masteron side effects

Undesirable effect of levosimendan on the 6-month survival rate was not revealed. Levosimendan in therapeutic doses ranging from 0.05 to 0.2 g / kg / min. is linear. Distribution The volume of distribution of levosimendan (Vss) is approximately 0.2 l / kg. Levosimendan is 97-98% bound to plasma proteins, mainly albumin. Binding active metabolites with the proteins -. 39% and 42% respectively Metabolism Levosimendan is mainly metabolized by conjugation with a cyclic or  conjugates tsisteinilglitsinom and cysteine.

Only about 5% of the dose of levosimendan in the small intestine are metabolized by oxidation to aminofenilpiridazinona , which after reabsorption biotransformed into the systemic circulation in the blood plasma by the action of masteron side effects metabolite to active . The rate of acetylation is genetically determined. In “fast acetylators” concentrations of the metabolite  are slightly higher than the “slow.” However, this is not reflected in clinically significant hemodynamic effects of the drug at the recommended doses. The systemic circulation in significant quantities determined only metabolite . The “slow” acetylators prevails , while the “fast» , however, the total amount of these metabolites and the incidence of hemodynamic effects in the same “fast” and “slow” acetylators these metabolites can have a lasting impact on hemodynamic parameters (for 7-9 days after discontinuation of a 24-hour infusion of levosimendan). with in vitro, metabolites of levosimendan and  aconcentration created in the application of the recommended doses, does not inhibit  levosimendan not inhibit  1A1, metabolism and it is not broken under the influence of masteron side effects inhibitors.

Excretion clearance of levosimendan is about 3.0 ml / min / kg, and the half-life – about 1 C. Over 95% of the dose levosimendan displayed for 1 week in the form of inactive metabolites. A small part of the dose (<0.05%) excreted by the kidneys unchanged. The circulating metabolites are formed and eliminated slowly, its half-life of about 75-80 hours. Concentrations plasma levels peak after about 2 days after cessation of the infusion of levosimendan. Active metabolites are subject to conjugation or renal filtration, and are derived primarily by the kidneys. Special groups Children: Limited evidence suggests that the pharmacokinetics of levosimendan after a single administration in children (aged 3 months to 6 years) is similar to that in adults. The pharmacokinetics of the active metabolite in children has not been studied. Levosimendan should not be used in children. Patients with renal impairment: The pharmacokinetics of levosimendan are similar in patients with mild or moderate renal impairment and in patients on hemodialysis. Patients with severe renal insufficiency pharmacokinetic parameters may be somewhat reduced.In patients with severe renal insufficiency, and those who are on hemodialysis, the free fraction of levosimendan is slightly increased, a (area under the curve “concentration-time”) metabolites . It is assumed that mild to moderate renal insufficiency have a smaller effect on the pharmacokinetics of metabolites masteron side effects.

Levosimendan does not appear in hemodialysis. Although metabolites are displayed in hemodialysis, their clearance is low (approximately 8-23 ml / min). Patients with hepatic impairment: In patients with mild to moderate hepatic insufficiency of levosimendan and its binding protein in cirrhosis of the liver pharmacokinetics They do not differ from those in healthy doborovoltsev. Pharmacokinetics of levosimendan and metabolite  is the same in healthy doborovoltsev and in patients with moderate hepatic impairment (class B classification Child-Pyuga) except that the half-life of the metabolite more elongated with moderate hepatic insufficiency. In a population the analysis did not reveal that the age, ethnicity or gender affect the pharmacokinetics of levosimendan. However, the amount and distribution of the total clearance depends on body weight.


Short-term treatment of acute decompensation of severe chronic heart failure  after failure of standard therapy and the need for inotropic therapy.


  • Hypersensitivity to levosimendan or any inactive components of the drug;
  • Mechanical obstruction that prevents filling and / or discharge of blood from the ventricles;
  • Severe renal impairment (creatinine clearance less than 30 ml / min)
  • Severe hepatic impairment (> 9 points on the classification of Child-Pyuga);
  • Severe hypotension (systolic blood pressure less than 90 mmHg)
  • Severe tachycardia (heart rate over 120 beats / min.);
  • Ventricular tachycardia of the type “pirouette” in history;
  • Age up to 18 years.
  • uncorrected hypokalemia masteron side effects
  • uncorrected hypovolemia