Instructions for Amiodarone-Darnitsa tablets 200 mg No. 30
Composition
active ingredient: amiodarone;
1 tablet contains amiodarone hydrochloride 200 mg;
Excipients: lactose monohydrate, potato starch, povidone, microcrystalline cellulose, crospovidone, magnesium stearate.
Dosage form
Pills.
Main physicochemical properties: tablets of white or white with a slightly creamy tint, flat-cylindrical shape, with a bevel and a score.
Pharmacotherapeutic group
Class III antiarrhythmic drugs.
ATX code C01B D01.
Pharmacological properties
Pharmacodynamics.
Class III antiarrhythmic agent. It exhibits antiarrhythmic and antianginal effects.
Antiarrhythmic properties:
prolongation of phase 3 of the cardiomyocyte action potential is mainly due to a decrease in the current of potassium ions (class III according to the Vaughan-Williams classification);
slowing of the heart rate due to inhibition of sinus node automaticity. This effect is not blocked by atropine;
non-competitive α- and β-antiadrenergic action;
slowing of sinoatrial, atrial, and nodal impulse conduction in the myocardium, which is more pronounced the faster the rhythm;
no changes in intraventricular conduction;
increase in the refractory period and decrease in myocardial excitability at the atrial, nodal and ventricular levels;
slowing of conduction and prolongation of refractory periods in accessory atrioventricular conduction pathways.
Other properties:
reduced oxygen consumption due to a moderate decrease in peripheral vascular resistance and a decrease in heart rate;
increasing coronary blood flow due to a direct effect on the smooth muscles of myocardial vessels and maintaining cardiac output against the background of reduced blood pressure and peripheral vascular resistance and in the absence of negative inotropic effects.
Pharmacokinetics.
Amiodarone is a drug with slow elimination and pronounced tissue affinity.
Bioavailability after oral administration varies from 30% to 80% (average 50%) in different patients. After a single dose, the maximum concentration in the blood plasma is reached after 3–7 hours. The therapeutic effect is achieved on average within 1 week after the start of taking the drug (from several days to two weeks).
The half-life of amiodarone is long, with a fairly high level of interindividual variability (from 20 to 100 days). During the first days of treatment, this drug accumulates in most tissues of the body, especially in adipose tissue. Elimination begins after a few days, and equilibrium between intake and excretion is reached within several months, with individual fluctuations.
Such characteristics explain the need to use an increased dose in order to quickly accumulate the drug in the body's tissues, which is necessary to achieve a therapeutic effect.
Some of the iodine is released from the drug and is found in the urine in the form of iodide; 6 mg of iodine per day corresponds to a daily dose of 200 mg of amiodarone. The remainder of the drug, i.e. most of the iodine, is excreted in the feces after metabolism in the liver.
The low urinary excretion of the drug allows for the administration of normal doses to patients with impaired renal function.
After discontinuation of treatment, elimination from the body continues for several months. It should be noted that after discontinuation of the drug, its effect continues from 10 days to 1 month.
Indication
Relapse prevention:
life-threatening ventricular tachycardia: AMIODARON-DARNYTSYA should be administered only in a hospital setting under supervision;
documented symptomatic and disabling ventricular tachycardia;
documented supraventricular tachycardia, if the need for the drug is determined in patients with a disease resistant to other treatment or with contraindications to other methods of treating ventricular fibrillation.
Treatment of supraventricular tachycardia: slowing or reducing atrial fibrillation or atrial flutter.
Amiodarone can be used in patients with ischemic heart disease and/or left ventricular dysfunction (see section "Pharmacodynamics").
Contraindication
Sinus bradycardia, sinoatrial heart block in the absence of an endocardial pacemaker (artificial pacemaker).
Sick sinus syndrome in the absence of an endocardial pacemaker (risk of sinus node arrest).
High-grade atrioventricular conduction disturbances in the absence of an endocardial pacemaker.
Thyroid dysfunction (hyperthyroidism) – may be exacerbated when taking amiodarone.
