Download Idiopathic fascicular left ventricular tachycardia: Linear

Idiopathic fascicular left ventricular tachycardia: Linear
ablation lesion strategy for noninducible or nonsustained
tachycardia
David Lin, MD,a Henry H. Hsia, MD,a Edward P. Gerstenfeld, MD,a Sanjay Dixit, MD,a
David J. Callans, MD,a Hemal Nayak, MD,a Andrea Russo, MD,b
Francis E. Marchlinski, MDa
a
From the Hospital of the University of Pennsylvania, University of Pennsylvania Health Systems, Department of
Medicine, Electrophysiology Section, Philadelphia, Pennsylvania, and
b
University of Pennsylvania-Presbyterian Medical Center, University of Pennsylvania Health Systems, Department of
Medicine, Electrophysiology Section, Philadelphia, Pennsylvania.
BACKGROUND Idiopathic “fascicular” left ventricular tachycardia (IFLVT) is frequently not inducible
or nonsustained at the time of planned catheter ablation. The mechanism of the arrhythmia has been
suggested to be reentry involving a sizable area of the LV inferior septum extending from base toward
the apex.
OBJECTIVE We tested the ability of a series of radiofrequency lesions delivered in a linear fashion to
the inferior-mid septum to control ventricular tachycardia not amenable to standard mapping ablation
strategies.
METHODS Programmed stimulation both at baseline state and with isoproterenol after heart rate was
increased by at least 25% was performed in all patients. The patients included in the study were either
non-inducible or only had brief nonsustained VT not amenable to “traditional” mapping. A detailed
electroanatomic map of the LV was performed in sinus rhythm. The location of the linear lesion along
the inferior septum was guided by the presence of Purkinje potentials, with pacemapping as an
additional guide. A linear lesion was placed perpendicular to the long axis of the ventricle approximately midway from the base to the apex in the region of the mid to mid-inferior septum. Radiofrequency lesions were delivered using a 4mm tip catheter at 50 Watts and 52 degrees for 60 –90 seconds.
RESULTS Of 122 consecutive patients who underwent ablation of idiopathic VT from 1999 to 2003, 15
had IFLVT based on standard diagnostic criteria. Six of the 15 patients (40%) had nonsustained or no
inducible VT in the EP lab. The number of RF lesions ranged from 7 to 15 (mean 9). The length of the
effective linear lesion ranged from 1.2 to 2.2 cm (mean 1.7 cm). Developement of left posterior
fascicular block was noted in two of the six patients. However, despite the absence of development of
left posterior fascicular block in the other four patients, no VT or premature ventricular beats could be
induced after ablation using the same provocation maneuvers as performed in the baseline state. No
spontaneous arrhythmias occurred during follow-up to 16 ⫾ 8 months (range 6 to 30 months).
CONCLUSION In patients with difficult to induce or nonsustained VT with the typical right bundle
branch block pattern and a superiorly directed axis on 12-lead ECG, RF energy ablation delivered in
a linear fashion approximately midway to two thirds toward the apex along the mid to inferior septum
and perpendicular to the plane of the septum is safe and effective for VT control.
KEYWORDS Ventricular tachycardia; Ablation; Fascicular
(Heart Rhythm 2005;2:934 –939) © 2005 Heart Rhythm Society. All rights reserved.
Introduction
Address reprint requests and correspondence: Dr. David Lin, Arrhythmia Section, Cardiovascular Division, Hospital of the University of
Pennsylvania, University of Pennsylvania Health Systems, 3400 Spruce
Street, Philadelphia, Pennsylvania 19104.
E-mail address: [email protected].
(Received March 8, 2005; accepted June 14, 2005.)
Idiopathic fascicular left ventricular tachycardia was first
described as an electrocardiographic entity by Zipes et al1
and subsequently as a clinical entity by Lin et al.2 The
tachycardia originates in the region of the left posterior
fascicle of the left bundle and is characterized by a right
1547-5271/$ -see front matter © 2005 Heart Rhythm Society. All rights reserved.
doi:10.1016/j.hrthm.2005.06.009
Lin et al
Idiopathic Fascicular Left Ventricular Tachycardia
Figure 1 ECG showing the right bundle branch block, left
superiorly directed axis pattern typical of left posterior fascicular
ventricular tachycardia. Despite administration of isoproterenol
10 ␮g/min, only infrequent premature ventricular complexes were
induced.
bundle branch block morphology with left-axis deviation
that is superiorly directed.1–5 Pharmacologic studies have
found that these tachycardias are often sensitive to verapamil.3 The mechanism of the sustained arrhythmia has
been suggested to be reentry involving a sizable area of the
left ventricular inferior septum extending from base toward
the apex, with the superficial endocardial Purkinje network
participating in the circuit. Application of radiofrequency
energy during ventricular tachycardia (VT) to the mid or
inferior apical left ventricular septum targeting presystolic
Purkinje potential is highly effective in treating this arrhythmia.6 –9 However, a major limitation of this technique is that
the VT must be inducible and sustainable to allow mapping.
