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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.
Even though initial studies suggested increased
automaticity as the mechanism of the tachycardia,
it is currently believed that the actual mechanism
is reentry. This is the result of abnormal Purkinje
ber conduction in a calcium- dependent circuit
[7–10]. The hypothesis of a false tendon-related
mechanism has also been evoked, with some evidence supporting it [11, 12].
The circuit of fascicular VT is comprised of an
antegrade limb, represented by verapamilsensitive bers situated at the level of the interventricular septum and of a retrograde limb,
represented by the fascicle of the left bundle
branch (Fig.8.16). The lower turnaround point is
usually situated at the junction of the proximal
two-thirds of the IVS with the distal third of the
IVS. The upper turnaround point is situated
below the bifurcation of the left bindle branch
into the anterior and the posterior fascicle [13].
Fascicular VT can arise both in the presence
and absence of structural heart disease. When no
underlying heart disease is present, the term
“idiopathic fascicular VT” is used. One suggested tool to differentiate between fascicular VT
in the presence and in the absence of heart disease is the 12-lead ECG. In patients with idiopathic fascicular VT, the RS interval during VT in
precordial leads is <80ms, unlike in patients with
structural heart disease, where the RS interval is
>80ms [3].
Fascicular VT is a form of VT that is verapamil sensitive [14]. The acute response to verapamil is superior to that of chronic verapamil
administration for the prevention of recurrence.
Propranolol has also been suggested as an alternative long-term treatment [3, 15]. Catheter ablation is an alternative to anti-arrhythmic treatment
in patients with VT recurrence under medical
treatment or in patients who do not desire longterm anti-arrhythmic medication. Its success rate
is reported to be around 80% [3].
Successful catheter ablation requires good
preparation for the procedure. Pre-procedural, a
high index of suspicion based on the 12-lead
ECG is required. At the time of the EP study,
arrhythmia initiation in order to allow activation
mapping during VT is desirable, but, as published
before, the VT may be non-inducible at the time
of the EP study in 25% to 40% of patients [3]. In
these cases, ablation during sinus rhythm is recommended, as described before [13, 16]. This
was also the choice for the above-presented case,
since mapping during VT was impossible, given
the mechanically induced polymorphic nonsustained VT by the Pentaray catheter (Fig.8.13).
When fascicular VT is inducible in the EP lab
and mapping is possible during VT, a Purkinje
potential (P2) is recorded when the mapping
catheter is situated at the level of the fascicle. A
pre-Purkinje (P1) potential is recorded at the
level of the entrance to the verapamil-sensitive
bers at the level of the interventricular septum.
Of note, ablation targeting the earliest ventricular
electrogram during VT has a low to zero chance
of success, since this is situated below the lower
turnaround point of the VT circuit. Entrainment
mapping with xed outputs and pacemapping at
xed outputs are also not helpful in ablating fascicular VT.The P2 potential is the most common
target of ablation. Targeting P1 is also possible,
but with a higher chance of LBBB or even complete AV block.
One particular aspect about the abovepresented case is the presence of fascicular VT in
the context of LBBB.In this particular patient,
LBBB was, most likely, the consequence of a
failed prior ablation procedure, probably due to
ablation performed too proximal on the IVS septum, close to the His bundle, above the upper
turnaround point. However, this case proves the
fact that fascicular VT can exist in the presence of
LBBB.
Learning Points
• Fascicular ventricular tachycardia is a
particular form of VT.
• The most common form is reentry in the
posterior fascicle of the left bundle
branch.
• It has a specic ECG aspect of RBBB
and superior axis, with narrow QRS
complexes.
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• The anti-arrhythmic treatment of choice
is verapamil.
• Catheter ablation is the treatment of
choice in patients refractory to medical
therapy or who do not desire long-term
anti-arrhythmic treatment.
References
1. Prystowsky EN, Padanilam BJ, Joshi S, Fogel
RI. Ventricular arrhythmias in the absence of
structural heart disease. J Am Coll Cardiol.
2012;59(20):1733–44.
2. Lerman BB, Stein KM, Markowitz SM.Mechanisms
of idiopathic left ventricular tachycardia. J Cardiovasc
Electrophysiol. 1997;8(5):571–83.
3. Kapa S, Gaba P, DeSimone CV, Asirvatham
SJ. Fascicular ventricular arrhythmias: pathophysiologic mechanisms, anatomical constructs,
and advances in approaches to management. Circ
Arrhythm Electrophysiol. 2017;10(1):e002476.
4. Al'Aref SJ, Ip JE, Markowitz SM, Liu CF, Thomas
G, Frenkel D, et al. Differentiation of papillary
muscle from fascicular and mitral annular ventricular arrhythmias in patients with and without structural heart disease. Circ Arrhythm Electrophysiol.