Hypersensitivity to iodine, amiodarone or any of the excipients.
Pregnancy.
Breastfeeding period.
Combination with drugs that can induce torsades de pointes (except antiparasitics, neuroleptics and methadone):
Class Ia antiarrhythmics (quinidine, hydroquinidine, disopyramide);
other medicines such as arsenic compounds, bepridil, cisapride, citalopram, escitalopram, diphemanil, dolasetron intravenously, domperidone, dronedarone, erythromycin intravenously, levofloxacin, mechitazine, mizolastine, vincamine intravenously, moxifloxacin, prucalopride, spiramycin intravenously, toremifene (see section “Interaction with other medicines and other types of interactions”);
telaprevir;
cobicistat.
Interaction with other medicinal products and other types of interactions
Antiarrhythmic drugs.
Many antiarrhythmic drugs inhibit cardiac automaticity, conduction, and myocardial contractility.
The simultaneous use of antiarrhythmic drugs belonging to different classes may
to ensure the achievement of a favorable therapeutic effect, but most often treatment with such a combination is a very delicate process that requires careful clinical and ECG monitoring.
Concomitant use of antiarrhythmics that may induce torsades de pointes (such as amiodarone, disopyramide, quinidine compounds, sotalol) is contraindicated.
The simultaneous use of antiarrhythmic drugs of the same class is not recommended, except in exceptional cases, as such treatment increases the risk of cardiac side effects.
Concomitant use with drugs that have a negative inotropic effect, contribute to slowing the heart rate and/or slow atrioventricular conduction is a delicate process that requires careful clinical and ECG monitoring.
Drugs that can induce the development of torsades de pointes.
This serious arrhythmia can be induced by certain drugs, whether or not they are antiarrhythmic drugs. Additional risk factors include hypokalemia (see section “Potassium-lowering drugs”), bradycardia (see section “Medicines that slow the heart rate”), or pre-existing congenital or acquired prolongation of the QT interval.
Drugs that may induce torsades de pointes include, in particular, class Ia and III antiarrhythmic drugs and some neuroleptics. For dolasetron, erythromycin, spiramycin and vincamicin, this interaction is realized only when using their dosage forms that are administered intravenously.
The simultaneous use of two drugs, each of which is a drug that contributes to the occurrence of torsades de pointes, is usually contraindicated.
However, methadone and some subgroups of drugs are exceptions to this rule:
antiparasitic drugs (halofantrine, lumefantrine, pentamidine) are also not recommended for use with other drugs that contribute to the occurrence of torsades de pointes;
Neuroleptics that can induce torsades de pointes are also not recommended for use with other agents that contribute to the occurrence of torsades de pointes, but such a combination is not contraindicated.
Medicines that slow the heart rate.
Many drugs can cause bradycardia. This includes class Ia antiarrhythmic drugs, β-blockers, some class III antiarrhythmic drugs, some calcium channel blockers, digitalis drugs, pilocarpine, and anticholinesterase drugs.
Effect of other drugs on amiodarone.
CYP3A4 and CYP2C8 inhibitors have the potential to inhibit the metabolism of amiodarone and thus increase its exposure.
Effects of amiodarone on other drugs.
Amiodarone and/or its metabolite desethylamiodarone inhibit CYP1A1, CYP1A2, CYP3A4, CYP2C9, CYP2D6 and P-glycoprotein and may increase exposure to their substrates. Since the effect of amiodarone is long-lasting, such interactions may be observed for several months after discontinuation of amiodarone treatment.
Contraindicated combinations (see section "Contraindications").
Medicinal products that may induce torsades de pointes (except antiparasitics, neuroleptics and methadone; see section “Combinations not recommended”):
Class Ia antiarrhythmics (quinidine, hydroquinidine, disopyramide);
class III antiarrhythmics (dofetilide, ibutilide, sotalol);
other medicines such as: arsenic compounds, bepridil, cisapride, citalopram, escitalopram, diphemanil, dolasetron intravenously, domperidone, dronedarone, erythromycin intravenously, levofloxacin, mechitazine, mizolastine, vincomycin intravenously, moxifloxacin, prucalopride, spiramycin intravenously, toremifene.
