Instruction for use: Egilok S

Trade name of the drug – Egilok S

Dosage Form: tablets

Active substance:Metoprololum

ATX

C07AB02 Metoprolol

Pharmacotherapeutic group: Beta1-selective blocker [Beta-blockers]

The nosological classification (ICD-10)

G43 Migraine: The pain of migraine; Migraine; hemiplegic migraine; Migraine headache; A migraine attack; Continuous headache; hemicrania

I10 Essential (primary) hypertension: hypertension; Arterial hypertension; Arterial hypertension crisis course; Essential Hypertension; Essential hypertension; Essential hypertension; Essential hypertension; Essential hypertension; Primary hypertension; Arterial hypertension, complications of diabetes; The sudden increase in blood pressure; Hypertensive disorders of blood circulation; hypertensive condition; hypertensive crises; arterial Hypertension; malignant Hypertension; Hypertonic disease; hypertensive crises; accelerated hypertension; malignant hypertension; The aggravation of hypertensive disease; Transient hypertension; Isolated systolic hypertension

I15 Secondary hypertension: Arterial hypertension, complications of diabetes; hypertension; The sudden increase in blood pressure; Hypertensive disorders of blood circulation; hypertensive condition; hypertensive crises; hypertension; arterial Hypertension; malignant Hypertension; hypertensive crises; accelerated hypertension; malignant hypertension; The aggravation of hypertensive disease; Transient hypertension; hypertension; Arterial hypertension; Arterial hypertension crisis course; renovascular hypertension; Hypertension symptomatic; Renal hypertension; Renovascular hypertension; renovascular hypertension; Symptomatic hypertension

I20 Angina [angina]: Heberden disease; Angina pectoris; The attack of angina pectoris; recurrent angina; Spontaneous angina; Stable angina pectoris; Angina rest; Angina progressing; Angina mixed; Angina spontaneous; stable angina; Chronic stable angina; Angina Syndrome X

I21 Acute myocardial infarction: Myocardial infarction in the acute phase; Acute Myocardial Infarction; Myocardial infarction with pathologic Q wave and without; Myocardial infarction complicated by cardiogenic shock; Infarction left ventricular; Transmural myocardial infarction; Myocardial infarction netransmuralny (subendocardial); Netransmuralny myocardial infarction; Subendocardial myocardial infarction; The acute phase of myocardial infarction; Acute myocardial infarction;Sub-acute phase of myocardial infarction; Subacute phase of myocardial infarction; Thrombosis of the coronary arteries (the arteries); Threatened myocardial infarction; Myocardial infarction without Q wave

I25.2 Transferred last myocardial infarction: Cardiac syndrome; Myocardial infarction; post-MI; Rehabilitation after myocardial infarction; Reocclusion of the operated vessel; Angina postinfarctnaya; Status after myocardial infarction; Status after myocardial infarction; myocardial infarction

I47.1 Supraventricular tachycardia: Supraventricular paroxysmal tachycardia; supraventricular tachyarrhythmia; supraventricular tachycardia; Supraventricular arrhythmias; Supraventricular paroxysmal tachycardia; supraventricular tachyarrhythmias; supraventricular tachycardia; Neurogenic sinus tachycardia; orthodromic tachycardia; Paroxysmal supraventricular tachycardia; Paroxysm of supraventricular tachycardia; Paroxysm of supraventricular tachycardia with WPW-syndrome; Paroxysm of atrial tachycardia; Paroxysmal supraventricular tachyarrhythmia; Paroxysmal supraventricular tachycardia; Politopnye atrial tachycardia; Atrial fibrillation; Atrial tachycardia is true; Atrial tachycardia; Atrial tachycardia with AV block; reperfusion arrhythmias; Reflex Bertsolda-Jarisch; Recurrent sustained supraventricular paroxysmal tachycardia; Symptomatic ventricular tachycardia; Sinus tachycardia; Supraventricular paroxysmal tachycardia; supraventricular tachyarrhythmia; supraventricular tachycardia; supraventricular arrhythmia; supraventricular arrhythmias; Tachycardia of AV connections; supraventricular tachycardia; Tachycardia orthodromic; sinus tachycardia; The nodal tachycardia; Chaotic atrial tachycardia politopnye; Wolff-Parkinson-White

