Ventricular Preex c it at io n

An Anomalous Wave Interfering with

the Ordered Ventricular Activation
Giuseppe Bagliani, MDa,b,c,*, Roberto De Ponti, MD, FHRSd,e,
Francesco Notaristefano, MDb, Claudio Cavallini, MDb,
Margherita Padeletti, MD, Phscf, Fabio M. Leonelli, MDg,h

KEYWORDS
 Ventricular preexcitation  Kent bundle  Mahaim fibers  ECG recording  Oesophageal pacing

KEY POINTS
 The presence of an accessory pathway, usually located between atria and ventricles, generates a
ventricular preexcitation.
 Short PR, delta wave, and wide QRS are the typical signs of ventricular preexcitation.
 A small preexcitation can be misleading, but an obvious pattern can be incorrectly diagnosed;
therefore, great care must be taken in the ECG interpretation.
 Precision electrocardiology, starting from basic electrophysiology, identifies a diagnostic method
that is the cornerstone for the clinician and for the interventional electrophysiologist.

INTRODUCTION involved in cardiac arrhythmias, which should be

The general, electrophysiologic concept of cardiac
preexcitation consists of the presence of an
accessory electrical path able to activate a portion
of the ventricular muscle or the conducting sys-
tem, earlier than normal.
Cardiac preexcitation refers to 2 conducting
fronts in equilibrium with each other, with an acti-
vation fusion well evident on surface electrocar-
diogram (ECG) (Fig. 1).
Depending on anatomic and physiologic condi-
tions, the preexcitation can be maximal or con-
cealed (Fig. 2). Independently from the degree of
preexcitation, an accessory pathway (AP) can be
carefully identified and investigated and, for this
aim, the ECG still represents the best tool.
In the past 3 decades, the knowledge of AP has
improved after the initial introduction of intracavi-
tary EP and later ablation; by this tool the complete
the AP anatomy and electrophysiology were
confirmed and fully characterized.1 Manifestations
of preexcitation on the ECG have been typically
associated with the presence of 3 different fea-
tures historically named with the first observer
(Fig. 3):
1. Short PR, Delta wave, wide QRS: a typical AP
connecting atria and ventricles (Kent bundle)

No funding sources to be acknowledged.

a
Arrhythmology Unit, Cardiology Department, Foligno General Hospital, Via Massimo Arcamone, Foligno,
Perugia 06034, Italy; b Cardiovascular Disease Department, University of Perugia, Piazza Menghini 1, Perugia
06129, Italy; c Arrhythmology and Electrophysiology Department, IRCCS Policlinico San Donato, San Donato
cardiacEP.theclinics.com

Milanese, Milano, Italy; d Department of Heart and Vessels, Ospedale di Circolo, Viale Borri, 57, Varese
21100, Italy; e Department of Medicine and Surgery, University of Insubria, Viale Guicciardini, 9, Varese
21100, Italy; f Cardiology Unit, Mugello Hospital, Viale della Resistenza, 60, Borgo San Lorenzo, Florence
50032, Italy; g Cardiology Department, James A. Haley Veterans’ Hospital, 13000 Bruce B Down Boulevard,
Tampa, FL 33612, USA; h University of South Florida FL, 4202 East Fowler Avenue, Tampa, FL 33620, USA
* Corresponding author. via Centrale Umbra 17, 06038 Spello (PG) - ITALY
E-mail address: giuseppe.bagliani@tim.it

