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F. Halbwachs et al.
Fig. 13.12 A 12-lead ECG recorded after the ablation
procedure showing sinus rhythm with a heart rate of
75bpm; QRS axis at −20°; Q waves in leads II, III, and
Commentary
The present case illustrates a RF catheter ablation
procedure of an electrical storm in a 77-year-old
male patient with ischemic cardiomyopathy and
a prior history of remote inferior myocardial
infarction. Several observations can be made
about the present case.
Electrical storm is dened by the presence of
three or more sustained episodes of ventricular
tachycardia/ventricular brillation/appropriate
ICD shocks within a period of 24h. Its incidence
varies between 4 and 20% of ICD recipients [1,
2]. It is an important cause of sudden cardiac
death, which raises a lot of therapeutic challenges, mostly related to the severity of the
arrhythmia, the underlying heart disease, and the
patient’s comorbidities. The ventricular arrhythmias responsible for electrical storm are represented by monomorphic VT in 86–97% of
patients, followed by ventricular brillation in
1–21% of patients, mixed (VT/VF) in 3–14% of
cases, and polymorphic VT in 2–8% of cases.
aVF compatible with remote inferior wall necrosis; attened T waves In leads II, III, and aVF; negative T waves
in leads V5 and V6
Electrical storm can arise in patients with a
chronic condition such as myocardial scar in
patients with previous myocardial infarction with
a superposed trigger and in patients with primary
cardiac inherited arrhythmia syndromes (such as
the Brugada syndrome), or it can arise in an
acute, reversible context, such as acute myocardial ischemia, acutely decompensated heart failure, electrolyte abnormalities (hypokalemia,
hypomagnesemia), drug toxicity/overdose
(including anti-arrhythmic drugs), sepsis, or
thyrotoxicosis.
Several decisional and therapeutic algorithms
have been proposed for the management of
patients with electrical storm [3–5]. Catheter
ablation is an efcient technique for the treatment of VT storm in patients with both ischemic
and nonischemic cardiomyopathy [6, 7]. It is
associated with elimination of VT episodes in up
to 89% of patients (number of catheter ablation
procedures needed between 1 and 3) and substantially reduces the number of ICD discharges during follow-up in survivors, with 66% of patients
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being free from VT recurrence after a median
follow-up period of 22months [6].
In patients with ischemic cardiomyopathy and
remote myocardial infarction, the most common
form of ventricular arrhythmia is sustained
monomorphic VT [5]. This usually originates in a
zone of myocardial scar or in a borderline zone
between the myocardial scar and normal myocardial tissue. Therefore, identication of the myocardial scar during the pre-ablation phase is
essential, in order to orient the cardiac electrophysiologist regarding the ablation strategy. This
can be done before the beginning of the ablation
procedure, using transthoracic 3D contrastenhanced echocardiography to identify zones of
akinesia [8], multidetector cardiac computed
tomography [9], nuclear techniques [10], and
cardiac MRI [11–15], the latter being able to
show areas of late gadolinium enhancement,
which are reliable markers of myocardial scar.
During the ablation procedure, this can be done
with the use of intracardiac echography [16] and
with electro-anatomical mapping systems, which
allow the creation of bipolar voltage maps, able
to differentiate healthy myocardium from myocardial scar [17]. It is widely accepted that dense
myocardial scar corresponds to areas of very low
bipolar voltage (conventionally dened as
≤0.5mV), normal myocardial tissue to areas of
voltage >1.5mV, and borderline areas to values
between 0.5mV and 1.5mV [18–21]. Creation
of high-density maps with the use of multipolar
electrodes (such as the Pentaray catheter) has
become the current standard [17]. For the abovepresented patient, this is illustrated in Fig.13.6.
The low-voltage area represented 22% of the
entire surface of the LV, compatible with a large
myocardial scar. The origin of VT was subsequently looked for in this area and in the regions
adjacent to it. This was done by performing activation mapping.
Activation mapping using a multielectrode
diagnostic catheter and an electro-anatomical
mapping system are the method of choice for
identication of the VT circuit [22–24]. However,
this method is not feasible in cases of fast VTs
with hemodynamic compromise or in cases when
the VT is not inducible during programmed ventricular stimulation. In all other cases, this is the
preferred method for tachycardia mapping, given
its high potential in describing the arrhythmia
mechanism (macro-reentry or focal) and in identifying the main components of the VT (see
Figs.13.7 and 13.8). Additional techniques, such
as entrainment mapping, pacemap during sinus
rhythm, and mapping of late potentials, should be
used as complements to activation mapping in
order to conrm the abovementioned ndings. In
the above-presented patient, the activation map
demonstrated the presence of a macro-reentry
circuit at the level of the infero-septal LV, with a
double-loop activation pattern, the VT isthmus
being situated in a borderline zone between the
dense myocardial scar and the healthy myocardium (see Fig.13.8).