I48 Atrial fibrillation and flutter: Permanent atrial tachyarrhythmias; Relief frequent ventricular rate during atrial flutter or blink; atrial fibrillation; Paroxysm of atrial fibrillation and flutter; Paroxysm of atrial fibrillation; Paroxysmal atrial fibrillation; Atrial premature beats; Tahiaritmicheskoy atrial fibrillation; Tahisistolicheskoy atrial fibrillation; auricular flutter; Life-threatening ventricular fibrillation; Atrial fibrillation; Chronic atrial fibrillation; supraventricular arrhythmia; Paroxysmal atrial fibrillation and flutter; Paroxysmal fibrilloflutter; Atrial premature beats

I49.3 Premature ventricular depolarization: Asynergia left ventricle; ventricular Arrhythmia; Pronounced PVCs; fibrillation; ventricular beat; ventricular beat; Ventricular arrhythmias; ventricular beat; Paroxysmal ventricular arrythmia; Recurrent ventricular arrhythmias; ventricular premature beats; Asynergia ventricular

I50.0 Congestive heart failure: anasarca heart; Decompensated congestive heart failure; Congestive heart failure; Congestive heart failure with high afterload; Congestive chronic heart failure; Cardiomyopathy with severe chronic heart failure; Compensated chronic heart failure; Swelling with circulatory failure; Edema of cardiac origin; Swelling of the heart; Edematous syndrome in diseases of the heart; Edematous syndrome in congestive heart failure; Edematous syndrome in heart failure; Edematous syndrome in heart failure or liver cirrhosis; right ventricular failure; Congestive Heart Failure; Heart failure stagnant; Heart failure with low cardiac output; Heart failure is a chronic; Cardiac edema; Chronic decompensated heart failure; Chronic Congestive Heart Failure; Chronic heart failure; Change of liver function in heart failure

I50.1 Left ventricular failure: Asthma heart; Asymptomatic left ventricular dysfunction; Asymptomatic left ventricular heart failure; Diastolic left ventricular dysfunction; Left ventricular dysfunction; Changes in left ventricular myocardial infarction; Left ventricular heart failure; Left ventricular dysfunction; Acute left ventricular failure; Acute cardiac left ventricular failure; cardiac asthma; Left ventricular heart failure; Changes in left ventricular failure with pulmonary; Precordial abnormal pulsation; Insufficiency of the left ventricle

R00.0 Unspecified Tachycardia: Tachycardia

Composition (per tablet): active substance: metoprolol succinate 23.75 mg, 47.5 mg, 95 mg

(Corresponding to 25, 50 and 100 g of metoprolol tartrate)

Other ingredients: MCC PH 101- 73,9 / 147,8 / 295,6 mg; methyl cellulose 15 mPa.s - 11.87 / 23.75 / 47.5 mg; glycerol - 0.24 / 0.48 / 0.95 mg; corn starch - 1.94 / 3.87 / 7.75 mg; ethyl cellulose 100 mPas - 11.43 / 22.85 / 45.7 mg; magnesium stearate - 1.87 / 3.75 / 7.5 mg

sheath film (coating Sepifilm LP 770 White - 3.75 / 7.5 / 15): MCC 20 microns (5-15%) - 0,19-0,56 / 0,38-1,13 / 0.75 2.25 mg hypromellose 5/15 mPa.s (60-70%) - 2,25-2,63 / 4,5-5,25 / 9-10.5 mg stearic acid (8-12%) - 0.3-0.45 / 0.6-0.9 / 1.2-1.8 mg titanium dioxide (E171) (10-20%) - 0,38-0,75 / 0.75 1.5 / 1.5-3 mg

Description

Tablets, 25, 50 and 100 mg: oval biconvex white film-coated with the notch on both sides.

Pharmacological Properties of Egilok S

Pharmachologic effect - antianginal, hypotensive, anti-arrhythmic.

