Case Study 2

Wolff-Parkinson White Syndrome with a Positive Maximal Exercise

Stress Test

Graduate Diploma of Clinical Physiology

(Clinical Measurements Science)
Griffith University
Nathan Campus

Mitchell Hollamby
5001226

Mitchell Hollamby Griffith University s5001226

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Introduction
A 24 year old male under doctor referral, arrived at The Prince
Charles Hospital for a maximal exercise stress test (MEST). MEST
was requested due to the patient experiencing chest pain upon
exertion along with syncope. Patient exercised regularly and began
feeling pain upon maximal exercise. Medical history showed the
patient had been previously diagnosed with Wolff-Parkinsons-White
Syndrome (WPW). This is classified as a syndrome as the patient
had been experiencing signs and symptoms concurrent with the
disease process(REF). Further investigation into case reports noted
that the patient experienced the Electrocardiogram changes
sporadically (ECG), with no known trigger or offset. WPW involves an
accessory pathway for the conduction of the heart to travel. The
Bundle of Kent is the most noted in literature and this arrises along
the atrioventricular groove (Lilly & School, 2011). ECG
characteristics concern a delta wave, seen in figure 1, which
indicates an accessory pathway allowing conduction to the
ventricles further down the pathway, however the causes are not
known. There are no literature supported risk factors other than a
heretic capacity, and WPW can affect 1.5 in every 1000 births
(Prem, 2008), study also found almost half can experience cardiac
conduction issues without being symptomatic.

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Figure 1: Delta Wave can be seen on initial upright inflection of R

wave. Image taken from (Tsugtoshi, 2014).
Case Presentation
Patient was referred for a MEST and was asymptomatic upon arrival,
no chest pain or syncope. Patient had not reported feeling any
palpitations throughout the day.

Patient Characteristics
Relevant Patient Information
Age- 24 y/o
Sex- Male
Height- 182cm
Weight- 91kg
BMI- 27.2kg/m2
Medications
Taking Nil.
Previous Medical History
Wolff-Parkinson-White Syndrome. Diagnosed at birth as father
presented with WPW.
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Presenting Signs and Symptoms

Resting Heart Rate- 72bpm
Resting Blood Pressure- 110/60mmHg
- ECG showed normal sinus rhythm and delta wave with normal
axis deviation.
- Patient had no complaints or concerns

Testing/ Outcomes
Patient participated in a MEST investigating the chest discomfort he
had been experiencing, to exclude any ischemia to the myocardium.
Also, to witness any dysrhythmias that may arise whilst exercising
From results of MEST patient was referred for computed tomography
coronary angiography.

Resting Electrocardiogram
ECG showed the delta waveform, indicating that there was an
accessory conductive pathway. This was substantiated with a short
(<120m/s) PR interval. Electrophysiology investigative report
concurred with presence of WPW. Patient had not been feeling any
symptoms prior to this episode, so further ablative measures were
not taken. Delta wave is expressed as a slurring of the initial R
wave inflection, usually in a normal sinus beat. Early conduction
causes the ventricles to initially depolarize then when the sinus
conduction following giving a delta wave affixed to the
corresponding R wave
Maximal Exercise Stress Test
Patient exercised according to the Bruce protocol at The Prince
Charles Hospital for 12:22, achiving a work level of 14.3 METS. Heart
rate rose to a maximum of 196bpm (100% APMHR). Blood pressure
rose to 180/80mmHg. Patient elected to stop due to fatigue and
max heart rate was achieved.
Although difficult to interoperate, patients delta wave intermittently
showed. Immediately post maximal exercise, delta waves were
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present appendix 1, however 1:45 post delta waves were no longer

visible on the trace.
Noted in the report, was the increasing frequency of isolated
unifocal ventricular ectopics correlated with increasing exercise
duration . This was also accompanied with unifocal ventricular
couplets. Patient did not report any presence of palpitations during
exercise however chest pain appeared near maximal capacity and
subsided upon rest. Expressed during maximal exercise, was
marked depression in inferolateral ST segments. This ceased with
exercise.
Computed Tomography Coronary Angiogram
The investigation returned negative for coronary stenosis, chamber
size and function were within normal ranges also.

Management/Treatment Options
Patient has been referred on to an electrophysiologist. Patient has
expressed concern for his wellbeing and sought that this syndrome
be dealt with whilst present. (Liu & Pusalkar, 2011)
Treatment and management options include antiarrhythmic agents
that block the accessory pathway and slow the ventricular rate.
Atrioventricular nodal blocking agents (adenosine) should be used
with caution, as it can cause atrial fibrillation in 10% of people WPW,
which has the capacity to be fatal. It is contraindicated in patients
with pre-existing atrial fibrillation (Liu & Pusalkar, 2011). This is due
to the decrease in the number of impulses entering the ventricles
through the AV node and allows for an increase in conduction within
accessory pathways. This process allows for an increase in
ventricular rate.

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More radical means include direct cardio version and radiofrequency

ablation of the accessory pathway (Liu & Pusalkar, 2011).

Discussion
Accessory Pathways
WPW is expressed when there is an accessory pathway pre-exciting
the ventricles, other than the normal conduction pathway through
the AV node and down the bundle of His (figure 2). Most common
accessory pathway is the bundle of kent (figure 3), which forms a
direct connection between the atria and the ventricles. The
formation of these accessory pathways is unknown in nature,
however speculated that they are formed when the atrioventricular
septum is not complete. The bundle of kent is comprised of
conductive myocardial fibers that bridge the fibrous layer between
the atria and ventricles (Scharf & Dang, 2013). This creates a
bypass of normal conduction and allows for premature ventricular
conduction, also the bundle of kent allows for more rapid conduction
of impulses (Scharf & Dang, 2013). This may allow for fatal
tachycardias to arise.

