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Electrophysiologic effects of 50 mg iv ajmaline were evaluated in 10 patients with atrioventricular nodal reentrant paroxysmal supraventricular tachycardia (PSVT) utilizing the slow pathway for antegrade and the fast pathway for retrograde conduction. Ajmaline terminated the PSVT in all 10 patients in 17 to 165 sec (mean 94 +/- 49 sec): by ventriculoatrial block in eight, AH block in one, and intra-atrial reentry in one patient. The predrug mean PSVT cycle length of 289 +/- 44 msec (range 240 to 350) increased significantly to 373.5 +/- 60 msec (range 263 to 464; p less than .01) before the tachycardia was terminated. The increase in cycle length was a function of both AH and HA prolongation. In all 10 patients ajmaline depressed conduction through the retrograde fast pathway, as evidenced by the increase in mean ventricular paced cycle length producing ventriculoatrial block from less than or equal to 280 +/- 40 to 438 +/- 93 msec (p less than .001), and the increase in the effective refractory period of the ventriculoatrial conduction system from less than or equal to 241 +/- 42 to less than or equal to 298 +/- 62 msec (p less than .05); the drug abolished ventriculoatrial conduction in four cases. The effective refractory period of the antegrade fast pathway was unchanged after ajmaline (less than or equal to 281 +/- 31 vs less than or equal to 275 +/- 38 msec; p = NS), but conduction through the antegrade slow pathway was depressed (atrial paced cycle length producing AH block 269 +/- 30 msec before and 312 +/- 44 msec after drug; p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

circulation

Salutary effects of intravenous ajmaline in patients with paroxysmal supraventricular tachycardia mediated by dual atrioventricular nodal pathways: blockade of the retrograde fast pathway.