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Cordarone 200 mg (30 tablets) Affairs.

$17.40

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Description

The instruction for medical use of Kordaron Torgovoye medicine a name Kordaron Mezhdunarodnoye the unlicensed name Amiodaronum Dosage Form of the Tablet divisible 200 mg Structure One tablet contains active agent – Amiodaronum a hydrochloride of 200 mg, excipients: lactoses monohydrate, starch corn, K90F povidone, silicon dioxide anhydrous colloidal, magnesium stearate. The description Round tablets from white till slightly cream color, with a notch for a break and an engraving in the form of a symbol of heart and 200 on one party of a tablet Pharmacotherapeutic group Drugs for treatment of diseases of a cardiovascular system. Drugs for treatment of heart diseases. Antiarrhytmic drugs I and III of classes. Antiarrhytmic drugs III of a class. Amiodaronum. ATX C01BD01 code. The pharmacological Pharmacokinetics Amiodaronum properties it is slowly soaked up, has big affinity to various fabrics. The oral bioavailability varies ranging from 30% up to 80% at different patients (average value about 50%). After reception of a single dose the peak concentration in plasma are reached in 3-7 hours. Therapeutic effects, on average, are observed in a week after the beginning of administration of drug (from several days to two weeks). Amiodaronum possesses long elimination half-life, taking into account individual distinctions at patients (from 20 to 100 days). During the first days of treatment, medicine collects in the majority of tissues of body, especially in fatty tissue. Elimination begins in several days and steady concentration in plasma are reached within several months, depending on individual reaction of the patient. These characteristics explain use of the saturating doses for the purpose of achievement of accumulation of drug in fabrics that is necessary for obtaining therapeutic effect. A part of the iodine which is contained in drug is released and found in urine in the form of iodide, it corresponds to 6 mg on each 200 mg of a dose of Amiodaronum a day. The rest of drug, and, therefore, and the most part of iodine, is removed with a stake after passing through a liver. As renal discharge of Amiodaronum is insignificant, patients with a renal failure can appoint usual doses. After drug withdrawal its removal from an organism continues within several months, it is necessary to take into account residual effect of drug during the period over 10 days and up to 1 month. Amiodaronum is generally metabolized by CYPP4503A4 cytochrome and also CYP2C8 cytochrome. Amiodaronum and its metabolite dezetilamiodaron are potentsilny in vitro inhibitors of CYP1A1, CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4, CYP2A6, CYP2B6 and CYP2C8 cytochromes. And dezetilamiodaron transport proteins such as P-glycoprotein and protein conveyor of organic cations 2 (OCT2) can also inhibit Amiodaronum. One research showed increase in concentration of creatinine by 1.1% (substrate of protein conveyor (OCT2).). These in vivo describes interaction between Amiodaronum and CYP3A4, CYP2C9, CYP2D6 and substrates of a P-glycoprotein. The pharmacodynamics Antiarrhytmic activity of drug is provided by means of the following mechanisms of action: – extends the 3rd phase of potential of activity of a cardiac muscle that is expressed, generally in decrease in potassium current (the III class on classification of Vaughan Williams), – reduces sinus automatism to the bradycardia which is not responding to influence with atropine – it is noncompetitive the alpha and beta and adrenergic activity suppresses, – slows down sinuatrial conductivity, conductivity in auricles and a node, in particular at the accelerated heart rhythm, – does not affect intra ventricular conductivity, – increases the refractory period and reduces atrial, atrioventricular and ventricular excitability of a myocardium, – slows down conductivity and extends the refractory period of additional atrioventricular ways. Other properties – the peripheric resistance and a warm rhythm moderately reduces that leads to decrease in consumption of oxygen, – increases coronary emission by direct impact on smooth muscles of arteries of a myocardium and supports warm emission by pressure decrease and peripheric resistance, without negative inotropic