Clinical and electrophysiologic observations in patients with concealed accessory atrioventricular bypass tracts

In 12 of 46 consecutive patients with paroxysmal supraventricular tachycardia or atrial flutter-fibrillation, without electrocardiographic evidence of ventricular preexcitation, electrophysiologic studies suggested the presence of accessory atrioventricular (A-V) pathways capable only of retrograde conduction (concealed Wolff-Parkinson-White syndrome). The ages of these patients ranged from 29 days to 71 years (mean 39.2 years). Most patients were clinically symptomatic with palpitations, dizziness, weakness or congestive heart failure. One patient had “cardiac dysrhythmia” described by an obstetrician during intrauterine life. Eleven patients manifested A-V reciprocating tachycardia involving the normal pathway for anterograde conduction and the accessory pathway for retrograde conduction. The remaining patient manifested recurrent paroxysms of atrial flutter-fibrillation as a result of rapid ventriculoatrial activation through the accessory pathway during the atrial vulnerable phase.

The electrophysiologic observations were analyzed with regard to clinical and electrocardiographic characteristics in these patients. The presence of concealed accessory pathways should be suspected in patients presenting with (1) an “incessant” form of tachycardia, (2) spontaneous onset of A-V reciprocal rhythms or reciprocating tachycardias after acceleration of the sinus rate without antecedent atrial extrasystoles or P-R interval prolongation, (3) slowing of the tachycardia rate consequent to the development of functional bundle branch block, (4) retrograde P waves (negative in leads II, III and aVF) discernible after the QRS complexes, with the R-P interval being shorter than the P-R interval during both A-V reciprocal rhythm and reciprocating tachycardia, and (5) oc-currence of atrial flutter-fibrillation in association with A-V reciprocal rhythms.

It is suggested that medical treatment in patients having concealed accessory pathways should be aimed at increasing the refractoriness of either the A-V node or the accessory pathway for reciprocating tachycardia, while increasing the refractoriness of the atrium and the accessory pathway in cases with atrial flutter-fibrillation. Pacemaker therapy and surgical intervention may be indicated in selected patients refractory to antiarrhythmic agents.     

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.     

The fast-slow form of atrioventricular nodal reentrant tachycardia in children

An unusual form of atrioventricular (A-V) nodal reentry is described as the underlying mechanism for incessant tachycardia in two children. During tachycardia a fast pathway was utilized for anterograde conduction and a slow pathway for retrograde conduction. This is the reverse of the usual form of A-V nodal reentrant tachycardia, in which the slow pathway is utilized for anterograde conduction and the fast pathway for retrograde conduction. One patient had a smooth ventriculoatrial (V-A) conduction curve demonstrating exclusive utilization of the slow pathway for retrograde conduction. The other had a discontinuous V-A conduction curve demonstrating failure of retrograde fast pathway conduction with resultant slow pathway conduction. In both cases the retrograde effective refractory period of the fast pathway was longer than that of the slow pathway, resulting in the establishment of this unusual reentry circuit. Both patients had a superior P axis with a P-R interval shorter than the R-P interval during tachycardia, features described in a significant number of children with incessant tachycardia. This unusual form of reentrant tachycardia can be suggested by its electrocardiographic pattern and is another mechanism for reentrant tachycardia not previously documented in children.     

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.     

Reciprocal tachycardias using accessory pathways with long conduction times.

Three patients with reentrant tachycardia are described who had an accessory pathway with a very long conduction time that was incorporated in the tachycardia circuit. The accessory pathway was able to conduct in one direction only, in retrograde manner in two patients and in anteriograde manner in the remaining patient. Evidence is presented that reveals that in the first two patients the accessory pathway was septally located, had completely bypassed the normal atrioventricular (A-V) conduction system, had properties of decremental conduction, and had an atrial exit close to the coronary sinus and a ventricular exit relatively far from the atrioventricular A-V ring. In the third patient, who manifested wide QRS complex during tachycardia, the ventricular end of the accessory pathway seemed to be located close to the right ventricular apex. The atrial end of the pathway could not be localized exactly.     

His bundle recordings in a case of complete atrioventricular block combined with pre-excitation syndrome.

