sustained bundle branch reentry as a mechanism of clinical

256

Sustained Bundle Branch Reentryas a Mechanism of Clinical Tachycardia

Jose Caceres, MD, Mohammad Jazayeri, MD, James McKinnie, MD, Boaz Avitall, MD,

Stephen T. Denker, MD, Patrick Tchou, MD, and Masood Akhtar, MD

The incidence of sustained bundle branch reentrant (BBR) tachycardia as a clinical or inducedarrhythmia or both continues to be underreported. At our institution, BBR has been theunderlying mechanism of sustained monomorphic ventricular tachycardia in approximately 6%of patients, whereas mechanisms unrelated to BBR were the cause in the rest. Data gatheredfrom 20 consecutive patients showed electrophysiologic characteristics that suggest this possi-bility. These include induction of sustained monomorphic tachycardia with typical left or rightbundle branch block morphology or both and atrioventricular dissociation or ventriculoatrialblock. On intracardiac electrograms, all previously published criteria for BBR were fulfilled,and in addition, whenever there was a change in the cycle length of tachycardia, the His to Hiscycle length variation produced similar changes in ventricular activation during subsequentcomplexes with no relation to the preceding ventricular activation cycles. Compared withpatients with ventricular tachycardia due to mechanisms unrelated to BBR, patients with BBRhad frequent combination of nonspecific intraventricular conduction defects and prolonged HVintervals (100% vs. 11%, p <0.001). When this combination was associated with a tachycardiashowing a left bundle branch block pattern, BBR accounted for the majority compared withmechanisms unrelated to BBR (73% vs. 27%, p<0.01). The above finding in patients withdilated cardiomyopathy should raise the suspicion of sustained BBR because dilated cardiomy-opathy was observed in 95% of the patients with BBR. Twelve of the 20 patients were treatedwith antiarrhythmic agents, and the other eight were managed by selective catheter ablation ofthe right bundle branch with electrical energy. Our data suggest that sustained BBR is not anuncommon mechanism of tachycardia; it can be induced readily in the laboratory and isamenable to catheter ablation by the very nature of its circuit. The clinical and electrophys-iologic features outlined in this study should enable one to correctly diagnose this importantarrhythmia. (Circulation 1989;79:256-270)

M acroreentry within the His-Purkinje sys-tem commonly referred to as bundlebranch reentry (BBR) is a frequently

observed phenomenon in the laboratory.1-3Althoughscattered cases of sustained BBR tachycardia havebeen reported, no large series dealing with thisphenomenon exists in the literature.4-11 The inci-dence of BBR as a mechanism of sustained ventric-ular tachycardia (VT), therefore, continues to beunderreported in the literature, and consequently,there is less awareness of sustained BBR tachycar-dia as a significant clinical arrhythmia.

In this study, we present our data from 20 con-secutive patients in whom sustained BBR as a

From the Electrophysiology Laboratory University of Wiscon-sin-Milwaukee Clinical Campus, Sinai Samaritan Medical Cen-ter, Milwaukee, Wisconsin.Address for correspondence: Masood Akhtar, MD, Electro-

physiology Laboratory, Sinai Samaritan Medical Center, 950North 12th Street, Milwaukee, WI 53201.

Received May 6, 1988; revision accepted September 20, 1988.

mechanism of VT was induced in the laboratory.The clinical and electrophysiologic substrate andthe rationale for the diagnosis of BBR as a mecha-nism of VT in these patients is presented.

MethodsPatientsThe patients included in this series are from those

referred to this institution for evaluation of docu-mented or suspected VT or ventricular fibrillationor both. After history and physical examinationwere obtained, diagnostic cardiac workup in allpatients included 12-lead electrocardiogram (ECG),echocardiogram, left and right heart catheteriza-tion, and coronary angiography. In addition, mostpatients also underwent radionuclide studies forassessment of left ventricular ejection fraction.

Electrophysiologic TestingBaseline electrophysiologic studies were per-

formed in patients in the unsedated postabsorptive

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Caceres et al Sustained Bundle Branch Reentry 257

state and who were not receiving antiarrhythmicagents except one patient who received amiodaronefor 1 month before admission to our institution.Multipolar electrode catheters were percutaneouslyintroduced through the antecubital or femoral veinsor both and positioned in the high right atrium forrecording and pacing the right atrium, across thetricuspid valve for recording His bundle or rightbundle electrograms or both, and in the right ven-tricle apex for recording and pacing the right ven-tricle. Three surface electrocardiographic leads (I,II, and V1), intracardiac electrograms (filtered at30-500 Hz), and time lines were simultaneouslydisplayed on a multichannel oscilloscope andrecorded on a Honeywell magnetic tape (Denver,Colorado) for later reproduction. Ventricular pac-ing was performed with a digital stimulator at twicediastolic threshold. The magnitude and duration ofthe electrical impulses remained the same through-out the study. All equipment was grounded, andisolation units were used for electrical stimulation.Programmed electrical stimulation was performed

at no less than two constant basic cycle lengths andfrom two right ventricular sites with up to twoextrastimuli. In addition, up to two extrastimuli weretested after an abrupt short-to-long cycle lengthchange that is a routine method of VT induction inour laboratory.12 As a matter of routine, in thislaboratory, single extrastimuli are tested first atconstant cycle length and then during a short-to-longcycle length change. A similar sequence is alsomaintained when two extrastimuli are used. Whenthe above did not induce sustained VT, three extra-stimuli were delivered at two constant cycle lengthsfrom the two right ventricular sites. Three extrastim-uli were not tested during a short-to-long cycle lengthchange. Inducibility of supraventricular tachycardiasand atrioventricular block in the His-Purkinje systemwith atrial pacing was also assessed in all patientsexcept those in atrial fibrillation. All pertinent con-duction and refractory period intervals were mea-sured as a part of the routine electrophysiologicstudy and have been previously published.13From the moment a sustained monomorphic VT

was induced, particular attention was paid to thefollowing. 1) Did the VT have a typical left or rightbundle branch block pattern? 2) Quality and reliabilityof recordings showing the His or right bundle branchpotentials or both were maintained. This was toensure that the disappearance of His bundle deflectionduring a wide QRS tachycardia was not due to poorquality of tracings. 3) The tachycardia cycle lengthwas carefully measured beat by beat until the arrhyth-mia became stable, that is, variation of 10 msec orless, and then again before and during termination. 4)Because the His or right bundle potentials or bothtypically precede the QRS complexes in all of thesecases, the relation between the consecutive HH (orright bundle to right bundle branch) intervals withthe preceding and succeeding RR intervals was care-fully analyzed. Similarly, the HV interval was also

