[Beta-blockers as antiarrhythmics drugs]

Catecholamines or increased sympathetic activity are arrhythmogenic by a) increasing the rate of diastolic depolarization of automatic pace-maker cells and thus increasing the rate of impulse formation; b) speeding the conduction process through the A-V node and shortening the refractory period and c) shortening the refractory period of ventricular cells and thus predisposing to extrasystoles by re-entry the threshold to ventricular fibrillation is lowered. The mode of action of beta-blockers may be broadly divided into two types: direct (effects on the electrophysiology of cardiac excitation and conduction) and indrect (involves a modification of a disease process which gives rise to arrhythmia production e.g., cardiac ischaemia, thyrotoxicosis, hypertrophic cardiomyopathy and mitral valve prolapse). Direct efects of beta-blockers are best seen in the presence of increased sympathetic activity; for supraventricular arrhythmias and less for venticular. Indirect effects of beta-blockers according to results of controlled clinical trials become very important in patients with coronary artery disease. At present, beta-blockers when given prophylactically, are the only antiarrhythmic agents that reduce the incidence of sudden death and reinfarction in survivors of myocardial infarction.