Long-Term Clinical Outcome of Right BundleBranch Radiofrequency Catheter Ahlation forTreatment of Bundle Branch ReentrantVentricular Tachycardia

ALI AKBAR MEHDIRAD, STEPHEN KEIM,* KEVIN RIST,**and PATRICK TCHOU+

From the Section of Cardiac Electrophysiology, Division of Cardiology, Department of Medicine,University of Pittsburgh School of Medicine, University of Pittsburgh Medical Center, Pittsburgh,the "Cardiology Associates of West Reading, Ltd., West Reading, Pennsylvania; 'The WatsonClinic, Lakeland, Florida; and ^The Cleveland Clinic Foundation, Cleveland, Ohio

MEHDIRAD, A.A., ET AL.: Long-Term Clinicat Outcome of Right Bundte Branch Radiofrequency CatheterAhtation for Treatment of Bundte Branch Reentrant Ventricutar Tachycardia. This study assessed thelong-term outcome of patients undergoing radiofrequency ablation of the right bundle for bundle branchreentrant ventricular tachycardia. Rundle branch reentrant tachycardia was diagnosed in 16 patients(ejection fraction 31% ± 15%) who underwent electrophysiology study in our laboratory. All patientshad His-Purkinje system conduction delay with mean HV interval of 68 ± 8 ms. After ablation, rightbundle branch block .developed in 15 patients. One patient developed complete heart block, which wasanticipated. One patient died of heart failure 9 months after ablation. Two patients were successfullybridged to heart transplantation 0.5 and 13 months, respectively, after ablation. Two patients receivedimplantable defibrillators for other ventricular tachycardias. One patient had syncope 11 months afterablation, but there was no evidence of ventricular tachycardia or heart block in repeat electrophysiologystudy. This patient died suddenly 29 months after ablation. The remaining nine patients were alive andwell for a mean follow-up of 19 ± 10 months. Radiofrequency ablation of the right bundle branch is aneffective therapy for treatment of bundle branch reentrant ventricular tachycardia. Survival is excellentprovided that other types of ventricular tachycardia, when present, are treated as well. This techniquemaybe helpful in management of patients who have unacceptable frequent shocks from their implanteddefibrillators and may be helpful in avoiding implantation of such a device completely in others. In somepatients with terminal heart failure and incessant ventricular tachycardia, this procedure can functionas a bridge to cardiac transplantation. (PACE 1995; 18:2135-2143)

radiofrequency ablation, bundle branch reentrant tachycardia, long-term follow-up

IntroductionCatheter ablation as a treatment of bundle

branch reentrant ventricular tachycardia was firstdescribed by Denker et al.^ and Wah et al.^ Subse-quently, Touboul et al.^ described another casewhere direct current shock ablation was used to

Address for reprints: Ali Akbar Mehdirad, M.D., The Ohio StatetJniversity Medical Center, 1654 Upham Dr., 6th Floor MeansHall, Columbus, OH 43210. Fax: (614) 293-5614.

Received August 17, 1994; accepted December 6, 1994.

ablate the right bundle branch in a patient withbundle branch reentrant ventricular tachycardia.Tchou et al.'' reported a series of seven patientstreated with this technique and established severaldiagnostic criteria for the identification of the bun-dle branch reentrant mechanism. More recently,radiofrequency has been used as a mean of accom-plishing right bundle branch ablation. Langberg etal.^ described the first reported case of radiofre-quency catheter ablation of the right bundlebranch for the treatment of this tachycardia. Cohenet al.® reported seven cases of right bundle ablationutilizing radiofrequency ablation technique. More

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MEHDIRAD, ET AL.

recently, Blanck et al.^ also included their experi-ence with this technique in a report of their overallexperience with bundle hranch reentrant tachy-cardia.

While the right hundle branch radiofrequencyablation appears to be effective in treating bundlebranch reentrant ventricular tachycardia, its long-term success in reducing arrhythmic events suchas sudden cardiac death or sustained ventriculartachyarrhythmias is unclear. A large proportion ofthese patients have depressed ventricular functionand are at risk for other types of ventriculararrhythmias as well. In this article, we describethe success and long-term outcome of patientsundergoing radiofrequency ablation of their rightbundle branch for bundle branch reentrant ven-tricular tachycardia at the University of PittsburghMedical Center.

