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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. 20.10 CARTO image in inferior view (same as in
Fig.20.8) showing the anatomical map of the left ventricle with a dilated LV (volume=206mL), with the superposed pacemap created with the roving/ablation catheter.
The best correlation between the QRS morphology during
VT and the locally induced QRS morphology produced
by local ventricular pacing is only 65%, failing to identify
the exit point of the VT at the endocardial level. This is
suggestive of an epicardial origin of the VT
Fig. 20.11 CARTO image in RAO 45° caudal 60° showing the anatomical map of the left ventricle with the superposed pacemap created with the roving/ablation catheter.
The best correlation between the QRS morphology during
VT and the locally induced QRS morphology produced
by local ventricular pacing is only 65%, failing to identify
the exit point of the VT at the endocardial level. This is
suggestive of an epicardial origin of the VT
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B. Bakouboula et al.
Fig. 20.12 A 12-lead ECG recorded after the EP study showing sinus rhythm with a heart rate of 58bpm, QRS axis at
+30°, absence of LV hypertrophy, and absence of ischemia
Figure 20.5 explained the ECG shows a wide
QRS complex tachycardia with a cycle length of
280ms, with an atypical LBBB aspect and superior axis, compatible with ventricular tachycardia. The ECG has several criteria in favor of an
epicardial origin of the VT. The pseudo-delta
wave (best visible in leads V3 to V6) ≥34 ms,
intrinsicoid deection time≥85ms (best visible
in leads V3 to V6), shortest RS complex ≥121ms,
and maximum deection index ≥0.55.
Question 3: How would you manage the
patient’s VT given the result of this cath-
eter ablation attempt?
A. Increase the dose of nadolol.
B. Initiate amiodarone treatment.
C. Perform an epicardial catheter ablation
procedure of the VT.
D. Upgrade the ICD to a triple-chamber
ICD.
E. I don’t know.
Given the absence of an evident VT substrate
on the endocardial bipolar voltage map, the morphology of the VT on the 12-lead ECG, the unipolar voltage map showing a potential VT
substrate at the epicardial level, and the failure of
identication of an optimal VT exit site at the
level of the VT endocardium, an epicardial origin
of the VT was suspected. The procedure was terminated and an epicardial ablation procedure was
scheduled. The ECG at the end of the ablation
procedure is presented in Fig.20.12.
Second Catheter Ablation
Procedure (Combined Endocardial
andEpicardial Approach)
The 12-lead ECG at the beginning of the ablation
procedure is shown in Fig.20.13.
The ICD detection and therapies were
switched off at the beginning of the procedure.
The ablation procedure was performed under
general anesthesia. Vascular access was obtained
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Fig. 20.13 A 12-lead ECG recorded at the beginning of the ablation procedure, showing sinus rhythm with a heart rate
of 60bpm, QRS axis at +30°, absence of LV hypertrophy, and absence of ischemia
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using the modied Seldinger technique, under
Doppler ultrasound guidance. A 6F bipolar nonsteerable 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 Cardiac Stimulator
of the Boston Scientic® system. Surface ECG
and intracavitary ECGs were recorded by the
LabSystem Pro (Boston Scientic®).
Programmed ventricular pacing was performed under basal conditions (no isoprenaline
administration) with induction of a wide QRS
complex tachycardia with a cycle length of
240 ms (Fig. 20.14). The tachycardia was not
well hemodynamically tolerated and was terminated by external electrical cardioversion
(Fig.20.15).
Given the result of the previous ablation procedure, with arguments in favor of an epicardial
origin of the VT, access to the LV epicardium was
considered necessary. This was obtained by performing a pericardial puncture using the retroster-
nal subxiphoid approach, with an 18 G Tuohy
needle. The iodinated contrast agent was sequentially injected during needle advancement, until it
was seen entering the pericardial space. Once
inside the pericardial space, a 0.32180cm guidewire was introduced inside the Tuohy needle, and
it was advanced inside the pericardial space until
several loops were visible, conrming its position outside the heart. The needle was then
retracted and replaced by an Agilis Epi (Abbott©)
sheath. A Pentaray catheter (Biosense Webster,
Johnson & Johnson) was used as the mapping
catheter. A Biosense Webster® SmartTouch SF
open-irrigated 3.5mm tip with double curve D/F
was used as the ablation catheter.
