Producer: Sanofi-Aventis Private Co.Ltd (Sanofi-Aventis Pravit. Co. Ltd.) France
Code of automatic telephone exchange: C01BD01
Release form: Firm dosage forms. Tablets.
General characteristics. Structure:
Active agent - Amiodaronum a hydrochloride of 200,0 mg;
excipients: lactoses monohydrate, starch corn, magnesium stearate, K90F povidone, silicon dioxide colloid anhydrous.
Description. Round tablets from color, white to white with a creamy shade, with the line of a break on the one hand and with a facet from two parties. There is an engraving: a symbol in the form of heart over the line of a break and 200 under the line of a break and a bevel from edges to the line of a break.
Pharmacodynamics. Amiodaronum belongs to the III class of antiarrhytmic drugs (a class of inhibitors of repolarization) and possesses the unique mechanism of antiarrhytmic action as in addition to properties of antiaritmik of the III class (blockade of potassium channels) it has effects of antiaritmik of the I class (blockade of natrium channels), antiaritmik of the IV class (blockade of calcium channels) and the non-competitive beta blocking action.
Except antiarrhytmic action it has anti-anginal, coronarodilator, alpha and beta and adrenoceptor blocking effects.
- increase in duration of the 3rd phase of action potential of cardiomyocytes, generally due to blocking of ionic current in potassium channels (effect of an antiaritmik Sh classes on Williams's classification);
- the reduction of automatism of a sinus node leading to reduction of heart rate;
- non-competitive blockade of alpha and beta adrenergic receptors;
- the delay of sinuatrial, atrial and atrioventricular conduction which was more expressed at tachycardia;
- lack of changes of conductivity of ventricles;
- increase in the refractory periods and reduction of excitability of a myocardium of auricles and ventricles, and also increase in the refractory period of an atrioventricular node;
- delay of carrying out and increase in duration of the refractory period in additional bunches of atrioventricular carrying out.
- lack of negative inotropic effect at intake;
- decrease in consumption of oxygen a myocardium due to moderate decrease in peripheric resistance and heart rate;
- increase in a coronary blood-groove due to direct impact on smooth muscles of coronary arteries;
- maintenance of cordial emission due to pressure decrease in an aorta and decrease in peripheric resistance;
- influence on exchange of thyroid hormones: inhibition of transformation of T3 into T4 (blockade of a thyroxine-5-deiodinase) both the blocking of capture of these hormones cardiocytes and hepatocytes leading to weakening of the stimulating influence of thyroid hormones on a myocardium.
Therapeutic effects are observed on average in a week after the beginning of administration of drug (from several days to two weeks). After the termination of its reception Amiodaronum is defined in a blood plasma for 9 months. It is necessary to take into account a possibility of preservation of pharmakodinamichesky action of Amiodaronum within 10-30 days after its cancellation.
Pharmacokinetics. Bioavailability after intake at different patients fluctuates from 30 to 80% (average value about 50%). After a single dose of Amiodaronum the maximum concentration in a blood plasma are reached in 3-7 hours. However therapeutic action usually develops in a week after the beginning of administration of drug (from several days to two weeks). Amiodaronum is drug with slow receipt in fabric and high affinity to them.
Communication with proteins of a blood plasma makes 95% (62% - with albumine, 33,5% - with beta lipoproteins). Amiodaronum has the large volume of distribution. During the first days of treatment drug collects almost in all fabrics, in particular in fatty tissue and except it in a liver, lungs, a spleen and a cornea.
Amiodaronum is metabolized in a liver. Its main metabolite - дезэтиламиодарон
- pharmacological is active and can strengthen antiarrhytmic effect of the main connection.
Amiodaronum is inhibitor of hepatic isoenzymes of a microsomal oxidation: CYP2C9, CYP2D6, CYP3A4, CYP3A5, CYP3A7.
Removal of Amiodaronum begins in several days, and achievement of balance between receipt and removal of drug (achievement of an equilibrium state) comes later from one to several months, depending on specific features of the patient. The main way of removal of Amiodaronum are intestines. Amiodaronum and its metabolites are not removed by means of a hemodialysis. Amiodaronum possesses a long elimination half-life with big individual variability
(therefore at selection of a dose, for example, its increase or reduction, it is necessary to remember that at least 1 month is necessary for stabilization of new plasma concentration of Amiodaronum). Removal at intake proceeds in 2 phases: an initial stage of semi-removal (the first phase) - 4-21 hour, an elimination half-life in the 2nd phase - 25-110 days. (20-100 days). After long oral administration an average elimination half-life - 40 days. After drug withdrawal full removal of Amiodaronum from an organism can continue within several months.
