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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. 14.8 Left panel: CARTO image in LAO 164° cau-
dal 12° showing the infero-lateral wall of the left ventricle. Pacemap of the left ventricle during sinus rhythm
depicting the critical components of the VT circuit: the
entrance zone (red color), the isthmus (the zone situated
between the two white lines), and the exit zone (violet).
The roving/ablation catheter is situated at the level of the
Pacing the LV in adjacent zones of the exit
zone identied sites with slightly different correspondence percentages, until a site was found
where the morphology of the paced QRS complex differed signicantly form 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.14.9).
exit zone of the VT circuit, represented in red. Pacing at
this site (yellow star) reproduces the QRS morphology of
the VT with a concordance of 99.4% (right panel). The
red curved arrows indicate the two outer loops of the VT,
corresponding to the activation wavefront during VT, traveling from red to yellow to green to blue and to violet
Once the exit zone and the entrance zone were
identied, the VT isthmus was considered present between these two zones. It measured 25mm
in length and 20mm in width.
Pacing the LV at the level of the VT isthmus
initiated a second non-sustained monomorphic
VT, with the same cycle length, but with a morphology different than that of the VT morphology
(Fig.14.10). Using the same pacemap technique,
several zones of the LV were paced at a xed
coupling interval of 600 ms using the ablation
catheter. The exit zone of the VT was identied in
the area of the entrance zone of VT 1 (Fig.14.10).
The entrance zone of the VT was identied in the
area of the exit zone of VT 1 (Fig.14.11). The VT
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Fig. 14.9 Left panel: CARTO image in LAO 164° cau-
dal 12°, same view as in Fig.14.8. Pacemap of the left
ventricle in sinus rhythm identifying the entrance zone of
the clinical VT (violet). Pacing with the roving/ablation
catheter at this site (yellow star) reproduces a QRS morphology very different from the morphology of the clinical VT (−28%, right panel), even though the catheter is
situated at a very short distance compared to its position in
isthmus was therefore the same as for VT 1. The
two VTs shared the same macro-reentry circuit,
but in an opposite direction, explaining the same
VT cycle length.
Having identied the critical components of
the VT (the entrance zone, the VT isthmus, and
the exit zone), RF ablation was performed by creating an ablation line which transected the VT
isthmus. The target parameters were power 35W
and ablation index 550. After ablation of the VT
isthmus, additional RF lesions were deployed in
order to create a line from the VT isthmus to the
mitral valve, in order to prevent potential future
Fig.14.8 (see text for further explanation). This is due to
the fact that the activation wavefront from this site propagates not through the VT isthmus where slow-conducting
myocardial bers are found but in the opposite direction,
through myocardial bers that conduct the activation
wavefront faster, therefore creating a QRS morphology
different from the QRS morphology during VT
peri-mitral reentry VT. Ablation of the LAVA
identied at the level of the scar was also performed. The bipolar voltage map of the LV with
the superimposed RF ablation lesions is presented in Fig.14.12.
Programmed ventricular stimulation was performed after the ablation, without the induction
of any sustained or non-sustained ventricular
arrhythmias. However, since no sustained VT
was induced before the ablation procedure, this
fact was not able to conrm the acute ablation
success.
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Fig. 14.10 Left panel: CARTO image in LAO 164° cau-
dal 12°, same view as in Figs.14.8 and 14.9. Pacemap of
the left ventricle during sinus rhythm identifying the exit
zone of the second VT (red color). The QRS morphology
during VT is shown in the right panel. The roving/ablation
catheter is situated at the level of the exit zone of the VT
circuit, represented in red. Pacing at this site reproduces a
QRS morphology with a concordance of 94% with the
morphology of VT 2 (right panel). The red curved arrows
indicate the two outer loops of the VT, corresponding to
There were no complications related to the
ablation procedure.
The 12-lead ECG recorded at the end of the
ablation procedure is presented in Fig.14.13.
The ICD interrogation performed at 3, 6, 12,
and 24 months post-ablation procedure showed
no tachycardia recurrence.
the activation wavefront during VT, traveling from red to
yellow to green to blue and to violet. It is worth noting that
the clinical VT (VT 1, with its mechanism presented in
Figs.14.5 and 14.6) and VT 2 share the same components
(isthmus, exit zone, and entrance zone) but with opposite
rotation direction of the wavefront: The exit zone of the
VT 1 corresponds to the entrance zone of the VT 2, and
the entrance zone of VT 1 corresponds to the exit zone of
the VT 2
Answers
Question 1: E.Ventricular tachycardia
Question 2: C.VT substrate identication using pacemapping in sinus
rhythm and ablation
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Fig. 14.11 Left panel: CARTO image in LAO 164° cau-
dal 12°, same view as in Figs. 14.8, 14.9, and 14.10.
