The effectiveness and tolerability of bisoprolol may affect the simultaneous reception of other drugs. Such interaction can also occur in cases where two LS are accepted after a short period of time.
Recommended combinations

General interactions between bisoprolol and amlodipine + bisoprolol

Amlodipine + Bisoprolol
Bisoprolol and amlodipine + bisoprolol are used together in the bisam
Bisoprolol and amlodipine + bisoprolol are used together in Niperthen Combi
Bisoprolol and amlodipine + bisoprolol are used together in Concorp AM
Bisoprolol and Amlodipine + Bisoprolol are used together in Bisoprolol AML

Interaction Amlodipine (enters Amlodipine + bisoprolol) ⇔ Bisoprolol

In bisoprolol (text from instruction) ⇒ Amlodipin (found him)

The effectiveness and tolerability of bisoprolol may affect the simultaneous reception of other drugs. Such interaction can also occur in cases where two LS are accepted after a short period of time.
Recommended combinations
Treatment of HSN. Antiarrhythmic LS I class (for example, County, dyspeciramide, lidocaine, phenytoin, freakinide, conpaphenon) while use with bisoprolol can reduce AV conductivity and myocardial contractility.
All indications for the use of bisoprolol. BKK type verapamil and to a lesser degree of diltiazem with simultaneous use with bisoprolol can lead to a decrease in the contractile ability of myocardium and violation of AV conduction. In particular, the introduction of verapamil to patients receiving β-adrenoblays can lead to a pronounced arterial hypotension and AV blockade. Hypotensive LS. central action (such as clonidine, methyldop, moxonidine, rylmidin) can cause heart rate and decrease heart EmissionAs well as to vasodilation due to a decrease in the central sympathetic tone. Sharp abolition, especially before the abolition of β-adrenoblockers, can increase the risk of ricochet arterial hypertension.
Combinations requiring special caution
Treatment of arterial hypertension and angina. Antiarrhythmic agents I class (for example, quinidine, dyspeyramide, lidocaine, phenytoin, freakinide, conpaphenon) while use with bisoprolol can reduce the AV conductivity and the contractility of myocardium.
All indications for the use of bisoprolol. BKK - Dihydropyridine derivatives (for example, nifedipine, feelodipine, amlodipine) - while simultaneous use with bisoprolol can increase the risk of arterial hypotension. In patients with CHF, it is impossible to eliminate the risk of subsequent deterioration of the contractile function of the heart.
Antiarrhythmic agents of class III (for example amiodar) can enhance violation of AV conduction.
Action of β-adrenoblockers for local application (eg eye drops For the treatment of glaucoma), it can enhance the systemic effects of bisoprolol (reduction of blood pressure, gentlemen of heart rate).
Parasympathomimetics while simultaneous use with bisoprolol can enhance the violation of AV conductivity and increase the risk of bradycardia.
The hypoglycemic effect of insulin or hypoglycemic drugs for intake can be intensified. Signs of hypoglycemia, in particular tachycardia, can be masked or suppressed. Such interaction is more likely to use nonitive of β-adrenoblocators.
HP for general anesthesia can increase the risk of cardiopractive action, leading to arterial hypotension (see "Precautions").
Cardiac glycosides while using bisoprolol simultaneously can lead to an increase in the time of the pulse and thus to the development of bradycardia. NSAIDs can reduce antihypertensive effect Bisoprolol.
The simultaneous use of bisoprolol with β-adreminimetics (for example isoprenaline, dobutamine) can lead to a decrease in the effect of both drugs. The use of bisoprolol with adrenomimetics that affect α- and β-adrenoreceptors (for example, norepinephrine, epinephrine) can enhance the vasoconstrictor effects of these agents arising from the participation of α-adrenoreceptors leading to an increase in blood pressure. Such interactions are more likely to use non-selective β-adrenoblockers.
Hypotensive LS. As well as other means with a possible antihypertensive effect (for example, tricyclic antidepressants, barbiturates, phenothiazines) can enhance the antihypertensive effect of bisoprolol.
MEFLOKHIN while simultaneously use with bisoprolol can increase the risk of bradycardia.
Mao inhibitors (. In addition to Mao B) inhibitors, the antihypertensive effect of β-adrenoblockers can enhance. Simultaneous use can also lead to the development of a hypertensive crisis.

In amlodipine (text from instruction) ⇒ Bisoprolol (found him)

Amlodipine can be safely used for arterial hypertension therapy along with thiazide diuretics, alpha-adrenoblockers, beta-adrenoblockers or aPF inhibitors. In patients S. stable angina Amlodipine can be combined with other antichangal means, for example, with nitrates of prolonged or short actionBeta-adrenoblockers.
Unlike other BKK, the clinically significant interaction of amlodipine (III generation of the BCC) was not detected during the joint use with the NSAID, in PM and with indomethacin.
It is possible to strengthen the anti-inanal and hypotensive effect of the BCC during co-use with thiazide and loop diuretics, ACE inhibitors, beta-adrenoblockers and nitrates, as well as enhancing their hypotensive effects with joint use with alpha1-adrenobloclars, neuroleptics.
Although, in the study of amlodipine, negative inotropic action was usually not observed, nevertheless, some of the BACK can enhance the severity of the negative inotropic effect of antiarrhythmic agents causing the elongation of the Qt interval (for example amiodarone and quinidine).
Amlodipine can also be safely used simultaneously with antibiotics and hypoglycemic agents for intake.
One-time reception of 100 mg of sildenafil in patients with essential hypertension does not affect the parameters of amlodipine pharmacokinetics.
The re-use of amlodipine at a dose of 10 mg and atorvastatin at a dose of 80 mg is not accompanied by significant changes in the indicators of the Pharmacokinetics of Atorvastatin.
Simvastatin: Simultaneous multiple use of amlodipine at a dose of 10 mg and simvastatin at a dose of 80 mg leads to an increase in the exposure of simvastatin by 77%. In such cases, it is necessary to limit the dose of simvastatin to 20 mg.
Ethanol (drinks containing alcohol): amlodipine for one-time and re-application At a dose of 10 mg does not affect the pharmacokinetics of ethanol.
Antiviral Means (Ritonavir): Increases plasma concentrations of BKK, in PM and amlodipine.
Neuroleptics and Isofluraran: Strengthening the hypotensive effect of dihydropyridine derivatives.
Calcium preparations can reduce BKK effect.
With the joint use of BKK with lithium preparations (for amlodipine, data is absent) It is possible to enhance the manifestation of their neurotoxicity (nausea, vomiting, diarrhea, ataxia, tremor, noise in the ears).
Studies of simultaneous use of amlodipine and cyclosporin in healthy volunteers and all groups of patients ,. In addition to patients after kidney transplantation, were not conducted. Various studies of amlodipine interaction with cyclosporin in patients after kidney transplantation show that the use of this combination may not lead to any effect or raise Cmin Cyclosporine in various degrees up to 40%. These data should be taken into account and control the concentration of cyclosporine in this group of patients with the simultaneous use of cyclosporine and amlodipine. It does not affect the concentration of Digoxin blood serum and its kidney clearance.
It does not have a significant effect on the action of warfarin (PV).
Cimetidine does not affect the pharmacokinetics of amlodipine.
In vitro studies, amlodipine does not affect the binding to the blood plasma proteins, phenytoin, warfarin and indomethacin.
Grapefruit juice: the simultaneous one-time reception of 240 mg of grapefruit juice and 10 mg of amlodipine inside is not accompanied by a significant change in amlodipine pharmacokinetics. However, it is not recommended to use grapefruit juice and amlodipine at the same time, because with the Genetic polymorphism of the CYP3A4 isoenzyme, it is possible to increase the bioavailability of amlodipine and as a result - an increase in the hypotensive effect.
Aluminum- or magnesium-containing antacids: their one-time reception does not have a significant impact on amlodipine pharmacokinetics.
Inhibitors of the CYP3A4 isoenzyme: while using a diltiazem at a dose of 180 mg and amlodipine at a dose of 5 mg in patients from 69 to 87 years old with arterial hypertension, an increase in amlodipine system exposure by 57% is noted. The simultaneous use of amlodipine and erythromycin in healthy volunteers (from 18 to 43 years) does not lead to significant changes in amlodipine exposure (an increase in AUC by 22%). Despite the fact that the clinical significance of these effects is completely unclear, they can be more pronounced in elderly patients.
The strong inhibitors of the CYP3A4 isoenzyme (for example ketoconazole, itraconazole) can lead to an increase in amlodipine concentration in the blood plasma to a greater extent than the diltia. Caution should be used amlodipine and inhibitors of the CYP3A4 isoenzyme.
Clarithromycin: CYP3A4 isoenzyme inhibitor. In patients taking at the same time clarithromycin and amlodipine, increased the risk of decline in blood pressure. Patients taking such a combination are recommended to be under careful medical supervision.
Inductors of the surgery of SUR 3A4: data on the effect of inductors of the CYP3A4 isoenzyme on amlodipine pharmacokinetics is not. The blood pressure should be carefully monitored with simultaneous use of amlodipine and inductors of the CYP3A4 isoenzyme.
Tacrolimus: With simultaneous use with amlodipine, there is a risk of increasing the concentration of tacrolimus in the blood plasma. In order to avoid the toxicity of the tacrolimus while simultaneously use with amlodipine, the concentration of tacrolimus in the blood plasma of patients should be monitored and adjust the tacrolimus dose if necessary.

Bisoprolol (Lat. Bisoprolol) is a drug, the testimony of which includes therapy with this medicine for the treatment of cardiovascular diseases. Tablets are often prescribed with hypertension to normalize increased pressure.

Also, the drug is able to shoot signs of tachycardia and angina, rehabilitates the vessels after infarction suffered, and also stabilizes bradycardia symptoms. In medical practice, it is customary to prescribe bisoprolol in chronic arrhythmias and such a disease as the deficiency of the heart type.