Table of Abbreviations

S,Sis,1

Beats of the basic driveThe basic ventricular drive at a short cyclelength (400 or 350 msec) followed by an abruptincrease in cycle length (S1S', =600 or 700msec) for one cycle before S2

S2,S3,S4 Single, double, or triple premature stimuli,respectively

SH Onset of stimulus artifact to the onset of Hisbundle deflection

HV Onset of His bundle deflection to the earliestdetectable ventricular activation on surfaceelectrocardiogram or intracardiac localelectrograms

RB-V Onset of right bundle deflection to the earliestdetectable ventricular activation on the surfaceelectrocardiogram or intracardiac electrograms

VH Onset of ventricular activation to the onset ofHis bundle potential

V-RB Onset of ventricular depolarization to the onsetof right bundle deflection

measured for all complexes associated with anychange in the cycle length of the tachycardia.

Catheter Ablation of the Right Bundle BranchThe details of this nonpharmacologic technique

for interruption of conduction along the right bundlebranch in our laboratory has been previously pub-lished and will not be detailed here.15

Statistical MethodsStatistical analyses were performed with the

Student's t test, x2 analysis, paired Wilcoxon'stest, and the Pearson's method. A value ofp lessthan 0.05 was considered significant. Descriptivedata are expressed as mean±SD.

ResultsOf the 285 patients with inducible sustained mono-

morphic VT analyzed between January 1980 andDecember 1987, 17 were diagnosed as having BBR,which is an incidence of 6.0%. Among the 285patients, the underlying structural heart disease wasatherosclerosis in 240, idiopathic dilated cardiomy-opathy in 22, and a variety of underlying causes inthe remaining 23. Three additional patients thatwere studied elsewhere were referred to us forfurther treatment, and these were already diag-nosed as having sustained BBR tachycardia. These20 patients, therefore, form the basis of this study.

Clinical CharacteristicsAmong the 20 patients, 18 were men and two were

women ranging in age from 32 to 81 years (mean,61.4± 12 years). All patients had cardiac enlargement(all four chambers in 16 and only left heart in fourpatients), confirmed by echocardiography and car-diac catheterization. The underlying structural heartdisease was atherosclerosis with previous myocar-dial infarction in 11, but in two of 11, the degree of



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258 Circulation Vol 79, No 2, February 1989

TABLE 1. Baseline Electrocardiogram

n t

RhythmSinus 16 80Atrial fibrillation 4 20

PR intervalFirst degree atrioventricular block(>210 msec) 14 88

Normal 2 12QRS duration (msec)Mean ± SD, 138 ± 22Range, 105-160

QRS patternNonspecific intraventricular conduction

delay 19 95Incomplete right bundle branch block 1 5

QRS axisLeft (< - 30° to - 90°) 15 75Normal (<300 to + 90°) 5 25

*Mean + SD; n =20 patients.

left ventricular dysfunction could not be explainedon the basis of coronary artery disease. Eight patientshad idiopathic congestive cardiomyopathy, and theremaining patient had aortic valve prosthesis forsignificant aortic regurgitation. Except the latterpatient, the left ventricular ejection fraction was

abnormal in all, ranging from 15% to 45% (mean,25 ± 10%). Therefore, by conventional criteria, 19 of20 patients (95%) had dilated cardiomyopathy. Sev-enteen of the patients (85%) had clinical symptoms ofcongestive heart failure.The majority of patients (17 of 20) had histories

of syncope. The number of syncopal episodes rangedfrom one to eight (mean, 2.4 ± 1.9). Three patients hadnear syncope and palpitations. In seven patients, an

immediate collapse due to rapid VT or degenerationinto ventricular fibrillation or both was documented,which required direct current cardioversion and car-

diopulmonary resuscitation.

Baseline Electrocardiogram andConduction Characteristics

Intermittent atrial fibrillation was previously docu-mented in 11 patients with an average RR cycle lengthof 795 msec, and fibrillation was persistent in four(Table 1). The baseline ECG variables depicted inTable 1 were obtained when patients were not beingtreated by antiarrhythmic drugs except one patientwho had been on amiodarone therapy for 1 month.

Because BBR circuit incorporates the intraven-tricular conduction (i.e., intramyocardial and His-Purkinje system conduction), the latter was analyzedin greater detail in search of a possible substrate,particularly during the last 3 years (1985-1987).During this 3-year period, 136 cases of patients withinducible sustained VT were studied in our labora-tory, and among those, eight patients (5.9%) had VTdue to sustained BBR (Table 2), which is an inci-dence remarkably similar to our total experience.

TABLE 2. Electrophysiologic Characteristics in Patients WithSustained Monomorphic Ventricular Tachycardia

Characteristic n %

BBR 8 5.9Non-BBR 128 94.1QRS duration

(128 patients with non-BBR)Normal 36 28Nonspecific IVCD (>100 msec) 81 63RBBB pattern 7 6LBBB pattern 4 3

HV interval(128 patients with non-BBR)Normal 106 83Prolonged (.60 msec) 22 17

Nonspecific IVCD+prolonged HVBBR (8 of 8) 8 100Non-BBR (14 of 128) 14 11

Nonspecific IVCD + prolonged HV+*LBBB configuration tachycardia 11BBR 8 73Non-BBR 3 27or

*RBBB configuration tachycardia 11BBR 0Non-BBR 11 100

Data from 1985 to 1987; n = 136 patients (unless otherwise noted).BBR, bundle branch block reentrant tachycardia; IVCD,

intraventricular conduction delay; RBBB, right bundle branchblock; LBBB, left bundle branch block; HV, His bundle toventricular electrogram interval.

