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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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4 Case 4
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gin of the left main coronary artery performed
during the procedure conrmed the origin of the
PVC at the level of the left sinus of Valsalva.
When ablating PVCs originating from the aortic sinus of Valsalva, an electro-anatomical mapping system is a very useful tool for guiding the
ablation procedure. Other tools that can be useful
for this kind of ablation procedure are intracardiac echocardiography [7]; CT angiography, performed before the ablation procedure; and
coronary angiography, performed during the procedure. Evaluating the distance between the ostia
of the coronary arteries and the desired ablation
site can be of crucial importance, in order to
avoid lesions to the coronary arteries. This is usually done by performing coronary angiography
during the procedure. However, ablation can still
be safely achieved in most cases even if no coronary angiography is performed, if an electroanatomical mapping system is used and ICE is
available. In the experience of Hoffmayer etal.
[8], ablation of PVCs originating from the aortic
cusps was safely achieved in 91% of their patients
without the need of performing intra-procedural
coronary angiography. The use of ICE conrmed
a safe distance between the tip of the ablation
catheter and the successful ablation site of more
than 10mm. In our patient, the use of the CARTO
system was enough to safely perform successful
ablation of the PVCs.
Concerning the ablation settings of PVC arising from the aortic root, it has been reported that
low power starting from 15W with energy titration of up to 30W has been enough in successfully
eliminating the PVCs [9]. Higher power is considered potentially dangerous, given the
proximity of the coronary arteries ostia. However,
when RF application in the aortic sinus of
Valsalva region is not possible due to the proximity of the origin of a coronary artery with implicit
risk of myocardial infarction in case of ablation
in this area, successful ablation can still be performed by applying RF energy in neighboring
structures, as demonstrated by this case. We present the case of successful ablation of a PVC originating in the left aortic sinus of Valsalva
performed from the LVOT.The origin of the PVC
was conrmed at the level of the left sinus of
Valsalva by the activation map, showing an earlier local activation compared to the onset of the
QRS complex on the surface ECG in the left
sinus of Valsalva versus in the LVOT.
As discussed in the commentary section of
Case 1, a high number of PVCs/24h can lead to
the development of dilated cardiomyopathy. The
generally accepted threshold for the arrhythmic
burden necessary to develop PVC-induced cardiomyopathy is 10% of the total number of QRS
complexes/24 h [10–12]. The probability
increases with the rise in the arrhythmic burden.
The procedure was performed without any
uoroscopic guidance. As described in the
“Electrophysiological Study and RF Catheter
Ablation Procedure” section of the case report,
the CARTO system can provide sufcient information for catheter positioning and RF ablation
in order to completely avoid utilization of uoroscopy. Experience with AVNRT ablation
guided by an electro-anatomical mapping system
[13] or by remote magnetic navigation [14] is
increasing.
Learning Points
• When ablating outow tract arrhythmias, careful mapping of the RVOT,
LVOT, the aortic sinus of Valsalva, and
the distal part of the great cardiac vein is
sometimes required in order to precisely
identify the origin of the arrhythmia.
This translates into unnecessary RF
applications in areas with suboptimal
ablation criteria and avoiding ablation
failure.
• When ablating PVCs originating from
the aortic sinus of Valsalva, either intracardiac echography or coronary angiography or images of 3D reconstructions
of the coronary arteries using a preablation performed CT angiography
should be used, in order to avoid com-
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plications (especially myocardial infarction) related to “blind” RF applications
at the origin of the coronary arteries.
• Zero uoroscopy ablation of PVC is
possible in selected cases, due to the use
of non-uoroscopic electro-anatomical
mapping systems, such as the CARTO
system.
References
1. Kanagaratnam L, Tomassoni G, Schweikert R,
Pavia S, Bash D, Beheiry S, et al. Ventricular
tachycardias arising from the aortic sinus of valsalva: an under- recognized variant of left outow
tract ventricular tachycardia. J Am Coll Cardiol.
2001;37(5):1408–14.
2. Yamada T, McElderry HT, Doppalapudi H, Murakami
Y, Yoshida Y, Yoshida N, etal. Idiopathic ventricular
arrhythmias originating from the aortic root prevalence, electrocardiographic and electrophysiologic
characteristics, and results of radiofrequency catheter
ablation. J Am Coll Cardiol. 2008;52(2):139–47.
3. de Groot JR. Ablation of idiopathic ventricular
arrhythmias. Neth Heart J. 2018;26(4):173–4.
