Coraxan tabs 5mg #56

Instruction for use of Coraxan

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Coraxan is an antianginal drug, a selective inhibitor of the If-channels of the sinus node.

Release form and composition

The dosage form of Coraxan is film-coated tablets: orange-pink in color, engraved, on one side - the company logo, on the other - for oval biconvex tablets with notches on two sides - the number 5, for triangular tablets - the number 7, 5 (14 pcs. In blisters, in a cardboard box 1, 2 or 4 blisters).
The active ingredient is ivabradine hydrochloride:
    1 oval tablet - 5.39 mg, which is equivalent to 5 mg of ivabradine;
    1 triangular tablet - 8.085 mg, which is equivalent to 7.5 mg of ivabradine.
Auxiliary components: magnesium stearate, lactose monohydrate, corn starch, colloidal anhydrous silicon dioxide, maltodextrin.
The composition of the film shell: hypromellose, glycerol, iron dye yellow oxide (E172), macrogol 6000, titanium dioxide (E171), iron dye red oxide (E172), magnesium stearate.

Pharmacodynamics

Ivabradine is a drug that slows down the heart rate. Its mechanism of action consists in the specific and selective suppression of the If-channels of the sinus node, which are responsible for spontaneous diastolic depolarization in the sinus node and control the heart rate (HR).
The effect on cardiac activity is specific for the sinus node and does not change the time of passage of impulses along the intraventricular, atrioventricular and intraatrial pathways, and also does not affect the contractility of the myocardium. In this case, the processes of repolarization of the ventricles proceed in the same way as in the absence of drug administration. Ivabradine can interact with Ih-channels localized in the retina and resembling the If-channels of the heart, which are involved in the development of transient metamorphosis of the visual perception system due to changes in the retinal response to light stimuli of high brightness. Provoking circumstances (for example, a rapid change in brightness) lead to partial inhibition of Ih channels by ivabradine, which in turn causes the so-called phenomenon of changes in light perception (photopsy). Photopsy is a temporary change in brightness observed in a limited area of ​​the visual field.
 The main clinical effects of ivabradine include its ability to reduce heart rate, which is dose-dependent. In a separate study, the dependence of the magnitude of the decrease in heart rate on the dose of Coraxan was studied. In the course of it, patients received a dose of ivabradine, gradually increasing to 20 mg per day, 2 times a day. The results indicated the achievement of a plateau effect (the therapeutic effect stopped increasing), which reduces the risk of developing severe bradycardia (heart rate less than 40 beats per minute), which is poorly tolerated by patients.
When using Coraxan in recommended doses, the decrease in heart rate is approximately 10 beats per minute, both during physical exertion and at rest. As a result, the functioning of the heart decreases and the need for myocardial oxygen supply decreases.
Ivabradine does not change the processes of repolarization of the ventricles, their contractility (no negative inotropic effect was found) and intracardiac conduction. In the course of clinical electrophysiological studies, ivabradine did not affect the transit time of impulses along the intraventricular or atrioventricular pathways, as well as the QT intervals that underwent correction. Special studies involving more than 100 patients with left ventricular dysfunction (ejection fraction ranged from 30 to 45%) showed that taking Coraxan does not affect myocardial contractility.
Four double-blind randomized studies (2 comparative studies using amlodipine and atenolol and 2 placebo-controlled studies) confirmed that the drug had a pronounced anti-ischemic and antianginal effect. The experiment involved 3222 patients suffering from chronic stable angina pectoris. Of these, 2,168 people took ivabradine. The results showed that ivabradine, taken at a dosage of 5 mg 2 times a day, had a beneficial effect on all parameters of stress tests as early as 3-4 weeks after the start of treatment. The effectiveness of the drug has been proven for a dosage of 7.5 mg 2 times a day. For example, an additional effect with an increase in the dose from 5 mg to 7.5 mg with the same frequency of administration was revealed in the course of a comparative study with atenolol: the time of physical activity increased by approximately 1 minute after 1 month of treatment with Coraxan, which was prescribed at a dosage of 5 mg 2 times a day. At the same time, additional intake of ivabradine at a dosage of 7.5 mg 2 times a day for 3 months led to a further increase in this indicator by 25 seconds. The results of this study also confirmed the anti-ischemic and antianginal efficacy of Coraxan for elderly patients (65 years and older). A pronounced therapeutic effect of ivabradine, used in dosages of 5 mg and 7.5 mg 2 times a day, was noted in the course of the above studies in relation to all parameters of stress tests (the time before the onset of ST segment depression is 1 mm below the isoline, the time before the onset of an attack of angina pectoris, time to the development of a limiting attack of angina pectoris, the total duration of physical activity). At the same time, the incidence of angina attacks decreased by approximately 70%. The dosage regimen, consisting in twice taking ivabradine throughout the day, provided equal efficacy within 24 hours.