Card Electrophysiol Clin 12 (2020) 447–464

https://doi.org/10.1016/j.ccep.2020.08.011
1877-9182/20/Ó 2020 Elsevier Inc. All rights reserved.
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448 Bagliani et al
2. Short PR and normal QRS: a possible connec-
tion between atrial and His bundle (James
bundle)
3. Normal PR, Delta wave, and wide QRS: an
atypical AP with slow conducting properties
connecting atria and ventricles (Mahaim fibers)
Wolff-Parkinson-White (WPW) syndrome is
defined as the combination of diagnostic ECG
pattern with arrhythmias in which the AP can be
either part of the tachycardia circuit or just a
bystandard.2
THE CONCEPT OF ORDERED VENTRICULAR
ACTIVATION
The normal conduction system is a complex struc-
ture that has the role of efficiently combining the
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Fig. 1. Unappreciable and obvious
Kent bundle preexcitation: ECG
criteria. On both sides of the figure
a Kent bundle (red tract) connecting
the atria and ventricles is present.
On the left side of the figure the KB
is unable to activate the ventricles
and preexcitation is unappreciable
(Normal values of PR and QRS). On
the right side the Kent bundle (red ar-
row) is able to preexcite the ventricles
generating the delta wave, short-
ening PR (110) and widening QRS
(160).
depolarization-contraction of the heart; this is
achieved optimizing heart rate, atrial activation,
atrioventricular conduction delay, and ventricular
depolarization. On the ECG, it is possible to iden-
tify the progression of the activation wavefront
from the atria to the ventricles through the atrio-
ventricular node (AVN)–His-Purkinje system
(HPS) and deduce the specific proprieties of the
conduction system and of the myocardium
(Fig. 4).
 Atrial activation and P wave (intra-interatrial
conduction)
From the sinus node bundles, the impulse
propagates along a bundle of atrial
muscular fibers specifically structured to
allow the orderly activation of the right
atrium at a conduction velocity that is
Fig. 2. Atrioventricular conduction in
the presence of a Kent bundle. This
ECG shows a very rare situation in
an 80-year-old man. Five atrial beats
(P1-P3-P5 sinus rhythm; P2 and P4 pre-
mature atrial beats) are conducted to
the ventricles in a different way: P1:
PR 110/QRS 160; Obvious ventricular
preexcitation (blue circle), P2: PR
100/QRS 180; Maximal ventricular
preexcitation (red circle), P3: PR 210/
QRS 90; Unappreciable ventricular
preexcitation (green circle), P4: No
QRS follows P4; this means that P4 is
blocked in both AV connections (AV-
Node and Kent bundle), P5: PR 140/
QRS 110; Minimal ventricular preexci-
tation (yellow circle); only the com-
parison with the other cardiac cycles
will be able to perform the diagnosis.

almost double most of the atria. The
Bachmann bundle and thin sleeves of
atrial muscle around the coronary sinus
guarantee interatrial activation and left
atrium activation occurs 40 to 50 ms later
in the right atrium.
 Atrioventricular junction (AVJ) and PR interval:
AVJ is deputed to conduction of the atrial
wavefront to the ventricles and the PR is the
corresponding segment on the ECG. Anatom-
ically, the AVJ is located within the triangle of
Koch, and can be divided in 3 portions with a
central portion (the compact node) connected
proximally with the atria (by the atrio-nodal
connections) and distally with the intraventric-
ular conducting system (by the bundle of His).
Features of the 3 structures are as follows:
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ECG and Preexcitations 449
Fig. 3. Three different features of
ventricular preexcitation. 1) Short
PR, Delta Wave, wide QRS: a typical
AP connecting atria and ventricles
(Kent bundle). 2) Short PR and normal
QRS: a possible connection between
atrial and His bundle (James bundle).
3) Normal PR, Delta Wave and wide
QRS: an atypical AP with slow con-
ducting properties connecting atria
and ventricles (Mahaim fibers).
 Atrio-nodal connections: The atrial input to
the AV node is a sodium-dependent con-
ducting system with a fast pathway anteri-
orly and a slow conducting pathway
posteriorly; the dynamic equilibrium be-
tween the 2 pathways is at the base of the
physiologic AV delay modulation mani-
fested on the ECG with PR variations.
 The compact AVN, due to its calcium-
dependent conduction, is the site where
most of the AV delay takes place.
 The bundle of His is a very short structure
with the fastest propagation velocity and
sodium-dependent conduction
 Intraventricular conduction and QRS com-
plex: The His bundle branches into a left and
right bundle propagating the wavefront to
the Purkinje network. The entire HPS is a
Fig. 4. The conducting system and
the activation of the cardiac cham-
bers. Time sequence of activation of
the heart; the normal value on the
ECG (see text for further explana-
tion). RA, right atrium; SVC, superior
vena cava; SN, sinus node; FO fossa
ovalis; IVC, inferior vena cava; CS, cor-
onary sinus; CN compact node; INE,
inferior nodal extensions.
450 Bagliani et al

Fig. 5. Electrogenesis of delta wave.

Delta wave is a partial anticipation
of the ventricular activation due to a
fast connecting AP (Kent Bundle, red
arrow).

high-speed sodium-dependent conducting In presence of a Kent bundle, a strand of

system that guarantees the well-ordered myocardial tissue directly connects atrial and ven-
time and spatial activation of the ventricles; tricular muscle across the AV grove, realizing an
this generates the QRS, which duration is electrical AP in parallel with the normal conducting
less than 120 ms. system (Fig. 5).
After atrial activation, the normal front of activa-
tion is delayed within the AVN, while proceeds
DOUBLE ACTIVATION OF THE VENTRICLES: faster along the Kent bundle to activate the sur-
COMMON AND UNCOMMON rounding ventricular myocardium with a cell-to-
OBSERVATIONS ON THE KENT BUNDLE AND cell “saltatory” conduction; this slow propagating
DELTA WAVE wavefront within the V will generate the classic
Overview of Delta Wave Inscription ECG features of WPW pattern: the characteristic
“Delta wave”, a short PR interval and a wide QRS
Ventricular preexcitation via a Kent bundle is the complex. After slowly traveling through the AVN,
most common form of this conduction abnormality the normally conducted wavefront will reach and
and its dynamics can be explained with simple rapidly depolarize the remaining ventricular mass
principles.

