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Warm up
The ECGs that will be read around the
world—and save lives of sportspeople
Karim M Khan
‘Having a heart attack? There’s an iPhone
App for that!’ is a true story. We congratulate its inventor Dr David Albert. This
issue of BJSM contains advances that are
equally exciting and which deserve as
much media attention. Sports cardiology
is one defining element of the sport and
exercise medicine specialty (http://bjsm.
bmj.com/content/46/Suppl_1/i2.full). Every
one of us has seen an athlete drop dead
on film—if not in real life. Whose heart
has not stopped on each such occasion?
“There but for the grace of God go I” as
physician, athlete, or parent. “Houston,
we have buy in.”
Sports cardiology is a BJSM ‘priority
topic’. We cover priority topics in each of
our three ‘pillars’—research, education and
implementation. Another way of labelling
the ‘pillars’ is innovation, education and
knowledge translation. We use BJSM and
partner ‘platforms’ (eg, see Partnering with
BMJ Learning section) to deliver the
content. Think of pages such as this one
you are reading, the education tab on the
BJSM home page with its popular podcasts
such as those by Mathew Wilson, Sanjay
Sharma, Jonathan Drezner, Jiri Dvorak
with Jonathan Tobin, etc. Helping to alert
the BJSM community to those riches is our
Twitter feed (@BJSM_BMJ) and Facebook
page. And our Senior Associate Editor,
Evert Verhagen is tasked with developing
BJSM’s Apps. He will not start with a
sports cardiology App but BJSM will land a
couple of Apps on this planet before the
end of the calendar year.
PARTNERING WITH BMJ LEARNING
A worldwide team led by Jonathan Drezner
(AMSSM) and listed in the ‘Seattle Criteria’
Department of Family Practice, The University of British
Columbia, Vancouver, British Columbia, Canada
Correspondence to Dr Karim M Khan, Department of
Family Practice, The University of British Columbia,
Vancouver, BC, Canada V6T 1Z3; [email protected]
Khan KM. Br J Sports Med February 2013 Vol 47 No 3
paper (bjsports-2012-092067) produced
the four key papers in this issue—four
papers that examine ECG findings in
sports people with more rigour than has
previously been managed. The experts
assembled in Seattle in 2012, they had the
compelling goal of clarifying the complexity of ECG interpretation in athletes among
different races to distinguish physiological
from pathological findings. The material is
very logically dished out in four courses:
(1) evidence of electrical disease (bjsports2012-092070), (2) evidence of cardiomyopathy (bjsports-2012-092069), (3) the
‘Seattle Criteria’ and (4) the old chestnut
now with new clarity—the ECG changes
that are physiological in athletes (bjsports2012-092068). A great innovation of this
team was to embed ‘implementation’ into
the plan from baseline. Thus, each of the
papers provides the foundation for online
education which will be available (in
English initially) for the entire world to
view. Because of the generosity of
sponsors—such as AMSSM, and FIFA, this
material will be free worldwide. The sports
cardiology team is partnering with BMJ
Learning—a branch of the BMJ Group
dedicated to CME in the imaginative,
broad sense of that term. Follow your
favourite mobile sites such as AMSSM,
FIFA or BJSM among others—to be
apprised of this free content as soon as it is
available.
PARTNERING WITH THE BMJ
The BMJ is deservedly an iconic brand and
BJSM is delighted to reprint key sport and
exercise medicine papers from recent BMJ
issues. We launched this in 2008 but had to
take a break to clear some backlog. Now
with 18 BJSM issues a year, the best of BMJ
is back for good! (bjsports-2012-e2672rep).
And remember BMJ’s active bloggers—
among them the evocative and provocative
Domhnall MacAuley (@DMacA).
WHAT’S IN A NAME 50 YEARS LATER?
A year from now, 2014, would have
marked the 50th anniversary of the
‘Bulletin of the British Association of Sport
and Medicine’ had not some iconoclasts
decided that a Journal was better than a
Bulletin. The 1964 ‘Bulletin of the British
Association of Sport and Medicine’ (http://
bjsm.bmj.com/content/1/1/1.full.pdf
+html) has had various iterations to reach
its present title of BJSM. In today’s sport
and exercise medicine setting, BJSM’s lack
of ‘E’ seems anachronistic. Britain’s BASM
readily become BASEM, Canada’s CASM
equally CASEM. The title of BJSM
mirrors neither the co-owner society name
(BASEM) nor does it reflect the paradigm
shift that has justified sport and exercise
medicine specialty status in many countries. In 2013, Exercise is Medicine.
Would ‘BJSEM’ make more sense and
more accurately signal to patients, policymakers and professional colleagues that
our field of medicine embraces exercise
(and physical activity)? Is it time to
advance, walk on the spot, or really
embrace our past and revert to a mighty
‘Bulletin’ again? If it’s time to advance,
then innovators would ‘open the
diamond’ and think bravely—consider
options that would add member society
value (ie, greater reach and brand value),
before refining and making a new choice.
The 2013 BJSM Management Meeting
heard that BASEM considers BJSM’s ratio
of ‘sports medicine’ content to ‘exercise
medicine’ about right. The editors have
heard that and are listening. But as for a
journal title, the BASEM executive welcomes members’ comments on how our
sport and exercise medicine community
thinks we should ring in our 50th year,
so let us know. You can Tweet
(@BJSM_BMJ), post a message on
Facebook, email, dial, or use Royal Mail.
Competing interests None.
Provenance and peer review Commissioned;
internally peer reviewed.
To cite Khan KM. Br J Sports Med 2013;47:121.
Received 19 December 2012
Revised 19 December 2012
Accepted 19 December 2012
Br J Sports Med 2013;47:121.
doi:10.1136/bjsports-2012-092108
121
Downloaded from bjsm.bmj.com on January 9, 2013 - Published by group.bmj.com
The ECGs that will be read around the world
−−and save lives of sportspeople
Karim M Khan
Br J Sports Med 2013 47: 121
doi: 10.1136/bjsports-2012-092108
Updated information and services can be found at:
http://bjsm.bmj.com/content/47/3/121.full.html
These include:
Email alerting
service
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Notes
To request permissions go to:
http://group.bmj.com/group/rights-licensing/permissions
To order reprints go to:
http://journals.bmj.com/cgi/reprintform
To subscribe to BMJ go to:
http://group.bmj.com/subscribe/
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Original articles
Electrocardiographic interpretation in athletes:
the ‘Seattle Criteria’
Jonathan A Drezner,1 Michael John Ackerman,2 Jeffrey Anderson,3 Euan Ashley,4
Chad A Asplund,5 Aaron L Baggish,6 Mats Börjesson,7 Bryan C Cannon,8
Domenico Corrado,9 John P DiFiori,10 Peter Fischbach,11 Victor Froelicher,4
Kimberly G Harmon,1 Hein Heidbuchel,12 Joseph Marek,13 David S Owens,14
Stephen Paul,15 Antonio Pelliccia,16 Jordan M Prutkin,14 Jack C Salerno,17
Christian M Schmied,18 Sanjay Sharma,19 Ricardo Stein,20 Victoria L Vetter,21
Mathew G Wilson22
For numbered affiliations see
end of article.
Correspondence to
Jonathan A Drezner,
Department of Family
Medicine, University of
Washington, 1959 NE Pacific
Street, Box 356390, Seattle,
Washington 98195, USA;
[email protected]
Received 7 December 2012
Revised 7 December 2012
Accepted 7 December 2012
This document was developed in collaboration between the American Medical Society for Sports Medicine (AMSSM),
the Section on Sports Cardiology of the European Association for Cardiovascular Prevention and Rehabilitation
(EACPR), a registered branch of the European Society of Cardiology (ESC), the FIFA Medical Assessment and Research
Center (F-MARC), and the Pediatric & Congenital Electrophysiology Society (PACES).
ABSTRACT
Sudden cardiac death (SCD) is the leading cause of death
in athletes during sport. Whether obtained for screening
or diagnostic purposes, an ECG increases the ability to
detect underlying cardiovascular conditions that may
increase the risk for SCD. In most countries, there is a
shortage of physician expertise in the interpretation of an
athlete’s ECG. A critical need exists for physician
education in modern ECG interpretation that distinguishes
normal physiological adaptations in athletes from
abnormal findings suggestive of pathology. On 13–14
February 2012, an international group of experts in sports
cardiology and sports medicine convened in Seattle,
Washington, to define contemporary standards for ECG
interpretation in athletes. The objective of the meeting
was to develop a comprehensive training resource to help
physicians distinguish normal ECG alterations in athletes
from abnormal ECG findings that require additional
evaluation for conditions associated with SCD.
INTRODUCTION
Cardiovascular-related sudden death is the leading
cause of mortality in athletes during sport.1 2 The
majority of disorders associated with increased risk
of sudden cardiac death (SCD), such as cardiomyopathies and primary electrical diseases, are suggested by abnormal findings present on a 12-lead
ECG. ECG interpretation in athletes requires
careful analysis to properly distinguish physiological changes related to athletic training from
findings suggestive of an underlying pathological
condition. Whether used for the diagnostic evaluation of cardiovascular-related symptoms, a family
history of inheritable cardiac disease or premature
SCD, or for screening of asymptomatic athletes,
ECG interpretation is an important skill for physicians involved in the cardiovascular care of athletes.
To cite: Drezner JA,
Ackerman MJ, Anderson J,
et al. Br J Sports Med
2013;47:122–124.
DISTINGUISHING NORMAL FROM ABNORMAL
A challenge in the interpretation of an athlete’s
ECG is the ability to accurately differentiate findings suggestive of a potentially lethal cardiovascular
Drezner JA, et al. Br J Sports Med 2013;47:122–124. doi:10.1136/bjsports-2012-092067
disorder from benign physiological adaptations
occurring as the result of regular, intense training
(ie, athlete’s heart). Several reports have outlined
contemporary ECG criteria intended to distinguish
normal ECG findings in athletes from ECG abnormalities requiring additional evaluation.3–8 Despite
the publication of these consensus guidelines, most
sports medicine and cardiology training programmes lack a standard educational curriculum on
ECG interpretation in athletes.
THE IMPACT OF STANDARDISED CRITERIA
Studies demonstrate that without further education
the ability of many physicians to accurately interpret
an athlete’s ECG is relatively poor and may lead to an
unacceptable rate of false-positive interpretations and
unnecessary secondary evaluations.9 10 However, providing physicians standardised criteria with which to
evaluate an ECG considerably improves accuracy.10 In
a study involving physicians across different specialties,
use of a simple two-page criteria tool to guide ECG
interpretation significantly improved accuracy to distinguish normal from abnormal findings, even in physicians with little or no experience.10 Therefore,
physician education in ECG interpretation is feasible
and accompanied by meaningful improvements in
accuracy when a reference standard is used to assist
interpretation. Further education is needed to produce
a larger physician infrastructure that is skilled and
capable of accurate ECG interpretation in athletes.
SUMMIT ON ECG INTERPRETATION IN
ATHLETES
On 13–14 February 2012, the American Medical
Society for Sports Medicine (AMSSM) co-sponsored
by the FIFA Medical Assessment and Research
Center
(F-MARC)
held
a
‘Summit
on
Electrocardiogram Interpretation in Athletes’ in
Seattle, Washington. Partnering medical societies
included the European Society of Cardiology (ESC)
Sports Cardiology Subsection and the Pediatric &
Congenital Electrophysiology Society (PACES), as
well as other leading cardiologists on ECG
1 of 3
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Original articles
interpretation in athletes from the USA, Europe and around the
world. The goals of the summit meeting were to:
1. define ECG interpretation standards to help physicians
distinguish normal ECG alterations in athletes from abnormal ECG findings that require additional evaluation for
conditions associated with SCD;
2. outline recommendations for the initial evaluation of
ECG abnormalities suggestive of a pathological cardiovascular disorder; and
3. assemble this information into a comprehensive resource and
online training course targeted for physicians around the world
to gain expertise and competence in ECG interpretation.
The consensus recommendations developed are presented in
three papers:
4. Normal Electrocardiographic Findings: Recognizing
Physiologic Adaptations in Athletes11
5. Abnormal Electrocardiographic Findings in Athletes:
Recognizing Changes Suggestive of Cardiomyopathy12
6. Abnormal Electrocardiographic Findings in Athletes:
Recognizing Changes Suggestive of Primary Electrical Disease13
Box 1 summarises a list of normal ECG findings in athletes
that are considered physiological adaptations to regular exercise
and do not require further evaluation. Table 1 summarises a list
of abnormal ECG findings unrelated to athletic training that
may suggest the presence of a pathological cardiac disorder and
should trigger additional evaluation in an athlete.
ONLINE E-LEARNING ECG TRAINING MODULE—FREE!
The Seattle Criteria will be used to develop a comprehensive
online training module for physicians to acquire a common
foundation in ECG interpretation in athletes. This state of the
art E-learning resource provides additional ECG examples,
figures and explanations, and is prepared in a user friendly
Box 1 Normal ECG findings in athletes
1.
2.
3.
4.
5.
6.
7.
8.
Sinus bradycardia (≥ 30 bpm)
Sinus arrhythmia
Ectopic atrial rhythm
Junctional escape rhythm
1° AV block (PR interval > 200 ms)
Mobitz Type I (Wenckebach) 2° AV block
Incomplete RBBB
Isolated QRS voltage criteria for LVH
▸ Except: QRS voltage criteria for LVH occurring with
any non-voltage criteria for LVH such as left atrial
enlargement, left axis deviation, ST segment
depression, T-wave inversion or pathological
Q waves
9. Early repolarisation (ST elevation, J-point elevation, J-waves
or terminal QRS slurring)
10. Convex (‘domed’) ST segment elevation combined with
T-wave inversion in leads V1–V4 in black/African athletes
These common training-related ECG alterations are
physiological adaptations to regular exercise, considered
normal variants in athletes and do not require further
evaluation in asymptomatic athletes.
AV, atrioventricular; bpm, beats per minute; LVH, left
ventricular hypertrophy; ms, milliseconds; RBBB, right bundle
branch block.
2 of 3
Table 1
Abnormal ECG findings in athletes
Abnormal ECG finding
Definition
T-wave inversion
>1 mm in depth in two or more leads V2–V6, II
and aVF, or I and aVL (excludes III, aVR and V1)
≥0.5 mm in depth in two or more leads
>3 mm in depth or >40 ms in duration in two or
more leads (except for III and aVR)
QRS ≥120 ms, predominantly negative QRS
complex in lead V1 (QS or rS), and upright
monophasic R wave in leads I and V6
Any QRS duration ≥140 ms
ST segment depression
Pathologic Q waves
Complete left bundle
branch block
Intraventricular conduction
delay
Left axis deviation
Left atrial enlargement
Right ventricular
hypertrophy pattern
Ventricular pre-excitation
Long QT interval*
Short QT interval*
Brugada-like ECG pattern
Profound sinus bradycardia
Atrial tachyarrhythmias
Premature ventricular
contractions
Ventricular arrhythmias
−30° to −90°
Prolonged P wave duration of >120 ms in leads I
or II with negative portion of the P wave ≥1 mm in
depth and ≥40 ms in duration in lead V1
R−V1+S−V5>10.5 mm AND right axis deviation
>120°
PR interval <120 ms with a delta wave (slurred
upstroke in the QRS complex) and wide QRS
(>120 ms)
QTc≥470 ms (male)
QTc≥480 ms (female)
QTc≥500 ms (marked QT prolongation)
QTc≤320 ms
High take-off and downsloping ST segment
elevation followed by a negative T wave in ≥2
leads in V1–V3
<30 BPM or sinus pauses ≥ 3 s
Supraventricular tachycardia, atrial-fibrillation,
atrial-flutter
≥2 PVCs per 10 s tracing
Couplets, triplets and non-sustained ventricular
tachycardia
Note: These ECG findings are unrelated to regular training or expected
physiological adaptation to exercise, may suggest the presence of
pathological cardiovascular disease, and require further diagnostic evaluation.
*The QT interval corrected for heart rate is ideally measured with heart rates of
60–90 bpm. Consider repeating the ECG after mild aerobic activity for borderline or
abnormal QTc values with a heart rate <50 bpm.
educational format to optimise learning. This online training
module is accessible at no cost to any physician world-wide at:
http://learning.bmj.com/ECGathlete
LIMITATIONS OF THE SEATTLE CRITERIA
While the ECG increases the ability to detect underlying cardiovascular conditions that place athletes at increased risk, ECG as
a diagnostic tool has limitations in both sensitivity and specificity. Even if properly interpreted, an ECG will not detect all
conditions predisposing to SCD. In addition, the true prevalence of specific ECG parameters in athletes and in diseases that
predispose to SCD is often unknown and requires further study.
The Seattle Criteria were developed with thoughtful attention
to balance sensitivity (disease detection) and specificity (falsepositives), while maintaining a clear and usable checklist of findings to guide ECG interpretation for physicians, including new
learners.
The criteria define ECG findings that warrant further cardiovascular evaluation for disorders that predispose to SCD. The
criteria were developed with consideration of ECG interpretation in the context of an asymptomatic athlete age 14–35. An
athlete is defined as an individual who engages in regular exercise or training for sport or general physical fitness, typically
with a goal of improving performance. In the presence of
Drezner JA, et al. Br J Sports Med 2013;47:122–124. doi:10.1136/bjsports-2012-092067
Downloaded from bjsm.bmj.com on January 9, 2013 - Published by group.bmj.com
Original articles
personal cardiac symptoms or a family history that is positive
for genetic cardiovascular disease or premature SCD, the criteria
may require modification. Physicians also may choose to deviate
from consensus standards based on their experience or practice
setting.
The evaluation of ECG abnormalities is performed ideally in
consultation with a specialist with knowledge and experience in
athlete’s heart and disorders associated with SCD in young athletes. As new scientific data become available, revision of the criteria may further improve the accuracy of ECG interpretation
within the athletic population.
CONCLUSIONS
Prevention of SCD in athletes remains a highly visible topic in
sports medicine and cardiology. Cardiac adaptation and remodelling from regular athletic training produces common ECG
alterations that could be mistaken as abnormal. Whether performed for screening or diagnostic purposes as part of the
cardiac evaluation in athletes, it is critical that physicians responsible for the cardiovascular care of athletes be guided by ECG
interpretation standards that improve disease detection and limit
false-positive results. The ECG interpretation guidelines presented and the online training programme serve as an important
foundation for improving the quality of ECG interpretations
and the cardiovascular care of athletes.
11
Children’s Healthcare of Atlanta, Department of Pediatrics, Emory University
School of Medicine, Atlanta, Georgia, USA
12
Department of Cardiovascular Sciences, University of Leuven, Leuven, Belgium
13
Midwest Heart Foundation, Oakbrook Terrace, Illinois, USA
14
Division of Cardiology, University of Washington, Seattle, Washington, USA
15
Department of Family and Community Medicine, University of Arizona, Tucson,
Arizona, USA
16
Department of Medicine, Institute of Sport Medicine and Science, Rome, Italy
17
Division of Cardiology, Seattle Children’s Hospital, Seattle, Washington, USA
18
Division of Cardiology, Cardiovascular Centre, University Hospital Zurich, Zurich,
Switzerland
19
Department of Cardivascular Sciences, St George’s University of London, London,
UK
20
Cardiology Department, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil,
Brazil
21
Division of Cardiology, The Children’s Hospital of Philadelphia, Philadelphia,
Pennsylvania, USA
22
Department of Sports Medicine, ASPETAR, Qatar Orthopedic and Sports Medicine
Hospital, Doha, Qatar
Funding None.
Competing interests None.
Provenance and peer review Commissioned; internally peer reviewed.
REFERENCES
1
2
Additional resources
For a free online training module on ECG interpretation in athletes,
please visit: http://learning.bmj.com/ECGathlete. For the November
2012 BJSM supplement on “Advances in Sports Cardiology,” please
visit: http://bjsm.bmj.com/content/46/Suppl_1.toc
3
Author affiliations
1
Department of Family Medicine, University of Washington, Seattle, Washington,
USA
2
Departments of Medicine, Pediatrics, and Molecular Pharmacology & Experimental
Therapeutics, Divisions of Cardiovascular Diseases and Pediatric Cardiology, Mayo
Clinic, Rochester, Minnesota, USA
3
Department of Athletics, University of Connecticut, Storrs, Connecticut, USA
4
Division of Cardiovascular Medicine, Stanford University School of Medicine, Palo
Alto, California, USA
5
Department of Family Medicine, Eisenhower Army Medical Center, Fort Gordon,
Georgia, USA
6
Division of Cardiology, Massachusetts General Hospital, Boston, Massachusetts,
USA
7
Department of Cardiology, Swedish School of Sports and Health Sciences,
Karolinska University Hospital, Stockholm, Sweden
8
Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota, USA
9
Department of Cardiac, Thoracic, and Vascular Sciences, University of Padua,
Padova, Italy
100
Division of Sports Medicine, Department of Family Medicine, University of
California Los Angeles, Los Angeles, California, USA
6
Drezner JA, et al. Br J Sports Med 2013;47:122–124. doi:10.1136/bjsports-2012-092067
4
5
7
8
9
10
11
12
13
Harmon KG, Asif IM, Klossner D, et al. Incidence of sudden cardiac death in
national collegiate athletic association athletes. Circulation 2011;123:1594–600.
Maron BJ, Doerer JJ, Haas TS, et al. Sudden deaths in young competitive athletes:
analysis of 1866 deaths in the United States, 1980–2006. Circulation
2009;119:1085–92.
Corrado D, Biffi A, Basso C, et al. 12-lead ECG in the athlete: physiological versus
pathological abnormalities. Br J Sports Med 2009;43:669–76.
Corrado D, Pelliccia A, Heidbuchel H, et al. Recommendations for interpretation of
12-lead electrocardiogram in the athlete. Eur Heart J 2010;31:243–59.
Uberoi A, Stein R, Perez MV, et al. Interpretation of the electrocardiogram of young
athletes. Circulation 2011;124:746–57.
Williams ES, Owens DS, Drezner JA, et al. Electrocardiogram interpretation in the
athlete. Herzschrittmacherther Elektrophysiol 2012;23:65–71.
Drezner J. Standardised criteria for ECG interpretation in athletes: a practical tool.
Br J Sports Med 2012;46(Suppl I):i6–8.
Marek J, Bufalino V, Davis J, et al. Feasibility and findings of large-scale
electrocardiographic screening in young adults: data from 32,561 subjects. Heart
Rhythm 2011;8:1555–9.
Hill AC, Miyake CY, Grady S, et al. Accuracy of interpretation of preparticipation
screening electrocardiograms. J Pediatr 2011;159:783–8.
Drezner JA, Asif IM, Owens DS, et al. Accuracy of ECG interpretation in competitive
athletes: the impact of using standised ECG criteria. Br J Sports Med
2012;46:335–40.
Drezner JA, Fischbach P, Froelicher V, et al. Normal electrocardiographic findings:
recognizing physiologic adaptations in athletes. Br J Sports Med 2013;47.
Drezner JA, Ashley E, Baggish AL, et al. Abnormal electrocardiographic findings in
athletes: recognizing changes suggestive of cardiomyopathy. Br J Sports Med
2013;47.
Drezner JA, Ackerman MJ, Cannon BC, et al. Abnormal electrocardiographic
findings in athletes: recognizing changes suggestive of primary electrical disease
2013;47.
3 of 3
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Electrocardiographic interpretation in
athletes: the 'Seattle Criteria'
Jonathan A Drezner, Michael John Ackerman, Jeffrey Anderson, et al.
Br J Sports Med 2013 47: 122-124
doi: 10.1136/bjsports-2012-092067
Updated information and services can be found at:
http://bjsm.bmj.com/content/47/3/122.full.html
These include:
References
This article cites 10 articles, 7 of which can be accessed free at:
http://bjsm.bmj.com/content/47/3/122.full.html#ref-list-1
Email alerting
service
Receive free email alerts when new articles cite this article. Sign up in
the box at the top right corner of the online article.