Conrmation of the localization of the VT circuit was subsequently done by creating a pacemap. For a detailed discussion about the technique
used for identication of the critical VT components (exit zone, entrance zone, and VT isthmus)
using pacing during sinus rhythm, as originally
described by de Chillou etal. [25], see the commentary section of cases 14, 16, 18, and 19.
Ablation of the VT isthmus plus ablation of
LAVA was successfully performed, and the
patient remains tachycardia-free 2years after the
ablation procedure.
Learning Points
• Catheter ablation is an important option
in the treatment of electrical storm.
• The bipolar voltage map performed during sinus rhythm offers important information about the substrate of ischemic
VT, due to its capability of identifying
myocardial scar.
• Performing activation mapping during
VT is the option of choice for ablation
guidance, provided that the VT is hemodynamically well tolerated.
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• In cases where activation mapping cannot be performed, pacemapping during
sinus rhythm can identify the critical
components of the VT (exit zone,
entrance zone, and VT isthmus). This
allows efcient catheter ablation, especially in patients for whom the VT is
not inducible during the ablation
procedure.
References
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9. Komatsu Y, Cochet H, Jadidi A, Sacher F, Shah A,
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11. Alcaine A, Jauregui B, Soto-Iglesias D, Acosta J,
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Ordonez A, Teres C, et al. Arrhythmogenic substrate
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14. Roca-Luque I, Van Breukelen A, Alarcon F, Garre P,
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Fernandez-Armenta J, Linhart M, et al. Cardiac
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T, Gurm G, etal. Assessment of ventricular tachycardia scar substrate by intracardiac echocardiography.
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17. Tschabrunn CM, Roujol S, Dorman NC, Nezafat R,
Josephson ME, Anter E.High-resolution mapping of
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2016;9(6):e003841.
18. Vergara P, Roque C, Oloriz T, Mazzone P, Della
BP.Substrate mapping strategies for successful ablation of ventricular tachycardia: a review. Arch Cardiol
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R, etal. Electroanatomic substrate and ablation outcome for suspected epicardial ventricular tachycardia
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21. Hsia HH, Lin D, Sauer WH, Callans DJ, Marchlinski
FE. Anatomic characterization of endocardial substrate for hemodynamically stable reentrant ventricular
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tachycardia: identication of endocardial conducting
channels. Heart Rhythm. 2006;3(5):503–12.
22. Waspe LE, Brodman R, Kim SG, Matos JA, Johnston
DR, Scavin GM, etal. Activation mapping in patients
with coronary artery disease with multiple ventricular
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23. Dixit S, Callans DJ.Mapping for ventricular tachycardia. Card Electrophysiol Rev. 2002;6(4):436–41.
24. Pandozi C, Lavalle C, Russo M, Galeazzi M, Ficili
S, Malacrida M, etal. Mapping of ventricular tachycardia in patients with ischemic cardiomyopathy: current approaches and future perspectives. Clin Cardiol.
2019;42(10):1041–50.
25. de Chillou C, Groben L, Magnin-Poull I, Andronache
M, MagdiAbbas M, Zhang N, et al. Localizing the
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Case 14
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RonanLe Bouar, FrédéricHalbwachs,
MatthieuGeorge, DidierBresson, JacquesLevy,
CrinaMuresan, SerbanSchiau, andCharlineDaval
14
Case Presentation
A 69-year-old male patient with a past medical
history of coronary artery disease (chronic total
occlusion of the RCA); remote inferior myocardial infarction at the age of 49years treated with
best medical therapy; recurrent sustained monomorphic ventricular tachycardia treated with ICD
implantation, complicated by ICD pocket infection treated with ICD removal and reimplantation
of the ICD in the right subclavian region at the
age of 52years; chronic obliterative arterial disease of the lower limbs treated by unilateral (left)
aortofemoral bypass surgery; gout; and hyperthyroidism secondary to amiodarone administration
was addressed to the cardiology department for
two electrical discharges from his ICD 2h prior
to his admittance to the hospital, which obliged
him to seek immediate medical care.
