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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. 7.8 CARTO image of the left ventricle in LAO 69°
caudal 14° showing an activation map of the LV during
PVCs. The red zone corresponds to an area of early endocardial activation, from which the activation wavefront
proceeds to the adjacent areas in a centrifugal manner (red
→yellow →green →blue →violet), suggesting a focal
Transthoracic echocardiography performed
3months after the RF procedure showed a stable
LVEF, at 43%. This was conrmed by a control
cardiac MRI, which showed an LVEF of 41%
(Fig.7.14).
Answers
Question 1: E.Catheter ablation.
Question 2: B. Anterolateral papil-
lary muscle area.
mechanism, in an anatomical area that could correspond
to the anterolateral papillary muscle region. The Pentaray
catheter situated at this level (center of the image) records
local ventricular electrograms which precede the onset of
the QRS complex on surface ECG (right side of the
image)
Question 3:
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
superposition of the locally generated
QRS morphology and that of the spontaneous QRS PVC of 95%.
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Fig. 7.9 A 12-lead ECG together with intracavitary leads
recorded from the distal and the proximal electrodes of
the roving/ablation catheter (ABL d, ABL p). The roving/
ablation catheter is positioned at the level of the anterolat-
eral papillary muscle region. During the frequent PVC,
the local ventricular electrogram precedes the surface
ECG by 7–10ms
Fig. 7.10 CARTO image of the left ventricle in LAO 134°
caudal 24° showing the bipolar voltage map of the LV
recorded in sinus rhythm (left panel). Middle panel: Same
view as in the left panel, showing the pacemap of the LV
created with the roving/ablation catheter. Pacing the LV at
the site of earliest endocardial activation during PVC reproduces a QRS morphology almost identical to the morphology of the PVC (concordance of 95%, right panel)
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Fig. 7.11 CARTO image in LAO 4° cranial 64° showing
the ablation catheter at the level of the earliest endocardial
activation during PVC and best pacemap site (right part of
the image, concordance between the locally generated
QRS complex and spontaneous PVC of 95%), corre-
sponding to the area of insertion of the anterolateral papillary muscle. The red and pink dots represent RF lesions.
Note the ash situated at the distal part of the ablation
catheter being perpendicular to the LW wall, conrming a
good orientation of the force vector
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Fig. 7.12 A 12-lead ECG after RF ablation showing sinus rhythm with a heart rate of 50bpm, QRS axis at +30°,
inverted T waves in lead I and aVL and absence of PVC
Fig. 7.13 A 24-h Holter ECG result recorded 4weeks after the RF ablation procedure showing the absence of PVCs
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Fig. 7.14 MRI images of FIESTA four-chamber view
recorded 12months after the ablation procedure showing
the end-diastolic (left panel) and the end-systolic diame-
Commentary
The present case illustrates a catheter ablation
procedure of PVCs originating from the anterolateral papillary muscle area. Several observations can be made about the present case.
The papillary muscles represent a potential
source of ventricular arrhythmias in both patients
with and without structural heart disease. The
spectrum of this type of ventricular arrhythmia is
wide, ranging from isolated PVCs to sustained
monomorphic VT. They are usually focal and
have characteristic ECG patterns. They can be
benign, but they can also serve as trigger for ventricular brillation and can precipitate SCD [1,
2]. Treatment options include anti-arrhythmic
drugs, with variable response, and catheter ablation. Given the complex anatomy of the papillary
muscles and the technical challenges associated
with this type of catheter ablation procedure
(especially catheter instability at the level of a
continuously moving structure), the success rate
of the ablation procedure is lower compared to
other origins of ventricular arrhythmias [3, 4].
