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Valsartan

Valsartan is an active specific angiotensin II receptor antagonist (ARA II), intended for oral administration.

Selectively blocks receptors of the AT1 subtype, which are responsible for the effects of angiotensin II. The consequence of AT1 receptor blockade is an increase in the plasma concentration of angiotensin II, which can stimulate unblocked AT2 receptors. Valsartan does not have any pronounced agonistic activity against AT1 receptors. The affinity of valsartan for receptors of the AT1 subtype is approximately 20,000 times higher than for receptors of the AT2 subtype. Valsartan does not interact with or block other hormone receptors or ion channels that are important in regulating the functions of the cardiovascular system.

The likelihood of coughing when using valsartan is very low, which is due to the lack of effect on angiotensin-converting enzyme (ACE), which is responsible for the degradation of bradykinin. Accordingly, when using angiotensin II receptor antagonists, ACE inhibition and accumulation of bradykinin or substance P do not occur. In comparative clinical studies of valsartan with an ACE inhibitor, the incidence of dry cough was significantly (p<0.05) lower in patients taking valsartan than in patients taking an ACE inhibitor (2.6% vs. 7.9%, respectively).

Use for arterial hypertension in patients over 18 years of age

When treating patients with arterial hypertension with valsartan, a decrease in blood pressure (BP) is observed, not accompanied by a change in heart rate (HR).

After oral administration of a single dose of valsartan, in most patients, the onset of the antihypertensive effect is observed within 2 hours, and the maximum reduction in blood pressure is achieved within 4-6 hours, lasting more than 24 hours. With repeated use of valsartan, the maximum reduction in blood pressure, regardless of the dose taken, is usually achieved within 2-4 weeks, and is maintained at this level during long-term therapy. Abrupt cessation of valsartan is not accompanied by a significant increase in blood pressure or other adverse events.

In patients with arterial hypertension, type 2 diabetes mellitus and nephropathy, taking valsartan at a dose of 160-320 mg per day, there is a significant decrease in proteinuria (36-44%).

Use after acute myocardial infarction in patients over 18 years of age

When using valsartan for 2 years in patients who began taking valsartan from 12 hours to 10 days after myocardial infarction (complicated by left ventricular failure and/or left ventricular systolic dysfunction), overall mortality and cardiovascular mortality are reduced and the time until the first hospitalization for exacerbation of chronic heart failure, repeated myocardial infarction, sudden cardiac arrest and stroke (without death) increases. The safety profile of valsartan in patients with acute myocardial infarction is similar to that in other conditions.

Chronic heart failure (CHF) in patients over 18 years of age

The mechanism of action of valsartan in CHF is based on its ability to eliminate the negative consequences of chronic hyperactivation of the renin-angiotensin-aldosterone system (RAAS) and its main effector, angiotensin II, namely: vasoconstriction; fluid retention in the body; cell proliferation leading to remodeling of target organs (heart, kidneys, blood vessels); stimulation of excess synthesis of hormones that act synergistically with the RAAS (catecholamines, aldosterone, vasopressin, endothelin). With the use of valsartan for CHF, preload decreases, wedge pressure in the pulmonary capillaries and diastolic pressure in the pulmonary artery decreases, and cardiac output increases. Along with hemodynamic effects, valsartan, due to indirect blockade of aldosterone synthesis, reduces sodium and water retention in the body.

When using valsartan (in an average daily dose of 254 mg) for 2 years in patients with CHF II (62%), III (36%) and IV (2%) functional class according to the NYHA classification with left ventricular ejection fraction (LV) ) less than 40% and LV intravenous diastolic diameter more than 2.9 cm/m2, receiving standard therapy, including ACE inhibitors (93%), diuretics (86%), digoxin (67%) and beta-blockers (36%), noted significant reduction (by 27.5%) in the risk of hospitalization due to exacerbation of CHF.

