Journal of Electrocardiology Vol. 33 No. 2 2000

Structure of the Reentrant Circuit of Idiopathic Left Ventricular Tachycardia:

N e w Insights Into the Role of the Purkinje N e t w o r k

T a k a s h i W a s h i z u k a , M D , M a s a o m i C h i n u s h i , M D ,

S h i n i c h i N i w a n o , M D , a n d Y o s h i f u s a A i z a w a , M D

Abstract: In idiopathic left ventricular tachycardia (ILVT), the reentrant circuit is considered to involve the Purkinje system, and the Purkinje potential (P-potential) appears to be a marker for successful ablation. However, the characteristics of the reentrant circuit in ILVT have not yet been defined. In 2 cases of ILVT, we performed detailed mapping along the left ventricular septum during VT and sinus rhythm. ILVTs were successfully ablated at the posteroapical area of the left ventricular septum where the high frequency P-potential was recorded and this portion was considered to be the exit site of the reentrant circuit. A small P-potential was also recorded at the portion proximal to the exit site, and it preceded the P-potential at the exit site. However, the local ventricular electrogram at the exit site preceded that at the proximal site during VT. Moreover, the small P-potential was orthodromically entrained by ventricular pacing from the proximal site. These findings suggest that the reentry circuit of ILVT appeared to have considerable size. Key words: Idiopathic left ventricular tachycardia, Purkinje potential, reentry, radiofrequency catheter ablation.

Idiopathic left ventr icular tachycardia (ILVT) has been character ized by a distinctive QRS morphol - ogy (right bundle branch block and superior axis), t e rminat ion by in t ravenous verapamil, and induc- tion and te rminat ion by p rog rammed st imulation (1,2). In ILVT, reen t ry is considered to be the mechan ism of tachycardia; en t r a inmen t is fre-

From the First Department of hTternal Medicine, Niigata University School of Medicine, Asahimachi, Niigata, Japan.

Reprint requests: Takashi Washizuka, MD, First Department of Internal Medicine, Niigata University School of Medicine, Asahi- mac.hi 1-754, Niigata 951, Japan; e-mail: washi@med.niigata-u.ac.jp

Copyright �9 2000 by Churchill Livingstone | 0022-073610013302-0011 $10.00f0 doi: 10.1054/xe.2000.6535

quent ly shown by ventr icular pacing and the area of slow conduct ion is thought to involve the Pur- kinje system (3-5). Moreover , the application of rad iof requency catheter ablation to the posteroapi- cal left ventr icular septum w h e re a high f requency Purkinje potent ial (P-potential) is recorded is highly effective (4,6,7). However , the electrophysiological proper ty or spatial or ienta t ion of the reen t ran t circuit and the association be tween the reen t ran t circuit and the P-potential of ILVT have not ye t been determined. In this article, detailed mapping along the poster ior left ventr icular septum during tachycardia and sinus r h y t h m provides a n e w in- sight into the reen t ran t circuit of ILVT.

