Is the Fascicle of Left Bundle Branch Involvedin the Reentrant Circuit of Verapamil-SensitiveIdiopathic Left Ventricular Tachycardia?JEN-YUAN KUO,* CHING-TAI TAI,† CHERN-EN CHIANG,† WEN-CHUNG YU,†JIN-LONG HUANG,§ MING-HSIUNG HSIEH,‡ CHARLES JIA-YIN HOU,*CHENG-HO TSAI,* YU-AN DING,† and SHIH-ANN CHEN†From the *Division of Cardiology, Department of Medicine, Mackay Memorial Hospital, Taipei Medical University,Taipei, †Division of Cardiology, Department of Medicine, National Yang-Ming University, School of Medicine, AndVeterans General Hospital-Taipei, Taipei, ‡Division of Cardiology, Department of Medicine, Wan-Fang Hospital,Taipei Medical University, Taipei, and the §Division of Cardiology, Department of Medicine, Veterans GeneralHospital-Taichung, Taichung, Taiwan

KUO, J.-Y., ET AL.: Is the Fascicle of Left Bundle Branch Involved in the Reentrant Circuit of Verapamil-Sensitive Idiopathic Left Ventricular Tachycardia? The exact reentrant circuit of the verapamil-sensitiveidiopathic left VT with a RBBB configuration remains unclear. Furthermore, if the fascicle of left bundlebranch is involved in the reentrant circuit has not been well studied. Forty-nine patients with verapamil-sensitive idiopathic left VT underwent electrophysiological study and RF catheter ablation. Group I in-cluded 11 patients (10 men, 1 woman; mean age 25 ± 8 years) with left anterior fascicular block (4 patients),or left posterior fascicular block (7 patients) during sinus rhythm. Group II included 38 patients (29 men,9 women; mean age 35 ± 16 years) without fascicular block during sinus rhythm. Duration of QRS com-plex during sinus rhythm before RF catheter ablation in group I patients was significant longer than thatof group II patients (104 ± 12 vs 95 ± 11 ms, respectively, P = 0.02). Duration of QRS complex duringVT was similar between group I and group II patients (141 ± 13 vs 140 ± 14 ms, respectively, P = 0.78).Transitional zones of QRS complexes in the precordial leads during VT were similar between group I andgroup II patients. After ablation, the QRS duration did not prolong in group I or group II patients (104 ±11 vs 95 ± 10 ms, P = 0.02); fascicular block did not occur in group II patients. Duration and transitionalzone of QRS complex during VT were similar between the two groups, and new fascicular block did notoccur after ablation. These findings suggest the fascicle of left bundle branch may be not involved in theantegrade limb of reentry circuit in idiopathic left VT. (PACE 2003; 26:1986–1992)

ventricular tachycardia, electrophysiology, ablation

IntroductionVerapamil-sensitive idiopathic left ventricu-

lar tachycardia (VT) with a right bundle branchblock (RBBB) configuration and left-axis devia-tion occurs predominantly in young male patientswithout structural heart disease. This VT wasdemonstrated to be due to reentry with an excitablegap and a slow conduction area. Radiofrequency(RF) ablation of idiopathic left VT can be guided bypacemapping, earliest presystolic Purkinje poten-tial (PP), or a diastolic potential (DP) during idio-pathic left VT.1−10 However, the exact reentrant cir-cuit of the verapamil-sensitive idiopathic left VTwith a RBBB configuration remains unclear. Fur-thermore, if the fascicle of the left bundle branchis involved in the reentrant circuit has not beenwell studied. If the left fascicles were involved in

Address for reprints: Shih-Ann Chen, M.D., Div. of Cardiol-ogy, Veterans General Hospital-Taipei, 201, Sec. 2, Shih-PaiRoad, Taipei, Taiwan. Fax: 886-2-2873-5656; e-mail: epsachen@ms41.hinet.net

Received November 12, 2002; revised January 10, 2003; ac-cepted January 15, 2002.

the antegrade limb of reentry circuit, the durationof the QRS complex during sinus rhythm wouldbe prolonged, and the new fascicular block wouldoccur after the successful ablation. The aim of thisstudy was to compare the duration of the QRS com-plex before and after RF catheter ablation betweenpatients with and without a left hemiblock in sinusrhythm.