Increased risk of developing ventricular arrhythmias, especially torsades de pointes.
Telaprevir: Cardiomyocyte automatism and conduction disorders with risk of excessive bradycardia.
Cobicistat: Risk of increased incidence of amiodarone-induced adverse events due to decreased metabolism.
Combinations are not recommended (see section "Special instructions for use").
Diltiazem for injection. Risk of bradycardia and atrioventricular block. If the combination cannot be avoided, close clinical supervision and ECG monitoring of cardiac function should be performed.
Fingolimod. Potentiation of bradycardia-induced effects, possible fatal outcome. This is especially true for β-blockers that inhibit adrenergic compensation mechanisms. After the first dose of the drug, clinical supervision and monitoring of cardiac activity by ECG for 24 hours is required.
Cyclosporine: Increased serum concentrations of cyclosporine due to impaired hepatic metabolism, with the risk of nephrotoxic effects.
Quantitative determination of serum cyclosporine concentrations, monitoring of renal function, and cyclosporine dose adjustment during amiodarone treatment.
Verapamil and diltiazem for injection. Risk of bradycardia and atrioventricular block.
If the use of this combination cannot be avoided, close clinical supervision and continuous ECG monitoring are essential.
Antiparasitic drugs that can induce torsades de pointes (halofantrine, lumefantrine, pentamidine). Increased risk of ventricular arrhythmias, especially torsades de pointes.
If possible, 1 or 2 drugs should be discontinued. If the combination cannot be avoided, it is extremely important to perform a preliminary assessment of the QT interval and perform ECG monitoring.
Neuroleptics that can induce torsades de pointes (amisulpride, chlorpromazine, cyamemazine, droperidol, flupentixol, fluphenazine, haloperidol, levomepromazine, pimozide, pipamperon, pipotiazine, sertindole, sulpiride, sultopride, tiapride, zuclopenthixol). Increased risk of ventricular arrhythmias, especially torsades de pointes.
Fluoroquinolones, except levofloxacin and moxifloxacin (contraindicated combinations). Increased risk of ventricular arrhythmias, especially torsades de pointes.
Stimulant laxatives. Increased risk of ventricular arrhythmias, especially torsades de pointes ventricular tachycardia (hypokalemia is a precipitating factor). Hypokalemia should be corrected before use, cardiac monitoring by ECG, and clinical supervision should be performed, including electrolyte monitoring.
Fidaxomicin: Increased plasma concentrations of fidaxomicin.
Methadone: Increased risk of ventricular arrhythmias, especially torsades de pointes.
Combinations requiring precautions for use.
P-glycoprotein substrates: Amiodarone is an inhibitor of P-glycoprotein. Concomitant use with P-glycoprotein substrates is expected to increase their blood concentrations.
Oral anticoagulants. Increased anticoagulant effect and increased risk of hemorrhagic complications.
More frequent monitoring of international normalized ratio. Possible adjustment of oral anticoagulant dose during amiodarone treatment and for 8 days after drug discontinuation.
β-blockers, except sotalol (contraindicated combination) and esmolol (combination requiring precautions for use). Disturbances of automaticity and conduction (suppression of compensatory sympathetic mechanisms). ECG and clinical monitoring.
β-blockers used to treat heart failure (bisoprolol, carvedilol, metoprolol, nebivolol). Disturbances in myocardial automatism and conduction with the risk of excessive slowing of the heart rate.
Increased risk of ventricular arrhythmias, especially torsades de pointes. Clinical and regular ECG monitoring.
Dabigatran: Increased plasma concentrations of dabigatran with increased risk of hemorrhagic events.
If dabigatran is used after surgery, clinical monitoring and dose adjustment of dabigatran should be performed if necessary, but not higher than 150 mg/day.
Since amiodarone has a long half-life, interactions may occur for several months after discontinuation of amiodarone treatment.
