions characterized by irregular heartbeat

Arrhythmias, also known as cardiac arrhythmias, are irregularities in the heartbeat, including when it is too fast or too slow. A resting heart rate that is too fast – above 100 beats per minute in adults – is called tachycardia, and a resting heart rate that is too slow – below 60 beats per minute – is called bradycardia. Some types of arrhythmias have no symptoms. Symptoms, when present, may include palpitations or feeling a pause between heartbeats. In more serious cases, there may be lightheadedness, passing out, shortness of breath, chest pain, or decreased level of consciousness. While most cases of arrhythmia are not serious, some predispose a person to complications such as stroke or heart failure. Others may result in sudden death.

<span class="mw-page-title-main">Celivarone</span> Experimental drug being tested for use in pharmacological antiarrhythmic therapy

Celivarone is an experimental drug being tested for use in pharmacological antiarrhythmic therapy. Cardiac arrhythmia is any abnormality in the electrical activity of the heart. Arrhythmias range from mild to severe, sometimes causing symptoms like palpitations, dizziness, fainting, and even death. They can manifest as slow (bradycardia) or fast (tachycardia) heart rate, and may have a regular or irregular rhythm.

<span class="mw-page-title-main">Budiodarone</span> Chemical compound

Budiodarone (ATI-2042) is an antiarrhythmic agent and chemical analog of amiodarone that is currently being studied in clinical trials. Amiodarone is considered the most effective antiarrhythmic drug available, but its adverse side effects, including hepatic, pulmonary and thyroid toxicity as well as multiple drug interactions, are discouraging its use. Budiodarone only differs in structure from amiodarone through the presence of a sec-butyl acetate side chain at position 2 of the benzofuran moiety. This side chain allows for budiodarone to have a shorter half-life in the body than amiodarone which allows it to have a faster onset of action and metabolism while still maintaining similar electrophysiological activity. The faster metabolism of budiodarone allows for fewer adverse side effects than amiodarone principally due to decreased levels of toxicity in the body.

References

  1. 1 2 3 4 5 6 7 "Pacerone- amiodarone hydrochloride tablet". DailyMed. Archived from the original on 29 December 2022. Retrieved 8 September 2021.
  2. 1 2 3 "Cordarone (amiodarone) tablets, for oral use Initial U.S. Approval: 1985". DailyMed. 30 October 2018. Archived from the original on 29 December 2022. Retrieved 8 September 2021.
  3. ↑ "Nexterone- Amiodarone HCl injection, solution". DailyMed. Archived from the original on 29 December 2022. Retrieved 8 September 2021.
  4. 1 2 3 4 5 6 7 8 9 10 11 "Amiodarone Hydrochloride". The American Society of Health-System Pharmacists. Archived from the original on 19 September 2016. Retrieved 22 August 2016.
  5. 1 2 Ali MU, Fitzpatrick-Lewis D, Kenny M, Raina P, Atkins DL, Soar J, et al. (November 2018). "Effectiveness of antiarrhythmic drugs for shockable cardiac arrest: A systematic review" (PDF). Resuscitation. 132: 63–72. doi:10.1016/j.resuscitation.2018.08.025. PMID   30179691. S2CID   52154562. Archived (PDF) from the original on 5 March 2020. Retrieved 17 December 2019.
  6. 1 2 Review of the Medical Use of Amiodarone (Nexterone, Pacerone). Xavier Research Press. 24 July 2018. ISBN   978-1-7242-7798-5.
  7. 1 2 Feduska ET, Thoma BN, Torjman MC, Goldhammer JE (May 2021). "Acute Amiodarone Pulmonary Toxicity". J Cardiothorac Vasc Anesth. 35 (5): 1485–1494. doi:10.1053/j.jvca.2020.10.060. PMID   33262034. S2CID   227253264.
  8. ↑ Analytical Profiles of Drug Substances and Excipients. Academic Press. 1992. p. 4. ISBN   978-0-08-086115-9. Archived from the original on 8 September 2017.
  9. 1 2 Fischer J, Ganellin CR (2005). Analogue-based Drug Discovery. John Wiley & Sons. p. 12. ISBN   978-3-527-60749-5. Archived from the original on 8 September 2017.
