Ethmozin. I. Effects of intravenous drug administration on paroxysmal supraventricular tachycardia in the ventricular preexcitation syndrome.

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.