Each dose of Amiodaronum (200 mg) contains 75 mg of iodine. A part of iodine is released from drug and it is found in urine in the form of iodide (6 mg in 24 hours at a daily dose of Amiodaronum of 200 mg). The most part of iodine remaining as a part of drug is removed with a fecal masses after passing through a liver, however at long reception of Amiodaronum, concentration of iodine can reach 60-80% of concentration of Amiodaronum.
Use of "load" doses which is directed to bystry achievement of necessary level of treatment of fabrics at which its therapeutic action is shown is explained by features of pharmacokinetics of drug.
Pharmacokinetics at a renal failure: in connection with insignificance of removal of drug kidneys dose adjustment of Amiodaronum is not required from patients with a renal failure.
Indications to use:
Prevention of a recurrence
• Life-threatening ventricular arrhythmias, including ventricular tachycardia and fibrillation of ventricles (treatment has to be begun in a hospital at careful cardiomonitor control).
• Supraventricular Bouveret's diseases:
- documentary attacks of a recurrent steady supraventricular Bouveret's disease at patients with organic heart diseases;
- documentary attacks of a recurrent steady supraventricular Bouveret's disease patients without organic heart diseases when antiarrhytmic drugs of other classes are not effective or have contraindications to their use;
- documentary attacks of a recurrent steady supraventricular Bouveret's disease at patients with a WPW-syndrome.
• A ciliary arrhythmia (fibrillation of auricles) and an atrial flutter Prevention of sudden arhythmic death at patients of group of high risk
• Patients after recently postponed myocardial infarction, the having more than 10 ventricular extrasystoles at 1 o'clock, clinical displays of chronic heart failure and reduced fraction of emission of a left ventricle (less than 40%).
Amiodaronum can be used at treatment of disturbances of a rhythm at patients with coronary heart disease and/or dysfunctions of a left ventricle.
Route of administration and doses:
Drug should be accepted only on doctor's orders!
Kordaron's pill is taken inside, before meal and is washed down with enough water.
The load ("sating") dose: various schemes of saturation can be used.
In a hospital: the initial dose divided into several receptions makes from 600 - 800 mg (to the maximum 1200 mg) in days before achievement of a total dose of 10 g (usually within 5-8 days).
On an outpatient basis: the initial dose divided into several receptions makes from 600 to 800 mg a day before achievement of a total dose of 10 g (usually within 10 - 14 days).
Maintenance dose: can vary at different sick from 100 to 400 mg/days. It is necessary to apply a minimal effective dose according to individual therapeutic result.
As Kordaron has very big elimination half-life, it can be accepted every other day or to do breaks in its reception 2 days a week.
Average therapeutic single dose - 200 mg. An average therapeutic daily dose - 400 mg. The maximum single dose - 400 mg. The maximum daily dose - 1200 mg.
Features of use:
As side effects of Amiodaronum are dozo-dependent, it is necessary to carry out treatment of patients by minimal effective doses to minimize a possibility of their emergence.
Patients should be warned about that they during treatment avoided influence of direct sunshine or took protective measures (for example, use of sunblock cream, wearing the corresponding clothes).
Before reception of Amiodaronum it is recommended to conduct research ECG and determination of level of potassium in blood. The hypopotassemia has to be corrected prior to use of Amiodaronum. During treatment it is regularly necessary to control an ECG (each 3 months) both the level of transaminases and other indicators of function of a liver.
Besides because Amiodaronum can cause a hypothyroidism or a hyperthyroidism, especially in patients with diseases of a thyroid gland in the anamnesis, before reception of Amiodaronum it is necessary to conduct clinical and laboratory (TTG) examination regarding identification of dysfunctions and diseases of a thyroid gland. During treatment by Amiodaronum and within several months after its termination it is regularly necessary to inspect the patient regarding identification of clinical or laboratory signs of change of function of a thyroid gland. At suspicion on dysfunction of a thyroid gland it is necessary to carry out determination of the TTG level in blood serum.