ter (right panel) of the LV.The measured LVEF using the
end-diastolic volume and the end-systolic volume of the
LV was 41%
The papillary muscles are muscular structures
that are part of the subvalvular apparatus that
ensure the correct function of the atrioventricular
valves. For the left ventricle, the anterolateral
papillary muscle inserts at the level of the lateral
LV wall and provides chordae tendineae to the
anterolateral half of both anterior and posterior
mitral leaets; the posteromedial papillary muscle provides chordae tendineae to the posteromedial half of both mitral leaets. The papillary
muscles receive blood supply from the LAD and
the CX coronary arteries or the RCA.The anterolateral papillary muscle receives blood supply
both from the LAD coronary artery and from a
marginal branch of the circumex coronary
artery. The posteromedial papillary muscle
receives blood supply either from the circumex
coronary artery or from the right coronary artery,
depending on dominance. In the above-presented
patient, the most likely cause of PVCs was the
myocardial infarction provoked by the occlusion
of the circumex coronary artery, which resulted
in necrosis at the level of the infero-lateral and
lateral wall of the LV, as evidenced by the scar
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identied by cardiac MRI (Fig.7.5). Other possible etiologies of PVCs arising from the papillary muscles besides myocardial ischemia
include mitral valve prolapse, myocarditis, and
hypertrophic cardiomyopathy, but some are idiopathic [5].
PVCs arising from the papillary muscles have
a distinct morphology on the 12-lead ECG.PVCs
from the anterolateral papillary muscle are characterized by a RBBB morphology and inferior
axis while those from the posteromedial papillary
muscle by a RBBB morphology and superior
axis. They both have a relatively late transition
zone in the precordial leads (in leads V3 or V4).
The differential diagnosis is made with PVCs
originating from the fascicles of the LBB and
with PVCs originating in the myocardium around
the mitral annulus. Elements in favor of fascicular arrhythmias include a narrower QRS width (<
130ms) and an “rR’” pattern in lead V1 [6], as
well as the presence of Q waves in leads I, aVL,
II, III, and aVF.A broader QRS complex and the
absence of an “rR’” aspect in lead V1 are in favor
of a papillary muscle origin. Also, an R/S
ratio<1in lead V6 for the anterolateral papillary
muscle origin and a QRS duration of >160ms for
the posteromedial papillary muscle origin are
other elements in favor of a papillary muscle origin. Q waves in leads I, aVL, II, III, and aVF are
not present in this location. PVCs originating
from the mitral annulus have a positive concordance in the precordial leads.
Catheter ablation of PVCs originating from
the papillary muscles is more difcult compared
to ablation of PVCs originating in other locations. This is mostly related to catheter instability
at the level of the papillary muscles. Useful tools
that can increase the accuracy of the mapping
phase are the use of an electro-anatomical mapping system and that of ICE [6–8]. Catheter stability at the level of the papillary muscle can be
increased using cryo-energy [6, 9, 10]. In the
above-presented case, the CARTO system was
used, which allowed proper identication of the
origin of the PVCs at the level of the anterolateral
papillary muscle.
In patients with a signicant ventricular
arrhythmia burden, the possibility of a PVCinduced cardiomyopathy should be taken into
account. This is a type of reversible cardiomyopathy that is (partially or completely) reversible
after the elimination of the PVC.The diagnosis is
therefore retrospective. The percentage of
patients who develop LV systolic dysfunction as
a consequence of PVCs is directly related to the
ventricular arrhythmia burden. Patients with a
burden of less than 1.000 PVCs/24h have a prevalence of 4% of PVC-induced CMP, compared to
patients who have a PVC burden between 1.000
and 10.000 PVC/24h who have a prevalence of
12%, different from those who have more than
10.000 PVC/24 h, who have a prevalence of
PVC-induced DCM of 34% [11]. In the experience of Baman etal. [12], the lowest PVC burden
that can result in a PVC-induced cardiomyopathy
is 10%. A catheter ablation procedure of PVCs in
a patient with PVCs-induced cardiomyopathy is
presented in Case 1. In the above-presented
patient, the moderate systolic dysfunction could
have been related to the myocardial infarction, to
the high number of PVCs, or both. Given the
absence of increase in the LV EF% post-ablation
after the complete elimination of the PVCs, the
hypothesis of a PVC-induced cardiomyopathy
was eliminated. Therefore, the systolic dysfunction was attributed to the myocardial infarction.
Learning Points
• PVCs originating from the anterolateral
papillary muscle area have a characteristic ECG aspect of RBBB morphology
inferior axis and a wide QRS.
• Treatment options include antiarrhythmic drugs and catheter ablation.