Pacemap of the left ventricle during sinus rhythm identifying the entrance zone of the second VT (violet). The
roving/ablation catheter is situated at the level of the
entrance zone of the VT circuit, represented in violet.
Fig. 14.12 CARTO image showing left ventricular bipolar voltage map after RF ablation. Red and pink dots correspond to the ablation lesions deployed at the level of the
VT isthmus transecting it (1), from the VT isthmus to the
mitral annulus in order to block the corridor around the
mitral valve that could sustain peri-mitral reentry (2) and
at the level of the LAVA (3), homogenizing the scar
Pacing with the roving/ablation catheter at this site produces a QRS morphology very different from the morphology of the clinical VT (negative concordance of
−34%, right panel), even though the catheter is situated
at a very short distance compared to its position in
Fig.14.10 (see text for further explanation)
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Fig. 14.13 A 12-lead ECG recorded after the ablation procedure showing sinus rhythm with a heart rate of 68bpm;
QRS axis at −30°; Q waves in leads II, III, and aVF; and negative T waves in V5, V6, lead I, and aVL
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Commentary
The present case illustrates a catheter ablation
procedure of monomorphic ventricular tachycardia in a 69-year-old male patient with ischemic
cardiomyopathy and remote inferior myocardial
infarction. Several observations merit further
discussion.
Ischemic heart disease with previous myocardial infarction is the number one cause of ventricular tachycardia in patients with structural
heart disease [4]. The myocardial scar postmyocardial infarction can be responsible for the
appearance of ventricular tachycardia even years
after the acute event. In the experience of de
Chillou et al., the average time interval after
myocardial infarction and VT diagnosis can be
almost 20 years (19.2 ± 5.6 years) [2]. This is
also the case of the above-presented patient, in
which the VT developed 20years after his myocardial infarction.
Treatment options for ventricular tachycardia
in the context of old myocardial infarction
include anti-arrhythmic drugs, catheter ablation,
and ICD implantation.
Catheter ablation is an effective treatment
option for VT in ischemic heart disease, usually
as complement to ICD implantation. A recent
systematic review and meta-analysis including
635 patients who were followed for a duration
ranging from 6 to 27.9months showed that catheter ablation signicantly decreased the odds of
appropriate ICD therapies (OR 0.49; 95% CI
0.28–0.87), appropriate ICD shocks (OR 0.52;
95% CI 0.28–0.96), VT storm (OR 0.64; 95% CI
0.43–0.95), and cardiac hospitalization (OR 0.67;
95% CI 0.46–0.97) [5]. Catheter ablation was
also the option of choice in our patient, since an
ICD had already been implanted and catheter
ablation is known to be superior to amiodarone in
terms of efcacy for the treatment of VT in ischemic heart disease [6]. The presence of
amiodarone- induced hyperthyroidism in our
patient represented a contraindication to its
administrations.
Regarding the technique used for guiding the
ablation procedure, a three-dimensional electroanatomical mapping system (such as the CARTO
system, Biosense Webster®) is currently widely
used in clinical practice, given its association
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with procedure time and uoroscopy time reduction [7–9].
Possible strategies described for VT ablation
in patients with remote myocardial infarction
include substrate mapping and ablation during
sinus rhythm [10–12], activation mapping [13–
15], pacemapping during sinus rhythm for identi-
cation of the VT components [6], and
entrainment mapping [16–18]. These strategies
are often combined, in order to maximize the
result of the ablation procedure. Among these,
activation mapping is the best option when the
VT is inducible during the procedure and when it
is hemodynamically well tolerated. However,
when this is not the case, the other ablation strategies are used, in variable combinations, depending on the operator’s experience.