  10. ↑ World Health Organization (2023). The selection and use of essential medicines 2023: web annex A: World Health Organization model list of essential medicines: 23rd list (2023). Geneva: World Health Organization. hdl: 10665/371090 . WHO/MHP/HPS/EML/2023.02.
  11. ↑ "The Top 300 of 2022". ClinCalc. Archived from the original on 30 August 2024. Retrieved 30 August 2024.
  12. ↑ "Amiodarone Drug Usage Statistics, United States, 2013 - 2022". ClinCalc. Retrieved 30 August 2024.
  13. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 Hamilton D, Nandkeolyar S, Lan H, Desai P, Evans J, Hauschild C, et al. (December 2020). "Amiodarone: A Comprehensive Guide for Clinicians". Am J Cardiovasc Drugs. 20 (6): 549–558. doi:10.1007/s40256-020-00401-5. PMID   32166725. S2CID   212682149.
  14. 1 2 Mori S, Tretter JT, Spicer DE, Bolender DL, Anderson RH (April 2019). "What is the real cardiac anatomy?". Clin Anat. 32 (3): 288–309. doi:10.1002/ca.23340. PMC   6849845 . PMID   30675928.
  15. 1 2 Larson J, Rich L, Deshmukh A, Judge EC, Liang JJ (June 2022). "Pharmacologic Management for Ventricular Arrhythmias: Overview of Anti-Arrhythmic Drugs". Journal of Clinical Medicine. 11 (11): 3233. doi: 10.3390/jcm11113233 . PMC   9181251 . PMID   35683620.
  16. 1 2 Ortiz M, Martín A, Arribas F, Coll-Vinent B, Del Arco C, Peinado R, et al. (May 2017). "Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study". European Heart Journal. 38 (17): 1329–1335. doi:10.1093/eurheartj/ehw230. PMC   5410924 . PMID   27354046.
  17. ↑ Laina A, Karlis G, Liakos A, Georgiopoulos G, Oikonomou D, Kouskouni E, et al. (October 2016). "Amiodarone and cardiac arrest: Systematic review and meta-analysis". International Journal of Cardiology. 221: 780–788. doi:10.1016/j.ijcard.2016.07.138. PMID   27434349.
  18. ↑ Lupton JR, Neth MR, Sahni R, Jui J, Wittwer L, Newgard CD, et al. (September 2023). "Survival by time-to-administration of amiodarone, lidocaine, or placebo in shock-refractory out-of-hospital cardiac arrest". Academic Emergency Medicine. 30 (9): 906–917. doi:10.1111/acem.14716. PMID   36869657.
  19. ↑ Perry E, Nehme E, Stub D, Anderson D, Nehme Z (June 2023). "The impact of time to amiodarone administration on survival from out-of-hospital cardiac arrest". Resuscitation Plus. 14: 100405. doi:10.1016/j.resplu.2023.100405. PMC   10250159 . PMID   37303855.
  20. 1 2 3 Medić F, Bakula M, Alfirević M, Bakula M, Mucić K, Marić N (August 2022). "Amiodarone and Thyroid Dysfunction". Acta Clin Croat. 61 (2): 327–341. doi:10.20471/acc.2022.61.02.20. PMC   9934045 . PMID   36818930.
  21. ↑ "Peri-arrest arrhythmias – Tachycardia algorithm]". Resuscitation Council (UK). Archived from the original on 3 January 2016. Retrieved 25 January 2016.
  22. ↑ "UpToDate". Archived from the original on 5 February 2024. Retrieved 5 February 2024.
  23. ↑ "Atrial fibrillation after surgery: Common and undertreated?". October 2022. Archived from the original on 5 February 2024. Retrieved 5 February 2024.
  24. ↑ "Amiodarone Reduction in Coronary Heart Trial". Archived from the original on 5 February 2024. Retrieved 5 February 2024.
  25. ↑ Guarnieri T, Nolan S, Gottlieb SO, Dudek A, Lowry DR (August 1999). "Intravenous amiodarone for the prevention of atrial fibrillation after open heart surgery: the Amiodarone Reduction in Coronary Heart (ARCH) trial". Journal of the American College of Cardiology. 34 (2): 343–347. doi:10.1016/S0735-1097(99)00212-0. PMID   10440143. S2CID   24714524.
