Termination of recurrent supraventricular tachycardia by right ventricular endocardial pacing but not by left ventricular epicardial pacing

Externally controlled ventricular pacing was employed in a patient with recurrent disabling supraventricular tachycardia and frequent sinus pauses between attacks of tachyarrhythmia. A permanent transthoracic demand pacemaker was inserted after electrophysiologic study demonstrated the effectiveness of ventricular stimulation in terminating induced supraventricular tachycardia. Subsequently, spontaneous recurrences of tachyarrhythmia failed to respond to fixed rate left ventricular stimulation accomplished by placing a magnet externally over the pacemaker pack. During an induced supraventricular tachycardia, repeat electrophysiologic study demonstrated that paced left ventricular beats failed to invade the A-V junctional area before it was depolarized previously by the corresponding tachycardia beat. Right ventricular stimulation from a transvenous pacemaker could depolarize the site of the reentrant circuit and terminate an induced supraventricular tachycardia. The addition of propranolol increased the ease by which spontaneous attacks of tachyarrhythmia could be terminated by right ventricular endocardial pacing.     

Initiation of two distinct forms of atrioventricular nodal reentrant tachycardia during programmed ventricular stimulation in man

Of 42 patients with supraventricular tachycardia related to dual atrioventricular (A-V) nodal pathway conduction, 8 had sustained tachycardia induced during programmed ventricular stimulation. The characteristics of the tachycardia in three patients suggested that the A-V nodal reentrant tachycardia used a slow pathway for anterograde conduction and a fast pathway for retrograde conduction (slow-fast form). In these patients, the retrograde effective refractory period was longer in the slow than in the fast pathway. Ventriculoatrial (V-A) conduction curves (V₁-V₂, A₁-A₂) were smooth. Ventricular premature beats, being conducted retrograde over the fast pathway, could activate the slow pathway in an anterograde direction, initiating the slow-fast form of A-V nodal reentrant tachycardia. In the remaining five patients, the tachycardia used a fast pathway for anterograde conduction and a slow pathway for retrograde conduction (fast-slow form). In these patients, the retrograde effective refractory period was longer in the fast than in the slow pathway. V-A conduction curves (V₁-V₂, A₁-A₂) could be either smooth or discontinuous if there was a sudden increase in V-A conduction time. Ventricular premature beats, conducted retrograde over the slow pathway, could activate the fast pathway in an anterograde direction, establishing a tachycardia circuit in reverse of the slow-fast form. In both groups of patients, the ventricular pacing cycle length appeared to be a crucial factor in the ability to expose functional discordance between the two A-V nodal pathways during retrograde conduction.The fast-slow form of A-V nodal reentrant tachycardia, similar to the slow-fast form, could also be induced during atrial premature stimulation in two patients. In this situation, the slow pathway having an anterograde effective refractory period longer, than that of the fast pathway was a requisite condition; anterograde A-V nodal conduction curves (A₁-A₂, H₁-H₂) were smooth. Atrial premature beats, conducted anterograde over the fast pathway, could activate the slow pathway in a retrograde direction resulting In an atrial echo or sustained fast-slow form of A-V nodal reentrant tachycardia.     

Retrograde dual atrioventricular nodal pathways

Thirty-one (3.5 percent) of 887 studied patients had retrograde dual atrioventricular (A-V) nodal pathways, as manifested by discontinuous retrograde A-V nodal conduction curves (29 patients) or by two sets of ventriculoatrial (V-A) conduction intervals at the same paced cycle length (2 patients). All patients had A-V nodal reentrant ventricular echoes of the unusual variety induced with ventricular stimulation (25 patients had single, 2 patients had double and 4 patients had more than three ventricular echoes). The weak link of the reentrant circuit was always the retrograde slow pathway. Eleven of the 31 patients also had anterograde dual A-V nodal pathways (bidirectional dual pathways). Eight patients (26 percent) had spontaneous as well as inducible A-V nodal reentrant paroxysmal supraventricular tachycardia (of the unusual type in three and the usual type in five). In addition, three patients (10 percent) had only inducible supraventricular tachycardia (two of the unusual and one of the usual type).Retrograde dual A-V nodal pathways are uncommon. They are associated with the finding of at least single A-V nodal reentrant ventricular echoes (all patients), anterograde dual pathways (one third of patients) and A-V nodal reentrant paroxysmal supraventricular tachycardia of the usual or unusual variety (one third of patients).     

