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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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141
Fig. 9.9 ECG recorded during VT showing surface leads
I, II, III, V1, V2, and V6 and intracavitary leads His d, His
p, Vp 1, and Vp 2. The cycle length of the VT is 250ms,
identical to that of the clinical VT.It is worth noting that a
His deection precedes every QRS complex (red arrows),
(Map 1,2 red color) is prolonged and the QRS is
narrow. The third QRS complex is wide (>
120 ms), and the PR interval narrows, even
though it remains prolonged >200ms. This is due
to the fact that the RB–V interval narrows, even
though the AH recorded by the proximal pair of
the roving/ablation catheter electrodes does not
change. But why does the RB–V interval narrow
with the widening of the QRS complex? Two
explanations are possible: The rst explanation is
that during the rst two QRS complexes there is
hidden retrograde conduction from the left anterior fascicle into the distal part of the right bundle
branch, and with the development of complete
left bundle branch block, there is no more retro-
one argument in favor of bundle branch reentry
VT. His = distal electrodes of the His catheter; His
p=proximal electrodes of the His catheter; Vp 1= the
distal electrodes of the RV catheter; and Vp 2=the proximal electrodes of the His catheter
grade conduction in the right bundle, which
recovers a normal antegrade conduction, which
explains the shorter RB–V interval recorded during the third QRS complex. However, this explanation would require the presence of a right
bundle branch block aspect for the rst two QRS
complexes, which is not the case. Therefore, this
explanation is probably not true. The second
explanation would be that of a late-coupled PVC,
mechanically induced by the ablation catheter
which is placed at the level of the right bundle
branch. This would explain both the QRS widening with the aspect of LBBB, and, since it is
occurring late, after the depolarization of the His,
the RB–V interval is short.
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Fig. 9.10 A 12-lead
ECG recorded from the
CARTO screen together
with the bipolar
recording of the distal
electrode of the roving/
ablation catheter placed
at the level of the right
bundle (MAP 1–2, in
red). The proximal pair
of the roving/ablation
catheter electrodes is
placed at the level of the
bundle of His
L. Muresan et al.
The hypothesis of ventricular preexcitation
is not conrmed; since this is the only beat with
a shorter HV interval, the rest of the times it is
prolonged. The ECG electrodes are not misplaced, since the P wave is positive in lead
I. And this is not left septal fascicular block
either, since the QRS width is over 120ms, and
there are no prominent anterior QRS forces in
the horizontal plane. This is therefore a latecoupled, mechanically induced PVC from the
area of the proximal right bundle branch. The
resulting QRS complex is a fusion between the
QRS in sinus rhythm and the locally induced
QRS morphology.
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Question 4: What would be the best
treatment option for this patient?
A. Catheter ablation of the right bundle
branch.
B. Catheter ablation of the left bundle
branch.
C. No ablation should be performed.
Amiodarone should be recommended
instead.
D. No ablation should be performed. ICD
implantation should be recommended
instead.
E. I don’t know.
The best treatment option for bundle branch
reentry VT is catheter ablation. Anti-arrhythmic
drugs are often not efcient and recurrences are
not rare. Therefore, catheter ablation was decided.
Considered options were (1) ablation of the right
bundle branch and (2) ablation of the left bundle
143
branch. Given the lower risk of vascular complications associated with ablation of the right bundle branch, the lower risk of systemic embolism,
and a potential less deleterious effect on the LV
function, ablation of the right bundle was therefore decided as the next step in the management
of the VT.
With the help of the CARTO system, an
anatomical map of the RV was initially created. Next, an activation map of the right ventricle during sinus rhythm was created.
Identication of the His bundle, the right bundle, and Purkinje network was subsequently
performed during sinus rhythm, by placing the
ablation catheter at the level of the septal wall
of the RV and carefully searching for sites
where a sharp local electrogram preceded the
local bipolar ventricular electrogram. This is
presented in Fig.9.11.
Next, programmed ventricular stimulation
was performed with the induction of the clinical
VT.
