Re-entry due to manifest and concealed. His bundle ectopic systoles. Report of a case.

Concealed (C) His bundle ectopic systoles (H') have been shown in man to give rise to first and second degree atrioventricular (A-V) block and to simulate nonconducted atrial premature beats (P'). This report outlines a hitherto undescribed electrophysiologic consequence of H' in a 69-year-old man with arteriosclerotic heart disease and a Wenckebach type second degree A-V block in the His-Purkinje system. During a His bundle study, H' were shown to conduct either to the atria and ventricles with varying relationships to P' and QRS, or to conduct only to the atria, simulating nonconducted P' or atrial fusion beats. Both types of H' could initiate a re-entrant arrhythmia during retrograde conduction. Of particular interest are late coupled H' that failed to conduct to the ventricles and also failed to activate the atria because of prior capture by the sinus impulse (CH'). These CH' could also initiate re-entry by conducting retrogradely to engage the subatrial re-entry circuit. Evidence is presented to suggest re-entry occurs by way of a retrograde concealed accessory pathway and antegrade conduction in the atrioventricular node.     

'Dual atrioventricular nodal pathways" in patients with Wolff-Parkinson-White syndrome.

'Dual atrioventricular nodal pathways" were found in five patients who also had the Wolff-Parkinson-White syndrome. All five patients had a re-entrant tachycardia that used the atrioventricular node for conduction in the anterograde direction and an accessory atrioventricular pathway for conduction in the retrograde direction. One of the patients also had a re-entrant tachycardia that originated within the atrium or the atrioventricular node. Dual atrioventricular nodal pathways were identified in three of the five patients during their first electrophysiological study because the effective refractory period of the accessory atrioventricular pathway in the anterograde direction was longer than the effective refractory period of the fast atrioventricular nodal pathway. In the other two patients the dual atrioventricular nodal pathways were found only after operative division of an accessory atrioventricular pathway. Re-entrant tachycardia that uses an accessory pathway may be cured by operative division of the accessory pathway. Tachycardia resulting from re-entry within the atrioventricular node cannot be cured by an operation unless the normal conduction system is divided and a permanent pacemaker implanted. These five patients indicate the importance of determining the aetiology of tachycardia by studying the tachycardia itself and not only the type of atrioventricular conduction present.     

Phase 3 and phase 4 block in the accessory pathway

Pacemaker activity at a site proximal to the area of a conduction disturbance has been postulated as depressing conduction in late diastole (phase 4 block). To elucidate the correlation between the site of phase 4 depolarization and that of a conduction disturbance, we examined seven patients with intermittent Wolff-Parkinson-White syndrome who had tachycardia (phase 3) and bradycardia (phase 4) dependent on block in the accessory pathway. In each patient, antegrade conduction over the accessory pathway was absent at the sinus rate. During premature atrial stimulation a "window" of accessory pathway conduction was identified in each patient. The outer limit of the window ranged from 420 to 670 ms; the inner limit, from 330 to 620 ms. The duration of the window ranged from 20 to 160 ms. Four patients with orthodromic atrioventricular reentrant tachycardia exhibited preserved retrograde accessory pathway conduction. In one patient with unsustained orthodromic atrioventricular reentrant tachycardia, retrograde accessory pathway conduction also exhibited phase 3 and phase 4 blocks. The remaining two patients had no retrograde accessory pathway conduction. In two patients, retrograde concealed conduction in the accessory pathway induced by ventricular stimulation eliminated a phase 4 block in antegrade accessory pathway conduction. These results suggest that 1) an antegrade phase 4 block may have phase 4 depolarization in the accessory pathway and block at the ventricular insertion of the accessory pathway; 2) a retrograde phase 4 block may have a conduction disturbance at the atrial insertion of the accessory pathway; and 3) a complete retrograde block may occur at the atrial insertion of the accessory pathway.     

