Instruction for use: AtacandI want this, give me price
Dosage form: tablets
Active substance: Candesartanum
Angiotensin II receptor antagonist [Angiotensin II receptor antagonists (AT1-subtype)]
Nosological classification (ICD-10)
I10 Essential (primary) hypertension: hypertension; Arterial hypertension; Arterial hypertension crisis course; Essential Hypertension; Essential hypertension; Essential hypertension; Essential hypertension; Essential hypertension; Primary hypertension; Arterial hypertension, complications of diabetes; The sudden increase in blood pressure; Hypertensive disorders of blood circulation; hypertensive condition; hypertensive crises; arterial Hypertension; malignant Hypertension; Hypertonic disease; hypertensive crises; accelerated hypertension; malignant hypertension; The aggravation of hypertensive disease; Transient hypertension; Isolated systolic hypertension
I15 Secondary hypertension: Arterial hypertension, complications of diabetes; hypertension; The sudden increase in blood pressure; Hypertensive disorders of blood circulation; hypertensive condition; hypertensive crises; hypertension; arterial Hypertension; malignant Hypertension; hypertensive crises; accelerated hypertension; malignant hypertension; The aggravation of hypertensive disease; Transient hypertension; hypertension; Arterial hypertension; Arterial hypertension crisis course; renovascular hypertension; Hypertension symptomatic; Renal hypertension; Renovascular hypertension; renovascular hypertension; Symptomatic hypertension
I50.0 Congestive heart failure: anasarca heart; Decompensated congestive heart failure; Congestive heart failure; Congestive heart failure with high afterload; Congestive chronic heart failure; Cardiomyopathy with severe chronic heart failure; Compensated chronic heart failure; Swelling with circulatory failure; Edema of cardiac origin; Swelling of the heart; Edematous syndrome in diseases of the heart; Edematous syndrome in congestive heart failure; Edematous syndrome in heart failure; Edematous syndrome in heart failure or liver cirrhosis; right ventricular failure; Congestive Heart Failure; Heart failure stagnant; Heart failure with low cardiac output; Heart failure is a chronic; Cardiac edema; Chronic decompensated heart failure; Chronic Congestive Heart Failure; Chronic heart failure; Change of liver function in heart failure
I50.1 Left ventricular failure: Cardiac asthma; Asymptomatic dysfunction of the left ventricle; Asymptomatic left ventricular heart failure; Diastolic dysfunction of the left ventricle; Left ventricular dysfunction; Changes in the left ventricle with myocardial infarction; Left ventricular heart failure; Violation of the function of the left ventricle; Acute left ventricular failure; Acute cardiac left ventricular failure; Cardiac asthma; Heart failure of left ventricular; Changes in the lungs with left ventricular failure; Precordial abnormal pulsation; Lack of left ventricle
Tablets -1 table.
active substance: Candesartan cilexetil 8 mg; 16 mg
Excipients: carmellose calcium (carmellose calcium salt) - 5.6 / 5.6 mg; Giprolose (hydroxypropylcellulose) - 4/4 mg; Iron dye oxide red (E172) - 0.065 / 0.26 mg; Lactose monohydrate - 89.4 / 81.4 mg; Magnesium stearate - 0.4 / 0.4 mg; Corn starch - 20/20 mg; Macrogol 2.6 / 2.6 mg
Description of dosage form
Atacand® 8 mg: light pink round biconvex tablets, with a risk and engraved "A / CG" - on one side and 008 on the other.
Atacand® 16 mg: pink round biconvex tablets, with a risk and engraved "A / CH" on one side and 016 on the other.
Mode of action - hypotensive, blocking AT1-receptors.
Angiotensin II is the main hormone of RAAS, which plays an important role in the pathogenesis of arterial hypertension, heart failure and other cardiovascular diseases. The main physiological effects of angiotensin II are vasoconstriction, stimulation of aldosterone production, regulation of water-electrolyte homeostasis and stimulation of cell growth. All these effects are mediated by the interaction of angiotensin II with angiotensin receptor type 1 (AT1 receptors).
Candesartan is a selective antagonist of angiotensin II type 1 receptors. Candesartan does not inhibit ACE which converts angiotensin I into angiotensin II and breaks down bradykinin; Does not affect the ACE and does not lead to the accumulation of bradykinin or P. In comparing candesartan with ACE inhibitors, the development of cough was less common in patients receiving candesartan cilexetil. Candesartan does not bind to the receptors of other hormones and does not block the ion channels involved in the regulation of CCC functions. As a result of blocking of AT1-receptors of angiotensin II, a dose-dependent increase in the level of renin, angiotensin I, angiotensin II and a decrease in plasma aldosterone concentration occurs.