Patients and Methods

Patient Population

Between October 1991 and April 1994,17 pa-tients undergoing electrophysiology study in ourlaboratory were identified to have inducible sus-

tained monomorphic ventricular tachycardia dueto bundle branch reentrant mechanism. Sixteen of17 underwent right bundle branch ablation andform the population of this report (1 patient choseantiarrhythmic therapy). There were 15 males and1 female with mean age of 60 ± 9 years (range43-75 years). Eight patients had undergone valvereplacement for valvular heart disease, one ofwhom also had significant coronary artery disease.Four patients had previous myocardial infarctionsand the remaining four had idiopathic dilated car-diomyopathy. All patients had coronary angiogra-phy, echocardiography, or nuclear imaging evalu-ation and the mean left ventricular ejection frac-tion was 31% ± 15% (range l l%-59%).

The clinical presentation (Table I) was syn-cope without rhythm documentation in 4, syncopewith documented sustained ventricular tachycar-dia in 4, presyncope with documented sustainedventricular tachycardia in 2, syncope or presyn-cope with documented nonsustained ventriculartachycardia in 2, cardiac arrest with documentedsustained ventricular tachycardia in 3, and cardiacarrest with no documented arrhythmias in 1 pa-tient. Two patients (patients 1 and 10) already had

Demographic

Patient No.

123456789

10111213141516

Table 1.

and Clinical Characteristics of 16 Patients with Bundle Branch Reentrant Ventricular Tachycardia

Age

56694964756764576554705461704543

Sex

MMMMMMMMMMMMFMMM

Presentation Pathology

syncope, sustained VT, multiple ICD shocks IDCMsyncopesyncope, sustained VTsyncopesyncopepresyncope, nonsustained VTsyncope, sustained VTcardiac arrest, sustained VTcardiac arrest, sustained VTcardiac arrest, multiple ICD shockssyncopepresyncope, sustained VTpresyncope, sustained VTcardiac arrest, sustained VTsyncope, nonsustained VTsyncope, sustained VT

AS, AVRIDGMCABG, MlHTN, MlAl, AVRRHD, AVR, MVRAS, AVRRHD, Al, AVRRHD, AVRAS, AVR, CABGMlIDCMCABG, MlIDCMMVR

EF

18%25%18%30%19%30%50%35%59%15%25%50%57%11%17%30%

Al = aortic insufficiency; AS = aortic stenosis; AVR = aortic valve replacement; CABG = coronary artery bypass grafting; EF = ejectionfraction; HTN = hypertension; ICD = implantable cardioverter defibrillator; IDCM = idiopathic dilated cardiomyopathy; Ml = history ofmyocardial infarction; MVR = mitral valve replacement; RHD = rheumatic heart disease; VT = ventricular tachycardia.

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LONG-TERM OUTCOME OE RIGHT BUNDLE ABLATION

implantable defibrillators at their initial evalua-tion, which were implanted at other hospitals.

Baseline Electrophysiological Studies

Electrophysiological studies and catheter ab-lations were performed utilizing standard tech-niques. Thirteen patients were taking no antiar-rhythmic medications at the time of study. In an-other patient (patient 3), amiodarone wasdiscontinued 6 months prior to ablation because

'of side effects. A second patient (patient 9) was onamiodarone for atrial flutter. The remaining pa-tient (patient 4) was taking quinidine for atrial fi-brillation. All studies were performed with the pa-tients in the fasting state, after obtaining informedconsent, and using two or three multipolar elec-trode catheters inserted through the antecubitaland femoral veins. Catheter tips were positionedin the high right atrium, across the tricuspid valvefor recording His and right bundle electrograms,and in the right ventricle. Electrical stimulationwas performed at twice diastolic threshold, utiliz-ing a digital stimulator (DTU-215, Bloom Assoc,Philadelphia, PA, USA) capable of delivering rec-tangular impulses of variable current and pulseduration. Programmed ventricular extrastimula-tion was performed during a ventricular basicdrive of 400- or 600-ms cycle length at two ventric-ular sites (right ventricular apex and right ventric-ular outflow tract) with up to five extrastimuli."Short-long-short" pacing pattern" was utilizedduring programmed stimulation if ventriculartachycardia was not inducible with constant basicdrive cycle length pacing. If ventricular tachycar-dia was not inducible, intravenous isoproterenoland/or procainamide infusion was utilized to fa-cilitate the induction. In addition to the intracar-diac electrograms, three electrocardiographicleads (I, II, and Vi) and time lines were simultane-ously displayed on a multichannel oscilloscopic(PPG, Midas, Overland Park, KS, USA) andrecorded on thermoprinter paper at 100 mm/sspeed.

