Ten patients with recurrent episodes of
ventricular tachycardia (VT) had electrophysiologic studies in the basal state and on chronic oral
ethmozin (12.1 +/- 0.6 SE mg/kg/day).
Ethmozin significantly prolonged the AH interval (basal: 75 +/- 8 SE msec;
ethmozin: 91 +/- 10 msec, p less than 0.05), the HV interval (51 +/- 3; 66 +/- 5 msec, p less than 0.01), and the QRS duration (101 +/- 4; 118 +/- 4 msec, p less than 0.001). Atrial and ventricular refractory periods and the corrected QT interval were not significantly affected by
ethmozin. VT was induced in 7 of 10 patients in the basal state by means of programmed right ventricular extrastimulation or rapid burst ventricular pacing. On oral
ethmozin nine patients had inducible VT. VT cycle length was consistently prolonged on
ethmozin (250 +/- 13; 326 +/- 14 msec, p less than 0.001). Four of the seven patients with VT on basal ambulatory monitoring had total abolition of spontaneous VT on
ethmozin.
Ethmozin failed to prevent induction of VT in most patients despite significant reductions in ventricular
arrhythmia on ambulatory monitoring. Further studies comparing VT induction with ambulatory monitoring in patients on
ethmozin are needed to confirm these findings and to define the clinical significance of this dissociation.