Regardless of existence or absence during treatment Amiodaronum of pulmonary symptomatology recommends to conduct each 6 months X-ray inspection of lungs and pulmonary functional trials.
At patients, it is long receiving treatment concerning disturbances of a rhythm it was reported about cases of increase in frequency of fibrillation of ventricles and/or increases in a threshold of operation of a pacemaker or the implanted defibrillator that can reduce their efficiency. Therefore before the beginning or during treatment by Amiodaronum it is necessary to check correctness of functioning of these devices regularly.
Emergence of an asthma or dry cough, as isolated, and accompanied by deterioration in the general state, has to indicate a possibility of pulmonary toxicity,
such as intersticial pneumopathy, suspicion on which development demands carrying out X-ray inspection of easy and pulmonary functional trials.
Owing to lengthening of the period of repolarization of ventricles of heart, pharmacological action of Kordaron vyzyvt certain changes of an ECG: lengthening of an interval of QT, QTc (korregirovanny), is possible emergence of waves of U. No more than 450 ms or no more than at 25% of initial size are admissible increase in an interval of Q-Tc. These changes are not manifestation of toxic effect of drug, however demand control for dose adjustment and assessment of possible proaritmogenny action of Kordaron.
At development of an atrioventricular block of II and III degrees, sinuatrial blockade or dvukhpuchkovy intra ventricular blockade, treatment has to be stopped. At emergence of an atrioventricular block of the I degree it is necessary to double the watch.
Though developing of arrhythmia or weighting of the available disturbances of a rhythm, proaritmogenny effect of Amiodaronum was noted weak it is, less, than at the majority of antiarrhytmic drugs, and is usually shown in a combination with some medicines or at disturbances of electrolytic balance.
At indistinct sight or at decrease in visual acuity it is necessary to conduct ophthalmologic examination, including survey of an eyeground. At development of neuropathy or optic neuritis, caused by Amiodaronum, drug needs to be cancelled because of danger of development of a blindness.
As Kordaron contains iodine, its reception can distort results of a radio isotope research of a thyroid gland, however the maintenance of T3, T4 and TTG in a blood plasma does not influence reliability of definition.
Before surgical intervention it is necessary to inform the anesthesiologist of what the patient receives Kordaron.
Long treatment by Kordaron can strengthen the hemodynamic risk inherent in local or general anesthesia. In particular it belongs to its bradikardichesky and hypotensive effects, decrease in cordial emission and disturbances of conductivity.
Besides, at the patients receiving Kordaron in rare instances directly after surgical intervention noted an acute respiratory distress a syndrome. At artificial ventilation of the lungs by such patient careful control is required.
Influence on ability to driving and other mechanisms
During treatment by Kordaron it is necessary to refrain from driving of the car and occupations potentially dangerous types of activity demanding the increased concentration of attention and speed of psychomotor reactions.
Frequency of side effects was determined as follows: very often (> 10%), it is frequent (> 1%, <10); infrequently (> 0,1%, <1%); seldom (> 0,01%, <0,1%) and it is very rare, including separate messages (<0,01%), frequency is not known (according to the available data frequency cannot be determined).
From cardiovascular system
- Moderate bradycardia which expressiveness depends on a drug dose. Infrequently
- Conductivity disturbances (sinuatrial blockade, atrioventricular block of various degrees).
- Aritmogenny action (there are messages on developing of the new arrhythmias, or aggravation existing in certain cases - with the subsequent cardiac standstill). In the light of the available data it is impossible to define whether it is caused by drug use, or it is connected with weight of damage of heart, or is a consequence of inefficiency of treatment. These effects are observed generally in cases of use of Kordaron together with the medicines extending the period of repolarization of ventricles of heart (QTc interval) or at disturbances of electrolytic balance (see. "Interaction with other medicines"). Very seldom
- The expressed bradycardia or, in exceptional cases, a stop of a sinus node which were noted at some patients (patients with dysfunction of a sinus node and patients of advanced age).
Frequency is not known
- Progressing of chronic heart failure (at prolonged use).
From the alimentary system
- Nausea, vomiting, a loss of appetite, obtusion or loss of flavoring feelings, heavy feeling in epigastriums, especially in an initiation of treatment; the doses passing after reduction.
