Torvacard pills 40mg №90

Dosage form

Coated tablets

Composition

1 coated pill contains: Atorvastatin (in the form of a Calcium salt) 40 mg.

Excipients: heavy Magnesium oxide, microcrystalline cellulose, lactose monohydrate, croscarmellose sodium, low substituted hydroxypropyl cellulose LH21, colloidal silicon dioxide, magnesium stearate.

Shell composition: hypromellose 2910/5, macrogol 6000, titanium dioxide, talc.

Packing

In the blister of 10 tablets. In a carton of 9 blisters.

Mechanism of action

Torvacardum is a lipid-lowering drug. Selective competitive inhibitor of HMG-CoA reductase - the main enzyme that converts 3-hydroxy-3-methylglutaryl-coenzyme A into mevalonic acid - the precursor of steroids, including cholesterol. In the liver, triglycerides and cholesterol are included in the composition of VLDL, enter the blood plasma and are transported to peripheral tissues. LDLs produce LDLs that are catabolized when interacting with high affinity LDL receptors. Atorvastatin lowers levels of cholesterol (Xc) and plasma lipoproteins by inhibiting HMG-CoA reductase in the liver and increasing the number of LDL receptors in the liver on the cell surface, which leads to increased cholesterol capture and catabolism - LDL.

Atorvastatin reduces the formation of cholesterol - LDL and the number of LDL particles.The drug causes a pronounced and persistent increase in the activity of LDL receptors, and also has a beneficial effect on the quality of circulating LDL. Atorvastatin effectively reduces the level of LDL cholesterol in patients with homozygous hypercholesterolemia, which usually is not amenable to treatment with other lipid-lowering drugs.

In studying the dose-dependence effect of atorvastatin, it was shown that the drug (at a dose of 10-80 mg) reduced the level of total cholesterol (by 30-46%), LDL cholesterol (by 41-61%), apolipoprotein B (by 34-50%) and triglycerides (14-33%). The results of treatment were similar in patients with heterozygous familial hypercholesterolemia, non-familial forms of hypercholesterolemia and mixed hyperlipidemia (including in patients with non-insulin dependent diabetes mellitus). Atorvastatin lowers total cholesterol, cholesterol - LDL, cholesterol-VLDL, apolipoprotein B, triglycerides, and non-HDL cholesterol, and increases HDL cholesterol in patients with isolated hypertriglyceridemia. Atorvastatin reduces the level of intermediate-density lipoprotein cholesterol (cholesterol-LNPP) in patients with dysbetalipoproteinemia. Like LDL, lipoproteins containing triglycerides (including VLDL, LPPP and their residues) also accelerate the development of atherosclerosis. Increased plasma triglycerides are often found in combination with a decrease in cholesterol-HDL cholesterol and the presence of small LDL particles, as well as in combination with non-lipid metabolic risk factors for coronary heart disease.It has not yet been proven that an increase in total plasma triglyceride levels is an independent risk factor for CHD. It has also not been proven that increasing HDL cholesterol or lowering triglyceride levels in itself affects the risk of coronary and other cardiovascular complications and patient mortality.

Atorvastatin and some of its metabolites are pharmacologically active. The primary target organ of the action of atorvastatin is the liver, where cholesterol synthesis and LDL clearance is performed.

The dynamics of the cholesterol level - LPNP correlates better with the dose of atorvastatin than with its concentration in the blood plasma. The dose of the drug should be selected based on the therapeutic effect.

Indications and usage

- In combination with a diet to reduce elevated levels of total cholesterol, LDL cholesterol, apolipoprotein B and triglycerides and increase cholesterol levels - HDL cholesterol in patients with primary hypercholesterolemia, heterozygous familial and non-familial hypercholesterolemia, and combined (mixed) hyperlipidemia, and combined heterozygous hypercholesterolemia and combined (mixed) hyperlipidemia, and hemoglobin, mixed heterozygous and cholesterol, and combined hyperinflammatory cholesterol cholesterol; ).
- In combination with a diet for the treatment of patients with elevated serum levels of triglycerides (type IV according to Fredrickson) and patients with dysbetalipoproteinemia (type III according to Fredrickson), in whom diet therapy does not give an adequate effect.
- To reduce total cholesterol and cholesterol levels - LDL in patients with homozygous familial hypercholesterolemia, when diet therapy and other non-pharmacological treatments are not effective enough.

