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R. Le Bouar et al.
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ventricular cardiomyopathy/dysplasia and no prior
ventricular brillation or sustained ventricular tachycardia. Circulation. 2010;122(12):1144–52.
12. Corrado D, Leoni L, Link MS, Della Bella P, Gaita F,
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therapy for prevention of sudden death in patients
with arrhythmogenic right ventricular cardiomyopathy/dysplasia. Circulation. 2003;108(25):3084–91.
13. Mathew S, Saguner AM, Schenker N, Kaiser L,
Zhang P, Yashuiro Y, et al. Catheter ablation of
ventricular tachycardia in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia: a sequential approach. J Am Heart Assoc.
2019;8(5):e010365.
14. Tschabrunn CM, Marchlinski FE.Ventricular tachycardia mapping and ablation in arrhythmogenic
right ventricular cardiomyopathy/dysplasia: lessons
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15. Scanavacca M, Sosa E. Epicardial ablation of ventricular tachycardia in chagas heart disease. Card
Electrophysiol Clin. 2010;2(1):55–67.
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left ventricular cardiomyopathy. Circ Arrhythm
Electrophysiol. 2011;4(1):49–55.
17. Waintraub X, Gandjbakhch E.My approach to ventricular tachycardia ablation in patient with arrhythmogenic right ventricular cardiomyopathy/dysplasia.
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18. Venlet J, Piers SRD, Kapel GFL, de Riva M, Pauli
PFG, van der Geest RJ, et al. Unipolar endocardial
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Case 11
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BabéBakouboula, FrédéricHalbwachs, RonanLe
Bouar, JacquesLevy, CrinaMuresan,
CharlineDaval, LaurentDietrich,
andLucienDiene
11
Case Presentation
A 36-year-old male patient with a past medical
history of arrhythmogenic cardiomyopathy diagnosed at the age of 21years, with repeated episodes of sustained monomorphic VT treated with
a single-chamber ICD implantation and a catheter ablation procedure, recurrent paroxysmal
atrial brillation, ICD replacement for battery
depletion at the age of 31years, electrical storm
Supplementary Information The online version contains supplementary material available at https://doi.org/
10.1007/978- 3- 031- 35579- 0_11.
B. Bakouboula (*)
“Rhena” Hospital, Strasbourg, France
F. Halbwachs
Biosense Webster, Mulhouse, France
R. Le Bouar · J. Levy · C. Muresan · C. Daval
L. Dietrich · L. Diene
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr; levyj@ghrmsa.fr;
crina.muresan@ghrmsa.fr; charline.daval@ghrmsa.fr;
laurent.dietrich@ghrmsa.fr;
lucien-leopold.diene@ghrmsa.fr
treated with a catheter ablation procedure at the
age of 33 years in another center, and several
symptomatic recurrences of monomorphic VT
treated with electrical cardioversion, was
addressed to the cardiology department for an
episode of palpitations with sudden onset and
regular rhythm that had started 30min prior to
this arrival at the hospital. The patient had no cardiovascular risk factors. His medication at home
consisted of ecainide 200 mg/day, nadolol
240 mg, and potassium supplements 3600 mg/
day. Physical examination at admission revealed
a blood pressure of 110/70mmHg, heart rate of
120 bpm, SpO2 of 96% breathing room air,
H=1.75m, W=77kg, and BMI=25.14kg/m2,
heart sounds were regular and rapid, cardiac auscultation did not reveal any murmurs, lung auscultation was clear, and there were no signs of
right heart failure. His 12-lead ECG at admittance is presented in Fig.11.1.
The tachycardia failed to terminate by ventricular overdrive pacing using the ICD was
accelerated and transformed into a faster VT
which required electrical cardioversion
(Fig.11.2).
The ECG recorded after the electrical cardioversion is presented in Fig.11.3.
His biological workup showed a Hb level of
15.9 g/dL, leukocytes 10.05 × 109/L, platelets
254 × 109/L, CRP 3mg/L, BUN 5.2mmol/L, creatinine78 μmol/L, glycemia 5.4 mmol/L,
Na+141mmol/L, K+ 4.1mmol/L, NT pro-BNP
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
L. Muresan (ed.), Clinical Cases in Cardiac Electrophysiology: Ventricular Arrhythmias,
https://doi.org/10.1007/978-3-031-35579-0_11
163
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Fig. 11.1 A 12-lead ECG showing a wide QRS complex tachycardia with LBBB morphology inferior axis with a heart
rate of 140bpm
B. Bakouboula et al.
Fig. 11.2 A 12-lead ECG showing electrical cardioversion (red arrow) of a fast monomorphic VT and conversion to
sinus rhythm
30 pg/mL, TSH 2.13 IU/L, total cholesterol
209 mg/dL, HDL 37 mg/dL, LDL 149 mg/dL,
triglycerides = 245 mg/dL, HbA1c 5.5%,
D-dimers 215mg/mL, and INR 1.2.
