American Journal of Emergency Medicine (2009) 27, 878–888

www.elsevier.com/locate/ajem

Diagnostics

Preexcitation syndromes: diagnostic consideration in the ED

Dustin G. Mark MD a , William J. Brady MD d , Jesse M. Pines MD, MBA, MSCE a,b,c,⁎
a
Department of Emergency Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
b
Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania School of Medicine,
Philadelphia, PA 19104, USA
c
The Leonard Davis Institute Of Health Economics, University of Pennsylvania, Philadelphia, PA 19104, USA
d
University of Virginia Health Sciences Center, Charlottesville, VA 22908, USA

Received 10 June 2008; accepted 16 June 2008

Abstract Preexcitation syndromes are a common cause of paroxysmal tachycardias presenting to the
ED. Emergency physicians should be familiar with the common electrocardiographic manifestations
of preexcitation, particularly the Wolff-Parkinson-White abnormality, as these conditions require
specific therapeutic management. This article reviews the pathophysiology of preexcitation, along
with the electrocardiographic findings of Wolff-Parkinson-White and its associated tachyarrhythmias.
© 2009 Elsevier Inc. All rights reserved.

1. Introduction of the ventricular fascicles), and other variations such as

Preexcitation is defined as a “premature activation of
the ventricular myocardium by an impulse that travels by
an anomalous path and…avoids physiologic delay in the
atrioventricular junction” [1]. Preexcitation as a finding on
electrocardiography (ECG) has come to be known as the
“Wolff-Parkinson-White abnormality,” after the authors
who first systematically described the appearance of
preexcitation and its association with paroxysmal tachy-
cardia. Several variations of preexcitation syndrome have
been described, being differentiated from one another by
the anatomy of the anomalous path, or accessory pathway.
Examples of accessory pathways include atrioventricular
(AV) tracks (extensions of atrial myocardium that connect
to ventricular myocardium by bridging the electrically
insulating fibrous AV septum), nodofascicular tracks
(connection between the AV node and a distal portion
⁎ Corresponding author. Tel.:+1 215 662 4050.
E-mail address: pinesjes@uphs.upenn.edu (J.M. Pines).
nodoventricular, fasciculoventricular, and atriofascicular
tracks. Most of these bypass tracts can result in
ventricular preexcitation and can predispose to reentry
arrhythmias manifested as the clinical syndrome of
preexcitation, paroxysmal tachycardia, and its associated
symptoms of palpitations, dizziness, and/or syncope.
Accessory AV pathways are responsible for most cases of
Wolff-Parkinson-White (WPW) syndrome. Wolff-Parkinson-
White syndrome is commonly used in reference to the finding
of preexcitation on the ECG, and syndrome is attached if
paroxysms of tachycardia occur. Findings suggestive of
WPW syndrome on 12-lead ECG analysis are found in 1.5 to
3.1 per 1000 persons in Western populations [2-4,8]. The
actual incidence of WPW syndrome may be higher because
not all cases of preexcitation are evident on standard 12-lead
ECG in the absence of paroxysmal tachycardia. Some cases
require high-resolution ECG or invasive electrophysiologic
studies for diagnosis (referred to as “concealed” WPW
syndrome) [5].
An accessory pathway creates ventricular preexcitation
by conducting atrial impulses to the ventricle faster than

0735-6757/$ – see front matter © 2009 Elsevier Inc. All rights reserved.
doi:10.1016/j.ajem.2008.06.013
Preexcitation syndromes: diagnostic consideration in the ED 879

Table 1 Syndromic associations with WPW syndrome 3. Demographics

Disease Examples Comments
classification
Although in most cases there is no strong pattern of
genetic inheritance, some cases of WPW syndrome occur
Congenital heart Ebstein's anomaly, 10% of Ebstein's either as part of a single inherited trait of preexcitation or as
disease tetralogy of Fallot anomaly have WPW
part of a broader genetic syndrome with more extensive
syndrome
cardiac disease [17]. Emergency physicians should have a
Familial Familial 5-10% have ECG
hypertrophic hypertrophic findings of heightened awareness for the possibility of preexcitation
cardiomyopathy cardiomyopathy preexcitation when evaluating these patients. Table 1 lists those syndromes
Metabolic and Tuberous sclerosis, Cases with tuberous associated with WPW syndrome.
mitrochondrial Pompe disease, sclerosis seen in
disorders Leber's hereditary association with
optic neuropathy cardiac
(LHON) rhabdomyoma 4. Pathophysiology