With arterial hypertension candesartan causes a dose-dependent long-term decline in blood pressure. The antihypertensive effect of the drug is due to a decrease in OPSS, without a change in heart rate. There were no cases of severe arterial hypotension after taking the first dose of the drug, as well as withdrawal syndrome ("ricochet" syndrome) after discontinuation of therapy.
The onset of antihypertensive action after taking the first dose of candesartan cilexetil usually develops within 2 hours. Against the background of continuing therapy with the drug at a fixed dose, the maximum decrease in blood pressure is usually achieved within 4 weeks and persists throughout the treatment. Candesartan tsileksetil, prescribed once a day, provides an effective and smooth decrease in blood pressure within 24 hours with minor fluctuations in blood pressure in the intervals between doses of the next dose of the drug. The use of candesartan cilexetil together with hydrochlorothiazide leads to an increase in the hypotensive effect. The combined use of candesartan cilexetil and hydrochlorothiazide (or amlodipine) is well tolerated.
The effectiveness of the drug does not depend on the age and sex of patients.
Candesartan cilexetil increases renal blood flow and does not change or increases the rate of glomerular filtration, whereas renal vascular resistance and filtration fraction decrease. The use of candesartan cilexetil in a dose of 8-16 mg for 12 weeks does not adversely affect glucose level and lipid profile in patients with arterial hypertension and type 2 diabetes mellitus.
The clinical effect of candesartan cilexetil on morbidity and mortality when taken at a dose of 8-16 mg (average dose of 12 mg) was tested once a day in a randomized clinical trial involving 4937 elderly patients (age 70 to 89 years, 21% of patients in Age 80 years and over) with mild to moderate arterial hypertension receiving cdesdesartan cilexetil for an average of 3.7 years (COPE study of cognitive function and prognosis in elderly patients). Patients received candesartan or placebo, if necessary, in combination with other antihypertensive agents. In the group of patients who received candesartan, BP was reduced from 166/90 to 145/80 mm Hg. Art. And in the control group - from 167/90 to 149/82 mm Hg. Art. There were no statistically significant differences in the incidence of cardiovascular complications (mortality due to cardiovascular disease, myocardial infarction and stroke, which did not result in death) between the two groups of patients.
In the group of patients receiving candesartan, there were 26.7 cases of cardiovascular complications per 1000 patient-years, compared to 30 cases per 1000 patient-years in the control group (risk ratio = 0.89, 95% confidence interval 0, 75-1.06, p = 0.19).
Chronic heart failure
According to the results of the CHARM study (Candesartan for Chronic Heart Failure - Assessment of Mortality and Morbidity Reduction), the use of candesartan cilexetil led to a reduction in the incidence of deaths and the need for hospitalization for chronic heart failure and an improvement in the systolic function of the left ventricle.
Patients with chronic heart failure in addition to the main therapy received candesartan cilexetil at a dose of 4-8 mg / day with a dose increase of up to 32 mg / day or up to the maximum tolerable therapeutic dose (average dose of candesartan was 24 mg). The median duration of follow-up was 37.7 months. After 6 months of therapy, 63% of patients who continued to take candesartan cilexetil (89%) received a therapeutic dose of 32 mg.
In another CHARM-Alternative study (n = 2028), patients with a reduced (≤40%) left ventricular ejection fraction (LVEF) who did not receive an ACE inhibitor because of intolerance (mainly due to a cough - 72%) participated; The rates of death from cardiovascular disease and the first hospitalization for chronic heart failure were significantly lower in the group of patients receiving candesartan compared with the placebo group (hazard ratio = 0.77, 95% confidence interval 0.67-0.89 ; P <0.001). The relative risk reduction was 23%. In this study, to prevent one death from cardiovascular complications or hospitalization for chronic heart failure, 14 patients were required to be treated throughout the study period. The combined criteria, including the incidence of deaths regardless of their cause, and the first hospitalization rate for chronic heart failure, also turned out to be significantly lower in the group of patients receiving candesartan (risk ratio = 0.80, 95% confidence interval 0.7- 0.92, p = 0.001). In this case, the positive effect of candesartan on each of the components of this combined criterion - the rate of deaths and incidence (the frequency of hospitalizations for chronic heart failure) was noted. The use of candesartan cilexetil led to an improvement in the functional class of chronic heart failure according to NYHA classification (p = 0.008).