His cardiovascular risk factors were represented by age (> 55 years old), smoking (40
pack-years), arterial hypertension, dyslipidemia,
R. Le Bouar (*) · D. Bresson · J. Levy · C. Muresan
S. Schiau · C. Daval
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr;
didier.bresson@ghrmsa.fr; levyj@ghrmsa.fr;
crina.muresan@ghrmsa.fr; serban.schiau@ghrmsa.fr;
charline.daval@ghrmsa.fr
F. Halbwachs · M. George
Biosense Webster, Mulhouse, France
grade 1 overweight, and a family history of early
atherosclerosis. His medication at home consisted of atorvastatin 20 mg, bisoprolol 5 mg,
aspirin 75 mg, valsartan 80 mg, esomeprazole
20mg, and febuxostat 80mg.
At physical examination, his blood pressure
was 123/63 mmHg, HR 67 bpm, H = 167 cm,
W=80kg, and BMI of 28.68kg/m2, heart sounds
were regular, there were no cardiovascular murmurs, lung auscultation was clear, peripheral
pulses were perceptible, and there were no signs
of right heart failure.
His blood workup showed a Hb level of
14.0 g/dL, leukocytes 8.08 × 109/L, platelets
194×109/L, CRP 2mg/L, BUN 6.5mmol/L, creatinine 82 μmol/L, glycemia 6.2 mmol/L,
Na+141mmol/L, K+ 4.5mmol/L, NT pro-BNP
571 pg/mL, troponin 0.089 ng/mL
(NV<0.042ng/mL), AST 18IU/L, ALT 42IU/L,
GGT 172IU/L, and proteins 62g/L.
His ECG is presented in Fig.14.1.
Telemetry recording during hospitalization
documented episodes of a wide QRS complex
tachycardia (Fig.14.2).
A 12-lead ECG was recorded during an episode of palpitations while in hospital (Fig.14.3).
Of note, the morphology of the PVC recorded in
limb leads in Fig.14.3 is very similar to the morphology of the wide QRS complex tachycardia
from the telemetry tracing presented in Fig.14.2,
and lead V1 shows morphology of RBBB in both
Figs.14.2 and 14.3. It is therefore likely that the
© 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_14
209
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R. Le Bouar et al.
Fig. 14.1 A 12-lead ECG showing sinus rhythm; heart
rate of 75bpm; QRS axis at −30°; Q waves in leads II, III,
and aVF, compatible with remote inferior wall necrosis;
initial R wave in V1 suggestive of remote lateral wall
necrosis [1]; and negative T waves in V5, V6, lead I, and
aVL suggesting lateral ischemia
Fig. 14.2 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
branch block, and inferior axis; P wave is best visible in
lead V1, with a 1:1 AV relationship
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Fig. 14.3 A 12-lead ECG with the limb leads showing sinus rhythm with ventricular trigeminy, followed by a wide
complex QRS tachycardia with a heart rate of 188bpm and RBBB aspect
211
tachycardias presented in Fig. 14.2 and in
Fig.14.3 are episodes of the same tachycardia.
Question 1: What is the nature of the
tachycardia from Fig. 14.3?
A. Antidromic tachycardia
B. AVNRT with RBBB
C. 2:1 atrial utter with RBBB
D. AVRT with RBBB
E. Ventricular tachycardia
Figure 14.3 explained. A 12-lead ECG with
the limb leads showing sinus rhythm with ventricular trigeminy, followed by a wide complex
QRS tachycardia with a heart rate of 188 bpm
and RBBB aspect. The aspect in lead V1 (R wave
taller than R’ wave) and the ratio of r/S<1in V6
suggest the diagnosis of ventricular tachycardia
Transthoracic echocardiography showed a
non-dilated LV (EDD of 51mm), with akinesia
of the inferior and lateral wall, with moderate
systolic dysfunction, a LVEF of 40% (Simpson
biplane method) (Fig.14.4). There was also type
1 diastolic dysfunction; the LV lling pressure
was within normal range; there was mild left
atrial dilation (LA area of 21cm2) and mild mitral
regurgitation by restriction of the posterior mitral
leaet; the cardiac index was 1.52L/min/m2; the
right ventricle was non-dilated; there was mild
tricuspid regurgitation, with sPAP of 28mmHg,
absence of pulmonary hypertension, and absence
of pericardial uid. The ventricular electrode of
the ICD was visible inside the right ventricle,
inserting in the region of the RV apex.
His chest X-ray is presented in Fig.14.5.
In order to rule out ongoing myocardial ischemia, coronary angiography was performed,
which demonstrated chronic occlusion of the
right coronary artery (Fig. 14.6), with no acute
atherosclerotic lesion, an aspect similar to his
coronary angiography performed 3years prior.
ICD interrogation (Medtronic Evera VR)
revealed the presence of 104 episodes of monomorphic ventricular tachycardia with a cycle
length of 310bpm during the 4months prior to
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R. Le Bouar et al.