effect. Meta-analysis of thirteen controlled randomized prospective studies with participation of 6,553 patients with a recent myocardial infarction (78%) or chronic heart failure (22%) was carried out. The average period of the subsequent observation of patients varied from 0.4 to 2.5 years. The daily maintenance dose averaged from 200 to 400 mg. Reliable decrease in the general mortality by 13% in favor of Amiodaronum (DI95 of % 0.78 – 0.99, p = 0.030) and an indicator of arrhythmic death for 29% was proved (DI95 of % 0.59 – 0.85, p = 0.0003). However, these results need to be interpreted with care, in view of the heterogeneity of the researches included in the analysis connected, mainly, with the chosen population, duration of the period of the subsequent observation, methodology and results of researches. Percentage of the cancelled treatment was higher in group of Amiodaronum (41%), than in group of placebo (27%). At 7% of the patients accepting Amiodaronum the hypothyroidism in comparison with 1% in group of placebo was revealed. The hyperthyroidism was diagnosed for 1.4% of the patients accepting Amiodaronum in comparison with 0.5% in group of placebo. The interstitial pneumopathy arose at 1.6% of the patients accepting Amiodaronum in comparison with 0.5% in group of placebo. Use at children’s age: At children safety and efficiency of Amiodaronum was not estimated by means of controlled clinical trials. In the published references the metaanalysis of safety of Amiodaronum on 1118 children with various types of arrhythmia was carried out. The following dosages were used in pediatric clinical trials: • load doses: 10-20 mg/kg/days, within 7-10 days (i.e. 500 mg/sq.m/days if the dose is calculated on body surface area) • maintenance dose: the minimal effective dose has to be used, depending on the patient can be in range of 5-10 mg/kg/days, (i.e. 250 mg/sq.m/days if the dose is calculated on body surface area). Indications Prevention of a recurrence: – the ventricular tachycardia posing a threat for life: treatment has to be begun in stationary conditions under careful monitoring the – clinically confirmed, symptomatic and causing disability ventricular arrhythmia the – clinically confirmed, supraventikulyarny tachycardia at the established need of treatment if at intake of other drugs the stability is observed or there are contraindications for their reception – fibrillation of ventricles Treatment of supraventricular tachycardia: delay or reduction of fibrillation or atrial flutter. A route of administration and doses Initial treatment the Usual mode of dosing – 3 tablets a day, within 8-10 days. In certain cases in an initiation of treatment higher doses (4 or 5 tablets a day), but only within a short period of time can be applied and at electrocardiographic control. The supporting treatment Should be defined a minimal effective dose, according to the individual answer, it can be ranging from ½ tablets a day (on 1 tablet every other day) up to 2 tablets a day. Safety and efficiency of use of Amiodaronum at children’s age was not established to children. Side effects Very often (≥10%) – microdeposits in a cornea, are almost always present at adults, and are usually localized in a zone under a pupil and are not a contraindication to treatment continuation. In exceptional cases can be followed by perception of color and dazzle light or misting of sight. Microdeposits in a cornea which are formed by a complex of lipids always disappear after the treatment termination. – photosensitization. Patients are recommended to avoid action of direct sunshine (and UV-radiations in general) during treatment. – in lack of any clinical symptoms of a dysthyroidea the level of the dissociated hormone of a thyroid gland (increase in T4 level at normal or a little reduced T3 level) is not the basis for treatment interruption. – in cases of injury of a liver, these cases were diagnosed on the increased transaminase levels in serum. As a rule, the moderated and isolated increase in level of transaminases (norms are from 1.5 to 3 times higher), decreases after reduction of a dose or is even spontaneous. – gastrointestinal disturbances (the nausea, vomiting, a dysgeusia) which are usually arising during initial treatment and disappearing at a dose decline. Often (≥1%, & lt, 10%) – the lilac or livid xanthopathy arising at the high daily doses appointed to a