Pharmacodynamics

Metoprolol - beta1-adrenergic blocker, beta1-adrenoceptor blocking at doses significantly lower than the doses required for beta2-adrenergic receptor blocking.

Metoprolol has an insignificant membrane-stabilizing effect and does not exhibit partial agonist activity.

Metoprolol reduces or inhibits the agonistic effect that has on cardiac function catecholamines released during neural and physical stress. This means that metoprolol has the ability to prevent an increase in heart rate, cardiac output and increased cardiac contractility, and increased blood pressure caused by sudden release of catecholamines.

Unlike conventional tablet dosage forms selective beta1-adrenergic blockers (including metoprolol tartrate), when using the drug metoprolol succinate prolonged action observed in the plasma constant concentration of the drug and provided a stable clinical effect (beta1-blockade) for more than 24 hours. Due to the absence Cmax important drug in blood plasma has a higher-beta1 selectivity compared to conventional tablet formulation of metoprolol. Moreover, substantially decreases the potential risk of side-effects observed at the highest concentrations of drug in blood plasma, for example bradycardia and weakness in the legs while walking. Patients with symptoms of obstructive pulmonary diseases can be administered metoprolol succinate sustained-release, if necessary, in combination with beta2- agonists. When combined with beta2-agonists metoprolol succinate sustained-release at therapeutic doses, to a lesser extent, it affects the beta2-agonists induced bronchodilation than non-selective beta-blockers. Metoprolol less than nonselective beta-blockers affect the production of insulin, and carbohydrate metabolism. Effect on CCC in terms of hypoglycemia is much less pronounced as compared to non-selective beta-blockers.

Use of the drug in hypertension causes a significant decrease in blood pressure for more than 24 hours, both lying and standing position, and during exercise. At the beginning of therapy with metoprolol there is an increase in vascular resistance. However, chronic administration may reduce blood pressure due to a decrease in vascular resistance with an unchanged cardiac output.

Pharmacokinetics

Each tablet formulation of metoprolol succinate sustained-release contains a large amount of microgranules (pellets), allowing for controlled release of metoprolol succinate. Outside each microgranule (pellet) is covered by a polymeric sheath, which allows for controlled release of the drug.

Action depot tablet comes quickly. Tablet disintegrates in the gastrointestinal tract to separate micropellets (pellets), which act as independent units and provide uniform controlled release metoprolol (zero order kinetics) for 20 hours. The rate of release of the active substance depends on the acidity of the medium. The duration of therapeutic effect after administration in the dosage form of tablets with prolonged action over 24 hours. T1 / 2 free metoprolol averages 3.5-7 hours.

The drug is completely absorbed after oral administration. Systemic bioavailability after oral administration of a single dose of about 30-40%. Metoprolol undergoes oxidative metabolism in the liver. Three main metabolites of metoprolol showed no clinically significant effect of beta-adrenoceptor blocking. About 5% of the dose for oral administration excreted by the kidneys in unchanged form, the remainder of the drug is excreted as metabolites. Communication with low plasma proteins, approximately 5-10%.

Indications

arterial hypertension;

angina;

stable chronic heart failure (CHF) with the presence of clinical manifestations (II-IV functional class NYHA classification) and a violation of left ventricular systolic function (as adjunct therapy to the main treatment of chronic heart failure);

decrease mortality and the frequency of reinfarction after the acute phase of myocardial infarction;

cardiac arrhythmias, including supraventricular tachycardia, reduction of ventricular rate during atrial fibrillation and ventricular arrhythmias;

functional cardiac abnormalities, accompanied by tachycardia;

prevention of migraine attacks.