Before discussing abnormal conduction, it is illustrative

the native atrioventricular node, potentially providing a
substrate for reentry arrhythmias and paroxysmal tachy-
cardia. Paroxysmal tachycardia can present clinically as
palpitations, dizziness, or frank syncope. Sudden death is
also possible with WPW syndrome in the setting of
extremely rapid and sustained tachycardia. However, this
is rare with an estimated incidence of 1 per 1000 patient-
years in persons with known ventricular preexcitation [6-
11]. This article will primarily focus on a description of
the pathophysiology of and 12-lead ECG manifestations
of WPW syndrome.
to review normal heart conduction and ECG findings
(Fig. 1). Preexcitation occurs when an atrial impulse is
conducted in an anterograde (atria to ventricle) fashion
down an AV accessory pathway before the AV node-His-
Purkinje axis begins depolarization. How this manifests
clinically and on the ECG depends on how much faster the
atrial impulse is conducted down the accessory pathway
into the ventricular myocardium as opposed to the AV node-
His-Purkinje axis. The classic “short P-R” interval descrip-
tion of WPW syndrome is a result of premature ventricular
depolarization mediated by the AV accessory pathway. This
early ventricular depolarization manifests on the ECG as
both a short P-R interval and a slurred upstroke in the R

2. A brief history of WPW syndrome

Drs Wolff, Parkinson, and White first described the

syndrome now known as WPW syndrome in 1930 in a report
of 11 patients with a short P-R interval, “bundle-branch
block,” and paroxysmal superventricular tachycardia and/or
atrial fibrillation [12]. Descriptions of similar ECG and
clinical findings had been published as early as 1915 but were
not ascribed to a single syndrome [13]. It was not until 1959
that accessory AV pathways were determined to be
responsible for the findings in WPW syndrome, although
such pathways had been described in 1893 by Stanley Kent
[14].This discovery has allowed electrophysiologists to map
out and ablate accessory pathways, albeit initially with
varying rates of success and complications depending on the
location of the pathway. The introduction of radiofrequency
energy for use in ablative procedures in the late 1980s Fig. 1 The impulse formation and conduction process in a patient
allowed for tremendous improvements in the success rates of with normal sinus rhythm. “A” denotes transmission of the impulse
through intraatrial pathways to the AV node. “B” denotes
this procedure. In clinical practice today, nearly all accessory
transmission of the impulse through the AV node and into the
pathway locations are amenable to attempts at ablative
His-Purkinje system. “C” represents the propagation of the impulse
therapy, with reported recurrence rates between 2% and 9% through the ventricular myocardium via the specialized conduction
[15]. More recently, advances in the understanding of WPW system. The ECG complex is the surface electrical manifestation of
syndrome have been made on the molecular level with the this process with a normal PR interval and QRS complex,
discovery of a familial form of WPW syndrome linked to a exhibiting the normal conduction through the atria to the AV
single gene [16]. node (“A” and “B”) and ventricles (“C”), respectively.
880
Fig. 2 The impulse formation and conduction process in a patient
with WPW syndrome in normal sinus rhythm. “A” denotes
transmission of the impulse through intraatrial pathways to the
AV node. “B” denotes transmission of the impulse through the AV
node and into the His-Purkinje system. “C” describes the rapid
conduction of the impulse through atrial tissues to the accessory
pathway, arriving at the ventricle sooner than anticipated had
normal transmission occurred via the AV node; this action is
manifested as a shortened PR interval on the ECG. “D,” the delta
wave, is the segment of ventricular myocardium that depolarizes
earlier than anticipated had normal conduction occurred. “E” is the
summation or fusion of the electrical waveforms transmitted to the
ventricular myocardium via both the accessory pathway and AV
node—as depicted by a widened QRS complex.
Fig. 3 Left lateral accessory AV pathway. Subtle delta waves are best seen in leads V3 and V4. A positive delta wave in V1 and the inferior
leads (II, III, aVF) along with a negative to isoelectric QRS in lead aVL point to this location in this ECG. This patient was admitted for atrial
fibrillation with a rapid ventricular response and wide QRS morphology.
D.G. Mark et al.
wave, referred to as the delta wave. The delta wave
represents relatively disorganized and slow ventricular
depolarization via the accessory AV pathway and ends at
the point at which AV nodal conduction begins to
successfully propagate, thus creating a terminal narrow
QRS complex (Fig. 2). Other ECG manifestations may
include a prolonged (N120 milliseconds) QRS complex and
secondary ST-T waves changes that are discordant to the
QRS vector.
The presence of a delta wave indicates that AV accessory
pathway conduction is faster than AV node conduction,
creating a substrate that can predispose to preexcitation
arrhythmias in the setting of either AV nodal blockade or
rapid rates of atrial depolarization, such as atrial fibrillation.
Rates of pre-excited tachycardias depend on the length of the
refractory period of the accessory pathway tissue, which is
usually longer than that of the AV nodal tissue. This
difference in refractory period length provides the substrate
by which a premature atrial depolarization can incite AV
reentry tachycardia (AVRT).
5. Electrocardiographic features of WPW
syndrome
There are 3 ECG criteria for diagnosing WPW
syndrome; a short (b120 milliseconds) PR interval, a
Preexcitation syndromes: diagnostic consideration in the ED 881