Notes
To request permissions go to:
http://group.bmj.com/group/rights-licensing/permissions
To order reprints go to:
http://journals.bmj.com/cgi/reprintform
To subscribe to BMJ go to:
http://group.bmj.com/subscribe/
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Original articles
Normal electrocardiographic findings: recognising
physiological adaptations in athletes
Scan to access more
free content
For numbered affiliations see
end of article.
Correspondence to
Jonathan A Drezner,
Department of Family
Medicine, University of
Washington, 1959 NE Pacific
Street, Box 356390, Seattle,
Washington 98195, USA;
[email protected]
Received 7 December 2012
Revised 7 December 2012
Accepted 7 December 2012
Jonathan A Drezner, Peter Fischbach,1,2 Victor Froelicher,3 Joseph Marek,4
Antonio Pelliccia,5 Jordan M Prutkin,6 Christian M Schmied,7 Sanjay Sharma,8
Mathew G Wilson,9 Michael John Ackerman,10 Jeffrey Anderson,11 Euan Ashley,3
Chad A Asplund,12 Aaron L Baggish,13 Mats Börjesson,14 Bryan C Cannon,15
Domenico Corrado,16 John P DiFiori,17 Kimberly G Harmon,1 Hein Heidbuchel,18
David S Owens,6 Stephen Paul,19 Jack C Salerno,20 Ricardo Stein,21 Victoria L Vetter22
This document was developed in collaboration between the American Medical Society for Sports Medicine (AMSSM),
the Section on Sports Cardiology of the European Association for Cardiovascular Prevention and Rehabilitation
(EACPR), a registered branch of the European Society of Cardiology (ESC), the FIFA Medical Assessment and Research
Center (F-MARC), and the Pediatric & Congenital Electrophysiology Society (PACES).
ABSTRACT
Electrocardiographic changes in athletes are common
and usually reflect benign structural and electrical
remodelling of the heart as a physiological adaptation to
regular and sustained physical training (athlete’s heart).
The ability to identify an abnormality on the 12-lead
ECG, suggestive of underlying cardiac disease associated
with sudden cardiac death (SCD), is based on a sound
working knowledge of the normal ECG characteristics
within the athletic population. This document will assist
physicians in identifying normal ECG patterns commonly
found in athletes. The ECG findings presented as normal
in athletes were established by an international
consensus panel of experts in sports cardiology and
sports medicine.
INTRODUCTION
To cite: Drezner JA,
Fischbach P, Froelicher V,
et al. Br J Sports Med
2013;47:125–136.
Sudden death from intrinsic cardiac conditions
remains the leading cause of mortality in athletes
during sport.1 2 A resting 12-lead ECG is utilised as
a diagnostic tool in the evaluation of both symptomatic and asymptomatic athletes for conditions
associated with sudden cardiac death (SCD). The
purpose of pre-participation cardiovascular screening is to provide medical clearance for participation
in sport through routine systematic evaluations
intended to identify pre-existing cardiovascular
abnormalities, and thereby reduce the potential
for adverse cardiac events and loss of life.3 Many
pre-participation screening programmes include an
ECG. Physicians responsible for the cardiovascular
care of athletes should be knowledgeable of the
physiological cardiac adaptations to regular exercise
that are manifested on the ECG.
ECG changes in athletes are common and
usually reflect the electrical and structural remodelling or autonomic nervous system adaptations that
occur as a consequence of regular and sustained
physical activity (ie, athlete’s heart). In fact, up to
60% of athletes demonstrate ECG changes (in isolation or in combination) such as sinus bradycardia,
sinus arrhythmia, first-degree atrioventricular (AV)
block, early repolarisation, incomplete right bundle
Drezner JA, et al. Br J Sports Med 2013;47:125–136. doi:10.1136/bjsports-2012-092068
branch block (IRBBB) and voltage criteria for left
ventricular hypertrophy (LVH).4 The extent of
these changes is also dependent on the athlete’s
ethnicity, age, gender, sporting discipline and level
of training and competition.5–7 Accordingly, the
ability to identify an abnormal ECG suggestive of
underlying cardiac disease is based on a sound
understanding of ECG normality within a broad
spectrum of athletic populations.
Concerns for the physician when interpreting an
athlete’s ECG include both missing a dangerous
cardiac condition and generating false-positive
interpretations that cause needless further investigations, increased economic cost and potentially
unnecessary activity restriction for the athlete.8
This paper focuses on the physiological ECG
adaptations commonly found in athletes to help
physicians distinguish normal ECG changes from
abnormal ECG findings related to a pathological
cardiac condition associated with SCD. Abnormal
ECG findings in athletes suggestive of underlying
cardiac disease are presented separately.9 10
OVERVIEW OF ATHLETE’S HEART
Regular and long-term participation in intensive
exercise (minimum of 4 h/week) is associated with
unique electrical manifestations that reflect
increased vagal tone and enlarged cardiac chamber
size. These ECG findings in athletes are considered
normal, physiological adaptations to regular exercise and do not require further evaluation (box 1).
Increased vagal tone
Common consequences of increased vagal tone
include sinus bradycardia, sinus arrhythmia and
early repolarisation (figure 1). Other, less common
markers of increased vagal tone are first-degree AV
block and Mobitz type I second-degree AV block.
Sinus bradycardia is defined as a heart rate of <60
beats/min and is present in up to 80% of highly
trained athletes.6 11 Heart rates ≥30 beats/min are
considered normal in highly trained athletes. Sinus
arrhythmia is also common, particularly in younger
athletes.
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Box 1 Normal ECG findings in athletes
1.
2.
3.
4.
5.
6.
7.
8.
Sinus bradycardia (≥30 bpm)
Sinus arrhythmia
Ectopic atrial rhythm
Junctional escape rhythm
First-degree AV block (PR interval>200 ms)
Mobitz type I (Wenckebach) second-degree AV block
Incomplete RBBB
Isolated QRS voltage criteria for LVH
▸ Except:QRS voltage criteria for LVH occurring with any
non-voltage criteria for LVH such as left atrial
enlargement, left axis deviation, ST segment depression,
T wave inversion or pathological Q waves
9. Early repolarisation (ST elevation, J-point elevation,
J waves, or terminal QRS slurring)
10. Convex (‘domed’) ST segment elevation combined with
T wave inversion in leads V1–V4 in black/African athletes.
These common training-related ECG alterations are
physiological adaptations to regular exercise, considered
normal variants in athletes, and do not require further
evaluation in asymptomatic athletes.
AV, atrioventricular; bpm, beats per minute; LVH, left
ventricular hypertrophy; RBBB, right bundle branch block.
Early repolarisation consists of concave ST segment elevation
most commonly observed in the precordial leads and present in
up to 45% of Caucasian athletes and 63–91% of black athletes
of African-Caribbean descent (hereto referred to as ‘black/
African’ athletes).11–13 Black/African athletes also commonly
demonstrate a repolarisation variant consisting of convex ST
segment elevation in the anterior leads (V1–V4) followed by T
wave inversion. On the basis of current data, T wave inversions
preceded by ST segment elevation are present in leads V1–V4 in
up to 13% of black/African athletes and do not require further
assessment in the absence of symptoms, positive family history
or abnormal physical examination.12 13
A junctional (nodal) rhythm or wandering atrial pacemaker
may be observed in up to 8% of all athletes under resting conditions.11 First-degree AV block (4.5–7.5%) and less commonly
Mobitz type I second-degree AV block are also seen in athletes
and a result of increased vagal tone.6 11 14
Increased cardiac chamber size
Voltage criterion for LVH is present in approximately 45% of
male athletes and 10% female athletes.6 11 15 Increased QRS
voltage is more common in black/African athletes.13 Although
there are several voltage criteria to define LVH, the
Sokolow-Lyon criterion is used most commonly. The
Sokolow-Lyon voltage criterion for LVH is defined as the sum
of the S wave in V1 and the R wave in V5 or V6 (using the
largest R wave) as >3.5 mV (35 small squares with a standard
amplification of the ECG at 10 mm/1 mV). The isolated presence of high QRS voltages fulfilling the Sokolow-Lyon voltage
criterion for LVH is regarded as a normal finding in athletes
related to physiological increases in cardiac chamber size and/or
wall thickness and does not in itself require additional evaluation (figure 1). However, the additional presence of nonvoltage criteria for LVH such as left atrial enlargement, left axis
deviation, ST segment depression, T wave inversion or pathological Q waves should raise the possibility of pathological LVH
and should prompt further evaluation.
IRBBB (commonly characterised as an rSR0 pattern in V1
with QRS duration <120 ms) is commonly present in athletes
(12–32%) and thought to reflect an increase in right ventricular
(RV) size secondary to regular training.6 11–14
Figure 1 ECG of a 29-year-old asymptomatic soccer player demonstrating sinus bradycardia, early repolarisation with ST elevation (arrows) and
peaked T waves, and voltage criteria for left ventricular hypertrophy. These are common findings related to regular training. This figure is only
reproduced in colour in the online version.
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NORMAL ECG FINDINGS IN ATHLETES
Sinus bradycardia
The normal heartbeat is initiated by the sinus node which is
located high in the right atrium near the junction of the superior vena cava and the right atrial appendage. To be classified as
sinus rhythm, three criteria must be met: (1) there must be a
P wave before every QRS complex, (2) there must be a QRS
complex after every P wave and (3) the P wave must have a
normal axis in the frontal plane (0–90°s). Assuming an intact
sinus node, the heart rate is set by the balance between the sympathetic and parasympathetic nervous systems. In healthy adults,
sinus rhythm < 60 beats/min is considered as ‘sinus bradycardia’
(figure 2). In well-trained athletes, resting sinus bradycardia is a
common finding due to increased vagal tone. In endurance athletes, aerobic training also may induce intrinsic adaptations in
the sinus node with decreased automaticity resulting in a high
prevalence of sinus bradycardia.16 17 In the absence of symptoms such as fatigue, dizziness or syncope, a heart rate ≥30
beats/min should be considered normal in a well-trained athlete.
Sinus bradycardia disappears with an increase in heart rate
during physical activity.
sinus syndrome). Differentiating features that suggest sinus node
dysfunction include lack of rhythmic changes in the heart rate,
abrupt sustained rate increases and decreases and an inappropriate rate response to exercise (both a slowed acceleration and an
inappropriately rapid deceleration), as well as any association
with clinical symptoms such as exercise intolerance, presyncope
and syncope. While the heart rhythm is quite irregular in sinus
arrhythmia, the P wave axis remains normal in the frontal
plane. Accelerating the heart rate with physical activity normalises the heart rhythm. Sinus arrhythmia is considered as a
normal finding in an athlete.
Junctional escape rhythm
A junctional or nodal rhythm occurs when the QRS rate is
faster than the resting P wave or sinus rate which is slowed in
athletes due to increased vagal tone (figure 4). The QRS rate for
junctional rhythms is typically less than 100 beats/min, and the
QRS complex usually narrow unless the baseline QRS has a
bundle branch block. Sinus rhythm resumes with increased
heart rates during exercise.
Ectopic atrial rhythm
Sinus arrhythmia
The heart rate usually increases slightly during inspiration and
decreases slightly during expiration (figure 3). This response
called sinus arrhythmia can be quite exaggerated in children and
in well-trained athletes resulting in an irregular heart rhythm
which originates from the sinus node. It has been estimated that
up to 55% of well-trained athletes have sinus arrhythmia.6 11
This should not be confused with sinus node dysfunction (sick
In an ectopic atrial rhythm, P waves are present but are a different morphology compared to the sinus P wave. Ectopic P waves
are most easily seen when the P waves are negative in the inferior leads (II, III and aVF; figure 5). The atrial rate is typically
less than 100 beats/min. There also may be more than two different P wave morphologies known as a wandering atrial pacemaker. Ectopic atrial rhythms occur due to a slowed resting
sinus rate from increased vagal tone in athletes, and sinus
Figure 2 ECG demonstrates sinus bradycardia with a heart rate of 40 bpm. The three required features of sinus bradycardia include: (1) P wave
before every QRS complex, (2) QRS after every P wave and (3) normal P wave axis (frontal plane 0–90°s). This figure is only reproduced in colour in
the online version.
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Figure 3 ECG demonstrates sinus arrhythmia. Note the irregular heart rate that varies with respiration. The P waves are upright in leads I and aVF
(frontal plane) suggesting a sinus origin. This figure is only reproduced in colour in the online version.
rhythm replaces the ectopic atrial rhythm when the heart rate is
increased during exercise.
increased vagal activity or intrinsic AV node changes, and typically resolves with faster heart rates during exercise.
Mobitz type I (Wenckebach) second-degree AV block
First-degree AV block
In first-degree AV block, the PR interval is prolonged (>200 ms)
but is the same duration on every beat (figure 6). This represents a delay in AV nodal conduction in athletes, due to
In Mobitz type I second-degree AV block, the PR interval progressively lengthens from beat to beat, until there is a nonconducted P wave with no QRS complex (figure 7). The first PR
interval after the dropped beat is shorter than the last conducted
Figure 4 ECG of a 28-year-old asymptomatic Caucasian handball player demonstrating a junctional escape rhythm. Note the constant RR interval
between beats. This figure is only reproduced in colour in the online version.
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Figure 5 ECG shows an ectopic atrial rhythm. The atrial rate is 63 beats/min and the P wave morphology is negative in leads II, III and aVF
(arrows), also known as a low atrial rhythm. This figure is only reproduced in colour in the online version.
PR interval before the dropped beat. This represents a greater
disturbance of AV nodal conduction than first-degree AV block,
but with exercise there should be a return of 1:1 conduction.
Incomplete right bundle branch block
IRBBB is defined by a QRS duration <120 ms with an RBBB
pattern: terminal R wave in lead V1 (rsR0 ) and wide terminal
S wave in leads I and V6 (figure 8). IRBBB is seen in less than 10%
of the general population but is observed in up to 40% of highly
trained athletes, particularly those engaged in endurance training
and mixed sport disciplines that include both aerobic and anaerobic
components.14 18 19 It has been suggested that the mildly delayed
RV conduction is caused by RV remodelling, with increased cavity
size and resultant increased conduction time, rather than an intrinsic delay within the His-Purkinje system itself.20
The occurrence of IRBBB in an asymptomatic athlete with a
negative family history and physical examination does not
require further evaluation. During the physical examination,
Figure 6 ECG shows first-degree AV block (PR interval >200 ms). The PR interval is measured from the beginning of the P wave to the beginning
of the QRS complex. This figure is only reproduced in colour in the online version.
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Figure 7 ECG shows Mobitz type I (Wenckebach) second-degree AV block demonstrated by progressively longer PR intervals until there is a
non-conducted P wave (arrows) and no QRS complex. Note the first PR interval after the dropped beat is shorter than the last conducted PR interval
prior to the dropped beat. This figure is only reproduced in colour in the online version.
particular care should be devoted to the auscultation of a fixed
splitting of the second heart sound because IRBBB can be an
associated ECG finding in patients with an atrial septal defect.
IRBBB may be seen in patients with arrhythmogenic RV cardiomyopathy (ARVC).21 However, in ARVC, the IRBBB pattern
is usually associated with other ECG abnormalities, such as T
wave inversion involving the mid-precordial leads beyond V2,
low limb-lead voltages, prolonged S wave upstroke and/or premature ventricular beats with a left bundle branch block (LBBB)
morphology (figure 9).
In some cases, IRBBB may be confused with a Brugada-ECG
pattern, which is characterised by a high take-off and downsloping ST segment elevation followed by a negative T wave in ≥2
leads in V1–V3.22 Unlike the R0 wave in IRBBB, the ‘J wave’
Figure 8 ECG demonstrates incomplete right bundle branch block (IRBBB) with rSR0 pattern in V1 and QRS duration of <120 ms. IRBBB is a
common and normal finding in athletes and does not require additional evaluation. This figure is only reproduced in colour in the online version.
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Figure 9 ECG from a patient with arrhythmogenic right ventricular cardiomyopathy showing delayed S wave upstroke in V1 (arrow), low voltages
in limb leads < 5 mm (circles) and inverted T waves in anterior precordial leads (V1–V4) and inferior leads (III and aVF). This figure is only
reproduced in colour in the online version.
seen in a Brugada-ECG pattern does not indicate delayed RV
activation, but reflects early repolarisation with J point elevation
and a high take-off with downsloping ST segment followed by a
negative T wave (figure 10).
Early repolarisation
Early repolarisation is an ECG pattern consisting of ST elevation
and/or a J wave (distinct notch) or slur on the downslope of the
R wave (figure 11). Traditional examples of early repolarisation
referred to ST elevation, but newer definitions also include
J waves or terminal QRS slurring (figure 12).23
Early repolarisation is a common finding in trained athletes
and considered a benign ECG pattern in apparently healthy,
asymptomatic individuals.24 25 Depending on how it is defined,
early repolarisation is reported in up to 35–91% of trained athletes and is more prevalent in young males and black/
Figure 10 (A) Brugada-ECG pattern mimicking IRBBB. The ‘J wave’ (arrows) of Brugada-ECG is confined to right precordial leads (V1 and V2)
without reciprocal ‘S wave’ (of comparable voltage and duration) in leads I and V6 (arrowheads). (B) IRBBB in a trained athlete. The RV conduction
interval is mildly prolonged (QRS duration=115 ms) with a typical rSR0 pattern in V1 (arrow). Note also the reciprocal ‘S wave’ in V6 (arrow).
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Figure 11 ECG from a 29-year-old asymptomatic soccer player demonstrating early repolarisation ( J-point and ST elevation) in I, II, aVF, V2–V6
(arrows) and tall, peaked T waves (circles). These are common, training-related findings in athletes and do not require more evaluation. This figure is
only reproduced in colour in the online version.
Africans.12 13 25 26 Early repolarisation is most common in the
precordial leads but can be present in any lead.27–29
Commercially available computer diagnostic ECG programmes
commonly misreport early repolarisation patterns in athletes as
acute ischaemia/myocardial infarction or pericarditis.
The early repolarisation pattern in athletes typically involves a
concave and ascending/upward ST segment elevation.24 28 Late
QRS slurring or notching with horizontal ST segment elevation
in the inferolateral leads has been associated with an increased
risk of arrhythmic death in one study of middle-aged, nonathletic Finnish citizens.30 However, a significant percentage of
young competitive athletes (25–30%) show early repolarisation
with similar morphological features in either the inferior or
lateral leads.27–29 These findings are more common in athletes
at times of peak fitness, suggesting early repolarisation is a
dynamic process and is at least in part a direct result of exercise
training.29 To date, no data support the presence of an association between early repolarisation and SCD in athletes.
Figure 12 (A and B) Classic
definition of early repolarisation based
on ST elevation at QRS end ( J-point).
Examples without (A) and with
(B) a J wave. (C and D) New
definitions of early repolarisation
showing slurred QRS downstroke
(C) and J-wave
(D) without ST elevation.
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Figure 13 ECG from a 19-year-old asymptomatic soccer player demonstrating voltage criteria for left ventricular hypertrophy (S-V1+R-V5>35 mm).
Note the absence of left atrial enlargement, left axis deviation, ST depression, T wave inversion, or pathological Q waves. Increased QRS amplitude
without other ECG abnormalities is a common finding in trained athletes and does not require additional testing. This figure is only reproduced in
colour in the online version.
Although further investigation is warranted to fully characterise
the prognostic implications of early repolarisation in competitive athletes, all patterns of early repolarisation, including inferolateral subtypes, should be considered normal variants in
athletes.24
QRS voltage criteria for LVH
The most commonly used voltage criterion for LVH is the
Sokolow-Lyon index. However, ECG QRS voltage may not be a
reliable predictor of LVH. The limitation of the ECG in identifying ventricular hypertrophy is due to the reliance of
Figure 14 Abnormal ECG from a patient with hypertrophic cardiomyopathy. In addition to voltage criteria for left ventricular hypertrophy, note the
deep T wave inversions extending to the lateral leads (I and aVL, V5–V6). These findings are abnormal, not related to regular training and require
additional evaluation. This figure is only reproduced in colour in the online version.
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Figure 15 ECG from a 24-year-old asymptomatic black/African soccer player demonstrating ‘domed’ ST elevation followed by T wave inversion in
leads V1–V4 (circles). This is a normal repolarisation pattern in black/African athletes. This figure is only reproduced in colour in the online version.
measuring the electrical activity of the heart by electrodes on
the surface of the body. Consequently, anything between the left
ventricular myocardium and the surface electrodes will affect
the voltage. ECG QRS voltage, therefore, can be influenced by a
variety of factors other than LV size or mass. Males, athletes
and black/African individuals have higher QRS voltage, while
obesity, older age and pulmonary disease may cause lower
voltage.31
The goal of identifying clinically relevant LVH by voltage criteria alone is particularly problematic in children. The standards
for QRS voltage have been derived from studies of populations
of clinically normal children. Furthermore, the limited studies
do not consistently include referencing to body size, gender or
ethnicity. Lastly, correlation with echocardiography is limited,
and reference standards from autopsy or MRI are not
available.31
Figure 16 (A) Normal variant repolarisation changes in a black/African athlete characterised by domed ST segment elevation and T wave inversion
in V1–V4. (B) Pathological T wave inversion and ST depression in the lateral leads. T wave inversion in V5–V6 is always an abnormal finding and
requires additional testing to rule out cardiomyopathy. This figure is only reproduced in colour in the online version.
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Figure 17 (A) Normal variant repolarisation changes in a black/African athlete characterised by domed ST segment elevation and T wave inversion
in V1–V4. (B) Pathological T wave inversion in V1–V3. Note the isoelectric ST segment. The absence of ST segment elevation prior to T wave
inversion makes this ECG abnormal. Additional testing is required to rule out arrhythmogenic right ventricular cardiomyopathy. This figure is only
reproduced in colour in the online version.
In athletes, intensive conditioning is also associated with morphological cardiac changes of increased cavity dimensions and wall
thickness that are reflected on the ECG. These changes constitute
physiological LVH in trained athletes and usually manifests as an
isolated increase in QRS amplitude (figure 13).32 ECGs with
increased QRS amplitudes meeting ECG voltage criteria for LVH
are prevalent and present in up to 45% of athletes and 25% of
sedentary young adults.11 14 As a result, the accuracy of increased
QRS voltage as an indicator of pathological LVH is poor.
Increased QRS voltage and HCM
Several studies have evaluated athletes and young adults with
isolated increased QRS voltage using echocardiography or
cardiac MRI and none had hypertrophic cardiomyopathy
Figure 18 (A) Normal variant repolarisation changes in a black/African athlete characterised by domed ST segment elevation and T wave inversion
in V1–V4. (B) A downsloping ST segment elevation followed by T wave inversion in V1–V2 suggestive of a Brugada-pattern ECG. Note the high-take
off and absence of upward convexity (‘dome’ shape) of the ST segment distinguishing this from the repolarisation variant in black/African athletes.
This figure is only reproduced in colour in the online version.
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(HCM).11 14 33–35 Furthermore, increased QRS voltage in the
absence of other ECG abnormalities is uncommon in subjects
with HCM being present in less than 2% of individuals with the
disease.36 However, when other ECG abnormalities such as ST
depression, T wave inversion, pathological Q waves, left axis
deviation or left atrial abnormalities are present, the possibility
of HCM should be investigated by additional testing (figure 14).
Therefore, isolated increased QRS voltage on the ECG in the
absence of other abnormalities in an asymptomatic athlete with
a negative family history is not a reliable indicator of LVH or
HCM and does not require further evaluation.
Repolarisation findings in black/African athletes
Growing attention has been paid to ethnic-related differences
in morphological and ECG features of the athlete’s heart.
Notably, there are specific repolarisation patterns in black/
African athletes that are normal variants and should be distinguished from abnormal findings suggestive of a pathological
cardiac disorder.