Fig. 9.11 CARTO image shoving a prolonged HV interval during SR of 74 ms (left panel). Right panel:
Activation map of the RV during SR from a postero-septal
view. Orange dot=the His bundle, the yellow line corresponds to the anatomical trajectory of the right bundle,
conrmed by the presence of right bundle branch poten-
tials at this level. The activation of the right ventricle in
sinus rhythm commences at the apex, at the site of insertion of the right bundle into the ventricular myocardium
(red area), and proceeds toward the base of the ventricle
(violet area). The color legend is presented in the top right
part of the image
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L. Muresan et al.
During VT, the ablation catheter was placed at
the level of the right bundle, where it recorded a
right bundle branch electrogram (Fig.9.12).
RF ablation of the right bundle was performed
with titration of power from 20W to 30W, with
an ablation index target of 330. Ablation was performed during VT.The tachycardia is terminated
during ablation and a complete right bundle
branch block was observed on the ECG.
The RV map post-ablation together with the
12-lead ECG post-ablation is shown in Fig.9.13.
Programmed ventricular stimulation of up to
three extrastimuli, at the level of the RV apex,
and RVOT did not induce any ventricular
arrhythmias.
The HV interval post-ablation measured
100ms. The 12-lead ECG post-ablation is shown
in Fig.9.14.
Given the presence of RBBB, LAFB, and
rst-degree AV block and of a prolonged HV
interval of 100ms, the implantation of a device
capable of ventricular pacing was decided.
Question 5: What kind of a device would
you implant in this patient?
A. A dual-chamber pacemaker.
B. A dual-chamber ICD.
C. A single-chamber ICD.
D. A CRT-D device.
E. A CRT-P device.
Given the normal LVEF%, implantation of a
CRT device was considered not justied. Also,
given the very low recurrence rate of bundle
Fig. 9.12 Left panel: Surface ECG during the wide QRS
complex tachycardia together with an intracavitary lead
(blue) recording from the roving/ablation catheter situated
at the level of the His bundle. This is conrmed by the His
potential recorded at this level (red arrow). The HV interval was 85 ms, identical to the HV interval in sinus
rhythm. Right panel: Anatomical map of the RV from a
posterior and septal view showing the His bundle (orange
dots) and the right bundle (light blue dots). The orange
line represents the theoretical position of the right bundle
branch
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Fig. 9.13 Left panel: The roving/ablation catheter
placed at the level of the His bundle. From this position,
the catheter is slightly and gently pushed toward the RV
apex, at the level of the right bundle, in an area away from
the His bundle, but where right bundle branch potentials
Fig. 9.14 A 12-lead ECG after the ablation of the right bundle branch, showing sinus rhythm heart rate of 75bpm,
QRS axis at −90°, RBBB, LAFB, and rst-degree AV block
are still recorded (H, V, but no A). White dots and red dot
represent RF lesions. Right panel: A 12-lead ECG after
the ablation of the right bundle branch. Note the presence
of RBBB, LPFB, and rst-degree AV block
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L. Muresan et al.
branch reentry VT post-ablation of the right bundle, an ICD implantation was not considered
compulsory. Therefore, implantation of a dualchamber pacemaker was decided.
The chest X-ray post-pacemaker implantation
is shown in Fig.9.15.
Fig. 9.15 Chest X-ray showing the presence of a dualchamber pacemaker with the distal part of the atrial lead at
the level of the right atrial appendage and the distal part of
the ventricular lead at the level of the right ventricular
septum
The 12-lead ECG recorded post-pacemaker
implantation is shown in Fig.9.16.
The patient was discharged from the hospital
48h after the pacemaker implantation.
Pacemaker follow-up at 24months showed no
VT recurrence.
Answers
Question 1: B. Bundle branch reentry
ventricular tachycardia.
Question 2: D.Figure 9.2 shows bundle branch reentry VT with LAFB and
Fig. 9.7 shows bundle branch reentry VT
with LPFB.
Question 3: E.This is a late PVC arising from the right ventricle, depolarizing
the ventricles after the sinus rhythm
antegradely depolarized the bundle of
His.
Question 4: A.Ablation of the right
bundle branch.
Question 5: A. A dual-chamber
pacemaker.