The HV interval was prolonged in all patients withsustained BBR but in only 22 of 128 (17%) patientswith sustained VT due to mechanisms not related toBBR. However, no direct evidence of intra-Hisdelay in the form of wide, slurred, or split His bundlepotentials was noted in patients with either the BBRor tachycardia not related to BBR. The HV intervalsin patients with sustained VT not due to BBR fromprevious years were not available in all patients, andfor this reason, the detailed analysis of intraventric-ular conduction was restricted to studies done duringthe last 3 years.None of the patients with BBR had either a

complete right or left bundle branch block patternon resting ECG, whereas in patients with VT notrelated to BBR, preexisting complex right bundlebranch block pattern occurred in 6% and left bundlebranch block occurred in 3%. Nonspecific intraven-tricular conduction delay was observed in 63% ofthe patients with VT not related to BBR and in100% of the patients with sustained BBR. A com-bination of nonspecific intraventricular conductiondelay and prolonged HV interval was significantlymore common in patients with sustained BBR (100%)compared with patients without BBR (11%,p <0.001). Eleven of the 136 patients had a combi-nation of nonspecific intraventricular conductiondelay, prolonged HV intervals, and a left bundlebranch block pattern tachycardia, and in eight ofthe 11 patients, BBR was diagnosed, which is anincidence of 73%. On the other hand, eleven patients



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TABLE 3. Induction of Sustained Bundle Branch Reentrant Tachycardia at Baseline Electrophysiologic Study

Basic cycle length (S,)Patient 600 msec 400 msec Short-to-long S2 S3 S41* + + +

2 + +

3t + +

4 + +

5 + NA +6 + +

7 + + +

8 + +

9 + + +

10 + NA +11 + +12 + +13 + +14 + NA +15t + +

16 + + +

17 + +

18§ + NA +19 + +20 + NA +

S2, S3, S4, right ventricular extrastimuli.*Received amiodarone 400 mg/day for 30 days before electrophysiologic study.In three patients, the right bundle branch block pattern tachycardia was initiated tfrom left ventricle, tatrial

pacing, and §right ventricle.

had intraventricular conduction delay, prolongedHV interval, and a right bundle branch block pat-tern tachycardia, and none had BBR as the mech-anism (Table 2).

Tachycardia InitiationThe pacing methods that resulted in the initiation

of sustained BBR are listed in Table 3. The detailsare as follows.Basic cycle length. As can be noted from the

table, most inductions occurred during basic cyclelengths incorporating a sudden short-to-long changebefore the introduction of extrastimuli. This methodof VT induction has been previously described andhas been routinely used in our laboratory since1982.12 In five patients (patients 5, 10, 14, 18, and20) who were studied earlier, this pacing methodwas not used. In 10 patients, a short-to-long cyclelength change was the only method of induction(Figure 1). In six patients (patients 5, 10, 11, 14, 18,and 20), the tachycardia was initiated at either aconstant basic cycle length of 600 or 400 msec, andin five of six patients, the short-to-long change wasnot even tested. When the constant cycle length anda short-to-long cycle length change were successfulin inducing the tachycardia (the remaining patients),the BBR was initiated at longer coupling intervalswith a short-to-long change. In three patients(patients 3, 15, and 18), another BBR tachycardiawith a right bundle branch block pattern was

induced. The induction method incorporated a short-to-long cycle length change while pacing from theleft ventricle in one (patient 3), a constant cyclelength with right ventricular pacing in one (patient18), and an incremental atrial pacing in the remain-ing patient (Figure 2). Aside from this latter patient,BBR could not be induced in any of the patientswith either incremental atrial pacing or atrial extra-stimulus technique. The shortest atrial cycle lengthsresulting in 1:1 conduction through the atrioven-tricular node exceeded the cycle length of tachy-cardia by at least 50 msec in patients without atrialfibrillation. In none of the patients in this serieswas a block in the His-Purkinje system observedduring electrophysiologic evaluation.Number of premature beats. Single ventricular

extrastimulus initiated sustained BBR (with a leftbundle branch block pattern) in 16 of 20 (80%)patients (Figure 1). In only one of these patients,the retrograde His deflection during the basic drive(i.e., HI) was identifiable. However, in all instances,the retrograde His bundle deflection (H2) emergedfrom the local V2 electrogram as the S1S2 intervalwas shortened, and there were measurable andprogressive retrograde delays in the His-Purkinjesystem (S2H2). In three patients, an S3 (patients 5,11, and 15), and in only one patient (patient 1 whowas on oral amiodarone), an S4 was required toinitiate the tachycardia. Among the three patientshaving a BBR with a right bundle branch block



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FIGURE 1. Tracings of initiation ofsustained bundle branch reentrant (BBR) tachycardia. Tracings in each panel, fromtop to bottom, are surface electrocardiographic leads 1, 2, V>, high right atrium (HRA), His bundle (HB) electrogram, andtime lines. Pertinent intervals are labeled, and all intervals are in milliseconds. At a constant basic cycle length of600 msec(Panels A and C) and 400 msec (Panel B) with up to two extrastimuli (S2, S3), no sustained tachycardia could be initiated.However, in Panel D, ventricular drive of400 msec is followed by an abrupt increase in cycle lengthfrom 400 to 600 msecfor one beat (S, - S', = 600 msec). A single ventricular extrastimulus (S2) initiates sustained BBR tachycardia. Note that thesame SJS2 interval of270 msec was introduced in PanelsA, C, and D. Note also the typical left bundle branch blockpatten,H-V interval equal to that ofsinus beats, and atrioventricular dissociation. The axis is leftward. Also note that when thereis a change in the cycle length of the tachycardia, the HH changes precede the WVchanges.

pattern, the tachycardia was induced with a singleextrastimulus in one (patient 18), two extrastimuliin one (patient 3), and incremental atrial pacing inthe remaining (patient 15). None of the patients inthis series demonstrated initiation of BBR when theinitiating premature beat terminated in the His-Purkinje system regardless of the method of induc-tion. Other types of sustained VT were initiated inonly one patient in this series. However, in thispatient, the sustained BBR was the clinical arrhyth-mia because it was identical to the clinical tachy-cardia recorded on the 12-lead ECG. In four patients(patients 2, 15, 16, and 18) in this series, threeextrastimuli were not tested. Supraventricular tachy-cardias were not induced in any of the patientsduring the electrophysiologic evaluation.Electrophysiologic characteristics oftachycardia

due to bundle branch reentry. All episodes of tachy-cardia showing a left bundle branch block config-uration were initiated during pacing from the right

ventricle (Table 4). As indicated above, anotherQRS morphology with a typical right bundle branchblock appearance was also observed in threepatients.The His bundle deflection in all patients preceded

the QRS complex by HV intervals equal to orexceeding those during baseline rhythms (Table4).1,3 Whenever recordings were obtained from theright bundle or left bundle deflection, these deflec-tions also preceded the QRS with an RB-V or LB-Vinterval or both greater than or equal to the baselinevalues (Figures 1D and 3). In 12 patients, His andright bundle branch recordings (obtained either simul-taneously or on separate occasions) were availableduring BBR with a left bundle branch block config-uration, the His bundle deflection preceded theright bundle deflection by H-RB intervals equal toor less than the H-RB during the baseline rhythm.3In two of three patients who had BBR with a rightbundle branch block pattern, the right bundle deflec-

1 1.

