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19 CATHETER ABLATION OF VENTRICULAR TACHYCARDIA

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Introduction

Antiarrhythmic surgery (ventriculotomy) was used in our institution between 1973 and 1980 to treat 15 patients with Arrhythmogenic Right Ventricular Dys- plasia (ARVC/D) who had ventricular tachycardia (VT) resistant to antiarrhythmic drug therapy. When catheter ablative procedures became available, we used fulguration (F) with DC energy shock alone in 27 patients between August 1983 and February 1992.

However, this technique was associated with serious complications. The causes of these complications are now understood and the problems associated with F have been corrected. We now use radiofrequency (RF) energy followed by F if RF ablation is not suc- cessful. This protocol has been used in 23 patients from 1992 until October, 1999. The results of abla- tion using these two approaches over 16 years has been reported [1]. We wish to report our most recent experience with 22 additional patients over 6 years using the combined treatment with RF ablation im- mediately followed by the use of F if necessary.

Selection of Cases

The study group consisted of all patients who met the criteria for ARVC/D established by the World Health Organization and the World Heart Federation (WHF) [2]. Most of these patients were referred from cardiology centers to La Salpêtrière Institute of Cardiology, Paris, France, for the treatment of VT re- sistant to antiarrhythmic drugs or because they were receiving frequent appropriate shocks from their im- plantable defibrillator, or because of failed RF abla- tions. Prior to their inclusion, all patients were reeval- uated with our pharmacologic protocols, including amiodarone alone or in combination with beta- blocking agents [3]. Only those patients, who could not be adequately controlled by antiarrhythmic drugs, as assessed by Holter monitoring, exercise

stress testing, and/or programmed pacing, were treat- ed by ablation. There was no exclusion due to age, clinical condition, or other factors.

Clinical Series

The study population consisted of 17 men and five women. The mean age at the time of the first abla- tion was 38±14 years (mean±SD), range 20 to 70 (Fig. 19.1). The mean left ventricular ejection fraction (LVEF) was 59±10%. It was below 45% in two pa- tients (Fig. 19.2).

Two patients who had an implantable defibrilla- tor had ablation for the treatment of frequent and poorly tolerated episodes of VT. Four patients had in- cessant VT at the time of the first ablation. One pa- tient had previous antiarrhythmic surgery performed at La Salpêtrière hospital, 23 years before the first ab- lation procedure.

CATHETER ABLATION OF

VENTRICULAR TACHYCARDIA

Guy Fontaine, Jérôme Lacotte, Françoise Hidden-Lucet, Robert Frank

CHAPTER

19

Fig. 19.1 • Distribution of age at first ablation in the present series of 22 patients. Note the wide spectrum at which the severe form of arrhythmia (resistant VT) occurred. It is possi- ble that this distribution may be skewed toward the younger age since some of the older patients may have died of con- gestive heart failure before developing severe arrhythmias

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Methods

Steerable catheters with 8 mm distal electrodes, some of them irrigated, were used for mapping and RF ab- lation [4]. The temperature-controlled catheters were manufactured by Medtronic Cardiorhythm (San Jose, CA), Biosense Webster (Baldwin Park, CA), and by Boston Scientific EPT (San Jose, CA).

The generators used for RF ablation were Medtronic Stockert and the EPT 1000XP generators.

Each of these generators incorporated a micro-com- puter with the appropriate software for impedance and temperature monitoring. The return radiofre- quency electrode was located on patients, back adja- cent to the indifferent electrode used for fulguration or defibrillation.

The fulgurator was a Fulgucor (Odam, Wissem- bourg, France) delivering a monophasic damped sine wave of 8ms duration at 10% of the baseline. In the fulguration sessions, bursts of two consecutive catho- dal shocks were programmed at 160J [5].

During the procedures, the fluoroscopic events were recorded on videodisc and the ECG and endo- cardial signals were recorded using a Cardiolab Sys- tem (GE Marquette Medical Systems, Houston, TX).

Mapping was performed with the Carto system (Biosense Webster, Baldwin Park, CA) or the Loca- Lisa Medtronic system.

Radial blood pressure was monitored continu- ously during the procedure. A SvO2 Swan-Ganz catheter was inserted in the pulmonary artery to monitor cardiac output and RV ejection fraction. A second SvO2 Swan-Ganz catheter was positioned in the coronary sinus to monitor myocardial oxygen

consumption during VT. This parameter was found to be a reliable marker for procedure tolerance [6].