A randomized placebo-controlled study, which involved 725 patients, showed the absence of any additional efficacy of Coraxan when added to amlodipine, taken at the maximum dose, on the decline in therapeutic activity (12 hours after oral administration), while during the period peak activity (3-4 hours after oral administration), additional efficacy of ivabradine was observed. The experiments in which the clinical efficacy of Coraxan was studied confirm the complete preservation of the effects of ivabradine during courses of treatment that lasted 3-4 months. During the course of therapy, no signs of pharmacological tolerance (decrease in effectiveness) were found, and after discontinuation of ivabradine, there was no withdrawal syndrome. The anti-ischemic and antianginal effect of the drug was expressed in a dose-dependent decrease in heart rate, as well as in a significant decrease in the work product (heart rate x systolic blood pressure), both during physical exertion and at rest. The drug had an insignificant effect on the resistance of the peripheral vascular system and the blood pressure indicator (the changes were not clinically pronounced).
Patients who took ivabradine for at least 12 months (n = 713) showed a sustained decrease in heart rate. At the same time, the drug did not affect the metabolism of lipids or glucose. In patients with diabetes mellitus (n = 457), ivabradine proved to be an effective drug, as in other groups of patients of comparable size.
A study in which patients with ischemic heart disease, not accompanied by signs of heart failure [left ventricular ejection fraction (LVEF)> 40%], who received maintenance therapy, showed that taking ivabradine in doses higher than recommended [initial dosage 7.5 mg 2 times a day (in patients over 75 years old - 5 mg 2 times a day), which was subsequently titrated to 10 mg 2 times a day], did not significantly affect the primary combined endpoint (diagnosis of nonfatal myocardial infarction or death due to cardiac - vascular causes). In the group of patients taking Coraxan, the incidence of bradycardia was 17.9%, 7.1% of the participants in the experiment additionally took diltiazem, verapamil, or potent inhibitors of the isoenzyme CYP3A4.
In patients with diagnosed class II angina or higher in accordance with the classification of the Canadian Cardiological Society, a slight increase in the number of cases of the onset of the primary combined endpoint was found when taking Coraxan, which is statistically significant. This effect was absent in the subgroup of all patients with angina pectoris (class I and above).
In the course of the study, which involved patients with left ventricular dysfunction (LVEF does not exceed 40%) and stable angina pectoris (86.9% of them also took beta-blockers), there were no differences between the groups of patients who took placebo or ivabradine on the background course of standard therapy, in terms of indicators such as increased symptoms of chronic heart failure (CHF), the total frequency of deaths due to cardiovascular diseases, hospitalization for the occurrence of new episodes of heart failure or hospitalization associated with acute myocardial infarction. In patients with symptomatic angina pectoris, no significant differences were found in the hospital room due to heart failure or the development of non-fatal myocardial infarction or in the incidence of deaths due to cardiovascular disease (the incidence was 15.5% in the placebo group and 12% in the ivabradine group. respectively). The intake of ivabradine by patients with a heart rate of at least 70 beats per minute led to a decrease in the frequency of hospitalizations caused by non-fatal and fatal myocardial infarction by 36% and the frequency of revascularization by 30%.
In patients with exertional angina pectoris during treatment with Coraxan, there was a decrease in the relative risk of complications (hospitalization due to increased symptoms of CHF or the occurrence of new episodes of heart failure, hospitalization associated with acute myocardial infarction, the frequency of deaths due to cardiovascular diseases) by 24%. This therapeutic benefit is achieved mainly by reducing the frequency of hospital admissions associated with acute myocardial infarction by 42%.
The frequency of hospitalization due to non-fatal and fatal myocardial infarction in patients with a heart rate of more than 70 beats per minute decreases even more significantly (by about 73%). In general, there is a relative safety of the drug in this category of patients and its good tolerance.
Against the background of ivabradine treatment of patients with CHF II ‒ IV functional class in accordance with the NYHA classification (LVEF does not exceed 35%), a clinically and statistically significant decrease in the relative risk of complications is recorded (a decrease in the number of hospitalizations associated with an increase in the symptoms of CHF, and the frequency of deaths). due to cardiovascular diseases) by 18%. At the same time, the absolute risk reduction was 4.2%. A pronounced therapeutic effect was noted approximately 3 months after the start of treatment.
A decrease in the number of hospitalizations due to increased symptoms of CHF, and deaths resulting from cardiovascular diseases, did not depend on the presence of arterial hypertension or diabetes mellitus in history, gender, age, ischemic or non-ischemic etiology of CHF, functional class of CHF, intake of beta adrenergic blockers.
Patients with a heart rate of at least 70 beats per minute and symptoms of CHF with sinus rhythm underwent a standard course of treatment, including aldosterone antagonists (60%), beta-blockers (89%), diuretics (83%), angiotensin II receptor antagonists and / or ACE inhibitors (91%).
It has been proven that the use of Coraxan for 12 months can prevent 1 hospitalization associated with cardiovascular disease, or 1 death for every 26 patients taking ivabradine. Against the background of its use, the functional class of CHF improves in accordance with the NYHA classification. In patients with a heart rate of 80 beats per minute, there was a decrease in this indicator by about 15 beats per minute.