4. Anderson RD, Kumar S, Parameswaran R, Wong G,
Voskoboinik A, Sugumar H, et al. Differentiating
right- and left-sided outow tract ventricular
arrhythmias: classical ECG signatures and prediction algorithms. Circ Arrhythm Electrophysiol.
2019;12(6):e007392.
5. Tada H. Idiopathic epicardial ventricular arrhythmias: diagnosis and ablation technique from the aortic sinus of Valsalva. Indian Pacing Electrophysiol J.
2005;5(2):96–105.
F. Halbwachs et al.
6. Xie S, Kubala M, Liang JJ, Hayashi T, Park J, Padros
IL, et al. Lead I R-wave amplitude to differentiate
idiopathic ventricular arrhythmias with left bundle
branch block right inferior axis originating from the
left versus right ventricular outow tract. J Cardiovasc
Electrophysiol. 2018;29(11):1515–22.
7. Lin D, Ilkhanoff L, Gerstenfeld E, Dixit S, Beldner
S, Bala R, et al. Twelve-lead electrocardiographic
characteristics of the aortic cusp region guided by
intracardiac echocardiography and electroanatomic
mapping. Heart Rhythm. 2008;5(5):663–9.
8. Hoffmayer KS, Dewland TA, Hsia HH, Badhwar N,
Hsu JC, Tseng ZH, et al. Safety of radiofrequency
catheter ablation without coronary angiography in
aortic cusp ventricular arrhythmias. Heart Rhythm.
2014;11(7):1117–21.
9. Jagadheesan KS, Satheesh S, Pillai AA, Jayaraman
B, Selvaraj RJ.Low power ablation for left coronary
cusp ventricular tachycardia-efcacy and long-term
outcome. Indian Heart J. 2018;70(Suppl 3):S384–S8.
10. Latchamsetty R, Bogun F. Premature ventricular
complex-induced cardiomyopathy. Revista espanola
de cardiologia. 2016;69(4):365–9.
11. Lee GK, Klarich KW, Grogan M, Cha YM.Premature
ventricular contraction-induced cardiomyopathy: a
treatable condition. Circ Arrhythm Electrophysiol.
2012;5(1):229–36.
12. Panizo JG, Barra S, Mellor G, Heck P, Agarwal
S. Premature ventricular complex-induced cardiomyopathy. Arrhythmia Electrophysiol Rev.
2018;7(2):128–34.
13. Earley MJ, Showkathali R, Alzetani M, Kistler PM,
Gupta D, Abrams DJ, etal. Radiofrequency ablation
of arrhythmias guided by non-uoroscopic catheter
location: a prospective randomized trial. Eur Heart J.
2006;27(10):1223–9.
14. Bhaskaran A, Albarri M, Ross N, Al Raisi S, Samanta
R, Roode L, et al. Slow pathway radiofrequency
ablation using magnetic navigation: a description of
technique and retrospective case analysis. Heart Lung
Circ. 2017;26(12):1297–302.
Case 5
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JustineHavard, FrédéricHalbwachs, RonanLe
Bouar, CrinaMuresan, TarekEl Nazer,
MarineKinnel, andNicolasBourrelly
5
Case Presentation
A 34-year-old female patient with no signicant
past medical history was addressed to the emergency department by her family doctor for two
episodes of malaise, accompanied by dizziness,
intermittent palpitations with short duration (seconds) and atypical chest pain. She had no cardiovascular risk factors and was on no chronic
medication at home. She reported a history of
palpitations with short duration, non-related to
physical effort that had been present for the past
6months.
Her ECG is presented in Fig.5.1.
At physical exam, her blood pressure was
111/71mmHg, HR of 63bpm, SpO2 99% breathing room air, H = 165 cm, W = 62 kg, and
BMI=22.77kg/m2, heart sounds were irregular,
there were no audible murmurs, peripheral pulses
were present bilaterally, lung auscultation was
normal, and there were no signs of right heart
failure.
J. Havard (*) · F. Halbwachs
Biosense Webster, Mulhouse, France
e-mail: jhavard@its.jnj.com
R. Le Bouar · C. Muresan · T. El Nazer · M. Kinnel ·
N. Bourrelly
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr;
crina.muresan@ghrmsa.fr; tarek.elnazer@ghrmsa.fr;
marine.kinnel@ghrmsa.fr; bourrellyn@ghrmsa.fr
Transthoracic echocardiography showed a
non-dilated LV, with preserved systolic ventricular function, and EF of 65% (Fig. 5.2). It also
showed normal diastolic function, absence of signicant valve disease, a non-dilated left atrium, a
non-dilated right ventricle, a non-dilated right
atrium, absence of pulmonary hypertension,
sPAP of 22 mmHg, a non-dilated IVC, and
absence of pericardial effusion.