2

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FIGURE 2. Tracings of initiation of bundle branch reentrant (BBR) tachycardia with atrial pacing. Tracings in eachpanel, from top to bottom, are surface electrocardiographic leads 1, 2, V,, high right atrium (HRA), His bundle (HB)electrogram, and time lines. Pertinent intervals are labeled, and all intervals are in milliseconds. A functional rightbundle branch block is initiated during atrial pacing at a cycle length of 400 msec (Panel A). Note further HVprolongation with the second paced beat to 120 msec (not labeled). The right bundle (RB) potential, which wasanterogradely depolarized with the firstpaced beat, is now activated retrogradely and hence follows the QRS, setting upa linkingphenomena between the His and the right bundles. Both His and right bundle activation result from the sameatrial paced impulse. However, the His bundle activation is anterograde through the atrioventricular node, and rightbundle depolarization is retrograde by way of transseptal conduction. This linking by interference continues until acapture ofHis bundle occurs by the retrograde impulse approaching through the right bundle as depicted by asterisk andsustained BBR tachycardia is initiated. The two perpendiculars drawn (Panel B) show the relative timing ofHis and rightbundle activation during the linking and the BBR, respectively. The HV interval during the tachycardia measures 80msec. There is atrioventricular dissociation and an appropriate RB-H activation sequence for a BBR tachycardiashowing a right bundle branch block pattern (Panel C). Continued atrial pacing after initiation of sustained BBRtachycardia does not result in capture of the His bundle and, therefore, has no influence on the tachycardia.



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-6-2' Circulation Vol 79, No 2, Februaty 1989

TABLE 4. Electrophysiologic Features of Sustained BundleBranch Reentrant Tachycardia Induced at Baseline Electro-physiologic Study

ConfigurationLB/LA 12 52LB/NA 8 35RB/LA 2 9RB/RA 1 4

Cycle length (msec)Mean ± SD, 279+ 26Range, 240-360

HV intervalIntrinsic rhythm (msec)Mean ± SD, 70+ 10Range, 60-90

Bundle branch reentrant tachycardiaMean± SD, 84± 22Range, 60-160

Atrioventricular dissociation 100% atrial rhythmSinus 78Atrial fibrillation 22

Symptoms during the tachycardiaSyncope 7 30Near syncope 15 65Palpitations 1 5

Reproducibility 1-10Mean--SD, 3.3+2.3

Data from 20 patients. Number of tachycardias was 23.LB/LA, left bundle branch block/left axis; LB/NA, left bundle

branch block/normal axis; RB/LA, right bundle branch block/leftaxis; RB/RA, right bundle branch block/right axis; HV, His tolocal ventriculogram potential interval.

tion preceded the His bundle potential (Figure 2). Adissociation between atrial and His bundle, as wellas ventricular activity, was clearly identifiable in allinduced tachycardias.At the beginning of tachycardia, the cycle length

variation (in the first 10 cycles) could be accountedfor by changes in the VH intervals (Figure iD),whereas the HV intervals were usually constant. Inall instances, however, the variations in the HH orRB-RB cycle length preceded the VV cycle lengthchanges (Figures 1-3). The relations of changes inconsecutive HH cycles to changes in the succeed-ing and preceding VV cycle are depicted in Figure4 It is apparent that correlation of changes in HHcycle lengths is excellent with the subsequent VV(Panels A and B), whereas there is no correlationwith the pi-eceding VV intervals (Panels C and D).The data in Figure 4 are from all patients and from23 tachycardias seen in this study. The high positivecorrelations in Panels A and B argue strongly againsta myocardial origin of these tachycardias with inci-dental His bundle activation. Reinduction of tachy-cardias were attempted in all patients whenever thepatient could tolerate the arrhythmia. On repeatinduction, the same type of tachycardia (i.e., QRSboiifiguration and axis) and similar HV relationswele observed. The main electrophysiologic inter-vals measured during these tachycardias are depictedin Table 4.

Spontaneous VT was documented in eight patients(rhythm strips in 6- and 12-lead ECG in twopatients), and the induced tachycardias were of thesame appearance in the corresponding leads. In theunmedicated state, the cycle length of the inducedtachycardias was within 10 msec of spontaneouslyoccurring VT.

Tachycardia termination. In situations where thetachycardia was well tolerated, isolated ventricularpremature beats were induced for termination(Figure 5). Tachycardia termination was accom-plished whenever the induced extrastimulus encoun-tered a block below the His bundle (i.e., no retro-grade His bundle deflection). In most instances,however, overdrive termination was preferentiallyused because of hemodynamic collapse. The tachy-cardias were terminated with overdrive (from rightventricle) in 14 patients. Like single extrastimulus,the overdrive termination was successful in termi-nating the tachycardia only when the last stimulusfailed to propagate to the His bundle (Figure 5B). Inanother five patients, some of the tachycardia epi-sodes could be immediately terminated with over-drive pacing, but because of hemodynamic col-lapse, other episodes required direct currentcardioversion when a quick termination was notaccomplished with overdrive. The remaining fourpatients required prompt direct current cardiover-sion because of rapid hemodynamic collapse. Over-drive atrial pacing was tried in only one patient whohad a well-tolerated tachycardia and was unsuccess-ful. In the patients in this series, an antegradecapture of the His bundle from dissociated atrialimpulses was never noted (Figures 1-3, 6).

