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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. 15.20 CARTO image in LAO 60° cranial 20° (same
as in Fig. 15.19) showing the activation map of the LV
during VT 3. The “gure of 8” mechanism is shown by the
red arrows. The exit zone of the VT is represented in red
and the entry zone is represented in violet. The propagation of the wavefront takes place from red to yellow to
green to blue and then violet (right upper corner of the
image)
235
Two more VT morphologies were induced
during catheter manipulation/ablation of the previously induced VTs (Figs.15.24, 15.25, 15.26,
and 15.27).
The activation map of VT 7 is presented in
Fig.15.28. This had a cycle length of 345ms and
was also hemodynamically tolerated by the
patient. This was in favor of a double-loop macroreentry circuit, forming a “gure of 8,” with an
identical isthmus as the isthmus used by the VT
3, but with an opposite rotation direction
(Fig. 15.28) (see Fig. 15.18 for comparison),
(Fig.15.29).
Ablation was performed at the level of the VT
isthmus, with transformation of the VT in VT 8
(Fig.15.30). This last VT was incessant.
Fig. 15.21 Surface ECG leads I, II, III, and V1 together
with intracavitary leads recorded by the Pentaray catheter
(P1–2 up to P19–20) and the right ventricular apex bipolar
catheter (VD 1,2) during VT 3. The Pentaray catheter is
placed at the level of an outer loop and records fragmented
diastolic potentials
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Fig. 15.22 A 12-lead ECG showing VT (VT4) initiated during ablation of VT 3. The VT has a cycle length of 388ms
and has a morphology of RBBB and inferior axis, very similar to VT 3
R. Le Bouar et al.
Fig. 15.23 A 12-lead ECG showing VT5, induced during
RF ablation of VT 3. The VT has a cycle length of 388ms
and has a morphology of atypical RBBB and inferior axis.
Question 4: What should be the end
point of this VT catheter ablation
procedure?
A. Ablation of the clinical VT
B. Ablation of all induced VTs
C. Ablation of VT substrate with elimina-
tion of all LAVA
D. Non-inducibility of the clinical VT
E. Non-inducibility of all induced VTs
Even though the cycle length is the same as VT 3 and 4,
the morphology is different. This may indicate a similar
VT circuit but with a different exit point
An activation map of the VT was commenced
(Fig. 15.31). However, despite the longer VT
cycle length, due to the long duration of the procedure, this map was incomplete.
Ablation of the VT substrate was therefore
decided, given the high number of sustained
monomorphic VTs induced. Ablation was accomplished during atrial brillation. Several lines of
ablation were created at the level of the myocardial scar, in an attempt to transect all the mapped
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Fig. 15.24 A 12-lead ECG showing another spontaneously initiated VT (VT6). The VT has a cycle length of 356ms
and has a morphology of atypical RBBB and inferior axis
237
Fig. 15.25 Surface ECG leads I, II, III, and V1 together
with intracavitary leads recorded by the Pentaray catheter
(P1–2 up to P19–20) and the right ventricular apex bipolar
catheter (VD 1,2) during VT 6. The Pentaray catheter is
placed at the level of the exit zone and records fragmented
presystolic potentials
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Fig. 15.26 A 12-lead ECG showing another spontaneously initiated VT (VT7). The VT has a cycle length of 345ms
and has a morphology of atypical RBBB and right inferior axis
R. Le Bouar et al.
Fig. 15.27 Surface ECG leads I, II, III, and V1 together
with intracavitary leads recorded by the Pentaray catheter
(P1–2 up to P19–20) and the right ventricular apex bipolar
catheter (VD 1,2) during VT 6. The Pentaray catheter is
placed at the level of the exit zone and electrodes 1–2 and
17–18 record local presystolic potentials
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239
Fig. 15.28 CARTO image in AP view showing the activation map of the LV during VT 7. This VT has a cycle
length of 356ms. The entire circuit was mapped in the left
ventricle. The underlying mechanism is represented by a
macro-reentry at the level of the LV apex, with an isthmus
oriented parallel to the mitral valve and the LV apex, with
a double-loop reentry creating a “gure of 8” circuit. The
exit zone of the VT is represented in red and the entry
Fig. 15.29 CARTO
image in LAO 15° (same
as in Fig.15.28)
showing the activation
map of the LV during
VT 7. The “gure of 8”
mechanism is shown by
the red arrows. The exit
zone of the VT is
represented in red and
the entry zone is
represented in violet.
The propagation of the
wavefront takes place
from red to yellow to
green to blue and then
violet (upper right
corner of the image)
zone is represented in violet. The propagation of the
wavefront takes place from red to yellow to green to blue
and then violet (upper right corner of the image). Lowfragmented diastolic potentials could be recorded in key
areas of the VT circuit (white arrows). Of note, this looks
like the same isthmus as for VT 3, but with an inverse
propagation direction
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Fig. 15.30 A 12-lead ECG showing the last spontaneously initiated VT (VT8), after several RF applications in the
isthmus zone of VT 7. The VT has a cycle length of 549ms and has a morphology of atypical RBBB and superior axis
R. Le Bouar et al.
Fig. 15.31 CARTO image in LAO 30° caudal 30° showing the activation map of the LV during VT 8. This VT has
a cycle length of 549 ms. The entire circuit was not
VT isthmi and to eliminate the LAVA situated at
the level of the anterior and apical wall of the
LV. The bipolar voltage map of the LV with
superposed RF ablation lesions at the end of the
ablation procedure is shown in Figs.15.32, 15.33
and 15.34.