His echocardiography revealed a non-dilated
left ventricle, with a LVEF of 68%, absence of
LV hypertrophy, normal diastolic function,
absence of signicant valve disease, and a nondilated right ventricle, with preserved longitudinal systolic function (TAPSE = 24 mm, lateral
tricuspid annulus S wave of 15 cm/s, FAC of
44%), a mild tricuspid regurgitation, absence of
pulmonary hypertension, sPAP of 25mmHg, and
no pericardial effusion (Fig.11.4).
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Fig. 11.3 A 12-lead ECG recorded at admittance to the cardiology department showing sinus rhythm with a heart rate
of 50bpm, QRS axis at +60°, absence of LV hypertrophy, and attened T waves in all 12 leads
165
Fig. 11.4 Left upper panel: Transthoracic echocardiog-
raphy image in parasternal long-axis view showing a nondilated LV and RV, with an end-diastolic diameter of
48 mm and 34 mm, respectively. Right upper panel:
Transthoracic echocardiography image in apical fourchamber view showing a non-dilated RV with a basal
diameter of 38 mm. Left lower panel: Apical fourchamber view showing mild tricuspid regurgitation with
the RV—RA pressure gradient of 20mmHg, in favor of
absence of pulmonary hypertension. Right lower panel:
Apical four-chamber view showing a non-dilated RV with
a fractional area change of 44%
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Question 1: What is the nature of the
tachycardia presented in Fig. 11.1?
A. AVNRT with phase 3 LBBB and iso-
lated PVC.
B. Antidromic tachycardia using a decre-
mentally conducting (Mahaim) bypass
tract.
C. Atrial utter with 2:1 AV conduction
and phase 3 LBBB, with isolated PVC.
D. Ventricular tachycardia.
E. Orthodromic tachycardia with phase 3
LBBB and isolated PVC.
F. Bundle branch reentry tachycardia.
B. Bakouboula et al.
Figure 11.1 explained: Fig. 11.1 shows a
wide QRS complex tachycardia with LBBB morphology inferior axis with a heart rate of 140bpm.
The QRS transition in the precordial leads takes
place in V5. The differential diagnosis of a wide
QRS complex tachycardia with LBBB and inferior axis comprises SVT with functional BBB
(AVNRT/orthodromic AVRT using a Kent accessory pathway or nodo-ventricular bers/atrial
utter/atrial tachycardia), preexcitation syndromes (antidromic AVRT using either a Kent or
a Mahaim accessory pathway), and ventricular
tachycardia (scar-related VT/ARVD VT/idiopathic VT/bundle branch reentry VT). The
patient’s history of arrhythmogenic cardiomyopathy is an argument in favor of a VT with origin
in the RVOT.Also, note that the ECG recorded in
sinus rhythm after the electrical cardioversion
shows ventricular bigeminy, with a LBBB inferior axis, suggesting an origin in the RVOT.
Given the patient’s history of several recur-
rences of VT after the catheter ablation procedure, the underlying heart disease, and the failure
of anti-arrhythmic medication, an electrophysiological study in view of another catheter ablation
procedure was offered and accepted by the
patient. A CT angiography scan was performed
prior to the ablation procedure; an image is presented in Fig.11.5. The 3D reconstruction of the
heart chambers was subsequently used by the
CARTO system (using the CARTOSEG module)
to guide mapping and ablation.
Fig. 11.5 Computed tomography angiography image
showing a non-dilated RV, with a LV/RV ratio>1
Electrophysiological Study andRF
Catheter Ablation Procedure
The ablation procedure was performed under
local anesthesia and conscious sedation. Vascular
access was obtained using the modied Seldinger
technique, under Doppler ultrasound guidance. A
6F bipolar non-steerable catheter (Viking, Boston
Scientic®) was introduced in a 6F 20cm vascular
sheath and was subsequently advanced via the
right common femoral vein up to the right ventricular apex. A Biosense Webster® SmartTouch
SF open-irrigated 3.5mm tip with double curve
D/F was used as the roving/ablation catheter,
which was introduced in a 9F 20 cm vascular
sheath in the right common femoral vein and
advanced up to the right ventricle. The CARTO®
3 electro-anatomic mapping system (Biosense
Webster, Johnson & Johnson) was used to guide
mapping and ablation.
Ventricular pacing was carried out at twice the
diastolic threshold using the EP-4™ Cardiac
Stimulator (Abbott®) system. Surface ECG and
intracavitary ECGs were recorded by the
WorkMate Claris™ System (Abbott®).
