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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. 17.1 A 12-lead ECG recorded at admittance to the cardiology department showing sinus rhythm, with a heart rate
of 78bpm, non-determined QRS axis, absence of LV hypertrophy, absence of ischemia, and incomplete RBBB
R. Le Bouar et al.
Fig. 17.2 Wide QRS complex tachycardia with a heart rate of 140bpm, RBBB morphology, and superior axis
Transthoracic echocardiography showed a
non-dilated LV (EDD of 55 mm), with mild
hypokinesia of the inferior and lateral wall of the
LV and of the basal IVS, with preserved systolic
function, a LVEF of 53% (Teichholz method)
(Fig. 17.3). The LV lling pressures were elevated; there were mild left atrial dilation and
moderate to severe functional mitral regurgitation (SRO=0.4cm2, PISA radius of 8mm); the
right ventricle was mildly dilated, with global
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Fig. 17.3 Transthoracic echocardiography image in M-mode showing a non-dilated LV (EDD of 55mm) with a preserved LV EF of 53%
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hypokinesia (TAPSE=11mm); there was moderate tricuspid regurgitation; the sPAP was
50 mmHg; and there was minimal pericardial
effusion and moderate pulmonary hypertension.
The ventricular electrodes of the ICD were visible inside the right ventricle and the right atrium.
ICD interrogation revealed the presence of
almost 16.000 episodes of non-sustained and sustained monomorphic VT with a cycle length of
around 415ms, during the past 12 months prior
to his admittance to the hospital, of which over
200 episodes during the past 24 hours, treated
with burst pacing by the ICD (Fig.17.4).
Given the presence of at least three episodes
of sustained VT over the last 24hours, the diagnosis of VT storm was established.
The patient’s chest X-ray is shown in Fig.17.5.
Question 1: What is the nature of the
tachycardia presented in Fig. 17.2?
A. Supraventricular tachycardia and
RBBB.
B. Antidromic tachycardia (WPW
syndrome).
C. Ventricular tachycardia.
D. Atrial utter with RBBB.
E. I don’t know.
Figure 17.2 explained. Fig. 17.2 shows a
wide QRS complex tachycardia with a heart rate
of 140 bpm, RBBB morphology, and superior
axis. The morphology of the tachycardia does not
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R. Le Bouar et al.
have a typical RBBB morphology, argument
against a supraventricular tachycardia with a
functional BBB.The amplitude of the R wave in
lead V1 is slightly more important than the amplitude of the R’ wave, argument in favor of ventricular tachycardia. The presence of Q waves in
lead V6 during a tachycardia with RBBB morphology also suggests the diagnosis of VT.There
is also a positive concordance in the precordial
leads, argument in favor of VT.
Given the high number of episodes of ventricular tachycardia that the patient experienced during the 12months prior to his hospital admittance,
an electrophysiological study in view of a catheter ablation procedure was scheduled.
• Question 2: What is the origin of the
ventricular tachycardia presented in
Fig. 17.2?
A. LV inferior and basal wall
B. LV superior and basal wall
C. LV lateral wall
D. RV septum
E. LV apex
Fig. 17.4 Upper panel: ICD tracing showing burst ventricular pacing with a coupling interval of 320ms with
termination of an episode of tachycardia, followed by
sinus rhythm with a rate of about 60bpm; an episode of
VT occurs (middle of the tracing), with VV intervals of
around 360–390 ms and the A-A intervals of around
700ms (A-V dissociation); the episode is treated unsuccessfully with two bursts of ventricular pacing of eight
beats each. Lower panel: from high to low: electrograms
for the atrial lead, the ventricular lead, and the lead with
markers and intervals showing A-V dissociation during an
episode of VT. At the end of the tracing, eight beats of
burst ventricular pacing are delivered by the ICD and the
VT episode is terminated. AP atrial paced, AR detection of
an atrial activity in the atrial refractory period, AS atrial
sensed, TD tachycardia detected, TP tachycardia paced TS
tachycardia sensed, and VP ventricular paced
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Fig. 17.4 (continued)
Fig. 17.5 Chest radiography image in posteroanterior
view showing the two leads of the ICD at the level of the
right atrial appendage and the lower RV septum. The cardiothoracic index is normal; there is no pleural effusion,
no signicant pulmonary stasis, and no evidence in favor
of a pulmonary infectious trigger
Electrophysiological Study andRF
Catheter Ablation Procedure
The ablation procedure 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 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.
