Acetacarol - instructions for use, reviews, analogs and formulations (tablets 50 mg, 100 mg and 300 mg) of the drug for the treatment of unstable angina, the prevention of heart attacks and strokes in adults, children and pregnancy

In this article, you can read the instructions for using the drug Acercarol. There are reviews of visitors to the site - consumers of this medication, as well as opinions of doctors of specialists on the use of acetylcholine in their practice. A big request is to actively add their feedback on the drug: the medicine helped or did not help get rid of the disease, which were observed complications and side effects, possibly not declared by the manufacturer in the annotation. Analogues of Acecardol in the presence of existing structural analogues.Use for the treatment of unstable angina, the prevention of heart attacks and strokes in adults, children, as well as during pregnancy and lactation.

Acercarol - the mechanism of antiplatelet action is based on irreversible inhibition of cyclooxygenase (COX-1), which blocks the synthesis of thromboxane A2 and suppresses platelet aggregation. Antiaggregant effect develops even after application of small doses of the drug and persists for 7 days after a single dose. It is believed that Acetylsalicylic acid or ASA (the active substance of the drug Accekarol) has other mechanisms for suppressing platelet aggregation.

In high doses ASA (over 300 mg per day) also has anti-inflammatory, antipyretic and analgesic effects.

Composition

Acetylsalicylic acid + auxiliary substances.

Pharmacokinetics

After ingestion Accekardol quickly and completely absorbed from the digestive tract. ASA is partially metabolized during absorption. During and after absorption, ASA is converted into a major metabolite, salicylic acid, which is metabolized mainly in the liver under the influence of enzymes to form such metabolites,such as phenyl salicylate, salicylic acid glucuronide and salicyluric acid, found in many tissues and in urine. In women, the metabolic process is slower (less enzyme activity in the blood serum). Due to the fact that the tablets are covered with an acid-resistant coating, ASA is not released in the stomach (the membrane effectively blocks the dissolution of the drug in the stomach), but in the alkaline medium of the duodenum. Thus, the absorption of ASA in the form of enteric coated tablets is delayed by 3 to 6 hours compared to conventional tablets (without such a coating). ASA and salicylic acid bind to blood plasma proteins (from 66% to 98% depending on the dose) and are quickly distributed in the body. Salicylic acid penetrates the placenta and into breast milk. Elimination of salicylic acid is dose-dependent, since its metabolism is limited by the possibilities of the enzymatic system. Unlike other salicylates, with repeated administration of the drug, unhydrolyzed ASA does not accumulate in the blood serum. Salicylic acid and its metabolites are excreted by the kidneys.In patients with normal kidney function 80-100% of a single dose of the drug is excreted by the kidneys within 24-72 hours.

Indications

• prevention of acute myocardial infarction in the presence of risk factors (for example, diabetes, hyperlipidemia, hypertension, obesity, smoking, old age);
• prevention of repeated myocardial infarction;
• unstable angina;
• prevention of ischemic stroke (including in patients with transient impairment of cerebral circulation);
• prevention of thromboembolism after surgery and invasive vascular interventions (eg, coronary artery bypass grafting, carotid endarterectomy, arteriovenous shunting, angioplasty and stenting of the coronary arteries, carotid angioplasty);
• prevention of deep vein thrombosis and thromboembolism of the pulmonary artery and its branches (including with prolonged immobilization as a result of extensive surgical intervention).

Forms of release

Tablets coated with 50 mg, 100 mg and 300 mg.

Instructions for use and dosage

Tablets should be taken before meals, washed down with plenty of liquid, once a day. Acetacarbol is intended for long-term use.The duration of therapy is determined by the doctor.

Prevention for suspected acute myocardial infarction: 100 mg daily or 300 mg every other day (the first tablet must be chewed for faster absorption).

Prevention of the first acute acute myocardial infarction in the presence of risk factors: 100 mg daily or 300 mg every other day.

Prevention of repeated myocardial infarction and unstable angina: 100-300 mg per day daily.

Prophylaxis of ischemic stroke and transient impairment of cerebral circulation: 100-300 mg per day daily.

Prevention of thromboembolism after surgery and invasive vascular interventions: 100-300 mg per day daily.

Prevention of deep vein thrombosis and thromboembolism of the pulmonary artery and its branches: 100 mg per day or 300 mg every other day.

Side effect

• nausea, vomiting;
• heartburn;
• stomach ache;
• ulcers of the mucous membrane of the stomach and duodenum;
• perforated ulcers of the stomach and duodenum;
• gastrointestinal bleeding;
• transient violations of liver function with increased activity of hepatic transaminases;
• increased risk of bleeding due to the inhibitory effect of ASA on aggregationthrombocytes;
• anemia;
• skin rash;
• itching;
• hives;
• angioedema;
• rhinitis;
• edema of the nasal mucosa;
• cardiorespiratory distress syndrome;
• anaphylactic shock;
• bronchospasm;
• dizziness;
• hearing loss;
• headache;
• noise in ears.

Contraindications

• erosive and ulcerative lesions of the gastrointestinal tract (in the phase of exacerbation);
• gastrointestinal bleeding;
• hemorrhagic diathesis;
• bronchial asthma induced by the intake of salicylates, a complete or incomplete combination of bronchial asthma, recurrent nasal polyposis and paranasal sinuses and ASA intolerance;
• marked renal failure (creatinine clearance (CK) less than 30 ml / min);
• marked hepatic insufficiency (class B and C on the Child-Pugh scale);
• chronic heart failure (3-4 functional classes according to NYHA classification);
• simultaneous reception of methotrexate in a dose of 15 mg per week or more;
• 1 and 3 trimesters of pregnancy;
• lactation period;
• children's age till 18 years;
• deficiency of lactase, lactose intolerance, glucose-galactose malabsorption;
• Hypersensitivity to ASA.

