Suppression of ouabain-induced ventricular rhythms with aprindine HCl. A comparison with other antiarrhythmic agents.

Three groups of dogs were given ouabain (mean 60 mug/kg) until an accelerated ventricular escape (AVE) and repetitive ventricular response (RVR) followed cessation of pacing. In a group of six control dogs, the AVE and RVR were found to occur at stable escape intervals for periods of at least three hours. A second group of dogs received various antiarrhythmic agents in an attempt to suppress the AVE and RVR. Quinidine, diphenylhydration, lidocaine, procainamide, and propranolol, were successful in only 0 to 33% of trials. Potassium canrenoate, 12 mg/kg was unsuccessful in three dogs. Verapamil, by bolus, suppressed RVR in 41% and AVE in 21% of trials. KCl, infused until AVE and RVR were suppressed, was successful when the mean serum potassium rose from 3.8 mEq/L to 7.2 mEq/L. Aprindine, 2.86 mg/kg, suppressed AVE and RVR in 14 of 14 dogs. In the third group of dogs, verapamil was infused continuously and suppressed RVR and AVE at a mean cumulative dose of 2.93 mg/kg. Calcium chloride reversed aprindine and verapamil-induced suppression of RVR and AVE. This study demonstrates that RVR and AVE resist suppression by available antiarrhythmic agents in clinically-used doses. Only aprindine was 100% successful at doses used in man. The ionic pathogenesis of RVR and AVE is unknown, but some data suggest the slow current may play an important role.