The medicine is not completely safe, for example, it is prohibited if there are some heart violations. And also not recommended therapy with drug during pregnancy.

The cost of the medication is not too high with respect to other drugs. But to meet it on the shelves of pharmaceutical networks, it is not always possible, so you should know how to replace bisoprolol if necessary.

Look analogs of bisoprolol, it also causes his complex method of reception, requiring the gradual start of treatment and smooth cancellation under the supervision of the doctor.

Basic drug substitutes with descriptions, contraindications and price

Initially, the manufacture of Bisoprolol is carried out by the German company Merck, however, the patent does not belong only to this company. The pharmaceutical market offers analogs and synonyms medical To reduce pressure from various manufacturers, ranging from Russian titans for the production of drugs and ending with the Belarusian "Pranophharm".

Among domestic manufacturers, you can allocate the following replacements to this medicine:

• Aritel. It is considered a complete analogue of bisoprolol, its price ranges from 150 to 200 rubles. It has contraindications, among which hypotension, various chronic heart diseases, including arrhythmias and flickering effects, bronchial asthma, psoriasis and other reception medicinal preparationsnot combined with the active component.

• Nipend. It has a similar bisoprolol formula, a distinctive feature of this medicine is the possibility of therapy in the presence of heart problems. However, the drug cannot be applied without medical testimony during diabetes mellitus.

The pharmaceuticals also offers Belarusian analogs of bisoprolol, which in its composition do not inferior to the original drug:

• Bisoprolol. Mick. The price of the medication is from 80 to 100 rubles. Available in powder, which helps the assimilation of the drug. It is prohibited for heart disease.

• Bisoprolol-Borimed. It has a low cost, you can purchase a medicine at a pharmacy in just 30-50 rubles, depending on the dosage. Despite the excellent hypertensive effect, can cause strong side effects In the form of allergic reactions.

• Bisoprolol FT. Allowed to use analogue with IBS ( ischemic disease Hearts), heart failure and increased arrhythmia, against the background of which arises arterial hypertension. The price of the drug can reach 200 rubles.

As an imported analogues of bisoprolol, pharmaceutical production offers the following drugs from high pressure:

Coronal. Price from 135 to 340 rubles. Among the contraindications should pay attention not only to bronchial asthma and problems heart Rhythm, but also a pregnancy followed by lactation period.

Locher. The French is a potent drug whose price can reach 1300 rubles. It is capable of adjusting pressure even in stress conditions during long-term reception. And also contraindicated in heart rate failures.

Sandoz. Full Ukrainian synonym for drug, worth 80 to 350 rubles, depending on the amount of medication and dosage. It has a large number of side effects, as well as forbidden during cardiac failures.

Carvedilol or bisoprolol - what is better

Similar therapeutic effects have such preparations such as carvedilol and bisoprolol. However, allocated by different compositions. The doctor should make a choice in favor of one or another medicine, depending on the patient's health features.

Bisoprolol is transferred to the human body better, while Carvedilol has a greater number of side effects, especially from nervous system. In addition, the bisoprolol has a simplified method of reception - a sufficient one dose per day.

The bisoprolol preparation used to treat hypertensive manifestations has many inexpensive analogs. However, the choice of this drug, even if it has similar composition with the original, is carried out by the doctor.

Amlodipine
Amlodipine can be safely used for arterial hypertension therapy along with thiazide diuretics, alpha-adrenoblockers, beta-adrenoblockers or ACE inhibitors. In patients with stable angina, amlodipine can be combined with other antichangal means, for example, prolonged or short-acting nitrates, beta-adrenoblockers.
Unlike other BCC, the clinically significant interaction of amlodipine (III generation of the BCC) was not detected during the joint use with the NSAID, in the PM Indomethacin. It is possible to strengthen the antichangal and antihypertensive effect of the BACK during co-use with tiazide and loop diuretics, ACE inhibitors, beta-adrenobloclars and nitrates, as well as enhancing their antihypertensive effects when used with alpha-adrenoblockers, neuroleptics.
Although, in the study of amlodipine, a negative inotropic effect was usually not observed, nevertheless, some of the BKK can enhance the severity of the negative inotropic effect of antiarrhythmic agents causing the elongation of the Qt interval (for example amiodarone and quinidine).

One-time reception of 100 mg of sildenafil in patients with essentially hypertension does not affect the parameters of amlodipine pharmacokinetics.

Simvastatin. The simultaneous multiple use of amlodipine at a dose of 10 mg and simvastatin at a dose of 80 mg leads to an increase in the exposure of simvastatin by 77%. In such cases, it is necessary to limit the dose of simvastatin to 20 mg.
Rosavastatin. With simultaneous repeated use of amlodipine at a dose of 10 mg and rosuvastatin at a dose of 20 mg, an increase in AUC was observed (about 28%) and CMAs (by 31%) Rosuvastatin. The exact interaction mechanism is unknown. It is expected that this effect will not have a clinical value in the daily use of the combination of amlodipine + lysinopril + rosevastatin, since it is shown only to the patients who are already obtained by leasest, amlodipine and rosavastatin in the same doses as in this combination.
Ethanol ( alcoholic beverages). Amlodipine during one-time and re-use at a dose of 10 mg does not affect the pharmacokinetics of ethanol.
Antiviral agents (ritonavir). Increases plasma concentrations of BKK, in PM amlodipine.
Neuroleptics and Isofluran. Strengthening the antihypertensive effect of dihydropyridine derivatives.
Calcium preparations. Can reduce the effect of BKK.
Lithium preparations. With the joint use of BKK with lithium preparations (for amlodipine, data is absent) It is possible to strengthen the manifestation of their neurotoxicity (nausea, vomiting, diarrhea, ataxia, tremor, noise in the ears).
Cyclosporin. Studies of simultaneous use of amlodipine and cyclosporin in healthy volunteers and all groups of patients ,. In addition to patients after kidney transplantation, were not conducted. Different studies of amlodipine interaction with cyclosporin in patients after kidney transplantation show that the use of this combination can either lead to any effect or increase CMIN cyclosporine to varying degrees to 40%. These data should be taken into account and control the concentration of cyclosporine in this group of patients with the simultaneous use of cyclosporine and amlodipine.
Amlodipine does not affect the concentration of Digoxin serum and its kidney clearance.
Amlodipine


Grapefruit juice. The simultaneous one-time reception of 240 mg of grapefruit juice and 10 mg of amlodipine inside is not accompanied by a significant change in amlodipine pharmacokinetics. Nevertheless, it is not recommended to use grapefruit juice and amlodipine at the same time, TD; With the genetic polymorphism of the CYP3A4 isoenzyme, it is possible to increase the bioavailability of amlodipine and as a result of which the increase in the antihypertensive effect.
Aluminum. Or magnesium-containing antacids. Their one-time reception does not have a significant impact on amlodipine pharmacokinetics.
Inhibitors of the CYP3A4 isoenzyme. With the simultaneous use of diltiazem at a dose of 180 mg and amlodipine at a dose of 5 mg in elderly patients (from 69 to 87 years) with arterial hypertension, an increase in amlodipine system exposure is noted by 57%. The simultaneous use of amlodipine and erythromycin in healthy volunteers (from 18 to 43 years) does not lead to significant changes in amlodipine exposure (an increase in AUC by 22%). Despite the fact that the clinical significance of these effects is not fully clear, they can be more pronounced in elderly patients.