long span. After treatment cancellation this pigmentation slowly disappears (from 10 to 24 months). – the hypothyroidism has the classical form: increase in body weight, sensitivity by cold, apathy, drowsiness, obvious increase in level of thyroid stimulating hormone is a signal for its diagnostics. Interruption of treatment leads to gradual return to normal function of a thyroid gland within 1-3 months therefore drug withdrawal is not of great importance. If it is offered in indications, treatment by Amiodaronum can be continued in combination with replaceable organotherapy on the basis of L-thyroxine with regulation of dosing depending on levels of thyroid stimulating hormone. The hyperthyroidism misleads more often: with several symptoms (small inexplicable loss of weight, reduction of efficiency of protivostenokardichesky and/or antiarrhytmic means), psychiatric forms at elderly people or even a thyrotoxicosis. Reduction of the levels of thyroid stimulating hormone measured by a supersensitive method confirms the diagnosis. It is important to suspend treatment by Amiodaronum: it is usually enough for initiation of clinical restoration within 3-4 weeks. Serious cases can lead to the death of the patient therefore it is necessary to begin appropriate treatment urgently. If the thyrotoxicosis causes concern or in itself, or in connection with its effects on unstable balance of a myocardium, and efficiency of synthetic anti-thyroid means non-constant, then direct corticosteroid therapy (1 mg/kg) during the sufficient long span (3 months) is recommended. It was reported about hyperthyroidism cases in several months after the treatment termination by Amiodaronum. – a diffusion interstitial or alveolar pneumopathy and an obliterating bronchiolitis with the organized pneumonia, sometimes with a lethal outcome. Appearance of the accruing dispnoe or dry cough – or separately, or in connection with deterioration in the general state (fatigue, loss of weight, a general malaise) demands radiological control and, if necessary, the treatment termination. These types of a pneumopathy can develop in pulmonary fibrosis. The early cancellation of Amiodaronum associated with corticosteroid therapy or untied with it leads to regression of disturbances. Clinical symptoms usually disappear in 3-4 weeks. Radiological and functional improvement usually happens more slowly (several months). It was reported about several cases of pleurisy mainly connected with an interstitial pneumopathy. – the tremor or other extrapyramidal symptoms – sleep disorders, including nightmares – touch, motive or mixed peripheral neuropathy – intense injury of a liver with increase in level of transaminases of blood and/or jaundice, sometimes with a lethal outcome, demanding the treatment termination – moderate bradycardia depending on a dose not often (≥0.1%, & lt, 1%) – a myopathy – the peripheral motive and touch or mixed neuropathy or a myopathy can arise after several months of treatment, but sometimes in several years. These disturbances are usually reversible at the treatment termination. However recovery can be incomplete, very slow and occur only after several months after the treatment termination. – disturbances of conductivity (sinoauricular block of different degree) it is rare (≥0.01, & lt, 0.1) – a hyponatremia which can indicate SNSADG/SIADH (syndrome of inadequate secretion of antidiuretic hormone) Is very rare (& lt, 0.01%) – optical neuropathy (optical neuritis) with the out-of-focus sight reduced by sight and papillary hypostasis in an eyeground. More or less strong reduction of visual acuity can be an outcome. The interrelation with Amiodaronum is not revealed today. Nevertheless, in case of any other obvious reason it is recommended to stop treatment – an erythema during radiotheraphy – skin rashes, as a rule, not really specific – exfoliative dermatitis, the interrelation with medicine is not accurately established – an alopecia – SNSADG/SIADH (syndrome of inadequate secretion of antidiuretic hormone), in particular at the combined use with drugs which can cause a hyponatremia. – the bronchospasm, especially at patients with asthma is a syndrome of acute respiratory insufficiency, sometimes with a lethal outcome or after operation (the interrelation with high doses is supposed) – a cerebellar ataxy – benign intracranial hypertensia, a headache. Appearance of