Pharmacokinetics

Ivabradine is rapidly released from tablet form and has very good water solubility (exceeding 10 mg / ml). The molecule of this substance is the S-enantiomer, which lacks bioconversion in accordance with the results of in vivo studies. It has been proven that when it enters the human body, ivabradine forms the main pharmacologically active metabolite - the N-desmethylated derivative.
Ivabradine is rapidly and almost 100% absorbed in the gastrointestinal tract after oral administration. Its maximum concentration in blood plasma is recorded 1.5 hours after oral administration on an empty stomach. Bioavailability reaches approximately 40%, which is associated with the effect of the first passage through the liver. Taking Coraxan with food increases the absorption time by about 1 hour and increases its concentration in blood plasma from 20% to 30%. To reduce interindividual variability, Coraxan is recommended to be taken together with meals.
Ivabradine binds to blood plasma proteins by approximately 70%. The volume of distribution is about 100 liters. The maximum content of the active substance in the blood plasma after long-term administration of the drug at the recommended dosage of 5 mg 2 times a day is approximately 22 ng / ml. On average, the equilibrium concentration in blood plasma reaches 10 ng / ml.
Ivabradine is predominantly metabolized in the liver and intestines through oxidation with the participation of the CYP3A4 isoenzyme of the cytochrome P450 system. The main metabolite showing pharmacological activity is the N-desmethylated derivative (S 18982). About 40% of the taken dose of ivabradine is converted into it, the pharmacodynamic and pharmacokinetic properties of which are almost identical to those of the metabolite. The metabolism of the N-desmethylated derivative is also carried out by the isoenzyme CYP3A4. Ivabradine is characterized by a low affinity for this isoenzyme, and there are no signs of its inhibition or induction. For this reason, it is unlikely that ivabradine affects the metabolism or the content of substrates of the CYP3A4 isoenzyme in blood plasma. However, the combination of ivabradine with strong inducers or inhibitors of the cytochrome P450 system can significantly change the content of the drug in the blood plasma.
The half-life of ivabradine averages about 2 hours (70-75% of the AUC - the area under the concentration-time curve), and the effective half-life reaches 11 hours. The total clearance is approximately 400 ml / min, and the renal clearance is 70 ml / min. Ivabradine in unchanged form (in small amounts) and its metabolites are excreted at the same rate through the gastrointestinal tract and kidneys. Approximately 4% of an oral dose taken is excreted in the urine.
The pharmacokinetics of the drug is linear when the drug is taken in the dose range of 0.5-24 mg.
When used in patients over 65 years old, over 75 years old and representatives of the general population, the pharmacokinetic parameters of ivabradine practically do not change.
In patients with renal insufficiency (CC 15-60 ml / min), the effect of this disease on the pharmacokinetics of the drug remains minimal.
In patients with mild hepatic insufficiency (5-7 points according to the Child-Pugh scale), the AUC of the active substance and its metabolite increases by 20% compared with patients with normal liver function.
Information on the use of ivabradine in patients with moderate hepatic impairment (7-9 points according to the Child-Pugh scale) is limited. Clinical data concerning patients with severe hepatic impairment (more than 9 points according to the Child-Pugh scale) are not available today.
As a result of the analysis of the relationship between pharmacodynamic and pharmacokinetic properties, it was found that the decrease in heart rate is in direct proportion to the increase in the level of ivabradine and its pharmacologically active metabolite S 18982 in the blood plasma when taking Coraxan at a dosage of up to 15–20 mg 2 times a day. At higher doses of the drug, there is no proportional dependence of the deceleration of the heart rate on the concentrations of ivabradine in the blood plasma, and the decrease in heart rate tends to achieve a plateau effect. Ivabradine in high concentrations, which can be achieved when Coraxan is combined with potent inhibitors of the isoenzyme CYP3A4, can provoke a pronounced decrease in heart rate, but the degree of risk decreases when combined with moderate inhibitors of CYP3A4.

