Cordinorm: instructions for use, indications, reviews, price and analogues

Pharmacodynamics and pharmacokinetics

Pharmacodynamics

Selective beta1-blocker without endogenous sympathomimetic action and membrane stabilizing properties. By inhibiting β1-adrenergic receptors of the heart , the active substance reduces the catecholamine-stimulated formation of cAMP from normal ATP and reduces the intracellular transport of calcium ions. It has a negative chronotropic, dromotropic, bathmotropic and inotropic effect, slows down AV conduction, inhibits conduction and excitability, reduces the heart's need for oxygen. Reduces heart rate at rest and during exercise. Reduces the effects renin .

With increasing doses, bisoprolol demonstrates a beta2-adrenergic blocking effect.

In the first 24 hours of using the drug, peripheral vascular resistance increases slightly, and after 2-3 days it returns to the original level, and with prolonged use it decreases.

The hypotensive effect of the active component is due to a decrease in the minute amount of blood, a decrease in the function of the renin-angiotensin system , sympathetic activation of peripheral vessels, restoration of feedback when blood pressure decreases and an effect on the brain. For arterial hypertension, the effect occurs after 2-6 days, and a stable effect occurs only after about 2 months.

The antiarrhythmic effect is caused by the elimination of factors that provoke arrhythmia, as well as a decrease in the speed of spread of pacemaker excitation and a slowdown in AV conduction.

The antianginal effect is caused by a decrease in myocardial oxygen demand due to a decrease in heart rate and weakened contractility, improved perfusion of heart tissue, and prolongation of diastole. Due to increased diastolic pressure and stretching of the muscles of both ventricles, the need for oxygen may increase.

When used in therapeutic dosages, in contrast to non-selective beta-blockers, Cordinorm has a less strong effect on target organs (skeletal muscles, uterus, smooth muscles of arteries, pancreas, bronchi) and on carbohydrate metabolism, and does not cause sodium accumulation in the body. The strength of the atherogenic action is the same as that of Propranolol .

When used in large doses, it exhibits a blocking effect on both types of β-adrenergic receptors.

Pharmacokinetics

After taking the drug orally, up to 90% of bisoprolol . Food does not affect absorption. The highest plasma levels occur after 2-3 hours.

Interaction with blood proteins reaches approximately 35%. Permeability through histohematic barriers and the degree of excretion during lactation are low.

Half of the dose taken is transformed in the liver with the production of inactive derivatives.

The half-life is 11-12 hours. Up to 98% of the substance is excreted by the kidneys, another approximately 2% - with bile.

Pharmacodynamics

Selective beta1-blocker without its own sympathomimetic activity. By blocking beta1-adrenergic receptors of the heart in low doses, it reduces the catecholamine-stimulated formation of cAMP from ATP, reduces the intracellular Ca2+ current, has a negative chrono-, dromo-, bathmo- and inotropic effect (reduces heart rate, inhibits conductivity and excitability, reduces myocardial contractility). With increasing dose, it has a beta2-adrenergic blocking effect. OPSS at the beginning of the use of beta-adrenergic blockers, in the first 24 hours, increases (as a result of a reciprocal increase in the activity of alpha-adrenergic receptors and the elimination of stimulation of beta2-adrenergic receptors), which after 1-3 days returns to the original level, and with long-term administration decreases.

The hypotensive effect is associated with a decrease in IOC, sympathetic stimulation of peripheral vessels, a decrease in the activity of the renin-angiotensin system (of greater importance for patients with initial hypersecretion of renin), restoration of the sensitivity of the baroreceptors of the aortic arch (there is no increase in their activity in response to a decrease in blood pressure) and an effect on CNS. In case of arterial hypertension, the effect occurs after 2–5 days, stable effect occurs after 1–2 months. The antianginal effect is due to a decrease in myocardial oxygen demand as a result of a decrease in heart rate and decreased contractility, prolongation of diastole, and improved myocardial perfusion. By increasing the final dBP in the left ventricle and increasing the stretching of the ventricular muscle fibers, it can increase the need for oxygen, especially in patients with chronic heart failure. The antiarrhythmic effect is due to the elimination of arrhythmogenic factors (tachycardia, increased activity of the sympathetic nervous system, increased cAMP content, arterial hypertension), a decrease in the rate of spontaneous excitation of sinus and ectopic pacemakers and a slowdown of AV conduction (mainly in the anterograde and to a lesser extent in the retrograde directions through the AV node) and along additional paths. In contrast to non-selective beta-blockers, when prescribed in average therapeutic doses, it has a less pronounced effect on organs containing beta2-adrenergic receptors (pancreas, skeletal muscles, smooth muscles of peripheral arteries, bronchi and uterus) and on carbohydrate metabolism, does not cause Na + retention in organism; the severity of the atherogenic effect does not differ from the effect of propranolol. When used in large doses, it has a blocking effect on both subtypes of beta-adrenergic receptors.

