Advances in Arrhythmia and Electrophysiology

Fascicular Ventricular Arrhythmias

Pathophysiologic Mechanisms, Anatomical Constructs,
and Advances in Approaches to Management
Suraj Kapa, MD; Prakriti Gaba, BS; Christopher V. DeSimone, MD, PhD; Samuel J. Asirvatham, MD

V entricular arrhythmias involving the fascicular system

may be seen in both structurally normal and abnormal
hearts. Idiopathic fascicular ventricular tachycardia represents
almost 10% to 15% of idiopathic ventricular tachycardia related
to the left ventricle.1,2 Cohen et al3 and subsequently Zipes et
al4 first described these arrhythmias in the 1970s as relatively
narrow right bundle left axis arrhythmias that arose close to
the posterior fascicle and could be induced with atrial pacing.
Belhassen et al5 later described the responsiveness of these
arrhythmias to verapamil. Although initial studies focused
on arrhythmias related to the left posterior fascicle, it is pos-
sible for arrhythmias to arise from any portion of the fascicular
system and in both structurally normal and abnormal hearts.
Furthermore, when approaching the patient presenting with
arrhythmias arising from the His-Purkinje system, it is impor-
tant to consider the unique complexities related to mapping
and ablation. In this review, we will focus on the mechanisms
of such arrhythmias, relevant embryology, anatomy and physi-
ology, and approaches to management in both the presence and
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Electrophysiological and
Anatomical Characteristics
In ablation of fascicular ventricular arrhythmias, an under-
standing of the normal anatomical course of the fascicles is
critical. However, variation in the anatomical course is com-
mon.6 In the normal human heart, the penetrating bundle of
His arises from the atrioventricular node and runs in the cen-
tral fibrous body as a cord-like structure, typically dividing
into the left and right bundles at the junction of the membra-
nous septum and the crest of the muscular interventricular
septum. The right bundle then arises at an obtuse angle with
the distal third of the right bundle being more superficial
and coursing to the right ventricular free wall in the modera-
tor band. The left bundle tends to be broader than the right
bundle and emerges just beneath the noncoronary cusp of
the aortic valve, giving rise to a thinner anterior fascicle and
broader posterior fascicle. Almost 60% of people may also
have a third fascicle termed the left septal, upper, or median
fascicle.7,8 The left bundle anatomy can exhibit considerable

absence of other structural heart disease. Broadly, fascicular
ventricular tachycardia in the absence of other structural heart
disease will be termed idiopathic fascicular ventricular tachy-
cardia (IFVT), whereas that related to structural disease will be
discussed in the context of the relevant disease state.
Generally, IFVT is separated into 3 types—left posterior
fascicular with a right bundle branch block pattern and left
axis deviation, left anterior with a right bundle branch block
and right axis deviation pattern, and left upper septal fascicu-
lar with a narrow QRS and normal axis but often with a right
bundle branch block morphology. There are rare reported cases
of left bundle branch block pattern, V3–V4 transition IFVT with
a normal axis arising from the right bundle branch. In addi-
tion, we will touch on other Purkinje- and fascicular-related
arrhythmias because they relate in diagnosis and mapping to
IFVT. However, by far, the most common form of IFVT is the
posterior fascicular type (≈90% of cases)1,2 (Table 1). We will
exclude consideration of premature ventricular contraction–
triggered ventricular fibrillation that may similarly involve
abnormalities in the His-Purkinje system from this review.
variation in the normal human heart with potential for sig-
nificant cross-linking between fascicles and variability in the
width, length, and degree of arborization9 (Figure 1). The
fascicular system ultimately terminates in a mesh-like Pur-
kinje network. The Purkinje fibers vary in density through-
out the heart, largely seen around the papillary muscles and
midventricle, and less so at the base of the heart. Further-
more, they can penetrate as deep as a third of the myocardial
thickness.10,11
Functionally, the electrophysiological tendency for the
fascicular–Purkinje system to participate in tachycardia may
be because of the unique physiology that allows the system to
overcome source–sink mismatch.12–15 On the basis of all exist-
ing data, electrical propagation from Purkinje to ventricular
myocyte depends on direct charge transfer. Thus, transmission
at the Purkinje–myocyte junction always has the potential to
be bidirectional (ie, anterograde and retrograde). In fact, given
the larger ventricular mass, the potential for retrograde activa-
tion may actually be higher than anterograde activation. This
has been demonstrated by work done by Joyner et al.14,15 One

Received March 17, 2016; accepted December 15, 2016.

The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.
From the Department of Cardiology (S.K., C.V.D., S.J.A.) and Division of Pediatric Cardiology, Department of Pediatrics (S.J.A.), Mayo Clinic College
of Medicine, Rochester, MN; and Mayo Clinic Medical School, Rochester, MN (P.G.).
The Data Supplement is available at http://circep.ahajournals.org/lookup/suppl/doi:10.1161/CIRCEP.116.002476/-/DC1.
Correspondence to Samuel J. Asirvatham, MD, Department of Cardiology and Cardiac Surgery, Mayo Clinic College of Medicine, 200 First St SW,
Rochester, MN 55905. E-mail asirvatham.samuel@mayo.edu
(Circ Arrhythm Electrophysiol. 2017;10:e002476. DOI: 10.1161/CIRCEP.116.002476.)
© 2017 American Heart Association, Inc.
Circ Arrhythm Electrophysiol is available at http://circep.ahajournals.org DOI: 10.1161/CIRCEP.116.002476

