© 2005 The European Society of Cardiology. Published by Elsevier Ltd. All rights reserved.
Non-contact mapping and linear ablation of the left posterior fascicle during sinus rhythm in the treatment of idiopathic left ventricular tachycardia
Department of Cardiology, First Affiliated Hospital of Nanjing Medical University Nanjing, 210029 Jiangsu, PR China
Manuscript submitted 14 June 2004. Accepted after revision 26 December 2004.
*Corresponding author. Fax: +86 25 83717168. E-mail address: chenminglong2001{at}163.com (M. Chen).
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Abstract |
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AIM: The reentry circuit of idiopathic left ventricular tachycardia (ILVT) has been demonstrated to be confined to the left posterior Purkinje network. We hypothesized that mapping and linear ablation of the left posterior fascicle (LPF) during sinus rhythm guided by non-contact mapping can effectively modify the arrhythmogenic substrate in patients with ILVT and abolish the tachycardia.
METHODS: Six patients with ILVT, consisting of one case in which conventional mapping failed three times, one recurrent case, one non-inducible case and three common cases, were included in the study. After a three-dimensional endocardial geometry of the left ventricle (LV) was created, the conduction system in the LV was mapped during sinus rhythm using a filter setting of 8 Hz. The His bundle area, left bundle branch, fascicles and sinus breakout point (SBO) were mapped in detail and tagged as special landmarks in the geometry. A linear lesion was placed perpendicular to the wave front propagation direction of the LPF, 1 cm above the SBO. There was a small Purkinje potential preceding the ventricular activation at its starting and ending point.
RESULTS: The mean tachycardia cycle length of ILVT in this study was 340.3±51.4 ms. After a mean of 5.5±1.6 radiofrequency deliveries, the clinical tachycardias could not be induced and the 12-lead surface ECG showed right QRS axis deviation (mean 39.7±26.0 degrees) in all patients. The total procedure time was 160.0±32.2 min with fluoroscopic time of 26.0±6.8 min. No ILVT was inducible during control stimulation, and none recurred during a mean follow-up of 13.0±4.8 months.
CONCLUSION: Mapping and linear ablation of the Purkinje network in LPF area guided by non-contact mapping is an effective and safe treatment of ILVT with radiofrequency energy, especially for those ILVTs which were unsuccessfully treated by conventional means or were non-inducible or non-sustained during the procedure.
Key Words: catheter ablation, non-contact mapping, tachycardia, electrophysiology
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Introduction |
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Catheter ablation guided by conventional contact mapping can effectively modify the arrhythmogenic substrate in patients with idiopathic left ventricular tachycardia (ILVT), resulting in elimination of the tachycardia. Nonetheless, there are still some cases in which the tachycardia is not eradicated, either because of the inability of conventional mapping methods to identify an appropriate target area or because the arrhythmia is non-inducible or non-sustained during the procedure. Previous studies [1–
5] suggest that the reentry circuit of ILVT is confined to the posterior Purkinje system in the left ventricle (LV) with an excitable gap and a slow conduction area. Therefore, we hypothesize that mapping and linear ablation of the left posterior fascicle (LPF) during sinus rhythm (SR) with the guidance of non-contact mapping (EnSite 3000, Endocardial Solutions, St. Paul, MN, USA) to destroy the substrate of ILVT is feasible, especially in cases where contact mapping either fails or cannot be applied. |
Methods |
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Patient characteristics
From July 2002 to June 2003, six consecutive patients (5 males, age 15–58 years, see Table 1) with ILVT were referred to our centre. ECG documentation during the clinical arrhythmia of all patients showed typical right bundle block morphology with left axis deviation. All examinations excluded the evidence of structural heart disease in all patients. Three previous ablation efforts were unsuccessful in one patient, making the tachycardia incessant and refractory to both verapamil and amiodarone. Another patient had a recurrence of tachycardia within 1 month of ablation. The remaining four patients had been treated intermittently with verapamil therapy before being admitted to our centre.
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Electrophysiological study
After withdrawing antiarrhythmic drugs and obtaining informed consent, electrophysiological evaluation was performed on all patients under intravenous sedation. Catheters were introduced to the right ventricular apex, right ventricular outflow tract, His bundle region and high right atrium via the femoral veins. A decapolar catheter was placed in the coronary sinus via a left subclavian vein approach. The stimulation protocol consisted of programmed ventricular stimulation from the right ventricular apex and right ventricular outflow tract including three drive rates with up to three extrastimuli and incremental burst pacing at a cycle length down to 250 ms. If sustained ILVT was not inducible at baseline, the stimulation protocol was repeated after isoprenaline infusion.
