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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3651_Библиотеки_им_академика_М_И_Перельмана
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Fig. 11.12 CARTO
image in LAO 60°
showing the bipolar
voltage map of the RV
next to the CT
angiography image with
the 3D reconstruction of
the LV.In dark red, the
CT angiography
reconstruction of the
coronary arteries. Note
the absence of lowvoltage areas at the level
of the endocardial RV,
present in red color, with
the exception of a small
area just below the level
of the pulmonary valve
B. Bakouboula et al.
Fig. 11.13 Left panel: Radioscopy image in LL 90°
showing the performance of pericardial puncture enabling
pericardial access, with the needle (red arrow) entering
the pericardial space, injecting a small amount of iodinated contrast agent inside the pericardial space (yellow).
The ICD is visible with the coil at the level of the RV
apex. Right panel: Radioscopy image of the heart in LAO
35° showing the Agilis Epi (Abbott©) sheath entering the
pericardium, with the guidewire present inside the pericardium, performing several loops extending from the left
cardiac border to the right cardiac border, demonstrating
the presence of the guidewire inside the pericardium, not
at the level of the RVOT.The ICD is visible with the coil
at the level of the RV apex
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Webster® SmartTouch SF catheter was introduced in a 9F 20cm 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
of the accessory pathway.
Ventricular pacing was carried out at twice the
diastolic threshold using the Cardiac Stimulator
of the Boston Scientic® system. Surface ECG
and intracavitary ECGs were recorded by the Lab
System Pro (Boston Scientic®).
First, a bipolar voltage map of the endocardial
RV was created. This showed the presence of
normal voltage in all areas of the RV with the
exception of two small areas at the level of the
anterior RV (Fig.11.14).
Programmed ventricular stimulation was then
performed with the induction of a monomorphic
VT, identical to the one from Fig. 11.9, which
remained inducible at the end of the previous
ablation procedure. Given the hemodynamically
moderately well-tolerated nature of the tachycardia, inotropic support with norepinephrine was
used at a dose of 0.1 μg/kg/min.
Mapping of the epicardial RVOT was then
performed. The activation map of the RVOT during tachycardia elucidated its mechanism: a
macro-reentry circuit at the level of the anterior
RVOT, with an exit zone at the level of the junction of the RVOT with the LVOT, an entrance
zone at the level of the junction of the anterior
RVOT with its lateral part, an isthmus parallel to
the pulmonic valve and two outer loops, creating
a “gure of 8” circuit (Fig.11.15).
Coronary angiography was subsequently performed, in order to rule out the proximity of a
major coronary artery branch to the VT isthmus.
No coronary artery was in close vicinity to the
key components of the VT circuit (Fig.11.16).
The bipolar voltage map of the epicardium
recorded during sinus rhythm is presented in
Fig. 11.17. This showed the presence of a very
wide area of low-voltage electrograms at the
level of the RV (< 0.5 mV), demonstrating an
advanced stage of the disease, with normal voltage at the level of the LV.
RF ablation was performed in a powercontrolled mode, with a target of 30 watts.
Several RF lesions were deployed at the level of
Fig. 11.14 CARTO image in LAO 60° showing the bipolar voltage map of the RV next to the CT angiography
image with the 3D reconstruction of the LV.Note the presence of three low-voltage areas at the level of the endocardial RV, present in red/yellow color at the level of the
anterior/septal part of the basal RVOT, probably as a con-
sequence of the previous catheter ablation procedure,
since these had not been present before the rst RF ablation of the VT (see Fig.11.11 for comparison). The yellow
star represents the VT endocardial exit site, determined by
activation mapping (see Fig.11.15)
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B. Bakouboula et al.
Fig. 11.15 CARTO image in AP view showing the epicardial activation map recorded during the clinical VT, in
favor of a macro-reentry circuit, with its key components:
the entrance zone (blue), the VT isthmus (light blue to
violet), the exit zone (violet), and the two outer loops (violet to red to green and back to light blue). The yellow
the VT isthmus, creating a line perpendicular to
it, transecting it.
The superposed epicardial and endocardial
maps of the RV at the end of the ablation procedure are presented in Fig.11.18.
Programmed ventricular stimulation was performed with up to three extrastimuli, which was
negative. ICD detection and therapies were
reactivated.
There were no complications related to the
procedure.
The ECG recorded after the ablation procedure is presented in Fig.11.19.
arrows are superposed for learning purpose. The yellow
star represents the VT exit site. Of note, this is situated in
an area just above the endocardial VT exit site, explaining
the good pacemap obtained by pacing the RV endocardium in this area
The anti-arrhythmic treatment was stopped.
