Atenolol, tablets 100 mg 30 pcs

It has antianginal, antihypertensive and antiarrhythmic effects. It does not have membrane stabilizing and intrinsic sympathomimetic activity. Reduces catecholamine-stimulated formation of cAMP from ATP.

In the first 24 hours after oral administration against the background of decreased cardiac output there is reactive increase of total peripheral vascular resistance, which gradually decreases during 1-3 days.

The hypotensive effect is associated with decreased cardiac output, decreased activity of the renin-angiotensin system, baroreceptor sensitivity and influence on the central nervous system. Hypotensive effect is manifested by both reduction of systolic and diastolic blood pressure (BP), reduction of stroke and minute volumes.

In medium therapeutic doses, it has no effect on the tone of the peripheral arteries. Hypotensive effect lasts for 24 hours and with regular use is stabilized by the end of the second week of treatment.

The antianginal effect is determined by decrease of myocardial oxygen demand as a result of decrease of heart rate (prolongation of diastole and improvement of myocardial perfusion) and contractility and decrease of myocardial sensitivity to sympathetic stimulation. It reduces heart rate (HR) at rest and during physical activity.

By increasing left ventricular end-diastolic pressure and increasing ventricular muscle fiber stretch may increase oxygen demand, especially in patients with chronic heart failure.

The antiarrhythmic action is manifested by suppression of sinus tachycardia and is associated with the elimination of arrhythmogenic sympathetic effects on the cardiac conduction system, decreased rate of propagation of excitation through the sinoatrial node and prolongation of the refractory period.

It suppresses conduction of impulses in antegrade and, to a lesser extent, in retrograde direction through the AV (atrioventricular) node and through additional conduction pathways.

The negative chronotropic effect appears 1 h after administration, reaches a maximum after 2-4 h, lasts up to 24 h.

Decreases automatism of the sinus node, decreases HR, slows down AV conduction, decreases myocardial contractility, and decreases myocardial oxygen demand. Reduces myocardial excitability. When used in medium therapeutic doses, it has less effect on the smooth muscle of the bronchi and peripheral arteries than non-selective beta-adrenoblockers.

Pharmacokinetics

Absorption from the gastrointestinal tract is fast, incomplete (50-60%), bioavailability is 40-50%, time of reaching maximum concentration in plasma – 2-4 hours. It poorly penetrates through the blood-brain barrier, passes in small amounts through the placental barrier and into breast milk.

Binding with blood plasma proteins is 6-16%. It is practically unmetabolized in liver. Half-life is 6-9 hours (increased in elderly patients). It is excreted by kidneys through glomerular filtration (85-100% unchanged).

Renal dysfunction is accompanied by prolongation of the half-life and cumulation: with creatinine clearance below 35 ml/min/1.73 m² the half-life is 16-27 h, with creatinine clearance below 15 ml/min/1.73 m² – more than 27 h (dose reduction is necessary). It is excreted during hemodialysis.

Indications

– Arterial hypertension;

– Prevention of angina attacks (except for Prinzmetal angina);

– Heart rhythm disorders: sinus tachycardia, prevention of supraventricular tachyarrhythmia, ventricular extrasystoles.

Active ingredient

Composition

1 tablet contains:
active ingredient:
atenolol – 0,1 g
excipients:
magnesium hydroxycarbonate – 0,08 g – 0,16 g
potato starch – 0,059 g – 0,118 g
gelatin – 0,009 g – 0,018 g
magnesium stearate – 0,001 g – 0,002 g
stearic acid – 0,001 g – 0,002

How to take, the dosage

Appoint orally before meals, without chewing, with a small amount of liquid.

Arterial hypertension. Treatment is started with 50 mg atenolol once daily. To achieve a stable hypotensive effect, 1 -2 weeks of therapy are required. If hypotensive effect is not sufficiently pronounced, the dose is increased to 100 mg per dose. Further increase of the dose is not recommended, as it is not accompanied by strengthening of the clinical effect.

In ischemic heart disease and tachycardia disorders of heart rhythm, 50 mg once daily.

In angina pectoris. The initial dose is 50 mg per day. If optimal therapeutic effect is not achieved within a week, the dose is increased to 100 mg per day.

In elderly patients and patients with impaired renal excretory function, the dosing regimen should be adjusted.

In patients with renal impairment, dose adjustment is recommended depending on creatinine clearance. In patients with renal insufficiency with creatinine clearance values higher than 35 ml/min./1.73 m2 (normal values are 100-150 ml/min./1.73 m2) there is no significant cumulation of atenololol.

Interaction

In concomitant use of atenolol with insulin, hypoglycemic agents for oral administration, their hypoglycemic effect is increased. When concomitant use with antihypertensive agents of different groups or nitrates the hypotensive effect is increased. Concomitant use of atenolol and verapamil (or diltiazem) may cause mutual enhancement of the cardiodepressant effect.