Patients and MethodsPatient Characteristics

Between July 1992 and September 2001,48 patients who had symptomatic monomorphicVT without recognizable structural heart diseasewere referred for electrophysiological study andRF ablation. Group I included 11 patients (10 men,1 woman; mean age 25 ± 8 years) with left anteriorfascicular block (4 patients) or left posterior fascic-ular block (7 patients) during sinus rhythm (Figs. 1and 2). Group II included 38 patients (29 men,9 women; mean age 35 ± 16 years) without fas-cicular block during sinus rhythm (Fig. 3). All pa-tients had clinically documented recordings of VTbefore referral.

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Figure 1. Tracings obtained from case 1.Twelve-lead electrocardiogram record-ings during (A) sinus rhythm, (B) ventric-ular tachycardia, and (C) sinus rhythmafter radiofrequency catheter ablation ina case with left anterior fascicular block.

Electrophysiological Study

All the patients gave written, informed con-sent. As described previously, electrophysiologi-cal study was performed while the patient was

Figure 2. Tracings obtained from case 5. Twelve-leadelectrocardiogram recordings during (A) sinus rhythm,(B) ventricular tachycardia, and (C) sinus rhythm afterradiofrequency catheter ablation in a case with left pos-terior fascicular block.

fasting and not sedated, and all antiarrhythmicmedications were discontinued for at least 5 half-lives before study. Details of the electrophysiolog-ical study have been described previously.2−4,7,11

Three 6 Fr quadripolar electrode catheters (USCI,

Figure 3. Tracings obtained from case 38. Twelve-leadelectrocardiogram recordings during (A) sinus rhythm,(B) ventricular tachycardia, and (C) sinus rhythm afterradiofrequency catheter ablation in a case without fas-cicular block.

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Billerica, MA, USA or Mansfield, Boston ScientificCorp., Watertown, MA, USA) were positioned inthe high right atrium, His-bundle area, and rightventricle via the femoral veins. Programmed stim-ulation was performed with atrial burst pacing,atrial single extrastimulus, ventricular burst pac-ing, or using up to three ventricular extrastimuliat two ventricular pacing cycle lengths (400 and600 ms) from the right ventricular apex, outflowtract, or left ventricle with delivery of stimuli attwice the diastolic threshold and 2-ms pulse dura-tion. Isoproterenol infusion (1–4 µg/min) was usedto facilitate the induction of VT if tachycardia wasnot inducible in the baseline state.

Catheter Ablation

Two methods were used to identify the tar-get site for ablation. Endocardial activation map-ping was performed during VT to identify the siteof earliest activation relative to the onset of theQRS complex with a sharp PP (Fig. 4). Pacemap-ping was done during sinus rhythm by pacingat the same rate as the clinical VT to obtain anidentical QRS morphology (Fig. 5). An optimalpacemapping was defined as a 12-lead electro-cardiograph (ECG) showing at least a match of11 leads with the QRS morphology of the clini-

Figure 4. Tracings obtained from case 38 showing theintracardiac electrogram at the successful site duringventricular tachycardia. A Purkinje potential (arrow-heads) of 16 ms preceding the onset of the surface elec-trocardiogram. ABL = ablation catheter; HRA = highright atrium; PCS = proximal coronary sinus; RVA =right ventricular apex.

Figure 5. Tracings obtained from case 16. Twelve-leadelectrocardiogram recordings during (A) ventriculartachycardia and (B) pacemapping from the distal bipo-lar electrodes of the ablation catheter at the suc-cessful site with the same cycle length of ventriculartachycardia.

cal VT. A 7 Fr quadripolar electrode catheter witha 4-mm distal electrode, interelectrode space of2 mm, deflectable curve, and thermistor-embeddedtip (Mansfield or EP Technologies, Inc., Sunny-valle, CA, USA) was used for ablation under fluo-roscopy. RF current (generated from the Radionics-3C, Radionics, Burlington, MA, USA, or EPT-500,−1000, EP Technologies, Inc.) was delivered be-tween the tip electrode and a standard adhesiveelectrosurgical dispersive pad applied to the pos-terior chest wall. RF energy was delivered with a

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power range of 30–50 W (or temperature setting of60–70◦C) and a pulse duration of 30–60 seconds.Successful ablation was defined as complete abo-lition of VT.