Intravenous heparin was given to patients with marked right ventricular dilatation according to well- established protocols. Monitoring of coagulation was performed during the procedure by APTT He- mochrom, Bard, US.

Before ablation, class I antiarrhythmic drugs were discontinued for at least 5 half-lives. Amio- darone was continued. Only monomorphic or mul- tiple monomorphic sustained ventricular tachycar- dias, either clinical or induced during the ablation session, were considered for attempted ablation.

The procedure was performed under general anes- thesia in order to have continuous assessment of myocardial function and in critical cases to moni- tor thrombogenicity by transesophageal echocar- diography. Ventricular tachycardia was induced by programmed pacing. In some cases pacing and iso- prenaline injection were required to induce VT.

Dobutamine was used in case of significant hypo- tension.

The classical approach of VT mapping was to record the earliest potentials before the QRS com- plex was seen on the surface tracing during ventric- ular tachycardia. This coupling interval was usually longer than 30 ms in patients with structural heart disease. Pacemapping was also used with the aim of reproducing the morphology of QRS complexes during spontaneous VT in all twelve leads. Pacemap- ping was achieved by slight overdrive pacing during VT using the same catheter used to deliver electrical energy for ablation. In addition, VT should be pre- sent after interruption of pacing. Special attention was paid to treat the area of slow conduction that was frequently represented by fragmented high fre- quency potentials located between two ventricular QRS complexes. There are additional features which facilitate the identification of the zone of slow con- duction that is a necessary link for the perpetuation of arrhythmia [7-11].

During the study period, RF was used first for all ablation attempts. When it was ineffective or if there was an impedance rise or lack of increase of temper- ature after multiple attempts of RV ablation, one or several F were delivered through the same catheter during the same session.

When the F technique was used, the DC ablation signal of voltage and current was displayed on the screen of a two-channel digital Tektronix 5116 oscil- loscope. This enabled to assess that the energy of each shock was correctly delivered, and that there was no damage to the catheter permitting its use for the next shock if necessary.

Fig. 19.2 • Left ventricular ejection fraction at the time of first ablation. Note the bimodal distribution with two cases below 45% (p<0.05)

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The In-Hospital Follow-Up Period

Postoperative hemodynamic surveillance consisted of monitoring the radial artery blood pressure for 24h.

After each ablation session, the surface ECG was monitored continuously by computerized telemetry (GE Marquette).

Control of VT was always assessed before hospi- tal discharge by 3 days of telemonitoring.

Definition of terms

The following definitions of the ablation results have been simplified from those used in the previous re- port [1]. If ventricular tachycardia identical or simi- lar to the previous attacks in rate as well as in mor- phology on the twelve-lead ECG occurred sponta- neously or was inducible by the same previously defined protocols, the case was considered a “failure”.

Any favorable change in the behavior of VT as com- pared to the features observed before ablation in- cluding decrease in the rate of VT (v10 bpm), num- ber of VT morphologies, sustained VT becoming nonsustained or effectiveness of antiarrhythmic drugs, was classified as a “partial success” because the ablation had prevented or clinically modified the ar- rhythmias by some alteration of the arrhythmogenic substrate. Effectiveness of drug treatment was as- sessed by EPS in case of rapid hemodynamically un- stable VTs or by monitoring in slower, well-tolerated VT episodes.

The case was classified as “success” when drugs were no longer needed and when patients were non- inducible after ablation. However, antiarrhythmic drugs were continued in the vast majority of cases for safety reasons (multiple episodes of rapid VT or VF documented prior to ablation or induced during the procedure, or to treat ventricular or supraventricular extrasystoles after ablation). The final clinical assess- ment of VT control was represented by the sum of

“success,” and “partial success.”

A repeat ablation session was always performed in patients in whom a session and previously defined drug therapy failed.

Follow-Up

After hospital discharge, follow-up was systematical- ly assessed by a computer-based system consisting of discussion with the referring physician or the refer- ring hospital, as well as by direct telephone calls to the patient or family members. Follow-up was based on

the time interval between the first ablation procedure and the latest information obtained for each patient.

Statistical Analysis

Statistical analysis and graphs have been performed with Statistica v6.0 (Statsoft, Tulsa, OK). The t-test was used for all statistical computations. A p value f0.05 was considered significant.

