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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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1 Case 1
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Fig. 1.6 CARTO image of the right ventricular outow
tract (RVOT) in left lateral view 100°. Pacemap conrming the origin of the PVC at the site of earliest endocardial
activation during PVCs, with a concordance of locally
was used to compare the resulting 12-lead ECG
during local pacing with the morphology of the
PVC. A superposed correlation of 98% was
observed at the earliest activation site of the
RVOT (Fig.1.6).
Question 5: Is this a good ablation site?
A. Yes. The earliest bipolar local electro-
gram precedes the surface QRS by
17ms, and this should be enough for a
successful site.
B. Yes. The pacemap of the RVOT indi-
cates a 98% correlation between the
spontaneous PVCs and the locally paced
QRS, indicating an optimal ablation
site.
generated QRS morphology and spontaneous PVC morphology of 98% (right side of the image). The roving/
ablation catheter was positioned at the site of the earliest
endocardial activation (yellow star)
C. Yes. The local unipolar electrogram
recorded by the distal electrode of the
roving/mapping catheter has a “QS”
pattern.
D. No. The earliest endocardial activation
in the RVOT precedes the beginning of
the QRS complex by only 17 ms, and
this is not good enough for a successful
lesion.
E. I don’t know.
The activation map of the RVOT during PVC
and the pacemap both indicate the same origin of
the PVC, in the high lateral and posterior part of
the RVOT.In fact, there are clues on the 12-lead
ECG, indicating the area of the RVOT where the
PVCs originate (see the comment section).
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R. Le Bouar et al.
Fig. 1.7 CARTO image of the right ventricular outow tract (RVOT) in left lateral view 98° with superposed RF ablation lesions at the successful ablation site
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.The RVOT
map with superposed RF ablation lesions is presented in Fig.1.7.
After a waiting period of 30min, isoprenaline
was infused, without reappearance of the PVC.
There were no complications related to the
procedure.
The ECG post-ablation is shown in Fig.1.8.
The patient was discharged from the hospital
48h later on heart failure treatment.
A transthoracic echocardiography performed
3months later revealed a LVEF of 55%. Heart
failure treatment was stopped and transthoracic
echocardiography was performed 3 months
later, which showed a non-dilated LV, with a
LVEF of 68%. The transthoracic echocardiography performed 2 years later is presented in
Fig.1.9.
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Fig. 1.8 A 12-lead ECG recorded after the RF ablation procedure, showing sinus rhythm with a heart rate of 48bpm,
QRS axis at +55°, no ischemia, and absence of premature ventricular contractions
Answers
Question 1: A.RVOT.
Question 2: D.Important.
Question 3: A. Yes. The PVCs are the
most likely cause of the LV systolic
dysfunction.
Question 4: E.Catheter ablation.
Question 5:
A. Yes. The earliest bipolar local electro-
gram precedes the surface QRS by
17ms, and this should be enough for a
successful site.
B. Yes. The pacemap of the RVOT indi-
cates a 98% correlation between the
spontaneous PVCs and the locally
paced QRS, indicating an optimal
ablation site.
C. Yes. The local unipolar electrogram
recorded by the distal electrode of the
roving/mapping catheter has an “QS”
pattern.
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R. Le Bouar et al.
Fig. 1.9 Transthoracic echocardiography performed
2years after the ablation procedure. Left upper panel:
M-mode echocardiography in parasternal long-axis view
showing a LVEF of 63% (Teicholtz method). Right upper
panel: Apical four-chamber view showing a LVEF of
68% (Simpson single-plane method). Left middle panel:
Parasternal long-axis view showing a non-dilated LV, with
an end-diastolic diameter of 48mm. Right middle panel:
Parasternal long-axis view showing a non-hypokinetic LV,
with an end-systolic diameter of 30 mm. Left lower
panel: Apical four-chamber view showing a non-dilated
LA, with an area of 19.7cm2. Right lower panel: Apical
four-chamber view showing the absence of pulmonary
hypertension, with a RV–RA pressure gradient of
13.7mmHg
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Commentary
The present case illustrates a catheter ablation
procedure of PVC arising from the RVOT in a
patient with PVC-induced cardiomyopathy.
Several aspects merit further comment.
