CardiASC, 100 mg 60 pcs

Cardiac Acetylsalicylic Acid is antiaggregative.

Pharmacodynamics

The mechanism of antiplatelet action of acetylsalicylic acid (ASA) is based on irreversible inhibition of COX-1, resulting in blocked synthesis of thromboxane A2 and suppressed platelet aggregation. The antiplatelet effect develops even after a low dose of the drug and lasts for 7 days after a single dose. It is believed that ASA has other mechanisms of platelet aggregation inhibition, which expands the field of its use in various vascular diseases. At high doses, ASK also has anti-inflammatory, antipyretic and analgesic effects.

Pharmacokinetics

Assoc is quickly and completely absorbed from the GI tract after oral administration. ASK is partially metabolized during absorption. During and after absorption ASA is converted to the main metabolite, salicylic acid, which is metabolized mainly in the liver under the influence of enzymes to form metabolites such as phenylsalicylate, salicylic acid glucuronide and salicyluric acid found in many tissues and in urine. In women, the metabolic process is slower (lower serum enzyme activity). T_max of ASA in plasma is 10-20 minutes after oral administration, of salicylic acid – 0.3-2 hours.

In view of the fact that the tablets are covered with an acid-resistant coating, ASK is not released in the stomach (the coating effectively blocks dissolution of the drug in the stomach), but in the alkaline environment of the duodenum. Thus, absorption of Asc in the form of tablets coated with an enteric coating is delayed by 3-6 hours compared to conventional (without such a coating) tablets. Asc and salicylic acid are bound to blood plasma proteins (from 66 to 93% depending on the dose) and are rapidly distributed in the body. Salicylic acid passes through the placenta and into the breast milk.

The excretion of salicylic acid is dose-dependent because its metabolism is limited by the enzyme system. T_1/2 ranges from 2-3 h when ASA is used in low doses and up to 16 h when the drug is used in high doses (common doses of acetylsalicylic acid as an analgesic). Unlike other salicylates, non-hydrolyzed ASA does not accumulate in the blood serum when taking the drug repeatedly. Salicylic acid and its metabolites are excreted by the kidneys. In patients with normal renal function 80-100% of a single dose of the drug is excreted by the kidneys within 24-72 hours.

Indications

Active ingredient

Composition

Active ingredient:

acetylsalicylic acid 100 mg;

Excipients:

Stearic acid;

Corn starch;

Lactose monohydrate (milk sugar);

Castor oil hydrogenated;

povidone (plasdon K90 or collidone 90F);

polysorbate (tween 80); MCC;

film wrapper:

Methacrylic acid and ethyl acrylate copolymer 1:1 (collicut MAE 100P);

macrogoal and polyvinyl alcohol copolymer (collicut IR);

p> copovidone (plasdon S630);

triethyl citrate;

talc;

Titanium dioxide.

How to take, the dosage

CardiASC should be taken orally before meals with plenty of fluid.
CardiASC is intended for long-term use. The duration of therapy is determined by the attending physician.

Prophylaxis in case of suspected acute myocardial infarction: 100-200 mg/day or 300 mg every other day (the first tablet should be chewed for faster absorption).

Prevention of first-time acute myocardial infarction in the presence of risk factors: 100 mg daily or 300 mg every other day.
Prevention of recurrent myocardial infarction, unstable angina pectoris, prevention of stroke and transient cerebral circulatory disorders, prevention of thromboembolic complications after surgical operations or invasive studies: 100-300 mg daily
Prevention of deep vein thrombosis and thromboembolism of the pulmonary artery and its branches: 100-200 mg daily or 300 mg every other day.

Interaction

When used concomitantly, CardIASC enhances the effects of methotrexate by reducing its renal clearance and displacement from plasma protein binding.

When used concomitantly, CardIASC increases the effects of heparin and indirect anticoagulants due to impaired platelet function and displacement of indirect anticoagulants from binding to plasma proteins.

CardIASC when combined use increases the effect of thrombolytic and antiplatelet drugs (including ticlopidine).

Cardiascan increases the plasma concentration of digoxin by reducing renal excretion and enhances its effects.

CardIASC enhances the effect of hypoglycemic drugs (insulin and sulfonylurea derivatives) due to the hypoglycemic effect of acetylsalicylic acid (in high doses) and displacement of sulfonylurea derivatives from plasma proteins binding.

CardIASC enhances the effect of valproic acid by displacing the latter from plasma protein binding.

When used together, CardIASC attenuates the effect of uricosuric drugs (benzbromaron) due to competitive tubular elimination of uric acid.

With concomitant use, GCS increases the excretion of salicylates and attenuates their effects.

Additive effect is noted when used concomitantly with ethanol.

Special Instructions

The drug CardiASC should be used after prescribing by a physician.

ASK may provoke bronchospasm, as well as causing attacks of bronchial asthma and other hypersensitivity reactions. Risk factors include a history of bronchial asthma, hay fever, nasal polyposis, chronic respiratory diseases, and allergic reactions to other drugs (e.g., skin reactions, itching, urticaria).

ASK can cause bleeding of varying severity during and after surgical interventions.

Combination of ASA with anticoagulants, thrombolytics and antiplatelet agents is accompanied by an increased risk of bleeding.

ASK in low doses may provoke development of gout in predisposed persons (who have reduced excretion of uric acid).
Combination of ASK with methotrexate is accompanied by an increased frequency of side effects from the hematopoietic organs.
High doses of ASA have hypoglycemic effect that should be kept in mind when prescribing it to patients with diabetes mellitus who receive hypoglycemic drugs.

When prescribing GCS and salicylates together, we must remember that during treatment, blood levels of salicylates decrease, and after withdrawal of GCS an overdose of salicylates is possible.

The combination of ASA with ibuprofen is not recommended because the latter worsens the beneficial effects of ASA on longevity.
Excessive doses of ASA are associated with a risk of gastrointestinal bleeding.
Overdose is especially dangerous in elderly patients.
When ASA is combined with alcohol, there is an increased risk of gastrointestinal mucosal damage and prolonged bleeding time.

Contraindications

Side effects

Allergic reactions: urticaria, Quincke’s edema.

Gastrointestinal tract: nausea, heartburn, vomiting, abdominal pain, gastric and duodenal ulcers, including perforative, gastrointestinal bleeding, increased activity of “liver” enzymes.

Respiratory system: bronchospasm.

Immune system disorders: anaphylactic reactions.

Hematopoietic system disorders: anemia (rare), increased bleeding.

Central nervous system disorders: dizziness, tinnitus.

Overdose

Symptoms of moderate overdose: nausea, vomiting, tinnitus, hearing impairment, dizziness, confusion.
Treatment: reduction of the drug dose.

The symptoms of severe overdose:
fever, hyperventilation, ketoacidosis, respiratory alkalosis, coma, cardiovascular and respiratory failure, severe hypoglycemia.

Treatment: immediate admission to specialized departments for emergency therapy – gastric lavage, determination of the acid-base balance, alkaline and forced alkaline diuresis, hemodialysis, administration of solutions, activated carbon, symptomatic therapy. When performing alkaline diuresis, it is necessary to achieve pH values between 7.5 and 8. Forced alkaline diuresis should be performed when plasma concentration of salicylates is more than 500 mg/l (3.6 mmol/l) in adults and 300 mg/l (2.2 mmol/l) in children.

Similarities