Results

During the ablation procedure, VT was monomor- phic in six patients, five patients had two morpholo- gies, four had three, and seven had from four to eight morphologies (Fig. 19.3).

Thirteen patients were successfully treated by a single session, four required two sessions, two re- quired three sessions, and one four. However, two pa- tients of the same cohort received eight and eleven sessions respectively, during the same study period (Fig. 19.4). They will be later referred to as Case #1 and Case #2 (Fig. 19.5).

Ablation was done only in the right ventricle in all patients. Four to 34 applications of RF energy (mean=17) were delivered as initial treatment. This approach alone proved to be successful in ten patients with “success” and three more patients with a “par- tial success” leading to a clinical success of 60%. F was used as secondary treatment in patients who failed from 17 to 34 RF applications. This approach was used in the nine remaining patients with the delivery of two to eight DC shocks.

Fig. 19.3 • Largest number of VT morphologies observed for each patient during the procedures

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Originally we changed catheters after two DC shocks. However at present, all catheters were able to withstand high-energy shocks. Repeat ablation ses- sions were performed during the same hospital stay in four patients (one had three sessions during the same stay). A new hospitalization was necessary in six pa- tients needing two to ten rehospitalizations. The time interval between these sessions is presented in detail for the two cases #1 and #2 in Figs. 19.6 and 19.7.

22 Session I

8 Session II

4 Session III

3 Session IV

2 Session VIII

1 Session XI

1 Surgery

3 P Success

1 P Success 1 P Success

2 F ailure 3 F ailure 4 F ailure 8 F ailure 11 Success

4 Success

1 Success

1 F ailure

1 F ailure

1 P Success

Fig. 19.4 • VT ablation in ARVC/D (including surgery) lead- ing to a final clinical success rate of 100%. Information in the boxes indicates number of patients and outcome.The roman numerals indicate the number of sessions of ablations

1 2 3 4 5 6 7 8 9 10 11

Number of Sessions 0

2 4 6 8 10 12 14 16

Number of Patients

Fig. 19.5 • Number of ablation sessions. The two cases re- quiring eight and eleven sessions are obvious outliers

0 1 2 3 4 5 6 7 8 9 10

Ablation Sessions in Case #1 0

5 10 15 20 25 30 35

Time Interval between Sessions (months)

3

2 1

7

2 2

2 (150)

(150)

(150) (220) (150)(160) (150) (145) (200) (180) (190)

(240) (220)

(150) (200)

(160) (180)

(140) (120)

(100) (160)

(220)

No more VT

Fig. 19.6 • Time intervals between successive ablation ses- sions. Numbers above the dots indicate the number of recorded VT morphologies. Numbers between brackets rep- resent the VT rate in beats per minute. Some long intervals wrongly suggesting control of VT were probably the result of disease progression finally controlled by ablation

0 2 4 6 8 10 12

Ablation Sessions in Case #2 0

5 10 15 20 25 30

Time Interval between sessions (months)

1 3

1

2 5

2

1 1

1 1 1

2 (100)

(100) (110)

(110)(100) (100)

(110)

(100)

(100) (117)

(160) (175)

(165)

(220) (200) (180)

(150) (150)

Surgical RF Ablation

Fig. 19.7 • Time intervals between successive ablation ses- sions. Numbers above the dots indicate the number of recorded VT morphologies. Numbers between brackets rep- resent the VT rate in beats per minute. Some long intervals wrongly suggesting control of VT were probably the result of disease progression finally controlled by ablation. Except for session 9, where four of the five morphologies were non- clinical, all the other VTs seemed to involve the same ar- rhythmogenic substrate which was finally controlled only after surgical epicardial RF ablation

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Patient Follow-Up After the Last Session

No patient was lost to follow-up. The mean follow- up period was 35 (±22 months, SD) ranging from 6 to 73 months.

Overall Results

VT catheter ablation failed only in one patient (Case

#2) finally controlled by surgery (Fig. 19.4).

Complications

No complications were observed in this study as compared to the patients treated before 1999, during which one patient (not ARVC/D) died when a per- cutaneous epicardial approach was used [1].