One of the most useful techniques for VT
ablation when the arrhythmia is non-sustained,
non-inducible, or not tolerated by the patient is
identication of the critical VT components using
the pacing technique during sinus rhythm
described by de Chillou etal. [2]. This was successfully used in the above-presented patient, in
whom the arrhythmia was non-sustained at the
beginning of the ablation procedure (likely due to
anti-arrhythmic administration in the cardiology
department before the procedure). In brief, the
technique of pacemapping during sinus rhythm
requires comparison between the QRS morphology resulted from local pacing at a specic site
and the morphology of the VT recorded by the
12-lead surface ECG. Using the PASO correlation algorithm of the CARTO system, the correlation between these two morphologies can be
estimated, and this can take values from −100%
(in case of complete discordance between the 2)
to 100% (perfect match). Several points from
areas located in the possible VT origin are paced
at twice the diastolic threshold at the VT cycle
length, and the percentage of correlation is represented on a CARTO map, with red color corresponding to the best match and violet to the
poorest match. Orange, yellow, green, and blue
colors represent intermediate matches. In the VT
exist zone and close to it, there will be good cor-
relations between the locally generated QRS
morphology and the 12-lead VT morphology.
This is due to the fact that the depolarization
wavefront travels in the same direction during
local pacing as during VT. In the VT entrance
zone, there will be a poor correlation between the
locally generated QRS morphology and the
12-lead VT morphology. This is due to the fact
that the depolarization wavefront travels in opposite direction during local pacing and during VT,
since during local pacing, the wavefront propagates faster from the entrance zone to the surrounding healthy myocardial tissue than during
myocardial scar, where conduction velocity is
signicantly decreased. According to de Chillou
etal., regarding VT isthmuses, the best correlation percentages are found in the VT exit zones
and isthmus exit part (89%±8% and 84%±7%,
respectively), and the poorest correlations are
found close to the scar border in the outer
entrance zones (23% ± 28%), in the entrance
zones (39%±34%), and in the entrance part of
the isthmus (32%±26%).
The VT isthmus orientation in the case of an
inferior basal myocardial infarction is usually
parallel to the mitral valve [19]. The VT circuit is
usually a dual loop in a “gure of 8” shape, with
one loop turning around the mitral annulus and
the other around a line of anatomical or functional line of block. Other possibilities are singleloop circuits, which are rarer. The average
dimensions of the VT isthmus are 31± 7 mm
(ranging from 18 to 41mm) long and 16±8mm
(ranging from 6 to 36mm) wide. Efcient ablation requires creating a line of RF lesions perpendicular to the VT isthmus. The end point of the
ablation procedure is non-inducibility of any sustained VT.For this reason, programmed ventricular stimulation should always be performed after
the ablation, in order to test the result of ablation.
Sometimes, other sustained VTs can be induced
during programmed ventricular stimulation,
which may or may not be favored by the RF
lesions deployed prior, for the ablation of the
clinical VT (for such an example, see Case 12).
In our presented patient, programmed ventricular
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stimulation was performed after the ablation,
without the induction of any sustained or nonsustained ventricular arrhythmias. However,
since no sustained VT was induced before the
ablation procedure, this fact was not able to conrm the acute ablation success. Nevertheless, the
patient presented no VT recurrence at his ICD
follow-up visits during the follow-up period of
2years.
Learning Points
• Catheter ablation is an efcient treatment option for ventricular tachycardia
in the context of ischemic heart disease
and prior myocardial infarction.
• When the VT is non-sustained, noninducible during the procedure, or
hemodynamically not tolerated, pacemapping during sinus rhythm can identify the VT critical components: the VT
isthmus, the entrance zone, and exit
zone and can allow a successful ablation
procedure.
• A three-dimensional electro-anatomical
mapping system is a very useful tool in
guiding the VT ablation procedure.
References
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A, Carreras F, Goldwasser D, et al. The end of an
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V1 is caused by a lateral not posterior myocardial
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cardiac magnetic resonance-electrocardiogram correlations. Eur Heart J. 2015;36(16):959–64.
2. de Chillou C, Groben L, Magnin-Poull I, Andronache
M, MagdiAbbas M, Zhang N, et al. Localizing the
critical isthmus of postinfarct ventricular tachycardia:
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Rhythm. 2014;11(2):175–81.
3. de Chillou C, Sellal JM, Magnin-Poull I.Pace mapping
to localize the critical isthmus of ventricular tachycardia. Cardiac Electrophysiol Clin. 2017;9(1):71–80.
4. Lopez EM, Malhotra R. Ventricular tachycardia in
structural heart disease. J Innov Card Rhythm Manag.
2019;10(8):3762–73.
5. Martinez BK, Baker WL, Konopka A, Giannelli D,
Coleman CI, Kluger J, et al. Systematic review and
meta-analysis of catheter ablation of ventricular
tachycardia in ischemic heart disease. Heart Rhythm.
