β-Adrenergic Receptor Blocking Drugs in Cardiac Arrhythmias

Summary

β-Adrenergic receptor blocking (β-blocking) drugs now have an established place in the elective and prophylactic treatment of many cardiac arrhythmias. In isolated preparations of heart muscle, these drugs inhibit spontaneous diastolic depolarisation and in high concentrations which are unlikely to have clinical relevance, they exhibit membrane-depressant properties. In intact animals and man they slow the rate of discharge of the sinus and ectopic cardiac pacemakers and increase the functional refractory period of the AV node. They also retard conduction, both anterograde as well as retrograde, in anomalous pathways of the heart.

Sinus tachycardia responds well to β-blocking drugs but they are particularly useful in atrial fibrillation in which their effect in reducing the ventricular rate by producing AV block is additive to that of digitalis. They do not, however, alter the atrial rate and sinus rhythm is restored in only a small number of cases. In atrial flutter, sinus rhythm is produced more frequently, but the usual response in this arrhythmia is an increase in AV block which may be useful as a diagnostic test in a complicated tachycardia.

Reversion of paroxysmal supraventricular tachycardias is frequently produced by β-adrenergic receptor antagonists which are also effective in reducing the frequency of recurrences especially in the Wolff-Parkinson-White syndrome. They are the drugs of choice in this situation. Digitalis-induced tachyarrhythmias respond well to β-blocking drugs as do arrhythmias provoked by exercise or by paroxysmal release of catecholamines in phaeochromocytoma. Resistant arrhythmias after acute myocardial infarction, cardiac surgery, or from other causes, may respond to β-blocking drugs especially when they are combined with other antiarrhythmic drugs or electrical pacing. Supraventricular and ventricular arrhythmias following acute myocardial infarction respond well to elective treatment with intravenous β-blocking drugs, but when these drugs are given orally for prophylaxis there is no reduction in acute mortality.

Pre-treatment with β-blocking drugs of patients having atrial fibrillation does not improve the conversion rate following DC countershock. Similarly, when they are given prophylactically to patients following successful cardioversion, relapse rate is not reduced except in combination with quinidine. β-Blocking drugs have been found useful in the treatment of arrhythmias occurring during anaesthesia and in the elimination of extrasystoles in patients during artificial cardiac pacemaking.

Clinical and experimental evidence tends to support the view that β-blockade is the main determinant of the antiarrhythmic action of β-adrenergic receptor blocking drugs. Their membrane-depressant properties appear to be irrelevant in most clinical situations. Thus, propranolol, oxprenolol, alprenolol, pindolol and practolol are all likely to have comparable antiarrhythmic potencies in adequate doses, and the therapeutic superiority of one agent over another is likely to be related essentially to the frequency of side-effects with the different drugs. Aggravation of heart failure and the development of atrioventricular block or airways obstruction, are the most frequent unwanted side-effects of β-blocking drugs used in antiarrhythmic therapy. Practolol, at present, is the only cardio selective compound and is less likely than other β-blocking drugs to cause airways obstruction. It also seems the least likely to cause severe haemodynamic depression and in situations where airways obstruction or cardiac decompensation are present, it is preferred to the conventional agents such as propranolol, oxprenolol, alprenolol and pindolol.