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achieved in 63.6% of patients with LV aneurysm
and partial success in 27.3%. This was achieved
with no major or life-threatening complication.
Absence of VT at follow-up after a median of
19 months (1–44 months) was not signicantly
lower compared to patients without LV aneurysm,
p= 0.40. However, this needs to be interpreted
with caution, given the large absolute difference
between the two groups and the small number of
patients included: 11 patients vs. 22 patients,
48.5% vs. 62.8%. In our experience, caution is
needed when deploying RF lesions for VT ablation inside a ventricular aneurysm, since the LV
wall is thinner at this level and cardiac perforations have been described in such a context [13].
In our patient, due to the high number of induced
VTs, not all circuits could be mapped. Several
isthmi were present, some shared by different
VTs, all in the apical LV region. Among the
described isthmi, the isthmus of VT 7 was located
in a septo-apical region (Fig.15.28).
Concerning the ablation strategy used in the
above-presented case (substrate ablation), several
comments can be made. In such cases, of multiple monomorphic VTs originating in the same
area, with some of the VTs sharing the same VT
isthmus, especially in patients with poor hemodynamic tolerance of VTs due to a low LV EF%
(such as the above-presented case) or fast rates of
VTs, substrate ablation is preferred. This is
because the alternatives, activation mapping and
pacemapping during sinus rhythm, would be very
time-consuming for eight different VT morphologies. There are several ablation strategies
described when performing substrate ablation.
Some of these are mapping and ablating late
potentials (LP) and local abnormal ventricular
activities (LAVA) [14–16], identifying and ablating channels and performing scar “dechanneling”
[17, 18], isolating the core of the scar [19, 20]
and scar homogenization [21–23]. Each of these
described techniques has their advantages and
shortcomings, and each might be more useful
than the others in a specic context. In our
patient, we chose to perform connecting lines of
ablation and create a box-shape lesion, with some
of the lines transecting the mapped VT isthmi.
The characteristics of the VT isthmi in the
case of anterior MI were described by de Chillou
etal. [24]. In their experience, the VT isthmi are
perpendicular to the mitral valve and the tachycardia mechanism is a dual-loop or “gure of 8”
type of circuit in the large majority of cases
(92.85%). Single-loop circuits are rare (7.15%).
In our patient, all three fully characterized isthmi
were perpendicular to the mitral valve
(Figs.15.16, 15.19, and 15.28).
The substrate ablation strategy chosen for this
patient was successful. No VT recurrence was
documented by the ICD interrogation 6 months
after the ablation procedure. However, given the
large area of myocardial scar and the large number
of VT induced, the recurrence risk remains high.
Learning Points
• Catheter ablation is a useful tool in the
treatment of sustained monomorphic
ventricular tachycardia in patients with
ischemic cardiomyopathy.
• Catheter ablation is associated with a
signicant reduction in the number of
ICD discharges in patients with VT
storm.
• Substrate ablation is a good ablation
strategy in patients with a high number
of monomorphic VT originating in the
same area of myocardial scar.
• An electro-anatomical mapping system
is very helpful in guiding the ablation
procedure.
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Tomogr. 2012;6(2):121–6.
12. Guo JR, Zheng LH, Wu LM, Ding LG, Yao
Y. Aneurysm-related ischemic ventricular tachycardia: safety and efcacy of catheter ablation. Medicine.
2017;96(13):e6442.
13. Tokuda M, Kojodjojo P, Epstein LM, Koplan BA,
Michaud GF, Tedrow UB, etal. Outcomes of cardiac
perforation complicating catheter ablation of ven-
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14. Sacher F, Lim HS, Derval N, Denis A, Berte B,
Yamashita S, et al. Substrate mapping and ablation
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15. Jais P, Maury P, Khairy P, Sacher F, Nault I, Komatsu
Y, et al. Elimination of local abnormal ventricular
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in patients with scar-related ventricular tachycardia.
Circulation. 2012;125(18):2184–96.
16. Komatsu Y, Daly M, Sacher F, Derval N, Pascale P,
Roten L, etal. Electrophysiologic characterization of
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ventricular tachycardia with respect to their anatomic
location. Heart Rhythm. 2013;10(11):1630–7.
17. Berruezo A, Fernandez-Armenta J, Andreu D, Penela
D, Herczku C, Evertz R, et al. Scar dechanneling:
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18. Andreu D, Penela D, Acosta J, Fernandez-Armenta
J, Perea RJ, Soto-Iglesias D, et al. Cardiac magnetic resonance-aided scar dechanneling: inuence
on acute and long-term outcomes. Heart Rhythm.
