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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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16 Case 16
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Fig. 16.9 CARTO
image in LAO 180°
caudal 3° view 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
and basal LV wall,
compatible with
myocardial scar. The
scar area represents 15%
of the total LV surface
and measures 36.1cm
2
255
The presence of LAVA was noticed at this
level on the Pentaray catheter during RV apical
pacing (Fig.16.14).
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. After ablation of the VT
isthmus, additional RF lesions were deployed in
order to eliminate the LAVA.The bipolar voltage
map of the LV with the superimposed RF ablation lesions is presented in Fig.16.15.
Programmed ventricular stimulation was performed after the ablation, with up to three extrastimuli, before and after isoprenaline
administration, without the induction of any sustained or non-sustained ventricular arrhythmias.
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.16.16.
The ICD interrogation performed at 3, 6, 12,
and 24 months post-ablation procedure showed
no ventricular tachycardia recurrence.
Answers
Question 1: D.Ventricular tachycardia
Question 2: A.LV inferior and basal
wall
Question 3: C.VT substrate identication using pacemapping in sinus
rhythm and ablation
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Fig. 16.10 CARTO
image in LAO 180°
showing the Pentaray
catheter positioned at
the level of the inferior
LV wall scar, recording
LAVA, as shown by the
poles 13–14
F. Halbwachs et al.
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257
Fig. 16.11 CARTO image showing the identication of
the exit point of the VT during sinus rhythm. Left panel:
PASO module image with superposition of the locally
generated QRS morphology and the morphology of the
clinical VT.A concordance of 97% at this point identied
the exit point of the VT circuit. Of note, the red area corresponds to the exit zone of the VT, which is rather wide.
Middle panel: LAO 180° view of the LV showing the
roving/ablation catheter positioned at a site on the 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. Right panel:
bipolar map of the LV in LAO 180° showing the corresponding position of the exit point of the VT circuit on
inside the myocardial scar
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F. Halbwachs et al.
Fig. 16.12 CARTO image showing the identication of
the entrance point of the VT during sinus rhythm. Left
panel: PASO module image with superposition of the
locally generated QRS morphology and the morphology
of the clinical VT. A concordance of 17% 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 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. Middle panel: LAO 180° view of
the LV showing the roving/ablation catheter positioned at
a site on the inferior and basal LV wall, close to the exit
zone of the VT, where the locally generated QRS was very
different from the QRS morphology during clinical VT,
therefore identifying the entrance point. Right panel:
bipolar map of the LV in LAO 180° view showing the corresponding position of the entrance point of the VT
circuit
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259
Fig. 16.13 Left panel: PASO module image with super-
position of the locally generated QRS morphology and the
morphology of the clinical VT.A concordance of 17% at
this point identied the entrance point of the VT circuit.
Middle panel: pacemap with superposed VT circuit (for
learning purposes): the VT isthmus is delineated by the
two white lines; the two outer loops are presented in red;
the entrance zone is represented by the red color; the
entrance zone is represented by the violet color. Right
panel: bipolar map of the LV in LAO 180° showing the
corresponding position of the exit point of the VT isthmus
on inside the myocardial scar
Fig. 16.14 CARTO image in LAO 180° view (same as in Fig.16.8) showing the Pentaray catheter positioned at the
level of the inferior LV wall scar, recording LAVA (left part of the image)
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F. Halbwachs et al.
Fig. 16.15 CARTO image showing left ventricular bipolar voltage map after RF ablation. Red and pink dots correspond to the ablation lesions deployed at the level of the
Fig. 16.16 A 12-lead ECG recorded after the ablation procedure showing atrial brillation with paced biventricular
rhythm with a heart rate of 70bpm
VT isthmus transecting it and at the level of the LAVA,
homogenizing the scar
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Commentary
The above-presented case illustrates a catheter
ablation procedure of sustained monomorphic
ventricular tachycardia in a 71-year-old male
patient with ischemic cardiomyopathy and
remote inferior myocardial infarction. Several
observations can be made about the present case.