Contraindications

Hypersensitivity to metoprolol, other ingredients or other beta-blockers;

atrioventricular block II and III degree, heart failure decompensation, patients receiving long-term or a term therapy with inotropic drugs and drugs acting on the beta-adrenergic receptors, clinically significant sinus bradycardia (heart rate less than 50 bpm. / min), a syndrome sick sinus, cardiogenic shock, severe peripheral circulatory disorders with risk of gangrene, arterial hypotension (Sad less than 90 mm Hg..), pheochromocytoma without simultaneous administration of alpha-blockers;

suspected acute myocardial infarction with heart rate less than 45 bpm. / min, the PQ interval is more than 0.24 with garden less than 100 mm Hg. Article .;

Simultaneous use of MAO inhibitors (except for MAO-B inhibitors);

BCCI type intravenous verapamil;

age of 18 years (effectiveness and safety have been established).

Precautions: atrioventricular block I degree, Prinzmetal angina, asthma, chronic obstructive pulmonary disease, diabetes, severe renal insufficiency, severe hepatic insufficiency, metabolic acidosis, the simultaneous application of cardiac glycosides, myasthenia gravis, pheochromocytoma (while taking alpha-blockers) , hyperthyroidism, depression, psoriasis, obliterating peripheral vascular disease (intermittent claudication, Raynaud's syndrome), advanced age.

Pregnancy and breast-feeding

A well-controlled studies on the use of metoprolol during pregnancy is not carried out, the use of the drug EgilokŪ C in the treatment of pregnant women is possible only if the benefit to the mother outweighs the risk to the embryo / fetus.

As with other antihypertensives, beta-blockers may cause side effects such as bradycardia in the fetus, newborn or a child who is breastfed. The amount of metoprolol, liberated into breast milk, and a beta-adrenoceptor blocking action of a child who is breastfed (while taking metoprolol mother in therapeutic doses), are minor. Despite the fact that children who are breastfed, the appointment of therapeutic doses the risk of side effects is low (with the exception of children with metabolic disorders) should be carefully monitored for the appearance of signs of their blockade of beta-adrenergic receptors.

Side effects

The drug was well tolerated, side effects are generally mild and reversible.

To assess the frequency of cases we used the following criteria: very common (> 10%); often (1-9,9%); rare (0.1-0.9%); rarely (0,01-0,09%) and very rare (<0.01%).

From the CCC: often - bradycardia, orthostatic hypotension (very rarely accompanied by syncope), cold extremities, palpitations; rarely - peripheral edema, pain in the heart, a temporary increase in heart failure symptoms, AV block of I degree; cardiogenic shock in patients with acute myocardial infarction; rarely - other disturbances of cardiac conduction, arrhythmias; very rarely - gangrene in patients with previous severe impairment of the peripheral circulation.

On the part of the central nervous system: very often - fatigue; often - dizziness, headache; rarely - paresthesia, convulsions, depression, weakening of attention, drowsiness or insomnia, nightmares; rarely - increased nervous irritability, anxiety, impotence / sexual dysfunction; very rarely - Amnesia / memory impairment, depression, hallucinations.

On the part of the digestive tract: often - nausea, abdominal pain, diarrhea, constipation; rarely - vomiting; rare - dryness of the oral mucosa.

Liver: rare - impaired liver function; very rarely - hepatitis.

For the skin: rarely - rash (in the form of urticaria), increased sweating; rare - hair loss; very rarely - photosensitivity, exacerbation of psoriasis flow.

From the respiratory system: often - shortness of breath during physical effort; rarely - bronchospasm; rarely - rhinitis.

From the sensory organs: rarely - visual disturbances, dry and / or irritated eyes, conjunctivitis; very rarely - ringing in the ears, impaired sense of taste.

From the musculoskeletal system: very rarely - arthralgia.

On the part of metabolism: rarely - weight gain.

On the part of the blood: very rarely - thrombocytopenia.

Interaction

Metoprolol is a substrate for the isoenzyme CYP2D6, and therefore drugs which inhibit isoenzyme CYP2D6 (quinidine, terbinafine, paroxetine, fluoxetine, sertraline, celecoxib, propafenone and diphenhydramine) may affect the plasma concentration of metoprolol.

Avoid joint use of the drug EgilokŪ With the following drugs

Barbituric acid derivatives: Barbiturates (the study was conducted with pentobarbital) enhance the metabolism of metoprolol as a result of enzyme induction.

