For adult patients without clinically expressed coronary heart disease, but with several risk factors for coronary heart disease, such as age, Smoking, hypertension, low HDL or early family history of coronary heart disease, etcet is indicated for: reducing the risk of myocardial infarction; reducing the risk of stroke; reducing the risk of revascularization and angina. For adult patients with type II diabetes mellitus and without clinically expressed coronary heart disease, but with several risk factors for coronary heart disease, such as retinopathy, albuminuria, Smoking, or hypertension, etset is indicated for: reducing the risk of myocardial infarction; reducing the risk of stroke. For adult patients with clinically expressed coronary heart disease, ATSAT is indicated for: reducing the risk of non-lethal myocardial infarction; reducing the risk of fatal and non-lethal stroke; reducing the risk of revascularization procedures; reducing the risk of hospitalization for congestive heart failure; reducing the risk of angina.
active substance: atorvastatin;
1 tablet contains atorvastatin calcium equivalent to atorvastatin 10 mg, 20 mg, 40 mg or 80 mg;
Excipients: lactose monohydrate, microcrystalline cellulose, calcium carbonate, povidone KZ0, croscarmellose sodium, colloidal anhydrous silica, magnesium stearate, Opadry 03F84827 pink *;
* Opadry 03F84827 pink: hypromellose, titanium dioxide (E 171), polyethylene glycol, talc, iron oxide red (E 172).
Etset Dosage form
Basic physical and chemical properties:
coated tablets 10 mg, 20 mg: round biconvex tablets coated with pink with the inscription “10” or “20” on one side;
coated tablets 40 mg, 80 mg: round biconvex coated tablets, pink, smooth on both sides.
Drugs that lower serum cholesterol and triglycerides.
HMG-CoA reductase inhibitors. ATX code C10A A05.
Etset® contains the active substance atorvastatin. Atorvastatin is a selective competitive inhibitor of MMC-CoA reductase, an enzyme that determines the rate of conversion of 3-hydroxy-3-methyl-glutaryl-coenzyme A to mevalonate, a precursor of sterols, in particular cholesterol. Triglycerides (TG) and cholesterol in the liver are incorporated into very low-density lipoprotein (VLDL) molecules, enter the blood plasma and are transported to peripheral tissues. Low-density lipoprotein (LDL) is formed from VLDL and is catabolized mainly by interaction with high-affinity LDL receptors (LDL receptors).
Atorvastatin reduces plasma serum cholesterol and lipoprotein concentrations by inhibiting MMC-CoA reductase and subsequently hepatic cholesterol biosynthesis, and increases the number of hepatic LDL receptors on the cell surface, leading to increased LD uptake and catabolism.
Atorvastatin reduces LDL formation and the number of LDL particles. Atorvastatin causes a marked and sustained increase in LDL receptor activity in combination with favorable changes in the quality of circulating LDL particles. Atorvastatin is effective in lowering LDL cholesterol in patients with homozygous familial hypercholesterolemia, a group that has not always responded to hypolipidemic therapy.
Liver disease in the acute phase, which may include a persistent increase in liver transaminases of unknown etiology.
Hypersensitivity to any of the components of this drug.