Non-cardioselective b-blockers (beta-blockers) / thiazide diuretics (thiazides).

pindolol, clopamide

Each tablet contains 10 mg pindolol and 5 mg clopamide.

Tablet. White, uncoated, round, flat, bevelled tablets, marked VISKALDIX on one side and with a score line on the other. The score line is only to facilitate breaking for ease of swallowing and not to divide into equal doses.

Mild to moderate hypertension.

One tablet daily in the morning. If blood pressure is not satisfactorily lowered after 2 to 3 weeks then two tablets daily as a single dose in the morning. Maximum dose of three tablets daily, if required.

There is no experience with Viskaldix in children.

There is no evidence that the dosage or tolerability of Viskaldix is directly affected by advanced age. However, because of the diuretic component, such patients should be carefully supervised as factors sometimes associated with aging, such as poor diet or impaired renal function may indirectly affect the dosage or tolerability.

• Untreated cardiac failure
• sick sinus syndrome (including sino-atrial block)
• second and third degree heart block
• Prinzmetal's 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
• metabolic acidosis
• pronounced bradycardia
• obstructive pulmonary disease
• cor pulmonale
• prolonged fasting hypokalaemia
• refractory hypokalaemia
• hyponatraemia
• hypercalcaemia
• Addison's disease
• severe renal or hepatic impairment and symptomatic hyperuricaemia.

Viskaldix should not be used with agents which inhibit calcium transport e.g. verapamil.

Especially in patients with ischaemic heart disease, treatment should not be discontinued suddenly. The dosage should be gradually reduced, i.e. over 1-2 weeks, if necessary at the same time initiating replacement therapy, to prevent exacerbation of angina pectoris.

Patients with a poor cardiac reserve should be stabilised with digitalis before treatment with Viskaldix to prevent impairment of myocardial contractility.

As with all beta-blockers, Viskaldix should be used with caution in patients with a history of non-asthmatic chronic obstructive lung disease or recent myocardial infarction.

Patients with spontaneous hypoglycaemia or diabetes should be monitored closely as concomitant use of beta-blockers may intensify the blood sugar lowering effect of insulin and other antidiabetic drugs and also as thiazide diuretics can lower insulin tolerance. Use of beta-blockers may mask the symptoms of hypoglycaemia (tachycardia, tremor). Beta blockers may also mask the symptoms of thyrotoxicosis.

During treatment with Viskaldix, patients should not undergo anaesthesia with agents causing myocardial depression (e.g. halothane, cyclopropane, trichloroethylene, ether, chloroform). Viskaldix should be gradually withdrawn before elective surgery. In emergency surgery or cases where withdrawal of Viskaldix would cause deterioration in cardiac condition, atropine sulphate 1 to 2mg 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. 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.

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 was 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.

In severe renal failure a further impairment of renal function following beta blockade has been reported in a few cases. Potassium levels should be checked in patients with renal or hepatic failure and urate levels should be checked in patients with gout.

Dilutional hyponatraemia may occur in hot weather in oedematous patients on Viskaldix.

The appropriate therapy is water restriction rather than the administration of salt, except in rare instances when the hyponatraemia is life-threatening. In true salt depletion, appropriate replacement is the treatment of choice.

Viskaldix should not be used during concomitant administration of lithium, or by patients with known hypersensitivity to sulphonamides.

Calcium-channel blocking agents: Viskaldix 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-blockers 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.

Cimetidine, hydralazine and alcohol may induce increased plasma level of 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.

Side-effects associated with beta-blockade: 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. Gastro-intestinal problems, nausea, vomiting, diarrhoea. 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.

Thiazide diuretics may cause postural hypotension and mild gastrointestinal effects; impotence (reversible on withdrawal of treatment); hypokalaemia, hypomagnesaemia, hyponatraemia, hypercalcaemia, hypochloraemic alkalosis, hyperuricaemia, gout, hyperglycaemia, and increases in plasma cholesterol. Less commonly rashes, photosensitivity; blood disorders (including neutropenia and thrombocytopenia), pancreatitis; intrahepatic cholestatis and hypersensitivity reactions (including pneumonitis, pulmonary oedema, severe skin reactions) have also been reported.

Amdipharm Plc

(POM)

16 February 2012