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
276
https://t.me/medicina_free
R. Le Bouar et al.
encountered. In the case of inferior myocardial
infarction, the orientation of the VT isthmus is
parallel to the mitral valve, and one loop is usually a peri-mitral loop [24]. Such is probably the
case of the above-presented patient (see
Fig.17.9). We use the word “probably” because
the activation map is incomplete and only the exit
zone was precisely identied with this technique.
Given the fact that not enough points were
acquired with the pacing during sinus rhythm
technique and that the VT was not induced during
the ablation procedure to allow the creation of a
complete activation map, the VT mechanism in
this particular patient (dual-loop macro-reentry
or single-loop macro-reentry) could not be fully
described. However, given the fact that the main
components of the VT circuit were identied
(entrance zone, VT isthmus, and exit zone), catheter ablation was successfully performed.
Another important observation is related to the
fact that our patient presented both sustained
monomorphic VT (as evidenced in Fig.17.2) and
frequent monomorphic PVCs, with the morphology being identical to the VT morphology.
Figure 17.8 shows the activation map of the LV
targeting the frequent PVCs and localizing their
origin at the level of the inferior and basal LV.One
would maybe be tempted to ablate the origin of
this PVC and, given the perfect match between the
PVC morphology and the VT morphology, consider the ablation procedure terminated. However,
given the macro-reentry mechanism of the VT, we
would like to draw attention to the fact that this
represents only the exit site of the VT and that
ablation of this region only, risks not to be efcient
in the treatment of VT. An efcient ablation of
macro-reentry VT requires transaction of the VT
isthmus by the ablation lesions, not of the exit
zone, since ablating the exit zone only can allow
for a different exit zone to develop, given the intact
nature of the VT isthmus. This is the reason for
which ablation was performed in this case both in
the exit zone of the VT (for PVC elimination) and
in the VT isthmus zone (for VT elimination).
The techniques used in this case in order to
identify the VT and the PVC origin were substrate mapping (identication of the zone of
myocardial scar, which represented the origin of
the PVCs and of the VT, Fig. 17.7), activation
mapping (for the PVC, Fig.17.8), and pacemapping during sinus rhythm (for identication of
the critical components of the VT, Figs.17.9 and
17.10), as described by de Chillou etal. [1, 2].
This technique is widely presented in the commentary section of Case 14. In brief, the technique of pacemapping during sinus rhythm
requires comparison between the QRS morphology resulted from local pacing at a specic site
and the morphology of the VT recorded by the
12-lead surface ECG. Using the PASO correlation algorithm of the CARTO system, the correlation between these two morphologies can be
estimated, and this can take values from −100%
(in case of complete discordance between the 2)
to 100% (perfect match). Several points from
areas located in the possible VT origin are paced
at twice the diastolic threshold at the VT cycle
length, and the percentage of correlation is represented on a CARTO map, with red color corresponding to the best match and violet to the
poorest match. Orange, yellow, green, and blue
colors represent intermediate matches. In the VT
exit zone and close to it, there will be good correlations between the locally generated QRS
morphology and the 12-lead VT morphology.
This is due to the fact that the depolarization
wavefront travels in the same direction during
local pacing as during VT. In the VT entrance
zone, there will be a poor correlation between the
locally generated QRS morphology and the
12-lead VT morphology. This is due to the fact
that the depolarization wavefront travels in opposite direction during local pacing and during VT,
since during local pacing, the wavefront propagates faster from the entrance zone to the surrounding healthy myocardial tissue than during
myocardial scar, where conduction velocity is
signicantly decreased. According to de Chillou
etal. [1, 2], regarding VT isthmuses, the best correlation percentages are found in the VT exit
zones and isthmus exit part (89% ±8% and
84%±7%, respectively), and the poorest correlations are found close to the scar border in the
outer entrance zones (23% ± 28%), in the
entrance zones (39%±34%), and in the entrance
part of the isthmus (32% ±26%).
In the above-presented patient, given the fact
that the mapping phase was performed with the
17 C ase 17
https://t.me/medicina_free
277
roving/ablation catheter only and no Pentaray
catheter was used, the bipolar voltage map of the
LV during sinus rhythm is incomplete (Fig.17.7).