  26. 1 2 3 4 5 Siddoway LA (December 2003). "Amiodarone: Guidelines for Use and Monitoring". American Family Physician. 68 (11): 2189–2197. PMID   14677664. Archived from the original on 5 February 2024. Retrieved 5 February 2024.
  27. ↑ Neff MJ (April 2005). "Practice Guideline Briefs". American Family Physician. 71 (7): 1434. Archived from the original on 5 February 2024. Retrieved 5 February 2024.
  28. ↑ King DE, Dickerson LM, Sack JL (15 July 2002). "Acute Management of Atrial Fibrillation: Part I. Rate and Rhythm Control". American Family Physician. 66 (2): 249–257. PMID   12152960. Archived from the original on 5 February 2024. Retrieved 5 February 2024.
  29. ↑ O'Bryan LJ, Redfern OC, Bedford J, Petrinic T, Young JD, Watkinson PJ (2020). "Managing new-onset atrial fibrillation in critically ill patients: A systematic narrative review". BMJ Open. 10 (3): e034774. doi:10.1136/bmjopen-2019-034774. PMC   7202704 . PMID   32209631. Archived from the original on 5 February 2024. Retrieved 5 February 2024.
  30. ↑ Letelier LM, Udol K, Ena J, Weaver B, Guyatt GH (2003). "Effectiveness of Amiodarone for Conversion of Atrial Fibrillation to Sinus Rhythm" . Archives of Internal Medicine. 163 (7): 777–785. doi:10.1001/archinte.163.7.777. PMID   12695268. Archived from the original on 5 February 2024. Retrieved 5 February 2024.
  31. ↑ "Recommendations | Atrial fibrillation: Diagnosis and management | Guidance | NICE". 27 April 2021. Archived from the original on 5 February 2024. Retrieved 5 February 2024.
  32. ↑ Johnston BW, Chean CS, Duarte R, Hill R, Blackwood B, McAuley DF, Welters ID. Management of new onset atrial fibrillation in critically unwell adult patients: a systematic review and narrative synthesis. British Journal of Anaesthesia. 2022 May 1;128(5):759-71.
  33. ↑ Centers for Disease Control (CDC) (June 1982). "Neonatal deaths associated with use of benzyl alcohol--United States". MMWR. Morbidity and Mortality Weekly Report. 31 (22): 290–291. PMID   6810084. Archived from the original on 30 August 2012.
  34. 1 2 3 Cappellani D, Bartalena L, Bogazzi F (September 2023). "Short review: novel concepts in the approach to patients with amiodarone-induced thyrotoxicosis". J Endocrinol Invest. 47 (2): 275–283. doi: 10.1007/s40618-023-02168-3 . PMC   10859339 . PMID   37731073. S2CID   262088052.
  35. 1 2 3 4 5 "Amiodarone". Drugs.com. 18 May 2022. Archived from the original on 25 July 2022. Retrieved 25 July 2022.
  36. 1 2 3 4 Chokesuwattanaskul R, Shah N, Chokesuwattanaskul S, Liu Z, Thakur R (April 2020). "Low-dose Amiodarone Is Safe: A Systematic Review and Meta-analysis". J Innov Card Rhythm Manag. 11 (4): 4054–4061. doi:10.19102/icrm.2020.110403. PMC   7192149 . PMID   32368381.
  37. ↑ Colunga Biancatelli RM, Congedo V, Calvosa L, Ciacciarelli M, Polidoro A, Iuliano L (July 2019). "Adverse reactions of Amiodarone". J Geriatr Cardiol. 16 (7): 552–566. doi:10.11909/j.issn.1671-5411.2019.07.004 (inactive 2 November 2024). PMC   6689516 . PMID   31447894.{{cite journal}}: CS1 maint: DOI inactive as of November 2024 (link)
  38. 1 2 Gašparini D, Raljević D, Pehar-Pejčinović V, Klarica Gembić T, Peršić V, Turk Wensveen T (2023). "When amiodarone-induced thyroiditis meets cardiomyopathy with excessive trabeculation: a case report". Front Cardiovasc Med . 10: 1212965. doi: 10.3389/fcvm.2023.1212965 . PMC   10401478 . PMID   37547257.
