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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. 12.3 Left panel: M mode echocardiography showing a non-dilated left ventricle, with an end-diastolic
diameter of 51 mm. Right panel: Apical four-chamber
Fig. 12.4 Left panel: Angiography image of the left coronary artery showing no major obstruction of the epicardial
vessel. Right panel: Chronic total occlusion of the epicardial right coronary artery in its proximal segment (red arrow)
view showing a non-dilated LV with severe systolic dysfunction, with a LVEF% of 33% (single-plane Simpson
method)
A 24-h period of rhythm monitoring was con-
Question 1: What is the next best diagnostic test in the management of this
patient?
A. A 24-h 12-lead Holter ECG recording.
B. A 7-day Holter ECG recording.
C. An electrophysiological study (with
programmed ventricular stimulation).
D. Transesophageal left atrial
stimulation.
E. Implantable loop recorder insertion.
sidered to have a low probability to record
another potential episode of tachycardia; therefore, the 24-h lead Holter ECG recording was not
the option chosen for this patient. A 7-day waiting period was considered too long and with no
guarantee of tachycardia reoccurrence.
Transesophageal stimulation is usually not useful
for inducing ventricular arrhythmias and was not
available in our hospital. An implantable loop
recorder does not allow making the differential
diagnosis between wide QRS complex tachycardias. Given the high likelihood of the diagnosis
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of ventricular tachycardia, an electrophysiological study was scheduled and subsequently performed, in order to guide a RF ablation
procedure.
Electrophysiological Study andRF
Catheter Ablation Procedure
The electrophysiological study and the ablation
procedure were 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 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
intracavitary ECGs were recorded by the
WorkMate Claris™ System (Abbott®).
Programmed ventricular pacing was performed under basal conditions (no isoprenaline
administration) with induction of a wide QRS
complex tachycardia with a cycle length of
250ms (Fig.12.5).
Question 2: What is the tachycardia pre-
sented in Fig. 12.5?
A. SVT with functional RBBB.
B. Antidromic tachycardia.
C. Ventricular tachycardia.
D. Atrial utter with 1:1 AV conduction.
E. Atrial brillation with RBBB.
Fig. 12.5 Wide QRS complex tachycardia with a heart rate of 240bpm, of indeterminate morphology and superior axis
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Figure 12.5 explained. A 12-lead ECG show-
ing a wide QRS complex tachycardia with a heart
rate of 240 bpm, of indeterminate morphology
(neither LBBB nor RBBB) and superior axis. Of
note, the aspect of the QRS is not compatible
with a typical BBB morphology, making SVT
with functional bundle branch block unlikely.
The R to S ratio of the QRS complex in V6 is <1,
element in favor of VT.The ratio between the initial part of the QRS complex and the terminal
part of the QRS complex (vi/vt) in lead V2 is <1,
also in favor of VT.
Once the diagnosis of VT was established
using the 12-lead ECG during VT, a Biosense
Webster® SmartTouch SF open-irrigated 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.
Question 3: Where is the origin of the
ventricular tachycardia presented in
Fig. 12.5?
A. LV lateral wall.
B. LV anterior wall.
C. LV inferior wall.
D. LV septum.
E. LV apex.
Given the personal history of ischemic heart
disease and remote inferior myocardial infarction, the indeterminate morphology on the
12-lead ECG during VT, and the relatively narrow QRS complex in the precordial leads, an origin at the level of the LV septal and inferior wall
was suspected. Mapping of the VT was therefore
commenced in the left ventricle.
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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 catheter was
used to perform RF ablation.
An anatomical map of the LV was rst created, which showed a non-dilated LV, with a
volume of 140mL. 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 wall of
the LV, measuring 20cm2, representing 15.3% of
the total LV surface, compatible with scar postmyocardial infarction (Fig.12.6).
Programmed ventricular stimulation was performed once again, with induction of the clinical
VT.This was hemodynamically tolerated by the
patient, which allowed the creation of an activation map with the Pentaray catheter. The activation map of the LV during VT is presented in
Fig. 12.7. This was in favor of a double-loop
macro-reentry circuit, forming a “gure of 8”,
each of the two outer loops using the same critical isthmus at the level of the inferior and septal
LV wall. The length of the VT isthmus was
17mm, with a width of 14mm, and it was situated at a distance of 18mm from the mitral valve
annulus.
