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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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5 Case 5
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Given the failure of ablation at this site, mapping of the coronary cusps was decided, given the
anatomical relationship between the aorta and the
posterior part of the RVOT.
Access to the coronary cusps was obtained
using the retrograde approach. The right common
femoral artery was punctured using the Seldinger
technique under ultrasonographic guidance, and
a 9F 20cm sheath was inserted.
Anticoagulation was obtained with unfractionated heparin 100 UI/kg as IV bolus, with a
target ACT between 300 and 350s.
Once anticoagulation was achieved, the roving/
ablation catheter was introduced in the common
femoral artery and retrogradely advanced to the
level of the aortic sinus of Valsalva. Subsequently,
an anatomical map of the coronary cusps region
and of the base of the aorta was performed. Next,
an activation map of the aortic cusps was created,
with identication of an early activation site at the
level of the junction between the right and the left
coronary cusp, which preceded the onset of the
QRS complex by 15ms, where the unipolar electrogram had a “QS” aspect (Fig.5.11).
Next, mapping of the distal part of the coronary sinus was decided, looking for a possible
better ablation site at the level of the LV summit.
An anatomical map of the coronary sinus was
rst created. Then, the roving/ablation catheter
was advanced inside the coronary sinus in its distal part, but no optimal ablation site was found at
this level (Fig.5.12).
Fig. 5.11 CARTO image in LAO 124° cranial 35° showing the RVOT (the transparent structure in the left side of
the image) and the base of the aorta (in gray, right side of
the image). The roving/ablation catheter records the elec-
trogram presented in blue, from the junction of the right
and the left coronary cusps (Map 1–2). The bipolar electrogram precedes the onset of the QRS by 11ms, and the
local unipolar electrogram has a “QS” aspect
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Fig. 5.12 CARTO
image in LAO 133°,
showing the activation
map of the RVOT, the
coronary cusps and the
coronary sinus during
the PVCs. The earliest
activation site is
recorded at the level of
the left coronary cusp
(red pin), from where
the activation wavefront
spreads in a radial
manner, strongly
suggesting a focal
mechanism
Question 4: What is the next best step at
this point of the procedure?
A. Ablate at the site of the earliest endocar-
dial activation at the level of the junction
of the right and left coronary cusps.
B. Map the LVOT looking for a better abla-
tion site.
C. Terminate the procedure, since ablation
at this site carries a considerable risk of
myocardial infarction.
D. Perform ablation at the earliest ablation
site in the RVOT with a higher power, in
order to avoid the risk of myocardial
infarction related to ablation in the left
coronary cusp.
E. I don’t know.
Given the optimal ablation criteria found at
the level of the junction of the right and left coronary cusps (the local bipolar electrogram preceding the onset of the QRS complex by 15ms and
the “QS” aspect of the unipolar electrogram—
Figs. 5.13 and 5.14), ablation at this site was
decided.
RF energy was applied at this site with titration of RF energy from 20 to 25W, with a target
ablation index of 350 (Figs. 5.15 and 5.16).
Disappearance of the PVC was immediately
J. Havard et al.
noticed 5s after the start of the rst RF delivery.
Two additional RF lesions were created, with no
recurrence of the PVC.
There were no complications related to the
procedure.
The ECG at the end of the ablation procedure
is presented in Fig.5.17.
The ECG recorded 24h later, before hospital
discharge, is presented in Fig.5.18. The patient
was discharged on no antiarrhythmic treatment.
A 24-h Holter ECG was recorded 1 month
after the ablation procedure, which showed the
presence of a low number of PVCs (Fig.5.19).
Answers
Question 1: C. Junction of the left and
right coronary cusp.
Question 2: C. No. The local unipolar
electrogram recorded by the roving/
ablation catheter at the earliest endocardial activation site has an “rS”
pattern.
Question 3: C.Map the coronary cusps.
Question 4: A.Ablate at the site of the
earliest endocardial activation at the
level of the junction between the right
and the left coronary cusps.