Inductors of the isoenzyme SUR 3A4. Data on the influence of inductors of the invention of CYP3A4 to the pharmacokinetics of amlodipine is absent. The blood pressure should be carefully monitored with simultaneous use of amlodipine and inductors of the CYP3A4 isoenzyme.
Lysinopril
With simultaneous use with potassium-saving diuretics (spironolactone, Eplenenone, triamteren, amyloride), potassium preparations, potassium-containing salt substitutes are increased by the risk of hypercalemia, especially in patients with impaired kidney function.
With simultaneous use with diuretics - a pronounced decrease in blood pressure. The simultaneous use of leasedid with beta-adrenoblockers, BKK, diuretics, tricyclic antidepressants / neuroleptics enhances the severity of antihypertensive action.
With simultaneous use with NSAIDs (in PM Indomethacin), including acetylsalicylic acid 3 g / day, estrogens, as well as adrenomimetics - a decrease in antihypertensive effect of lysinopril.
With simultaneous use with lithium preparations, a slowdown in the removal of lithium from the body.
Simultaneous use with antacids and skewers slows down suction from the gastrointestinal tract.
Ethanol enhances the effect of the leaser.
The double blockade of Raas through the simultaneous use of ARA II), ACE inhibitors or alianity is associated with the increased frequency of the development of arterial hypotension, hypercalemia and renal impairments (in PM renal failure) Compared to the use of one means acting on Raas.
With simultaneous use with insulin and hypoglycemic agents, the risk of hypoglycemia is increased.
With the simultaneous use of APE inhibitors and gold preparations for in / in administration (sodium aurochiomalat), a symptom complex, which includes hyperemia of the face, nausea, vomiting and decreased blood pressure.
It is not contraindicated simultaneous use of leasing with acetylsalicylic acid as an angiogenic agent, thrombolytic, beta-adrenobloclars and / or nitrates.
Simultaneous use with SIRES can lead to severe hyponatremia.
Simultaneous use with allopurinol, procanamide, cytostatics can increase the risk of leukopenia.
Rosavastatin
Effect of other drugs on rosavastatin
Transport protein inhibitors. Rosavastatin binds to some transport proteins, in particular the OAST1B1 and BCRP. The concomitant use of drugs, which are inhibitors of these transport proteins, can be accompanied by an increase in the concentration of rosuvastatin in the blood plasma and an increased risk of myopathy development (see "Precautions").
Cyclosporin. With the simultaneous use of Rosuvastatin and Cyclosporine AUC Rosuvastatin was on average 7 times higher than the value, which was noted in healthy volunteers. Rosavastatin does not affect the plasma concentration of cyclosporine. Rosevastatin is contraindicated in patients taking cyclosporin (see "Contraindications").
HIV protease inhibitors. Despite the fact that the exact interaction mechanism is unknown, the joint taking of HIV protease inhibitors can lead to a significant increase in the exposition of Rosuvastatin. Pharmacokinetic study on the simultaneous use of 20 mg of rosuvastatin and a combined means containing two inhibitors of HIV proteases (400 mg of Lopinavir / 100 mg of ritonavir), in healthy volunteers led to approximately two-time and five-time increase in AUC0-24 and Cmax Rosuvastatin, respectively. Therefore, simultaneous reception of rosuvastatin and inhibitors of HIV proteases in the treatment of patients with HIV infection is not recommended (see "Precautions").
Hemfibrosyl and other hypolypidemic drugs. Sharing Rosuvastatin and hemfibrosyl leads to an increase in 2 times Cmax Rosuvastatin in the blood plasma, as well as an increase in AUC Rosuvastatin (see "Precautions"). Based on data on specific interaction, pharmacokinetically significant interaction with fenofibrate is not expected, pharmacodynamic interaction is possible.
Hemfibrosyl, fenofibrate, other fibrates and a nicotinic acid In lipid lining doses (more than 1 g / day), the risk of myopathy increases while using inhibitors of the GMG-Coa reductase, possibly due to the fact that they can cause myopathy and when using them in monotherapy (see "Precautions").
Ezetimib. The simultaneous use of rosuvastatin at a dose of 10 mg and esetimib at a dose of 10 mg was accompanied by an increase in Rosuvastatan AUC in patients with hypercholesterolemia. It is impossible to exclude an increase in the risk of side effects due to pharmacodynamic interaction between rosuvastatin and ezetimib.
Antacids. The simultaneous use of rosuvastatin and suspensions of antacids containing aluminum or magnesium hydroxide leads to a decrease in the plasma concentration of rosuvastatin by about 50%. This effect is less pronounced if antacids are used 2 hours after taking Rozuvastatin. The clinical significance of this interaction has not been studied.
Erythromycin. The simultaneous use of rosuvastatin and erythromycin leads to a decrease in the AUC0-T Rosuvastatin by 20% and Cmax Rosuvastatin by 30%. Such interaction may occur as a result of increased intestinal motility caused by erythromycin intake.
Fussidic acid. Research on the study of the interaction of rosuvastatin and fusidic acid was not conducted. As with the reception of other GMG-Coa-reductase inhibitors, post-marketing reports were obtained on rabbadomyolysis cases with the joint use of rosuvastatin and fusidic acid. It is necessary to intently observe patients. If necessary, a temporary cessation of rosuvastatin reception is possible.
P450 cytochrome isoenzyme. The results of studies in vivo and in vitro showed that rosevastatin is neither an inhibitor nor the inducer of the isoenzyme of cytochrome P450. In addition, Rosavastatin is a weak substrate for these enzymes. Therefore, the interaction of Rosuvastatin with other drugs at the metabolism level with the participation of cytochrome P450 is not expected. There was no clinically significant interaction between rosuvastatin and fluconazole (inhibitor of CYP2C9 and CYP3A4 inhibitor) and ketoconazole (inhibitor of CYP2A6 and CYP3A4 isoenzytes).
Interaction with LS, which requires a dose correction Rosuvastatin
The dose of Rosuvastatin should be adjusted if it is necessary for its joint use with drugs that increase the exposure of Rosuvastatin. If an increase in exposure is expected 2 times or more, the initial dose of rosuvastatin should be 5 mg 1 time per day. You should also adjust the maximum daily dose of Rosuvastatan so that the expected exposure of Rosuvastatin does not exceed that for a dose of 40 mg taken without simultaneously assigning drugs that interact with Rosuvastatin. For example, the maximum daily dose Rosuvastatin, while simultaneous use with a hemfibrosyl is 20 mg (an increase in exposure by 1.9 times), with ritonavir / atazanavir - 10 mg (an increase in exposure by 3.1 times).
Below are data on the influence of concomitant therapy on the exposition of Rosuvastatin (AUC Rosuvastatin) in descending order by the results of published clinical studies.
Cyclosporine (75-200 mg 2 times a day, 6 months) + Rosavastatin (10 mg 1 time per day, 10 days) - an increase in AUC is 7.1 times.
Atazanavir / Ritonavir (300/100 mg 1 time per day, 8 days) + Rosavastatin (10 mg once) - an increase in AUC 3.1 times.
Lopinavir / Ritonavir (400/100 mg 2 times a day, 17 days) + rosevastatin (20 mg 1 time per day, 7 days) - an increase in AUC 2.1 times.
Hemfibrosyl (600 mg 2 times a day, 7 days) + rosevastatin (80 mg once) - an increase in AUC 1.9 times.
Elrombopag (75 mg 1 time per day, 10 days) + rosevastatin (10 mg once) - an increase in AUC 1.6 times.
Darunavir / Ritonavir (600/100 mg 2 times a day, 7 days) + Rosavastatin (10 mg 1 time per day, 7 days) - an increase in AUC 1.5 times.
Typinavir / ritonavir (500/200 mg 2 times a day, 11 days) + rosevastatin (10 mg once) - an increase in AUC 1.4 times.
DRONEDARON (400 mg 2 times a day) + Rosavastatin (no data) - an increase in AUC 1.4 times.
Itraconazole (200 mg 1 time per day, 5 days) + rosevastatin (10 or 80 mg once) - an increase in AUC 1.4 times.
Ezetimib (10 mg 1 time per day, 14 days) + rosevastatin (10 mg 1 time per day, 14 days) - an increase in AUC 1.2 times.
FOSPRENAVIR / RITONAVIR (700/100 mg 2 times a day, 8 days) + rosevastatin (10 mg once) - unchanged.
Aleglytazar (0.3 mg, 7 days) + rosevastatin (40 mg, 7 days) - no change.
Silimarine (140 mg 3 times a day, 5 days) + rosevastatin (10 mg once) - unchanged.
Fenofibrate (67 mg 3 times a day, 7 days) + rosevastatin (10 mg, 7 days) - no change.
Rifampicin (450 mg 1 time per day, 7 days) + rosevastatin (20 mg once) - unchanged.
Ketoconazole (200 mg 2 times a day, 7 days) + rosevastatin (80 mg once) - unchanged.
Flukonazole (200 mg 1 time per day, 11 days) + rosevastatin (80 mg once) - unchanged.
Erythromycin (500 mg 4 times a day, 7 days) + rosevastatin (80 mg once) - Reduced AUC by 28%.
Baikalin (50 mg 3 times a day, 14 days) + rosevastatin (20 mg once) - AUC decrease by 47%.
Clopidogrel (300 mg (load dose), then 75 mg after 24 hours) + rosevastatin (20 mg once) - an increase in AUC 2 times.
SimePrevir (152 mg 1 time per day, 7 days) + rosevastatin (10 mg once) - an increase in AUC 2.8 times.
Effect of Rosuvastatin on Other LS
Vitamin K. antagonists as in the case of other GMG-Coa-reductase inhibitors, the beginning of rosuvastatin therapy or an increase in Rosuvastatan's dose in patients receiving vitamin K antagonists (for example, warfarin or other coumarin anticoagulants) can lead to an increase in many. Cancellation or reduction of the dose of Rosuvastatin can cause a decrease in many. In such cases, monitoring changes.
Oral contraceptives / hormone-plating therapy. The simultaneous use of rosuvastatin and oral contraceptives increases the AUC of Ethinyl Estradiol and Northetrel at 26 and 34%, respectively. Such an increase in plasma concentration should be taken into account when selecting the dose of oral contraceptives. Pharmacokinetic data on the simultaneous use of rosuvastatin and hormone-plating therapy are absent. It is impossible to exclude a similar effect with the simultaneous use of rosuvastatin and hormone-plating therapy. However, such a combination was widely used during clinical studies and was well tolerated by patients.
Other hops. The clinically significant interaction between Rosuvastatin with Digoxin is not expected.

Interaction Amlodipine ⇔ Amlodipine + leasing + rosevastatin (enters bisoprolol)

In amlodipine (text from instruction) ⇒ Amlodipine + leasing + rosevastatin (found him)

Amlodipine can also be safely used simultaneously with antibiotics and hypoglycemic agents for intake.

The re-use of amlodipine at a dose of 10 mg and atorvastatin at a dose of 80 mg is not accompanied by significant changes in the indicators of the Pharmacokinetics of Atorvastatin.







It does not have a significant effect on the action of warfarin (PV).
Cimetidine does not affect the pharmacokinetics of amlodipine.
In vitro studies, amlodipine does not affect the binding to the blood plasma proteins, phenytoin, warfarin and indomethacin.



The strong inhibitors of the CYP3A4 isoenzyme (for example ketoconazole, itraconazole) can lead to an increase in amlodipine concentration in the blood plasma to a greater extent than the diltia. Caution should be used amlodipine and inhibitors of the CYP3A4 isoenzyme.

General interactions between amlodipine and amlodipine + leasing + rosevastatin

BKK - Drug Dihydropyrididi derivatives (for example Nifedipine, Felodipine, amlodipine) - while simultaneous use with bisoprolol can increase the risk of arterial hypotension
Amlodipine + Bisoprolol
Amlodipine and bisoprolol are used together in the BIVAM
Amlodipine and bisoprolol are used together in Niperthen Combi
Amlodipine and bisoprolol are used together in Concorp
Amlodipine and bisoprolol are used together in Bisoprolol AML

Interaction Amlodipine (enters Amlodipine + leasing + rosevastatin) ⇔ Lysinopril (enters bisoprolol)

In Lysinopril (text from instruction) ⇒ Amlodipin (found him)

Double blockade Raas

General interactions between amlodipine and lysinopril

Hypotensive LS.

