cal entity.
4 Paroxysmal tachycardias are estimated to occur
Ventricular Preexcitation
Practical Considerations
James M. Richardson, MD
preexcitation syndromes are important be-
\s=b\ Ventricular
cause they are associated with paroxysmal tachycardias that
can result in serious cardiovascular complications and sud-
den death. These syndromes are also important because the
ECG findings, if unrecognized, are frequently misdiagnosed as
something else. With the use of "classic" syndrome names,
for example, the Wolff-Parkinson-White (WPW) syndrome,
physicians tend to think of ventricular preexcitation in a rigidly
defined sense (short PR interval, delta wave, and abnormal
QRS). A broader view of ventricular preexcitation allows one to
think of it as an entity with endless variations. Failure to
recognize the wide ECG variations in which ventricular preex-
citation occurs may have substantial clinical consequences
relative to misdiagnosis and treatment.
(Arch Intern Med 1983;143:760-764)
is generally given to Wolff, Parkinson, and
Recognition
White1 who in 1930 first described the clinical syn¬
drome that bears their names. This syndrome was de¬
scribed as having a bundle-branch block with a short PR
interval occurring in healthy young people prone to parox¬
ysmal tachycardia. Aberrantly conducted ventricular com¬
plexes had been described as early as 1909, but it was Wolff
et al1 who observed the association of such aberrantly
conducted complexes with paroxysmal tachycardias.
We now recognize that WPW syndrome is just a part of
the broader entity called ventricular preexcitation. Preex-
citation, as defined by Durrer et al,2 "exists if, in relation to
atrial events, the whole or some part of the ventricular
muscle is activated earlier by the impulse originating from
the atrium than would be expected if the impulse reached
the ventricles by way of the normal specific conduction
system only." The resulting QRS complexes are fusion
beats, and all gradations of fusion can occur. This makes
classifications by syndrome, such as the WPW syndrome,
less rigid and less than totally satisfactory. Two other
widely known types of ventricular preexcitation syndromes
are the Mahaim syndrome (normal or prolonged PR inter¬
val, delta wave, and abnormal QRS complexes) and the
Lown-Ganong-Levine (LGL) syndrome (short PR interval,
absent delta waves, and normal QRS complexes).3
The term syndrome, when related to ventricular preex¬
citation, does not apply until the ECG or other elec-
trographic evidence (His bundle studies, etc) is associated
with paroxysmal tachycardia. The development of tachy¬
cardias makes ventricular preexcitation an important clini-
Accepted for publication Dec 6,1982.
From the Departments of Medicine, University of California School of
Medicine, San Francisco, and the Fairmont Hospital, San Leandro.
Reprint requests to Fairmont Hospital, 15400 Foothill Blvd, San Leandro,
CA 94578 (Dr Richardson).
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in 40% to 80% of cases with ventricular preexcitation, most
of which are reentrant supraventricular tachycardia (75%
to 80%), with atrial fibrillation occurring in 20% to 25% of
cases. Atrial flutter occurs rarely.5 On the other hand,
approximately 5% to 10% or more of all patients with attacks
of paroxysmal tachycardia have ventricular preexcitation.
The ultimate concern about paroxysmal tachyarrhyth-
mias is the possible development of angina, acute myocar-
dial infarction, congestive heart failure, syncope, circula¬
tory compromise with shock, cerebral vascular accidents,
ventricular tachycardia, ventricular fibrillation, and sud¬
den death.6"8
The reentrant supraventricular tachycardia most com¬
monly is conducted over the normal atrioventricular (AV)
system for antegrade conduction and over the accessory
pathway for retrograde conduction. This results in a tachy¬
cardia with a normal QRS duration. A tachycardia mimick¬
ing ventricular tachycardia associated with a wide QRS is
less frequent. It results when the reentrant circuit is
antegrade over the accessory pathway and retrograde over
the normal conduction system.9
Patients with ventricular preexcitation in whom atrial
fibrillation and atrial flutter develop are more likely to
deteriorate into ventricular fibrillation than those with any
other arrhythmia. This may result in a ventricular response
of 250 to 300 beats per minute.5·810 This is usually due to a
very short refractory period in the accessory pathway by
either antegrade and/or retrograde bypass conduction. In
adults without ventricular preexcitation, untreated atrial
fibrillation and atrial flutter usually conduct to the ventri¬
cles via the AV node, which results in a ventricular response
of less than 180 beats per minute.5,9 Very high ventricular
rates may, therefore, be of diagnostic and prognostic value
in ventricular preexcitation. In addition, patients with
atrial fibrillation are very likely to be receiving digitalis
(48%)10 and digitalis can, by blocking the AV node, increase
antegrade conduction over the accessory pathway.11 In this
manner, digitalis can increase the ventricular rate in atrial
fibrillation and atrial flutter and further complicate the
medical treatment of these patients.
