Cardiolip, 10 mg 60 pcs

Cardiolip is a hypolipidemic drug, a selective competitive inhibitor of HMG-CoA reductase.

It is effective in adult patients with hypercholesterolemia, with or without hypertriglyceridemia (regardless of race, sex or age), including patients with diabetes and familial hypercholesterolemia.

Additive effect is noted in combination with fenofibrate (with respect to reduction of TG concentration) and nicotinic acid in lipid-lowering doses (with respect to reduction of HDL-C concentration).

Indications

– Primary Fredriksen hypercholesterolemia (type IIa, including familial heterozygous hypercholesterolemia) or mixed hypercholesterolemia (type IIb) as an adjunct to diet when diet and other non-drug treatments (exercise, weight loss) are insufficient.

– Familial homozygous hypercholesterolemia as an adjunct to diet and other lipid-lowering therapy (eg, LDL apheresis), or in cases where such therapy is not sufficiently effective.

– Hypertriglyceridemia (Fredriksen type IV) as an adjunct to diet.

– To slow the progression of atherosclerosis as an adjunct to diet in patients who are indicated for therapy to reduce the concentration of total cholesterol and LDL-C.

– Primary prevention of major cardiovascular complications (stroke, myocardial infarction, arterial revascularization) in adult patients without clinical signs of coronary artery disease, but with an increased risk of its development (age over 50 years for men and over 60 years for women, increased concentration of C-reactive protein (more than 2 mg/l) in the presence of at least one of the additional risk factors, such as arterial hypertension, low HDL-C concentration, smoking, family history of early onset ischemic heart disease).

Pharmacological effect

Cardiolip is a lipid-lowering drug, a selective competitive inhibitor of HMG-CoA reductase.

Effective in adult patients with hypercholesterolemia, with or without hypertriglyceridemia (regardless of race, gender or age), including patients with diabetes mellitus and familial hypercholesterolemia.

An additive effect is observed in combination with fenofibrate (in relation to reducing the concentration of TG) and nicotinic acid in lipid-lowering doses (in relation to reducing the concentration of HDL-C).

Special instructions

Before starting therapy and throughout the entire period of treatment, you should follow a standard lipid-lowering diet. During treatment, the lipid profile should be monitored every 2 to 4 weeks and the dose of the drug should be adjusted accordingly if necessary.

When using rosuvastatin at all doses, and especially at doses exceeding 20 mg, short-term proteinuria may occur. In patients taking the drug at a dose of 40 mg, it is recommended to monitor renal function indicators.

Patients taking rosuvastatin at a dose exceeding 20 mg may experience myalgia, myopathy, and rarely rhabdomyolysis. Determination of CPK activity should not be carried out after intense physical activity or in the presence of other possible reasons for the increase in CPK, which may lead to incorrect interpretation of the results obtained. If CPK increases 5 times above the upper limit of normal, a repeat measurement should be taken after 5-7 days. Therapy should not be started if a repeat test confirms an initial increase in CPK activity of more than 5 times the upper limit of normal.

In patients at risk of developing myopathy/rhabdomyolysis, it is necessary to consider the balance of risk and possible benefit of therapy and carry out clinical monitoring throughout the course of treatment.

The patient should be informed to immediately report to the doctor in cases of unexpected onset of muscle pain, muscle weakness or spasms, especially in combination with malaise and fever. In such patients, CPK activity should be monitored. Therapy should be discontinued if CPK activity is increased by more than 5 times the upper limit of normal, or if muscle symptoms are severe and cause daily discomfort (even if CPK activity is 5 times less than the upper limit of normal). If symptoms disappear and CPK activity returns to normal, re-use of the drug or other HMG-CoA reductase inhibitors in lower doses should be considered under close medical supervision. Routine monitoring of CPK in the absence of symptoms of rhabdomyolysis is impractical.

An increased incidence of myositis and myopathy has been reported in patients taking other HMG-CoA reductase inhibitors in combination with fibric acid derivatives, including gemfibrozil, cyclosporine, niacin in lipid-lowering doses, azole antifungals, HIV protease inhibitors and macrolide antibiotics. Gemfibrozil increases the risk of myopathy when combined with certain HMG-CoA reductase inhibitors. Therefore, concomitant use of rosuvastatin and gemfibrozil is not recommended. The risk/benefit ratio should be carefully weighed when using rosuvastatin and fibrates or nicotinic acid in lipid-lowering doses together.

