Journal of Interventional Cardiac Electrophysiology 10, 255–259, 2004C© 2004 Kluwer Academic Publishers. Manufactured in The Netherlands.

Case Report

Bundle Branch Reentrant Tachycardia in a Patientwith Normal Ventricular Function

Simon P. Fynn and Jonathan M. KalmanThe Royal Melbourne Hospital Department of Cardiologyand Department of Medicine,University of Melbourne,Royal Parade, Parkville, Victoria 3050, Australia

Abstract. We report an unusual case of bundle branchreentrant tachycardia, in a patient with normal leftventricular function, cured by radiofrequency catheterablation. However, the long-term prognosis of thesepatients is uncertain. We discuss the indications for animplantable defibrillator in this group.

Key Words. bundle branch reentrant tachycardia, im-plantable defibrillator

Introduction

Bundle branch reentrant tachycardia (BBRT) isan uncommon form of ventricular tachycardia(VT), accounting for approximately 6% of sus-tained monomorphic VTs [1,2]. This type of VTis typically associated with significant left ven-tricular dysfunction and conduction system dis-ease [3,4], although on rare occasions, patientswith normal ventricular function [5] and appar-ently normal cardiac conduction [6] can presentwith this arrhythmia. BBRT is amenable to ra-diofrequency ablation and this approach has beenshown to be curative [5]. We report an unusualcase of BBRT in a patient with aortic valve dis-ease and a hypertrophied left ventricle with nor-mal systolic function, who had both right bundlebranch block (RBBB) and left bundle branch block(LBBB) tachycardia morphologies.

Case

A 30 yr. old man presented to the emergency de-partment with a broad complex tachycardia witha RBBB morphology and right axis deviation, anda ventricular rate of 200 bpm (Fig. 1A). There wasevidence on the electrocardiogram (ECG) of disso-ciated P waves. He was hypotensive with the ar-rhythmia and required DC cardioversion. A subse-quent ECG revealed sinus rhythm with a normalPR interval and QRS morphology consistent withcomplete RBBB (QRS duration 162 ms) (Fig. 1B).All biochemical markers of myocardial ischaemia,

and electrolytes, were within normal limits. Sub-sequent transthoracic echocardiogram showed abicuspid aortic valve, with a mean transvalvu-lar gradient of 25 mmHg, and aortic regurgita-tion of a moderate severity. The aortic valve andring showed unusually heavy calcification. The leftventricle was mildly concentrically hypertrophied(1.3 cm) but of normal size and function. The pa-tient was admitted to hospital for continuous am-bulatory ECG monitoring. Over the course of thefollowing few days, whilst monitored in the Coro-nary Care Unit, he experienced frequent episodesof broad complex tachycardia with multiple sus-tained and non-sustained episodes occurring daily.Twelve lead ECG’s of these tachycardias revealed2 differing morphologies. One of these had thesame morphology as the initial tachycardia whilstthe other tachycardia was broad complex withLBBB morphology and left axis deviation. How-ever, the rates of each tachycardia were very simi-lar (Fig. 2). The RBBB morphology was induced byatrial premature beats and the LBBB morphologyby ventricular ectopic beats.

At electrophysiologic (EP) study all baseline in-tervals were within normal limits, specifically theHV interval was 50 ms. Atrial premature stimu-lation and overdrive pacing were performed andshowed no evidence of pre-excitation. Followingstimulation from the right atrium (both with andwithout isoproterenol infusion), only brief, non-sustained episodes of a RBBB tachycardia wereinduced. No reliable His recording was discernibleduring this tachycardia, which showed VA dis-sociation strongly suggestive of VT (Fig. 3A).Due to the non-sustained nature of this rhythm,no further diagnostic maneuvers were possible.

Address for correspondence: Dr. Simon P. Fynn, MD, Dept. ofCardiology, The Royal Melbourne Hospital, Parkville, Victoria3050, Australia. E-mail: simon.fynn@mh.org.au

Received 16 October 2003; accepted 24 November 2003

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Fig. 1. (A) Twelve lead electrocardiogam of the presenting broad complex tachycardia. There is a right bundle branch blockmorphology (RBBB) with right axis deviation, and a ventricular rate of 200 bpm. (B) After DC cardioversion, the patient reverted tosinus rhythm with complete RBBB morphology. Paper speed 25 mm/sec.

Fig. 2. Twelve lead electrocardiograms of the broad complex tachycardias recorded during monitoring. (A) There is a right bundlebranch block morphology with right axis deviation and a rate of approximately 165 bpm. (B) Further monitoring revealed anadditional tachycardia with left bundle branch block morphology, left axis deviation and a similar rate of 165 bpm. Paper speed 25mm/sec.