Fig. 14.4 Left upper panel: M-mode echocardiography
showing a non-dilated left ventricle (end-diastolic diameter of 51mm) with moderately reduced LV EF% of 42%.
Right panel upper: LV EF% quantied by Simpson
biplane method at 39.88%, compatible with moderate systolic dysfunction. Left lower panel: pulsed Doppler inter-
Fig. 14.5 Chest X-ray in anteroposterior
projection showing an enlarged cardiac
silhouette with an increased
cardiothoracic index. The ICD is visible
in the right subclavian region, with the
distal end of the ventricular lead visible
at the level of the right ventricular apex.
The sternal wires post-sternotomy are
also visible. The proximal coil of the
abandoned ICD lead is visible in the left
innominate vein, entering the SVC.The
distal part of the old ICD lead had been
removed
rogation of the transmitral ux showing an E/A ratio<1,
with a E wave deceleration time>200ms, in favor of type
1 diastolic dysfunction. Right lower panel: Apical fourchamber view showing a mildly dilated left atrium, with a
surface of 21.5cm
2
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Fig. 14.6 Left panel: angiography image of the left cor-
onary artery showing no major obstruction of the epicardial vessel. The coil of the ventricular electrode of the
ICD is also visible, inserting in the apical region of the
right ventricle. The sternal wires post-sternotomy are visible in the upper left side of the image. Right panel:
his admittance to the hospital, efciently treated
with burst pacing by the ICD, 99 episodes of sustained monomorphic ventricular tachycardia in
the “monitor-only” zone, and two episodes of
sustained monomorphic VT treated with electrical cardioversion (35 Joules) after failed burst
ventricular pacing, corresponding to the electrical discharges felt by the patient the day of his
admittance to the hospital.
Given the high number of episodes of ventricular tachycardia that the patient experienced during the 4months prior to his hospital admittance
that lately required internal cardioversion for
termination, an electrophysiological study in
view of a catheter ablation procedure was
scheduled.
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
chronic obstruction of the epicardial right coronary artery
in its proximal segment (red arrow). The coil of the ventricular electrode of the ICD is visible in the inferior right
part of the image. The sternal wires post-sternotomy are
visible in the left side of the image
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 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 and after isoprenaline infusion, up to three extrastimuli, at two
coupling intervals, 600 ms and 400 ms, at the
level of RV apex and RVOT, without induction of
any sustained ventricular tachycardia. This was
probably due to the anti-arrhythmic drugs that the
patient received in the intensive care unit. Only
short runs of the clinical monomorphic V were
induced.
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Question 2: Given the fact that the VT
was not inducible during the EP study,
what would be an appropriate ablation
strategy in this case?
A. Substrate ablation—“carpet bombing”
the suspected area of origin.
B. Substrate ablation—entire “scar
isolation.”
C. VT substrate identication using pace-
mapping in sinus rhythm and ablation.
D. LAVA ablation.
E. No ablation should be performed in
this case.
A decision to perform mapping of the VT sub-
strate and identify the VT circuit using pacing
during sinus rhythm was taken.
Given the personal history of ischemic heart
disease and remote inferior myocardial infarction, and the morphology on the 12-lead ECG
during VT, an origin in the LV was suspected.
Mapping of the VT was therefore commenced in
the left ventricle.
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
was used to perform RF ablation.
An anatomical map of the LV was rst cre-
ated, which showed a non-dilated LV, with a volume of 143 ml. A bipolar voltage map was
subsequently created during sinus rhythm, which
showed the presence of a large area of lowvoltage electrograms at the level of the inferior
wall of the LV, extending from the mitral valve to
the LV apex, measuring 32 cm2, representing
20.0% of the total LV surface, compatible with
scar post-myocardial infarction (Fig.14.7).
R. Le Bouar et al.
Fig. 14.7 CARTO image in LAO 180° showing the
infero-lateral wall of the left ventricle. Bipolar voltage
map of the left ventricle revealing a large area of low voltage (< 0.5mV, red color) at the level of the infero-lateral
wall, compatible with myocardial scar post-myocardial
infarction
Given the fact that the clinical VT was not
induced during PVS, an activation map during
VT was impossible to create. However, the morphology of the induced non-sustained VT during
PVS was used during the creation of the pacemap, in order to compare the QRS morphology
resulted from local LV pacing with the QRS morphology during VT, in order to identify the critical components of the VT circuit.
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. [2, 3]. 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 99.4% was observed in
an area of the mid-inferior LV wall, at the level of
the myocardial scar, at the junction of the two
distal thirds with the proximal third, identifying
the exit zone of the VT (Fig.14.8). This good correlation 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.
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