Effects of quinidine on atrioventricular nodal reentrant paroxysmal tachycardia.

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Abstract
Electrophysiologic studies were performed in 14 patients with atrioventricular nodal reentrant paroxysmal tachycardia (PSVT) before and after oral administration of 1.2-1.6 g quinidine sulfate over a 24-hour period (0.3-0.4 g every 6 hours). Studies were performed after 0.5-1 mg i.v. atropine before and after quinidine. All 14 patients had induction of sustained PSVT before quinidine, with or without atropine. After quinidine, 11 patients lost the ability to induce echoes or sustain PSVT, reflecting depression of the retrograde pathway with either absence of atrial echoes (six patients) or induction of nonsustained PSVT, with termination of echoes or PSVT occurring after QRS (block in retrograde pathway) (five patients). In only one of these 11 patients was sustained PSVT inducible after addition of atropine. All 11 were discharged on the same dose of quinidine. In three patients, quinidine was discontinued because of side effects. Follow-up in the remaining eight patients for 8 +/- 2 months showed no recurrence of sustained PSVT. Three of the 14 patients had induction of sustained PSVT after quinidine. Ventricular paced cycle length producing ventriculoatrial block was 314 +/- 7 msec (mean +/- SEM) before and 392 +/- 13 msec after quinidine (p less than 0.01) in the 14 patients, suggesting depression of the retrograde pathway with quinidine. In summary, quinidine inhibited induction of sustained atrioventricular nodal reentrant tachycardia with depression of the retrograde pathway. It is very effective in preventing recurrence of PSVT in most patients.

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