1
 2  Kapa et al  Fascicular Ventricular Tachycardia Management
Table 1.  Types of Idiopathic Fascicular Ventricular Tachycardia
ECG
Type of Tachycardia QRS Width, ms QRS Morphology
Posterior fascicle (most <120–140 RBBB
common)
Anterior fascicle <120–140 RBBB
Upper septal fascicle <120 RBBB or normal
LBBB indicates left bundle branch block; and RBBB, right bundle branch block.
mechanism by which retrograde activation is prevented is best
understood by the gating hypothesis proposed by Myerburg
et al,16 wherein the action potential duration increases as one
moves distally from the point of initial stimulus, thus result-
ing in the region of greatest refractoriness being at the distal
2 to 3 mm of the Purkinje fiber, which as a result serves as
a gate against retrograde conduction. However, during every
conducted beat, not all Purkinje–myocyte junctions are acti-
vated, with quiescent junctions existing among activated junc-
tions that may be later recruited based on cycle variability of
anterogradely conducted signals.12 Thus, although certain pro-
tective mechanisms may exist within the Purkinje–myocyte
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junction to prevent retrograde propagation, the potential
for retrograde activation still exists and may further explain
Figure 1. The variability of origin of the anterior, posterior, and
median fascicles observed in 20 normal human hearts and their
interconnections. Reprinted from Demoulin and Kulbertus7 with
permission of the publisher. Copyright © 1972 BMJ Publishing
Group Ltd.
QRS Axis Circuit Components
Left Starts in upper septum near bundle of His/proximal LBBB in
verapamil-sensitive slow zone, travels toward apex. Posterior
fascicle is the antegrade limb.
Right Starts in upper septum near bundle of His/proximal LBBB in
verapamil-sensitive slow zone, travels toward anterior fascicle exit.
Anterior fascicle is the antegrade limb.
Normal Circuit likely to involve reverse path of others (namely the fascicle is
the antegrade limb). Although not fully characterized, the reason for
the narrow QRS may be because of near simultaneous antegrade
activation of the left anterior and posterior fascicles with the septal
fascicle serving as the retrograde limb.
why reentry may occur in otherwise normal ventricular and
Purkinje myocardium.
Embryological Considerations
The bundle of His and Purkinje cells have distinct embryolog-
ical origins, which may underlie potential arrhythmogenicity.
Although the bundle of His develops from a cluster of peri-
odic acid–Schiff positive cells around the primitive atrioven-
tricular node, which then travel down the septal ridge to form
the bundle branches, the Purkinje cells are derived from con-
tractile cardiac myocytes and embryonic ventricular cells.17,18
Once the bundle of His and ventricular trabeculae consisting
of Purkinje cells have, respectively, developed on day 11 to 12
of embryogenesis, both structures connect to one another to
complete the formation of the primary ventricular conduction
system.19 One limitation in modeling an embryologic basis
for IFVT is the great interspecies variability both in anatomi-
cal distribution and in number of Purkinje fibers.12 However,
given the different embryological origins and interfacing
that occurs late in embryogenesis, the potential for myocar-
dial disarray during this complex period of development may
partly contribute to arrhythmogenesis. Furthermore, although
genetic factors may increase the arrhythmogenic potential of
Purkinje fibers, specific relationship to the pathogenesis of
IFVT has not been well characterized.20
Pathophysiologic Mechanisms of
Fascicular Ventricular Tachycardia
Automatic Versus Reentrant
Initial studies suggested automaticity as the mechanism of
fascicular ventricular arrhythmias, especially given associa-
tion with exercise, the ability to induce with burst pacing, and
characteristics of the His-Purkinje system that could confer
the potential for both normal and abnormal automaticity.4 For
example, in the setting of digoxin toxicity, the mechanism of
ventricular tachycardia (VT) is thought to be enhanced auto-
maticity in the region of the fascicles. However, the majority
of studies have laid more weight on there being a reentrant
basis for IFVT.21–23 VT that appears morphologically similar
to IFVT but exhibits features more suggestive of automaticity
may be more consistent with focal Purkinje VT.24
 3  Kapa et al  Fascicular Ventricular Tachycardia Management

The reentrant theory suggests that IFVT is the result of a
calcium-dependent circuit because of abnormal Purkinje fiber
conduction.25 In this setting, the reentrant zone is thought to
involve retrogradely activated fast conduction fibers during
tachycardia along with antegrade conduction through a vera-
pamil-sensitive zone. Ouyang et al26 elegantly demonstrated
this association, with unidirectional block and resulting mac-
roreentry within the Purkinje network subtending arrhythmia
initiation. Although it is fairly consistent that the upper turn-
around of the reentrant circuit is likely located near the His
or proximal left bundle/fascicle area, the retrograde limb of
the circuit may vary from patient to patient.27 Previous studies
have also suggested the role of a fibromuscular false tendon
in the pathophysiology of fascicular VT as ablation of this
tendon has led to elimination of the reentrant form of IFVT
in several cases.28 Further supporting reentry is the ability to
entrain with ventricular and atrial pacing, with the use of the
latter supporting involvement of the fascicles given the easy
access over the conduction system into the reentry circuit.21
However, it is possible that in some cases of apparent IFVT,
the fascicle may act as a bystander with the retrograde limb
comprising the left ventricular myocardium.29 Thus, it may be
important to also recognize the contribution of false tendons
or other structures in arrhythmogenesis.
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Role for the False Tendon?
Many of the studies concerning IFVT occurred before the
widespread use of intracardiac echocardiography (ICE).
The suggestion that a false tendon may underlie the patho-
physiology of IFVT in some patients has been supported by
several investigators.28 The false tendons are thought to be
noncompacted extensions of the His-Purkinje system and are
electrophysiologically active (Figure 2; Movie I in the Data
Supplement). Pathologically, they have been shown to con-
tain Purkinje fibers and that their electric properties (action
potential duration and refractory period) vary with changes
in the degree of length–tension application.30–32 Furthermore,
there is a significant association between the incidence of
false tendons on echocardiography and that of idiopathic left
ventricular tachycardia. Perry et al33 reported a 0.8% over-
all incidence of false tendons in a group of 3847 patients,
although 37% of those with false tendons had exercise-asso-
ciated premature ventricular contractions. The false tendon
as a mechanism for macroreentry, given different conduc-
tion characteristics from the remaining myocardium, makes
physiological sense. However, close attention to imaging
(transthoracic echocardiography, ICE, and magnetic reso-
nance imaging) may be necessary to identify these structures
in patients presenting with IFVT.