Fig. 4 Right posteroseptal accessory AV pathway. Occasional narrow QRS complexes without evidence of preexcitation are seen (arrows). The
QRS and delta waves in the inferior leads are negative during preexcitation, simulating prior inferior myocardial infarction. The right ventricular
origin is indicated by the negative delta wave in V1, which promptly becomes upright in V2. Delta waves are best seen in the lateral precordial leads.

delta wave, and an anomalous QRS configuration. The locations for accessory AV pathways are, in decreasing
last of these is the most variable factor and depends on order of frequency, left lateral (free wall), posteroseptal,
the location of the bypass tract. The most common right free wall, and anteroseptal.

Fig. 5 Left posteroseptal accessory AV pathway. As in Fig. 4, negative delta and QRS deflections are seen in leads III and aVF, mimicking
prior inferior myocardial infarction. The left ventricular origin of this pathway is indicated by the positive delta wave in V1.
882 D.G. Mark et al.

Fig. 6 The same patient in Fig. 4, now with suppressed accessory pathway conduction. Procainamide was administered to this patient after
an episode of atrial fibrillation with rapid ventricular conduction and a wide QRS complex. Note the inverted T waves in the inferior leads,
which are the result of ventricular memory of preexcitation in these leads.

5.1. Left lateral accessory pathway ECG, preexcitation via this pathway results in a positive
delta wave and QRS in V1, upright delta and QRS in the
The most commonly found accessory AV pathways insert inferior leads (as opposed to posteroseptal locations, see
into the lateral free wall of the left ventricle (Fig. 3). On the below), and Q waves with negative to isoelectric deflections

Fig. 7 Wide QRS complex tachycardia (WCT) with retrograde

AV node conduction in the patient with WPW syndrome, an ART.
This form of WCT uses the accessory pathway as the anterograde
limb of the reentry loop (“A”) with the AV node functioning as the
retrograde limb (“C”). The reentry loop involves the ventricular
(“B”) and atrial (“D”) myocardium. The impulse arrives at the
ventricle via the accessory pathway and is propagated distally via
the ventricular myocardium; the QRS complex is widened in that
the His-Purkinje system is not used to rapidly and efficiently
propagate the impulse, thereby producing a wide QRS complex.
Fig. 8 Narrow QRS complex tachycardia (NCT) with antero-
grade AV node conduction in the patient with WPW syndrome, an
orthodromic reciprocating tachycardia (ORT). This form of NCT
uses the AV node as the anterograde limb of the reentry loop (“A”)
with the accessory pathway functioning as the retrograde limb
(“C”). The reentry loop involves the ventricular (“B”) and atrial
(“D”) myocardium. The impulse arrives at the ventricle via the AV
node and is propagated distally using the His-Perkinje system,
thereby producing a narrow QRS complex.
Preexcitation syndromes: diagnostic consideration in the ED 883