In the CHARM-Added study (n = 2548) in patients with reduced LVEF <40% who received ACE inhibitors, the combined criteria including the mortality from cardiovascular disease and the first hospitalization for chronic heart failure was significantly lower in the group of patients Who received candesartan compared with the placebo group (risk ratio = 0.85, 95% confidence interval 0.75-0.96, p = 0.011), which corresponded to a 15% relative risk reduction. In this study, to prevent one death from cardiovascular complications or hospitalization for chronic heart failure, it was necessary to treat 23 patients throughout the study period. The value of the combined effectiveness criterion, which included an estimate of the frequency of deaths regardless of their cause or frequency of first hospitalization for chronic heart failure, was significantly lower in the group of patients receiving candesartan (risk ratio = 0.87, 95% confidence interval 0, 78-0.98, p = 0.021), which also indicated a positive effect with candesartan. The use of candesartan cilexetil led to an improvement in the functional class of chronic heart failure according to the NYHA classification (p = 0.02).
In the CHARM-Preserve study (n = 3023), in patients with preserved systolic function (LVEF> 40%), there was no statistically significant difference in the value of the combined efficacy test, which included the incidence of fatal outcomes and the frequency of first hospitalization for chronic heart failure, In the groups candesartan and placebo (risk ratio = 0.89, 95% confidence interval 0.77-1.03, p = 0.118). A small numerical decrease in this criterion was due to a decrease in the frequency of hospitalizations for chronic heart failure. In this study, the effect of candesartan on the incidence of death was not shown.
In a separate analysis of the results of 3 studies of the CHARM program, there was no significant difference in the incidence of fatal outcomes in the candesartan and placebo groups. However, the death rate was assessed in the combined CHARM-Alternative and CHARM-Added studies and in all 3 studies (hazard ratio = 0.91, 95% confidence interval 0.83-1.0, p = 0.055). The reduction in the frequency of deaths and the frequency of hospitalizations for chronic heart failure with candesartan therapy did not depend on age, sex and concomitant therapy. Candesartan was also effective in patients taking beta-blockers in combination with ACE inhibitors, and the efficacy of candesartan was not dependent on whether the patient was receiving the optimal dose of an ACE inhibitor or not.
In patients with chronic heart failure and reduced left ventricular systolic function (LVEF ≤ 40%), candesartan administration contributed to a reduction in OPSS and capillary pressure in the lungs, an increase in renin activity and an angiotensin II concentration in the blood plasma, and a decrease in aldosterone levels.
Suction and distribution
Candesartan cilexetil is a prodrug for oral administration. Rapidly turns into an active substance - candesartan by ether hydrolysis when absorbed from the digestive tract, firmly binds to AT1 receptors and dissociates slowly, does not have the properties of an agonist. Absolute bioavailability of candesartan after oral administration of a solution of candesartan cilexetil is about 40%. The relative bioavailability of the tablet preparation as compared to the oral solution is approximately 34%. Thus, the calculated absolute bioavailability of the tablet form of the drug is 14%. Cmax in the blood serum is achieved 3-4 hours after taking the tablet form of the drug. With an increase in the dose of the drug within the recommended range candesartan increases linearly. The pharmacokinetic parameters of candesartan do not depend on the sex of the patient. Eating does not have a significant effect on AUC, i.e. Simultaneous intake of food does not significantly affect the bioavailability of the drug. Candesartan actively binds to blood plasma proteins (> 99%). Vd candesartan is 0.1 l / kg.
Metabolism and excretion from the body
Candesartan, basically, is excreted from the body by the kidneys and bile in unchanged form and is only slightly metabolized in the liver. T1 / 2 candesartan is approximately 9 hours. Cumulation in the body is not observed.
Candesartan has a total clearance of about 0.37 ml / min / kg, with a kidney clearance of about 0.19 ml / min / kg. Renal excretion of candesartan is carried out by glomerular filtration and active tubular secretion. When ingestion of radio-labeled candesartan cilexetil, about 26% of the administered amount is excreted by the kidneys in the form of candesartan and 7% - in the form of an inactive metabolite, whereas in feces 56% of the administered amount in the form of candesartan and 10% in the form of an inactive metabolite is detected.
In elderly patients (over 65 years of age), Cmax and AUC of candesartan increase by 50 and 80%, respectively, compared with young patients. However, the hypotensive effect and frequency of side effects when using Atacand® do not depend on the age of the patients.