However, it was complete enough in order to
uncover the low-voltage area which served as
substrate both for the frequent monomorphic
PVCs and for the VT.
Regarding the approach of the left ventricle
used in this case, we chose the retrograde aortic
approach. The transseptal approach is the alternative to the retrograde aortic approach, which has
its advantages (lower percentage of vascular
complications since no arterial puncture is
needed) and disadvantages (limitation in catheter
manipulation at the level of the IV septum). The
two approaches can be combined during the same
procedure and often offer better access to different areas of the left ventricle. The choice between
one or the other is very operator dependent. In the
above-presented case, the retrograde transaortic
approach was enough to map the LV area around
the mitral valve.
Learning Points
• Catheter ablation is a viable treatment
option for ventricular tachycardia in
patients with ischemic heart disease.
• Creation of a pacemap during sinus
rhythm is a viable strategy for identifying the mechanism and origin of ventricular tachycardia.
• An electro-anatomical mapping system
is a very useful tool in guiding the ablation procedure.
References
1. 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.
2. de Chillou C, Sellal JM, Magnin-Poull I.Pace mapping
to localize the critical isthmus of ventricular tachycardia. Card Electrophysiol Clin. 2017;9(1):71–80.
3. Antunes E, Brugada J, Steurer G, Andries E, Brugada
P.The differential diagnosis of a regular tachycardia
with a wide QRS complex on the 12-lead ECG: ven-
tricular tachycardia, supraventricular tachycardia with
aberrant intraventricular conduction, and supraventricular tachycardia with anterograde conduction over
an accessory pathway. Pacing Clin Electrophysiol.
1994;17(9):1515–24.
4. Brady WJ, Skiles J. Wide QRS complex tachycardia: ECG differential diagnosis. Am J Emerg Med.
1999;17(4):376–81.
5. Miller JM, Das MK, Yadav AV, Bhakta D, Nair G,
Alberte C. Value of the 12-lead ECG in wide QRS
tachycardia. Cardiol Clin. 2006;24(3):439–51, ix-x.
6. Patil R, Rawat A, Ravikishore AG. Practical guide
to ECG diagnosis of wide QRS tachycardia. Indian
Heart J. 2011;63(4):312–5.
7. Vereckei A. Current algorithms for the diagnosis of
wide QRS complex tachycardias. Curr Cardiol Rev.
2014;10(3):262–76.
8. Vereckei A, Duray G, Szenasi G, Altemose GT, Miller
JM.Application of a new algorithm in the differential diagnosis of wide QRS complex tachycardia. Eur
Heart J. 2007;28(5):589–600.
9. Vereckei A, Duray G, Szenasi G, Altemose GT, Miller
JM. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia.
Heart Rhythm. 2008;5(1):89–98.
10. Steurer G, Gursoy S, Frey B, Simonis F, Andries E,
Kuck K, etal. The differential diagnosis on the electrocardiogram between ventricular tachycardia and preexcited tachycardia. Clin Cardiol. 1994;17(6):306–8.
11. Wellens HJ, Brugada P. Diagnosis of ventricular
tachycardia from the 12-lead electrocardiogram.
Cardiol Clin. 1987;5(3):511–25.
12. Ozin B. Differential diagnosis of wide QRS complex tachycardias by ECG.Turk Kardiyol Dern Ars.
2012;40(6):552–6.
13. Szelenyi Z, Duray G, Katona G, Frituz G, Szego E,
Kovacs E, etal. Comparison of the "real-life" diagnostic value of two recently published electrocardiogram methods for the differential diagnosis of
wide QRS complex tachycardias. Acad Emerg Med.
2013;20(11):1121–30.
14. Katritsis DG, Brugada J. Differential diagnosis of
wide QRS tachycardias. Arrhythmia Electrophysiol
Rev. 2020;9(3):155–60.
15. Shlevkov NB, Salami HF, Kiktev VG, Sokolov
SF. New ECG criteria for differential diagnosis of
wide QRS complex tachycardias with right bundle
branch block pattern. Ter Arkh. 2019;91(4):83–9.
