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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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Fig. 6.13 Transthoracic
echocardiography image
showing a LVEF of 52%
evaluated by singleplane Simpson method
99
Commentary
The present case illustrates a catheter ablation
procedure of PVCs originating from the junction
of the left and right coronary cusps in a patient
with ischemic heart disease. Several observations
merit further discussion.
Ventricular arrhythmias in structurally normal
hearts represent about 10% [1] to 30% [2] of
diagnosed ventricular arrhythmias. The most
common origins of idiopathic ventricular
arrhythmias are the RVOT in about 70% of cases
[3], followed by LVOT and the aortic root region,
the latter being responsible for 16.6% of cases
[4]. In the experience of Yamada etal. [4], the left
coronary cusp is responsible for more than half of
the cases (54.5%) and the right coronary cusp for
approximately one-third of cases (31.8%), the
non-coronary cusp origin is exceptional (2.3% of
cases), and at the junction between the LCC and
RCC (L-RCC) is responsible for about 10% of
cases (11.4%, more precisely).
The spectrum of these ventricular arrhythmias varies from isolated PVCs to sustained
VT.The most common forms are isolated PVCs,
which have a higher prevalence in females than
in males [1].
A 12-lead ECG clues in favor of an aortic cusp
origin of PVC are an early transition in the
precordial leads (V1 or V2) and the presence of
an “rS” pattern in lead V1 for PVCs originating
from the right coronary cusp [5, 6], a transition in
lead V3 and the presence of a “QS” notch in lead
V1 for PVCs originating from the junction of the
right and left coronary cusps, and the presence of
multiphasic “M” or “W” in lead V1 for PVCs
originating in the left coronary cusp region. Other
features distinguishing the origin of the PVC at
the level of the coronary cusps are the maximum
amplitude of the R-wave in the inferior leads,
which is signicantly greater in the case of a
LCC origin than of a RCC origin; the ratio of the
R-wave amplitude in leads II and III, which is
signicantly greater for LCC origin than for the
RCC origin and signicantly smaller for NCC
origin than in the other sites; the ventricular electrogram recorded by the His catheter is signicantly later compared to the surface QRS in the
case of a LCC origin or L-RCC origin than with
an RCC or NCC origin; and the ratio of the A to
V deection amplitude is greater in the NCC origin than in the other sites [4]. In the abovepresented patient, the ECG presented in Fig.6.1
shows a “QS” pattern in lead V1, with a QRS
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transition in lead V3, in favor of an origin at the
junction of the left and right coronary cusps. A
similar case is presented in Case 5.
The exact location of the PVC origin is best
determined with intracardiac echography [7, 8].
However, an electro-anatomical mapping system,
as demonstrated by this case, is an excellent diagnostic and mapping tool also capable of precisely
identifying the PVC origin at the level of the aortic cusps. Combining ICE with an electroanatomical mapping system is even better, when
both tools are available.
As discussed in the commentary section of
Case 5, one of the main challenges of ablating
PVCs originating from the coronary cusp region
is performing safe ablation, without injuring the
coronary arteries. The site of origin of PVCs
from the aortic cusps is sometimes situated in
close proximity to the coronary arterial ostia. It is
considered that a distance of minimum 10 mm
should be respected between the ablation site and
the ostium of a coronary artery [9]. Some authors
have described a lower safety margin, of 5mm
[10]. The appreciation of the safety margin generally requires performing coronary angiography
before RF ablation. However, in most of the
cases, when ICE is available, this is not strictly
necessary, since in more than 90% of cases, the
safety margin can safely be identied with ICE,
as demonstrated by Hoffmayer etal. [9]. A 3D
reconstruction of the CT angiography of the coronary arteries can also be integrated in the working platform by the CARTO system and can serve
the same purpose.
The success rate of catheter ablation of VA
originating from the coronary cusps is usually
lower than VA originating from the RVOT, but, in
experienced hands, it can reach 90% [11]. This is
dened as a reduction of at least 80% of the
arrhythmia burden on follow-up Holter ECG
monitoring. In our patient, neither ICE nor coronary angiography was used as additional tools to
the CARTO system for ablation of the PVCs. We
do believe that these are important elements in
increasing the safety of the procedure and should
be systematically used when available. Holter
monitoring performed 2months after the ablation
procedure conrmed the midterm success of this
patient.
Learning Points
• The aortic cusp region represents a possible origin for PVCs.
• Catheter ablation, if possible using an
electro-anatomical mapping system ± intracardiac echography, is the
treatment of choice, given its high success rate and its low complication rate.
References
1. Brooks R, Burgess JH.Idiopathic ventricular tachycardia. A review. Medicine. 1988;67(5):271–94.
2. Sirichand S, Killu AM, Padmanabhan D, Hodge
DO, Chamberlain AM, Brady PA, et al. Incidence
of idiopathic ventricular arrhythmias: a populationbased study. Circ Arrhythm Electrophysiol.
2017;10(2):e004662.
3. de Groot JR. Ablation of idiopathic ventricular
arrhythmias. Neth Heart J. 2018;26(4):173–4.