It is recommended to determine liver function indicators before starting therapy and 3 months after starting therapy. If the activity of ‘liver’ transaminases in the blood serum is 3 times higher than the upper limit of normal, the dose of the drug should be reduced or discontinued.

When hypercholesterolemia is combined with hypothyroidism or nephrotic syndrome, therapy for underlying diseases should be carried out before starting treatment with rosuvastatin.

There was an increase in plasma concentrations of rosuvastatin in Asian patients compared to Caucasian patients.

In patients with blood glucose concentrations between 5.6 and 6.9 mmol/L, rosuvastatin therapy was associated with an increased risk of developing type 2 diabetes mellitus.

Women of reproductive age should use adequate methods of contraception.

During the treatment period, dizziness and weakness may occur, so care must be taken when driving vehicles and engaging in other potentially hazardous activities that require increased concentration and speed of psychomotor reactions.

Active ingredient

Rosuvastatin

Composition

One film-coated tablet contains:

active ingredient:

rosuvastatin calcium in terms of rosuvastatin 10.00 mg;

excipients:

microcrystalline cellulose,

pregelatinized starch,

colloidal silicon dioxide (Aerosil),

magnesium stearate;

tablet shell:

opadry II pink (polyvinyl alcohol, titanium dioxide, macrogol (polyethylene glycol), talc, carmine red dye (E120)).

Contraindications

Hypersensitivity to rosuvastatin or any of the components of the drug;
liver disease in the active phase, including a persistent increase in serum transaminase activity and any increase in serum transaminase activity (more than 3 times the upper limit of normal);
severe renal dysfunction (creatinine clearance (CC) less than 30 ml/min);
myopathy;
simultaneous use of cyclosporine;
in women: pregnancy, lactation, lack of adequate methods of contraception;
patients predisposed to the development of myotoxic complications;
children under 18 years of age.

With caution:

There is a risk of developing myopathy/rhabdomyolysis – renal failure, hypothyroidism, personal or family history of hereditary muscle diseases and a previous history of muscle toxicity when using other HMG-CoA reductase inhibitors or fibrates; alcohol addiction; age over 65 years; conditions in which an increase in plasma concentration of rosuvastatin is noted; race (Asian race – Japanese and Chinese); simultaneous use with fibrates; history of liver disease; sepsis; arterial hypotension; major surgery, trauma, severe metabolic, endocrine or electrolyte disturbances, or uncontrolled seizures.

Patients with hepatic impairment: There are no data or experience with the drug in patients with a Child-Pugh score above 9.

Use during pregnancy and breastfeeding: Rosuvastatin is contraindicated during pregnancy and lactation. Since cholesterol and substances synthesized from cholesterol are important for fetal development, the potential risk of inhibiting HMG-CoA reductase outweighs the benefit of using the drug during pregnancy.

If pregnancy is diagnosed during therapy, the drug should be discontinued immediately.

Women of reproductive age should use adequate methods of contraception.

Side Effects

From the central nervous system: often – headache, dizziness, asthenic syndrome; very rarely – polyneuropathy, memory loss.

From the digestive system: often – constipation, nausea, abdominal pain; rarely – pancreatitis; very rarely – jaundice, hepatitis; unspecified frequency – diarrhea.

From the respiratory system: unspecified frequency – cough, shortness of breath.

From the musculoskeletal system: often – myalgia; rarely – myopathy (including myositis), rhabdomyolysis with or without acute renal failure; very rarely – arthralgia.

From the urinary system: proteinuria (less than 1% of cases – for doses of 10 mg and 20 mg, 3% of cases – for a dose of 40 mg); unspecified frequency – peripheral edema; very rarely – hematuria.

From the endocrine system: diabetes mellitus type 2.

Allergic reactions: rarely – hypersensitivity reactions, including angioedema; uncommon – skin itching, rash, urticaria; unspecified frequency – Stevens-Johnson syndrome.

Laboratory indicators: transient dose-dependent increase in creatine phosphokinase (CPK) activity (if CPK activity increases more than 5 times compared to the upper limit of normal, therapy should be temporarily suspended); reversible transient dose-dependent increase in the activity of ‘liver’ transaminases; increased concentrations of glucose, bilirubin, activity of gamma-glutamyl transpeptidase, alkaline phosphatase, changes in the level of thyroid hormones.