Propafenone: the appointment of propafenone to four patients treated with metoprolol, showed an increase in plasma concentrations of metoprolol by 2-5 times, while two patients had side effects that are typical of metoprolol. Probably due to inhibition of the interaction of propafenone, like quinidine, metoprolol metabolism by CYP2D6 isoenzyme of cytochrome P450. Taking into account the fact that propafenone has the properties of a beta blocker, metoprolol, and co-administration of propafenone is not recommended.

Verapamil: The combination of beta-blockers (atenolol, propranolol and pindolol) and verapamil may cause bradycardia and lead to a reduction in blood pressure. Verapamil and beta-blockers are mutually inhibitory effect on AV conduction and sinus node function.

Combination drug EgilokŪ With the following drugs may require dose adjustment

Amiodarone: concomitant use of amiodarone and metoprolol may lead to severe sinus bradycardia. Taking into account the extremely long T1 / 2 of amiodarone (50 days), to consider the possible interaction after a long time after the abolition of amiodarone.

Class I antiarrhythmics: Class I antiarrhythmic drugs and beta-blockers can lead to the summation of negative inotropic effect, which may result in serious haemodynamic side effects in patients with impaired left ventricular function. Also avoid such a combination in patients with sick sinus syndrome and AV conduction disorder.

The interaction is described by the example of disopyramide.

NSAIDs: NSAIDs weaken the antihypertensive effect of beta-blockers. This interaction is documented for indomethacin. Probably, described the interaction will not be celebrated in cooperation with sulindac. Negative interaction has been observed in studies with diclofenac.

Diphenhydramine: Diphenhydramine reduces the metabolism of metoprolol to alpha-gidroksimetoprolola 2.5 times. At the same time strengthening the metoprolol action observed.

Diltiazem: Diltiazem and beta-blockers reinforce inhibitory effect on AV conduction and sinus node function. When combined with metoprolol diltiazem were cases of severe bradycardia.

Epinephrine: reports of 10 cases of severe hypertension and bradycardia in patients treated with non-selective beta-blockers (including pindolol and propranolol) and treated with epinephrine. Interaction observed in the group of healthy volunteers. It is assumed that these reactions can also occur when using epinephrine in conjunction with local anesthetics Accidental contact with the bloodstream. It is expected that this risk is much lower with cardioselective beta-blockers.

Phenylpropanolamine: phenylpropanolamine (norephedrine) in single doses of 50 mg may cause increased Dad to pathological values in healthy volunteers. Propranolol generally prevents the increase in blood pressure caused by phenylpropanolamine. However, beta-blockers can cause paradoxical reaction of hypertension in patients receiving high doses of phenylpropanolamine. A few cases of hypertensive crisis in patients receiving phenylpropanolamine.

Quinidine: Quinidine inhibits the metabolism of metoprolol have a special group of patients with rapid hydroxylation (in Sweden about 90% of the population), mainly causing a significant increase in plasma concentrations of metoprolol and increased beta-adrenoblockade. It is believed that such interaction is typical for other beta-blockers, which participating in the metabolism of CYP2D6 isoenzyme of cytochrome P450.

Clonidine: hypertensive reactions during abrupt cancellation of clonidine may be increased when co-administered beta-blockers. In a joint application, in the case of clonidine, discontinuation of beta-blockers should start several days before clonidine.

Rifampicin: rifampicin may enhance the metabolism of metoprolol by reducing the plasma concentration of metoprolol.

Patients simultaneously receiving metoprolol and other beta-blockers (in the dosage form of eye drops) or MAO inhibitors should be kept under close supervision. While taking beta-blockers inhalation anesthetics enhance cardiodepressive action. While taking beta-blockers to patients receiving hypoglycemic agents for oral administration,

Dosage and Administration

Inside. EgilokŪ designed for the daily administration once a day, it is recommended to take the drug in the morning. The tablet should be swallowed EgilokŪ C, with some liquid. The tablets (or tablets, divided in half) should not chew or crumble. Food does not affect the bioavailability. In the selection of the dose necessary to avoid the development of bradycardia.