Digitalis preparations. Suppression of automatism (excessive slowing of the heart rate) and disturbances of atrioventricular conduction.
When using digoxin, an increase in blood digoxin levels is observed due to a decrease in digoxin clearance, which requires monitoring of cardiac activity using ECG and clinical observation, quantitative determination of blood digoxin levels and appropriate adjustment of the digoxin dose.
Oral diltiazem. Risk of bradycardia or atrioventricular block, especially in elderly patients. ECG and clinical monitoring.
Some macrolides (azithromycin, clarithromycin, roxithromycin). Increased risk of ventricular arrhythmias, especially torsades de pointes. ECG and clinical monitoring during concomitant use of these drugs.
Oral verapamil. Risk of bradycardia and atrioventricular block, especially in elderly patients. ECG and clinical monitoring.
Potassium-depleting drugs: potassium-depleting diuretics (alone or in combination), stimulant laxatives, amphotericin B (intravenous), glucocorticoids (systemic), tetracosactide. Increased risk of ventricular arrhythmias, especially torsades de pointes (hypokalemia is a predisposing factor).
Hypokalemia should be corrected before prescribing the drug and ECG, electrolytes and clinical monitoring should be performed.
Lidocaine. Risk of increased plasma concentrations of lidocaine, with possible neurological and cardiac side effects, due to inhibition of hepatic metabolism by amiodarone. Clinical and ECG monitoring, and, if necessary, quantitative determination of plasma lidocaine concentrations. If necessary, adjustment of the lidocaine dose during treatment with amiodarone and after its withdrawal.
Orlistat. Risk of decreased plasma concentrations of amiodarone and its active metabolite. Clinical monitoring and, if necessary, ECG monitoring.
Phenytoin (by extrapolation – fosphenytoin). Increased plasma concentrations of phenytoin with signs of overdose, especially neurological signs (inhibition of phenytoin metabolism in the liver). Clinical monitoring, quantification of plasma concentrations of phenytoin and possible dose adjustment.
Tacrolimus. Increased blood concentrations of tacrolimus due to inhibition of its metabolism by amiodarone. Quantitative determination of tacrolimus blood concentrations, monitoring of renal function and adjustment of tacrolimus dose during concomitant use of amiodarone and its withdrawal.
Tamsulosin: Risk of increased adverse effects of tamsulosin due to inhibition of its metabolism in the liver. Clinical monitoring and, if necessary, dose adjustment of tamsulosin should be performed during treatment with an enzyme inhibitor and after its discontinuation.
Voriconazole: Increased risk of ventricular arrhythmias, especially torsades de pointes, due to possible decreased metabolism of amiodarone. Clinical supervision and ECG monitoring of cardiac function are required, and amiodarone dose adjustment is required if necessary.
CYP2D6 substrates.
Flecainide: Amiodarone increases plasma concentrations of flecainide due to inhibition of cytochrome CYP 2D6. Therefore, the dose of flecainide should be adjusted.
Drugs metabolized by cytochrome P450 3A4 (fentanyl, sildenafil, midazolam, triazolam, dihydroergotamine, ergotamine, statins, including atorvastatin, lovastatin). Their administration with amiodarone, which is an inhibitor of this enzyme, increases the concentration of these drugs in the blood plasma and, as a result, may increase their toxicity.
Cyclosporine: Combination with amiodarone may lead to increased plasma levels of cyclosporine. Dose adjustment is required.
Fentanyl: combination with amiodarone may enhance the pharmacological effects of fentanyl and increase the risk of its toxicity.
CYP3A4 substrates.
Amiodarone is a CYP3A4 inhibitor and increases the plasma concentration of substrates of this cytochrome, as a result, the toxic effect of these substrates increases.
Statins: Concomitant use of amiodarone and statins metabolised by CYP3A4, such as simvastatin, atorvastatin and lovastatin, increases the risk of muscle toxicity (e.g. rhabdomyolysis). When used concomitantly with amiodarone, statins not metabolised by CYP3A4 are recommended.