Fig. 6. Electrogenesis of the “Pure

Delta wave,” advanced concepts on
the preexcited QRS. Red line and bar
show the first component of the delta
wave (Pure Delta Wave).

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generating a fused QRS. The degree of fusion, is a
dynamic process varying from a stable to progres-
sive increase (see Fig. 2) or beat to beat changes
(see Fig. 1).
If V preexcitation occurs late, it may be possible
to identify a tardive inscription of the delta wave
modifying the terminal QRS vector. Some investi-
gators have propose a number of ECG features
allowing identification of the presence and location
of the AP.3
“Pure Delta Wave” and the Multicomponent
of a Totally Preexcited QRS
During sinus rhythm, a completely preexcited QRS
can occur following a complete AV-block induced
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ECG and Preexcitations 451
Fig. 7. The QRS and preexcitation:
from fusion to total preexcitation. In
basic conditions we can observe a
fusion between the Kent bundle
(red arrow) and the normal con-
ducting system (green arrow). Fast
Adenosine infusion blocks the AVN
conduction and Kent bundle totally
activates the ventricles (see text for
further details).
by adenosine infusion or during antidromic tachy-
cardia (see the article “Accessory-Pathway medi-
ated Tachycardias: ‘Precision Electro Cardiology’
through standard and advanced ECG recording
techniques” elsewhere in this issue; Fig. 6). In
both situations, we have the opportunity to study
the complete delta wave propagation in the ventri-
cles. If waveform progression was only due to
myocyte to myocyte activation (saltatory conduc-
tion) given its low velocity would last for a very
long period with a resulting QRS of approximately
400 ms or more.
Preexcitation behaves as other rhythms origi-
nating in the ventricle such as ventricular tachycar-
dias or pacemaker rhythms where the initial slow
Fig. 8. relationship between AP loca-
tion and the percentage of preexcita-
tion. During normal sinus rhythm,
right AP shows a more prominent
delta wave with respect to the left
side; this last shows maximum degree
of preexcitation by a single left atrial
pacing (second QRS on the right
panel).
452 Bagliani et al

Fig. 9. Ventricular preexcitation and QRS normalization. The normalization occurs after a long cycle (A) or after a
short cycle (B). Further explanation in text.

saltatory conduction will increase due to penetra-
tion into the peripheral ramifications of the normal
conducting system Fig. 6.
Likewise, the initial wavefront originated by the
AP, initially traveling at low velocity (0.3 m/s), will,
at some point, encounter the peripheral arboriza-
tions of the HPS and, having penetrated it, it will
markedly increase its propagation velocity (around
2 m/s). This change of velocities is manifested on
the ECG with variations of waveform slope and po-
larity (see Fig. 6). These alterations could be
confusing when attempting to identify the AP vec-
tor and define its localization. This is why in the
diagnostic algorithms (see the article “Algorithms
to Identify Accessory Pathways’ Location on the
12-lead ECG,” elsewhere in this issue; see Fig. 3)
the vectorial analysis is restricted to the first 20
ms of QRS, the “Pure Delta Wave”. Fig. 6

Fig. 10. Concertina effect. A continuous, fluctuating degree of the preexcitation is due to modulation of AVN
conduction secondary to vagal-mediated breathing phases.

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demonstrates how, after the first 20 ms (the “pure”
delta wave), there is an increase in voltage/time as
the Purkinje fibers become involved in spreading
the V wavefront. The duration of the “pure” delta
wave can vary depending on the relationship be-
tween peripheral HPS divisions and the KB intra-
mural branching.
In Fig. 7, the totally preexcited QRS induced by
adenosine infusion evidences an initial slow prop-
agating wavefront followed by 2 very fast compo-
nents (V1 and V2) explained by hypothesizing the
following:
A. An initial cell-to-cell propagation, typically
slow: the pure delta wave (red arrow in Fig. 7)
B. A wavefront penetration in the subendocardial
His-Purkinje fibers producing an initial fast
component of the QRS (V1 in Fig. 7)
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ECG and Preexcitations 453
Fig. 11. “Source and sink effect” and
unappreciable preexcitation. On in-
tracavitary recordings the AP depolar-
ization can be recorded as a “local
preexcitation” (red arrow) failing to
proceed past that point (the QRS is
normal). RF ablation abolishes the po-
tential of Kent bundle (green arrow).
C. A period of slow propagation probably due to
transseptal conduction
D. Reengagement of the HPS in the other
ventricle and inscription of the second fast
component of the ECG (V2 in Fig. 7)
This hypothesis is supported by similar observa-
tions made during ventricular tachycardias and
pacemaker rhythms.
FROM MAXIMAL TO CONCEALED
PREEXCITATION: A DYNAMIC EQUILIBRIUM
BETWEEN 2 PATHWAYS
Anatomic Factors Influencing Kent Bundle
Conduction
1. Kent bundle location on the AV grove (Fig. 8): A
right AP will shows a maximal degree of preex-
citation being very close to the initial activation
Fig. 12. Linking in AP and the func-
tional translation of the refractory
period of the AP. See text for
explanation.
454 Bagliani et al