4. 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.
5. 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.
6. 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.
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. Liu CF.The evolving utility of intracardiac echocardiography in cardiac procedures. J Atr Fibrillation.
2014;6(6):1055.
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9. 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.
10. 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.
11. Im SI, Lee SH, Gwag HB, Park Y, Park SJ, Kim JS,
et al. Electrocardiographic characteristics for successful radiofrequency ablation of right coronary
cusp premature ventricular contractions. Medicine.
2020;99(11):e19398.
Case 7
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RonanLe Bouar, FrédéricHalbwachs,
Jean- YvesWiedemann, JacquesLevy, MaximTissier,
DavidKenizou, andLaurentDietrich
7
Case Presentation
A 57-year-old female patient with a past medical
history of infero-lateral myocardial infarction
4months prior (thrombotic occlusion of the circumex coronary artery in the distal segment,
with a severe stenosis of the proximal segment
caused by a ruptured plaque) treated with PTCA
+ stent implantation (Fig.7.1), ischemic cardiomyopathy with mild to moderate LV systolic dysfunction (LVEF of 42%), paroxysmal
symptomatic atrial brillation, PVCs with a high
ventricular arrhythmic burden at the 24-h Holter
ECG monitoring (40% PVC/24h, mostly monomorphic) despite successful coronary revascularization, and subclinical hyperthyroidism was
admitted to the cardiology department 4months
after her acute coronary syndrome complaining
of intermittent palpitations, dyspnea on exertion,
and fatigue. Her cardiovascular risk factors were
represented by active smoking (30 pack-years),
grade 2 overweight, and dyslipidemia. Her medi-
R. Le Bouar (*) · J.-Y. Wiedemann · J. Levy ·
D. Kenizou · L. Dietrich
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr; wiedemannjy@
ghrmsa.fr; levyj@ghrmsa.fr; kenizoud@ghrmsa.fr;
laurent.dietrich@ghrmsa.fr
F. Halbwachs · M. Tissier
Biosense Webster, Mulhouse, France
cation at home consisted of apixaban 2×2.5mg,
clopidogrel 75 mg, aspirin 75 mg, bisoprolol
2.5 mg, furosemide 40 mg, atorvastatin 40 mg,
ezetimibe 10mg, and esomeprazole 20mg.
At physical examination, her blood pressure
was 92/67mmHg, HR 80bpm, SpO2 97% breathing room air, H = 1.65 m, W = 85 kg, and
BMI=31.22kg/m2, heart sounds were irregular,
there was a mild systolic murmur in the mitral
auscultation region, lung auscultation was clear,
and there were no signs of right heart failure.
Her ECG at presentation is showed in Fig.7.2.
The result of her 24-h Holter ECG monitoring
is presented in Fig.7.3.
Her biological workup showed a Hb level of
12.2g/dL, leukocytes 7.64 × 109/L, platelets 131
× 109/L, CRP 5mg/L, BUN 6.7mmol/L, creatinine 94 μmol/L, glycemia 5.0 mmol/L,
Na+143mmol/L, K+ 4.2mmol/L, NT pro-BNP
1136pg/mL, TSH 0.38IU/L, FT4 10.5pmol/L,
total cholesterol 186 mg/dL, HDL 82 mg/dL,
LDL 85mg/dL, and triglycerides 210mg/dL.
Transthoracic echocardiography showed the
presence of moderate LV systolic dysfunction,
with a LVEF of 42%, with akinesia of the apical
lateral wall and antero-median and apical segments and hypokinesia of the inferior-median
and apical posterior basal segments (Fig.7.4). It
also showed moderate mitral regurgitation, a
mildly dilated left atrium (LA surface of 25cm2),
a non-dilated right ventricle, mild to moderate
tricuspid regurgitation, mild pulmonary hyper-
© 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_7
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Fig. 7.1 Left panel: Coronary angiography image showing the presence of a signicant stenosis (70–90%) of the
ostium of the CX artery and a large intraluminal thrombus
(green arrow) at the level of the proximal CX coronary
artery; there is acute thrombotic occlusion of the distal
Fig. 7.2 A 12-lead ECG showing sinus rhythm with a heart rate of 44bpm, QRS axis at +15°, negative T waves in leads
I, aVL, and V6
CX coronary artery (red arrow). Right panel: Coronary
angiography image post-PTCA and stent implantation at
the level of the ostium of the CX coronary artery and
thrombus aspiration and PTCA of the distal coronary
artery, showing TIMI 3 ow
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Fig. 7.3 A 24-h Holter ECG showing a high ventricular arrhythmia burden: 34233 isolated PVCs, mostly monomorphic, representing 39.9% of the total number of QRS complexes/24h
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Fig. 7.4 Transthoracic echocardiography image showing
a mildly dilated and hypokinetic LV, with moderate systolic dysfunction, LV EF% of 42%, type 2 diastolic dysfunction, a mildly dilated left atrium, mild to moderate
mitral regurgitation, mild to moderate tricuspid regurgitation, mild pulmonary hypertension, sPAP of 48 mmHg,
and mild pericardial effusion
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Fig. 7.5 Left panel: Cardiac MRI image (cine SSFP
four-chamber view) showing a non-dilated left ventricular
end-diastolic diameter. Right panel: Cardiac MRI image
tension, sPAP of 48mmHg, and mild pericardial
effusion (3mm in subcostal view).