Interaction Amlodipine (enters Amlodipine + leasing + rosevastatin) ⇔ Bisoprolol

In bisoprolol (text from instruction) ⇒ Amlodipin (found him)

Recommended combinations














Mao inhibitors (. In addition to Mao B) inhibitors, the antihypertensive effect of β-adrenoblockers can enhance. Simultaneous use can also lead to the development of a hypertensive crisis.

In amlodipine (text from instruction) ⇒ Bisoprolol (found him)

Amlodipine can be safely used for arterial hypertension therapy along with thiazide diuretics, alpha-adrenoblockers, beta-adrenoblockers or ACE inhibitors. In patients with stable angina, amlodipine can be combined with other antichangal means, for example, with nitrates of prolonged or short action, beta-adrenobloclars.
Unlike other BKK, the clinically significant interaction of amlodipine (III generation of the BCC) was not detected during the joint use with the NSAID, in PM and with indomethacin.
It is possible to strengthen the anti-inanal and hypotensive effect of the BCC during co-use with thiazide and loop diuretics, ACE inhibitors, beta-adrenoblockers and nitrates, as well as enhancing their hypotensive effects with joint use with alpha1-adrenobloclars, neuroleptics.
Although, in the study of amlodipine, negative inotropic action was usually not observed, nevertheless, some of the BACK can enhance the severity of the negative inotropic effect of antiarrhythmic agents causing the elongation of the Qt interval (for example amiodarone and quinidine).
Amlodipine can also be safely used simultaneously with antibiotics and hypoglycemic agents for intake.
One-time reception of 100 mg of sildenafil in patients with essential hypertension does not affect the parameters of amlodipine pharmacokinetics.
The re-use of amlodipine at a dose of 10 mg and atorvastatin at a dose of 80 mg is not accompanied by significant changes in the indicators of the Pharmacokinetics of Atorvastatin.
Simvastatin: Simultaneous multiple use of amlodipine at a dose of 10 mg and simvastatin at a dose of 80 mg leads to an increase in the exposure of simvastatin by 77%. In such cases, it is necessary to limit the dose of simvastatin to 20 mg.
Ethanol (drinks containing alcohol): Amlodipine during one-time and reuse in a dose of 10 mg does not affect the pharmacokinetics of ethanol.
Antiviral Means (Ritonavir): Increases plasma concentrations of BKK, in PM and amlodipine.
Neuroleptics and Isofluraran: Strengthening the hypotensive effect of dihydropyridine derivatives.
Calcium preparations can reduce BKK effect.
With the joint use of BKK with lithium preparations (for amlodipine, data is absent) It is possible to enhance the manifestation of their neurotoxicity (nausea, vomiting, diarrhea, ataxia, tremor, noise in the ears).
Studies of simultaneous use of amlodipine and cyclosporin in healthy volunteers and all groups of patients ,. In addition to patients after kidney transplantation, were not conducted. Various studies of amlodipine interaction with cyclosporin in patients after kidney transplantation show that the use of this combination may not lead to any effect or increase CMIN cyclosporine to varying degrees to 40%. These data should be taken into account and control the concentration of cyclosporine in this group of patients with the simultaneous use of cyclosporine and amlodipine. It does not affect the concentration of Digoxin blood serum and its kidney clearance.
It does not have a significant effect on the action of warfarin (PV).
Cimetidine does not affect the pharmacokinetics of amlodipine.
In vitro studies, amlodipine does not affect the binding to the blood plasma proteins, phenytoin, warfarin and indomethacin.
Grapefruit juice: the simultaneous one-time reception of 240 mg of grapefruit juice and 10 mg of amlodipine inside is not accompanied by a significant change in amlodipine pharmacokinetics. However, it is not recommended to use grapefruit juice and amlodipine at the same time, because with the Genetic polymorphism of the CYP3A4 isoenzyme, it is possible to increase the bioavailability of amlodipine and as a result - an increase in the hypotensive effect.
Aluminum- or magnesium-containing antacids: their one-time reception does not have a significant impact on amlodipine pharmacokinetics.
Inhibitors of the CYP3A4 isoenzyme: while using a diltiazem at a dose of 180 mg and amlodipine at a dose of 5 mg in patients from 69 to 87 years old with arterial hypertension, an increase in amlodipine system exposure by 57% is noted. The simultaneous use of amlodipine and erythromycin in healthy volunteers (from 18 to 43 years) does not lead to significant changes in amlodipine exposure (an increase in AUC by 22%). Despite the fact that the clinical significance of these effects is completely unclear, they can be more pronounced in elderly patients.
The strong inhibitors of the CYP3A4 isoenzyme (for example ketoconazole, itraconazole) can lead to an increase in amlodipine concentration in the blood plasma to a greater extent than the diltia. Caution should be used amlodipine and inhibitors of the CYP3A4 isoenzyme.
Clarithromycin: CYP3A4 isoenzyme inhibitor. In patients taking at the same time clarithromycin and amlodipine, increased the risk of decline in blood pressure. Patients taking such a combination are recommended to be under careful medical supervision.
Inductors of the surgery of SUR 3A4: data on the effect of inductors of the CYP3A4 isoenzyme on amlodipine pharmacokinetics is not. The blood pressure should be carefully monitored with simultaneous use of amlodipine and inductors of the CYP3A4 isoenzyme.
Tacrolimus: With simultaneous use with amlodipine, there is a risk of increasing the concentration of tacrolimus in the blood plasma. In order to avoid the toxicity of the tacrolimus while simultaneously use with amlodipine, the concentration of tacrolimus in the blood plasma of patients should be monitored and adjust the tacrolimus dose if necessary.

Interaction Lysinopril (enters Amlodipine + leasing + rosevastatin) ⇔ Bisoprolol

In Lysinopril (text from instruction) ⇒ Bisoprolol (found him)

With the simultaneous use of lysinopril with potassium-saving diuretics (spironolactone, EPRELENON, TRIMENTEN, AMILORID), potassium drugs, substitutes of salts containing potassium, cyclosporin increases the risk of hypercalemia, especially when the kidney function is impaired, so they can be jointly used only with regular control of potassium content in Serum and kidney function.
Simultaneous use with beta-adrenobloclars, BKK, diuretics and other hypotensive means enhances the severity of antihypertensive effects.
Lysinopril slows down the removal of lithium preparations. Therefore, when co-use, it is necessary to regularly control the concentration of lithium in serum.
Antacids and swiverars reduce the suction of the leasedor into the gastrointestinal tract.
Hypoglycemic agents (insulin, hypoglycemic drugs for intake). The use of ACE inhibitors can enhance the hypoglycemic effect of insulin and hypoglycemic agents for intro, up to the development of hypoglycemia. As a rule, this is observed in the first weeks of simultaneous therapy and in patients with impaired kidney function.
NSAIDs (in PM selective inhibitors COG-2), estrogens, adrenomimetics reduce the antihypertensive effect of lysinopril. The simultaneous use of ACE and NSAID inhibitors can lead to a deterioration in the kidney function, including the development of acute renal failure, and an increase in the content of potassium in serum, especially in patients with reduced kidney function. Care should be taken when appointing this combination, especially in elderly patients. Patients should receive an adequate amount of fluid, and it is recommended to carefully monitor the kidney function, both at the beginning and in the process of treatment.
With the simultaneous use of ACE inhibitors and gold preparations (sodium ahurohythomalat), a symptom complex comprising hyperemia, nausea, vomiting and decreased blood pressure.
Co-use with SSORS can lead to pronounced hyponatremia.
Co-use with allopurinol, procanamide, cytostatics can lead to leukopenia.
Double blockade Raas
The literature reported that in patients with an asset atherosclerotic disease, heart failure or diabetes With the defeat of target organs, simultaneous therapy of the ACE and ARA II inhibitor is associated with a higher frequency of the development of arterial hypotension, fainting, hypercalemia and deterioration of the kidney function (including acute renal failure) compared to the use of only one LAN affecting Raas. A double blockade (for example, with a combination of an ACE inhibitor with Ara II), it must be limited to individual cases with careful monitoring of the kidney function, potassium and blood pressure.
Simultaneous use is contraindicated (see "Contraindications")
Alisian. In patients with diabetes or impaired kidney function (SCF less than 60 ml / min) increases the risk of hypercalemia, deterioration of the kidney function and increase the frequency of cardiovascular morbidity and mortality.
Estramustine. Simultaneous use can lead to an increase in the risk of side effects, such as angioedery edema.
Baclofen. Enhances the antihypertensive effect of ACE inhibitors. It is necessary to carefully control the blood pressure and, if necessary, the dosage of antihypertensive LS.
Gliptins (Linagliptin, Saxagliptin, Sitagliptin, Vitagliptin). Co-use with ACE inhibitors can increase the risk of developing angioedema edema due to the suppression of the activity of DPP-4 Glipticin.
Sympathomimetics. Can weaken the antihypertensive effect of ACE inhibitors.
Tricyclic antidepressants, neuroleptics and means for general anesthesia. Simultaneous use with ACE inhibitors can lead to an increase in antihypertensive action (see "Precautions").