  39. ↑ Scaramozzino MU, Sapone G, Plastina UR, Nucara M (March 2023). "Amiodarone-Induced Lung Toxicity: A Case Initially Not Correctly Framed". Cureus . 15 (3): e36818. doi: 10.7759/cureus.36818 . PMC   10146449 . PMID   37123694.
  40. ↑ Tsai IL, Huang LT, Yu YT, Lee CT, Huang TH (June 2023). "Variable radiographic and histologic presentations of amiodarone-related interstitial lung disease and the importance of avoiding re-exposure". Respirol Case Rep. 11 (6): e01165. doi:10.1002/rcr2.1165. PMC   10209837 . PMID   37249923.
  41. ↑ Budin CE, Cocuz IG, Sabău AH, Niculescu R, Ianosi IR, Ioan V, et al. (December 2022). "Pulmonary Fibrosis Related to Amiodarone-Is It a Standard Pathophysiological Pattern? A Case-Based Literature Review". Diagnostics . 12 (12): 3217. doi: 10.3390/diagnostics12123217 . PMC   9777900 . PMID   36553223.
  42. ↑ Mitrofan CE, Cretu A, Mitrofan C, Bar C, Ghiciuc CM (2022). "Amiodarone induced lung disease". Arch Clin Cases. 9 (3): 126–132. doi:10.22551/2022.36.0903.10217. PMC   9512125 . PMID   36176494.
  43. ↑ Duineveld MD, Kers J, Vleming LJ (September 2023). "Case report of progressive renal dysfunction as a consequence of amiodarone-induced phospholipidosis". Eur Heart J Case Rep . 7 (9): ytad457. doi:10.1093/ehjcr/ytad457. PMC   10516635 . PMID   37743903.
  44. 1 2 "Amiodarone Side Effects". Drugs.com. 25 April 2021. Archived from the original on 24 February 2016. Retrieved 25 July 2022.
  45. 1 2 3 Tsang W, Houlden RL (July 2009). "Amiodarone-induced thyrotoxicosis: a review". Can J Cardiol. 25 (7): 421–4. doi:10.1016/s0828-282x(09)70512-4. PMC   2723027 . PMID   19584973.
  46. 1 2 3 4 Florek JB, Lucas A, Girzadas D (2024). Amiodarone. PMID   29489285. NCBI   NBK482154.
  47. ↑ Lombardi A, Inabnet WB, Owen R, Farenholtz KE, Tomer Y (January 2015). "Endoplasmic reticulum stress as a novel mechanism in amiodarone-induced destructive thyroiditis". The Journal of Clinical Endocrinology and Metabolism. 100 (1): E1-10. doi:10.1210/jc.2014-2745. PMC   4283007 . PMID   25295624.
  48. ↑ Hall GM, Hunter JM, Cooper MS (2010). Core Topics in Endocrinology in Anaesthesia and Critical Care. Cambridge University Press. p. 170. ISBN   978-1-139-48612-5. Archived from the original on 8 September 2017.
  49. ↑ Venturi S (2011). "Evolutionary Significance of Iodine". Current Chemical Biology. 5 (3): 155–162. doi:10.2174/187231311796765012 (inactive 17 November 2024). ISSN   1872-3136.{{cite journal}}: CS1 maint: DOI inactive as of November 2024 (link)
  50. ↑ Venturi S (2014). "Iodine, PUFAs and Iodolipids in Health and Disease: An Evolutionary Perspective". Human Evolution. 29 (1–3): 185–205. ISSN   0393-9375.
  51. ↑ Bartalena L, Bogazzi F, Chiovato L, Hubalewska-Dydejczyk A, Links TP, Vanderpump M (March 2018). "2018 European Thyroid Association (ETA) Guidelines for the Management of Amiodarone-Associated Thyroid Dysfunction". European Thyroid Journal. 7 (2): 55–66. doi:10.1159/000486957. PMC   5869486 . PMID   29594056.
  52. ↑ Batcher EL, Tang XC, Singh BN, Singh SN, Reda DJ, Hershman JM (October 2007). "Thyroid function abnormalities during amiodarone therapy for persistent atrial fibrillation". The American Journal of Medicine. 120 (10): 880–885. doi:10.1016/j.amjmed.2007.04.022. PMID   17904459. Archived from the original on 9 August 2020. Retrieved 27 August 2020.