As aforementioned, early repolarisation is common in athletes
and usually characterised by an elevated ST segment with upward
concavity, ending in a positive (upright ‘peaked’) T wave
(figure 11). There is also a normal variant early repolarisation
pattern found in some black/African athletes, characterised by an
elevated ST segment with upward convexity (‘dome’ shaped), followed by a negative T wave confined to leads V1–V4 (figure 15).
The presence of either repolarisation pattern in an asymptomatic
black/African athlete does not require additional testing.
Differentiating normal repolarisation variants from pathological
findings
The presence of early repolarisation and T wave inversion in the
anterior leads in black/African athletes probably represents a
specific, ethnically dependent adaption to regular exercise.
More than two-thirds of black athletes exhibit ST segment elevation and up to 25% show T wave inversions.12 13 However,
normal repolarisation changes in black/African athletes do not
extend beyond V4. Thus, T wave inversion in the lateral leads
(V5–V6) is always considered as an abnormal finding and
requires additional testing to rule out HCM or other cardiomyopathies (figure 16).
Repolarisation variants in black/African athletes also must be
distinguished from pathological repolarisation changes in the
anterior precordial leads found in ARVC and Brugada-pattern
ECGs. In ARVC, the ST segment is usually isoelectric prior to
T wave inversion, in contrast to the ‘domed’ ST segment elevation which is the hallmark feature of the normal repolarisation
variant in black/African athletes (figure 17). In Brugada-pattern
ECGs, the high take-off and downsloping ST segment prior to
T wave inversion distinguishes this from the ‘domed’ ST segment
elevation preceding the negative T wave in black/African athletes
(figure 18). Pathological repolarisation changes in the anterior
precordial leads suggesting either ARVC or Brugada-pattern
require additional testing.
Additional resources
For a free online training module on ECG interpretation in athletes,
please visit:http://learning.bmj.com/ECGathlete. For the November
2012 BJSM supplement on ‘Advances in Sports Cardiology’, please
visit:http://bjsm.bmj.com/content/46/Suppl_1.toc.
Author affiliations
1
Department of Family Medicine, University of Washington, Seattle, Washington,
USA
2
Department of Pediatrics, Emory University School of Medicine, Children’s
Healthcare of Atlanta, Atlanta, Georgia, USA
3
Division of Cardiovascular Medicine, Stanford University School of Medicine, Palo
Alto, California, USA
4
Midwest Heart Foundation, Oakbrook Terrace, Illinois, USA
5
Department of Medicine, Institute of Sport Medicine and Science, Rome, Italy
6
Division of Cardiology, University of Washington, Seattle, Washington, USA
7
Division of Cardiology, University Hospital Zurich, Zurich, Switzerland
8
Department of Cardivascular Sciences, St. George’s University of London, London,
UK
9
Department of Sports Medicine, ASPETAR, Qatar Orthopedic and Sports Medicine
Hospital, Doha, Qatar
10
Divisions of Cardiovascular Diseases and Pediatric Cardiology, Departments of
Medicine, Pediatrics, and Molecular Pharmacology & Experimental Therapeutics,
Mayo Clinic, Rochester, Minnesota, USA
11
Department of Athletics, University of Connecticut, Storrs, Connecticut, USA
12
Department of Family Medicine, Eisenhower Army Medical Center, Fort Gordon,
Georgia, USA
13
Division of Cardiology, Massachusetts General Hospital, Boston, Massachusetts,
USA
14
Department of Cardiology, Swedish School of Sports and Health Sciences,
Karolinska University Hospital, Stockholm, Sweden
15
Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota, USA
16
Department of Cardiac, Thoracic, and Vascular Sciences, University of Padua,
Padua, Italy
17
Division of Sports Medicine, University of California Los Angeles, Los Angeles,
California, USA
18
Department of Cardiovascular Sciences, University of Leuven, Leuven, Belgium
19
Department of Family and Community Medicine, University of Arizona, Tucson,
Arizona, USA
20
Division of Cardiology, Seattle Children’s Hospital, Seattle, Washington, USA
21
Cardiology Department, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil,
Brazil
22
Division of Cardiology, The Children’s Hospital of Philadelphia, Philadelphia,
Pennsylvania, USA
Competing interests None.
Provenance and peer review Commissioned; internally peer reviewed.
REFERENCES
1
2
3
4
5
CONCLUSIONS
Fundamental to the cardiovascular care of athletes is an understanding of the physiological cardiac adaptations in athletes that
are manifested on the ECG. The ECG can provide valuable
information when interpreted properly, accounting for the electrical and structural changes that are a common result of regular
training. Distinguishing ECG findings related to athlete’s heart
from changes suggestive of an underlying pathological disorder
is critical to the identification of athletes at risk of SCD.
12 of 13
6
7
8
9
Harmon KG, Asif IM, Klossner D, et al. Incidence of sudden cardiac death in
national collegiate athletic association athletes. Circulation 2011;123:1594–600.
Maron BJ, Doerer JJ, Haas TS, et al. Sudden deaths in young competitive athletes:
analysis of 1866 deaths in the United States, 1980–2006. Circulation
2009;119:1085–92.
Wilson MG, Basavarajaiah S, Whyte GP, et al. Efficacy of personal symptom and
family history questionnaires when screening for inherited cardiac pathologies: the
role of electrocardiography. Br J Sports Med 2008;42:207–11.
Pelliccia A, Culasso F, Di Paolo FM, et al. Prevalence of abnormal
electrocardiograms in a large, unselected population undergoing pre-participation
cardiovascular screening. Eur Heart J 2007;28:2006–10.
Sharma S. Athlete’s heart—effect of age, sex, ethnicity and sporting discipline.
Exp Physiol 2003;88:665–9.
Sharma S, Whyte G, Elliott P, et al. Electrocardiographic changes in 1000 highly
trained junior elite athletes. Br J Sports Med 1999;33:319–24.
Wilson MG, Chatard JC, Carre F, et al. Prevalence of electrocardiographic
abnormalities in West-Asian and African male athletes. Br J Sports Med
2011;46:341–7.
Papadakis M, Sharma S. ECG screening in athletes: the time is now for universal
screening. Br J Sports Med 2009;43:663–8.
Drezner JA, Ashley E, Baggish AL, et al. Abnormal electrocardiographic findings in
athletes: recognizing changes suggestive of cardiomyopathy. Br J Sports Med
2013;47.
Drezner JA, et al. Br J Sports Med 2013;47:125–136. doi:10.1136/bjsports-2012-092068
Downloaded from bjsm.bmj.com on January 9, 2013 - Published by group.bmj.com
Original articles
10
11
12
13
14
15
16
17
18
19
20
21
22
23
Drezner JA, Ackerman MJ, Cannon BC, et al. Abnormal electrocardiographic
findings in athletes: recognizing changes suggestive of primary electrical disease.
2013;47.
Papadakis M, Basavarajaiah S, Rawlins J, et al. Prevalence and significance of
T-wave inversions in predominantly Caucasian adolescent athletes. Eur Heart J
2009;30:1728–35.
Papadakis M, Carre F, Kervio G, et al. The prevalence, distribution, and clinical
outcomes of electrocardiographic repolarization patterns in male athletes of African/
Afro-Caribbean origin. Eur Heart J 2011;32:2304–13.
Di Paolo FM, Schmied C, Zerguini YA, et al. The athlete’s heart in adolescent
Africans: an electrocardiographic and echocardiographic study. J Am Coll Cardiol
2012;59:1029–36.
Pelliccia A, Maron BJ, Culasso F, et al. Clinical significance of abnormal
electrocardiographic patterns in trained athletes. Circulation 2000;102:278–84.
Rawlins J, Carre F, Kervio G, et al. Ethnic differences in physiological cardiac
adaptation to intense physical exercise in highly trained female athletes. Circulation
2010;121:1078–85.
Stein R, Medeiros CM, Rosito GA, et al. Intrinsic sinus and atrioventricular node
electrophysiologic adaptations in endurance athletes. J Am Coll Cardiol
2002;39:1033–8.
Stein R, Moraes RS, Cavalcanti AV, et al. Atrial automaticity and atrioventricular
conduction in athletes: contribution of autonomic regulation. Eur J Appl Physiol
2000;82:155–7.
Moore EN, Boineau JP, Patterson DF. Incomplete right bundle-branch block.
An electrocardiographic enigma and possible misnomer. Circulation
1971;44:678–87.
Fagard R, Aubert A, Lysens R, et al. Noninvasive assessment of seasonal variations
in cardiac structure and function in cyclists. Circulation 1983;67:896–901.
Langdeau JB, Blier L, Turcotte H, et al. Electrocardiographic findings in athletes:
the prevalence of left ventricular hypertrophy and conduction defects. Can J Cardiol
2001;17:655–9.
Corrado D, Basso C, Thiene G. Arrhythmogenic right ventricular cardiomyopathy:
diagnosis, prognosis, and treatment. Heart 2000;83:588–95.
Gussak I, Bjerregaard P, Egan TM, et al. ECG phenomenon called the J wave.
History, pathophysiology, and clinical significance. J Electrocardiol 1995;28:49–58.
Perez MV, Friday K, Froelicher V. Semantic confusion: the case of early
repolarization and the J point. Am J Med 2012;125:843–4.
Drezner JA, et al. Br J Sports Med 2013;47:125–136. doi:10.1136/bjsports-2012-092068
24
25
26
27
28
29
30
31
32
33
34
35
36
Tanguturi VK, Noseworthy PA, Newton-Cheh C, et al. The electrocardiographic
early repolarization pattern in athletes: normal variant or sudden death risk factor?
Sports Med 2012;42:359–66.
Leo T, Uberoi A, Jain NA, et al. The impact of ST elevation on athletic screening.
Clin J Sport Med 2011;21:433–40.
Uberoi A, Jain NA, Perez M, et al. Early repolarization in an ambulatory clinical
population. Circulation 2011;124:2208–14.
Junttila MJ, Sager SJ, Freiser M, et al. Inferolateral early repolarization in athletes.
J Interv Card Electrophysiol 2011;31:33–8.
Tikkanen JT, Junttila MJ, Anttonen O, et al. Early repolarization: electrocardiographic
phenotypes associated with favorable long-term outcome. Circulation
2011;123:2666–73.
Noseworthy PA, Weiner R, Kim J, et al. Early repolarization pattern in competitive
athletes: clinical correlates and the effects of exercise training. Circ Arrhythm
Electrophysiol 2011;4:432–40.
Tikkanen JT, Anttonen O, Junttila MJ, et al. Long-term outcome associated with
early repolarization on electrocardiography. N Engl J Med 2009;361:2529–37.
Hancock EW, Deal BJ, Mirvis DM, et al. AHA/ACCF/HRS recommendations for the
standardization and interpretation of the electrocardiogram: part V: electrocardiogram
changes associated with cardiac chamber hypertrophy: a scientific statement from the
American Heart Association Electrocardiography and Arrhythmias Committee, Council
on Clinical Cardiology; the American College of Cardiology Foundation; and the
Heart Rhythm Society: endorsed by the International Society for Computerized
Electrocardiology. Circulation 2009;119:e251–61.
Corrado D, Biffi A, Basso C, et al. 12-lead ECG in the athlete: physiological versus
pathological abnormalities. Br J Sports Med 2009;43:669–76.
Sohaib SM, Payne JR, Shukla R, et al. Electrocardiographic (ECG) criteria for
determining left ventricular mass in young healthy men; data from the LARGE Heart
study. J Cardiovasc Magn Reson 2009;11:2.
Sathanandam S, Zimmerman F, Davis J, et al. Abstract 2484: ECG screening
criteria for LVH does not correlate with diagnosis of hypertrophic cardiomyopathy.
Circulation 2009;120:S647.
Weiner RB, Hutter AM, Wang F, et al. Performance of the 2010 European
Society of Cardiology criteria for ECG interpretation in the athlete. Heart
2011;97:1573–7.
Ryan MP, Cleland JG, French JA, et al. The standard electrocardiogram as a
screening test for hypertrophic cardiomyopathy. Am J Cardiol 1995;76:689–94.
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Normal electrocardiographic findings:
recognising physiological adaptations in
athletes
Jonathan A Drezner, Peter Fischbach, Victor Froelicher, et al.
Br J Sports Med 2013 47: 125-136
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Original articles
Abnormal electrocardiographic findings in athletes:
recognising changes suggestive of cardiomyopathy
Scan to access more
free content
For numbered affiliations see
end of article
Correspondence to
Jonathan A Drezner,
Department of Family
Medicine, University of
Washington, 1959 NE Pacific
Street, Box 356390, Seattle,
Washington 98195, USA;
[email protected]
Received 7 December 2012
Revised 7 December 2012
Accepted 7 December 2012
Jonathan A Drezner,1 Euan Ashley,2 Aaron L Baggish,3 Mats Börjesson,4
Domenico Corrado,5 David S Owens,6 Akash Patel,7 Antonio Pelliccia,8
Victoria L Vetter,7 Michael J Ackerman,9,10 Jeff Anderson,11 Chad A Asplund,12
Bryan C Cannon,13 John DiFiori,14 Peter Fischbach,15 Victor Froelicher,2
Kimberly G Harmon,1 Hein Heidbuchel,16 Joseph Marek,17 Stephen Paul,18
Jordan M Prutkin,6 Jack C Salerno,19 Christian M Schmied,20 Sanjay Sharma,21
Ricardo Stein,22 Mathew Wilson23
This document was developed in collaboration between the American Medical Society for Sports Medicine (AMSSM),
the Section on Sports Cardiology of the European Association for Cardiovascular Prevention and Rehabilitation
(EACPR), a registered branch of the European Society of Cardiology (ESC), the FIFA Medical Assessment and Research
Center (F-MARC), and the Pediatric & Congenital Electrophysiology Society (PACES).
ABSTRACT
Cardiomyopathies are a heterogeneous group of heart
muscle diseases and collectively are the leading cause of
sudden cardiac death (SCD) in young athletes. The
12-lead ECG is utilised as both a screening and
diagnostic tool for detecting conditions associated with
SCD. Fundamental to the appropriate evaluation of
athletes undergoing ECG is an understanding of the ECG
findings that may indicate the presence of an underlying
pathological cardiac disorder. This article describes ECG
findings present in cardiomyopathies afflicting young
athletes and outlines appropriate steps for further
evaluation of these ECG abnormalities. The ECG findings
defined as abnormal in athletes were established by an
international consensus panel of experts in sports
cardiology and sports medicine.
INTRODUCTION
To cite: Drezner JA,
Ashley E, Baggish AL, et al.
Br J Sports Med 2013;47:
137–152.
The cardiomyopathies are a diverse group of heart
muscle diseases that are defined and subdivided in
clinical practice by different structural and functional characteristics. As a family of related diseases,
the cardiomyopathies are the leading cause of
sudden cardiac death (SCD) in young competitive
athletes.1–3 Athletes with an underlying cardiomyopathy may present with disease-related symptoms
or may be asymptomatic and thus only identified by
abnormal testing during pre-participation screening.
Although a definitive diagnosis may require extensive evaluation by a cardiovascular specialist, the
12-lead ECG is commonly abnormal among athletes
with an underlying cardiomyopathy. Therefore, it is
of paramount importance that clinicians responsible
for ECG interpretation in athletes be familiar with
key findings associated with underlying diseases of
the heart muscle. This paper will review the principal ECG findings associated with the most common
forms of cardiomyopathy relevant to the care of the
young athlete. Initial testing for further evaluation
of abnormal ECG findings is also presented.
Drezner JA, et al. Br J Sports Med 2013;47:137–152. doi:10.1136/bjsports-2012-092069
DISTINGUISHING NORMAL FROM ABNORMAL
A challenge in the use of ECG for screening or
diagnostic evaluations in athletes is the ability to
accurately differentiate findings suggestive of a
potentially lethal cardiovascular disorder from
benign physiological adaptations occurring as the
result of regular and sustained intensive training
(ie, athlete’s heart). Several reports have outlined
ECG criteria intended to distinguish normal ECG
findings in athletes from ECG abnormalities requiring additional evaluation.4–9
On 13–14 February 2012, an international
group of experts in sports cardiology and sports
medicine convened in Seattle, Washington, to
define contemporary standards for ECG interpretation in athletes. The objective of the meeting was
to help physicians distinguish normal ECG alterations in athletes from abnormal ECG findings that
require additional evaluation for conditions that
predispose to SCD.10 A review of normal ECG
findings in athletes is presented separately.11
In this paper, abnormal ECG findings are presented relative to the most common cardiomyopathies associated with SCD in athletes:
hypertrophic cardiomyopathy (HCM), arrhythmogenic right ventricular cardiomyopathy (ARVC),
dilated cardiomyopathy (DCM) and left-ventricular
non-compaction (LVNC). Table 1 summarises a list
of abnormal ECG findings unrelated to athletic
training that may suggest the presence of an underlying cardiomyopathy and should trigger additional
evaluation in an athlete.
HYPERTROPHIC CARDIOMYOPATHY
HCM is a genetic disease of the heart muscle. It is
characterised by ventricular hypertrophy in the
absence of a recognisable cause such as aortic valve
disease or hypertension. A common pattern of
hypertrophy in HCM is an asymmetric septal
hypertrophy where the interventricular septum is
thicker than the rest of the left ventricle. However,
many other patterns of pathological hypertrophy
are consistent with HCM such as apical
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Original articles
Table 1 Abnormal ECG findings suggestive of cardiomyopathy
Abnormal ECG finding
Definition
T wave inversion
>1 mm in depth in two or more leads V2–V6, II and
aVF or I and aVL (excludes III, aVR and V1)
≥0.5 mm in depth in two or more leads
>3 mm in depth or >40 ms in duration in two or
more leads (except III and aVR)
QRS≥120 ms, predominantly negative QRS complex
in lead V1 (QS or rS), and upright monophasic R
wave in leads I and V6
Any QRS duration ≥140 ms
ST segment depression
Pathological Q waves
Complete left bundle
branch block
Intraventricular
conduction delay
Left axis deviation
Left atrial enlargement
Right ventricular
hypertrophy pattern
Premature ventricular
contractions
Ventricular arrhythmias
−30° to −90°
Prolonged P wave duration of >120 ms in leads I or
II with negative portion of the P wave≥1 mm in
depth and ≥40 ms in duration in lead V1
R-V1+S-V5>10.5 mm AND right axis deviation
>120°
≥2 PVCs per 10 s tracing
Couplets, triplets and non-sustained ventricular
tachycardia
Note: These ECG findings are unrelated to regular training or expected
physiological adaptation to exercise, may suggest the presence of
pathological cardiovascular disease, and require further diagnostic evaluation.
hypertrophy, concentric hypertrophy and proximal septal hypertrophy. Poor ventricular compliance (diastolic dysfunction) is
characteristic, along with microvascular dysfunction which contribute to ischaemia during exercise. Some patients have
dynamic left ventricular (LV) outflow tract obstruction caused
by the combination of hypertrophy and abnormalities of the
mitral valve which leads to systolic anterior motion of the anterior leaflet. However, only about 25% of patients with HCM
have a murmur from LV outflow tract obstruction during resting
examination.12 Symptoms of HCM include chest pain, syncope
and exercise intolerance, but for many persons the disease can
be asymptomatic and SCD may be the clinical presentation of
the disease.13 Fibrosis of the heart muscle is characteristic and
may underlie ventricular arrhythmias and sudden death. On
histopathological analysis, disorganised cellular architecture with
cardiac myocyte disarray is a hallmark feature.12
Prevalence
HCM is among the most common inherited cardiovascular disorders and may occur in 1 : 500 adults and at equal prevalence in
men and women.12 However, the reported prevalence of HCM in
competitive athletes is apparently lower, approximately 1 in 1000
to 1 in 1500 athletes.3 14 HCM is inherited primarily as autosomal
dominant with variable penetrance, and morphological expression
of HCM may appear in childhood but typically develops in early
adolescence through young adulthood. This may contribute to the
lower prevalence of HCM found in younger athletes.
Contribution as a cause of SCD
In most case series, HCM is among the most common causes of
SCD in young athletes. In the USA, HCM accounts for approximately one-third of identified causes of SCD in athletes, and in
the UK HCM represents 11% of cases.1 15 HCM is a less
common cause of sudden death in other populations. In US
military personnel, HCM accounted for only 6% of SCD, and
in the US general population (less than 35 years old) only 5% of
cases of sudden cardiac arrest were attributed to HCM.16 17
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Diagnostic criteria
HCM can be diagnosed by ECG in combination with echocardiography or cardiac MRI. An LV wall thickness of 1.5 cm or
greater is normally required to make the diagnosis, but marked
asymmetry with lower absolute wall thickness measurement is
also compatible with HCM. The upper limit of normal wall
thickness in most echocardiography laboratories is 1.2 cm.
A ‘grey area’ is defined between 1.2 and 1.5 cm. In borderline
cases, other features favouring a diagnosis of HCM include
impaired diastolic function, small LV cavity size, LV wall thickness asymmetry, mitral valve pathology (leaflet redundancy and
systolic anterior motion) and the presence of myocardial fibrosis
(late gadolinium enhancement) on cardiac MRI.18
Abnormal ECG findings in HCM
Over 90% of patients with HCM will have an abnormal
ECG.19–21 ECG abnormalities include T wave inversion (TWI),
ST segment depression, pathological Q waves, conduction delay,
left-axis deviation (LAD) and left atrial enlargement (LAE).
T wave inversion
TWI in the lateral or inferolateral leads is seen commonly in
HCM (figures 1–3). In a series of asymptomatic patients
≤35 years old with HCM confirmed by cardiac MRI, 62%
exhibited TWI.21 Similarly, in patients with a positive HCM
genetic test and overt morphological HCM, 54% demonstrate
TWI.22 In black patients with HCM, TWI occurs more commonly in the lateral leads (77%) and less frequently in the inferior leads (2%).23 Abnormal TWI is defined as >1 mm in depth
in two or more leads V2–V6, II and aVF, or I and aVL (excludes
leads III, aVR and V1). Deep TWI in the mid-precordial to
lateral precordial leads (V4–V6) should raise the possibility of
apical HCM.
In healthy athletes, TWI in the lateral or inferior leads is
uncommon. TWI beyond V2 is a rare abnormality found in
only 0.1% of Caucasian adolescent athletes older than
16 years.24 In a college athletic population of mixed ethnicity,
TWI in the lateral or inferolateral leads is reported in 2% of
athletes.25 In Caucasian elite athletes, the prevalence of TWI in
the lateral or inferior leads is also about 2%.26 However, TWI is
more common in black athletes of African-Caribbean descent
(hereto referred to as ‘black/African’ athletes). TWI in the lateral
or inferior leads is reported in 8–10% of black/African
athletes.23 27
Repolarisation variant in black/African athletes
TWI in the anterior precordial leads should be distinguished
from TWI in the lateral or inferior leads in black/African athletes. TWI in the anterior precordial leads may be part of a
normal variant pattern of repolarisation in black/African athletes
consisting of convex (‘dome’ shaped) ST segment elevation followed by TWI in V1–V4 (figure 4). On the basis of current
data, TWI preceded by ST segment elevation are present in the
anterior precordial leads in up to 13% of black/African athletes
and do not require further assessment in the absence of symptoms, positive family history or abnormal physical examination.23 27 However, TWI in the lateral or inferolateral leads
(V5–V6, I and aVL, II and aVF), regardless of ethnicity, is considered abnormal and requires additional testing to rule out
HCM (figures 1–3).
Drezner JA, et al. Br J Sports Med 2013;47:137–152. doi:10.1136/bjsports-2012-092069
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Figure 1 Abnormal ECG in a patient with hypertrophic cardiomyopathy. Note the T wave inversion and ST depression in the inferolateral leads
(arrows). This figure is only reproduced in colour in the online version.
