Review
Electrocardiography in athletes: normal and
1
Department of Medicine/
Cardiology, University
of Washington, Seattle,
Washington, USA
2
Sports Medicine Department,
ASPETAR Orthopaedic and
Sports Medicine Hospital, Doha,
Qatar
3
Athlete Health and
Performance Research Centre,
ASPETAR Orthopaedic and
Sports Medicine Hospital, Doha,
Qatar
Correspondence to
Dr Jordan M Prutkin, Division
of Cardiology, University of
Washington, Seattle 1959 NE,
USA; j​ prutkin@​cardiology.​
washington.​edu
Received 7 May 2018
Revised 16 July 2018
Accepted 23 July 2018
© Author(s) (or their
employer(s)) 2018. No
commercial re-use. See rights
and permissions. Published
by BMJ.
To cite: Prutkin JM,
Wilson MG. Heart Epub
ahead of print: [please
include Day Month
Year]. doi:10.1136/
heartjnl-2017-312901
abnormal findings
Jordan M Prutkin,1 Mathew G Wilson2,3
Abstract
Many sporting organisations recommend a pre-
participation ECG to screen for disorders which
predispose to sudden cardiac arrest (SCA). The ability
of the ECG to perform accurately is dependent on the
ECG criteria used and the experience of the operator.
There have been several ECG criteria over the last
decade, though these were recently superseded with
the publication of the ’International Consensus Criteria
for ECG Interpretation in Athletes’. These criteria
use the latest evidence to improve specificity while
maintaining sensitivity for ECG-detectable pathologies
associated with SCA. Accordingly, this review describes
the normal, borderline and abnormal ECG findings in an
asymptomatic athlete aged 12–35 years.
Introduction
The pre-participation evaluation of the athlete has
traditionally involved a history and physical exam,
though many sporting organisations now recom-
mend the inclusion of an ECG as it may be more
accurate than the history and physical in picking up
disorders which predispose to sudden cardiac arrest
(SCA).1 2 The ability of the ECG to perform accu-
rately is dependent on the ECG criteria used and
the experience of the operator.3 4 Initial attempts
to create athlete-specific ECG criteria by the Euro-
pean Society of Cardiology (ESC) divided findings
into normal training related and abnormal unre-
lated to training.5 Based on consensus opinion, the
ESC criteria suffered greatly from high false posi-
tive rates, especially in black athletes.6While other
groups have attempted ECG criteria ‘refinement’,6–8
including the ‘Seattle Criteria’,9 all were superseded
in 2017 with the publication of the ‘International
Consensus Criteria for ECG Interpretation in
Athletes’ (International Criteria).10 These criteria
use the latest evidence to improve specificity while
maintaining sensitivity for ECG-detectable pathol-
ogies associated with SCA. Accordingly, this review
describes the normal, borderline and abnormal
ECG findings in an asymptomatic athlete aged
12–35 years with no concerning family history of
cardiomyopathy, channelopathy, syncope or SCA.
Normal findings
Conduction system findings
The normal athletic heart has elevated vagal tone
that may manifest as sinus bradycardia, ectopic
atrial rhythm and accelerated junctional rhythm,10
although mechanisms other than increased vagal
tone have also been implicated.11 For instance, in
animal models, exercise training was associated
with decreased expression of HCN4 and decreased
density of If.12 In addition, first-degree AV block
Prutkin JM, Wilson MG. Heart 2018;0:1–8. doi:10.1136/heartjnl-2017-312901
Heart: first published as 10.1136/heartjnl-2017-312901 on 18 August 2018. Downloaded from http://heart.bmj.com/ on 23 September 2018 by guest. Protected by copyright.
with a PR interval >200 ms and second-degree,
type 1 AV block (Wenckebach) are also normal.8 13
If there is any concern, having the athlete do
brief aerobic exercise such as running in place and
repeating the ECG should show sinus P waves and
normal AV conduction.
Left and right ventricular hypertrophy
Voltage criteria for left ventricular hypertrophy
(LVH) in the absence of ST segment or T-wave
repolarisation changes is common in athletes. In
contrast, those with hypertrophic cardiomyopathy
(HCM) usually have additional ECG abnormal-
ities.14 15 For instance, one study of mostly male
Caucasian athletes showed that 45% met Sokolow-
Lyon voltage criteria for LVH.15 Similarly, voltage
criteria for right ventricular (RV) hypertrophy in
the absence of other ECG findings are present in
up to 12% of athletes and do not correlate with
pathological disease.16 17
Early repolarisation pattern
The early repolarisation pattern consists of J-point
and convex ST segment elevation, often with a
notch at the intersection of the two.18 It is frequently
seen in athletes, up to 35% in one study,19 and is
more common in those who are younger, male or
of African-Caribbean descent (figure 1).19 20 While
the early repolarisation pattern has been associ-
ated with SCA in the general population, especially
if present in the inferior leads, it is enhanced by
exercise training and there are no data suggesting
an increased risk of SCA in young athletes.19 No
secondary evaluation is needed for these athletes.
Normal T-wave inversion patterns
T-wave inversion in leads V1–V4 when preceded by
J-point elevation and convex ST segment elevation
is normal in African-Caribbean athletes and does
not require secondary investigation in the absence
of other clinical or ECG features of cardiomyop-
athy.6 16 Interestingly, there does seem to be some
geographic variation from within Africa in the prev-
alence of this pattern.21
T-wave inversion may be present in leads V1–
V3 in those <16 years of age(or prepubertal).10 15
Lastly, a biphasic T-wave may be seen in isolation in
V3 only and is a normal finding.10
Borderline findings
Recent studies have demonstrated that certain ECG
findings previously categorised as abnormal may
also represent normal variants for athletes and do
not usually represent pathological cardiac disease
if they are the sole abnormality.6 However, the
  1
 Review

