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F. Halbwachs et al.
20. Plank F, Stowasser B, Till D, Schgor W, Dichtl W,
Hintringer F, etal. Reduction of uoroscopy dose for
cardiac electrophysiology procedures: a feasibility
and safety study. Eur J Radiol. 2019;110:105–11.
21. Pathak RK, Ariyarathna N, Garcia FC, Sanders
P, Marchlinski FE. Catheter ablation of idiopathic ventricular arrhythmias. Heart Lung Circ.
2019;28(1):102–9.
22. Oomen A, Dekker LRC, Meijer A. Catheter ablation
of symptomatic idiopathic ventricular arrhythmias : a
ve-year single-Centre experience. Netherlands Heart
J. 2018;26(4):210–6.
23. Peichl P, Wichterle D, Pavlu L, Cihak R, Aldhoon
B, Kautzner J. Complications of catheter ablation of ventricular tachycardia: a single-center experience. Circ Arrhythm Electrophysiol.
2014;7(4):684–90.
24. Kitamura T, Nakajima M, Kawamura I, Ohbe H,
Sasabuchi Y, Matsui H, et al. Patient characteristics, procedure details including catheter devices,
and complications of catheter ablation for ventricular tachycardia: a nationwide observational study. J
Arrhythm. 2020;36(3):464–70.
Case 3
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RonanLe Bouar, FrédéricHalbwachs,
EmmanuelleGain, CharlineDaval, DidierBresson,
MihaelaCalcaianu, AubrietiaLawson,
andMarineKinnel
3
Case Presentation
A 25-year-old female patient with no signicant past medical history is addressed to the
emergency department by the ambulance squad
for an episode of ongoing palpitations with sudden onset, with rapid and regular rhythm that
had started 15 min before the arrival of paramedics at her home, accompanied by dizziness,
dyspnea at rest, and anxiety. She was 28weeks’
pregnant, and up to that day, she had had a normal pregnancy, with no signicant elements
reported by her gynecologist during routine
visits. Her other two children from her two previous pregnancies were in good health. She had
no cardiovascular risk factors. Her medication
at home consisted of calcium and iron supplements. By the time physical examination was
performed by the emergency unit physician, the
palpitations had stopped abruptly. At physical
examination, her blood pressure was
R. Le Bouar (*) · C. Daval · D. Bresson ·
M. Calcaianu · A. Lawson · M. Kinnel
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr;
charline.daval@ghrmsa.fr; didier.bresson@ghrmsa.fr;
mihaela.calcaianu@ghrmsa.fr;
bree.lawson@ghrmsa.fr
F. Halbwachs · E. Gain
Biosense Webster, Mulhouse, France
118/71 mmHg, heart rate was 82 bpm, SaO2
was 98% breathing room air, heart sounds were
regularly irregular, there was no audible murmur, she had no signs of left or right heart failure, peripheral pulses were present, and she had
mild bilateral edema of the lower limbs. Her
ECG is presented in Fig.3.1.
Her biological workup showed a Hb level of
11.8 g/dL, leukocytes 13.32 × 109/L, platelets
360×109/L, CRP 3mg/L, BUN 3.4mmol/L, creatinine 50 μmol/L, glycemia 5.7 mmol/L, Na+
131mmol/L, K+ 4.5mmol/L, and TSH 2.9IU/L.
She was transferred to the cardiology depart-
ment for further tests and appropriate treatment.
Telemetry tracing in the ICU showed repeated
episodes of non-sustained VT (Fig.3.2).
Transthoracic echocardiography showed a
non-dilated LV with preserved LV EF %, absence
of LV hypertrophy, normal diastolic function,
absence of signicant valve disease, non-dilated
right heart chambers, no pulmonary hypertension, and absence of pericardial effusion
(Fig.3.3).
Given the symptomatic nature of her PVCs,
she was prescribed oral metoprolol 50 mg bid,
but with little benet. She was prescribed oral ecainide 150mg daily on top of metoprolol, after
discussing the potential risks and benets of the
antiarrhythmic treatment, and, after 48h of surveillance, the non-sustained VT episodes ceased.
She was discharged 24h later and did ne for
another 9weeks, after which she was admitted to
© 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_3
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Fig. 3.1 A 12-lead ECG at admittance to the cardiology department showing sinus rhythm with a heart rate of 72bpm,
QRS axis at +80°, absence of LVH, absence of ischemia, and monomorphic PVC—ventricular trigeminy
R. Le Bouar et al.
Fig. 3.2 A 3-lead telemetry tracing recorded during hospitalization showing sinus rhythm and coupled PVCs, triplets,
and a run of non-sustained monomorphic VT
the emergency department for an episode of sustained VT.At this time, she was 37weeks’ pregnant. After the acute treatment of VT, she
underwent emergency cesarian section under
general anesthesia and was subsequently admitted
to the intensive care unit. She was transferred to
the cardiology department 3 days later, but,
despite antiarrhythmic treatment, telemetry tracing showed repeated episodes of sustained VT
(Fig. 3.4), which required IV amiodarone for
termination.
