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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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R. Le Bouar et al.
Fig. 3.12 X-ray image in posteroanterior view showing the position of the roving/ablation catheter at the level of the earliest activation site during PVCs
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Fig. 3.13 CARTO image in a superior and septal view (same as in Fig.3.10) showing the activation map of the LV
during PVCs with superposed RF ablation lesions
Fig. 3.14 CARTO image in a superior and septal view (same as in Fig.3.11) showing the pacemap of the LV with
superposed RF ablation lesions
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Fig. 3.15 A12-lead ECG recorded after the end of the ablation procedure showing sinus rhythm with a heart rate of
76bpm, QRS axis at +60°, absence of LV hypertrophy, absence of ischemia, and no PVC
R. Le Bouar et al.
Fig. 3.16 A 24-hour Holter ECG performed 5weeks after the ablation procedure showing the absence of any ventricular arrhythmia
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Answers
Question 1: B.LVOT
Question 2: E.Catheter ablation
Question 3: D.All of the above
Commentary
The present case describes a catheter ablation
procedure of PVCs arising from the LVOT in a
patient without structural heart disease. Several
observations can be made about the present case.
Ventricular arrhythmias in patients without
structural heart disease, the so-called idiopathic,
are typically encountered in young individuals,
are considered benign, and have a good longterm prognosis [1, 2]. However, they can be disturbing by producing a variety of symptoms,
from mild palpitations to syncope, and can negatively impact the patient’s quality of life. They
can manifest as isolated PVCs or organized
ventricular arrhythmias, such as NSVT or even
sustained VT. They are sometimes refractory to
medical treatment, and this is mostly the reason
for which catheter ablation has become the treatment option of choice, given its high efcacy and
low complication rate [3, 4].
The most common site of origin of idiopathic
ventricular arrhythmias is the outow tract region
(RVOT in 70–80% [5] of cases and LVOT in
15–25% of cases [6]), followed by the aortic
sinus of Valsalva region. Examples of PVC originating from the RVOT are presented in cases 1
and 2 and from the aortic sinus of Valsalva in
cases 4, 5, and 6. There are four regions described
when evaluating the origin of a PVC arising from
the LV: (1) the aorto-mitral continuity, (2) the
anterior site around the mitral annulus, (3) the
coronary cusp region, and (4) the epicardial
LV.For the above-presented patient, the origin of
the PVC would correspond to the anterior site
around the mitral annulus (Fig.3.10).
Several papers have been published up to date
regarding the presence of specic elements on
the 12-lead ECG that help the electrophysiologist
41
localize the origin of the PVC [6–9].
Differentiating RVOT PVC from LVOT PVC is
sometimes not easy, but several characteristic
features distinguish one origin from the other.
The RVOT is situated more anterior than the
LVOT, and therefore, the QRS transition in the
precordial leads for PVCs originating in the
RVOT takes place later than for PVCs originating
in the LVOT.For RVOT PVCs, the transition in
the precordial leads takes places in V3 or V4; for
PVCs originating in the LVOT region, this takes
place not later than V3 (usually V1 or V2). PVCs
originating from the aorto-mitral continuity are
characterized by a “qR” aspect in lead V1 and
have a positive precordial concordance. PVCs
from LV summit usually have a V2 pattern break,
are negative in lead I, and are more negative in
aVL than in aVR.PVCs originating from the LV
septum have a somewhat more narrow LBBB
pattern; they have a “QS” ratio in leads II and III
>1. And nally, PVCs originating from the
anterolateral mitral annulus have a late-phase
notching in the inferior leads. This was the case
for our above-presented patient (see the 12-lead
ECG from Fig.3.1).
Another important criterion that helps differentiate RVOT from LVOT PVCs is the comparison of the QRS transition in the precordial leads
of the PVC to the one of the QRS complex 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.This is known as the
V2 criteria [10]. In the above-presented patient,
the ECG in Fig.3.1 shows a QRS transition in the
precordial leads for the PVC in lead V2 and for
the QRS complex during sinus rhythm in lead
V3. This localizes the origin of the PVC in the
LVOT, fact conrmed by the activation map done
with the CARTO system and presented in
Fig.3.10.