Simvastatin: Increased risk of concentration-dependent side effects such as rhabdomyolysis (inhibition of simvastatin metabolism in the liver). Given this type of interaction, the dose of simvastatin should not exceed 20 mg per day or another statin should be used.
Other drugs metabolized by CYP3A4 include lidocaine, sirolimus, tacrolimus, sildenafil, fentanyl, midazolam, triazolam, dihydroergotamine, ergotamine, and colchicine.
Vitamin K antagonists. Enhancement of the effects of vitamin K antagonists and increased risk of bleeding. Monitoring of international normalized ratio (INR) is required. The dose of the vitamin K antagonist should be adjusted during treatment with amiodarone and for 8 days after the end of treatment.
Amiodarone is a CYP3A4 inhibitor and increases the concentrations of these molecules in the blood plasma, which leads to an increase in their toxicity.
It is recommended to avoid the use of CYP3A4 inhibitors (e.g. grapefruit juice and certain medications) during treatment with amiodarone.
Drugs that slow the heart rate. Increased risk of ventricular arrhythmias, especially torsades de pointes. Clinical and ECG monitoring.
CYP2C9 substrates: Amiodarone increases the concentrations of substances that are CYP2C9 substrates, such as warfarin or phenytoin, due to inhibition of cytochrome P4502C9 enzymes.
Combinations that require special attention.
Pilocarpine: risk of excessive slowing of the heart rate (additive effects of drugs that slow the heart rate).
Application features
The frequency and severity of adverse effects are dose-dependent, so the minimum effective maintenance dose should be used.
Heart effects.
Before starting the drug, an ECG should be performed and serum potassium levels should be determined.
Elderly patients may experience an increase in heart rate decelerations while taking the drug. Caution should be exercised in elderly patients due to the risk of bradycardia. Amiodarone induces ECG changes. These changes include prolongation of the QT interval due to prolonged repolarization, with possible appearance of a U wave. This is a sign of the therapeutic effect of the drug, and not its toxicity.
If second- or third-degree sinoatrial block or atrioventricular block or bifascial bundle branch block occurs, treatment should be discontinued.
The occurrence of second or third degree AV block, sinoatrial block or bifascicular block during treatment requires discontinuation of the drug. The development of first degree AV block requires increased patient monitoring.
Cases of arrhythmia or exacerbation of pre-existing and treated arrhythmia have been reported (see section 4.8).
The risk of drug-induced torsades de pointes with amiodarone is low or even lower than with most antiarrhythmics in patients with the same degree of QT prolongation and usually occurs with certain drug combinations (see section 4.5) or in the presence of electrolyte imbalance (hypokalemia).
Thyroid disorders.
This medicine contains iodine, which affects the results of some thyroid function tests (radioactive iodine binding, protein-bound iodine). However, thyroid function tests (TSH, T4, TSH) can still be performed.
Amiodarone may cause thyroid dysfunction, especially in patients with a history of thyroid dysfunction. Quantitative determination of TSH is recommended in all patients before starting the drug, then regularly during treatment and for several months after discontinuation of the drug, as well as in case of clinical suspicion of thyroid dysfunction (see section "Adverse reactions").
Lung disorders.
The appearance of dyspnea or dry cough, either isolated or associated with a deterioration in the general condition, should be considered as a possible sign of pulmonary toxicity of the drug, for example the development of interstitial pneumopathy, and requires a radiological examination of the patient (see section "Adverse reactions").
Liver disorders.
Regular monitoring of liver function is recommended at the beginning of treatment with the drug, then periodically during treatment with amiodarone (see section "Adverse reactions"). The dose of amiodarone should be reduced or the drug should be discontinued if transaminase levels increase by more than 3 times compared to the norm of these indicators.
Acute liver disorders (including severe hepatocellular insufficiency or liver failure, sometimes fatal) and chronic liver disorders may develop with the use of amiodarone.
Neuromuscular disorders.
Amiodarone may cause sensory, motor or mixed peripheral neuropathy and myopathy (see section "Adverse reactions").
Visual impairment.
