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Fig. 19.23 Chest X-ray in posteroanterior view showing
the presence of a single-chamber ICD with the lead placed
at the level of the apical part of the RV
R. Le Bouar et al.
Fig. 19.24 A 12-lead ECG recorded after the ablation procedure showing sinus rhythm with a heart rate of 72bpm,
QRS axis at +80°, absence of LV hypertrophy, and negative T waves in leads III and aVF
Commentary
The present case illustrates a catheter ablation
procedure of a sustained monomorphic ventricular tachycardia in a 55-year-old male patient with
ischemic cardiomyopathy and prior inferior myocardial infarction with nonobstructive coronary
arteries (MINOCA). Several observations can be
made about the present case.
A rst observation would be that patients with
MINOCA can, as a consequence of myocardial
infarction, subsequently develop a myocardial
arrhythmogenic substrate than can sustain myocardial reentry and give rise to sustained monomorphic ventricular tachycardia, similar to
patients with myocardial infarction with
obstructive coronary arteries. In the experience of
Biere et al. [3], who performed an observation
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study on patients with MINOCA and normal
LVEF%, the percentage of patients developing
ventricular arrhythmias during hospitalization in
the acute phase was 13.8%. There was a statistically signicant difference between patients with
late gadolinium enhancement demonstrated by
cardiac MRI and those without: 26.5% vs. 4.0%
developed ventricular arrhythmias during the
follow-up period of 1year. On multivariate analysis, late gadolinium enhancement transmural
extent [OR=1.52 (1.08–2.15), p=0.017] was an
independent predictor of ventricular arrhythmic
events, emphasizing the role of myocardial scar
in increasing the risk of future ventricular
arrhythmias. Our above-presented patient demonstrated the presence of late gadolinium
enhancement on cardiac MRI, as seen in
Fig. 19.6. Another risk factor for ventricular
arrhythmia development in our patient was the
severe systolic dysfunction (LV EF%) of 35%.
The association of severe ventricular dysfunction, prior myocardial infarction, and the future
risk of signicant ventricular arrhythmias is well
known [4–9]. Furthermore, even though patients
with MINOCA are considered to have a better
prognosis than patients with myocardial infarction and obstructive coronary arteries, cases of
sudden cardiac death have been reported in
patients after MINOCA [10]. In the VIRGO trial
[11], there were 299 patients with MINOCA
included, which represented 11% of the entire
population. Four of these patients (1.3%) presented with SCD and required ICD
implantation.
MINOCA patients presenting as STEMI may
develop heart failure and recurrent VT, even after
catheter ablation [12]. This is another strong
argument supporting the role of ICD implantation
in the secondary prevention of SCD in this population of patients.
Another aspect related to this case that merits
discussion is the aspect of the 12-lead ECG
recorded during VT (Fig.19.1). The differential
diagnosis of ventricular tachycardia with RBBB
morphology and superior axis is scar-related VT,
fascicular ventricular tachycardia (reentry in the
posteroinferior fascicle), and interfascicular
reentry VT [13]. This is extremely important,
since the last two entities can exist both in patients
with and without structural heart disease. For an
example of a catheter ablation procedure performed for fascicular ventricular tachycardia
(reentry in the posteroinferior fascicle), the reader
is invited to see Case 8. In the absence of a myocardial substrate (in patients with structurally
normal hearts), implantation of an ICD has a
class III recommendation (not recommended)
according to the current guidelines on the management of patients with ventricular arrhythmias
and prevention of sudden cardiac death [14]. The
situation is different in patients with structural
heart disease, such as in the present case, where
the VT arises from a zone of myocardial scar
post-myocardial infarction. In such cases, even
after a successful catheter ablation procedure,
implantation of an ICD is recommended [14],
since the existence of a myocardial scar can give
rise to other VT circuits in the future. In the
above-presented patient, both the activation map
(Fig. 19.16) and the pacemaps recorded while
pacing during sinus rhythm (Figs. 19.12 and
19.14) indicated the presence of a VT isthmus at
the level of the inferior and posterior LV wall.
These maps, together with the substrate map (the
bipolar voltage map recorded during sinus
rhythm presented in Figs.19.9, 19.10, and 19.11),
conrmed the mechanism of the VT: a dual-loop
or “gure of 8” macro-reentry circuit, related to
the presence of myocardial scar post-myocardial
infarction, despite the 12-lead ECG aspect of the
VT that might have suggested the presence of
fascicular ventricular tachycardia (reentry in the
posteroinferior fascicle) and interfascicular reentry VT.
