Ethmozin. II. Effects of intravenous drug administration on atrioventricular nodal reentrant tachycardia.

Electrophysiologic studies were performed in 11 patients with atrioventricular (AV) nodal reentrant tachycardia (SVT) before and after intravenous administration of 1.5 to 2 mg/kg ethmozin. Initially, 9 of 11 patients had induction of sustained SVT, and two remaining patients had nonsustained SVT and atrial echoes, respectively. Ethmozin terminated induced SVT in six of nine patients. In six of nine patients ethmozin prevented the development of sustained SVT, indicating that ethmozin depressed retrograde fast pathway AV nodal conduction. In four of these patients atrial echoes were abolished. In the two remaining cases ethmozin prevented the induction of nonsustained SVT. In only three of these nine patients was sustained SVT induced. Anterograde fast and slow pathway properties did not significantly change with ethmozin administration. Effective refractory period (ERP) of the ventriculoatrial (VA) conduction system and ventricular paced cycle length producing VA block was 305 +/- 40 (mean +/- SEM) and 347 +/- 38 msec before and 424 +/- 105 and 475 +/- 71 msec after ethmozin administration, respectively (p less than 0.01, n = 8), suggesting depression of retrograde pathway with ethmozin administration. Ethmozin significantly (p less than 0.05) lengthened PA, AH, HV, and PR intervals (36 +/- 11 to 45 +/- 14 msec, 84 +/- 21 to 93 +/- 17 msec, 42 +/- 8 to 50 +/- 7 msec, and 163 +/- 23 to 190 +/- 31 msec, respectively). No significant change was observed in sinus rate, QRS and QT intervals, or ERP of atrium and ventricle. Thus, a single intravenous dose of ethmozin terminated induced SVT and prevented induction of sustained SVT in most patients, reflecting depression of retrograde fast pathway conduction.