Bundle branch reentrant mechanism was de-termined based on the previously published crite-ria* described briefly as follows:

1. A His or right bundle (RB) electrogram pre-ceded each QRS complex during tachycardia.

2. HH or RB-RB interval variations precededV-V variation during tachycardia.

3. Duration of the HV interval was the sameor longer during tachycardia as compared to thesinus beats.

4. The absence of consistent H or RB poten-tials between QRS complexes during ventricularpacing at the rate of ventricular tachycardia.

5. Tachycardia was terminated by sponta-neous or pacing induced His-Purkinje systemblock and was not inducible after ablation of rightbundle.

6. QRS morphology during tachycardia onsurface ECG, as well as activation sequence of in-tracardiac electrograms, was consistent with depo-larization of the ventricle via one of the hundlebranches.

Utilizing these criteria, supraventriculartachycardia with aberrancy, ventricular tachycar-dia without bundle branch reentrant mechanism,and preexcited tachycardia utilizing Mahaim fi-bers were excluded.

Right Bundle Branch Ablation

A 7 French steerable quadripolar catheterwith a large distal electrode (Mansfield Scientific,Watertown, MA, USA) was inserted through thefemoral vein and positioned at ventricular septumfor right bundle electrogram recording.^ The rightbundle potential was distinguished ftom the Hispotential by: (1) absence or minimal atrial elec-trogram on the recording; and (2) an H-RB intervalof at least 15 ms. Positioning ofthe catheter for theright bundle recording was verified in the rightanterior oblique view.

Radiofrequency energy was delivered utiliz-ing a LIZ-88 (American Cardiac Ablation Corp.,Foxboro, MA, USA). This device generates a sine-wave output at 550 kHz. The resistance, voltage,and wattage were continuously monitored. Radio-frequency current was delivered up to 65 volts be-tween the distal tip catheter electrode and a stan-dard adhesive backplate placed under the left sca-pula.

The energy was delivered during baselinerhythm, that is, sinus rhythm, atrial fibrillation, oratrial flutter. The ablation was considered success-ful when complete right bundle branch block ap-peared on the surface ECG.

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MEHDIRAD, ET AL.

Thirty minutes after successful right bundleablation, the same ventricular extrastimulationprotocols were utilized to investigate the induc-ibility of the tachycardia. In addition, decrementalas well as programmed premature atrial stimula-tion was utilized to evaluate the conduction prop-erties of the His-Purkinje system and to assess thepropensity to develop infra-Hisian block. Ante-grade His-Purkinje system conduction was also as-sessed following atropine infusion and procai-namide infusion of up to 10 mg/kg.

Patient FoUow-Up

After ablation all patients were monitored forat least 48 hours. Each patient was asked to reportto our service for any recurrence of arrhythmiasymptomatology similar to those experiencedprior to ablation. Some patients had follow-upelectrophysiology study 2-7 days after ablation. Inaddition, all patients who were discharged wereseen in our electrophysiology outpatient clinic 1week and 6 weeks after ablation. A history, physi-cal exam, and 12-lead ECG were obtained duringeach visit. The long-term follow-up of these pa-tients was achieved through phone contact to pa-tients and if necessary their referring physicians.Patients were questioned regarding occurrence ofventricular tachycardia, palpitation, functionalclass, presyncope, syncope, treatment with antiar-rhythmic drugs, hospitalization, pacemaker or de-fibrillator implantation, or heart transplantation.

Statistical Analysis

Descriptive statistics are reported as means ±standard deviations. All statistical comparisonswere performed in a pair wise fashion using theWilcoxon's matched pair test.

Results

All electrocardiographic, electrophysiologi-cal, and follow-up data are presented in Table II.

Electrocardiographic Data

At the time of electrophysiological studies,three patients had atrial fibrillation and one pa-tient had atrial flutter. Twelve patients had normalsinus rhythm with mean PR interval of 211 ± 32

ms preablation, which increased to 237 ± 36 ms(P < 0.008) after ablation. Seven of 12 patients hadfirst-degree atrioventricular block.