Another observation related to this catheter
ablation procedure would be the ablation strategy
used in this case. The identication of the VT origin and its critical components: VT isthmus,
entrance zone, and exit zone were accomplished
by creating different maps with the CARTO system. As presented in the commentary section of
Case 18, we rst performed substrate mapping in
sinus rhythm, in order to identify the myocardial
scar evidenced by the cardiac MRI presented in
Fig.19.6. Most of sustained monomorphic ventricular tachycardias in patients with ischemic
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cardiomyopathy and prior myocardial infarction
originate in the zone of myocardial scar, not in
the zone of dense myocardial scar, but in zones
where surviving intact myocardial bers coexist
with disrupted myocardial bers, or in borderline
zones, at the junction of myocardial scar with
healthy myocardial tissue. Such is the case in the
above-presented case (see for comparison
Figs.19.9, the bipolar voltage map recorded during sinus rhythm, and Fig.19.16, the activation
map recorded during VT). After the substrate
map identied the presence of myocardial scar,
pacemapping during sinus rhythm was performed
according to the technique described by de
Chillou et al. [1, 2]. The identication of the
myocardial scar during the previous phase,
together with the aspect of the VT on the 12-lead
ECG, allowed the performing physician to concentrate the pacemapping phase on the area
around the myocardial scar. This is time-saving,
since creating a pacemap for the entire left ventricle, especially in patients with dilated LV can
be very time-consuming.
Once the critical components of the VT were
identied with this technique, initiation of ventricular tachycardia during programmed electrical stimulation was performed. Activation
mapping conrmed the ndings of the pacemaps
acquired during sinus rhythm. Catheter ablation
was subsequently performed, at the level of the
VT isthmus, with a good result.
Another observation that can be made about
this case is a technical observation related to the
approach of the left ventricle. We chose to perform a retrograde approach of the mitral valve,
via the aorta, since this is the most commonly
used technique performed in our center for this
type of ablation procedure. The alternative is the
transseptal approach, which is accompanied by
similar results [15]. This is related to the operator’s experience and preference, with some operators performing both types of approaches in all
patients. The transseptal approach has been
claimed to provide a somewhat limited access to
the interventricular septum [15].
R. Le Bouar et al.
Learning Points
• Patients with MINOCA can develop a
ventricular substrate as a consequence
of myocardial infarction that can sustain
myocardial reentry and give rise to sustained monomorphic ventricular
tachycardia.
• The differential diagnosis of ventricular
tachycardia with RBBB morphology
and superior axis is scar-related VT and
fascicular tachycardia (reentry in the
posteroinferior fascicle).
• Catheter ablation with the help of an
electro-anatomical mapping system of
sustained monomorphic ventricular
tachycardia is a good treatment option
in these cases.
• A good ablation strategy is to create several different maps, providing complementary information: 1. the substrate
map (the bipolar voltage map) recorded
during sinus rhythm, 2. the activation
map recorded during ventricular tachycardia, and 3. the pacemap(s) created
while pacing during sinus rhythm.
• In the presence of structural heart disease, especially in ischemic heart disease with prior myocardial infarction,
implantation of an ICD remains recommended even in cases of successful
catheter ablation procedure, given the
risk of VT recurrence.
References
1. de Chillou C, Groben L, Magnin-Poull I, Andronache
M, MagdiAbbas M, Zhang N, et al. Localizing the
critical isthmus of postinfarct ventricular tachycardia:
the value of pace-mapping during sinus rhythm. Heart
Rhythm. 2014;11(2):175–81.
2. de Chillou C, Sellal JM, Magnin-Poull I.Pace mapping
to localize the critical isthmus of ventricular tachycardia. Card Electrophysiol Clin. 2017;9(1):71–80.
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3. Biere L, Niro M, Pouliquen H, Gourraud JB, Prunier
F, Furber A, et al. Risk of ventricular arrhythmia
in patients with myocardial infarction and nonobstructive coronary arteries and normal ejection
fraction. World J Cardiol. 2017;9(3):268–76.
4. Lane RE, Cowie MR, Chow AW.Prediction and prevention of sudden cardiac death in heart failure. Heart.
2005;91(5):674–80.