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Fig. 5.13 CARTO
image in LAO 64°
projection of the base of
the aorta showing the
earliest activation site at
the level of the junction
of the right and left
coronary cusps during
PVC, with a “QS”
aspect at the level of the
unipolar electrogram
recorded by the distal
electrode of the roving/
ablation catheter
81
Fig. 5.14 A 12-lead ECG together with intracavitary
leads recorded from the distal and the proximal bipolar
electrode of the ablation catheter (ABL d and ABL p) and
from the right ventricular apical catheter showing the ear-
liest activation site at the level of the junction of the right
and left coronary cusps (Map 1–2), preceding the onset of
the QRS complex by 15ms
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J. Havard et al.
Fig. 5.15 CARTO image in LAO 119° projection showing the anatomical relationship between the earliest endocardial activation site at the level of the RVOT and the
earliest activation site at the level of the junction between
the right and left coronary cusps. The close proximity of
the posterior part of the RVOT to this site explains why
the posterior and inferior wall of the RVOT is activated
Fig. 5.16 A 12-lead ECG together with intracavitary
leads recorded from the distal and the proximal bipolar
electrode of the ablation catheter (ABL d and ABL p) and
from the right ventricular apical catheter showing rapid
rapidly after the depolarization of the left coronary cusp.
The pink and red dots represent ablation lesions, both at
the level of the RVOT and at the level of the left coronary
cusp. The presented bipolar and unipolar electrograms are
recorded from the earliest activation site in the left coronary cusp
disappearance of the PVC immediately after the start of
RF delivery at the earliest activation site at the junction
between the right and the left coronary cusp
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Fig. 5.17 A 12-lead ECG after the RF ablation procedure showing sinus rhythm with a heart rate of 74bpm, QRS axis
at 0°, absence of LV hypertrophy, absence of ischemia, and absence of PVC
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Fig. 5.18 A 12-lead ECG after the RF ablation procedure showing sinus rhythm with a heart rate of 68bpm, QRS axis
at 0°, absence of LV hypertrophy, absence of ischemia, and absence of PVC
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Fig. 5.19 Holter ECG recorded 1month after the RF ablation procedure showing the presence of a low number of
PVCs 1024, representing 1.2% of the total number of QRS complexes during 24h
J. Havard et al.
Commentary
The present case illustrates a catheter ablation
procedure of PVCs originating from the junction
of the right and the left coronary cusps in a patient
with no cardiovascular risk factors and no structural heart disease. Several observations merit
further comment.
The aortic root region can give rise to PVCs in
patients with structurally normal hearts and is
responsible for about 16.6–18% of cases of idiopathic ventricular arrhythmias [1, 2]. The left and
the right coronary cusps are known potential
sources of PVC and VTs, while the noncoronary
cusp may give rise to atrial tachycardias [3–5].
The exact identication of the site of origin of
PVCs is done during the electrophysiological
study, during the mapping phase that precedes
catheter ablation. Currently, this is best guided by
an electro-anatomical mapping system. However,
prior to the ablation procedure, the 12-lead ECG
remains a valuable tool in orienting the electrophysiologist in nding the likely origin of the
PVC. Our patient presented with frequent PVC
originating from the junction of the right and the
left coronary cusps. A 12-lead ECG arguments in
favor of an origin at this site are a QRS transition
in precordial leads in V3 and the presence of a
“QS” notch in lead V1 [6]. This aspect can be
observed in the ECG presented in Fig.5.1.
Another very valuable diagnostic clue on the
12-lead ECG that can orient the physician about
the origin of the PVC (right side of the heart vs.
left side of the heart) is the comparison between
the QRS transition in the precordial leads of the
PVC and the QRS transition during sinus rhythm.