Heart: first published as 10.1136/heartjnl-2017-312901 on 18 August 2018. Downloaded from http://heart.bmj.com/ on 23 September 2018 by guest. Protected by copyright.
Figure 1  Early repolarisation pattern in a 20-year-old African-American basketball player. There is J-point and ST segment elevation diffusely with
notching (arrows) seen.

presence of two or more of these borderline findings warrants
secondary investigation (figure 2).
Complete right bundle branch block
While one study of US collegiate athletes showed that in
the 2.5% of athletes who had right bundle branch block
(RBBB) there was a greater RV size with decreased RV
function, the significance of these findings is unclear as
no adverse events occurred. 22 Other studies have shown
normal imaging in these athletes, 23 and for now, RBBB
should be considered normal if no other abnormality is
present.

Figure 2  Right bundle branch block and left axis deviation in an 18-year-old soccer player. The presence of these findings in conjunction requires
further evaluation. If they were seen in isolation, no evaluation would be necessary.
2 Prutkin JM, Wilson MG. Heart 2018;0:1–8. doi:10.1136/heartjnl-2017-312901
 Review
Axis deviation and atrial enlargement Abnormal findings

Compared with non-athletic controls, athletes are more likely to
present left axis deviation or left atrial enlargement.24 Gati et al
examined almost 600 athletes and demonstrated no correlation
between any axis deviation or atrial enlargement and pathology
on cardiac imaging.24 Therefore, if axis deviation or atrial
enlargement is the sole finding, these changes do not require
further evaluation in an otherwise asymptomatic athlete.
Heart: first published as 10.1136/heartjnl-2017-312901 on 18 August 2018. Downloaded from http://heart.bmj.com/ on 23 September 2018 by guest. Protected by copyright.
Abnormal ECG findings deserve further evaluation with echo-
cardiography, cardiac MRI, ambulatory ECG monitoring, exer-
cise ECG testing and/or signal averaged ECG, as appropriate.
The reader is referred to table 1 which summarises how athletes
with each of the abnormalities described in the following section
should be further evaluated. Consideration for referral to an
expert in cardiac disease or sports cardiology may be reasonable.

