Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3651_Библиотеки_им_академика_М_И_Перельмана
.pdf
15 C as e 15
https://t.me/medicina_free
Fig. 15.3 A 12-lead ECG showing a wide QRS complex tachycardia with a heart rate of 150bpm, atypical RBBB
morphology, and superior axis
225
Fig. 15.4 A 12-lead ECG recorded at admittance to the cardiology department showing atrial brillation with biventricular pacing, with a heart rate of 70bpm and an isolated PVC (second QRS complex in leads V1–V6)
226
https://t.me/medicina_free
Question 1: Are there elements on the
12-lead ECG presented in Fig. 15.1 in
favor of a specic diagnosis?
A. Initial R wave in lead aVR in favor of
ventricular tachycardia
B. R/S ratio < 1 in V6, in favor of ven-
tricular tachycardia
C. The RBBB morphology and “north-
west” axis deviation, in favor of ventricular tachycardia
D. Typical right bundle branch block in
favor of a supraventricular tachycardia
with aberrancy
E. Ventricular preexcitation
Figure 15.1 explained. The ECG shows a
wide QRS complex tachycardia with a heart rate
R. Le Bouar et al.
of 160 bpm, with atypical RBBB morphology,
and “northwest” axis deviation, compatible with
ventricular tachycardia. As a general rule, a wide
QRS complex tachycardia in a patient with a personal history of myocardial infarction has nine
times higher likelihood of being ventricular in
origin compared to a supraventricular tachycardia. Several clues are visible on this ECG and
support the diagnosis of VT: the association of a
RBBB aspect and “northwest” axis deviation, the
presence of an initial R wave in lead aVR (the
Vereckei criteria), the R/S ratio in V6<1, and the
atypical RBBB morphology (this does not support the diagnosis of SVT with aberrancy).
A transthoracic echocardiography was performed, which showed a dilated left ventricle,
with a severely depressed LVEF of 25% and akinesia of the anterior LV wall (Fig.15.5). It also
showed elevated LV lling pressure (E/e’ of 12);
Fig. 15.5 Left upper panel: transthoracic ECG image in
parasternal long-axis view showing a dilated LV with an
ESD of 72mm. Right upper panel: apical two-chamber
view showing a dilated LV with severe systolic dysfunction and a LV EF of 25%. Left lower panel: apical fourchamber view showing interrogation of the transmitral
ow, showing a unique E wave (no A wave) explained by
the presence of atrial brillation. Right lower panel: apical four-chamber view showing tissue Doppler imaging at
the level of the lateral mitral annulus with an E/e’ ratio of
12, in favor of increased LV lling pressure
15 C as e 15
https://t.me/medicina_free
227
absence of LV hypertrophy; a moderately dilated
LA (surface of 36cm2); mild to moderate mitral
regurgitation; mild aortic regurgitation; a cardiac
index of 2.2L/min/m2; a non-dilated right ventricle, with TAPSE of 18 mm; mild pulmonary
hypertension; sPAP of 38mmHg; and absence of
pericardial uid.
Laboratory workup showed no electrolyte
imbalance (Na 141 mmol/L, K 3.8 mmol/L),
mild renal dysfunction (BUN 4.3mmol/L, creatinine 134μmol/L), normal hepatic (AST 38IU/L,
ALT 38 IU/L) and thyroid function (TSH
2.8 IU/L), and mildly elevated cTnI (0.063 ng/
mL, interpreted in the context of repeated episodes of ventricular tachycardia requiring electrical cardioversion).
In order to rule out ongoing ischemia, coronary angiography was performed, which showed
chronic obstruction of the proximal LAD coronary artery; moderate stenosis of the circumex
coronary artery, with permeable bypass grafts;
and no acute lesion in favor of an acute coronary
syndrome (Fig.15.6).
Chest X-ray showed no argument in favor of a
pulmonary infectious trigger (Fig.15.7).
Question 2: What is the best treatment
option for this arrhythmic storm in this
patient?
A. Increase the dose of carvedilol to
50mg/day.
B. Add amiodarone.
C. Add mexiletine.
D. Change carvedilol to sotalol 40 mg
bid.
E. Perform catheter ablation.
Given the presence of the arrhythmic storm,
after discussing the potential benets and risks of
an ablation procedure and after having obtained
informed consent, an electrophysiological study
in view of a catheter ablation procedure was
rapidly scheduled, due to its superior efcacy
compared to anti-arrhythmic drugs in the treatment of this condition.
