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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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R. Le Bouar et al.
Fig. 18.23 CARTO image in RAO 70° caudal 30° showing the bipolar voltage map (left panel) and the unipolar volt-
age map (right panel), with superposed RF ablation lesions (pink and red dots)
Fig. 18.24 A 12-lead ECG showing the absence of VT induction during PVS after the ablation of the clinical VT
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Fig. 18.25 A 12-lead ECG recorded at the end of the ablation procedure showing sinus rhythm with a heart rate of
50bpm, QRS axis at +60°, absence of LV hypertrophy, and inferior wall necrosis
Fig. 18.26 Chest
radiography in a
posteroanterior position
showing the presence of
a subcutaneous ICD
(ICD lead, single arrow;
ICD can, double arrow)
297
Commentary
The present case illustrates a catheter ablation
procedure for two monomorphic ventricular
tachycardias in a 43-year-old male patient with
ischemic cardiomyopathy and remote inferior
myocardial infarction. Several observations can
be made about the present case.
Among all structural heart disease, ischemic
heart disease with prior myocardial infarction
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R. Le Bouar et al.
represents the number one case of sustained
monomorphic ventricular tachycardia [2, 3].
Patients with VT after myocardial infarction
often have multiple morphologies of inducible
VT during the electrophysiological study, with an
average of 3.6±2, in the experience of Stevenson
etal. [4]. Induction of several VT morphologies
during the electrophysiological study that precedes the catheter ablation phase may prolong
the duration of the ablation procedure, since the
goal of a catheter ablation procedure of ventricular tachycardia is ablation of all sustained monomorphic VTs and non-inducibility of any
sustained VT at the end of the ablation procedure
[5]. In the above-presented patient, a nonpreviously documented sustained VT was
induced during PVS. However, given its sustained nature, this was considered signicant and
a decision to performed catheter ablation was
taken. The activation mapping performed during
VT demonstrated its origin in the area of previous myocardial infarction, at the level of the low
interventricular septum, conrming the presence
of substrate for this VT also.
The site of origin of VT can be approximated
from the 12-lead ECG.Several papers have been
currently published proposing several algorithms
for identication of the VT site of origin [6–8].
By applying some of the criteria from these algorithms to the present case, the negative QRS morphology during the clinical VT in the inferior
leads, the “double transition” recorded in precordial leads (rS in lead V1, R in lead V2, and RS in
lead V3), and the unique “R” wave in leads I and
aVL, the suggested origin of the VT from
Fig.18.1 is at the level of the infero-septal wall of
the LV. This fact was conrmed by the electrophysiological study. The same criteria apply to
the second VT, which has a 12-lead ECG close to
that of the rst VT.
The strategies used in the above-presented
case for identifying the VT isthmus for the two
monomorphic VTs were 1. substrate mapping
(for both VTs), 2. activation mapping for the rst
VT (see Figs. 18.12, 18.3, 18.4, and 18.15 and
video 18.1), and 3. pacemapping during sinus
rhythm for the second VT (Figs. 18.19 and
18.20).
Substrate mapping during sinus rhythm has as
goal identication of areas of scar slow conduction which might serve as origin for the ventricular tachycardia. In cases of previous myocardial
infarction, the identication of myocardial scar is
the rst step inlocalizing the potential VT circuit,
since most of VTs in this context originate in
areas of slow conduction/low-amplitude local
electrograms, corresponding to areas of myocardial brosis or in borderline areas (the junction
between brotic areas and healthy myocardium)
[9, 10]. In the above-presented case, Fig.18.15
illustrates the anatomical relationship between
the location of the VT isthmus and the location of
the myocardial scar. The VT isthmus is situated
in such an area of myocardial scar, displayed
between the two white lines on the bipolar voltage map. Given the possible large areas of scar
post-myocardial infarction, with the presence of
late potential in several wide areas of the ventricles, substrate mapping alone is not likely to sufce in identifying the VT isthmus, and other
additional mapping techniques are usually
required.
Activation mapping is the preferred ablation
technique, since it allows understanding of the
VT mechanism (macro-reentry vs. focal) and
accurately identies the VT isthmus with the
entrance and exit zones [11, 12]. However, this
requires a good hemodynamic tolerance of the
VT by the patient [13]. The activation map can be
created relatively fast, in a matter of minutes,
especially if multielectrode diagnostic catheters
are used [14]. The development of such diagnostic catheters created the concept of high-density
mapping, where thousands of local electrograms
are recorded and put together in order to create an
activation map [15]. The exit point of the VT is
dened by the earliest activation site on the map
recorded during VT, from where the activation
spreads toward other areas of ventricular myocardium. A presystolic local potential is usually
observed at the exit site of the slow conduction
zone during VT.The entrance point of the VT is
dened by the latest activation site during ventricular systole (corresponding to the duration of
the QRS complex), where the VT isthmus begins.