Table 1  Recommendations for further evaluation depending on ECG finding

ECG criteria Evaluation Possible disorders
T-wave inversion
 Anterior leads Echocardiography, CMR, Holter ECG ARVC, DCM Further evaluation may be considered for ARVC may
monitor, signal averaged ECG, exercise be considered.
ECG test
 Lateral leads Echocardiography, CMR, Holter ECG ARVC, DCM, HCM, LVNC, myocarditis If T-wave inversions are present in V5–6, apical HCM
monitor, exercise ECG test must be excluded.
This is best identified with CMR.
 Inferior leads Echocardiography ARVC, DCM, HCM, LVNC, myocarditis CMR may be considered.
ST segment depression Echocardiography, CMR ARVC, DCM, HCM, LVNC, myocarditis
Pathological Q-waves Echocardiography, CAD risk factor DCM, HCM, LVNC, MI, myocarditis Echocardiography should include assessment of
assessment coronary artery ostia. Evaluation for coronary artery
disease preferably should include exercise stress
testing with or without imaging.
LBBB or widened QRS Echocardiography, CMR DCM, HCM, LVNC, myocarditis, cardiac
sarcoidosis
WPW pattern Echocardiography, exercise Abrupt cessation of the bypass pathway on exercise
ECG test testing suggests a low risk for sudden cardiac
arrest. Gradual disappearance of the pathway is
a non-diagnostic test result. Consideration for an
electrophysiology study is appropriate to assess
conduction speed of the bypass pathway and
ablation if high-risk features are seen.
Prolonged QT interval Repeat ECG LQTS Medications should be reviewed for any that may
prolong QT interval. Review ECGs of family members.
Consider ECG stress testing or genetic testing.
Two or more PVCs Holter ECG monitor, echocardiography, ARVC, DCM, HCM, LVNC, myocarditis, CMR should be considered if>2000 PVCs present in
ECG stress test cardiac sarcoidosis 24 hours
Non-sustained ventricular Echocardiography, CMR, Holter ECG Myocardial or electrical disease Consider referral to cardiac electrophysiologist.
tachycardia, ventricular couplets monitor, ECG stress test
Sinus bradycardia<30 beats/min or Repeat ECG after brief aerobic exercise Myocardial or electrical disease ECG stress test may be considered.
PR interval>400 ms
Second-degree, type 2 or complete Echocardiography Primary electrical disease, myocarditis, Consider CMR, Holter ECG monitor or exercise ECG
heart block cardiac sarcoidosis, Lyme disease test depending on urgency of treatment.
Epsilon wave Echocardiography, CMR, exercise ARVC, cardiac sarcoidosis Rarely seen in the absence of other ECG
ECG test, Holter ECG monitor, signal abnormalities such as T-wave inversion.
averaged ECG
Brugada pattern
 Type 1 Referral to expert Brugada syndrome A repeat ECG with leads in the second intercostal
space may elicit the pattern if it is indeterminate.
 Type 2 No further evaluation Consideration for sodium channel blockade to elicit
a type 1 pattern may be considered if symptoms are
present.
Sinus tachycardia Repeat ECG with HR slower
Atrial fibrillation/flutter or Echocardiography, ambulatory ECG Myocardial or electrical disease CMR may be considered. Atrial fibrillation may be
supraventricular tachycardia monitor, exercise ECG test, laboratory associated with WPW.
testing
Two (or more) borderline findings Echocardiography Myocardial disease Further testing based on initial results and clinical
suspicion.
Work-up should be completed by an expert in cardiovascular disease. Not every test needs to be completed but should be chosen based on clinical context, results of initial
testing, and local expertise. Additional testing including evaluation of family members or genetic testing may be considered. See text for definitions of specific ECG criteria.
Modified from Sharma et al.10
ARVC, arrhythmogenic right ventricular cardiomyopathy; CAD, coronary artery disease; CMR, cardiac magnetic resonance; DCM, dilated cardiomyopathy; HCM, hypertrophic
cardiomyopathy; LBBB, left bundle branch block; LQTS, long QT syndrome; LVNC, left ventricular non-compaction; MI, myocardial infarction; PVC, premature ventricular
contraction; WPW, Wolff-Parkinson-White.