Fig. 9.16 A 12-lead ECG post-pacemaker implantation showing sinus rhythm with paced ventricular QRS complexes
(As Vp), with a heart rate of 70bpm
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Commentary
The present case illustrates a catheter ablation
procedure of bundle branch reentrant ventricular
tachycardia in a 79-year-old male patient with no
signicant past medical history. Several observations merit further comments.
Bundle branch reentrant ventricular tachycardia is a rare type of VT that has as a specic trait
the involvement of the conduction system in the
mechanism of the tachycardia [1]. It is usually
present in patients with structural heart disease,
such as dilated or ischemic cardiomyopathy, or in
patients with valvular heart disease [2–4], but
exceptionally it can be present in patients without
structural heart disease [5, 6]. The presence of
His–Purkinje disease can, under certain circumstances, determine the appearance of transient
unidirectional block in one of the bundle
branches, and this can favor the development of
reentry between the two branches.
The 12-lead ECG of patients with bundle
branch reentrant VT recorded during sinus
rhythm typically shows conduction delay, usually
right or left bundle branch block [3, 7]. Clinical
manifestations include pre-syncope or syncope,
due to the fast heart rates of the VT, but palpitations, dyspnea, or chest pain can also be present.
The 12-lead ECG during ventricular tachycardia
shows a wide QRS complex tachycardia, usually
of a LBBB aspect, which may be identical to that
recorded during sinus rhythm. RBBB morphology is also possible but is rarer [8].
When LBBB pattern is present during VT, the
differential diagnosis of the wide QRS complex
tachycardia includes ventricular tachycardia
(myocardial VT, bundle branch reentry VT, or
interfascicular reentry VT), supraventricular
tachycardia (atrial tachycardia, AVNRT, ORT)
with aberrancy, atrial utter with 1:1 AV conduction, and ventricular preexcitation. For a denite
diagnosis, an electrophysiological study is most
of the times needed. In the case of bundle branch
reentrant VT, this usually shows the presence of a
prolonged HV interval during sinus rhythm (>
70 ms), even though rare cases of HV interval
within normal limits have been reported. The HV
interval during tachycardia is equal to or greater
than the HV interval recorded during sinus
rhythm. The denite diagnosis of VT is established by proving the participation of the His–
Purkinje system to the tachycardia mechanism.
The presence of a His electrogram before each V
during tachycardia should raise suspicion of bundle branch reentrant VT.VA dissociation can rule
out ORT with aberrancy (even though ORT using
nodo-fascicular/ventricular bers can exist in the
presence of VA dissociation [9]). PPI—TCL at
the RV apex is usually <30ms. Atrial pacing during tachycardia can entrain bundle branch reentry
VT.
The differential diagnosis of bundle branch
reentry VT and interfascicular reentry VT (reentry between the superior and inferior fascicles of
the left bundle) can be challenging. Patients with
interfascicular reentry VT usually exhibit right
bundle branch block and left anterior or left posterior fascicular block during sinus rhythm. The
tachycardia usually has RBBB morphology. The
antegrade limb of the tachycardia is either the left
anterior or the left posterior fascicle, and the posterior limb is the opposite fascicle. Features that
distinguish bundle branch reentry VT from interfascicular reentry VT are a shorter HV interval
during VT than during sinus rhythm in the case of
interfascicular reentry VT and the presence of a
left bundle branch potential before each His
deection during VT for interfascicular reentry
VT. In the case of our patient, the HV interval
during VT was the same as that during sinus
rhythm, argument in favor of bundle branch reentry VT. Also, he had no RBBB during sinus
rhythm, and the tachycardia did not have a RBBB
aspect (even though this does not exclude interfascicular reentry).
The best treatment option of bundle branch
reentrant VT is catheter ablation, due to the poor
response of this type of VT to anti-arrhythmic
drugs [10–14]. Any of the two bundles can be targeted, but the right bundle is usually the bundle
of choice. The risk of developing high-degree AV
block or complete AV block requiring pacemaker
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implantation is reported to be up to 30%. The
long-term prognostic of the patient is dependent
on the underlying heart disease. Patients with
severely depressed LV systolic function are candidates for ICD implantation.