Indications for use

According to the instructions, the drug is indicated for the treatment of stable angina pectoris in patients with normal sinus rhythm:
    The presence of contraindications to beta-blockers or their intolerance;
    Inadequate control of stable angina pectoris with optimal doses of beta-blockers, for combination with beta-blockers.
In addition, Coraxan is prescribed for chronic heart failure in patients with a heart rate (HR) of 70 or more beats per minute and sinus rhythm in order to reduce the incidence of possible cardiovascular complications.

Contraindications

    Sinoatrial blockade;
    Bradycardia, with a resting heart rate of less than 60 beats per minute;
    Acute myocardial infarction;
    Unstable angina
    Cardiogenic shock;
    Severe hypotension (systolic blood pressure (BP) below 90 mm Hg (Hg) and diastolic blood pressure below 50 mm Hg);
    Sick sinus syndrome (SSS);
    Acute or unstable heart failure;
    Atrioventricular block (AV block) III degree;
    Constant stimulation by an artificial pacemaker;
    Concomitant use of strong inhibitors of isoenzymes of the cytochrome P450 3A4 system, such as nefazodone, macrolide antibiotics (telithromycin, clarithromycin, josamycin, oral erythromycin), antifungal drugs of the azole group (itraconazole, ketoconazole) (riftonavir HIV-inhibitors, HIV-inhibitors);
    Severe liver failure (on the Child-Pugh scale more than 9 points);
    Glucose-galactose malabsorption syndrome, lactose intolerance, lactase deficiency;
    The period of pregnancy and breastfeeding;
    Age under 18;
    Hypersensitivity to the components of Coraxan.
The drug is contraindicated in women of reproductive age who do not use reliable contraception.
It is recommended to prescribe the drug with caution to patients with arterial hypotension, AV block II degree, chronic heart failure class IV (NYHA classification), moderate hepatic failure, severe renal failure (with creatinine clearance (CC) less than 15 ml / min), congenital lengthening QT interval, recent stroke, retinal pigment degeneration.
Under close medical supervision, it is necessary to take the drug in combination with moderate inhibitors and inducers of CYP3A4 isoenzymes, drugs that lengthen the QT interval, grapefruit juice, slow calcium channel blockers that reduce heart rate (diltiazem, verapamil), potassium-sparing diuretics.

Instructions for the use of Coraxan: method and dosage

The tablets are taken orally, with meals, 2 times a day (morning and evening).
With stable angina pectoris, the initial daily dose is 10 mg (1 tablet 5 mg in the morning and in the evening). Based on clinical indications, after 3-4 weeks of administration, the daily dose can be increased to 15 mg. In the case of a decrease in resting heart rate to less than 50 beats per minute or the appearance of symptoms of bradycardia (dizziness, a strong decrease in blood pressure, increased fatigue), the daily dose of the drug should be reduced to 5 mg. In the absence of a therapeutic effect after a dose reduction, the use of Coraxan should be canceled.
In chronic heart failure, the recommended starting daily dose is 10 mg. After 2 weeks of use, if the resting heart rate remains stable at more than 60 beats per minute, the dose can be increased to 15 mg.
Correction of the daily dose of Coraxan depends on the patient's heart rate stability at rest:
    50 beats per minute or less - 5 mg (against the background of the onset of symptoms of bradycardia);
    50 to 60 beats per minute - 10 mg;
    Above 60 beats per minute - 15 mg.
If the heart rate is 50 beats per minute or less, or the symptoms of bradycardia in the patient persist, the question of discontinuing the drug should be considered.
For patients aged 75 years and older, the recommended initial daily dose is 5 mg, its further increase is possible.
For patients with impaired renal function (CC more than 15 ml / min), the initial daily dose is recommended to be prescribed in the amount of 10 mg, in the case of a therapeutic effect, its increase to 15 mg is possible after 3-4 weeks of taking Coraxan.
Patients with mild hepatic impairment (up to 7 points on the Child-Pugh scale) do not need to adjust the usual recommended dosage.
In case of severe renal dysfunction and moderate hepatic impairment, the drug is recommended to be prescribed with caution.