Figure 2: normal conduction of the heart with an accessory pathway

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Figure 3: Bundle of Kent and abnormal conduction

Other causes of pre-excitation may also arise due to pathways such
as James fibers, fibers that connect the atria to the inferior portion
of the AV node allowing for sporadic His fiber conduction. Another is
Mahaim fibres, that, connect the inferior portion of the AV node to
the ventricles or the His bundle directly to the ventricles. Accessory
pathways appear most commonly on the left free wall then less
commonly on the posterior septum. A 12 lead ECG may assist in the
discovery of location, however an electrophysiologist is more
precise.
Atrioventricular Re-entrant Tachycardia
In atrioventricular re-entrant tachycardia, this uses the AV node and
an accessory pathway to for a re-entry circuit, this is classified as
either orthodromic or antidromic (Almendral, Castellanos, & Ortiz,
2012). The characteristics can have high variability and influence
different arrhythmias. The conduction may be either; anterograde,
retrograde or both similtanously (figure 4). The most common is
orthodromic and accounts for supraventricular tachycardias such as
AF (figure 5). anterograde conduction occurs through the AV node
causing a narrow QRS and short PR interval. The conduction then
re-enters the atria through the accessory pathway (Almendral,
Castellanos, & Ortiz, 2012). Impulse circulates causing a narrow
complex tachycardia figure.

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Figure 4: Conduction pathway direction as it can manifest

Figure 5: Orthodromic Conduction through an accessory pathway

Antidromic is less common and impulses through the accessory
pathway and then circulates through the AV node (figure 5). This
produces a wide complex tachycardia (Almendral, Castellanos, &
Ortiz, 2012).

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Figure 6:Antidromic Conduction through an accessory pathway

Atrial Fibrillation
Atrial fibrillation is the uncoordinated conduction of the atria with
rate up to 500bpm. With the AV node acting as a gatekeeper and
only allowing specific rates through to the ventricles, this arrhythmia
is compatible with life (figure 7). The accessory pathway, present in
WPW, allow for extra conduction into the ventricles and can allow for
rhythms such as ventricular tachycardia and ventricular flutter,
which arent always compatible with life (Almendral, Castellanos, &
Ortiz, 2012).

Figure 7: Image representing atrial fibrillation

Intermittent Wolff-Parkinson-White Syndrome
This patient does not present with a consistent accessory pathway
and is causing the intermittent nature (Hoyt & Snyder, 2013). The
pathway may present with both directions of conduction. This
concealed the WPW ECG recording. This is caused by the pathway
being retrogradely conducted while not manifesting, as it can only
conduct from the ventricles to the atria. This does not pre-excite the
ventricles and give the manifestation of the delta wave, that WPW is
characterized (Hoyt & Snyder, 2013).
ST Depression and Negative Ischemia
ST Segment and T-wave changes can occur due to the abnormal
conduction of the ventricles. This is due to ventricular depolarization
does not follow a normal sequence and is delayed, the repolarization
may also be out of its normal conduction pattern (Ceresnack &
Dubin, 2015). In this case and most commonly, ST segment and Twave polarity are generally opposite to the conduction of the delta
wave (Ceresnack & Dubin, 2015).
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Summary
Wolff-Parkinson-White is caused by an accessory pathway allowing
for abnormal conduction within the heart and can potentially lead
death. In this patients case, WPW has been dormant and
asymptomatic. It is critical that this patient is monitored carefully
through out his life to ensure that death is not caused, or his
abilities are limited by his conduction defect.

Appendix

Appendix 1: <1min Post MEST in patient with WPW note the

presence of a Delta wave

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Appendix 2: >1min Post MEST in patient with WPW note the

absence of a Delta wave.

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References
Almendral, J., Castellanos, E., & Ortiz, M. (2012). Paroxymal
supreventricular tachycardias and pre-excitation syndromes.
Arrhythmias , 456-469.
Ceresnack, S., & Dubin, A. (2015). Wolff-Parkinson-White Syndrome
and athletes. Journal of electrocardiology , 356.
Hanna, E., & Glancy, D. (2011). ST-segment depression and T-Wave
inversion: classification,. Cleveland CLinical Journal of
Medicine , 404-414.
Hoyt, W., & Snyder, C. (2013). The asymptomatic Wolff-ParkinsonWhite Syndrome. Progress in padiatric cardiology , 17.
Lilly, L., & School, H. (2011). Pathophysiology of Heart Disease: A
collaborative project of medical student and faculty. Wolters
Kluwer/Lippencott Williams and Wilkins.
Liu, A., & Pusalkar, P. (2011). Asymptomatic Wolff-Parkinson White
Syndrome: incidental ECG diagnosis and a review of literature
regarding current treatment. Brittish Medical Journal .
Prem, S. (2008). Epidemiology of arrhythmias in children. Indian
Packing and electrophysiology , 8-13.
Scharf, C., & Dang, L. (2013). Epicardial Wolff-Parkinson-White
ablation. European Heart Journal , 2738.
Tsugtoshi, S. (2014). Differentiating fasciculoventricular pathway
fromo Wolff-Parkingson-White syndrome by ECG. Heart
Rhythm Society , 686-690

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