Programmed ventricular stimulation
(S1=600ms, S2=270ms, S4=340ms) induced
a sustained monomorphic ventricular tachycardia
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with a cycle length of 297ms, with LBBB and
inferior axis, which spontaneously transitioned to
the clinical VT (Fig.11.5). V-A dissociation was
present during the tachycardia. The clinical VT
was well tolerated by the patient.
Given the 12-lead aspect of the VT (LBBB
morphology inferior axis and a precordial transition in V5, with a “QS aspect” in V1–V4 and
unique R in V5, V6, a QRS width of 160ms), the
diagnosis of arrhythmogenic cardiomyopathy, an
origin at the level of the RVOT, was suspected.
Mapping RV was therefore commenced basal in
the RVOT.
An anatomical map of the RV was initially
created. This showed an RV with a volume of
120mL.Next, given the well-tolerated nature of
the VT, an activation map of the RV was created
during the tachycardia. This showed the presence
of an early activation zone at the level of the anterior basal and septal RVOT, from where the ventricular activation spread in a radial manner, in
favor of a focal mechanism (Fig.11.6). At this
level, the local bipolar electrogram recorded during VT had an amplitude of >1.5mV and pre-
ceded the onset of the QRS complex by 15ms.
The unipolar electrogram had a “QS” aspect. The
tachycardia terminated with mechanically
induced PVCs.
Next, a pacemap was subsequently created by
pacing from the distal electrode of the roving/
ablation catheter at a xed coupling interval of
600ms in several areas of the RVOT, with emphasis on the area of the earliest activation site
recording during VT. The PASO module of the
CARTO system was used to compare the resulting 12-lead ECG during local pacing with the
morphology of the PVC.A superposed correlation of 98% was observed at the level of the exit
zone of the VT, conrming it (Fig.11.7).
Given the good concordance between the activation map recorded during VT and the pacemap,
but indicating the same exit zone of the VT, RF
ablation was decided. This was performed with a
power of 30 watts. Of note, catheter stability was
an issue in this area. The activation map of the
RV and the bipolar voltage map of the RV with
superposed ablation lesions are shown in
Fig.11.8.
Fig. 11.6 A 12-lead ECG showing programmed ventricular stimulation with induction of a wide QRS complex
tachycardia with LBBB and inferior axis (VT 2), with a
cycle length of 297ms, different from the clinical VT (VT
1), spontaneously transitioning to a different morphology
of wide QRS complex tachycardia with LBBB and inferior axis, with a cycle length of 400ms, identical to the
clinical VT
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B. Bakouboula et al.
Fig. 11.7 CARTO image in LAO 41° cranial 17° showing in the left panel: The activation map of the RV during
the clinical VT (VT 1), with an exit zone situated in the
anterior and septal part of the RVOT (red zone, surrounded
by the red circle). On the lateral and the septal side of the
RVOT, the CT angiography images of the coronary arteries can be seen (dark red). Right panel: Pacemap of the
RVOT showing a correlation of 98% between the locally
Programmed ventricular stimulation was subsequently performed, after several RF lesions
were deployed in the area of the earliest endocardial activation (Fig.11.7). The clinical VT was no
longer inducible. However, the VT from the rst
part of the tracing in Fig. 11.6 was repeatedly
induced (VT 2, Fig.11.9).
Question 2: What is the origin of this
ventricular tachycardia?
A. Anteroseptal RVOT.
B. Posterior RVOT.
C. Lateral RVOT.
D. LVOT.
E. Epicardial RVOT.
induced QRS morphology (induced by local pacing of the
RV myocardium with the roving/ablation catheter) and
the morphology of the VT 2, indicating the exit zone of
the VT in this area. Of note, both the activation map and
the pacemap indicate the same exit site of the VT, conrming its location in this narrow area of the RVOT
This VT was hemodynamically moderately
tolerated. For this reason, activation mapping
was not performed. A pacemap was created for
this tachycardia (Figs. 11.10 and 11.11). This
was created by pacing from the distal electrode of
the roving/ablation catheter at a xed coupling
interval of 600ms in several areas of the RV, with
emphasis on the area of slow conduction during
sinus rhythm, based on the technique described
by de Chillou etal. [1, 2]. The PASO module of
the CARTO system was used to compare the
resulting 12-lead ECG during local pacing with
the morphology of the PVC.The best correlation
site between the locally induced QRS morphology and the morphology of the VT 2 was found in
an area at the level of the high septal part of the
RVOT, where the correlation between the 12-lead
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Fig. 11.8 CARTO image in LAO 30° view showing from
left to right: The 12-lead ECG aspect of the clinical VT
(VT 1), together with the bipolar local signal recorded by
the roving/ablation catheter (MAP 1–2), placed at the
level of the VT exit zone, the activation map of the RV
during VT 1 with superposed RF ablation lesions (white,
pink, and red dots) at the level of the clinical VT exit zone;
the bipolar voltage map of the RV with superposed RF
ablation lesions (white, pink, and red dots). Of note, no
low voltage area was found at the level of the endocardial
exit site of the VT
Fig. 11.9 A 12-lead ECG showing a monomorphic ventricular tachycardia (VT 2), with a cycle length of 292ms and
a QRS width of 140ms
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B. Bakouboula et al.
