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
12 C ase 12
https://t.me/medicina_free
193
References
1. Lo R, Chia KK, Hsia HH. Ventricular tachycardia
in ischemic heart disease. Card Electrophysiol Clin.
2017;9(1):25–46.
2. Cronin EM, Bogun FM, Maury P, Peichl P, Chen
M, Namboodiri N, etal. 2019 HRS/EHRA/APHRS/
LAHRS expert consensus statement on catheter
ablation of ventricular arrhythmias. Heart Rhythm.
2020;17(1):e2–e154.
3. Priori SG, Blomstrom-Lundqvist C, Mazzanti A,
Blom N, Borggrefe M, Camm J, et al. 2015 ESC
Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden
cardiac death: the task force for the management of
patients with ventricular arrhythmias and the prevention of sudden cardiac death of the European Society
of Cardiology (ESC) endorsed by: Association for
European Paediatric and Congenital Cardiology
(AEPC). Europace. 2015;17(11):1601–87.
4. Sapp JL, Wells GA, Parkash R, Stevenson WG, Blier
L, Sarrazin JF, etal. Ventricular tachycardia ablation
versus escalation of antiarrhythmic drugs. N Engl J
Med. 2016;375(2):111–21.
5. Deyell MW, Steinberg C, Doucette S, Parkash R,
Nault I, Gray C, et al. Mexiletine or catheter ablation after amiodarone failure in the VANISH trial. J
Cardiovasc Electrophysiol. 2018;29(4):603–8.
6. Morawski S, Pruszkowska P, Sredniawa B, Lenarczyk
R, Kalarus Z. Long-term outcome of catheter ablation and other form of therapy for electrical storm in
patients with implantable cardioverter-debrillators. J
Interv Card Electrophysiol. 2017;50(3):227–34.
7. Palaniswamy C, Kolte D, Harikrishnan P, Khera S,
Aronow WS, Mujib M, et al. Catheter ablation of
postinfarction ventricular tachycardia: ten-year trends
in utilization, in-hospital complications, and inhospital mortality in the United States. Heart Rhythm.
2014;11(11):2056–63.
8. Hendriks AA, Khan M, Geller L, Kardos A, de Vries
LJ, Yap SC, etal. Ventricular tachycardia in ischemic
cardiomyopathy; a combined endo-epicardial ablation as the rst procedure versus a stepwise approach
(EPILOGUE)- study protocol for a randomized controlled trial. Trials. 2015;16:487.
9. Marchlinski FE, Haffajee CI, Beshai JF, Dickfeld
TL, Gonzalez MD, Hsia HH, et al. Long-term success of irrigated radiofrequency catheter ablation
of sustained ventricular tachycardia: post-approval
THERMOCOOL VT trial. J Am Coll Cardiol.
2016;67(6):674–83.
10. de Chillou C, Groben L, Magnin-Poull I, Andronache
M, MagdiAbbas M, Zhang N, et al. Localizing the
critical isthmus of postinfarct ventricular tachycardia:
the value of pace-mapping during sinus rhythm. Heart
Rhythm. 2014;11(2):175–81.
Case 13
https://t.me/medicina_free
FrédéricHalbwachs, RonanLe Bouar,
CharlineDaval, TarekEl Nazer, LaurentJacquemin,
LucienDiene, andJacquesLevy
13
Case Presentation
A 77-year-old male patient with a past medical
history of remote infero-lateral myocardial
infarction at the age of 56 years treated with
thrombolysis, ischemic cardiomyopathy with
severe LV systolic dysfunction (LVEF of 30%),
severe coronary artery disease (chronic total
occlusion of the right coronary artery, chronic
total occlusion of the circumex coronary artery,
severe stenosis of the proximal LAD and the rst
diagonal branch– treated with PTCA and stent
Supplementary Information The online version contains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 35579- 0_13.
F. Halbwachs (*)
Biosense Webster, Mulhouse, France
R. Le Bouar · C. Daval · T. El Nazer · L. Jacquemin ·
L. Diene · J. Levy
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr;
charline.daval@ghrmsa.fr; tarek.elnazer@ghrmsa.fr;
jacqueminl@ghrmsa.fr;
lucien-leopold.diene@ghrmsa.fr; levyj@ghrmsa.fr
implantation at the age of 64 years, intra-stent
restenosis of the rst diagonal branch treated
with PTCA + stent implantation at the age of
69years), and cardiac arrest at the age of 69 due
to ventricular brillation with subsequent ICD
implantation for the secondary prevention of sudden cardiac death was admitted to the emergency
department for electrical storm. ICD interrogation (Boston Teligen) revealed 34 episodes of
sustained monomorphic VT which required ICD
intervention: 30 episodes treated with burst ventricular pacing and four episodes requiring internal electrical cardioversion. His cardiovascular
risk factors were represented by age>55years
old, a history of smoking (35 pack-years), and
grade 1 overweight.