In a patient with complete A-V block suffering from attacks of dizziness an intermittent A-V conduction with a short P-R interval and a delta wave of the conducted ventricular complex were observed. After accelerating the sinus rate by atropine and by exercise, one-to-one conduction was established with QRS complexes of WPW type A configuration. His bundle recordings revealed a complete block within the normal conduction system at the level of the A-V node. A slow junctional rhythm with a normal H-V interval was activating the ventricle. During atrial pacing a one-to-one conduction through an accessory pathway could be documented at cycle lengths between 800 and 380 msec. sandwiched in between zones of complete block at smaller or longer cycle lengths. During ventricular stimulation no retrograde V-A conduction could be observed. The findings support the thesis of at least two functionally different A-V pathways in patients with pre-excitation syndrome.     

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.     

The postponed compensatory pause as a manifestation of positive feedback in atrioventricular conduction.

A patient with hypertensive cardiovascular disease was found to have unusual varieties of premature atrial and ventricular contractions. If the premature atrial contraction resulted in a greatly prolonged P-R interval, such that the increment in P-R exceeded the decrement in the preceding R-P, the next sinus P wave, occurring after a normal P-P interval, was found to be blocked. Also, numerous interpolated ventricular extrasystoles were observed in which the postextrasystolic P-R intervals were markedly prolonged and in which the compensatory pauses were postponed for one or two beats. We also present data from one dog in which a premature atrial activation produced a chain reaction such that complete A-V block occurred three beats later. We propose that the chain reaction which evoked the delayed block in the dog and the postponed compensatory pauses in the patient reflects the operation of a positive feedback mechanism in A-V conduction. Positive feedback is initiated by an extremely long P-R, which results in a very short R-P before the next cycle. This then leads to a still longer P-R, which then elicits a still shorter R-P. Block ultimately supervenes when the atrial activation wave arrives at the A-V junction during its effective refractory period.     

Reciprocal rhythm in patients with normal electrocardiogram: Evidence for dual conduction pathways.

The present study refers to six patients in whom an A-V reciprocal rhythm could be documented; in four cases it took the form of sustained tachycardia. None of the patients showed any ECG feature of ventricular pre-excitation (PR interval of more than 0.12 sec. and normal QRS configuration). The extrastimulus method showed, at first, that the A-V conduction time of the premature beat varied only slightly with the decrease of the coupling interval. From a critical A1A2 interval there was a sudden lengthening of A2H2 preceding the occurrence of re-entrant beats. The curve of H1H2 responses reflected these changes, showing two distinct parts. The second part following the slowing of the impulse included the initiation zone of atrial echoes and of reciprocating tachycardia. These results suggest the existence of two A-V pathways, one fast and the other slow. The point at which the break between the two parts of the curve occurred might be related to the effective refractory period of the fast pathway. In the same way, when atrial pacing reached a critical rate, it induced an abrupt increase of AH in five cases. In the sixth patient, A-V conduction time remained unchanged up to 170 per minute. Ventriculoatrial conduction was always observed, the delay of which did not lengthen with the rate. In one case tachycardia could be induced by a premature ventricular beat without lengthening of the V-A time. It is concluded that in spite of a normal PR interval, the presence of dual A-V pathways may be implied in the genesis of reciprocal rhythm.     

Observations on the antidromic type of circus movement tachycardia in the Wolff-Parkinson-White syndrome

In the differential diagnosis of tachycardias showing a wide QRS complex and having a 1 to 1 relation between ventricular and atrial events, a supraventricular tachycardia with anterograde conduction over an accessory pathway and retrograde conduction by way of the specific conduction system must be considered. Five patients showing this type of circus movement tachycardia were studied by programmed electrical stimulation of the heart. Sudden changes in the tachycardia cycle length were observed in these patients that were based on changes in the VH interval. This finding suggested a change in the reentrant circuit with anterograde conduction over the accessory pathway but retrograde conduction sometimes occurring over the right bundle branch and at other times over one of the two divisions of the left bundle branch system. Characteristically, the tachycardia cycle length changed suddenly depending on the bundle branch used in retrograde direction. In one patient, an important difference was also observed between the anterograde effective refractory period of the accessory bypass (280 ms) and the shortest RR interval between preexcited QRS complexes during atrial fibrillation (measuring 190 ms). It is postulated that the short RR intervals during atrial fibrillation in the Wolff-Parkinson-White syndrome could result from bundle branch reentry after activation of the ventricles over the accessory pathway.     

Effect of atropine and isoproterenol on tachycardia induction in asymptomatic patients with Wolff-Parkinson-White electrocardiographic pattern.