PVCs in the absence of structural heart dis-
ease (also called idiopathic) usually originate
from the outow tract region, either the RVOT or
the LVOT, from the aortic cusp region or from the
aortomitral continuity. Other possible but less
frequently encountered origins include the periHis bundle region, the mitral annulus, the tricuspid annulus, the papillary muscles, or the
perivascular epicardial region [1]. Almost 70% of
idiopathic PVCs originate in the RVOT [2]. The
mechanism of these PVCs is calcium-dependent
triggered activity [3]. PVCs in the absence of
structural heart disease are usually benign. Their
prognosis is generally good, since they are not
usually associated with a higher risk of sudden
cardiac death [2], even though exceptions exist
[4, 5]. They can provoke a series of symptoms
from dyspnea to palpitations, fatigue, nearsyncope, or syncope and, if frequent, can sometimes lead to dilated cardiomyopathy [6–9]. The
treatment of choice is catheter ablation, because
of its positive benet to risk ratio. The success
rate is high, reaching 90–95% in experienced
hands [10–12] and the complication rate is low
[13].
PVC-induced cardiomyopathy is a reversible
form of dilated cardiomyopathy that can develop
as a consequence of frequent PVC, desynchronizing the two ventricles [14]. Predictors of PVCinduced cardiomyopathy include a high PVC
burden (more than 26%/24 h), the presence of
non-sustained ventricular tachycardia, and the
presence of a retrograde P wave following the
PVC [15]. In the experience of Kanei etal., the
percentage of patients who develop LV systolic
dysfunction as a consequence of PVCs is related
to the ventricular arrhythmia burden. Therefore,
patients with a burden of less than 1000
PVCs/24 h have a prevalence of 4% of PVCinduced CMP, compared to patients who have a
PVC burden between 1000 and 10,000 PVC/24h
who have a prevalence of 12%, different from
those who have more than 10,000 PVC/24h, who
have a prevalence of PVC-induced DCM of 34%
[8]. In the experience of Baman etal. [16], the
lowest PVC burden that can result in a PVCinduced cardiomyopathy is 10%. The PVC burden in our patient was 38.2%, explaining the
development of DCM.
Our patient had all the abovementioned predictors of developing PVC-induced DCM: a very
high arrhythmia burden, with a total of 50.117
PVC/24 h, episodes of NSVT on Holter ECG,
and retrograde P waves following the PVCs, best
seen on the Holter ECG tracing from Fig.1.2.
The diagnosis of PVC-induced DCM is retrospective. It requires an increase in the LV EF%
after the elimination of the PVCs [17]. However,
if the PVCs persist for long periods of time, the
recovery of the LV systolic function may be
incomplete or absent, probably due to the
development of myocardial brosis. The only
predictor of failure of LV EF% recovery despite
successful ablation is PVC QRS duration [18]. In
the above-presented patient, the recovery was
complete.
Regarding the localization of the PVC origin
using the surface ECG, several criteria have been
described up to present which can help the cardiac electrophysiologist decide in which ventricle the mapping phase preceding the catheter
ablation procedure should be begun [3, 19, 20].
The presence of a notch on the peak of the R
wave in inferior leads is most likely associated
with a lateral origin in the RVOT [21–23]. The
presence of a “QS” aspect in lead aVL is associated with a high origin in the RVOT, less than
3 cm from the pulmonary valve [21–23]. This
was also the case of our patient, which had the
origin of the PVC in the high lateral part of the
RVOT and presented the abovementioned criteria
on the surface ECG (see Fig.1.1).
Another important aspect worth mentioning is
the fact that DCM of other origins can give rise to
ventricular arrhythmias, from isolated PVCs to
NSVT and sustained VT. In fact, up to 85% of
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patients with DCM have ventricular arrhythmias
on the 24-h Holter ECG [24]. Therefore, in
patients presenting with DCM and a high ventricular arrhythmia burden, it is sometimes difcult to know if the DCM provokes the PVCs or if
they have a PVC-induced DCM.Since the diagnosis of PVC-induced DCM is retrospective, the
most important aspect is elimination of the PVCs.
If the increase in the LV EF% occurs after treatment of the PVCs, it was most likely PVCinduced DCM, such as in the case of the
above-presented patient, in which the LV EF
increased from 31% to 68%. The increase in the
LV EF post-catheter ablation of PVCs is however
variable. Sometimes full recovery is observed;
sometimes an incomplete recovery exists. This is
most likely due to induced irreversible changes,
such as myocardial brosis. In Marchlinski’s
series, the average post-ablation increase in the
EF% post-catheter ablation of PVCs was 14%
[25].
And last but not least, the presence (or
absence) of an underlying heart disease in
patients with PVCs determines the prognosis of
the patient. The absence of an underlying heart
disease is associated with a good prognosis,
unlike the presence of a heart disease, such as
arrhythmogenic cardiomyopathy, in which the
prognosis is more reserved. From this point of
view, the prognosis of the above-presented
patient is good, given the normalization of the LV
EF% post-ablation.