Prutkin JM, Wilson MG. Heart 2018;0:1–8. doi:10.1136/heartjnl-2017-312901 3

 Review
Table 2  T-wave inversions in ECG leads associated with potential
cardiomyopathy
ECG leads Potential cardiomyopathy
Anterior V2–V4* ARVC, DCM
Lateral I, aVL, V5, V6† DCM, HCM, LVNC, ARVC (if extensive or
LV involvement), myocarditis
Inferior II and aVF DCM, HCM, LVNC
Inferolateral I, II, aVL, aVF and DCM, HCM, LVNC, myocarditis
V5–6
Inversions must be ≥1 mm deep in two or more contiguous leads, excluding III,
aVR and V1. Modified from Sharma et al.10
*Excludes juvenile T-wave pattern in those  <16 years of age , African-Caribbean
athlete repolarisation pattern  and biphasic T-wave isolated to V3 only.
†T-wave inversion in V5 or V6 alone is abnormal.
ARVC, arrhythmogenic right ventricular cardiomyopathy; DCM, dilated
cardiomyopathy; HCM, hypertrophic cardiomyopathy; LV, left ventricular; LVNC, left
ventricular non-compaction.
T-wave inversions
Abnormal T-wave inversions are defined as ≥1 mm and described
by anatomic location (table 2). When assessing biphasic T-waves,
the negative portion should be considered abnormal if ≥1 mm as
if the T-wave was solely inverted. Note that aVR, III and V1 can
normally have inverted T-waves and are excluded from analysis.
One of the most sensitive findings for cardiomyopathy is
T-wave inversions (figure 3).6 14 25 One study of 81 athletes
with T-wave inversions in  ≥3 leads followed for a mean of 9
years showed that 6% developed a cardiomyopathy, including
two patients who suffered SCA.14 However, the specificity is
less good, especially in African-Caribbean athletes. For instance,
10%–15% of normal athletes of African-Caribbean descent
present with T-wave inversion.16 Another study found a positive
predictive value for T-wave inversions of 22.2% in white athletes
and only 8.3% in African-Caribbean athletes.6 This suggests that
further refinement or characterisation of T-wave morphology
Figure 3  Abnormal T-wave inversions in leads V2–V4 (arrows) in a 16-year-old child diagnosed with arrhythmogenic right ventricular
cardiomyopathy. The T-wave inversion in V1 is normal.
4 Prutkin JM, Wilson MG. Heart 2018;0:1–8. doi:10.1136/heartjnl-2017-312901
will be necessary in the future to improve the accuracy of this
Heart: first published as 10.1136/heartjnl-2017-312901 on 18 August 2018. Downloaded from http://heart.bmj.com/ on 23 September 2018 by guest. Protected by copyright.
criterion. Serial testing over time may be necessary if initial
evaluation of T-wave inversions is negative, as a morphological
phenotype may later develop.
While the arrhythmogenic right ventricular cardiomyopathy
(ARVC) diagnostic criteria do include T-wave inversions in V1–2
as a minor criterion,26 in the absence of another concerning
finding such as symptoms, ventricular arrhythmias or family
history, this is unlikely to represent true disease.27 28 The height
of the J-point and location of T-wave inversions can also be used
to guide decision making. J-point elevation >1 mm and T-wave
inversion only in leads V1–4 are highly unlikely to represent
cardiac pathology.29 However, if there is no J-point elevation or
more diffuse T-wave inversion, then a cardiomyopathy may be
present.
T-wave inversions are commonly observed in the lateral leads
in those with HCM, though may also be present in the inferior
leads (figure 4).16 A study of African-Caribbean patients with
HCM demonstrated that 77% had lateral and 1.9% had inferior
T-wave inversions, though 4.1% and 6% of African-Caribbean
athletes and 0.3% and 1.5% of white athletes without HCM
also presented with lateral and inferior repolarisation patterns,
respectively.16 If the initial evaluation is normal, athletes with
lateral T-wave inversions should be followed annually with
imaging to determine if HCM manifests at a later date.
The clinical significance of isolated inferior T-wave inver-
sions is not well understood, but one study suggested this might
be a normal finding.6 Until more data are available, however,
those with inverted T-waves in leads II and aVF should undergo
further evaluation.
ST segment depression
ST segment depression  ≥0.5 mm in two or more contiguous
leads is always considered an abnormal finding. Approximately
50% of young people with HCM have ST depression, though it