In the above-presented patient, a particular
nding is the presence of a structurally normal
heart, as evidenced by the transthoracic echocardiography, the coronary angiography, and the
cardiac MRI.The LV EF was 61%. Also, interestingly, the 12-lead ECG during sinus rhythm
did not show the presence of BBB.It showed the
presence of rst-degree AV block and left anterior fascicular block. The EP study conrmed the
presence of a prolonged HV interval, of 74ms.
The intracavitary ECGs during tachycardia
showed in Figs. 9.9 and 9.11 demonstrate the
presence of a His electrogram before each ventricular electrogram. Ablation of the RBBB was
performed, with appearance of a typical RBBB
aspect on the 12-lead ECG, without complete AV
block. However, given the presence of prolonged
HV interval post-ablation of 100ms, implantation of a pacemaker was considered appropriate.
Given the non-inducibility of VT post-ablation
and the normal LV EF%, as well as the low recurrence rate post-ablation, no ICD was implanted.
The preserved LV EF% did not justify the implantation of a CRT device.
Learning Points
• Bundle branch reentrant ventricular
tachycardia is a particular rare type of
VT that involves the conduction system
of the heart.
• It is more frequently found in patients
with structural heart disease.
• It usually has fast heart rates, which
explains its clinical poorly tolerated
nature.
• The 12-lead ECG during sinus rhythm
usually shows bundle branch block.
• The ECG during tachycardia usually
shows LBBB and may be identical to
the one in sinus rhythm.
L. Muresan et al.
• The differential diagnosis of a wide
QRS complex tachycardia with LBBB
morphology should always take into
account bundle branch reentrant VT.
• During the EP study, the HV interval is
usually prolonged during sinus rhythm.
The HV interval during VT is equal to or
greater than the HV during sinus rhythm.
• Catheter ablation is the treatment of
choice. The RBB is usually targeted for
ablation.
• A high number of patients will require a
pacemaker or an ICD implantation postablation, due to advanced AV block
post-ablation and the underlying heart
disease, which dictate prognosis.
References
1. Tchou P, Jazayeri M, Caceres JA.Bundle branch reentrant ventricular tachycardia. Am Heart J. 1988;116(6
Pt 1):1647–8.
2. Barra S, Moreno N, Providencia R, Goncalves H,
Primo JJ. Incessant slow bundle branch reentrant
ventricular tachycardia in a young patient with
left ventricular noncompaction. Rev Port Cardiol.
2013;32(6):523–9.
3. Mazur A, Kusniec J, Strasberg B. Bundle branch
reentrant ventricular tachycardia. Indian Pacing
Electrophysiol J. 2005;5(2):86–95.
4. Shan QJ, Chen ML, Zou JG. The incessant bundle
branch reentrant ventricular tachycardia in a patient
with aortic valve replacement: a case report. Zhonghua
Xin Xue Guan Bing Za Zhi. 2007;35(10):960–2.
5. Chen H, Shi L, Yang B, Ju W, Zhang F, Yang G,
et al. Electrophysiological characteristics of bundle
branch reentry ventricular tachycardia in patients
without structural heart disease. Circ Arrhythm
Electrophysiol. 2018;11(7):e006049.
6. Mazur A, Iakobishvili Z, Kusniec J, Strasberg
B.Bundle branch reentrant ventricular tachycardia in a
patient with the Brugada electrocardiographic pattern.
Ann Noninvasive Electrocardiol. 2003;8(4):352–5.
7. Balasundaram R, Rao HB, Kalavakolanu S,
Narasimhan C. Catheter ablation of bundle branch
reentrant ventricular tachycardia. Heart Rhythm.
2008;5(6 Suppl):S68–72.
8. Mizusawa Y, Sakurada H, Nishizaki M,
Ueda- Tatsumoto A, Fukamizu S, Hiraoka
M. Characteristics of bundle branch reentrant ven-
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tricular tachycardia with a right bundle branch block
conguration: feasibility of atrial pacing. Europace.
2009;11(9):1208–13.
9. 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.