A cardiac computed tomography was performed before the ablation procedure, in order
to better dene the LV anatomy and to exclude
the presence of an apical thrombus. This
showed the absence of LV thrombus and the
presence of calcications at the level of the LV
apex (Fig.15.8).
Question 3: What would be your abla-
tion strategy in this patient at the begin-
ning of the procedure?
A. Perform PVS and perform activation
mapping of the induced VT.Ablate the
VT isthmus.
B. Perform a bipolar voltage map of the
LV during atrial brillation and substrate ablation.
C. Perform a bipolar voltage map of the
LV during RV pacing and substrate
ablation.
D. Perform an activation map of the LV
during RV pacing and ablate the zones
with the latest activation.
E. Perform an activation map of the LV
during atrial brillation and ablate the
zones with the latest activation.
228
https://t.me/medicina_free
R. Le Bouar et al.
Fig. 15.6 Coronary angiography image showing: left
upper panel type C chronic occlusion of the proximal
LAD coronary artery; type B1 moderate stenosis of the
proximal circumex coronary artery. Right upper panel:
mild stenosis (<50%) of the proximal right coronary
artery. Left lower panel: the left internal mammary
artery: LAD bypass graft presents no signicant stenosis;
however, the distal part of the LAD has a small caliber and
is diffusely inltrated. Right lower panel: the left internal
mammary artery: second marginal branch presents no signicant stenosis. The distal part of the second marginal
branch has no signicant stenosis. The atrial, right ventricular, and left ventricular ICD leads are also visible
15 C as e 15
https://t.me/medicina_free
Fig. 15.7 Chest radiography image in posteroanterior
view showing the three leads of the ICD at the level of the
right atrial appendage, lower RV wall, and a posterolateral
branch of the coronary sinus
Fig. 15.8 Computed tomography image of the heart with
emphasis on the left heart chambers. The left ventricle is
dilated and presents calcications in its apical part (red
arrow)
RF Catheter Ablation Procedure
The ICD was programmed in mode VVI 40bpm
and VT detection and therapies were switched
off.
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
229
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®).
The ECG at the beginning of the ablation procedure is presented in Fig.15.9.
Programmed ventricular pacing was performed under basal conditions (no isoprenaline
administration) with induction of a wide QRS
complex tachycardia with a cycle length of
308ms (Fig. 15.10), different from the patient’s
clinical ventricular tachycardia.
Given the personal history of ischemic heart
disease and of remote anterior myocardial infarction and also the morphology on the 12-lead ECG
during VT, an origin in the LV was suspected.
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.A Biosense
Webster® SmartTouch SF open-irrigated 3.5mm
tip with double curve was used to perform RF
ablation.
An anatomical map of the LV was rst created, which showed a severely dilated LV, with a
volume of 387mL.
A bipolar voltage map was subsequently created during atrial brillation, which showed the
presence of a very large area of low-voltage electrograms at the level of the anterior wall of the
LV, the upper half of the IV septum, and the inferior LV apex, measuring 144cm2, representing
49% of the total LV surface, compatible with scar
230
https://t.me/medicina_free
R. Le Bouar et al.
Fig. 15.9 A 12-lead ECG at the beginning of the ablation
procedure, showing atrial brillation with a heart rate of
110bpm, QRS axis at −75°, and nonspecic intraventricu-
lar conduction defect. Of note, the ICD detection and therapies have been switched off, and the device was programed
in mode VVI 40bpm in view of the ablation procedure
Fig. 15.10 A 12-lead ECG showing induction of VT 1
during programmed ventricular stimulation. VT 1 was
induced with two extrastimuli (S1=600ms, S2=260ms,
S3= 250ms). The VT has a cycle length of 308ms and
has a RBBB and superior axis
15 C as e 15
https://t.me/medicina_free
231
post-myocardial infarction (Figs. 15.11, 15.12,
15.13, and 15.14).
Catheter manipulation of the Pentaray cathe-
ter during creation of the LV bipolar voltage map
Fig. 15.11 CARTO image in LAO 20° cranial 26° showing the bipolar voltage map of the LV recorded during
sinus rhythm. The red area represents myocardial tissue
with a voltage of <0.5mV, compatible with dense myocardial scar. Yellow, green, and blue areas represent bor-
mechanically induced the tachycardia in
Fig.15.15.