Contraindications

Collapse.
Acute heart failure.
AV block above 2 degrees without the use of a pacemaker.
Prinzmetal's angina.
Shock.
Raynaud's disease.
Pulmonary edema.
Sinoatrial block.
Metabolic acidosis.
Weakness of the sinus node.
Chronic decompensated heart failure.
Severe bradycardia.
Cardiomegaly without symptoms characteristic of heart failure.
Arterial hypotension.
Joint use of MAO blockers.
Bronchial asthma or obstructive chronic pulmonary disease .
Late stages of peripheral circulatory disorders.
Pheochromocytoma (without the use of alpha-blockers ).
Hypersensitivity to the components of the drug or other beta-blockers.
Age up to 18 years.

It is recommended to use the drug with caution in myasthenia gravis, liver or kidney failure, diabetes mellitus, thyrotoxicosis, 1st degree AV block, psoriasis, depression, and elderly patients.

Overdose

Symptoms: arrhythmia, ventricular extrasystole, severe bradycardia, AV block, decreased blood pressure, chronic heart failure, cyanosis of fingernails or palms, difficulty breathing, bronchospasm, dizziness, fainting, convulsions.

Treatment: gastric lavage and administration of adsorbent drugs; symptomatic therapy: in case of developed AV block - intravenous administration of 1-2 mg of atropine, epinephrine or installation of a temporary pacemaker; for ventricular extrasystole - lidocaine (class Ia drugs are not used); when blood pressure decreases, the patient should be in the Trendelenburg position; if there are no signs of pulmonary edema - intravenous plasma replacement solutions, if ineffective - administration of epinephrine, dopamine, dobutamine (to maintain chronotropic and inotropic effects and eliminate the pronounced decrease in blood pressure); for heart failure - cardiac glycosides, diuretics, glucagon; for convulsions - intravenous diazepam; for bronchospasm - beta2-adrenergic stimulants by inhalation.

Side effects

Disorders from the sensory organs: decreased secretion of tear fluid, blurred vision, soreness and dryness of the eyes, conjunctivitis .
Nervous system disorders: weakness, fatigue, dizziness , nightmares, sleep disorders, headache , depression, myasthenia gravis, confusion, memory loss, anxiety, asthenia , hallucinations , paresthesia, tremor.
Circulatory disorders: palpitations, decreased myocardial contractility, sinus bradycardia, changes in myocardial conductivity, arrhythmias , impaired AV conduction, progression of chronic heart failure, orthostatic hypotension , decreased pressure, manifestation of vasospasm, chest pain.
Respiratory disorders: respiratory distress, nasal congestion, laryngospasm or bronchospasm.
Digestive disorders: dry mouth, abdominal pain, vomiting, constipation or diarrhea , changes in taste, nausea, changes in liver function, changes in enzymes , triglycerides , bilirubin levels.
Hormonal disorders: hypoglycemia, hyperglycemia, hypothyroid state.
Dermatological reactions: redness of the skin, psoriasis-like reactions on the skin, increased sweating, exanthema, alopecia, exacerbation of psoriasis .
Allergic reactions : rash, urticaria , itching.
Hematopoietic disorders: agranulocytosis, leukopenia, thrombocytopenia.
Sexual disorders: weakened libido , decreased potency.
Disorders of the musculoskeletal system: muscle cramps in the legs, muscle weakness, arthralgia, lumbodynia.
Effect on the fetus: hypoglycemia , fetal growth restriction, bradycardia.
Other disorders: withdrawal syndrome.

Instructions for use of Cordinorm (Method and dosage)

Instructions for use of Cordinorm prescribe taking the medicine in the morning, on an empty stomach, orally, without chewing. A single dose is 2.5-5 mg. Typically the initial dose is 5 mg per day. If necessary, the dose is increased to 10 mg per day. The maximum daily dose is 20 mg.

Interaction

In persons receiving bisoprolol , immunotherapeutic and diagnostic allergens, the risk of systemic severe allergic reactions .

Iodine-containing intravenous radiocontrast agents increase the risk of anaphylactic reactions.

When used simultaneously, bisoprolol can change the effectiveness of insulin and hypoglycemic agents , as well as mask the symptoms of emerging hypoglycemia.

Phenytoin, when administered intravenously and inhalational anesthetics, increases the strength of the cardiodepressive effect and the likelihood of lowering blood pressure.