Fig. 13. Supernormal conduction at

the base of alternant conduction in
the AP a retrograde conducted AVN-
HPS impulse modifies the ERP of the
Kent bundle activating the supernor-
mal mechanism for the conduction.

of the right atrium. The propagating wavefront Factors Influencing Normal Atrioventricular
will rapidly proceed to the right ventricle shortly Node Conduction
after being generated by the sinus node. The
The compact AVN is the site where AV conduction
location of a left side Kent bundle is far from
delay occurs. This property is highly dynamic
right atrial activation origin: the more lateral its
determining, for example, each R-R interval during
location the less obvious the degree of preexci-
atrial arrhythmias such as atrial fibrillation. Struc-
tation decreases until the Kent bundle becomes
turally, the AVN presents a slow and a fast atrial
electrically silent (inapparent Kent bundle).
input with different electrophysiological character-
2. Intrinsic Kent bundle conduction properties: an
istics. The latter runs, in some cases, a completely
AP consists of small fibers of ordinary myocar-
extranodal course and in so doing conducts very
dium linking the atrium with the basal ventricu-
rapidly across the AVJ: a situation indistinguish-
lar myocardium, across the AV groove. They
able from atrio-His connections able to generate
function as a sort of an electrical wire and
short PR and normal QRS (in the past called
obey a number of the laws of electricity. Vol-
“James bundle”) (see Fig. 3). Autonomic tone
ume, course, and atrial and ventricular ramifica-
and many drugs affect AVN with opposite effects.
tions are some of the variables affecting the AP
likelihood to be successfully depolarized (see
later in this article).

Fig. 14. Suspected preexcitation:

deep ECG analysis. Two ECG with sus-
pected preexcitation: PR 5 110 ms,
QRS 120; No clear delta wave. Anal-
ysis of PR dispersion (PRmax-PRmin)
on 12 leads and initial vector in lead
aVR. (A) A short PR dispersion (less
of 20 ms) and the initial “r” in V1
(green circle) excludes the diagnosis
of ventricular preexcitation. (B) A
long PR dispersion (more of 20 ms)
and the absence of the initial “r” in
aVR strongly suggests the presence
of a ventricular preexcitation.

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 ECG and Preexcitations 455

Fig. 15. Vagal hypertonia increases

the preexcitation degree.

Accessory Pathway and Atrioventricular single source depolarization (in case of block of
Node–His-Purkinje System Refractoriness and AP or AVN) or no conduction at all (in case of AP
Conduction and AVN-HPS block). Catecholaminergic increase
of the heart rate is able to improve conductivity
The refractory period, the time required to restore
and shorten refractoriness in both AVN and AP:
excitability, is an important variable determining
the comparative effects on each limb is often
the degree of preexcitation (see Fig. 2). Although
different and individually determined creating the
the AP behaves with a “all or none” response to
conditions for an increase (Fig. 9A) or a
premature stimulation,4 the AVN, with its decre-
decrease/block (Fig. 9B) of the preexcitation.
mental properties, has a more varied response.
“Concertina effect” is a continuous variation of
This different refractoriness in the 2 AV connec-
preexcitation degree, often synchronous with the
tions can be demonstrated during APC of
breathing. In this case the variable delta wave is
increasing prematurity.
due to modulation of AVN conduction secondary
The responses will include a modulation of AVN-
HPS contribution to overall V depolarization, a

Fig. 16. Transesophageal atrial pac-

ing and the differential diagnosis of
cardiac preexcitation. (A) A single
atrial pacing (asterisk) is associated
with PR prolongation and normal
QRS (green arrow) or PR prolonga-
tion and BBB (blue arrow): cardiac
preexcitation can be excluded. (B) Af-
ter a drive (black asterisks) a single
premature atrial stimulus (red
asterisk) shows a delta wave and
wide QRS: ventricular preexcitation
is confirmed.