Juvenile pattern of TWI
TWI in the anterior precordial leads in younger, prepubertal
athletes often reflects a persistent juvenile pattern and requires
careful interpretation. In Caucasian adolescent athletes, anterior
precordial TWI extending beyond V2 was present in 1.2% of
athletes <16 years but only 0.1% of athletes ≥16 years.24 In a
study of Italian adolescent athletes, incomplete pubertal development was an independent predictor for right precordial
TWI.28 The prevalence of right precordial TWI decreased significantly with increasing age, 8.4% in children <14 years of
age versus 1.7% in those ≥14 years.28
Biphasic T waves
Biphasic T waves create a challenge and currently there is no consensus regarding the definition of TWI when a large positive
deflection precedes a negative portion below the isoelectric line. If
Figure 2 Markedly abnormal ECG in a patient with hypertrophic cardiomyopathy. Note deep T wave inversion and ST depression in the
inferolateral leads. This figure is only reproduced in colour in the online version.
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Figure 3 Markedly abnormal ECG in a patient with hypertrophic cardiomyopathy. Note the deep T wave inversions in the inferolateral leads (V4–
V6, I and aVL, II and aVF). This ECG pattern may represent apical hypertrophic cardiomyopathy which is not adequately evaluated by
echocardiography. Cardiac MRI is recommended. This figure is only reproduced in colour in the online version.
the negative portion of the T wave is >1 mm in depth in two or
more leads (excluding leads III, aVR, and V1), it is reasonable to
consider this pattern as abnormal until more data are obtained.
ST segment depression
ST segment depression is a common abnormality in HCM but
extremely rare in otherwise healthy athletes, making it a
concerning indicator of disease if identified on an athlete’s
ECG. ST segment depression is reported in 46–50% of patients
with HCM, but in <1% of apparently healthy athletes or
adolescents undergoing ECG screening.9 22–25 Any degree of
ST depression beyond 0.5 mm in two or more leads is significant and requires further investigation for cardiomyopathy
(figures 1 and 2).
Pathological Q waves
Q waves have been defined in different ways in different populations. In patients with overt HCM, pathological Q waves are
Figure 4 ECG from a 17-year-old black/African soccer player demonstrating ‘domed’ ST elevation followed by T wave inversion in leads V1–V4
(circles). This is a normal repolarisation pattern in black/African athletes and does not require further investigation in asymptomatic athletes. Note
the T wave inversion does not extend to the lateral leads beyond V4. This figure is only reproduced in colour in the online version.
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reported in 32–42% of patients.19 22 In one series of asymptomatic patients with HCM, 42% demonstrated pathological Q
waves.21 The consensus of this group is to define Q waves for
HCM as >3mm in depth or >40 ms in duration in at least two
leads (excluding leads III and aVR; figure 5). This detects HCM
with a sensitivity of 35% and a specificity of 95% in patients
with preclinical HCM based on molecular genetic diagnosis.29
Intraventricular conduction delay
Left bundle branch block (LBBB) is an abnormal finding
detected in 2% of patients with HCM but not reported in
screening populations of athletes or adolescents.9 22 25 LBBB
pattern with a QRS duration of 120 ms or greater should
prompt further evaluation (figure 6). Right bundle branch block
(RBBB) is found more commonly in HCM than in athletes but
the frequency of incomplete and complete RBBB in athletes is
felt to limit its differentiating value.23 30 The significance of a
non-specific intraventricular conduction delay (IVCD) with
normal QRS morphology is uncertain. However, marked nonspecific IVCD >140 ms is considered abnormal and should
prompt further evaluation.
Left axis deviation
LAD, defined as −30° to −90°, is present in almost 12% of
HCM patients but less than 1% of athletes (figure 7).9 23 25
LAD can be a secondary marker for pathological LV hypertrophy (LVH) and if present warrants additional evaluation.
Left atrial enlargement
ECG findings suggestive of LAE have been defined in different
ways. Overall, LAE on ECG is present in approximately 10–
21% of HCM patients but has been reported in up to 44% of
black patients with HCM (figure 8).21–23 LAE is defined as a
prolonged P wave duration of >120 ms in leads I or II with
negative portion of the P wave ≥1 mm in depth and ≥40 ms in
duration in lead V1. LAE on ECG is an uncommon finding in
athletes and should prompt additional investigation.
Increased QRS voltage in athletes and HCM
The isolated presence of high QRS voltages fulfilling voltage criterion for LVH is regarded as a normal finding in athletes
related to physiological increases in cardiac chamber size and/or
wall thickness and does not in itself require additional evaluation.5 6 As expected, voltage criteria for LVH also are commonly identified in individuals with HCM. However, the
presence of isolated increased QRS voltage in the absence of
other ECG abnormalities is uncommon and present in <2% of
individuals with the disease.19 Several studies have evaluated
athletes and young adults with isolated increased QRS voltage
using echocardiography or cardiac MRI and none had
HCM.24 26 31–33 Therefore, isolated increased QRS voltage on
the ECG in the absence of other abnormalities in an asymptomatic athlete with a negative family history is not a reliable indicator of HCM and does not require further evaluation.
Co-existing ECG abnormalities such as TWI, ST segment
depression, pathological Q waves, IVCD, LAD or LAE should
be investigated by additional testing.
Evaluation of suspected HCM
If HCM is suspected based on ECG abnormalities, evaluation of
LV morphology and function is required.34 Echocardiography
provides assessment of LV cavity size and wall thickness, systolic
and diastolic function and valvular structure and function, and
is the first test of choice under most circumstances. HCM can
be diagnosed when wall thickness is ≥1.5 cm with normal or
small LV cavity size in the absence of other causes capable of
causing myocardial hypertrophy. Diastolic dysfunction, mitral
valve pathology and LV outflow tracts obstruction are other findings that support the diagnosis of HCM.
However, echocardiographic quality is variable based on
numerous factors, including operator proficiency and patient
acoustic windows, and may have limited ability to detect hypertrophy of the anterolateral LV wall and apex (figure 9).35
Cardiac MRI provides superior assessment of myocardial hypertrophy and may demonstrate late gadolinium enhancement
which is a non-specific marker suggesting myocardial fibrosis.
Cardiac MRI should be considered when echocardiography is
insufficient to assess all myocardial segments or when
Figure 5 Abnormal ECG in a patient with hypertrophic cardiomyopathy. Note the abnormal Q waves (>3 mm in depth) in V5–V6, II and aVF. This
figure is only reproduced in colour in the online version.
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Figure 6 Abnormal ECG in a patient with hypertrophic cardiomyopathy showing complete left bundle branch block (QRS≥120 ms with
predominantly negative QRS complex in lead V1).
myocardial hypertrophy falls into the ‘grey zone’ between 1.2
and 1.5 cm. Cardiac MRI is recommended for markedly abnormal ECGs suggestive of apical HCM, specifically ECGs with
deep TWI and/or ST depression in the inferolateral leads (V4–
V6, I, aVL, II and aVF), in which echocardiography often does
not provide an adequate assessment of the LV apex or inferior
septum (figures 1–3).
A common clinical dilemma is the detection of myocardial
hypertrophy in an athlete in which the hypertrophy may be due
to physiological adaptation to exercise. Differentiating athlete’s
heart from HCM requires careful clinical evaluation by an
experienced provider.36–38 Cardiac MRI, cardiopulmonary exercise testing and Holter monitoring should be considered.
Findings suggestive of HCM include the presence of unusual
patterns of hypertrophy with substantial differences in wall
thickness of the LV segments, normal or reduced LV cavity size,
extreme LAE, diastolic dysfunction, family history of HCM or
SCD, below normal peak oxygen consumption ( peak VO2), and
the presence of ventricular arrhythmias. When diagnostic uncertainty remains, genetic testing and/or a period of deconditioning
followed by reassessment to document regression (or lack
thereof ) of exercise-induced LVH may be considered.
Long-term follow-up of markedly abnormal ECGs
Highly trained athletes occasionally present markedly abnormal
ECG patterns instinctively suggesting the presence of a cardiomyopathy.39 40 Such abnormal ECGs raise the question of differentiating between the initial, subtle expression of cardiac
disease or the extreme but innocent ECG expression of the ‘athlete’s heart’.26 41 42
Investigators researched the clinical outcomes of 81
athletes presenting initially with markedly abnormal repolarisation patterns in the absence of detectable cardiac abnormalities.43 After an average 9-year follow-up, a new diagnosis of
Figure 7 ECG demonstrates abnormal left-axis deviation defined as frontal plane QRS axis of less than −30°. The QRS is positive in lead I and
negative in aVF and lead II. The QRS axis shown here is about −70°. This figure is only reproduced in colour in the online version.
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Figure 8 Abnormal ECG in a patient with hypertrophic cardiomyopathy showing left atrial enlargement, defined as a prolonged P wave duration
>120 ms in leads I or II with negative portion of the P wave≥1 mm in depth and ≥40 ms duration in lead V1. This figure is only reproduced in
colour in the online version.
cardiomyopathy was made in five athletes (6%), including three
with HCM, one with ARVC and one with DCM.43 Two athletes
experienced adverse events (0.3% per year), including one
cardiac arrest from HCM and one sudden death related to
ARVC.43 Markedly abnormal ECGs, therefore, may represent
the initial expression of cardiomyopathy, preceding by many
years the phenotypic or morphological expression of structural
heart disease.
Athletes presenting with distinctly abnormal ECGs (ie, deep
TWI in the lateral leads) and no evidence of structural heart
disease after a thorough work-up may be permitted to participate in competitive athletics. However, these athletes should
undergo serial clinical evaluation on an annual basis, even in the
absence of symptoms, including repeat imaging tests such as
echocardiography and/or cardiac MRI to evaluate for the development of cardiomyopathy.
Figure 9 ECG (left panel) and cardiac MRI (right panel) of apical hypertrophic cardiomyopathy. Deep T wave inversions across the precordial leads
are a characteristic ECG finding. The region of hypertrophy (red arrow) is isolated to the left ventricular (LV) apex, which can be challenging to
detect by echocardiography. This figure is only reproduced in colour in the online version.
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ARRHYTHMOGENIC RIGHT VENTRICULAR
CARDIOMYOPATHY
ARVC is an inherited heart muscle disease characterised by
fibro-fatty replacement of right ventricular myocardium and corollary life-threatening ventricular arrhythmias or SCD, mostly in
young people and athletes. Progressive dilation/dysfunction predominantly involves the right ventricle with involvement of the
left ventricle in late-stage disease. Variants with predominantly
LV involvement are described in about 10% of patients (hence
the alternative term of arrhythmogenic cardiomyopathy).
Mutations in the desmosomal genes account for approximately
50% of ARVC cases.44 45 In addition, there is emerging evidence that intense endurance sports may lead to a similar
phenotype (with similar prognosis) in the absence of desmosomal mutations, so-called exercise-induced ARVC, which may
be the result of increased RV wall stress during exercise.46–48
The prevalence of familial ARVC is estimated at 1 : 2000–1 :
5000 persons.44 45
Contribution as a cause of SCD
According to data from the Veneto region of Italy where postmortem investigation of young sudden death victims is performed systematically, ARVC is a leading cause of sport-related
sudden death accounting for approximately one-fourth of fatalities in young competitive athletes.3 Data from the USA, notably
without a mandatory registry for SCD in athletes, suggest that
ARVC is a less common cause of SCD.1
voltage in limb leads and premature ventricular beats with an
LBBB morphology and superior axis. If there is primarily LV
involvement, the TWI involves the lateral precordial leads and
the premature ventricular beats can have an RBBB morphology.
T wave inversion
TWI in the anterior precordial leads (V1–V3/V4) is present in
approximately 85% of patients with ARVC in the absence of
RBBB (figures 10 and 11).50 TWI occasionally extends to the
left precordial leads V5–V6 or inferior limb leads II, III and
aVF. TWI in V1–V3 or beyond in individuals >14 years of age
(in the absence of complete RBBB) represent a major diagnostic
criterion for ARVC, while TWI confined to just leads V1 and
V2 in individuals >14 years of age (in the absence of complete
RBBB) represents a minor diagnostic criterion.49 In Italian children ≥14 years with TWI in the anterior precordial leads
beyond V2 (ie, V3 or V4), 3 of 26 (11%) fulfilled diagnostic criteria for ARVC (1 definitive, 2 borderline).28
In the presence of complete RBBB, right precordial (V1–V3)
TWI is more likely secondary to RBBB rather than a sign of
underlying ARVC. TWI extending beyond V3 is uncommon in
patients with RBBB and represents a minor diagnostic criterion
for ARVC.49
Thus, TWI involving at least two consecutive precordial
leads, excluding V1, should prompt further investigation in the
athlete.
Epsilon waves
Diagnostic criteria
The original (1994) and the revised (2010) Task Force Criteria
for diagnosis of ARVC are based on major and minor criteria
encompassing familial/genetic, ECG, arrhythmic, morphofunctional ventricular and histopathological features.49 The diagnosis
is fulfilled in the presence of two major criteria, one major plus
two minor criteria, or four minor criteria from different
groups.49
Abnormal ECG findings in ARVC
Over 80% of patients with ARVC will have an abnormal
ECG.45 50 51 ECG abnormalities include TWI in the anterior
precordial leads, epsilon waves, delayed S wave upstroke, low-
Epsilon waves are defined as distinct low-amplitude potentials
localised at the end of the QRS complex. Epsilon waves are
challenging to detect and appear as a small negative deflection
just beyond the QRS in V1–V3 (figure 10). The presence of
epsilon waves in the right precordial leads V1–V3 represents a
major diagnostic criterion for ARVC.49
Delayed S wave upstroke
Delayed S wave upstroke of >55 ms in leads V1–V3 in the
absence of complete RBBB represents a minor diagnostic criterion for ARVC (figure 11).49 This feature is most commonly
observed among ARVC patients with mild QRS prolongation
(100–120 ms). The S wave upstroke is measured from the nadir
Figure 10 ECG from a patient with arrhythmogenic right ventricular cardiomyopathy. (A) Inverted T waves in leads V1–V5. (B) A subtle epsilon
wave with notching in V1 at the terminal portion of the QRS complex. This figure is only reproduced in colour in the online version.
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Figure 11 ECG from a patient with arrhythmogenic right ventricular cardiomyopathy showing delayed S wave upstroke in V1 (arrow), low voltages
in limb leads <5 mm (circles), and inverted T waves in anterior precordial leads (V1–V4) and inferior leads (III and aVF). This figure is only
reproduced in colour in the online version.
of the S wave to the end of the QRS (including epsilon wave if
present). Prolonged S wave upstroke may be present in up to
95% of patients with ARVC in the absence of RBBB.50
Low voltage in limb leads
Low voltage in limb leads, defined as a QRS amplitude ≤5 mm
in each of the limb leads (I, II and III), also can be suggestive of
ARVC (figure 11).
Premature ventricular contractions
Premature ventricular contractions (PVCs) originating from the
right ventricle typically show an LBBB pattern with a predominantly negative QRS complex in V1. On the basis of the QRS
axis in the limb leads the origin of the PVC can be further suggested. PVCs with LBBB morphology and an inferior axis
( positive in the inferior leads) originate from the right ventricular outflow tract consistent with idiopathic right ventricular outflow tract arrhythmia which is a benign condition,
non-familial and not associated with structural ventricular
abnormalities. PVCs with an LBBB morphology and superior
axis (negative in the inferior leads) originate from the right
ventricular free wall or apex and are more suggestive of ARVC
(figure 12).
Evaluation of suspected ARVC
Disease expression in ARVC is variable, and clinical manifestations vary with age and stage of disease.49 Similarly, the extent
of ECG abnormalities are associated with the severity of
disease.51 In patients with diagnosed ARVC (‘overt stage’) or
known desmosome mutation positive subjects, 95% have an
Drezner JA, et al. Br J Sports Med 2013;47:137–152. doi:10.1136/bjsports-2012-092069
abnormal ECG marked by abnormal TWI, a prolonged S wave
upstroke in the anterior precordial leads (V1–V3), and/or an
epsilon wave.50–52 However, in cardiac screening, physicians
may encounter asymptomatic athletes in the early ‘concealed
stage’ of the disease, showing less pronounced ECG changes.
The extent of evaluation is dependent on the specific ECG
findings suggestive of ARVC and will be more extensive in the
presence of warning symptoms or significant family history. A
combination of tests is needed to effectively make the diagnosis
or to rule out ARVC. Echocardiography, ambulatory ECG
(Holter) monitoring, signal-averaged ECG (SAECG), and ventricular angiography provided optimal evaluation, while cardiac
MRI (false-positives) and biopsy (low-sensitivity) were considered less useful for diagnosis in suspected ARVC.53 54
The evaluation of major diagnostic ECG findings according
to the 2010 Task Force criteria of TWI in the right precordial
leads (V1–V3) or beyond in ages >14 years (in the absence of
complete RBBB) should be extensive. In addition to a comprehensive symptom history, family history and physical examination, evaluation of TWI in V1–V3 or beyond should include
echocardiography, Holter monitoring, SAECG, maximal
exercise-ECG test and possibly a cardiac MRI.49 Isolated epsilon
waves in the right precordial leads, a less specific major ECG
criteria, still require an echocardiography and ECG monitoring
for an arrhythmia (Holter or exercise-ECG test).49
Evaluation of minor diagnostic ECG-findings according to the
Task Force criteria (without accompanying positive family
history or alarming symptoms), may be less extensive.49 TWI in
V1–V2 may require simply a careful personal and family history
and physical examination.
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Figure 12 ECG from a patient with arrhythmogenic right ventricular cardiomyopathy. Note multiple premature ventricular complexes with a left
bundle branch pattern and superior axis (negative QRS vector in inferior leads). This figure is only reproduced in colour in the online version.
Repolarisation variants in the anterior precordial leads in
black/African athletes must be distinguished from pathological
repolarisation changes found in ARVC. In ARVC, the ST
segment is usually isoelectric prior to TWI, in contrast to the
‘domed’ ST segment elevation which is the hallmark feature of
the normal repolarisation variant in black/African athletes
(figure 13). TWI involving at least two consecutive precordial
leads from V2 to V6 with an isoelectric ST segment, regardless
of ethnicity, requires additional investigation.
DILATED CARDIOMYOPATHY
DCM is a heart muscle disorder characterised by weakened
myocardial contraction, which over time leads to cavity enlargement and eccentric heart muscle hypertrophy. It is a common
Figure 13 (A) Normal variant repolarisation changes in a black/African athlete characterised by domed ST segment elevation and T wave inversion
in V1–V4. (B) Pathological T wave inversion in V1–V3. Note the isoelectric ST segment. The absence of ST segment elevation prior to T wave
inversion makes this ECG abnormal. Additional testing is required to rule out arrhythmogenic right ventricular cardiomyopathy. This figure is only
reproduced in colour in the online version.
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cause of heart failure, the inability of the heart to meet the
demands of the body. DCM can be caused by a variety of aetiologies ranging from coronary artery disease, infections/myocarditis, toxins (alcohol and other drugs), metabolic or endocrine
abnormalities, autoimmune disorders, infiltrative processes and
a variety of genetic/inheritable disorders. In many cases, a distinct cause of the compromised heart muscle is never found.
DCM can be asymptomatic, or it can result in symptoms of
exercise intolerance, shortness of breath, swelling, congestive
heart failure or SCD from ventricular arrhythmia.
Prevalence
The exact prevalence of DCM in the general population is not
known and estimates depend on the population demographics
and the cut-off used to define LV dysfunction.55 The majority of
cases with early stages of LV dysfunction may be asymptomatic.56 DCM prevalence is increased with older age, male
gender and the presence of cardiovascular risk factors. Among a
relatively young, healthy population without coronary risk
factors, asymptomatic LV dysfunction was present in about
0.2% of individuals.57
Contribution as a cause of SCD
DCM is associated with an increased risk of ventricular arrhythmias and sudden cardiac arrest, with highest risk seen among
individuals with severe LV dysfunction. Notably, SCD can occur
even in the absence of heart failure symptoms. In the
Framingham Heart Study, the death rate from asymptomatic LV
dysfunction was 6.5% per 100 person-years, with 53% of
deaths occurring prior to the onset of symptoms, emphasising
the importance of screening for this disorder.58 DCM accounts
for about 2% of cases in a series of young athletes with sudden
cardiac arrest.2
Diagnostic criteria
DCM is diagnosed on non-invasive imaging (echocardiography
or cardiac MRI) by detecting LV chamber enlargement and
decreased LV systolic (contractile) function. Systolic function is
usually quantified using either fractional shortening (FS) or ejection fraction (EF), but there is no consensus cut-off definition of
DCM based on these parameters. Normal ranges vary by lab
and imaging modality.
Abnormal ECG findings in DCM
Several studies have examined ECG abnormalities in patients
with symptomatic DCM, but few have reported findings among
non-ischaemic DCM or among individuals with asymptomatic
LV dysfunction.59–61 Overall, approximately 90% of individuals
with DCM have abnormal ECG findings (figures 14 and 15).
Patients with prior myocardial infarction may manifest pathological Q waves. Among individuals with non-ischaemic cardiomyopathy, the most common abnormalities seen include voltage
criteria for LVH (33–40%), TWIs (25–45%), LAE (15–33%),
LAD (15–25%), pathological Q waves (10–25%), LBBB (9–
25%), premature ventricular contractions (5–10%) and RBBB
(4%).62 These findings are non-specific for DCM. Goldberger
has proposed a triad of findings that may offer more specificity:
(1) LVH in the anterior precordial leads; (2) low limb lead
voltage and (3) poor precordial R wave progression.63 Given
the overlap of some of these findings with physiological ECG
changes found in athlete’s heart, distinctly abnormal ECG criteria unrelated to regular training and requiring additional
evaluation to rule out an underlying cardiomyopathy are listed
in table 1.
Evaluation of suspected DCM
When DCM is suspected, further evaluation of LV size and
function is required. Echocardiography provides assessment of
cardiac structure and function, including FS and/or EF, and is
the first test of choice under most circumstances. Contrast echocardiography or cardiac MRI should be considered when image
resolution is reduced.
Athletes may have LV chamber enlargement as a part of
physiological adaptation to exercise.64 This is most often seen in
Figure 14 ECG from a patient with idiopathic dilated cardiomyopathy. Note the resting sinus tachycardia, left atrial enlargement, T wave
inversions in the lateral limb (I and aVL) and precordial (V5–V6) leads and deep S waves in V1–V3 ( part of Goldberger’s triad). This figure is only
reproduced in colour in the online version.
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Figure 15 ECG of a young patient with dilated cardiomyopathy. Note inferior Q waves (II, III and aVF), poor R wave progression across the
precordial leads with deep S waves in V1–V3, and a single premature ventricular complex. High-degree AV block is also present. This figure is only
reproduced in colour in the online version.
athletes participating in endurance sports such as cycling, crosscountry skiing or rowing. Mild reduction in LV contractility (EF
40–50%) is seen in a minority of athletes with LV cavity dilation, but is not an invariable component of physiological adaptation to exercise.64 65 Stress echocardiography can assess
myocardial performance at submaximal or peak exercise which
may help differentiate those with low normal or borderline systolic function, as systolic function is more likely to normalised
in athlete’s heart than in DCM. Thus, LV dilatation and measures of systolic function should be interpreted carefully and in
the context of the athlete’s level and amount of endurance training. All patients with DCM should be referred to a cardiologist
for further aetiological evaluation, including assessment for
myocardial ischaemia and infiltrative disorders.
Contribution as a cause of SCD
LVNC is associated with an increased risk of abnormal heart
rhythms and sudden cardiac arrest.68 LVNC is a rare (<1%)
cause of SCD in a series of young athletes.2
Diagnostic criteria
Several sets of diagnostic criteria for isolated LVNC exist, but
remain controversial.69–73 These criteria are based generally on
echocardiography or cardiac MRI findings of an increased ratio
of trabeculations to compact myocardium. These criteria have
LV NON-COMPACTION
LVNC is a heart muscle disorder in which loosely organised
myocardial fibres fail to condense into a compact layer resulting
in increased myocardial trabeculations and thinning of the
compact myocardium (figure 16).66 67 LVNC can occur along
with other congenital or embryological abnormalities, or can be
found in isolation, and can be due to underlying gene mutations. However, the majority of LVNC remains genetically
elusive. This disturbance of myocardial structure leads to progressive weakening of heart muscle contraction (lower EF) with
ventricular dilation. Therefore, LVNC should be distinguished
from DCM. Blood clots may also form within the trabecular
recesses, increasing the risk for embolic strokes.