When used together, bisoprolol reduces the clearance of xanthines and lidocaine , and also increases their content in the blood.

The hypotensive effect of the drug when used together is weakened by non-steroidal anti-inflammatory drugs, glucocorticosteroids and estrogens.

Cardiac glycosides, Reserpine, Methyldopa, Guanfacine, slow calcium channel inhibitors, Amiodarone and other antiarrhythmic drugs, when used simultaneously with bisoprolol , increase the risk of developing AV block, bradycardia and even cardiac arrest.

When used together, Nifedipine can significantly reduce blood pressure.

Diuretics, Clonidine, sympatholytics, Hydralazine and other antihypertensive drugs when used together can cause an excessive decrease in blood pressure.

Cordinorm increases the duration of action of non-depolarizing muscle relaxants and coumarins.

and tetracyclic antidepressants and hypnotics enhance the suppressive effect of bisoprolol on nervous function.

Concomitant use with MAO blockers (as well as the use of Cordinorm within a two-week period after taking them) is not recommended due to the increased hypotensive effect.

Ergotamine, when used simultaneously, increases the risk of developing peripheral circulatory disorders.

Non-hydrogenated ergot alkaloids, when used together, increase the risk of peripheral circulatory disorders.

Rifampicin, when used together, shortens the half-life of the active component.

Sulfasalazine increases the level of bisoprolol in the blood.

Cordinorm 5mg n30 tab

Dosage form:

film-coated tablets, film-coated tablets, tablets

Pharmachologic effect:

Selective beta1-blocker without its own SMA; has hypotensive, antiarrhythmic and antianginal effects. By blocking beta1-adrenergic receptors of the heart in low doses, it reduces the catecholamine-stimulated formation of cAMP from ATP, reduces the intracellular Ca2+ current, has a negative chrono-, dromo-, bathmo- and inotropic effect (reduces heart rate, inhibits conductivity and excitability, reduces myocardial contractility). With increasing dose, it has a beta2-adrenergic blocking effect. OPSS at the beginning of the use of beta-blockers, in the first 24 hours, increases (as a result of a reciprocal increase in the activity of alpha-adrenergic receptors and the elimination of stimulation of beta2-adrenergic receptors), which after 1-3 days returns to the original level, and with long-term administration decreases. The hypotensive effect is associated with a decrease in IOC, sympathetic stimulation of peripheral vessels, a decrease in the activity of the RAAS (more important for patients with initial hypersecretion of renin), restoration of the sensitivity of the baroreceptors of the aortic arch (there is no increase in their activity in response to a decrease in blood pressure) and an effect on the central nervous system. In case of arterial hypertension, the effect occurs after 2-5 days, a stable effect occurs after 1-2 months. The antianginal effect is due to a decrease in myocardial oxygen demand as a result of a decrease in heart rate and decreased contractility, prolongation of diastole, and improved myocardial perfusion. By increasing the end-diastolic pressure in the left ventricle and increasing the stretching of the ventricular muscle fibers, it can increase the need for oxygen, especially in patients with CHF. The antiarrhythmic effect is due to the elimination of arrhythmogenic factors (tachycardia, increased activity of the sympathetic nervous system, increased cAMP content, arterial hypertension), a decrease in the rate of spontaneous excitation of sinus and ectopic pacemakers and a slowdown of AV conduction (mainly in the antegrade and to a lesser extent in the retrograde directions through the AV node ) and along additional paths. Unlike non-selective beta-blockers, when prescribed in average therapeutic doses, it has a less pronounced effect on organs containing beta2-adrenergic receptors (pancreas, skeletal muscles, smooth muscles of peripheral arteries, bronchi and uterus) and on carbohydrate metabolism, does not cause Na+ retention in body; the severity of the atherogenic effect does not differ from the effect of propranolol. When used in large doses, it has a blocking effect on both subtypes of beta-adrenergic receptors.

Indications:

Arterial hypertension; IHD, angina pectoris, myocardial infarction (secondary prevention), CHF. Rhythm disturbances - sinus tachycardia, supraventricular and ventricular extrasystole; arrhythmias due to mitral valve prolapse, thyrotoxicosis.

Contraindications:

Hypersensitivity, acute HF or decompensated CHF, cardiogenic shock, AV block II-III stage, SA block, SSSU, bradycardia (heart rate less than 60 beats/min - in the treatment of CHF, less than 50/min - for other indications), cardiomegaly ( without signs of heart failure), arterial hypotension (systolic blood pressure less than 100 mmHg - in the treatment of CHF and 90 mmHg - for other indications), COPD (including bronchial asthma), impaired peripheral circulation (late stages); lactation period, simultaneous use of MAO inhibitors (with the exception of MAO-B inhibitors).