OBJECTIVE: To determine if pharmacological interventions aimed at altering autonomic tone would allow induction of orthodromic atrioventricular reentrant tachycardia in asymptomatic patients with the Wolff-Parkinson-White electrocardiographic pattern. DESIGN: Prospective interventional protocol in consecutive eligible patients. SETTINGS: University hospital. PATIENTS: Eighteen asymptomatic patients (13 male and five female) with the Wolff-Parkinson-White electrocardiographic pattern without inducible tachycardia in the drug-free state. INTERVENTION: Electrophysiological assessment was performed at baseline, after intravenous administration of atropine (0.03 mg/kg) and during isoproterenol infusion (0.5 to 2 micrograms/min). RESULTS: Orthodromic reciprocating tachycardia was not inducible at baseline because of absent retrograde accessory pathway conduction in seven patients. In five patients, orthodromic atrial echo beats could be induced (which blocked retrogradely in the accessory pathway in three patients and anterogradely in the atrioventricular node in two). In the remaining six patients, neither orthodromic echo beats nor reciprocating tachycardia could be induced despite intact retrograde accessory pathway conduction. Following atropine administration (mean dose 1.9 +/- 0.3 mg), anterograde and retrograde accessory pathway effective refractory periods decreased from 360 +/- 172 to 284 +/- 62 ms and from 340 +/- 38 to 296 +/- 32 ms, respectively (both P < 0.05 versus control). Orthodromic reciprocating tachycardia was induced in two patients (nonsustained in one). During isoproterenol infusion (mean dose 1.0 +/- 0.3 micrograms/min), anterograde and retrograde accessory pathway effective refractory periods decreased further to 243 +/- 23 and 248 +/- 22 ms, respectively (both P < 0.05 versus after atropine); two further patients had inducible orthodromic reciprocating tachycardia (nonsustained in one). No patient with absent retrograde accessory pathway conduction developed retrograde accessory pathway conduction or reciprocating tachycardia with isoproterenol and/or atropine. CONCLUSIONS: Isoproterenol and/or atropine allowed tachycardia induction in four of 18 asymptomatic patients with the Wolff-Parkinson-White electrocardiographic pattern. In the majority of these patients, tachycardia is not inducible because of deficient retrograde accessory pathway conduction which does not improve with autonomic facilitation.     

Termination of circus movement tachycardia utilizing an accessory atrioventricular pathway by retrograde concealed penetration of the atrioventricular node through the bundle branch system: A mechanism of tachycardia termination in Wolff-Parkinson-White syndrome

A 30 year old woman with Wolff-Parkinson-White syndrome underwent electrophysiologic study for investigation of circus movement tachycardia utilizing the accessory pathway for retrograde conduction. The accessory pathway was located on the right side. Episodes of circus movement tachycardia with left and right bundle branch block were induced. Some episodes of circus movement tachycardia with left bundle branch block terminated spontaneously. Two episodes of spontaneous termination at the level of the atrioventricular (A-V) node were preceded by prolongation of the H-V interval causing delay in atrial activation. This delayed atrial cycle was then followed paradoxically by spontaneous termination of the tachycardia in the A-V node. A similar phenomenon could be demonstrated reproducibly with single echo beats induced by coronary sinus extrastimuli. It appears that retrograde concealed penetration of the A-V node through the bundle branch system during anterograde left bundle branch block is the most likely mechanism for this phenomenon.     

Atypical termination of simultaneous sino-atrial and atrio-ventricular Wenckebach type conduction caused by atrial premature beats

This is a case report of a patient with group beating characterized by progressively shortening P-P intervals and at the same time gradually increasing P-R intervals showing R-P/P-R interval reciprocity due to the simultaneous occurrence of sino-atrial (S-A) Wenckebach and atrio-ventricular (A-V) Wenckebach-like periodicities. All group beatings are terminated by atrial premature beats elicited by a critical P-P interval shortening during S-A Wenckebach type conduction preventing the typical termination of Wenckebach periods.     