The following side effects have been reported with some HMG-CoA reductase inhibitors (statins): depression, sleep disturbances including insomnia and nightmares, sexual dysfunction. Isolated cases of interstitial lung disease have been reported, especially with long-term use of the drugs.

When taking several daily doses simultaneously, the pharmacokinetic parameters of rosuvastatin do not change. Treatment of overdose is symptomatic; monitoring of liver function and CPK activity is necessary; There is no specific antidote, hemodialysis is ineffective.

Interaction

Cyclosporine: with simultaneous use of Cardiolip and cyclosporine, the AUC of rosuvastatin is on average 7 times higher than the value observed in healthy volunteers. Combined use with rosuvastatin leads to an 11-fold increase in Cmax in blood plasma. Does not affect plasma concentrations of cyclosporine.

Vitamin K antagonists: Initiating rosuvastatin therapy or increasing the dose of the drug in patients receiving concomitant vitamin K antagonists (eg, warfarin) may lead to an increase in prothrombin time (International Normalized Ratio – INR). Discontinuation of rosuvastatin or reduction of the drug dose may lead to a decrease in INR (INR monitoring is recommended).

Gemfibrozil and other lipid-lowering drugs: the combined use of rosuvastatin and gemfibrozil leads to a 2-fold increase in Cmax and AUC of rosuvastatin. Based on specific interaction data, no pharmacokinetically significant interaction with fenofibrates is expected; pharmacodynamic interaction is possible.

Gemfibrozil, fenofibrate, other fibrates and lipid-lowering doses of nicotinic acid (large doses or equivalent to 1 g per day) increase the risk of myopathy when used concomitantly with HMG-CoA reductase inhibitors, possibly due to the fact that they can cause myopathy when used in monotherapy. When taking the drug simultaneously with gemfibrozil, fibrates, nicotinic acid at a dose of more than 1 g/day, patients are recommended to start with an initial dose of 5 mg (1/2 tablet of 10 mg).

Ezetimibe: Concomitant use of rosuvastatin and ezetimibe was not accompanied by changes in the AUC and Cmax of both drugs.

HIV protease inhibitors: Although the exact mechanism of interaction is unknown, coadministration of HIV protease inhibitors may result in a significant increase in rosuvastatin exposure. Therefore, simultaneous use of rosuvastatin and HIV protease inhibitors in the treatment of patients with human immunodeficiency virus (HIV) is not recommended.

Antacids: simultaneous use of rosuvastatin and antacid suspensions containing aluminum and magnesium hydroxide leads to a decrease in plasma concentrations of rosuvastatin by approximately 50%. This effect is less pronounced if antacids are used 2 hours after taking rosuvastatin. The clinical significance of this interaction has not been studied.

Erythromycin: simultaneous use of rosuvastatin and erythromycin leads to a decrease in AUC of rosuvastatin by 20% and Cmax by 30%. This interaction may occur as a result of increased intestinal motility caused by erythromycin.

Oral contraceptives/hormone replacement therapy: Concomitant use of rosuvastatin and oral contraceptives increases ethinyl estradiol AUC and norgestrel AUC by 26% and 34%, respectively. This increase in plasma concentration should be taken into account when selecting the dose of oral contraceptives. There are no pharmacokinetic data on the simultaneous use of rosuvastatin and hormone replacement therapy; therefore, a similar effect cannot be excluded when using this combination.

Other medicinal products: No clinically significant interaction between rosuvastatin and digoxin is expected.

Cytochrome P450: results of in vivo and in vitro studies showed that rosuvastatin is neither an inhibitor nor an inducer of cytochrome P450 isoenzymes. In addition, rosuvastatin is a non-core substrate for these isoenzymes. There was no clinically significant interaction between rosuvastatin and fluconazole and ketoconazole. The combined use of rosuvastatin and itraconazole increases the AUC of rosuvastatin by 28% (clinically insignificant). Thus, interactions related to metabolism via the cytochrome P450 system are not expected.

Storage conditions

At a temperature not exceeding 25 °C.

Keep out of the reach of children.

Shelf life

2 years.

Manufacturer

ALSI Pharma, Russia