Method of action:
Medically reviewed by Fedorchenko Olga Valeryevna, PharmD. Last updated on 2020-04-10
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Top 20 medicines with the same components:
a. Management of hypertension
b. Management of angina pectoris
c. Management of cardiac dysrhythmias
d. Management of myocardial infarction. Early intervention in the acute phase and long-term prophylaxis after recovery from myocardial infarction
The dose must always be adjusted to individual requirements of the patients, with the lowest possible starting dosage. The following are guidelines:
One tablet daily. Most patients respond to 100 mg daily given orally as a single dose. Some patients, however, will respond to 50 mg given as a single daily dose. The effect will be fully established after one to two weeks. A further reduction in blood pressure may be achieved by combining Korus-Atenolol tablets with other antihypertensive agents. For example, co-administration of Korus-Atenolol tablets with a diuretic provides a highly effective and convenient antihypertensive therapy.
Most patients with angina pectoris will respond to 100 mg given orally once daily or 50 mg given twice daily. It is unlikely that additional benefit will be gained by increasing the dose.
Having controlled the dysrhythmias with intravenous Korus-Atenolol a suitable maintenance dosage is 50 mg - 100 mg daily, given as single dose.
For patients suitable for treatment with intravenous beta-blockade and presenting within 12 hours of the onset of chest pain, Korus-Atenolol 5-10 mg should be given by slow intravenous injection (1 mg/minute) followed by Korus-Atenolol 50 mg orally about 15 minutes later, provided no untoward effects have occurred from the intravenous dose. This should be followed by a further 50 mg orally 12 hours after the intravenous dose, and then 12 hours later by 100 mg orally, once daily. If bradycardia and/or hypotension requiring treatment, or any other untoward effects occur, Korus-Atenolol should be discontinued.
Dosage requirements may be reduced, especially in patients with impaired renal function.
There is no paediatric experience with Korus-Atenolol and for this reason it is not recommended for use in children.
Since Korus-Atenolol is excreted via the kidneys, the dosage should be adjusted in cases of severe impairment of renal function.
No significant accumulation of Korus-Atenolol occurs in patients who have a creatinine clearance greater than 35 ml/min/1.73 m2 (normal range is 100-150 ml/min/1.73 m2).
For patients with a creatinine clearance of 15-35 ml/min/1.73 m2 (equivalent to serum creatinine of 300-600 micromol/litre), the oral dose should be 50 mg daily and the intravenous dose should be 10 mg once every two days.
For patients with a creatinine clearance of less than 15 ml/min/1.73 m2 (equivalent to serum creatinine of greater than 600 micromol/litre), the oral dose should be 25 mg daily or 50 mg on alternate days and the intravenous dose should be 10 mg once every four days.
Patients on haemodialysis should be given 50 mg orally after each dialysis; this should be done under hospital supervision as marked falls in blood pressure can occur.
Method of administration
For administration by the oral route.
- Korus-Atenolol, as with other beta-blockers, should not be used in patients with any of the following:
- Cardiogenic shock
- Uncontrolled heart failure
- Sick sinus syndrome (including sino-atrial block)
- Second-or third-degree heart block
- Untreated phaeochromocytoma
- Metabolic acidosis
- Bradycardia (< 50 bpm before treatment initiation)
- Known hypersensitivity to the active substance, or any of the excipients
- Severe peripheral arterial circulatory disturbances
- Severe asthma and severe chronic obstructive pulmonary disorders, such as airway obstructions
- The intravenous application of calcium channel blockers (verapamil / diltiazem type) is contraindicated in patients who use Korus-Atenolol (except in intensive care unit)
Korus-Atenolol as with other beta-blockers:
- Should not be withdrawn abruptly. The dosage should be withdrawn gradually over a period of 7-14 days, to facilitate a reduction in beta-blocker dosage. Patients should be followed during withdrawal, especially those with ischaemic heart disease. Furthermore there is a risk on myocardial infarction and sudden death.
- When a patient is scheduled for surgery, and a decision is made to discontinue beta-blocker therapy, this should be done at least 24 hours prior to the procedure. Continuation of beta-blockade reduces the risk of arrhythmias during induction and intubation, however the risk of hypotension may be increased as well. The risk-benefit assessment of stopping beta-blockade should be made for each patient. If treatment is continued, an anaesthetic with little negative inotropic activity should be selected to minimise the risk of myocardial depression. The patient may be protected against vagal reactions by intravenous administration of atropine.
- Although contraindicated in uncontrolled heart failure , may be used in patients whose signs of heart failure have been controlled. Caution must be exercised in patients whose cardiac reserve is poor.