One to one atrioventricular conduction during atrial pacing at rates of 300/minute in absence of wolff-parkinson-white syndrome

One to one atrioventricular (A-V) or atrio-His bundle (A-H) conduction occurred during right atrial pacing at rates of 300/min in two patients with short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias. Patient 1 had episodes of reciprocating A-V tachycardia and of atrial fibrillation with very fast rates (270 to 290/min) that were slowed to 100 to 135/min after administration of intravenous verapamil. Enhanced A-V (A-H) conduction was exposed only during stimulation from the high right atrium, but not from the low lateral right atrium or coronary sinus. Patient 2 had episodes of atrial flutter with 1:1 A-V conduction and rates of 290/min. The H-V interval was short (25 ms) during sinus rhythm and atrial pacing presumably because conduction occurred through an atrio-“distal” His bundle (atriofascicular) tract. In contrast, the H-V interval was normal (40 ms) in echo beats or when the “proximal” His bundle was stimulated.In these two patients, having as “common denominators” short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias, enhanced A-V (A-H) conduction was (1) possibly due to different electrogenetic mechanisms; (2) pacing-site dependent; (3) manifested, during atrial fibrillation and atrial flutter, by extremely fast ventricular rates; and (4) unrelated to the rate of reciprocating A-V tachycardias because the latter was predominantly a function of anterograde conduction through the “slow” nodal pathway.     

Incidence, determinants and significance of fixed retrograde conduction in the region of the atrioventricular node. Evidence for retrograde atrioventricular nodal bypass tracts.

Of 104 consecutive patients studied in our laboratory with His bundle electrograms, atrial and ventricular pacing and the atrial and ventricular extrastimulus techniques, 18 patients in whom the existence and utilization of ventriculoatrial (V-A) bypass tracts were excluded demonstrated evidence for fixed and rapid retrograde conduction in the region of the atrioventricular node (A-V) as suggested by the following: (1) short (36 +/- 2 msec [mean +/- standard error of mean]) and constant retrograde H2-A2 intervals during retrograde refractory period studies; (2) significantly (P less than 0.025) better V-A than A-V conduction; (3) significantly (P less than 0.025) shorter retrograde functional refractory period of the V-A conducting system than of the A-V conduction system; and (4) the retrograde effective refractory period of the A=V nodal region was not attainable in any of the 18 patients. Fourteen of the 18 patients (77 percent) had a history of palpitations and 10 (51 percent) had documented paroxysmal supraventricular tachycardia; in 13 (72 percent) single echoes or sustained reentrant supraventricular tachycardia, or both, could be induced during atrial pacing or atrial premature stimulation studies, or both. During tachycardia all these 13 patients had a short (37 +/- 2.4 msec) and constant conduction time in the retrograde limb (H-Ae interval) of the reentrant circuit that was identical to the H2-A2 interval. In conclusion, fixed and rapid retrograde conduction in the region of the A-V node (1) is seen in approximately 17 percent of patients, (2) is associated with a large incidence of reentrant paroxysmal supraventricular tachycardia, and (3) suggests the presence of A-V nodal bypass tracts (intranodal or extranodal functioning in retrograde manner).     

Quintuple pathways participating in three distinct types of atrioventricular reciprocating tachycardia in a patient with Wolff-Parkinson-White syndrome

Electrophysiologic studies were performed in a patient with recurrent supraventricular tachyarrhythmias. Sinus and paced atrial beats had QRS complexes characteristic of atrioventricular (A-V) conduction through a manifest left lateral accessory pathway (Wolff-Parkinson-White syndrome, type A). Three distinct types of A-V reciprocating tachycardia and three different modes of retrograde atrial activation were demonstrated. Type 1 tachycardia involved the slow A-V nodal pathway and a second (left lateral or left paraseptal) accessory A-V pathway capable of retrograde conduction only. Type 2 tachycardia was of the slow-fast A-V nodal pathway type. Type 3 tachycardia involved a heretofore undescribed circuit in that retrograde conduction occurred through an accessory A-V pathway with long retrograde conduction times and anterograde conduction through both the manifest left lateral accessory A-V pathway and fast A-V nodal pathway. Premature ventricular beats delivered late in the cycle of this tachycardia advanced (but did not change) the retrograde atrial activity without affecting the timing of the corresponding anterograde H deflection. In summary, this patient had five (three accessory and two intranodal) pathways participating in three different types of A-V reciprocating tachycardia; the recurrence of these were prevented with oral amiodarone therapy.     