Postablation Follow-Up

As previously described, all patients were ob-served in the intensive care unit and were moni-tored by ECG for 24 hours. After discharge fromthe hospital, patients returned to the outpatientclinic at 2 weeks, 1 month, and subsequently ev-ery 2–4 months. If the patients experienced palpi-tation, another 24-hour Holter monitoring or car-diac event recording was used to evaluate thesesymptoms.

ECG Criteria for Fascicular Block

Left anterior fascicular block was defined asthe (1) frontal plane mean QRS axis of −45 to −90degrees; (2) rS patterns in leads II, III, and aVF,and a qR pattern in leads I and aVL; and (3) QRSduration < 0.12 seconds.12,13

Left posterior fascicular block was defined as a(1) right-axis deviation greater than + 120 degrees;(2) rS pattern in leads I and aVL with qR patternsin inferior leads; (3) QRS duration < 0.12 seconds;and an (4) exclusion of other factors causing right-axis deviation (e.g., right ventricular overload pat-terns, lateral infarction).12,13

Statistical Analysis

Quantitative data were expressed as mean ±SD. Parametric data were compared with t-test,

Table I.

Clinical Features and Electrocardiographic Characteristics in Patients with Left Fascicular Blocks During Sinus Rhythm

SR VT

Group I QRSD-B QRSD-A Transition QRSD-VT TransitionPt. No. Age Sex Axis (ms) (ms) Zone Axis (ms) Zone

1 27 M LAD 110 110 V3–V4 RAD 153 V2–V3

2 19 M LAD 118 120 V3–V4 I 155 V2–V3

3 20 M LAD 110 108 V3–V4 LAD 160 V2–V3

4 30 M LAD 115 112 V2–V3 I 135 V2–V3

5 35 M RAD 110 110 V1–V2 I 135 V1–V2

6 14 F RAD 90 92 V5–V6 RAD 155 V2–V3

7 25 M RAD 87 90 V4 I 120 V1–V2

8 43 M RAD 85 85 V3–V4 I 135 V2–V3

9 26 M RAD 110 108 V2–V3 I 130 V3–V4

10 20 M RAD 110 110 V2–V3 I 135 V2–V3

11 20 M RAD 100 100 V2–V3 LAD 140 V2–V3

F = female; I = indeterminate axis; LAD = left-axis deviation; M = male; QRSD = duration of QRS complex during ventriculartachycardia; QRSD-A = duration of QRS complex during sinus rhythm after ablation; QRSD-B = duration of QRS complex during sinusrhythm before ablation; RAD = right-axis deviation; SR = sinus rhythm; VT = ventricular tachycardia.

and categorical data were analyzed by the chi-square test with Yates’ correction or Fisher’s ex-act test. P < 0.05 was considered statisticallysignificant.

ResultsCharacteristics of VT Patients with Left Anterioror Posterior Fascicular Block (Table I)

The mean duration of QRS complex during si-nus rhythm before and after RF catheter ablationand during VT were 104 ± 12 ms, 104 ± 11 ms, and141 ± 13 ms, respectively. The transitional zonesof QRS complexes in the precordial leads duringsinus rhythm were at or before V3 in five (45%)patients, and after V3 in six (55%) patients. Thetransitional zones of QRS complexes in the pre-cordial leads during VT were at or before V3 in ten(91%) patients, and after V3 in one (9%) patient.The transitional zones of QRS complexes in theprecordial leads during VT were earlier (54.5%),equal to (36.6%), or later (9.1%) than those of dur-ing sinus rhythm.