Side effects:

Frequency: very often (more than or equal to 1/10); often (more than 1/100, less than 1/10); uncommon (more than 1/1000, less than 1/100); rare (more than 1/10000, less than 1/1000); very rare (less than 1/10000, including individual reports). From the nervous system: infrequently - increased fatigue, asthenia, dizziness, headache, drowsiness or insomnia, depression, rarely - hallucinations, nightmares, convulsions. From the senses: rarely - blurred vision, decreased secretion of tear fluid, dryness and soreness of the eyes; very rarely - conjunctivitis. From the cardiovascular system: very often - sinus bradycardia, often - decreased blood pressure, manifestation of vasospasm (increased peripheral circulatory disorders, coldness of the lower extremities, paresthesia), infrequently - impaired AV conduction, orthostatic hypotension, decompensation of CHF, peripheral edema. From the digestive system: often - dryness of the oral mucosa, nausea, vomiting, diarrhea, constipation; rarely - hepatitis. From the respiratory system: infrequently - difficulty breathing when prescribed in high doses (loss of selectivity) and/or in predisposed patients - laryngo- and bronchospasm; rarely - nasal congestion. From the endocrine system: hyperglycemia (in patients with non-insulin-dependent diabetes mellitus), hypoglycemia (in patients receiving insulin). Allergic reactions: rarely - itching, rash, urticaria. From the skin: rarely - increased sweating, skin hyperemia, very rarely - psoriasis-like skin reactions, exacerbation of psoriasis symptoms, alopecia. From the musculoskeletal system: infrequently - muscle weakness, cramps in the calf muscles, arthralgia. Laboratory indicators: rarely - increased activity of liver transaminases, hypertriglyceridemia, in some cases - thrombocytopenia, agranulocytosis. Effect on the fetus: intrauterine growth retardation, hypoglycemia, bradycardia. Other: impaired potency, “smokers” syndrome; the effectiveness of beta-blockers is lower. Patients using contact lenses should take into account that during treatment the production of tear fluid may decrease. When used in patients with pheochromocytoma, there is a risk of developing paradoxical arterial hypertension (if effective alpha-blockade is not previously achieved). In thyrotoxicosis, bisoprolol may mask certain clinical signs of thyrotoxicosis (for example, tachycardia). Abrupt withdrawal in patients with thyrotoxicosis is contraindicated because it can increase symptoms. In diabetes mellitus, it can mask tachycardia caused by hypoglycemia. Unlike non-selective beta-blockers, it practically does not enhance insulin-induced hypoglycemia and does not delay the restoration of blood glucose to normal levels. When taking clonidine concomitantly, it can be discontinued only a few days after bisoprolol is discontinued. It is possible that the severity of the hypersensitivity reaction may increase and the absence of effect from usual doses of epinephrine against the background of a burdened allergic history. If planned surgical treatment is necessary, the drug should be discontinued 48 hours before the start of general anesthesia. If the patient took the drug before surgery, he should select a drug for general anesthesia with minimal negative inotropic effect. Reciprocal activation of the n.vagus can be eliminated by intravenous administration of atropine (1-2 mg). Drugs that reduce catecholamine reserves (for example, reserpine) can enhance the effect of beta-blockers, so patients taking such combinations of drugs should be under constant medical supervision to detect arterial hypotension or bradycardia. Patients with bronchospastic diseases can be prescribed cardioselective adrenergic blockers in case of intolerance and/or ineffectiveness of other antihypertensive drugs, but the dosage should be strictly monitored. An overdose is dangerous due to the development of bronchospasm. If elderly patients develop increasing bradycardia (less than 50/min), arterial hypotension (systolic blood pressure below 100 mm Hg), AV block, bronchospasm, ventricular arrhythmias, severe liver and kidney dysfunction, it is necessary to reduce the dose or stop treatment . It is recommended to discontinue therapy if depression caused by taking beta-blockers develops. Treatment should not be abruptly interrupted due to the risk of developing severe arrhythmias and myocardial infarction. Cancellation is carried out gradually, reducing the dose over 2 weeks or more (reduce the dose by 25% in 3-4 days). Use during pregnancy and lactation is possible if the benefit to the mother outweighs the risk of side effects in the fetus and child. Should be discontinued before testing the content of catecholamines, normetanephrine and vanillylmandelic acid in the blood and urine; antinuclear antibody titers. During the treatment period, care must be taken when driving vehicles and engaging in other potentially hazardous activities that require increased concentration and speed of psychomotor reactions.

