Acute electrophysiologic effects of rotundium were studied with programmed electrical cardiac stimulation in 14 patients with paroxysmal tachyarrhythmias due to preexcitation syndrome after intravenous infusion of 2 mg/kg. The results showed that the drug depressed the function of the atrioventricular node markedly. Significant lengthening of A-H interval (from 75 +/- 19ms to 88 +/- 21ms, P < 0.01), AVNERP (from 246 +/- 47ms to 290 +/- 45ms, P < 0.01), AVNWCL (from 326 +/- 23ms to 388 +/- 42ms, P < 0.01) were seen. But no significant influence on SNRT, CSNRT and SACT (P < 0.05) were observed. Rotundium lengthened A-delta interval (from 97 +/- 18 ms to 106 +/- 19ms, P < 0.05) and the anterograde effective refractory period (ERP) of the accessory pathway (from 287 +/- 36ms to 320 +/- 43ms P < 0.05). It slightly lengthened V-A interval and the retrograde ERP of the accessory pathway. Rotundium lengthened AERP significantly (from 216 +/- 37ms to 244 +/- 41ms, P < 0.02). The effective rate of prevention of supraventricular tachycardia (SVT) by PES in this study was 77.8% (7/9). Rotundium showed no severe side effect in this study.