195

196 Journal of Electrocardiology Vol. 33 No. 2 April 2000

Case Presentation

Case 1

A 21-year-old man had experienced episodes of paroxysmal palpitation and faintness for 5 years. During 1 episode of palpitation, an electrocardio- gram (ECG) documented a wide QRS tachycardia at a rate of 180/min with a QRS morphology of right bundle branch block and left axis deviation. This episode was terminated by intravenous administra- tion of verapamil (5 mg). Although he received oral verapamil at a dose of 240 mg/d prophylactically, symptomatic episodes repeated. Thus, he was re- ferred to our hospital for further evaluation. Phys- ical examination, chest roentgenogram, surface ECG, and echocardiogram were normal. After obtaining informed consent, electrophysiological study was performed in the postabsorptive non- sedated state. Under fluoroscopic guidance, 5 6-F quadripolar catheters with a 5-mm interelectrode distance (USCI Inc., Division of C.R. Bard, Boston, MA) were positioned against the His-bundle elec- trogram recording site, the apex, and the outflow tract of the right ventricle for pacing and recording of the local electrogram. A 7-F quadripolar steerable electrode catheter with a 4-ram tip (Cordis/Web- ster, Boston Scientific International, Boston, MA) was retrogradely introduced into the left ventricle through the aorta for pacing, recording of local electrogram, and ablation. Programmed stimulation induced ventricular tachycardia, which showed an identical QRS morphology to the clinical arrhyth- mia. The phenomenon of transient entrainment of tachycardia was shown by overdrive pacing from the right ventricular outflow tract. Endocardial mapping of the left ventricle was performed during VT. A sharp high frequency P-potential was re- corded before ventricular activation from the distal pair of electrodes at the posteroapical left ventricu- lar septum during VT. Rapid ventricular pacing from site A during VT resulted in acceleration to the pacing rate without change in the configuration of the QRS complex in all 12 ECG leads and the first postpacing return cycle was identical to the VT cycle length (Fig. 1A). When the mapping catheter was moved along the inferoposterior septum, a small P-potential was registered 1.0 cm proximal to the first position (Fig. 1B). Rapid ventricular pacing in Figure 1B did not show any change in the config- uration 'of the QRS complex and the small P- potential was orthodromically captured by rapid ventricular pacing. The P-potential in Figure 1B preceded the QRS onset (P-QRS interval) by 60 ms during tachycardia, whereas the P-QRS interval in

Vl

H B E i r q - - 1 ] l] . ] ~ . ~ ~ .

, ,p ~ , ~ k l ,I

t

M,p ~ - ~ 1 ~ . . . ~ 1 ~

I.i%

Fig. 1. Endocardial mapping in Case I. Surface leads V1 are shown with intracardiac electrograms from the map- ping catheter in the left ventricle. See text for details. Map, mapping catheter.

Figure 1A was shorter (45 ms). In Figure 1B, VT was terminated by radiofrequency catheter ablation (RF), but VT with a slightly different QRS configu- ration was induced by programmed stimulation. VT was finally ablated in Figure 1A.

Case 2

A 27-year-old man had experienced episodes of paroxysmal palpitation for 2 years. During an epi- sode of palpitation, an ECG documented wide QRS tachycardia with a rate of 160/min with a QRS morphology of the right bundle branch block and left axis deviation. The episode was terminated by intravenous administration of verapamil (5 mg) or procainamide (200 mg). He was referred to our hospital for electrophysiological evaluation because antiarrhythmic therapy with oral verapamil at a dose of 120 mgld could not prevent palpitation attack. Physical examination, chest roentgenogram, surface ECG, and echocardiogram were normal at the time of hospital admission. After obtaining informed consent, electrophysiological study was similarly performed as described in Case 1. The programmed stimulation induced ventricular tachy- cardia with an identical QRS morphology to the clinical arrhythmia. Tachycardia was entrained by overdrive pacing from the right ventricular outflow tract. Endocardial mapping of the left ventricle was performed during sinus rhythm and VT. The acti- vation sequence of sharp P-potential was from site D to site C, and the activation of local ventricular electrogram was from site C to site D (Fig. 2B).

A.

B I a: during sinus rhythm b: during VT

: : : . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

V1 - -

RVOT - "-~

HBE - ' ~ . ; Jl,, l i 200 m s e c i

Fig. 2. Intracardiac recording and catheter position dur- ing sinus rhythm and ventricular tachycardia in Case 2. (A) White and black arrowheads show the proximal and distal pair of the mapping catheter at the LV, respectively. See text for details. (B) Surface leads I, II, and V1 are shown with intracardiac electrograms from the right ventricular outflow tract (RVOT), the His bundle electro- gram recording site (HBE), site C, and site D.

While the P-QRS interval was longer at site D, and the local ventricular electrogram at site C preceded that at site D by 5 ms (Fig. 2Bb). RF was first attempted at site C and the VT was ablated. During sinus rhythm, the activation sequence of P-poten- tial was from site D to site C, and the local ventric- ular electrogram was from site C to site D (Fig. 2Ba). These findings suggested that site C was the exit site of the VT while site D was upstream to the wave- front.