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456 Bagliani et al
to shifting vagal tone induced by the respiratory
phases (Fig. 10).
COMPLEX ELECTROPHYSIOLOGICAL
PHENOMENA INFLUENCING PREEXCITATION
The degree of preexcitation cannot be fully
explained by the dynamic interplay of the 2 AV
conducting paths. Some other phenomena that
are a combination of electrical properties and elec-
trophysiological behavior also need to be
considered.
“Source- Sink” Phenomenon and Concealment
A propagating wavefront through myocardial tis-
sue (source), needs to have a level of charge
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Fig. 17. Suspected ventricular preex-
citation: a 3-step diagnostic algo-
rithm. (1) ECG analysis: in case of PR
interval less of 120 ms, ventricular
preexcitation can be confirmed if
dispersion of PR is longer of 20
msec, or if R wave is absent in aVR
or if QRS transition is in V1 or before.
(2) Vagal stimulation (or adenosine):
see Fig. 15 and text. (3) Programmed
atrial pacing: see Fig. 16 and text.
sufficiently high to depolarize the tissue in front
(the sink). When 2 structures with different electric
characteristics merge, there is a potential for
source-sink mismatch and the propagation will
fail.5,6 This is the case of an AP, which, although
activated on time to preexcite the ventricles,
carries a charge too low to depolarize the ventri-
cles. The amount of charge depends, in part, on
the anatomic characteristics of the AP (see the
article “Anatomy of the AV Junction, AV Grooves,
and Accessory Pathways,” elsewhere in this issue)
and the direction of the depolarizing wavefront. On
intracavitary recordings the AP depolarization can
be recorded as a “local preexcitation” (red arrow in
Fig. 11) failing to proceed past that point.
Fig. 18. Electrogenetic mechanisms of
ventricular repolarization in normal
conditions and preexcitation. On the
left side, the normal sequence of ven-
tricular depolarization/repolarization
is represented. On the right side, in
presence of ventricular preexcitations
an asynchronous depolarization/
repolarization process realizes shift-
ing the J point, ST segment, and T
wave.

Linking
Extended ECG recordings can, at times, show a
number of puzzling QRS variations. An alternans
of maximum and no preexcitation at a stable
rate, disappearance of preexcitation following an
increase in atrial rate, QRS normalization persist-
ing at longer atrial cycle length normally associ-
ated with ventricular preexcitation (Fig. 12).
The phenomenon cannot be explained by sim-
ple competitive conduction between AVN and
AP; it is instead due to retrograde concealed de-
polarization of the AP by the antegrade wavefront
proceeding from the AVN-HPS. This retrograde
penetration will render the AP refractory to the
subsequent antegraded depolarization. For linking
to occur in sinus rhythm, a subtle combination of
timing, refractoriness and AP location must be
combined.7 The phenomenon is much more com-
mon during atrial fibrillation where the high fre-
quency of stimulation allows concealment to
occur both in proximal and distal end of the AP.
Supernormal Conduction
At times, AP block on alternate beats (Fig. 13) is
shown during a Holter monitoring. The mechanism
of block cannot be explained with the previously
discussed mechanisms as preexcitation starts to
alternate when the intrinsic heart rate increases.
The best explanation for this uncommon obser-
vation is super normal conduction through the AP
when the effective refractory period (ERP) of this
bundle has been modified by a retrograde conduc-
tion of an AVN-HPS conducted impulse.8
Rate, retrograde penetration, and a baseline
long ERP of the AP all play a role in the induction
of a phenomenon infrequently observed.
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ECG and Preexcitations 457
ELECTROCARDIOGRAM IN PREEXCITATION:
LIMITS AND FINE POINTS
The classic ECG triad associated with preexcita-
tion includes short PR (P-delta wave) lasting
120 ms, slurring of the QRS upstroke (delta
wave), and wide QRS (>120 ms). These parame-
ters can be measured when the QRS is maximally
preexcited or when the degree of preexcitation is
obvious because the delta wave is at least 40 ms
in duration.9 Maximal preexcitation is easily recog-
nized on ECG in the presence of a right AP (see
Fig. 8). On the contrary, in the presence of left
AP, the path is located far away from the emergent
sinus impulse and therefore unable to generate an
appreciable pattern of preexcitation with a minimal
delta wave. On the base of the percentage of
fusion between KB and normal QRS we can iden-
tify 4 patterns of ventricular preexcitation identifi-
able in 4 well-distinct ECG patterns (see Fig. 2):
1. Maximum preexcitation: the QRS is totally or
almost totally preexcited and the PR interval is
extremely short (and the QRS very wide).
2. Obvious preexcitation: a delta wave is well
evident lasting 40 ms or more; a pattern due
to a ventricular fusion is usually well evident,
the PR interval is clearly short.
3. Minimal preexcitation: this is a situation in
which the delta wave is only a smooth wave
lasting less than 40 ms, the PR is, in most
cases, near the normal range. This represents
a very confounding situation.
4. Unappreciable preexcitation: The delta wave is
absent, PR interval and QRS are completely
normal; it is possible that preexcitation may
become noticeable in other situations such as
Fig. 19. Left BBB (LBBB) with short
PR. Short PR (110 ms) and an LBBB
morphology of the QRS. After an
ectopic beat the QRS normalizes and
PR remains stable (110) excluding
the presence of cardiac preexcitation.
458 Bagliani et al
during an arrythmia, a change in autonomic
tone, or drug effect.
The most important clinical determinant of sud-
den coronary death in WPW syndrome is not the de-
gree of preexcitation but the presence of it. This
makes identification of the presence of a delta
wave the most import clinical observation in the
management of these patients. Although in obvious
preexcitation, ECG-based AP localization is the next
step well aided by effective algorithms (Derek Crin-
ion and colleague’ article, Algorithms to Identify
Accessory Pathways’ Location on the 12-Lead
Electrocardiogram,” in this issue); in the presence
of minimal preexcitation an algorithm may be neces-
sary to confirm the presence of a Kent bundle.
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Fig. 20. Vagal hypertonia and preex-
citation. Vagal hypertonia unmasks
ventricular preexcitation; PR: 80 ms,
delta wave (red arrow).
MINIMAL PREEXCITATION: THE NEED FOR AN
ALGORITHM
A minimal preexcitation is observed when only a
small portion of ventricular muscle is activated by
the Kent bundle; in this case, the vectorial force
of the delta wave is too weak to “imprint” every
ECG lead and it can be appreciated only in leads
nonperpendicular to the axis of the delta wave. In
case of minimal preexcitation, the classic criteria
for the diagnosis of cardiac preexcitation may
not be completely fulfilled; that is, PR interval
may not necessarily be 120 ms or QRS wider
than 120 ms. Other criteria have been proposed
to confirm a suspected AP in this case based on
Fig. 21. Mahaim preexcitation. An
apparent LBBB. The presence of rS in
lead III together with a very small Q
waves in V6, alerts about the possibil-
ity of Mahaim fibers.