If blurred vision or decreased visual acuity occurs, a complete ophthalmological examination, including fundoscopy, should be performed immediately. The development of optic neuropathy or neuritis caused by amiodarone requires discontinuation of the drug, as continued treatment may lead to progression of the disorders up to blindness (see section "Adverse reactions").
Severe bradycardia.
Severe, potentially life-threatening bradycardia and severe cardiac conduction abnormalities have been reported in patients taking amiodarone in combination with sofosbuvir, alone or in combination with other direct-acting antivirals for the treatment of hepatitis C, such as daclatasvir, simeprevir or ledipasvir. Therefore, concomitant use of these medicinal products with amiodarone is not recommended.
If concomitant use of these medicinal products with amiodarone cannot be avoided, patients should be closely monitored when initiating sofosbuvir (alone or in combination with other direct-acting antivirals). Patients at high risk of bradyarrhythmia should be monitored for at least 48 hours after initiation of sofosbuvir.
Patients receiving such drugs for the treatment of hepatitis C in combination with amiodarone, regardless of the intake of other drugs that reduce heart rate, should be warned about the symptoms that occur with bradycardia and severe cardiac conduction disorders, and that they should seek emergency medical attention if they occur.
Disorders associated with interactions with other drugs.
Combinations (see section "Interaction with other medicinal products and other forms of interaction") with medicinal products such as β-blockers, except sotalol (a combination contraindicated) and esmolol (a combination requiring precautions for use), verapamil and diltiazem, should only be considered for the prevention of life-threatening ventricular arrhythmias.
The use of amiodarone is not recommended in combination with cyclosporine, diltiazem (for injection) and verapamil (for injection), some antiparasitic agents (halofantrine, lumefantrine and pentamidine), some neuroleptics (amisulpride, chlorpromazine, cyamemazine, droperidol, flupentixol, fluphenazine, haloperidol, levomepromazine, pimozide, pipamperon, pipotiazine, sertindole, sulpiride, sultopride, tiapride, zuclopenthixol), fluoroquinolones (except levofloxacin and moxifloxacin), stimulant laxatives, methadone or fingolimod (see section "Interaction with other medicinal products and other types of interactions").
Electrolyte disturbances, especially hypokalemia.
Hypokalemia may contribute to the manifestation of proarrhythmic effects of the drug.
The use of amiodarone with β-blockers, calcium channel inhibitors that reduce heart rate (verapamil, diltiazem), and stimulant laxatives that can cause hypokalemia is not recommended.
Hypokalemia should be corrected before initiating amiodarone therapy. Serum potassium levels should be monitored.
The side effects listed below are most often associated with excessive use of the drug; they can be avoided or minimized by using the minimum maintenance dose.
The safety and efficacy of amiodarone in children have not been evaluated in controlled clinical trials.
Due to the possible increase in the defibrillation threshold and/or stimulation by implanted cardiac defibrillators or artificial pacemakers, this threshold should be checked before treatment with amiodarone and several times after starting its use, as well as each time the dose of the drug is adjusted.
Effects on the skin and subcutaneous tissue.
During treatment with amiodarone, patients are advised to avoid ultraviolet radiation.
Severe bullous reactions.
Amiodarone should be used with caution in patients at high risk of serious skin reactions, including Stevens-Johnson syndrome and toxic epidermal necrolysis. Amiodarone should be discontinued immediately at the first appearance of skin rash, mucosal lesions, or any other sign of hypersensitivity.
Anesthesia.
The anesthesiologist should be informed before surgery that the patient is taking amiodarone.
Long-term treatment with amiodarone may increase the haemodynamic risks associated with general and local anaesthesia, which will be manifested by adverse effects. These adverse effects include, in particular, bradycardia, hypotension, decreased cardiac output and cardiac conduction disturbances. In addition, several cases of acute respiratory distress syndrome have been observed in patients receiving amiodarone in the early postoperative period. Therefore, it is recommended that such patients be closely monitored during mechanical ventilation (see section "Adverse reactions").