5. Bhar-Amato J, Davies W, Agarwal S. Ventricular
arrhythmia after acute myocardial infarction: ‘The
perfect Storm’. Arrhythmia Electrophysiol Rev.
2017;6(3):134–9.
6. Bardy GH, Lee KL, Mark DB, Poole JE, Packer
DL, Boineau R, etal. Amiodarone or an implantable
cardioverter- debrillator for congestive heart failure.
N Engl J Med. 2005;352(3):225–37.
7. Stecker EC, Chugh SS.Prediction of sudden cardiac
death: next steps in pursuit of effective methodology.
J Interv Card Electrophysiol. 2011;31(2):101–7.
8. Hohnloser SH, Kuck KH, Dorian P, Roberts
RS, Hampton JR, Hatala R, et al. Prophylactic
use of an implantable cardioverter-debrillator
after acute myocardial infarction. N Engl J Med.
2004;351(24):2481–8.
9. Moss AJ, Zareba W, Hall WJ, Klein H, Wilber DJ,
Cannom DS, et al. Prophylactic implantation of
a debrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med.
2002;346(12):877–83.
10. Kosmas N, Manolis AS, Dagres N, Iliodromitis
EK. Myocardial infarction or acute coronary syndrome with non-obstructive coronary arteries and sudden cardiac death: a missing connection. Europace.
2020;22(9):1303–10.
11. Spatz ES, Curry LA, Masoudi FA, Zhou S, Strait KM,
Gross CP, etal. The variation in recovery: role of gender on outcomes of young AMI patients (VIRGO)
classication system: a taxonomy for young women
with acute myocardial infarction. Circulation.
2015;132(18):1710–8.
12. Li B, Ming Z, Wu J, Zhang M. Nonobstructive
coronary artery myocardial infarction complicated
by heart failure, ventricular aneurysm, and incessant ventricular arrhythmia: a case report. Medicine.
2019;98(2):e13995.
13. Chen H, Shi L, Yang B, Ju W, Zhang F, Yang G,
et al. Electrophysiological characteristics of bundle
branch reentry ventricular tachycardia in patients
without structural heart disease. Circ Arrhythm
Electrophysiol. 2018;11(7):e006049.
14. Priori SG, Blomstrom-Lundqvist C, Mazzanti A,
Blom N, Borggrefe M, Camm J, et al. 2015 ESC
guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden
cardiac death: the task force for the management of
patients with ventricular arrhythmias and the prevention of sudden cardiac death of the European Society
of Cardiology (ESC) Endorsed by: Association for
European Paediatric and Congenital Cardiology
(AEPC). Europace. 2015;17(11):1601–87.
15. Pluta S, Lenarczyk R, Pruszkowska-Skrzep P,
Kowalski O, Sokal A, Sredniawa B, etal. Transseptal
versus transaortic approach for radiofrequency
ablation in patients with cardioverter-debrillator
and electrical storm. J Interv Card Electrophysiol.
2010;28(1):45–50.
Case 20
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BabéBakouboula, FrédéricHalbwachs, RonanLe
Bouar, YasmineDoghmi, LaurentDietrich,
AubrietiaLawson, DidierBresson,
andJacquesLevy
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Case Presentation
A 69-year-old male patient with a past medical
history of ischemic heart disease from the age of
50years (but with nonobstructive coronary arteries demonstrated during coronary angiography),
with dilated cardiomyopathy with moderate systolic dysfunction (LV EF of 42% on cardiac
MRI), with remote infero-lateral myocardial
infarction (with an area of necrosis at the level of
the inferior and infero-lateral LV wall demonstrated by cardiac MRI and absence of myocardial viability in these territories), with aborted
sudden cardiac death due to fast VT at the age of
58 years, with subsequent implantation of a
Boston Scientic single-chamber ICD for the
secondary prevention of sudden cardiac death,
and highly differentiated locally invasive adenocarcinoma of the colon (T1N1M0) at the age of
65years treated with surgery and chemotherapy
B. Bakouboula (*)
“Rhena” Hospital, Strasbourg, France
F. Halbwachs
Biosense Webster, Mulhouse, France
R. Le Bouar · Y. Doghmi · L. Dietrich · A. Lawson ·
D. Bresson · J. Levy
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr;
yasmine.hadjidj@ghrmsa.fr;
laurent.dietrich@ghrmsa.fr; bree.lawson@ghrmsa.fr;
didier.bresson@ghrmsa.fr; levyj@ghrmsa.fr
was admitted to the cardiology department due to
an episode of electrical discharge by the ICD preceded by palpitations that occurred during mild
physical effort (walking). His cardiovascular risk
factors were represented by age>55years, arterial hypertension, dyslipidemia, overweight, a
past history of smoking, and a family history of
heart disease (father with myocardial infarction
at the age of 55years). His medication at home
consisted of nadolol 80mg, atorvastatin 20mg,
aspirin 75mg, and perindopril 4mg.