Multiple reentry tachycardia in patients with ventricular preexcitation: report of three cases

The electrophysiologic studies of three patients with accessory pathways and multiple reentrant circuits are reported. The first patient had two atrioventricular accessory pathways: a left posterior capable of bidirectional conduction and a right paraseptal with retrograde conduction only. Four atrioventricular reentry circuits were documented: left and right orthodromic circuits and a left antidromic circuit with retrograde conduction over the right paraseptal accessory pathway. The second patient had a left lateral atrioventricular accessory pathway with type A preexcitation. Two reentrant tachycardias were noted: an atrial tachycardia where the accessory pathway remained concealed and an orthodromic atrioventricular tachycardia. The third patient had dual atrioventricular nodal pathways and a right nodofascicular accessory pathway. The accessory pathway became manifest only when a critical atrioventricular delay was reached, indicating its association with the slow atrioventricular nodal pathway. Wide QRS tachycardia with left bundle branch block contour was documented, by means of the slow atrioventricular nodal pathway and nodofascicular fiber antegradely, and the proximal right bundle branch, the His bundle, and the fast atrioventricular nodal pathway retrogradely.     

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.     

Paroxysmal supraventricular tachycardia with complete atrio-ventricular block or dissociation]

Recent studies have shown the high incidence of concealed Bundles of Kent in the reentry circuits of paroxysmal supraventricular tachycardia. Arguments in favour of the nodal or junctional level of reentry were observed in supraventricular tachycardia with complete atrioventricular dissociation. Two such cases under went electrophysiological investigation. In the first case, tachycardia was terminated by a complete infrahisian block. However, during atrioventricular dissociation, tachycardia could be initiated by a single atrial stimulus after an increased nodal conduction time and terminated by a single atrial stimulus or cardiac message. In the second case the supraventricular tachycardia presented with complete atrioventricular dissociation due to a retrograde ventriculo-atrial block. Atrial stimulation at progressively higher rates and premature atrial extra stimuli initiated the tachycardia but could not terminate it, so confirming the non-participation of the atrium in the reentry circuit. These two cases suggest that the ventricle (case I) and the atrium (case II) are not indispensable links in junctional or nodal reentry circuits. Case II was suggestive of a common initial pathway developing retrograde unidirectional block during tachycardia.     

Supraventricular tachycardia in patients without overt preexcitation

In this article, the authors discuss the features and differential diagnosis of supraventricular tachycardia with a regular ventricular rate that occurs in patients without overt preexcitation during sinus rhythm. In the authors' experience, the two most common mechanisms of these tachycardias are reentry within the atrioventricular node (AV nodal reentry) and atrioventricular reentry using a concealed accessory pathway for retrograde conduction and the AV node/His-Purkinje system for antegrade conduction (AV reentry). Sinus nodal reentry, intra-atrial reentry, automatic atrial tachycardia, and nonparoxysmal junctional tachycardia account for the remaining episodes of regular supraventricular tachycardia. Therapy for AV and AV nodal reentry is also discussed.     

Rate-dependent accessory pathway conduction due to phase 3 and phase 4 block. Antegrade and retrograde conduction properties.

Six patients who had antegrade phase 3 and phase 4 block in the accessory pathway were examined. In each patient, antegrade conduction over the accessory pathway was absent both at the sinus rate and at slower heart rates. During premature atrial stimulation a "window" of accessory pathway conduction was identified in all patients. The outer limits of the window ranged from 480 ms to 670 ms. The inner limits ranged from 410 ms to 620 ms. The durations of the window ranged from 20 ms to 160 ms. Three patients with orthodromic atrioventricular reentrant tachycardia showed preserved retrograde accessory pathway conduction. The remaining three patients had impaired retrograde accessory pathway conduction. One of the patients showed retrograde phase 4 block in the accessory pathway. In two patients, retrograde concealed conduction in the accessory pathway induced by ventricular stimulation prolonged the outer limit of the window in the antegrade accessory pathway conduction. These findings suggest that the mechanism of antegrade phase 3 and phase 4 block in the accessory pathway may be spontaneous diastolic depolarization in the accessory pathway and conduction disturbance at the ventricular and/or atrial insertion of the accessory pathway.     

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.     

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.     