Ablation of ventricular arrhythmias arising
from the LVOT below the coronary cusp region
can be accomplished most often by the retrograde
transaortic approach, but transseptal approach
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has also been described [11]. Success rate is high
in experienced hands, but slightly lower than for
VA originating from the RVOT [12].
A 3D non-uoroscopic mapping system, such
as the CARTO system, is a very useful tool in
guiding the mapping phase, in identifying the
PVCs origin, and is associated with a reduced
uoroscopy time and dose [13–15]. In the abovepresented patient, the CARTO system allowed
the creation of an activation map during PVCs
and of a pacemap. The latter conrmed the origin
of the PVCs at the level of the anterior LVOT.The
total uoroscopy time was 1.92min and the total
uoroscopy dose was 125.2cGycm2.
A CT angiography performed before the ablation procedure can also be very helpful for a catheter ablation procedure of ventricular arrhythmias.
Integration of CT angiography images in the
CARTO platform and performing a 3D reconstruction of the heart chambers, coronary arteries,
and sometimes other structures (such as the coronary sinus, the vein of Marshall, or the esophagus)
are of great help during the rst phase of an ablation procedure (the creation of the anatomical
map), when dening the borders of a specic anatomical structure is needed. It is also very useful
during the ablation phase itself, allowing the performing physician to assess the anatomical relationships with neighboring structures. For
example, the juxtaposition of the coronary arteries with the anatomical/activation map of the LV
can allow the evaluation of the safety distance
between a desired ablation site and a coronary
artery. A good example is presented in Figs.3.13
and 3.14. It can also avoid the need to perform of
coronary angiography during the procedure.
Potential complications related to a catheter
ablation procedure of ventricular arrhythmias
arising from the LVOT include vascular accessrelated complications (hematoma, hemorrhage,
pseudoaneurysm, arteriovenous stula), pericardial effusion with or without cardiac tamponade,
ischemic stroke, damage to the aortic valve in
case of a retrograde approach, deep vein thrombosis, pulmonary embolism, and sepsis. These
possible complications need to be well known by
the performing physician, promptly recognized
when present and promptly treated.
R. Le Bouar et al.
Learning Points
• PVCs originating from the LVOT are
characterized by the presence of a
LBBB morphology inferior axis, with a
QRS transition in the precordial leads
not later than in V3. The QRS transition
in the precordial leads of the PVC QRS
takes places earlier than the transition of
the QRS complex during sinus rhythm.
• The treatment of choice is catheter ablation, if possible guided by an electroanatomical mapping system.
References
1. Yamada T. Idiopathic ventricular arrhythmias: relevance to the anatomy, diagnosis and treatment. J
Cardiol. 2016;68(6):463–71.
2. Kim RJ, Iwai S, Markowitz SM, Shah BK, Stein KM,
Lerman BB. Clinical and electrophysiological spectrum of idiopathic ventricular outow tract arrhythmias. J Am Coll Cardiol. 2007;49(20):2035–43.
3. Heeger CH, Hayashi K, Kuck KH, Ouyang F.Catheter
ablation of idiopathic ventricular arrhythmias arising
from the cardiac outow tracts- recent insights and
techniques for the successful treatment of common
and challenging cases. Circ J. 2016;80(5):1073–86.
4. Pathak RK, Ariyarathna N, Garcia FC, Sanders
P, Marchlinski FE. Catheter ablation of idiopathic ventricular arrhythmias. Heart Lung Circ.
2019;28(1):102–9.
5. de Groot JR. Ablation of idiopathic ventricular
arrhythmias. Neth Heart J. 2018;26(4):173–4.