subtle ECG alterations induced by a minimal de-
gree of V preexcitation.
Because the PR interval is variable among the
12 ECG leads (Fig. 14), some investigators pro-
posed to define the difference between maximal
and minimal PR as “PR dispersion” (PRd: differ-
ence between longest and shortest PR).
Combining a PRd 20 ms with a PR interval
120 ms achieved, in the same study, a specificity
of 100%.
Other criteria that appeared to be highly predic-
tive when used to confirm the presence of preexci-
tation in case of negative PRd were the absence of
septal vector in aVR (red arrow in Fig. 14) and a
transition in V1 or before in left lateral APs.2
In presence of a suspected delta wave,
increasing vagal tone or infusing adenosine, it is
possible to decrease or block the AV node con-
duction and so obtain the classic pattern of ven-
tricular preexcitation (short PR and wide
preexcited QRS) (Fig. 15). In the same way,
Fig. 16 shows it is possible to use the pro-
grammed atrial pacing (delivered by esophageal
catheter) to obtain the classic pattern of ventricu-
lar preexcitation (see Fig. 16B) or exclude it (see
Fig. 16A).
We propose a 3-arm algorithm (Fig. 17) to
confirm or exclude a ventricular preexcitation
when a suspect exists. At first we do a meticulous
ECG analysis. In the second step, we propose
vagal maneuvers or fast adenosine infusion and,
as third step, programmed atrial pacing.
MULTIPLE ACCESSORY PATHWAYS
Multiple AP are present in approximately 10% of
patients and are rarely suspected although their
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ECG and Preexcitations 459
presence is relevant in terms of risk of SCD and
in planning the approach to ablation. Their pres-
ence is most often suspected during AF when
changing preexcited ECG morphologies strongly
suggest the presence of more than one AP
spatially separated (see the article “Arrhythmias
with By-stander Accessory Pathways,” elsewhere
in this issue; see Fig. 3). This needs to be distin-
guished from variable degrees of single AP preex-
citation due to variable fusion. Spontaneous
change of different antidromic AVRTs or shifting
from an antidromic to orthodromic tachycardia
can be explained only by the presence of at least
2 APs. More difficult to identify, but equally diag-
nostic, is the evidence of changing retrograde P
morphology during orthodromic tachycardia.
In SR the signs may be more subtle and suspi-
cion of the presence of more than one AP is
heightened by the fact that the delta wave
morphology is not consistent with one of the
described patterns. This should also be consid-
ered in the light of left ventricular hypertrophy, pre-
vious myocardial infarction (MI), or congenital
heart disease that may alter the expected ECG
pattern.
VENTRICULAR PREEXCITATION AND
REPOLARIZATION
The Paradigm of Normal Cardiac
Repolarization
Normal ventricular repolarization begins from the J
point, continuing with the ST segment and T wave.
The J point and ST segment are on an isoelectric
line and T wave is monophasic with a polarity
“on-phase” with the QRS (Fig. 18).
Normal repolarization is initially isoelectric due
Fig. 22. Postero-septal pathways
mimics a previous inferior MI.
460 Bagliani et al