His medication at home consisted of lisinopril
20mg, carvedilol 2 × 25mg, clopidogrel 75mg,
atorvastatin 40mg, and eplerenone 25mg.
In the emergency department, at physical
examination, his blood pressure was
100/60mmHg, HR 190bpm, and SpO2 94% with
4 L O2/min via nasal cannula, his heart sounds
were rapid and regular, he was in respiratory distress with 28 breaths/min, lung auscultation
revealed mild bilateral crepitant rales, and he had
no signs of right heart failure.
His ECG at presentation is showed in
Fig.13.1.
In the emergency department, he had several
episodes of the same wide QRS complex tachycardia (Fig.13.1), treated unsuccessfully by burst
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
L. Muresan (ed.), Clinical Cases in Cardiac Electrophysiology: Ventricular Arrhythmias,
https://doi.org/10.1007/978-3-031-35579-0_13
195
196
https://t.me/medicina_free
Fig. 13.1 A 12-lead ECG showing a wide QRS complex tachycardia with a heart rate of 190bpm, left bundle branch
morphology, and left superior axis
F. Halbwachs et al.
Fig. 13.2 A 12-lead ECG showing sinus rhythm, heart rate of 75bpm, QRS axis at −20°, Q waves in leads II, III, and
aVF compatible with remote inferior wall necrosis, and attened T waves In leads II, III, and aVF and V5 and V6
ventricular pacing by the ICD, which required
repeated electrical cardioversion, due to their
hemodynamically unstable nature. An ECG was
recorded between electrical cardioversions
(Fig.13.2).
Amiodarone, magnesium sulfate, and lido-
caine were administered, but the tachycardia
recurred. The patient was sedated, intubated, and
transferred to the intensive care unit, where his
condition stabilized.
A transthoracic echocardiography was performed, which showed a dilated left ventricle,
with a severely depressed LVEF of 18% and akinesia of the LV basal posterior wall (Fig.13.3)
13 C ase 13
https://t.me/medicina_free
197
Fig. 13.3 Left panel: M-mode echocardiography showing a dilated left ventricle (EDD of 72.8 mm), with a
severely depressed LVEF of 18% (Teicholz) and akinesia
Fig. 13.4 Left panel: Angiography image of the left
coronary artery showing chronic total occlusion of the circumex coronary artery (red arrow), with no acute lesion
at the level of the LAD.The coil of the ventricular electrode of the ICD is also visible, inserting in the apical
of the LV basal posterior wall. Right panel: Apical fourchamber view showing a severely depressed LVEF of
31%
region of the right ventricle. Right panel: Chronic
obstruction of the epicardial right coronary artery in its
proximal segment (red arrow). The coil of the ventricular
electrode of the ICD is visible in the inferior right part of
the image
and severe global hypokinesia. It also showed
type 1 diastolic dysfunction; elevated LV lling
pressure (E/e′ of 14); moderate LV hypertrophy;
a mildly dilated LA (surface of 28 cm2; mild
mitral regurgitation; mild aortic regurgitation; a
cardiac index of 2.53 L/min/m2; a non-dilated
right ventricle, with TAPSE of 19 mm; absence
of pulmonary hypertension; sPAP of 30mmHg;
and absence of pericardial uid.
Laboratory workup showed mild thrombocytopenia (100 × 109/L), with no electrolyte imbalance (Na 140 mmol/L, K 4.1 mmol/L); normal
renal function (BUN 2.3 mmol/L, creatinine
86μmol/L), hepatic function (AST 29IU/L, ALT
32IU/L), and thyroid function (TSH 3.13IU/L);
and mild elevation of cTnI (0.863ng/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 circumex and right
coronary arteries, but no acute lesion in favor of
an acute coronary syndrome (Fig.13.4).
198
https://t.me/medicina_free
F. Halbwachs et al.
An electrophysiological study in view of a
catheter ablation procedure was subsequently
performed.
Question 1: What is the origin of the ven-
tricular tachycardia presented in Fig.
13.1?
A. LV infero-septal wall.
B. LV superior wall.
C. LV lateral wall.
D. LV septum.
E. LV apex.
EP Study andRF 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
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
350ms (Fig.13.5).
Given the personal history of ischemic heart
disease and remote inferior myocardial infarction, and the morphology on the 12-lead ECG
during VT, an origin in the LV was suspected.
Mapping of the VT was therefore commenced in
the left ventricle.
Fig. 13.5 A 12-lead ECG showing a wide QRS complex tachycardia with a cycle length of 349ms, corresponding to
a heart rate of 171bpm, left bundle branch morphology, and left superior axis
13 C ase 13
https://t.me/medicina_free
Question 2: What would be your ablation strategy for this patient?
A. Perform activation mapping during
VT.
B. Perform a bipolar voltage map during
sinus rhythm to identify the myocardial scar post-myocardial infarction.
C. Perform pacemapping during sinus
rhythm in order to identify the critical
components of the VT circuit: exit
zone, entrance zone, and VT isthmus.