Figure 12.8 shows the relationship between
the anatomical substrate of the tachycardia (the
low-voltage area situated at the level of the
inferior LV wall, seen on the bipolar voltage
map of the LV, right panel) and the critical components of the VT: the two outer loops and the
VT isthmus superposed on the activation map
of the LV.
Once the VT mechanism was elucidated, RF
ablation was subsequently performed by creating
an ablation line which transected the VT isthmus.
Fig. 12.6 Left panel: A 12-lead ECG showing sinus
rhythm at the beginning of the ablation procedure. Right
panel: CARTO image in LAO 6° caudal 49° showing the
inferior wall of the left ventricle. Bipolar voltage map of
the left ventricle revealing a large area of low voltage (<
0.5mV, red color) at the level of the inferior wall, compatible with myocardial scar post-myocardial infarction. The
low-voltage area represents 20cm2 or 15% of the entire
surface of the LV
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Fig. 12.7 Left panel: A 12-lead ECG of the induced VT
during programmed ventricular stimulation, VT which is
identical to the clinical VT. Right panel: CARTO image
of the left ventricle in LAO 90° caudal 80° showing the
inferior LV wall. 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). Left side of
the image: Surface ECG leads and intracavitary electrograms; the yellow arrow indicates far-eld ventricular
electrogram, and green arrow indicates near-eld ventricular electrogram, recorded during early diastole at the
level of the isthmus by the Pentaray catheter
Fig. 12.8 CARTO image showing the inferior wall of the
left ventricle in LAO 164° Caudal 74°. Left panel:
Activation map of the LV during ventricular tachycardia,
showing the critical components of the VT, same as in
Fig. 12.6. Right panel: Bipolar voltage map of the left
ventricle showing the anatomical relationship between the
VT circuit and the scar– the former is present at the border between the scar and normal myocardial tissue (voltage >1.5mV)
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The target parameters were power of 35W and
ablation index 550. The VT is terminated during
RF ablation.
Programmed ventricular stimulation was performed after the ablation, with induction of a sustained ventricular tachycardia, with a different
morphology compared to the rst VT. Since the
end point of the VT ablation procedure is noninducibility of any sustained monomorphic ventricular arrhythmias, mapping and ablation of this
second VT were performed.
Given the fact that this VT was also hemodynamically tolerated, an activation map of the VT
was subsequently created. This, together with the
12-lead ECG morphology of the VT, is shown in
Fig.12.9. The activation map was in favor of a
single-loop macro-reentry circuit turning in a
clockwise direction around a line of block possibly created by the RF lesions previously deployed
at the level of the inferior LV wall.
Figure 12.10 shows the relationship between
the anatomical substrate of the tachycardia (the
low-voltage area situated at the level of the inferior LV wall, seen on the bipolar voltage map of
the LV, right panel) and the critical components
of the VT: the single loop turning around the line
of block, superposed on the activation map of the
LV.
RF ablation was performed by creating an
ablation line joining the mitral annulus and the
line of block around which the activation wavefront propagated (Fig.12.11). The target parameters were power of 35W and ablation index 550.
The VT is terminated during RF ablation.
Programmed ventricular stimulation was performed after the ablation, before and after isoprenaline infusion, at two coupling intervals
(600ms et 400ms), up to three extrastmuli, this
time without induction of any ventricular
arrhythmia.
Fig. 12.9 Left panel: A 12-lead ECG recorded during
VT 2, induced during programmed ventricular stimulation
after successful ablation of VT 1, together with the intracavitary leads recorded by the Pentaray catheter placed at
the level of the VT isthmus; the yellow arrow indicates
near-eld ventricular electrogram recorded during late
diastole (pre-systole) by the electrodes 5–6 of the Pentaray
catheter, situated in the red zone of the map; the green
arrow indicates near-eld ventricular electrogram
recorded in early diastole by the poles 11–12 of the
Pentaray catheter, situated in the entrance zone of the
map. The activation time difference between the two sites
is 178ms. Right panel: CARTO image of the left ventricle in LAO 173° caudal 60° showing the infero-septal LV
wall. Activation map of the LV during ventricular tachycardia, showing a different macro-reentry circuit compared to VT 1. The exit zone (red color) is close to the
mitral valve; the outer loop is represented in yellow,
green, and blue, indicated by the curved red arrows; and
the entrance zone is represented in violet. The VT isthmus
is represented by the white line, around which the activation wavefront propagates
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Fig. 12.10 CARTO image showing the inferior wall of
the left ventricle in LAO 170° caudal 60°. Left panel:
Activation map of the LV during ventricular tachycardia,
showing the critical components of the VT, same as in
Fig. 12.8. Right panel: Bipolar voltage map of the left
Fig. 12.11 CARTO
image showing the
inferior wall of the left
ventricle in LAO 170°
caudal 60°. Activation
map of the LV during
VT 2 after RF ablation.
