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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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F. Halbwachs et al.
Fig. 2.3 Left upper panel: Echocardiography image in
parasternal long-axis view showing a mildly dilated LV,
with an EDD of 58mm. Right upper panel: Apical fourchamber view showing a mildly dilated LV, with a basal
diameter of 58 mm. Left middle panel: Apical fourchamber view showing a non-dilated RV, with a basal
diameter of 30 mm. Right middle panel:
Echocardiography image in apical four-chamber view
showing a mildly dilated left atrium, with an area of
20.2cm2. Left lower panel: Pulsed Doppler evaluation of
the transmitral ow in apical four-chamber view showing
normal diastolic function. Right lower panel: Tissue
Doppler imaging showing normal LV lling pressure,
with an E/e′ ratio of 4
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Fig. 2.4 Exercise stress showing disappearance of PVC during physical effort (upper panel), with reappearance dur-
ing the recovery phase (lower panel)
Fig. 2.5 Chest X-ray in
posteroanterior view showing a
non-enlarged cardiac silhouette,
with a normal cardiothoracic
index, absence of pleural
effusion, and no pulmonary
stasis
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F. Halbwachs et al.
Fig. 2.6 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
Figure 2.1 explained. A 12-lead ECG showing sinus rhythm with a heart rate of 68 bpm,
QRS axis at 0°, absence of LV hypertrophy,
absence of ischemia, frequent monomorphic
PVC, and normal QT interval. The PVC morphology is “notched R” in lead I, “notched R” in
leads II, III, and aVF with a LBBB morphology,
panel: Absence of late gadolinium enhancement at the
level of the right and left ventricle. No major or minor
criteria in favor of arrhythmogenic cardiomyopathy
and a precordial transition in V4, in favor of a
RVOT origin. Of note, the PVC QRS transition in
precordial leads (V4) takes place later than the
QRS transition in sinus rhythm (V3), also an
argument in favor of a RVOT origin. The aspect
of the QRS complex in lead I—unique “R” wave
is in favor of an origin in the posterior part of the
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Fig. 2.7 Signal-averaged ECG showing a QRS duration of 100ms, the amplitude of the last 40ms of the QRS complex
of 35μV, and a duration of less than 40μV of 36ms (within normal values)
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RVOT.The “QS” aspect in lead aVL suggests an
origin at less than 3 cm from the pulmonary
valve.
Given the presence of a moderate arrhythmia
burden and the patient’s occupation, an electrophysiological study in view of a catheter ablation
procedure was offered and accepted by the
patient. A cardiac CT angiography was performed prior to the ablation procedure and subsequently used for guiding the mapping phase
during the EP study.
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. 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 ven-
tricular apex. A Biosense Webster® SmartTouch
SF open-irrigated 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 right ventricle. The CARTO ® 3 electro-anatomic mapping system (Biosense Webster, Johnson &
Johnson) 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®).
Given the 12-lead aspect of the PVC (“notched
R” in lead I, “R” in leads II, III, and aVF with a
LBBB morphology, and a precordial transition in
V4), an origin in the RVOT was suspected.
Mapping of the PVC was therefore commenced
in the RVOT.
The ECG at the beginning of the electrophysiological study is presented in Fig.2.8.
An anatomical map of the RVOT was initially
created. Next, an activation map of the RVOT
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Fig. 2.8 A 12-lead ECG at the beginning of the ablation procedure, showing the presence of frequent isolated PVC,
identical to the patient’s clinical PVCs
F. Halbwachs et al.
during the frequent PVCs was created. This
showed the presence of an early activation site at
the level of the high posterior and lateral RVOT,
just below the pulmonary valve, from where the
activation of the RVOT spread in a radial manner,
suggesting a focal activation pattern (Fig.2.9). At
this site, the unipolar electrogram recorded by the
roving/ablation catheter had a “QS” aspect.
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 98.1% was
observed at the earliest activation site of the
RVOT, conrming the origin of the PVC at this
level (Fig.2.10).
RF energy was applied at this site with a target
power of 30W and a target ablation index of 450,
with rapid disappearance of the PVC.
After a waiting period of 30min, isoprenaline
was infused, without reappearance of the PVC.
A comparison of the pacemap and the activa-
tion map of the RVOT is presented in Fig.2.11.
There were no complications related to the
procedure.
The ECG at the end of the ablation procedure
is shown in Fig.2.12.
The ECG recorded 24h after the ablation pro-
cedure is shown in Fig.2.13.
The patient was discharged from the hospital
on no antiarrhythmic treatment.
His 24-h Holter ECG performed 10 weeks
after the ablation procedure showed the presence
of only 30 PVC during 24 h of recording
(Fig.2.14).
Answers
Question 1: A.RVOT
Question 2: A.High RVOT and C. poste-
rior RVOT
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Fig. 2.9 CARTO image of the right ventricle in PA view
cranial 10° showing the superposed cardiac CT angiography 3D reconstruction image and the anatomical map of
the RV acquired with the roving/ablation catheter. The
activation map of the RVOT during PVCs is also presented, showing an area of early endocardial activation
(red color at the top of the roving/ablation catheter), preceding the onset of the QRS onset on the surface ECG by
38ms, with a “QS” aspect of the local unipolar electrogram. The area is situated in the upper lateral posterior
part of the RVOT
Fig. 2.10 CARTO image of the right ventricular outow
tract (RVOT) in RAO view 140° (right side of the image).
Pacemap conrming the origin of the PVC at the site of
earliest endocardial activation during PVCs, with a concordance of locally generated QRS morphology and spontaneous PVC morphology of 98.1% (left side of the
image). The roving/ablation catheter was positioned at the
site of the earliest endocardial activation. Pacing from this
specic site produced a QRS morphology that had a concordance of 98.1% with that of the spontaneous PVC,
conrming the optimal ablation site
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F. Halbwachs et al.