2015;8(3):616–24.
5. Good E, Desjardins B, Jongnarangsin K, Oral H,
Chugh A, Ebinger M, etal. Ventricular arrhythmias
originating from a papillary muscle in patients without prior infarction: a comparison with fascicular
arrhythmias. Heart Rhythm. 2008;5(11):1530–7.
6. Deyell MW, Park KM, Han Y, Frankel DS, Dixit S,
Cooper JM, etal. Predictors of recovery of left ventricular dysfunction after ablation of frequent ventricular premature depolarizations. Heart Rhythm.
2012;9(9):1465–72.
131
7. Okumura K, Matsuyama K, Miyagi H, Tsuchiya
T, Yasue H. Entrainment of idiopathic ventricular
tachycardia of left ventricular origin with evidence
for reentry with an area of slow conduction and
effect of verapamil. Am J Cardiol. 1988;62(10 Pt
1):727–32.
8. Lau CP. Radiofrequency ablation of fascicular tachycardia: efcacy of pace-mapping and
implications on tachycardia origin. Int J Cardiol.
1994;46(3):255–65.
9. Nogami A, Naito S, Tada H, Oshima S, Taniguchi
K, Aonuma K, et al. Verapamil-sensitive left anterior fascicular ventricular tachycardia: results of
radiofrequency ablation in six patients. J Cardiovasc
Electrophysiol. 1998;9(12):1269–78.
10. Ouyang F, Cappato R, Ernst S, Goya M, Volkmer
M, Hebe J, et al. Electroanatomic substrate of idiopathic left ventricular tachycardia: unidirectional
block and macroreentry within the purkinje network.
Circulation. 2002;105(4):462–9.
11. Thakur RK, Klein GJ, Sivaram CA, Zardini M,
Schleinkofer DE, Nakagawa H, et al. Anatomic
substrate for idiopathic left ventricular tachycardia.
Circulation. 1996;93(3):497–501.
12. Perry LW, Ruckman RN, Shapiro SR, Kuehl KS,
Galioto FM Jr, Scott LP 3rd. Left ventricular false
tendons in children: prevalence as detected by
2- dimensional echocardiography and clinical signicance. Am J Cardiol. 1983;52(10):1264–6.
13. Ramprakash B, Jaishankar S, Rao HB, Narasimhan
C. Catheter ablation of fascicular ventricular tachycardia. Indian Pacing Electrophysiol J.
2008;8(3):193–202.
14. Belhassen B, Rotmensch HH, Laniado S. Response
of recurrent sustained ventricular tachycardia to verapamil. Br Heart J. 1981;46(6):679–82.
15. Nogami A. Idiopathic left ventricular tachycardia:
assessment and treatment. Card Electrophysiol Rev.
2002;6(4):448–57.
16. Creta A, Chow AW, Sporton S, Finlay M,
Papageorgiou N, Honarbakhsh S, etal. Catheter ablation for fascicular ventricular tachycardia: a systematic review. Int J Cardiol. 2019;276:136–48.
Case 9
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LucianMuresan, FrédéricHalbwachs,
RonanLe Bouar, DidierBresson, LucienDiene,
SerbanSchiau, CrinaMuresan,
andThomasRobein
9
Case Presentation
A 79-year-old male patient was admitted to the
cardiology department for malaise accompanied
by palpitations. He had a past medical history of
two episodes of intracranial hemorrhage, peripheral arterial disease (nonobstructive bilateral
carotid atherosclerosis), COPD, gastroduodenal
ulcer, and gout. His cardiovascular risk factors
were represented by age > 55 years old, a past
history of smoking, arterial hypertension, dyslipidemia, and grade 1 overweight. His medication
at home consisted of clopidogrel 75mg, hydrochlorothiazide 25 mg, lercanidipine 10 mg,
omeprazole 20mg, simvastatin 40mg, allopurinol 200 mg, and oxazepam 10 mg. At physical
examination, his blood pressure was
75/52mmHg, HR 240bpm, and SpO2 97% under
5 L O2/min via nasal cannula, his heart sounds
L. Muresan (*) · R. Le Bouar · D. Bresson
L. Diene · S. Schiau · C. Muresan
Cardiology Department, “Emile Muller” Hospital,
Mulhouse, France
e-mail: LEBOUARR@ghrmsa.fr;
didier.bresson@ghrmsa.fr;
lucien-leopold.diene@ghrmsa.fr;
serban.schiau@ghrmsa.fr; crina.muresan@ghrmsa.fr
F. Halbwachs · T. Robein
Biosense Webster, Mulhouse, France
were rapid and regular, there was no audible murmur, he was in respiratory distress with 25
breaths/min, and he had no signs of right heart
failure.