The VT isthmus is dened by the area delineated
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by two functional or anatomical barriers, situated
between the entrance and the exit points. During
VT, the mapping or the ablation catheter can
record local diastolic potentials, propagating
from the entrance point to the exit point.
In cases where the VT is hemodynamically
not tolerated, non-sustained, or non-inducible
during the electrophysiological study, pacemapping during sinus rhythm can accurately identify
the VT isthmus, with the exit and entrance zone
[1, 16, 17]. A number of electrogram characteristics (the bipolar voltage, the number of positive
peaks, and the spike to QRS interval) can successfully identify a VT isthmus entrance in postinfarct patients [18]. This technique is presented
widely in the commentary section of cases 14,
16, and 17.
Whatever the mapping technique used to identify the VT isthmus, once this is accomplished,
the most efcient ablation technique is ablation
of the VT isthmus [1, 13, 19]. In the abovepresented patient, the VT isthmi of both ventricular tachycardias were situated at the level of the
interventricular septum, in an area of scar postmyocardial infarction. The isthmus of the clinical
VT was close to the mitral valve, and transecting
it required creation of an ablation line joining the
area of previously deployed RF lesions and the
mitral valve annulus. This prevented any perimitral macro-reentry.
The patient remains VT-free 4 months after
the ablation procedure.
Learning Points
• Catheter ablation is an efcient treatment option for monomorphic sustained
ventricular tachycardia post-myocardial
infarction.
• Programmed ventricular stimulation
performed during the electrophysiological study often induces multiple VT
morphologies, with an average of
3.6±2.
• The goal of a catheter ablation procedure of ventricular tachycardia is ablation of all sustained monomorphic VTs
299
and non-inducibility of any sustained
VT at the end of the ablation
procedure.
• When ablating ventricular tachycardias
with origin in the interventricular septum area of the left ventricle, care must
be exercised not to damage the left bundle branch and its ramications.
References
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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. Miller JM, Altemose GT, Jayachandran JV.Catheter
ablation of ventricular tachycardia in patients
with structural heart disease. Cardiol Rev.
2001;9(6):302–11.
3. Zeppenfeld K, Stevenson WG.Ablation of ventricular
tachycardia in patients with structural heart disease.
Pacing Clin Electrophysiol. 2008;31(3):358–74.
4. stevenson WG, Friedman PL, Ganz LI.
Radiofrequency catheter ablation of ventricular tachycardia late after myocardial infarction. J
Cardiovasc Electrophysiol. 1997;8(11):1309–19.
5. Fukunaga M, Goya M, Hiroshima K, Hayashi K, Ohe
M, Makihara Y, et al. Impact of catheter ablation of
ventricular tachycardia in patients with prior myocardial infarctions. J arrhythm. 2016;32(6):462–7.
6. Josephson ME, Callans DJ. Using the twelve-lead
electrocardiogram to localize the site of origin of ventricular tachycardia. Heart Rhythm. 2005;2(4):443–6.
7. Haqqani HM, Morton JB, Kalman JM. Using the
12-lead ECG to localize the origin of atrial and ventricular tachycardias: part 2—ventricular tachycardia.
J Cardiovasc Electrophysiol. 2009;20(7):825–32.
8. Ushijima S, Kamata E, Saito H, Mitsui T, Kobayashi
H, Iwa T.Diagnosis of the origin of ventricular tachycardia by 12-lead electrocardiogram—evaluation
of ECG of clinical cases of VT. Kokyu to Junkan.
1984;32(6):619–25.
9. Arruda M, Fahmy T, Armaganijan L, Di Biase L, Patel
D, Natale A.Endocardial and epicardial mapping and
catheter ablation of post myocardial infarction ventricular tachycardia: a substrate modication approach. J
Interv Card Electrophysiol. 2010;28(2):137–45.
10. Verma A, Marrouche NF, Schweikert RA, Saliba W,
Wazni O, Cummings J, et al. Relationship between
successful ablation sites and the scar border zone
dened by substrate mapping for ventricular tachycardia post-myocardial infarction. J Cardiovasc
Electrophysiol. 2005;16(5):465–71.
