Electrophysiologic effects of intravenous
ethmozin (1.5 to 2 mg/kg) were evaluated in 16 patients (10 with Wolff-Parkinson-White [
WPW] syndrome and six with
concealed accessory pathway [AP]) with ventricular
preexcitation syndrome.
Ethmozin terminated induced
supraventricular tachycardia (SVT) in 9 of 14 patients and
atrial flutter with anterograde conduction 2: 1 over AP in one patient. The
drug prevented induction of sustained SVT in 8 of 14 patients (four with
WPW syndrome and four with concealed AP). The
drug significantly lengthened the cycle length of induced SVT in
WPW syndrome (381 +/- 24 to 421 +/- 27 msec) and in concealed AP (313 +/- 19 to 343 +/- 15 msec), mainly because of prolongation of the ventriculoatrial (VA) interval; the
drug increased SVT atrial zone in
WPW syndrome and removed or decreased it in patients with concealed AP. The
drug abolished anterograde (6 of 10 patients) and retrograde (3 of 16 patients) conduction over AP, and/or increased anterograde and retrograde refractoriness of AP in all patients.
Ethmozin significantly lengthened the following: PA (27 +/- 2 to 40 +/- 3 msec), AH (92.6 +/- 6 to 107 +/- 8 msec), and PR intervals (175 +/- 9 to 202 +/- 15 msec), and refractoriness of VA conduction systems. The refractoriness of atrioventricular node, HV, QRS, and QT intervals and the spontaneous sinus cycle length did not change significantly. Thus intravenous
ethmozin terminated induced SVT and prevented the induction of sustained SVT in most patients with
preexcitation syndrome due to a suppressive effect of the
drug on AP.