Interaction:

Allergens used for immunotherapy or allergen extracts for skin testing increase the risk of severe systemic allergic reactions or anaphylaxis in patients receiving bisoprolol. Iodine-containing radiopaque drugs for intravenous administration increase the risk of developing anaphylactic reactions. Phenytoin with intravenous administration, drugs for inhalation general anesthesia (hydrocarbon derivatives) increase the severity of the cardiodepressive effect and the likelihood of lowering blood pressure. Changes the effectiveness of insulin and oral hypoglycemic drugs, masks the symptoms of developing hypoglycemia (tachycardia, increased blood pressure). The hypotensive effect is weakened by NSAIDs (Na+ retention and blockade of Pg synthesis by the kidneys), corticosteroids and estrogens (Na+ retention). Cardiac glycosides, methyldopa, reserpine and guanfacine, BMCC (verapamil, diltiazem), amiodarone and other antiarrhythmic drugs increase the risk of developing or worsening bradycardia, AV block, cardiac arrest and HF. Nifedipine can lead to a significant decrease in blood pressure. Diuretics, clonidine, sympatholytics, hydralazine and other antihypertensive drugs can lead to an excessive decrease in blood pressure. Prolongs the effect of non-depolarizing muscle relaxants and the anticoagulant effect of coumarins. Tri- and tetracyclic antidepressants, antipsychotic drugs (neuroleptics), ethanol, sedative and hypnotic drugs increase CNS depression. Concomitant use with MAO inhibitors is not recommended due to a significant increase in the hypotensive effect; the break in treatment between taking MAO inhibitors and bisoprolol should be at least 14 days. Non-hydrogenated ergot alkaloids increase the risk of developing peripheral circulatory disorders. Ergotamine increases the risk of developing peripheral circulatory disorders; Rifampicin shortens T1/2.

special instructions

It is not recommended to suddenly stop treatment or change the recommended dose without consulting your doctor.

Monitoring of persons taking Cordinorm includes monitoring heartbeat and blood pressure levels, conducting an ECG , and testing glucose in patients with diabetes (once every 4 months). In elderly patients, it is recommended to monitor kidney function (every 4 months).

Before starting treatment in patients with a significant pulmonary history, it is necessary to conduct an external respiration study.

In approximately 20% of patients suffering from angina , beta blockers are ineffective.

When smoking, the effects of beta-blockers are weakened.

When using Cordinorm in people with pheochromocytoma , there is a risk of developing arterial hypertension of the paradoxical type.

Increased hypersensitivity reactions and ineffectiveness of usual dosages of Epinephrine in case of a burdened allergic history. If surgical treatment is necessary, discontinuation of the drug is carried out two days before the start of anesthesia.

Medicines that reduce catecholamine can stimulate the effect of beta-blockers , therefore, patients taking these combinations of drugs should be under regular medical supervision.

Persons with bronchospastic diseases are allowed to prescribe selective adrenergic blockers if other antihypertensive drugs , but the dosage must be strictly controlled. An overdose may cause bronchospasm.

It is recommended to discontinue therapy if depression caused by the use of beta blockers .

It is forbidden to abruptly interrupt therapy due to the risk of myocardial infarction and life-threatening arrhythmias .

Cancellation is carried out gradually, reducing the dose over 2 weeks or more.

During therapy, patients need to be careful when driving.

Cordinorm 5 mg 30 pcs. film-coated tablets

pharmachologic effect

Beta1-adrenergic blocker selective.

Composition and release form Cordinorm 5 mg 30 pcs. film-coated tablets

Tablets - 1 tablet:

active substance; bisoprolol fumarate 5 mg;
excipients: microcrystalline cellulose 21.10 mg, mannitol 148.50 mg; croscarmellose sodium 1.80 mg, magnesium stearate 3.60 mg, hypromellose 2.19 mg, titanium dioxide 0.88 mg, macrogol 6000 0.53 mg.

10 tablets in blisters made of PVC/PVDC/aluminum foil or 100 tablets in a PE container.

3.6, 9 blisters or 1 container each, placed in a cardboard box with instructions for use.

Description of the dosage form

Round, convex, film-coated, white tablets with a score line on one side, side lines and an engraving “B 5” on the other side.

Directions for use and doses

Take orally, in the morning on an empty stomach, without chewing, 2.5-5 mg once. Usually the initial dose is 5 mg 1 time per day. If necessary, the dose is increased to 10 mg 1 time per day. The maximum dose for adults is 20 mg/day.

Treatment of hypertension and angina: Treatment of patients with mild or moderate hepatic or renal impairment usually does not require dose adjustment.

In patients with severe renal impairment (creatinine clearance less than 20 ml/min) or with severe liver dysfunction, the maximum daily dose is 10 mg.