- The isolated increase in activity of transaminases in blood serum, usually moderate (1,5-3 multiple exceeding of normal values) and decreasing at reduction of a dose or is even spontaneous.
- Acute damage of a liver with increase in transaminases and/or jaundice, including development of a liver failure, sometimes fatal (see. Special instructions).
- Chronic diseases of a liver (pseudo-alcoholic hepatitis, cirrhosis) sometimes fatal. Even at the moderate increase in activity of transaminases in blood which is observed after the treatment continuing over 6 months it is necessary to suspect chronic damage of a liver.
From respiratory system
- It was reported about the cases of development of an intersticial or alveolar pneumonitis and an obliterating bronchiolitis with pneumonia which sometimes are coming to an end with a lethal outcome. Several cases of pleurisy are noted. These changes can lead to development of pulmonary fibrosis, however they are generally reversible at early cancellation of Amiodaronum with purpose of corticosteroids or without from appointment. Clinical manifestations usually disappear within 3-4 weeks. Recovery of a X-ray pattern and function of lungs happens more slowly (several months). Emergence in the patient receiving Amiodaronum, the expressed asthma or dry cough, both followed, and not followed by deterioration in the general state (increased fatigue, decrease in body weight, fervescence) demands carrying out a X-ray analysis of a thorax and, if necessary, drug withdrawal.
- A bronchospasm at patients with heavy respiratory insufficiency, especially at patients with bronchial asthma.
- An acute respiratory distress a syndrome, sometimes with a lethal outcome and sometimes directly after surgical interventions (the possibility of interaction with high doses of oxygen is supposed) (see. "Special instructions").
Frequency is not known
- Pulmonary bleeding
From sense bodys
- The microdeposits in a cornea epithelium consisting of difficult lipids including lipofuscin, they are usually limited to area of a pupil and do not demand the termination of treatment and disappear after drug withdrawal. They can sometimes cause vision disorders in the form of emergence of a color aura or an illegibility of contours at bright lighting.
- Several cases of neuritis of a visual nerve / visual neuropathy were described. Their connection with Amiodaronum is so far not established. However, as the optic neuritis can lead to a blindness, at emergence of an illegibility of sight or decrease in visual acuity against the background of Kordaron's reception, it is recommended to conduct full ophthalmologic examination, including a fundoskopiya, and in case of detection of an optic neuritis to stop reception of Amiodaronum.
- A hypothyroidism with its classical manifestations: increase in body weight, a chill, the apathy reduced by activity, drowsiness bradycardia, excessive in comparison with the expected action of Amiodaronum. The diagnosis is confirmed by identification of the increased level of thyritropic hormone (TTG) of blood serum. Normalization of function of a thyroid gland is usually observed within 1-3 months after the treatment termination. In the situations connected with danger to life treatment by Amiodaronum can be continued, with simultaneous additional purpose of L-thyroxine under control of the TTG level in blood sera.
- A hyperthyroidism which emergence is possible during treatment and after it (cases of the hyperthyroidism which developed in several months after cancellation of Amiodaronum were described). The hyperthyroidism proceeds is more reserved with a small amount of symptoms: insignificant inexplicable loss of body weight, reduction of antiarrhytmic and/or anti-anginal efficiency; mental disorders at patients of advanced age or even the phenomenon of a thyrotoxicosis. The diagnosis is confirmed by identification of the TTG reduced level of blood serum (supersensitive criterion). At identification of a hyperthyroidism Amiodaronum has to be cancelled. Normalization of function of a thyroid gland usually happens within several months after drug withdrawal. At the same time the clinical symptomatology is normalized earlier (in 3-4 weeks), than there is a normalization of level of hormones of a thyroid gland. Hard cases can lead to a lethal outcome therefore in such cases urgent medical intervention is required. Treatment in each separate case is selected individually. If the condition of the patient worsens, both because of the thyrotoxicosis, and in connection with a dangerous imbalance between the need of a myocardium for oxygen and its delivery, it is recommended to begin immediately treatment with corticosteroids (1 mg/kg), continuing it long enough (3 months), instead of use of synthetic anti-thyroid drugs which can not always be effective in this case.
- Syndrome of disturbance of secretion of antidiuretic hormone.
- Photosensitization. Often
- In case of long use of drug in high daily doses the grayish or bluish xanthopathy can be observed; after the treatment termination this pigmentation slowly disappears.