Due to the unstable hemodynamical nature of
the tachycardia, electrical cardioversion was performed after sedation of the patient (one biphasic
shock of 200J). The ECG post-cardioversion is
presented in Fig.9.1. His ECG before cardioversion is presented in Fig.9.2.
The 12-lead ECG recorded during palpitations
shows a wide QRS complex tachycardia with
LBBB morphology and left inferior axis, with a
HR of 230bpm.
Laboratory tests revealed a Hb of 13.3g/dL,
leukocytes 7.26 × 109/L, platelets 299 × 109/L,
BUN 6.5 mmol/L, creatinine 119 μmol/L, Na
138mmol/L, K 4.3mmol/L, CRP 3mg/dL, glycemia 5.4mmol/L, HbA1c 6.1%, proteins 74g/L,
NT-pro BNP 474pg/mL, cTnI 0.387ng/mL, and
TSH 1.24 mIU/L.
Transthoracic echocardiography was performed, which showed a non-dilated LV, with a
preserved LV EF% of 61% (Fig. 9.3). It also
showed mild hypokinesia of the apical and septoapical segments, slightly increased LV lling
pressure (E/e′ = 12), mild aortic regurgitation,
mild to moderate mitral regurgitation, a mildly
dilated LA (surface of 23 cm2), a non-dilated
right atrium (surface of 16 cm2), a non-dilated
right ventricle, no signs of pulmonary hypertension, and absence of pericardial uid.
© 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_9
133
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Fig. 9.1 A 12-lead ECG showing sinus rhythm with a heart rate of 60bpm, QRS axis at +120°, LAFB, and rst-degree
AV block
L. Muresan et al.
the cTn I, and the presence of localised hypoki-
Question 1: What is the nature of the
tachycardia presented in Fig. 9.1?
A. Scar-related ventricular tachycardia.
B. Bundle branch reentry ventricular
tachycardia.
C. Antidromic tachycardia in WPW
syndrome.
D. AVNRT + functional LBBB.
E. Mahaim-mediated tachycardia.
nesia ony transthoracic echocardiography, ongoing myocardial ischemia was suspected. Coronary
angiography was therefore performed, which
showed no major atherosclerotic plaques at the
level of the epicardial coronary arteries (Fig.9.4).
A cardiac MRI was also performed, which
showed a normal LV systolic function of both
ventricles, absence of arguments in favor of
arrhythmogenic cardiomyopathy, but with an
area of late enhancement present at the level of
the inferior wall of the LV (Fig.9.5).
Based on the 12-lead ECG aspect of the wide
QRS complex tachycardia that raised suspicion
of ventricular tachycardia, the elevated level of
In order to establish the correct diagnosis of
the tachycardia presented in Fig.9.1, an electrophysiological study was performed.
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135
Fig. 9.2 A 12-lead ECG showing a wide QRS complex tachycardia with LBBB morphology and left superior axis,
with a HR of 230bpm
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L. Muresan et al.
Fig. 9.3 Left panel: Echocardiography image showing
in parasternal short-axis view a non-dilated LV with an
end diastolic diameter of 52mm. Right panel: Parasternal
Fig. 9.4 Angiography images of the coronary arteries showing the absence of signicant stenosis of the epicardial vessels. Left panel: Left coronary artery. Right panel: Right coronary artery
short-axis view showing an end systolic diameter of
35mm and a preserved LV EF% of 61%
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137
Fig. 9.5 Left panel: Cardiac MRI image (cine SSFP
short-axis view) showing a non-dilated left and right ventricle, absence of hypertrophy. Right panel: Area of late
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 ventricular 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 in the right common femoral vein and
advanced up to the right atrium. A 6F quadripolar
steerable catheter (Dynamic Extrem, Microport®)
was introduced in a 9F 20cm vascular sheath and
was subsequently advanced via the right common
femoral vein up to the bundle of His. The
CARTO® 3 electro-anatomic mapping system
(Biosense Webster, Johnson & Johnson) was
enhancement present at the level of the inferior wall of the
LV (red arrow)
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®).
The ECG at the beginning of the EP study is
presented in Fig.9.6.
Baseline intervals were AH = 180 ms,
HV=21ms, and HV=74ms.
Programmed ventricular stimulation
(S1=400ms, S2=240ms, S4=280ms) induced
a wide QRS complex tachycardia with a cycle
length of 260ms, with LBBB and right inferior
axis (Fig. 9.7), which was hemodynamically
moderately tolerated (dyspnea, palpitations, and
a systolic blood pressure of 90mmHg). Of note,
the QRS aspect in the precordial leads is identical
to that of the clinical tachycardia, but the limb
leads show a different morphology: inferior axis
for this wide QRS complex tachycardia vs. superior axis for the clinical VT.
