Retrograde His bundle deflection in bundle-branch re-entry.

Atrial echo beats resulting from a reciprocating mechanism involving the bundle-branches were produced by premature atrial impulses in a patient with an A-V nodal bypass tract. The mechanism of the arrhythmia was suggested by the presence of a retrograde His bundle deflection which appeared 'sandwiched' in between a QRS complex with complete right bundle-branch morphology and a negative P wave. Though at a shorter cycle length the His bundle was still activated retrogradely echo beats were not seen because the retrograde H deflection occurred too early, when both bypass tract and A-V node were still effectively refractory. At the faster driven rate concealed retrograde activation of the right branch (by the premature impulse) was responsible for the right bundle-branch block patterns shown by the post-premature driven beat.     

The junctional premature beat: an instructional exercise in modes of concealment.

?The relative brevity of the main His bundle refractory period compared with that of the A-V node above, and the trifascicular system below, makes it likely that premature beats originating in the His bundle will encounter physiologic delay, or block in both antegrade and retrograde modes. Two clinical cases of junctional premature beats are presented, which demonstrate many facets of concealment (antegrade, retrograde and bidirectional). Hitherto unreported is a ventricular echo which was induced by a junctional premature beat, the antegrade concealment of which was due to functional trifascicular block.     

Ventriculo-atrial conduction associated with ventricular premature beats. Study with his bundle electrography

In a group of eight patients with ventricular premature beats, ventriculoatrial conduction, with retrograde activation of the His bundle and the atria could be demonstrated by His bundle electrograms in four subjects. All had early ventricular premature beats with coupling indices between 210 and 350 msec. In the other four cases, concealed retrograde conduction could be demonstrated in the A-V nodal area. The ventricular ectopic beats were late, and depending upon the refractory period of the A-V node these extrasystoles were interpolated or followed by compensatory pauses.     

Intermittent AV conduction disturbances in patients with AV nodal bypass tracts. Possible mechanisms of unusual variant of tachycardia-bradycardia syndrome.

His bundle recordings were performed in 2 patients in whom AV nodal bypass tracts coexisted with intermittent AV conduction disturbances occurring below the site from which the His bundle deflection was recorded. Case 1 had: (a) tachycardia dependent right bundle-branch block, (b) persistent HV prolongation, and (c) bradycardia dependent AV block. Case 2 showed: (a) intra-atrial conduction delay, (b) tachcardia dependent left bundle-branch block with HV prolongation, (c) bradycardia dependent HV conduction disturbance, (d) tachycardia-bradycardia syndrome of an unusual type; the latter presumably resulted, during atrial flutter, from the alternation of rapid AH conduction through the bypass tract with intermittent (complete) distal His bundle block or bilateral bundle-branch block.     

Gap in bundle-branch conduction elicited by programmed His bundle stimulation

The gap phenomenon in right bundle-branch conduction was elicited during programmed stimulation of the His bundle. Premature beats with short and long coupling intervals showed undisturbed intraventricular conduction, while the premature beat with intermediate coupling interval blocked within the right bundle branch. The electrophysiologic mechanism of "supernormal" conduction of the earliest beats was conduction delay at a proximal site within the His bundle which allowed recovery of the right bundle branch. This study shows that programmed His bundle stimulation is a valuable method in analyzing conduction characteristics of the distal atrioventricular conduction system in cases where atrioventricular nodal refractoriness would preclude this by atrial stimulation.     

His bundle electrocardiography in manifest and concealed right bundle branch extrasystoles.