If the transition of the PVC takes place later than
the QRS transition during sinus rhythm, the origin of the PVC is in the RVOT.If the transition of
the PVC takes places earlier than the QRS complex during sinus rhythm, the origin of the PVC
is in the LVOT [6, 7]. In the above-presented
patient, the ECG in Fig.5.1 shows a precordial
lead transition of the PVC in lead V3 and for the
QRS complex during sinus rhythm in lead V4.
This localizes the origin of the PVC in the left
outow tract region, fact conrmed by the activation map recorded with the CARTO system and
presented in Fig. 5.12. The reader is invited to
view cases 1–4 and 6 for an analysis of this criterion on other ECGs presenting cases of outow
tract ventricular arrhythmias.
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As proposed by Lin etal. [8], in patients with
PVCs/VT exhibiting “qrS” pattern or “QS” pattern with a notch on the descending limb in lead
V1 (such in the case of our patient), the presence
of “m,” “r,” “R,” or “Rs” morphology in lead I
predicted the origin of the PVC at the level of the
left–right coronary cusp and right coronary cusp
with sensitivity of 94.44%, specicity of 60%,
PPV of 89.47%, and NPV of 75%. As can be seen
in Fig.5.1, our patient had an “R” morphology in
lead I, compatible with an origin at the level of
the junction between the right and the left coronary cusps.
In what concerns mapping of VA originating
in the outow tract region, as a general rule, this
should always be started in the RVOT. This is
especially true for PVCs with a QRS transition in
V3, since approximately 50% of them will have
an RVOT origin and 50% will have a LVOT/coronary cusp origin [8].
It should be acknowledged that the exact site
of origin of the PVCs at the level of the coronary
cusps is best identied by intracardiac echography [9]. This technique was not used in the
above-presented case, but only the CARTO system. ICE allows direct visualization of the ablation catheter at the level of the aortic cusps and is
also able to show the distance between it and the
ostia of the coronary arteries.
Coronary angiography is recommended to be
performed during the catheter ablation procedure, just before RF application, since ablation of
the PVC site of origin should be performed at
least 5mm away from the ostium of a coronary
artery in order to avoid coronary artery injury
[10]. However, as described by Hoffmayer etal.
[11], ablation of PVCs originating from the aortic
cusps can be safely achieved in 91% of the
patients without the need of performing intraprocedural coronary angiography, if an electroanatomical mapping system is used and ICE is
available. In their experience, the use of ICE can
conrm a necessary safety distance of more than
10 mm between the tip of the ablation catheter
and the successful ablation site. In our patient,
the use of the CARTO system was enough to
safely perform successful ablation of the PVCs.
However, we do recommend the use of ICE for
the ablation of PVCs/VTs originating in the aortic root region, when this is available.
Learning Points
• PVCs arising from the junction of the
right coronary cusp and the left coronary cusp are characterized by an early
transition in the precordial leads and by
the presence of an “rS” aspect in lead
V1.
• 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. 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. Beukema RJ, Smit JJ, Adiyaman A, Van Casteren L,
Delnoy PP, Ramdat Misier AR, etal. Ablation of focal
atrial tachycardia from the non-coronary aortic cusp:
case series and review of the literature. Europace.
2015;17(6):953–61.
4. Wang Z, Liu T, Shehata M, Liang Y, Jin Z, Liang M,
etal. Electrophysiological characteristics of focal atrial
tachycardia surrounding the aortic coronary cusps.
Circ Arrhythm Electrophysiol. 2011;4(6):902–8.
5. Rillig A, Meyerfeldt U, Birkemeyer R, Jung
W.Ablation within the sinus of valsalva for treatment
of supraventricular and ventricular tachycardias: what
is known so far? Europace. 2009;11(9):1142–50.
6. 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.
7. Betensky BP, Park RE, Marchlinski FE, Hutchinson
MD, Garcia FC, Dixit S, et al. The V(2) transition ratio: a new electrocardiographic criterion
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J. Havard et al.
for distinguishing left from right ventricular outow tract tachycardia origin. J Am Coll Cardiol.
2011;57(22):2255–62.