Excipient-related disorders.
This medicinal product contains lactose. Therefore, it should not be administered to patients with galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption syndrome (rare hereditary diseases).
Use during pregnancy or breastfeeding
Pregnancy: No teratogenic effects have been observed in animals, therefore no malformative effects are expected in humans.
There are insufficient clinical data to assess the possible teratogenic or fetotoxic effects of amiodarone when administered in therapeutic doses during the first trimester of pregnancy.
Since the fetal thyroid gland begins to bind iodine from the 14th week, no effect on the fetal thyroid gland is expected if the drug is used before this time. Excessive iodine intake during the period of drug administration may lead to hypothyroidism in the fetus. Given the effect of amiodarone on the fetal thyroid gland, this drug is contraindicated for use during pregnancy.
Breastfeeding. Amiodarone and its metabolites, together with iodine, are excreted in breast milk in concentrations higher than those in maternal plasma. Breastfeeding is contraindicated during treatment with amiodarone due to the risk of hypothyroidism in the newborn.
Ability to influence reaction speed when driving vehicles or other mechanisms
During treatment, caution should be exercised when driving or working with other mechanisms that require increased concentration and speed of psychomotor reactions due to the possible development of adverse reactions from the organs of vision or the nervous system.
Method of administration and doses
Administer to adults orally, during or after meals, without chewing, with a small amount of liquid.
Initial treatment.
The usual dosage regimen of the drug is 3 tablets per day for 8–10 days.
In some cases, higher doses (4–5 tablets per day) should be used for initial treatment, but always for a short period of time and with electrocardiogram monitoring.
Supportive treatment.
The minimum effective dose should be determined, which may vary depending on the patient and range from 0.5 tablet per day (1 tablet every 2 days) to 2 tablets per day.
Children.
The safety and efficacy of amiodarone in children have not been evaluated at this time, therefore, the use of this drug in children is not recommended.
Overdose
Cases of overdose with amiodarone are not well documented. Several cases of sinus bradycardia, ventricular arrhythmias, especially torsades de pointes, and liver damage have been reported. Treatment should be symptomatic. Given the pharmacokinetic profile of this drug, monitoring of the patient's condition, especially cardiac function, for a sufficiently long period of time is recommended. AMIODARON-DARNYTSYA and its metabolites are not removed by dialysis.
Side effects
Adverse reactions were classified by system organ class and frequency as follows: very common (> 10%); common (> 1%, < 10%); uncommon (> 0.1%, < 1%); rare (> 0.01%, < 0.1%); very rare (< 0.01%).
On the part of the organs of vision: very often - microdeposits in the cornea, in almost all adults, usually within the subpupillary area, which do not require discontinuation of amiodarone. In exceptional cases, they are associated with colored halos in bright light or with blurred vision. Microdeposits in the cornea are complex lipid deposits and are always completely reversible after discontinuation of the drug; very rarely - optic neuropathy (optic neuritis) with blurred vision and visual impairment, as well as, according to the results of fundus examination, with swelling of the optic nerve head, which may progress to a more or less complex decrease in visual acuity. The causal relationship of this side effect with amiodarone has not been established at this time.
However, in the absence of other obvious reasons for the development of this side effect, it is recommended to discontinue amiodarone.
Respiratory, thoracic and mediastinal disorders: Common: Interstitial or diffuse alveolar lung disease and bronchiolitis obliterans with organizing pneumonia (BOOP), sometimes fatal, have been reported. The appearance of dyspnea on exertion or dry cough, either isolated or associated with deterioration in general health (increased fatigue, weight loss and a slight increase in body temperature), requires radiological examination and, if necessary, discontinuation of the drug, since these lung diseases can lead to pulmonary fibrosis.
Early withdrawal of amiodarone, with or without corticosteroid therapy, results in gradual resolution of symptoms. Clinical signs usually resolve within 3–4 weeks; improvement in radiographic and pulmonary function is slower (over several months).
A few cases of pleurisy have been reported, usually associated with interstitial pneumopathy; very rarely,