The QRS morphology on baseline 12-leadECG was left bundle branch block in 8 patients,intraventricular conduction delay with left bundlebranch block pattern in 6 patients, and incompleteright bundle branch block in 1 patient. The re-maining patient had normal QRS morphology butshowed Q waves consistent with old inferior myo-cardial infarction. After ablation the QRS mor-phology was right bundle branch block in 15 pa-tients. In these 15 patients, mean QRS durationwas 140 ± 24 ms (range 100-188 ms) prior to abla-tion and increased to 168 ± 13 ms (range 144-196ms; P < 0.005) after ablation. In 1 of these 15, QRSduration decreased from 160 ms preablation to 144ms after ablation. The remaining patient had nor-mal sinus rhythm with left bundle branch blockQRS morphology prior to electrophysiology study.During manipulation of His-bundle catheter priorto the delivery of radiofrequency ablation, the pa-tient developed traumatic right bundle branchblock associated with atrioventricular dissociationand intermittent 2:1 antegrade conduction throughthe left bundle branch. This traumatic right bundlebranch block resolved shortly, and the ablationprocedure was performed the following day. Afterablation she developed complete atrioventricularblock. However, with ventricular premature stim-ulation, intact retrograde conduction through theleft bundle branch was documented.

Electrophysiology Data

At baseline study all patients had prolongedHV interval with mean HV interval of 68 ± 8 ms(range 60-90 msec). Preablation, bundle branchreentrant ventricular tachycardia was induced uti-lizing constant basic drive cycle pacing followedby premature right ventricular stimulation in ninepatients and a "short-long-short" pacing patternin the remaining seven. Intravenous infusion ofprocainamide was required in two patients andisoproterenol in another one to induce ventriculartachycardia. The tachycardia had left bundlebranch block QRS morphology in all patients withmean cycle length of 266 ms (range 220-320 ms).Tachycardia was terminated by overdrive pacingin 11 patients, electrical cardioversion in 3 pa-

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LONG-TERM OUTCOME OF RICHT BUNDLE ABLATION

Table II.

Electrocardiographic, Electrophysiological, and Follow-Up Data of 16 Patients with Bundle BranchReentrant Ventricular Tachycardia

Patient

1

2

3

4

5

6

7

8

9

10

11

12

13

14

15

16

ECG Findings

Pre-Ablation

NSR, NLaxis, LBBB

NSR, 1AVB,ICRBBB,

AFib, LAD,LBBB

NSR, NLaxis, IMI,LVH

NSR, 1AVB, LAD,LBBBpattern

AFib, LAD,LVH, LBBB

NSR, 1AVB, NLaxis, LBBB

NSR, 1AVB, NLaxis, LBBB

AFIutter, NLaxis, LBBB

AFib, NLaxis, LBBB

NSR, 1AVB, NLaxis, LBBBpattern

NSR, NLaxis, LBBB

NSR, NLaxis, LBBB

NSR, 1AVB, LAD,LBBB

NSR, NLaxis, LBBBpattern

NSR, NLaxis, LVH,LBBBpattern

Post-Abiation

NSR, 1 AVB,RBBB,LPHB

NSR, 1 AVB,RBBB,LAHB

ATach, RBBB,LAHB

NSR, 1 AVB,NL axis.RBBB

NSR, RBBB,LAHB

NSR, RBBB,LAHB, LVH

NSR, 1 AVB,NL axis.RBBB

NSR, 1 AVB,RBBB,LAHB

AFib, RBBB,LAHB

AFib, RBBB,LAHB

NSR, RBBB,LAHB

NSR, 1 AVB,RBBB,LAHB

CHB

NSR, 1 AVB,RBBB,LAHB

NSR, RBBB,extremeLAD

NSR, RBBB,RAD

QRS Duration (ms)

Pre-Abiation

172

116

164

100

140

128

150

120

164

188

124

124

144

160

112

130

Post-Abiation

176

160

168

152

172

164

160

156

168

196

152

184

—

144

160

184

PR Intervai (ms)

Pre-Abiation

192

248

196

284

—

240

216

—

—

204

188

192

208

156

204

Post-Abiation

220

264

208

288

—

250

226

—

—

232

230

—

308

180

204

HV intervai (ms)

