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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. 19.6 (Panel a) Cardiac MRI image cine SSFP four-
chamber view showing a mildly dilated LV, with an EDD
of 64 mm (Panel b) Short-axis view showing late
enhancement at the level of the inferior LV wall (red
arrow). (Panel c) Two-chamber view showing late
Electrophysiological Study andRF
Catheter Ablation Procedure
The electrophysiological study 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
enhancement at the level of the infero-basal LV wall (red
arrow). (Panel d) Four-chamber view showing late
enhancement at the level of the basal and lateral LV wall
(red arrow)
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
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Fig. 19.7 A 12-lead ECG recorded at the beginning of the ablation procedure showing sinus rhythm with a heart rate
of 78bpm, QRS axis at +90°, absence of LV hypertrophy, and absence of ischemia
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intracavitary ECGs were recorded by the
WorkMate Claris™ System (Abbott®).
The ECG at the beginning of the ablation pro-
cedure is presented in Fig.19.7.
Programmed ventricular pacing was performed under basal conditions with repeated
induction of a wide QRS complex tachycardia
with a cycle length of 300ms, with an identical
morphology to that of the clinical VT (Fig.19.8).
A Biosense Webster® SmartTouch SF openirrigated 3.5mm tip with double curve D/F was
placed in the right atrium via a 6F 20cm vascular
sheath inserted at the level of the right common
femoral vein. It conrmed A-V dissociation during the tachycardia and the diagnosis of VT.The
tachycardia was terminated by burst ventricular
pacing.
Given the monomorphic aspect of the VT and
its repeated induction during programmed ventricular stimulation, ablation of this VT was
decided.
Its RBBB aspects with superior axis and with
late transition in the precordial leads (V5) were in
favor of an origin at the level of the infero-basal
left ventricle. Therefore, mapping of the LV was
decided.
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 map, the bipolar voltage
map, and the activation map of the LV. The
Biosense Webster® SmartTouch SF openirrigated 3.5mm tip with double curve was used
to perform RF ablation.
An anatomical map of the LV was rst created, which showed a mildly dilated LV, with a
volume of 195mL.A bipolar voltage map was
subsequently created during sinus rhythm, which
showed the presence of an area of low-voltage
electrograms at the level of the inferior basal and
middle part of the LV inferior wall (Figs.19.9
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Fig. 19.8 A 12-lead ECG showing the induction of the VT during programmed ventricular stimulation. Of note, the
morphology is identical to that of the clinical VT
R. Le Bouar et al.
Fig. 19.9 CARTO image in RAO 135° caudal 14° showing the bipolar voltage map of the left ventricle revealing
a large area of low voltage (< 0.5mV, red color) at the
level of the inferior basal and mid-wall, compatible with
myocardial scar post-myocardial infarction. The CT angi-
ography three-dimensional reconstruction of the basal
aorta and the coronary arteries (in red) is superposed in
order to show the anatomical relationship between the
coronary arteries and the zone of myocardial scar. Of
note, the LV is dilated, with a volume of 195mL
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and 19.10), measuring 19.3cm2 (Fig.19.11), representing 10% of the total LV surface, compatible
with scar post-myocardial infarction.
Identication of the VT circuit was performed
using pacemapping in sinus rhythm, according to
the technique described by de Chillou etal. [1, 2].
Fig. 19.10 CARTO
image in RAO 135°
caudal 14° showing the
bipolar voltage map of
the left ventricle
revealing the absence of
myocardial scar at the
level of the anterior LV
wall (no zone of voltage
<0.5mV, represented by
the color red). The CT
angiography threedimensional
reconstruction of the
basal aorta and the
coronary arteries (in red)
is superposed
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 at the level of
the inferior basal LV wall. The PASO module of
Fig. 19.11 CARTO
image in RAO 140°
caudal 25° showing the
bipolar voltage map of
the left ventricle
revealing a large area of
low voltage (< 0.5mV,
red color) at the level of
the inferior basal and
mid-wall, compatible
with myocardial scar
post-myocardial
infarction. The
low-voltage area
represents 19.3cm2, or
10% of the entire
surface of the LV
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R. Le Bouar et al.
Fig. 19.12 Left panel: CARTO image in RAO 151° cau-
dal 19° showing the inferior wall of the left ventricle.
Pacemap of the left ventricle in sinus rhythm conrming
the exit zone of the clinical VT (red color). Pacing with
the roving/ablation catheter at this site reproduces a QRS
morphology almost identical to the morphology of the
the CARTO system was used to compare the
resulting 12-lead ECG during local pacing with
the morphology of the VT.A superposed correlation of 97.3% was observed in an area of the
basal inferior wall, at the level of the myocardial
scar, close to the mitral valve, identifying the exit
zone of the VT (Fig.19.12). This 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.
This site recorded during sinus rhythm a fragmented local potential, of small amplitude and
prolonged duration that was present after the end
of the QRS complex (Fig.19.13).
clinical VT (concordance of over 97%, right panel). This
is explained by the fact that the depolarisation wavefront
of the LV myocardium during pacing from this site
spreads in a manner which is similar to that during VT.
The resulting QRS morphology is therefore identical to
the QRS morphology during VT
Pacing the LV in adjacent zones of the exit
zone identied sites with slightly different correspondence percentages. Pacing was continued at
more and more remote sites, until a site was found
where the morphology of the paced QRS complex
differed signicantly from 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.19.14).