Unfortunately, idiopathic fascicular left ventricular tachycardia frequently is not inducible or is nonsustained at the
time of planned catheter ablation. Given the anticipated
anatomically determined nature and location of the VT
circuit in this setting, we hypothesized that creation of
radiofrequency lesions in a linear fashion targeting the endocardial mid-inferior septum of the left ventricle (LV)
would be an effective strategy for targeting nonsustained or
noninducible idiopathic left ventricular tachycardia.
935
Figure 2 Intracardiac electrograms showing the presence of
Purkinje potentials during both sinus beats (solid arrows) and
premature ventricular complexes (broken arrows).
nonsustained or noninducible VT in the electrophysiology
laboratory. Twelve-lead ECG from each of these patients
documented a wide complex tachycardia with a typical right
bundle branch block morphology and left-axis deviation
that was superiorly directed, consistent with a left posterior
fascicular VT (Figure 1). These six patients are the subject
of this report.
The study patients underwent electrophysiologic evaluation after providing informed consent. All procedures were
performed following the institutional guidelines of the University of Pennsylvania Health System. After discontinuation of the antiarrhythmic agents for at least five half-lives,
vascular access was obtained via the right femoral vein and
artery. Three standard 6Fr Josephson quadripolar electrode
nondeflectable catheters were placed percutaneously via the
femoral veins to the high right atrium, His-bundle region,
and right ventricular apex. A deflectable 4-mm CARTO
ablation catheter (Biosense-Webster, Diamond Bar, CA,
USA) was placed via the right femoral artery and advanced
retrograde into the LV. A bolus of heparin (80 U/kg) was
Methods
A total of 122 patients underwent ablation of idiopathic VT
at our center between January 1999 and December 2003. Of
this group, 88 (72%) of the 122 patients had a site of origin
localized to the outflow tract region. Of the remaining patients, 15 had fascicular VT based on standard diagnostic
criteria.
Of the 15 patients with fascicular VT, nine had inducible
and sustainable VTs that were successfully ablated using
“traditional” methods.6 –11 The remaining six patients (one
female; age range 17 to 46 years) had structurally normal
hearts and clinically documented VT but had only brief
Figure 3 Intracardiac recordings showing the presence of Purkinje potentials at the site of best pace map at site of radiofrequency delivery.
936
Heart Rhythm, Vol 2, No 9, September 2005
pared to the clinical VT (Figures 4 and 5). Attempts to
reinduce VT via ventricular programmed electrical stimulation were repeated using the protocol described from the
mapping catheter at the sites where Purkinje potentials were
localized during sinus rhythm to confirm their presence
during VT.
Mapping and ablation
Figure 4 Pace map obtained at the site of Purkinje potential
recordings (left) closely resembling, but not a perfect match to, the
clinical premature ventricular complexes (right).
administered intravenously with access of the systemic circulation and titrated to maintain an activated clotting time
between 250 and 300 seconds.
Baseline electrophysiologic measurements were obtained. Programmed stimulation at twice diastolic threshold
amplitude with 2-ms pulse width from the high right atrium
and the right and left ventricles was performed with up to
three extrastimuli, followed by ventricular burst pacing for
15 intervals at cycle lengths of 350 to 250 ms. If VT was not
induced, an infusion of isoproterenol (1–10 ␮g/min) was initiated and titrated until a heart rate increase ⬎25% from baseline or maximum tolerated dose (up to 10 ␮g/min) was
achieved. The mean isoproterenol dose was 5 ␮g/min (range
2–10 ␮g/min). Repeat programmed stimulation was performed
once an adequate heart rate response was noted. If VT was
induced and sustained and was hemodynamically tolerated,
three-dimensional electroanatomic activation mapping was
performed using the CARTO system. Right and left ventricular
voltage mapping was performed during sinus rhythm to confirm the absence of abnormal myocardium characterized by
confluent areas of low voltage (⬍1.5 mV) and to establish a
template for localizing radiofrequency lesion placement. If the
VT was either noninducible or nonsustained despite the
described methodologies, mapping of the LV to localize
regions with Purkinje potentials was performed during sinus
rhythm (Figures 2 and 3). Pace mapping at sites where
Purkinje potentials were recorded was performed and com-
A detailed (⬎150 points) three-dimensional electroanatomic map of the LV was performed in each patient. Radiofrequency energy lesions were placed perpendicularly to
the long axis of the ventricle, approximately midway from
the base to the apex in the region of the mid to mid-inferior
apical septum of the LV (Josephson site 2/3), and further
guided by the presence of Purkinje potentials (Figure 6).