Pre-Abiation

70

60

60

75

70

70

70

70

60

60

90

60

70

60

75

65

Post-Abiation

100

80

100

80

95

80

130

80

90

90

105

80

—

105

80

75

QRSiUorpiioiogyof BBRVT

LBBB, NLaxis

LBBB, LAD

LBBB, RAD

LBBB, U D

LBBB, LAD

LBBB, LAD

LBBB, NLaxis

LBBB, NLaxis

LBBB, LAD

LBBB, NLaxis

LBBB, LAD

LBBB, LAD

LBBB, NLaxis

LBBB, LAD

LBBB, LAD

LBBB, NLaxis

Long-TermFoiiow-Up

NBBRVT, transplant13 months afterRFA

A& W

Transplant 0.5months after RFA

NBBRVT, iCD 1week after RFA

syncope 11 monthsafter-RFA,negative EPstudy

A& W

VVI pacer, died ofCHF 9 monthsafter RFA

A& W

A& W

A& W

A& W

A& W

DDD pacer, A & W

AS W

NBBRVT & awaitsheart transpianf

A& W

Foiiow-Up

(months)

32

32

32

31

29

29

9

25

24

23

22

19

18

16

2

2

A & W = alive and well; AFib = atrial fibrillation; ATach = atrial tachycardia; 1 AVB = first-degree atrioventricular block; BBRVT = bundle branch reentrant ventricular tachycardia; CHB= complete heart block; CHF = congestive heart failure; ICD = implantable cardioverter defibrillator; ICRBBB = incomplete right bundle branch block; IMI = inferior myocardial infarction;LAD = left axis deviation; LAHB = left anterior hemiblock; LBBB = left bundle branch block; LAHB = left anterior hemiblock; LPHB = left posterior hemiblock; LVH = left ventricularhypertrophy; NBBRVT = non bundle branch reentrant ventricular tachycardia; NBBRVT = non bundle branch reentrant ventricular tachycardia; NL axis; = normal axis; NSR = normal sinusrhythm; RAD = right axis deviation; RBBB = right bundle branch block; RFA = radiofrequency ablation.

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tients, and self-terminated in the remaining 2 pa-tients. In addition, three patients had inducihleventricular tachycardia of right hundle hranchhlock QRS morphology, which did not have hun-dle hranch reentrant mechanism.

Ablation

Radiofrequency catheter ahlation of the rightbundle produced complete right hundle branchblock in all patients. The mean number of deliv-ered radiofrequency pulses was 2.4 (range 1-14pulses) with mean duration of 58 ± 5 seconds(range 40-60 s) and mean voltage of 55 ± 5 volts(range 50-65 V).

The mean HV interval prolonged from 68 ±8 ms (range 60-90 ms) preablation to 91 ± 15 ms(range 75-130 ms; P < 0.002) after ablation in 15patients. The remaining patient had left hundlebranch block with QRS duration of 144 ms and HVinterval of 70 ms prior to ablation. After deliveryof radiofrequency energy, the patient developedcomplete heart hlock. She underwent a dual cham-ber pacemaker implant 1 hour after the ahlation.

In one patient HV interval prior to ahlationwas 70 ms and increased to 130 ms after ahlation.After infusion of 300 mg of procainamide, it in-creased to 180 ms. Despite this long HV interval,there was no evidence of infra-Hisian hlock withdecremental atrial pacing. Because of significantHV prolongation after ahlation and the responseto intravenous procainamide, the patient under-went a ventricular pacemaker implantation on aprophylactic basis. Fourteen patients underwentrepeat atrial and ventricular stimulation studies 30minutes after radiofrequency ahlation. There wasno evidence of conduction hlock helow His or in-ducihle hundle hranch reentrant ventricular tachy-cardia. In addition, five patients underwent repeatelectrophysiology study 2-7 days after radiofre-quency ahlation. In these studies there was no evi-dence of hlock helow His or inducihle ventriculartachycardia with hundle branch reentrant mecha-nism.