No dose adjustment is required in elderly patients.

Pharmacodynamics

A selective beta1-blocker, without its own sympathomimetic activity, does not have a membrane-stabilizing effect. Reduces plasma renin activity, reduces myocardial oxygen demand, and reduces heart rate (heart rate) (at rest and during exercise). It has hypotensive, antiarrhythmic and antianginal effects. By blocking beta1-adrenergic receptors of the heart in low doses, it reduces the formation of cAMP from ATP stimulated by catecholamines, reduces the intracellular current of calcium ions, has a negative chrono-, dromo-, bathmo- and inotropic effect, inhibits conductivity and excitability, and slows down atrioventricular conduction.

With increasing dose, it has a beta2-adrenergic blocking effect.

The total peripheral vascular resistance at the beginning of the use of the drug, in the first 24 hours, increases slightly (as a result of a reciprocal increase in the activity of alpha-adrenergic receptors and the elimination of stimulation of beta2-adrenergic receptors), which returns to the original level after 1-3 days, and decreases with long-term administration.

The hypotensive effect is associated with a decrease in minute blood volume, sympathetic stimulation of peripheral vessels, a decrease in the activity of the renin-angiotensin system (of great importance for patients with initial hypersecretion of renin), restoration of sensitivity in response to a decrease in blood pressure (BP) and an effect on the central nervous system ( CNS). In case of arterial hypertension, the effect occurs after 2-5 days, a stable effect occurs after 1-2 months.

The antianginal effect is due to a decrease in myocardial oxygen demand as a result of a decrease in heart rate and decreased contractility, prolongation of diastole, and improved myocardial perfusion. By increasing end-diastolic pressure in the left ventricle and increasing the stretch of ventricular muscle fibers, it can increase oxygen demand, especially in patients with chronic heart failure.

The antiarrhythmic effect is due to the elimination of arrhythmogenic factors (tachycardia, increased activity of the sympathetic nervous system, increased cAMP content, arterial hypertension), a decrease in the rate of spontaneous excitation of sinus and ectopic pacemakers and a slowdown in atrioventricular (AV) conduction (mainly in the antegrade and, to a lesser extent, in retrograde directions through the AV node) and along additional pathways.

Unlike non-selective beta-blockers, when prescribed in average therapeutic doses, it has a less pronounced effect on organs containing beta2-adrenergic receptors (pancreas, skeletal muscles, smooth muscles of peripheral arteries, bronchi and uterus) and on carbohydrate metabolism, does not cause Na+ retention in organism; the severity of the atherogenic effect does not differ from the effect of propranolol.

When used in large doses, it has a blocking effect on both subtypes of beta-adrenergic receptors.

Pharmacokinetics

Absorption - 80-90%, food intake does not affect absorption. The maximum concentration in blood plasma is observed after 1-3 hours, the connection with blood plasma proteins is about 35%. Permeability through the blood-brain barrier and placental barrier, secretion into breast milk is low. 50% of the dose is metabolized in the liver with the formation of inactive metabolites, the half-life is 9-12 hours. About 98% is excreted by the kidneys, 50% unchanged, less than 2% with bile.

Indications for use Cordinorm 5 mg 30 pcs. film-coated tablets

Arterial hypertension; coronary heart disease (prevention of angina attacks).

Contraindications

Hypersensitivity to bisoprolol or to any of the components of the drug, other beta-blockers, shock (including cardiogenic), collapse, pulmonary edema, acute heart failure, chronic heart failure in the stage of decompensation, atrioventricular block (AV block) stage II-III . (without pacemaker), sinoatrial block, sick sinus syndrome, severe bradycardia (heart rate less than 50 beats/min), Prinzmetal's angina, cardiomegaly (without signs of heart failure), arterial hypotension (systolic blood pressure less than 100 mm Hg, especially with myocardial infarction); history of bronchial asthma and chronic obstructive pulmonary disease; simultaneous use of monoamine oxidase inhibitors (MAO) (with the exception of MAO-B), late stages of peripheral circulatory disorders, Raynaud's disease, pheochromocytoma (without simultaneous use of alpha-blockers), metabolic acidosis, age under 18 years (efficacy and safety have not been established).

With caution: liver failure, chronic renal failure, myasthenia gravis, thyrotoxicosis, diabetes mellitus, first degree atrioventricular block, depression (including a history), psoriasis, old age.

Application of Cordinorm 5 mg 30 pcs. film-coated tablets during pregnancy and breastfeeding

Use during pregnancy and lactation is possible if the benefit to the mother outweighs the risk of side effects in the fetus and child.

special instructions

Do not stop treatment abruptly or change the recommended dosage without first consulting your doctor.