- May increase the number and duration of angina attacks in patients with Prinzmetal's angina due to unopposed alpha-receptor mediated coronary artery vasoconstriction. Korus-Atenolol is a beta1-selective beta-blocker; consequently, its use may be considered although utmost caution must be exercised.
- Although contraindicated in severe peripheral arterial circulatory disturbances , may also aggravate less severe peripheral arterial circulatory disturbances (Raynaud's disease or syndrome, intermittent claudication).
- Due to its negative effect on conduction time, caution must be exercised if it is given to patients with first-degree heart block.
- May mask the symptoms of hypoglycaemia, in particular, tachycardia. Insulin sensitivity may be reduced in patients treated with Korus-Atenolol.
- May mask the signs of thyrotoxicosis.
- Will reduce heart rate as a result of its pharmacological action. In the rare instances when a treated patient develops symptoms, which may be attributable to a slow heart rate and the pulse rate drops to less than 50-55 bpm at rest, the dose should be reduced.
- May cause a more severe reaction to a variety of allergens when given to patients with a history of anaphylactic reaction to such allergens. Such patients may be unresponsive to the usual doses of adrenaline (epinephrine) used to treat the allergic reactions.
- May cause a hypersensitivity reaction including angioedema and urticaria.
- Should be used with caution in the elderly, starting with a lesser dose.
Since Korus-Atenolol is excreted via the kidneys, dosage should be reduced in patients with a creatinine clearance of below 35 ml/min/1.73 m2.
Although cardioselective (beta1) beta-blockers may have less effect on lung function than non-selective beta-blockers, as with all beta-blockers, these should be avoided in patients with reversible obstructive airways disease, unless there are compelling clinical reasons for their use. Where such reasons exist, Korus-Atenolol may be used with caution. Occasionally, some increase in airways resistance may occur in asthmatic patients however, and this may usually be reversed by commonly used dosage of bronchodilators such as salbutamol or isoprenaline. The label and patient information leaflet for this product state the following warning: â€œIf you have ever had asthma or wheezing, you should not take this medicine unless you have discussed these symptoms with the prescribing doctorâ€.
As with other beta-blockers, in patients with a phaeochromocytoma, an alpha-blocker should be given concomitantly.
Patients with anamnestically known psoriasis should take Korus-Atenolol only after careful consideration.
Use is unlikely to result in any impairment of the ability of patients to drive or operate machinery. However, it should be taken into account that occasionally dizziness or fatigue may occur
Korus-Atenolol is well tolerated. In clinical studies, the undesired events reported are usually attributable to the pharmacological actions of Korus-Atenolol.
The following undesired events, listed by body system, have been reported with the following frequencies: very common (>1/10), common (>1/100 to <1/10), uncommon (>1/1,000 to <1/100), rare (>1/10,000 to <1/1,000), very rare (<1/10,000) including isolated reports, not known (cannot be estimated from the available data).Blood and lymphatic system disorders:
Rare: Purpura, thrombocytopenia, leucopenia.
Uncommon: Sleep disturbances of the type noted with other beta-blockers.
Rare: Mood changes, depression, anxiety, nightmares, confusion, psychoses and hallucinations.
Nervous system disorders:
Rare: Dizziness, headache, paraesthesia of extremities.
Rare: Dry eyes, impaired vision, visual disturbances.
Rare: Heart failure deterioration, precipitation of heart block.
Common: Cold extremities.
Rare: Postural hypotension, which may be associated with syncope, intermittent claudication, may be increased if already present, in susceptible patients Raynaud's phenomenon.
Respiratory, thoracic and mediastinal disorders:
Rare: Bronchospasm may occur in patients with bronchial asthma or a history of asthmatic complaints.
Common: Gastrointestinal disturbances, constipation.
Rare: Dry mouth.
Uncommon: Elevations of transaminase levels.
Rare: Hepatic toxicity including intrahepatic cholestasis.
Skin and subcutaneous tissue disorders:
Rare: Alopecia, psoriasiform skin reactions, exacerbation of psoriasis, skin rashes.
Not known: Hypersensitivity reactions, including angioedema and urticaria.
Musculoskeletal and connective tissue disorders:
Not known: Lupus like syndrome
Reproductive system and breast disorders:
General disorders and administration site conditions:
Common: Fatigue, sweating.
Very rare: An increase in ANA (Antinuclear Antibodies) has been observed, however the clinical relevance of this is not clear.