Long-Term Clinical FoUow-Up

These 16 patients were followed for a meanduration of 22 ± 10 months (range 2-32 months).One patient, the one who had undergone prophy-lactic ventricular pacemaker implantation after ra-

diofrequency ahlation, died secondary to progres-sive heart failure 9 months after the ablation with-out any recurrent ventricular arrhythmia. Theremaining 15 patients were followed for 22 ± 10months (range 2-32 months). One patient experi-enced an episode of syncope 11 months after ra-diofrequency ahlation. He underwent repeat elec-trophysiology study hut there was no evidence ofheart hlock or inducible ventricular tachycardia.His syncopal episode was attributed to overzeal-ous doses of vasodilators. These were reduced andhe remained asymptomatic for a follow-up of 14months since the repeat electrophysiology study.At this time, he developed episodes of recurrentheadaches with unknown etiology. This patientdied suddenly 4 months later, 29 months after ah-lation. One patient who had incessant ventriculartachycardia prior to ahlation remained arrhyth-mia-free and underwent heart transplantation 15days after radiofrequency ahlation of the right bun-dle branch. He was alive and well following trans-plant at a follow-up of 32 months. One patient hadmultiple implantable defibrillator discharges 1year after radiofrequency ahlation. His defibrilla-tor was implanted 3 years before the ablation. Atthat time, he had multiple episodes of clinical sus-tained ventricular tachycardia that did not re-spond to drug therapy. Two years following im-plantation, he had frequent shocks, which necessi-tated treatment with amiodarone. Seven monthsafter starting amiodarone treatment, this drug hadto he discontinued due to side effects. Six monthslater, he again experienced multiple shocks forwhich he underwent repeat electrophysiologystudy and right bundle ablation. He remainedasymptomatic for 11 months following the ahla-tion. At this time, however, he again presentedwith multiple shocks. This time, he had a nonhun-dle branch reentrant ventricular tachycardia,which had not heen seen previously. He was re-started on amiodarone and metoprolol. A monthlater he underwent heart transplantation hecauseof progressive congestive heart failure. At the timeof this report, he is alive and well 18.5 monthsafter transplant for a total follow-up since the ahla-tion of 32 months.

Another patient had a defibrillator implanted3 years prior to the ahlation procedure. Before theahlation, he was receiving frequent shocks fromhis device due to ventricular tachycardia. At elec-

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LONG-TERM OUTCOME OF RIGHT BUNDLE ABLATION

trophysiology study, he was found to have a bun-dle branch reentrant tachycardia for which heunderwent right bundle ablation. After ablationhe has received only occasional shocks and hasnot required antiarrhythmic therapy. Fourteenmonths after ablation, he was admitted withcongestive heart failure and was found to haveatrial fibrillation with slow ventricular responseof 60 beats/min. He underwent a single chamberpacemaker implantation to increase his cardiacoutput. He presented with progressive heart fail-ure 4 months later and is currently awaiting hearttransplantation 23 months after ablation.

Another patient had a sustained ventriculartachycardia induced at the follow-up electrophysi-ology study after right bundle ablation. This tachy-cardia did not have a bundle branch reentrantmechanism and its induction was not suppressedwith antiarrhythmic drugs. He underwent defibril-lator implantation 1 week after radiofrequency ab-lation. Twenty-six months after implant, he re-ceived the first shock from his defibrillator for arapid tachycardia with a rate of 200 beats/min.This data was derived from the memory of the defi-brillator, which could store only the cycle lengthsof the tachycardia prior to shock delivery. One pa-tient had episodes of sustained polymorphic ven-tricular tachycardia approximately 1 month afterablation and is currently awaiting heart transplan-tation 2 months after radiofrequency ablation.

The remaining nine patients have not receivedantiarrhythmic therapy for ventricular tachycardiaand have not had recurrent syncope, presyncope,or documented ventricular tachyarrhythmias for amean follow-up period of 19 ± 10 months (range2-32 months).

Discussion

Single bundle branch reentrant beats (the V3phenomenon) elicited with right ventricular pre-mature stimulation in the human heart was firstdescribed by Akhtar et al. '̂̂ ° Bundle branch reen-try can also be a potential mechanism for sustainedventricular tachycardia in patients with conduc-tion delay within the His-Purkinje system usuallyassociated with structural heart disease. Reddy etal.̂ ^ and Touboul et al.^^ reported cases of sus-tained bundle branch reentrant ventricular tachy-cardia. Caceres et al.^^ reported that 6% of all in-

duced sustained monomorphic ventricular tachy-cardia, in their laboratory, was due to bundlebranch reentrant mechanism. From the same labo-ratory, Tchou et al.̂ "* reported that bundle branchreentry was the mechanism in 40% of induced sus-tained monomorphic ventricular tachycardia inpatients with idiopathic dilated cardiomyopathy.