Effects of verapamil on supraventricular tachycardia in children

Thirteen patients, aged 6 weeks to 16 years, with uncontrolled recurrent Supraventricular tachycardia were given intravenous verapamil in an attempt to abolish an episode of Supraventricular tachycardia. All patients had had intracardiac electrophysiologic studies to define the mechanism of their tachycardia. In seven patients conversion to sinus rhythm occurred after administration of verapamil: Five of the seven had atrioventricular (A-V) nodal reentry as the mechanism of their supraventricular tachycardia; the other two had reentrant tachycardia involving an accessory pathway. Verapamil was effective in abolishing the Supraventricular tachycardia in these patients, probably by prolonging the A-V nodal refractory period and conduction, thus breaking the reentrant circuit. In six patients there was no conversion to sinus rhythm: Four of the six had automatic atrial ectopic tachycardia and two had automatic junctional ectopic tachycardia. Among the four patients with automatic atrial ectopic tachycardia, a junctional escape rhythm developed in one, and second degree A-V block developed in the others. The two patients with junctional ectopic tachycardia had severe symptomatic arterial hypotension after verapamil and required resuscitation with intravenous calcium chloride. In spite of the good response to intravenous verapamil in the seven patients with reentrant tachycardia, only four of the seven could be maintained successfully on long-term oral therapy. The patients who experienced conversion to sinus rhythm with an intravenous bolus dose of verapamil but in whom Supraventricular tachycardia could still be induced with programmed stimulation could not be maintained successfully on oral therapy.It is concluded that verapamil is an effective antiarrhythmic agent that can (1) abolish the acute episode of Supraventricular tachycardia only in cases due to reentrant mechanisms, and (2) be used as an oral medication to prevent recurrences of supraventricular tachycardia in patients in whom the arrhythmia cannot be induced with programmed stimulation after intravenous doses of the drug.     

Continuous rapid atrial pacing to control recurrent or sustained supraventricular tachycardias following open heart surgery.

A technique is described to control recurrent or sustained supraventricular tachycardia associated with rapid ventricular rates following open heart surgery. The technique utilizes a pair of temporarily implanted atrial epicardial wire electrodes to pace the heart. In one group of patients with recurrent atrial flutter and 2:1 A-V conduction, continuous rapid atrial pacing at 450 beats/min produced and sustained atrial fibrillation. The ventricular response rate immediately slowed when compared to that during atrial flutter, and if further slowing was required, it was easily accomplished by the administration of digitalis. Another group of patients with different arrhythmias (recurrent paroxysmal atrial tachycardia, sustained ectopic atrial tachycardia, or sinus rhythm with premature atrial beats which precipitated runs of atrial fibrillation) was treated with continuous rapid atrial pacing to produce 2:1 A-V block. In all instances, the continuous rapid atrial pacing suppressed the supraventricular tachycardia and maintained the ventricular response rate in a therapeutically desirable range. It was demonstrated that the technique is safe, effective, and reliable.     

Simultaneous anterograde fast-slow atrioventricular nodal pathway conduction after procainamide

Three patients with paroxysmal supraventricular tachycardia underwent electrophysiologic studies that included His bundle recordings, incremental atrial and ventricular pacing and extrastimulation before and after intravenous infusion of 500 mg of procainamide. In all three patients the tachycardia was induced during atrial pacing or premature atrial stimulation, or both. Two of the three patients had discontinuous atrioventricular (A-V) nodal curves with induction of a slow-fast tachycardia during failure in anterograde fast pathway conduction and one patient had a smooth A-V nodal curve with induction of a slow-fast tachycardia at critical A-H interval delays. After procainamide: (1) in all three patients atrial pacing induced A-V nodal Wenckebach periodicity (cycle length 300 to 400 ms) resulting in simultaneous anterograde fast and slow pathway conduction (one atrial beat resulting in two QRS complexes) and retrograde fast pathway conduction initiating an echo response or a slow-fast tachycardia, or both; (2) in all three patients there was enhanced conduction and shortening of refractoriness of the anterograde fast pathway and depressed conduction and lengthening of refractoriness of the retrograde fast pathway; and (3) in two patients there was inability to sustain tachycardia because of selective block within the retrograde fast pathway. In conclusion: (1) procainamide altered conduction and refractoriness of the anterograde fast and slow pathways so that simultaneous conduction could occur during atrial pacing, resulting in a double ventricular response and a slow-fast echo or tachycardia, or both; and (2) the differential effects of procainamide on anterograde fast and retrograde fast pathways suggests two functional A-V nodal fast pathways, one for anterograde and the other for retrograde conduction.     