In patients not receiving ACE inhibitors, there was a significant reduction in overall mortality (by 33%), cardiovascular mortality and morbidity associated with CHF (time to the onset of the first cardiovascular event), which are assessed by the following indicators: death, sudden death with resuscitation, hospitalization for exacerbation of CHF, intravenous administration of inotropic or vasodilator drugs for 4 or more hours without hospitalization (44%). In the group of patients receiving ACE inhibitors (without beta-blockers), during treatment with valsartan there was no reduction in overall mortality, but cardiovascular mortality and morbidity associated with CHF decreased by 18.3%.

In general, the use of valsartan leads to a decrease in the number of hospitalizations for CHF, a slowdown in the progression of CHF, an improvement in the functional class of CHF according to the NYHA classification, an increase in left ventricular ejection fraction, as well as a decrease in the severity of signs and symptoms of heart failure and an improvement in quality of life compared with placebo.

Use in patients over 18 years of age with arterial hypertension and impaired glucose tolerance

When using valsartan and changing lifestyle, there was a statistically significant reduction in the risk of developing diabetes mellitus in this category of patients. Valsartan had no effect on the incidence of deaths due to cardiovascular events, myocardial infarction and non-fatal ischemic attacks, hospitalizations due to heart failure or unstable angina, arterial revascularization, in patients with impaired glucose tolerance and arterial hypertension, differing in age, gender and race. In patients receiving valsartan, the risk of developing microalbuminuria was significantly lower than in patients not receiving this therapy. The recommended starting dose of valsartan in patients with arterial hypertension and impaired glucose tolerance is 80 mg once daily. If necessary, the dose can be increased to 160 mg.

Use in children and adolescents aged 6 to 18 years with arterial hypertension

In children and adolescents from 6 to 18 years of age, valsartan provides a dose-dependent, smooth reduction in blood pressure. When using valsartan, the maximum reduction in blood pressure, regardless of the dose taken, is usually achieved within 2 weeks and is maintained at this level during long-term therapy.

Valsartan, 30 pcs., 80 mg, film-coated tablets

Active specific angiotensin II receptor antagonist, intended for oral administration. Selectively blocks receptors of the AT1 subtype, which are responsible for the effects of angiotensin II. The consequence of AT1 receptor blockade is an increase in the plasma concentration of angiotensin II, which can stimulate unblocked AT2 receptors. Valsartan does not have any pronounced antagonistic activity against AT1 receptors. The affinity of valsartan for receptors of the AT1 subtype is approximately 20,000 times higher than for receptors of the AT2 subtype.

Valsartan does not interact with or block other hormone receptors or ion channels that are important for regulating the function of the cardiovascular system.

The likelihood of coughing when using valsartan is very low, which is due to the lack of influence on the angiotensin converting enzyme (ACE), which is responsible for the degradation of bradykinin.

A comparison of valsartan with an ACE inhibitor showed that the incidence of dry cough was significantly (p < 0.05) lower in patients receiving valsartan than in patients receiving an ACE inhibitor (2.6% versus 7.9%, respectively). In the group of patients who had previously developed a dry cough during treatment with an ACE inhibitor, during treatment with Valsartan this complication was noted in 19.5% of cases, and during treatment with a thiazide diuretic - in 19% of cases, while in the group of patients receiving treatment ACE inhibitor, cough was observed in 68.5% of cases (p < 0.05).

Use for arterial hypertension in patients over 18 years of age

When treating patients with arterial hypertension with valsartan, a decrease in blood pressure (BP) is observed, not accompanied by a change in heart rate (HR).

After taking a single dose of the drug, in most patients, the onset of the antihypertensive effect is noted within 2 hours, and the maximum reduction in blood pressure is achieved within 4-6 hours. After taking the drug, the antihypertensive effect lasts more than 24 hours.

With repeated prescriptions of the drug, the maximum reduction in blood pressure, regardless of the dose taken, is usually achieved within 2-4 weeks and is maintained at the achieved level during long-term therapy.

When the drug is combined with hydrochlorothiazide, a significant additional reduction in blood pressure is achieved. Abrupt cessation of valsartan is not accompanied by a sharp increase in blood pressure or other undesirable consequences.