Side effects

The use of Coraxan can cause side effects:
    From the side of the cardiovascular system: often - bradycardia; infrequently - supraventricular extrasystole, palpitations; very rarely - SSSU, atrial fibrillation, AV block II and III degree; the frequency is unknown - a pronounced decrease in blood pressure (may be associated with bradycardia);
    From the senses: very often - changes in light perception (photopsia); often - blurred vision; infrequently - vertigo; frequency unknown - visual impairment, diplopia;
    From the digestive system: infrequently - nausea, diarrhea or constipation;
    From the respiratory system: infrequently - shortness of breath;
    From the nervous system: often - headache (especially the first 4 weeks of therapy), dizziness; frequency unknown - fainting;
    From the musculoskeletal system: infrequently - muscle spasms;
    On the part of the skin and subcutaneous fat: the frequency is unknown - itching, skin rash, erythema, urticaria, angioedema;
    On the part of laboratory and instrumental parameters: infrequently - eosinophilia, hyperuricemia, prolongation of the QT interval on the electrocardiogram (ECG), an increase in the level of creatinine concentration in the blood;
    General disorders: frequency unknown - fatigue, asthenia, malaise.
The most often undesirable effects from taking ivabradine are dose-dependent and associated with the mechanism of clinical action of the drug.

Overdose

An overdose of Coraxan may be accompanied by severe prolonged bradycardia, which is poorly tolerated by patients. In this case, symptomatic treatment is prescribed, which is carried out exclusively in specialized hospitals. If bradycardia is combined with unfavorable changes in hemodynamic parameters, symptomatic therapy with intravenous administration of beta-adrenergic agonists (for example, isoprenaline) is recommended. If necessary, it is possible to temporarily install an artificial pacemaker.

Special instructions

Coraxan has no clinical effect in the treatment or prevention of arrhythmias; against the background of supraventricular or ventricular tachycardia, its effect decreases.
It is not recommended to prescribe ivabradine to patients with atrial fibrillation (atrial fibrillation) and other types of arrhythmias caused by dysfunction of the sinus node.
Patients with chronic heart failure taking the drug, and patients with other diseases, are more at risk of developing atrial fibrillation against the background of simultaneous use with amiodarone or class I antiarrhythmic drugs. The use of Coraxan in patients with impaired intraventricular conduction (blockade of the left or right bundle branch), chronic heart failure and ventricular dyssynchrony should be closely monitored by a physician.
With bradycardia with a resting heart rate of less than 60 beats per minute, unstable heart failure and immediately after a stroke, the administration of the drug is contraindicated.
If you experience visual impairment, you should consult your doctor.
If it is necessary to prescribe Coraxan to patients with congenital syndrome of an extended QT interval, treatment should be carried out under strict ECG control.
In patients with atrial fibrillation, the risk of developing severe bradycardia in pharmacological cardioversion of restoration of sinus rhythm has not been confirmed. You should stop taking the drug 24 hours before the planned electrical cardioversion.
Changes in antihypertensive therapy in chronic heart failure in patients taking Coraxan should be monitored by blood pressure.

Influence on the ability to drive vehicles and complex mechanisms

Coraxan does not affect the patient's ability to drive vehicles and mechanisms, however, one should take into account the possible visual impairment in the form of a temporary change in light perception and be careful during the period of a sharp change in light intensity, mainly at night.