16. Colin Lizalde Lde J. Electrocardiogram in the differential diagnosis of wide-QRS tachycardias. Arch
Cardiol Mex. 2004;74(Suppl 1):S44–9.
17. Kaiser E, Darrieux FC, Barbosa SA, Grinberg R,
Assis-Carmo A, Sousa JC, et al. Differential diagnosis of wide QRS tachycardias: comparison of
two electrocardiographic algorithms. Europace.
2015;17(9):1422–7.
18. Brugada P, Brugada J, Mont L, Smeets J, Andries
EW. A new approach to the differential diagnosis
of a regular tachycardia with a wide QRS complex.
Circulation. 1991;83(5):1649–59.
278
https://t.me/medicina_free
R. Le Bouar et al.
19. Alcaine A, Jauregui B, Soto-Iglesias D, Acosta J,
Penela D, Fernandez-Armenta J, et al. Automatic
detection of slow conducting channels during substrate ablation of scar-related ventricular arrhythmias.
J Interv Cardiol. 2020;2020:4386841.
20. Andreu D, Penela D, Acosta J, Fernandez-Armenta
J, Perea RJ, Soto-Iglesias D, et al. Cardiac magnetic resonance-aided scar dechanneling: inuence
on acute and long-term outcomes. Heart Rhythm.
2017;14(8):1121–8.
21. Berruezo A, Fernandez-Armenta J, Andreu D, Penela
D, Herczku C, Evertz R, et al. Scar dechanneling:
new method for scar-related left ventricular tachycardia substrate ablation. Circ Arrhythm Electrophysiol.
2015;8(2):326–36.
22. Codreanu A, Odille F, Aliot E, Marie PY, MagninPoull I, Andronache M, etal. Electroanatomic char-
acterization of post-infarct scars comparison with
3-dimensional myocardial scar reconstruction based
on magnetic resonance imaging. J Am Coll Cardiol.
2008;52(10):839–42.
23. Anderson RD, Ariyarathna N, Lee G, Virk S, Trivic
I, Campbell T, etal. Catheter ablation versus medical
therapy for treatment of ventricular tachycardia associated with structural heart disease: systematic review
and meta-analysis of randomized controlled trials
and comparison with observational studies. Heart
Rhythm. 2019;16(10):1484–91.
24. de Chillou C, Lacroix D, Klug D, Magnin-Poull I,
Marquie C, Messier M, etal. Isthmus characteristics
of reentrant ventricular tachycardia after myocardial
infarction. Circulation. 2002;105(6):726–31.
Case 18
https://t.me/medicina_free
RonanLe Bouar, FrédéricHalbwachs,
DidierBresson, AubrietiaLawson, MarineKinnel,
LaurentDietrich, DavidKenizou,
andLaurentJacquemin
18
Case Presentation
A 43-year-old male patient with a history of
remote inferior myocardial infarction at the age
of 33 years (thrombotic occlusion of the right
coronary artery in the proximal segment) treated
with PTCA + stent implantation 4h after symptoms onset; intra-stent restenosis 1 year after,
treated with PTCA + stent implantation; ischemic cardiomyopathy with mild to moderate LV
systolic dysfunction (LVEF of 44%); pulmonary
Supplementary Information The online version contains supplementary material available at https://doi.org/
10.1007/978- 3- 031- 35579- 0_18.
R. Le Bouar (*) · D. Bresson · A. Lawson
M. Kinnel · L. Dietrich · D. Kenizou · L. Jacquemin
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr;
didier.bresson@ghrmsa.fr; bree.lawson@ghrmsa.fr;
marine.kinnel@ghrmsa.fr;
laurent.dietrich@ghrmsa.fr;
kenizoud@ghrmsa.fr; jacqueminl@ghrmsa.fr
F. Halbwachs
Biosense Webster, Mulhouse, France
embolism at the age of 38 years with negative
thrombophilia tests; NONSTEMI at the age of
42 years with occlusion of the right coronary
artery in the third segment; and gastroduodenal
ulcer at the age of 35years was admitted to the
emergency department for an episode of palpitations with sudden onset accompanied by dizziness that had started 25min prior.