D i s c u s s i o n

ILVT is characterized by a distinctive QRS config- uration with a right bundle branch block and supe- rior axis, and a specific response to verapamil (1-3). Whether the detailed structure of the reentrant circuit of this VT involves microreentry or macro-

The Reentrant Circuit of ILVT �9 Washizuka et al. 197

reentry remains unknown. Kottkamp et al. (8) reported that it was a microreentrant circuit in the left posterior fascicle and fragmented potentials scanning the whole diastole during VT were ob- served. Nakagawa et al. (6) also suggested that tachycardia originated from the Purkinje network of the left posterior fascicle and the P-potential recorded at the left posterior fascicle was the marker of successful ablation. However, we previ- ously reported that the entrance to the reentrant circuit was located toward the base of the interven- tricular septum, whereas the exit was located at the posteroapical area: the successful ablation site (4). Moreover, Wen et al. (9) recently reported that successful ablation of ILVT could be achieved at sites away from the tachycardia exit site: the usual ablation site. Furthermore, their ablation site was considered to be close to the entrance of the reen- trant circuit (8). These findings suggest that the reentrant circuit of ILVT has considerable size.

In the present study, we performed a detailed mapping along the posterior septum in the left ventricle. In both cases, the exit site was deter- mined at the posteroapical left ventricular septum where a high frequency P-potential preceded the QRS complex and the postpacing interval during VT was identical to the VT cycle length. Ventricular activation was earliest at this site (Fig. 2). Along the septum we also recorded a small P-potential at a site proximal to the exit site where the potential was earlier than that at the exit site, while local ventric- ular activation was delayed in comparison with that at the exit site by 5 ms (Fig. 2). During sinus rhythm, small deflections were also recorded at 2 sites and the sequence of activation proceeded from the proximal to distal pair. These findings suggest that the conduction of impulses during VT was similar to the normal activation sequence of the Purkinje system. Because the interval from the proximal to distal pairs occupies only a small frac- tion of the cycle length of ILVT, the Purkinje fiber involved in the VT reentrant circuit seems relatively normal. The identical interval between the 2 re- cording sites during sinus rhythm and VT also suggest the absence of a decremental conduction property in the Purkinje fiber. However, some part of the Purkinje network must be dysfunctioned because the wave fronts via normal myocardium reenter the Purkinje system at the proximal site (Fig. 3). Thus, the reentrant circuit of rLVT would have considerable size and defective insulation, thought we could not determine the critical slow conduction zone.

If ILVT originated from the microreentry in the left posterior fascicle, the activation sequence of

198 Journal of Electrocardiology Vol. 33 No. 2 April 2000

I V S L ~ e n t r a n c e

RV ~ LV )

~N~: main delay site

~ : normal myocardium

. . . . . : Purkinje fiber

Fig. 3. Schematic representation of the reentrant circuit of the idiopathic left ventricular tachycardia. RV, right ventricle; IVS, intraventricular septum.

Purkinje fibers would be reversed. Because Kott- kamp et al. (8) had reported that the fragmented middiastolic potentials were recorded from a small area during VT and they could ablate the VT at that site, a critical delay might occur at this level of Purkinje fiber (Fig. 3). Further investigation is nec- essary in a larger number of patients with ILVT.

References

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2. Ohe T, Shimomura K, Aihara N, et al: Idiopathic left ventricular tachycardia: Clinical and electrophysi- ologic characterization. Circulation 77:360, 1988

3. Okumura K, Matsuyama K, Miyagi H, et al: Entrain- ment of idiopathic ventricular tachycardia of left ven- tricular origin with evidence for reentry with an area of slow conduction and effect of verapamil. Am J Cardiol 62:727, 1988

4. Washizuka T, Aizawa Y, Chinushi M, et al: Alteration of QRS morphology and effects of radiofrequency ablation in idiopathic ventricular tachycardia. Pacing Clin Electrophysiol 18:18, 1995

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