Discontinuance of the drug should be considered if, according to clinical judgement, the well-being of the patient is adversely affected by any of the above reactions
Reporting of suspected adverse reactions
Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme website: www.mhra.gov.uk/yellowcard.
The symptoms of overdosage may include bradycardia, hypotension, acute cardiac insufficiency and bronchospasm.
General treatment should include: close supervision; treatment in an intensive care ward; the use of gastric lavage; activated charcoal and a laxative to prevent absorption of any drug still present in the gastrointestinal tract; the use of plasma or plasma substitutes to treat hypotension and shock. The possible uses of haemodialysis or haemoperfusion may be considered.
Excessive bradycardia can be countered with atropine 1-2 mg intravenously and/or a cardiac pacemaker. If necessary, this may be followed by a bolus dose of glucagon 10 mg intravenously. If required, this may be repeated or followed by an intravenous infusion of glucagon 1-10 mg/hour depending on response. If no response to glucagon occurs or if glucagon is unavailable, a beta-adrenoceptor stimulant such as dobutamine 2.5 to 10 micrograms/kg/minute by intravenous infusion may be given. Dobutamine, because of its positive inotropic effect could also be used to treat hypotension and acute cardiac insufficiency. It is likely that these doses would be inadequate to reverse the cardiac effects of beta-blocker blockade if a large overdose has been taken. The dose of dobutamine should therefore be increased if necessary to achieve the required response according to the clinical condition of the patient.
Bronchospasm can usually be reversed by bronchodilators.
Pharmacotherapeutic group: Beta-blocking agents, plain, selective.
ATC code: CO7A B03.
Mechanism of action
Korus-Atenolol is a beta-blocker, which is beta1-selective, (i.e. acts preferentially on beta1-adrenergic receptors in the heart). Selectivity decreases with increasing dose.
Korus-Atenolol is without intrinsic sympathomimetic and membrane-stabilising activities and as with other beta-blockers, has negative inotropic effects (and is therefore contraindicated in uncontrolled heart failure).
As with other beta-blockers, the mode of action of Korus-Atenolol in the treatment of hypertension is unclear. It is probably the action of Korus-Atenolol in reducing cardiac rate and contractility, which makes it effective in eliminating, or reducing the symptoms of patients with angina.
It is unlikely that any additional ancillary properties possessed by S (-) Korus-Atenolol, in comparison with the racemic mixture, will give rise to different therapeutic effects.
Clinical efficacy and safety
Korus-Atenolol is effective and well tolerated in most ethnic populations although the response may be less in black patients.
Korus-Atenolol is effective for at least 24 hours after a single oral dose. The drug facilitates compliance by its acceptability to patients and simplicity of dosing. The narrow dose range and early patient response ensure that the effect of the drug in individual patients is quickly demonstrated. Korus-Atenolol is compatible with diuretics, other hypotensive agents and antianginals. Since it acts preferentially on beta-receptors in the heart, Korus-Atenolol may, with care, be used successfully in the treatment of patients with respiratory disease, who cannot tolerate non-selective beta-blockers.
Early intervention with Korus-Atenolol in acute myocardial infarction reduces infarct size and decreases morbidity and mortality. Fewer patients with a threatened infarction progress to frank infarction; the incidence of ventricular arrhythmias is decreased and marked pain relief may result in reduced need of opiate analgesics. Early mortality is decreased. Korus-Atenolol is an additional treatment to standard coronary care.
Absorption of Korus-Atenolol following oral dosing is consistent but incomplete (approximately 40-50%) with peak plasma concentrations occurring 2-4 hours after dosing. The bioavailability is decreased by 20% when taken with food. There is a linear relationship between dosage and plasma concentration. The inter-subject variability in AUC and Cmax is about 30-40%. There is no significant hepatic metabolism of Korus-Atenolol and more than 90% of that absorbed reaches the systemic circulation unaltered.
Korus-Atenolol penetrates tissues poorly due to its low lipid solubility and its concentration in brain tissue is low. The volume of distribution is 50 to 75 L. The protein binding is low (approximately 3%). Most of an absorbed dose (85-100%) is excreted unchanged via the urine.
The clearance is about 6 l/h and the half-life is about 6 to 9 hours. In elderly patients, clearance is decreased and elimination half-life increased. The clearance is correlated to renal function and the elimination is prolonged in patients with renal impairment. Impaired liver function does not influence the pharmacokinetics of Korus-Atenolol.
Korus-Atenolol is a drug on which extensive clinical experience has been obtained. Relevant information for the prescriber is provided elsewhere in the Prescribing Information.
No special requirements
However, we will provide data for each active ingredient