Pace mapping before each radiofrequency energy delivery
was performed and compared with the clinically documented VT. However, a “perfect” pace map was not a
necessary requirement for energy delivery. The maximum
line length extended from the mid septum to the junction of
the septum with the inferior free wall of the LV. Each
radiofrequency lesion was delivered via a 4-mm-tip electrode for 60 to 90 seconds at 50 W achieving a maximum
temperature of 52°C.
Programmed stimulation and isoproterenol infusion were
repeated after a single point lesion in three patients and after
the line was completed in all six patients. Successful ablation was defined as noninducibility of any VT or premature
ventricular complexes (PVCs) both with and without isoproterenol using the same protocol as preablation.
Figure 5 Different patient demonstrating a perfect pace map (12
of 12 lead match) obtained at the site of Purkinje potential recordings (left) compared with the clinical ventricular tachycardia
(right).
Lin et al
Idiopathic Fascicular Left Ventricular Tachycardia
937
in all but the last patient studied far exceeds the anticipated
spontaneous VT frequency noted prior to the study.
Discussion
Figure 6 Three-dimensional electroanatomic map of the left
ventricle from the left anterior oblique (LAO) and right anterior
oblique (RAO) projections and the corresponding fluoroscopic
images at 45° LAO and 30° RAO. The line of small red circles
represents the location of radiofrequency energy delivery in a
linear fashion.
Results
Baseline intracardiac measurements demonstrated normal
AH and HV intervals. Two of the six patients had undergone previous ablation attempts at other institutions. Three
of the patients had easily inducible VT with burst pacing at
baseline. However, after initial activation mapping, the VT
became nonsustained despite all attempts at aggressive
pharmacologic stimulation and programmed stimulation.
Two of the patients had only brief nonsustained VT that was
induced. The last patient had VT that terminated and became noninducible while mapping along the apical inferior
portion of the left ventricular septum. The number of RF
lesions ranged from 7 to 15 (mean 9). The length of the
effective linear lesion ranged from 1.2 to 2.2 cm (mean 1.7).
Development of left posterior fascicular block was noted in
two of the six patients. However, despite the absence of
development of left posterior fascicular block in the other
four patients, no VT or PVCs were inducible postablation
using the same provocation maneuvers as performed in the
baseline state and after a single point lesion in the three
patients tested. Mean fluoroscopy time was 39.6 minutes
(range 22– 68). Mean duration time as defined by catheter
insertion to time of catheter removal was 75 minutes (range
55–145). There were no procedure-related complications.
Of the six patients who underwent the ablation procedure
using the technique described, none experienced recurrence
after follow-up of 16 ⫾ 8 months (range 6 –30). Follow-up
We describe a new technique for ablation of idiopathic left
posterior fascicular VT. Although many patients have inducible sustained VT in the electrophysiology laboratory,
the VTs in some patients are noninducible or are only brief
and characterized by nonsustained paroxysms that preclude
detailed activation mapping. Pace mapping alone can be
successful in some of these patients. However, the limitations of pace mapping and the difficulty in achieving a 12 of
12 ECG match forced us to consider an alternative strategy.
Based on the evidence supporting (1) a reentrant mechanism
for the VT, (2) a circuit that likely is of considerable size
involving the apical to basal extent of the inferior left
interventricular septum, and (3) a circuit that either incorporated or was in close proximity to the Purkinje network,
we hypothesized that such a circuit of considerable dimension should be effectively interrupted by a linear ablation
lesion that transected this region.
In a consecutive series of six patients, we found that we
could provide VT control by targeting a region of the left
ventricular mid-inferior septal endocardium marked by the
presence of Purkinje potentials in sinus rhythm and the best
pace map match of the VT and then creating a linear lesion of
significant dimension perpendicular to the long axis of the
septum in this region from the mid septum to the inferior wall.