In patients with mild and moderate renal impairment, Cmax and AUC of candesartan increased by 50 and 70%, respectively, whereas T1 / 2 of the drug did not change as compared to patients with normal renal function. In patients with severe renal dysfunction, Cmax and AUC of candesartan increased by 50% and 110%, respectively, and T1 / 2 of the drug increased 2-fold. Patients on hemodialysis were found to have the same pharmacokinetic parameters of candesartan as in patients with severe renal dysfunction.
In patients with mild and moderate impairment of liver function, AUC of candesartan was increased by 23%.
Indications of the drug Atacand
Chronic heart failure and a violation of left ventricular systolic function (reduction of the left ventricular ejection fraction ≤40%) as adjunctive therapy to ACE inhibitors or intolerant ACE inhibitors (see the section "Pharmacodynamics").
Increased sensitivity to candesartan cilexetil or other components included in the preparation;
Severe violations of liver function and / or cholestasis;
Pregnancy and lactation (see the section on "Application during pregnancy and lactation").
With caution: in patients with severe renal failure (Cl creatinine <30 ml / min), bilateral renal artery stenosis or stenosis of the single kidney, with hemodynamically significant stenosis of the aortic and mitral valve, after a kidney transplant in history, in patients with cerebrovascular disease and IHD, hyperkalemia, in patients with reduced bcc, primary hyperaldosteronism (there is insufficient data on clinical studies), hypertrophic cardiomyopathy, under the age of 18 (effe Quality and safety are not established).
Application of pregnancy and breastfeeding
In a human embryo, the kidney blood supply system, which depends on the development of RAAS, begins to form in the second trimester of pregnancy. Thus, the risk to the fetus increases with the appointment of Atakand® in the II and III trimesters of pregnancy. Drugs that have a direct effect on RAAS can cause fetal developmental disorders or have a negative effect on the newborn, up to a lethal outcome when the drug is used in the second and third trimesters of pregnancy.
In animal studies, kidney damage in the embryonic and neonatal periods was identified with candesartan cilexetil. It is assumed that the mechanism of damage is due to the pharmacological effect of the drug on RAAS.
Based on the information received, Atacand® should not be used during pregnancy. If the pregnancy is detected during treatment with Atacand®, therapy should be discontinued (see section "Contraindications").
Now it is not known whether candesartan penetrates into breast milk. Due to possible undesirable effects on infants, Atacand® should not be used during breastfeeding.
Side effects in clinical trials were mild and transient and were comparable in frequency with the placebo group. The overall incidence of side effects with Atacand® was independent of the dose and age of the patient. The incidence of discontinuation due to side effects was similar when using candesartan cilexetil (2.4%) and placebo (2.6%).
During the analysis of these studies, the following side effects were reported, often (> 1/100) occurring against the background of administration of candesartan cilexetil. The described side effects were observed with a frequency of at least 1% more than in the placebo group.
From the side of the central nervous system: dizziness, weakness, headache.
From the osteomuscular system, connective tissue: back pain.
Infections: Respiratory infections.
Laboratory indices: in general, when Atakand® was used, clinically significant changes in standard laboratory parameters were not observed. As with other RAAS inhibitors, a slight decrease in hemoglobin concentration can be observed. There was an increase in creatinine, urea or potassium and a decrease in the sodium content. The increase in ALT levels was noted somewhat more frequently with Atacand® compared with placebo (1.3% instead of 0.5%). When using Atacand®, there is usually no need for regular monitoring of laboratory indicators. However, in patients with impaired renal function it is recommended to periodically monitor the level of potassium and creatinine in the serum.
Chronic heart failure
The side effects detected with Atacand® in patients with chronic heart failure corresponded to the pharmacological properties of the drug and depended on the patient's condition. Clinical studies of CHARM compared Atakand® at doses of 32 mg (n = 3803) with placebo (n = 3796), 21% of patients treated with candesartan cilexetil, and 16.1% of patients in the placebo group , Discontinued treatment due to the occurrence of adverse reactions.
The most common side effects (≥1 / 100, <1/10).
From the CVS: a marked decrease in blood pressure.
On the part of the urinary system: a violation of kidney function.
Laboratory changes: increase in the level of creatinine, urea and potassium. It is recommended to monitor the level of creatinine and potassium in the blood serum.
About the following side effects during the postmarketing use of the drug reported very rarely (<1/10000).