The hypotensive effect is weakened by estrogens (sodium retention) and nonsteroidal anti-inflammatory drugs, glucocorticosteroids. Concomitant use of atenolol and cardiac glycosides increases the risk of bradycardia and atrioventricular conduction disorders.

The simultaneous use of atenolol with reserpine, methyldopa, clonidine, verapamil may result in marked bradycardia.

Concomitant intravenous administration of verapamil and diltiazem may provoke cardiac arrest; nifedipine may lead to a significant decrease in BP. If atenolol is concomitantly administered with ergotamine derivatives, xanthine, its efficacy is reduced.

If combined use of atenolol and clonidine is discontinued, treatment with clonidine continues for several more days after atenolol is withdrawn.

Simultaneous use with lidocaine may decrease its excretion and increase the risk of lidocaine toxicity.

The use together with phenothiazine derivatives, increases the serum concentrations of each drug.

Phenytoin when administered by IV, general anesthesia drugs (hydrocarbon derivatives) increase the severity of cardiodepressant effects and the likelihood of BP reduction.

When co-administered with eufylline and theophylline, mutual suppression of therapeutic effects is possible.

The concomitant use with MAO inhibitors is not recommended because of the significant increase in hypotensive effect; a break in treatment between MAO inhibitors and atenolol should be at least 14 days.

Allergens used for immunotherapy or allergen extracts for skin tests increase the risk of severe systemic allergic reactions or anaphylaxis.

Inhaled anesthetics (hydrocarbon derivatives) increase the risk of myocardial depression and arterial hypertension. Amiodarone increases the risk of bradycardia and inhibition of AV conduction. Cimetidine increases plasma concentrations (inhibits metabolism). Iodine-containing radiopaque agents for IV administration increase the risk of anaphylactic reactions.

Longens the effects of nondepolarizing myorelaxants and the anticoagulant effect of coumarins.

Tri- and tetracyclic antidepressants, antipsychotics (neuroleptics), ethanol, sedatives and hypnotics increase central nervous system depression.

Non-hydrogenated ergot alkaloids increase the risk of peripheral circulatory disorders.

Special Instructions

Control of patients taking atenolol should include monitoring of HR and BP (at the beginning of treatment – daily, then once every 3-4 months), blood glucose content in diabetic patients (once every 4-5 months). In elderly patients it is recommended to monitor kidney function (once every 4-5 months).

The patient should be trained in the method of heart rate calculation and instructed to consult a physician if the heart rate is less than 50 bpm. In thyrotoxicosis, atenolol may mask certain clinical signs of thyrotoxicosis (e.g., tachycardia). Abrupt withdrawal in patients with thyrotoxicosis is contraindicated, since it can aggravate the symptoms. In patients with diabetes mellitus it can mask tachycardia caused by hypoglycemia. Unlike non-selective beta-adrenoblockers practically does not increase insulin-induced hypoglycemia and does not delay the recovery of blood glucose to normal concentrations.

In patients with coronary heart disease (CHD), abrupt withdrawal of beta-adrenal blockers may increase the frequency or severity of angina attacks, so discontinuation of atenololol in CHD patients should be done gradually.

In comparison with non-selective beta-adrenoblockers, cardioselective beta-adrenoblockers have less effect on lung function, however, atenololol is only prescribed in obstructive airway disease when absolutely indicated. The use of beta2-adrenomimetics may be recommended in some cases if their prescription is necessary.

Patients with bronchospastic disorders may be prescribed cardioselective adrenoblockers in cases of intolerance and/or ineffectiveness of other hypotensive drugs, but the dosage should be strictly observed. Overdose is dangerous with the development of bronchospasm.

Particular attention is necessary in cases where surgery under anesthesia is required in patients taking atenolol. Administration of the drug should be discontinued 48 hours before the intervention. As an anesthetic, a drug with as little negative inotropic effect as possible should be chosen.

In concomitant use of atenolol and clonidine, atenolol should be discontinued several days before clonidine in order to avoid the withdrawal symptoms of the latter. Hypersensitivity reactions may become more pronounced and there may be no effect from usual doses of epinephrine against a background of a history of aggravated allergy.

Drugs that reduce catecholamine stores (e.g., reserpine) can potentiate the effects of beta-adrenoblockers, so patients taking these combinations of drugs should be under constant medical monitoring for evidence of marked BP reduction or bradycardia.

In elderly patients with increasing bradycardia (less than 50ud/min), hypotension (systolic BP below 100 mmHg), atrioventricular block, bronchospasm, ventricular arrhythmias, and severe hepatic or renal impairment, the dose should be reduced or treatment should be stopped.

It is recommended that therapy be discontinued if depression develops induced by taking beta-adrenoblockers.

If intravenous verapamil administration is necessary, this should be done at least 48 hours after atenolol administration.

The use of atenolol may decrease tear fluid production, which is important in patients who wear contact lenses.