  53. 1 2 3 Ylli D, Wartofsky L, Burman KD (January 2021). "Evaluation and Treatment of Amiodarone-Induced Thyroid Disorders". The Journal of Clinical Endocrinology and Metabolism. 106 (1): 226–236. doi:10.1210/clinem/dgaa686. PMID   33159436. S2CID   226275566.
  54. ↑ Chew E, Ghosh M, McCulloch C (June 1982). "Amiodarone-induced cornea verticillata". Canadian Journal of Ophthalmology. Journal Canadien d'Ophtalmologie. 17 (3): 96–99. PMID   7116220.
  55. ↑ Passman RS, Bennett CL, Purpura JM, Kapur R, Johnson LN, Raisch DW, et al. (May 2012). "Amiodarone-associated optic neuropathy: a critical review". The American Journal of Medicine. 125 (5): 447–453. doi:10.1016/j.amjmed.2011.09.020. PMC   3322295 . PMID   22385784.
  56. ↑ Roy FH (2012). Ocular differential diagnosis (9th ed.). Panama City, Panama: Jaypee Highlights Medical Publishers. p. 94. ISBN   978-93-5025-571-1. Archived from the original on 8 September 2017.
  57. ↑ Flaharty KK, Chase SL, Yaghsezian HM, Rubin R (1989). "Hepatotoxicity associated with amiodarone therapy". Pharmacotherapy. 9 (1): 39–44. doi:10.1002/j.1875-9114.1989.tb04102.x. PMID   2646621. S2CID   37972060.
  58. ↑ Singhal A, Ghosh P, Khan SA (March 2003). "Low dose amiodarone causing pseudo-alcoholic cirrhosis". Age and Ageing. 32 (2): 224–225. doi: 10.1093/ageing/32.2.224 . PMID   12615569.
  59. ↑ Puli SR, Fraley MA, Puli V, Kuperman AB, Alpert MA (November 2005). "Hepatic cirrhosis caused by low-dose oral amiodarone therapy". The American Journal of the Medical Sciences. 330 (5): 257–261. doi:10.1097/00000441-200511000-00012. PMID   16284489.
  60. ↑ Murphy RP, Canavan M (January 2020). "Skin Discoloration from Amiodarone". The New England Journal of Medicine. 382 (3): e5. doi:10.1056/NEJMicm1906774. PMID   31940702. S2CID   210333420.
  61. 1 2 "Amiodarone Pregnancy and Breastfeeding Warnings". Drugs.com. Archived from the original on 15 October 2020. Retrieved 8 December 2021.
  62. ↑ Fraser AG, McQueen IN, Watt AH, Stephens MR (June 1985). "Peripheral neuropathy during long-term high-dose amiodarone therapy". Journal of Neurology, Neurosurgery, and Psychiatry. 48 (6): 576–578. doi:10.1136/jnnp.48.6.576. PMC   1028375 . PMID   2989436.
  63. ↑ Thomas A, Woodard C, Rovner ES, Wein AJ (February 2003). "Urologic complications of neurologic medications". The Urologic Clinics of North America. 30 (1): 123–131. doi:10.1016/S0094-0143(02)00111-8. PMID   12580564.
  64. ↑ Bembo SA, Carlson HE (June 2004). "Gynecomastia: its features, and when and how to treat it" (PDF). Cleveland Clinic Journal of Medicine. 71 (6): 511–7. doi:10.3949/ccjm.71.6.511 (inactive 24 November 2024). PMID   15242307. Archived from the original (PDF) on 9 July 2009.{{cite journal}}: CS1 maint: DOI inactive as of November 2024 (link)
  65. 1 2 Su VY, Hu YW, Chou KT, Ou SM, Lee YC, Lin EY, et al. (May 2013). "Amiodarone and the risk of cancer: a nationwide population-based study". Cancer. 119 (9): 1699–1705. doi: 10.1002/cncr.27881 . PMID   23568847. S2CID   24144312.
  66. ↑ Lesko LJ (August 1989). "Pharmacokinetic drug interactions with amiodarone". Clinical Pharmacokinetics. 17 (2): 130–140. doi:10.2165/00003088-198917020-00005. PMID   2673606.