A cardiac MRI searching for an underlying
heart disease was performed but found no argument in favor of a structural heart disease
(Fig.3.5). A cardiac CT angiography showed no
obstruction at the level of the coronary arteries
and, as an incidental nding, revealed a pulmonary embolus at the level of a lobar branch of the
right pulmonary artery (Fig.3.6). Venous Doppler
ultrasonography found no evidence of thrombus
at the level of the lower limbs or IVC.The patient
was anticoagulated with enoxaparin 1mg/kg bid.
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Fig. 3.3 Left panel: Transthoracic echocardiography image in parasternal long-axis view showing a non-dilated left and right ventricle, with no LV hypertrophy. Right panel:
Tissue Doppler imaging in apical four-chamber view showing normal LV lling pressure with an E/e′ ratio at the level of the lateral mitral annulus of 3.1
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Fig. 3.4 A 7-lead telemetry tracing recorded during hospitalization showing an episode of sustained monomorphic VT
R. Le Bouar et al.
Fig. 3.5 Left panel: Cardiac MRI image FIESTA
sequence in cine SSFP short-axis view showing a nondilated LV and RV with absence of LV hypertrophy. Right
Question 1: What is the origin of the
PVC shown in Fig. 3.1?
A. RVOT
B. LVOT
C. Coronary cusp
D. Epicardial LV (LV summit)
E. Left anterior fascicle of the left bundle
branch
panel: Short-axis view showing no late gadolinium
enhancement areas. There are no criteria in favor of
arrhythmogenic cardiomyopathy
Question 2: What is the best treatment
option for this patient’s PVCs?
A. High-dose beta blockers
B. Flecainide
C. Amiodarone
D. Sotalol
E. Catheter ablation
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Fig. 3.6 Left panel: Cardiac CT angiography image showing the presence of pulmonary embolism (red arrow) at the level of a branch of the right inferior pulmonary artery.
Right panel: No criteria in favor of acute cor pulmonale (non-dilated right ventricle, with the ration RV/LV<1)
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R. Le Bouar et al.
Interpretation of the ECG in Fig.3.1: The
ECG shows sinus rhythm with a heart rate of
72 bpm, QRS axis at +80° with ventricular trigemini. Concerning the PVC morphology, the
presence of a unique R wave in leads II, III, and
aVF suggests an outow tract origin (RVOT or
LVOT). The presence of an S wave in lead I
together with a precordial transition in V1 or V2
suggests a LVOT origin. The presence of small s
waves in leads V5 and V6 suggests an LVOT origin below the aortic cusps (the absence of s wave
in V5 and V6 suggests a coronary cusp region).
Given the failure of antiarrhythmic drugs, the
non-suitable patient prole for amiodarone
administration, after discussing the benets and
potential risks, an ablation procedure was offered
and accepted by the patient.
Electrophysiological Study andRF
Catheter Ablation Procedure
The ablation procedure was performed under
local anesthesia and conscious sedation. Vascular
access was obtained using the modied Seldinger
technique, under Doppler ultrasound guidance.
Given the presence of recent pulmonary embolism, despite a normal venous ultrasound of the
lower limbs, a decision not to puncture the femoral vein was taken, in order to minimize the risk
of a subsequent pulmonary embolism episode.
Given the 12-lead ECG aspect of the PVC, a
LVOT origin was considered highly likely and
the common right femoral artery was punctured.
A Biosense Webster® SmartTouch SF openirrigated 3.5mm tip with double curve D/F was
used as the roving/ablation catheter, which was
introduced in a 9F 20 cm vascular sheath and
advanced at the level of the left ventricle. The
CARTO ® 3 electro- anatomic mapping system
(Biosense Webster, Johnson & Johnson) was
used to guide mapping and ablation. Given the
fact that the PVCs had an identical morphology
on the 12-lead ECG to that of the sustained VT,
targeting the PVCs was considered an appropriate aim of the procedure. For reasons presented
before, mapping of the PVC was commenced in
the LVOT.
The ECG at the beginning of the electrophysi-
ological study is presented in Fig.3.7.
The 12-lead ECG recorded before local anes-
thesia administration is shown in Fig.3.8.