Fig. 9 Atrioventricular reentry tachycardia. A reentry circuit in which an electrical impulse is conducted down the AV node-His-Purkinje
axis, forming a narrow QRS complex, and reentering the atria via retrograde conduction through an AV accessory pathway distant from the AV
node. Note the distinct p waves following the QRS complex in lead V1 (red arrow; pseudo-r′ waves) and in leads II, III, and AVF (blue arrow;
pseudo-S waves), thus creating a “short r-p” tachycardia pattern. This patient manifested ventricular preexcitation on resting ECGs. (For
interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

in any of the lateral leads (I, aVL, V5, or V6). These Q waves
can give the mistaken impression of a former high lateral
myocardial infarction and can give the appearance of right
axis deviation.

5.2. Posteroseptal accessory pathway

The second most common location for an AV bypass tract

is in the posteroseptal region of the AV groove. Ventricular
preexcitation from this pathway manifests on the ECG with
negative deflecting delta waves and QRS complexes in the
inferior leads (II, III, aVF). Preexcitation via this pathway is
thus often mistaken for prior inferior myocardial infarction
and can give the appearance of left axis deviation. Those that
are situated in the right ventricle show negative delta and
QRS deflections in V1 (Fig. 4), whereas those in the left
ventricle show positive deflections (Fig. 5). Acute suppres-
sion of accessory pathway conduction can also result in ST-T Fig. 10 Irregular, wide QRS complex tachycardia consistent with
preexcited atrial fibrillation in the patient with WPW syndrome.
wave abnormalities suggestive of ischemia (Fig. 6).
This form of atrial fibrillation uses the AV node (“A”) and accessory
pathway (“B”) for anterograde conduction to the ventricular
myocardium. “C” is the segment of ventricular myocardium
6. Electrocardiographic features of WPW which depolarizes earlier than anticipated had normal conduction
occurred. “D” is the summation or fusion of the electrical
syndrome
waveforms transmitted to the ventricular myocardium via both
the accessory pathway and AV node—as depicted by a widened
Accessory AV pathway activity is determined by the QRS complex. The resultant ECG waveform is an irregular, wide
electrophysiological properties of the pathway tissue, includ- QRS complex tachycardia with delta wave and beat-to-beat
ing the rate of tissue depolarization, length of the refractory variation in QRS complex morphology.
884
Fig. 11 Preexcited atrial fibrillation in the patient with WPW
syndrome. The ECG waveform is an irregular, wide QRS complex
tachycardia with delta wave and beat-to-beat variation in QRS
complex morphology. The delta wave, not present in all beats,
signifies the depolarization of the ventricular myocardium due to
the impulse arriving via the accessory pathway. The beat-to-beat
variation in the QRS complex results from the varying contribution
to ventricular depolarization arriving via the accessory pathway and
the AV node.
period, and differentials in these properties when confronted
with anterograde (atria to ventricle) or retrograde (ventricle to
atria) directions of conduction. An accessory AV pathway can
be seen as 2 separate tracks, one running from the atria to the
ventricle and the other heading in the opposite direction. The
clinical syndrome of WPW can likewise be categorized into 2
separate disorders: (1) those arrhythmias that result from
anterograde accessory AV pathway conduction (resulting in a
wide QRS complex) and (2) those that use retrograde
Fig. 12 Atrial fibrillation with WPW syndrome. Note the variety of QRS morphologies, but the relatively constant amplitude of voltages, in
contrast to the wide variation in QRS voltages seen with PVT. A probable fusion beat is seen (arrow).
D.G. Mark et al.
accessory AV pathway conduction (resulting in a narrow
QRS complex). Examples of the first include atrial
tachycardias (ie, atrial fibrillation) that result in premature
and disorganized ventricular depolarization via the accessory
AV pathway or the uncommon antidromic reciporicating
tachycardia (ART) in which an impulse becomes entrained in
a circuit involving the accessory pathway and the AV node,
traveling in a retrograde (ie, antidromic) fashion up the AV
node from ventricle to atria, and in turn down the accessory
pathway from atria to ventricle (Fig. 7). The same circuit may
run in the opposite direction, in which case it is called
orthodromic reciporicating tachycardia (ORT), in which the
retrograde conduction from ventricle to atria occurs through
the accessory AV pathway instead of through the AV node
(Fig. 8). Orthodromic reciporicating tachycardia is much
more common than ART and largely encompasses the narrow
QRS complex variety of WPW syndromes. These 2 entities
are clinically distinct, as the acute management of wide and
narrow QRS arrhythmias mediated by accessory AV path-
ways is different in the acute setting. However, the therapeutic
implications of ablative therapy are the same for both entities
and both warrant referral for electrophysiologic evaluation.
6.1. Orthodromic reciporicating tachycardia or AVRT
ORT, or AVRT, is a common presentation of WPW
syndrome, as most accessory AV pathways are in fact only
capable of retrograde conduction. Atrioventricular reentry
tachycardia can be initiated in the setting of a premature atrial
complex when the refractory period of the accessory AV
Preexcitation syndromes: diagnostic consideration in the ED 885
886 D.G. Mark et al.