Endocardial non-contact mapping of the left ventricle
The details of the EnSite 3000 System have been previously described [6,7]. The 9 French balloon catheter of the non-contact mapping system was advanced through the left femoral artery into the LV in a retrograde fashion. The multielectrode array (MEA) was then deployed within the chamber supported by the balloon which was inflated with 7.5 ml of contrast to provide 64 non-contact electrodes with a fixed geometry. The other end of the balloon catheter, which was outside the body, was sutured and fixed to the local skin to avoid dislocation during the entire procedure. A deflectable catheter with a 4-mm electrode tip (Biosense Webster) was introduced into the chamber via the right femoral artery to sweep throughout the LV to establish three-dimensional endocardial geometry. Particular attention was paid to the geometry detail in the areas of the His bundle, the septum and the apex of the LV. Once the ventricular geometry had been generated, the system could then calculate electrograms from 3000 endocardial points simultaneously by reconstructing far-field signals to create the isopotential map of sinus rhythm (SR) using a single cardiac cycle. Non-depolarized myocardium was shown in purple in the three-dimensional isopotential map. The activation of the left bundle branch, fascicles and the whole ventricle was analysed using a filter setting of 8 Hz. The His bundle, the left bundle branch, fascicles and sinus breakout point (SBO) were tagged as special landmarks in the geometry.
RF ablation
A linear lesion was created perpendicular to the activation direction of LPF and 1 cm above SBO. There was a small Purkinje potential preceding the ventricular activation at its starting and ending point. RF energy was delivered from the distal electrode of the mapping catheter for 90 s with a preselected temperature of 60 °C at each point. Each delivery of RF started from 20 W and increased up to 40 W to reach the target temperature. After finishing the linear lesion, reinduction of the ILVT was performed by the programmed stimulation protocol described above. Heparin was administered to maintain the activated coagulation time (ACT) at the level of 250–300 s during the whole procedure.
Control stimulation and follow-up
The procedure was considered successful if ILVT was not inducible at the end of ablation and during a second control stimulation, which was performed 3 days later. Follow-up information was obtained either from the referring physician or our outpatient clinic.
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Results |
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Electrophysiological study
Clinical tachycardia could be induced in all patients before the balloon catheter was placed in the LV with a mean tachycardia cycle length of 340.3±51.4 ms. The tachycardia was incessant in patient 1 and was accidentally terminated when the MEA was deployed in the ventricle. The tachycardia in patient 2 became non-inducible after the geometry was created. In patient 3, whose tachycardia was recurrent after a previous ablation, only a short run of 3–5 beats of tachycardia could be induced after constructing the geometry. In the remaining three patients, we did not induce tachycardia after the MEA was placed.
Non-contact mapping of the conduction system in LV
Sinus activation began in the His bundle area and then propagated down the septum until it bifurcated into two wavefronts, one going anteriorly to the left free wall and the other going down to the inferobasal part of the ventricle before the entire ventricle was finally activated (see Fig. 1). SBO was located in the mid-posterior septum and the local virtual electrogram presented with a QS morphology in all patients. Virtual electrograms at points from the His down to the SBO showed a sharp, low-amplitude potential preceding the ventricular potential. The interval between these two potentials became progressively shorter as the activation proceeded from the His to the SBO until the two potentials finally fused together at the SBO (Fig. 2, left). Virtual electrograms recorded from the points placed in the pattern of block above the SBO showed the whole Purkinje network in the LPF area (Fig. 2, right).
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RF ablation and follow-up
Linear lesions were created along the predefined line (Fig. 3). The mean length of the deployed line was 2.0±0.4 cm. After a mean of 5.5±1.6 RF deliveries, the clinical tachycardias could not be induced and the 12-lead surface ECG showed a significant shift of QRS axis to the right with a mean deviation of 39.7±26.0 degrees in all patients (Fig. 4). The total procedure time was 160.0±32.2 min (range 125–205 min) with 26.0±6.8 min (range 19–37 min) of fluoroscopy. No dislocation of the balloon catheter happened and no complications occurred during the procedure. ILVT was not inducible with or without isoprenaline infusion during the second stimulation 3 days after the first procedure in all patients. All patients were free of symptoms without antiarrhythmic drugs at a mean follow-up of 13.0±4.8 months (range 7–19 months).
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Discussion |
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Probable mechanisms of ILVT
Previous studies [1–
5,8–10] suggested that ILVT with the configuration of right bundle branch block and left axis deviation originates within the Purkinje network of the LPF. The mechanism of this tachycardia is believed to be reentry because of its induction and termination characteristics as well as its entrainment properties during tachycardia, though direct evidence is lacking. By using electroanatomic mapping, Ouyang et al, [10] provided evidence for a slow conduction area with passive retrograde activation along the posterior fascicle during ILVT. They suggested that ILVT reentry may be a small macroreentrant circuit consisting of one antegrade Purkinje fibre with Purkinje potential, one retrograde Purkinje fibre with retrograde Purkinje potential, and ventricular myocardium as a bridge.