- During radiation therapy erythema cases can meet, there are messages on the skin rash, usually low-specific, separate cases of exfoliative dermatitis (connection with drug is not established).
From the central nervous system
- Tremor or other extrapyramidal symptoms.
- Sleep disorders, including, dreadful dreams. Seldom
- Sensomotor, motor and mixed peripheral neuropathy and/or a myopathy, usually reversible after drug withdrawal.
- Cerebellar ataxy, benign intracranial hypertensia (brain pseudoneoplasm), headache.
- A vasculitis, an epididymite, several cases of impotence (connection with drug is not established), thrombocytopenia, hemolitic anemia, aplastic anemia.
Interaction with other medicines:
- With the drugs capable to cause polymorphic ventricular tachycardia like "pirouette" (torsade de pointes) (at their combination to Amiodaronum the risk of development of potentially lethal ventricular tachycardia like "pirouette" increases):
- antiarrhytmic means: 1A of a class (quinidine, hydroquinidine, Disopyramidum, procaineamide), III class (дофетилид, ибутилид, bretylium tosylate), соталол;
- other (not antiarrhytmic) drugs, such as bepridit; Vincaminum; some neuroleptics: fenotiazina (Chlorpromazinum, циамемазин, levomepromazinum, thioridazine, трифлуоперазин, Fluphenazin), benzamides (амисульприд, сультоприд, сульприд, тиаприд, вералиприд), phenyl propyl ketones (Droperidolum, haloperidol), сертиндол, Pimozidum; tricyclic antidepressants; цизаприд; makrolidny antibiotics (erythromycin at intravenous administration, Spheromycinum); azoles; protivomyalyariyny means (quinine, chloroquine, мефлохин, галофантрин, лумефантрин); pentamidine at parenteral administration; difemanit methyl sulfate; мизоластин; астемизол; терфенадин; ftorkhinolona (in particular moxifloxacin).
Not recommended combinations
- With beta adrenoblockers, with the blockers of "slow" calcium channels which are slowing down ChSS (verapamil, diltiazem) as there is a risk of development of disturbances of automatism (the expressed bradycardia) and conductivity.
- With the laxatives stimulating an intestines peristaltics which can cause a hypopotassemia which increases risk of development of ventricular tachycardia like "pirouette". At a combination to Amiodaronum it is necessary to use laxatives of other groups.
The combinations demanding care at use
- With the drugs capable to cause a hypopotassemia:
- the diuretics causing a hypopotassemia (in monotherapy or a combination);
- Amphotericinum In (in/in);
- system glucocorticosteroids;
Increase in risk of development of ventricular disturbances of a rhythm, in particular ventricular tachycardia like "pirouette" (the hypopotassemia is the contributing factor). Control of the level of electrolytes in blood if necessary correction of a hypopotassemia and constant clinical and electrocardiographic observation of the patient is necessary. In case of development of ventricular tachycardia like "pirouette" it is not necessary to apply antiarrhytmic means (ventricular cardiostimulation, perhaps intravenous administration of salts of magnesium has to be begun).
- With procaineamide (see. "interaction. Contraindicated combinations"
Amiodaronum can increase plasma concentration of procaineamide and its metabolite of N-atsetilprokainamida that can increase risk of development of side effects of procaineamide.
- With anticoagulants of indirect action
Amiodaronum increases concentration of warfarin at the expense of inhibition of P450 2C9 cytochrome. At a warfarin combination with Amiodaronum strengthening of effects of indirect anticoagulant is possible that increases risk of development of bleedings. The thicket should control a prothrombin time (MNO) and to carry out correction of doses of anticoagulant both during treatment by Amiodaronum, and after its cancellation.
- With cardiac glycosides (foxglove drugs)
Possibility of disturbances of automatism (the expressed bradycardia) and atrioventricular conductivity. Besides, at a digoxin combination with Amiodaronum increase in concentration of digoxin in a blood plasma is possible (because of decrease in its clearance). Therefore at a digoxin combination to Amiodaronum it is necessary to define concentration of digoxin in blood and to control possible clinical and electrocardiographic displays of digitalis intoxication. Decrease in doses of digoxin can be required.
- With esmololy
Disturbances of contractility, automatism and conductivity (suppression of compensatory reactions of a sympathetic nervous system). Carrying out clinical and ECG control is required.
