1. Name Of The Medicinal Product
Visken Tablets 5 mg
2. Qualitative And Quantitative Composition
Each tablet contains 5 mg pindolol.
3. Pharmaceutical Form
Tablet.
4. Clinical Particulars
4.1 Therapeutic Indications
Essential hypertension: For reduction in blood pressure in essential hypertension. Onset of action of Visken is usually rapid, most patients showing a response within the first one to two weeks of treatment. However, maximum response may take several weeks to develop.
Prophylactic treatment of angina pectoris: Prophylactic treatment with Visken reduces the frequency and severity of anginal attacks and increases work capacity.
4.2 Posology And Method Of Administration
Adults
Hypertension: Initially one 5 mg tablet two or three times a day. According to the response of the patient the dose may be increased at weekly intervals to a maximum of 45 mg given in divided doses twice or three times daily.
Once daily dosage schedule: Further work shows that many patients respond to a once daily dosage regime. Initially 15 mg (3 tablets) should be taken once a day with breakfast and adjusted according to individual response up to a maximum of 45 mg (9 tablets). Most patients respond to a once daily dose of between 15-30 mg (3-6 tablets).
Angina pectoris: Usually 2.5 mg to 5 mg orally three times a day according to response.
Use in children
Experience with Visken in children is limited. Its use is therefore not recommended.
Use in the elderly
No evidence exists that elderly patients require different dosages or show different side-effects from younger patients.
Route of administration
Oral.
4.3 Contraindications
Untreated cardiac failure, cardiogenic shock, sick sinus syndrome, second and third degree heart block, Prinzmetals angina, history of bronchospasm and bronchial asthma (a warning stating "do not take this medicine if you have a history of wheezing or asthma" will appear on the label), untreated phaeochromocytoma, peripheral circulatory disease, pronounced bradycardia, obstructive pulmonary disease, history of cor pulmonale, metabolic acidosis, prolonged fasting, severe renal failure. Visken should not be taken in conjunction with agents which inhibit calcium transport e.g. verapamil.
4.4 Special Warnings And Precautions For Use
Patients with a poor cardiac reserve should be stabilised with digitalis before treatment with Visken to prevent impairment of myocardial contractility.
As for other beta-blockers, and especially in patients with ischaemic heart disease, treatment should not be discontinued suddenly. The dosage should gradually be reduced, i.e. over 1-2 weeks, if necessary at the same time initiating replacement therapy, to prevent exacerbation of angina pectoris.
As with all beta-blockers, Visken should be used with caution in patients with a history of non-asthmatic chronic obstructive lung disease or recent myocardial infarction. Caution must be exercised when beta-blocking agents are administered to patients with spontaneous hypoglycaemia or diabetes under treatment with insulin or oral hypoglycaemic agents, since hypoglycaemia may occur during prolonged fasting and some of its symptoms (tachycardia, tremor) may be masked. Beta-blockers may also mask the symptoms of thyrotoxicosis.
During treatment with Visken, patients should not undergo anaesthesia with agents causing myocardial depression (e.g. halothane, cyclopropane, trichloroethylene, ether, chloroform). Visken should be gradually withdrawn before elective surgery. In emergency surgery or cases where withdrawal of Visken would cause deterioration in cardiac condition, atropine sulphate 1 to 2 mg intravenously should be given to prevent severe bradycardia.
If a beta-blocker is indicated in a patient with phaeochromocytoma it must always be given in conjunction with an alpha-blocker. Pre-existing peripheral vascular disorders may be aggravated by beta-blockers.
In severe renal failure a further impairment of renal function following beta blockade has been reported in a few cases.
There have been reports of skin rashes and/or dry eyes associated with the use of beta-adrenoceptor blocking drugs. The reported incidence is small and in most cases the symptoms have cleared when treatment is withdrawn. Discontinuance of the drug should be considered if any such reaction is not otherwise explicable.
Cessation of therapy with a beta-blocker should be gradual.
Patients with known psoriasis should take beta-blockers only after careful consideration.
Beta-blockers may increase both the sensitivity towards allergens and the seriousness of anaphylactic reactions.
4.5 Interaction With Other Medicinal Products And Other Forms Of Interaction
Calcium-channel blocking agents: Visken should not be used with calcium-channel blockers with negative inotropic effects e.g. verapamil and to a lesser extent diltiazem. The concomitant use of oral beta-blockers and calcium antagonists of the dihydropyridine type can be useful in hypertension or angina pectoris. However, because of their potential effect on the cardiac conduction system and contractility, the i.v. route must be avoided. The concomitant use with dihydropyridines e.g. nifedipine may increase the risk of hypotension. In patients with cardiac insufficiency, treatment with beta-blocking agents may lead to cardiac failure.
Use of digitalis glycosides, in association with beta-adrenoceptor blocking drugs, may increase atrio-ventricular conduction time.
Clonidine: when therapy is discontinued in patients receiving a beta-blocker and clonidine concurrently, the beta-blockers should be gradually discontinued several days before clonidine is discontinued, in order to reduce the potential risk of a clonidine withdrawal hypertensive crisis.
MAO inhibitors: concurrent use with beta-blockers is not recommended. Possibly significant hypertension may theoretically occur up to 14 days following discontinuation of the MAO inhibitor.
Caution should be exercised in the concurrent use of beta-blocking agents with class 1 antiarrhythmics (e.g. disopyramide, quinidine) and amiodarone.