Telemetry tracings did not record any VT recurrence. The patient was discharged home 48h later.
ICD interrogation of up to 18months after the
ablation procedure showed no VT recurrence.
Answers
Question 1: D.Ventricular tachycardia.
Question 2: E.Epicardial RVOT.
Question 3: D.Perform epicardial VT
ablation.
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Fig. 11.16 Left upper panel: Radioscopy image in
anteroposterior view showing the anatomy of the left main
coronary artery with its branches. There is no stenosis of
the epicardial left coronary artery. The roving/ablation
catheter is placed in the upper part of RVOT, and the
Agilis Epi (Abbott ©) sheath is placed inside the pericardium. The ICD is visible in the upper right corner of the
image and the ventricular lead is inserted at the level of
the RV apex. Right upper panel: Same projection as in
the left upper panel, with the roving/ablation catheter at
the level of the anterior and septal part of the RVOT. Left
lower panel: Radioscopy image in anteroposterior view
with the roving/ablation catheter positioned at the level of
the endocardial exit site of the VT. Right lower panel:
The roving/ablation catheter positioned at the level of the
epicardial exit site of the VT
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Fig. 11.17 CARTO image in LAO 30°, cranial 30°
showing the epicardial bipolar voltage map of the RV and
LV demonstrating the presence of a large area of low voltage electrograms (< 0.5mV, in red color) situated at the
level of the entire anterior and lateral wall of the RV.The
CT angiography 3D reconstruction of the coronary arteries is superposed, with the LAD artery showing the delimitation between the RV and the LV. Note the difference
Fig. 11.18 CARTO
image in LAO 30°,
cranial 35° showing the
endocardial bipolar
voltage map of the RV
with superposed RF
ablation lesions (pink/
red dots) deployed at the
level of the epicardial
anterior wall of the
RV.The CT angiography
3D reconstruction of the
LV is presented next to
the RV bipolar voltage
map. In glass color, the
superposed epicardial
anatomical map of the
RV and the LV
between the RV and the LV epicardium voltage, with the
LV having a wide area of normal (> 1.5mV) voltage (violet). The yellow star represents the VT exit site. The pink/
red dots represent RF ablation lesions deployed at the
level of the epicardial VT isthmus and exit site. In glass
color, the CT angiography 3D reconstruction of the RV,
LV, and the aorta are superposed
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Fig. 11.19 A 12-lead ECG recorded after the ablation procedure
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Commentary
The present case illustrates two catheter ablation
procedures of two sustained monomorphic ventricular tachycardia in a 36-year-old male patient
with arrhythmogenic cardiomyopathy. Several
observations merit further discussion.
Ventricular arrhythmias represent the major
manifestation of arrhythmogenic cardiomyopathy. These range from isolated premature ventricular beats to sustained episodes of ventricular
tachycardia and ventricular brillation. Clinical
manifestations include palpitations, dyspnea,
pre-syncope, syncope, and sudden cardiac death.
Arrhythmogenic cardiomyopathy is one of the
primary causes of sudden cardiac death in young
adults, accounting for 11% of causes and 22% of
cases in competitive athletes [3].
The most common origin of sustained monomorphic ventricular tachycardia is the
RVOT. As discussed in the Commentary section of Case 10, other potential origins include
the RV apex, the RV lateral wall, and LV sites.
The most common VT morphology in patients
with arrhythmogenic cardiomyopathy is LBBB
with superior axis (36.8%), followed by LBBB
inferior axis (26.3%), LBBB indeterminate axis
(21%), indeterminate morphology (13%), and
RBBB pattern in 2.6% [4]. Recently,
Marchlinski etal. [5] showed in their population of 110 patients with arrhythmogenic cardiomyopathy that TV with RBBB morphology
can be found in 17% of patients and that the
majority of these VTs actually originate in the
right ventricle (62%). An early precordial QRS
transition (in leads V2 of V3) with a superiorly
and typically leftward axis deviation in the
frontal plane is indicative of a RV origin,
despite a RBBB morphology. The authors
explain this by an exit VT site from the dilated
RV close to the inferior LV septum.
Treatment options for arrhythmias in the context of arrhythmogenic cardiomyopathy include
anti-arrhythmic drugs, namely, beta-blockers (in
particular sotalol [6]), class I anti-arrhythmic
drugs (ecainide [7]), and class III anti-
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B. Bakouboula et al.
arrhythmic drugs (amiodarone [8]), alone or in
association [7]. However, their efcacy is limited
and side effects represent limitations in their
widespread use. ICD implantation is currently
indicated in patients with aborted SCD and
hemodynamically poorly tolerated VT, in patients
with hemodynamically well-tolerated sustained
VT, and may be considered in patients with one
or more risk factors for ventricular arrhythmias in
patients with a life expectancy of at least 1year
[9]. Besides these two treatment options, catheter
ablation has emerged as an attractive strategy in
reducing the VT arrhythmia burden and in reducing the number of ICD discharges [10].