- With Phenytoinum (and, on extrapolation, with fosfenitoiny)
Amiodaronum can increase plasma concentration of Phenytoinum at the expense of inhibition of P450 2C9 cytochrome therefore at Phenytoinum combination to Amiodaronum development of overdose of Phenytoinum is possible that can lead to emergence of neurologic symptoms; clinical monitoring is necessary and, at the first signs of overdose, Phenytoinum dose decline, definition of concentration of Phenytoinum in a blood plasma is desirable.
- With flekainidy
Amiodaronum increases plasma concentration of a flekainid at the expense of inhibition of CYP 2D6 cytochrome. In this connection correction of doses of a flekainid is required.
- With the drugs which are metabolized by means of P450 3A4 cytochrome
At a combination of Amiodaronum, CYP 3A4 inhibitor, to these drugs increase in their plasma concentration is possible that can lead to increase in their toxicity and/or strengthening of pharmakodinamichesky effects and can demand decrease in their doses. Such drugs are listed below.
The increase in level of cyclosporine in a blood plasma connected with decrease in metabolism of drug in a liver that can increase nephrotoxic effect of cyclosporine is possible. Definition of concentration of cyclosporine in blood, control of function of kidneys and correction of the mode of dosing of cyclosporine during treatment by Amiodaronum and after drug withdrawal is necessary.
The combination with Amiodaronum can increase pharmakodinamichesky effects of fentanyl and increase risk of development of its toxic effects.
- Other drugs which are metabolized by means of CYP 3A4: lidocaine (risk of development of a sinus bradycardia and neurologic symptoms), такролимус (risk of nephrotoxicity), sildenafit (risk of increase in its side effects), midazolam (risk of development of psychomotor effects), to triazoles, dihydroergotamine, ergotamine, симвастатин and other statines which are metabolized by means of CYP 3A4 (increase in risk of muscular toxicity, a rabdomioliz in this connection the dose of a simvastatin should not exceed 20 mg a day, at its inefficiency should be passed to reception of other statine which is not metabolized by means of CYP 3A4).
- With orlistaty
Risk of decrease in concentration of Amiodaronum and its active metabolite in a blood plasma. ECG control is necessary clinical and, if necessary.
- With a clonidine, guanfatsiny, cholinesterase inhibitors (donepezil, Galantaminum, rivastigminy, takriny, an ambenoniya chloride, pyridostigmine bromide, a neostigmina bromide), Pilocarpinum
Risk of development of excessive bradycardia (cumulative effects).
- With Cimetidinum, grapefruit juice
Delay of metabolism of Amiodaronum and increase in its plasma concentration, is possible increase in pharmakodinamichesky and side effects of Amiodaronum.
- With drugs for an inhalation anesthesia
It was reported about a possibility of development of the following heavy complications in the patients receiving Amiodaronum when receiving the general anesthesia by them: bradycardia (resistant to administration of atropine), arterial hypotension, disturbances of conductivity, decrease in cordial emission.
Very exceptional cases of heavy complications from respiratory system were observed (an acute respiratory distress a syndrome of adults), sometimes fatal which developed directly after surgical intervention which emergence contacts high concentration of oxygen.
- With a radioiodine
Amiodaronum contains iodine in the structure and therefore can break absorption of a radioiodine that can distort results of a radio isotope research of a thyroid gland.
- With rifampicin
Rifampicin is the powerful inductor CYP3A4, at combined use with Amiodaronum it can reduce plasma concentration of Amiodaronum and dezetilamiodaron.
- With St. John's Wort drugs
The St. John's Wort is the powerful inductor SUR3A4. In this regard decrease in plasma concentration of Amiodaronum and reduction of its effect is theoretically possible (clinical data are absent).
- With HIV protease inhibitors (including индинавир)
Inhibitors of HIV protease are SUR3A4 inhibitors. At simultaneous use with Amiodaronum can increase concentration of Amiodaronum in blood.
- With klopidogrely,
Klopidogrel, being the inactive tiyenopirimidinovy drug which is metabolized in a liver with formation of active metabolites. Interaction between klopidogrely and Amiodaronum which can lead to decrease in efficiency of a klopidogrel is possible.