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Fig. 9.6 A 12-lead ECG at the beginning of the electrophysiological study showing sinus rhythm, QRS axis at +120°,
LPFB, and rst-degree AV block. Paper speed at 50mm/s
L. Muresan et al.
Fig. 9.7 A 12-lead ECG showing a wide QRS complex tachycardia with LBBB morphology and left inferior axis
induced during programmed ventricular stimulation
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Question 2: What is the explanation for
the identical aspect of the precordial
leads but different aspect in the limb
leads for the two wide QRS complex
tachycardias from Figs. 9.2 and 9.7?
A. Misplacement of the ECG electrodes.
This is actually one and the same
tachycardia.
B. These are two different SVTs with
LBBB aberrancy.
C. This is the same SVT with different
functional bundle branch block.
D. Figure 9.2 shows bundle branch reentry
VT with LAFB and Fig.9.7 shows bundle branch reentry VT with LPFB.
E. I don’t know.
Explanation
The ECG from Fig.9.1 shows sinus rhythm with
LAFB and the ECG from Fig. 9.6 shows sinus
rhythm with LPFB.Given the presence of a positive QRS complex in lead I in Fig.9.1 and of a
negative QRS complex in lead I in Fig.9.6, one
might think that the ECG electrodes are misplaced for the ECG presented in Fig. 9.6.
However, the ECG electrodes are placed correctly for both ECGs, since the P wave is positive
in lead I in both ECGs. This is therefore alternating fascicular block. The ECG recorded during
the wide QRS complex tachycardia from Fig.9.2
has the same fascicular block aspect as in sinus
rhythm in Fig.9.1, and the ECG recorded during
the wide QRS complex tachycardia from Fig.9.7
has the same fascicular block aspect as in sinus
rhythm in Fig.9.6. However, the QRS aspect in
precordial leads during both wide QRS complex
tachycardia is identical. The explanation for the
tachycardia mechanisms is presented in Fig.9.8.
This is therefore bundle branch reentry VT
with LAFB (Fig.9.2) and with LPFB (Fig.9.7).
Ventricular—atrial dissociation was noted
during the tachycardia, conrming its ventricular
origin.
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The tachycardia was terminated by ventricular
overdrive pacing. Programmed ventricular stimulation was performed once again, with the induction of the clinical VT. This is presented in
Fig.9.9. Of note, the His catheter recorded a His
bundle potential preceding each QRS complex
during tachycardia.
Entraining maneuvers were performed: PPI—
TCL at the RV apex was 10ms.
Based on the morphology of the VT on the
12-lead ECG and the abovementioned observations, the diagnosis was bundle branch reentry
tachycardia.
The VT was terminated by two ventricular
extrastimuli.
Next, the ECG in Fig.9.10 was recorded.
Question 3: What is the explanation for
the widening of the third QRS complex
accompanied by the shortening of the
right bundle to ventricle (RB–V)
interval?
A. This is a strong argument in favor of
ventricular preexcitation.
B. This is development of complete septal
fascicular block.
C. The ECG electrodes are misplaced, so
no correct explanation can be offered.
D. Development of complete LBBB, which
abolishes (hidden) retrograde conduction in the right bundle, which recovers
a normal antegrade conduction.
E. This is a late PVC arising from the right
ventricle, depolarizing the ventricles
after the sinus rhythm antegradely depolarized the bundle of His.
Explanation: The rst two QRS complexes
show sinus rhythm with left posterior fascicular
block and rst-degree AV block. The AH and the
HV intervals recorded by the proximal electrodes
of the roving/ablation catheter (Map 3–4) are
prolonged (both suprahisian and infrahisian conduction delays are present). On note, the RB—V
interval recorded by the roving/ablation catheter
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RB
RB
LPF
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Fig. 9.8 Left upper
panel: Diagram
representing the
depolarization of the LV
during sinus rhythm in
Fig.9.1. Right upper
panel: Diagram
representing the
depolarization of the LV
during VT in Fig.9.2.
Left lower panel:
Diagram representing
the depolarization of the
LV during sinus rhythm
in Fig.9.6. Right lower
panel: Diagram
representing the
depolarization of the LV
during VT in Fig.9.7.
AVNatrioventricular
node, HBhis bundle,
RBright bundle, LBleft
bundle, LAFleft anterior
fascicle, LPFleft
posterior fascicle
AVN
HB
AVN
LAF
LB
LPF
RB
L. Muresan et al.
AVN
HB
LB
LPF
LAF
AVN
HB
LAF
LB
LPF
RB
HB
LB
LAF
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