Other arrhythmias that have been observed to occur with
ventricular preexcitation are supraventricular ectopie
beats, with or without aberrant conduction, ventricular
premature beats, AV dissociation, and atrial and ventricu¬
lar parasystole.5 Premature contractions occur with in¬
creased frequency in ventricular preexcitation and range
Fig 1.—Ventricular preexcitation with "classic" Wolff-Parkinson-
White pattern, type A, mimicking inferior wall myocardial infarction.
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 Fig 3.—Top, 12-lead ECG tracing shows small delta waves in leads I, III, aVL, and aVF. Bottom,
Rhythm strip on same patient illustrates blocked wave occurring immediately after third QRS
complex. This is followed by atrial escape beat with aberrant conduction, premature ventricular
contraction (PVC), second escape beat, premature atrial contraction with aberrant conduction, and
then return to sinus rhythm. Ventricular preexcitation then occurs, alternately demonstrating
concertina effect, and mimicking PVCs. With concertina effect, PR interval varies in association with
changes in magnitude of delta waves and occurs progressively. In other words, PR interval gradually
becomes shorter with more prominent delta waves, and conversely, it becomes longer, with less
prominent delta waves caused by varying degrees of fusion. Three types have been described.67

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 from 18% to 63%. The higher figure may result if 24-hour
ECG monitoring is done.1 The occurrence of ectopy has
importance because both spontaneous or induced ectopy
can initiate and terminate tachyarrhythmias, thereby in¬
creasing the likelihood of paroxysmal tachycardia in this
clinical entity.912'13
MISDIAGNOSIS
A second major reason why it is important to recognize
ventricular preexcitation when it exists is because an
erroneous diagnosis usually means that a nonexistent myo¬
cardial disease is diagnosed. The misdiagnosis will usually
be either myocardial infarction, bundle-branch block, or
ventricular hypertrophy. Up to approximately 50% of pa¬
tients with ventricular preexcitation are thought to have
their conditions misdiagnosed.3
A number of theories exist to explain ventricular preex¬
citation, but anatomical studies give support to the belief
that embryologie faults" (embryonal rests),3 in partitioning
of the atrium from the ventricle, with persisting muscular
bridges passing through the faulty ring,14 account for the
phenomenon in most cases. In an effort to understand ven¬
tricular preexcitation, it is desirable to be familiar with a
classification of ventricular preexcitation based on anatomi¬
cal and physiologic features of the disorder, as Gallagher et
aP have proposed. The Kent's bundle, which is the most
common anatomical substrate, would then become the
accessory AV connection; the atrio-Hisian fiber becomes
the atriofascicular bypass tract; the James fiber becomes
the internodal bypass tract; Mahaim fibers become the
nodo-ventricular connection; and the Paladino tract be¬
comes the septal accessory AV muscle bundle and the
transitional nodo-ventricular bundle.9,1215 Gallagher et al16
also thought that accelerated conduction in the AV node
may account for some of the cases of ventricular preexcita¬
tion.16
The 12-lead ECG is the primary modality for diagnosing
ventricular preexcitation, and the delta wave is the hall¬
mark. Diagnosis can be supplemented by ambulatory ECG
(Holter) monitoring, stress testing, vectorcardiography,
His bundle electrography, and epicardial mapping.310·1417'18
The surface ECG is of benefit only in approximating the
location of bypass tracts and connections. It does not allow
discrimination of free wall accessory pathways from septal
accessory pathways.7 The ECG, though, is of considerable
benefit to the ECG interpreter, by providing a basis for
understanding why certain patterns occur and why they
mimic or mask specific unrelated organic cardiac disease.