His bundle electrocardiography was helpful in the diagnosis of impulse formation in the right bundle branch. Ten patients with narrow QRS complexes had ectopic beats with an "incomplete" left bundle branch pattern and almost simultaneous activation of His bundle and ventricles. Both QRS morphology and H- - V intervals depended on the more proximal or distal location of the ectopic focus. In four patients with "complete" right bundle branch block the morphology of ectopic ventricular complexes and H- - V intervals also depeneded on the presence or absence of retrograde block and differential degrees of forward and/or retrograde conduction delays. Nine patients with "complete" right bundle branch block and four with "complete" left bundle branch block had premature beats which could have originated in the proximal right bundle branch, proximal left bundle branch, or distal His bundle. In one patient with "complete" left bundle branch block, "concealed" His bundle depolarizations (probably originating in an ectopic focus located in the right bundle branch) produced pseudo Type II (Mobitz) A-V block. Although lidocaine appeared to have been more effective in patients with bundle branch block than in those with narrow QRS complexes, further studies are necessary to corroborate this impression.     

Familial occurrence of sinus bradycardia, short PR interval, intraventricular conduction defects, recurrent supraventricular tachycardia, and cardiomegaly.

Four members of a family presenting with sinus bradycardia, a short P-R interval, intraventricular conduction defects, recurrent supraventricular tachycardia (SVT), syncope, and cardiomegaly had His bundle studies and were found to have markedly shortened A-H intervals (30 to 55 msec.) with normal H-V times (35 to 50 msec.). Right atrial pacing at rates as high as 170 to 215 per minute failed to increase the A-H or H-V intervals significantly. The data are compatible with the presence of an A-V nodal bypass tract (James bundle) or even complete absence of an A-V node. Ventricular pacing and spontaneous ventricular premature beats resulted in a short ventriculoatrial conduction time (110 msec.) suggesting that if A-V nodal bypass tracts exist, they are utilized in an antegrade and retrograde fashion. None of the features of WPW syndrome was present. The mechanism of syncope in the mother and daughter was intermittent third-degree heart block. Both went on to develop permanent complete heart block despite electrophysiologic studies demonstrating 1:1 A-V conduction at extremely rapid atrial pacing rates and both required implantation of permanent pacemakers. The mechanism of syncope in the two brothers was possibly marked sinus bradycardia, but transient complete heart block has not been ruled out. Permanent pacemaker therapy was recommended for both. The nature of the cardiomegaly, which was mild in three patients, is not known. Although not well documented, several maternal relatives have had enlarged hearts, SVT, complete heart block, and syncope.     

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.     

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.     

Bundle branch reentrant tachycardia treated by electrical ablation of the right bundle branch

A 66 year old man presented with multiple episodes of tachycardia. Some had QRS complexes with a right bundle branch block configuration identical to those of sinus beats. The onset of the tachycardia was preceded by premature His bundle depolarizations. There was a His potential before each QRS complex of the tachycardia. Atrial activity was dissociated. Occasionally the appearance of sinus beats with a left bundle branch block pattern announced a tachycardia with an identical configuration and atrioventricular dissociation. His bundle activity occurred before the QRS complex and was followed by a right bundle branch deflection. A reentrant mechanism within the bundle branch system was invoked. One 200 J shock was delivered through an electrode catheter to the site of the right bundle branch. The postprocedure course was uneventful (follow-up 10 months).     

Limitation of tachycardia zone resulting from longitudinal dissociation of the atrioventricular node in concealed pre-excitation.

Two cases with a concealed left-sided accessory atrioventricular bypass tract are described. In both, functional longitudinal dissociation of the atrioventricular node narrowed the range of atrial premature beat coupling intervals which could initiate re-entry using the accessory pathway. In case 1 early premature atrial beats were followed by an atrioventricular nodal re-entrant echo. The atrial echo pre-empted retrograde conduction over the Kent bundle and thus limited the development of paroxysmal supraventricular tachycardia. In case 2 atrioventricular nodal conduction showed typical features ascribed to dual atrioventricular nodal pathways. In addition there was a bradycardia-related retrograde block in the concealed accessory pathway. Early premature atrial beats, because of exclusive "slow pathway" anterograde conduction, arrived at the ventricles during the period of bradycardia-dependent retrograde block and failed to initiate a macro re-entrant tachycardia. This study shows that (1) longitudinal dissociation within the atrioventricular node may limit the ability to initiate tachycardia in patients with concealed pre-excitation; and (2) discontinuous atrioventricular nodal conduction curves occasionally help to reveal bradycardia-related retrograde block in a concealed accessory pathway.     