Figure 2. An example of a patient with incessant ventricular tachycardia, which was thought to arise near the left anterior fascicle. How-
ever, mapping along the false tendon demonstrated mid-diastolic potentials (top left—potentials labeled) The intracardiac echocardiog-
raphy (ICE) image (right) demonstrated contact of the distal tip with the tendon. The bottom left image depicts entrainment at this site
along the false tendon, where ablation was successful in terminating tachycardia. See Movie I in the Data Supplement for ICE video.
 4  Kapa et al  Fascicular Ventricular Tachycardia Management
Structurally Normal Versus Structurally Abnormal
Hearts With VT Suggesting Fascicular Involvement
Fascicular VT can occur in both structurally normal and abnor-
mal hearts. Arrhythmias related to the His-Purkinje system in
structurally abnormal or ischemic hearts are often caused by
Purkinje fibers with abnormal automaticity. In the setting of
structural heart disease (in particular infarct or nonischemic
involvement of the septum), changes in health of components
of the His-Purkinje system may also lead to unidirectional
block in one component of the fascicular system and result-
ing interfascicular or bundle branch reentry that may appear
as IFVT on the basis of 12-lead electrocardiography.6,34 One
way to distinguish VT attributable to the presence of structural
heart disease from idiopathic causes is the RS interval, with
fascicular VT generally demonstrating an RS interval <80 ms
in all precordial leads.25
Electrocardiographic Differentiation of Fascicular
From Other Arrhythmias
Fascicular ventricular arrhythmias are commonly narrow (ie,
110–140 ms in QRS duration) and have typical morphologi-
cal characteristics on 12-lead electrocardiography. Gener-
ally, arrhythmias arising from a specific fascicle will have a
QRS morphology similar to that seen in sinus rhythm with
block in the remaining portions of the His-Purkinje system
(eg, IFVT arising from the posterior fascicle may have a rep-
resentative right bundle branch block/left anterior deviation-
type morphology). However, this need not always be the case
because of arborization of the distal Purkinje fibers resulting
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in opportunity for varying QRS morphology depending on the
exact path of distal myocardial activation. This phenomenon
is similar to that seen with papillary muscle-related or other
VT where a focus that is insulated from the rest of the myocar-
dium may have variable exits (and thus the exact site of ear-
liest myocardial exit may not reflect the arrhythmia source).
When reviewing the ECG of a patient presenting with pos-
sible fascicular VT, it is important to not confuse the arrhythmia
with supraventricular tachycardia with aberrancy. Evidence
of ventriculo-atrial dissociation is one useful characteris-
tic but is not always present, especially in younger patients.
Furthermore, at the time of the electrophysiology study, initial
induction of a supraventricular tachycardia should not imme-
diately rule out possible IFVT given that as many as 10% to
25% of patients with IFVT may also have supraventricular
tachycardia.34,35 It is important to note that one key method of
differentiating the two is by comparing H-V intervals during
sinus rhythm versus tachycardia (see below).
Two arrhythmias that may commonly be confused with
IFVT are arrhythmias arising from the papillary muscles and
arrhythmias arising from the mitral annulus. This is because
of the relatively small anatomical area that separates these
structures. The role of a mismatch in conduction character-
istics between fascicular, Purkinje, and myocardial tissue in
the pathogenesis of IFVT has also been described in papil-
lary muscle ventricular arrhythmias, in which Purkinje fibers
that penetrate deep into the tissue have been implicated in
the source–sink mismatch responsible for arrhythmogen-
esis. Several authors have published criteria to differenti-
ate specifically left posterior fascicular VT from ventricular
arrhythmias arising from the posteromedial papillary mus-
cle.36–38 However, it is important to recognize that electrocar-
diographic distinction between these arrhythmias is artificial.
Specifically, Purkinje and fascicular tissue exist on the papil-
lary muscle and components of the papillary muscle may arise
on the septum close to where the conduction system normally
transitions from fascicle to Purkinje tissue. Furthermore,
Purkinje tissue and remnant Purkinje-like tissue may exist in
many areas of the heart, including the outflow tracts, papil-
lary muscles, and close to the mitral annulus.39 Thus, attempts
to identify distinguishing electrocardiographic characteristics
must be considered in the context of normal anatomical vari-
ability of fascicular, Purkinje, and papillary muscle tissue.
Thus, although electrocardiographic criteria may be useful,
recognizing its limitations is important as well.
Pharmacological Management Options
In cases of IFVT, verapamil has proven a mainstay of therapy
(thus the term verapamil-sensitive idiopathic left ventricular
tachycardia). The mechanism of action of verapamil is via the
slow inward calcium channel. Unfortunately, chronic treat-
ment with oral verapamil is not as effective as acute treatment
with intravenous verapamil. Propranolol has also been pro-
posed as an effective treatment. Generally, fascicular VT does
not respond to adenosine, although case reports have been
published suggesting rare responsiveness. Although use of
drug therapy may be useful, ablation, particularly in IFVT, has
been suggested to have a high success rate (as high as 80%).
Pre- and Intraprocedural Set-Up
The approach to mapping and ablation of any arrhythmia relies
on 3 principles: preoperative recognition of the arrhythmia
and presumptive substrate; ability to induce the arrhythmia at
the time of invasive mapping; and appropriate mapping of the
relevant signals with targeted ablation. Fascicular ventricular
arrhythmias comprise a unique problem for several reasons:
(1) the substrate is often normal macroscopically and, thus,
traditional methods of substrate mapping used in other scar-
related arrhythmias may not be applicable; (2) earliest myo-
cardial activation does not necessarily indicate arrhythmia
source; and (3) variable anatomy and degree of endocardial
penetration of the fascicle and relevant Purkinje fibers may
make typical mapping and ablation techniques technically dif-
ficult. Thus, a systematic approach to preoperative recogni-
tion, induction, mapping, and ablation is critical.
Substrate Considerations
An important consideration is whether or not the heart is
truly structurally normal. In the presence of previous infarct,
Purkinje-related VT is not uncommon and may present with
similar rapid upstroke to that of fascicular VT. However, some-
times substrate may not necessarily be obvious via traditional
imaging methods such as echocardiography and may not be
sufficiently extensive to cause a decrease in ejection fraction.
In a recent study, magnetic resonance imaging in patients pre-
senting with fascicular VT and preserved ejection fractions
demonstrated total absence of delayed enhancement in only 4
out of 9 patients.40 Among the remaining patients, either uni-
focal or multifocal fibrosis was identified and was associated
 5  Kapa et al  Fascicular Ventricular Tachycardia Management
with the sites of successful ablation of IFVT. Thus, it is possi-
ble that some patients with apparently normal cardiac function
and IFVT may, in fact, have corresponding substrate. Whether
there is a threshold in terms of degree of substrate needed to
confer an increased risk of VT recurrence or whether the pres-
ence of fibrosis signifies a progressive process (eg, sarcoid-
osis) or a fixed substrate from a previous subclinical event (eg,
myocarditis) is unknown. and further study is required. The
relevance to mapping, however, lays in that the recognition of
pre-existing substrate that may offer an approach to mapping
a potentially targetable fixed substrate even if the arrhythmia
is noninducible.
Induction at Electrophysiology Study
As with any electrophysiological procedure, induction of the
arrhythmia at the time of ablation is critical to mapping. How-
ever, dependence on sympathetic activity and effects of seda-
tion and subcutaneous lidocaine on inducibility may make
induction difficult. Reports have suggested that VT may be
noninducible in as many as 25% to 40% of cases. Gopi et
al41 published a stepwise approach to inducing IFVT. In addi-
tion, preoperative cessation of antiarrhythmics, β-blockers,
and calcium channel blockers at least 3 half-lives before the
procedure is important.
Considerations in Mapping
An array of modalities may be used when mapping fascicular
VT. However, use of fluoroscopy, ICE, and an electroanatomic
mapping system may help optimize the likelihood of success.42
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Although fluoroscopy has been most traditionally used, and
the skilled electrophysiologist can make excellent anatomical
determinations with fluoroscopy alone, it lacks fine definition
(in particular for endocavitary structures, catheter contact, etc)
that ICE has. As a result, modern-day diagnostic strategies
have shifted focus toward greater utilization of ICE.43