Characteristics of VT Patients Without LeftFascicular Block (Table II)

The mean duration of QRS complex duringsinus rhythm before and after RF catheter abla-tion, and during VT was 95 ± 11 ms, 95 ± 10 ms,and 140 ± 14 ms, respectively. The transitionalzones of QRS complexes in the precordial leadsduring VT were at or before V3 in 18 (47%) patientsand after V3 in 20 (53%) patient. The transitional

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Table II.

Clinical Features and Electrocardiographic Characteristics in Patients Without Left Fascicular Blocks During Sinus Rhythm

SR VT

Group II QRSD-B QRSD-A Transition QRSD-VT TransitionPt. No. Age Sex Axis (ms) (ms) Zone Axis (ms) Zone

1 30 M N 100 100 V3–V4 LAD 124 V3–V4

2 41 M N 90 88 V2–V3 LAD 120 V5–V6

3 69 M N 87 90 V2–V3 RAD 126 V1–V2

4 57 M N 86 90 V3–V4 RAD 143 V1–V2

5 26 M N 100 96 V3–V4 I 140 V3–V4

6 16 F N 100 100 V2–V3 LAD 152 V2–V3

7 19 M N 100 102 V1–V2 I 135 V2–V3

8 27 M N 78 80 V3–V4 I 148 V3–V4

9 29 M N 110 108 V3–V4 LAD 150 ALL +10 26 M N 82 85 V3–V4 I 160 V2–V3

11 45 M N 100 96 V2–V3 I 150 V2–V3

12 32 M N 94 98 V3–V4 LAD 139 V2–V3

13 8 F N 98 100 V4–V5 LAD 120 V2–V3

14 15 F N 77 80 ALL+ I 120 V2–V3

15 31 M N 90 86 V2–V3 LAD 118 V3

16 8 F N 94 94 V2–V3 I 139 V3–V4

17 53 M N 94 96 V3–V4 I 155 V2–V3

18 34 M N 110 108 V1–V2 I 155 V2–V3

19 32 M N 95 96 V3–V4 RAD 114 V5–V6

20 38 M N 98 100 V1–V2 I 145 V3–V4

21 25 F N 98 96 V4 I 140 V2–V3

22 38 M N 105 100 V3–V4 LAD 120 V2–V3

23 28 M N 69 70 V2–V3 LAD 151 V1–V2

24 16 M N 118 116 V4–V5 I 155 V1–V2

25 26 M N 85 90 V3–V4 LAD 151 V1–V2

26 57 F N 102 100 V3 I 155 V2–V3

27 67 M N 90 90 V3–V4 LAD 155 V5–V6

28 34 M N 110 105 V3–V4 I 145 V2–V3

29 30 M N 95 100 V2–V3 I 130 V2–V3

30 32 F N 87 90 V2–V3 LAD 138 V2–V3

31 76 M N 90 88 V2–V3 I 158 V3–V4

32 57 F N 115 110 V3–V4 I 145 V4–V5

33 18 M N 102 100 V2–V3 LAD 130 V2–V3

34 36 M N 82 80 V2–V3 I 125 V1–V2

35 34 M N 100 96 V3–V4 LAD 158 V2–V3

36 22 F N 106 104 V2–V3 LAD 126 V2–V3

37 46 M N 88 86 V4–V5 I 150 V2–V3

38 35 M N 82 82 V3–V4 I 131 V1–V2

See Table I for definitions.

zones of QRS complexes in the precordial leadsduring VT were at or before V3 in 27 (71%) pa-tients and after V3 in 11 (29%) patients. The tran-sitional zones of QRS complexes in the precor-dial leads during VT were earlier (47.4%), equal to(26.3%), or later (26.3%) than those of during sinusrhythm.

Comparisons of Patients BetweenGroups I and II (Table III)

Mean age and sex were similar between groupI and group II patients. The duration of QRScomplex during sinus rhythm before and afterRF catheter ablation in group I patients was sig-nificantly longer than that of group II patients

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Table III.