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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 stimulation was performed under basal conditions at the level of RV
apex and easily induced the clinical ventricular
tachycardia, which reproduced the patient’s
symptoms (palpitations and dyspnea). The VT
was terminated by burst ventricular pacing.
Based on the morphology of the QRS complex during VT on the 12-lead ECG (RBBB
aspect, superior axis), an origin in the basal
inferior LV was suspected. A decision to perform
mapping of the basal LV was taken.
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 Biosense Webster® SmartTouch SF
open-irrigated 3.5mm tip with double curve D/F
catheter (Biosense Webster, Johnson & Johnson)
was introduced in a 9F 20cm vascular sheath and
was subsequently advanced via the aorta to the
LV.It was used to perform the anatomical map,
the bipolar voltage map, the pacemap, and the
activation map of the LV and subsequently the
RF ablation.
The ECG at the beginning of the ablation procedure is shown in Fig.17.6.
An anatomical map of the LV was rst created, which showed a non-dilated LV, with a volume of 150 mL. A bipolar voltage map was
subsequently created during sinus rhythm, which
showed the presence of a small area of low-
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R. Le Bouar et al.
Fig. 17.6 A 12-lead ECG recorded at the beginning of the ablation procedure
voltage electrograms at the level of the lateral
basal and inferior wall of the LV (Fig.17.7).
The patient presented frequent PVCs identical
to the clinical VT morphology. Therefore, activation mapping of the PVC was decided. During
the frequent PVCs, the roving/ablation catheter
recorded the timing of several sites in the LV
compared to the beginning of the QRS complex
on the surface ECG.The earliest activation site
was recorded at the level of the low-fragmented
ventricular electrograms in sinus rhythm, at the
level of the infero-lateral basal wall of the LV,
where the local ventricular bipolar electrogram
preceded the surface QRS by 45 ms. The local
unipolar electrogram recorded a “QS” signal
(Fig. 17.8). Given the identical morphology of
the PVC to that of the patient’s VT, this was considered to be the exit zone of the VT.The pres-
ence of ischemic heart disease in the patient’s
past medical history and the presence of a small
zone of low-amplitude potentials at the level of
the exit zone of the VT and the VT induction during programmed ventricular stimulation with
extrastimuli were all arguments in favor of a
reentry mechanism. The identication of the
entrance zone of the VT was performed during
sinus rhythm, using the technique described by
de Chillou etal. [1, 2].
A 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. The PASO
module of the CARTO system was used to compare the resulting 12-lead ECG during local pacing with the morphology of the PVC. A
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Fig. 17.7 CARTO
image in posteroanterior
view showing the
bipolar map of the LV
during sinus rhythm. A
small area of lowvoltage electrograms
was identied at the
level of the infero-lateral
basal wall of the LV.A
voltage <0.5mV was
considered compatible
with myocardial scar,
values between 0.5 and
0.5mV correspond to
borderline tissue, and
values over 0.5mV are
dened as normal
myocardial tissue
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Fig. 17.8 CARTO image of the left ventricle in a pos-
teroanterior view showing the infero-lateral LV wall.
Activation map of the LV during the frequent PVCs,
showing the origin of the PVC.Since the morphology of
the PVC was identical to that of the clinical VT, this was
considered to be the exit zone of the VT.The earliest acti-
vation site was recorded at the level of the low-fragmented
ventricular electrograms in sinus rhythm, at the level of
the infero-lateral basal wall of the LV, where the local ventricular bipolar electrogram preceded the surface QRS by
45ms. The local unipolar electrogram recorded a “QS”
signal
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R. Le Bouar et al.
Fig. 17.9 CARTO image showing the identication of
the exit point of the VT during sinus rhythm. Left side of
the image: PASO module image with superposition of the
locally generated QRS morphology and the morphology
of the clinical VT. A concordance of 97.8% at this point
identied the exit point of the VT circuit. Right side of
the image: posteroanterior view of the LV showing the
superposed correlation of 97.8% was observed in
an area of the infero-lateral basal LV wall, in the
area of the low-amplitude electrograms, corresponding to the earliest local activation site during PVCs, identifying the exit zone of the VT
(Fig.17.9). 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.