• Catheter ablation is challenging, but
with the existing additional tools such as
the use of an electro-anatomical mapping system and ICE, the success rate
has improved.
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References
1. Van Herendael H, Zado ES, Haqqani H, Tschabrunn
CM, Callans DJ, Frankel DS, etal. Catheter ablation
of ventricular brillation: importance of left ventricular outow tract and papillary muscle triggers. Heart
Rhythm. 2014;11(4):566–73.
2. Santoro F, Di Biase L, Hranitzky P, Sanchez JE,
Santangeli P, Perini AP, etal. Ventricular brillation
triggered by PVCs from papillary muscles: clinical
features and ablation. J Cardiovasc Electrophysiol.
2014;25(11):1158–64.
3. Latchamsetty R, Yokokawa M, Morady F, Kim HM,
Mathew S, Tilz R, etal. Multicenter outcomes for catheter ablation of idiopathic premature ventricular complexes. JACC Clin Electrophysiol. 2015;1(3):116–23.
4. Enriquez A, Supple GE, Marchlinski FE, Garcia
FC.How to map and ablate papillary muscle ventricular arrhythmias. Heart Rhythm. 2017;14(11):1721–8.
5. Kobashi A, Suwa M, Ito T, Otake Y, Hirota Y,
Kawamura K.Solitary papillary muscle hypertrophy
as a possible form of hypertrophic cardiomyopathy.
Jpn Circ J. 1998;62(11):811–6.
6. Kautzner J, Peichl P. Papillary muscle ventricular
tachycardia or ectopy: diagnostics, catheter ablation and the role of intracardiac echocardiography.
Arrhythmia Electrophysiol Rev. 2019;8(1):65–9.
7. Proietti R, Rivera S, Dussault C, Essebag V, Bernier
ML, Ayala-Paredes F, et al. Intracardiac echo-
facilitated 3D electroanatomical mapping of ventricular arrhythmias from the papillary muscles: assessing
the ‘fourth dimension’ during ablation. Europace.
2017;19(1):21–8.
8. Lee A, Hamilton-Craig C, Denman R, Haqqani
HM. Catheter ablation of papillary muscle arrhythmias: implications of mitral valve prolapse and
systolic dysfunction. Pacing Clin Electrophysiol.
2018;41(7):750–8.
9. Gordon JP, Liang JJ, Pathak RK, Zado ES, Garcia
FC, Hutchinson MD, et al. Percutaneous cryoablation for papillary muscle ventricular arrhythmias after
failed radiofrequency catheter ablation. J Cardiovasc
Electrophysiol. 2018;29(12):1654–63.
10. Rivera S, Tomas L, Ricapito MP, Nicolas V, Reinoso
M, Caro M, et al. Updated results on catheter ablation of ventricular arrhythmias arising from the
papillary muscles of the left ventricle. J Arrhythm.
2019;35(1):99–108.
11. Kanei Y, Friedman M, Ogawa N, Hanon S, Lam
P, Schweitzer P. Frequent premature ventricular
complexes originating from the right ventricular
outflow tract are associated with left ventricular dysfunction. Ann Noninvasive Electrocardiol.
2008;13(1):81–5.
12. Baman TS, Lange DC, Ilg KJ, Gupta SK, Liu TY,
Alguire C, et al. Relationship between burden of
premature ventricular complexes and left ventricular
function. Heart Rhythm. 2010;7(7):865–9.
Case 8
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FrédéricHalbwachs, RonanLe Bouar,
CharlineDaval, SerbanSchiau, JacquesLevy,
CrinaMuresan, LucienDiene, ArthurKholer,
andDidierBresson
8
Case Presentation
A 40-year-old male patient was addressed to the
cardiology department for recurrent palpitations. He had a history of fascicular ventricular
tachycardia (reentry in the posterior fascicle)
treated with catheter ablation at the age of 30
years old in another center. Ablation was carried
out in an anatomical manner, since the VT was
not inducible during the electrophysiological
study preceding the ablation. During the ablation procedure, the patient developed complete
LBBB and the HV interval increased to 87ms.