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. Zheng J, Fu G, Anderson K, Chu H, Rakovski C.A
12-Lead ECG database to identify origins of idiopathic ventricular arrhythmia containing 334 patients.
Sci Data. 2020;7(1):98.
8. Yamada T, Yoshida N, Litovsky SH, Itoh T,
Doppalapudi H, Kay GN. Idiopathic ventricular arrhythmias originating from the infundibular
muscles: prevalence, electrocardiographic and electrophysiological characteristics, and outcome of
catheter ablation. Circ Arrhythm Electrophysiol.
2018;11(3):e005749.
9. Ludwik B, Deutsch K, Mazij M, Sledz J, Morka A,
Labus M, et al. Electrocardiographic algorithms to
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guide the management strategy of idiopathic outow
tract ventricular arrhythmias. Pol Arch Intern Med.
2017;127(11):749–57.
10. Betensky BP, Park RE, Marchlinski FE, Hutchinson
MD, Garcia FC, Dixit S, et al. The V(2) transition ratio: a new electrocardiographic criterion
for distinguishing left from right ventricular outow tract tachycardia origin. J Am Coll Cardiol.
2011;57(22):2255–62.
11. Ouyang F, Mathew S, Wu S, Kamioka M, Metzner
A, Xue Y, et al. Ventricular arrhythmias arising from
the left ventricular outow tract below the aortic sinus
cusps: mapping and catheter ablation via transseptal
approach and electrocardiographic characteristics.
Circ Arrhythm Electrophysiol. 2014;7(3):445–55.
12. Latchamsetty R, Yokokawa M, Morady F, Kim
HM, Mathew S, Tilz R, et al. Multicenter out-
comes for catheter ablation of idiopathic premature
ventricular complexes. JACC Clin Electrophysiol.
2015;1(3):116–23.
13. Knecht S, Sticherling C, Reichlin T, Pavlovic N, Muhl
A, Schaer B, etal. Effective reduction of uoroscopy
duration by using an advanced electroanatomicmapping system and a standardized procedural protocol for ablation of atrial brillation: ‘the unleaded
study’. Europace. 2015;17(11):1694–9.
14. 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.
15. Yamagata K, Aldhoon B, Kautzner J. Reduction
of uoroscopy time and radiation dosage during
catheter ablation for atrial brillation. Arrhythmia
Electrophysiol Rev. 2016;5(2):144–9.
Case 4
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FrédéricHalbwachs, RonanLe Bouar,
ThomasRobein, Jean-YvesWiedemann,
LaurentDietrich, TarekEl Nazer, andJacquesLevy
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Case Presentation
A 60-year-old female patient with a past medical
history of peripheral arterial disease (moderate
stenosis of the right subclavian artery), type 2
diabetes mellitus on insulin, PVCs with a moderate ventricular arrhythmic burden at the 24-h
Holter ECG monitoring, and goiter with normal
thyroid function was admitted to the cardiology
department complaining of intermittent palpitations, dyspnea on exertion, and fatigue.
Her cardiovascular risk factors were represented by arterial hypertension, overweight, and
diabetes mellitus. Her medication at home consisted of telmisartan 40 mg, ezetimibe10 mg,
metformin 850mg tid, sitagliptin 100mg, rosuvastatin 20 mg, aspirin 75 mg, betaxolol 20 mg,
and long-lasting insulin 48IU/day.
Supplementary Information The online version contains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 35579- 0_4.
F. Halbwachs (*) · T. Robein
Biosense Webster, Mulhouse, France
R. Le Bouar · J.-Y. Wiedemann · L. Dietrich ·
T. El Nazer · J. Levy
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr;
wiedemannjy@ghrmsa.fr; laurent.dietrich@ghrmsa.fr;
tarek.elnazer@ghrmsa.fr; levyj@ghrmsa.fr
At physical examination, her blood pressure
was 129/76 mmHg, HR 67 bpm, SpO2 99%
breathing room air, H=1.65m, W=75kg, and
BMI=27.54kg/m2, heart sounds were irregular,
there were no audible murmurs, lung auscultation
was clear, and there were no signs of right heart
failure.