Approach to Mapping
Ideally, induction and maintenance of tachycardia will best
assist the operator in both defining the mechanism of tachycar-
dia and identifying critical components amenable to ablation.
There are several different approaches to mapping and ablat-
ing IFVT that may be used, which are summarized in Table 2,
and discussed in further detail below. Traditional approaches,
including pace and entrainment mapping, mapping the earliest
ventricular electrogram during VT, and mapping the earliest
fascicular electrogram during VT, have been well described
but carry potential limitations. We also discuss the potential
role of comparative mapping techniques.
Intraoperative Definition of Tachycardia Circuit
Several reviews of approaches to mapping and ablation have
been published.44–46 We would encourage the reader to review
these in detail as we seek to put them in broader context here.
During mapping of the tachycardia circuit, 2 distinct potentials
may be observed, typically termed the Purkinje potential (P2)
and pre-Purkinje potential (P1) (Figure 3). The relative activa-
tion times vary in described studies between 5 to 25 and 30 to
70 ms pre-QRS, respectively. P2 reflects activation of the fas-
cicle and Purkinje fiber near the fascicle and appears as a sharp,
high-frequency potential. P1 reflects excitation at the entrance
to the verapamil-sensitive zone in the septum. This potential is
often lower in frequency than P2 and, when pacing at higher
pacing rates, may be captured antidromically during tachycardia
but captured orthodromically in sinus rhythm and thus may fol-
low the ventricular complex. It is this association between fast
conducting Purkinje fibers (P1) and slow conducting verapamil-
sensitive fibers (P2) that characterize the substrate for reentry.
Figure 4 demonstrates the putative reentry circuit and the elec-
trograms to which P1 and P2 refer. Interestingly, although the
above is true in left anterior and posterior fascicular VT, some
have suggested that the upper septal fascicle works in the
reverse direction, with Purkinje potentials activated in the
reverse direction to that of common forms of IFVT (ie, P1 is
activated retrogradely but P2 is activated antegradely).45
The classic schema for mapping has been previously well
described by Nogami et al.46 To achieve the best discrimina-
tion of P1 and P2 potentials and their participation in tachy-
cardia, use of a multipolar electrode catheter to help define
antegrade and retrograde activation patterns followed by
attempts to entrain the fascicles to prove they are part of the
circuit provides an excellent initial means of (1) defining the
circuit and (2) determining whether the fascicle in question is
involved in the circuit.
Critical Considerations When Mapping
First, performing rigorous maneuvers to define the arrhythmia
mechanism is critical, such as pacing from a distant site to
support whether the underlying mechanism is reentry or auto-
maticity. If a diagnosis of reentry is supported, the operator
must be careful to not solely rely on tagging sites of earliest
myocardial activation. Because of the fact that there may be
arborization of Purkinje fibers beyond the region of reentry,
there may be several early myocardial sites with relatively
late sites in between. Thus, the earliest site is characterized
not only by the earliest myocardial signal but also by defin-
ing earliest P1 and P2 (ie, conduction signals). Furthermore,
use of ICE and fluoroscopy to define close by endocavitary
structures and to optimize catheter contact is critical, as the
Purkinje signals may be small, easily missed, and occur on the
surface of other structures. Given that critical elements of the
circuit are normally superficial, careful catheter manipulation
so as not to cause mechanical injury and thus render the VT
noninducible is important.
Simultaneous use of a multielectrode catheter along with
point-to-point mapping may further help when mapping IFVT.
The goal when using both together is to be able to discriminate
myocardial and conduction signals across a large region of
myocardium with closely spaced electrodes to optimize signal
discrimination. Using 1-mm electrodes with 1- to 2-mm spac-
ing oriented along the path of the fascicle would optimize both
signal discrimination and timing of relative activation. Thus, 2
points of access to the left ventricle, whether by 2 trans-septal
punctures or a combined retrograde and trans-septal approach,
may be needed to facilitate placement of both the multielec-
trode catheter and the ablation catheter.
One of the main limitations to the use of a multielectrode
catheter is being able to line it up with the course of the fas-
cicle. Typically in human hearts, the angle between the bundle
 6  Kapa et al  Fascicular Ventricular Tachycardia Management
Table 2.  Approaches to Mapping and Ablating Fascicular Ventricular Tachycardia
Utility for
Approach Fascicular VT How to Do
Map earliest ventricular Zero to low Map earliest myocardial
electrogram during VT signals during arrhythmia and
identify/ablate the earliest
area
Entrainment mapping Zero to low Stimulate at a fixed cycle
with fixed output at length at various sites to
various sites determine whether in circuit
Pace mapping at fixed Zero to low Deliver electric stimulation
output at multiple sites to identify
regions with similar QRS
morphology to clinical
arrhythmia
Target earliest Low to Map earliest fascicular and
fascicular signal moderate Purkinje potentials during VT
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Pace mapping at Low to Identify fiducial reference on
variable (ie, high, low, moderate QRS complex (see caveats
and very low output) in text) and identify sites at
combined with similar which fascicle/Purkinje signal
stim to QRS and to QRS equal to stim to QRS
concurrent abnormal during pacing at variable
fascicular/Purkinje output
signals
Fascicular entrainment High Stimulate locally at sites
where fascicular/Purkinje
signals seen to capture local
fasciscle/Purkinje fiber (not
just myocardium). Cycle
length of pacing should be
determined by fascicle–
fascicle timing rather than
QRS–QRS timing because
of potential for multiple
secondary exits/variable
cycle length
Benefits
Identifying a relatively fixed
earliest ventricular electrogram
can serve as a fiducial
reference for other mapping
May help define if arrhythmia
mechanism reentrant or
automatic when performed at
varying distances from circuit
Does not rely on arrhythmia
sustainability
Mapping critical components
of circuit (ie, fascicles/
Purkinje fibers) rather than
secondarily activated region (ie,
myocardium)
May be effective for automatic
arrhythmias
Does not rely on arrhythmia
sustainability (although still
must be inducible)
More likely to
differentially capture local
myocardium versus local
myocardial+fascicle
Able to determine if activating
elements that are proximal to
the circuit based on different
stim to QRS
Depend on a definite return
electrogram (not ventricular but
fascicular)
More accurate reflection of
circuit because ensuring
fascicular and not myocardial
entrainment
Pitfalls
Earliest myocardial signal is not a critical part
of the circuit
Potential for multiple early areas of myocardial
activation because of arborization of Purkinje
system distal to VT circuit
Needs to be a discrete area of stimulation
because if one captures sites that are both in
and out of the circuit, results of entrainment
may be flawed
If one records signals that have mixed
components (eg, ventricular and Purkinje
signals), it may be difficult to impossible to
interpret the return signal
May be multiple distal means of exit and return
because of the extensive arborization of the
Purkinje system, thus making the timing of the
return difficult to interpret
May or may not be capturing fascicle/Purkinje
fibers during stimulation
Will capture surrounding myocardium not
involved in circuit leading to difference in QRS
morphology
Potential for variable QRS morphology during
VT→inability to use a fixed QRS morphology
against which to map
Most fascicular VT reentrant and thus earliest
signal is relative
If earliest signal identified above level of
circuit because of low density of mapping, this
may not eliminate circuit despite eliminating
fascicular conduction proximally
Will capture surrounding myocardium not
involved in circuit leading to difference in QRS
morphology from VT
Potential for variable earliest QRS during
VT→inability to use a fixed portion of QRS (even
earliest portion of QRS) against which to map
Earliest QRS may vary both during pacing and
during VT when capturing conduction fibers
because of multiple secondary exits through
distal Purkinje system
Local fascicular or Purkinje signal may be
normal in appearance even in patients with
fascicular VT
Arrhythmia must be sustainable to allow for
entrainment
Will need to use a multielectrode catheter
to define fascicular activation sequence to
differentiate concealed vs manifest (cannot
depend on QRS morphology)
Need to ensure capture of local fascicular
signals
If multiple means of secondary exit and return,
there may be shifts in timing of the return beat
Need to be able to differentiate local fascicular/
Purkinje from myocardial signal
(Continued )
 7  Kapa et al  Fascicular Ventricular Tachycardia Management