Hypertension: 50-100 mg once daily. If necessary, the dose may be increased to 200 mg per day, or add another antihypertensive, a diuretic and BCCI preferable. The maximum daily dose in hypertension - 200 mg / day.

Angina pectoris: 100-200 mg EgilokŪ With once daily. other antianginal drug could be added if necessary to the therapy.

Stable chronic heart failure with the presence of clinical manifestations and impaired left ventricular systolic function. Patients should be on a stable chronic heart failure without acute stage of episodes during the past 6 weeks and no change in the basic therapy during the past 2 weeks.

CHF therapy beta-blockers may sometimes cause a temporary worsening of heart failure flow. In some cases continued therapy or dose reduction, in some cases you may need discontinuation of the drug.

Stable heart failure, II functional class. The recommended initial dose of the drug EgilokŪ With the first 2 weeks - 25 mg once daily. After 2 weeks of treatment dose can be increased to 50 mg once daily and further to double every 2 weeks.

The maintenance dose for long-term treatment - 200 mg of the drug EgilokŪ With once daily.

Stable heart failure, III-IV functional class. The recommended starting dose of the first two weeks - 12.5 mg EgilokŪ C (2.1 Table 25 mg.) Once a day. The dose is adjusted individually. During the period of increasing the dose the patient should be monitored, because some patients with CHF symptoms can progress.

After 1-2 weeks the dose may be increased to 25 mg drug EgilokŪ C once daily. Then, after two weeks, the dose may be increased to 50 mg once a day. Patients who tolerate the drug, it is possible to double the dose every 2 weeks up to a maximum dose of 200 mg drug EgilokŪ C once daily. In the case of arterial hypotension and / or bradycardia may need correction of dose primary therapy or reduction in dose EgilokŪ C. Arterial hypotension at the beginning of therapy does not necessarily indicate that the dose of the drug EgilokŪ C will not be carried on further long-term treatment. However, increasing the dose only possible after stabilization of the patient. You may need to monitor renal function.

Cardiac arrhythmias: 100-200 mg once daily.

Maintenance treatment after myocardial infarction. The target dose - 100-200 mg / day, in one (or two) reception.

Functional disorders of cardiac activity, accompanied by palpitations 100 mg once a day. If necessary, the dose may be increased to 200 mg per day.

Prophylaxis of migraine: 100-200 mg once a day.

Impaired renal function. There is no need to adjust the dose in patients with impaired renal function.

Abnormal liver function. Typically, due to the low degree of correlation with plasma proteins correction dose is not required. However, in severe hepatic impairment (patients with severe liver cirrhosis or portocaval anastomosis) may require dose reduction.

Elderly age. There is no need to adjust the dose in elderly patients.

Overdose

Symptoms: an overdose of metoprolol most serious are the symptoms of the cardiovascular system, but sometimes, especially in children and adolescents, may predominate symptoms of the central nervous system and the suppression of lung function, bradycardia, AV block I-III degree, asystole, marked reduction in blood pressure, poor peripheral perfusion, cardiac failure, cardiogenic shock; inhibition of lung function, sleep apnea, as well as fatigue, altered mental status, loss of consciousness, tremors, convulsions, sweating, paresthesia, bronchospasm, nausea, vomiting, possible oesophageal spasm, hypoglycaemia (especially in children), or hyperglycemia, hyperkalemia; impairment of renal function; transient myasthenic syndrome; concomitant use of alcohol, antihypertensives, quinidine or barbiturates may aggravate the patient's condition. The first signs of overdose can be observed after 20 min - 2 h after dosing.

Treatment: The purpose of the activated carbon, if necessary - gastric lavage.