The activation map recorded during VTs 2, 3,
and 7 are shown in Figs.15.34, 15.35, 15.36 and
15.37 respectively.
mapped, and the activation map is incomplete. However,
the exit zone of the VT seems to be in the apical region
The ECG recorded at the end of the ablation
procedure is shown in Fig.15.38.
There were no complications related to the
procedure.
The CRT-D was reprogrammed in VVI biV
pacing 70 bpm and detection of ventricular
arrhythmias and therapies were switched on. The
ECG recorded 24h after the ablation procedure is
shown in Fig.15.39.
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Fig. 15.32 CARTO
image in LAO 45°
showing the bipolar
voltage map of the LV
with superposed RF
ablation lesions at the
end of ablation
Fig. 15.33 CARTO
image in LAO 105°
cranial 7° showing the
bipolar voltage map of
the LV with superposed
RF ablation lesions at
the end of ablation
241
Fig. 15.34 CARTO
image in RAO 30°
showing the bipolar
voltage map of the LV
with superposed RF
ablation lesions at the
end of ablation
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Fig. 15.35 CARTO
image in LAO 45°
showing the activation
map of the LV recorded
during VT 2 with
superposed RF ablation
lesions at the end of
ablation
Fig. 15.36 CARTO
image in LAO 60°
showing the activation
map of the LV recorded
during VT 3 with
superposed RF ablation
lesions at the end of
ablation
R. Le Bouar et al.
Fig. 15.37 CARTO
image in AP view
showing the activation
map of the LV recorded
during VT 7 with
superposed RF ablation
lesions at the end of
ablation
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Fig. 15.38 A 12-lead ECG at the end of the ablation procedure showing atrial brillation with a heart rate of 100bpm,
QRS axis at- 60°, and atypical LBBB
243
Fig. 15.39 A 12-lead ECG recorded 24h after the ablation procedure, after reprogramming the CRT-D in biventricular
pacing mode 70bpm, showing atrial brillation with biventricular pacing
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R. Le Bouar et al.
Telemetry recordings during the next 72h did
not show any VT recurrence.
The patient was discharged 12h later.
Six months later, he had no VT recurrence.
Answers
Question 1:
A.Initial R wave in lead aVR in favor
of ventricular tachycardia.
B.R/S ratio<1in V6, in favor of ven-
tricular tachycardia.
C. The RBBB morphology and
“northwest” axis deviation, in favor of
ventricular tachycardia.
Question 2: E. Perform catheter
ablation.
Question 3: All answers are acceptable, depending on the operator’s experience, on the patient’s characteristics,
and on several elements of the ablation
procedure (such as VT inducibility, VT
tolerability, number of VTs induced).
Question 4: Non-inducibility of all
induced VTs.
Commentary
The present case illustrates a catheter ablation
procedure of eight monomorphic VTs in a
70-year-old male patient with ischemic cardiomyopathy and remote large anterior myocardial
infarction. Several observations can be made
about the present case.
The most common cause of VT in patients
with structural heart disease is coronary artery
disease with remote myocardial infarction [1–3].
The myocardial scar post-infarction can, under
certain circumstances, favor the appearance of
unidirectional block across functional or anatomical boundaries, which can sustain macro- or
micro-reentry VT.The most common form of VT
in patients with ischemic cardiomyopathy and
remote myocardial infarction is a “gure of 8”
dual-loop macro-reentry circuit. Ventricular
tachycardia can appear early after myocardial
infarction, but it usually develops many years
after the index event [4].
Catheter ablation is a useful tool in the treatment of sustained monomorphic ventricular
tachycardia in patients with ischemic
cardiomyopathy. It is associated with a signicant reduction in the number of ICD discharges
in patients with VT storm [5–8]. A systematic
review and meta-analysis conducted by Anderson
etal. [1] demonstrated that, in randomized control trials, compared to anti-arrhythmic medication, catheter ablation reduced VT recurrence and
electrical storm (RR 0.78, 95% CI 0.64–0.95,
p=0.01; RR 0.70, 95% CI 0.51–0.94, p=0.02,
respectively) after a mean follow-up of 22months
in predominantly post-myocardial infarction
scar-related VT.In data pooled from four observational studies on 3065 patients, catheter ablation reduced VT recurrence and mortality, as
compared to RCTs (28.6% vs 39%, p < 0.001;
13.2% vs. 18%, p = 0.01, respectively). This
reduction was observed in spite of a greater incidence of electrical storm (33.2% vs. 17%,
P<0.001), a higher prevalence of nonischemic
substrate (46.4% vs 3.6%, p<0.001), and a lower
rate of implanted ICDs (68% vs. 94.7%,
p < 0.001). The mean follow- up period was
18.2months.
A pertinent observation related to the abovepresented case would be that cardiac imaging has
an important role in preparing for the ablation
procedure. A CT angiography of the left ventricle
is especially useful in patients with remote myocardial infarction and large VT aneurysms undergoing ablation, in order to rule out the presence
of thrombi at this level [9–11]. LV thrombus is an
absolute contraindication to catheter ablation,
due to the risk of embolic stroke during the
procedure.
Concerning the safety and efcacy of catheter
ablation of ventricular tachycardia in patients
with left ventricular aneurysm, Guo et al. [12]
conducted a study on 33 patients (11 with and 22
without LV aneurysm) with VT and found that in
patients with LV aneurysm, more than one-third
of clinical VTs (36.4%) had their origin in the
ventricular septum scar zone. Acute success was
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