Access to the endocardial left ventricle was
obtained using a combined retrograde and antegrade approach. Retrograde approach was
achieved by puncturing the right common femoral artery using the modied Seldinger technique.
The antegrade approach of the LV was achieved
by performing a single transseptal puncture. The
right common femoral vein was punctured under
Doppler ultrasound guidance and an 8F 20 cm
vascular sheath was inserted. This was then
exchanged for a Swartz SL0™ transseptal sheath
(Abbott®), which was advanced over a 0.32 wire
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Fig. 20.14 A 12-lead ECG showing the morphology of the VT, with RBBB and superior axis, with a cycle length of
240ms.
B. Bakouboula et al.
Fig. 20.15 Left side of the tracing: the induced fast VT
with RBBB and superior axis, hemodynamically unstable,
which required electrical cardioversion (middle part of the
tracing). Right side of the tracing: idioventricular rhythm
with RBBB morphology and superior axis
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inside the superior vena cava. The transseptal
puncture was performed under uoroscopic and
transesophageal echocardiography guidance. The
Swart SL0 sheath was then placed inside the left
atrium and exchanged for a Direx (Boston
Scientic©) deectable sheath.
After the transseptal puncture, anticoagulation
was obtained with unfractionated heparin 100IU/
kg given as bolus, followed by continuous infusion of 12 IU/kg/h, with a target ACT of over
300seconds.
An anatomical map of the LV was rst created. A bipolar voltage map was subsequently
created during sinus rhythm, which conrmed
the absence of myocardial scar, with a possible
exception of a very small area of low-amplitude
signals at the level of the LV apex, of uncertain
signicance (Fig.20.16).
A bipolar voltage map of the epicardium was
then created, which showed the presence of a
low-voltage area (< 0.5mV) at the level of the
inferior and basal wall of the LV and at the level
of the lateral wall of the right ventricle
(Figs.20.17 and 20.18).
Under dobutamine up to 10 μg/kg/min and
noradrenaline 0.1 μcg/kg/min vasopressor support, programmed ventricular stimulation was
performed again, with induction of the same VT
from Fig. 20.13. This was again not well tolerated from a hemodynamical point of view, requiring external electrical cardioversion. However,
this time activation mapping of the tachycardia
was performed in short repeated sequences,
between the moment of VT induction and electrical cardioversion (four in total), which allowed
the characterization of the VT mechanism: a
macro-reentry circuit at the level of the inferior
and basal epicardial LV, with a VT isthmus perpendicular to the mitral valve, between an
entrance and an exit zone and two outer loops
(Fig.20.19).
Figure 20.20 shows the anatomical relationship between the VT key components (VT isthmus, entrance and exit zone, and the two outer
loops) on the epicardial activation map and the
VT substrate (the junction of the low-voltage
area and the healthy myocardial tissue) on the
epicardial bipolar voltage map.
Fig. 20.16 Left panel: CARTO image in LAO 60°
showing the endocardial bipolar voltage map of the LV,
with a normal voltage (> 1.5mV) at the endocardial level,
with the exception of a small area at the level of the LV
apex. The superposed image of the CT angiography
reconstruction of the LV, coronary arteries, and of the
aorta can be seen in dark red (glass-like appearance).