Ventricular pacing at rapid rates equal to orexceeding the tachycardia rates did not result in astable retrograde His bundle or right bundle deflec-tion (Figure 3B). When rapid ventricular pacingproduced a retrograde His bundle potential (usuallyat the onset of pacing), it had no consistent relationwith the succeeding QRS complex, and His-Purkinje system accommodation quickly ensued.Spontaneous termination of BBR occurred in

only two patients with a left bundle branch blockconfiguration tachycardia and was usually in theretrograde limb as indicated by the absence of Hisbundle deflection after the last V (Figures IC and6B). In one of these patients, an anterograde blockbetween the His and right bundle recording sites(Figure 6, Panel A) terminated some episodes.

Treatment and Follow-upTherapy consisted of antiarrhythmic agents in 12

patients (60%) (Table 5), whereas the remainingeight were treated by nonpharmacologic means.15Seven patients received type la agents alone or incombination with type lb drugs. Control was doc-umented with serial drug testing in five of sevenpatients. The other two patients (patients 7 and 15)did not undergo repeat studies for the followingreasons. The first patient had severe heart failure



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B

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FIGURE 3. Tracings of His-Purkinje system activation during bundle branch reentrant (BBR) tachycardia andventricularpacing. Tracings in eachpanel, from top to bottom, are surface electrocardiographic leads 1, 2, V,, high rightatrium (HRA), His bundle (HB) electrogram, and time lines. Pertinent intervals are labeled, and all intervals are inmilliseconds. Sustained BBR tachycardia is initiated by a short-to-long change in the basic cycle length and S2. Note theprolonged right bundle (RB)-V interval of 45 msec (compared with 20 msec during sinus beat, not labeled) remainsunchanged despite variations in tachycardia cycle length. His-Purkinje system involvement in tachycardia initiation andmaintenance is indicated by the RB-RB interval changes that precede the W intervals before the tachycardia cyclelength became stable at 220-230 msec (Panel A). In Panel B, ventricularpacing at the same cycle length as the inducedtachycardia fails to show right bundle activation between the ventricular electrograms.

and died of pump failure 6 days after the initialelectrophysiologic study without tachycardia recur-rence. The second patient refused to be retestedand died suddenly at home, 35 days after hospitaldischarge. The remaining five patients receivedamiodarone after trying an average of three (range,2-4) antiarrhythmic agents. Amiodarone preventedtachycardia induction in three patients, whereastwo patients (patients 6 and 9) continued to haveinducible VT related to BBR, albeit at slower rate.Percutaneous catheter ablation of the right bundlewas successfully performed in the remaining eightpatients, and not a single beat of BBR could beinduced after right bundle ablation in these patients.15Follow-up period ranged from 6 to 2,985 days

with a mean of 614±847 days. Eleven of the 12patients who received antiarrhythmic agents werestill taking these drugs at the time of death orfollow-up. The remaining patient (patient 18), whohad aortic valve replacement, had received amio-darone for 20 months. He spontaneously developedcomplete atrioventricular block in the His-Purkinjesystem, and the drug was discontinued. He received

a permanent pacemaker, and subsequent electro-physiologic study did not result in the induction ofVT related to BBR. None of the eight patients whounderwent right bundle branch ablation subse-quently received antiarrhythmic drugs.

Recurrent sustained VT attributed to BBR wasobserved in the two patients who had inducibletachycardia while receiving amiodarone. Tenpatients (50%) died primarily because of low car-diac output (Table 5) without recurrence of bundlebranch reentry tachycardia. Eight of the ten werefrom those who were treated with antiarrhythmicdrugs. Two of the patients treated by right bundleablation also died of progressive congestive heartfailure. The mean baseline left ventricular ejectionfraction in patients who underwent right bundleablation and in the remaining 11 patients receivinglong-term drug therapy were 26.12± and 24.81±,respectively (p= NS). Of the 10 patients still living,six are still working.

DiscussionThis study shows that sustained BBR is the

underlying mechanism in approximately 6% of

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-L-0 ---50

FIGURE 4. Plots relations ofHH cycle length with preceding and succeeding WVintervals. Panels A and B depict thechanges in the HH intervals of the second, third, and fourth bundle branch reentrant tachycardia beats plotted againstsucceedingW interval changes in 23 tachycardias. The correlation coefficient is 0.98 and 1.00, respectively. However,when a similar graph was plotted against the W intervals of the preceding beats (Panels C and D), there is little (andnegative) correlation (correlation coefficient is -0.29 and -0.46, respectively). These data strongly argue againstmyocardial origin of these tachycardias.

induced sustained monomorphic VT in our patientpopulation. The incidence of this tachycardia in ourlaboratory has remained essentially the samethroughout the years (1980-1987). Before acceptingthe patients here as, indeed, examples of sustainedBBR, we should examine some important issuesoften raised.

Mechanisms of Induced TachycardiaThe first aspect relates to the possibility that

induced tachycardias may be of different origin thanBBR. For example, one could argue that the inducedtachycardia represents the usual form of VT (arisingfrom diseased ventricular myocardium) and that theretrograde His bundle activation is incidental. Thiswould imply that the induced tachycardias repre-sent VT of myocardial origin with secondary His

bundle activation due to one of the following mech-anisms: 1) retrograde functional delays in the His-Purkinje system, 2) linking phenomenon, and 3)retrograde ipsilateral bundle branch block. Withretrograde functional delays or block or both, accom-modation is frequent, causing the His bundle deflec-tion to merge with the corresponding ventricularelectrogram.16 Similarly, the linking phenomenon isdependent upon critical timing of the events, andfrequently, accommodation follows with forwardmigration of the site of linking.17 Regarding thepresence of retrograde bundle branch block, that is,a retrograde right bundle branch block with a tachy-cardia originating in the right ventricle (displaying aleft bundle branch block configuration) and a retro-grade left bundle branch block with a tachycardiaarising in the left ventricle (i.e., a right bundle

AH4H5- H5H6

(D

W)

20 30 40 50

C

U)