Contraindications

- Active liver disease or increased serum transaminase activity (more than 3 times compared with the upper limit of normal) of unclear genesis.
- Pregnancy.
- Lactation period.
- Children and adolescents under 18 years of age (efficacy and safety have not been established).
- Hypersensitivity to the drug.

Caution should be used when:

- Chonic alcoholism.
- A history of liver diseases.
- Severe electrolyte imbalance.
- Endocrine and metabolic disorders.
- Arterial hypotension.
- Severe acute infections (sepsis).
- Uncontrolled epilepsy.
- Extensive surgical injuries.
- Diseases of the skeletal muscles.

Pregnancy and Breastfeeding

Atorvastatin is contraindicated for use during pregnancy and lactation (breastfeeding).

It is not known whether atorvastatin is excreted in breast milk. Given the possibility of adverse events in infants, if necessary, use of the drug during lactation should decide on the termination of breastfeeding.

Women of reproductive age during treatment should use adequate methods of contraception. Atorvastatin can be prescribed to women of reproductive age only if the probability of pregnancy is very low and the patient is informed about the possible risk of treatment for the fetus.

Dosage and administration

Before prescribing Torvacard, the patient should be advised to recommend a standard lipid-lowering diet, which he must continue to follow throughout the entire period of therapy.

The initial dose is an average of 10 mg 1 time / day. The dose varies from 10 to 80 mg 1 time / day. The drug can be taken at any time of the day with food or regardless of meal times. The dose is selected based on the initial levels of LDL-C, the goal of therapy and the individual effect. At the beginning of treatment and / or during the dose increase of Torvacard, it is necessary to monitor plasma lipid levels every 2-4 weeks and correct the dose accordingly.

With primary hypercholesterolemia and mixed hyperlipidemia, in most cases, it is enough to give a dose of 10 mg of the drug Torvacard 1 time / day. A significant therapeutic effect is observed after 2 weeks, as a rule, and the maximum therapeutic effect is usually observed after 4 weeks. With long-term treatment, this effect persists.

When determining the goal of treatment, you can use the following recommendations.

Recommendations of the National Cholesterol Education Program (USA). Diagnosed vascular atherosclerosis * Cholesterol - LDL, mg / dL (mmol / l).

Objectives of lipid-lowering therapy of the European Society of Atherosclerosis In patients with a confirmed diagnosis of coronary artery disease and other patients with a high risk of ischemic complications, the goal of treatment is to reduce LDL cholesterol less than 115 mg / dL (less than 3 mmol / l) and less than 190 mg / dL 5 mmol / l).

National treatment guidelines Homozygous familial hypercholesterolemia. In a study in adult patients with homozygous familial hypercholesterolemia, atorvastatin therapy at a dose of 80 mg in most cases resulted in a decrease in the level of LDL-C LDL by more than 15% (18-45%). The use of the drug in patients with renal insufficiency and kidney disease does not affect the level of atorvastatin in the blood plasma or the degree of cholesterol - LDL cholesterol when it is used, therefore, changing the dose of the drug is not required. When using the drug in elderly patients, there were no differences in safety, efficacy, or achievement of lipid-lowering therapy goals in comparison with the general population.

Before starting treatment with Torvacard, the patient should be prescribed a standard hypocholesterol diet, which he must follow during the entire period of treatment.

The use of HMG-CoA reductase inhibitors to reduce the level of lipids in the blood can lead to changes in biochemical parameters reflecting the function of the liver. Liver function should be monitored before starting therapy, 6 weeks, 12 weeks after starting to take Torvacard and after each dose increase, as well as periodically (for example, every 6 months). An increase in the activity of liver enzymes in the serum may be observed during therapy with Torvacard. Patients with increased transaminase levels should be monitored until the level of enzymes returns to normal.In the event that the values ​​of ALT or AST are more than 3 times higher than the higher limit of normal, it is recommended to reduce the dose of Torvacard or discontinue treatment.

Treatment with Torvacard can cause myopathy. In patients with common myalgia, muscle soreness or weakness and / or a pronounced increase in CPK activity, one should bear in mind the possibility of developing myopathy (pain and weakness in muscles combined with an increase in CPK activity of more than 10 times compared with the higher limit of normal). Patients should be warned that they should immediately inform the doctor about the appearance of unexplained pain or weakness in the muscles, if they are accompanied by indisposition or fever.