Table 2.  Continued

Utility for
Approach Fascicular VT How to Do
Comparative mapping High Look at timing of local
between sinus rhythm, fascicle/Purkinje signal
high output pacing, compared with earliest V in
and VT using a fiducial sinus rhythm, during pacing,
electrogram reference and during VT. If timing is
(ie, earliest V) same as during VT, then
signals are in or distal to
circuit. If not, then likely
proximal to circuit
VT indicates ventricular tachycardia.
Benefits
Depend on the earliest V (not
QRS) against which to compare
Does not depend on arrhythmia
sustainability (though should be
inducible)
May be used to define circuit
length from most proximal
portion onward
Pitfalls
Portions distal to the circuit will exhibit similar
timing to earliest V (Figure 5D) and thus
matching retrograde sequence of activation
with pacing versus tachycardia should be
evaluated
Depends on having a dependable fiducial
ventricular reference
Need to be able to differentiate local fascicular/
Purkinje from myocardial signal

of His and left bundle is around 15°, the angle between the
left bundle and the takeoff of the left anterior fascicle is 50°
to 75°, and the angle between the left bundle and the takeoff
of the posterior fascicle is 15° to 30°. If one appreciates the
natural angle between the His bundle and the left posterior
or left anterior fascicle takeoff, positioning the multielectrode
catheter to approximate the course of the desired fascicle may
be made more straightforward.
extensive arborization of the Purkinje system, thus making the
timing of the return similarly difficult to interpret.
Consideration must also be given to atrial entrainment
during IFVT. Entrainment by atrial pacing may suggest easy
access of the conduction system to the circuit. This, in turn,
supports a role for the fascicles. Thus, although ventricu-
lar entrainment may support a reentrant mechanism, atrial
entrainment may suggest a critical role of the fascicles.21

Pace and Entrainment Mapping for IFVT
Pace Mapping
In many atrial and ventricular arrhythmias, pace mapping to
try and reproduce the same activation pattern/QRS morphol-
ogy may be used as a surrogate for the target site. The issue
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Defining the Earliest Ventricular Activation
One of the main limitations during mapping of IFVT is the
potential for variable activation of the ventricle. It is well rec-
ognized that during activation of the His-Purkinje system, not
all Purkinje–myocyte junctions are activated with every beat.
Thus, there is the potential for variable QRS morphology and