The treatment should not be stopped abruptly because of the risk of severe arrhythmias and myocardial infarction. Withdrawal is done gradually, reducing the dose over 2 weeks or more (reduce the dose by 25% every 3 to 4 days).

The dose should be discontinued before blood and urine catecholamine, normetanephrine, and vanillylmindalic acid; and antinuclear shggitel titers are investigated. In smokers, the efficacy of beta-adsnoblockers is lower. Pregnancy and lactation period.

Pregnant women should prescribe atenolol only when the benefit to the mother exceeds the potential risk to the fetus. Atenolol is excreted with breast milk, so if the drug is indicated while breastfeeding, it is better to stop breastfeeding for a while.

Impact on driving and operating machinery

At the time of treatment, one must refrain from engaging in potentially hazardous activities requiring increased concentration and quick psychomotor reactions.

Contraindications

– Cardiogenic shock;

– atrioventricular (AV) block of II-III stage;

– pronounced bradycardia (heart rate less than 40 beats/min.

– sinus node weakness syndrome;

– sinoauricular blockade;

– acute or chronic heart failure in decompensation stage;

– cardiomegaly without evidence of heart failure;

– Prinzmetal angina;

– arterial hypotension (if used for myocardial infarction;

– systolic BP less than 100 mm Hg.

– concomitant use of monoamine oxidase inhibitors (MAOIs);

– Age less than 18 years (efficacy and safety of the drug have not been established);

– hypersensitivity to the drug.

With caution: diabetes mellitus, metabolic acidosis, hypoglycemia, allergic reactions in anamnesis, chronic obstructive pulmonary disease (including pulmonary emphysema). Pulmonary emphysema), 1st degree AV blockade, chronic heart insufficiency (compensated), peripheral vascular obliterating diseases (“intermittent claudication”, Raynaud’s syndrome), pheochromocytoma, liver insufficiency, chronic renal insufficiency, myasthenia, thyrotoxicosis, depression (including in anamnesis), psoriasis, elderly age, pregnancy.

Side effects

Cardiovascular system: development (aggravation) of symptoms of chronic heart failure (swelling of ankles, feet; dyspnea), atrioventricular conduction disorders, arrhythmias, bradycardia, marked BP decrease, palpitation, myocardial contractility weakening, orthostatic hypotension, angiospasm symptoms (coldness of lower extremities, Raynaud’s syndrome), vasculitis, chest pain.

CNS: Dizziness, decreased ability to concentrate, decreased reaction speed, drowsiness or insomnia, depression, hallucinations, increased fatigue, headache, weakness, “nightmare” dreams, anxiety, confusion or short-term memory loss, paresthesias in extremities (in patients with “intermittent” claudication and Raynaud syndrome), muscle weakness, seizures.

Gastrointestinal: dry mouth, nausea, vomiting, diarrhea, abdominal pain, constipation or diarrhea, change in taste.

Respiratory system: dyspnea, bronchospasm, apnea, nasal congestion.

Hematological reactions: thrombocytic purpura, anemia (aplastic), thrombosis.

Endocrine system: decreased potency, decreased libido, hyperglycemia (in patients with insulin-independent diabetes), hypoglycemia (in patients receiving insulin), hypothyroidism.

Skin reactions: urticaria, dermatitis, skin itching, photosensitivity, increased sweating, skin hyperemia, exacerbation of psoriasis, reversible alopecia.

Sensory organs: visual impairment, decreased tear fluid secretion, dry and painful eyes, conjunctivitis.

Fetal effects: intrauterine growth retardation, hypoglycemia, bradycardia. Laboratory parameters: agranulocytosis, leukopenia, increased activity of “liver” enzymes, hyperbilirubinemia, thrombocytopenia (unusual bleeding and hemorrhage).

Others: back pain, arthropathy, “withdrawal” syndrome (tachycardia, increased frequency of angina pectoris attacks, increased BP, etc.).

The frequency of side effects increases with increasing the dose of the drug.

Overdose

Symptoms: expressed bradycardia, grade II-III AV blockade, increasing symptoms of heart failure, excessive BP decrease, difficulty breathing, bronchospasm, dizziness, fainting, arrhythmia, ventricular extrasystole, cyanosis of finger or palm nails, seizures.

Treatment:Gastric lavage and administration of adsorptive medications; inhalation or intravenous administration of the beta2-adrenomimetic salbutamol is indicated if bronchospasm occurs.

In case of AV conduction disorders, bradycardia – intravenous injection of 1-2 mg of atropine, epinephrine or placement of a temporary pacemaker; in ventricular extrasystole – lidocaine (Class 1A drugs are not used); if BP decreases – the patient should be in Trendelenburg position.

If there are no signs of pulmonary edema – IV plasma exchange solutions, if ineffective – injection of epinephrine, dopamine, dobutamine; in chronic heart failure – cardiac glycosides, diuretics, glucagon; in convulsions – IV diazepam. Dialysis is possible.

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