Concomitant use of beta-blockers may intensify the blood sugar lowering effect of insulin and other antidiabetic drugs. Use of beta-blockers may prevent appearance of the signs of hypocalcaemia (tachycardia).
Cimetidine, hydralazine and alcohol may induce increased plasma levels of hepatically metabolised beta-blockers.
Prostaglandin synthetase inhibiting drugs may decrease the hypotensive effects of beta-blockers.
Sympathomimetics with beta-adrenergic stimulant activity and xanthines: concurrent use with beta-blockers may result in mutual inhibition of therapeutic effects; in addition, beta-blockers may decrease theophylline clearance.
Concomitant use of beta-blockers with tricyclic antidepressants, barbiturates and phenothiazines as well as other anti-hypertensive agents may increase the blood pressure lowering effect.
Reserpine: concurrent use may result in an additive and possibly excessive beta-adrenergic blockade.
4.6 Pregnancy And Lactation
Visken is contraindicated in pregnancy and passes in small quantities into breast milk. Breastfeeding is therefore not recommended following administration.
4.7 Effects On Ability To Drive And Use Machines
Because dizziness or fatigue may occur during initiation of treatment with beta-adrenoceptor blocking drugs, patients driving vehicles or operating machinery should exercise caution until their individual reaction to treatment has been determined.
4.8 Undesirable Effects
Bradycardia, a slowed AV-conduction or increase of an existing AV-block, hypotension, heart failure, cold and cyanotic extremities, Raynaud's phenomenon, paraesthesia of the extremities, increase of an existing intermittent claudication. Fatigue, headaches, impaired vision, hallucinations, psychoses, confusion, impotence, dizziness, sleep disturbances, depression, nightmares. Gastrointestinal disturbances (including diarrhoea, nausea and vomiting). Bronchospasm in patients with bronchial asthma or a history of asthmatic complaints. Disorder of the skin, especially rash. Dry eyes. Beta-blockers may mask the symptoms of thyrotoxicosis or hypoglycaemia. An increase in ANA (anti-nuclear antibodies) has been seen; its clinical relevance is not clear.
4.9 Overdose
Treat by elimination of any unabsorbed drug and general supportive measures. Marked bradycardia as a result of overdosage or idiosyncrasy should be treated with atropine sulphate 1 or 2 mg intravenously. If necessary, isoprenaline hydrochloride can be administered by a slow intravenous injection, under constant supervision, beginning with 25 mcg (5 mcg/min) until the desired effect is achieved. A cardiac pacemaker may be required, i.v. glucagon (5-10 mg) has been reported to overcome some of the features of serious overdosage and may be useful.
5. Pharmacological Properties
5.1 Pharmacodynamic Properties
Visken is a potent beta-adrenoceptor antagonist (beta-blocker). It blocks both B- and B2-adrenoceptors for more than 24 hours after administration. It has negligible membrane-stabilising activity. As a beta-blocker, Visken protects the heart from beta-adrenoceptor stimulation by acetecholamines during physical exercise and mental stress, and also reduces the sympathetic drive to the heart at rest. Its intrinsic sympathomimetic activity (ISA), however, provides the heart with basal stimulation similar to that elicited by normal resting sympathetic activity, with the result that heart rate and contractility at rest and intracardiac conduction are not unduly depressed. The risk of bradycardia is therefore small and normal cardiac output is not reduced.
Visken is a beta-blocker with clinically relevant vasodilator activity. This results from the ISA exerted on B2-adrenoceptors in blood vessels. The high vascular resistance of established hypertension is lowered by Visken; tissue and organ perfusion is not impaired, and may even be improved.
In contrast to the potentially adverse changes in blood lipoprotein profiles seen during treatment with other beta-blockers (a decrease in the HDL/LDL ratio), the ratio of high density lipoproteins (HDL) to low density (for further information see product licence file).
5.2 Pharmacokinetic Properties
The rapid, nearly complete absorption ( >95%) and the negligible hepatic first-pass effect (13%) of Visken result in a high bioavailability (87%). Maximum plasma concentration is reached within one hour after oral administration. Visken has a plasma protein binding of 40%, a volume of distribution of 2-3 l/Kg and a total clearance of 500 ml/min. The elimination half-life of Visken is 3-4 hours. 30-40% is excreted unchanged in the urine, while 60-70% is excreted via kidney and liver as inactive metabolites. Visken crosses the placental barrier and passes in small quantities into breast milk.
Patients with impaired kidney or liver function may usually be treated with normal doses. Only in severe cases may a reduction of the daily dose be necessary.
5.3 Preclinical Safety Data
There are no pre-clinical data of relevance to the prescriber which are additional to that already included in other sections of the SmPC.
6. Pharmaceutical Particulars
6.1 List Of Excipients
Microcrystalline cellulose, starch, colloidal anhydrous silica, magnesium stearate.
6.2 Incompatibilities
None.
6.3 Shelf Life
5 years.
6.4 Special Precautions For Storage
None.
6.5 Nature And Contents Of Container
PVC/PVDC clear blister packs in a cardboard carton containing 56, 60 or 100 tablets.
6.6 Special Precautions For Disposal And Other Handling
None.
7. Marketing Authorisation Holder
Amdipharm Plc
Regency House
Miles Gray Road
Basildon
Essex
SS14 3AF
United Kingdom
8. Marketing Authorisation Number(S)
PL 20072/0021
9. Date Of First Authorisation/Renewal Of The Authorisation
1 January 2005
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