Prevalence
The exact prevalence of isolated LVNC is unknown, but is
thought to be <0.1–0.2%. Reasons for the uncertainty in prevalence include challenges in imaging the non-compaction and disagreement regarding diagnostic criteria.
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Figure 16 Echocardiographic (left panel) and cardiac MRI (right
panel) of isolated left ventricular non-compaction. Note the prominent
trabeculations in the left ventricular apex (red arrow), with a thin layer
of compact myocardium (blue arrow) and prominent intertrabecular
recesses. This figure is only reproduced in colour in the online version.
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been called into question recently for being non-specific, particularly among black individuals who have relatively greater
degrees of myocardial trabeculations and among athletes.74
Abnormal ECG findings in isolated LVNC
ECG abnormalities in isolated LVNC are common but nonspecific (figures 17 and 18). In a series of 78 patients with a
clinical diagnosis of LVNC, only 13% had a normal ECG.75
The most common abnormalities in this series included repolarisation changes (72%), QT prolongation (52%), ST segment
depression (51%), TWI (41%), LVH voltage criteria (38%),
IVCD (31%) including LBBB (19%) and RBBB (3%), and LAE
(26%).75 Given the overlap of some of these findings with
physiological ECG changes found in athlete’s heart, abnormal
ECG criteria requiring additional evaluation to rule out an
underlying cardiomyopathy are listed in table 1.
Evaluation of suspected isolated LVNC
Echocardiography is usually the first investigation in the evaluation of ECG abnormalities suggestive of cardiomyopathy. The
diagnosis and evaluation of suspected LVNC is quite challenging, and therefore patients should be referred to a cardiovascular specialist familiar with LVNC. Cardiac MRI provides a more
detailed and accurate assessment of myocardial trabeculations
and is recommended in cases with concerning or borderline
findings on echocardiography. A smaller absolute thickness of
compacted myocardium and the presence of LV dysfunction
favour the diagnosis of LVNC. In select cases, LV angiography
may be used to help delineate hypertrabeculation from compacted myocardium. Holter monitoring or more extended
ambulatory monitoring for arrhythmias also should be
considered. In some cases, genetic testing may inform the diagnostic evaluation.
OTHER ECG FINDINGS POSSIBLY SUGGESTIVE OF A
CARDIOMYOPATHY
Several additional ECG abnormalities including RBBB, nonspecific IVCD with QRS duration <140 ms, and isolated (one
per tracing) ectopic/premature ventricular contractions (PVCs)
have been associated with an underlying cardiomyopathy in
non-athletic populations.76–83 However, these findings are also
more common in trained athletes without an underlying heart
disease than among the general population.26 84–87 Each of
these findings, particularly when observed in an asymptomatic
athlete with no family history suggestive of heritable heart
disease, has a low-positive predictive value for the cardiomyopathic conditions associated with an increased risk of SCD
during exercise. As such, none of these ECG patterns, when
found in isolation in asymptomatic athletes, clearly necessitate
further evaluation. However, in athletes with cardiovascularrelated symptoms or a family history of sudden death or suspected cardiomyopathy, each of these findings should prompt
additional evaluation to evaluate for cardiomyopathy.
Right bundle branch block
RBBB is defined as a QRS complex ≥120 ms in association with
a terminal (final component of the QRS complex) R0 wave in
lead V1 and terminal S waves in leads I, aVL and V6 (figure 19).
The R0 may extend into lead V2 but is typically absent in
other precordial leads. T waves in typical RBBB are in the same
direction as the terminal QRS forces and are thus inverted
in leads with an R0 (V1±V2). A QRS complex duration of
Figure 17 ECG from a patient with isolated left ventricular non-compaction. Note the ST segment depression in the inferolateral leads (II, III, aVF
and V5–V6). This figure is only reproduced in colour in the online version.
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Figure 18 ECG from a patient with isolated left ventricular non-compaction, demonstrating left atrial enlargement with a left bundle branch block.
An isolated premature ventricular complex is also present. These findings warrant further testing to evaluate for cardiomyopathy. This figure is only
reproduced in colour in the online version.
100–119 ms with these morphological features is termed an
incomplete RBBB.
Although RBBB may be present in various forms of heart
disease, complete and incomplete RBBB are found commonly
among trained athletes without underlying heart disease. This
ECG pattern has been shown to reflect the exercise-induced
right ventricular remodelling common in endurance sport athletes.88 In asymptomatic athletes with an isolated complete or
incomplete RBBB, no further diagnostic evaluation is required.
In contrast, athletes presenting with symptoms suggestive of
cardiomyopathy, a family history of sudden death or suspected
cardiomyopathy, an RBBB with atypical features (extensive
TWIs, ST-segment elevation or a markedly prolonged R0 ), or a
RBBB in conjunction with other abnormal ECG findings should
be further evaluated.
Non-Specific intra-ventricular conduction delay
IVCD is defined as a QRS complex >110 ms that does not have
morphological features consistent with either LBBB or RBBB.
IVCD has been documented among patients with
Figure 19 ECG showing complete right bundle branch block with an R0 wave in V1, terminal S wave in V6, and a QRS duration of 128 ms. This
figure is only reproduced in colour in the online version.
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cardiomyopathy, but is also frequently seen in healthy athletes.
The physiology underlying IVCD in athletes remains incompletely understood but likely includes some combination of
neurally mediated conduction fibre slowing and increased myocardial mass.
Digital analysis of QRS duration can outperform standard
visual measurement because the first onset and last offset in all
of the leads can be considered.6 In asymptomatic athletes with
an isolated IVCD with a QRS duration of 100–139 ms, no
further diagnostic evaluation is required. In contrast, athletes
presenting with symptoms suggestive of cardiomyopathy, a
family history of sudden death or suspected cardiomyopathy, an
IVCD with marked QRS prolongation (≥140 ms) or an IVCD
in tandem with other abnormal ECG findings should be further
evaluated.
more) during a single ECG tracing (10 s), multifocal PVCs or
PVCs found in tandem with other abnormal ECG findings
should be further evaluated.
PULMONARY HYPERTENSION
Pulmonary hypertension (PHT) is caused by a variety of aetiologies that result in elevation in the pulmonary artery pressure
(mean pulmonary artery pressure greater than or equal to
25 mm Hg) and elevation in the pulmonary vascular resistance.89 As a result of the increased afterload on the right heart,
patients are predisposed to develop right heart failure and are at
risk for sudden death. PHT is a rare cause of sudden death in
athletes but may be suggested by ECG abnormalities and thus a
clinically relevant finding in the cardiovascular care of athletes.
ECG findings in pulmonary hypertension
Isolated premature ventricular contractions
PVCs are electrical impulses that originate from myocardial
tissue below the AV node. They are defined as QRS complexes
>100 ms that are not preceded by a triggering p-wave. PVCs
may reflect pathological myocardial ‘irritability’ due to a cardiomyopathy, an underlying systemic disease process, or may be a
completely benign normal variant. PVCs are common in athletes
with high vagal tone and resting bradycardia and may increase
in frequency in parallel with physical fitness. A single PVC captured during a routine 12-lead ECG in an asymptomatic athlete
does not require further evaluation, unless the athlete performs
a high-intensity endurance sport (mainly cycling, triathlon,
rowing or swimming). In this select group of high-intensity
endurance athletes, a single PVC, especially if it has an LBBB
morphology, may be a hallmark of ‘exercise-induced’ ARVC,
and further evaluation should be considered.46–48 The presence
of PVCs in an athlete with cardiovascular symptoms or a family
history of sudden death or suspected cardiomyopathy should
prompt further evaluation. In addition, multiple PVCs (2 or
The ECG findings in PHT are due to physiological and anatomic
adaptions of the right heart as a result of elevated pulmonary
artery pressures and/or pulmonary vascular resistance. Findings
suggestive of PHT include right ventricular hypertrophy (RVH),
right axis deviation, right ventricular strain and right atrial
enlargement (figure 20).89–91 In adults with idiopathic PHT,
87% demonstrated RVH and 79% demonstrated right axis deviation.89 However, in patients with PHT, the ECG remains an
inadequate screening tool to completely rule out the presence of
this disease.92
Right ventricular hypertrophy pattern
RVH pattern is defined as an R wave in lead V1 plus S wave in
V5 greater than 1.05 mV (10.5 mm at standard amplification)
AND right axis deviation >120° (figure 20). Additional criteria
for RVH associated with PHT include a tall R wave and small S
wave with R/S ratio greater than 1 in lead V1 and a qR complex
in lead V1. The presence of RHV pattern on ECG should
prompt further investigation in the athlete.
Figure 20 ECG from a patient with pulmonary hypertension demonstrating evidence of right-axis deviation >120° (A), right ventricular
hypertrophy (B), right atrial enlargement (C) and right ventricular strain (D). This figure is only reproduced in colour in the online version.
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Right axis deviation
Right-axis deviation is defined as a frontal plane QRS axis of
>120° (figure 20).
Right atrial enlargement
Right atrial enlargement is defined as a P wave greater than or
equal to 2.5 mm in leads II, III and aVF (figure 20).
RV strain
Right ventricular ‘strain’ is defined as ST depression and TWI in
the right precordial leads (V1–V3) (figure 20). As with LVH,
these ST-T changes are referred to as ‘secondary ST-T
abnormalities.’
Evaluation of suspected pulmonary hypertension
Evaluation should include clinical assessment with appropriate
diagnostic testing. Pulmonary artery pressures often can be
assessed by Doppler echocardiography, and both echocardiography and cardiac MRI can evaluate RVH and function, and
assess for secondary causes of PHT such as intracardiac shunts.
Definitive diagnosis of PHT is made by cardiac catheterisation.
CONCLUSIONS
The cardiomyopathies are a heterogeneous group of heart
muscle diseases associated with important clinical implications.
In aggregate, HCM, ARVC, DCM and LVNC underlie the majority of autopsy-positive sudden death cases in young athletes. Each
of these cardiomyopathies can manifest in athletes with a broad
spectrum of clinical severity ranging from completely asymptomatic to markedly symptomatic disease with associated exercise
limitations. The ECG plays an important role in the cardiovascular assessment of athletes given its capacity to detect cardiomyopathies. As delineated in this paper, there is a concise list of ECG
findings that may indicate the presence of an underlying cardiomyopathic condition. Importantly, these ECG findings are not
characteristic of the benign exercise-induced cardiac remodelling
common in athletes, and, thus, the ECG can be useful for differentiating physiological cardiac enlargement in athletes from
pathological myocardial disease.
Clinicians charged with the cardiovascular care of athletes
should be familiar with the ECG findings associated with cardiomyopathy. During pre-participation screening that includes
the use of ECG, asymptomatic athletes with any of these abnormal findings should undergo further testing. Athletes presenting
with symptoms that may be indicative of an underlying cardiomyopathy (ie, exercise intolerance, inappropriate exertional dyspnoea, chest pain, palpitations or syncope) should undergo a
prompt evaluation including an ECG. The symptomatic athlete
with an ECG suggestive of a cardiomyopathy requires a comprehensive and definitive assessment that will include some combination of non-invasive cardiac imaging, exercise testing and
ambulatory rhythm monitoring. This evaluation should be conducted by a sports medicine team that includes a cardiovascular
specialist familiar with cardiomyopathic diseases and with
experience in caring for athletes.
Additional resources
For a free online training module on ECG interpretation in athletes, please visit: http://learning.bmj.com/ECGathlete
For the November 2012 BJSM supplement on ‘Advances in
Sports Cardiology,’ please visit: http://bjsm.bmj.com/content/46/
Suppl_1.toc
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Author affiliations
1
Department of Family Medicine, University of Washington, Seattle, Washington,
USA
2
Division of Cardiovascular Medicine, Stanford University School of Medicine, Palo
Alto, California, USA
3
Division of Cardiology, Massachusetts General Hospital, Boston, Massachusetts,
USA
4
Department of Cardiology, Swedish School of Sports and Health Sciences,
Karolinska University Hospital, Stockholm, Sweden
5
Department of Cardiac, Thoracic, and Vascular Sciences, University of Padua,
Padova, Italy
6
Division of Cardiology, University of Washington, Seattle, Washington, USA
7
Division of Cardiology, The Children’s Hospital of Philadelphia, Philadelphia,
Pennsylvania, USA
8
Department of Medicine, Institute of Sport Medicine and Science, Rome, Italy
9
Departments of Medicine, Pediatrics, and Molecular Pharmacology and
Experimental Therapeutics, Mayo Clinic, Rochester, Minnesota, USA
10
Divisions of Cardiovascular Diseases and Pediatric Cardiology, Mayo Clinic,
Rochester, Minnesota, USA
11
Department of Athletics, University of Connecticut, Storrs, Connecticut, USA
12
Department of Family Medicine, Eisenhower Army Medical Center, Fort Gordon,
Georgia, USA
13
Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota, USA
14
Division of Sports Medicine, University of California Los Angeles, Los Angeles,
California, USA
15
Department of Pediatrics, Emory University School of Medicine, Children’s
Healthcare of Atlanta, Atlanta, Georgia, USA
16
Department of Cardiovascular Sciences, University of Leuven, Leuven, Belgium
17
Midwest Heart Foundation, Oakbrook Terrace, Illinois, USA
18
Department of Family and Community Medicine, University of Arizona, Tucson,
Arizona, USA
19
Division of Cardiology, Seattle Children’s Hospital, Seattle, Washington, USA
20
Division of Cardiology, University Hospital Zurich, Zurich, Switzerland
21
Department of Cardivascular Sciences, St. George’s University of London, London,
UK
22
Cardiology Department, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil
23
Department of Sports Medicine, ASPETAR, Qatar Orthopedic and Sports Medicine
Hospital, Doha, Qatar
Competing interests None.
Funding None.
Provenance and peer review Commissioned; internally peer reviewed.
REFERENCES
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
Maron BJ, Doerer JJ, Haas TS, et al. Sudden deaths in young competitive athletes:
analysis of 1866 deaths in the United States, 1980–2006. Circulation
2009;119:1085–92.
Maron BJ. Sudden death in young athletes. N Engl J Med 2003;349:1064–75.
Corrado D, Basso C, Schiavon M, et al. Screening for hypertrophic cardiomyopathy
in young athletes. N Engl J Med 1998;339:364–9.
Corrado D, Biffi A, Basso C, et al. 12-Lead ECG in the athlete: physiological versus
pathological abnormalities. Br J Sports Med 2009;43:669–76.
Corrado D, Pelliccia A, Heidbuchel H, et al. Recommendations for interpretation of
12-lead electrocardiogram in the athlete. Eur Heart J 2010;31:243–59.
Uberoi A, Stein R, Perez MV, et al. Interpretation of the electrocardiogram of young
athletes. Circulation 2011;124:746–57.
Williams ES, Owens DS, Drezner JA, et al. Electrocardiogram interpretation in the
athlete. Herzschrittmacherther Elektrophysiol 2012;23:65–71.
Drezner J. Standardised criteria for ECG interpretation in athletes: a practical tool.
Br J Sports Med 2012;46(Suppl I): i6–8.
Marek J, Bufalino V, Davis J, et al. Feasibility and findings of large-scale
electrocardiographic screening in young adults: data from 32 561 subjects. Heart
Rhythm 2011;8:1555–9.
Drezner JA, Ackerman MJ, Anderson J, et al. Electrocardiographic interpretation in
athletes: the ‘seattle criteria’. Br J Sports Med 2013;47.
Drezner JA, Fischbach P, Foelicher V, et al. Normal electrocardiographic findings:
recognizing physiologic adaptations in athletes. Br J Sports Med 2013;47.
Maron BJ. Hypertrophic cardiomyopathy. Lancet 1997;350:127–33.
Maron BJ, Shirani J, Poliac LC, et al. Sudden death in young competitive athletes.
Clinical, demographic, and pathological profiles. JAMA 1996;276:199–204.
Basavarajaiah S, Wilson M, Whyte G, et al. Prevalence of hypertrophic
cardiomyopathy in highly trained athletes: relevance to pre-participation screening. J
Am Coll Cardiol 2008;51:1033–9.
de Noronha SV, Sharma S, Papadakis M, et al. Aetiology of sudden cardiac death
in athletes in the United Kingdom: a pathological study. Heart 2009;95:1409–14.
Drezner JA, et al. Br J Sports Med 2013;47:137–152. doi:10.1136/bjsports-2012-092069
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16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
Eckart RE, Shry EA, Burke AP, et al. Sudden death in young adults an
autopsy-based series of a population undergoing active surveillance. J Am Coll
Cardiol 2011;58:1254–61.
Meyer L, Stubbs B, Fahrenbruch C, et al. Incidence, causes, and survival trends from
cardiovascular-related sudden cardiac arrest in children and young adults 0 to
35 years of age: a 30-year review. Circulation 2012;126:1363–72.
Maron BJ. Distinguishing hypertrophic cardiomyopathy from athlete’s heart
physiological remodelling: clinical significance, diagnostic strategies and implications
for preparticipation screening. Br J Sports Med 2009;43:649–56.
Ryan MP, Cleland JG, French JA, et al. The standard electrocardiogram as a
screening test for hypertrophic cardiomyopathy. Am J Cardiol 1995;76:689–94.
Maron BJ, Roberts WC, Epstein SE. Sudden death in hypertrophic cardiomyopathy: a
profile of 78 patients. Circulation 1982;65:1388–94.
Rowin EJ, Maron BJ, Appelbaum E, et al. Significance of false negative
electrocardiograms in preparticipation screening of athletes for hypertrophic
cardiomyopathy. Am J Cardiol 2012;110:1027–32.
Lakdawala NK, Thune JJ, Maron BJ, et al. Electrocardiographic features of
sarcomere mutation carriers with and without clinically overt hypertrophic
cardiomyopathy. Am J Cardiol 2011;108:1606–13.
Papadakis M, Carre F, Kervio G, et al. The prevalence, distribution, and clinical
outcomes of electrocardiographic repolarization patterns in male athletes of African/
Afro-Caribbean origin. Eur Heart J 2011;32:2304–13.
Papadakis M, Basavarajaiah S, Rawlins J, et al. Prevalence and significance of
T-wave inversions in predominantly Caucasian adolescent athletes. Eur Heart J
2009;30:1728–35.
Le VV, Wheeler MT, Mandic S, et al. Addition of the electrocardiogram to the
preparticipation examination of college athletes. Clin J Sport Med 2010;20:
98–105.
Pelliccia A, Maron BJ, Culasso F, et al. Clinical significance of abnormal
electrocardiographic patterns in trained athletes. Circulation 2000;102:278–84.
Di Paolo FM, Schmied C, Zerguini YA, et al. The athlete’s heart in adolescent
Africans: an electrocardiographic and echocardiographic study. J Am Coll Cardiol
2012;59:1029–36.
Migliore F, Zorzi A, Michieli P, et al. Prevalence of cardiomyopathy in Italian
asymptomatic children with electrocardiographic T-wave inversion at preparticipation
screening. Circulation 2012;125:529–38.
Konno T, Shimizu M, Ino H, et al. Diagnostic value of abnormal Q waves for
identification of preclinical carriers of hypertrophic cardiomyopathy based on a
molecular genetic diagnosis. Eur Heart J 2004;25:246–51.
Pelliccia A, Culasso F, Di Paolo FM, et al. Prevalence of abnormal
electrocardiograms in a large, unselected population undergoing pre-participation
cardiovascular screening. Eur Heart J 2007;28:2006–10.
Sohaib SM, Payne JR, Shukla R, et al. Electrocardiographic (ECG) criteria for
determining left ventricular mass in young healthy men; data from the LARGE Heart
study. J Cardiovasc Magn Reson 2009;11:2.
Sathanandam S, Zimmerman F, Davis J, et al. Abstract 2484: ECG screening
criteria for LVH does not correlate with diagnosis of hypertrophic cardiomyopathy.
Circulation 2009;120:S647.
Weiner RB, Hutter AM, Wang F, et al. Performance of the 2010 European Society
of Cardiology criteria for ECG interpretation in the athlete. Heart 2011;97:1573–7.
Gersh BJ, Maron BJ, Bonow RO, et al. ACCF/AHA guideline for the diagnosis and
treatment of hypertrophic cardiomyopathy: a report of the American College of
Cardiology Foundation/American Heart Association Task Force on Practice
Guidelines. Circulation 2011;124:e783–831.
Maron MS, Maron BJ, Harrigan C, et al. Hypertrophic cardiomyopathy phenotype
revisited after 50 years with cardiovascular magnetic resonance. J Am Coll Cardiol
2009;54:220–8.
Pelliccia A, Maron MS, Maron BJ. Assessment of left ventricular hypertrophy in a
trained athlete: differential diagnosis of physiologic athlete’s heart from pathologic
hypertrophy. Prog Cardiovasc Dis 2012;54:387–96.
Rawlins J, Bhan A, Sharma S. Left ventricular hypertrophy in athletes. Eur J
Echocardiogr 2009;10:350–6.
Maron BJ. Distinguishing hypertrophic cardiomyopathy from athlete’s heart: a
clinical problem of increasing magnitude and significance. Heart 2005;91:1380–2.
Maron BJ, Wolfson JK, Ciro E, et al. Relation of electrocardiographic abnormalities
and patterns of left ventricular hypertrophy identified by 2-dimensional
echocardiography in patients with hypertrophic cardiomyopathy. Am J Cardiol
1983;51:189–94.
Thiene G, Nava A, Corrado D, et al. Right ventricular cardiomyopathy and sudden
death in young people. N Engl J Med 1988;318:129–33.
Maron BJ, Niimura H, Casey SA, et al. Development of left ventricular hypertrophy
in adults in hypertrophic cardiomyopathy caused by cardiac myosin-binding protein
C gene mutations. J Am Coll Cardiol 2001;38:315–21.
Maron BJ, Seidman JG, Seidman CE. Proposal for contemporary screening strategies
in families with hypertrophic cardiomyopathy. J Am Coll Cardiol 2004;44:2125–32.
Pelliccia A, Di Paolo FM, Quattrini FM, et al. Outcomes in athletes with marked
ECG repolarization abnormalities. N Engl J Med 2008;358:152–61.
Drezner JA, et al. Br J Sports Med 2013;47:137–152. doi:10.1136/bjsports-2012-092069
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
61
62
63
64
65
66
67
68
69
70
71
72
Basso C, Corrado D, Marcus FI, et al. Arrhythmogenic right ventricular
cardiomyopathy. Lancet 2009;373:1289–300.
Corrado D, Basso C, Thiene G. Arrhythmogenic right ventricular cardiomyopathy: an
update. Heart 2009;95:766–73.
Heidbuchel H, Hoogsteen J, Fagard R, et al. High prevalence of right ventricular
involvement in endurance athletes with ventricular arrhythmias. Role of an
electrophysiologic study in risk stratification. Eur Heart J 2003;24:1473–80.
La Gerche A, Robberecht C, Kuiperi C, et al. Lower than expected desmosomal
gene mutation prevalence in endurance athletes with complex ventricular
arrhythmias of right ventricular origin. Heart 2010;96:1268–74.
Heidbuchel H, Prior DL, Gerche AL. Ventricular arrhythmias associated with
long-term endurance sports: what is the evidence? Br J Sports Med 2012;46(Suppl
1):i44–50.
Marcus FI, McKenna WJ, Sherrill D, et al. Diagnosis of arrhythmogenic right
ventricular cardiomyopathy/dysplasia: proposed modification of the task force
criteria. Circulation 2010;121:1533–41.