Cardiac MRI conrmed the moderate systolic
dysfunction and showed the presence of late gadolinium enhancement at the level of the lateral
LV wall (Fig.7.5, right panel, red arrow).
Question 1: How would you treat the
patient’s ventricular arrhythmia?
A. Flecainide 200mg SR/day.
B. Propafenone 150mgt.i.d.
C. Sotalol 80mg b.i.d.
D. Amiodarone 200mg od.
E. Catheter ablation.
(short-axis view) showing late gadolinium enhancement
at the level of the infero-lateral and lateral LV wall
Given the presence of myocardial infarction
in her past medical history, both ecainide and
propafenone were considered contraindicated.
Given the presence of bradycardia, the low values of her blood pressure (92/67mmHg), and
the presence of moderate LV systolic dysfunction, sotalol was considered as not being the
best option either. Given the relatively young
age of the patient, the presence of bradycardia,
and the presence of subclinical hyperthyroidism, amiodarone was considered as the secondbest treatment option. Given the high arrhythmia
burden at 24 h Holter ECG, the presence of
symptoms, and LV dysfunction, a catheter ablation procedure was offered and accepted by the
patient.
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Electrophysiological Study andRF
Catheter Ablation Procedure
The ECG at the beginning of the ablation procedure is shown in Fig.7.6.
Question 2: What is the origin of the
PVC presented in Fig. 7.3?
A. Posteromedial papillary muscle area.
B. Anterolateral papillary muscle area.
C. Left posterior fascicle.
D. Left anterior fascicle.
E. Aortomitral continuity.
Figure 7.6 explained. A 12-lead ECG at the
beginning of the ablation procedure, showing
sinus rhythm with ventricular bigeminy. It is
worth noting the morphology of PVC: RBBB
morphology with an “Rs” pattern in leads II, III,
aVF, and “rS” in leads I and aVL and a late precordial transition in V5/V6, suggesting an origin
at the level of the anterolateral papillary muscle
region.
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 of the
PVCs.
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®).
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
Fig. 7.6 A 12-lead ECG at the beginning of the procedure showing sinus rhythm with ventricular bigeminy
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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, the bipolar voltage and
the activation maps of the LV. A Biosense
Webster® SmartTouch SF open-irrigated 3.5mm
tip with double curve D/F was used to perform
RF ablation.
An anatomical map of the LV was rst created, which showed a slightly dilated LV, with a
volume of 178mL.A bipolar voltage map was
subsequently created during sinus rhythm, which
showed the presence of several low-voltage areas
at the level of the lateral and inferior wall of the
LV and at the level of the anterolateral papillary
muscle region (Fig.7.7).
An activation map of the LV was subsequently
created during the frequent PVCs, with emphasis
on the anterolateral papillary muscle area
(Fig. 7.8). This demonstrated an area of early
ventricular activation at the level of the anterior
papillary muscle, where the local bipolar electro-
gram preceded the beginning of the PVC QRS on
the surface ECG by 10ms (Fig.7.9).
A pacemap was subsequently created by pacing from the distal electrode of the roving/ablation catheter at a xed coupling interval of
600 ms in several regions of the anterolateral
papillary muscle area, 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 95% was observed at
the earliest activation site, conrming the origin
of the PVC at this level (Fig.7.10).
Question 3: Is this a good ablation site?
A. Yes. The ablation catheter records a
local electrogram that precedes the surface QRS by 10ms, and this should be
enough for a successful ablation lesion.
B. Yes. The pacemap conrms a superposi-
tion of the locally generated QRS morphology and that of the spontaneous
QRS PVC of 95%.
C. No. The ablation catheter records a local
electrogram that precedes the surface
QRS by 10ms, and this should not be
enough for a successful ablation lesion.
D. No. The pacemap shows a superposition
of the locally generated QRS morphology and that of the spontaneous QRS
PVC of 95%, which is not good enough.
E. I don’t know.
Fig. 7.7 CARTO image in LAO 134° caudal 24° showing the infero-lateral wall of the left ventricle. The bipolar
voltage map recorded in sinus rhythm shows an area of
low (<0.5 mV, in red) and borderline (0.5–1.5 mV, in
green and blue) voltage in the territory of the circumex
coronary artery, corresponding to the area of late gadolinium enhancement shown with cardiac MRI, and to the
myocardial scar post-myocardial infarction
RF ablation was applied at this site with a target power of 30W and a target ablation index of
450 (Fig.7.11), with rapid disappearance of the
PVCs. A few additional RF lesions were applied
at this site.
There were no complications related to the
procedure.
The ECG post-RF ablation is shown in
Fig.7.12.
The 24-h Holter ECG performed 1 month
after the procedure showed the absence of PVC
(Fig.7.13).
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