in the case of any Purkinje or fascicle-related arrhythmia,
whether automatic or reentrant, is that it is almost impossi-
ble to capture the specialized conduction fibers without also
capturing surrounding myocardium and perhaps other nearby
Purkinje fibers with disparate exits. Thus, 1 of 2 events can
happen—(1) a similar pace map is seen, but because of a large
virtual electrode capturing critical circuit elements that are far-
ther away, ablation locally would not necessarily be successful
or (2) a significantly different pace map is seen despite being
at the site of a critical circuit component because of simulta-
neous capture of local ventricular myocardium or differences
in ventricular activation through distal components of the
fascicular–Purkinje system during pacing versus tachycardia.
Although several authors have suggested the ability to specifi-
cally capture Purkinje fibers during both pace and entrainment
mapping, the potential limitations of this approach need to be
understood.47
Entrainment Mapping
The same issues noted for pace mapping apply to entrainment
mapping. For entrainment mapping to succeed, there needs
to be a discrete area of stimulation, and one should be able to
record a dependable return electrogram with the assumption
that return can only occur through a single retrograde limb of
the reentry circuit. However, if one captures sites that are both
in and out of the circuit, results of entrainment may be flawed.
In addition, if one records signals that have mixed components
(eg, ventricular and Purkinje signals), it may be difficult to
impossible to interpret the return signal. Finally, there may
be multiple distal means of exit and return because of the
coupling intervals. One of 3 events can occur during IFVT as
a result: (1) the QRS morphology and earliest ventricular acti-
vation can be fixed; (2) the QRS morphology may be slightly
variable, but the earliest intracardiac activation is fixed with
variable recruitment of surrounding Purkinje fibers causing
a slightly variable morphology; or (3) the QRS morphology
and earliest intracardiac electrogram may both vary signifi-
cantly over time. Attempting to define each of these situations
will help the operator in identifying a reasonable fiducial ref-
erence—whether the earliest surface QRS in case 1, a fixed
intracardiac reference in case 2, or no reliable fiducial refer-
ence in case 3. It is important to note than when stating earliest
ventricular activation, we are referring to the earliest local V
during tachycardia and not the earliest V during sinus rhythm.
Defining the Earliest Fascicular Signal
Defining the earliest fascicular signal is necessary when map-
ping IFVT because they reflect critical components of the cir-
cuit rather than secondarily activated regions (ie, ventricular
myocardium). However, fascicular signals may or may not be
easily differentiated from the associated ventricular signals. For
example, depending on the activation of the fascicle relative to
the immediately surrounding myocardium, there may not be an
apparent isoelectric period during tachycardia thus impeding
appropriate signal discrimination. Furthermore, most IFVT is
reentrant, and, thus, the concept of early is relative. Finally, if
the earliest signal is mistakenly thought to be above the level of
critical components of the circuit because of low-density map-
ping, the VT circuit may not be eliminated despite elimination
of proximal fascicular conduction.
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Figure 3. An example from a case of left posterior fascicular ventricular tachycardia (VT). Top, Signals during tachycardia, including P1
(blue dot), the low-frequency signal, and P2 (orange dot), the high-frequency signal. Bottom, Block in components of the circuit with
return to P1 but without conduction back to P2.

Additional Approaches Requiring Validation
Comparative Mapping
Although the previously mentioned approaches (defining P1
and P2, using pace and entrainment mapping, identifying the
earliest diastolic and presystolic signals) have been widely
reported, fewer authors have discussed the role of compara-
tive mapping techniques.48,49 The principles of comparative
mapping to define the tachycardia circuit are natural exten-
sions of those previously reported by Nogami et al but may
offer a systematic approach to defining critical circuit compo-
nents to IFVT. The main limitation, however, is the need for
dependable comparative analysis of individual signals during
sinus rhythm versus tachycardia. The purpose of this section
is to highlight principles that may be useful for assessment of
fascicular VT but require further study to determine (1) their
efficacy relative to other approaches and (2) the percentage of
patients in whom they can be realistically used. Specifically,
whether such rigorous evaluation affords incremental value
above other techniques is unclear and requires further study.
Although these methods still require systematic validation, the
concepts are critical to consider and relevant to all arrhythmias.
Comparative Timing Against Sinus Rhythm
One method of defining whether the mapping site is in the
circuit may be using comparative timing of the local signals
against sinus rhythm. If a catheter is placed at a site along the
fascicle and the P2 signal is recorded, one can measure the
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Figure 4. An example of the reentry circuit thought to occur during fascicular ventricular tachycardia (VT). P1 reflects the low-frequency
signal during tachycardia that is earlier pre-QRS (bottom left) and occurs right after the turn around close to the proximal left bundle and
bundle of His. P2 reflects the sharper signal closer to the start of the QRS. Following P2 comes the ventricular signal (V) in association
with generation of the QRS complex.