Rosenbaum et al19 provided what is now known to be a
useful though incomplete classification of WPW syndrome,
which divides the ECG findings into two types, types A and
B. In type A, the delta wave is directed anteriorly and
usually to the right, resulting in tall R waves in V2 disclosing
patterns of R, RS, Rs, RSr^andRsr1. Leads V5 and V6 show
Rs or R deflections. These complexes mimic right ventricu¬
lar hypertrophy, right bundle-branch block, true posterior
wall myocardial infarction,5 simple counterclockwise rota¬
tion, and electrode misplacement (Fig 1).
Type has the delta wave directed posteriorly and
usually to the left, resulting in the precordial leads, V4
through V6 along with leads I and aVL, disclosing tall
R waves along with delta waves. Leads V, and V2 show
negative QRS complexes (negative delta waves) manifest¬
ing QS waves. These complexes mimic a left bundle-branch
block, anteroseptal myocardial infarction, and left ventric¬
ular hypertrophy5 (Fig 2). An inferior wall myocardial
infarction may be mimicked by negative delta waves occur¬
ring in inferior leads (II, III, and aVF).
Ventricular preexcitation can also give false-positive
ECG abnormalities during stress testing for ischemie heart
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Fig 4.—Ventricular preexcitation with "classic" Lown-Ganong-Le-
vine pattern, namely, short PR interval, absent delta wave, and
normal QRS.
disease.18 The ST segment depression apparently occurs
because of the basic conduction disturbance seen in this
disorder, especially in type B.517
No other set of ECG findings mimic so perfectly such a
large number of important organic cardiac diseases. Ven¬
tricular preexcitation is truly the "great masquerader" in
electrocardiography.
THINGS TO KNOW THAT SHOULD INCREASE
THE ACCURACY OF DIAGNOSIS
IN VENTRICULAR PREEXCITATION
1. "Classic" ECG findings are often not present (Fig 1).
2. Delta waves may be small or even notched. The delta
wave should be observed in two or more QRS complexes in a
lead, in at least two separate leads. The "Eiffel Tower"
pattern,20 or what I prefer to call the "reversed h" configura¬
tion, is often not typical (Fig 2).
3. Delta waves often have a negative component in addi¬
tion to the well-known positive component. This negative
component may mimic the q or QS pattern of infarction (Fig
1).
4. Delta may occur in any lead, in different sizes,
waves
at differenttimes, even in the same patient, or they may
disappear completely. Multiple tracings or cardiac monitor¬
ing may be necessary before ventricular preexcitation can
be diagnosed (Figs 2 and 3).
5. Delta waves may be manifested only in premature
contractions.
6. Ventricular preexcitation may occur intermittently
during an ECG tracing and can mimic premature beats that
are occurring late. The PP interval usually is unchanged in
these cases (Fig 3, bottom).
7. Delta waves may not be seen during tachyarrhythmia
but may reappear after the rhythm and rate have returned
to normal.
8. The delta wave may be characteristically absent as in
LGL syndrome (Fig 4).
9. Notching relatively high on the left side of the R waves
may be a clue that it is a delta wave.
10. Q waves in leads I, aVL, V6, and V5 may be absent (Fig
1). This is an important clue. It mimics a left bundle-branch
block.
 11. The PR interval may be less than, equal to, or greater
than 0.12-s duration (Fig 2). Many physicians look only for
the short PR interval.
12. The PR interval will usually be shortest before the
QRS complex demonstrating the delta wave. Measurement
of the PR interval in the complex without a delta wave may
result in missing the short PR interval and the diagnosis of
ventricular preexcitation (Fig 1).
13. Tall R waves in Vi and V2 should alert one to the
possibility of ventricular preexcitation (Fig 1). This may be a
very striking feature in Vj, mimicking a right bundle-
branch block, right ventricular hypertrophy, or true pos¬
terior infarction.