Her ECG at presentation is showed in Fig.4.1.
A 24-h Holter ECG showed the presence of
20.422 PVC/24h, of which 17,644 isolated PVCs
of two morphologies, 1370 couplets, with six
runs but no episodes of sustained VT.The result
of her 24-h Holter ECG monitoring is presented
in Fig.4.2.
Transthoracic echocardiography showed a
non-dilated LV, with preserved systolic ventricular function, EF of 53%. It also showed mild
LV hypertrophy, 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 39mmHg, a non-dilated
IVC, and absence of pericardial effusion
(Fig.4.3).
Her biological workup showed a Hb level of
13.6 g/dL, leukocytes 5.77 × 109/L, platelets
251×109/L, CRP 3mg/L, BUN 4.9mmol/L, creatinine 43μmol/L, glycemia 15.2mmol/L, Na+
137 mmol/L, K+ 4.0 mmol/L, NT pro-BNP
279 pg/mL, TSH 1.10 IU/L, total cholesterol
168 mg/dL, HDL 33 mg/dL, LDL 130 mg/dL,
and triglycerides 408mg/dL.
© 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_4
45
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F. Halbwachs et al.
Fig. 4.1 A 12-lead ECG recorded at admittance to the
cardiology department showing sinus rhythm with a heart
rate of 88bpm, QRS axis at +60°, absence of LV hypertro-
Her chest X-ray showed a normal cardiothoracic index, absence of pleural effusion, and
absence of a possible pulmonary infectious trigger (Fig.4.4).
Question 1: What is the best step in the
management of this patient?
A. Increase the dose of betaxolol to 40mg
and perform another 24-h Holter ECG.
B. Replace betaxolol treatment with meto-
prolol 200mg/day.
C. Add amiodarone200 mg/day on top of
betaxolol.
D. Initiate ecainide treatment 200mg/day
on top of betaxolol.
E. Perform catheter ablation.
phy, absence of ischemia, two isolated PVCs, and one
polymorphic ventricular couplet
Betaxolol is a beta blocker used for the treatment of arterial hypertension and angina pectoris,
at doses of 20 mg daily. There is no reason to
augment the dose at 40mg/day in this patient, for
the treatment of her PVCs. Switching to metoprolol may be considered, but this is not very
likely to suppress her symptoms, given the
absence of betaxolol’s efcacy. Amiodarone was
offered but not desired by the patient, due to possible long- term side effects. Both ecainide and
catheter ablation were presented as treatment
options to the patient, who preferred the latter.
Therefore, an ablation procedure was subsequently scheduled and performed.
A cardiac computed tomography was performed before the ablation procedure, in order to
better dene the LV anatomy. This showed the
absence of mild LV hypertrophy and the absence
of LV thrombus (Fig.4.5).
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Fig. 4.2 A 24-hour Holter ECG recording showing frequent PVCs of two morphologies (red stars), with a moderate
ventricular arrhythmia burden, representing 21.2% of the total QRS complexes/24h
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F. Halbwachs et al.
Fig. 4.3 Left upper panel: Transthoracic echocardiog-
raphy image in parasternal long-axis view showing a nondilated LV, with an EDD of 46mm. Right upper panel:
M-mode echocardiography image showing a preserved
LVEF of 53%. Left middle panel: Pulsed Doppler transmitral ow interrogation showing type 1 diastolic dysfunction. Right middle panel: Tissue Doppler at the level
of the lateral part of the mitral valve showing non-dilated
LV lling pressure, with an E/e′ ratio of 8. Left lower
panel: Continuous Doppler wave interrogation of the
trans-tricuspid ow, evaluating a RV-RA pressure of
39mmHg. Right lower panel: Apical four-chamber view
showing a mildly dilated left atrium of 25.4cm
2
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