His cardiovascular risk factors were represented by a past history of smoking (20 packyears), arterial hypertension, dyslipidemia, and
grade 2 obesity. His medication at home consisted of ramipril 10 mg, atorvastatin 40 mg,
aspirin 75mg, bisoprolol 5mg, ivabradine 5mg
twice daily, and pantoprazole 40mg.
At physical examination, his blood pressure
was 112/71 mmHg, HR 145 bpm, SpO2 96%
breathing room air, H=1.74m, W=110kg, and
BMI=36.33kg/m2, heart sounds were rapid and
regular, there were no audible murmurs, lung
auscultation was clear, and there were no signs of
right heart failure.
His biological workup showed a Hb level of
13.3 g/dL, leukocytes 6.63 × 109/L, platelets
314×109/L, CRP 4mg/L, BUN 5.7mmol/L, creatinine 101 μmol/L, glycemia 5.9 mmol/L
(non- fasting), Na+143mmol/L, K+ 4.0mmol/L,
cTnI 0.07ng/mL, TSH 3.13IU/L, total cholesterol 168mg/dL, HDL 46 mg/dL, LDL 98 mg/
dL, and triglycerides 120mg/dL.
His ECG at presentation is showed in
Fig. 18.1. His ECG recorded 30 s later is presented in Fig.18.2. He presented several episodes
© 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_18
279
280
https://t.me/medicina_free
Fig. 18.1 A 12-lead ECG recorded at admission showing a wide QRS complex tachycardia with a heart rate of
145bpm, with a LBBB aspect, and superior axis
R. Le Bouar et al.
Fig. 18.2 A 12-lead ECG showing the spontaneous termination of the wide QRS complex tachycardia with conversion to sinus rhythm with a heart rate of 76bpm; QRS
axis at 60°; Q waves in leads II, III, and aVF suggestive of
of the same wide QRS complex tachycardia that
were incessant.
Transthoracic echocardiography was per-
formed during one of such episodes, which dem-
remote inferior myocardial infarction; negative T waves in
leads II, III, and aVF, and attened in V5 and V6, suggestive of possible infero-lateral ischemia
onstrated a non-dilated LV, but with akinesia of
the inferior LV wall and with moderate systolic
dysfunction, absence of pericardial effusion, and
a non-dilated IVC (Fig.18.3).
18 Case 18
https://t.me/medicina_free
281
Fig. 18.3 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. 18.4 Left panel: M mode echocardiography showing a non-dilated left ventricle, with an end-diastolic
diameter of 56 mm. Right panel: Apical four-chamber
Intravenous amiodarone was administered at a
dose of 300mg, with cessation of the tachycardia. Transthoracic echocardiography was
repeated during sinus rhythm, which showed a
non-dilated LV with moderate systolic dysfunction (LVEF of 44%), non-elevated LV lling
pressure, mild septal LV hypertrophy, absence of
mitral regurgitation, a non-dilated right ventricle,
mild tricuspid regurgitation with sPAP of
27 mmHg, absence of pericardial uid, and
absence of LV thrombus (Fig.18.4).
The patient’s chest X-ray is presented in
Fig.18.5.
view showing a non-dilated LV with severe systolic dysfunction, with a LVEF% of 33% (single-plane Simpson
method)
view showing pulsed Doppler interrogation of the transmitral ux, showing a pseudo-normal LV diastolic
dysfunction
Question 1: What is the nature of the
tachycardia presented in Fig. 18.1?
A. SVT with functional RBBB
B. Antidromic tachycardia
C. Ventricular tachycardia
D. Atrial utter with 1:1 AV conduction
E. Atrial brillation with BBB
Figure 18.1 explained (see below): This
shows a wide QRS complex tachycardia with a
heart rate of 145bpm, with a LBBB aspect, and
282
https://t.me/medicina_free
Fig. 18.5 Chest radiography image in posteroanterior
view showing a normal cardiothoracic index, absence of
pleural effusion, and absence of an obvious infections
which trigger at the level of the pulmonary parenchyma
R. Le Bouar et al.
superior axis. Capture beats (*) and fusion beats
can be observed (**), favoring the diagnosis of
ventricular tachycardia. Of note, the aspect of the
QRS complex is not that of a typical LBBB, with
transition of the QRS complex in precordial leads
in V2, another argument in favor of VT.A-V dissociation is also observed, with blue arrows
pointing to P waves.