From the blood and lymphatic system: leukopenia, neutropenia and agranulocytosis.
Disturbance of metabolism and diseases caused by a metabolic disorder: hyperkalemia, hyponatremia.
From the nervous system: dizziness, weakness, headache.
From the digestive tract: nausea.
From the liver and biliary tract: increased activity of liver enzymes, a violation of liver function or hepatitis.
Allergic reactions: angioedema, skin rash, hives, itching.
From the musculoskeletal system, connective tissue: back pain, arthralgia, myalgia.
On the part of the urinary system: a violation of kidney function, including renal failure in predisposed patients.
In pharmacokinetic studies, the combined use of Atacand® with hydrochlorothiazide, warfarin, digoxin, oral contraceptives (ethinyl estradiol / levonorgestrel), glibenclamide, nifedipine, and enalapril has been studied. Clinically significant drug interactions were not identified.
Candesartan is metabolized in the liver to an insignificant extent (CYP2C9). The conducted studies on the interaction did not reveal the effect of the drug on CYP2C9 and CYP3A4; The effect on other isoenzymes of the cytochrome P450 system has not been studied.
The combined use of Atacand® with other antihypertensive agents potentiates the hypotensive effect.
The experience of using other drugs that act on RAAS shows that concomitant therapy with potassium-sparing diuretics, potassium preparations, salt substitutes containing potassium, and other agents that can increase serum potassium levels (for example, heparin) can lead to the development of hyperkalemia.
With the combined use of lithium preparations with ACE inhibitors, a reversible increase in serum lithium concentration and the development of toxic reactions were reported. Similar reactions can occur with the use of angiotensin II receptor antagonists, and therefore, it is recommended to monitor the level of lithium in the serum when combined use of these drugs.
The bioavailability of candesartan is not dependent on food intake.
Dosing and Administration
Inside, 1 time per day, regardless of food intake.
The recommended initial and maintenance dose of Atacand® is 8 mg once a day. Patients who require a further reduction in blood pressure, it is recommended to increase the dose to 16 mg once a day. The maximum antihypertensive effect is achieved within 4 weeks from the start of treatment.
If Atakand ® therapy does not lead to a decrease in blood pressure to the optimal level, it is recommended to add a thiazide diuretic to therapy.
Patients of advanced age. In elderly patients, there is no need to adjust the initial dose of the drug.
Patients with impaired renal function. In patients with mild to moderate renal impairment (Cl creatinine ≥30 mL / min / 1.73 m2 body surface area), no change in the initial dose of the drug is required.
Clinical experience of the drug in patients with severe renal dysfunction (Cl creatinine <30 ml / min / 1.73 m2 body surface area) is limited; In this case, you should consider starting treatment with a daily dose of 4 mg.
Patients with impaired hepatic function. In patients with impaired liver function of mild and moderate severity, it is recommended to begin treatment with a daily dose of 2 mg once a day. It is possible to increase the dose if necessary. Clinical experience in patients with severe liver damage is limited.
Concomitant therapy. The use of Atakand® together with thiazide type diuretics (eg hydrochlorothiazide) can enhance the antihypertensive effect of Atacand®.
Chronic heart failure
The recommended initial dose of Atacand® is 4 mg once a day. An increase in the dose to 32 mg once a day or up to the maximum tolerated dose is performed by doubling it at intervals of not less than 2 weeks (see section "Special instructions").
Special patient groups. Elderly patients and patients with impaired renal or hepatic function do not need to change the initial dose of the drug.
Use in children and adolescents. Safety and effectiveness of Atakanda® in children and adolescents (under the age of 18 years) have not been established.
Concomitant therapy. Atakand® can be administered together with other agents used in the therapy of chronic heart failure, for example, ACE inhibitors, beta-blockers, diuretics and cardiac glycosides (see sections "Special instructions", "Pharmacodynamics").
Symptoms: an analysis of the pharmacological properties of the drug suggests that the main manifestation of an overdose may be a clinically pronounced decrease in blood pressure and dizziness. Individual cases of drug overdose (up to 672 mg of candesartan cilexetil), which resulted in the recovery of patients without severe consequences, were described.
Treatment: with the development of clinically pronounced arterial hypotension, it is necessary to carry out symptomatic treatment and monitor the patient's condition. Lay the patient, raise the head end of the bed. If necessary, increase the volume of circulating plasma, for example, by iv administration of an isotonic sodium chloride solution. If necessary, sympathomimetic preparations may be prescribed. The withdrawal of candesartan by hemodialysis is unlikely.