The most common approach method for VT
ablation is the endocardial approach. However,
this has been associated with a high acute failure
rate and high recurrence rates in patients with
arrhythmogenic cardiomyopathy, given the frequent epicardial nature of the arrhythmic substrate. An epicardial-only approach has been
described, but a combined epicardial and endocardial approach is the most efcient ablation
strategy in these patients. This has been associated with a higher rate of acute and long-term
success. The preferred strategy is scar dechanneling or scar homogenization [11].
In a recent meta-analysis conducted by Shen
etal. including 24 studies on 717 patients [12],
epicardial ablation of VT in patients with arrhythmogenic cardiomyopathy had an acute success
rate of 89.8%, a long-term success evaluated
after a follow-up period of 28.9months of 75.3%,
with a major complication rate of 5.2%. When
only the main ten studies were analyzed, compared to an endocardial-only approach, epicardial VT ablation signicantly decreased VT
recurrence (OR 0.5; 95% CI 0.30–0.85, p=0.01),
but with an increase in the major complication
rate (OR 4.64, 95% CI 1.28–16.92, p=0.02) and
with no signicant reduction in all-cause mortality (OR 0.87, 95% CI 0.09–8.31, p=0.9).
In our above-presented patient, the rst
endocardial- only ablation procedure did not
result in acute termination of VT. Programed
ventricular stimulation demonstrated VT inducibility at the end of the procedure, and an epicardial substrate was considered to be the most
likely cause of acute ablation failure. The presence of an epicardial substrate for the VT was
identied during the second ablation procedure
(Fig.11.14). The activation map of the RV epicardial surface demonstrated the VT isthmus in
an area of low voltage of the epicardial RVOT.RF
ablation of the VT substrate terminated the VT
and rendered it non-inducible.
Learning Points
• Sustained monomorphic ventricular
tachycardia is a frequent manifestation
in patients with arrhythmogenic
cardiomyopathy.
• Catheter ablation is a useful complement to ICD implantation in the treatment of these patients.
• An epicardial approach is necessary in
almost half of the patients in order to
achieve acute success.
• A combined endocardial—epicardial
approach has the highest success rate in
the catheter-based treatment of these
patients.
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.
3. Gemayel C, Pelliccia A, Thompson
PD. Arrhythmogenic right ventricular cardiomyopathy. J Am Coll Cardiol. 2001;38(7):1773–81.
4. Marcus FI, Zareba W. The electrocardiogram in
right ventricular cardiomyopathy/dysplasia. How
can the electrocardiogram assist in understanding the
pathologic and functional changes of the heart in this
disease? J Electrocardiol. 2009;42(2):136.e1–5.
5. Marchlinski DF, Tschabrunn CM, Zado ES, Santangeli
P, Marchlinski FE.Right bundle branch block ventricular tachycardia in arrhythmogenic right ventricular
cardiomyopathy more commonly originates from the
right ventricle: criteria for identifying chamber of origin. Heart Rhythm. 2021;18(2):163–71.
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179
6. Wichter T, Borggrefe M, Haverkamp W, Chen X,
Breithardt G. Efcacy of antiarrhythmic drugs in
patients with arrhythmogenic right ventricular disease. Results in patients with inducible and noninducible ventricular tachycardia. Circulation.
1992;86(1):29–37.
7. Ermakov S, Gerstenfeld EP, Svetlichnaya Y,
Scheinman MM. Use of ecainide in combination
antiarrhythmic therapy in patients with arrhythmogenic right ventricular cardiomyopathy. Heart
Rhythm. 2017;14(4):564–9.
8. Marcus GM, Glidden DV, Polonsky B, Zareba W,
Smith LM, Cannom DS, etal. Efcacy of antiarrhythmic drugs in arrhythmogenic right ventricular cardiomyopathy: a report from the North American ARVC
registry. J Am Coll Cardiol. 2009;54(7):609–15.
9. 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.
10. 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.
11. Romero J, Mejia-Lopez E, Manrique C, Lucariello
R.Arrhythmogenic right ventricular cardiomyopathy
(ARVC/D): a systematic literature review. Clin Med
Insights Cardiol. 2013;7:97–114.
12. Shen LS, Liu LM, Zheng LH, Hu F, Hu ZC,
Liu SY, et al. Ablation strategies for arrhythmogenic right ventricular cardiomyopathy: a systematic review and meta-analysis. J Geriatr Cardiol.
