Betaxolol

Betaxolol belongs to the beta-blocker family, and more specifically to the so-called cardioselective beta-blockers. It selectively blocks the beta-1 adrenergic receptors of the heart, without intrinsic sympathomimetic activity and with a weak membrane-stabilising effect. By occupying these receptors, it prevents adrenaline and noradrenaline from binding to them and transmitting their acceleration signal. Its selectivity means that at usual doses it targets mainly the heart, more than the beta-2 receptors of the bronchi and the vessels.

Deprived of this stimulation, the heart slows its rate, which is the negative chronotropic effect, and contracts with less force, which is the negative inotropic effect. Cardiac output falls, and with it the pressure exerted on the artery walls. It is this double brake, on the rhythm and on the contraction, that lowers blood pressure and that defines the entire pharmacology of the medicine.

The marketing authorisation indication for oral betaxolol is the management of arterial hypertension, alone or in combination with other antihypertensive agents. By reducing cardiac output and pressure, it eases the workload imposed on the heart and the arteries, which is the objective sought when pressure remains persistently too high. Depending on each person’s profile, it may therefore be prescribed on its own or alongside another blood-pressure treatment.

Its effect does not settle in with a single dose. With an elimination half-life of about 14 to 22 hours, betaxolol accumulates gradually in the blood and reaches its plasma steady state in 5 to 7 days. It is over this period that the fall in pressure stabilises, which explains why the doctor reassesses the response after one to two weeks rather than in the first days of treatment.

Betaxolol is taken once a day. The usual starting dose is 10 mg per day, increased to 20 mg after 7 to 14 days if pressure warrants it; beyond 20 mg, the additional benefit remains minimal. Its oral absorption is complete and its absolute bioavailability is around 89 %, with neither food nor alcohol altering these figures. It can therefore be taken with or without a meal, provided the same time is kept from one day to the next in order to cover the twenty-four hours.

Regularity also applies to stopping, which must never be abrupt. In a person with coronary disease, suddenly interrupting a beta-blocker can worsen angina pectoris and, in some cases, trigger a myocardial infarction. If treatment must be stopped, the dose is reduced gradually, over several days, under the doctor’s supervision. This decision rests with the doctor, and not with the patient alone.

In the US studies, considering the effects reported in at least 2 % of people, those most often observed are bradycardia, that is to say a heart beating slowly, fatigue, difficulty breathing, lethargy and dizziness. Bradycardia is clearly dose-dependent. Discontinuation of treatment concerned about 3.5 % of people, mainly because of bradycardia, but also fatigue, dizziness, headaches and erectile disorders.

In people with diabetes, beta-blockers can raise blood sugar and mask certain signs of a drop in blood sugar, such as the acceleration of the heart, so that a hypoglycaemia may pass more unnoticed. Betaxolol nonetheless keeps an advantage linked to its cardioselectivity: unlike non-selective beta-blockers, it does not prolong the hypoglycaemia caused by insulin.

The blockade of beta receptors also affects the way the body handles potassium. Stimulation of the beta-2 receptors normally drives potassium into the cells, to the point that beta-2 agonists are used to treat an excess of potassium in the blood. A beta blockade may therefore, conversely, slow this transfer into the cells and let potassium accumulate a little more in the blood. This effect passes through the beta-2 receptors: yet betaxolol targets mainly the beta-1 receptors of the heart, so that its influence on potassium remains minimal. Potassium then becomes a marker to monitor rather than to load without measure.

This mineral is found mainly in everyday fruits and vegetables: dried apricots and raisins, lentils and beans, the potato, spinach and chard, broccoli, the avocado, the banana, citrus fruits and the tomato, but also salmon, yoghurt and almonds. Knowing where it concentrates helps to keep control of the quantities, together with the doctor, who monitors your blood potassium throughout treatment.

Some combinations call for caution. Adding an oral calcium channel blocker such as verapamil or diltiazem exposes to hypotension, to disturbances of atrioventricular conduction that can go as far as complete block, and to left ventricular failure. Medicines that deplete catecholamine stores, such as reserpine, can have an additive effect. With clonidine, the beta-blocker is first stopped over several days before clonidine is gradually withdrawn.

The person’s terrain counts just as much. Patients with bronchospastic disease, including asthma, should generally not receive a beta-blocker, and a bradycardia, a hypotension or a risk of heart block constitute other precautions or contraindications. Monitoring therefore bears on heart rate, blood pressure and, in people with diabetes, on blood sugar. Betaxolol is eliminated mainly by the liver, but more than 80 % of the dose is found again in the urine, of which about 15 % in unchanged form, which guides the adjustment of doses according to each situation.