Problems of conventional mapping and RF ablation of ILVT
Nakagawa et al. [8] reported that distinct potentials could be recorded before QRS onset at the site of ILVT origin during tachycardia and that the earliest distinct potential precedes the QRS by 15–42 ms during ILVT. They emphasized the importance of the earliest Purkinje potential as a marker for successful ablation, because the site of this potential is believed to be the exit site of the reentrant circuit. Recently, a diastolic potential preceding the Purkinje potential during ILVT was demonstrated by endocardial mapping [3–5,9]. ILVT can be successfully ablated at the site where the diastolic potential was recorded, which is far from the recording site of the earliest Purkinje potential. The conventional activation mapping, either guided by the earliest Purkinje potential or the diastolic potential, though very effective, depends on the inducibility and endurance of ILVT. However, the critical substrate of ILVT is amenable to mechanical injury due to catheter manipulation, which will make the tachycardia non-inducible. In the absence of inducibility, the only technique available is pace mapping, which has proved to be unreliable in this arrhythmia [8]. Furthermore, the reentry circuit in some patients may have multiple entrances and exits because of a complex Purkinje network. RF delivery guided by the earliest Purkinje potential or diastolic potential cannot create enough damage to destroy the substrate of ILVT. This will result both in failed cases and early recurrence.
Findings of the present study
According to the probable mechanisms of ILVT, we hypothesized that making linear lesions perpendicular to the conduction direction of LPF, 1 cm above the SBO, could produce enough damage to destroy the substrate of ILVT, and thus abolish the tachycardia. This can only be done with the guidance of a three-dimensional mapping system. To our knowledge, this is the first study of a series of patients where mapping and linear ablation of the LPF Purkinje network during SR was performed using a three-dimensional mapping system. Our study has the following findings: (1) this approach is especially suitable for ILVT that is non-inducible during the procedure; (2) for cases where conventional mapping has failed, this approach can provide an effective way to eradicate the tachycardia by catheter ablation, thus improving the success rate of the treatment of ILVT with RF ablation; (3) as mapping and ablation can be performed during SR, it is easy and also time saving; (4) 12-lead ECG after the linear lesion has been created only shows a significant shift of the QRS axis to the right, without the morphology of real LPF block, suggesting that the approach in this study only modifies the conduction properties of the Purkinje network of the LPF area, without blocking the conduction of the LPF, and thus does not affect the global activation of the LV; (5) conversely proves that the Purkinje network or the myocardium of the LPF area is the arrhythmogenic substrate of ILVT.
Study limitations
Activation mapping was not performed after non-contact mapping of the conduction system in LV, so we could not check whether the earliest activation of ILVT is coming from the LPF area and going across the linear lesion line.
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References |
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[1] Okumura K, Matsuyama K, Miyaji H, Tsuchiya T, Yasue H. Entrainment of idiopathic ventricular tachycardia of left ventricular origin with evidence for re-entry with an area of slow conduction and effects of verapamil. Am J Cardiol 1988; 62: 727–732.[CrossRef][Web of Science][Medline]
[2] Okumura K, Yamabe H, Tsuchiya T, Tabuchi K, Iwasa A, Yasue H. Characteristics of slow conduction zone demonstrated during entrainment of idiopathic ventricular tachycardia of left ventricular origin. Am J Cardiol 1996; 77: 379–383.[CrossRef][Web of Science][Medline]
[3] Wen MS, Yeh SJ, Wang CC, Lin FC, Wu D. Successful radiofrequency of ablation of idiopathic left ventricular tachycardia at a site away from the tachycardia exit. J Am Coll Cardiol 1997; 30: 1024–1031.[Abstract]
[4] Nogami A, Naito S, Tada H, Taniguchi K, Okamoto Y, Nishimura S, et al. Demonstration of diastolic and presystolic Purkinje potentials as critical potentials in a macroreentry circuit of verapamil-sensitive idiopathic left ventricular tachycardia. J Am Coll Cardiol 2000; 36: 811–823.
[5] Tsuchiya T, Okumura K, Honda T, Honda T, Iwasa A, Yasue H, et al. Significance of late diastolic potential preceding Purkinje potential in verapamil-sensitive idiopathic left ventricular tachycardia. Circulation 1999; 99: 2408–2413.
[6] Schilling RJ, Davies DW, Peters NS. Characteristics of sinus rhythm electrograms at sites of ablation of ventricular tachycardia relative to all other sites: a noncontact mapping study for the entire left ventricle. J Cardiovascular Electrophysiol 1998; 9: 921–933.[Web of Science][Medline]
[7] Friedman PA, Beinborn DA, Schultz J, Hammill SC. Ablation of noninducible idiopathic left ventricular tachycardia using a noncontact map acquired from a premature complex with tachycardia morphology. Pacing Clin Electrophysiol 2000; 23: 1311–1314.[CrossRef][Medline]
[8] Nakagawa H, Beckmann KJ, McClelland JH, Wang X, Arruda M, Santoro I, et al. Radiofrequency catheter ablation of idiopathic left ventricular tachycardia guided by a Purkinje potential. Circulation 1993; 88: 2607–2617.
[9] Kottkamp H, Chen X, Hindricks G, Willems S, Haverkamp W, Wichter T, et al. Idiopathic left ventricular tachycardia: new insights into electrophysiological characteristics and radiofrequency catheter ablation. Pacing Clin Electrophysiol 1995; 18: 1285–1297.[Medline]
[10] Ouyang F, Cappato R, Ernst S, Goya M, Volkmer M, Hebe J, et al. Electroanatomic substrate of idiopathic left ventricular tachycardia: Unidirectional block and macroreentry within the Purkinje network. Circulation 2002; 105: 462–469.
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