抄録
A method to evaluate the clinical effect of antiarrhythmic agents by artificial induction of the paroxysmal supraventricular tachycardia (PSVT) has been developed. The present study was carried out in thirty-five patients with a history of documented PSVT, including 8 cases of WPW syndrome.
In all cases, PSVT was induced with complete reproducibility by a single or paired electrical stimulation (an interval of 250 to 300 msec), which was applied to the right atrium, and terminated by rapid right atrial pacing.
The procedures of the developed method were as follows : (a) PSVT was induced by the electrical stimulation of the right atrium during sinus rhythm. After confirming the persistence of PSVT, the induced tachycardia (PSVT) was converted to the original sinus rhythm by means of the rapid right atrial pacing. The reproducibility of PSVT induction was proved by repeated electrical stimulations. (a) Two or three minutes after the intravenous administration of one of the agents, the induction of PSVT was tried again.
The drugs were evaluated as having a preventive effect on PSVT, when either PSVT was not induced or only one to five echo beats occurred after its administration. By this method, PSVT was successfully prevented in 11 out of 16 patients (68.8%) with disopyramide, in 8 out of 14 (57.1%) with verapamil, and in 4 Out of 5 (80.0%) with ajmaline, indicating the effectiveness of these drugs. This test was completed within an hour, showing no serious adverse effects.
The electrophysiological studies revealed that disopyramide significantly prolonged the effective refractory period of the right atrium, but not the effective refractory period and functional refractory period of the AV node. Verapamil produced no significant changes in the refractory periods.
His bundle electrogram showed that AH and HV intervals increased significantly after either disopyramide or verapamil administration. After ajmaline, AH and HV intervals were prolonged in most patients, but it was not statistically significant.
The RR interval during PSVT was significantly longer when PSVT was induced despite the administration of the drugs because of their ineffectiveness than when it was induced prior to the administration of drugs. This lengthening may be ascribed to the increase in AH, HV and/or VA intervals.
In conclusion, the method proposed here is a very efficient and safe procedure for evaluating the effectiveness of antiarrhythmic agents.