CI

*10.-50 -40 -30 -20 -10

a a v A

a 5. a a a9 5 Xa -i - X1r101

_-10

ha a



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A12vi

H- H = 300 260 250 260 260 - *HB

RB - RB = 300 260 250 260 260 *RB ~~~~~~~~~RB2RB3 RB RB RBRBE

S2 -H2 =230 V3 V V V V VRV

TJ 400 400 600 270 V-V=300 260 250 260 260 -T

B

H-H = 260 260 260 260

RB-RB=260 RB

V -V = 260 260 260 260 260 -

FIGURE 5. Tracings oftermination ofsustained bundle branch reentrant (BBR) tachycardia with block in the His-Purkinjesystem. Tracings in each panel, from top to bottom, are surface electrocardiographic leads 1, 2, Vb, high right atrium(HRA), His bundle (HB) electrogram, and time lines. Pertinent intervals are labeled, and all intervals are in milliseconds.In Panel A, sustained BBR tachycardia displaying a left bundle branch block configuration is induced with a short-to-longbasic cycle length change and a single extrastimulus. The His bundle activation (H2) precedes activation ofthe right bundle(RB2), which, in turn, is followed by ventricular muscle activation (13), that is, the first tachycardia beat. The RB-Vof20msec compared with 30 msec during the baseline (last complex in Panel B) is typical ofH-RB activation through the leftbundle during BBR. In Panel B, a premature ventricular extrastimulus is introduced immediately after the His bundledeflection (arrow at A), retrograde His activation follows, and the tachycardia continues. An earlier ventricularextrastimulus (arrow at B) terminates the tachycardia. Note termination ofthepremature impulse below the His bundle (noH or RB), which was essential for termination of this and other tachycardias in this series.

branch block configuration), the following can be The reason for the diagnosis of BBR (versus otherstated. In 19 of 20 patients having the BBR tachy- mechanisms) in these patients is discussed below.cardia with a left bundle branch block pattern, therewas no evidence of preexisting anterograde right Distinction From Ventricular Tachycardiabundle branch block, which often coexists with the During the sustained tachycardias observed inretrograde counterpart. 18 Furthermore, evidence of this study, His bundle activation appeared neces-retrograde bundle branch block is usually present sary before the inscription of subsequent QRS. Thisduring the basic drive beats, which was not evident could be deduced from 1) the excellent correlationin most patients in this series during right ventricu- of changes in HH cycles to succeeding but notlar stimulation.18 preceding ORS cycles (Figure 4). A reverse of the



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A 1

2vi

A1 A1 A, A2 Ar Ar AHRA

1J VJ Vi V2 V3 A V

HB _ H W=60

RB-RB-210 240 V

RBRRBV 25

400 400 250 S3 V-V-210 240T .1..... L 1 -- AL LL . ..... LL

B

A1 A1 A1 A2 Ar Ar Ar

RB-RB - 220 210 210 210

400 400 250 210 xS3 V-V-220 210 210 210

C

A, A, A, A2 Ar Ar Ar

RB-RB-240 215 215 215 215 230

400 400 250 210 S3 V-V-240 215 215 215 215 230

FIGURE 6. Tracings ofspontaneous ternination ofbundle branch reentrant (BBR) tachycardia. A tachycardia terminationin the anterograde limb (between H and RB) is depicted in Panel A. The H-RB activation sequence is typical ofBBRtachycardia. The last QRS of the tachycardia is followed by His but no right bundle deflection, and the site of block isbetween the two recording sites. The episode ofBBR in Panel B terminates in the retrograde limb (no His deflection). PanelC shows initiation ofa sustained episode. Again, HH variation precedes theWby the same magnitude.



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TABLE 5. Sustained Bundle Branch Reentrant Tachycardia: Treatment and Follow-up

Treatment Follow-up

RightAntiarrhythmic bundle VT induced Antiarrhythmic VT

Patient agents ablation on treatment Days agents recurrence Cause of death

7 Procainamide NA 6 Procainamide Congestive heart failure10 Procainamide No 120 Procainamide Myocardial infarction12 Procainamide No 682 Procainamide15 Procainamide NA 35 Procainamide Sudden death syndrome5 Quinidine +mexiletine No 110 Quinidine +mexiletine Pneumonia8 Quinidine +mexiletine No 128 Quinidine +mexiletine Congestive heart failure

14 Quinidine + mexiletine No 1,860 Quinidine + tocainide2 Amiodarone No 2,090 Amiodarone4 Amiodarone No 152 Amiodarone Congestive heart failure6 Amiodarone Yes 350 Amiodarone + Mitral valve thrombosis9 Amiodarone Yes 16 Amiodarone + Myocardial infarction18 Amiodarone No 2,9851 + No 3003 + No 280

11 + No 100 Congestive heart failure13 + No 180 Congestive heart failure16 + No 1,73017 + No 56819 + No 11020 + No 48

VT, ventricular tachycardia; NA, electrophysiologic testing was not performed.

above would be expected if activation of the Hisbundle was incidental and related to the previousQRS complex. 2) Retrograde block of spontaneousor paced ventricular impulses below the His bundleterminated the tachycardia (Figures 5 and 6), andsimilarly in one individual, anterograde blockbetween the His bundle and right bundle recordingsites also resulted in spontaneous termination (Figure6A). 3) A consistent relation between the His deflec-tion and subsequent QRS with a constant HVinterval despite varying VV intervals would beunlikely with VT not related to BBR. A dissociationbetween the H and V would occur during severalcycles as has been demonstrated previously duringrapid ventricular pacing, and this was also seen inthis study.16 It is important to point out that aconsistent relation between the QRS and the Hisbundle (with HV greater than or equal to baselinevalues) has never been demonstrated in VT notrelated to BBR. Therefore, an argument suggestingan incidental relation between ventricular and His-Purkinje system activation during a ventricular tachy-cardia (mimicking the patterns in this study) remainspurely a hypothetical one for which no documentedsupport exists. 4) The activation sequence of Hisand right bundle in all instances (where the tworecordings were available) suggested impulse prop-agation through the His-Purkinje system before thenext QRS (Figure 5A). Because of these reasonsand the fact that noninducibility was achieved in100% of the patients (eight of eight) with a localized

ablation attempt, these tachycardias very likelywere from BBR mechanisms.15 Of note, in thiscontext, the tachycardia spontaneously ceased inthe patient with aortic prosthesis when he devel-oped atrioventricular block within the His-Purkinjesystem with progression of the His-Purkinje systemdisease.From the arguments above, ventricular tachy-

cardia not related to BBR probably would notproduce the patterns seen here. On the otherhand, it will be more logical to consider tachycar-dias arising in or above the level of the His bundlebecause these will constitute more important dif-ferential diagnoses as detailed below.