Figure 4  T-wave inversions in the inferior and lateral leads (arrows) in a baseball player with hypertrophic cardiomyopathy. ST depression is also
seen in I, II, V5 and V6.
is commonly associated with other ECG abnormalities such as
T-wave inversions and pathological Q-waves.6 16
Pathological Q-waves
Abnormal Q-waves are observed in up to 45% of patients
with HCM,30 as well has those with ARVC or Wolff-Parkin-
son-White (WPW) pattern. While the definition of an abnormal
Q-wave differed in previous criteria,5 9 it is currently considered
abnormal if the Q/R ratio ≥0.25 or Q-wave duration is ≥40 ms
in two or more contiguous leads (except III and aVR).6 Even
with this definition, however, optimal Q-wave criteria are still
a challenge. One computer analysis study demonstrated that
a Q-wave  ≥30 ms in lead I may offer the best discriminatory
ability for HCM.31
LBBB or QRS >140 ms
In most ECG screening studies of athletes, no cases of left bundle
branch block (LBBB) were found.1 8 32 33 The few studies that had
patients with LBBB found a high prevalence of cardiac abnor-
malities.34–36 For instance, in one study it was present in 5.9% of
patients with HCM but in no normal athletes.37 Consequently,
LBBB is always considered abnormal and requires secondary
evaluation.
The prognostic value of a non-specific intraventricular
conduction delay of ≥140 ms in athletes is unclear. It may be a
physiological adaptation to exercise with increased ventricular
mass or conduction system slowing, but cardiomyopathies may
also have QRS widening. In the absence of clear data, a QRS
duration of ≥140 ms regardless of morphology should prompt
further evaluation.
WPW pattern
The WPW pattern occurs in about 0.1%–0.3% of people,
though it may be more prevalent if a family member also has
WPW.38 Over half of adolescents with WPW and 40% over age
Prutkin JM, Wilson MG. Heart 2018;0:1–8. doi:10.1136/heartjnl-2017-312901
Review
Heart: first published as 10.1136/heartjnl-2017-312901 on 18 August 2018. Downloaded from http://heart.bmj.com/ on 23 September 2018 by guest. Protected by copyright.
30 years are asymptomatic.38 Up to 4% of symptomatic patients
with WPW may have a risk of SCA in their lifetime,39 the mech-
anism of which is thought to be rapid condition of atrial fibrilla-
tion down the pathway leading to ventricular fibrillation. Some
forms of WPW are known to be associated with structural heart
disease including Ebstein anomaly, L-transposition of the great
arteries and LVH due to LAMP2 or PRKAG2 mutations. There-
fore, an athlete exhibiting a WPW pattern should undergo echo-
cardiography to look for structural heart disease.
Prolonged QT interval
Congenital long QT syndrome (LQTS) is an inherited channelo-
pathy associated with prolonged QT interval and risk of torsade
de pointes, syncope and SCA. Prevalence is estimated as 1 in
2000. At least 17 genes have been associated with LQT, though
KCNQ1 (LQT1), KCNH2 (LQT2) and SCN5A (LQT3) repre-
sent about 80% of cases.
There is overlap in the QTc between those with genetic
confirmed LQTS and normal individuals. A value of ≥480 ms in
women and ≥470 ms in men was chosen as the best trade-off to
find those with LQTS while not excluding normal individuals and
these individuals should undergo further evaluation. These cut-offs
represent the 99th percentile of QTc values in normal individuals.
Those with a QTc ≥500 ms are more suggestive of LQTS.40
The recommended method to measure the QT interval is to
‘teach the tangent’ or ‘avoid the tail’, to avoid including the
U-wave.41 A straight line is drawn on the downslope of the
T-wave to where it intersects the isoelectric line (figure 5). The
QT interval is measured from the beginning of the QRS to where
this intersection of the baseline occurs. Bazett’s QT correction
(QTc) for heart rate (HR) should be used, though it becomes less
accurate when the HR is <50 or >90 bpm.
There can be variation in measurement of QT interval between
readers,41 42 and the computer read of the QT interval is only
about 90%–95% accurate.10 T-wave morphology can also be
5
 Review

Heart: first published as 10.1136/heartjnl-2017-312901 on 18 August 2018. Downloaded from http://heart.bmj.com/ on 23 September 2018 by guest. Protected by copyright.
Figure 5  Prolonged QT interval measuring 510 ms in a 21-year-old long-distance runner with syncope. The inset shows the ‘teach the tangent’
method where a tangent line is drawn on the downslope of the T-wave to the intersection of the isoelectric line. This is the end of the QT interval. The
average heart rate is 59 beats/min, giving a QTc of 506 ms using Bazett’s formula. This is a markedly prolonged QT interval.

important as notching of the T-wave in lateral precordial leads, Two or more premature ventricular contractions
where the second portion of the notch is larger than the first, Premature ventricular contractions (PVCs) may be observed in
may suggest LQT2 even with a normal QTc interval.43 normal individuals, but an increased frequency may represent