This VT (VT 2) had a morphology identical to
the clinical VT of the patient. It had a cycle length
of 361ms and was hemodynamically tolerated by
derline tissue with values between 0.5 and 1.5mV.Violet
zones represent areas with a local voltage of >1.5 mV,
compatible with normal myocardial tissue. Note that the
dense scar area represents 143.6cm2 or 49% of the entire
LV, covering almost the entire LV anterior wall
Fig. 15.12 CARTO image in inferior view showing the
bipolar voltage map of the LV during sinus rhythm. The
red area represents myocardial tissue with a voltage of
<0.5mV, compatible with dense myocardial scar. Yellow,
green, and blue areas represent borderline tissue with values between 0.5 and 1.5mV.Violet zones represent areas
with a local voltage of >1.5mV, compatible with normal
myocardial tissue. The inferior wall of the LV has normal
myocardial voltage in its proximal two-thirds (violet)
Fig. 15.13 CARTO image in RAO 20° view showing the
bipolar voltage map of the LV recorded during sinus
rhythm. The red area represents myocardial tissue with a
voltage of <0.5 mV, compatible with dense myocardial
scar. Yellow, green, and blue areas represent borderline
tissue with values between 0.5 and 1.5mV.Violet zones
represent areas with a local voltage of >1.5mV, compatible with normal myocardial tissue. The inferior septal LV
wall contains normal myocardial tissue, while the superior septal LV wall contains borderline and scar tissue
232
https://t.me/medicina_free
R. Le Bouar et al.
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. 15.16. 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 LV apex.
The local ventricular potentials recorded by the
Fig. 15.14 CARTO image in LAO 60° showing the bipolar voltage map of the LV recorded during sinus rhythm.
The red area represents myocardial tissue with a voltage
of <0.5 mV, compatible with dense myocardial scar.
Yellow, green, and blue areas represent borderline tissue
with values between 0.5 and 1.5mV.Violet zones represent areas with a local voltage of >1.5 mV, compatible
with normal myocardial tissue
Pentaray catheter at the level of the LV apex are
shown in Fig.15.17.
RF ablation at the level of the VT isthmus was
commenced, with a power of 30 watts and an
ablation index of 550. During RF ablation of VT,
the tachycardia presented in Fig. 15.18 was
induced.
This VT (VT 3) had a cycle length of 388ms
and was also hemodynamically tolerated by the
patient, which also allowed the creation of an
activation map with the Pentaray catheter. The
activation map of the LV during VT is presented
in Fig.15.19. 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 anterior and apical LV wall
(Fig. 15.20). The local ventricular potentials
recorded by the Pentaray catheter at the level of
an outer loop are shown in Fig.15.21.
RF ablation at the level of the VT isthmus was
commenced, with a power of 30 watts and an ablation index of 550. During RF ablation of VT, the
tachycardia presented in Fig.15.22 was induced.
Ablation at the level of the VT isthmus was
continued, with induction of another VT
(Fig.15.23).
Fig. 15.15 A 12-lead ECG showing the catheter-induced VT (VT2) during the creation of the anatomical map of the
LV.The VT has a cycle length of 361ms and has a morphology identical to the clinical VT
15 C as e 15
https://t.me/medicina_free
233
Fig. 15.16 CARTO image in LAO 30° caudal 26° showing the activation map of the LV during VT 2. This VT has
a cycle length, after stabilization of the heart rate, of
400ms. The entire circuit was mapped in the left ventricle. The underlying mechanism is represented by a macroreentry at the level of the LV apex, with an isthmus
oriented perpendicular to the mitral valve and the LV
Fig. 15.17 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 2 (the clinical VT). The
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 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).
Low-fragmented diastolic potentials could be recorded in
key areas of the VT circuit (white arrows)
Pentaray catheter is placed close to the exit zone of the VT
and records fragmented, low-amplitude presystolic
potentials
234
https://t.me/medicina_free
Fig. 15.18 A 12-lead ECG showing the VT (VT3) induced during RF ablation of the clinical VT (VT 2). The VT has
a cycle length of 388ms and has a morphology of RBBB and inferior axis
R. Le Bouar et al.
Fig. 15.19 CARTO image in LAO 60° cranial 20° showing the activation map of the LV during VT 3. This VT has
a cycle length of 388ms. 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 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).
Low-fragmented diastolic potentials could be recorded in
key areas of the VT circuit (white arrows). The VT isthmus is wide, measuring 20mm
Соседние файлы в папке Библиотека им академика М.И. Перельмана