Distinction From Atrioventricular Nodal ReentryWith Retrograde Block

Intranodal reentry localized to part of the atrio-ventricular node with retrograde atrioventricularnodal block (and hence atrioventricular dissocia-tion) particularly in the setting of atrial fibrillationwould appear rather unlikely. To initiate intranodalreentry with V2, the impulse has to activate the Hisbundle twice, that is, once in the retrograde andthen in the anterograde direction, and this was notobserved during this study.19,20 Furthermore, inonly one patient was the tachycardia initiated withatrial pacing, and even then, it was unrelated toatrioventricular nodal delays (Figure 2). Other argu-ments against atrioventricular nodal reentry include,first, relatively short cycle lengths of the tachycar-



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dia compared with the ability of the atrioventricularnode to maintain 1: 1 response during either atrialpacing or spontaneous atrial fibrillation. Second,spontaneous or induced termination of tachycardiawith impulses that terminated in the His-Purkinjesystem and, therefore, failed to reach the atrioven-tricular node would be unable to terminate a proc-ess localized within that structure. Third, H-RBsequence in many patients suggested His bundleactivation retrogradely through one of the bundlebranches and not the atrioventricular node; that is,with a left bundle branch block morphology tachy-cardia, the H-RB frequently measured less than theH-RB of baseline rhythm.3

Distinction From Reentry Within the His BundleReentry within the His bundle is the most difficult

to distinguish from sustained BBR. However, somereasons can be offered that argue against this pos-sibility. 1) No direct evidence of intra-His delay(i.e., wide or split His potentials) was seen duringbaseline studies, atrial pacing, or after extrastimuliinitiating the tachycardia. Similarly, wide or splitHis potentials also were not seen during the tachy-cardia. 2) Termination of tachycardia occurred bypremature ventricular impulse that failed to reachthe His bundle (i.e., terminated below the Hisbundle), which is an unlikely event if intra-Hisreentry was the mechanism. 3) Catheter ablationof the right bundle without associated atrioventric-ular block in the His bundle abolished the induc-tion of the tachycardia.15 4) The sequence of Hisbundle and right bundle activation was compatiblewith impulse arrival at the His bundle through thebundle branches. This, again, would be an unlikelyrecurring coincidence if intra-His reentry was thecause.

Reentry With Retrograde Conduction Through aNodoventricular MahaimOne can visualize at least theoretically a circuit

where the anterograde conduction occurs over theHis-Purkinje system and retrograde activationthrough a nodoventricular Mahaim. A patient(patient 5 from Gallagher et a121) has been reportedin whom such a circuit was hypothesized. How-ever, the possibility of BBR was not convincinglyexcluded in that patient, and the example shown isquite similar to the BBR tachycardia induced withatrial pacing (Figure 2 from Gallagher et a121).Furthermore, none of the patients in this series hadanterograde conduction along a nodoventricularMahaim, and exclusive retrograde conduction througha nodoventricular Mahaim has never been demon-strated in the literature. Recent data also shed somedoubt concerning the existence of proposed circuitsin patients with so-called -"nodoventricular Mahaimfibers."22,23 Such patients may have atriofascicularconnection, and therefore, atrial activation may bean important link in the tachycardia circuit. This

would cast further doubt concerning the circuits oftachycardia reported by Gallagher et al.2'

Sustained Bundle Branch Reentry as aClinical TachycardiaFrom these data and the arguments already offered,

there is little doubt that sustained BBR can be amechanism of induced tachycardia. However, onemay still argue whether these tachycardias wereclinical or simply laboratory-induced phenomena.

In eight patients, clinical tachycardias wererecorded, and the ECG appearance and rate weresimilar to the induced ones. Tracings in other patientswere either not available or showed ventricular fibril-lation, and sustained BBR was the only form of VTinduced in the laboratory. In all patients, however,the serious symptoms previously experienced by thepatient were noted during induced BBR despite thefact that patients were in the supine position and thatquick termination of tachycardia was often accom-plished. Of note, the sustained BBR tachycardiastend to be rapid and often produce serious symp-toms, can be associated with rapid hemodynamiccollapse, and can also lead to ventricular fibrillation.A 12-lead ECG of clinical VT due to BBR, therefore,is seldom recorded. Also, other arrhythmic causessuch as block in the His-Purkinje system or rapidsupraventricular tachycardia were not found toexplain the serious symptoms experienced by thesepatients.Of the 12 patients treated with drugs, eight died,

of whom six died from pump failure (Table 5). Twohad VT recurrences, and one died suddenly, pre-sumably from ventricular arrhythmias. The patientwith the longest follow-up (2,985 days) was initiallycontrolled with amiodarone, but his long-term suc-cess was due to development of spontaneous blockwithin the His-Purkinje system because amiodaronewas discontinued after 20 months. Excluding thispatient, patients treated with antiarrhythmic drugshad a follow-up of 504 ± 754 days. For a comparablefollow-up period of 414 ± 556 days in the eightpatients treated with right bundle branch ablation,there were two deaths from congestive heart failureand no recurrence of VT.

Arrhythmogenic Substrate for SustainedBundle Branch Reentry

In patients with normal intraventricular conduc-tion, BBR is a self-terminating phenomenon. On theother hand, the presence of a complete right or leftbundle branch block would not be expected topermit this type of reentry as also evidenced by itsabolition with ablation of the right bundle branch.However, conduction delay in the His-Purkinjesystem without complete block would provide anideal milieu for sustenance of BBR. It is, therefore,not surprising that all patients in this series hadprolonged HV intervals, and one patient also had anincomplete right bundle branch block. In addition tothe observed delays in the His-Purkinje system,



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some degree of intramyocardial conduction delaymay also be playing an important role in facilitatingBBR because transseptal intramyocardial conduc-tion does constitute an essential part of the circuit.This would explain why HV prolongation and non-specific intraventricular conductance delay wereobserved in nearly all of these patients. Nonethe-less, critical degree of His-Purkinje system delaysalone may be sufficient to cause sustained BBR asoccurred in one patient with aortic valve prosthesis.