Fig. 2.11 Comparison of the pacemap and the activation
map of the RVOT after RF ablation of the PVC, showing
the anatomical relationship between the earliest activation
site on the activation map (right panel) and the best correlation site between the locally induced QRS morphology while pacing from the distal electrode of the roving/
Fig. 2.12 A 12-lead ECG at the end of the ablation procedure showing sinus tachycardia (explained by the IV isoprenaline infusion) with no PVC
ablation catheter and the spontaneous PVC (left and
middle panel). Pink and red lesions represent RF lesions.
The left panel shows concordance of locally generated
QRS morphology and spontaneous PVC morphology of
98.1%
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Fig. 2.13 A 12-lead ECG recorded after the RF ablation procedure, showing sinus rhythm with a heart rate of 71bpm,
QRS axis at 0°, no ischemia, and absence of premature ventricular contractions
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Fig. 2.14 A 24-hour Holter ECG performed 10weeks after the ablation procedure showing the presence of only 30
PVC/24h
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F. Halbwachs et al.
Commentary
The present case illustrates a catheter ablation
procedure of PVC arising from the RVOT in a
patient with structurally normal heart. Several
aspects merit further comment.
Few, isolated PVCs are common ndings in
the adult population, with a prevalence of
40–75% on the 24–48-h Holter ECG monitoring
[1]. In the absence of an underlying heart disease
and of symptoms, when the arrhythmia burden is
low, they do not require treatment. However,
when the arrhythmia burden is signicant and
they represent more than 10% of the total number
of QRS complexes/24h, the risk of developing
PVC-induced cardiomyopathy increases signicantly [2] (see Case 1).
In the presence of an underlying heart disease,
PVCs represent a marker of adverse prognosis
[3–8]. Therefore, in patients with frequent PVCs,
a complete cardiology workup, including careful
history taking, physical examination, 12-lead
ECG, Holter ECG, transthoracic echocardiography, tests evaluating the presence of coronary
artery disease and inducible myocardial ischemia, and cardiac MRI evaluating the possible
presence of several cardiomyopathies (especially
arrhythmogenic cardiomyopathy) is appropriate.
Ventricular arrhythmias in the absence of
heart disease are called idiopathic. They can present in a wide range of forms, from isolated PVCs
to sustained ventricular tachycardia. They can
cause a variety of symptoms, from mild palpitations to dyspnea, chest pain, asthenia, fatigue, to
near-syncope, and syncope. The most common
form of idiopathic ventricular arrhythmias are
isolated PVCs. Their most common origin is the
RVOT in 70% of cases [9], followed by the
LVOT, the aortic cusp region, and the aorto- mitral
continuity. Other locations do exist but are less
frequent. Treatment options include antiarrhythmic medication and catheter ablation. Due to the
variable response to antiarrhythmic drugs and to
their possible adverse effects when prescribed for
long periods of time, catheter ablation has
become the preferred treatment option in symptomatic patients with a signicant arrhythmia
burden and in those with PVC-induced cardio-
myopathy [9]. The origin of the PVC can be identied using the 12-lead ECG [10–14]. Several
diagnostic clues have been validated, with the
purpose of guiding the electrophysiologist when
preparing for the catheter ablation procedure.
The characteristics of PVCs originating in the
RVOT are (1) LBBB morphology and inferior
axis, (2) QRS transition in the precordial leads in
V3 or V4, and (3) QRS transition of the PVC in
the precordial leads that takes places later than
the transition of the QRS complex in sinus
rhythm [15]. Several other clues have been
described, which can identify a specic region in
the RVOT where the PVCs originate. Therefore,
the presence of a notch on the top of the R wave
in leads II, III, and aVF, together with a late QRS
transition in the precordial leads (V4) and a wider
QRS duration, characterizes the lateral wall origin. Septal origins are characterized by a narrower QRS complex and a transition earlier than
V4 [11, 13]. A “QS” aspect in lead aVL is in
favor of a high RVOT origin, less than 2cm from
the pulmonary valve [16]. The presence of an “R
wave” in lead I points to an origin at the level of
the posterior RVOT, while the presence of a “Q
wave” in lead I usually indicates an origin at the
level of the anterior RVOT [17].
In our patient, the 12-lead ECG presented in
Fig.2.1 shows the presence of a “QS” aspect in
lead aVL and the presence of an “R wave” in lead
I, suggesting an origin in the high posterior
RVOT, fact conrmed by the activation map performed with the CARTO system (Fig.2.9).
Catheter ablation of PVCs can be performed
using simple uoroscopy, or it can be guided by
an electro-anatomical mapping system, such as
the CARTO system. The latter has the advantage
of reducing the uoroscopy time and dose
[18–20].
The success rate of the catheter ablation procedure is high, over 90% in experienced hands [9,
21]. Recurrences are rare and the complication
rate is low. These are mostly related to the vascular access site (hematoma, hemorrhage, pseudoaneurysm, arteriovenous stula), but cases of
pericardial effusion, cardiac tamponade, and pulmonary embolism have also been described
[22–24].
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Given the absence of a structural heart disease
in our patient and the good result of the catheter
ablation procedure, the long-term prognosis is
excellent.
Learning Points
• PVCs arising from the RVOT are characterized by LBBB morphology and
superior axis, with QRS transition in the
precordial leads usually in V3 or V4.
• PVCs originating from the posterior
part of the RVOT show an “R” wave in
lead I.
• Cather ablation of the PVC guided by an
electro-anatomical mapping system is
the treatment of choice, given its high
success and its low complication rate.
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