Intravenous diltiazem in patients with paroxysmal re-entrant supraventricular tachycardia

The electrophysiologic effects and efficacy of diltiazem were evaluated with programmed electrical stimulation of the heart in 12 patients with supraventricular re-entrant tachycardia (five with atrioventricular nodal tachycardia and seven with circus movement tachycardia the accessory pathway being concealed in 4). Diltiazem was infused over 1 minute at the dose of 0.25 mg/kg and the electrophysiologic parameters were evaluated at 5 and 30 minutes. Diltiazem prolonged the AH interval from 83.5 +/- 58 to 99 +/- 55 msec (P less than 0.05), effective and functional refractory periods of atrioventricular node from 244 +/- 40 to 268 +/- 56 msec (P less than 0.05) and from 432 +/- 124 to 468 +/- 130 msec (P less than 0.005) respectively, lowered the atrial pacing rate inducing second-degree atrioventricular block from 159 +/- 32 to 134 +/- 33 beats/min (P less than 0.005) and decreased systolic and diastolic blood pressure from 143.5 +/- 33 to 132.5 +/- 22 mm Hg (P less than 0.05) and from 90 +/- 15 to 82.5 +/- 9 (P less than 0.05), respectively. Diltiazem prevented the reinduction of the tachycardia in 4 of 5 patients with atrioventricular nodal tachycardia and in 4 of 7 with circus movement tachycardia. The mechanism of action of diltiazem consisted of depression of conduction in atrioventricular node in anterograde fashion while there were no effects on refractoriness of the accessory pathway. The drug was well tolerated with no adverse effects. Diltiazem, therefore, appears an effective and safe drug in the acute treatment of re-entrant supraventricular tachycardia.     

Electrophysiologic effects and mechanisms of termination of supraventricular tachycardia by intravenous amiodarone

Electrophysiologic studies were performed in nine patients with reentrant paroxysmal supraventricular tachycardia (PSVT) during a control period and following 5 mg/kg body weight of intravenous amiodarone (Cordarone, Labaz) administered as a slow continuous infusion over 15 to 20 minutes. All nine patients had induction of sustained PSVT during control studies. In seven of nine patients (group 1) the tachycardia was due to atrioventricular (AV) nodal reentry, and in two of nine patients (group 2) a concealed retrograde bypass tract was incorporated in the reentrant process. In group 1, following amiodarone, all seven patients lost the ability to sustain PSVT with either absence of atrial echoes (one patient) or induction of ≤3 echo beats (six patients) with termination of PSVT in the antegrade pathway (three patients) or retrograde pathway (two patients) or both (one patient). In group 2, following amiodarone, both patients lost the ability to sustain PSVT with absence of atrial echoes (one patient) on induction of a single echo beat (one patient) with block in the retrograde pathway (i.e., the concealed retrograde bypass tract). Amiodarone significantly increased (1) atrial cycle length for AV nodal Wenckebach block, (2) antegrade functional refractory period of the AV node, (3) antegrade effective refractory period of the AV node, (4) ventricular paced cycle length for ventricular atrial block, and (5) the retrograde functional refractory period of the ventricular-atrial conducting system. Thus intravenous-amiodarone inhibited induction of sustained reentrant PSVT by inducing block in the antegrade or retrograde or both limbs of the reentrant circuit and was shown to have significant depressant effects on both antegrade and retrograde AV nodal conduction and refractory periods.     

Retrograde dual atrioventricular nodal pathway in patients with atrioventricular reciprocating tachycardia using concealed accessory pathways

We present electrophysiological studies in two patients with atrioventricular reciprocating tachycardias. The first patient had anterograde dual atrioventricular nodal pathways with a right-sided concealed accessory pathway. The retrograde atrioventricular nodal pathway showed evidence suggestive of slow pathway properties. After block was induced with ajmaline in the accessory pathway, a typical pattern of discontinuous retrograde atrioventricular nodal conduction curves was recognized. We then observed three types of induced atrioventricular reentry. The other patient had continuous anterograde atrioventricular nodal conduction, a fast-conducting retrograde atrioventricular nodal pathway and a left-sided concealed accessory pathway. After refractoriness had been induced in the accessory pathway with ajmaline, a typical pattern of retrograde dual atrioventricular nodal pathways was recognized, and it proved impossible to induce atrioventricular nodal echoes. Induction of block or impairment of conduction with ajmaline in the concealed accessory pathway proved helpful in the disclosure of retrograde dual atrioventricular nodal pathways by means of the ventricular extrastimulus method.     