A cardiac MRI performed post-catheter ablation
showed gadolinium late enhancement at the
level of the infero-septal wall of the LV
(Fig. 8.6). Coronary angiography showed no
atherosclerotic lesion at the level of the epicardial coronary arteries. The VT recurred soon
after the ablation procedure. Given the presence
F. Halbwachs (*) · A. Kholer
Biosense Webster, Mulhouse, France
R. Le Bouar · C. Daval · S. Schiau · J. Levy
C. Muresan · L. Diene · D. Bresson
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr;
charline.daval@ghrmsa.fr; serban.schiau@ghrmsa.fr;
levyj@ghrmsa.fr; crina.muresan@ghrmsa.fr;
lucien-leopold.diene@ghrmsa.fr;
didier.bresson@ghrmsa.fr
of LBBB, the long HV interval, and the presence of late gadolinium enhancement at the
level of the inferior wall of the LV, compatible
with myocardial scar, structural heart disease
was considered present, and a single- chamber
ICD was subsequently implanted in the same
center. The patient was treated with verapamil
LR 240mg/day and was discharged home. He
was stable during the following years and presented no VT recurrence at his regular follow-up
visits. However, several years later, he started
presenting palpitations with a rapid rhythm and
regular heart rate.
At physical exam, his blood pressure was
110/68mmHg, heart rate of 75 bpm, SpO2 99%
breathing room air, H=185cm, W=65kg, and
BMI= 18.99 kg/m2, heart sounds were regular,
there were no cardiovascular murmurs, lung auscultation was clear, and there were no signs of
right heart failure.
His ECG at admittance at the cardiology
department is shown in Fig.8.1.
His biological workup showed a Hb level of
13.8g/dL, leukocytes 5.33 × 109/L, platelets 266
× 109/L, CRP<3mg/L, BUN 5.7mmol/L, creatinine 69 μmol/L, glycemia 4.8 mmol/L,
Na+140mmol/L, K+ 3.7mmol/L, NT pro-BNP
168 pg/mL, TSH = 0.87 IU/L, troponin
I < 0.015 ng/mL, total bilirubin 7 μmol/L, and
direct bilirubin 2μmol/L.
© 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_8
117
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Fig. 8.1 A 12-lead ECG showing sinus rhythm with a heart rate of 75bpm, QRS axis at −75°, complete LBBB
F. Halbwachs et al.
Fig. 8.2 Left panel: Transthoracic echocardiography
image showing a mildly dilated left ventricle with an endsystolic diameter of 57mm and paradoxical movement of
Transthoracic echocardiography showed a
mildly dilated left ventricle, ventricle with an
end-systolic diameter of 57 mm with moderate
LV systolic dysfunction, LVEF of 43% (Simpson
biplane method) (Fig.8.2), absence of LV hypertrophy, normal diastolic function, absence of signicant valve disease, non-dilated right ventricle
the interventricular septum. Right panel: Apical twochamber view showing moderate LV systolic dysfunction
with a LVEF of 43% (Simpson biplane method)
and right atrium, and absence of pericardial
effusion.
The chest X-ray showed no signs of heart failure, with the presence of the ventricular lead of
the single-chamber ICD placed at the level of the
RV apex (Fig.8.3).
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Fig. 8.3 Chest X-ray in posteroanterior projection showing the single-chamber ICD with the distal part of the ventricular lead at the level of the RV apex
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Interrogation of his ICD showed the presence
of multiple episodes of sustained VT, treated efciently with burst ventricular pacing (Fig.8.4).
Such an episode is shown in Fig.8.5.
His cardiac MRI from 2010 is shown in
Fig.8.6.
Given the presence of recurrent monomorphic
episodes of ventricular tachycardia, the nonsuitable patient prole for long-term amiodarone
administration, a catheter ablation procedure was
offered and accepted. A cardiac CT angiography
was performed before the ablation procedure,
and the 3D reconstruction of the images was integrated into the CARTO system and used throughout the procedure for guiding the ablation.
Fig. 8.4 Telemetry tracing showing interrogation of the ICD memory demonstrating the presence of a tachycardia
episode classied as VT (episode number 13), treated efciently with one burst ventricular pacing (outlined in red)
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