Recent Insights into Paroxysmal Supraventricular Tachycardia– An Integrated Approach to Diagnosis and Therapy

Summary: Paroxysmal supraventricular tachycardia may result from re-entrance in the AV node, the norma/ A-V pathway with an accessory AV connection, in the sino-atrial node, in the atria, or else reflect ectopic impulse formation in a spontaneously automatic supraventricular focus. Electrocardiographic criteria which are helpful in differentiating these mechanisms involve an analysis of cycle length, changes in cycle length with intermittent bundle branch block, P wave morphology and the relationship of P wave to QRS complex, P-R interval, the presence of A-V block during tachycardia and the influence of autonomic tone on the tachycardia. Electrophysiologic studies further elucidate mechanism by demonstrating the mode of induction and termination of the tachycardia, the characteristics of antegrade and retrograde A-V conduction curves and refractory periods, atrial activation sequence of echo beats and the influence of premature beats introduced during tachycardia. These features are summarised in Table 1. Therapy can be accurately planned according to the results of experimental administration of antiarrhythmic agents and of pacing sequences upon induction and termination of tachycardia in the catheterisation laboratory.     

Supraventricular tachycardia in lown-ganong-levine syndrome: Atrionodal versus intranodal reentry

The mechanism of the abbreviated atrioventricular (A-V) nodal conduction time and paroxysmal Supraventricular tachycardia in the LownGanong-Levine syndrome was evaluated in six patients. In each the A-H interval increased in response to rapid atrial pacing and atrial extrastimuli; typical dual A-V nodal pathways were demonstrated. In five patients studied at two cycle lengths prolongation of conduction and refractoriness of the “fast” pathway was noted at the shorter basic cycle length. Propranolol prolonged conduction and refractoriness of the “fast” pathway in three patients and in one produced Wenckebach conduction during atrial pacing which did not occur prior to its administration. In three patients the atrium did not appear necessary to sustain Supraventricular tachycardia. These findings suggest that preferential rapidly conducting A-V nodal fibers and intranodal reentry are the responsible mechanisms in those patients with Lown-Ganong-Levine syndrome and reciprocating tachycardia.     

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.     

Effect of catheter position on the initiation of atrial echoes with atrial pacing and premature stimulation in patients with accessory pathways

Eleven patients with an accessory pathway and reciprocating tachycardia were studied using both fixed rate atrial pacing and the atrial extrastimulus technique. Six of the patients had an accessory pathway that conducted in both the anterograde and retrograde direction; but the effective refractory period of their accessory pathway in the anterograde direction was relatively long and was greater than the longest coupling intervals that initiated atrial echoes. Five patients had an accessory pathway that conducted only in the retrograde direction.The extrastimulus technique could be used with stimulation sites near to and remote from the accessory pathway in 10 of the 11 patients. Atrial echoes were initiated by a single atrial extrastimulus at both sites in 7 of the 10 patients, and in each patient the upper limit of the echo zone was longer with stimulation at the site near the accessory pathway. In the other three patients atrial echoes were initiated only during stimulation at the site near the acessory pathway because either atrial refractoriness or atrioventricular nodal refractoriness was encountered before the echo zone was entered during stimulation at the site remote from the accessory pathway.Differences in the longest cycle length that initiated an atrial echo during fixed rate atrial pacing were similarly demonstrated in three patients. In these three patients, pacing at the site near the accessory pathway initiated echoes at a longer cycle length than pacing at the site remote from the accessory pathway. In three other patients the electrophysiologic characteristics of atrioventricular conduction prevented a demonstration of these differences. Catheter position is an important variable in the initiation of atrial echoes in patients with accessory pathways.     

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).     

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.     

Retrograde block during dual pathway atrioventricular nodal reentrant paroxysmal tachycardia

There are limited reported data regarding the occurrence of retrograde block during dual pathway atrioventricular (A-V) nodal reentrant paroxysmal tachycardia. This study describes two patients with this phenomenon. The first patient had 2:1 and type 1 retrograde ventriculoatrial block during the common variety of A-V nodal reentrance (slow pathway for anterograde and fast pathway for retrograde conduction). Fractionated atrial electrograms suggested that the site of block was within the atria. The second patient had type 1 retrograde block (between the A-V node and the low septal right atrium) during the unusual variety of A-V nodal reentrance (stow pathway for retrograde and fast pathway for anterograde conduction). The abolition of retrograde block by atropine suggested that the site of block was within A-V nodal tissue. Both cases demonstrate that intact retrograde conduction is not necessary for the continuation of A-V nodal reentrant paroxysymal tachycardia. Case 2 supports the hypothesis that the atria are not a requisite part of the A-V nodal reentrant pathway.