Direct current catheter ablation was the initialreported approach to right bundle ablation.^-^However, because of concerns with potential com-plications, radiofrequency ablation has becomethe preferred approach. The first case of radiofre-quency catheter ablation of the right bundle wasreported by Langberg et al.^ in 1989. Since then,two different groups^'' have reported their experi-ence with radiofrequency catheter ablation of theright bundle. In the study by Cohen et al.,^ sevenpatients underwent radiofrequency ablation of theright bundle. They had no recurrence of tachycar-dia in their follow-up period of 12 months. Onepatient died of congestive heart failure and uremia29 months after ablation. One patient died of sep-sis 3 months after ablation. Two patients alreadyhad pacemakers before ablation. In the study byBlanck et al.,'' radiofrequency was utilized in 11of 28 patients who underwent catheter ablation ofthe right bundle for sustained bundle branch reen-trant tachycardia. However, a separate follow-upduration on these 11 patients was not available intheir report.

In those two reports, as well as ours, the suc-cess rate of radiofrequency ablation of the rightbundle was 100%. In spite of this success rate andlow incidence of short-term complications, thelong-term outcome of these patients has been ofmajor concern. In fact, the majority of these pa-tients have poor left ventricular function and NewYork Heart Association Class III-IV symptomatol-ogy. Therefore, the long-term efficacy of the rightbundle ablation in improving event-free survivalin this patient population has been questioned.

In the 16 patients reported here, the only im-mediate complication was complete heart block inone patient (1/16 patients). This was an antici-pated complication as complete antegrade leftbundle branch block was documented at the elec-trophysiology study before the ablation. Perhapsin this patient, left bundle branch ablation couldhave been attempted. However, in the absence of aleft bundle potential (no anterograde conduction)

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localization of left bundle by fluoroscopic guid-ance and delivery of radiofrequency energy couldhave been problematic. Another patient developedsignificant HV prolongation and underwent per-manent pacemaker implantation on a prophylacticbasis. This low incidence of complications is con-sistent with previous reports. Given the significantleft ventricular dysfunction of this group of pa-tients, their survival was quite good.

Fourteen of 16 patients were alive and well ata mean follow-up of 22 ± 10 (range 2-32 months).One patient died suddenly 29 months after abla-tion. There was no autopsy performed. Anotherpatient died at 9-months follow-up due to progres-sive heart failure. In two patients right bundle ab-lation played an important role in their clinicalmanagement so as to bridge them to heart trans-plantation. With a mean follow-up of 22 ± 10months, there was only one heart failure death andone sudden death. Given the poor cardiac functionof this population, this outcome is quite favorable.

Four of 16 patients (25%) also had ventriculartachycardia of a mechanism other than bundlebranch reentry (sustained monomorphic ventricu-lar tachycardia induced in electrophysiology labo-ratory in 3 patients and clinical sustained poly-morphic ventricular tachycardia in another 1).Therefore, elimination of bundle branch reentryclearly does not prevent other types of tachycar-dia. Gonversely, all stimulation protocols that fa-cilitate the induction of bundle branch reentrantventricular tachycardia should be utilized duringan electrophysiological study even though othermechanisms of ventricular tachycardia have beenidentified. Our experience with these four patientssuggests that follow-up electrophysiology studiesare important in patients after ablation to assessfor the presence of ventricular tachycardias withmechanisms other than bundle branch reentry.Where these tachycardia are present, the implanta-ble defibrillator can be an important additionaltherapy. Similarly, catheter ablation may be a use-ful additional therapy in patients who alreadyhave an implantable defibrillator. When such a pa-tient experiences excessively frequent device dis-charges, the ablation of a demonstrable bundlebranch reentrant tachycardia could readily allowcontrol of frequent shocks without the need forantiarrhythmic drug administration. In the threepatients who had implantable defibrillators, two

had the implantation prior to right bundle abla-tion. The ablation was performed to prevent fre-quent device discharges triggered by clinical bun-dle branch reentrant tachycardias. The third pa-tient received a device due to persistence of aninducible ventricular tachycardia (nonbundlebranch reentrant) after bundle branch ablationeven though his clinical tachycardia was the bun-dle branch reentrant one. Indeed, 26 months afterthe implant, he received a shock for a rapid tachy-cardia with a rate of approximately 200 beats/min.Persistence of right bundle branch block on hissurface EGG made it highly unlikely that the tachy-cardia was bundle branch reentry.