2020;17(11):694–703.
Case 12
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FrédéricHalbwachs, RonanLe Bouar,
MatthieuGeorge, TarekEl Nazer,
LaurentJacquemin, LaurentDietrich,
SerbanSchiau, andJacquesLevy
12
Case Presentation
A 40-year-old female patient with a history of
remote inferior myocardial infarction at the age
of 35 years (thrombotic occlusion of the right
coronary artery in the second segment) treated
with PTCA + stent implantation, ischemic cardiomyopathy with moderate to severe LV systolic
dysfunction (LVEF of 36%), chronic total occlusion of the right coronary artery due to in-stent
restenosis, and systemic lupus erythematosus,
and former heroin addict on methadone, was
Supplementary Information The online version contains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 35579- 0_12.
F. Halbwachs (*) · M. George
Biosense Webster, Mulhouse, France
R. Le Bouar · T. El Nazer · L. Jacquemin · L. Dietrich
S. Schiau · J. Levy
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr;
tarek.elnazer@ghrmsa.fr; jacqueminl@ghrmsa.fr;
laurent.dietrich@ghrmsa.fr;
serban.schiau@ghrmsa.fr; levyj@ghrmsa.fr
admitted to the emergency department for an episode of palpitations with sudden onset accompanied by dizziness, retrosternal chest pain, nausea,
anxiety, and near syncope that had started 15min
prior to her presentation at the hospital. Her palpitations had spontaneously stopped before arriving in the emergency department. Her
cardiovascular risk factors were represented by
active smoking (20 pack-years) and type 2 diabetes mellitus. Her medication at home consisted of
ramipril 1.25mg, spironolactone 12.5mg, metoprolol long release 97 mg, pravastatin 60 mg,
venlafaxine 75 mg, quetiapine LR 400 mg,
paracetamol 3000 mg, hydroxychloroquine
400mg, prednisone 5mg, alprazolam 2mg, and
mycophenolic acid 2000 mg. The patient was
addressed to the cardiology department for further investigations and treatment.
At physical examination, her blood pressure
was 105/67 mmHg, HR 72 bpm, SpO2 96%
breathing room air, H=1.60m, W=63kg, and
BMI = 24.6kg/m2, heart sounds were regular,
there was a mild systolic murmur in the mitral
auscultation region, lung auscultation was clear,
and there were no signs of right heart failure.
Her ECG at presentation is showed in
Fig.12.1.
Her biological workup showed a Hb level of
12.3g/dL, leukocytes 6.03 × 109/L, platelets 233
× 109/L, CRP 5mg/L, BUN 5.6mmol/L, creatinine 70 μmol/L, glycemia 4.7 mmol/L,
Na + 136 mmol/L, K+ 3.9 mmol/L, cTnI
© 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_12
181
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F. Halbwachs et al.
Fig. 12.1 A 12-lead ECG at admittance to the hospital
showing sinus rhythm with a heart rate of 72bpm; QRS
axis at −35°; Q waves in leads II, III, and aVF suggestive
Fig. 12.2 A 3-lead ECG telemetry tracing showing wide QRS complex tachycardia with a heart rate of 179bpm,
RBBB, and superior axis, with A:V dissociation (P waves indicated by red arrows), in favor of ventricular tachycardia
0.150 ng/mL, INR 2.1, NT pro-BNP 1997 pg/
mL, TSH 1.04IU/L, total cholesterol 108mg/dL,
HDL 42 mg/dL, LDL 60 mg/dL, and triglycerides 88mg/dL.
While in the cardiology department, the
patient presented another episode of palpitations,
which was recorded by telemetry monitoring
(Fig.12.2).
Transthoracic echocardiography was performed, which demonstrated a non-dilated LV,
with akinesia of the inferior LV wall and with
severe systolic dysfunction, LVEF of 33%
of remote inferior myocardial infarction; and negative T
waves in leads II, III, aVF, and V3–V6, suggestive of possible infero-lateral ischemia
(Fig. 12.3). It also showed a cardiac output of
3.7 L/min, non-elevated LV lling pressure,
absence of LV hypertrophy, mild mitral regurgitation, a non-dilated right ventricle, mild tricuspid
regurgitation with sPAP of 24mmHg, absence of
pericardial uid, and absence of LV thrombus.
In order to rule out ongoing myocardial ischemia, given the diagnostic of ventricular tachycardia and the elevated troponin level, coronary
angiography was performed, which demonstrated
chronic total occlusion of the RCA in its proximal segment (Fig.12.4).
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