THERAPY AND PREVENTION ARRHYU[ Salutary effects of intravenous ajmaline in patients with paroxysmal supraventricular tachycardia mediated by dual atrioventricular nodal pathways: blockade of the retrograde fast pathway

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 < .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 '280 40 to 438 + 93 msec (p < .001), and the increase in the effective refractory period of the ventriculoatrial conduction system from .241 + 42 to '298 + 62 msec (p < .05); the drug abolished ventriculoatrial conduction in four cases. The effective refractory period of the antegrade fast pathway was unchanged after ajmaline ('281 ± 31 vs '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 < .05). PSVT could not be reinduced in eight subjects, predominantly because of inhibition of the retrograde pathway, although suppression of the antegrade slow pathway also contributed in one patient. In the remaining two subjects depression of retrograde conduction was insufficient to prevent sustenance of tachycardia. We conclude that ajmaline terminates atrioventricular nodal reentrant PSVT by blockade of the retrograde fast pathway, although effects on the antegrade slow pathway are also observed. Circulation 70, No. 5, 876-883, 1984. AJMALINE, an alkaloid derived from the Indian plant Rauwolfia serpentina, has been found useful in experimental and clinical atrial and ventricular arrhythmias.1-3 By virtue of its strong depressant action on accessory pathways, the drug has been extremely successful in management of arrhythmias associated with Wolff-Parkinson-White syndrome.4 5 No information is available concerning the efficacy of ajmaline in patients with paroxysmal supraventricular tachycardia (PSVT) that is mediated by dual atrioventricular nodal pathways. The present study was designed to evaluate the elfects of ajmaline on termination and reinduction From the Department of Cardiology and Electrophysiology Laboratory, G. B. Pant Hospital, New Delhi. Address for correspondence: Kamal K. Sethi, Department of Cardiology, G. B. Pant Hospital, J. L. Nehru Marg. New Delhi 110002, India. Received June 13, 1983; revision accepted July 12. 1984. 876 of PSVT resulting from reentry within the atrioventricular node. Subjects and methods Ten patients, one man and nine women from 18 to 60 years old (mean 45.4 ± 13), comprised the study group and were selected on the following criteria: (1) history of electrocardiographically documented recurrent PSVT, (2) absence of preexcitation during sinus rhythm on all available electrocardiograms, and (3) electrophysiologic documentation of atrioventricular nodal reentry during PSVT. All patients were free of organic heart disease. Two patients (Nos. 2 and 10) had incomplete right bundle branch block; all others had normal 12lead electrocardiograms. Electrophysiologic studies were performed in patients in the postabsorptive nonsedated state. All cardioactive drug therapy was stopped a week before the study. Informed written consent was obtained from all. The method of study has been published elsewhere.' Six No. 6F bipolar catheters were introduced transvenously and positioned at high, mid, and low right atrium, proximal coronary sinus, tricuspid valve (for His bundle electrogram), and right CIRCULATION by gest on M ay 0, 2017 http://ciajournals.org/ D ow nladed from THERAPY AND PREVENTION-ARRHYTHMIA ventricular apex of each subject. Multiple surface and intracardiac electrograms were recorded on a VR-12 photographic recorder (Electronics for Medicine) or on a Mingograf 8-channel ink-jet recorder (Siemens Elema) at paper speeds of 100 and 50 mm/sec. Stimuli 2 msec in duration and approximately twice diastolic threshold were delivered by a programmable stimulator (Digitimer arrhythmia investigating system, Neurolog 4279). Conduction intervals and refractory periods were measured as defined by Wu et al.7 The study protocol included: (1) incremental ventricular pacing to a paced cycle length producing ventriculoatrial block, (2) programmed ventricular extrastimulation at decreasing coupling intervals at a driven cycle length shorter than the sinus cycle length, (3) incremental atrial pacing to a paced cycle length producing AH block, (4) programmed atrial extrastimulus testing at decreasing coupling intervals during one or more atrial paced cycle lengths, (5) induction of PSVT by rapid atrial pacing, atrial extrastimulation, or rapid ventricular pacing, and delineation of the limbs of the reentrant circuit by analysis of mode of initiation of PSVT, antegrade and retrograde conduction times, and sequence of retrograde atrial activation, and (6) ventricular programmed extrastimulation during PSVT. In one patient (No. 4) intravenous atropine was required to induce sustained PSVT. After the verification of the participation of the dual atrioventricular nodal pathway in PSVT, 50 mg of ajmaline was injected intravenously over a period of 30 sec. Blood pressure was closely monitored by cuff. Intracardiac and surface electrograms were continuously recorded at a paper speed of 100 (eight patients) or 50 mm/sec (two patients) from the beginning of the injection to allow study of the mode of break of PSVT. The last 10 cycles preceding the break were analyzed in detail to identify electrophysiologic events leading to termination of the tachycardia. After break of PSVT was achieved, atrial and ventricular pacing and extrastimulus studies were repeated in the same sequence described earlier and an attempt was made to reinduce PSVT. Driving cycle lengths during extrastimulus testing were kept identical before and after the drug. All postdrug studies were completed within 25 min after administration of ajmaline. Diagnosis of atrioventricular nodal reentrant tachycardia was made as previously described.6' 8 9 Since this is mainly a diagnosis made by exclusion of other causes, care was taken to exclude patients in whom there was participation of concealed accessory pathways during tachycardia.9 Specifically, in all of the 10 patients atrial activation occurred either simultaneously with or slightly before the onset of ventricular activation during the tachycardia, suggesting that the ventricle was not an essential component of the reentry circuit. '° Statistical analysis was done with Student's t test for paired data. All results are expressed as mean ± SD.