Background and rationale
VT occurring in the absence of structural heart disease or
any identifiable cause accounts for approximately 10% to
15% of clinical VTs. An uncommon type of idiopathic VT
can originate from the left posterior fascicle of the left
bundle branch. Various techniques involving activation
mapping and identification of the earliest pre-QRS Purkinje
potentials during VT have been described, and focal ablation at these sites has been shown to be highly effective.6 –10
However, many of the previously described mapping techniques are dependent on inducibility of sustained VT. Because many of the fascicular VTs involve a rather superficial circuit in the inferior apical region of the septum, it is
not unusual for the VT to be rendered nonsustained or even
noninducible by virtue of mechanical “bump” during the
mapping process. This observation has also been described
by others.11–13 Furthermore, VT sometimes is nonsustained
or is not inducible despite pharmacologic provocation.
These obstacles often lead to aborted radiofrequency ablation procedures or VT recurrences after initial apparent
success.
The underlying mechanism of idiopathic fascicular left
ventricular tachycardia is still not well understood. Although most findings have supported a reentrant mecha-
938
nism,14 –18 other studies have suggested triggered activity as
the underlying mechanism.1,19,20 Several characteristics of
idiopathic fascicular left ventricular tachycardia support reentry as the mechanism: (1) VT can be induced and terminated by ventricular programmed stimulation, (2) an inverse
relationship exists between the coupling interval of the
ventricular extrastimulus and the first tachycardia return
cycle, (3) entrainment with progressive fusion with shorter
pacing cycle lengths can be demonstrated, and (4) VT can
be entrained with concealed fusion over a region of the septum
with entrance sites at the more basal septum and exit sites
described toward the more mid to apical inferior septum.
Characteristics supporting a smaller reentrant or possibly
a triggered mechanism include (1) the His bundle can be
activated in an anterograde fashion without influencing the
tachycardia and (2) the ventricle can be captured by extrastimuli without resetting the tachycardia, suggesting that
much of the ventricle does not participate in the arrhythmia
circuit.1,15 A false tendon extending from the posteroinferior LV to the septum found in patients with idiopathic
fascicular left ventricular tachycardia also has been postulated to be responsible for this tachycardia.21 The exact
mechanism by which the false tendons may potentiate the
VT is unclear, but the hypotheses include (1) conduction
through the false tendon as part of the circuit and (2) stretch
of the Purkinje fiber network on the interventricular septum
caused by the tendon.
As indicated, characteristically for the sustained VT,
detailed mapping is performed to identify the earliest preQRS Purkinje potential. Successful ablation has occurred
with single point lesions targeting these sites. Pace mapping
has met with some success for targeting more limited forms
of VT. Some of the possible explanations for the difficulties
encountered and the “imperfect” pace map are the variable
current strength that is used for pacing, the variability in the
conduction system, and, more importantly, the amount of
surrounding myocardium “captured.” Furthermore, it is possible to obtain a pace map with a similar QRS morphology
at a site remote from the origin of the tachycardia due to
selective capture of the Purkinje network. Because of these
limitations of point lesion application based on pace mapping alone, a new strategy for providing more uniform
success for unmappable forms of this VT was desirable.
Linear ablation lesions for control of unmappable VT in
patients with ischemic and nonischemic cardiomyopathy
have been described.22–25 It is believed that these lesions
guided by pace maps, which mimic and approximate the
exit site of VT, are successful because they interrupt a
circuit of considerable dimension. This technique can also
be applied to patients with idiopathic fascicular left ventricular tachycardias that are difficult to induce or that are
nonsustained or noninducible for which “traditional” mapping techniques may not work. We found that a linear lesion
transecting through the inferior mid to mid-apical left ventricular septum guided by electroanatomic mapping, the
best pace map, and the presence of Purkinje potentials in
Heart Rhythm, Vol 2, No 9, September 2005
sinus rhythm and self-limited VT was effective in eliminating tachycardia in these patients. Achievement of left posterior fascicular block on surface ECG was not a necessary
prerequisite for a successful endpoint, suggesting that conduction through the posterior fascicle is not a necessary
prerequisite for the development of clinical VT. The success
of the procedure supports a reentrant mechanism for these
VTs, with the circuit having significant apical to basal
dimension along the inferior septum and thus vulnerable to
the effects of the linear lesion.
Conclusion
In patients with difficult to induce or nonsustained VT with
the typical right bundle branch block pattern and a superiorly directed axis on 12-lead ECG, radiofrequency energy
ablation delivered in a linear fashion approximately midway
to two thirds toward the apex along the mid to inferior
septum and perpendicular to the plane of the septum is safe
and effective for VT control.
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