Monitoring of patients taking Cordinorm should include monitoring heart rate and blood pressure (at the beginning of treatment - daily, then once every 3-4 months), an ECG, determination of blood glucose in patients with diabetes (once every 4-5 months) . In elderly patients, it is recommended to monitor renal function (once every 4-5 months).

The patient should be taught how to calculate heart rate and instructed about the need for medical consultation if the heart rate is less than 50 beats/min.

Before starting treatment, it is recommended to conduct a study of external respiratory function in patients with a burdened bronchopulmonary history.

In approximately 20% of patients with angina, beta blockers are ineffective. The main causes are severe coronary atherosclerosis with a low ischemic threshold (heart rate less than 100 beats/min) and increased end-diastolic volume of the left ventricle, impairing subendocardial blood flow.

In smokers, the effectiveness of beta-blockers is lower.

Patients using contact lenses should take into account that during treatment the production of tear fluid may decrease.

When used in patients with pheochromocytoma, there is a risk of developing paradoxical arterial hypertension (if effective alpha-blockade is not previously achieved).

In case of thyrotoxicosis, Cordinorm can mask certain clinical signs of thyrotoxicosis (for example, tachycardia). Abrupt withdrawal in patients with thyrotoxicosis is contraindicated because it can increase symptoms.

In diabetes mellitus, it can mask tachycardia caused by hypoglycemia. Unlike non-selective beta-blockers, it practically does not enhance insulin-induced hypoglycemia and does not delay the restoration of blood glucose to normal levels.

When taking clonidine simultaneously, it can be discontinued only a few days after Cordinorm is discontinued.

It is possible that the severity of the hypersensitivity reaction may increase and there will be no effect from usual doses of epinephrine against the background of a burdened allergic history. If planned surgical treatment is necessary, the drug should be discontinued 48 hours before the start of general anesthesia. If the patient took the drug before surgery, he should choose a drug for general anesthesia with minimal negative inotropic effect.

Reciprocal activation of the vagus nerve can be eliminated by intravenous atropine (1-2 mg).

Medicines that reduce the supply of catecholamines (for example, reserpine) may enhance the effect of beta-blockers, so patients taking such combinations of drugs should be under constant medical supervision to detect arterial hypotension or bradycardia.

Patients with bronchospastic diseases can be prescribed cardioselective adrenergic blockers in case of intolerance and/or ineffectiveness of other antihypertensive drugs, but the dosage should be strictly monitored. An overdose is dangerous due to the development of bronchospasm.

In case of increasing bradycardia (less than 50 beats/min), arterial hypotension (systolic blood pressure below 100 mm Hg), AV blockade, bronchospasm, ventricular arrhythmias, severe liver and kidney dysfunction in elderly patients, it is necessary to reduce the dose or stop treatment.

It is recommended to discontinue therapy if depression caused by taking beta-blockers develops.

Treatment should not be abruptly interrupted due to the risk of developing severe arrhythmias and myocardial infarction. Cancellation is carried out gradually, reducing the dose over 2 weeks or more (reduce the dose by 25% in 3-4 days).

Should be discontinued before testing the content of catecholamines, normetanephrine and vanillinmandelic acid in the blood and urine; antinuclear antibody titers.

Impact on the ability to drive vehicles and operate machinery

During the treatment period, care must be taken when driving vehicles and engaging in other potentially hazardous activities that require increased concentration and speed of psychomotor reactions.

Overdose

Treatment: gastric lavage and administration of adsorbent drugs; symptomatic therapy: in case of developed AV block - intravenous (IV) administration of 1-2 mg of atropine, epinephrine or installation of a temporary pacemaker; for ventricular extrasystole - lidocaine (class IA drugs are not used); when blood pressure decreases, the patient should be in the Trendelenburg position; if there are no signs of pulmonary edema, intravenous plasma-substituting solutions; if ineffective, administration of epinephrine, dopamine, dobutamine (to maintain chronotropic and inotropic effects and eliminate a pronounced decrease in blood pressure); for heart failure - cardiac glycosides, diuretics, glucagon; for convulsions - intravenous diazepam; for bronchospasm - beta2-adrenergic stimulants by inhalation.

Side effects Cordinorm 5 mg 30 pcs. film-coated tablets

From the central nervous system: increased fatigue, weakness, dizziness, headache, drowsiness or insomnia, nightmares, depression, anxiety, confusion or short-term memory loss, hallucinations, asthenia, myasthenia, paresthesia in the extremities (in patients with " intermittent claudication and Raynaud's syndrome), tremor.