As discussed in the commentary section of
cases 12–15, coronary artery disease with prior
myocardial infarction is the most common cause
of ventricular tachycardia in patients with structural heart disease [3]. According to the current
ESC guidelines on the management of patients
with ventricular arrhythmias and the prevention
of sudden cardiac death, catheter ablation of ventricular tachycardia in patients with ischemic
heart disease has a class I indication level of evidence B in patients with ICD and recurrent
shocks due to sustained VT [4]. Other treatment
options include anti-arrhythmic drugs and ICD
implantation [4]. In the above-presented patient,
given the presence of a severe systolic dysfunction and his past medical history of amiodaroneinduced hyperthyroidism, no class I or class III
anti-arrhythmic drugs could be administered. He
was already an ICD carrier; therefore, the best
remaining treatment option was catheter
ablation.
Presently, three-dimensional electroanatomical mapping systems have become universally present in the electrophysiology labs and
are widely used to guide catheter ablation procedures [5, 6]. This is especially true for ablation
procedures of ventricular tachycardia, where substrate mapping is very important in identifying
the tachycardia circuit.
Regarding the ablation strategy, several
options have been proposed by different working
groups. These include ablation of late potentials
(LP) and local abnormal ventricular activities
(LAVA) [7, 8], identifying and ablating channels
and performing scar “dechanneling” [9, 10], isolating the core of the scar [11, 12] and scar
homogenization [13–15]. In the above-presented
patient, mapping of the tachycardia by creating
an activation map during VT was not possible,
due to the risk of hemodynamic compromise,
given his very severe LV dysfunction (LV EF%
of 17%). Instead, the technique described by de
Chillou etal. [1] using pacemapping during sinus
rhythm was considered the best strategy is this
case. We consider this to be very useful in cases
where the target ventricular tachycardia is nonsustained, non-inducible, or not tolerated by the
patient or when the activation map performed
during VT is incomplete or needs conrmation.
As presented in Case 14, 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., 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%),
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F. Halbwachs et al.
in the entrance zones (39% ± 34%), and in the
entrance part of the isthmus (32%±26%).
Another important observation is related to
the localization of the VT isthmus in this case. As
in most patients with prior inferior wall myocardial infarction and peri-mitral VTs, the VT isthmus was parallel to the mitral valve [16]. As
described by de Chillou etal., the VT circuit is
usually a dual-loop “gure of 8,” with one loop
turning around the mitral annulus and the other
around a line of anatomical or functional line of
block, which represents the lower boundary of
the VT isthmus. A minority of patients will have
single-loop circuits, but these are less common
than “gure of 8” circuits. In the experience of de
Chillou etal., the average dimensions of the VT
isthmus are 31 ± 7 mm (ranging from 18 to
41mm) long and 16±8mm (ranging from 6 to
36mm) wide.
In the present patient, RF ablation of the VT
isthmus plus LAVA elimination rendered the VT
non-inducible.
Learning Points
• Coronary artery disease with prior myocardial infarction is the most common
cause of ventricular tachycardia in
patients with structural heart disease.
• Catheter ablation with the help of an
electro-anatomical mapping system is a
very good treatment option in patients
with recurrent episodes of sustained
monomorphic ventricular tachycardia.
• In patients in whom the ventricular
tachycardia is non-inducible during the
ablation procedure, non-sustained or
hemodynamically poorly tolerated, creation of a pacemap during sinus rhythm
can identify the critical components of
the VT and allows performance of the
ablation.
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. Miller JM, Altemose GT, Jayachandran JV.Catheter
ablation of ventricular tachycardia in patients
with structural heart disease. Cardiol Rev.
2001;9(6):302–11.
4. 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.
5. Maury P, Monteil B, Marty L, Duparc A, Mondoly
P, Rollin A.Three-dimensional mapping in the electrophysiological laboratory. Arch Cardiovasc Dis.
2018;111(6–7):456–64.
6. Merino JL.Tools or toys? The 20-year anniversary of
the nonuoroscopic mapping system dilemma. Rev
Esp Cardiol. 2017;70(9):690–3.
7. Sacher F, Lim HS, Derval N, Denis A, Berte B,
Yamashita S, et al. Substrate mapping and ablation
for ventricular tachycardia: the LAVA approach. J
Cardiovasc Electrophysiol. 2015;26(4):464–71.
8. Jais P, Maury P, Khairy P, Sacher F, Nault I, Komatsu
Y, et al. Elimination of local abnormal ventricular
activities: a new end point for substrate modication
in patients with scar-related ventricular tachycardia.
Circulation. 2012;125(18):2184–96.
9. 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.
10. 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.