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11. Fiala M, Chovanzik J, Neuwirth R, Nykl I, Szymeczek
H, Nevralova R, etal. Sustained monomorphic ventricular tachycardia in patients with structural heart
disease. Different arrhythmogenic substrates, different options of palliative and curative treatment
in the era of three-dimensional mapping. Vnitr Lek.
2006;52(6):577–89.
12. Kitamura T, Martin CA, Vlachos K, Martin R,
Frontera A, Takigawa M, et al. Substrate mapping
and ablation for ventricular tachycardia in patients
with structural heart disease: how to identify ventricular tachycardia substrate. J Innov Cardiac Rhythm
Manag. 2019;10(3):3565–80.
13. Dixit S, Callans DJ.Mapping for ventricular tachycardia. Card Electrophysiol Rev. 2002;6(4):436–41.
14. Schalij MJ, van Rugge FP, Siezenga M, van der Velde
ET. Endocardial activation mapping of ventricular
tachycardia in patients: rst application of a 32-site
bipolar mapping electrode catheter. Circulation.
1998;98(20):2168–79.
15. Martin R, Hocini M, Haisaguerre M, Jais P, Sacher
F. Ventricular tachycardia isthmus characteristics:
insights from high-density mapping. Arrhythmia
Electrophysiol Rev. 2019;8(1):54–9.
16. 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.
17. Brunckhorst CB, Delacretaz E, Soejima K, Maisel
WH, Friedman PL, Stevenson WG.Identication of
the ventricular tachycardia isthmus after infarction by
pace mapping. Circulation. 2004;110(6):652–9.
18. Battaglia A, Odille F, Magnin-Poull I, Sellal JM,
Hoyland P, Hooks D, et al. An efcient algorithm
based on electrograms characteristics to identify ventricular tachycardia isthmus entrance in post-infarct
patients. Europace. 2020;22(1):109–16.
19. de Chillou C, Lacroix D, Klug D, Magnin-Poull I,
Marquie C, Messier M, etal. Isthmus characteristics
of reentrant ventricular tachycardia after myocardial
infarction. Circulation. 2002;105(6):726–31.
Case 19
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RonanLe Bouar, FrédéricHalbwachs,
ThomasRobein, OlivierRoth, CrinaMuresan,
TarekEl Nazer, andYasmineDoghmi
19
Case Presentation
A 55-year-old male patient with a past medical
history of remote inferior myocardial infarction
at the age of 40years, with no lesion at the level
of the epicardial coronary arteries evidenced by
coronary angiography (MINOCA), complicated
by Dressler pericarditis that required surgical
drainage, with dilated cardiomyopathy and moderate LV systolic dysfunction (LVEF of 43%)
was admitted to the emergency department for
recurrent episodes of palpitations with sudden
onset accompanied by dyspnea and dizziness that
had started 3days prior to his presentation to the
emergency department. He described the presence of several such episodes during the past
18months.
His cardiovascular risk factors were represented by a past history of tobacco smoking, dyslipidemia, and grade 3 obesity. His medication at
home consisted of nebivolol 5mg, atorvastatin
40mg, and aspirin 75mg.
R. Le Bouar (*) · O. Roth · C. Muresan · T. El Nazer
Y. Doghmi
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr; rotho@ghrmsa.fr;
crina.muresan@ghrmsa.fr; tarek.elnazer@ghrmsa.fr;
yasmine.hadjidj@ghrmsa.fr
F. Halbwachs · T. Robein
Biosense Webster, Mulhouse, France
At physical examination, his blood pressure
was 123/74 mmHg, HR 190 bpm, SpO2 92%
breathing room air, H=1.79m, W=135kg, and
BMI=42.13kg/m2, heart sounds were rapid and
regular, there were no audible murmurs, lung
auscultation revealed bilateral crepitant rales, and
there were no signs of right heart failure.
His ECG at presentation is showed in Fig.19.1.
His biological workup showed a Hb level of
13.6 g/dL, leukocytes 7.41 × 109/L, platelets
167×109/L, CRP 7mg/L, BUN 8.9mmol/L, creatinine 161μmol/L, glycemia 7.1mmol/L (nonfasting), Na+135mmol/L, K+ 3.8mmol/L, cTnI
0.12 ng/mL, TSH 2.47 IU/L, total cholesterol
192 mg/dL, HDL 42 mg/dL, LDL 120 mg/dL,
and triglycerides 148mg/dL.