the isolated headaches demands a research of the reason which is the cornerstone of this disturbance – chronic injury of a liver during long-term treatment Histology corresponds to pseudo-alcoholic hepatitis. The abstract nature of a clinical and biological picture (the non-constant hepatomegalia, increase in level of transaminases of blood is 1.5-5 times higher than norm) is the basis for regular monitoring of function of a liver. The diagnosis of chronic injury of a liver should be considered in a case even of moderate increase in the level of transaminases of blood arising later treatments, lasting more than 6 months. Clinical and biological disturbances usually regress after the treatment termination. It was reported about several cases of an irreversible outcome. – profound bradycardia and seldom refusal of a sinus node (dysfunction of a sinus node, elderly patients). – the epididymite, interrelation with medicine is not established. – a vasculitis – a renal failure with moderate increase in creatinine – thrombocytopenia. Frequency is unknown (it is impossible to estimate on the basis of the available data) – the pulmonary hemorrhages sometimes found in connection with a pneumorrhagia. – Ventricular tachycardia like ‘pirouette’ – Pakreatit / acute pancreatitis – cases of a Quincke’s disease and/or small tortoiseshell – Cases of a granuloma of marrow of Reportirovaniye of the suspected side reactions the reportirovaniye about the suspected undesirable phenomena after medicine registration is important. It allows to continue monitoring of a ratio advantage/risk of medicine. Workers of health care we ask to report about any suspected undesirable phenomena through national reporting system the French National agency on safety of medicines and goods for health (ANSM) and network of the Regional centers of pharmacovigilance via the website: www.ansm.sante.fr. Contraindications – sinus bradycardia and sinuatrial heart block at patients without artificial pacemaker of heart – a sick sinus syndrome at patients without artificial pacemaker of heart (risk of a stop of sinus node) – disturbances of atrioventricular conductivity of high degree at patients without artificial pacemaker of heart – a hyperthyroidism, in connection with the possible aggravation caused by Amiodaronum use – the known hypersensitivity to iodine, Amiodaronum or one of excipients – a 2-y and 3rd trimester of pregnancy – the lactation period – a combination with the following medicines: – which can cause piruetny ventricular tachycardia like torsade de pointes (except, antiparasitic drugs, neuroleptics, and methadone): – antiarrhytmic means of the class Ia (quinidine, hydroquinidine, Disopyramidum) – antiarrhytmic means of class III (sotalol, dofetilid, ibutilid) – other medicines, such, as: compounds of arsenic, bepridit, tsizaprid, difemanit, dolazetron in/in, erythromycin in/in, mizolastin, moxifloxacin, Spheromycinum in/in, toremifen, Vincaminum in/in, to tsitalopra, estsitalopra, domperidon, dronedaron, levofloxacin, mekvitazin, prukat
Read (see. Medicinal interactions). – telaprevir – kobitsistat Medicinal interactions Antiarrhytmic means Many antiarrhytmic means reduce automatism, conductivity and sokratitelny ability of heart. The combined purpose of antiarrhytmic means of different classes demands fixed clinical observation and the ECG of monitoring. The combined use of antiarrhytmic means which cause piruetny ventricular tachycardia (Amiodaronum, Disopyramidum, hinidinovy connections, sotalol, etc.) is contraindicated. The combined use of antiarrhytmic means of one class is not recommended, except exceptional cases, in connection with the increased risk of adverse effects on heart. The combined use of Amiodaronum with the medicines having negative inotropic properties which cause bradycardia and/or slow down atrioventricular conductivity, is problematic and demands clinical and the ECG of monitoring. Medicines which can cause piruetny ventricular tachycardia This severe form of arrhythmia can be near is caused medicines irrespective of whether they are antiaritmika. The hypopotassemia is the contributing factor, as well as bradycardia or the congenital or acquired previous lengthening of QT of an interval. Medicines which can cause piruetny ventricular tachycardia are antiarrhytmic means of the class Ia and III and some neuroleptics. Concerning a