timing from the local signal to the earliest ventricular electro-
gram during tachycardia. If this timing during sinus rhythm is
the same as during tachycardia, then that spot is likely either
the target site or distal to it because one would assume that
regardless of whether one was in tachycardia or in sinus, the
time to get from that local signal to the ventricular myocar-
dium should be about the same. The timing of more proximal
elements (eg, the His bundle) compared with ventricular acti-
vation, however, will be shorter during tachycardia than that
during sinus rhythm (Figure 5A).
Thus, one could identify a site where the fascicle-to-ven-
tricular electrogram timing is the same during both tachycar-
dia and sinus rhythm and sequentially map back to the more
proximal elements of the fascicle/bundle until the timing starts
to become earlier during tachycardia. The point at which the
timing goes from being equal in both rhythms to different may
indicate the most proximal elements of the circuit.
However, this method does have its limitations. First, a
point ablation is unlikely to be effective, and one might have
to cross through the fascicle at or below this spot somewhere
along the circuit. In addition, if during sinus rhythm there
is a secondary exit that is getting to the local ventricular
electrogram faster than that during tachycardia, one may never
get an exact timing match. One way to avoid this issue of sec-
ondary exits is to keep a separate fiducial reference for earliest
ventricular activation against which to compare. This would
be the ideal method for mapping. The limitation, of course, is
creating a stable reference, in which case a screw in electrode
may be considered.
Comparative Mapping During Pacing
One method of mapping that may be complementary to com-
paring signal timing during sinus is to use a surrogate of para-
Hisian pacing—high versus low output pacing in the region
of the fascicle or Purkinje tissue. The use of this is most rel-
evant for certain more microreentrant causes of IFVT. In the
fascicular region, high output pacing would be expected to
capture both the insulated fascicle and the local ventricular
myocardium, but one would expect a paced QRS morphology
different from that of tachycardia. If the stimulus to the earli-
est ventricular signal is similar during high output pacing and
during tachycardia, then this suggests that the fascicle is part
of the circuit, as long as the QRS morphology during pacing is
different. However, if one paces proximal to critical portions
 10  Kapa et al  Fascicular Ventricular Tachycardia Management
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Figure 5. A, A simplified schematic of mapping during sinus rhythm and tachycardia during left posterior fascicular ventricular tachycar-
dia (VT). This is meant to highlight comparative mapping principles given that the circuit in the Purkinje network is not necessarily linear
and there is extensive potential for bystander conduction during VT. Numbered sites are mapping sites where the catheter is placed. V
indicates the earliest ventricular signal during tachycardia being used as a fiducial reference. Proximal to the circuit site, the timing from the
fascicular signal (f) to V will be longer in sinus than in tachycardia. In the circuit, it will be equal. However, given the potential for multiple
secondary exits, a catheter placed within the distal Purkinje system (3) may exhibit the same timing to the earliest V during sinus and
tachycardia, but ablation here would not necessarily terminate tachycardia given it acts as a secondary exit site. Note fascicular and Pur-
kinje fibers are in red for purposes of discriminating between the two. P refers to local Purkinje signal seen during point-to-point mapping,
not specifically P1 vs P2. Note that the schematic diagram is meant to point out timing and that both fascicular and ventricular electro-
gram morphologies will necessarily be different during tachycardia and sinus. B, Actual tracings from a patient with fascicular VT. The first
pair of ablation electorgrams (1) show a site proximal to the VT circuit during mapping, where the fascicle (f) to ventricular electrogram
time was longer during sinus than tachycardia. Below that was the electrogram at the first spot where there is a Purkinje/fascicle (P) tim-
ing to the local V equal in sinus and tachycardia. Ablation here resulted in termination of the arrhythmia. (Continued )
 11  Kapa et al  Fascicular Ventricular Tachycardia Management
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Figure 5 Continued. C, Effects of high, low, and very low output pacing on signal characterization. The examples are most relevant to
focal and microreentrant versions of idiopathic fascicular ventricular tachycardia (IFVT), with schema 2 not necessarily being relevant for
cases of macroreentrant IFVT. The pacing sites are blue and the overlying earliest ventricular electrogram is overlaid in purple. With high
output pacing on the fascicle, one will capture both the insulated fascicular fiber and local ventricular myocardium. Proximal to the circuit,
fascicular signal to the earliest V will always be greater than during tachycardia. If, however, one is in the circuit, with high output pacing,
the stim to earliest V will be equal to fascicle to V during tachycardia, but when the fascicle is not captured, stim to V will then be longer
(although fascicle to V will remain similar). In case (3) where one is pacing at the earliest Purkinje exit, high and low output pacing may
capture both Purkinje and local ventricular myocardium, resulting in a different QRS morphology than tachycardia. However, if very low
output pacing only captured the distal Purkinje fiber, this may result in the same QRS morphology as tachycardia (please note even at
very low outputs, it may be impossible to only capture the Purkinje fiber and not the surrounding ventricular myocardium). Because this
site is in the circuit, pV and SV should be the same for all pacing situations. However, if one paces at a distal, secondary exit site (case 4),
one might expect that the stim to earliest V during pacing might actually be greater than during tachycardia given that now the stimulus to
earliest V must get back to the site either via retrograde conduction through the Purkinje system or via ventricular myocardium. However,
given the rapid nature of Purkinje conduction, it is possible that the difference will be minimal/not measurable. The paced QRS morphol-
ogy during very low output pacing in case (4), if only the Purkinje fiber was captured, will likely exhibit subtle differences given the exit
site is different than that during tachycardia. fV, fascicle to earliest ventricular electrogram timing; pV, Purkinje to earliest ventricular elec-
trogram timing; SV, stimulus to earliest recorded ventricular electrogram timing. Subscripts refer to intervals as noted during high output
(high), low output (low), and very low output (very) pacing done during sinus and during tachycardia (tach). D, Pacing to look at retrograde
activation sequence when pacing at 2 different sites where local fascicular/Purkinje potential timing to the local earliest recorded ventricu-
lar electrogram (V) was the same in both sinus and during tachycardia. In the case of (1), we are in the circuit, and the retrograde activa-
tion sequence is the same as the P2 activation sequence during tachycardia. However, when pacing at site (2), the activation sequence is
different despite a similar local signal to earliest ventricular electrogram (V) timing. Note that the fascicular/Purkinje signals are highlighted
in red. The numbers 1 to 6 indicate individual bipoles along a multipolar catheter (green) placed along the left posterior fascicle. Also, note
that the earliest recorded ventricular electrogram (V) may or may not have a Purkinje potential identified.
 12  Kapa et al  Fascicular Ventricular Tachycardia Management
of the circuit, the timing will be shorter during tachycardia.
In turn, if the pace map is identical to that of tachycardia with
high output and low output pacing, one has to suspect that
either the tachycardia is, in fact, not IFVT and traditional
myocardial approaches to mapping may be needed or one is at
the myocardial exit site (Figure 5C).
One caveat to this approach is when pacing directly on the
Purkinje fibers, which are not insulated. There, very low out-
put may capture Purkinje fibers alone without capturing the
surrounding myocardium. If the paced morphology is identi-
cal to that of tachycardia during very low output pacing, but
at higher outputs the morphology is different, and the stim
to QRS is very short similar to that seen during tachycardia,
then one knows the particular Purkinje fiber is of value to the
circuit (Figure 5C).
Of note, this schematic idea requires validation but adopts
many of the principles of high and low output pacing used in
other areas of VT mapping. One key factor to consider is that
all the schemas described in Figure 5C are likely to work dur-
ing focal or microreentrant causes of VT. However, as with
any macroreentrant VT, schema number 2 in Figure 5C may