Fig. 13 Continued.
Preexcitation syndromes: diagnostic consideration in the ED 887

pathway is longer than that of the AV node. For this to occur,
the premature atrial complex must occur early enough in the
cardiac cycle to be blocked from anterograde conduction
down the accessory pathway but late enough to allow for
successful conduction through the AV node. As a result, a
normally conducted impulse from the atria is spread
throughout the ventricles by the AV node-His-Purkinje axis
(referred to as orthodromic conduction) and passes back into
the atria in a retrograde fashion though the now excitable
accessory AV pathway (Fig. 8). As long as the atrial fibers are
not refractory to depolarization at the time this impulse
arrives, the atria will depolarize prematurely (ie, before the
sinus node depolarizes), setting up a reentrant circuit. Rates of
ventricular depolarization typically range between 150 and
250 beats per minute. A representative ECG of AVRT is
shown (Fig. 9). Note that the p wave is distinctly seen
following the QRS, giving a “short r-p interval” tachycardia.
This is in contrast to the typical form of AV nodal reentry
tachycardia (AVNRT), in which the p wave is often buried in
the QRS complex due to simultaneous activation of both atria
and ventricles. However, a discrete p wave can be appreciated
following the QRS complex in up to 30% of AVNRT, making
this an imperfect discriminator between AVRT and AVNRT,
and thus a nonspecific indicator for the presence of an
accessory AV pathway [18].
Another confounding factor in detecting the presence or
absence of an accessory AV pathway is that accessory AV
pathways do not always conduct in an anterograde direction
and thus do not demonstrate preexcitation on standard 12-lead
ECGs [5]. These are commonly referred to as “concealed”
accessory pathways. Concealed accessory AV pathways may
still facilitate arrhythmias or simply lay inactive and/or
dormant. Atrioventricular reentry tachycardia in the absence
of findings of WPW syndrome on a sinus rhythm ECG is thus
also referred to as “concealed” WPW syndrome.
6.2. Wolff-Parkinson-White syndrome with atrial
fibrillation
Another concerning feature of AVRT is that it can
disorganize into atrial fibrillation, which can have disastrous
consequences in patients with accessory AV pathways
capable of anterograde conduction (Fig. 10). Atrial impulses
can reach an accessory pathway at a rate of 300 to 400 times
per minute and may result in hemodynamic instability due to
rapid rates of ventricular response, far in excess of that
allowed by the AV node-His-Purkinje axis. Although
accessory pathways typically have longer refractory periods
than the AV node, and thus should not be capable of pacing
the ventricles faster than the AV node, this refractory period
can shorten markedly at high rates and allow for a rapider rate
of conduction than the AV node. This manifests as a wide
QRS complex tachyarrhythmia with an irregular rate, the
differential of which includes WPW syndrome with atrial
fibrillation, polymorphic ventricular tachycardia (PVT), and
atrial fibrillation with interventricular conduction delay.
Distinguishing between these rhythms can be extremely
difficult. Having access to a previously recorded ECG in
these cases is critical.
Polymorphic ventricular tachycardia tends to exhibit
chaotic and haphazard QRS complex voltages as opposed
to the other 2 entities and thus is the most likely diagnosis if
wide voltage variation in QRS complexes is present. These
patients may have a history of alcoholism, poor nutritional
status, or excessive diuretic use, all of which predispose to
hypomagnesemia and the torsades de pointes variety of PVT.
An ECG obtained before the tachycardia may reveal a
prolonged QT interval in these individuals. Alternatively,
PVT can be sequelae of preexisting ischemic heart disease,
congenital long QT syndrome, or acute coronary syndromes.
In most cases, the ECG will suggest the correct diagnosis
based on the chaotic electrical nature of this rhythm.
In contrast, AF with interventricular conduction delay
usually manifests QRS complexes that are consistent in
appearance across the ECG. Rates of ventricular depolariza-
tion in these cases tend not to exceed 190 to 200 beats per
minute, which is usually the upper limit of AV nodal
conduction cycles. Such ECGs in rare instances may also
show an occasional narrow complex QRS without a delta
wave if the conduction delay is rate induced, which would
alternatively suggest the correct diagnosis. Prior ECGs
showing sinus rhythms with similar morphologies of
ventricular conduction delays strongly suggest this diagnosis.
Wolff-Parkinson-White syndrome with AF should be
suspected based on clinical history and ECG features.
Patients who present with a history of multiple episodes of
sudden syncope in the absence of known cardiovascular
disease are particularly suspicious. The ECG can demon-
strate a variety of findings, with QRS morphologies varying
widely depending on the location of the accessory pathway
and the relative rate of AV nodal conduction (Fig. 11). The
presence of any simultaneous conduction via the AV nodal