Evidence for an incomplete mitral isthmus block after failed ablation of a left postero-inferior concealed accessory pathway.

We report the case of a young woman in whom previous ablation of a concealed left-sided accessory pathway (AP) created an iatrogenic mitral block. The mitral block was responsible for a split retrograde atrial activation pattern during orthodromic atrioventricular re-entrant tachycardia (AVRT). The differential diagnoses are discussed. The AP was ablated at the site with the shortest interval between the ventricular signal and the earliest component of the retrograde atrial activation. Meticulous mapping is paramount during AVRT with an unusual retrograde atrial activation pattern.     

Electrophysiologic mechanisms of adverse effects of class I antiarrhythmic drugs (cibenzoline,pilsicainide, disopyramide,procainamide) in induction of atrioventricular re-entrant tachycardia

Summary We evaluated the electrophysiological mechanisms of adverse effects of class I antiarrhythmic drugs (cibenzoline in seven patients, pilsicainide in two, and disopyramide in two, and procainamide in three) in the induction of orthodromic atrioventricular re-entrant tachycardia (AVRT). In 14 patients (10 males, 4 females; mean age 37±18 years) who had inducible AVRT despite the administration of class I drugs, electrophysiological effects of class I antiarrhythmic drugs were evaluated using programmed electrical stimulation techniques. In 4 out of 6 patients with a manifest accessory pathway, class I drugs induced unidirectional conduction block of the accessory pathway (antegrade conduction block associated with preserved retrograde conduction) and enhanced the induction of AVRT with atrial extrastimulation. In eight patients with a concealed accessory pathway, the outward or inward expansion of the tachycardia induction zone was observed in patients who had greater prolongation of the conduction time than the refractory period of the retrograde accessory pathway after class I drugs. During ventricular extrastimulation, the induction of bundle branch reentry after class I drugs initiated the AVRT in patients with either manifest or concealed accessory pathways. We conclude that the adverse effects of class I drugs are mainly due to induction of unidirectional retrograde conduction of the manifest accessory pathway and the greater prolongation of the retrograde conduction time of the concealed accessory pathway than the refractory period, regardless of the subclassification of class I drugs.     

Concealed retrograde bypass tracts and enhanced atrioventricular nodal conduction: An unusual subset of patients with refractory paroxysmal supraventricular tachycardia

The clinical and electrophysiologic features of eight patients with unusually rapid, medically refractory paroxysmal supraventricular tachycardia are described. Exercise induction of tachycardia and functional bundle branch block patterns during tachycardia were common. Tachycardia resulted from anterograde enhanced atrioventricular nodal conduction combined with retrograde conduction by a concealed left atrial-left ventricular accessory pathway producing rates ranging from 200 to 300 beats/min. Management and late follow-up study were characterized by generally unsuccessful electrophysiologic-pharmacologic testing and inconsistent rhythm control with continued drug therapy. Three patients underwent successful surgical interruption of the concealed accessory pathway, with elimination of recurrent tachycardias. These patients represent a unique subgroup with an identifiable electrophysiologic basis for unusually rapid tachycardias, potentially benefiting from invasive study and aggressive therapy.     

Pharmacological observations in patients with nodoventricular pathways.

Three patients with accessory nodoventricular pathways and re-entry tachycardia are reported. In all three patients the accessory nodoventricular pathway formed the anterograde limb of the re-entry circuit while the His-Purkinje-atrioventricular node axis formed the retrograde limb of the tachycardia in two of the patients and a concealed accessory pathway formed the retrograde limb in the remaining patient. All three patients also manifested dual anterograde atrioventricular nodal pathways with conduction through the accessory nodoventricular pathways being associated with the atrioventricular nodal fast pathway. Type I antiarrhythmic drugs, especially disopyramide and quinidine, were effective for the treatment of the re-entry tachycardia because of their depressive action on the nodoventricular pathway. Beta blockers were also effective because of their action on the atrioventricular nodal portion of the re-entry circuit in one patient and most probably due to atypical (atrioventricular nodal like) properties of a retrogradely conducting accessory pathway in a second patient.     