Right panel: the bipolar voltage map of the LV (same as
in the left panel), in LAO 155°, showing a normal endocardial voltage, with the exception of a small zone of borderline voltage, at the level of the basal and lateral LV wall
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Fig. 20.17 Left panel: CARTO image in LAO 60°
showing the epicardial bipolar voltage map of the LV,
demonstrating several areas of low voltage (< 0.5mV) at
the level of the LV apex and posteroinferior LV. The
superposed image of the CT angiography reconstruction
Fig. 20.18 Left panel: CARTO image in LAO 95°
showing the epicardial bipolar voltage map of the LV,
demonstrating several areas of low voltage (< 0.5mV) at
the level of the LV apex and posteroinferior LV. The
superposed image of the CT angiography reconstruction
of the LV, coronary arteries, and of the aorta can be seen
of the LV, coronary arteries, and of the aorta can be seen
in dark red (glass-like appearance). Right panel: the epicardial bipolar voltage map of the LV (same as in the left
panel), in LAO 144°, showing the presence of a lowvoltage area at the level of the posteroinferior LV
in dark red (glass-like appearance). Right panel: the epicardial bipolar voltage map of the LV (same as in the left
panel), in LAO 60° caudal 70°, showing the presence of a
low-voltage area at the level of the posteroinferior LV and
at the level of the lateral-inferior wall of the RV
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Fig. 20.19 Left panel: CARTO image in LAO 60° cau-
dal 70° showing the epicardial activation map of the left
ventricle during VT. The Pentaray catheter is situated at
the level of the basal and inferior LV, recording an early
mid-diastolic potential (represented by the red color), corresponding to the VT exit zone. The depolarization
sequence of the LV epicardial during VT is symbolized by
the color transition from red to yellow to green to blue and
to violet. This supports the existence of a macro-reentry
circuit at the level of the inferior and basal LV epicardium,
The localization of the VT isthmus was conrmed using the PASO module of the CARTO
system (Fig. 20.21) and the pattern matching
software of the LabSystem Pro System
(Fig.20.22).
Once the VT circuit was identied and characterized, coronary angiography was performed
using the femoral approach, which excluded the
presence of any major epicardial vessel in the
close proximity of the VT isthmus.
Next, RF ablation was performed, with a target power of 30watts at the level of the LV epicardium. Several RF lesions were deployed at the
level of the VT isthmus, transecting it (Figs.20.23
and 20.24).
Programmed ventricular stimulation with up
to three extrastimuli performed after RF ablation
of the VT was negative.
There were no complications related to the
procedure.
with an exit zone (in red), entrance zone (violet), an isthmus (between the entrance zone and the exit zone), and
two outer loops (see right panel). Right panel: CARTO
image in LAO 60° caudal 70° (same as in left panel)
showing the epicardial activation map of the left ventricle
during VT, with superposed arrows representing the two
outer loops, for learning purpose. The Pentaray catheter is
situated at the level of the basal and inferior LV, recording
an early mid-diastolic potential (represented by the violet
color), corresponding to the VT entrance zone
ICD detection and therapies were activated.
The ECG recorded after the ablation proce-
dure is presented in Fig.20.25.
Beta blocker treatment with nadolol was continued. The 48-hour telemetry tracings did not
record any VT recurrence. The patient was discharged home 48h later.
ICD interrogation of up to 12months after the
ablation procedure showed no VT recurrence.
Answers
Question 1: C.Perform a catheter abla-
tion procedure of the VT.
Question 2: E.Epicardial origin.
Question 3: C.Perform an epicardial
catheter ablation procedure of the VT.
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Fig. 20.20 CARTO image in LAO 60°, caudal 70° showing the activation map of the VT (left panel) in relationship with the VT substrate depicted by the epicardial
bipolar voltage map (right panel). The VT isthmus (white
lines) is situated at the junction of the low-voltage area
and healthy myocardial tissue, represented in violet on the
bipolar voltage map (voltage >1.5mV)
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Fig. 20.21 CARTO image in LAO 84° caudal 55° showing the epicardial bipolar voltage map of the LV, with the
Pentaray catheter situated at the junction of the area of
low-voltage electrograms at the level of the posteroinferior LV, corresponding to the VT isthmus. Pacing is performed at this level from electrodes 5–6, producing
myocardial capture. The correlation of the resulting QRS
morphology during pacing (right side of the image, yellow color) and the VT morphology (green color) is 90%,
with a short spike to QRS, conrming the exit zone of the
VT
Fig. 20.22 A 12-lead ECG showing the VT morphology
(left side of the image) and the correlation between the
locally generated QRS morphology resulting by pacing
from the Pentaray catheter at the level of the exit zone of
the VT and the VT morphology. With the exception of
lead I, there is very good concordance between the QRS
complexes, with an average of 95.54%
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Fig. 20.23 CARTO image in LAO 60°, caudal 70° showing the activation map of the VT (left panel) in relationship with the VT substrate depicted by the epicardial
bipolar voltage map (right panel), same as in Fig.20.19,
with superposed RF ablation lesions (pink and red dots) at
the level of the VT isthmus
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