In bisoprolol (text from instruction) ⇒ Lysinopril (found him)

The effectiveness and tolerability of bisoprolol may affect the simultaneous reception of other drugs. Such interaction can also occur in cases where two LS are accepted after a short period of time.
Recommended combinations
Treatment of HSN. Antiarrhythmic LS I class (for example, County, dyspeciramide, lidocaine, phenytoin, freakinide, conpaphenon) while use with bisoprolol can reduce AV conductivity and myocardial contractility.
All indications for the use of bisoprolol. BKK type verapamil and to a lesser degree of diltiazem with simultaneous use with bisoprolol can lead to a decrease in the contractile ability of myocardium and violation of AV conduction. In particular, the introduction of verapamil to patients receiving β-adrenoblays can lead to a pronounced arterial hypotension and AV blockade. Hypotensive LS of the central action (such as clonidine, methyldop, moxonidine, RylMidin) can lead to heart rate and reduce heart emissions, as well as to vasodilation due to a decrease in the central sympathetic tone. Sharp cancellation, especially before the cancellation of β-adrenoblastors, can increase the risk of ricochetic arterial hypertension.
Combinations requiring special caution
Treatment of arterial hypertension and angina. Antiarrhythmic agents I class (for example, quinidine, dyspeyramide, lidocaine, phenytoin, freakinide, conpaphenon) while use with bisoprolol can reduce the AV conductivity and the contractility of myocardium.
All indications for the use of bisoprolol. BKK - Dihydropyridine derivatives (for example, nifedipine, feelodipine, amlodipine) - while simultaneous use with bisoprolol can increase the risk of arterial hypotension. In patients with CHF, it is impossible to eliminate the risk of subsequent deterioration of the contractile function of the heart.
Antiarrhythmic agents of class III (for example amiodar) can enhance violation of AV conduction.
The action of β-adrenoblockers for local application (for example, eye drops for the treatment of glaucoma) can enhance the systemic effects of bisoprolla (decreased blood pressure, gentlement of heart rate).
Parasympathomimetics while simultaneous use with bisoprolol can enhance the violation of AV conductivity and increase the risk of bradycardia.
The hypoglycemic effect of insulin or hypoglycemic drugs for intake can be intensified. Signs of hypoglycemia, in particular tachycardia, can be masked or suppressed. Such interaction is more likely to use nonitive of β-adrenoblocators.
HP for general anesthesia can increase the risk of cardiopractive action, leading to arterial hypotension (see "Precautions").
Cardiac glycosides while using bisoprolol simultaneously can lead to an increase in the time of the pulse and thus to the development of bradycardia. NSAIDs can reduce the antihypertensive effect of bisoprolol.
The simultaneous use of bisoprolol with β-adreminimetics (for example isoprenaline, dobutamine) can lead to a decrease in the effect of both drugs. The use of bisoprolol with adrenomimetics that affect α- and β-adrenoreceptors (for example, norepinephrine, epinephrine) can enhance the vasoconstrictor effects of these agents arising from the participation of α-adrenoreceptors leading to an increase in blood pressure. Such interactions are more likely to use non-selective β-adrenoblockers.
Hypotensive LS. As well as other means with a possible antihypertensive effect (for example, tricyclic antidepressants, barbiturates, phenothiazines) can enhance the antihypertensive effect of bisoprolol.
MEFLOKHIN while simultaneously use with bisoprolol can increase the risk of bradycardia.
Mao inhibitors (. In addition to Mao B) inhibitors, the antihypertensive effect of β-adrenoblockers can enhance. Simultaneous use can also lead to the development of a hypertensive crisis.

Citation:Rosin A.N., Rosina N.A. The clinical efficacy of bisoprolol and its fixed combination with amlodipine // RMG. 2015. №5. P. 294.

Beta blockers are one of the main classes. medicinesused in modern cardiology and therapeutic practice. Knowledge of the mechanisms of drugs, their individual characteristics, in particular bisoprolol, determines the application of these funds.

Β-adrenoreceptor antagonists are selectively associated with receptors, carrying out a reversible competitive effect of the β-adrenergic blockade of various organs. Them pharmacological effect It can be explained by response reactions of receptor data in various tissues and a sympathetic tone (Table 1).

β-blockers have a relatively small effect on the frequency and strength of heart abbreviations in humans alone, but reduce these indicators when sympathetic system Activated, including during the load or stress.

Interestingly, β-blockers do not inhibit the cardiosulting effect of cardiac glycosides, theophylline, calcium ions, and also do not affect the vasodilating effect of acetylcholine.

Classification of β-blockers

β-blockers are divided into two groups:

1) non-selective β-blockers, i.e., equally blocking both β1 and β and β 2-adrenoreceptors;

2) β 1-selective β-blockers, i.e. having greater affinity to β 1-adrenoreceptors.

Selectivity, however, depends on the dose and decreases or disappears at all when the use of large doses of drugs.

Bisoprolol is highly selective with respect to β 1-adrenoreceptors with the ratio of antagonistic activity β1 to β2 more than 119. This exceeds the selectivity of the metoprolol of succinate (its ratio - 45).

Some β-blockers can cause a weak agonistic response (internal sympathomimetic activity), as well as stimulate and block β-adrenoreceptors. Bisoprolol does not have its own sympathomimetic activity and membrane-stabilizing effect.

In some β-blockers, peripheral vasodilative activity is observed, mediated by the α 1-adrenoreceptor blockade (carvedilol, labetalol), agonism β 2-adrenoreceptors (clerk) or mechanisms of independent blockade of adrenoreceptors (bucindolol, nebivolol).

In addition, β-blockers can be divided into lipophilic, amphophilic and hydrophilic.

Lipophilic drugs

Lipophilic preparations (metoprolol, propranolol, thymolol) quickly and completely absorbed in gastrointestinalBut at the same time quickly metabolized in the intestinal wall and in the liver (First Pass Effect), therefore, with oral administration, their effectiveness is small (10-30%). These drugs can accumulate in patients with reduced hepatic blood flow (including in older people, in patients with chronic heart failure and cirrhosis of the liver). Lipophilic drugs are characterized by a short half-life (1-5 h), they easily penetrate the central nervous system, which can explain frequent cases of the occurrence of central side effects.

Hydrophilic drugs

Hydrophilic preparations (atenolol, esmolol) are not completely absorbed in the gastrointestinal tract and are removed either in the initial state or as active metabolites by the kidneys. Their half-life longer (6-24 hours), and they do not interact with other medicines, metabolizing liver. They almost do not penetrate the hematorencephalic barrier. The half-life increases at low speed of glomerular filtering (including the elderly and with renal failure).

Amfophilic drugs

Grease and water-soluble β-blockers have two ways to eliminate - liver metabolism and renal excretion. Bisoprolol is an amphophilic β-blocker, since it is dissolved in fats and in water. As a result, he slightly penetrates through the hematorencephalic barrier and has two equivalent paths of elimination. Due to its amphophilic properties (i.e., solubility, both in fats and water), is well absorbed in the gastrointestinal tract, has a high bioavailability. Bisoprolol is partially metabolized in the liver, and its main part is distinguished by the kidneys unchanged. Due to the long period of half-life (10-12 hours), the drug is prescribed 1 r. / Day, the peak of its action occurs after 2-4 hours after the reception, the duration of the effect is 24 hours. Bisoprollane pharmacokinetics does not depend on food intake. The violation of the kidney function almost does not affect the concentration of the drug in the blood, only with pronounced renal failure, its dose is required. The dependence of the pharmacokinetics of bisoprolol from the dose is linear in nature, individual and mixing oscillations is small, which ensures the constant and predictable therapeutic effect of the drug.

Mechanism of action

The mechanisms of action of β-blockers are diverse and not fully studied. Most likely, there are significant differences between the mechanisms of action of various agents. An important role is played by preventing cardiotoxic effects of catecholamines.

The following mechanisms are also considered:

1) Antihypertensive effect associated with a decrease in the performance of the heart, inhibiting the secretion of renin and angiotensin II, blocking the presynaptic α-adrenoreceptors, which stimulate the emission of norepinephrine in sympathetic nerve endings and reduce central vasomotor activity.

2) Anti-Hichke action. β-blockers reduce the consumption of oxygen myocardium by reducing the heart rate, the contractile ability of the heart muscle, systolic blood pressure. In addition, the elongation of diastole caused by a decrease in heart rate can increase myocardial perfusion.

3) Reducing the emission of renin and angiotensin II and the synthesis of aldosterone by blocking β 1-adrenoreceptors of YuCstaglomelar cells of the kidneys.

4) Improving the structure and function of LV due to a decrease in its size and increasing the emission fraction.

β-blockers are able to improve the heart function, because they are:

a) reduce heart rate, diastolic volume and increase the coronary diastolic time of perfusion;

b) reduce the need of myocardium in oxygen;

c) increase myocardial energy by inhibiting catecholamine-induced emission of free fatty acids from adipose tissue;

d) stimulate β-adrenergic receptors;

e) reduce myocardial oxidative stress.

5) Antiarrhythmic effect, which is the result of direct heart electrophysiological effects (decrease in CCC, the oppression of the spontaneous activity of ectopic pacemaker cells, slowing down the conductivity and an increase in the refractory period of an atrioventricular node), a reduction in sympathetic regulation and myocardial ischemia, improve the barraflex function and preventing catecholamine-induced hypokalemia.

Other mechanisms of action include: inhibition of cardiac apoptosis, mediated by the activation of β-adrenergic pathways, inhibition of platelet aggregation, reduced mechanical stress, preventing the breaking of plaques, reacitization of β-adrenergic pathways and a change in myocardial gene expression.

Some β-blockers have antioxidative properties and inhibit the proliferation of smooth muscle cells of the vessels.

Interestingly, the use of β-blockers, and bisoprolol in particular, was associated with a favorable effect on inflammatory activity markers (tumor necrosis factor (TNF-α), its receptors, interleukins) in animals and in clinical studies.

Features of application in some clinical situations

In general, the β-blockers are moved well, but may also have serious side effects, especially when using large doses of drugs.

In patients with insulin-dependent diabetes (SD) of the 1st type, non-selective β-blockers suppress some important symptoms of hypoglycemia (tremor, tachycardia) associated with adrenergic conjunral activity; The remaining signs of hypoglycemia (for example, sweating) are saved. Therefore, the use of selective β-blockers is preferable, in any case for insulin-dependent patients.