In this context, it is important to note thatsustained BBR seems to be a relatively morecommon tachycardia in patients with idopathicdilated cardiomyopathy compared with patientswith atherosclerotic heart disease (i.e., 8 of 22 vs.11 of 240 patients; p < 0.001). These observationssuggest that in association with idiopathic dilatedcardiomyopathy, sustained BBR is a rather fre-quent cause of monomorphic VT (i.e., 36% of thepatients) at least in our patient population.

Summary and ConclusionsData from this series of patients indicate that sus-

tained BBR is not an uncommon mechanism of sus-tained monomorphic VT, occurring in approximately6% of the patients. It can be readily recognized by itstypical bundle branch block pattern and His activa-tion preceding the QRS with HV intervals approxi-mating those during the baseline rhythms. The typicalsubstrate appears to be abnormal His-Purkinje systemconduction manifested by prolonged HV intervalsand intramyocardial delay of conduction suggested bynonspecific intraventricular conduction delay. Theserequirements seem to be typically met in patients withdilated cardiomyopathy.Why BBR is associated primarily with dilated

cardiomyopathy is unclear. This issue obviouslyneeds further exploration, but it is quite possiblethat a combination of intramyocardial and His-Purkinje system delays are more common in dilatedcardiomyopathy compared with patients with pre-vious infarct but no cardiac dilation. In any case,the present results and analysis of previously pub-lished studies indicate that sustained BBR is animportant clinical arrhythmia in patients with dilatedcardiomyopathy. Recognition of this clinical phe-nomenon is obviously important because effectivenonpharmacologic therapy is available for thesepatients, and it would be preferable to pharmaco-logic therapy.15

This arrhythmia is most often initiated with ashort-to-long cycle length change preceding a singleextra stimulus and may not be noticed if such atechnique is not used in the pacing protocol.

Note added in proof: Since the submission of thismanuscript, three additional patients with sustainedbundle branch reentry have been diagnosed at ourinstitution. Two were treated with ablation of theright bundle, and the remaining patient was treated

AcknowledgmentsWe are grateful to Brian Miller, Jane Powell, and

Jane Wellenstein for their assistance in the prepa-ration of this manuscript.

References1. Akhtar M, Damato AN, Batsford WP, Ruskin JN, Ogunkelu

JB, Vargas G: Demonstration of reentry with the His-Purkinje system in man. Circulation 1974;50:1150

2. Zipes DP, De Joseph RL, Rothbaum DA: Unusual proper-ties of accessory pathways. Circulation 1974;49:1200

3. Akhtar M, Gilbert C, Wolf FG, Schmidt DH: Reentry withinthe His-Purkinje system: Elucidation of reentrant circuitusing right bundle branch and His bundle recordings. Circu-lation 1978;58:295

4. Reddy CP, Slack JD: Recurrent sustained ventricular tachy-cardia: Report of a case with His-bundle branches reentry asthe mechanism. Eur J Cardiol 1980;11:23

5. Welch WJ, Strasberg B, Coelho A, Rosen K: Sustainedmacroreentrant ventricular tachycardia. Am Heart J 1982;104:166

6. Lloyd EA, Zipes DP, Heger JJ, Prystowsky EN: Sustainedventricular tachycardia due to bundle branch reentry. AmHeartJ 1982;104:1095

7. Akhtar M: Electrophysiologic base for wide QRS complextachycardia. PACE 1983;6:81

8. Touboul P, Kirkorian G, Atallah G, Moleur P: Bundlebranch reentry: A possible mechanism of ventricular tachy-cardia. Circulation 1983;67:674

9. Denker S, Gilbert CJ, Lehmann MH, Mahmud R, Akhtar M:Ablation of right bundle for prevention of ventricular tachy-cardia due to sustained macro-reentry within the His-Purkinje system (abstract). Clin Res 1984;32:159A

10. Wah J, Friday K, Olson E, Khan A, Probhu S, Jackman W:Selective percutaneous catheter ablation of the right bundlebranch in patients with sustained bundle branch reentranttachycardia (abstract). JAm Coll Cardiol 1986;7:243A

11. Touboul P, Kirkorian G, Atallah G, Lavaud P, Moleur P,Lanraud M, Mathiev M: Bundle branch reentrant tachycar-dia treated by electrical ablation of the right bundle branch.JAm Coll Cardiol 1986;7:1404

12. Denker S, Lehmann M, Mahmud R, Gilbert C, Akhtar M:Facilitation of ventricular tachycardia induction with abruptchanges in ventricular cycle length. Am J Cardiol 1984;53:508

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15. Tchou P, Jazayeri M, Denker S, Dongas J, Caceres J,Akhtar M: Transcatheter electrical ablation of the rightbundle branch: A method of treating macro-reentrant ven-tricular tachycardia due to bundle branch reentry. Circula-tion 1988;78:246

16. Lehmann MH, Denker S, Mahmud R, Akhtar M: FunctionalHis-Purkinje system behavior during sudden ventricular rateacceleration in man. Circulation 1983;68:767

17. Lehmann MH, Denker S, Mahmud R, Addas A, Akhtar M:Linking: A dynamic electrophysiologic phenomenon in mac-roreentry circuits. Circulation 1985;71 :254

18. Saleem T, Akhtar M, Gilbert CJ: Bidirectional block: Acommon finding in patients with anterograde bundle branchblock. Circulation 1980;62(suppl III):III-46

19. Akhtar M, Damato AN, Ruskin JN, Ogunkelu JB, ReddyCP, Leeds CJ: Characteristics and coexistence of two formsof ventricular echo phenomena. Am Heart J 1976;92:174

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21. Gallagher JJ, Smith WM, Kasell JH, Benson DW, Sterba R,Grant AO: Role of Mahaim fibers in cardiac arrhythmias inman. Circulation 1981;64:176

22. Klein GJ, Guiraudon GM, Kerr Ch.R, Sharma AD, Yee R,Szabo T, Yeung J: The "nodoventricular" accessory path-way: Evidence for a distinct accessory atrioventricular path-way with AV node-like properties. JAm Coll Cardiol 1988;11:1035

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KEY WORDS * macroreentry * ventricular tachycardia



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J Caceres, M Jazayeri, J McKinnie, B Avitall, S T Denker, P Tchou and M AkhtarSustained bundle branch reentry as a mechanism of clinical tachycardia.

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