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.
• PVC-induced cardiomyopathy can
develop if at least a moderate PVC burden is present (>10%/24h).
• Predictors of PVC-induced cardiomyopathy include a high PVC burden
(more than 26%/24h), the presence of
non-sustained ventricular tachycardia,
R. Le Bouar et al.
and the presence of a retrograde P wave
following the PVC.
• Catheter ablation of the PVC guided by
an electro-anatomical mapping system
is the treatment of choice, since elimination of the PVC is associated most of the
times with a decrease in LV end-systolic
and end-diastolic volumes and an
increase in the LV EF%.
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tract are associated with left ventricular dysfunction.
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S, etal. Electrocardiographic predictors of long-term
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Shah BK, Cheung JW, et al. Reversal of cardiomyopathy in patients with repetitive monomorphic ventricular ectopy originating from the right ventricular
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Case 2
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FrédéricHalbwachs, MatthieuGeorge,
LucienDiene, MarineKinnel, JacquesLevy,
andLaurentJacquemin
2
Case Presentation
A 30-year-old male patient, volunteer reghter,
with no cardiovascular risk factors and no signicant past medical history, was addressed by
his reghter unit physician for a complete cardiology checkup due to three episodes of palpitations that had occurred during physical effort
during the past 6weeks while training. An ECG
recorded at rest after interruption of physical
training showed frequent PVC. A cardiology
consultation was organized and performed,
which conrmed the presence of frequent,
monomorphic PVC.
Physical examination revealed a BP of
156/75mmHg, an HR of 70bpm, irregular heart
sounds, no cardiovascular murmur, clear lung
upon auscultation, and no signs of left or right
heart failure.
The 12-lead ECG is presented in Fig.2.1.
A 24-h Holter ECG was subsequently performed, which showed a moderate ventricular
arrhythmia burden at 24-h Holter ECG (11,414
isolated PVC, with no couplets, runs, or sustained
episodes of VT, representing 10.3% of the total
QRS complexes/24h) (Fig.2.2).
His transthoracic echocardiography showed a
normal LV systolic function, with an EF of 58%.
It also showed absence of regional hypokinesia,
with a non-dilated LV (EDD of 48 mm), nonelevated LV lling pressure, a preserved cardiac
index of 4.2L/min/m2, nonsignicant valve disease, non-dilated left atrium and right ventricle,
mild tricuspid regurgitation, absence of pulmonary hypertension, sPAP of 29 mmHg, and
absence of pericardial effusion (Fig.2.3).
An exercise stress test did not show any signs
of myocardial ischemia. It demonstrated disappearance of PVC during effort, with reappearance during the recovery phase (Fig.2.4).
His biological workup showed a Hb level of
14.3 g/dL, leukocytes 6.44 × 109/L, platelets
277×109/L, CRP<3mg/L, BUN 3.8mmol/L,
creatinine 65μmol/L, glycemia 4.3mmol/L, Na+
138 mmol/L, K+ 3.8 mmol/L, NT proBNP<30pg/mL, and TSH 2.0IU/L.
F. Halbwachs (*) · M. George
Biosense Webster, Mulhouse, France
L. Diene · M. Kinnel · J. Levy · L. Jacquemin
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: lucien-leopold.diene@ghrmsa.fr;
marine.kinnel@ghrmsa.fr; levyj@ghrmsa.fr;
jacqueminl@ghrmsa.fr
© 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_2
15
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Fig. 2.1 A 12-lead ECG at admittance to the cardiology department
F. Halbwachs et al.
His chest X-ray is presented in Fig.2.5.
Given the ECG aspect of the PVC, a cardiac
MRI was performed, searching for arguments in
favor of arrhythmogenic cardiomyopathy
(Fig.2.6).
Signal-averaged ECG was negative (0 positive
criteria out of 3, Fig.2.7).
Question 1: Where is the most likely ori-
gin of the PVC presented in Fig. 2.1?
A. RVOT
B. LVOT
C. LV summit
D. Right coronary cusp
E. Left coronary cusp
Question 2: In which area of the RVOT
does the PVC originate?
A. High RVOT.
B. Low RVOT.
C. Posterior RVOT.
D. Anterior RVOT.
E. I don’t know.
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Fig. 2.2 A 24-hour Holter ECG recording showing frequent, monomorphic PVC, with a moderate ventricular arrhythmia burden, representing 10.3% of the total QRS complexes/24h
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