Survival

In this series, no patient died suddenly after hospital discharge and there were no deaths due to congestive heart failure. Of note, two patients had a left ven- tricular ejection fraction below 45% (Fig. 19.2). This was clearly different from other patients and sug- gested the role of a superimposed episode of my- ocarditis as we have previously described [12-14].

Comments

RF ablation of ventricular tachycardia is used world- wide with acceptable results [15-17]. It is confirmed by this study that its effectiveness (used in combina- tion with F) leads to a success rate of 95%. However, failure in one patient after eleven attempts and the need of eight ablation sessions in other patients are intriguing.

Case #1 had diffuse involvement of the right ven- tricle with severe dilatation and total akinesia of the right ventricle. Almost the entire right ventricle in- cluding the RV septum was involved in the arrhyth- mogenic process. Clinical success was obtained only when each of the critical areas were ablated.

In Case #2, the explanation of ablation failure is different. The zone of VT origin was not disseminat- ed in multiple areas of the RV. It was on the free wall of the right ventricle easily accessible to the ablation catheter. In addition, the techniques of mapping, per- formed by two different pieces of advanced electro- anatomical equipments, indicated the same critical

area. The endocardial ablation procedure failed whereas epicardial ablation during open-chest surgery proved effective. It confirmed that the re-entrant phe- nomenon was located on the surviving epicardial fibers. Recording of a distinct high amplitude epicar- dial potential in middiastole suggested a layer of my- ocardium exhibiting slow conduction properties. This feature was similar to delayed potentials observed on the epicardium of a patient with Uhl’s anomaly, rather than ischemic myocardium.

The ventricular arrhythmias of all the other pa- tients were finally controlled with fewer ablation at- tempts. It is necessary to propose a particular mech- anism to explain this ablation failure. The surgeon discovered a large zone of fibrosis. This could not be the result of the previous ablations scar. In that case the thinness of RV myocardial free wall (especially in ARVD) should have not prevented successful abla- tion. The only explanation was suggested by the pathology observed in the most severe forms of the disease with major dilatation and akinesia as shown in Fig. 19.6 and color plate 14 of reference 18. This illustration shows whitish plaques consisting of hya- line fibrosis on the endocardium. Histologic study demonstrated this represented an old organized mur- al thrombus.

Therefore, this case illustrates that chronic VT re- sistant to endocardial ablation can be managed by epicardial RF ablation without extracorporeal circu- lation. A previous transcutaneous epicardial ablation failed for unclear reasons.

To the best of our knowledge this is the first re- port of this technique for the antiarrhythmic treat- ment of severe ventricular tachycardia.

Overview of VT Management

It seems important to stress that ablation of VT is one aspect of the treatment of ventricular tachycardia.

The high success rate of ablation is also due to the ex- pertise of our group in the use of antiarrhythmic drugs, especially in the preparation of patients before the ablative techniques. For example, in a patient with poorly tolerated fast VT, or VT that degenerates rapidly to ventricular fibrillation, low-rate continu- ous injection of IV amiodarone or an oral loading dose is the first approach to therapy. In most cases, this causes a slower and more stable sustained monomorphic VT amenable to precise mapping and effective treatment by ablation.

The number of different morphologies of VT may vary during the follow-up due to disease pro- gression or simple modification of the arrhythmo-

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genic substrate without clear anatomic changes.

However, in some patients, multiple ablation at- tempts were necessary during the same session and it was confirmed that multiple morphologies of VT is not a deterrent for successful ablation.

In this study only two patients had an ICD be- fore ablation. However, ICD was frequently im- planted after the ablation or during the follow-up in order to protect the patient because of disease progression leading to new episodes of rapid VT or VF. Therefore ICD implantation was performed in nine patients. All patients with ICD had follow-up every 6 months. VTs were detected in the two ex- ceptional patients and led to rehospitalizations.

One patient had well tolerated asymptomatic VT interrupted by antitachycardia pacing (ATP), fol- lowed by two appropriate shocks in December, 2005, several VT episodes, and one appropriate shock in early 2006. Since then the patient has not had recurrent VT. Two patients had nonsustained VT. Three patients received inappropriate shocks.

One patient had palpitations but no recording of VT by the device.

New forms of VT observed during the follow-up may be related to disease progression and may re- quire additional ablation. In our experience, no pa- tient needed heart transplant for arrhythmia man- agement but one (in the low LVEF group), who re- cently had heart transplant for heart failure.