D. All of the above.
E. None of the above.
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 D/F was used to perform
RF ablation.
199
An anatomical map of the LV was rst created, which showed a severely dilated LV, with a
volume of 327mL.A bipolar voltage map was
subsequently created during sinus rhythm, which
showed the presence of a very large area of lowvoltage electrograms at the level of the inferior
wall of the LV, measuring 58.7cm2, 22.1% of the
total LV surface, compatible with scar postmyocardial infarction (Fig.13.6).
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. 13.7. 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 situated at the level of the inferior LV wall.
The length of the VT isthmus was 20mm, with a
width of 16mm, and it was situated at the level of
the mid-part of the inferior and septal wall.
Figure 13.8 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.
Fig. 13.6 CARTO
image in LAO 142°
caudal 13° 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 22% of the
entire surface of the LV
200
https://t.me/medicina_free
F. Halbwachs et al.
Fig. 13.7 Left side of the image: CARTO image show-
ing the infero-septal wall of the left ventricle. 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 pur-
The tachycardia was terminated by a run of
mechanically induced PVCs, provoked by the
Pentaray catheter.
A pacemap was subsequently created by pacing from the distal electrode of the roving/ablation catheter at a xed coupling interval of
600ms in several areas of the LV, with emphasis
on the area of the VT isthmus, entrance zone, and
exit zone. 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 superposed correlation of 99% was
pose), being parallel to the mitral valve. Right side of the
image: Surface ECG leads II, aVR, and V1, together with
the intracavitary leads recorded by the Pentaray catheter;
the yellow arrow indicates far-eld ventricular electrogram, and green arrow indicates near-eld ventricular
electrogram, recorded during diastole at the level of the
isthmus by the Pentaray catheter
observed in the exit zone of the VT, conrming it
(Fig.13.9). This is explained by the fact that activation of the LV 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 the zone corresponding to
the entrance zone during VT produced a QRS
morphology very different from the QRS morphology during VT.This is explained by the fact
that during ventricular pacing, the depolarization
of the LV takes place in the direction opposite to
13 C ase 13
https://t.me/medicina_free
201
Fig. 13.8 CARTO image showing the infero-septal wall
of the left ventricle (same view as in Fig. 13.6). Left
panel: Activation map of the LV during ventricular tachycardia, showing the critical components of the VT, same
as Fig.13.6. Right panel: Bipolar voltage map of the left
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. 13.10) from that of the QRS morphology
during VT.
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 = 35 W and ablation index 550. Before
ablation, VT was reinduced during programmed
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)
ventricular stimulation. Ablation was performed
during VT. The VT is terminated during RF
ablation.
Ablation of the LAVA identied at the level
of the scar was subsequently performed. The
anatomical map of the LV with the superimposed RF ablation lesions is presented in
Fig.13.11.
Programmed ventricular stimulation was performed after the ablation, without the induction
of any sustained ventricular arrhythmias.
The ICD was reprogrammed in VVI mode,
40bpm, and detection of ventricular arrhythmias
and therapies were switched on.
202
https://t.me/medicina_free
F. Halbwachs et al.
Fig. 13.9 CARTO image showing the infero-septal wall
of the left ventricle (same view as in Figs.13.6 and 13.7).
Pacemap of the left ventricle in sinus rhythm conrming
the exit zone of the clinical VT (red color). Pacing with
the roving/ablation catheter at this site reproduces a QRS
There were no complications related to the
ablation procedure.
The 12-lead ECG recorded at the end of the
ablation procedure is presented in Fig.13.12.
The ICD interrogation performed at 3, 6, 12,
and 24 months post-the ablation procedure
showed no tachycardia recurrence.
morphology identical to the morphology of the clinical
VT (concordance of 99%, right side of the image). The
red contour represents the border of the myocardial scar;
green dots represent LAVA; the two white lines delineate
the VT isthmus
Answers
Question 1: A.LV infero-septal wall.
Question 2: D.All of the above.
13 C ase 13
https://t.me/medicina_free
203
Fig. 13.10 CARTO image showing the infero-septal
wall of the left ventricle (same view as in Figs.13.6, 13.7,
and 13.8). Pacemap of the left ventricle in sinus rhythm
conrming the entrance zone of the clinical VT (blue
color). Pacing with the roving/ablation catheter at this site
reproduces a QRS morphology substantially different to
the morphology of the clinical VT (concordance of 21.9%,
Fig. 13.11 CARTO image showing left ventricular anatomical map after RF ablation. Red and pink dots correspond to the ablation lesions deployed at the level of the
VT isthmus transecting it (1) and at the level of the LAVA
(2), homogenizing the scar
right side of the image), this zone being close to the exit
zone of the VT (red color), where pacing produced a morphology identical to the VT QRS morphology (Fig.13.8).
The red contour represents the border of the myocardial
scar; green dots represent LAVA; the two white lines
delineate the VT isthmus (same as in Fig.13.8)
Соседние файлы в папке Библиотека им академика М.И. Перельмана