Comparisons of QRS Complex Duration and Precordial Transitional Zone Between Two Groups

Precordial TransitionalZone During VT

QRSD-B QRSD-VT QRSD-A(ms) (ms) (ms) V1–V3 ≥ V3–V4

Group I 104 ± 12 141 ± 13 104 ± 11 10 (91%) 1 (9%)Group II 95 ± 11 140 ± 14 95 ± 10 27 (71%) 11 (29%)P value 0.02 0.78 0.007 P > 0.05

Values are expressed as mean ± SD, number, or percentage (in parenthesis). See Table I for definition.

(104 ± 12 vs 95 ± 11 ms, respectively, P = 0.02before RF catheter ablation; 104 ± 11 ms vs 95 ±10 ms, respectively, after RF catheter ablation). Theduration of QRS complex during VT was similarbetween group I and group II patients (141 ± 13ms vs 140 ± 14 ms, respectively, P = 0.78). Tran-sitional zones of QRS complexes in the precor-dial leads during VT were similar between groupI and group II patients. After ablation, QRS du-ration did not prolong in group I or group IIpatients (104 ± 11 ms vs 95 ± 10 ms, respec-tively); fascicular block did not happen in group IIpatients.

DiscussionMajor Findings

This study showed that transitional zones ofQRS complexes in the precordial leads during VTwere similar between patients with or without leftfascicular block, and new fascicular block did notappear after ablation. These findings suggest thefascicles of the left bundle branch may not be in-volved in the antegrade limb of reentry circuit inidiopathic left VT.

Reentry Circuit in Patientswith Idiopathic Left VT

The exact entity of the reentry circuit in id-iopathic left VT remains unclear. This study didnot systematically do entrainment from the rightventricular apex or outflow tract or left ventricu-lar ablation site. Therefore, it could not be deter-mined how much of the circuit is involved andparticipates in the VT. This as study limitation.Kottkamp et al.14 suggest that it is a microreen-try circuit in the region of the posterior fascicle.Nakagawa et al.3 suggest that the tachycardia orig-inates from the Purkinje fiber network of the leftposterior fascicle, which is insulated from the sur-rounding myocardium. The earliest PP was useful

in guiding successful RF ablation. Previous studiesdemonstrated that the slow conduction zone of thereentry circuit is of considerable size and extend-ing from the mid-septum to the inferior apical sep-tum of the LV. The entrance and exit sites of slowconduction zone may be different, and the discretesharp spikes of PP were likely to represent the fas-cicular potentials rather than a specific marker forthe reentry circuit of this tachycardia.7,9,10,15

In this study, the QRS duration did not pro-long in both groups, and new fascicular block didnot appear after ablation. These findings suggestedthat the fascicle of left bundle branch or Purkinjefiber may not be involved in the antegrade limb ofthe reentry circuit in idiopathic left VT. These re-sults were consistent with the report from Nogamiet al.10 They recorded both mid-DP and presystolicPP during VT from the mid-septal region in 15 of20 patients with idiopathic left VT. Entrainmentpacing captured mid-DP orthodromically and resetthe VT. After successful ablation, mid-DP appearedafter the QRS complex during sinus rhythm withan identical sequence to that during VT. Whetherthe Purkinje fiber or left fascicle was involvedin the retrograde limb of the reentrant circuit re-mained unclear. Ouyang et al.15 suggested that id-iopathic left VT reentry may be a small macroreen-trant circuit consisting of one antegrade Purkinjefiber with PP, one retrograde Purkinje fiber withretrograde PP, and ventricular myocardium as thebridge.

This study found that the transitional zones ofQRS complexes in the precordial leads during VTwere similar between patients with or without leftfascicular block. The transitional zones were het-erogeneous in both groups. The transitional zonesof QRS complexes in the precordial leads duringVT were earlier than those during sinus rhythm in24 (49%) patients. The transitional zones of QRScomplexes in the precordial leads during VT wereequal to those during sinus rhythm in 14 (29%)

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patients. The transitional zones of QRS complexesin the precordial leads during VT were later thanthose of during sinus rhythm in 11 (22%) patients.There were several possible explanations. First,the ventricular depolarization sequences were dif-ferent between sinus rhythm and VT. Second, theexit sites of idiopathic left VTs were heteroge-neous. Some were higher, some were lower, andthe others were in between. These results werecompatible with the previous reports that idio-pathic left VT could be ablated successfully from

inferior apical septum, mid-septum, or the anteriorlateral wall of the left ventricle.3−5,7−11,15

ConclusionsTransitional zones of QRS complexes in the

precordial leads during VT were similar betweenpatients with or without left fascicular block, andnew fascicular block did not appear after ablation.These findings suggest the fascicle of the left bun-dle branch may be not involved in the antegradelimb of reentry circuit in idiopathic left VT.