18 Case 18
https://t.me/medicina_free
283
Fig. 18.6 Left upper panel: angiography image of the
left coronary artery in LAO view showing no major
obstruction of the LAD and CX epicardial vessels. Right
upper panel: angiography image of the left coronary
artery in posteroanterior view showing no major obstruction of the left main, LAD and CX coronary arteries. Left
In order to rule out ongoing myocardial ischemia, given the diagnostic of ventricular tachycardia and the slightly elevated troponin level,
coronary angiography was performed, which
demonstrated chronic total occlusion of the RCA
in its distal segment (Fig.18.6), an aspect already
described during the last coronary angiography
performed 1year prior. Of note, no PTCA was
lower panel: chronic total occlusion of the epicardial
right coronary artery in its third segment (red arrow).
Right lower panel: retrograde lling of the distal part of
the right coronary artery from the left coronary artery (red
arrow), in favor of a chronic occlusion of the right coronary artery
performed at that time, given the lack of myocardial viability at the level of the inferior LV wall
demonstrated by the stress echocardiography
performed prior to the coronary angiography.
A cardiac MRI was subsequently performed,
which conrmed the lack of myocardial viability
at the level of the LV inferior wall and the absence
of inducible ischemia in the other territories and
284
https://t.me/medicina_free
Fig. 18.7 Left panel: cardiac MRI image in cine SSFP three-chamber view showing a non-dilated left ventricle. Right
panel: cardiac MRI image in cine SSFP short-axis view showing a non-dilated left and right ventricle
R. Le Bouar et al.
which conrmed the moderate LV systolic dysfunction (Fig.18.7).
Given the diagnosis of ventricular tachycardia, the presence of remote inferior myocardial
infarction, the young age of the patient and the
high rate of adverse effects associated with
long- term amiodarone administration, and the
superiority of catheter ablation to anti-arrhythmic drugs in the treatment of VT, an electrophysiological study in view of a catheter
ablation procedure was scheduled and subsequently performed.
Question 2: Where is the origin of the
ventricular tachycardia?
A. Septal right ventricle
B. Infero-septal left ventricle
C. LV apex
D. Infero-lateral left ventricle
E. Infero-septal right ventricle
Electrophysiological Study andRF
Catheter Ablation Procedure
The electrophysiological study 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®). The ECG
at the beginning of the ablation procedure is presented in Fig.18.8.
18 Case 18
https://t.me/medicina_free
Fig. 18.8 A 12-lead ECG recorded at the beginning of the ablation procedure showing sinus rhythm with a heart rate
of 63bpm, QRS axis at +60°, absence of LV hypertrophy, and inferior wall necrosis
285
Programmed ventricular pacing was performed under basal conditions with repeated
induction of a wide QRS complex tachycardia
with a cycle length of 320ms (Fig.18.9), with
a morphology different from that of the clinical VT.
Question 3: Given the fact that this ven-
tricular tachycardia is different from
the patient’s clinical VT, should this
VT be treated with catheter
ablation?
A. No. This is not the patient’s clinical
VT; therefore, no indication for
catheter ablation exists.
B. No. This is probably related to the
stimulation protocol and should not
be ablated.
C. Yes. This should also be ablated,
since the goal of a catheter ablation
procedure for VT is ablation of all
monomorphic sustained VTs.
D. Yes. This should be ablated during a
second catheter ablation procedure.
E. I don’t know.
A Biosense Webster® SmartTouch SF openirrigated 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.The
tachycardia was stopped by burst ventricular
pacing.
Given the monomorphic aspect of the VT and
its repeated induction during programmed ventricular stimulation, ablation of this VT was
decided.
Question 4: Where is the origin of the
ventricular tachycardia presented in
Fig. 18.5?
A. LV lateral wall
B. LV anterior wall
C. LV inferior wall
D. LV septum
E. LV apex
Its RBBB aspect and its relatively narrow
QRS complex were in favor of a septal origin in
Соседние файлы в папке Библиотека им академика М.И. Перельмана