Use after acute myocardial infarction in patients over 18 years of age

When using the drug for 2 years in patients who began taking it from 12 hours to 10 days after acute myocardial infarction (complicated by left ventricular failure and/or left ventricular systolic dysfunction), the rates of overall mortality and cardiovascular mortality are reduced and the time until the first hospitalization for exacerbation of CHF, repeated myocardial infarction, sudden cardiac arrest and stroke (without death) increases. The safety profile of valsartan in patients with acute infarction is similar to that in other conditions.

CHF in patients over 18 years of age

The mechanism of action of valsartan in chronic heart failure (CHF) is based on its ability to eliminate the negative consequences of hyperactivation of the renin-angiotensin-aldosterone system (RAAS) and its main effector, angiotensin II, namely vasoconstriction; fluid retention in the body; cell proliferation leading to remodeling of target organs (heart, kidneys, blood vessels); stimulation of excess synthesis of hormones that act synergistically with the RAAS (catecholamines, aldosterone, vasopressin, endothelin, etc.).

With the use of valsartan for CHF, preload decreases, pulmonary capillary wedge pressure (PCWP) and diastolic pressure in the pulmonary artery decrease, and cardiac output increases. Along with hemodynamic effects, valsartan, due to indirect blockade of aldosterone synthesis, reduces sodium and water retention in the body.

It was found that the drug did not have a significant effect on the concentration of total cholesterol, uric acid, and also, when studied on an empty stomach, on the concentration of triglycerides and glucose in the blood plasma.

When using valsartan (in an average daily dose of 254 mg) for 2 years in patients with CHF II (62%), III (36%) and IV (2%) functional class according to the NYHA classification with left ventricular ejection fraction (LV) less than 40% and LV internal diastolic diameter more than 2.9 cm/m2, receiving standard therapy, including ACE inhibitors (93%), diuretics (86%), digoxin (67%) and beta-blockers (36%) there is a significant decrease (by 27.5%) risk of hospitalization due to exacerbation of CHF.

In patients not receiving ACE inhibitors, there was a significant reduction in overall mortality (by 33%), cardiovascular mortality and CHF-related morbidity (time to first cardiovascular event), assessed by the following indicators: death, sudden death with resuscitation, hospitalization for exacerbation of CHF, intravenous administration of inotropic and vasodilator drugs for 4 or more hours without hospitalization (44%). In the group of patients receiving ACE inhibitors (without beta-blockers), during treatment with valsartan there is no reduction in overall mortality, but cardiovascular mortality and morbidity associated with CHF decrease by 18.3%.

In general, the use of valsartan leads to a decrease in the number of hospitalizations for CHF, a slowdown in the progression of CHF, an improvement in the functional class of CHF according to the NYHA classification, an increase in LV ejection fraction, as well as a decrease in the severity of signs and symptoms of heart failure and an improvement in quality of life compared to placebo.

Use in patients over 18 years of age with arterial hypertension and impaired glucose tolerance

When using valsartan and changing lifestyle, there was a statistical reduction in the risk of developing diabetes mellitus in this category of patients. Valsartan had no effect on the incidence of deaths due to cardiovascular events, myocardial infarction and non-fatal ischemic attacks, hospitalizations due to heart failure or unstable angina, arterial revascularization, in patients with impaired glucose tolerance and arterial hypertension, differing in age, gender and race.

In patients receiving valsartan, the risk of developing microalbuminuria was significantly lower than in patients not receiving this therapy. The recommended initial dose of Valsartan in patients with arterial hypertension and impaired glucose tolerance is 80 mg once a day. If necessary, the dose can be increased to 160 mg.

Use in children and adolescents from 6 to 18 years of age with arterial hypertension

In children and adolescents from 6 to 18 years of age, valsartan provides a dose-dependent, smooth reduction in blood pressure. When using valsartan, the maximum reduction in blood pressure, regardless of the dose taken, is usually achieved within 2 weeks, and is maintained at this level during long-term therapy.