Figure 6  Frequent premature ventricular contractions (PVCs) and slow non-sustained ventricular tachycardia in an 18-year-old basketball player.
This is not originating from the right ventricular outflow tract as the QRS is positive throughout the precordial leads. Evaluation showed 3000 PVCs in
24 hours but no abnormality on cardiac imaging. Serial follow-up was recommended for this patient.
6 Prutkin JM, Wilson MG. Heart 2018;0:1–8. doi:10.1136/heartjnl-2017-312901

an underlying cardiomyopathy or myocarditis.44 45 Two or more
PVCs on a 10 s ECG were chosen as a surrogate for an increased
number over a 24-hour period (figure 6), knowing there can be
significant variability in PVC burden throughout the day or even
day-to-day.44 45 For instance, an Italian study of 120 compet-
itive athletes with no personal or family history of cardiomy-
opathy demonstrated a median of 3760 PVCs in 24 hours on
initial testing, but even in those who continued playing sport
in the absence of treatment, the number of PVCs significantly
decreased to 1240.44 Another study of 5011 athletes undergoing
exercise testing showed that 367 athletes had exercise-induced
PVCs and demonstrated a reduction on repeat exercise testing
even if allowed to continue playing sports.45 It may simply be
regression to the mean that explains the decrease in PVC burden.
Miscellaneous findings
Type 2 second degree AV block (Mobitz II) and complete AV
block are abnormal finding suggesting cardiac conduction
system disease, as is sinus bradycardia <30 beats/min and a PR
interval  >400 ms.10
An epsilon wave is a low-amplitude, high-frequency deflection
seen at the end of QRS complex in leads V1–3 and is associated
with ARVC.26 However, it is rare to see an epsilon wave in the
absence of other ECG abnormalities such as T-wave inversions in
the anterior precordial leads.
The Brugada type 1 pattern is defined by a coved rsR’, ST
segment elevation ≥2 mm and T-wave inversions in V1–3. The
Corrado index quantifies this finding by examining the ratio
of the height of the start of the ST segment/J point versus 80
ms afterwards.46 If this ratio is <1, it means the ST segment is
upsloping and it is not the Brugada pattern. If it is >1, it is consis-
tent with a Brugada pattern. A type 2 Brugada pattern is defined
by a high take-off of the r’≥2 mm, convex ST elevation ≥0.5 mm
and positive T wave in V2 though variable morphology in V1.47
Because event rates are low in asymptomatic patients with a type
2 pattern, this does not require evaluation.48
Sinus tachycardia is frequently seen on resting ECG, espe-
cially if the athlete is anxious. Giving the athlete a few minutes
to relax almost always slows the HR down to normal. Atrial
tachyarrhythmias, including paroxysmal supraventricular tachy-
cardia, atrial fibrillation and atrial flutter are very rare and are
abnormal.8 These are not life-threatening, but can be associated
with other syndromes such as cardiomyopathies and channel-
opathies. Non-sustained ventricular tachycardia or ventricular
couplets may also represent underlying cardiac pathology.
Conclusion
There are only limited studies on the accuracy of the new ECG
criteria. Improved accuracy was seen with the International
Criteria versus the Seattle Criteria in National Basketball Asso-
ciation players, though 15.8% of African-American and 11.5%
of white athletes still had abnormal ECGs with no imaging
evidence of cardiac disease.49 Another study of almost 5000
athletes showed only 3.0% had an abnormal ECG with the new
criteria, which was a 50% reduction compared with the Seattle
Criteria.50 The 15 athletes found to have significant cardiac
disease were picked up with both criteria. Future studies will be
needed to confirm the accuracy of the International Criteria, but
also to refine them. In addition, there is a need to evaluate these
criteria in older athletes, retired athletes and those of different
ethnicities.
Those who intensely exercise may have ECG findings that
would be considered abnormal in a less athletically trained
Prutkin JM, Wilson MG. Heart 2018;0:1–8. doi:10.1136/heartjnl-2017-312901
Review
individual. Many of these abnormal ECG findings do not neces-
Heart: first published as 10.1136/heartjnl-2017-312901 on 18 August 2018. Downloaded from http://heart.bmj.com/ on 23 September 2018 by guest. Protected by copyright.
sarily represent disease but are a flag for further evaluation.
Referral to a provider experienced with the possible diagnoses
may aid in evaluation or management.
Contributors  Both authors wrote and revised the manuscript.
Funding  The authors have not declared a specific grant for this research from any
funding agency in the public, commercial or not-for-profit sectors.
Competing interests  None declared.
Patient consent  Not required.
Provenance and peer review  Commissioned; externally peer reviewed.
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