Atorvacor (atorvastatin) coated tablets 20 mg. №30

active ingredient : atorvastatin;

1 tablet contains atorvastatin calcium trihydrate 10.82 mg in terms of 100% substance (which is equivalent to atorvastatin) 10 mg;

excipients : calcium carbonate; lactose monohydrate, microcrystalline cellulose sodium croscarmellose; polysorbate 80, hydroxypropyl cellulose; magnesium stearate Opadry II 85F18422 white (polyvinyl alcohol, polyethylene glycol, talc, titanium dioxide (E 171)).

Film-coated tablets.

Basic physical and chemical properties: round-shaped tablets with a biconvex surface, film-coated white or almost white.

Drugs that lower the level of cholesterol and triglycerides in the blood serum. HMG-CoA reductase inhibitors.

ATX code C10A A05.

Atorvacor (atorvastatin) is a synthetic lipid-lowering drug. Atorvastatin is an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, an early step in cholesterol biosynthesis that limits the rate of its formation.

Atorvacor (atorvastatin) is a selective competitive inhibitor of HMG-CoA reductase, an enzyme that determines the rate of conversion of 3-hydroxy-3-methylglutaryl-coenzyme A to mevalonate, a precursor of sterols, including cholesterol. Cholesterol and triglycerides circulate in the bloodstream in combination with lipoproteins. These complexes are separated by ultracentrifugation into HDL (high density lipoprotein), LDLP (intermediate density lipoprotein), LDL (low density lipoprotein) and VLDL (very low density lipoprotein) fractions. Triglycerides (TG) and cholesterol in the liver are incorporated into VLDL and released into the blood plasma for transport to peripheral tissues. LDL is formed by VLDL and catabolized by interaction with high-affinity LDL receptors.

In animal models, atorvastatin lowers plasma cholesterol and lipoprotein levels by inhibiting hepatic HMG-CoA reductase and cholesterol synthesis and by increasing hepatic LDL receptors on cell surfaces to enhance LDL uptake and catabolism; atorvastatin also reduces the production of LDL and the number of these particles. Atorvastatin lowers LDL cholesterol levels in some patients with homozygous familial hypercholesterolemia, i.e. those who rarely respond to treatment with other lipid-lowering drugs.

Numerous clinical studies have shown that elevated levels of total cholesterol, LDL cholesterol and apo B (membrane complex for LDL cholesterol) provoke the development of atherosclerosis. Similarly, reduced levels of HDL cholesterol (and its transport complex – a by A) are associated with the development of atherosclerosis. Epidemiological studies have established that cardiovascular morbidity and mortality vary in direct proportion to the level of total cholesterol and LDL cholesterol and inversely with the level of HDL cholesterol.

Atorvastatin reduces total cholesterol, LDL cholesterol and apo B in patients with homozygous and heterozygous familial hypercholesterolemia, non-familial forms of hypercholesterolemia and mixed dyslipidemia. Atorvastatin also lowers VLDL and TG cholesterol levels, and also causes an unsustainable increase in HDL cholesterol and apolipoprotein A-1. Atorvastatin lowers total cholesterol, LDL cholesterol, VLDL cholesterol, apo B, triglycerides and HDL-C, and increases HDL cholesterol in patients with isolated hypertriglyceridemia. Atorvastatin reduces LDL-C in patients with dysbetalipoproteinemia.

Like LDL, lipoproteins rich in cholesterol and triglycerides, including VLDL, LDL and others, can also contribute to the development of atherosclerosis. Elevated plasma triglyceride levels are often found in the triad of low HDL cholesterol and small LDL lobules, and in association with non-lipid metabolic risk factors for coronary artery disease. Total plasma triglycerides per se have not been consistently shown to be an independent risk factor for coronary artery disease. In addition, an increase in HDL or a decrease in triglycerides has been found to have an independent effect on the risk of coronary and cardiovascular morbidity and mortality.

Atorvastatin, as well as some of its metabolites, is pharmacologically active in humans. The main site of action of atorvastatin is the liver, which plays a major role in cholesterol synthesis and LDL clearance. The dose of the drug, in contrast to the systemic concentration of the drug, better correlates with a decrease in LDL cholesterol. Individual dose selection should be carried out depending on the therapeutic response.

Indications.

Prevention of cardiovascular disease

For adult patients without symptomatic coronary artery disease but with multiple risk factors for coronary artery disease such as age, smoking, hypertension, low HDL-C, or a family history of early coronary artery disease, Atorvacor (atorvastatin) is indicated for:

– reduced risk of myocardial infarction

– reducing the risk of stroke;

– reducing the risk of revascularization procedures and angina pectoris.

For patients with type II diabetes mellitus and without symptomatic coronary heart disease, but with several risk factors for coronary heart disease, such as retinopathy, albuminuria, smoking or arterial hypertension, Atorvacor is indicated for:

– reduced risk of myocardial infarction

– reducing the risk of stroke.