The QRS morphology of the induced bundlebranch reentrant ventricular tachycardia in all ofour patients showed a left bundle branch blockpattern. In those that had clinical tachycardiasdocumented, the QRS morphology was the same.These findings are consistent with other reports^'^and suggest that retrograde conduction via the leftbundle branch and antegrade conduction via theright bundle branch may be the preferred reentrantpathway for a diseased His-Purkinje system. Sucha reentrant pathway is also seen in a large majorityof bundle branch reentrant beats elicited in thenormal human heart with right ventricular apexpremature stimulation.^-^" Recent findings in thenormal human heart suggest that even with leftventricular extrastimulation, the preferred retro-grade route of reentry is via the left bundlebranch." If this finding could be extrapolated tothe abnormal His-Purkinje system, it could explainwhy left bundle branch block pattern is the pre-dominant QRS morphology of bundle branch reen-trant ventricular tachycardia.

Four of the patients reported here had rela-tively normal left ventricular systolic functionwith left ventricular ejection fractions of 50% orbetter. Two of these patients had valvular disease.One underwent aortic valve replacement and theother, mitral valve replacement. The third patienthad an inferior wall myocardial infarction, but leftventricular function was well preserved. The lastpatient had a history of a mild dilated cardiomyop-athy (left ventricular ejection fraction of 47%) pre-sumably due to excessive alcohol consumption.One and a half years after cessation of alcohol in-take, her left ventricular ejection fraction was 57%with no wall-motion abnormalities. However, all

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LONG-TERM OUTCOME OF RIGHT BUNDLE ABLATION

four of these patients had His-Purkinje system con-duction delay.

Gonsistent with previous reports, this reportindicates that ventricular tachycardia with bundlebranch reentrant mechanism can be seen in a vari-ety of pathological states as in ischemic, rheu-matic, or valvular cardiomyopathy and is not lim-ited to idiopathic dilated cardiomyopathy. Thistachycardia can even be seen in patients with nor-mal ventricular function but who have abnormalHis-Purkinje system conduction.^®

Although less common than ventriculartachycardia associated with ischemic scarring,this mechanism should always be considered dur-ing electrophysiological studies. Techniques thatfacilitate induction of this arrhythmia including"short-long-short" pacing pattern, intravenous in-fusion of isoproterenol and/or procainamide, andeven left ventricular pacing if clinical ground sug-

References

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2. Wah J, Friday K, Olson E, et al. Selective percutane-ous catheter ablation of the right bundle branch inpatients with sustained bundle branch reentranttachycardia, (abstract) J Am Coll Cardiol 1986; 7:243A.

3. Touboul P, Kirkorian G, Atallah G, et al. Bundlebranch reentrant tachycardia treated by electricalablation ofthe right bundle branch. J Am Goll Gar-diol 1986; 7:1404-1409.

4. Tchou P, Jazayeri M, Denker S, et al. Transcatheterelectrical ablation of the right bundle branch: Amethod of treating macro-reentrant ventriculartachycardia due to bundle branch reentry. Gircula-tion 1988; 78:246-257.

5. Langberg JJ, Desai J, Dullet N, et al. Treatment ofmacroreentrant ventricular tachycardia with ra-diofrequency ablation of the right bundle branch.J Am Goll Gardiol 1989; 63:1010-1013.

6. Gohen TJ, Ghien WW, Lurie KG, et al. Radiofre-quency catheter ablation for treatment of bundlebranch reentrant ventricular tachycardia: Resultsand long-term follow-up. J Am Coll Cardiol 1991;7:1767-1773.

7. Blanck Z, Dhala A, Deshpande S, et al. Bundlebranch reentrant ventricular tachycardia: Cumula-tive experience in 48 patients. J Cardiol Elec-trophysiol 1993; 4:253-262.

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gests this arrhythmia should be considered. Re-gardless of etiology, patients with His-Purkinjesystem conduction delay appear to be predisposedto have clinical or induced sustained bundlebranch reentrant ventricular tachycardia.

Summary

Our data suggest that radiofrequency ablationof tbe right bundle for treatment of bundle branchreentrant tachycardia can play an important role inthe management of patients with this arrhythmia.The ablation can cure this arrhythmia. In addition,this technique can reduce the frequency of tachy-arrhythmic episodes even in patients who haveother types of ventricular tachycardia.

Acknowledgment: The authors would like to thank MimiRanallo for preparation of this manuscript.

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