Fig. 11.10 CARTO image in LAO 98° cranial 36° showing the pacemap of the RV for VT 2. The red narrow zone
present at the level of the RV septum represents the site
with a correlations of 93% to 96% between the locally
induced QRS morphology (induced by local pacing of the
RV myocardium with the roving/ablation catheter) and
ECG during VT and the locally induced electrogram was of 96%. This was considered to be the
exit zone of the VT (Figs.11.10 and 11.11).
RF ablation was performed at the site with a
power of 30 watts. However, the VT remained
inducible each time during programmed ventricular stimulation. Of note, the best correlation site
between the locally induced QRS morphology
and that of the VT was constantly found elsewhere after each RF application, in a slightly different area compared to the one before the
ablation. The VT exit site seemed therefore to
move downward, toward the apical part of the IV
septum. This was strongly suggestive of an epicardial origin of the VT, with the tachycardia
arising from the epicardial surface of the RVOT,
with slightly different endocardial breakthrough
sites, modied by the RF lesions. The procedure
the morphology of the VT 2, indicating the exit zone of
the VT in this area (superposed electrograms visible in the
right side of the image). Note the proximity of the LAD
coronary artery (dark red) present in between the LV and
the RV.The yellow dots represent the bundle of His
was terminated. The bipolar voltage map of the
RV with superposed RF ablation procedure at the
end of the ablation is presented in Fig.11.12.
Question 3: Given the result of the
above-described ablation procedure,
what is the next best step in the management of this patient?
A. Stop ecainide + nadolol and start
sotalol treatment.
B. Replace ecainide with amiodarone.
C. Continue ecainide +nadolol, but
increase the dose of ecainide to
300mg/day.
D. Perform epicardial ablation of the VT.
E. Perform radioablation of the VT.
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Fig. 11.11 CARTO image in LAO 97° cranial 41° showing the CT angiography 3D reconstruction of the LV, the
RV, and the LAD coronary artery. The pacemap of the RV
for VT 2 is superposed with the 3D reconstruction of the
CT angiography image of the RV. The red narrow zone
present at the level of the RV septum represents the site
with a correlation of 96% between the locally induced
Given the fact that VT 2 remained inducible at
the end of the ablation procedure, the underlying
heart disease (arrhythmogenic cardiomyopathy),
the high likelihood of an epicardial origin of the
VT, the failure of anti-arrhythmic drugs in controlling VT recurrence (ecainide + a high dose
of nadolol), and the young age of the patient
which did not favor the administration of longterm amiodarone, an epicardial ablation procedure of the VT was programmed.
This was performed 1 month later, under general anesthesia. ICD detection was turned off.
Pericardial access was obtained using the
retrosternal subxiphoid approach, with an 18 G
Tuohy needle (Fig.11.13). The iodinated contrast
agent was sequentially injected during the puncture, until it entered the pericardial space. Once
QRS morphology (induced by local pacing of the RV
myocardium with the roving/ablation catheter) and the
morphology of the VT 2, indicating the exit zone of the
VT in this area (superposed electrograms visible in the
right side of the image). Note the proximity of the LAD
coronary artery (dark red) present in between the LV and
the RV.Yellow dots represent the bundle of His
inside the pericardial space, a 0.32180cm guidewire was introduced inside the Tuohy needle, and
it was advanced inside the pericardial space until
several loops were visible, conrming its position outside the heart. The needle was then
retracted and replaced by an Agilis Epi (Abbott©)
sheath. A Biosense Webster® SmartTouch SF
open-irrigated 3.5mm tip with double curve D/F
was used as the roving/ablation catheter for mapping the endocardial and epicardial RV.
Vascular access was then obtained using the
modied Seldinger technique, under Doppler
ultrasound guidance. A 6F bipolar non-steerable
catheter (Viking, Boston Scientic®) was introduced in a 6F 20cm vascular sheath and was subsequently advanced via the right common femoral
vein up to the right ventricular apex. The Biosense
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