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19. Santangeli P, Frankel DS, Marchlinski FE.End points
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for unstable ventricular tachycardia. Heart Rhythm.
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W, Yamakawa K, et al. Electrical homogenization
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Case 16
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FrédéricHalbwachs, RonanLe Bouar,
DidierBresson, Jean-YvesWiedemann,
LaurentDietrich, CharlineDaval,
RomaricBouillard, andJacquesLevy
16
Case Presentation
A 71-year-old male patient with a past medical
history of ischemic cardiomyopathy, with 90%
stenosis of the right coronary artery and 99% of
the circumex coronary artery treated with stent
implantation at the age of 59years; severe systolic dysfunction (LV EF% of 25%), in functional
class II NYHA; a single-chamber ICD implanted
at the age of 60years for the primary prevention
of sudden cardiac death, upgraded to a Saint Jude
Quadra Assura CRT-D at the age of 69 years;
repeated episodes of sustained monomorphic
ventricular tachycardia complicated by syncope
with cranial trauma and subdural hematoma; VT
treated with amiodarone administration; perma-
F. Halbwachs (*) · R. Bouillard
Biosense Webster, Mulhouse, France
R. Le Bouar · D. Bresson · J.-Y. Wiedemann
L. Dietrich · C. Daval · J. Levy
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr;
didier.bresson@ghrmsa.fr; wiedemannjy@ghrmsa.fr;
laurent.dietrich@ghrmsa.fr;
charline.daval@ghrmsa.fr; levyj@ghrmsa.fr
nent atrial brillation; and hyperthyroidism
related to amiodarone treatment which required
its interruption was addressed to the cardiology
department for repeated episodes of palpitations
with a rapid heart rate accompanied by dyspnea
at rest and anxiety that had started 2weeks prior
to his presentation at the hospital.
His cardiovascular risk factors were represented by age (> 55years old), a history of smoking (10 pack-years), arterial hypertension and
dyslipidemia.
His medication at home consisted of atorvastatin 40mg, bisoprolol 5mg, aspirin 75mg, fosinopril 10mg, esomeprazole 40mg, furosemide
500mg, and potassium supplements 2400mg.
At physical examination, the patient was in
respiratory distress; his blood pressure was
90/50 mmHg, HR 170 bpm, H = 175 cm,
W=65kg, and BMI of 21.22kg/m2; heart sounds
were rapid and regular; there were no cardiovascular murmurs; lung auscultation revealed bilateral basal crepitant rales; peripheral pulses were
barely perceptible; there were bilateral edema of
the lower limbs; and there was moderate hepatomegaly and jugular venous distension.
His ECG is presented in Fig.16.1.
After the spontaneous termination of the
tachycardia, the ECG in Fig.16.2 was recorded.
His blood workup showed a Hb level of
11.6 g/dL, leukocytes 4.16 × 109/L, platelets
126×109/L, CRP 3mg/L, BUN 8.8mmol/L, creatinine 124 μmol/L, glycemia 5.1 mmol/L,
© 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_16
247
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F. Halbwachs et al.
Fig. 16.1 A 12-lead ECG showing a wide QRS complex tachycardia with a heart rate of 180bpm, RBBB, and axis
at 0°
Fig. 16.2 A 12-lead ECG showing atrial brillation with biventricular pacing, with a heart rate of 70bpm and a ventricular couplet seen in leads V4 to V6
16 Case 16
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249
Fig. 16.3 Telemetry tracing (leads I, II, III, V1, aVR,
aVL, aVF) showing initiation of a wide QRS complex
tachycardia with a heart rate of 180 bpm, right bundle
Na+141mmol/L, K+ 3.6mmol/L, NT pro-BNP
2430 pg/mL, troponin 0.058 ng/mL
(NV<0.042ng/mL), TSH 0.39IU/L, total cholesterol 1.16 g/L, triglycerides 0.70 g/L, HDL
0.48g/L, and LDL 0.68g/L.
Telemetry tracings showed repeated episodes
of sustained and non-sustained episodes of the
wide QRS complex tachycardia. One of such episodes is presented in Fig.16.3.
Question 1: What is the nature of the
tachycardia presented in Fig. 16.1?