Nasir K, Bomma C, Tandri H, et al. Electrocardiographic features of arrhythmogenic
right ventricular dysplasia/cardiomyopathy according to disease severity: a need to
broaden diagnostic criteria. Circulation 2004;110:1527–34.
Steriotis AK, Bauce B, Daliento L, et al. Electrocardiographic pattern in
arrhythmogenic right ventricular cardiomyopathy. Am J Cardiol 2009;103:1302–8.
Protonotarios N, Anastasakis A, Antoniades L, et al. Arrhythmogenic right
ventricular cardiomyopathy/dysplasia on the basis of the revised diagnostic criteria in
affected families with desmosomal mutations. Eur Heart J 2011;32:1097–104.
Kamath GS, Zareba W, Delaney J, et al. Value of the signal-averaged
electrocardiogram in arrhythmogenic right ventricular cardiomyopathy/dysplasia.
Heart Rhythm 2011;8:256–62.
Marcus FI, Zareba W, Calkins H, et al. Arrhythmogenic right ventricular
cardiomyopathy/dysplasia clinical presentation and diagnostic evaluation:
results from the North American Multidisciplinary Study. Heart Rhythm
2009;6:984–92.
Atherton JJ. Screening for left ventricular systolic dysfunction: is imaging a solution?
JACC Cardiovasc Imaging 2010;3:421–8.
Ammar KA, Jacobsen SJ, Mahoney DW, et al. Prevalence and prognostic
significance of heart failure stages: application of the American College of
Cardiology/American Heart Association heart failure staging criteria in the
community. Circulation 2007;115:1563–70.
Galasko GI, Barnes SC, Collinson P, et al. What is the most cost-effective strategy
to screen for left ventricular systolic dysfunction: natriuretic peptides, the
electrocardiogram, hand-held echocardiography, traditional echocardiography, or
their combination? Eur Heart J 2006;27:193–200.
Wang TJ, Evans JC, Benjamin EJ, et al. Natural history of asymptomatic left
ventricular systolic dysfunction in the community. Circulation 2003;108:977–82.
Baig MK, Goldman JH, Caforio AL, et al. Familial dilated cardiomyopathy: cardiac
abnormalities are common in asymptomatic relatives and may represent early
disease. J Am Coll Cardiol 1998;31:195–201.
Grunig E, Tasman JA, Kucherer H, et al. Frequency and phenotypes of familial
dilated cardiomyopathy. J Am Coll Cardiol 1998;31:186–94.
Mahon NG, Murphy RT, MacRae CA, et al. Echocardiographic evaluation in
asymptomatic relatives of patients with dilated cardiomyopathy reveals preclinical
disease. Ann Intern Med 2005;143:108–15.
Surwicz B, Knilan T, eds. Chou’s electrocardiography in clinical practice.
Philadelphia: WB Saunders Company, 2001:256–8.
Goldberger AL. A specific ECG triad associated with congestive heart failure. Pacing
Clin Electrophysiol 1982;5:593–9.
Pelliccia A, Culasso F, Di Paolo FM, et al. Physiologic left ventricular cavity
dilatation in elite athletes. Ann Intern Med 1999;130:23–31.
Abergel E, Chatellier G, Hagege AA, et al. Serial left ventricular adaptations in
world-class professional cyclists: implications for disease screening and follow-up. J
Am Coll Cardiol 2004;44:144–9.
Paterick TE, Umland MM, Jan MF, et al. Left ventricular noncompaction: a 25-year
odyssey. J Am Soc Echocardiogr 2012;25:363–75.
Sarma RJ, Chana A, Elkayam U. Left ventricular noncompaction. Prog Cardiovasc
Dis 2010;52:264–73.
Steffel J, Duru F. Rhythm disorders in isolated left ventricular noncompaction. Ann
Med 2012;44:101–8.
Chin TK, Perloff JK, Williams RG, et al. Isolated noncompaction of left ventricular
myocardium. A study of eight cases. Circulation 1990;82:507–13.
Jenni R, Oechslin E, Schneider J, et al. Echocardiographic and pathoanatomical
characteristics of isolated left ventricular non-compaction: a step towards
classification as a distinct cardiomyopathy. Heart 2001;86:666–71.
Jacquier A, Thuny F, Jop B, et al. Measurement of trabeculated left ventricular mass
using cardiac magnetic resonance imaging in the diagnosis of left ventricular
non-compaction. Eur Heart J 2010;31:1098–104.
Petersen SE, Selvanayagam JB, Wiesmann F, et al. Left ventricular non-compaction:
insights from cardiovascular magnetic resonance imaging. J Am Coll Cardiol
2005;46:101–5.
17 of 18
Downloaded from bjsm.bmj.com on January 9, 2013 - Published by group.bmj.com
Original articles
73
74
75
76
77
78
79
80
81
Stollberger C, Kopsa W, Tscherney R, et al. Diagnosing left ventricular
noncompaction by echocardiography and cardiac magnetic resonance imaging and
its dependency on neuromuscular disorders. Clin Cardiol 2008;31:383–7.
Kohli SK, Pantazis AA, Shah JS, et al. Diagnosis of left-ventricular non-compaction
in patients with left-ventricular systolic dysfunction: time for a reappraisal of
diagnostic criteria? Eur Heart J 2008;29:89–95.
Steffel J, Kobza R, Oechslin E, et al. Electrocardiographic characteristics at initial
diagnosis in patients with isolated left ventricular noncompaction. Am J Cardiol
2009;104:984–9.
Corrado D, Basso C, Buja G, et al. Right bundle branch block, right precordial
ST-segment elevation, and sudden death in young people. Circulation
2001;103:710–17.
Schneider JF, Thomas HE, Kreger BE, et al. Newly acquired right bundle-branch
block: the Framingham Study. Ann Intern Med 1980;92:37–44.
Brugada J, Brugada R, Antzelevitch C, et al. Long-term follow-up of individuals
with the electrocardiographic pattern of right bundle-branch block and ST-segment
elevation in precordial leads V1 to V3. Circulation 2002;105:73–8.
Steffel J, Kobza R, Namdar M, et al. Electrophysiological findings in patients with
isolated left ventricular non-compaction. Europace 2009;11:1193–200.
Nelson GS, Curry CW, Wyman BT, et al. Predictors of systolic augmentation from
left ventricular preexcitation in patients with dilated cardiomyopathy and
intraventricular conduction delay. Circulation 2000;101:2703–9.
Xiao HB, Brecker SJ, Gibson DG. Relative effects of left ventricular mass and
conduction disturbance on activation in patients with pathological left ventricular
hypertrophy. Br Heart J 1994;71:548–53.
18 of 18
82
83
84
85
86
87
88
89
90
91
92
Baman TS, Lange DC, Ilg KJ, et al. Relationship between burden of premature
ventricular complexes and left ventricular function. Heart Rhythm 2010;7:865–9.
Braunwald E, Brockenbrough EC, Morrow AG. Hypertrophic subaortic stenosis—a
broadened concept. Circulation 1962;26:161–5.
Marek JC. Electrocardiography and preparticipation screening of competitive high
school athletes. Ann Int Med 2011;153:131–2.
Baggish AL, Hutter AM Jr, Wang F, et al. Cardiovascular screening in college
athletes with and without electrocardiography: a cross-sectional study. Ann Intern
Med 2010;152:269–75.
Biffi A, Maron BJ, Verdile L, et al. Impact of physical deconditioning on ventricular
tachyarrhythmias in trained athletes. J Am Coll Cardiol 2004;44:1053–8.
Biffi A, Pelliccia A, Verdile L, et al. Long-term clinical significance of frequent and
complex ventricular tachyarrhythmias in trained athletes. J Am Coll Cardiol
2002;40:446–52.
Kim JH, Noseworthy PA, McCarty D, et al. Significance of electrocardiographic right
bundle branch block in trained athletes. Am J Cardiol 2011;107:1083–9.
Rich S, Dantzker DR, Ayres SM, et al. Primary pulmonary hypertension. A national
prospective study. Ann Intern Med 1987;107:216–23.
Bossone E, Paciocco G, Iarussi D, et al. The prognostic role of the ECG in primary
pulmonary hypertension. Chest 2002;121:513–18.
Henkens IR, Gan CT, van Wolferen SA, et al. ECG monitoring of treatment response
in pulmonary arterial hypertension patients. Chest 2008;134:1250–7.
Ahearn GS, Tapson VF, Rebeiz A, et al. Electrocardiography to define clinical status
in primary pulmonary hypertension and pulmonary arterial hypertension secondary
to collagen vascular disease. Chest 2002;122:524–7.
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Abnormal electrocardiographic findings in
athletes: recognising changes suggestive of
cardiomyopathy
Jonathan A Drezner, Euan Ashley, Aaron L Baggish, et al.
Br J Sports Med 2013 47: 137-152
doi: 10.1136/bjsports-2012-092069
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Original articles
Abnormal electrocardiographic findings in athletes:
recognising changes suggestive of primary electrical
disease
Jonathan A Drezner,1 Michael J Ackerman,2 Bryan C Cannon,3 Domenico Corrado,4
Hein Heidbuchel,5 Jordan M Prutkin,6 Jack C Salerno,7 Jeffrey Anderson,8
Euan Ashley,9 Chad A Asplund,10 Aaron L Baggish,11 Mats Börjesson,12
John P DiFiori,13 Peter Fischbach,14 Victor Froelicher,9 Kimberly G Harmon,1
Joseph Marek,15 David S Owens,6 Stephen Paul,16 Antonio Pelliccia,17
Christian M Schmied,18 Sanjay Sharma,19 Ricardo Stein,20 Victoria L Vetter,21
Mathew G Wilson22
For numbered affiliations see
end of article.
Correspondence to
Jonathan A Drezner,
Department of Family
Medicine, University of
Washington, 1959 NE Pacific
Street, Box 356930, Seattle,
Washington, 98195, USA;
[email protected]
Received 7 December 2012
Revised 7 December 2012
Accepted 7 December 2012
This document was developed in collaboration between the American Medical Society for Sports Medicine (AMSSM),
the Section on Sports Cardiology of the European Association for Cardiovascular Prevention and Rehabilitation
(EACPR), a registered branch of the European Society of Cardiology (ESC), the FIFA Medical Assessment and Research
Center (F-MARC), and the Pediatric & Congenital Electrophysiology Society (PACES).
ABSTRACT
Cardiac channelopathies are potentially lethal inherited
arrhythmia syndromes and an important cause of sudden
cardiac death (SCD) in young athletes. Other cardiac
rhythm and conduction disturbances also may indicate
the presence of an underlying cardiac disorder.
The 12-lead ECG is utilised as both a screening and a
diagnostic tool for detecting conditions associated with
SCD. Fundamental to the appropriate evaluation of
athletes undergoing ECG is an understanding of the ECG
findings that may indicate the presence of a pathological
cardiac disease. This article describes ECG findings
present in primary electrical diseases afflicting young
athletes and outlines appropriate steps for further
evaluation of these ECG abnormalities. The ECG findings
defined as abnormal in athletes were established by an
international consensus panel of experts in sports
cardiology and sports medicine.
INTRODUCTION
To cite: Drezner JA,
Ackerman MJ, Cannon BC,
et al. Br J Sports Med
2013;47:153–167.
Inherited primary arrhythmia syndromes are known
causes of sudden cardiac death (SCD) in young athletes. Channelopathies represent a heterogeneous
group of genetically distinct cardiovascular disorders
associated with sudden death and ventricular arrhythmias from disturbed function of the cardiac ion
channel.1–3 Ventricular pre-excitation and other disturbances of cardiac conduction also are associated
with diseases predisposing to SCD in young athletes.4
Primary electrical disorders may present with
disease-related symptoms or be asymptomatic and
thus only identified by abnormal testing during preparticipation screening. The 12-lead ECG is commonly abnormal among athletes with pathological
cardiac disease, and clinicians responsible for ECG
interpretation in athletes must be familiar with key
findings associated with conditions at risk for SCD.
This paper will review ECG findings associated with
primary electrical diseases relevant to the care of the
Drezner JA, et al. Br J Sports Med 2013;47:153–167. doi:10.1136/bjsports-2012-092070
young athlete. Initial testing for further evaluation of
abnormal ECG findings is also presented.
DISTINGUISHING NORMAL FROM ABNORMAL
A challenge in the use of ECG for screening or
diagnostic evaluations in athletes is the ability to
accurately differentiate findings suggestive of a
potentially lethal cardiovascular disorder from
benign physiological adaptations occurring as the
result of regular, intense training (ie, athlete’s
heart). Several reports have outlined ECG criteria
intended to distinguish normal ECG findings in
athletes from ECG abnormalities requiring additional evaluation.5–10
On 13–14 February 2012, an international
group of experts in sports cardiology and sports
medicine convened in Seattle, Washington, to
define contemporary standards for ECG interpretation in athletes. The objective of the meeting was
to assist physicians distinguish normal ECG alterations in athletes from abnormal ECG findings that
require additional evaluation for conditions that
predispose to SCD.11 A review of normal ECG
findings in athletes is presented separately.12
In this paper, abnormal ECG findings suggestive
of an ion channel or conduction disorder associated
with SCD in athletes are presented including congenital long and short QT syndromes (LQTS and
SQTS), catecholaminergic polymorphic ventricular
tachycardia (CPVT), Brugada syndrome (BrS), ventricular pre-excitation, supraventricular tachycardias
(SVT), atrioventricular (AV) blocks and premature
ventricular contractions (PVCs). Table 1 summarises
a list of abnormal ECG findings unrelated to athletic
training that may suggest the presence of a pathological cardiac disorder and should trigger additional evaluation in an athlete.
THE CONGENITAL QT SYNDROMES
Congenital long QT syndrome (LQTS) and short
QT syndrome (SQTS) are potentially lethal,
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Original articles
Table 1 Abnormal ECG findings suggestive of primary electrical
disease
Abnormal ECG Finding
Definition
Ventricular pre-excitation
PR interval <120 ms with a delta wave (slurred
upstroke in the QRS complex) and wide QRS
(>120 ms)
QTc ≥470 ms (male)
QTc ≥480 ms (female)
QTc ≥500 ms (marked QT prolongation)
QTc ≤320 ms
High take-off and downsloping ST segment
elevation followed by a negative T wave in ≥2 leads
in V1–V3
<30 bpm or sinus pauses ≥3 s
Long QT interval*
Short QT interval*
Brugada-like ECG pattern
Profound sinus
bradycardia
Atrial tachyarrhythmias
Premature ventricular
contractions
Ventricular arrhythmias
Supraventricular tachycardia, atrial-fibrillation,
atrial-flutter
≥2 PVCs per 10 s tracing
Couplets, triplets, and non-sustained ventricular
tachycardia
Note: These ECG findings are unrelated to regular training or expected
physiological adaptation to exercise, may suggest the presence of
pathological cardiovascular disease, and require further diagnostic evaluation.
*The QT interval corrected for heart rate is ideally measured with heart rates of
60–90 bpm. Consider repeating the ECG after mild aerobic activity for borderline or
abnormal QTc values with a heart rate <50 bpm.
genetically mediated ventricular arrhythmia syndromes with the
hallmark electrocardiographic feature of either QT prolongation
(LQTS) or markedly shortened QT intervals (SQTS) (figures 1–3).
Symptoms if present include arrhythmic syncope, seizures or
aborted cardiac arrest/sudden death stemming from either
torsades de pointes (LQTS) or ventricular fibrillation (SQTS).
The pathophysiology of the QT syndromes is understood as
either delayed ventricular repolarisation (LQTS) or accelerated
ventricular repolarisation (SQTS) originating primarily from
loss-of-function (LQTS) or gain-of-function (SQTS) mutations in
genes encoding voltage-gated potassium channels (Kv7.1 and
Kv11.1) that govern phase 3 repolarisation in the ventricular
myocytes. Currently, 13 LQTS-susceptibility genes and
3 SQTS-susceptibility genes have been identified and account for
over 75% of LQTS and <20% of SQTS.1
Prevalence
SQTS is extremely uncommon affecting less than 1:10 000 individuals. Although once considered similarly rare, LQTS is now
estimated to affect 1 in 2000 individuals and given the subpopulation of so-called ‘normal QT interval’ or ‘concealed’ LQTS,
this may be an underestimate.13
Contribution as a cause of SCD
Among individuals between 1 and 40 years of age, approximately 25–40% of sudden unexpected deaths are classified as
autopsy negative sudden unexplained death (SUD) lacking necropsy findings to establish the cause and manner of death.14–16
Here, cardiac channelopathies such as LQTS, SQTS, CPVT and
BrS are considered as possible culprits and have been implicated
by postmortem genetic testing as the root cause for up to
25–35% of SUD in selected cohorts.17–19 LQTS is the most
common channelopathy responsible for about 15–20% of
SUD.20 SQTS is a very rare cause of autopsy negative SUD.14
In a series of young athletes with SCD from the USA
(n=1049), a precise cause of death was identified in 690 cases.4
LQTS was implicated in less than 4% of cases (23/690) with an
identified cause.4 However, this estimate does not include
one-third of the total cases in the series (359/1049) with no
precise diagnosis but in whom post-mortem genetic testing was
not documented. Thus, it is likely ion channelopathies or
Figure 1 ECG demonstrating a profoundly prolonged QT interval. The computer derived a QTc measurement of 362 ms which was inaccurate.
Manual measurement of the QTc was 760 ms.
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Original articles
Figure 2 ECG from a 27-year-old man with long QT syndrome (QTc=520 ms). Heart rate is 52 bpm. Bazett’s formula: QTc=QT/√RR. Note the RR
interval is measured in seconds. This figure is only reproduced in colour in the online version.
accessory electrical pathways represent a larger percentage of
SCD in young athletes than previously reported.
Diagnostic criteria
Both QT syndromes are diagnosed based on a combination of
symptoms, family history, electrocardiographic findings and
genetic testing. The Gollob score is used for SQTS while the
Schwartz-Moss score is used to invoke low, intermediate and
high probability for LQTS.21–23 For LQTS, genetic testing is
recommended for: (1) any patient where a cardiologist has an
index of suspicion for LQTS (intermediate or high probability
score), or (2) an asymptomatic patient with no family history
Figure 3 ECG from a patient with short QT syndrome. The QT interval is 250 ms and the QTc 270 ms. Note the tall, peaked T waves across the
precordial leads characteristic of short QT syndrome. (ECG courtesy of Professor P Mabo).
Drezner JA, et al. Br J Sports Med 2013;47:153–167. doi:10.1136/bjsports-2012-092070
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Original articles
but an incidental ECG finding with a QTc >480 ms prepuberty
and >500 ms postpuberty that is confirmed on repeat ECG
testing.1 Genetic testing may be considered for individuals with
an incidental QTc finding (repeated) of ≥460 ms prepuberty and
≥480 ms postpuberty.1
Calculating the QTc
Whether the ECG was obtained for screening or diagnostic purposes, the heart rate corrected QT interval (QTc) derived by the
computer must be confirmed manually because the accuracy of
the computer generated QTc is only about 90–95%. Notably,
the computer-derived QTc for the ECG in figure 1 was off by
about 400 ms as the true QTc was around 760 ms but was read
as 360 ms. Although this is an extreme example of an inaccurate
computer QTc calculation, studies have also suggested that the
ability of cardiologists and even heart rhythm specialists to
accurately measure the QTc is suboptimal.24 However, an accurate assessment of the QTc can be taught and achieved by adhering to the following six principles.25
First, most ECG machines utilise the Bazett’s heart rate correction formula (QTc=QT/√RR; note the RR interval is measured
in seconds).26 Although there are many heart rate correction formulas for the QTc, it is recommended to use Bazett’s correction
to confirm the computer’s QTc as the population-based QTc distributions most frequently used Bazett-derived QTc values.
Second, Bazett’s formula loses accuracy at slow heart rates
and can underestimate the individual’s inherent QTc at heart
rates <60 bpm, especially at heart rates <50 bpm. Accordingly,
if an athlete has a heart rate <50 bpm, repeat the ECG after
some mild aerobic activity to get his/her heart rate into a range
(60–90 bpm) where the formula is most accurate.
Third, if there is beat-to-beat variation in heart rate (sinus
arrhythmia) which is common among athletes, do not take the
maximum QT interval on the ECG and divide it by the square
root of the shortest RR interval,27 which will grossly overestimate the QTc. Instead, it is more accurate to derive an average
QT interval and average RR interval.
Fourth, to perform a manual confirmation, the critical issue is
identifying the end of the T wave since the onset of the QRS is
seen easily. The rhythm strip at the bottom of the ECG generally includes leads II, V1 and/or V5, and lead II and V5 usually
provide the best delineation of the T wave.
Fifth, it is incorrect to include the commonly seen lowamplitude U wave in the QT calculation. Such U wave inclusion
will inflate greatly the QTc. Instead, follow the ‘Teach-the-Tangent’
or ‘Avoid-the-Tail’ method as shown in figure 4.25
Sixth, the morphology of the T waves, not just the length of
the QT interval, can suggest the presence of a QT syndrome.28
As shown in figure 5, a notched T wave in the lateral precordial
leads may be a tip off to LQTS even in the absence of overt QT
prolongation.
With this framework, the easiest and most efficient way to
confirm the computer-derived QTc is to examine lead II and/or
V5 and determine if the manually measured QT interval
matches the computer’s QT measurement. If there is concordance within about 10 ms of each other, one can trust that the
computer can derive accurately an average RR interval and complete Bazett’s calculation. As such, the computer generated QTc
has been confirmed manually. If, however, the manually measured QT interval is >10 ms different than the computer’s QT
measurement, calculate an average RR interval and recalculate
the QTc using Bazett’s formula.
QTc cut-offs: how long is too long? How short is too short?
Figure 6 shows the overlap between the distribution of QTc
values in population-derived cohorts of healthy individuals
Figure 4 This figure illustrates the ‘Teach-the-Tangent’ or ‘Avoid-the-Tail’ method for manual measurement of the QT interval. A straight line is
drawn on the downslope of the T wave to the point of intersection with the isoelectric line. The U wave is not included in the measurement. This
figure is only reproduced in colour in the online version.
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Figure 5 ECG of a patient with long QT syndrome. Note the notched T waves (arrows) in the lateral precordial leads (V4–V5) that are typical of
long QT type-2. This figure is only reproduced in colour in the online version.
compared to patients with genetically confirmed LQTS.29–31
Considering that 25–40% of genotype positive individuals
(mostly relatives of the index cases/probands) have normal QT
interval/concealed LQTS, it must be acknowledged that no
screening programme will identify all persons with either LQTS
or SQTS.32 Instead, the QTc cut-off values, where the QTc
Figure 6 Distribution and overlap of QTc values for healthy
individuals compared to patients with genetically confirmed LQTS.
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measurement requires further evaluation, must be chosen carefully to balance the frequency of abnormal results and the positive predictive value that an SQTS or LQTS host has been
identified.
