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Active specific angiotensin II receptor antagonist intended for oral administration. Selectively blocking receptor subtype  , which is responsible for the effects of angiotensin II. The consequence of the blockade of the  receptor is to increase the plasma concentrations of angiotensin II, which may stimulate the unblocked – receptors. does not have any agonist activity expressed in relation to  receptors. affinity receptor subtype testosterone cypionate reviews in about 20 times higher Ltd. than AT receptor subtype 2 . The probability of occurrence of cough in applying valsartan is very low, due to the lack of effect on angiotensin converting enzyme (ACE), which is responsible for the degradation of bradykinin. Comparison of with ACE inhibitor, showed that the incidence of dry cough was significantly (p <0.05) lower in patients treated with than in patients treated with an ACE inhibitor (2.6% versus 7.9%, respectively). In the group of patients who previously in the treatment of an ACE inhibitor developed dry cough, in the treatment om this complication was observed in 19.5% of cases, and in the treatment of a thiazide diuretic – in 19.0% cases – while in the group of patients treated with inhibitor ACE cough was observed in 68.5% of cases (p <0.05). Valsartan does not interact and does not block other hormone receptors or ion channels that are important for the regulation of the cardiovascular system functions. When treating om patients with hypertension is marked reduction of blood pressure (BP) is not accompanied by a change in heart rate (HR). After setting the inside of a single dose of the drug, most patients start antihypertensive effect observed within 2 hours and maximum reduction of blood pressure is achieved within 4-6 hours. After ingestion antihypertensive effect persists for more than 24 hours.Repeated use of the drug the maximum reduction in blood pressure, regardless of the dose, usually achieved within 2-4 weeks and maintained at that level during prolonged therapy. In the case of the drug combination with hydrochlorothiazide achieved a significant additional reduction in blood pressure. Sudden discontinuation of is not accompanied by a sharp increase in blood pressure or other adverse clinical effects. The mechanism of action of in patients with chronic heart failure (CHF) is based on its ability to eliminate the negative effects of chronic hyperactivation of the renin-angiotensin-aldosterone system (RAAS), and its main effector -angiotenzina II namely, – vasoconstriction; fluid retention; cell proliferation that leads to remodeling of the target organs (heart, kidneys, blood vessels);excessive stimulation of the synthesis of hormones, acting synergistically with the RAAS (catecholamines, aldosterone, vasopressin, endothelin, etc..). Against the background of the use of valsartan in CHF decreased preload, reduced pressure pulmonary capillary wedge (PCWP) and diastolic blood pressure in the pulmonary arteries, increased cardiac output. Along with the hemodynamic effects of valsartan by mediated blockade of the synthesis of aldosterone reduces the retention of sodium and water in the body. It is found that the drug had no significant effect on the concentration of total cholesterol, uric acid, and also in the study of fasting – the concentration of triglycerides and serum glucose . Chronic heart failure (CHF), hemodynamics and neurohormones . In patients with chronic heart failure (II-IV functional class NYHA classification) and the pressure in the pulmonary capillary wedge (PCWP)> 15 mm Hg. Art. We studied the concentration of neurohormones hemodynamics and blood serum. Patients continually receiving ACE inhibitors, valsartan, appointed on the background of an ACE inhibitor in a single and repeated doses, leads to an improvement of hemodynamic parameters, including reduction of PCWP and diastolic pressure in the pulmonary artery, and systolic blood pressure (SBP). After 28 days of treatment there was a reduction of concentrations of aldosterone and norepinephrine in the blood. In patients not receiving an ACE inhibitor for at least 6 months after 28 days of therapy, valsartan significantly reduced PCWP, systemic testosterone cypionate reviews vascular resistance, systolic and cardiac output. The morbidity and mortality . The effects of Valsartan as compared with placebo on morbidity and mortality in patients with chronic heart failure II (62%), III (36%) and IV (2%) functional class classification NYHA with left ventricular ejection fraction (LVEF) < 40% and internal diastolic diameter of the left ventricle (VDDLZH)> 2.9 cm / m 2 located on conventional therapy, which included ACE inhibitors (93% o), diuretics (86%), digoxin (67%) and beta-blockers (36 %). The mean duration of follow-up of almost 2 years; average daily dose of 254 mg a-. The two primary efficacy criterion included all-cause mortality (time to death) and morbidity associated with heart failure (time to first event), which were evaluated by the following indicators: death, sudden death with resuscitation, hospitalization for heart failure, I / administration of inotropic or vasodilator agents for four hours or more without hospitalization. Mortality from all causes in the