Three minutes after subcutaneous lidocaine
was administered for local anesthesia
(20mL=200mg), the number of PVCs signicantly dropped (Fig. 3.9). This represented a
Fig. 3.7 A 12-lead ECG at the beginning of the ablation
procedure showing sinus rhythm with ventricular trigemini. The PVCs are monomorphic and the morphology is
identical to the morphology of the PVC present on the
ECG recorded at admittance to the hospital
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Fig. 3.8 A 12-lead ECG at the beginning of the ablation procedure showing sinus rhythm with a ventricular triplet
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Fig. 3.9 A 12-lead ECG recorded a few minutes after administering local anesthesia (lidocaine 200mg) with disappearance of PVCs
challenge for the mapping phase, since an activation map of the LV during PVCs was more difcult to create.
During the rst part of the procedure, an anatomical map of the LV was created. This showed
the presence of a non-dilated LV.
Subsequently, after isoprenaline administration, the number of PVCs slightly increased.
Therefore, an activation map of the LVOT was
created during the rare PVCs, which showed a
small area at the level of the anterior LVOT of
early local ventricular activation, where the local
bipolar electrogram preceded the onset of the
QRS complex on the surface ECG by 20 ms
(Fig.3.10). At this site, the unipolar EGM has a
“QS” aspect.
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R. Le Bouar et al.
Fig. 3.10 CARTO image in a superior and septal view
showing the activation map of the LV during PVCs. This
is in favor of an ectopic focus situated at the level of the
anterior LVOT (red zone, tip of the roving/ablation catheter), at 7 mm distance from the aortic valve, where the
local ventricular electrogram preceded the beginning of
the QRS complex on the surface ECG by 20ms. Note the
A pacemap was subsequently created, by pacing from the distal electrode of the roving/ablation catheter at different areas at the level of the
LV, at a xed coupling interval of 600ms, 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 QRS morphology with that of the QRS of the
PVCs, and the correlation percentage was displayed in absolute values but also in colors from
violet to red, depending of the degree of correlation between the two morphologies, with violet
representing a very weak correlation percentage
close proximity of the LAD coronary artery (red), situated
at 10mm distance from this site. The inner and outer layers of LV myocardium as recorded by the cardiac CT
angiography (green layers) are superposed with the actual
anatomical map of the LV created during the procedure by
the direct contact of the roving/ablation catheter with the
LV wall
and red an excellent one. Colors were displayed
on a map superposed on the anatomical map of
the LV.Absolute correlation values could range
from −100%, in case of a complete mismatch
between the locally generated QRS morphology
and that of the PVC, to 100%, in case of a perfect
match between the two. The pacemap showed a
correlation of 98% between the locally generated
QRS morphology in a small area at the level of
the anterior LVOT and the morphology of the
PVC (Fig. 3.11). This zone corresponds to the
earliest activation site displayed on the activation
map recorded during PVCs from Fig.3.10.
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Fig. 3.11 Left side of the image: CARTO image in a
superior and septal view (same as in Fig.3.10) showing
the pacemap of the LV conrming the origin of the PVC
at the site of a small area in the anterior and basal LVOT,
Question 3: Is this a good ablation site?
A. Yes. The local ventricular bipolar elec-
trogram precedes the onset of the QRS
on the surface ECG by 20ms.
B. Yes. The local ventricular unipolar elec-
trogram recorded a “QS” aspect at this
site.
C. Yes. The pacemap conrmed the origin of
the PVC at this site, given the 98% correlation between the locally generated QRS
morphology and the PVC morphology.
D. All of the above.
E. No. 20ms is not enough for a successful
ablation site. Mapping of the coronary
cusps should be the next step at this
stage of the procedure.
RF energy was applied at this site starting
from a power of 25W and increasing the energy
to 30W, with a target ablation index of 550. A
total of seven ablation lesions were applied, with
total elimination of the PVCs.
corresponding to the area of the earliest endocardial activation during PVCs (Fig. 3.10). The concordance of
locally generated QRS morphology and spontaneous PVC
morphology is of 98% (right side of the image)
The position of the ablation catheter at the earliest ventricular activation site in the LVOT is
presented in Fig.3.12. At this site, the distance
from the LAD coronary artery was 10mm.
The activation map of the LV and the pacemap
of the LV with superposed RF ablation lesions
are shown in Figs.3.13 and 3.14.
After a waiting period of 60 min, no PVC
recurrence was observed. Intravenous isoprenaline was given, and programmed ventricular
stimulation with up to three extra stimuli was
performed, with no VT induction.
There were no complications related to the
ablation procedure.
The ECG recorded after the procedure is presented in Fig.3.15.
Telemetry recording in the ICU for 48 h
showed no PVC recurrence.
The patient was discharged from the hospital
72 h later under anticoagulant treatment, given
her recent episode of pulmonary embolism.
Her 24-h Holter ECG recorded 5weeks later
showed no PVC or VT (Fig.3.16).
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