Question 1: What is the nature of the
tachycardia presented in Fig. 19.1?
A. SVT with functional RBBB
B. Antidromic tachycardia
C. Ventricular tachycardia
D. Atrial utter with 1:1 AV conduction
E. Atrial brillation with RBBB
His ECG recorded after the administration
of amiodarone 300 mg IV is presented in
Fig.19.2.
Figure 19.1 explained: This shows a wide
QRS complex tachycardia with a heart rate of
© 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_19
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Fig. 19.1 A 12-lead ECG at admission to the emergency department showing a wide QRS complex tachycardia with
RBBB and superior axis, with a heart rate of 191bpm
R. Le Bouar et al.
Fig. 19.2 A 12-lead ECG at admittance to the cardiology
department showing sinus rhythm with a heart rate of
75bpm, QRS axis at +60°, absence of LV hypertrophy,
191bpm, with a RBBB aspect, and superior axis.
The differential diagnosis includes SVT with
functional bundle branch block, antidromic
tachycardia (ventricular preexcitation syndrome),
and ventricular tachycardia. Given the absence of
attened T waves in V5, negative in V6, attened in lead
II, negative in lead III and aVF, two isolated PVC, and
incomplete RBBB
ventricular preexcitation on the ECG in sinus
rhythm (Fig.19.2), antidromic tachycardia is not
highly likely (even though not impossible).
Arguments in favor of ventricular tachycardia are
the presence of myocardial infarction in the
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Fig. 19.3 Chest X-ray in posteroanterior view showing
an enlarged cardiac silhouette with an increased cardiothoracic index, no pleural effusion, and no sign of infection in the pulmonary parenchyma
patient’s medical history and the morphological
criteria on the patient’s ECG: R wave taller than
R’ wave in lead V1 and a ration of R/S in lead
V5<1.
The patient’s chest X-ray is presented in
Fig.19.3.
Transthoracic echocardiography was performed, which demonstrated a mildly dilated LV,
with akinesia of the inferior basal and middle
segment of the LV wall and with moderate to
severe systolic dysfunction, type 1 diastolic dysfunction, absence of any major valvular disease,
a mildly dilated left atrium, non-dilated right
atrium and right ventricle, a non-dilated IVC,
sPAP of 30 mmHg, and absence of pericardial
effusion (Fig.19.4).
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Question 2: What is the origin of the ventricular tachycardia presented in Fig.
19.1?
A. LV inferior wall
B. LV superior wall
C. LV lateral wall
D. LV septum
E. LV apex
In order to rule out ongoing myocardial ischemia, given the diagnosis of ventricular tachycardia and the slightly elevated troponin level,
coronary angiography was performed, which
demonstrated no signicant obstructive lesion at
the level of the epicardial coronary arteries
(Fig.19.5).
A cardiac MRI was subsequently performed,
which conrmed the presence of subendocardial
myocardial necrosis at the level of the inferior
basal and middle LV wall and moderate LV systolic dysfunction (Fig.19.6).
Given the diagnosis of ventricular tachycardia, the presence of remote inferior myocardial
infarction, the young age of the patient and the
high rate of potential adverse effects associated
with long-term amiodarone administration, and
the superiority of catheter ablation to antiarrhythmic drugs in the treatment of VT, an electrophysiological study in view of a catheter ablation
procedure was scheduled and subsequently
performed.
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R. Le Bouar et al.
Fig. 19.4 Left upper panel: Transthoracic echocardiog-
raphy showing M mode in parasternal long-axis view,
with a mildly dilated LV (EDD of 65mm), global hypokinesia (ESD of 53mm), with severe LV systolic dysfunction and a LVEF of 35% (Teicholtz). Right upper panel:
Trans-mitral Doppler ow interrogation showing type 1
diastolic dysfunction (E wave < A wave). Left lower
panel: Tissue Doppler analysis with the cursor placed at
the septal part of the mitral annulus, showing a e’ wave of
8.3 cm/s with a ratio of E/e’ of 3.5, in favor of nonaugmented LV lling pressure. Right lower panel: Apical
ve-chamber view showing a preserved cardiac output of
4.37L/min
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305
Fig. 19.5 Coronary angiography image showing absence
of signicant stenosis at the level of the left main coronary
artery, as well as at the level of the LAD and circumex
coronary arteries (left panel) and at the level of the right
coronary artery (right panel)
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