10. Blanck Z, Deshpande S, Jazayeri MR, Akhtar
M. Catheter ablation of the left bundle branch for
the treatment of sustained bundle branch reentrant
ventricular tachycardia. J Cardiovasc Electrophysiol.
1995;6(1):40–3.
11. Blanck Z, Dhala A, Deshpande S, Sra J, Jazayeri
M, Akhtar M. Bundle branch reentrant ventricular
tachycardia: cumulative experience in 48 patients. J
Cardiovasc Electrophysiol. 1993;4(3):253–62.
12. Cohen TJ, Chien WW, Lurie KG, Young C, Goldberg
HR, Wang YS, etal. Radiofrequency catheter ablation
for treatment of bundle branch reentrant ventricular
tachycardia: results and long-term follow-up. J Am
Coll Cardiol. 1991;18(7):1767–73.
13. Mehdirad AA, Keim S, Rist K, Tchou P. Long-term
clinical outcome of right bundle branch radiofrequency catheter ablation for treatment of bundle
branch reentrant ventricular tachycardia. Pacing Clin
Electrophysiol. 1995;18(12 Pt 1):2135–43.
14. Petrac D, Radic B, Vukosavic D.Radiofrequency catheter ablation of the bundle branch reentrant ventricular
tachycardia. Acta Med Austriaca. 2001;28(1):16–20.
Case 10
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RonanLe Bouar, FrédéricHalbwachs,
Jean- YvesWiedemann, TarekEl Nazer,
NicolasBourrelly, LaurentJacquemin,
andOlivierRoth
10
Case Presentation
A 59-year-old male patient with no signicant
past medical history was addressed to the cardiology department for cardiovascular evaluation and
treatment due to one recent episode of syncope
on exertion (table tennis match). The syncope
was preceded by a short episode of palpitations
with sudden onset, with a rapid and regular
rhythm. Recovery was spontaneous, and there
was no post-critical neurologic decit or postcritical confusion. His cardiovascular risk factors
were represented by age (> 55years). He was on
no chronic treatment. Physical examination at
admission revealed a blood pressure of
112/63 mmHg, heart rate of 64 bpm, SpO2 of
Supplementary Information The online version contains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 35579- 0_10.
R. Le Bouar (*) · J.-Y. Wiedemann · T. El Nazer ·
N. Bourrelly · L. Jacquemin · O. Roth
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr;
wiedemannjy@ghrmsa.fr; tarek.elnazer@ghrmsa.fr;
bourrellyn@ghrmsa.fr; jacqueminl@ghrmsa.fr;
rotho@ghrmsa.fr
F. Halbwachs
Biosense Webster, Mulhouse, France
98% breathing room air, H=1.74m, W=70kg,
and BMI=23.12kg/m2, heart sounds were regular, cardiac auscultation did not reveal any murmurs, lung auscultation was clear, and there were
no signs of right heart failure.
His 12-lead ECG is presented in Fig.10.1.
His echocardiography revealed a non-dilated
left ventricle, with a LVEF of 75%, absence of
LV hypertrophy, normal diastolic function,
absence of signicant valve disease, a mildly
dilated right ventricle, with preserved longitudinal systolic function (TAPSE of 26mm, lateral
tricuspid annulus S wave of 13cm/s), mild tricuspid regurgitation, absence of pulmonary hypertension, sPAP of 20 mmHg, and no pericardial
effusion (Fig.10.2).
His biological workup showed a Hb level of
14.6g/dL, leukocytes 5.92 × 109/L, platelets 165
× 109/L, CRP 5mg/L, BUN 5.2mmol/L, creatinine79 μmol/L, glycemia 5.1 mmol/L,
Na+139mmol/L, K+ 4.2mmol/L, NT pro-BNP
56 pg/mL, TSH 4.37 IU/L, total cholesterol
259 mg/dL, HDL 48 mg/dL, LDL 184 mg/dL,
triglycerides 131mg/dL, troponin I 0.026ng/mL,
and HbA1c 5.8%.
An exercise stress test was performed which
was stopped at 101% of the theoretical maximum
heart rate for fatigue, 8.6 METS, 175W, which
showed absence of inducible ischemia, with persistence of isolated polymorphic PVC during
© 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_10
151
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