Therapy with Torvacard should be discontinued in the case of a pronounced increase in the activity of CPK or in the presence of a confirmed or suspected myopathy. The risk of myopathy in the treatment of other drugs of this class increased with the simultaneous use of cyclosporine, fibrates, Erythromycin, nicotinic acid or azole antifungal agents. Many of these drugs inhibit the metabolism mediated by the CYP3A4 isoenzyme and / or the transport of drugs. Atorvastatin is biotransformed by CYP3A4. By prescribing atorvastatin in combination with fibrates, erythromycin, immunosuppressants, azole antifungal drugs, or nicotinic acid in lipid-lowering doses,Expected benefit and risk of treatment should be carefully weighed and patients should be regularly monitored to detect pain or weakness in muscles, especially during the first months of treatment and during periods of increasing the dose of any drug. In such situations, periodic determination of CPK activity can be recommended, although such monitoring does not prevent the development of severe myopathy.

When using atorvastatin, as well as other drugs of this class, cases of rhabdomyolysis with acute renal failure due to myoglobinuria are described. Therapy with Torvacard should be temporarily stopped or completely canceled if there are signs of possible myopathy or a risk factor for the development of renal failure in the presence of rhabdomyolysis (for example, severe acute infection, hypotension, serious surgery, trauma, severe metabolic, endocrine and electrolyte disturbances and uncontrolled seizures). Before starting treatment with Torvacard, it is necessary to try to control hypercholesterolemia by adequate diet therapy, increasing physical activity, reducing body weight in patients with obesity and treating other conditions. Patients should be warned that they should immediately consult a doctor if they develop unexplained pains or weakness in the muscles, especially if they are accompanied by indisposition or fever.

The risk of myopathy during treatment with other drugs of this class is increased with simultaneous use of cyclosporine, fibrates, erythromycin, antifungal drugs related to azoles, and niacin.

With simultaneous ingestion of atorvastatin and a suspension containing magnesium and aluminum hydroxide, plasma concentrations of atorvastatin decreased by approximately 35%, however, the extent to which LDL cholesterol levels were reduced did not change.

With simultaneous use of atorvastatin does not affect the pharmacokinetics of antipyrine, therefore, interactions with other drugs metabolized by the same cytochrome isoenzymes are not expected.

With simultaneous use of colestipol, the concentration of atorvastatin in the blood plasma decreased by approximately 25%. However, the lipid-lowering effect of the combination of atorvastatin and colestipol was superior to that of each drug separately.

When repeated administration of Digoxin and atorvastatin at a dose of 10 mg, the equilibrium concentration of digoxin in the blood plasma did not change. However, when using digoxin in combination with atorvastatin at a dose of 80 mg / day, the concentration of digoxin increased by about 20%. Patients receiving digoxin in combination with atorvastatin require monitoring.

With simultaneous use of atorvastatin and erythromycin (500 mg 4 times / day) or Clarithromycin (500 mg 2 times / day), which inhibit the CYP3A4 isoenzyme, an increase in the concentration of atorvastatin in the blood plasma was observed.

With simultaneous use of atorvastatin (10 mg 1 time / day) and Azithromycin (500 mg 1 time / day), the concentration of atorvastatin in the blood plasma did not change.

Atorvastatin did not have a clinically significant effect on the concentration of terfenadine in plasma, which is metabolized mainly with the participation of CYP3A4; therefore, it seems unlikely that atorvastatin can significantly affect the pharmacokinetic parameters of other CYP3A4 substrates.

Simultaneous use of atorvastatin and oral contraceptive containing norethindrone and ethinyl estradiol. With simultaneous use of atorvastatin and oral contraceptive containing norethindrone and ethinyl estradiol, there was a significant increase in the AUC of norethindrone and ethinyl estradiol by about 30% and 20%, respectively. This effect should be considered when choosing an oral contraceptive for a woman receiving atorvastatin.

When studying the interaction of atorvastatin with Warfarin and cimetidine signs of a clinically significant interaction was not found.

With simultaneous use of atorvastatin 80 mg and Amlodipine 10 mg, the pharmacokinetics of atorvastatin in an equilibrium state did not change.

The simultaneous use of atorvastatin with protease inhibitors, known as inhibitors of the CYP3A4 isoenzyme, was accompanied by an increase in plasma atorvastatin concentrations.

No clinically significant undesirable interaction of atorvastatin and antihypertensive drugs, as well as with estrogens. Studies of the interaction with all specific drugs were not conducted.

Symptoms: possible hypotension.
Treatment: conducting symptomatic therapy. There is no specific antidote. Hemodialysis is ineffective.

Store at temperatures from 10 ° to 30 ° C.

2 years.