The pink and red dots
represent ablation
lesions
ventricle showing the anatomical relationship between the
VT circuit and the scar– the former is present at the border between the scar and normal myocardial tissue (voltage >1.5mV)
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There were no complications related to the
procedure.
The 12-lead ECG recorded after the ablation
is shown in Fig.12.12.
Given the presence of remote myocardial
infarction and sustained recurrent monomorphic
VT, the patient presented a class IIa indication for
an ICD implantation.
Question 4: What type of ICD would you
implant in this particular patient?
A. A single-chamber ICD.
B. A dual-chamber ICD.
C. A CRT-D device.
D. A subcutaneous ICD.
E. I would not implant an ICD, given the
good result of the ablation procedure.
Given the success of the RF ablation procedure and the age of the patient, as well as the
patient’s desire, a subcutaneous ICD was
implanted (Fig.12.13). There was no indication
for implanting a CRT-D device given the presence of a narrow QRS complex on the ECG.
The patient was discharged from the hospital
48h later.
Answers
Answer to Question 1: C. An electro-
physiological study (with programmed
ventricular stimulation).
Answer to Question 2: C.Ventricular
tachycardia.
Answer to Question 3: C.LV Inferior
wall.
Answer to Question 4: D.A subcutaneous ICD (but answer A and B are possible answers too).
Fig. 12.12 A 12-lead ECG recorded at the end of the ablation procedure showing sinus rhythm with a heart rate of
60bpm; QRS axis at −45°; Q waves in leads II, III, and aVF; and negative T waves in leads II, III, aVF, and V3–V6
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Fig. 12.13 Chest X ray, posteroanterior view showing
the position of the subcutaneous ICD implanted after the
RF procedure of VT in the secondary prevention of sudden cardiac death. The device is indicated by the yellow
arrow; the ICD subcutaneous lead is indicated by the red
arrows
Commentary
The present case illustrates a catheter ablation
procedure of two sustained monomorphic ventricular tachycardias in a young female patient
with a personal history of ischemic cardiomyopathy and remote inferior myocardial infarction.
Several observations merit further discussion.
Ischemic heart disease is the most common
cause of ventricular tachycardia in patients with
structural heart disease. The presence of VT in
patients with structural heart disease has a signicant impact on the patients’ morbidity and
mortality [1]. Treatment options for VT in the
context of ischemic heart disease (outside of an
acute setting) include anti-arrhythmic drugs,
catheter ablation and ICD implantation. In
patients with ischemic heart disease and recurrent symptomatic monomorphic ventricular
tachycardia despite anti-arrhythmic drug therapy,
or when anti-arrhythmic drugs are contraindicated or not tolerated, according to the 2019
HRS/EHRA/APHRS/LAHRS expert consensus
statement on catheter ablation of ventricular
arrhythmias [2], catheter ablation has a class I
recommendation, level of evidence B-NR, to
reduce VT recurrence. The 2015 ESC Guidelines
on the management of patients with ventricular
arrhythmias state that in patients with recurrent
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VT or VF despite complete revascularization and
optimal medical treatment, radiofrequency catheter ablation should be considered, class IIa recommendation, level of evidence C [3].
Several clinical trials have shown the superiority of catheter ablation to anti-arrhythmic drugs
in the treatment of VT. In the case of VT recurrence despite the use of anti-arrhythmic drugs,
treatment options include increasing the dose,
switching to another anti-arrhythmic drug, or
performing catheter ablation. The VANISH trial
(Ventricular Tachycardia Ablation versus
Escalated Antiarrhythmic Drugs) [4] compared
the efcacy of anti-arrhythmic drugs (either an
increased dose compared to the patients’ usual
dose or the introduction of a different antiarrhythmic drug) to catheter ablation on a population of 259 patients. The mean follow-up was
28 ± 17 months. Patients treated with catheter
ablation had a signicant reduction in the composite primary end point of death, VT storm, or
appropriate ICD shocks. Patients who had the
most benet were those who were on amiodarone
at the inclusion in the trial, in whom the strategy
consisted in increasing the amiodarone dose or
adding mexiletine (HR 0.55; 95% CI 0.38–0.80;
p < 0.001). Interestingly, patients who were on
sotalol at the inclusion in the trial and the strategy
was switching to amiodarone did not have the
same benet (HR 1.14; 95% CI 0.65–2.02;
p=0.64) [4]. Compared to patients who received
mexiletine on top of high dose of amiodarone (>
300mg/day), those who underwent catheter ablation had a signicant benet [5].