Direct and reflex cardiac bradydysrhythmias from small vagal nerve stimulations

Alterations in cardiac pacemaker location, its rate of discharge, and A-V conduction patterns were induced in anesthetized adult dogs by electrical stimulation of the thoracic vagi and their small cardiac branches before and after cervical vagotomy. Electrical activity from small, contiguous bipolar silver electrodes was amplified and recorded by an optical oscillograph. The electrodes were located over the SA node, the three internodal pathways, the left atrium, and ventricular epicardium. A Hoffman-type plaque electrode was placed over the A-V node to record a His bundle electrogram simultaneously with a Lead II electrocardiogram. Electrical stimulation of the intact left recurrent laryngeal nerve and its cardiac branches before and after vagotomy induced both direct and reflex effects on SA nodal cycle length. Efferent dromotropic effects on the A-V node varied from first- to third-degree heart block during stimulation of individual left recurrent cardiac branches. Stimulation of the right recurrent cardiac nerve induced atrial bradycardia with heart block above the His bundle. Stimulation of individual right vagal branches near the heart induced bradycardia, cardiac asystole, shifts in atrial pacemaker location, or activation of His pacemakers. Establishment of the His rhythm probably indicates selective inhibition of supraventricular pacemakers but not of the His bundle. Asystole and His rhythms induced during stimulation of the more caudal branches of the right cardiac vagal nerves were generally reflexly mediated and were abolished by cervical vagotomy.     

Electrophysiologic effects of ouabain in patients with preexcitation and circus movement tachycardia

Effects of intravenous ouabain were evaluated in 19 patients with an anomalous conduction pathway (14 with manifest and 5 with concealed preexcitation) utilizing intracardiac stimulation and recording. Anterograde conduction through the anomalous pathway was present in all 14 patients with manifest preexcitation at a maximal atrial paced rate of 140 to 250 beats/min (mean ± standard error of the mean 214 ± 7.2) before and at 150 to 240 beats/min (mean 206 ± 7.1) after ouabain (difference not significant [NS]). The anterograde effective refractory period of the anomalous pathway, measured at an equivalent atrial paced rate in 10 patients, was 250 to 450 ms (mean 309 ± 19.7) before and 260 to 450 ms (mean 300 ± 17.2) after ouabain (NS). Retrograde conduction through the anomalous pathway was possible at maximal ventricular paced rates (17 patients) of 160 to 250 beats/min (mean 222 ± 6.6) before and 190 to 250 beats/min (mean 221 ± 4.4) after ouabain (NS). Sustained atrioventricular (A-V) reentrant paroxysmal supraventricular tachycardia was inducible in all 19 patients before and in 17 patients (89 percent) after ouabain (tachycardia could not be induced in two patients because of increased A-V nodal refractoriness). The mean cycle length of tachycardia in the 17 patients was 320 ± 6.7 ms before and 340 ± 8.1 ms after ouabain (p <0.01).In conclusion, ouabain has no significant effect on either anterograde or retrograde anomalous pathway refractoriness. Although ouabain slightly increases the cycle length of tachycardia, it does not interfere with induction of tachycardia in most patients with preexcitation. Oral cardiac glycosides alone would appear to be of limited value in patients with preexcitation and recurrent supraventricular tachycardia.     