Physical examination at admission revealed a
blood pressure of 111/62 mmHg, heart rate of
55 bpm, SpO2 of 98% breathing room air,
H=1.83m, W=92kg, and BMI=27.47kg/m2;
heart sounds were regular, cardiac auscultation
did not reveal any murmurs, lung auscultation
was clear, and there were no signs of right heart
failure.
His 12-lead ECG is presented in Fig.20.1.
ICD interrogation revealed an episode of fast
monomorphic VT with a cycle length of 260ms,
classied in the VF window, unsuccessfully
treated with anti-tachycardia pacing, converted to
sinus rhythm by a single internal electric shock of
40J.
Transthoracic echocardiography revealed a
non-dilated LV with an end-systolic diameter of
55mm, with moderate systolic dysfunction (LV
EF of 40%), with hypokinesia of the inferolateral basal LV wall, with type 1 diastolic dysfunction, non-elevated LV lling pressure,
© 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_20
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Fig. 20.1 A 12-lead ECG showing sinus rhythm, with a heart rate of bpm, QRS axis at +30°, absence of LV hypertrophy, absence of ischemia, and one isolated PVC
B. Bakouboula et al.
Fig. 20.2 Left panel: transthoracic echocardiography
image in parasternal long-axis view showing a non-dilated
LV and RV, with a LV end-diastolic diameter of 55mm.
absence of signicant valve disease, non-dilated
right heart chambers, absence of pulmonary
hypertension, with a non-dilated aorta, and
absence of pericardial effusion (Fig.20.2).
His chest X-ray demonstrated a silhouette,
absence of pulmonary stasis, absence of pleural
effusion, no image compatible with an infectious
trigger at the level of the pulmonary parenchyma,
the presence of a single-chamber ICD with the
distal end of the electrode at the level of the IVS
septum, and the presence of an implantable
Right panel: transthoracic echocardiography image in
apical four- chamber view showing a moderately
depressed LV EF of 39%
venous access device (IVAD) at the level of the
right subclavian vein (Fig.20.3).
His biological workup showed a Hb level of
14.5 g/dL, leukocytes 7.63 × 109/L, platelets
190×109/L, CRP<3mg/L, BUN 5.0mmol/L,
creatinine 94 μmol/L, glycemia 5.6 mmol/L
(non-fasting), Na+141mmol/L, K+ 4.1mmol/L,
cTnI 0.03ng/mL, TSH 2.76IU/L, total cholesterol 176mg/dL, HDL 41mg/dL, LDL 108mg/
dL, triglycerides 135 mg/dL, and NT-pro BNP
160pg/mL.
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Fig. 20.4 CT angiography image performed before the
ablation procedure showing the ratio between the LV and
the RV>1 and the absence of an intracavitary thrombus
Fig. 20.3 Chest X-ray image in posteroanterior view
showing a non-enlarged cardiac silhouette with a normal
cardiothoracic index, the presence of a single-chamber
ICD with the distal end of the electrode at the level of the
IVS septum, and the presence of an implantable venous
access device (IVAD) at the level of the right subclavian
vein
Question 1: What would be your sug-
gested management of this patient, given
his past medical history and his current
reason of admittance?
A. Increase the dose of nadolol for pre-
venting VT recurrence.
B. Initiate amiodarone treatment for pre-
venting VT recurrence.
C. Perform a catheter ablation procedure
of the VT.
D. Upgrade the ICD to a triple-chamber
ICD.
E. Perform an electrophysiological study
with the ICD, and, if positive (induction of monomorphic VT), perform
catheter ablation.