For patients with clinically significant ischemic heart disease, Atorvacor (atorvastatin) is indicated for:

– reduced risk of non-fatal myocardial infarction

– reducing the risk of fatal and non-fatal stroke;

– reducing the risk of revascularization procedures;

– reduced risk of hospitalization due to congestive heart failure

– reducing the risk of angina pectoris.

hyperlipidemia

– As an adjunct to diet to reduce elevated levels of total cholesterol, LDL cholesterol, apolipoprotein B and triglycerides, as well as to increase HDL cholesterol levels in patients with primary hypercholesterolemia (heterozygous familial and non-familial) and mixed dyslipidemia (Fredrickson types IIa and IIb) ).

– As an adjunct to diet for the treatment of patients with elevated serum triglyceride levels (Fredrickson type IV).

– For the treatment of patients with primary dysbetalipoproteinemia (Fredrickson type III), in cases where dieting is not effective enough.

– To reduce total cholesterol and LDL cholesterol in patients with homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering treatments (such as LDL apheresis) or when such treatments are not available.

– As an adjunct to a diet to reduce levels of total cholesterol, LDL cholesterol and apolipoprotein B in boys and girls after the onset of menstruation at the age of 10 to 17 years with heterozygous familial hypercholesterolemia, if, after appropriate dietary therapy, the test results are:

a) LDL cholesterol remains ³ 190 mg/dl or

b) LDL cholesterol ³ 160 mg/dl and:

Have a family history of early cardiovascular disease or

Two or more other risk factors for cardiovascular disease are present

in a pediatric patient.

Contraindications.

– Active liver disease, which may include a persistent increase in liver transaminases of unknown etiology.

– hypersensitivity to any of the components of Atorvacor (atorvastatin) 20 mg..

– During pregnancy and breastfeeding.

– Women of childbearing age not using contraceptives.

Method of application and dose.

Hyperlipidemia (heterozygous familial and non-familial) and mixed dyslipidemia (Fredrickson type IIa and IIb)

The recommended starting dose of Atorvacor (atorvastatin) is 10 or 20 mg once daily. For patients requiring a significant reduction in LDL cholesterol (greater than 45%), therapy may be started with a dose of 40 mg once daily. The dosing range of Atorvacor® is 10 to 80 mg once daily. The drug can be taken as a single dose at any time and regardless of food intake. Initial and maintenance doses of Atorvacor® are selected individually, depending on the goal of treatment and response. After initiation of treatment and / or after dose titration of Atorvacor®, lipid levels should be analyzed over a period of 2 to 4 weeks and the dose adjusted accordingly.

Heterozygous familial hypercholesterolemia in pediatric patients (aged 10-17 years)

The recommended starting dose of Atorvacor (atorvastatin) is 10 mg/day; the maximum recommended dose is 20 mg/day (doses greater than 20 mg have not been studied in this group of patients). Doses of the drug should be selected individually, for the purpose of treatment. Dose adjustments should be made at intervals of 4 weeks or more.

Homozygous familial hypercholesterolemia

The dose of Atorvacor (atorvastatin) for patients with homozygous familial hypercholesterolemia is 10 to 80 mg per day. Atorvacor should be used as an adjunct to other lipid-lowering therapies (eg, LDL apheresis) or if lipid-lowering therapies are not available.

Simultaneous lipid-lowering therapy

Atorvacor (atorvastatin) can be used with bile acid sequestrants. The combination of HMG-CoA reductase inhibitors (statins) and fibrates should generally be used with caution.

Dosing for patients with impaired renal function

Kidney disease does not affect either plasma concentrations or the reduction in LDL cholesterol when using Atorvacor®; therefore, dose adjustment of the drug for patients with impaired renal function is not required.

Dosing for patients taking ciclosporin, clarithromycin, itraconazole, or certain protease inhibitors

Treatment with Atorvacor (atorvastatin) 20 mg. should be avoided in patients taking cyclosporine or HIV protease inhibitors (tipranavir + ritonavir) or an inhibitor of hepatitis C virus protease (telaprevir). Atorvacor (atorvastatin) should be used with caution in HIV patients taking lopinavir + ritonavir and used at the most appropriate dose. In patients taking clarithromycin, itraconazole, and patients with HIV taking saquinavir + ritonavir, darunavir + ritonavir, fosamprenavir or fosamprenavir + ritonavir in combination, the therapeutic dose of Atorvacor (atorvastatin) should be limited to 20 mg, and appropriate clinical evaluations are recommended to ensure the use of the slightest the required dose of Atorvacor®. For patients taking the HIV protease inhibitor nelfinavir or the hepatitis C protease inhibitor boceprevir.