Electrophysiology and pharmacology of cardiac arrhythmias. VI. Cardiac effects of verapamil

Abstract

It is clear from clinical and experimental data that have been reported thus far that verapamil is highly effective in the therapy of cardiac arrhythmias, and that it acts by a different mechanism than most of the commonly used antiarrhythmic drugs. The available clinical data indicate that on intravenous administration verapamil is as good as and perhaps superior to quinidine, procainamide and propranolol for the therapy of many atrial arrhythmias. Unfortunately the extent to which it is useful as longterm prophylaxis has not yet been reported, nor has its toxicity during protracted oral administration. The effects of verapamil on cardiac action potentials clearly indicate that it modifies the slow response to a much greater extent than the fast response. Studies of cardiac tissues from diseased human atria have indicated that slow response action potentials occur frequently. It is possible that such action potentials are responsible for the reentrant and automatic arrhythmias which occur in association with clinical cardiac disease. Whether the efficacy of verapamil in the therapy of atrial arrhythmias is primarily due to abolishing slow response activity in diseased atrial tissues or to suppression of propagation through the atrioventricular node is uncertain. However, it is likely that the therapeutic action of the drug may result from altered propagation of an arrhythmia through the atrioventricular junction as well as from the effects of the drug on diseased atrial and ventricular tissues.