dolazerton, erythromycin, Spheromycinum and Vincaminum this interaction happens only for injection forms. Use of two torsadogenny means is contraindicated. However, some drug which are absolutely necessary are not contraindicated, but are not recommended for combined use with other torsadogenny srestvo. Treat them: – methadone – antiparasitic means (galofantrin, lumefantrin, pentamidine) – the Means neuroleptics causing bradycardia a Number of medicines can cause bradycardia, in particular, antiarrhytmic means of the class Ia, beta-blockers, some protivoary means of class III, some antagonists of calcium, foxglove drugs, pilocarpine and antikholinesterazny means. Effect of Amiodaronum on other medicines Amiodaronum and/or its metabolite, dezetilamiodaron, inhibit CYP1A1, CYP1A2, CYP3A4, CYP2C9, CYP2D6 and a P-glycoprotein and can strengthen influence of these substrates. Considering long-term effect of Amiodaronum, these interactions can be observed within several months after the treatment termination. Effect of other medicines on Amiodaronum CYP3A4 Inhibitors and CYP2C8 inhibitors can potentially inhibit Amiodaronum metabolism, and, thus, increase its influence. CYP3A4 inhibitors (for example, grapefruit juice and certain medicines) preferably should not be used during treatment by Amiodaronum. Contraindicated combinations (see. Contraindications) Medicines which are capable to cause piruetny ventricular tachycardia (except antiparasitic means, neuroleptics and methadone, see. Not recommended combinations), – antiarrhytmic means of the class Ia (quinidine, hydroquinidine, Disopyramidum) – antiarrhytmic means of class III (dofetilid, ibutilid, sotalol) – other medicines, such, as: compounds of arsenic, bepridit, tsizaprid, to tsitalopra, estsitalopra, difemanit, dolazetron in/in, domperidon, dronedaron, erythromycin in/in, levofloxacin, mekvitazin, mizolastin, moxifloxacin, prukaloprid, Spheromycinum in/in, toremifen, Vincaminum in / century. The increased risk of developing ventricular arrhythmia, in particular piruetny ventricular tachycardia. Telaprevir Narusheniya of conductivity and automatism of heart with risk of strengthening of bradycardia. Kobitsistat Povysheniye of risk of the side effects caused by Amiodaronum because of reduced metabolism. Not recommended combinations Sofosbuvir Tolko at the patients receiving double therapy daklatazvir/sofosbuvir or ledipazvir/sofosbuvir development of bradycardia, symptomatic or even deadly is possible. If use of these combinations it is impossible to avoid, clinical control and the ECG, especially within the first several weeks of double therapy are necessary. CYP3A4 substrates Amiodaronum is CYP3A4 inhibitor and increases plasma concentration of CYP3A4 substrates, potentially increasing toxicity of these substrates. Povysheniye’s cyclosporine of concentration of cyclosporine in blood because of decrease in metabolism of a liver with risk of emergence of nephrotoxic effects. The analysis of concentration of cyclosporine in blood, monitoring of renal function and correction of a dose of cyclosporine during treatment by Amiodaronum. Injection diltiazem Risk of developing of bradycardia and atrioventricular heart block. If this combination cannot be avoided, an important role will be played by careful clinical observation and constant the ECG monitoring. Fingolimod Usileniye of the effects causing bradycardia with possible lethal result. In particular it belongs to beta-blockers which inhibit adrenergic mechanisms of compensation. Control of clinical indicators and continuous control of the ECG within 24 hours after reception of the first dose is necessary. Injection verapamil Risk of developing of bradycardia and atrioventricular heart block. If this combination cannot be avoided, careful clinical observation and the ECG monitoring is necessary. Antiparasitic means which can cause piruetny ventricular tachycardia (galofantrin, lumefantrin, pentamidine) the Increased risk of developing of ventricular arrhythmia, in particular piruetny ventricular tachycardia. If it is possible, stop one or the other treatments. If this combination cannot be avoided, preliminary control of an interval of QT and the ECG monitoring is necessary. Neuroleptics which are capable to cause piruetny ventricular tachycardia: (amisulprid, Chlorpromazinum, tsiamemazin, Droperidolum, flupentiksol, Fluphenazin, haloperidol, levomepromazinum, Pimozidum, pipamperon, pipotiazin, sertindol, Sulpiridum, sultoprid, tiaprid, zuklopentiksol). The increased risk of developing of ventricular arrhythmia, in particular piruetny ventricular tachycardia. Methadone the Increased risk of developing of ventricular arrhythmia, in particular piruetny ventricular tachycardia. Ftorkhinolona, except a levofloksatsin and a moksifloksatsin (contraindicated combinations): The increased risk of ventricular arrhythmia, especially the pirouette type. The stimulating depletive the Increased risk of developing ventricular arrhythmia, especially the pirouette type (the hypopotassemia is the contributing factor). Before intake of medicine the correction of any hypopotassemia is necessary, to remove the ECG, to carry out clinical control together with electrolyte control. Fidaksomitsin Uvelicheniye of concentration of a fidoksomitsin in blood plasma. The combinations demanding taking measures of precaution when using P-glycoprotein substrates Amiodaron is inhibitor of a P-glycoprotein (P-gp). The combined appointment with P-gp substrates can lead to the increased influence of these substrates. Foxglove medicines the Weakened automatism (excessive bradycardia) and disturbance of atrioventricular conductivity. At use of digoxin the increase in its level in blood connected with decrease in its clearance is noted. The ECG and clinical monitoring and also control of levels of digoxin in blood and correction of a dose of digoxin if necessary. Dabigatran Povyshennye of concentration of a dabigatran in serum with the increased risk of bleeding. Clinical monitoring and correction of a dose of a dabigatran if necessary, without exceeding 150 mg/day. CYP2C9 substrates Amiodaron increases concentration of CYP2C9 substrates in blood plasma, such as antagonists of vitamin K and Phenytoinum. Antagonists of vitamin K the Increased action as antagonist of vitamin K and high risk of bleeding. The thicket should check the international coefficient of normalization (INR). The dosage of agonist of vitamin K has to be corrected during the treatment period by Amiodaronum and within 8 days after the treatment termination. Phenytoinum (and with extrapolation on fosfenitoin) Povysheniye of concentration of Phenytoinum in plasma with overdose symptoms, in particular neurologic symptoms (reduced metabolism of Phenytoinum a liver). Clinical monitoring, control of concentration of Phenytoinum in plasma and, perhaps, correction of a dose). CYP2D6 substrates Flekainid Amiodaron increases concentration of a flekainid in plasma by means of CYP2D6 cytochrome inhibition. The dosage of a flekainid should be corrected. CYP3A4 substrates Amiodaron is CYP3A4 inhibitor and increases concentration of substrates of this cytochrome in plasma that potentially increases toxicity of these substrates. Statines (simvastatin, atorvastatin, lovastatin) the Risk of muscular toxicity (for example, a rhabdomyolysis) increases because of joint prescribing of Amiodaronum as statines break up under the influence of CYP3A4. Use of other statine which is not affected by this interaction is recommended. Other drugs which are metabolized under the influence of CYP3A4 (lidocaine, takrolimus, sildenafit, midazolam, dihydroergotamine, ergotamine, colchicine, to triazoles) Amiodaron is CYP3A4 inhibitor and increases concentration of these molecules in plasma, potentially increasing risk of toxicity of these substances. Lidocaine Risk of increase in concentration of lidocaine in plasma with a possibility of emergence of neurologic and warm undesirable effects in connection with his lowered hepatic metabolism caused by Amiodaronum. Clinical and the ECG monitoring, if necessary control of concentration of lidocaine in plasma. If necessary correction of dosing of lidocaine during treatment by Amiodaronum and after its cancellation. Takrolimus Povysheniye of the level of a takrolimus in blood in connection with inhibition of its metabolite Amiodaronum. Measurement of levels of a takrolimus in blood, monitoring of function of kidneys and correction of a dose of a takrolimus at the combined appointment with Amiodaronum and after Amiodaronum cancellation. Beta-blockers, except a sotalol (contraindicated combination) and an esmolol (the combination demanding taking measures of precaution when using) of Disturbance of conductivity and automatism (oppressed compensatory