The mechanisms of exercise provocation of supraventricular tachycardia

Treadmill exercise tests, electrophysiologic studies, and isoproterenol infusions were performed in 14 patients with exercise provocable supraventricular tachycardia to delineate the mechanisms of exercise provocation of paroxysmal supraventricular tachycardia. Treadmill exercise tests reproducibly provoked supraventricular tachycardia in all patients. Supraventricular tachycardia similar to that provoked by exercise occurred spontaneously during isoproterenol infusions in 9 of 11 patients tested. The specific supraventricular tachycardia diagnoses of all patients were atrial reentrant tachycardia (two patients), automatic atrial tachycardia (three), atrial flutter-fibrillation (one), atypical junctional tachycardia (two), and orthodromic atrioventricular (AV) reentrant tachycardia (six) as defined by electrophysiologic studies. Various mechanisms of exercise or isoproterenol induction of supraventricular tachycardia were identified. A critical heart rate and/or appropriate sympathetic state was found to provoke all instances of reentrant or automatic atrial tachycardia and atypical junctional tachycardia. A properly timed atrial premature beat provoked five of six cases of AV reentrant tachycardia and the only case of atrial flutter-fibrillation. The remaining case of AV reentrant tachycardia was induced by a ventricular premature beat. In conclusion, the mechanisms of exercise provocation of reentrant or automatic supraventricular tachycardia are multiple and include a critical sinus rate, increased sympathetic tone, and properly timed atrial or ventricular premature beats.     

Initiation of atrioventricular nodal reentrant tachycardia in patients with discontinuous anterograde atrioventricular nodal conduction curves with and without documented supraventricular tachycardia: Observations on the role of a discontinuous retrograde conduction curve

To evaluate factors playing a role in initiation of atrioventricular (AV) nodal reentrant tachycardia utilizing anterogradely a slow and retrogradely a fast conducting AV nodal pathway, 38 patients having no accessory pathways and showing discontinuous anterograde AV nodal conduction curves during atrial stimulation were studied. Twenty-two patients (group A) underwent an electrophysiologic investigation because of recurrent paroxysmal supraventricular tachycardia (SVT) that had been electrocardiographically documented before the study. Sixteen patients (group B) underwent the study because of a history of palpitations (15 patients) or recurrent ventricular tachycardia (one patient); in none of them had SVT ever been electrocardiographically documented before the investigation. Twenty-one of the 22 patients of group A demonstrated continuous retrograde conduction curves during ventricular stimulation. In 20 tachycardia was initiated by either a single atrial premature beat (18 patients) or by two atrial premature beats. Fifteen of the 16 patients of group B had discontinuous retrograde conduction curves during ventricular stimulation, with a long refractory period of their retrograde fast pathway. Tachycardia was initiated by multiple atrial premature beats in one patient. Thirteen out of the remaining 15 patients received atropine. Thereafter tachycardia could be initiated in three patients by a single atrial premature beat, by two atrial premature beats in one patient, and by incremental atrial pacing in another patient. In the remaining eight patients tachycardia could not be initiated. Our observations indicate that the pattern of ventriculoatrial conduction found during ventricular stimulation is a marker for ease of initiation of AV nodal tachycardia in patients with discontinuous anterograde AV nodal conduction curves.     

Diagnostic and therapeutic use of adenosine in patients with supraventricular tachyarrhythmias

Adenosine has been shown to affect both sinus node automaticity and atrioventricular (AV) nodal conduction. The effects of increasing doses of intravenous adenosine were assessed in 46 patients with supraventricular tachyarrhythmias. Adenosine reliably terminated episodes of supraventricular tachycardia in all 16 patients with AV reciprocating tachycardia, in 13 of 13 patients with AV nodal reentrant tachycardia and in 1 of 2 patients with junctional tachycardia with long RP intervals. Adenosine produced transient high grade AV block without any effect on atrial activity in six patients with intraatrial reentrant tachycardia, four patients with atrial flutter, three patients with atrial fibrillation and in single patients with either sinus node reentry or an automatic atrial tachycardia. The dose of adenosine required to terminate episodes of supraventricular tachycardia was variable (range 2 to 23 mg). Side effects were minor and of short duration. These results demonstrate that adenosine is useful for the acute therapy of supraventricular tachycardia whenever reentry through the AV node is involved. When arrhythmia termination is not affected, atrial activity may be more readily analyzed during adenosine-induced transient AV block.     