valsartan and placebo groups was comparable. Compared with the placebo group, the incidence in patients treated with valsartan significantly decreased by 13.2%. The primary efficacy parameter was the decrease by 27.5% of the time to first hospitalization for heart failure. This effect was most pronounced in patients not receiving ACE inhibitors or beta-blockers. Exercise capacity. In patients with chronic heart failure II-IV NYHA functional class classification with left ventricular dysfunction (LVEF ≤40%) evaluated the effect of valsartan, assigned in addition to the conventional treatment of heart failure, in the exercise tolerance using the Modified Naughton Protocol. In all treatment groups showed an increase in exercise time from baseline. Compared with placebo, patients receiving valsartan, there was more average increase from baseline exercise time, although this difference was not significant. The most significant improvement in exercise tolerance observed in a subgroup of patients not receiving an ACE inhibitor: Mean change in time of physical activity in the valsartan group 2 times superior to those in the placebo group. Effect of valsartan on exercise tolerance, compared with enalapril, according six-minute walking test was studied in patients with heart failure II-IV NYHA functional class classification with left ventricular dysfunction (LVEF ≤45%), treated with previous (at least within 3 months) treatment with ACE inhibitors. Patients transferred to treatment with an ACE inhibitor, or to receive valsartan or enalapril.Valsartan in doses ranging from 80 mg to 160 mg 1 time per day was at least as effective as enalapril doses ranging from 5 mg to 10 mg 2 times a day. NYHA class, symptoms, quality of life, ejection fraction . patients treated with valsartan, there was a significant, compared to placebo, the improvement of the functional class of heart failure of NYHA classification, as well as signs and symptoms of heart failure, including such as shortness of breath, fatigue, peripheral edema, wheezing. Compared to placebo, patients treated with valsartan, there was a significant increase in ejection fraction and a significant decrease VDDLZH compared to baseline before treatment. The use of reduces the number of hospitalizations for heart failure, slow the progression of chronic heart failure, improved NYHA functional class , an increase in ejection fraction and reduces the severity of signs and symptoms of heart failure and improve the quality of life compared with placebo. The use after acute myocardial infarction in the study VALIANT included 14,703 patients with acute myocardial infarction complicated by left ventricular failure and / or systolic dysfunction of the left ventricle. Randomization was performed via 0.5-10 days after an acute myocardial infarction, in groups, in which, in addition to the conventional treatment, the treatment was started either valsartan (4909 patients), or a combination of captopril and valsartan (4885 patients), or captopril (4909 patients). mortality rates from any cause and death from specific causes have been similar in all three treatment groups. A total of 979 died in the valsartan group (19.9%) in the combination therapy group – 941 (19.3%) and in the group of captopril – 958 (19.5%) patients. The ratio of the risk of death from cardiovascular causes and risk ratio for a composite index that included, along with cases of cardiovascular death, serious non-fatal cardiovascular events (recurrent myocardial infarction, hospitalization for heart failure, resuscitation after cardiac arrest and stroke) were similar for the groups of valsartan and captopril group as well as combination therapy group and captopril group. In the combination therapy group revealed the highest incidence of adverse events associated with taking drugs. When valsartan monotherapy in the group were more frequent hypotension and renal dysfunction, captopril group -. Cough, rash and taste disturbance Research has proven the effectiveness of valsartan, equal to that of captopril in reducing total and cardiovascular mortality. The calculated effectiveness of valsartan on the impact on the overall mortality rate was 99.6% that of captopril. Additional analysis conducted using the method of placebo assumptions showed that valsartan lowers the risk of death by 25%. Valsartan is as effective a drug as captopril, in patients at high risk for cardiovascular complications after myocardial infarction. Adding valsartan with captopril therapy leads to an increase in adverse events, without causing further improve the survival of patients.


  • arterial hypertension.
  • Chronic heart failure (CHF) (II-IV functional class NYHA classification) in patients receiving standard therapy, including diuretics, digitalis preparations, as well as ACE inhibitors or beta-blockers (not simultaneously). Use of each of these drugs is not necessary.
  • to improve survival in testosterone cypionate reviews patients with acute myocardial infarction complicated by left ventricular failure and / or left ventricular systolic dysfunction, the presence of a stable hemodynamic parameters.Contraindications
  • Hypersensitivity to any component of .
  • Pregnancy, lactation.

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