In one of the works, it was demonstrated that the bisoprolol does not change the blood glucose level in patients with diabetes, and no correction of doses of hypoglycemic agents is required, which indicates its metabolic neutrality.

β-blockers can lead to life-threatening increase in respiratory resistance. Asthma is a contraindication to the use of any β-blockers, and chronic obstructive pulmonary disease (COPD) in the absence of significant reactivity respiratory tract Contraindication is not.

At the same time, it is shown that the use of selective β-blockers (including bisoprolol) in order to control the heart rate in patients with COPD and the development of acute respiratory failure did not lead to an increase in the treatment time in the intensive care departments and increase mortality compared to other Class of preparations used to control the heart rate.

When comparing bisoprollaol with carvedilol in the treatment of patients with heart failure and COPD, an improvement in the function of external respiration and a decrease in the severity of broncho-referee in the bisoprolol group is shown.

A sharp cessation of taking β-blockers after long-term treatment can lead to ricochetic symptoms (including arterial hypertension (AG), arrhythmias, angina complications). This increased risk is associated with the enhancement of the activity of β-adrenoreceptors over a long period of treatment.

CD or intermittent chromota are not absolute contraindications to the use of β-blockers.

Bisoprolol in the treatment of heart failure

The use of β-blockers in the treatment of heart failure led to a significant breakthrough in understanding the mechanisms of pathogenesis of this syndrome. Previously, the basis of the development of heart failure was considered to be a violation of hemodynamics, and the activation of the sympathetic nervous system was considered as a favorable reaction aimed at an increase in the contractile ability of myocardium and cardiac output. And, following this logic, the use of drugs with a negative inotropic effect in the conditions of violation of the pump function of myocardium should lead to further aggravation of heart failure phenomena (which is completely fair in decompensation and acute heart failure). Subsequent studies, however, showed an independent prognostic role of sympathetic activation in heart failure and its long-term negative impact on the function of myocardium and the outcome of the disease. An increase in sympathetic activity is associated with an increase in myocardial energy expenditures and, possibly, ischemia. Subsequently, it was shown that the stimulation of β 1-adrenoreceptors is a powerful mechanism of the apoptosis stimulation, which leads to accelerated cell death and serious changes in the qualitative characteristics of cardiomyocytes - aggravate reduction in the reduction of the contractility and disorders of intracellular calcium exchange (Table 2).

The role of sympathetic stimulation in quantitative and qualitative changes in myocardium is indirectly confirmed by their reversibility in the treatment of β-blockers.

The positive properties of β-blockers in the treatment of chronic heart failure (CXN) include the ability:

a) reduce dysfunction and death of cardiomyocytes as by necrosis and apoptosis;

b) reduce the number of hibernating cardiomyocytes;

c) for long use Improve hemodynamic indicators by increasing the zones of the reduced myocardial;

d) increase the density and affinity of β-adrenoreceptors sharply reduced in patients in patients;

e) reduce myocardial hypertrophy;

e) reduce heart rate;

g) reduce the degree of myocardial ischemia alone and, especially in physical activity;

h) somewhat reduce the frequency of ventricular arrhythmias;

and) to have an antifibrillator action leading to risk reduction sudden death.

The effectiveness of the use of bisoprolol in the treatment of CHSN is proved in the CIBIS Studies Series (Cardiac Insufficiency Bisoprolol Study), which were the first large-scale project that studied the influence of the β-blockade for mortality and the course of heart failure.

When carrying out a double-blind randomized placebo-controlled study on the use of bisoprolol with heart failure of class III or IV on NYHA (CIBIS) caused by a violation of the systolic function of LV (LVEF<40%), оценивалась эффективность и переносимость данного препарата у 641 пациента . В результате проведенного исследования было показано отсутствие значимого влияния бисопролола на смертность. 67 (20,9%) летальных исходов наблюдались в группе плацебо и 53 (16,6%) - в группе бисопролола (p=0,22). Положительные эффекты бисопролола наблюдались в других конечных точках: уменьшалась частота госпитализаций в сравнении с плацебо (61 vs 90, p<0,01) и снижался функциональный класс по NYHA (21% vs 15%, p=0,03). Переносимость β-блокатора была сопоставима с плацебо .

In Cibis, the effect of bisoprolol on mortality was less expected, which could be associated with the dose of the drug (5 mg / day), which could be too low to achieve an adequate β-blockade. In a few years earlier, the "Metoprolol in dilatation cardiomyopathy" (MDC), the effect of metoprolol tartrate on mortality and the need for heart transplantation turned out to be unreliable. Thus, the conducted studies did not finally estimate the effect of β-blockers on mortality in heart failure, and therefore the double-blind randomized placebo-controlled multicenter study of CIBIS-II was planned, which included 2647 heart failure patients (NYHA class III-IV) and the fraction of emissions of LV ≤35%. In this study, the main phase of 564 patients with 42.5% was obtained 10 mg of bisoprolol, 152 (11%) - 7.5 mg and 176 (13%) - 5 mg daily. In addition, standard therapy with diuretics and ACE inhibitors (IAPF) was carried out. In the CIBIS-II study, the answer was obtained to the question, not solved in the previous protocol, was an assessment of the influence of the β-blockade on mortality. The study was prematurely stopped after the average period of observation of 1.3 years due to a significant decrease in the mortality rate in patients receiving bisoprolol, compared with the placebo group - 11.8% against 17.3%, p<0,0001. Прогнозируемая смертность в течение года должна была составить 8,8% в группе бисопролола и 13,2% - в группе плацебо (ОШ; 95% ДИ) .

The decrease in mortality was due mainly with a decrease in the frequency of sudden cardiac death (48 patients in the bisoprolol group and 83 in the placebo group, HR 95% Ci, 0.56, 0.39-0.80; p \u003d 0.0011). The mortality rate from heart failure itself was reduced, but this result did not have a statistical value due to a small number of events (36 VS 47 patients, HR; 95% Ci, 0.74; 0.48-1.14; p \u003d 0, 17). This, as well as relatively low annual mortality among the studied patients, is consistent with the fact that people with relatively non-heavy heart failure, the main cause of mortality there was a sudden heartfelt death.

Bisoprolol also had a significant impact on all cardiovascular diseases. It was reduced as the total number of hospitalizations (440 (33%) VS 513 (39%), HR; 95% Ci, 0.80, 0.71-0.91; p \u003d 0.0006) and the number of hospitalizations due to Decompensation of heart failure (12% VS 18%, HR; 95% Ci, 0.64, 0.53-0.79; p \u003d 0.0001) and ventricular disorders of rhythm and hypotension.

The positive effects of bisoprolol are also identified in high-risk groups - good tolerability of the drug was noted, which contrasted with a widespread opinion on poor tolerability of β-blockers.

Upon completion of the meta-analysis, which included the results of CIBIS and CIBIS-II (n \u003d 3288), the effect of bisoprolol on a decrease in both overall death (p \u003d 0.0003) and cardiovascular mortality and all hospitalization cases were confirmed (P \u003d 0.0001 ). The results of CIBIS-II were confirmed by studies with metoprolol succinate and carvedilla.

Despite the high importance of the results obtained in the treatment of heart failure by β-blockers, all data were collected in the appointment of β-blockers against the background of standard therapy, including the IAPF, according to national recommendations. Nevertheless, there is reason to believe that the beginning of treatment with β-blockers, and not with the IAPF, may be no less favorable. First, in heart failure, the activation of the sympathetic nervous system can precede the activation of the renin-angiotensin system. Secondly, β-blockers can reduce the activity of the renin angiotensin system to a greater extent than this can be achieved against the background of the use of the IAPP under conditions of sympathetic activation. Thirdly, the most common cause of death in patients with CXN is a sudden heartfelt death, and β-blockers, in contrast to the IAPF, largely have a protective effect.

The idea of \u200b\u200bstudying CIBIS-III was the assumption that the initiation of the treatment of HSN from bisoprolol with the subsequent addition of enalapril is as effective and safe, as well as the beginning of therapy from the appointment of Enalapril with the subsequent addition of bisoprolol. Thus, the main purpose of the study was to prove that the beginning of the therapy from bisoprolol followed by combined therapy with enalapril after 6 months. It was also effectively (no worse), as well as the beginning of treatment with an ENALAPRIL, followed by a combination with bisoprolol, in relation to the prevention of all the causes of death and hospitalization.

The study included 1010 patients (the average age of 72 years), suffering from HSN light and moderate severity and previously not taking β-blockers nor IAPF. In the first 6 months. Participants were randomized into two parallel groups who received monotherapy with bisoprolol or enalapril. In the next 6-24 months. All participants received combined therapy with both drugs. At the end of the study, cases of death or hospitalization of patients were taken into account.

In the CIBIS-III study, it was shown that there is no difference in terms of efficiency and safety between the beginning of treatment with bisoprolol or enalapril in patients with NYHA II or III class of heart failure and a low fraction of LV emission. The results of the study allowed us to assume a greater impact on the level of mortality and sudden cardiac death when initiating treatment with bisoprolol, and not by enalapril. The main disadvantage of research is that it is built on an artificial continuation of monotherapy for 6 months. Before the combo treatment. In clinical practice, patients either begin to take both drugs at the same time, or the treatment of the IAPF followed by the rapid purpose of β-blockers.

The studies have demonstrated that the treatment of bisoprolol on tolerance is comparable to placebo. The recent episode of the decompensation of heart failure is contraindicated to the appointment of the drug, although research against carvedilol has shown that treatment can be started immediately when compensation is reached, followed by an increase in the dose, which leads to an improvement in the forecast.

It is important to remember that β-blockers do not apply to the number of ambulances and cannot extend patients from the state of decompensation and hyperifolding. β-blockers should be used in all patients with HSN with FV<40%, не имеющих противопоказаний (обычных для этой группы лекарств). При обычных клинических ситуациях β-блокаторы должны использоваться только вместе с иАПФ и у больных, у которых достигнута стабилизация состояния .