A technique for the rapid diagnosis of atrial tachycardia in the electrophysiology laboratory

OBJECTIVE: The purpose of this study was to determine if the atrial response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction during paroxysmal supraventricular tachycardia is a useful diagnostic maneuver in the electrophysiology laboratory. BACKGROUND: Despite various maneuvers, it can be difficult to differentiate atrial tachycardia from other forms of paroxysmal supraventricular tachycardia. METHODS: The response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction was studied during four types of tachycardia: 1) atrioventricular nodal reentry (n = 102), 2) orthodromic reciprocating tachycardia (n = 43), 3) atrial tachycardia (n = 19) and 4) atrial tachycardia simulated by demand atrial pacing in patients with inducible atrioventricular nodal reentry or orthodromic reciprocating tachycardia (n = 32). The electrogram sequence upon cessation of ventricular pacing was, categorized as "atrial-ventricular" (A-V) or "atrial-atrial-ventricular" (A-A-V). RESULTS: The A-V response was observed in all cases of atrioventricular nodal reentrant and orthodromic reciprocating tachycardia. In contrast, the A-A-V response was observed in all cases of atrial tachycardia and simulated atrial tachycardia, even in the presence of dual atrioventricular nodal pathways or a concealed accessory atrioventricular pathway. CONCLUSIONS: In conclusion, an A-A-V response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction is highly sensitive and specific for the identification of atrial tachycardia in the electrophysiology laboratory.     

Incessant atrioventricular tachycardia involving an accessory pathway: preoperative and intraoperative electrophysiologic studies and surgical correction.

In three patients with incessant supraventricular tachycardia, the anatomic substrate was a left-sided atrioventricular (A-V) accessory pathway. In two patients there was no expression of anterograde conduction through this pathway during spontaneous or induced atrial rhythms. The three patients had had increasingly frequent palpitations for more than 10 years despite adequate antiarrhythmic drug therapy.Preoperative intracardiac studies indicated that a left lateral accessory pathway was utilized in the retrograde limb of supraventricular tachycardia in all three patients. The spontaneous initiation of supraventricular tachycardia was due to (1) frequent spontaneous ventricular premature beats in two patients, (2) increase in sinus rate in two patients, and (3) ventriculoatrial reentry without preceding changes in sinus rate or intracardiac conduction intervals in one patient.At operation the accessory pathway was located in two patients with epicardial and endocardial electrographic mapping and cryothermal mapping. In one patient the His bundle was located with electrographic and cryothermal mapping. The accessory pathway (two patients) or the His bundle (one patient) were cryoablated by freezing over the area of the conducting tissue for 120 seconds at a temperature of ?65 ° C. Attempts to reinitiate supraventricular tachycardia after this procedure were unsuccessful. The operation was without significant morbidity. During follow-up for 3 to 10 months, no patient has experienced any further attacks of supraventricular tachycardia or required antiarrhythmic drugs.These observations confirm that an A-V accessory pathway may be the anatomic substrate for incessant or persistently repetitive tachycardias that may be resistant to medical and pacing therapy. Surgical interruption or cryothermal ablation of part of the reentrant circuit may abolish tachycardia, thus providing proof of the underlying mechanism.     

Induction of atrioventricular nodal reentrant tachycardia after atropine. Report of five cases.

After intravenous administration of 0.5 mg of atropine sustained atrioventricular (A-V) nodal reentrant tachycardia could be produced in five patients who had no prior historical or electrocardiographic evidence of supraventricular tachycardia. During the control period single atrial echo beats could be demonstrated in four of the five patients, but no instance of sustained tachycardia occurred. Atropine, known to enhance A-V nodal conduction, allowed achievement of longer A-H intervals (Case 1) and provided the necessary balance of conduction and refractoriness within the A-V nodal reentrant pathways (Cases 1 to 5) to sustain A-V nodal reentry in these patients.     

Electrophysiologic evidence for selective retrograde utilization of a specialized conducting system in atrioventricular nodal reentrant tachycardia.