Published definitions of a ‘prolonged QTc’ requiring further
evaluation have varied. Guidelines from the European Society
of Cardiology for ECG interpretation in athletes define a QTc
value of >440 ms in men and >460 ms in women (but
<500 ms) as a ‘grey zone’ requiring further evaluation, and a
QTc ≥500 ms, otherwise unexplained and regardless of family
history and symptoms, as indicative of unequivocal LQTS.6 In
the USA, the AHA/ACC/HRS guideline has dropped the term
‘borderline’ QT prolongation and instead now annotates a QTc
≥450 ms in men and ≥460 ms in women as ‘prolonged QTc’.33
Concern has been raised that these QTc cut-offs will produce a
high number of false-positive test results if followed in a screening population of athletes.29 However, one study of 2000 elite
athletes age 14–35 in the UK found that only 0.4% of athletes
had a QTc >460 ms, and another study detailing ECG findings
in 32 561 young adults from the USA undergoing screening
reported only 0.3% had a QTc >460 ms.10 34 Nonetheless,
these QTc thresholds (440–460 ms) represent the approximate
90–95th percentile values for QTc distribution in the general
population, and utilisation of these QTc cut-offs in a screening
programme of athletes will have a <1% positive predictive
value for LQTS in the absence of any personal or family history
to indicate disease.29 31 In 2011, an international statement on
ECG interpretation in athletes recommended that all athletes
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with a QTc >470 ms in men and >480 ms in women undergo
further evaluation for LQTS to better balance false-positive and
false-negative findings.7
Accordingly, it seems prudent to shift the QTc cut-off values
that should trigger further evaluation in asymptomatic athletes
with no concerning family history. This consensus group recommends cut-off values around the 1st percentile (QTc ≤320 ms)
for a short QTc and around the 99th percentile (≥470 ms in
men and ≥480 ms in postpubertal women) to indicate a prolonged QTc. These cut-offs will improve the positive predictive
value if ECG is used for athlete screening while still identifying
the most overt QT abnormalities and those individuals most like
to experience QTc-related adverse events. These cut-offs are
also consistent with thresholds defined by the 36th Bethesda
Conference.35
However, it is critical that an athlete should not be obligated
to a diagnosis of either SQTS or LQTS for falling below or
above these QTc cut-off values, but rather these cut-off values
should trigger the need for further evaluation. In other words, a
prolonged QTc measurement on a single ECG does not equal
LQTS. Further evaluation as outlined below and the use of
scoring systems that account for personal symptoms, family
history, as well as electrocardiographic features are helpful in
clarifying the diagnosis.
QTc cut-offs: relative versus absolute risk of a QT syndrome
By definition, the 99th percentile cut-off for genetically confirmed LQTS assumes 1% of those with a value outside of this
QTc threshold (≥470 ms in men, ≥480 ms in women) have a
false-positive result. If one assumes that the prevalence of LQTS
is 1 : 2000 individuals, and approximately half of these individuals will have a QTc above and half below these QTc thresholds (1 : 4000), then the positive predictive value of detecting
true disease for a QTc outside the cut-off value is about
2.5%.29 30 However, once a prolonged QTc is identified, that
individual has a 1 in 40 (rather than 1 : 2000) chance of having
true disease. In other words, with no additional corroborative
evidence, a single prolonged QTc value above the defined
cut-off would suggest a 50-fold increase in relative risk for
LQTS but only a 2.5% absolute risk. However, in an athlete
with a QTc ≥500 ms, the predictive value now favours the presence of not only LQTS but possibly higher risk LQTS.34 36
Evaluation of a possible long or short QT syndrome
An athlete identified as crossing the aforementioned QTc thresholds (≥470 ms men, ≥480 ms women) should have their personal history (exercise/emotion/auditory-triggered syncope or
seizures) and family history (exertional syncope, exercise/
auditory-triggered ‘epilepsy’, postpartum-timed syncope/seizure,
unexplained motor vehicle accidents, unexplained drowning,
and premature, unexplained sudden death <50 years of age)
reviewed. If their personal/family history is positive, then the
athlete should be referred to a heart rhythm specialist for
further evaluation. If the personal/family history is negative,
then a repeat ECG should be obtained. If the follow-up ECG is
within the QTc cut-off values, then no additional evaluation is
needed and the athlete should be reassured and may continue
sports participation.
On the other hand, if the repeat ECG still exceeds the QTc
cut-off values, then a screening ECG of the athlete’s first-degree
relatives ( parents and siblings) should be considered and the
athlete should be referred to a heart rhythm specialist or cardiologist as the possibility for newly discovered LQTS or SQTS
has increased. Reversible, extrinsic factors, such as electrolyte
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abnormalities (hypokalaemia) or the presence of QT prolonging
medications, must also be evaluated. If an athlete’s ECG shows
a QTc ≥500 ms and no reversible causes are identified, then the
athlete should be referred immediately to a heart rhythm specialist or cardiologist as the probability of LQTS and future
adverse events has increased.36 Further testing including provocative treadmill stress and/or epinephrine QT stress testing
along with genetic testing need to be considered carefully and
should be performed and interpreted by a cardiologist familiar
to the disease.
CATECHOLAMINERGIC POLYMORPHIC VENTRICULAR
TACHYCARDIA
CPVT is an inherited arrhythmogenic disorder characterised by
ventricular ectopy induced by exercise or emotional stress.
CPVT is a primary electrical disease involving cardiac channels,
particularly the RYR2-encoded cardiac ryanodine receptor/
calcium release channel, and typically occurs in patients with
structurally normal hearts. Exercise or acute emotion can lead
to progressive ventricular ectopy eventually causing a fast ventricular tachycardia. This tachycardia may lead to syncope and
in some cases ventricular fibrillation and sudden death. The
average age of presentation of CPVT is between 7 and 9 years
old, but onset as late as the fourth decade of life has been
reported.37 If untreated, approximately 30% of individuals
experience cardiac arrest and up to 80% have at least one
episode of syncope.38
Prevalence and contribution as a cause of SCD
The prevalence of CPVT is estimated to be around 1 in 10 000
people, although the true prevalence of this condition is not
known.39 The incidence of SCD in athletes from CPVT is also
not known. However, one study showed a prevalence of 9.4%
in adults with sudden unexplained death and a pooled analysis
found 4–10% of autopsy negative SCD could be attributed to
CPVT.20 40 41
Diagnostic criteria and ECG findings in CPVT
CPVT should be considered in any person who experiences
syncope during exercise or extreme emotion, particularly in
those who experience syncope during maximal exertion or have
repeated episodes of syncope with exercise. CPVT cannot be
diagnosed on the basis of a resting ECG, as the resting ECG is
normal. An echocardiogram is also typically normal. As ventricular ectopy occurs only in the face of increased emotion or
exercise, exercise stress testing is the key test in the evaluation
CPVT. As exercise workload increases, there is typically an
increase in the amount of ventricular ectopy which ultimately
may result in polymorphic ventricular tachycardia42 (figure 7).
This graded, exercise-induced ventricular ectopy differentiates
CPVT from benign PVCs which typically suppress with
exercise.
The ventricular tachycardia in CPVT can be bidirectional with
a 180° rotation of the QRS complex alternating from beat to
beat. However, exercise-induced bidirectional ventricular tachycardia is uncommonly seen in patients with genetically proven
CPVT. Instead, as heart rate increases during exercise there will
be increasing ventricular ectopy initially with isolated PVC’s,
then ventricular bigeminy, progressing to ventricular couplets
and ventricular tachycardia if exercise persists.43
Evaluation of possible CPVT
Evaluation of possible CPVT should be referred to a cardiologist. An exercise stress ECG such as an exercise treadmill test
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Figure 7 15-year-old boy undergoing exercise stress test for evaluation of CPVT. Polymorphic ventricular ectopy is evident late in stage 3 of the
exercise stress test. Heart rate 148 bpm. This figure is only reproduced in colour in the online version.
may be diagnostic in CPVT. Infusion of intravenous catecholamines (isoproterenol) during ECG monitoring or CPVT genetic
testing may confirm the diagnosis in questionable cases.1 44
channel, accounts for approximately 20–25% of BrS and
approximately 40% of BrS accompanied by prolonged PR
intervals.1 45–47
BRUGADA SYNDROME
Prevalence and contribution as a cause of SCD
BrS is a primary electrical disease which is characterised by the
distinctive ECG pattern of ‘high take-off“ ST segment elevation
in the right precordial leads and predisposes to ventricular fibrillation and sudden death in the absence of clinically demonstrable structural heart disease.45 Loss-of-function defects in the
SCN5A gene, which encodes for the α-subunit of the sodium
The syndrome is estimated to account for up to 4% of all
sudden deaths in the general population and 5–20% of sudden
deaths victims with a structurally normal heart at autopsy.20 45
Ventricular fibrillation and sudden death in patients with BrS
occurs more commonly during rest and sleep and is unrelated to
exercise.
Figure 8 Brugada pattern ECGs. Type 1 Brugada pattern ECG is defined as a high-take off and downsloping ST segment elevation ≥2 mm
followed by a negative T-wave in at least two contiguous leads (V1–V3). Type 2 and 3 Brugada pattern ECGs have a ‘saddleback’ appearance with
J-point elevation ≥2 mm, ST segment elevation >1 mm in type 2 and ≤1 mm in type 3, and either a positive or biphasic T-wave.
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Diagnostic criteria
VENTRICULAR PRE-EXCITATION
In 2002, a consensus conference endorsed by the Heart Rhythm
Society and the European Heart Rhythm Association proposed
ECG criteria for the diagnosis of BrS.48 Three types of Brugada
ECG (Br-ECG) patterns were defined: the ‘diagnostic’ (type 1)
which is characterised by a ‘coved-type’ ST segment elevation in
the right precordial leads, and the ‘non-diagnostic’ (types 2 and 3)
which show a ‘saddle-back’ configuration. (figure 8) The type 1
Br-ECG may be unmasked or worsened by sodium channel blockers such as ajmaline, flecainide and procainamide.49 Higher placement of the V1 and V2 electrodes in the second intercostal space
(rather than the fourth intercostal space) also can precipitate a type
1 Brugada ECG pattern. Conversion of type 2 and 3 Br-ECG to
type 1 by sodium channel blocker administration is considered
diagnostic for a positive Brugada ECG pattern and is used in clinical practice for diagnosis and management of BrS according to
current guidelines.49
The PR interval is the time required for the electrical impulse to
travel from the sinus node through the AV node to the Purkinje
fibres, and it is measured from the beginning of the P wave to
the beginning of the QRS. Ventricular pre-excitation occurs
when an accessory pathway of electrical activation bypasses the
AV node. As a result, there is abnormal conduction to the ventricle ( pre-excitation) with shortening of the PR interval and
widening of the QRS. This is evident on the ECG as the Wolf–
Parkinson–White (WPW) pattern.
ECG findings in Brugada syndrome
Type 1 Brugada pattern ECG is defined as a high-take off and
downsloping ST segment elevation ≥2 mm followed by a negative T-wave in at least two contiguous leads (V1–V3) (figure 8).
Type 2 and 3 Brugada pattern ECGs have a ‘saddleback’ appearance with J-point elevation ≥2 mm, ST segment elevation
>1 mm in type 2 and ≤1 mm in type 3, and either a positive or
biphasic T-wave (figure 8).
The downsloping ST elevation in Brugada type-1 ECG should
be distinguished from the ‘convex’ ST segment elevation characteristic of early repolarisation in a trained athlete (figure 9).
Measuring the ST elevation at the start of the ST segment/
J-point (STJ) and 80 ms after the start of the ST segment (ST80)
can help differentiate the slope of the ST segment. In Brugada
type-1 pattern the downsloping ST segment will have a STJ/
ST80 ratio >1. In early repolarisation patterns in an athlete the
initial upsloping of the ST segment will produce a STJ/ST80
ratio <1 (figure 9).
Evaluation of possible brugada syndrome
Patients with a type 1 Brugada pattern ECG should be referred
to a cardiac electrophysiologist for further evaluation and
management.
Prevalence and contribution as a cause of SCD
WPW pattern occurs in approximately 1 : 1000 athletes.50 The
presence of an accessory pathway can predispose an athlete to
sudden death if the athlete also goes into atrial fibrillation.
Rapid conduction of atrial fibrillation across the accessory
pathway can result in ventricular fibrillation. The risk of sudden
death associated with asymptomatic WPW pattern in most
population-based studies is 0.1% per year in adults.51 There is
evidence to suggest a higher risk of sudden death in asymptomatic children and younger adults with WPW pattern.52–54
Overall, WPW accounted for 1% of cardiovascular deaths in a
long-term registry of sudden death in athletes.4
Diagnostic criteria and ECG findings in ventricular
pre-excitation
WPW pattern is defined as a short PR interval (<120 ms), the
presence of a delta wave (slurring of the initial QRS) and a wide
QRS (>120 ms).55 (figure 10)
WPW pattern should be differentiated from a low atrial
rhythm with a short PR interval that is a common finding in
athletes (figure 11). The short PR is a result of the impulse
being generated by an atrial focus outside the sinus node and
closer to the AV node. Due to the proximity to the AV node,
atrial conduction time is reduced and the PR interval is shortened. Findings that can help differentiate this from preexcitation include an atypical P wave axis (negative P wave in
the inferior leads) suggesting the atrium is activated from
bottom to top rather than top to bottom as in sinus rhythm
(figure 11). No further evaluation is recommended for asymptomatic athletes with only a short PR interval and no other
ECG abnormality.
Figure 9 Brugada type-1 ECG (left) should be distinguished from early repolarisation with ‘convex’ ST-segment elevation in a trained athlete
(right). Vertical lines mark the J-point (STJ) and the point 80 ms after the J-point (ST80), where the amplitudes of the ST segment elevation are
calculated. The ‘downsloping’ ST segment elevation in Brugada pattern is characterised by a STJ/ST80 ratio >1. Early repolarisation patterns in an
athlete show an initial ‘upsloping’ ST segment elevation with STJ/ST80 ratio <1.
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Figure 10 ECG demonstrating the classic findings of Wolff–Parkinson–White with a short PR interval (<120 ms), delta wave (slurred QRS upstroke)
and prolonged QRS (>120 ms). This figure is only reproduced in colour in the online version.
Evaluation of WPW
The diagnostic evaluation of asymptomatic athletes with WPW
pattern remains controversial and is conducted usually by an
electrophysiologist. Stratification methods for the risk of sudden
death include invasive and non-invasive tests. Non-invasive measures of a low-risk accessory pathway include intermittent
pre-excitation during sinus rhythm and abrupt, complete loss of
pre-excitation during an exercise stress test.56 57
If non-invasive testing is inconclusive, electrophysiology
testing should be considered. Characteristics of a high-risk
pathway are generally determined during an electrophysiology
study by the shortest pre-excited RR interval during induced
atrial fibrillation. If the shortest pre-excited RR interval is measured as ≤250 ms [240 beats/min (bpm)] then the pathway is
deemed high risk.52 Young athletes with a shortest pre-excited
RR interval ≤250 ms should proceed with transcatheter
ablation.58 An echocardiogram should also be considered due to
the association of WPW with Ebstein’s anomaly and
cardiomyopathy.
SUPRAVENTRICULAR TACHYCARDIAS
Figure 11 ECG demonstrating a low atrial rhythm with short PR
interval. Since the impulse is initiated adjacent to the AV node the
atrial conduction time is decreased and the PR interval shortened. The
P wave is also negative in the inferior leads (II, III, aVF) which confirms
this as a low atrial rhythm and differentiates it from Wolf–Parkinson–
White. This figure is only reproduced in colour in the online version.
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SVT are heart rhythms >100 bpm, originating from the sinus
node, atrial tissue or involving the AV node. The most common
SVT is sinus tachycardia, seen during exercise, anxiety, fever,
infection, dehydration, hyperthyroidism, anaemia, pulmonary
disease, heart failure, stimulant use and other causes.
Paroxysmal SVT includes AV nodal re-entrant tachycardia
(AVNRT), AV reciprocating tachycardia (AVRT), atrial tachycardia and other rare tachycardias (figure 12). AVNRT is a circuit
involving a slow and fast pathway entering and exiting the AV
node. The electrical circuit usually travels down the slow
pathway and up the fast pathway, but can be reversed or even
involve multiple slow pathways. AVRT involves an accessory AV
bypass pathway where the circuit typically conducts down the
AV node and up the bypass pathway, producing a narrow
complex tachycardia. In WPW pattern, the circuit also may
conduct down the bypass pathway and up the AV node. Since
the ventricular myocardium is activated by the bypass tract and
not the His-Purkinje system, there is a resultant wide complex
tachycardia. More commonly in AVRT there is a concealed
bypass pathway that only conducts retrograde and, therefore, is
not seen on ECG. Lastly, atrial tachycardia occurs from an
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Figure 12 Paroxysmal supraventricular tachycardia (SVT) refers to narrow complex tachycardias including atrioventricular nodal re-entrant
tachycardia (AVNRT), atrioventricular reciprocating tachycardia (AVRT), atrial tachycardia and other rare tachycardias. Atrial fibrillation and flutter are
types of SVT but do not fall into the paroxysmal classification. Here, there is a narrow complex tachycardia at 240 bpm, which was later found to be
AVRT. This figure is only reproduced in colour in the online version.
abnormal focus within the atrium that activates faster than the
sinus node.
Atrial fibrillation and flutter are other types of SVT. Atrial fibrillation is the most common abnormal SVT and is defined by
the rapid and irregular atrial electrical activation with the resultant dysfunctional atrial mechanical activation. Atrial flutter is
characterised by a macro-reentrant circuit within the atrium and
is more organised than atrial fibrillation.
Prevalence of SVT
The incidence of SVT is difficult to determine because of the
various study populations and ascertainment methods. Many
studies have included elderly patients, with coronary disease or
heart failure, which are not relevant to a younger athletic population. SVT is rarely found on a screening ECG, as most young
athletes are symptomatic with SVT. In a study of 32 652 Italian
subjects, 29 (0.09%) had SVT and 5 (0.02%) had atrial
Figure 13 The top row demonstrates atrioventricular nodal re-entrant tachycardia (AVNRT) and the bottom row is in normal sinus rhythm in the
same patient. In lead II, retrograde P waves are present at the end of the QRS complex. In lead V1, a pseudo-R0 with right bundle branch block
pattern is present due to the retrograde P waves. These deflections are not seen on the ECG when in sinus rhythm. This figure is only reproduced in
colour in the online version.
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fibrillation or flutter.50 Uncontrolled supraventricular arrhythmias led to disqualification in 73 of 42 386 subjects in the
Veneto region of Italy from 1982 to 2004.59 In 32 561 screening ECGs, an ectopic atrial tachycardia was found in only 4
(0.01%) and atrial fibrillation in 2 (<0.01%).10 These studies
suggest the presence of SVT to be quite rare on a screening
ECG.
rate. The ventricular response to atrial fibrillation is irregular
with varying QRS intervals. Atrial flutter, however, has regular
atrial activity characterised by flutter waves. Counterclockwise
typical atrial flutter, the most common type, shows negative,
sawtooth flutter waves in leads II, III and aVF and a positive
deflection in lead V1 (figure 15). The atrial activity in atrial
flutter is almost always continuous with no isoelectric segment.
Contribution as a cause of SCD
Evaluation of SVT
SVT, atrial fibrillation and atrial flutter very rarely lead to SCD,
but are more likely to lead to symptoms (ie, palpitations) that
prevent intense physical activity due to uncontrolled ventricular
rates or lack of adequate AV mechanical synchronisation.
Another concern is whether SVT or atrial fibrillation/flutter is
reflective of an underlying cardiomyopathy or channelopathy
that would place the athlete at risk for SCD. These may include
hypertrophic or other cardiomyopathies, BrS, myocarditis, short
QT syndrome or WPW.60
If paroxysmal SVT is seen, carotid sinus massage, Valsalva manoeuver or facial dunking in an ice bath should be completed
while recording the ECG to determine if the rhythm terminates
(suggestive of AVNRT or AVRT) or ventricular rate slows to
reveal hidden P waves (suggestive of an atrial tachycardia or
atrial flutter). Once the patient is no longer in SVT, a baseline
ECG should be completed to assess for WPW, and if seen, an
electrophysiologist should be consulted to discuss electrophysiology study and possible ablation. If the baseline ECG is
normal, it is reasonable to obtain an echocardiogram to look for
structural heart disease and consider an electrophysiology consultation to discuss possible ablation.
If the rhythm is atrial fibrillation or atrial flutter, an echocardiogram and 24 h Holter monitor should be completed to look
for structural heart disease and assess the heart rate throughout
the day, including with exercise. If a Holter cannot be performed during exercise, treadmill testing should be completed
to assess maximum heart rate while in atrial fibrillation/flutter.
Thyroid, liver and renal laboratory testing also should be
completed.
ECG findings in SVT
SVT is usually narrow complex, but in the presence of a bundle
branch block can be wide complex. It is often difficult to see
P waves in AVNRT, since the atrium and ventricles activate near
simultaneously, but it is sometimes possible to see inverted
P waves in the inferior leads and a pseudo R0 in V1 suggesting
right bundle branch block, which are not present when in sinus
rhythm (figure 13). AVRT will also usually show retrograde P
waves, but they do not necessarily have to be inverted in the
inferior leads. Some patients with AVRT will have a WPW
pattern on their baseline ECG. Atrial tachycardia demonstrates a
regular atrial rhythm which is faster than 100 bpm with P waves
all of the same morphology.
The ECG in atrial fibrillation shows fibrillation waves instead
of P waves (figure 14). These vary in size, morphology and frequency, but are usually low amplitude with changing shape and
OTHER ABNORMAL ECG FINDINGS
Profound sinus bradycardia
Diagnostic criteria
Sinus bradycardia is one of the hallmark features of a wellconditioned athlete’s heart. It is the result of increased vagal
Figure 14 ECG demonstrating atrial fibrillation with no clear P waves and an ‘irregularly’ irregular QRS response. Fibrillatory activity is best seen in
V1, as the fibrillation waves are irregular and of changing morphology. This figure is only reproduced in colour in the online version.
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Figure 15 ECG demonstrating atrial flutter, as evidenced by regular, sawtooth flutter waves in the inferior leads and a positive deflection in V1.
No isoelectric segment is present between the flutter waves. The QRS response is regular, in this case a 4 : 1 pattern. This figure is only reproduced
in colour in the online version.
tone and possible structural atrial remodelling.61 The sinus rate
only rarely falls below 30 bpm or shows pauses of ≥3 s during
an ECG recording at rest.
Evaluation
Profound sinus bradycardia (<30 bpm) at rest in an athlete
should be evaluated further but is not necessarily pathological
(figure 16). If asymptomatic and the sinus rate quickly accelerates with an increase in sympathetic tone (ie, small exercise
load), then additional testing is not usually necessary. The presence of symptoms, such as decreased exercise capacity or a predisposition for vasovagal syncope, may prompt additional
testing to exclude primary sinus node disease. One might also
consider temporary cessation of sports activity to evaluate
Figure 16 ECG in an asymptomatic long-distance runner showing profound sinus bradycardia (30 bpm) compatible with high vagal tone. The
athlete showed a normal chronotropic response during exercise testing.
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Figure 17 ECG showing Mobitz type II second-degree AV block. Note the presence of P waves with loss of conduction and no QRS complex
(arrows) and without PR prolongation in the beats prior, nor PR shortening in the beats after (which would suggest Mobitz type I). Mobitz type II
second-degree AV block in an athlete is not due to increased vagal tone and should prompt evaluation for underlying conduction disease. This
figure is only reproduced in colour in the online version.
reversibility, although even adaptive athlete’s heart sinus bradycardia may not be fully reversible.62 63
Mobitz type II second-degree AV block
Diagnostic criteria
Profound first-degree AV block
Diagnostic criteria
An abrupt loss of P wave conduction (P wave with no ensuing
QRS complex), without prior PR prolongation, represents
Mobitz type II second-degree AV block (figure 17). If Mobitz
type II or more advanced types of AV block including 2:1 or
3:1 occur during sinus rhythm, it may be indicative of underlying structural heart disease.
The high vagal tone in athletes also leads to a slowing of AV
nodal conduction, and hence a lengthening of the PR interval.
It is not uncommon to see PR intervals longer than 200 ms in
athletes at rest. Even significant PR prolongation ≥300 ms may
occur, although this by itself is not necessarily pathological and
is usually asymptomatic.
Evaluation
In asymptomatic athletes with a profound first-degree AV block
(≥300 ms), the athlete should undergo a minimal exercise load
(ie, like climbing a flight of stairs) to increase sympathetic tone.