11. Santangeli P, Frankel DS, Marchlinski FE.End points
for ablation of scar-related ventricular tachycardia.
Circ Arrhythm Electrophysiol. 2014;7(5):949–60.
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12. Santangeli P, Marchlinski FE. Substrate mapping
for unstable ventricular tachycardia. Heart Rhythm.
2016;13(2):569–83.
13. Briceno DF, Romero J, Gianni C, Mohanty S,
Villablanca PA, Natale A, etal. Substrate ablation of
ventricular tachycardia: late potentials, scar dechanneling, local abnormal ventricular activities, Core
isolation, and homogenization. Card Electrophysiol
Clin. 2017;9(1):81–91.
14. Gokoglan Y, Mohanty S, Gianni C, Santangeli P,
Trivedi C, Gunes MF, et al. Scar homogenization
versus limited-substrate ablation in patients with non-
ischemic cardiomyopathy and ventricular tachycardia. J Am Coll Cardiol. 2016;68(18):1990–8.
15. Yagishita D, Ajijola OA, Vaseghi M, Nsair A, Zhou
W, Yamakawa K, et al. Electrical homogenization
of ventricular scar by application of collagenase: a
novel strategy for arrhythmia therapy. Circ Arrhythm
Electrophysiol. 2013;6(4):776–83.
16. 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 17
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RonanLe Bouar, FrédéricHalbwachs,
ThomasRobein, CharlineDaval, SerbanSchiau,
MihaelaCalcaianu, BergamotteThinot,
andJacquesLevy
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Case Presentation
An 83-year-old male patient with a past medical
history of ischemic heart disease; severe stenosis
of the proximal LAD treated with CABG (IMALAD) at the age of 52years; severe stenosis of
the CX artery and of the rst marginal branch
treated with PTCA + stent implantation at the age
of 73years; intrastent restenosis of the CX artery
and severe stenosis of the RCA, both treated with
stent implantation at the age of 77years; LV EF%
of 50%; dual-chamber pacemaker implanted at
the age of 73years for symptomatic sinus node
disease; upgrade of the device to a dual-chamber
ICD at the age of 75years for the secondary prevention of sudden cardiac death due to repeated
episodes of sustained monomorphic VT; ICD
replacement for battery depletion at the age of
83years (Medtronic Evera MRI XT DR); ischemic stroke at the age of 73years due to a 99%
stenosis of the left common carotid artery treated
with bypass graft; and chronic renal failure
R. Le Bouar (*) · C. Daval · S. Schiau
M. Calcaianu · J. Levy
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr;
charline.daval@ghrmsa.fr; serban.schiau@ghrmsa.fr;
mihaela.calcaianu@ghrmsa.fr; levyj@ghrmsa.fr
F. Halbwachs · T. Robein · B. Thinot
Biosense Webster, Mulhouse, France
e-mail: Bergamotte.thinot@its.jnj.com
(GFR=40mL/min) presented to the cardiology
department for repeated episodes of palpitations
with sudden onset and offset, accompanied by
dyspnea at rest and anxiety that had aggravated
during the past 3days prior to his presentation at
the hospital.
His cardiovascular risk factors were represented by age (> 55years old), arterial hypertension, and dyslipidemia. His medication at home
consisted of atorvastatin 20 mg, bisoprolol
10mg, and aspirin 75mg.
At physical examination, his blood pressure
was 113/76 mmHg, HR 76 bpm, H = 170 cm,
W=62kg, and BMI of 21.45kg/m2, heart sounds
were regular, there were a mild systolic murmur
in the apical region, lung auscultation revealed
bilateral basal crepitant rales, peripheral pulses
were barely perceptible, there were mild bilateral
edema of the lower limbs, and there were no
signs of right heart failure.
His ECG is presented in Fig.17.1. A second
ECG, recorded several minutes after his admittance, during an episode of palpitations is presented in Fig.17.2.
His blood workup showed a Hb level of
11.8 g/dL, leukocytes 9.19 × 109/L, platelets
128×109/L, CRP 19mg/L, BUN 17.8mmol/L,
creatinine 184 μmol/L, glycemia 5.2 mmol/L,
Na+141mmol/L, K+ 3.9mmol/L, NT pro-BNP
15100 pg/mL, troponin 0.063 ng/mL
(NV<0.042ng/mL), and TSH 2.03IU/L.
© 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_17
265
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