Atropine (0.25-0.5 mg / in adults, 10-20 mg / kg for children) must be assigned to gastric lavage (the risk of stimulation of the vagus nerve). If necessary, maintain the airway (intubation) and adequate ventilation. Restores BCC and glucose infusion. ECG monitoring. Atropine 1.2 mg / in repeated administration (particularly in the case of vagal symptoms) as needed. In the case of (suppression), depression of the myocardium shown infusion dobutamine or dopamine. Glucagon can also be used 50-150 mg / kg / in intervals of 1 min. In some cases, it may be effective to add to the treatment of epinephrine (adrenaline). When extensive fibrillation and ventricular (QRS) complex is administered by infusion of 0.9% sodium chloride or sodium bicarbonate. The possibility of setting an artificial pacemaker. During cardiac arrest due to overdose may require resuscitation for several hours. terbutaline can be used for the relief of bronchospasm (by injection or via inhalation). Symptomatic treatment.

special instructions

Patients taking beta-blockers should not be administered in / in BCCI type verapamil.

Patients with obstructive lung disease is not recommended to prescribe beta-blockers. In case of poor tolerability of other antihypertensives or inefficiency metoprolol can be administered as it is a selective drug. It is necessary to assign the minimum effective dose, if necessary, you can assign beta2-agonists.

Not recommended to prescribe non-selective beta-blockers in patients with Prinzmetal angina. This group of patients, selective beta-blockers should be used with caution.

In applying the beta1-adrenergic blockers risk of their influence on carbohydrate metabolism or the ability to mask the symptoms of hypoglycemia is much less than with non-selective beta-blockers.

In patients with heart failure in a decompensation stage is necessary to achieve the stage of compensation, both before and during treatment with EgilokŪ S.

Very rarely patients with AV conduction disorders deterioration may occur (possible outcome - AV block). If during treatment developed bradycardia, the dose of the drug EgilokŪ C must be reduced or the drug should be phased out.

Metoprolol may aggravate the symptoms of peripheral circulatory disorders are mainly due to a decrease in blood pressure.

Caution should be exercised when administered to patients of the drug with severe renal insufficiency, metabolic acidosis, concomitant use with cardiac glycosides.

Patients taking beta-blockers, anaphylactic shock occurs in more severe. Adrenaline in therapeutic doses do not always achieve the desired results in a clinical benefit in patients receiving metoprolol. In patients with pheochromocytoma, in parallel with the preparation EgilokŪ C should be given an alpha-blocker.

In the case of surgery should inform the anesthetist that the patient is taking EgilokŪ C patients undergoing surgery, discontinue treatment for beta-blockers is not recommended.

Data from clinical studies for efficacy and safety in patients with severe stable heart failure patients (IV class NYHA classification) are limited.

Patients with symptoms of heart failure in combination with acute myocardial infarction and unstable angina were excluded from the study, which were determined on the basis of the indications. The efficacy and safety of the preparation is not described for this group of patients. Application for heart failure decompensation contraindicated.

Abrupt withdrawal of beta-blocker can lead to increased heart failure symptoms and an increased risk of myocardial infarction and sudden death, especially in high-risk patients, and therefore should be avoided. If necessary, drug withdrawal should be carried out gradually, over at least two weeks, with a twofold reduction of the dose in each stage to achieve a final dose of 12.5 mg (Table 2.1. 25 mg), which should be at least 4 days to complete withdrawal of the drug. When symptoms recommended a slower withdrawal of the drug regime.

Effects on ability to drive and use machines. Be careful when driving and occupations potentially hazardous activities that require high concentration of attention, because of the risk of dizziness and fatigue when using the drug EgilokŪ S.

Release Form

The long-acting tablets, film-coated, 25 mg, 50 mg, 100 mg. According to Table 10. in a blister made of PVC / PE / PVDC // aluminum foil. 3 or 10 blisters in a carton box.

Manufacturer

INTAS Pharmaceuticals Ltd. - India.

Registration Certificate Holder: CJSC "Pharmaceutical plant EGIS." 1106 Budapest, ul. Keresturi, 30-38, Hungary.

Representative office of JSC "Pharmaceutical plant EGIS" (Hungary) in Moscow. 121108, Moscow, st. Ivan Franko, 8.

Conditions of supply of pharmacies

On prescription.

Storage conditions of Egilok S

The temperature is not above 30 ° C.

Keep out of the reach of children.

Shelf life

3 years.

Do not use beyond the expiration date printed on the package.