From the senses: blurred vision, decreased secretion of tear fluid, dry and sore eyes, conjunctivitis.

From the cardiovascular system: sinus bradycardia, palpitations, impaired myocardial conduction, impaired AV conduction (up to the development of complete transverse block and cardiac arrest), arrhythmias, weakened myocardial contractility, development (worsening) of chronic heart failure (swelling of the ankles, feet; shortness of breath), decreased blood pressure, orthostatic hypotension, manifestation of vasospasm (increased peripheral circulatory disorders, coldness of the lower extremities, Raynaud's syndrome), chest pain.

From the gastrointestinal tract: dryness of the oral mucosa, nausea, vomiting, abdominal pain, constipation or diarrhea, liver dysfunction (dark urine, yellowness of the sclera or skin, cholestasis), changes in taste.

From the respiratory system; nasal congestion, difficulty breathing when prescribed in high doses (loss of selectivity) and/or in predisposed patients - laryngo- and bronchospasm.

From the endocrine system: hyperglycemia (in patients with non-insulin-dependent diabetes mellitus), hypoglycemia (in patients receiving insulin), hypothyroid state.

Allergic reactions: skin itching, rash, urticaria.

From the skin: increased sweating, skin hyperemia, exanthema, psoriasis-like skin reactions, exacerbation of psoriasis symptoms, alopecia.

Laboratory indicators: thrombocytopenia (unusual bleeding and hemorrhage), agranulocytosis, leukopenia, changes in the activity of liver enzymes (increased ALT, AST), bilirubin levels, triglycerides.

Effect on the fetus: intrauterine growth retardation, hypoglycemia, bradycardia.

From the musculoskeletal system: muscle weakness, cramps in the calf muscles.

Other: back pain, arthralgia, decreased libido; rarely - decreased potency, withdrawal syndrome (increased angina attacks, increased blood pressure).

Drug interactions

Allergens used for immunotherapy or allergen extracts for skin testing increase the risk of severe systemic allergic reactions or anaphylaxis in patients receiving bisoprolol.

Iodine-containing radiocontrast drugs for intravenous administration increase the risk of anaphylactic reactions.

Phenytoin when administered intravenously, drugs for inhalation general anesthesia (hydrocarbon derivatives) increase the severity of the cardiodepressive effect and the likelihood of lowering blood pressure.

Changes the effectiveness of insulin and oral hypoglycemic drugs, masks the symptoms of developing hypoglycemia (tachycardia, increased blood pressure).

Reduces the clearance of lidocaine and xanthines (except diphylline) and increases their concentration in plasma, especially in patients with initially increased clearance of theophylline under the influence of smoking.

The hypotensive effect is weakened by nonsteroidal anti-inflammatory drugs (NSAIDs), sodium ion retention and blockade of prostaglandin synthesis by the kidneys), glucocorticosteroids and estrogens (Na+ retention).

Cardiac glycosides, methyldopa, reserpine and guanfacine, slow calcium channel blockers (verapamil, diltiazem), amiodarone and other antiarrhythmic drugs increase the risk of developing or worsening bradycardia, AV block, cardiac arrest and heart failure.

Nifedipine can lead to a significant decrease in blood pressure.

Diuretics, clonidine, sympatholytics, hydralazine and other antihypertensive drugs can lead to an excessive decrease in blood pressure.

Prolongs the effect of non-depolarizing muscle relaxants and the anticoagulant effect of coumarins.

Tri- and tetracyclic antidepressants, antipsychotics (neuroleptics), ethanol, sedatives and hypnotics increase depression of the central nervous system.

Concomitant use with MAO inhibitors is not recommended due to a significant increase in the hypotensive effect; the break in treatment between taking MAO inhibitors and bisoprolol should be at least 14 days.

Non-hydrogenated ergot alkaloids increase the risk of developing peripheral circulatory disorders.

Ergotamine increases the risk of developing peripheral circulatory disorders; sulfasalazine increases the concentration of bisoprolol in plasma; Rifampin shortens the half-life.

Analogs

Level 4 ATC code matches:
Biol

Metocard

Metozok

Nebilet

Nebilong

Betaxolol

Bisogamma

Aritel

Vasocardin

Corvitol

Bidop

Bisoprolol

Nebivolol

Biprol

Bisoprol

Concor Cor

Lokren

Concor

Niperten

Betaloc ZOK

Analogues of Cordinorm: Aritel, Bidop, Aritel Cor, Biol, Coronal, Bisogamma, Niperten, Bisocard, Concor, Bisomore, Biprol, Bisoprolol, Corbis, Bisoprolol-Teva, Bisoprolol-OBL, Tirez.