Fig. 13 Series of ECGs from a patient with WPW syndrome and atrial fibrillation, treated with procainamide (courtesy of Ralph Verdino,
MD). A, WPW syndrome with atrial fibrillation on presentation to the ED. Irregular wide QRS complex tachycardia with varying QRS
configurations representing varying degrees of accessory pathway mediated ventricular preexcitation and concomitant AV node mediated
conduction. This is differentiated from PVT by its relatively nonchaotic pattern and from SVT with aberrant conduction by both the
heterogeneity of QRS complexes and the lack of a stereotypical bundle-branch pattern. B, ECG recorded after initiation of treatment with
procainamide in the ED. Note intermittent narrow QRS complexes due to Na+ channel–mediated blockade of accessory pathway conduction.
C, ECG obtained later that day showing normal sinus rhythm with a narrow QRS complex. The procainamide infusion was discontinued at this
time. D, ECG from the following day demonstrating a return of ventricular preexcitation. The patient was subsequently taken to the
electrophysiology laboratory for a successful radiofrequency ablation.
888
pathway may manifest as a fusion beat QRS complex,
which can be an additional clue to this rhythm (Fig. 12).
Patients in this rhythm can deteriorate quickly and require
emergent management, either with antiarrhythmic therapy
(Figs. 13A-D) or electrical cardioversion.
7. Pediatric considerations
Wolff-Parkinson-White syndrome is a relatively common
cause of superventricular tachycardia (SVT) in young
children. Approximately 60% of children with SVT will
manifest their arrhythmia within the first year of life, most
often by 3 to 4 months of life [19]. Up to 20% of newly
diagnosed SVT in children will reveal WPW syndrome after
conversion to sinus rhythm [20]. Many of these children will
lose their predisposition to tachycardia, as the electrical
properties of the accessory pathways can change with age.
These patients may present with new onset tachyarrhythmias
to the ED, and emergency physicians should be familiar with
the treatment in this population. Major deviations from adult
management include a higher reliance on vagal maneuvers
(ie, ice bags applied to the face to stimulate a diving reflex),
more reliance on medical management, and the use of digoxin
as a means of arrhythmia suppression. Syndromic associa-
tions are of particular importance in this group (Table 1).
8. Summary
Wolff-Parkinson-White syndrome is a rare but potentially
lethal conduction disturbance that requires specific emergency
management. Emergency physicians should thus be intimately
familiar with common ECG manifestations. Asymptomatic
cases warrant prompt cardiology referral on an outpatient
basis, whereas symptomatic cases should be hospitalized in
conjunction with electrophysiologic evaluation.
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