Fig. 3. (A) During electrophysiological (EP) study, a non-sustained broad complex tachycardia of right bundle branch blockmorphology was initiated with programmed ventricular stimulation. This had the same morphologic characteristics as thepresenting arrhythmia. There is no discernible His potential on the His catheter. The VA dissociation is suggestive of VT. Paperspeed 100 mm/sec. (B) A left bundle branch block tachycardia was also induced by ventricular stimulation during EP study. Paperspeed 200 mm/sec. A right bundle (RB) potential can be seen immediately preceding each ventricular electrogram in the RVchannel. The spontaneous variation in ventricle-to-ventricle intervals (upper row of numbers) are preceded by identical changes inthe RB-RB intervals (lower row of numbers), suggestive of BBRT. Subsequent ablation at the site of the RB potential rendered bothmorphologies of tachycardia non-inducible. HBE denotes His bundle electrogram, CS denotes coronary sinus, RV denotes rightventricle. All intervals are in ms.

Bundle Branch Reentrant Tachycardia in a Patient with Normal Ventricular Function 257

However, with stimulation from the right ventric-ular apex, a sustained LBBB morphology tachy-cardia was easily and reproducibly inducible andwas identical to one of the clinical arrhythmias(Fig. 3B). During this tachycardia, a right bundle(RB) potential was recorded preceding every QRScomplex, with changes in RB-RB interval preced-ing those changes in V-V interval. A diagnosis ofBBRT was made based on previously publishedcriteria [1–4]. Unsuccessful attempts were madeto induce the RBBB morphology tachycardia bystimulation of the left ventricle via a coronary si-nus branch vein. The aortic valve was not crosseddue to marked calcification.

This patient underwent a successful ablationof the right bundle branch (RBB) after which, us-ing a standard programmed stimulation protocolwith up to 4 extra-stimuli at 2 sites and 2 cyclelengths, no further tachycardia was inducible. TheHV interval pre and post ablation of the RBB wasidentical (50 msec). During in-patient monitoringover the following week the patient experiencedno further episodes of either morphology of VT. Apre-discharge maximal exercise test did not pro-voke a recurrent arrhythmia. There were no fur-ther episodes of either tachycardia over a 1 monthfollow-up period, the patient previously having nu-merous daily episodes. Following the procedurethe option of an implantable cardiac defibrillator(ICD) was discussed with the patient. However, inthe absence of definitive data, he decided againstundergoing implantation of the device.

Discussion

This case report highlights the occurrence ofBBRT in the presence of normal ventricular sys-tolic function and with an HV interval at the up-per limit of normal. The patient had both reentrygoing down the RBB and up the LBB (LBBB mor-phology) and probably the reverse circuit; downthe LBB and back up the RBB (RBBB morphol-ogy). While the latter circuit was not proven atEP study, it remains highly likely in the clinicalcontext. Although the patient was cured of bothtachycardias by ablation of the RBB, uncertaintyexists as to whether patients with normal left ven-tricular function and BBRT should also undergoimplantation of an ICD.

Presentation of BBRT

Previous reports have shown that BBRT, althougha relatively rare form of VT, is typically asso-ciated with poor left ventricular function and ahistory of congestive cardiac failure. Such pa-tients often have a dilated cardiomyopathy of ei-ther unknown aetiology or secondary to signifi-

cant coronary artery disease [1,3,4]. Specifically inthe group with the former, BBRT may account forup to 40% of all inducible monomorphic VT’s [2].BBRT has also been shown to be associated withsignificant valvular disease, both with [3,7,8], andwithout [8], concomitant ventricular dysfunction.In the current case, we presume that calcifica-tion invading the proximal bundle branches fromthe aortic ring created the substrate for bundlebranch reentry. Although the patient presentedhere had normal ventricular function, the valvu-lar pathology may, in time, have resulted in a car-diomyopathy as seen in the majority of patientswho present with this arrhythmia. There have alsobeen reports of cases of BBRT in patients withoutventricular dysfunction or valvular disease, whoseonly underlying substrate for this arrhythmia is asignificant abnormality of the His-Purkinje Sys-tem (HPS) [5]. Indeed, baseline HV prolongationhas previously been thought to be necessary forthe development of sustained BBRT [1,2,4]. How-ever, it is becoming increasingly recognised thatthis is not the case. In a recent review of 13 pa-tients with BBRT [6], 6 patients were found tohave an HV ≤ 55 ms during sinus rhythm. In thisreview, significant prolongation of the HV intervalin these 6 patients only developed during tachy-cardia suggesting functional, rather than fixed,conduction block in the HPS. Interestingly, only1 of this group of 6 had QRS duration >120 ms insinus rhythm. Our case reported here is of note inthat, in the setting of a resting ECG showing anapparent complete RBBB (QRS duration 162 ms),there was the subsequent development of BBRTwith a LBBB morphology. Indeed, although thiscombination has been recognised as being theoret-ically possible (ie. RBBB in sinus rhythm, LBBBmorphology BBRT), there are few reported casesof this in the literature [9,10].