Her biological workup showed a Hb level of
12.0 g/dL, leukocytes 5.54 × 109/L, platelets
245×109/L, CRP 3mg/L, BUN 3.1mmol/L, creatinine 56 μmol/L, glycemia 5.7 mmol/L, Na+
137 mmol/L, K+ 3.9 mmol/L, NT proBNP<30pg/mL, and TSH 1.5IU/L
An exercise stress test was also performed,
stopped at a heart rate of 143bpm (representing
77% of her maximal theoretical heart rate) for
fatigue, 6.1 METS, with disappearance of her
PVC during physical effort, with reappearance of
ventricular bigeminy at the end of the effort,
showing no signs of myocardial ischemia, with
normal adaptation of the blood pressure (Fig.5.3).
A 24-h Holter ECG showed the presence of
12,000 isolated PVC/24h, with no couplets, runs,
or episodes of sustained VT (Fig.5.4).
Given the 12-lead ECG aspect of the PVC, a
cardiac MRI was performed, searching for arguments in favor of arrhythmogenic cardiomyopathy (Fig. 5.5), which showed a non-dilated left
ventricle (volume of 100mL/m2), with preserved
LV EF of 60%, a non-dilated right ventricle (vol-
© 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_5
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Fig. 5.1 A 12-lead ECG showing sinus rhythm with a heart rate of 60bpm, QRS axis at −10°, absence of hypertrophy,
absence of ischemia, and two isolated monomorphic PVCs
J. Havard et al.
Fig. 5.2 Transthoracic echocardiography image showing a normal global longitudinal strain, with absence of local or
regional kinetic disorders
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Fig. 5.3 Upper gure: Exercise stress test showing the
12-lead ECG during the peak of physical effort, with no
PVC. Lower gure: A 12-lead ECG recorded during the
ume of 85mL/m2) with a RV EF of 52%, with no
late gadolinium enhancement areas. No criteria
in favor of arrhythmogenic cardiomyopathy were
found.
Question 1: What is the origin of the
PVC shown in Fig. 5.1?
A. RVOT
B. LVOT
C. Junction of the left and right coronary
cusp
D. Noncoronary cusp
E. Epicardial LV (LV summit)
recovery phase of the stress test demonstrating ventricular
bigeminy
Figure 5.1 explained: Fig. 5.1 shows sinus
rhythm with a heart rate of 60bpm, QRS axis at
−10°, two isolated monomorphic PVCs, with a
unique “R wave” morphology in leads II, III, and
aVF, “QS” morphology in lead V1, rS in V2,
unique R in V3–V6 (sudden transition from V2 to
V3!), notched R in lead I, suggesting an outow
tract origin. Of note, the transition of the PVC in
precordial leads takes place earlier than the transition of the QRS complex during sinus rhythm
(V3 vs. V4), argument in favor of a left-sided
origin.
Given the presence of a moderate arrhythmia
burden on the 24-h Holter ECG (>10,000/24h)
and the highly symptomatic nature of the PVCs,
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J. Havard et al.
Fig. 5.4 A 24-hour Holter ECG recording showing frequent, monomorphic PVC, with a moderate ventricular arrhythmia burden, representing 26% of the total QRS complexes/24h
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Fig. 5.5 Left panel: Cardiac MRI image (cine SSFP
four-chamber view) showing a non-dilated LV and no
global or localized dilation of the right ventricle. Right
an electrophysiological study in view of a catheter ablation procedure was offered and accepted
by the patient.
Electrophysiological Study andRF
Catheter Ablation Procedure
The ablation procedure was performed under
local anesthesia. No conscious sedation was performed, in order not to inhibit the PVCs. Vascular
access was obtained using the modied Seldinger
technique, under Doppler ultrasound guidance.
A bipolar 6F 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. A Biosense Webster®
SmartTouch SF open-irrigated 3.5 mm tip with
double curve (D/F) was used as the roving/ablation catheter, which was introduced in a 9F 20cm
vascular sheath and advanced at the level of the
right ventricle.