A. Antidromic tachycardia
B. Atrial utter with 2:1 AV conduction
and RBBB
C. Atrial brillation with RBBB
D. Ventricular tachycardia
E. Mahaim tachycardia
branch block, and inferior axis; P waves are best visible in
lead V1, with a 1:1 AV relationship
Figure 16.1 explained. The ECG in Fig.16.1
shows a wide QRS complex tachycardia with
RBBB aspect and axis at 0°. The aspect in lead
V1 (R wave taller than R’ wave) and the positive
concordance in precordial leads suggest the diagnosis of ventricular tachycardia. No ventricular–
atrial dissociation can be observed since the
patient is in permanent atrial brillation. The end
of the tracing shows the spontaneous termination
of the tachycardia.
Transthoracic echocardiography showed a
dilated LV (EDD of 72mm), with akinesia of the
inferior and lateral wall and severe global hypokinesia, with severe systolic dysfunction, a LVEF
of 17% (Simpson biplane method) (Fig. 16.4).
The LV lling pressures were elevated; there
were severe left atrial dilation (LA area of 40cm2)
and moderate functional mitral regurgitation
(SRO=0.14cm2), the cardiac index was 2.3L/
min/m2; the right ventricle was dilated, with an
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Fig. 16.4 Left panel: M-mode echocardiography showing a dilated left ventricle (end-diastolic diameter of 72mm).
Right panel: LV EF% quantied by biplane Simpson method at 17%, compatible with severe systolic dysfunction
F. Halbwachs et al.
EDS of 33cm2, an ESS of 21cm2, with a SF of
35%, and S wave amplitude TDI of 8cm/s; the
right atrium was dilated with a surface of 34cm2;
there were severe tricuspid regurgitation and
minimal pericardial effusion. The ventricular
electrode of the ICD was visible inside the right
ventricle, inserting in the region of the RV apex.
ICD interrogation revealed the presence of 38
episodes of sustained and non-sustained monomorphic ventricular tachycardia with a cycle
length of around 360–370ms during the 14days
prior to his admittance to the hospital, efciently
treated with burst pacing by the ICD, and 13 episodes of sustained monomorphic ventricular
tachycardia in the “monitor-only” zone. One of
such episodes is shown in Fig.16.5.
The patient’s chest X-ray is shown in Fig.16.6.
In order to rule out ongoing myocardial ischemia, coronary angiography was performed,
which demonstrated a nonsignicant lesion of
the distal part of the left common coronary artery,
an intermediate lesion of the proximal part of the
LAD coronary artery, intra-stent stenosis of the
proximal CX coronary artery, chronic occlusion
of the second marginal branch of the CX coronary artery, and absence of intra-stent restenosis
of the right coronary artery (Fig. 16.7).
Importantly, there were no signs of any unstable
acute atherosclerotic lesion.
Given the high number of episodes of ventricular tachycardia that the patient experienced during the 14days prior to his hospital admittance
and his past medical history of hyperthyroidism
due to amiodarone treatment, an
electrophysiological study in view of a catheter
ablation procedure was scheduled.
Question 2: What is the origin of the ven-
tricular tachycardia presented in Fig.
16.1?
A. LV inferior and basal wall
B. LV superior and basal wall
C. LV lateral wall
D. RV septum
E. LV apex
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251
Fig. 16.5 ICD interrogation showing the initiation of an episode of monomorphic VT (upper panel) with a cycle length
of around 360–370ms.
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Fig. 16.6 Chest X-ray in anteroposterior projection
showing an enlarged cardiac silhouette with an increased
cardio-thoracic index. The ICD is visible in the right subclavian region, with the distal end of the right ventricular
lead visible at the level of the right ventricular apex, the
left ventricular lead visible in the distal part of a lateral
vein of the coronary sinus, and the atrial lead with its distal end at the level of the right atrial appendage
F. Halbwachs et al.
Fig. 16.7 Left panel: Angiography image of the left
coronary artery showing no major obstruction of the
LAD.The coil of the ventricular electrode of the ICD is
also visible, inserting in the apical region of the right ventricle. The ICD is visible in the upper right side of the
image. Right panel: Absence of intra-stent restenosis of
the right coronary artery, a vessel of small caliber. The coil
of the ventricular electrode of the ICD is visible in the
inferior part of the image, and the LV lead is visible in the
middle part of the image
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Electrophysiological Study andRF
Catheter Ablation Procedure
The electrophysiological study and the ablation
procedure were performed under local anesthesia
and conscious sedation. Vascular access was
obtained using the modied Seldinger technique,
under Doppler ultrasound guidance. A 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 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 pacing was performed under basal conditions at the level of RV
apex easily induced the clinical ventricular tachycardia, which was rapidly accompanied by a drop
in the arterial blood pressure of 30 mmHg and
that required prompt termination by programmed
ventricular stimulation.