References1. Ohe T, Shimomura K, Aihara N, et al. Idiopathic sustained left

ventricular tachycardia: Clinical and electrophysiological charac-teristics. Circulation 1988; 77:560–568.

2. Okumura K, Matsuyama K, Miyagi H, et al. Entrainment of idio-pathic ventricular tachycardia of left ventricular origin with evi-dence for reentry with an area of slow conduction and effect ofverapamil. Am J Cardiol 1988; 62:727–732.

3. Nakagawa H, Beckman KJ, McClelland JH, et al. RF catheter abla-tion of idiopathic left ventricular tachycardia guided by a Purkinjepotential. Circulation 1993; 88:2607–2617.

4. Wen MS, Yeh SJ, Wang CC, et al. Successful RF ablation of idio-pathic left ventricular tachycardia at a site away from the tachycar-dia exit. J Am Coll Cardiol 1997; 30:1024–1031.

5. Klein LS, Shih HT, Hackett K, et al. RF catheter ablation of ven-tricular tachycardia in patients without structural heart disease.Circulation 1992; 85:1666–1674.

6. Okumura K, Yamabe H, Tsuchiya T, et al. Characteristics of slowconduction zone demonstrated during entrainment of idiopathicventricular tachycardia of left ventricular origin. Am J Cardiol1996; 77:379–383.

7. Aiba T, Suyama K, Matsuo K, et al. Mid-diastolic potential is re-lated to the reentrant circuit in a patient with verapamil-sensitiveidiopathic left ventricular tachycardia. J Cardiovasc Electrophysiol1998; 9:1004–1007.

8. Tada H, Nogami A, Naito S, et al. Retrograde Purkinje potentialactivation during sinus rhythm following catheter ablation of id-iopathic left ventricular tachycardia. J Cardiovasc Electrophysiol1998; 9:1218–1224.

9. Tsuchiya T, Okumura K, Honda T, et al. Significance of late dias-tolic potential preceding Purkinje potential in verapamil-sensitiveidiopathic left ventricular tachycardia. Circulation 1999; 99:2408–2413.

10. Nogami A, Naito S, Tada H, et al. Demonstration of di-astolic and presystolic Purkinje potentials as critical poten-tials in a macroreentry circuit of verapamil-sensitive idiopathicleft ventricular tachycardia. J Am Coll Cardiol 2000; 36:811–823.

11. Tsai CF, Chen SA, Tai CT, et al. Idiopathic monomorphic ventric-ular tachycardia: Clinical outcome, electrophysiologic character-istics and long-term results of catheter ablation. Cardiology 1997;62:143–150.

12. Willems JL, Robles ME, Bernard R. WHO task force on criteria forinterventricular conduction disturbances and pre-excitation. J AmColl Cardiol 1985; 5:1261.

13. Rosenbaum MB, Elizari MV, Lazzari JO. Intraventricular trifasci-cular block: The syndrome of right bundle branch block with in-termittent left anterior and posterior hemiblock. Am Heart J 1969;78:306.

14. Kottkamp H, Chen X, Hindricks G, et al. RF catheter ablation of idio-pathic left ventricular tachycardia: Further evidence for microreen-try as the underlying mechanism. J Cardiovasc Electrophysiol 1994;5:268–273.

15. Ouyang F, Cappato R, Ernst S, et al. Electroanatomic substrateof idiopathic left ventricular tachycardia: Unidirectional blockand macroreentry within the Purkinje network. Circulation 2002;105:462–469.

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