  67. ↑ Marcus FI (October 1983). "Drug interactions with amiodarone". American Heart Journal. 106 (4 Pt 2): 924–930. doi:10.1016/0002-8703(83)90017-0. PMID   6137140.
  68. 1 2 3 4 5 6 7 8 9 10 11 12 Brunton LL, Knollmann BC (1 November 2022). Goodman & Gilman's the Pharmacological Basis of Therapeutics. McGraw Hill. ISBN   978-1264258079.
  69. ↑ Tisdale JE, Chung MK, Campbell KB, Hammadah M, Joglar JA, Leclerc J, et al. (October 2020). "Drug-Induced Arrhythmias: A Scientific Statement From the American Heart Association". Circulation. 142 (15): e214–e233. doi: 10.1161/CIR.0000000000000905 . PMID   32929996.
  70. 1 2 3 Holbrook A, Schulman S, Witt DM, Vandvik PO, Fish J, Kovacs MJ, et al. (February 2012). "Evidence-based management of anticoagulant therapy: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines". Chest. 141 (2 Suppl): e152S–e184S. doi:10.1378/chest.11-2295. PMC   3278055 . PMID   22315259.
  71. ↑ "UpToDate: Warfarin Drug Information". Archived from the original on 10 September 2024. Retrieved 17 November 2024.
  72. 1 2 "Amiodarone hydrochloride (Marketed as Cordarone and Pacerone) Information". FDA. 18 June 2019. Archived from the original on 7 October 2024. Retrieved 17 November 2024.
  73. 1 2 3 "Cordarone (amiodarone HCl) tables" (PDF). FDA. 2010. Archived (PDF) from the original on 3 August 2023. Retrieved 22 March 2024.
  74. ↑ John E. Murphy (27 August 2021). Clinical Pharmacokinetics. American Society of Health-System Pharmacists. ISBN   978-1585287000.
  75. ↑ Hansten PD, Horn JR (12 April 2014). Drug Interaction Analysis and Management 2014. Wolters Kluwer Health. ISBN   978-1574393644.
  76. ↑ West S (21 March 2015). "Gilead Warns After Hepatitis Patient on Heart Drug Dies". Bloomberg. Archived from the original on 22 March 2017.
  77. ↑ "Amiodarone | Deranged Physiology". Archived from the original on 5 December 2023. Retrieved 22 March 2024.
  78. ↑ Lesko L (1989). "Pharmacokinetic Drug Interactions with Amiodarone". Clinical Pharmacokinetics. 17 (2): 130–140. doi:10.2165/00003088-198917020-00005. PMID   2673606.
  79. ↑ Bressler R (2006). "Grapefruit juice and drug interactions. Exploring mechanisms of this interaction and potential toxicity for certain drugs". Geriatrics. 61 (11): 12–18. PMID   17112309.
  80. ↑ "Information on Simvastatin/Amiodarone". Food and Drug Administration . Archived from the original on 21 September 2008. Retrieved 21 September 2008.
  81. ↑ Palleria C, Di Paolo A, Giofrè C, Caglioti C, Leuzzi G, Siniscalchi A, et al. (July 2013). "Pharmacokinetic drug-drug interaction and their implication in clinical management". Journal of Research in Medical Sciences. 18 (7): 601–610. PMC   3897029 . PMID   24516494.
  82. ↑ VandenBrink BM, Isoherranen N (January 2010). "The role of metabolites in predicting drug-drug interactions: focus on irreversible cytochrome P450 inhibition". Current Opinion in Drug Discovery & Development. 13 (1): 66–77. PMC   2898504 . PMID   20047147.
  83. 1 2 Latini R, Tognoni G, Kates RE (April 1984). "Clinical pharmacokinetics of amiodarone". Clinical Pharmacokinetics. 9 (2): 136–156. doi:10.2165/00003088-198409020-00002. PMID   6370540.
  84. ↑ Haverkamp W, Israel C, Parwani A (September 2017). "[Clinical aspects of treatment with amiodarone]". Herzschrittmacherther Elektrophysiol (in German). 28 (3): 307–316. doi:10.1007/s00399-017-0516-0. PMID   28643175.