A case of paroxysmal rate dependent intra-His bundle block

We present a symptomatic bradycardia-dependent paroxysmal atrio-ventricular (A-V) block occurred within the bundle of His. Paroxysmal A-V block was caused by atrial or ventricular premature beats and also by sinus slowing. This case also showed tachycardia-dependent A-V block within the bundle of His. We also discussed the controversial mechanisms of paroxysmal A-V block.     

Right atrial versus left atrial echo zones: A proposed new criterion for determining the atrial site of retrograde preexcitation

In a patient whose electrocardiogram (ECG) initially (1966) showed a Type A Wolff-Parkinson-White pattern, recurrent supraventricular tachycardia (SVT) developed but never subsequently showed antegrade bypass conduction. Intracardiac pacing studies (1975) revealed that premature high right atrial (induced 250–450 msec after atrial depolarization) or coronary sinus depolarization (250–550 msec) resulted in SVT. Late coronary sinus depolarization resulted in SVT without A-H prolongation. During SVT, P wave morphology changed and the coronary sinus atrial electrogram preceded that from the low right atrium; retrograde ventriculoatrial conduction time was 240 msec. Neither pacing the high right atrium or coronary sinus up to rates of 200 beats/min nor progressive atrial premature depolarizations from the high right atrium or coronary sinus resulted in antegrade bypass conduction. Failure of antegrade bypass conduction does not preclude SVT due to retrograde pre-excitation and must be distinguished from atrioventricular (A-V) nodal reentry. Atrial effective refractory period (200 msec) was shorter than the minimal time required for an atrial impulse to return to the atrium (380 msec), suggesting concealed antegrade bypass conduction. Stimulation of the atrium linked to the A-V bypass results in earlier bypass activation and recovery and explains the differing high right atrial vs coronary sinus echo zones.     

Tachycardia caused by an accessory nodoventricular tract: a clinico-pathologic correlation

Paroxysmal tachycardia with widened QRS complexes was recordedin an eleven-year old boy who had suffered from brain damage,which had resulted from an episode of ventricular fibrillation.Atrial stimulation produced an increased AV conduction, suddendisappearance of the His bundle deflection and a complete leftbundle branch block pattern. Tachycardias of this morphologywere initiated by early atrial and ventricular premature beats.The findings suggested the presence of a macro re-entry circuit,utilizing a slow A V node-nodoventricular bypass tract as theanterograde limb and the His-Purkinje system–fast A Vnode as the retrograde limb. This supposition found furthersupport by serial sectioning of the A V junctional area of theheart, which revealed a nodoventricular tract, which originatedfrom the posterior extension of the compact part of the atrioventricularnode and inserted into the crest of the ventricular septum.     

Mechanism and significance of widened QRS complexes during complete atrioventricular block in acute inferior myocardial infarction

Twelve of 35 consecutive patients admitted with complete, atrioventricular (A-V) block complicating acute inferior myocardial infarction manifested widened QRS complexes. The escape beats had the pattern of left bundle branch block in four patients, right bundle branch block in five patients and both left and right bundle branch block in three patients.

His bundle recordings in five patients with escape beats that had a left bundle branch block configuration revealed a His bundle potential preceding the widened QRS complex at His-V intervals of 45 to 60 msec. Bradycardia-dependent left bundle branch block was demonstrated in two patients by His bundle pacing. In three patients the conducted beats had a left bundle branch block configuration after critical lengthening of the R-R interval during second degree A-V block before or after the episode of complete A-V block. In six patients whose escape beats had a right bundle branch block configuration, His bundle recordings did not reveal a His bundle potential preceding these beats.

Our observations suggest that widened QRS complexes with a left bundle branch block configuration could be due to an A-V junctional escape rhythm with phase 4 left bundle branch block. Alternatively in association with a right bundle branch block configuration it is possible that the widened QRS complexes represent a ventricular or fascicular escape rhythm.