Using bisoprolol in a fixed combination with amlodipine

The advantages and features of the bisoprolol make it attractive for use in combination therapy in the treatment of cardiovascular diseases. One of the rational combinations is the use of β-blockers with calcium antagonists of a dihydropyridine row. This combination can be used both in the treatment of ischemic heart disease and ag.

The use of amlodipine in combination with Bisoprolol (KONCOR AM, "Takeda") justifies and by virtue of the similarity of their pharmacokinetic features. Both drugs have a long action and in one-time reception provide adequate control over the course of day, there are no pharmacokinetic interactions - plasma concentrations, bioavailability, the speed of metabolism does not change significantly, the combination does not increase the risk of insulin resistance and SD.

Bisoprolol and amlodipine in combination mutually complement each other:

• to the effects of the β-blocker, a pronounced vasodilative effect of calcium antagonist is added;
• tachycardia, developing in response to vasodilation, is controlled by adrenergic blockade;
• the extension of the vessels under the action of amlodipine additionally protects against the occurrence of peripheral spasm, which is potentially possible against the background of the use of bisoprolol.

In addition, amlodipine is one of the most applied calcium antagonists of a dihydropyridine row. It was studied in a variety of clinical studies as a reference hypotensive drug. In the AllHAT study with the participation of more than 40 thousand elderly patients with AG, a greater efficiency of amlodipine was shown in respect of decrease in blood pressure in comparison with the lease drive throughout the observation period. In addition, the ASCOT-BPLA study demonstrates a reliable reduction in the frequency of stroke, ischemic heart disease, as well as cardiovascular mortality.

According to A. I. Cherishnoy and Sovat. (2014), the use of a fixed combination of bisoprolol and amlodipine (Concor AM) in the outpatient treatment of patients with hypertension and ischemic heart disease was accompanied by a pronounced and resistant decrease in blood pressure with the achievement of the target level of systolic blood pressure in 90%, diastolic blood pressure - in 97% of cases, as well as a decrease in manifestations of myocardial ischemia and the demolition of heart rate, which, of course, helps to reduce the risk of developing cardiovascular complications and improving the forecast. The inclusion of the Preparation of Concor AM into the treatment regimen led to a significant increase in the commitment of patients therapy.

The combination of two drugs in fixed doses in one tablet is preferred, since the adherence to treatment is improved, which is confirmed by the use of bisoprolol / amlodipine. So, in March 2015, the results of a large study conducted in Poland were published on the use of a fixed combination of bisoprolol / amlodipine in the treatment of hypertension, in which the good adherence of patients, leading to better control of blood pressure and reduction of cardiovascular events.

Literature

1. CruckShank J.M., Prichard B.N.C. Beta-AdrenoCeptors / Cruickshank J.M., Prichard B.N.C. ED. // Beta-Blockers in Clinical Practice. London: Churchill Livingstone, 1996. P. 9-86.
2. Tamargo J.L., Delpon E. Optimisation of B-Blockers Pharmacology // J. Cardiovasc. Pharmacol. 1990. Vol. 16 (Suppl. 5). S. 8-10.
3. Metelitsa V.I. Handbook on clinical pharmacology of cardiovascular funds. M., 2005. p.162.
4. Bristow M.r. Beta-Adrenergic Receptor Blockade in Chronic Heart Failure // Circulation. 2000. Vol. 101. P. 558-569.
5. Lupanov V.P. Cardooselective beta blocker Bisoprolol in the treatment of patients with ischemic heart disease // Russian cardiology magazine. 2011. No. 3. P. 96-100.
6. Kryzhanovsky S.A., Vititious M.B. Medicinal products for the treatment of coronary heart disease (fundamental, clinical and evidence pharmacology). Lecture 4. Part 1. Beta-adrenoblays and their place in pharmacotherapy of the coronary heart disease // Therapist. 2012. No. 2. P. 26-36.
7. Tsolpugina S.N., Martsevich S.Yu. The place of bisoprolol in the treatment of cardiovascular diseases // Cardiovascular therapy and prevention. 2008. No. 7. P. 111-118.
8. Lukina Yu.V., Martsevich S.Yu. Bisoprolol is a highly selective beta-adrenoblocator from the position of evidence-based medicine // rational pharmacotherapy in cardiology. 2010. № 6 (1). P. 103-107
9. Bristow M.r. Pathophysiologic and Pharmacologic Rationale for Clinical Management of Chronic Hart Failure with Beta-Blocking Agents // AM. J. Cardiol. 1993. Vol. 71. P.12-22C.
10. Waagstein F. Beta-Blocket In Congestive Heart Failure: The Evolution of a New Treatment Concept-Mechanism of Action and Clinical Implications // J. Clin. Basic Cardiol. 2002. Vol. 5. P. 215-223.
11. β-Adrenergic Receptor Blockers // EUROPEAN Heart Journal. 2004. Vol. 25. P. 1341-13621-9.
12. Bouzamondo A., Hulot J.S., Sanchez P. et al. Beta-Blocker Treatment in Heart Failure // Fundam. CLIN. Pharmacol. 2001. Vol. 15. P. 95-109.
13. Opie L.h. Effect of Beta-Adrenergic Blockade on Biochemical and Metabolic Response to Exercise // AM. J. Cardiol. 1985. Vol. 55. P. 95D.
14. KUKIN M.L., KALMAN J., Charney R. et al. Prospective, Randomized COMPARISON OF EFFECT OF LONG-TERM TREATMENT WITH METOPROLOLOL OR CARVEDILOL ON SYMPTOMS, EXERCISE, EJECTION FRACTION, AND OXIDATIVE STRESS IN HEART FAILURE // CIRCULATION. 1999. Vol. 102. P.2646-2451.
15. Cleland J.g., Dargie H.J. Arrhythmias, Catechlamines and Electrolytes // AM. J. Coll. Cardiol. 1988. Vol. 62. P. 55-59.
16. Shizukuda Y., Buttrick P.M., Geenen D. et al. Beta-Adrenergic Stimulation Causes Cardioocyte Apoptosis: Influence of Tachycardia and Hypertrophy // AM. J. Physiol. 1998. Vol. 275. P. 961-968.
17. Lowes B.D., Gilbert E.M., Abraham W.T. et al. Myocardial Gene Expression in Dilated Cardiomyopathy Treated with Beta-Blocking Agents // N. Engl. J. Med. 2002. Vol. 346. P. 1357-1365.
18. Frishman W.H. CARVEDILOL // N. engl. J. Med. 1998. Vol. 339. P. 1759-1765.
19. Ohtsuka T., Hamada M., Hiasa G. et al. Effect of Beta-Blockers on Circulating Levels of Inflammatory and Anti-Inflammatory Cytokines in Patients with Dilated Cardiomyopathy // J. Am. Coll. Cardiol. 2001. Vol. 37 (2). P. 412-417.
20. Kuzes V.G., Ostrumova OD, Baturina A.M., Zykova A.A. Beta-blockers in the treatment of arterial hypertension in patients with diabetes mellitus: contraindications or preparations of choice? // RMW. 2002. No. 10. P. 446-449.
21. EXPERT CONSENSUS Document On B-Adrenergic Receptor Blockers. The Task Force On Beta-Blockers of the European Society of Cardiology // European Heart Journal. 2004. Vol. 25. P. 1341-1362.
22. Feyza Kargin, Huriye Berk Takir, Cuneyt Salturk et al. The Safety of Beta Blocker Use In Chronic Obstructive Pulmonary Disease Patients with Respiratory Failure in The Intensive Care Unit // Multidiscip. Respir. Med. 2014. Vol. 9 (1). P. 8.Published Online 2014 Feb 4. Doi: 10.1186 / 2049-6958-9-8
23. Lainscak M., Podbregar M., Kovacic D., Rozman J. Differences Between Bisoprolol and Carvedilol in Patients with Chronic Heart Failure and Chronic Obstructive Pulmonary Disease: A Randomized Trial // Respir. Med. 2011. Vol. 105. S1, S. 44-49.
24. Marco M., Nodari S., Bordonali T. et al. Bisoprolol in The Treatment of Chronic Heart Failure: From Pathophysiology to Clinical Pharmacology and Trial Results // Ther. CLIN. Risk. Manag. 2007. Vol. 3 (4). P. 569-578.
25. Metra M., Nodari S., D'Aloia A. et al. A Rationale for the Use of Beta Blockers AS Standard Treatment for Heart Failure // AM. Heart J. 2000B. Vol. 139. P. 511-521.
26. National Recommendations OSSN, RKO and RNMMS on the diagnosis and treatment of HSN (fourth revision) // Heart failure. 2013. T. 14, No. 7 (81).
27. Cibis Investigators and Committees 1994. A Randomized Trial of Beta-Blockade in Heart Failure. The Cardiac Insufficiency Bisoprolol Study (Cibis) // Circulation. Vol. 90. P. 1765-1773.
28. Waagstein F., Bristow M.R., Swedberg K. et al. Beneficial Effects of Metoprolol in IDIOPATHIC DILATED CARDIOMYOPATHY. Metoprolol in Dilated Cardiomyopathy (MDC) Trial Study Group // LanCet. 1993. Vol. 342. P. 1441-1446.
29. CIBIS-II INVESTIGATORS AND COMMITTEES. The Cardiac Insufficiency Bisoprolol Study: A Randomised Trial // LanCet. 1999. Vol. 353. P. 9-13.
30. Leizorovicz A., Lechat P., Cucherat M. Bisoprolol for Treatment of Chronic Heart Failure: A Meta-Analysis on Individual Data Of Two Placebo-Controlled Studies-Cibis and Cibis II // AM. Heart J. 2002. Vol. 143. P. 301-307.
31. Merit-HF Study Group. Effect of Metoprolol CR / XL in Chronic Heart Failure: Metoprolol CR / XL Randomised Intervention Trial In CONGESTIVE HEART FAILURE (MERIT-HF) // LANCET. 1999. Vol. 353. P. 2001-2007.
32. Packer M., Coats A., Fowler M. et al. Effect of Carvedilol on Survival in Severe Chronic Heart Failure (Copernicus Trial) // N. engl. J. Med. 2001. Vol. 344. P. 1651-1658.
33. Hunt S.A., Abraham W.T., Chin M.h. et al. ACC / AHA. Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: a report of the American College of Cardiology / American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): Developed in Collaboration with the American College of CHEST PHYSICIANS AND THE INTERNATIONAL SOCIETY FOR HEART AND LUNG TRANSPLANTATION: Endorsed by The Heart Rhythm Society // Circulation. 2005. Vol.112. P. E154-235.
34. Swedberg K., Cleland J., Dargie H. et al. Task Force For the Diagnosis and Treatment of Chronic Heart Failure of the European Society of Cardiology. Guidelines for the Diagnosis and Treatment of Chronic Heart Failure: Executive Summary (UPDATE 2005) // EUR. Heart J. 2005. Vol. 26. P. 1115-1140.
35. Francis G.S., Benedict C., Johnstone et al. COMPARISON OF NEUROENOCRINE ACTIVATION IN PATIENTS WITH LEFT VENTRICULAR DYSFUNCTION WITH AND WITHOUT CONGESTIVE HEART FAILURE. A SUBSTUDY OF THE STUDIES OF LEFT VENTRICULAR DYSFUNCTION (SOLVD) // CIRCULATION. 1990. Vol. 82. P. 1724-1729.
36. Campbell D.J., Aggarwal A., Esler M. et al. Beta-Blockers, Angiotensin II, and Ace Inhibitors in Patients with Heart Failure // LanCet. 2001. Vol. 358. P. 1609-1610.
37. Willenheimer R., Van Veldhuisen D.J., Silke B. et al. Effect on Survival and Hospitalization of Initiating Treatment for Chronic Heart Failure with Bisoprolol Followed by Enalapril, AS Compared with the Opposite Sequence. Results of the Randomized Cardiac Insufficiency Bisoprolol Study (CIBIS) III // Circulation. 2005. Vol. 112. P. 2426-2435.
38. Gattis W.A., O'Connor C.M., Gallup D.S. et al. Impact-hf Investigators and Coordinators. PREDISCHARGE INITIATION OF CARVEDILOL IN PATIENTS HOSPITALIZED FOR DECOMPENSATED HEART FAILURE: RESULTS OF THE INITIATION MANAGEMENT OF CARVEDILOL THERAPY IN HEART FAILURE (IMPACT-HF) TRIAL // J. am Coll. Cardiol. 2004. Vol. 43. P. 1534-1541.
39. Gradman A.H. et al. Combination Therapy In Hypertension // J. Am. SOC. Hypertens. 2010. Vol. 4 (1). P. 42-50.
40. Ostergren J. et al. Effect of Amlodipine Versus Felodipine Extended Release ON 24-Hour Ambulatory Blood Pressure in Hypertension // AM. J. Hypertens. 1998. Vol. 11 (6 pt1). P. 690-696.
41. MINUSHINA L.O. Rational therapy of arterial hypertension in patients with diabetes mellitus: the possibilities of using new fixed combinations // Hard patient. December 2013.
42. Cooper-dehoff R.M., Bird S.T., Nichols G.A. et al. AntiHypertensive Drug Class Interactions and Risk for Incident Diabetes: A Nested Case-Control Study // J. AM. Heart Assoc. 2013. Vol. 2 (3). P. E000125.
43. Officers A., A.c.r.g.t.a. Coordinators for the, and T. Lipid-Lowering Treatment to Prevent Heart Attack, Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (Allhat) // jama. 2002. Vol. 288 (23). P. 2981-2997.
44. Dahlof B., WEDEL H. ET AL. Prevention of cardiovascular events with an antihypertensive regimen of amlodipine adding perindopril as required versus atenolol adding bendroflumethiazide as required, in the Anglo-Scandinavian Cardiac Outcomes Trial-Blood Pressure Lowering Arm (ASCOT-BPLA): a multicentre randomised controlled trial // Lancet. 2005. Vol. 366. P. 895-906.
45. Chesnikova A.I., Safronenko V.A., Kolomatskaya O.E. Evaluation of the effectiveness of the fixed combination of bisoprolol and amlodipine in the outpatient treatment of patients with arterial hypertension and ischemic heart disease // Cardiology. 2014. No. 9. P. 30--36.
46. Recommendations for the treatment of arterial hypertension. ESH / ESC // Russian Cardiology Journal. 2014. No. 1 (105).
47. Czarnecka D., Koch E.m.w., Hostalek U. Benefits of a Fixed Dose Combination of Bisoprolol and Amlodipine (Concoram) In The Treatment of Hypertension In Daily Practice: Results of More Than 4,000 Patients // Current Med. Research and Opinion. 2015. Mar 9.