Application during pregnancy and lactation

Pregnancy is a contraindication to the use of the drug. At the moment, information regarding the use of the drug by pregnant women is considered insufficient. The results of preclinical studies of ivabradine prove the presence of a teratogenic and embryotoxic effect.
The appointment of Coraxan during lactation is contraindicated. Animal studies confirm that ivabradine passes into breast milk. Patients requiring the drug therapy should stop breastfeeding.
During treatment with the drug, women of reproductive age should use reliable methods of contraception.

Childhood use

Due to the lack of data on the efficacy and safety of Coraxan in children and adolescents under the age of 18, the drug is not used in pediatrics.

With impaired renal function

With severe renal failure [creatinine clearance (CC) below 15 ml / min], the drug is prescribed with caution. With CC above 15 ml / min, it is not required to adjust the dosage regimen of the drug.

For violations of liver function

    mild liver failure: no dosage adjustment is required;
    moderate hepatic impairment: care must be taken when taking the drug;
    severe liver failure: drug therapy is contraindicated.

Use in the elderly

Patients aged 75 years and older should not exceed the initial daily dose of Coraxan, which is 5 mg (2.5 mg 2 times a day). Depending on the tolerance of the drug and the patient's condition, a further increase in the daily dose is possible.

Drug interactions

Combinations with inducers and inhibitors of the CYP3A4 isoenzyme are not recommended, since they cause a decrease and an increase (respectively) in the level of ivabradine concentration in blood plasma.
The combination of Coraxan with strong inhibitors of the isoenzyme CYP3A4 is contraindicated, since they can cause an increase in average concentrations of ivabradine in blood plasma by 7-8 times.
Concomitant administration of fluconazole and other moderate inhibitors of the CYP3A4 isoenzyme is possible if the resting heart rate exceeds 60 beats per minute. The initial dose of the drug is recommended in the amount of 5 mg per day; treatment must be accompanied by heart rate control.
Additional prolongation of the QT interval is caused by the combination of ivabradine with disopyramide, quinidine, bepridil, ibutilide, sotalol, amiodarone and other antiarrhythmics; ziprasidone, pimozide, sertindole, cisapride, halofantrine, pentamidine, mefloquine, erythromycin (when administered intravenously). Treatment in this combination must be carried out under careful and regular ECG monitoring.
Hypokalemia may increase the risk of arrhythmia, therefore, caution should be exercised when the drug is prescribed while taking non-potassium-sparing diuretics (loop and thiazide diuretics).
The combined use of rifampicin, barbiturates, phenytoins, herbal remedies including St. John's wort or other inducers of the CYP3A4 isoenzyme can reduce the concentration and effect of ivabradine.
There is no clinically significant effect on the pharmacokinetics and pharmacodynamics of the drug in combination with warfarin, digoxin, proton pump inhibitors (lansoprazole, omeprazole), HMG-CoA reductase inhibitors (simvastatin), PDE5 inhibitors (sildenafil), calcium channel blockers (sildenafil) amlodipine).
Coraxan does not affect the pharmacokinetics of amlodipine, warfarin, digoxin, simvastatin, lacidipine and the pharmacodynamics of warfarin, digoxin, acetylsalicylic acid.
Grapefruit juice increases the concentration of ivabradine in blood plasma by 2 times, therefore, it is recommended to avoid its use during the treatment period.
Shown is the use of Coraxan in combination with angiotensin II receptor antagonists, ACE inhibitors, beta-blockers, aldosterone antagonists, diuretics, long-acting and short-acting nitrates, fibrates, HMG-CoA reductase inhibitors, proton pump inhibitors, oral antiglycemic agents, hypoglycemic agents ...

Terms and conditions of storage

Store at room temperature. Keep out of the reach of children.
Shelf life is 3 years.

Reviews about Coraxan

On the network, there are mainly positive reviews about Coraxan, since it eliminates disturbances in the work of the heart muscle of an unclear etiology, that is, when the reason remains unknown to a specialist. Some patients call the drug a "life buoy", as it helps in cases when the use of beta-blockers is ineffective and does not lead the rhythm of myocardial contractions to sinus.
However, Coraxan's side reactions are also mentioned, which are most pronounced on the part of the organ of vision. Many patients complain of severe photopsy, which significantly impairs their quality of life.
Doctors consider Coraxan a fairly effective drug that copes in situations where similar drugs are unable to help the patient. They advise stopping unwanted side effects while taking ivabradine with a medication, since when the drug is canceled, a relapse of the underlying disease is often observed.

Terms of sell

You don't need a prescription to buy Coraxan.