In 12 patients with atrioventricular (A-V) nodal reentrant tachycardia, the existence and utilization of retrograde ventriculoatrial bypass tracts in the reentrant process were excluded, and the characteristics of the anterograde and retrograde limbs of the reentrant circuits were studied using His bundle electrograms, incremental atrial and ventricular pacing and atrial and ventricular extrastimulus techniques before and after the administration of 0.01 mg/kg of intravenous ouabain. Similar studies were also performed in five control patients without tachycardia. Paroxysmal supraventricular tachycardia could be induced in all 12 patients during atrial pacing-induced A-V nodal Wenckebach periods or premature atrial stimulation, or both. On the basis of conduction time in the retrograde limb during tachycardia and during retrograde studies, two groups were identified. Group I (seven patients) had (1) short (39 ± 10 msec) and constant conduction time in the retrogarde limb measured from the anterograde His bundle deflection to the retrograde atrial echo response (H-Ae interval), (2) no change in ventriculoatrial conduction time up to maximal ventricular pacing rates, (3) H₂-A₂ intervals during retrograde refractory period studies that were identical to the H-Ae intervals and that did not increase with decreasing V₁-V₂ intervals, and (4) increased conduction time of the anterograde limb (Ae-H intervals) after the administration of ouabain without any effect on retrograde limb conduction (H-Ae and H₂-A₂ intervals) and refractoriness. Group II (five patients) had (1) long and variable H-Ae intervals (60 to 180 msec), (2) a progressive increase in ventriculoatrial intervals during incremental ventricular pacing, (3) an increase in H₂-A₂ intervals in response to decreasing V₁-V₂ intervals, and (4) increased anterograde (Ae-H interval) and retrograde limb (H-Ae and H₂-A₂ intervals) conduction and refractoriness after the administration of ouabain. Changes in the H₂-A₂ interval corresponded to the changes in four of the five control patients. These findings suggest that (1) in group I the anterograde limb was the A-V node, whereas the retrograde limb was an A-V nodal bypass tract or an insulated intranodal tract physiologically unlike the A-V node; and (2) in group II the A-V node comprised both the anterograde and retrograde limbs of the reentrant circuit.     

Reanalysis of the "pseudo A-A-V" response to ventricular entrainment of supraventricular tachycardia: importance of his-bundle timing

BACKGROUND: The sequence of atrial and ventricular electrograms following termination of ventricular pacing during supraventricular tachycardia has been shown to reliably differentiate atrial tachycardia from atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT). However in patients with long HV intervals, this may be misleading due to a pseudo "A-A-V" response. The aim of the present study is to see if inclusion of the timing of the His-bundle in the electrogram response (ER) following ventricular pacing would reliably identify the mechanism of tachycardia in patients with long HV intervals. METHODS: Eight patients (7 men) with AVNRT and underlying bundle branch block and long HV (>55 msec) intervals underwent ventricular pacing at 10-40 msec shorter than the tachycardia cycle length during SVT. The ER was classified as "A-A-H" or "A-H" depending on the number of atrial electrograms (A) prior to His deflection following VEP. RESULTS: The ER following ventricular pacing was classified as A-H in all 8 patients. However, using conventional classification the response was A-A-V in 5 of 8 patients due to delayed ventricular activation secondary to long HV intervals and would erroneously suggest atrial tachycardia. The ER was A-V in only 1 of 8 patients. In the remaining 2 patients the A and V electrograms were simultaneous. CONCLUSIONS: Incorporating the His-bundle in the ER following ventricular pacing would eliminate the pseudo "A-A-V" response in patients with AVNRT and long HV intervals. Labeling the response to ventricular pacing as "A-H" or "A-A-H" is simple and more accurate.     

Effects of intravenous verapamil on cardiac arrhythmias and on the electrocardiogram.

The effects of intravenous verapamil on the electrocardiogram in 15 patients with heart disease in sinus rhythm and in 44 patients with supraventricular and ventricular tachyarrhythmias were evaluated. Verapamil prolonged the P-R interval without effect on the QRS duration or the Q-Tc interval. In patients with atrial flutter and fibrillation, A-V block was increased, with slowing of the ventricular rate, in almost all cases but sinus rhythm was restored in only 1 of 12 patients in atrial fibrillation and in 2 of the 11 patients with flutter. Verapamil had no effect in 3 patients with atrial fibrillation complicating WPW syndrome; in 1 of 5 patients with ventricular tachycardia it caused reversion to sinus rhythm. Sinus rhythm was restored promptly by verapamil in 13 of 17 patients with paroxysmal supraventricular tachycardias; in 2 others, sinus rhythm became established 1 to 2 hours after administration of the drug. Transient hypotension, not requiring treatment, was the only side effect noted but not in the patients with supraventricular tachycardias, in whom blood pressure generally increased after reversion to sinus rhythm by verapamil.