Hypertensive disease is the problem of many middle-aged people. Elevated blood pressure is available in most people whose age over 50 years old. However, recently, the disease has grown out, and people of younger age suffer high pressure. It is impossible to fully cure the disease, but you can reduce the pressure using medicines.

Pharmacological companies are constantly developing new drugs. Relatively new are amlodipine and bisoprolol. Some patients are asked what drugs to choose for the treatment of arterial hypertension. To do this, it is necessary to study both medications in detail, as well as their similarities and differences.

Pharmacological group: calcium channel blockers. Active substance amlodipine Besilat. Available in tablets in the dosage 5 and 10 mg. The medicine has a hypotensive and antianginal effect.

Antianginal action occurs due to expansion of vessels. This increases the amount of oxygen entered myocardium.

A long hypotensive effect is caused by influence on the smooth muscles of the vessels. Daily dose provides a significant decrease in blood pressure in 24 hours.

Meal does not affect the absorption of medicinal substances. The average bioavailability is 64%.

Applied at:

1. Hypertension.
2. Angina.
3. Heart failure.
4. Ischemic heart disease.

The use of amplodipine when angina can prevent the appearance of an attack. This allows you to increase the duration of physical exertion, as well as reduce the reception of nitroglycerin.

The initial dosage is 5 mg per day. If necessary, the dose gradually increases. Maximum dosage 10 mg per day.

Contraindications for the use of amlodipine are:

• Individual intolerance to the substances that are part of.
• Pregnancy.
• Arterial hypotension.
• Cardiogenic shock.
• Collapse.
• Children under 18.
• Lactation period.

Patients with aortic stenosis, myocardial infarction and renal pathologies - amlodipine is appointed with caution.

Refers to a group of beta adrenobloclars. Active substance: bisoprolol Fumarat. Tablets are produced in a dosage of 5 and 10 mg.

It has antianginal, antiarrhythmic and hypotensive effect.

The hypotensive effect is associated with a decrease in the minute volume of blood circulating in vessels. After taking medication, the effect occurs through 3-5 days. The resistant hypotensive effect is observed after 1-2 months at regular reception of the drug.

The antianginal effect is determined by a decrease in the needs of myocardium in oxygen. An antiarrhythmic effect is associated with the elimination of arrhythmogenic factors.

Eliminates symptoms and improves the general condition of the patient. Regular reception allows you to achieve a resistant hypotensive effect and avoid a hypertonic crisis.

Indications for the use of bisoprolol are:

1. Hypertonic disease.
2. Coronary artery disease.
3. Heart failure.

The dosage is appointed by the doctor individually. The initial dose is 5 mg per day. Take it in the morning, before taking food, not chewing. If necessary, the dose is doubled, but the reception is carried out once in the morning. Maximum daily dose - 20 mg.

Contraindications are:

• Individual intolerance to the drug.
• Acute heart failure.
• Cardiogenic shock.
• Pulmonary edema.
• Bradycardia.
• Heavy form of arterial hypotension.
• Bronchial asthma.
• COPL.
• Diabetes.

The effectiveness and safety of bisoprolol has not been studied in relation to children, so it does not apply to pediatrics.

What kind of drug is better?

Both drugs are used in cardiology in the treatment of hypertensive disease, heart failure or angina. Medicines should be taken daily even with a satisfactory condition of the patient and normal blood pressure. In compliance with the rules of application, both drugs are transported quite well patients.

Distinctive features of drugs are as follows:

1. Different pharmacological groups and action mechanism.
2. Bisoprolol can be taken with acute myocardial infarction at normal arterial pressure, and amlodipine - no.
3. Amlodipine does not affect the conduct of impulses and can be taken with various types of arrhythmia.
4. Bisoprolol can not be taken to patients with bronchial asthma and diabetes.
5. For diseases of peripheral vessels, amlodipine preference is given.

Many are interested in which drug is better to choose. If we talk about efficiency, then Bisoprolol is much stronger. However, it is able to cause sufficiently severe side effects. It is also rarely used in the composition of combined therapy, as it is poorly combined with a variety of drugs, and with some incompatible at all.

Amlodipine is often prescribed to patients with uncomplicated hypertension. Bisoprolol is recommended for patients with severe heart failure. It is also an important element of treatment after a myocardial infarction. Sometimes these drugs are combined into a single treatment scheme.

Reception of drugs allows reduce the load on the heart musclethat allows it to work in a calm mode.

Thus, these are two sufficiently strong drug with their advantages and disadvantages. It is impossible to say exactly what drug is better, since it should choose the doctor individually for each patient. Do not deal with self-medication.

Medicinal preparations must be taken regularly, and not only at the time of increase of pressure. The effectiveness of therapy depends on the regularity of the drug intake. Regular reception allows you to maintain the tone of vessels in good condition, as well as prevent the development of heart attack and stroke.