- With dextromethorphan
Dextromethorphan is SUR2B6 and CYP3A4 substrate. Amiodaronum inhibits SUR2B6 and can theoretically increase plasma concentration of a dektrometorfan.
- Hypersensitivity to iodine, Amiodaronum or excipients of drug.
- A sick sinus syndrome (a sinus bradycardia, sinuatrial blockade), except for cases of their correction by an artificial pacemaker (danger of "stop" of a sinus node).
- An atrioventricular block of the II-III degree, two - and trekhpuchkovy blockade in the absence of an artificial pacemaker (pacemaker).
- Hypopotassemia, hypomagnesiemia
- A combination to the drugs capable to extend an interval of QT and to cause development of Bouveret's diseases, including polymorphic ventricular tachycardia like "pirouette" (torsade de pointes) (see. "Interaction with other medicines"):
- antiarrhytmic means: 1A of a class (quinidine, hydroquinidine, Disopyramidum procaineamide); antiarrhytmic means of the III class (дофетилид, ибутилид, bretylium tosylate); соталол;
- other (not antiarrhytmic) drugs, such as bepridit; Vincaminum; some neuroleptics: fenotiazina (Chlorpromazinum, циамемазин, levomepromazinum, thioridazine, трифлуоперазин, Fluphenazin), benzamides (амисульприд, сультоприд, сульприд, тиаприд, вералиприд), phenyl propyl ketones (Droperidolum, haloperidol), сертиндол, Pimozidum; цизаприд; tricyclic antidepressants; makrolidny antibiotics (in particular erythromycin at intravenous administration, Spheromycinum); azoles; antimalarial means (quinine, chloroquine, мефлохин, галофантрин); pentamidine at parenteral administration; difemanit methyl sulfate; мизоластин; астемизол, терфенадин; ftorkhinolona.
- The inborn or acquired lengthening of an interval of QT.
- Dysfunction of a thyroid gland (hypothyroidism, hyperthyroidism).
- Intersticial pulmonary disease.
- Pregnancy (see. "Pregnancy and period of a lactation").
- The lactation period (see. "Pregnancy and period of a lactation").
- Age up to 18 years (efficiency and safety are not established).
With care to apply at dekompensirovanny or heavy chronic (the III-IV FC on NYHA classification) heart failure, a liver failure, bronchial asthma, heavy respiratory insufficiency, at patients of advanced age (high risk of development of the expressed bradycardia), at an atrioventricular block of the I degree.
Pregnancy and period of a lactation Pregnancy
Clinical information available now is insufficient for definition of an opportunity or impossibility of developing of malformations at an embryo at use of Amiodaronum in the first trimester of pregnancy.
As the thyroid gland of a fruit begins to connect iodine only from 14th week of pregnancy (amenorrhea), influence of Amiodaronum on it in case of its earlier use is not expected. Excess of iodine at use of drug after this period can lead to emergence of laboratory symptoms of a hypothyroidism in the newborn or even to formation at it clinically significant craw.
In view of impact of drug on a thyroid gland of a fruit, Amiodaronum it is contraindicated during pregnancy, except for special cases when the expected advantage exceeds risks (at zhizneugrozhayushchy ventricular disturbances of a heart rhythm).
Amiodaronum is allocated in breast milk in significant amounts therefore it is contraindicated during feeding by a breast (therefore during this period drug it is necessary to cancel or stop breastfeeding).
At oral administration of very high doses several cases of a sinus bradycardia, a cardiac standstill, attacks of ventricular tachycardia, a Bouveret's disease like "pirouette" and damages of a liver are described. Delay of atrioventricular conductivity, strengthening of already being available heart failure is possible.
Treatment has to be symptomatic (the gastric lavage, purpose of absorbent carbon (if drug is accepted recently), in other cases carry out symptomatic therapy: at bradycardia - beta адреностимуляторы or installation of a pacemaker, at tachycardia like "pirouette" - in/in administration of salts of magnesium or cardiostimulation. Neither Amiodaronum, nor its metabolites are removed at a hemodialysis. There is no specific antidote.
To store at a temperature not above 30 °C. To store in the place, unavailable to children. List B.
Period of validity 3 years. Not to use drug after the period of validity specified on packaging.
According to the recipe
Tablets of 200 mg.
On 10 tablets in the PVC/ave blister. On 3 blisters together with the application instruction in a cardboard pack.