Diagnosis of BBRT

Our patient had BBRT with LBBB morphologyand a VT with RBBB morphology. The latter wasnon-sustained at EP study and therefore no formaldiagnosis of its mechanism was possible. Whilstalternative explanations for the tachycardia withRBBB and right axis deviation might include reen-try originating in the left anterior fascicle of theHPS [11], a myocardial VT [12], or a VT from afocal origin in the left ventricular outflow tract orcoronary cusp [13], these possibilities would seemless likely than a “reverse” BBRT. Prior to the ab-lation, the rates of the 2 morphologies of the tachy-cardia, when they occurred one following the other,were similar. Furthermore, following the ablationof the RBB, neither tachycardia was inducibleor observed clinically. This was in the context

258 Fynn and Kalman

of multiple daily paroxysms prior to the ablationprocedure. Therefore, it would seem likely thatboth tachycardias utilised the right bundle branchas part of the circuit.

Management of Patients with BBRT

The management of patients with BBRT presentsa specific problem. Although this arrhythmia iscurable by catheter ablation, there is a recog-nised association between BBRT and myocardialVT, with between 6% and 30% of patients withBBRT having the latter [2,6,8]. Although there areno guidelines, implantation of an ICD would ap-pear appropriate in patients who have other in-ducible VT’s. An ICD is also probably warrantedin patients without other inducible VT’s who havesignificant left ventricular dysfunction [14]. How-ever, the management of those patients with noinducible VT post ablation and normal left ven-tricular function (such as our patient) is difficult.BBRT is rare in patients with normal ventricu-lar function and consequently there have been nostudies that have systematically addressed this is-sue. The only available data on the prognosis ofpatients with BBRT come from published retro-spective analyses and case reports, in which themajority of patients had significant ventriculardysfunction.

In the largest series of patients with BBRT,Blanck et al. [5] reported on 48 patients, only 3of whom had normal left ventricular function. Inthis series, the only patients to receive an ICDwere those with documented myocardial VT in ad-dition to BBRT. The outcome of those patients withnormal ventricular function is not clear althoughduring a follow-up over a mean of 16 months,there were 10 deaths in the group who under-went catheter ablation only. Seven of these weresecondary to cardiac failure, 2 due to non-cardiaccauses and one patient died suddenly. Mehdiradet al. [10] reported on 16 patients who underwentright bundle ablation for BBRT, and who were fol-lowed up over 22 ± 10 months. Four of this grouphad normal left ventricular systolic function, and2 of these had valvular disease (as in our patient).All 4 of these patients remained alive and well atthe end of the follow up period, with no recurrenceof VT of any nature. The authors suggested thatright bundle ablation may have a role in avoidingthe implantation of an ICD in this patient group.

Narasimhan et al. [8] reported on a group of9 patients with BBRT and no other inducible VTfollowing valvular surgery. Eight were treated bycatheter ablation of the right bundle branch and1 received an ICD. Four of the group had normalventricular function and were alive and well at amean follow up of 30 ± 29 months. Two of the re-

maining 5 patients (all with poor left ventricularfunction) died during this time from progressivecardiac failure. In the other studies that have re-ported on ablation of BBRT, all patients had ab-normal left ventricular function [3,4].

Conclusion

BBRT is curable by catheter ablation. We presentan unusual case of 2 different morphology tachy-cardias in a patient with normal ventricular func-tion and an HV interval within normal limits. Bothtachycardias (BBRT proven for only one) were suc-cessfully eliminated by ablation of the right bun-dle branch. In those patients who have a myocar-dial VT, in addition to BBRT, or in whom thereis significant left ventricular dysfunction, the im-plantation of an ICD would appear to be war-ranted. However, the further management of apatient with normal ventricular function and noother inducible VT is difficult. The little data avail-able in the published literature would suggest thatthese patients do not require prophylactic ICD im-plantation. However, as it is unlikely that ran-domised, controlled trials will ever be conducted,such cases will continue to present both physicianand patient with a difficult choice.

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