Levosimendan increases the calcium sensitivity of contractile proteins by binding to troponin C. infarction (calcium dependent binding) increases the strength of heart contraction opens masteron enanthate potassium channels in vascular smooth muscle and induces the expansion of arteries, including coronary, and veins. In vitro demonstrated selective inhibitory activity against phosphodiesterase levosimendan III. The significance of this effect when used in therapeutic concentrations of the drug is not established. In patients with chronic heart failure, the positive inotropic and vasodilatory calcium-effects of levosimendan increases the strength of cardiac contractions and decrease preload and afterload, without worsening diastolic function. It activates the ischemic myocardium in patients after percutaneous transluminal coronary angioplasty or thrombolysis. Study of hemodynamics in healthy volunteers and in patients with chronic heart failure have shown a dose-dependent effect of loading dose (3 mg / kg body weight) and continuous infusion (0.05 – 0.2 ug / kg body weight for 1 minute). Levosimendan increases cardiac output, stroke volume, ejection fraction and increases the heart rate (HR), reduces systolic and diastolic blood pressure, wedge pressure in the capillaries of the lungs, right atrial pressure and total peripheral vascular resistance. When administered at the recommended dose of the drug is formed one active metabolite that gives similar to levosimendan hemodynamic effects. They persist for 7-9 days after discontinuation of a 24-hour infusion of levosimendan. The infusion of levosimendan causes an increase in coronary blood flow in patients undergoing coronary intervention, and improves myocardial perfusion in patients with chronic heart failure. These positive effects are not accompanied by a significant increase in myocardial oxygen consumption. Significantly reduces the content of endothelin 1 in patients with chronic heart failure. At observance of the recommended rate of administration the drug does not increase the concentration of catecholamines in the blood plasma. Masteron enanthate II and I of the Programme. REVIVE Programme levosimendan compared with placebo in combination with standard therapy in patients with acute decompensation of chronic heart failure with left ventricular ejection fraction ≤35% and shortness of breath at rest. The continuation of the previous therapy masteron enanthate with the exception of intravenous milrinone. The results showed that most of the patients began to improve, fewer patients worsened.
Under Simdaksa there was a slight increase in mortality rate on day 90 as compared to the control group (15% and 12% respectively). It is shown that the initial level of systolic blood pressure <100 mm Hg. Article or diastolic blood pressure <60 mm Hg. Art. increase the risk of mortality.
In a double-blind, multicenter, comparative study of levosimendan and dobutamine in 1327 patients with acute decompensated chronic heart failure and ineffectiveness of previous therapy with diuretics and vasodilators compared the performance of 180-day mortality. The interest rate was preimushestv of levosimendan on Day 5 (4% levosimendan, 6% dobutamine). This benefit was maintained for 31 days (12% levosimendan, dobutamine 14%), especially in those patients who initially received beta-blockers. In patients with initially lower levels of blood pressure were worse mortality in both groups. The masteron enanthateIn a double-blind, multicenter study of 203 patients with severe chronic heart failure with low cardiac output (ejection fraction <0.35 cardiac index <2.5 L / min / m, the pressure pulmonary capillary wedge> 15 mm Hg. v.) in need of inotropic therapy received levosimendan (loading dose of 24 mg / kg for 10 min., followed by a continuous infusion of 0.1-0.2 ug / kg / min for 24 hours) or dobutamine 5-10 mcg / kg / min for 24 hours. The increase in cardiac output> 30% and simultaneously reduce wedge pressure in the pulmonary capillaries of 25% or more after 24 hours was achieved in 28% of patients receiving levosimendan and 15% of patients receiving dobutamine (p = 0.025). Dyspnea decreased 68% and 59%, respectively, fatigue – 63 and 47%. Performance 31-day mortality was 7.8% in the levosimendan group and 17% in the dobutamine group. Russlan In a double-blind, multicenter study, the primary purpose of which was safety study, 504 patients with decompensated chronic heart failure after acute myocardial infarction, need of inotropic therapy gave levosimendan or placebo for 6 hours. Groups did not differ significantly in the incidence of hypotension and myocardial ischemia. In a retrospective analysis of the results of the two studies.