14. Tachyarrhythmias should alert one to the possibility
of ventricular preexcitation, especially if the ventricular
rate is greater than 200 beats per minute.
15. Atrial fibrillation in association with ventricular pre¬
excitation may have ventricular rates of 250 to 300 beats per
minute with broad bizarre complexes. This is one of the few
clinical situations in which the ventricular rate can occur
that rapidly. Another situation may occur when quinidine-
like drugs are given for atrial fibrillation in the absence of
digitalization.
THERAPY
Electrophysiologic studies can provide information about
the mechanism of arrhythmias and demonstrate functional
properties of therapeutic importance by localizing the site
of preexcitation and allowing the drug of choice to be
determined.5,7 These studies are indicated for those pa¬
tients whose pattern of living continues to be disrupted by
tachyarrhythmias despite medical therapy.12
In most instances, paroxysmal supraventricular tachy¬
cardia associated with ventricular preexcitation syndromes
will convert spontaneously to normal sinus rhythm. Initia¬
tion of reflex mechanisms by means of breath holding,
performing Valsalva's maneuver or carotid sinus massage
may often terminate the tachycardia.4,5,8,12 Intravenously
administered verapamil (Isoptin)21,22 is the drug of choice for
most cases of paroxysmal supraventricular tachycardia. It
works by interrupting reentry at the AV node. Verapamil
has no effect on conduction across accessory bypass tracts,
nor does it alter normal atrial action potential or intra-
ventricular conduction time (as reported in the October 1981
Primary Cardiology Supplement [pp A-25-A-28], Hospital
Physician). Intravenous propranolol hydrochloride (In¬
derai) is a second major drug used in the treatment of
paroxysmal supraventricular tachycardia with normal QRS
in ventricular preexcitation.5,7,12 Propranolol has no effect on
antegrade conduction or refractoriness in the accessory
pathway and is useless in the situation that is manifested by
rapid irregular ventricular complexes aberrantly con¬
ducted with a rate greater than 200 beats per minute.
Cardioversion is indicated in this instance.12
The use of digitalis is controversial in the treatment of
tachycardias associated with ventricular preexcitation, but
there seems to be general agreement regarding the recom¬
mendation that digitalis is contraindicated in atrial fibrilla¬
tion and atrial flutter. This is especially the case if there is
aberrant conduction over anomalous AV conduction path¬
ways,5,8,12 resulting in a broad bizarre QRS complex.
Ventricular fibrillation is more frequent in this circum¬
stance.9 On the other hand, digitalis is considered to be the
drug of choice by many physicians for the treatment of
paroxysmal supraventricular tachycardia when it occurs in
newborns and infants with this disorder.17
Intravenously administered lidocaine hydrochloride is an
important drug to consider in ventricular preexcitation
when there is anomalous conduction, particularly with
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atrial fibrillation or atrial flutter. Procainamide hydro-
chloride or quinidine sulfate in some circumstances may be
equally effective, especially with supraventricular tachy¬
cardia. An alternate form of therapy is cardioversion.5
In severe tachyarrhythmias resistant to medical treat¬
ment or in patients intolerant to medication, radio frequen¬
cy-activated pacemaker therapy may be feasible and effec¬
tive. Its use is based on the fact that premature stimulation
of the atrium or the ventricle can initiate and terminate
tachyarrhythmias. By introducing a premature depolariza¬
tion, especially near the preexcitation connection, a portion
of the reentrant circuit can be made refractory, resulting in
termination of the tachycardia.512 These pacemakers are
activated by the patient when he is aware of the tachycar¬
dia. Pacing would not be used for the treatment of atrial
fibrillation.
Surgical interruption of ventricular preexcitation has
been proved to be effective, particularly in free wall AV
connections. Surgery can be considered for the rare cases
with life-threatening tachyarrhythmias that are medication
and pacemaker refractory. The surgery is performed only
after precise localization of the anomalous connections.4'512
Ventricular preexcitation occurs approximately once in
500 individuals (0.15% to 0.2%5). It is, therefore, not as rare
as some may think.
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