8. Lin C, Zheng C, Zhou DP, Li XW, Wu SJ, Lin
JF. Origins location of the outow tract ventricular arrhythmias exhibiting qrS pattern or QS pattern
with a notch on the descending limb in lead V1. BMC
Cardiovasc Disord. 2017;17(1):124.
9. 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.
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. 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.
Case 6
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RonanLe Bouar, FrédéricHalbwachs,
Jean- YvesWiedemann, JacquesLevy,
DavidKenizou, andRomaricBouillard
6
Case Presentation
A 66-year-old male patient with a history of
dilated cardiomyopathy with mild LV systolic
dysfunction (LVEF of 46%) and ventricular
arrhythmia (PVCs with a high ventricular
arrhythmia burden at 24-h Holter ECG: 38,613
isolated PVC, couplets, and short runs, representing 37% of the total QRS complexes/24h) was
admitted to the cardiology department complaining of aggravated palpitations during the past few
days. His cardiovascular risk factors were represented by age>55years old, arterial hypertension, dyslipidemia, and overweight. His
medication at home consisted of ramipril 10mg,
metoprolol 200mg, aspirin 75mg, and atorvastatin 40mg. For the treatment of his ventricular
arrhythmia, ecainide and propafenone were
tried but failed to reduce his symptoms, and amiodarone was refused by the patient due to potential side effects. At physical exam, his blood
pressure was 116/74 mmHg, HR of 68 bpm,
SpO2 99% breathing room air, H = 179 cm,
W= 83 kg, and BMI= 26 kg/m2, heart sounds
R. Le Bouar (*) · J.-Y. Wiedemann · J. Levy ·
D. Kenizou
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr; wiedemannjy@
ghrmsa.fr; levyj@ghrmsa.fr; kenizoud@ghrmsa.fr
F. Halbwachs · R. Bouillard
Biosense Webster, Mulhouse, France
were irregular, there were no audible murmurs,
peripheral pulses were bilaterally present, lung
auscultation was normal, and he had mild bilateral peripheral edema, no jugular vein distention,
and no hepatojugular reux. His ECG is presented in Fig.6.1. The result of the 24h Holter
ECG is presented in Fig.6.2.
Transthoracic echocardiography showed a
mildly dilated LV with mild systolic ventricular
dysfunction, EF of 46% (Fig.6.3). It also showed
type 1 diastolic dysfunction, absence of signicant valve disease, a mildly dilated left atrium, a
non-dilated right ventricle, a non-dilated right
atrium, mild pulmonary hypertension, sPAP of
37 mmHg, a non-dilated IVC, and absence of
pericardial effusion.
His biological workup showed a Hb level of
13.7 g/dL, leukocytes 9.57 × 109/L, platelets
170×109/L, CRP 5mg/L, BUN 7.2mmol/L, creatinine 96 μmol/L, glycemia 4.7 mmol/L, Na+
140 mmol/L, K+ 4.0 mmol/L, NT pro-BNP
539pg/mL, and TSH 1.0IU/L.
Coronary angiography was performed, showing a signicant stenosis of the LAD coronary
artery (stenosis of the second segment of the
LAD, FFR of 0.66 during hyperemia vs. 0.90 at
rest, red arrow), which was treated with PTCA
and stent implantation (Fig.6.4).
Three months after the PTCA procedure, the
LVEF did not improve and the ventricular
arrhythmia burden was unchanged at his 24-h
Holter ECG.
© 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_6
87
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Fig. 6.1 A 12-lead ECG recoded at admittance to the cardiology department
A cardiac MRI was performed, searching for a
potential ventricular arrhythmia substrate, which
demonstrated the presence of large areas of
delayed enhancement at the intramyocardial level
of the septal and anterior wall of the left ventricle
(Fig.6.5).
Question 1: What is the origin of the
PVC presented in Fig. 6.1?
A. RVOT
B. LVOT
C. LV summit
D. Right coronary cusp
E. Junction of the left and right coronary
cusp
R. Le Bouar et al.
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