Pacing the LV in adjacent zones of the exit
zone identied sites with slightly different correspondence percentages. Pacing of the different
adjacent sites was continued 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
roving/ablation catheter positioned at a site on the lateral
inferior and basal LV wall, where the locally generated
QRS was almost identical to the QRS morphology during
clinical VT, therefore identifying the exit point (red zone).
This corresponds to the area of the earliest activation zone
during the PVCs (Fig. 17.6), which represents the exit
zone of the VT
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.17.10).
Between the entrance and the exit zones, the
VT isthmus was delineated. This was parallel to
the mitral valve, with an activation wavefront
turning clockwise around the mitral valve
(Fig.17.11).
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.
The activation map of the LV during the PVCs
with superposed RF ablation lesions is presented
in Fig.17.12.
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Fig. 17.10 CARTO image showing the identication of
the entrance point of the VT during sinus rhythm. Left
side of the image: PASO module image with superposition of the locally generated QRS morphology and the
morphology of the clinical VT. A concordance of 0% at
this point identied the entrance point of the VT circuit.
This is explained by the fact that during ventricular pacing, the depolarization of the LV takes place in the direc-
tion 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. Right side of the
image: posteroanterior view of the LV showing the roving/ablation catheter positioned at the entry zone of the
VT (violet zone)
Fig. 17.11 CARTO image in posteroanterior view
describing the VT mechanism: the red area represents the
exit point of the VT, the purple area represents the entrance
point, the white lines represent the VT isthmus, and the
red curved lines show the depolarization wavefront of the
macro-reentry around the mitral valve
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Fig. 17.12 CARTO image in posteroanterior view showing the activation map of the LV during the PVCs with superposed RF ablation lesions
Programmed ventricular stimulation was performed after the ablation, without the induction
of any sustained or non-sustained ventricular
arrhythmias.
There were no complications related to the
Answers
Question 1: C.Ventricular tachycardia
Question 2: A.LV inferior and basal
wall
ablation procedure.
The ECG post-ablation is presented in
Fig.17.13.
The patient was discharged home 48 hours
after the ablation procedure.
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Fig. 17.13 A 12-lead ECG post-ablation showing sinus rhythm with a heart rate of 75bpm, undetermined QRS axis,
absence of LV hypertrophy, and absence of ischemia
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Commentary
The above-presented case illustrates a catheter
ablation procedure of monomorphic ventricular
tachycardia in an 83-year-old male patient with a
past medical history of ischemic heart disease
and preserved LV EF%. Several observations can
be made about this case.
The diagnosis of ventricular tachycardia relies
on the correct interpretation of the 12-lead
ECG.Up to date, several diagnosis criteria found
on the 12-lead ECG have been published, which
offer arguments in favor against a ventricular origin of a wide QRS complex tachycardia [3–18],
with variable sensitivity and specicity. Most of
these algorithms do well in differentiating VT
from SVT with aberrancy. However, there are
less specic in differentiating VT from ventricular
preexcitation. In the present case, according to
the Brugada algorithm [18], the positive concordance in the precordial leads is a strong argument
in favor of VT.The initial R wave in lead aVR is
also in favor of a ventricular origin of the tachycardia [8, 9].
Catheter ablation is a viable treatment option
for ventricular tachycardia in patients with ischemic heart disease. In cases of severe coronary
artery disease, such in the above-presented case,
even in the absence of a clinical diagnosis of
myocardial infarction, the bipolar voltage map
created during sinus rhythm sometimes nds
zones of low local voltage, compatible with myocardial scar. These zones correlate well with
zones of late gadolinium enhancement evidenced
by cardiac MRI [19–22] and most likely represent small areas of brosis. These areas can subsequently serve as substrate for ventricular
arrhythmias.
The most common mechanism of ventricular
tachycardia in patients with ischemic heart disease and prior myocardial infarction is reentry
[23]. Macro-reentry circuits are more common
than micro-reentry circuits. In the case of macroreentry circuits, these can be dual-loop circuits in
a “gure of 8” shape, with the two loops turning
in opposite directions around lines of anatomical
or functional block; or these can have a singleloop mechanism, which is less frequently
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