Circulation, Vol 70, 876-883, Copyright © 1984 by American Heart Association
KK Sethi, S Jaishankar and MP Gupta
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)
ARTICLES
Salutary effects of intravenous ajmaline in patients with paroxysmal supraventricular tachycardia mediated by dual atrioventricular nodal pathways: blockade of the retrograde fast pathway
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