Two of 12 patients with widened QRS complexes died. There were no significant differences in immediate mortality, 6 month mortality or mean peak serum glutamic oxaloacetic transaminase (SGOT) values between patients with narrow and widened QRS complexes. This finding suggests that widened QRS complexes during complete A-V block in acute inferior myocardial infarction have no prognostic significance.     

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.     

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.     

Concealed intraventricular conduction in the His bundle electrogram.

Multiple areas of concealed intraventricular conduction are deduced on the basis of aftereffects observed in His bundle recordings. Electrocardiograms and His bundle recordings are presented from two patients with unstable bilateral bundle branch block, the instability of which depended on the interval at which ventricular depolarization was initiated by sinus or paced impulses. This circumstance allows postulation of 1) concealed transseptal retrograde penetration of the left bundle branch system; 2) concealed transseptal retrograde penetration of the right bundle branch system; 3) alternate beat Wenckebach phenomenon with two areas of block in the bundle branch system with concealed penetration of the proximal area; 4) concealed re-entry in the right bundle branch system during an H-V Wenckebach cycle with resetting of the sequence of 2:1 H-V block and return of the re-entry wave to the A-V node causing subsequent A-H block; 5) proximal 2:1 block and distal Wenckebach block producing only two consecutively blocked beats; and 6) infrahisian Wenckebach block with changes both in A-V conduction and QRS contour.     

Intracardiac electrode catheter recordings of atrioventricular bypass tracts in Wolff-Parkinson-White syndrome: techniques, electrophysiologic characteristics and demonstration of concealed and decremental propagation

Atrioventricular bypass tract deflections were recorded in five patients with the Wolff-Parkinson-White syndrome using standard, closely spaced (5 mm) electrode catheters. Three right paraseptal and two left-sided Kent bundles were recorded at the level of the tricuspid valve on the His bundle catheter and in the coronary sinus, respectively. Characteristics of the bypass tracts were studied during atrial pacing, programmed premature atrial stimulation, induction of supraventricular tachycardias and programmed ventricular stimulation. During atrial pacing, as pre-excitation increased, the stimulus to bypass tract deflection time remained unchanged. In five patients normalization of the QRS complex coincided with loss of the bypass tract deflection during incremental atrial pacing. Two patients demonstrated fragmentation of the bypass tract deflection before block. In one patient fragmentation of the bypass deflection coincided with normalization of the QRS complex. The effective refractory periods of the bypass tracts coincided with loss of bypass tract deflections in three of the five patients. In one patient, the effective refractory period of the bypass tract at its ventricular insertion preceded that at its atrial insertion, whereas in the remaining patient, the effective refractory period of the bypass tract was not attained because of atrial refractoriness. During orthodromic supraventricular tachycardia, the bypass tract deflections disappeared in the anterograde limb in all patients. In one patient, the bypass tract deflection was recorded during atrial fibrillation with pre-excitation. In conclusion: Bypass tract deflections can be recorded with a closely spaced electrode catheter. Right paraseptal bypass tracts are located close to the His bundle. The anterograde effective refractory period of the bypass tract usually reflects its atrial insertion, but concealment through the bypass tract can occur with block at the ventricular insertion. Decremental conduction within the bypass tract can occur before block, suggesting concealed and overt Wenckebach block within the bypass tract. Recordings of bypass tract deflections increase the potential of closed chest ablation of right paraseptal and left-sided bypass tracts.     

Combined intra-Hisian block and A-V nodal bypass

A patient with first and second degree atrio-ventricular (A-V) block and left bundle branch block was shown on electrophysiological study to have an intra and infra-His bundle branch block. In addition, this patient also had an A-V nodal bypass tract. The intra-Hisian block was concealed on the resting His bundle electrogram and became evident only during atrial pacing. The A-V nodal bypass was masked on the surface electrocardiogram (ECG) by the associated A-V conduction defect. The clinical significance of A-V bypass and combined block below the A-V node is discussed. The diagnostic value of His bundle electrocardiography in a patient with complex electrophysiological abnormalities is stressed.