The CARTO ® 3 electro-anatomic mapping
system (Biosense Webster, Johnson & Johnson)
panel: cine SSFP short-axis view showing a non-dilated
RV.No major or minor criteria in favor of arrhythmogenic
cardiomyopathy
was used to guide mapping and ablation of the
accessory pathway. 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 electrophysi-
ological study is presented in Fig.5.6.
Mapping of the PVC was commenced in the
right ventricle.
An anatomical map of the RVOT was initially
created, which showed the presence of a nondilated RVOT, with a volume of 40mL.Next, an
activation map of the RVOT during the frequent
PVCs was created. This showed the presence of
an early activation site at the level of the posterior
and inferior wall of the RVOT, at 12mm distance
from the right bundle, from where the activation
of the RVOT spread in a radial manner, suggesting a focal activation pattern (Figs.5.7 and 5.8).
At this site, the unipolar electrogram recorded by
the roving/ablation catheter had a “rS” aspect.
The local bipolar ventricular electrogram preceded the surface ECG QRS complex by 9ms.
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Fig. 5.6 A 12-lead ECG at the beginning of the ablation procedure, showing sinus rhythm with a heart rate of 60bpm
QRS axis at −10° and the presence of frequent isolated PVC
Fig. 5.7 CARTO image
in LAO 104° caudal 3
showing the activation
map of the RVOT during
PVC.The roving/
ablation catheter is
positioned at the level of
the posterior inferior
wall of the RVOT, at a
distance of 12mm from
the right bundle branch
(orange dots). The His
bundle is represented by
the yellow dot situated
at the level of the
tricuspid valve
J. Havard et al.
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 RVOT, with emphasis on
the area of the earliest activation during the PVCs.
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 97% was observed at
the earliest activation site of the RVOT (Fig.5.9).
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Fig. 5.8 A 12-lead ECG together with intracavitary leads
recorded from the distal and the proximal electrodes of
the ablation catheter (ABL d and ABL p) as well as from
the bipolar electrode of the diagnostic catheter positioned
the level of the RV apex showing the local activation time
at the level of the earliest ventricular activation site in the
RVOT compared to the beginning of the surface ECG
QRS complex. The roving/ablation catheter electrogram
precedes the QRS onset by 9ms
Fig. 5.9 CARTO image of the RVOT in a LAO 104° caudal 3° view showing the pacemap of the RVOT, with a
maximal correlation between the paced QRS complex and
the clinical PVC morphology of 97%, in the posterior and
inferior area of the RVOT (red zone)
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Question 2: Given the presented activa-
tion map and the pacemap of the RVOT,
is this a good ablation site?
A. Yes. The earliest local bipolar electro-
gram precedes the onset of the QRS
complex by 9 ms, and this should be
enough for a good ablation site.
B. Yes. The pacemap conrms the earliest
activation site on the activation map,
with a correlation of 97% at this site.
C. No. The local unipolar electrogram
recorded by the roving/ablation catheter
at the earliest endocardial activation site
has a “rS” pattern.
D. No. The transition of the QRS PVC in
the precordial leads takes place earlier
than the transition of the QRS complex
during sinus rhythm, in favor of a leftsided origin.
E. I don’t know.
RF energy was applied at this site with a target
power of 30W and a target ablation index of 450,
J. Havard et al.
with rapid disappearance of the PVC, but with
reappearance 1min later.
A comparison of the activation map and the
pacemap of the RVOT with superposed RF
lesions is presented in Fig.5.10.
Question 3: Given the reappearance of
PVC after the ablation at this site in the
RVOT, what is the next best step at this
stage of the procedure?
A. Perform additional RF ablation at the
site of the earliest activation in the
RVOT during the PVC with higher
power, of 40–50W.
B. Perform additional RF ablation at the
site of the earliest activation in the
RVOT during the PVC with a longer
duration, of 120s per application.
C. Map the coronary cusps.
D. Map the LVOT.
E. Terminate the procedure and suggest
chronic antiarrhythmic treatment.
Fig. 5.10 CARTO image in LAO 172° showing the activation map of the RVOT (left panel) and the pacemap of
the RVOT (right panel) with superposed RF lesions at the
site of the earliest endocardial activation at the level of the
RVOT during the PVC (left panel) and the best correlation
site between the locally paced QRS electrogram and the
PVC electrogram. Note that both sites indicate the same
small area (red) as the optimal ablation site in the RVOT
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