Successful elimination of concealed accessory pathway-mediated tachycardia by ablation of AV nodal slow pathway

We report a case of atrioventricular reentrant tachycardia (AVRT) using a concealed para-Hisian accessory pathway for retrograde conduction, which also required anterograde conduction over the AV nodal slow pathway to maintain the tachycardia. The shortest VA interval during AVRT (70 ms) was noted at a site with His bundle electrogram amplitude of 0.25 mV. The AVRT was cured by radiofrequency ablation of the AV nodal slow pathway without affecting accessory pathway conduction. The patient has not reported any sustained palpitations at 2 years after ablation while receiving no medications. The case presented in this report illustrates a para-Hisian AVRT that was successfully eliminated by an unconventional approach of ablation of the atrial inputs to the AV nodal slow pathway.     

Pharmacological observations in patients with nodoventricular pathways

Three patients with accessory nodoventricular pathways and re-entry tachycardia are reported. In all three patients the accessory nodoventricular pathway formed the anterograde limb of the re-entry circuit while the His-Purkinje-atrioventricular node axis formed the retrograde limb of the tachycardia in two of the patients and a concealed accessory pathway formed the retrograde limb in the remaining patient. All three patients also manifested dual anterograde atrioventricular nodal pathways with conduction through the accessory nodoventricular pathways being associated with the atrioventricular nodal fast pathway. Type I antiarrhythmic drugs, especially disopyramide and quinidine, were effective for the treatment of the re-entry tachycardia because of their depressive action on the nodoventricular pathway. Beta blockers were also effective because of their action on the atrioventricular nodal portion of the re-entry circuit in one patient and most probably due to atypical (atrioventricular nodal like) properties of a retrogradely conducting accessory pathway in a second patient.     

Unusual induction of slow-fast atrioventricular nodal reentrant tachycardia. Report of two cases

INTRODUCTION: Generally, the induction of typical atrioventricular nodal reentrant tachycardia (AVNRT) occurs with a premature atrial stimulus that blocks in the fast pathway and proceeds down the slow pathway slowly enough to allow the refractory fast pathway time to recover. We describe two cases in which a typical AVNRT was induced in an unusual fashion. RESULTS: The first case is a 41-year-old man with paroxysmal supraventricular tachycardia. During the electrophysiology study, the atrial extrastimulus inducing the typical AVNRT was conducted simultaneously over the fast (AH) and the slow pathway (AH'). A successful ablation of the slow pathway was performed. During the follow-up no recurrence was noted. The second case is a 52-year-old woman with a Wolff-Parkinson-White syndrome due to a left posterior accessory pathway. After 5 minutes of atrioventricular reentrant tachycardia (AVRT) induced by a ventricular extrastimulus, a variability of the antegrade conduction was noted in presence of the same VA conduction. In fact, a short AH interval (fast pathway) alternated with a more prolonged AH intervals (slow pathway) that progressively lengthened until a typical AVNRT was induced. The ablation of the accessory pathway eliminated both tachycardias. DISCUSSION: A rare manifestation of dual atrioventricular nodal pathways is a double ventricular response to an atrial impulse that may cause a tachycardia with an atrioventricular conduction of 1:2. In our first case, an atrial extrastimulus was simultaneously conducted over the fast and the slow pathway inducing an AVNRT. This nodal reentry implies two different mechanisms: 1) a retrograde block on the slow pathway impeding the activation of the slow pathway from the impulse coming down the fast pathway, and 2) a critical slowing of conduction in the slow pathway to allow the recovery of excitability of the fast pathway. Interestingly, in the second case, during an AVRT the atrial impulse suddenly proceeded alternately over the fast and the slow pathway. The progressive slowing of conduction over the slow pathway until a certain point which allows the recovery of excitability of the fast pathway determines the AVNRT. This is a case of "tachycardia-induced tachycardia" as confirmed by the fact that the ablation of the accessory pathway eliminated both tachycardias.