Given the patient’s past medical history of
aborted sudden cardiac death, the presence of
ischemic cardiomyopathy with a remote inferior
myocardial infarction, of a fast monomorphic
VT, and the occurrence of VT despite beta
blocker treatment, a catheter ablation procedure
was offered and subsequently performed.
A CT angiography was performed (Fig.20.4),
in order to guide the catheter ablation procedure
and to exclude the presence of an LV thrombus.
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.
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 (no isoprenaline
administration) with induction of a wide QRS
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Fig. 20.5 A 12-lead ECG showing the induction of a monomorphic ventricular tachycardia during programmed ventricular stimulation, with a cycle length of 287ms, with an atypical LBBB aspect and superior axis
B. Bakouboula et al.
complex tachycardia with a cycle length of
280ms (Fig.20.5). The tachycardia was not well
hemodynamically tolerated and was terminated
by burst ventricular pacing.
Question 2: What is the origin of the
tachycardia presented in Fig. 20.5?
A. Infero-lateral wall of the LV
B. Infero-septal wall of the LV
C. Epicardial origin
D. Anterolateral wall of the LV
E. Anteroseptal wall of the LV
Given the personal history of ischemic heart
disease and remote inferior myocardial infarction
and the LBBB morphology on the 12-lead ECG
during VT with a double transition in the precordial leads suggesting a septal origin, mapping of
the VT substrate was 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 20cm
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.The Biosense Webster® SmartTouch SF openirrigated 3.5mm tip with double curve D/F was
used to perform the pacemap.
An anatomical map of the LV was rst created, which showed a mildly dilated LV, with a
volume of 210mL.A bipolar voltage map was
subsequently created during sinus rhythm, which
showed the absence of myocardial scar, with a
possible exception of a very small area of borderline voltage at the level of the postero-septal and
inferior wall of the LV, of uncertain signicance
(Figs.20.6 and 20.7). The unipolar voltage map
of the LV revealed a much wider area of lowvoltage electrograms situated at the level of the
posterior and inferior wall of the LV, possibly
suggesting the presence of an epicardial substrate
of the VT (Figs.20.8 and 20.9).
Given the fact that an activation map of the VT
during VT was not possible to perform due to the
hemodynamically unstable character of the VT, a
pacemap of the LV was decided.
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Fig. 20.6 CARTO image in RAO 45° caudal 50° showing the anatomical map of the left ventricle with a dilated
LV (volume of 206mL), with the superposed bipolar voltage map created with the Pentaray catheter. Of note, there
is no area of low voltage, compatible with myocardial
scar, with the exception of a very small area of borderline
voltage at the level of the postero-septal and inferior wall
of the LV, of uncertain signicance. The orange dots represent the bundle of His
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Fig. 20.8 CARTO image in inferior view showing the
anatomical map of the left ventricle with a dilated LV
(volume of 206mL), with the superposed bipolar voltage
map created with the Pentaray catheter. A small area of
low voltage at the level of the posteroinferior wall of the
LV, of uncertain signicance. The orange dots represent
the bundle of His
Fig. 20.7 CARTO image in RAO 45° caudal 50° (same
as in Fig.20.6) showing the anatomical map of the left
ventricle with a dilated LV (volume of 206mL), with the
superposed unipolar voltage map created with the
Pentaray catheter. An area of low voltage situated at the
level of the posterior and inferior wall of the LV can be
seen, possibly suggesting the presence of an epicardial
substrate of the VT.The orange dots represent the bundle
of His
Fig. 20.9 CARTO image in inferior view (same as in
Fig.20.8) showing the anatomical map of the left ventricle with a dilated LV (volume of 206mL), with the superposed bipolar voltage map created with the Pentaray
catheter. An area of low voltage situated at the level of the
posterior and inferior wall of the LV can be seen, possibly
suggesting the presence of an epicardial substrate of the
VT.The orange dots represent the bundle of His
The pacemap 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 LV, with emphasis on the
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B. Bakouboula et al.
basal inferior wall of the LV, as initially
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 superposed correlation of (only)
64% between the locally induced QRS mor-
phology and the VT morphology was observed
in a small area of the basal inferior wall
(Figs.20.10 and 20.11). No higher correlation
was found elsewhere in the LV.
A careful analysis of the ECG from Fig.20.5
is subsequently presented. This shows elements
in favor of an epicardial origin of the VT.
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