  85. ↑ Di L, Balesano A, Jordan S, Shi SM (January 2021). "The Role of Alcohol Dehydrogenase in Drug Metabolism: Beyond Ethanol Oxidation". AAPS J. 23 (1): 20. doi:10.1208/s12248-020-00536-y. PMID   33415501.
  86. ↑ Shleghm MR, Mircioiu C, Voicu VA, Mircioiu I, Anuta V (2020). "Estimation of the In Vivo Release of Amiodarone From the Pharmacokinetics of Its Active Metabolite and Correlation With Its In Vitro Release". Front Pharmacol. 11: 621667. doi: 10.3389/fphar.2020.621667 . PMC   7917713 . PMID   33658939.
  87. ↑ "Amiodarone". Drugbank. Archived from the original on 23 May 2019. Retrieved 28 May 2019.
  88. 1 2 Harris L, Williams RR, eds. (1986). Amiodarone: pharmacology, pharmacokinetics, toxicology, clinical effects. Paris: Médecine et sciences internationales. p. 12. ISBN   978-2-86439-125-8.
  89. ↑ "FDA Drug Label". Archived from the original on 27 March 2017.
  90. ↑ Ghovanloo MR, Abdelsayed M, Ruben PC (2016). "Effects of Amiodarone and N-desethylamiodarone on Cardiac Voltage-Gated Sodium Channels". Frontiers in Pharmacology. 7: 39. doi: 10.3389/fphar.2016.00039 . PMC   4771766 . PMID   26973526.
  91. ↑ Brunton LL, Lazo JS, Parker K, eds. (2005). Goodman & Gilman's The Pharmacological Basis of Therapeutics (11th ed.). New York: McGraw-Hill. ISBN   0-07-142280-3.[ page needed ]
  92. ↑ Anrep GV, Barsoum GS, Kenawy MR, Misrahy G (October 1946). "Ammi Visnaga in the Treatment of the Anginal Syndrome". British Heart Journal. 8 (4): 171–177. doi:10.1136/hrt.8.4.171. PMC   503580 . PMID   18610042.
  93. ↑ Deltour G, Binon F, Tondeur R, Goldenberg C, Henaux F, Sion R, et al. (September 1962). "[Studies in the benzofuran series. VI. Coronary-dilating activity of alkylated and aminoalkylated derivatives of 3-benzoylbenzofuran]". Archives Internationales de Pharmacodynamie et de Therapie (in French). 139: 247–254. PMID   14026835.
  94. ↑ Charlier R, Deltour G, Tondeur R, Binon F (September 1962). "[Studies in the benzofuran series. VII. Preliminary pharmacological study of 2-butyl-3-(3,5-diiodo-4-beta-N-diethylaminoethoxybenzoyl)-benzofuran]". Archives Internationales de Pharmacodynamie et de Therapie (in French). 139: 255–264. PMID   14020244.
  95. 1 2 Antiarrhythmic Agents. Books LLC. ISBN   978-1-156-39374-1.
  96. ↑ Singh BN, Vaughan Williams EM (August 1970). "The effect of amiodarone, a new anti-anginal drug, on cardiac muscle". British Journal of Pharmacology. 39 (4): 657–667. doi:10.1111/j.1476-5381.1970.tb09891.x. PMC   1702721 . PMID   5485142.
  97. ↑ Rosenbaum MB, Chiale PA, Halpern MS, Nau GJ, Przybylski J, Levi RJ, et al. (December 1976). "Clinical efficacy of amiodarone as an antiarrhythmic agent". The American Journal of Cardiology. 38 (7): 934–944. doi:10.1016/0002-9149(76)90807-9. PMID   793369.
  98. ↑ Rosenbaum MB, Chiale PA, Haedo A, Lázzari JO, Elizari MV (October 1983). "Ten years of experience with amiodarone". American Heart Journal. 106 (4 Pt 2): 957–964. doi:10.1016/0002-8703(83)90022-4. PMID   6613843.
  99. ↑ "Drug Approval Package: Cordarone (Amiodarone Hydrochloride) Tablets. NDA #018972". U.S. Food and Drug Administration. Archived from the original on 21 February 2014. Retrieved 6 February 2014.
  100. ↑ "Compound summary for CID 2157". pubchem.ncbi.nil.nih.gov. Archived from the original on 24 March 2016.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.