not be effective, in part because of the fact that antidromic
capture/activation also needs to be considered.
Pacemapping of Retrograde Activation to Identify
Critical Circuit Elements
In addition to comparative mapping of the antegrade activa-
tion characteristics noted above, comparing retrograde activa-
tion is similarly critical. Although antegrade activation during
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pace mapping may be of little value because of simultaneous
capture of ventricular myocardium, retrograde conduction
does not care whether or not the ventricular myocardium is
captured. One would expect, when pacing at the target site,
the timing of the pacing stimulus to the retrograde His should
be similar during pacing as would be the local fascicular sig-
nal to the retrograde His during tachycardia. In isolation, this
approach is of limited value, but when used in combination
with comparative mapping approaches noted above, it may
help further confirm the target site.
Evaluation of this retrograde sequence during pacing
serves as an adjunct. Using comparative mapping, similar-
ity in timing between local fascicular or Purkinje and earliest
local ventricular electrogram timing implies one is at a point
within or distal to the proximal end of the circuit. However,
it is still possible that there may be multiple exits and that
the catheter is at a secondary exit site. However, if one also
compares retrograde activation during pacing at this site, if
the retrograde activation sequence is different during pacing
than tachycardia, this implies the site was a secondary exit
but not a critical portion of the circuit. The finding of retro-
grade Purkinje/fascicular activation sequence being similar
during tachycardia and pacing along with similar fascicular/
Purkinje to ventricular timing during both sinus rhythm and
tachycardia implies that this is at a critical portion of the cir-
cuit (Figure 5D). If the latter is seen but not the former, map-
ping may be done more proximally along the fascicle course
until this finding occurs. This approach is essentially the
same as pace mapping for other arrhythmias, except instead
of comparing the surface QRS during pacing versus during
tachycardia, instead here we use the intracardiac electrograms
given the aforementioned potential for a high degree of vari-
ability in surface QRS morphology during fascicular VT.
Approach to Ablation of IFVT
Once the mechanism and the responsible fascicle is defined,
it is critical to consider how one approaches ablation. One
option given aforementioned limitations of traditional map-
ping techniques and particularly if there is high suspicion
of IFVT but it proves noninducible or nonsustained is to
go upstream of the presumed critical site and simply ablate
through the proximal aspect of the fascicle, thus prevent-
ing conduction through all distal elements.50,51 However,
there are 3 issues related to this: (1) this may require more
ablation than otherwise necessary; (2) if there is interlink-
ing between components of the more distal fascicle and
Purkinje fibers, there may still exist potential for reentry
despite elimination of the conduction through more prox-
imal elements; and (3) proarrhythmia may occur because
of excessive ablation. Thus, having a systematic approach
to mapping, defining the electrograms and the circuit and
deciding where to ablate is critical.
Another commonly used ablative approach is to identify
the earliest presystolic or diastolic fascicular or Purkinje sig-
nal relative to the QRS during tachycardia and ablate there,
which will likely work in >50% of cases.45 Alternatively,
one could map the earliest ventricular electrogram and,
near that, ablate a fascicular or Purkinje signal. The limi-
tations of these approaches are several, including the fact
that for reentry a point ablation for a wide isthmus may not
be effective and, if ablating upstream of the circuit, there
may be other connections to the muscle or within the fas-
cicular–Purkinje network. In addition, discriminating these
signals can be difficult. Although fascicular signals may be
well separated from local ventricular activation because of
the presence of a fibrous coat insulating the fibers (result-
ing in a reasonable isoelectric period), there may not be a
similar isoelectric period separating Purkinje and ventricular
activation. Furthermore, particularly when mapping during
sinus rhythm, if there is slow conduction through a fascicle
or Purkinje fiber such that local ventricular activation occurs
before those fibers can reach their target, then there may be
significant obfuscation of the signal. However, one method
of better differentiating myocardial from fascicular/Purkinje
signals would be to interpolate premature ventricular con-
tractions during tachycardia to separate the signals, although
this would have to be repeated at every mapped point. This
will afford 2 benefits: (1) we can define whether the mecha-
nism is reentrant or automatic based on resetting characteris-
tics and (2) based on which signals were moved and whether
the tachycardia reset or not we can determine whether the
perceived signals are critical to the arrhythmia and may be
reasonable ablation targets.
Ideally, if one can map during tachycardia using any or all
of the techniques previously mentioned and compare signals
against those seen during sinus rhythm to identify the por-
tions of the fascicles most critical to arrhythmia propagation,
then ablation can be targeted at these most critical sites while
salvaging areas that may not be as relevant. However, these
 13  Kapa et al  Fascicular Ventricular Tachycardia Management
approaches need to be balanced against the limitations, which
include the need to repeatedly induce tachycardia and having
a well-placed multipolar catheter.
Several final key points need to be considered during abla-
tion. First, given that the fascicular and Purkinje fibers are
relatively superficial, transmural lesions are typically not nec-
essary to achieve success. In addition, during ablation, there
is potential to cause activation of the Purkinje tissue and to
induce ventricular fibrillation. Finally, premature ablation
without fully defining the circuit elements first should not be
done as ablating prematurely proximally or distally may make
further analysis/acquisition of signals difficult (eg, ablation
of a secondary exit during more distal ablation leading to a
change in QRS morphology but with continued tachycardia).
Ablation Outcomes
Overall success rates for ablation of IFVT range from 70% to
90% over long-term follow-up.52,53 Over a follow-up of almost
5 years, in those who recurred, a shorter VT cycle length at
baseline was the only predictor of recurrence, and most com-
monly recurrence involved the same fascicle, although in a
third involved the left upper septal fascicle. The upper sep-
tal fascicle in IFVT has been suggested to be an orthodromic
form of IFVT and ≈50% of patients presenting with this form
of IFVT will have had a previous ablation for a more com-
mon form related to the left anterior or posterior fascicles.44
The role of creating fascicular or partial fascicular block in
patients with IFVT is unclear, although it has been suggested
that in patients with noninducible tachycardia, creation of at
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least partial fascicular block may serve as a reasonable end
point.54 However, others have suggested that in cases in which
mapping during tachycardia can be performed, the develop-
ment of fascicular block may be unnecessary.55
Conclusions
IFVT is a common source of arrhythmia. Fascicular ven-
tricular arrhythmias may occur in both structurally normal
and abnormal hearts. However, the traditional paradigm
of IFVT consists of verapamil-sensitive tachycardias that
occur in the setting of an otherwise structurally normal
heart. Although pharmacological therapy may be effective,
ablation, especially when VT is inducible at the time of
electrophysiology study, has a high success rate. Differenti-
ation of VT due to the fascicular system versus surrounding
structures (eg, the mitral annulus or papillary muscle) can
be difficult but possible with careful mapping and character-
ization of the mechanism of arrhythmia. Although ablation
undertaken during sinus rhythm may be effective, ideally
ablation should be done in VT to optimize likelihood of suc-
cess but requires careful mapping of fascicular, Purkinje,
and myocardial potentials. Future therapies may allow for
improved targeting of the critical circuits of IFVT while
avoiding damage to adjacent myocardium, but use of such
therapies and whether they may improve outcomes of abla-
tion remains to be seen.
Acknowledgments
We would like to acknowledge the contributions of Dr Siva Mulpuru
in providing relevant case slides and figures.
Sources of Funding
S. Kapa is supported by a Mayo Clinic Department of Medicine
Career Development Grant.
Disclosures
None.
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KEY WORDS: anatomy ◼ arrhythmias, cardiac ◼ electrophysiology ◼ tachycardia,
ventricular