RF Antiarrhythmic Epicardial Surgery

Histologic material of the native heart of this trans- planted patient showed presence of fibro fatty re- placement of the myocardium of both ventricles.

Lymphocytes also involved both ventricles with the pattern of multifocal clusters mostly located in the subepicardial layers of the right ventricle.

RF antiarrhythmic epicardial surgery may prove effective in the most difficult cases resistant to endo- cardial RF ablation.

Overview of VT Ablation in the Literature

Several studies have reported a similar success rate in patients with ARVC/D. Verma et al. obtained a suc- cess rate of 82% on a series of 22 cases [19]. Several less clear studies concerning the definitions of cases included under the term of ARVC/D have been re-

ported by Marchlinski et al. on a series of 21 cases with a success rate of 89% [20]. Manaka et al. have reported a series of 41 patients with a success rate of 80% [21]. These results seems better than those ob- tained in idiopathic dilated cardiomyopathy in the study of Soejima et al., with a success rate of only 54% [22]. This is probably related to the anatomic structure of diseased myocardium in this particular entity. It should be noted that the definition of suc- cess is not uniform in the literature.

In summary:

1. Radiofrequency alone or in combination with fulguration is appropriate as a first approach for VT ablation in ARVD with a success rate of 90%.

2. In a resistant case it was possible to control in- cessant VT with surgical epicardial radiofrequen- cy ablation.

3. Overview of RF ablation of VT from the literature shows a similar success rate 80%-90% with the same long-term occurrence of new VTs during the follow-up.

Conclusions

ARVC/D is a structural heart disease, affecting young adults, leading to cardiac rhythm disorders, mostly ventricular arrhythmias. Sudden death may be the first presentation of the disease. Ablation techniques have been used for the treatment of VT cases resis- tant to drug therapy. The use of radiofrequency en- ergy is appropriate as a first approach for VT abla- tion in ARVC/D. Fulguration is effective for VT ab- lation and can be used after ineffective RF ablation.

However, these techniques requires expertise, gener- al anesthesia, and more than one session in half of patients.

Radiofrequency and/or fulguration plus other common forms of treatment, including pacemakers and ICDs, provided a clinical success rate of 95% in a series of 22 consecutive patients studied over 6 years. This result is in agreement with data re- ported by other centers and presented in the litera- ture. However, successful ablation achieved by epi- cardial surgical RF ablation was only obtained in one patient after failure of four consecutive ablation sessions incorporating both endocardial RF and DC energy.

This new technique of surgical epicardial ra- diofrequency ablation can be extended to other catheter-resistant arrhythmogenic substrates.

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Addendum

After submission of this chapter, Case #2 had two ap- propriate shocks for rapid VT documented by inter- rogation of the ICD memory. The drug regimen was not changed and no further arrhythmias were ob- served until the present time, three months after the ICD shocks. However, the patient developed increas- ing signs of heart failure and is now on the waiting list for heart transplant.

Acknowledgements

This work has been supported by grant N°99B0691 from the “Ministère de l’Education, de la Recherche et de la Technologie.” We would like to extend our gratitude to the team of colleagues who have per- formed the ablation procedures: J. Tonet, G. Jauvert, F. Halimi, Ph. Aouate, G. Lascault, F. Poulain, and N.

Johnson with special mention for our anesthesiolo- gist Y. Gallais, C. Himbert, V. Bors, cardiac surgeon are also acknowledged.

We also appreciate the work of Mrs. Samia Riguet, and Mrs. Deanna Bammer for their contribution in the preparation of the manuscript.

References

1. Fontaine G, Tonet J, Gallais Y et al (2000) Ventricular tachycardia catheter ablation in arrhythmogenic right ventricular dysplasia: A 16-year experience. Curr Car- diol Rep 2:498-506

2. McKenna WJ, Thiene G, Nava A et al (1994) Diagno- sis of arrhythmogenic right ventricula dysplasia/car- diomyopathy. Br Heart J 71:215-218

3. Tonet J, Himbert C, Johnson N et al (2000) Prolonga- tion of ventricular refractoriness and ventricular tachy- cardia cycle length by the combination of oral beta- blocker – Amiodarone in patients with ventricular tachycardia. PACE 23:565