If this results in shortening and normalisation of the PR interval,
the PR prolongation is due to functional (vagal) mechanisms
and hence benign. If the PR interval does not normalise to
≤200 ms with exercise, a structural cause of AV conduction disturbance (such as Lyme disease or sarcoidosis) should be investigated. Athletes with a profound first-degree AV block (≥300 ms)
who have symptoms (ie, syncope, palpitations) or a positive
family history of cardiac disease or sudden death require additional evaluation to rule out pathological causes of heart block.
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Evaluation
Suspected Mobitz type II second-degree AV block or other more
advanced types of AV block (2:1 or 3:1 block) should first be
differentiated from Wenckebach (Mobitz type I) second-degree
AV block. Wenckebach (Mobitz type I) block is present when
there is PR prolongation before a blocked P wave and a shorter
PR in the first conducted beat after the block. Mobitz type I
second-degree AV block is usually a functional block from
increased vagal tone and does not constitute pathology in an
athlete. Further diagnostic evaluation can be done with an ECG
after minor exercise, as a slight increase in sympathetic tone
will resolve the conduction disturbance in physiological cases.
A Holter monitor (or other form of long-term ECG recording)
also can assist in clarifying the type of AV block. Mobitz type II
or higher degree (2:1 or 3:1) AV block requires further evaluation for underlying pathological cardiac disease.
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Figure 18 ECG showing third-degree (complete) AV block and a junctional escape rhythm. With third-degree AV block, there are more P waves
than QRS complexes and the ventricular rhythm is perfectly regular due to an undisturbed junctional pacemaker. Complete heart block is not an
expression of athlete’s heart and requires additional evaluation. This figure is only reproduced in colour in the online version.
Third-degree AV block/complete heart block
Diagnostic criteria
Complete heart block is not an expression of athlete’s heart and
should be considered an abnormal finding requiring additional
evaluation.
Evaluation
With true third-degree AV block, there are more P waves than
QRS complexes and the ventricular rhythm is perfectly
regular due to an undisturbed junctional or ventricular pacemaker (figure 18). Complete heart block can easily be
Figure 19 ECG of a 35-year-old cyclist shows two premature ventricular contractions which should trigger further evaluation for underlying
structural heart disease and/or more complex arrhythmias. This asymptomatic athlete had inducible ventricular tachycardia during EP study, and later
received appropriate shocks from an implanted ICD.
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Original articles
confused with AV dissociation without block—a situation
where the junctional pacemaker is faster than the sinus node,
leading to more QRS complexes than P waves. Intermittent
ventricular capture by sinus P waves (resulting in an irregular
ventricular response) excludes complete AV block. AV dissociation without block is the expression of autonomic mismatch
between AV and sinus nodal modulation, but is not pathological. Like all other functional disturbances, a small exercise
load with repeat ECG recording will show resolution of the
ECG findings in AV dissociation. Complete heart block
requires further evaluation for underlying cardiac disease.
≥2 premature ventricular contractions
Diagnostic criteria
When two PVCs are recorded on a baseline (10 s) ECG, the
likelihood is very high that the athlete has >2000 PVCs per
24 h. In athletes with >2000 PVCs per 24 h, underlying structural heart disease which may predispose to more lifethreatening ventricular arrhythmias was found in 30% of cases,
compared to only 3% of athletes with 100–2000 PVCs, and
0% of athletes with <100 PVCs on a 24 h Holter.64 Over half
of the athletes with >2000 PVCs also had bursts of nonsustained ventricular tachycardia. Therefore, a structural
cardiac abnormality should be ruled out in athletes with
>2000 PVCs per 24 h.64
Evaluation
Documentation of ≥2 PVCs on baseline ECG should prompt
more extensive evaluation to exclude underlying cardiac disease
(figure 19). However, excluding pathology may be difficult and
the extent of the evaluation is controversial. At a minimum, a 24
Holter monitor, echocardiogram and exercise stress test should
be done. If the Holter and echocardiogram are normal and the
PVCs suppress with exercise, some experts recommend no
further evaluation for an asymptomatic athlete. However, in
cases with >2000 PVCs per 24 h or episodes of non-sustained
ventricular tachycardia, and depending on the level of clinical
concern, morphology of the PVCs and type of sport, additional
evaluation may also include cardiac MRI and more extensive
electrophysiological (EP) evaluation with signal averaged ECG,
long-term ECG recording, invasive EP study and/or cardiac
biopsy.65 66 Therefore, many such cases require referral to a heart
rhythm specialist.
Considerations in high-level endurance athletes with PVCs
In high-level adult endurance athletes (such as cyclists, triathlon athletes, marathon runners and rowers), concern has
been raised about right ventricular changes that may resemble
familial arrhythmogenic right ventricular cardiomyopathy
(ARVC), but in the absence of demonstrable desmosomal
mutations or a familial history.66 67 There is evolving evidence that persistent high volume and pressure load on the
right ventricle from such long-term endurance exercise may
result in ‘exercise-induced’ ARVC in such athletes.68 Its prognosis is not benign and may result in major ventricular
arrhythmias or sudden death, although many athletes with
exercise-induced ARVC initially present with minor arrhythmias or symptoms. PVCs originating from the right ventricle
typically show a left bundle branch block (LBBB) pattern
with a predominantly negative QRS complex in V1.
Therefore, in high-level adult endurance athletes, it may be
reasonable to consider a single PVC, especially with LBBB
morphology and superior axis, sufficient to warrant further
investigation similar to that discussed above.
Drezner JA, et al. Br J Sports Med 2013;47:153–167. doi:10.1136/bjsports-2012-092070
CONCLUSIONS
The ECG plays an important role in the cardiovascular assessment
of athletes given its capacity to detect inherited primary arrhythmia
syndromes and other diseases of disturbed cardiac conduction. As
outlined in this paper, there is a concise list of ECG findings that are
associated with the presence of a primary cardiac channelopathy or
other disorder predisposing to ventricular arrhythmias. Clinicians
charged with the cardiovascular care of athletes should be familiar
with abnormal ECG findings indicative of primary electrical disease.
During preparticipation screening that includes the use of ECG,
asymptomatic athletes with any of these abnormal findings should
undergo additional testing. Athletes presenting with symptoms (ie,
palpitations, exercise, or emotion related syncope or seizure-like
activity) should undergo prompt evaluation including an ECG. The
evaluation of an athlete with abnormal ECG findings is conducted
ideally in consultation with a cardiovascular specialist familiar with
primary electrical diseases and with experience caring for athletes.
Additional Resources
For a free online training module on ECG interpretation in athletes,
please visit: http://learning.bmj.com/ECGathlete. For the November
2012 BJSM supplement on ‘Advances in Sports Cardiology’, please
visit: http://bjsm.bmj.com/content/46/Suppl_1.toc.
Author affiliations
1
Department of Family Medicine, University of Washington, Seattle, Washington,
USA
2
Departments of Medicine, Pediatrics, and Molecular Pharmacology and
Experimental Therapeutics; Divisions of Cardiovascular Diseases and Pediatric
Cardiology, Mayo Clinic, Rochester, Minnesota, USA
3
Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota, USA
4
Department of Cardiac, Thoracic, and Vascular Sciences, University of Padua,
Padova, Italy
5
Department of Cardiovascular Sciences, University of Leuven, Leuven, Belgium
6
Division of Cardiology, University of Washington, Seattle, Washington,
USA
7
Division of Cardiology, Seattle Children’s Hospital, Seattle, Washington, USA
8
Department of Athletics, University of Connecticut, Storrs, Connecticut, USA
9
Division of Cardiovascular Medicine, Stanford University School of Medicine, Palo
Alto, California, USA
10
Department of Family Medicine, Eisenhower Army Medical Center, Fort Gordon,
Georgia, USA
11
Division of Cardiology, Massachusetts General Hospital, Boston, Massachusetts,
USA
12
Swedish School of Sports and Health Sciences and Department of Cardiology,
Karolinska University Hospital, Stockholm, Sweden
13
Division of Sports Medicine, University of California Los Angeles, Los Angeles,
California, USA
14
Department of Pediatrics, Emory University School of Medicine, Children’s
Healthcare of Atlanta, Atlanta, Georgia, USA
15
Midwest Heart Foundation, Oakbrook Terrace, Illinois, USA
16
Department of Family and Community Medicine, University of Arizona, Tucson,
Arizona, USA
17
Department of Medicine, Institute of Sport Medicine and Science, Rome, Italy
18
Division of Cardiology, University Hospital Zurich, Zurich, Switzerland
19
Department of Cardiovascular Sciences, St George’s University of London, London,
UK
20
Department of Cardiology, Hospital de Clínicas de Porto Alegre, Porto Alegre,
Brazil
21
Division of Cardiology, The Children’s Hospital of Philadelphia, Philadelphia,
Pennsylvania, USA
22
Department of Sports Medicine, ASPETAR, Qatar Orthopedic and Sports Medicine
Hospital, Doha, Qatar
Competing interests None.
Provenance and peer review Commissioned; internally peer reviewed.
▸ References to this paper are available online at http://bjsm.bmjgroup.com
REFERENCES
1
Ackerman MJ, Priori SG, Willems S, et al. HRS/EHRA expert consensus statement on
the state of genetic testing for the channelopathies and cardiomyopathies this
15 of 17
Downloaded from bjsm.bmj.com on January 9, 2013 - Published by group.bmj.com
Original articles
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
document was developed as a partnership between the Heart Rhythm Society (HRS)
and the European Heart Rhythm Association (EHRA). Heart Rhythm
2011;8:1308–9.
Bastiaenen R, Behr ER. Sudden death and ion channel disease: pathophysiology
and implications for management. Heart 2011;97:1365–72.
Richard P, Denjoy I, Fressart V, et al. Advising a cardiac disease gene positive yet
phenotype negative or borderline abnormal athlete: is sporting disqualification really
necessary?. Br J Sports Med 2012;46(Suppl 1):i59–68.
Maron BJ, Doerer JJ, Haas TS, et al. Sudden deaths in young competitive athletes:
analysis of 1866 deaths in the United States, 1980–2006. Circulation
2009;119:1085–92.
Corrado D, Biffi A, Basso C, et al. 12-lead ECG in the athlete: physiological versus
pathological abnormalities. Br J Sports Med 2009;43:669–76.
Corrado D, Pelliccia A, Heidbuchel H, et al. Recommendations for interpretation of
12-lead electrocardiogram in the athlete. Eur Heart J 2010;31:243–59.
Uberoi A, Stein R, Perez MV, et al. Interpretation of the electrocardiogram of young
athletes. Circulation 2011;124:746–57.
Williams ES, Owens DS, Drezner JA, et al. Electrocardiogram interpretation in the
athlete. Herzschrittmacherther Elektrophysiol 2012;23:65–71.
Drezner J. Standardised criteria for ECG interpretation in athletes: a practical tool.
Br J Sports Med 2012;46(Suppl I):i6–8.
Marek J, Bufalino V, Davis J, et al. Feasibility and findings of large-scale
electrocardiographic screening in young adults: data from 32,561 subjects. Heart
Rhythm 2011;8:1555–9.
Drezner JA, Ackerman MJ, Anderson J, et al. Electrocardiographic interpretation in
athletes: the ‘Seattle Criteria’. Br J Sports Med 2013;47.
Drezner JA, Fischbach P, Froelicher V, et al. Normal electrocardiographic findings:
recognizing physiologic adaptations in athletes. Br J Sports Med 2013;47.
Schwartz PJ, Stramba-Badiale M, Crotti L, et al. Prevalence of the congenital
long-QT syndrome. Circulation 2009;120:1761–7.
Tester DJ, Ackerman MJ. Cardiomyopathic and channelopathic causes of sudden
unexplained death in infants and children. Annu Rev Med 2009;60:69–84.
Eckart RE, Shry EA, Burke AP, et al. Sudden death in young adults an
autopsy-based series of a population undergoing active surveillance. J Am Coll
Cardiol 2011;58:1254–61.
Meyer L, Stubbs B, Fahrenbruch C, et al. Incidence, causes, and survival trends from
cardiovascular-related sudden cardiac arrest in children and young adults 0 to
35 years of age: a 30-year review. Circulation 2012;126:1363–72.
Behr E, Wood DA, Wright M, et al. Cardiological assessment of first-degree relatives
in sudden arrhythmic death syndrome. Lancet 2003;362:1457–9.
Tester DJ, Spoon DB, Valdivia HH, et al. Targeted mutational analysis of the
RyR2-encoded cardiac ryanodine receptor in sudden unexplained death: a
molecular autopsy of 49 medical examiner/coroner’s cases. Mayo Clin Proc
2004;79:1380–4.
Tan HL, Hofman N, van Langen IM, et al. Sudden unexplained death: heritability
and diagnostic yield of cardiological and genetic examination in surviving relatives.
Circulation 2005;112:207–13.
Tester DJ, Medeiros-Domingo A, Will ML, et al. Cardiac channel molecular autopsy:
insights from 173 consecutive cases of autopsy-negative sudden unexplained death
referred for postmortem genetic testing. Mayo Clin Proc 2012;87:524–39.
Gollob MH, Redpath CJ, Roberts JD. The short QT syndrome: proposed diagnostic
criteria. J Am Coll Cardiol 2011;57:802–12.
Schwartz PJ, Moss AJ, Vincent GM, et al. Diagnostic criteria for the long QT
syndrome. An update. Circulation 1993;88:782–4.
Schwartz PJ, Crotti L. QTc behavior during exercise and genetic testing for the
long-QT syndrome. Circulation 2011;124:2181–4.
Viskin S, Rosovski U, Sands AJ, et al. Inaccurate electrocardiographic interpretation
of long QT: the majority of physicians cannot recognize a long QT when they see
one. Heart Rhythm 2005;2:569–74.
Postema PG, De Jong JS, Van der Bilt IA, et al. Accurate electrocardiographic
assessment of the QT interval: teach the tangent. Heart Rhythm 2008;5:1015–18.
Bazett HC. An analysis of the time-relations of electrocardiograms. Heart 1920;
(7):353–70.
Johnson JN, Ackerman MJ. The prevalence and diagnostic/prognostic utility of sinus
arrhythmia in the evaluation of congenital long QT syndrome. Heart Rhythm
2010;7:1785–9.
Malfatto G, Beria G, Sala S, et al. Quantitative analysis of T wave abnormalities
and their prognostic implications in the idiopathic long QT syndrome. J Am Coll
Cardiol 1994;23:296–301.
Johnson JN, Ackerman MJ. QTc: how long is too long? Br J Sports Med
2009;43:657–62.
Taggart NW, Haglund CM, Tester DJ, et al. Diagnostic miscues in congenital
long-QT syndrome. Circulation 2007;115:2613–20.
Mason JW, Ramseth DJ, Chanter DO, et al. Electrocardiographic reference ranges
derived from 79,743 ambulatory subjects. J Electrocardiol 2007;40:228–34.
Vincent GM, Timothy KW, Leppert M, et al. The spectrum of symptoms and QT
intervals in carriers of the gene for the long-QT syndrome. N Engl J Med
1992;327:846–52.
16 of 17
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
Rautaharju PM, Surawicz B, Gettes LS, et al. AHA/ACCF/HRS recommendations for
the standardization and interpretation of the electrocardiogram: part IV: the ST
segment, T and U waves, and the QT interval: a scientific statement from the
American Heart Association Electrocardiography and Arrhythmias Committee,
Council on Clinical Cardiology; the American College of Cardiology Foundation; and
the Heart Rhythm Society: endorsed by the International Society for Computerized
Electrocardiology. Circulation 2009;119:e241–50.
Basavarajaiah S, Wilson M, Whyte G, et al. Prevalence and significance of an
isolated long QT interval in elite athletes. Eur Heart J 2007;28:2944–9.
Maron BJ, Zipes DP. 36th Bethesda Conference: eligibility recommendations for
competitive athletes with cardiovascular abnormalities. J Am Coll Cardiol
2005;45:1312–77.
Goldenberg I, Moss AJ, Peterson DR, et al. Risk factors for aborted cardiac arrest
and sudden cardiac death in children with the congenital long-QT syndrome.
Circulation 2008;117:2184–91.
Mohamed U, Napolitano C, Priori SG. Molecular and electrophysiological bases of
catecholaminergic polymorphic ventricular tachycardia. J Cardiovasc Electrophysiol
2007;18:791–7.
Kontula K, Laitinen PJ, Lehtonen A, et al. Catecholaminergic polymorphic
ventricular tachycardia: recent mechanistic insights. Cardiovasc Res
2005;67:379–87.
Napolitano C, Priori SG, Bloise R. Catecholaminergic polymorphic ventricular
tachycardia. In: Pagon RA BT, Dolan CR, Stephens K, Adam MP. GeneReviews™:
National center for biotechnology information, 2004 Oct 14. Seattle, Washington:
University of Washington (updated 2012 Feb 16).
Larsen MK, Berge KE, Leren TP, et al. Postmortem genetic testing of the ryanodine
receptor 2 (RYR2) gene in a cohort of sudden unexplained death cases. Int J Legal
Med 6 Jan 2012 [Epub ahead of print].
Ferrero-Miliani L, Holst AG, Pehrson S, et al. Strategy for clinical evaluation and
screening of sudden cardiac death relatives. Fundam Clin Pharmacol
2010;24:619–35.
Liu N, Ruan Y, Priori SG. Catecholaminergic polymorphic ventricular tachycardia.
Prog Cardiovasc Dis 2008;51:23–30.
Horner JM, Ackerman MJ. Ventricular ectopy during treadmill exercise stress testing
in the evaluation of long QT syndrome. Heart Rhythm 2008;5:1690–4.
Pflaumer A, Davis AM. Guidelines for the diagnosis and management of
catecholaminergic polymorphic ventricular tachycardia. Heart Lung Circ
2012;21:96–100.
Antzelevitch C, Brugada P, Borggrefe M, et al. Brugada syndrome: report of the
second consensus conference: endorsed by the Heart Rhythm Society and the
European Heart Rhythm Association. Circulation 2005;111:659–70.
Kapplinger JD, Tester DJ, Alders M, et al. An international compendium of
mutations in the SCN5A-encoded cardiac sodium channel in patients referred for
Brugada syndrome genetic testing. Heart Rhythm 2010;7:33–46.
Crotti L, Marcou CA, Tester DJ, et al. Spectrum and prevalence of mutations
involving BrS1- through BrS12-susceptibility genes in a cohort of unrelated patients
referred for Brugada syndrome genetic testing: implications for genetic testing. J Am
Coll Cardiol 2012;60:1410–18.
Wilde AA, Antzelevitch C, Borggrefe M, et al. Proposed diagnostic criteria for the
Brugada syndrome: consensus report. Circulation 2002;106:2514–19.
Zorzi A, Migliore F, Marras E, et al. Should all individuals with a nondiagnostic
Brugada-electrocardiogram undergo sodium-channel blocker test? Heart Rhythm
2012;9:909–16.
Pelliccia A, Culasso F, Di Paolo FM, et al. Prevalence of abnormal
electrocardiograms in a large, unselected population undergoing pre-participation
cardiovascular screening. Eur Heart J 2007;28:2006–10.
Munger TM, Packer DL, Hammill SC, et al. A population study of the natural history
of Wolff-Parkinson-White syndrome in Olmsted County, Minnesota, 1953–1989.
Circulation 1993;87:866–73.
Klein GJ, Bashore TM, Sellers TD, et al. Ventricular fibrillation in the
Wolff-Parkinson-White syndrome. N Engl J Med 1979;301:1080–5.
Deal BJ, Beerman L, Silka M, et al. Cardiac arrest in young patients with
Wolff-Parkinson-White syndrome. PACE 1995;18:815(a).
Russell MW, Dick MD. Incidence of catastrophic events associated with the
Wolff-Parkinson-White syndrome in young patients: diagnostic and therapeutic
dilemma. Circulation 1993;(1993):484(a).
Surawicz B, Childers R, Deal BJ, et al. AHA/ACCF/HRS recommendations for the
standardization and interpretation of the electrocardiogram: part III: intraventricular
conduction disturbances: a scientific statement from the American Heart Association
Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the
American College of Cardiology Foundation; and the Heart Rhythm Society:
endorsed by the International Society for Computerized Electrocardiology. Circulation
2009;119:e235–40.
Klein GJ, Gulamhusein SS. Intermittent preexcitation in the Wolff-Parkinson-White
syndrome. Am J Cardiol 1983;52:292–6.
Daubert C, Ollitrault J, Descaves C, et al. Failure of the exercise test to predict the
anterograde refractory period of the accessory pathway in Wolff Parkinson White
syndrome. Pacing Clin Electrophysiol 1988;11:1130–8.
Drezner JA, et al. Br J Sports Med 2013;47:153–167. doi:10.1136/bjsports-2012-092070
Downloaded from bjsm.bmj.com on January 9, 2013 - Published by group.bmj.com
Original articles
58
59
60
61
62
Cohen MI, Triedman JK, Cannon BC, et al. PACES/HRS expert consensus statement
on the management of the asymptomatic young patient with a
Wolff-Parkinson-White (WPW, ventricular preexcitation) electrocardiographic pattern:
developed in partnership between the Pediatric and Congenital Electrophysiology
Society (PACES) and the Heart Rhythm Society (HRS). Endorsed by the governing
bodies of PACES, HRS, the American College of Cardiology Foundation (ACCF), the
American Heart Association (AHA), the American Academy of Pediatrics (AAP), and
the Canadian Heart Rhythm Society (CHRS). Heart Rhythm 2012;9:1006–24.
Corrado D, Basso C, Pavei A, et al. Trends in sudden cardiovascular death in young
competitive athletes after implementation of a preparticipation screening program.
JAMA 2006;296:1593–601.
Corrado D, Basso C, Schiavon M, et al. Pre-participation screening of young
competitive athletes for prevention of sudden cardiac death. J Am Coll Cardiol
2008;52:1981–9.
Stein R, Medeiros CM, Rosito GA, et al. Intrinsic sinus and atrioventricular node
electrophysiologic adaptations in endurance athletes. J Am Coll Cardiol
2002;39:1033–8.
Jensen-Urstad K, Bouvier F, Saltin B, et al. High prevalence of arrhythmias in
elderly male athletes with a lifelong history of regular strenuous exercise. Heart
1998;79:161–4.
Drezner JA, et al. Br J Sports Med 2013;47:153–167. doi:10.1136/bjsports-2012-092070
63
64
65
66
67
68
Baldesberger S, Bauersfeld U, Candinas R, et al. Sinus node disease and arrhythmias
in the long-term follow-up of former professional cyclists. Eur Heart J 2008;29:71–8.
Biffi A, Pelliccia A, Verdile L, et al. Long-term clinical significance of frequent and
complex ventricular tachyarrhythmias in trained athletes. J Am Coll Cardiol
2002;40:446–52.
Heidbuchel H, Corrado D, Biffi A, et al. Recommendations for participation in
leisure-time physical activity and competitive sports of patients with arrhythmias and
potentially arrhythmogenic conditions. Part II: ventricular arrhythmias,
channelopathies and implantable defibrillators. Eur J Cardiovasc Prev Rehabil
2006;13:676–86.
Heidbuchel H, Hoogsteen J, Fagard R, et al. High prevalence of right
ventricular involvement in endurance athletes with ventricular arrhythmias. Role
of an electrophysiologic study in risk stratification. Eur Heart J 2003;24:
1473–80.
La Gerche A, Robberecht C, Kuiperi C, et al. Lower than expected desmosomal
gene mutation prevalence in endurance athletes with complex ventricular
arrhythmias of right ventricular origin. Heart 2010;96:1268–74.
Heidbuchel H, Prior DL, Gerche AL. Ventricular arrhythmias associated with
long-term endurance sports: what is the evidence? Br J Sports Med
2012;46(Suppl 1):i44–50.
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Abnormal electrocardiographic findings in
athletes: recognising changes suggestive of
primary electrical disease
Jonathan A Drezner, Michael J Ackerman, Bryan C Cannon, et al.
Br J Sports Med 2013 47: 153-167
doi: 10.1136/bjsports-2012-092070
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