Question 3: Given the fact that the VT
was not tolerated by the patient during
the EP study, what would be an appro-
priate ablation strategy in this case?
A. Substrate ablation– “carpet bombing”
of the suspected area of origin.
B. Substrate ablation – entire “scar
isolation.”
C. VT substrate identication using pace-
mapping in sinus rhythm and subse-
quent ablation.
D. LAVA ablation.
E. No ablation should be performed in
this case.
Based on the morphology of the QRS complex during VT on the 12-lead ECG, an origin in
the basal inferior LV was suspected. A decision
to perform mapping of the VT substrate and identify the VT circuit during sinus rhythm was taken.
Access to the left ventricle was obtained using
a retrograde approach by puncturing the right
common femoral artery using the modied
Seldinger technique, under Doppler ultrasound
guidance. A Pentaray catheter (Biosense Webster,
Johnson & Johnson) was introduced in a 9F
20 cm vascular sheath and was subsequently
advanced via the aorta to the LV.It was used to
perform the anatomical and the bipolar voltage
map of the LV.A Biosense Webster® SmartTouch
SF open-irrigated 3.5mm tip with double curve
D/F was used to perform RF ablation.
An anatomical map of the LV was rst created, which showed a severely dilated LV, with a
volume of almost 300mL.A bipolar voltage map
was subsequently created during RV apical pacing, which showed the presence of a large area of
low-voltage electrograms at the level of the inferior wall of the LV, extending from the mitral
valve to the mid-LV inferior wall, measuring
36.1cm2, representing 15.0% of the total LV surface, compatible with scar post-myocardial
infarction (Figs.16.8 and 16.9).
Inside the myocardial scar at the level of the
inferior LV wall, LAVA could be recorded by the
Pentaray catheter (Fig.16.10).
Given the fact that the clinical VT was poorly
tolerated by the patient, an activation map during
VT was considered difcult to create. A decision
to identify the critical components of the VT
(entrance point, exit point, and the critical isthmus) during sinus rhythm, with the help of a
pacemap, using an already described technique
[1] was taken.
The pacemap was created by pacing from the
distal electrode of the roving/ablation catheter at
a xed coupling interval of 600 ms in several
areas of the LV, with emphasis on areas situated
in or close to the myocardial scar, as initially
described by de Chillou etal. [1, 2]. The PASO
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Fig. 16.8 CARTO
image in AP view
showing the bipolar map
of the LV during RV
apical pacing. A voltage
<0.5mV was considered
compatible with
myocardial scar, values
between 0.5 and 0.5mV
correspond to borderline
tissue, and values over
0.5mV are dened as
normal myocardial
tissue. Of note, no
low-voltage area could
be identied at the level
of the anterior LV wall
F. Halbwachs et al.
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 97% was observed in
an area of the basal inferior wall, inside the myocardial scar, at the junction with the lateral inferior wall of the LV, identifying the exit zone of
the VT (Fig.16.11). This is explained by the fact
that activation of the LV during pacing proceeds
from this site in a manner similar as that during
VT.The resulting QRS morphology is therefore
identical to the QRS morphology during VT.
Pacing the LV in adjacent zones of the exit
zone identied sites with slightly different correspondence percentages. Pacing of the different
adjacent sites was continued until a site was found
where the morphology of the paced QRS complex
differed signicantly from the morphology of the
QRS during VT. This identied the area corresponding to the entrance zone during VT.This is
explained by the fact that during ventricular pacing, the depolarization of the LV takes place in the
direction opposite to that of the VT isthmus
(where slow conduction is present), toward
healthy ventricular myocardium, where the conduction velocity is superior to the conduction at
the level of the VT isthmus. The resulting morphology is therefore very different (Fig.16.12).
Between the entrance and the exit zones, the
VT isthmus was delineated (white parallel lines
in Fig. 16.12). The schematic representation of
the VT circuit is shown in Fig.16.13. This is a
double-loop “gure of 8” circuit, with one loop
rotating around the mitral annulus and the other
loop rotating in the opposite direction, around the
lower boundary of the VT isthmus.
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