Impaired renal function
Against the background of Atakand® therapy, as with other agents that oppress RAAS, some patients may have impaired renal function.
When using Atacand® in patients with arterial hypertension and severe renal failure, it is recommended that the serum levels of potassium and serum creatinine be monitored periodically. The clinical experience of the drug in patients with severe renal dysfunction or terminal renal failure is limited (Cl creatinine <15 mL / min).
Patients with chronic heart failure need periodic monitoring of kidney function, especially in patients aged 75 years and older, as well as in patients with impaired renal function. When the dose of Atakand® is increased, it is also recommended to monitor the level of potassium and creatinine.
Clinical studies of Atacand® in chronic heart failure did not include patients with a creatinine level> 265 μmol / L (> 3 mg / dL).
Co-administration with ACE inhibitors in chronic heart failure
When using candesartan in combination with ACE inhibitors, the risk of side effects may increase, especially kidney and hyperkalemia (see "Side effects" section). In these cases, careful monitoring and monitoring of laboratory indicators is necessary.
Stenosis of the renal artery
In patients with bilateral renal artery stenosis or stenosis of the single kidney artery, drugs that affect RAAS, in particular ACE inhibitors, can cause an increase in the level of urea and creatinine in the serum. Similar effects can be expected with the appointment of angiotensin II receptor antagonists.
Data on the use of Atacand® in patients who have recently undergone a kidney transplant are not available.
Patients with chronic heart failure with Atacand® therapy may develop hypotension. As with the use of other drugs that affect RAAS, the cause of the development of arterial hypotension in patients with hypertension may be a decrease in BCC, as observed in patients receiving high doses of diuretics. Therefore, at the beginning of therapy, care should be taken and, if necessary, correct hypovolemia.
General anesthesia and surgery
Patients receiving angiotensin II antagonists may develop arterial hypotension as a result of blockade of the renin-angiotensin system during general anesthesia and during surgical interventions. Very rarely there can be cases of severe arterial hypotension, requiring intravenous fluids and / or vasopressors.
Stenosis of the aortic and mitral valve (obstructive hypertrophic cardiomyopathy)
Caution should be exercised in appointing Atakand®, like other vasodilators, in patients with obstructive hypertrophic cardiomyopathy or hemodynamically significant stenosis of the aortic or mitral valve.
Patients with primary hyperaldosteronism are usually resistant to therapy with antihypertensive drugs that affect RAAS. In this regard, Atacand® is not recommended for such patients.
The clinical experience of using other drugs that affect RAAS shows that the simultaneous administration of Atakand® with potassium-sparing diuretics, potassium preparations or salt substitutes containing potassium, or other drugs that can increase the potassium content in the blood (eg heparin) can lead to the development of Hyperkalemia in patients with arterial hypertension.
In patients with chronic heart failure with Atacand ® therapy, hyperkalemia may develop. When assigning Atakand® to patients with chronic heart failure, regular monitoring of potassium levels in the blood is recommended, especially when co-administered with ACE inhibitors and potassium-sparing diuretics.
Patients in whom vascular tone and renal function predominantly depend on the activity of RAAS (for example, patients with severe chronic heart failure or kidney disease, including renal artery stenosis) are particularly sensitive to drugs acting on RAAS. The appointment of such drugs is accompanied in these patients by severe arterial hypotension, azotemia, oliguria and, more rarely, acute renal failure. The possibility of developing these effects cannot be ruled out when using angiotensin II receptor antagonists. A sharp decrease in blood pressure in patients with ischemic cardiopathy or cerebrovascular disease of ischemic origin, with the use of any antihypertensive drugs, may lead to the development of myocardial infarction or stroke.
Influence on the ability to drive a car or perform work that requires an increased speed of physical and mental reactions. Impact on the ability to drive a car or work with machinery has not been studied, but the pharmacodynamic properties of the drug indicate that such an effect is absent.
When driving vehicles and engaging in potentially dangerous activities that require an increased concentration of attention and speed of psychomotor reactions, it should be taken into account that when using the drug, dizziness and fatigue can occur.
Tablets, 8 mg and 16 mg. On the 14 table. In a blister of PVC / aluminum; 2 blisters in a cardboard box.
Conditions of supply of pharmacies
Storage conditions of the drug Atacand
At temperatures below 30 ° C.
Keep out of the reach of children.
The shelf life of the drug Atacand
Do not use beyond the expiration date printed on the package.