With caution when:

• gout, hyperuricemia, t.p.ASA in low doses reduces the excretion of uric acid; it should be borne in mind that ASA in low doses can provoke the development of gout in predisposed patients (having decreased urinary acid excretion);
• gastric ulcer and duodenal ulcer or gastrointestinal bleeding (in the anamnesis);
• impaired liver function (class A on the Child-Pugh scale);
• impaired renal function (QC more than 30 ml / min);
• bronchial asthma, chronic respiratory diseases, hay fever, nasal polyposis, drug allergy;
• simultaneous reception of methotrexate in a dose less than 15 mg / week;
• concomitant therapy with anticoagulants;
• 2 trimester of pregnancy;
• the proposed surgical intervention (including small, for example, extraction of the tooth); ASA can cause a tendency to develop bleeding within a few days after taking the drug.

Application in pregnancy and lactation

The use of salicylates in large doses in the first 3 months of pregnancy is associated with an increased frequency of fetal development defects (split sky, heart defects). The appointment of salicylates in the first trimester of pregnancy is contraindicated.

In the 2nd trimester salicylates can only be assigned with the rigorous assessment of risk to the fetus and the mother for use, preferably in doses not exceeding 150 mg a day and short.

In the 3 trimester of pregnancy salicylates in high doses (more than 300 mg per day) causes a weakening of labor, premature closure of the ductus arteriosus in the fetus, increased bleeding in the mother and the fetus, and the appointment just before birth may cause intracranial hemorrhage, especially in preterm infants. The appointment of salicylates in the 3 trimester of pregnancy is contraindicated.

Salicylates and their metabolites penetrate into breast milk in small amounts, so breastfeeding should be abolished during lactation.

Use in children

Accekarol is contraindicated in children and adolescents under the age of 18 years.

special instructions

Accekarol can provoke bronchospasm, as well as cause seizures of bronchial asthma and other reactions of hypersensitivity. Risk factors are the availability of a history of asthma, hay fever, nasal polyposis, chronic diseases of the respiratory system as well as of allergic reactions to other drugs (e.g., skin reactions, pruritus, urticaria).

The inhibitory effect of ASA on platelet aggregation persists for several days after admission, which may increase the risk of bleeding during surgery or in the postoperative period. If absolute elimination of bleeding is necessary in the course of surgical intervention, it is necessary, if possible, to completely abandon the use of ASA in the preoperative period.

ASA in low doses can provoke the development of gout in predisposed individuals (having a decreased excretion of uric acid).

When combined glucocorticosteroids (glucocorticosteroids) and salicylates should be remembered that during treatment, the concentration of salicylates in the blood is reduced, and after the withdrawal of GCS, an overdose of salicylates is possible.

Excess dose of ASA is associated with a risk of gastrointestinal bleeding.

Impact on the ability to drive vehicles and manage mechanisms

Caution should be exercised when administering the drug Accekarol while controlling vehicles, mechanisms and other potentially hazardous activities requiring increased concentration and speed of psychomotor reactions.

Drug Interactions

Acekardol with simultaneous use enhances the effect of the following medicines:

• methotrexate by reducing renal clearance and displacing it from the bond with plasma proteins; also a combination of acetylsalicylic acid with methotrexate is accompanied by an increased incidence of side effects on the part of the hematopoiesis;
• heparin and indirect anticoagulants due to impaired platelet function and the displacement of indirect anticoagulants from the connection with plasma proteins;
• thrombolytic agents and antiplatelet agents;
• digoxin due to a decrease in its renal excretion;
• hypoglycemic agents (insulin and sulfonylurea derivatives) due to hypoglycemic properties of ASA itself at high doses and displacement of sulfonylurea derivatives from the connection with plasma proteins;
• valproic acid by displacing it from the bond with plasma proteins.

The combination of ASA with anticoagulants, thrombolytics and antiaggregants is accompanied by an increased risk of bleeding.

With simultaneous reception of Acecardol with alcohol, there is an increase in the toxic effect of alcohol on the central nervous system,the risk of damage to the mucous membrane of the gastrointestinal tract increases and the time of bleeding prolongs.

ASC at simultaneous use weakens the effect of the following drugs:

• uricosuric drugs - benzbromarone (reduction of uricosuric effect due to competitive suppression of renal tubular excretion of uric acid);
• ACE inhibitors (a dose-dependent decrease in the glomerular filtration rate due to inhibition of prostaglandins with vasodilating action is observed, and accordingly, weakening of hypotensive action is observed);
• diuretics (when combined with ASA in high doses, there is a decrease in the glomerular filtration rate as a result of a decrease in the synthesis of prostaglandins in the kidneys).

By enhancing the elimination of salicylates, systemic GCSs weaken their action.

Analogues of the drug Acecaradol

Structural analogs for the active substance:

• Anopyrine;
• ASA cardio;
• Aspicor;
• Aspen;
• Aspirin York;
• Aspirin;
• Aspirin 1000;
• Aspirin Cardio;
• Aspirin Express;
• Acentene;
• Acetylsalicylic acid;
• Acylpyrine;
• Acsbyrin;
• Bufferin;
• KardiASK;
• Cardiomagnet;
• Collorite;
• Myristin;
• Plolidol 100;
• Plolidol 300;
• Polokard;
• Taspir;
• Trombo ACC;
• Thrombogard 100;
• Thrombopol;
• Walsh Asalgin;
• Upsarin of the UPSA;
• Hack el-Payne.

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