Besides the VANISH trial [4], several other
prospective, multicenter cohort studies support
the ruse of catheter ablation in the treatment of
VT in patients with ischemic heart disease on
anti-arrhythmic drugs. The main benet is a
reduction in VT recurrence [6, 7]. In these studies, a signicant reduction in the number of VT
episodes was observed during the follow-up
period of 6 months post-ablation, comparing to
the 6months period prior to the catheter ablation
procedure. In the Euro-VT study, absence of VT
recurrence was observed in almost half of the
patients treated with catheter ablation (51%) [8].
A signicant reduction in ICD therapies was
observed in almost 80% of the patients (from
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60± 70 to 14±15, p< 0.2). In the Multicenter
Thermocool VT Ablation Trial, the number of
VT episodes was reduced by the catheter ablation
procedure from a median of 11.5 to 0 episodes
(p<0.0001) [9].
In the above-presented patient, the bipolar
voltage map identied the myocardial scar postmyocardial infarction, which was situated at the
level of the inferior LV wall. This represented
15% of the LV surface. In patients with remote
MI, the VT circuit is usually situated not inside
the dense myocardial scar but at the junction
between the myocardial scar and healthy myocardial tissue, in borderline zones, where the surviving cardiac myocytes are able to conduct
electricity but in abnormal ways, much slower,
favoring unidirectional block and the appearance
of macro-reentry. After the creation of the bipolar
voltage map (Fig.12.6), given the good toleration
of the clinical VT, creation of an activation map
during VT was possible. This is not always the
case when performing VT ablation, since faster
VTs, especially in patients with low LV EF%, are
usually not well hemodynamically tolerated, and
activation mapping cannot be used; other techniques such as the creation of a pacemap by pacing during sinus rhythm for the identication of
the VT isthmus, entrance zone, and exit zone
have been described [10] (see cases 13, 14, 16,
17, 18, and 19). This allowed the identication of
the VT isthmus at the level of the inferior LV
wall. RF ablation of the VT isthmus terminated
the VT.What is important to notice is that the VT
isthmus of the second VT was situated in the
zone where RF had been applied for termination
of VT 1. This raises the possibility of an iatrogenic origin of VT 2, since modication of conduction of the level of the LV wall created by RF
lesions might have created the VT isthmus for VT
2. Another argument in favor of this possibility is
the fact that programmed ventricular stimulation
did not induce this sustained monomorphic VT
prior to catheter ablation. The ablation strategy of
this VT was to create a line of ablation up to an
anatomical structure serving as a block in the
propagation of the electrical wavefront, in this
case the mitral annulus. This strategy rendered
the second VT non-inducible.
As recommended by the current international
guidelines, an ICD was implanted in the secondary prevention of sudden cardiac death [3]. Of
note, one could say that the patient also had an
ICD implantation indication based on the low LV
EF of 33%. However, she was not on optimal
medical therapy mainly (no K+-sparing diuretic
and no sacubitril-valsartan and on the minimal
dose of ACE-I). Given the young age of the
patient and the lack of a need for ventricular pacing or CRT, a subcutaneous ICD was considered
to be the device of choice. This has a class IIa
indication, level of recommendation C in the
2015 ESC Guidelines on the management of
patients with ventricular arrhythmias [3].
Learning Points
• Ischemic heart disease is the most common cause of ventricular tachycardia in
patients with structural heart disease.
• The most common VT mechanism in
this setting is macro-reentry, even
though enhanced automatism is also
possible.
• The bipolar voltage map is useful in
identifying myocardial scar, which usually contains the origin of the VT
circuit.
• When the VT is hemodynamically tolerated, activation mapping is the method
of choice in understanding the tachycardia circuit.
• The end point of a catheter ablation procedure of ventricular tachycardia is
elimination of all sustained VTs, not
only of the clinical VT.
• Programmed ventricular stimulation
after the ablation of the clinical VT is
compulsory, in order to identify other
potential ablation targets.
• Despite a successful ablation, an ICD
implantation is indicated, given the
presence of a myocardial substrate
which places the patient at risk for
future VT recurrence or development of
other VT circuits.
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