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Fig. 19.13 A 12-lead ECG together with intracavitary
leads recorded from the distal and the proximal electrodes
of the roving/ablation catheter (ABL d and ABL p) and
from the bipolar electrode of the RV catheter. The roving/
ablation catheter is placed at the level of the exit zone of
the VT and records a fragmented local late potential that
terminates after the end of the QRS complex
Fig. 19.14 Left panel: CARTO image showing the infe-
rior wall of the left ventricle. Pacemap of the left ventricle
in sinus rhythm conrming the entrance zone of the clinical VT (blue color). Pacing with the roving/ablation catheter at this site reproduces a QRS morphology substantially
different to the morphology of the clinical VT (concordance of 33.4%, right panel), this zone being close to the
exit zone of the VT (red color). 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 QRDS morphology during VT.The red contour represents the border of the myocardial scar; the two white lines
delineate the VT isthmus (same as in Fig.19.12), drawn for
learning purpose. The yellow star indicates that pacing
from the roving/ablation catheter is performed
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R. Le Bouar et al.
The area between the entrance and the exit
zones identied the VT isthmus.
In order to conrm the key VT components
(entrance zone, exit zone, and VT isthmus) identied with pacemapping during sinus rhythm,
programmed ventricular stimulation was performed once again, with induction of the clinical
VT (Fig.19.15). This was hemodynamically tolerated by the patient, which allowed the creation
of an activation map with the ablation catheter.
The activation map of the LV during VT is
presented in Fig. 19.16. This was in favor of a
double- loop macro-reentry circuit, forming a
“gure of 8,” each of the two loops using the
same critical isthmus at the level of the basal LV
inferior wall. The length of the VT isthmus was
20mm, with a width of 18mm, and it was situated at a distance of 5mm from the mitral valve.
Fig. 19.15 A 12-lead ECG recorded during VT showing a wide QRS complex tachycardia identical to the clinical VT,
with RBBB and superior axis, with a cycle length of 300ms.
Fig. 19.16 CARTO image in RAO 144° caudal 19°
showing the inferior wall of the left ventricle. Activation
map of the LV during ventricular tachycardia, showing the
critical components of the VT: the exit zone (red color),
the two outer loops (represented in yellow, green, and
blue, indicated by the curved and straight red arrows), and
the entrance zone (in violet). The VT isthmus is delineated
by the two white lines (manually added for learning purpose), being parallel to the mitral valve
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The ablation catheter recorded the presence of
presystolic local potentials when placed at the level
of the distal part of the VT isthmus, close to the exit
zone (Fig. 19.17), and early diastolic potentials
when placed at the level of the proximal part of the
VT isthmus identied by pacing during sinus
rhythm, close to the entrance zone (Fig.19.18).
Having conrmed the location of the VT isthmus, RF ablation was subsequently performed by
creating several ablation lesions which transected
the VT isthmus (Fig.19.19). The target parameters were power 30W and ablation index 550. The
VT is terminated during RF ablation (Fig.19.20).
The bipolar voltage map of the LV with superposed RF ablation lesions is presented in
Fig.19.21.
The ECG recorded at the end of the ablation
procedure is presented in Fig.19.22.
Fig. 19.17 A 12-lead ECG together with intracavitary
leads recorded from the distal and the proximal electrodes
of the roving/ablation catheter (ABL d and ABL p) and
from the bipolar electrode of the RV catheter. The roving/
Fig. 19.18 A 12-lead ECG together with intracavitary
leads recorded from the distal and the proximal electrodes
of the roving/ablation catheter (ABL d and ABL p) and
from the bipolar electrode of the RV catheter. The roving/
ablation catheter is placed at the level of the proximal part
ablation catheter is placed at the level of the terminal part
of the VT isthmus, close to the exit zone, and records a
local presystolic potential indicated by the red arrow; the
blue arrow indicates the far-eld ventricular electrogram
of the VT isthmus, close to the entrance zone, and records
a local early diastolic potential indicated by the red arrow;
the blue arrow indicates the far-eld ventricular
electrogram
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Fig. 19.19 CARTO
image in RAO 144°
caudal 19° showing left
ventricular activation
map after RF ablation.
Red and pink dots
correspond to the
ablation lesions
deployed at the level of
the VT isthmus
transecting it and at the
level of the LAVA (green
dots), homogenizing the
scar
R. Le Bouar et al.
Fig. 19.20 A 12--lead ECG recorded during RF application at the level of the VT isthmus recorded during RF application showing the termination of the VT, conrming its origin at this site
There were no complications related to the
procedure.
The arterial puncture site was closed with a
ProGlide and a FemoSeal vascular system. The
venous access site was closed with a “gure of 8”
supercial suture.
Given the presence of remote inferior myocardial infarction and the scar at the level of the inferior LV wall which could serve as a potential
future VT substrate, a single-chamber ICD was
implanted for the secondary prevention of SCD.
The patient’s chest X-ray after implantation is
presented in Fig.19.23.
The ECG recorded before hospital discharge
is presented in Fig.19.24.
The patient was discharged 48h later.
Answers
Question 1: C.Ventricular tachycardia
Question 2: A.LV inferior wall
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Fig. 19.21 CARTO
image in RAO 147°
caudal 13° 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 and at the
level of the LAVA (green
dots), homogenizing the
scar
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Fig. 19.22 A 12-lead ECG recorded at the end of the ablation procedure showing sinus rhythm with a heart rate of
93bpm, QRS axis at +90°, absence of LV hypertrophy, and negative T waves in leads II, III, and aVF
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