sympathetic mechanisms). The ECG and clinical monitoring is required. Beta-blockers in heart failure (bisoprolol, karvedilol, metoprolol, nebivolol) Disturbances of automatism and warm conductivity with risk of developing of excessive bradycardia. The increased risk of developing of ventricular arrhythmia, in particular piruetny ventricular tachycardia. Monitoring is necessary regular clinical and the ECG. Esmolol Narusheniya of sokratitelny function, automatism and conductivity of heart (suppression of compensatory sympathetic mechanisms). The ECG and clinical monitoring is required. Oral diltiazem of Risk of developing of bradycardia or atrioventricular heart block, in particular at elderly patients. The ECG and clinical monitoring is required. Oral verapamil of Risk of developing of bradycardia and atrioventricular heart block, in particular at elderly patients. Some macroleads (azithromycin, klaritromitsin, roksitromitsin) Povyshenny risk of ventricular arrhythmia, in particular piruetny ventricular tachycardia. The ECG and clinical monitoring during combined use with Amiodaronum. Gipokaliyemichesky means: gipokaliyemichesky diuretics (in monotherapy or in a combination), Amphotericinum B (in/in a method of administration), glucocorticoids (system way), tetrakozaktid Povyshenny risk of developing of ventricular arrhythmia, in particular piruetny ventricular tachycardia (the hypopotassemia is the contributing factor). It is necessary to carry out correction of a hypopotassemia before administration of the medicine and also it is necessary to carry out the ECG, monitoring of electrolytes of blood and clinical monitoring. The means causing bradycardia Povyshenny risk of ventricular arrhythmia, in particular piruetny ventricular tachycardia. Also the ECG monitoring is required clinical. Orlistat Risk of decrease in concentration of Amiodaronum and its active metabolite in plasma. Monitoring is required clinical and in need of the ECG. Tamsulozin Risk of the adverse effects caused tamsuloziny because of inhibition (delay) of hepatic metabolism. It is necessary to make clinical observation and to correct a dosage of a tamsulozin during the treatment period using inhibitor of enzyme and after completion of use, if necessary. Vorikonazol Povyshenny risk of ventricular arrhythmia, in particular tachycardias like pirouette as metabolism of Amiodaronum can be reduced. It is necessary to make clinical observation and the ECG and, if necessary, to correct Amiodaronum dosage. Combinations which it is necessary to take Risk Pilocarpine of developing of excessive bradycardia (additional effects of the means causing bradycardia) into account. Special indications of Prevention Cardiological diseases – prior to treatment need to be carried out by the ECG – the urezheniye of heart rate can amplify at elderly patients. – the electrocardiogram changes against the background of treatment by Amiodaronum. This change caused by Kordaron consists in lengthening of an interval of QT that reflects repolarization lengthening, it is possible with the advent of U waves, it is sign of therapeutic saturation, but not toxicity. – approach of atrioventricular blockade of the 2nd and 3rd degree, sinuatrial heart block or bifastsikulyarny blockade have to be the basis for the treatment termination. Atrioventricular blockade of the 1st degree has to be the basis for carrying out more fixed monitoring. – it was reported about cases of new arrhythmias or deteriorations in the previous, treated arrhythmia (see. Side effects). – such proaritmogenny effect can arise especially in the presence of factors which promote lengthening of an interval of QT, such as combination with some medicines and a hypopotassemia. Risk of developing of tachycardia like pirouette lower at intake of Amiodaronum in comparison with other antiarrhytmic drugs at patients with the identical level of lengthening of an interval of QT. Impacts on a thyroid gland – the iodine which is contained in medicine influences some tests for function of a thyroid gland (radioiodine binding, the proteinaceous and connected iodine), however, assessment of tests of function of a thyroid gland is still possible (T3, T4, USTSH). – Amiodaronum can cause diseases of a thyroid gland, in particular, in patients with dysfunctions of a thyroid gland in the anamnesis. Prov
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