to the presence of a long plateau (Phase 1–2 of
the action potential) of similar voltage across
the different myocardial layers; during this period
there will be no differential potential or transmu-
ral currents in the heart: this corresponds to an
iso-electric J point and ST segment. On the con-
trary, during the final stage of repolarization
(Phase 3 of the AP), the epicardial layers repo-
larize before the corresponding endocardial
layers with resultant transmural voltage gradient.
A current is therefore generated giving origin to
the T wave.
Ventricular Repolarization Following
Preexcitation
In presence of preexcitations, as during bundle
branch block (BBB) or single-chamber pacing,
asynchronous depolarization of an area of
myocardium is accompanied by an equally asyn-
chronous repolarization process (see Fig. 18).
This will lead to a shifting of the J point-ST
segment and T wave changes.
Specific patterns can be generated: pseudo-ST
elevation MI, pseudo-non-ST elevation MI, ven-
tricular overload, or nonspecific inverted T wave;
at times these abnormalities can be more obvious
than preexcitation itself.
Electrical Memory
Electrical memory is a phenomenon related to
ions-channels conditioning during repolarization
that can continue to remain impaired after depolar-
ization normalizes. The phenomenon can be
extremely insidious, as these repolarization abnor-
malities can coexist with a perfectly normal QRS
and so leading the diagnostic process in a wrong
direction.
PREEXCITATION DIFFERENTIAL DIAGNOSIS:
THE BIG MIMES OF CARDIOLOGY
Ventricular preexcitation represents, for the clini-
cian, a diagnostic challenge to identify the anat-
omy of the AP its electrophysiological properties
and manifestations.

Fig. 23. Ventricular preexcitation mimics acute MI. From normal conduction (green box) to obvious preexcitation
(red box). The secondary impairment of ventricular repolarization (yellow arrow) simulates acute inferior MI.

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 ECG and Preexcitations 461

The immediate recognition of the ECG anomaly
together with its deductive analysis is the basis of
any successful ECG interpretation. Superficial
analysis of the tracing in a setting of a busy prac-
tice can often miss the subtle manifestations of
preexcitation or confuse it with other more com-
mon pathologies, such as conduction delays,
ischemic or hypertensive cardiomyopathies, or
premature ventricular beats. A step-by-step
approach where observation is followed by inter-
pretation and final synthesis requires some time
fully dedicated to this diagnostic aim.
ECG pathologies potentially mimicking preexci-
tation include the following.
recording of the initial saltatory conduction is
more in keeping with a ventricular origin of the im-
pulse than with a supraventricular beat with con-
duction block (Fig. 20). A close examination of
an ECG during ventricular preexcitation will also
identify the features of 2 fusing wavefronts of acti-
vation with a slow initial component followed by a
very fast late one.
Vagal maneuvers or adenosine challenge will
quickly dispel any remaining doubt by
1. Shortening the PR and widening the QRS in the
case of preexcitation
2. Prolonging the PR with unchanged QRS in the
case of BBB

Conduction Delays or Blocks The diagnosis is more difficult is the case of

A trouble of intraventricular conduction (delay or
block) in presence of a PR interval at lower limits
can mime a ventricular preexcitation Fig. 19.
In a fully manifested AP conduction with a delta
wave lasting over 40 ms does not offer any diag-
nostic dilemma, as this feature is associated with
a marked PR shortening. Furthermore, the
Mahaim fibers, which present with a normal PR
due to the decremental AP properties and an un-
usual QRS without a classic delta wave and a
configuration resembling left BBB (Fig. 21). Preex-
citation is rarely present and it is very subtle. The
presence of rS in lead III together with Q waves
in I, aVL and V6, although at times observed in

Fig. 24. Acute MI in patient with preexcitation. (A) Obvious preexcitation with minimal impairment of ST-T in V3-
V4-V5-V6. (B) Acute MI (inferior, red arrow), without any change of the preexcitation degree.