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6. Sapp JL, Wells GA, Parkash R, Stevenson WG, Blier
L, Sarrazin JF, etal. Ventricular tachycardia ablation
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7. Knecht S, Sticherling C, Reichlin T, Pavlovic N, Muhl
A, Schaer B, etal. Effective reduction of uoroscopy
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10. Kella DK, Sheldon SH, Noheria A, Padmanabhan
D, Munger T, Asirvatham SJ, etal. Dening the substrate for ventricular tachycardia ablation: the impact
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11. Kitamura T, Martin CA, Vlachos K, Martin R,
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2019;10(3):3565–80.
12. Kumar S, Baldinger SH, Romero J, Fujii A, Mahida
SN, Tedrow UB, etal. Substrate-based ablation versus
ablation guided by activation and entrainment mapping for ventricular tachycardia: a systematic review
and meta-analysis. J Cardiovasc Electrophysiol.
2016;27(12):1437–47.
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Parson I. Activation sequence of ventricular tachycardia: endocardial and epicardial mapping studies in the human ventricle. J Am Coll Cardiol.
1987;10(5):1040–7.
14. Hooks DA, Yamashita S, Capellino S, Cochet H,
Jais P, Sacher F. Ultra-rapid Epicardial activation mapping during ventricular tachycardia using
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15. Waspe LE, Brodman R, Kim SG, Matos JA, Johnston
DR, Scavin GM, etal. Activation mapping in patients
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16. Stevenson WG, Friedman PL, Ganz
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1997;8(11):1309–19.
17. Stevenson WG, Friedman PL, Sager PT, Saxon
LA, Kocovic D, Harada T, et al. Exploring
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18. Stevenson WG, Khan H, Sager P, Saxon LA,
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Case 15
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RonanLe Bouar, FrédéricHalbwachs,
ThomasRobein, JacquesLevy,
LaurentJacquemin, CharlineDaval,
andCrinaMuresan
15
Case Presentation
A 70-year-old male patient with a past medical
history of remote anterior myocardial infarction
at the age of 50years treated with CABG (right
internal mammary artery, LAD coronary artery
,and left internal mammary artery, CX coronary
artery); ischemic cardiomyopathy with severe
LV systolic dysfunction (LVEF of 25%); singlechamber ICD implantation for the primary prevention of sudden cardiac death at age 53years,
upgraded to CRT-D at the age of 65years; and
permanent atrial brillation was admitted to the
emergency department for electrical storm. ICD
interrogation of his Biotronik ILIVIA 7 HF-T
R. Le Bouar (*) · J. Levy · L. Jacquemin · C. Daval
C. Muresan
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr; levyj@ghrmsa.fr;
jacqueminl@ghrmsa.fr; charline.daval@ghrmsa.fr;
crina.muresan@ghrmsa.fr
F. Halbwachs · T. Robein
Biosense Webster, Mulhouse, France
ICD (Fig.15.1) revealed several episodes of sustained monomorphic VT which required ICD
intervention: burst ventricular pacing which
were sometimes unsuccessful (Fig. 15.2) and
several episodes requiring internal electrical
cardioversion.
His cardiovascular risk factors were represented by age > 55years old, a past history of
smoking (30 pack-years), and grade 1 obesity.
His medication at home consisted of sacubitril/valsartan 49/51 mg/day, carvedilol
3×12.5 mg, atorvastatin 40mg, and uindione
30mg/day.
In the emergency department, at physical
examination, his blood pressure was
83/52mmHg, HR 155bpm, and SpO2 98% with
3 L O2/min via nasal cannula, his heart sounds
were rapid and regular, he was in mild respiratory
distress with 20 breaths/min, lung auscultation
revealed mild bilateral crepitant rales, and he had
mild bilateral edema.
His ECG at presentation is showed in
Fig.15.3.
Overdrive ventricular pacing (ramp) was performed which stopped the tachycardia and converted the ventricular rhythm to biventricular
pacing (Fig.15.4).
© 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_15
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Fig. 15.1 ICD interrogation showing repeated episodes
of a tachycardia with a cycle length of 375–383 ms,
detected in the VT1 window, successfully (episode 67)
Fig. 15.2 ICD electrograms showing unsuccessful ATP (the rst ten electrograms marked VDp and VGp) during an
episode of VT.At the end of ventricular pacing, the tachycardia continues with a cycle length around 390ms
and unsuccessfully (episode 71–83) treated with antitachycardia pacing (ATP)
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