4 Langberg J, Lee MA, Chin M, Rosenqvist M (1990) Ra- diofrequency catheter ablation: The effect of electrode size on lesion volume in vivo. PACE 13:1242-1248 5. Fontaine G, Cansell A, Lampe L et al (1987) Endocav-

itary fulguration (electrode catheter ablation): Equip- ment-related problems. In: Fontaine G, Scheiman MM (eds) Ablation in cardiac arrhythmias. Futura, Kisko, NY pp 85-100

6. Gallais Y, Lascault G, Tonet J et al (1993) Continuous measurement of coronary sinus oxygen saturation dur- ing ventricular tachycardia (abstract). Eur Heart J 14:368

7. Morady F, Frank R, Kou WH et al (1988) Identification and catheter ablation of a zone of slow conduction in the reentry. Circuit of ventricular tachycardias in hu- mans. J Am Coll Cardiol 11:775-782

8. Fontaine G, Frank R, Tonet J, Grosgogeat Y (1989) Identification of a zone of slow conduction appropri- ate for VT ablation. Theoretical and practical consid- erations. PACE 12:262-267

9. Stevenson WG, Khan H, Sager P et al (1993) Identi- fication of reentry circuit sites during catheter map- ping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction. Circula- tion 88:1647-1670

10. Man KC, Daoud E, Knight BP et al (1997) Accuracy of the unipolar electrogram for identification of the site of origin of ventricular activation. J Cardiovasc Elec- trophysiol 8:974-979

11. Harada T, Aonuma K, Yamauchi S et al (1998) Catheter ablation of ventricular tachycardia in patients with right ventricular dysplasia: Identification of tar- get sites by entrainment mapping techniques. PACE 21:2547-2550

12. Fontaliran F, Arkwright S, Vilde F, Fontaine G (1998) Arrhythmogenic right ventricular dysplasia and car- diomyopathy. Clinical and anatomic-pathologic as- pects, nosologic approach. Arch Anat Cytol Pathol 46:171-177

13. Fontaine G, Fontaliran F, Rosas Andrade F et al (1995) Arrhythmogenic right ventricle: Dysplasia or car- diomyopathy? Value of left ventricle ejection fraction.

Ann Cardiol Angeiol 44:321-331

14. Hulot JS, Jouven X, Empana JP et al (2004) Natural his- tory and risk stratification of arrhythmogenic right ventricular dysplasia/cardiomyopathy. Circulation 110:1879-1884

15. Feld GK (1998) Expanding indications for radiofre- quency catheter ablation: Ventricular tachycardia in as- sociation with right ventricular dysplasia. J Am Coll Cardiol 32:729-731

16. Wichter T, Hindricks G, Kottkamp H et al (1997) Catheter ablation of ventricular tachycardia. In: Ar- rhythmogenic right ventricular cardiomyopathy/dys- plasia. Nava A, Rossi L, Thiene G (eds) Elsevier Science BV, Amsterdam, pp 376-391

17. Marchlinski FE, Zado E, Dixit S et al (2004) Elec- troanatomic substrate and outcome of catheter ablative therapy for ventricular tachycardia in setting of right ventricular cardiomyopathy. Circulation 110:2293- 2298

18. Fontaine G, Fontaliran F, Lascault G et al (1994) Arrhythmogenic right ventricular dysplasia. In:

Cardiac electrophysiology. From cell to bedside.

Zipes DP, Jalife J (eds) WB Saunders, Philadelphia, pp 754-768

19. Verma A, Kiliscaslan F, Schweikert RA et al (2005) Short- and long-term success of substrate-based map- ping and ablation of ventricular tachycardia in ar- rhythmogenic right ventricular dysplasia. Circulation 111:3209-3216

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20. Marchlinski FE, Zado E, Dixit S et al (2004) Elec- troanatomic substrate of catheter ablation therapy for ventricular tachycardia in setting of right ventricular cardiomyopathy. Circulation 110:2293-2298

21. Manaka T, Shoda M, Tanisaki K et al (2005) Electro- physiological properties and long term outcome of catheter ablation for ventricular tachycardia ablation in

arrhythmogenic right ventricular cardiomyopathy – A single center experience. Circulation 112:624

22. Soejima K, Stevenson WG, Sapp JL et al (2004) Endo- cardial and epicardial Radiofrequency ablation of ven- tricular tachycardia with dilated cardiomyopathy: The importance of low voltage scars. J Am Coll Cardiol 43:1834-1842

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