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462 Bagliani et al

healthy individuals, should alert the clinician to the
possibility of Mahaim fibers especially in patients
with unexplained palpitations.10 The clinical risk
of this condition is low in view of the slow AP ante-
grade conduction.
Previous Myocardial Infarction
A preexcited ECG can show deep Q waves in the
leads where the polarity of the delta wave is nega-
tive. Postero-septal pathways typically show
negative delta waves in inferior leads and they
are often misinterpreted as a previous inferior MI
Fig. 22. The clinical evaluation and the echocardi-
ography are usually able to differentiate the 2 con-
ditions and further tests (eg, vagal maneuvers,
adenosine, stress test) are seldom required.
Acute Ischemia
Secondary repolarization abnormalities associ-
ated with ventricular preexcitation can mimic con-
ditions associated with ST segment elevation or
depression either acute such as acute MI
Fig. 23, or chronic such as ventricular overload
or stable ischemic cardiomyopathy. The
previously proposed diagnostic algorithm and the
clinical evaluation are of paramount importance
to confirm or exclude the presence of an AP to
provide the proper treatment without forgetting
that, in rare circumstances, preexcitation and
acute pathologies can coexist (Fig. 24). The ECG
should be carefully evaluated even after ablation
because repolarization changes associated with
cardiac memory can be erroneously interpreted
as an expression of structural cardiac diseases.
Ectopic Beats
Ventricular ectopic beats frequently begin with a
prolonged intrinsicoid deflection due to slow myo-
cyte to myocyte propagation. This delay can be
confused with a delta wave particularly if a P
wave in a preceding T wave cannot be excluded
or if a late VPC occurs immediately after a P
causing a “pseudo” short PR Fig. 25. In the un-
usual and confusing case of persisting PR relation-
ship some observations will help. Preexcitation is a
dynamic phenomenon and it is closely correlated
with PR variations. Observing multiple unfused
VPCs will demonstrate a fixed morphology despite

Fig. 25. Ventricular ectopic beats miming ventricular preexcitation. ECG recording of a parasystolic rhythm (beats
with color circles). The red circle shows a P wave casually occurring before QRS miming ventricular preexcitation;
the green circles evidences that the wide QRSs are independent from the atrial activity so excluding ventricular
preexcitation.

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 ECG and Preexcitations 463

Fig. 26. Idioventricular rhythm miming ventricular preexcitation. Red circle shows an apparent preexcitation
(short PR, wide QRS) that will be excluded by the next sequence: yellow circle is a fusion beat, blue circle is a cap-
ture, green circle is a beat in which the ventricular activity is dissociated from the atrial one.

changes in PR duration excluding the possibility of SUMMARY

AP conduction. Furthermore, vectorial analysis of
a delta wave is consistent with a specific site,
whereas the ectopic QRS has a morphology that
does not match any possible AP location.
An idioventricular rhythm competing with sinus
rhythm can pose a diagnostic challenge as the
QRS complexes can be, at times, preceded by
a P wave (Fig. 26). The resulting “pseudo” PR in-
tervals vary in subsequent beats and the QRS
morphology changes because of variable degree
of fusion between the ectopic beat and the
sinus activation wavefront. Observing a long
rhythm strip will identify periods of varying sinus
rate showing the opposite response of idioven-
tricular rhythm and AP conduction to these
variations.
As sinus rate increases P-P interval shortens
making fusion more common while in the presence
of an AP the degree of preexcitation should
decrease due to improved AVN conduction during
slowing of sinus rates. The opposite is true during
periods of increased sinus rates.
The presence of AV dissociation excludes the
presence of typical AP.
The ECG interpretation of patients with ventricular
preexcitation reveals enthusiastic moments of
reflection regarding the conductive phenomena
of the heart. An anomalous wave interferes with
the ordered ventricular activation and vice versa:
from the detailed analysis of a simple ECG-signal
we can meticulously reconstruct all stages of the
process.
The ECG continues to be the main tool and this
will also be so in the future.
The ECG analysis of APs is a return to the origins
of cardiac electrophysiology and of ECG
recording, but with a modern approach that looks
to the future. This is precision electrocardiology
that incorporates the analysis of the electrophysi-
ological phenomena of the heart at 360 : from
anatomy to electrophysiology, both macroscopic
and cellular. The biophysics of individual ion chan-
nels is the fundamental element of cardiac con-
duction, under normal and preexciting conditions.
Although an accessory connection deals with a
problem concerning the processes of depolariza-
tion of the heart, even ventricular repolarization is

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464 Bagliani et al
consequently impaired: this must absolutely be
considered.
The "precision ECG interpretation" is so funda-
mental for diagnostic orientation, differential diag-
nosis, anatomic localization, and
electrophysiological characterization of specific
accessory connections.
No clinical, prognostic, and therapeutic process
can rule out such a precision interpretation pro-
cess of ECG.
DISCLOSURE
Dr R. De Ponti has received lecture fees from Bio-
sense Webster and Biotronik; educational grants
from Biosense Webster, Biotronik, Medtronic,
Abbott, Boston Scientific, Bayer, Pfizer, Boeh-
ringer Ingelheim; and research grants from Acte-
lion. None for the other authors.
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