A Pelliccia

AP Burke

BJ Maron

D Corrado

IA Rijsingen Van

JA Drezner

JE Madias

M Papadakis

N Chandra

S Basavarajaiah

S Sharma

English

PubMed

J. K. Jongman

N. Sheikh

A. Zaidi

S. Sharma

Crossref

Netherlands Heart Journal

Recurrent repolarisation abnormalities in an athlete

Jongman, JK

Sheikh, N

Zaidi, A

Sharma, S

St George's Online Research Archive

CASE REPORTRecurrent repolarisation abnormalities in an athleteJ. K. Jongman & N. Sheikh & A. Zaidi & S. SharmaPublished online: 9 November 2013# The Author(s) 2013. This article is published with open access at Springerlink.comIntroductionElectrocardiographic changes due to regular physical exerciseare well recognised and result from a combination of structuralcardiac changes and increased vagal tone [1–6]. However,abnormalities on the athlete’s resting electrocardiogram(ECG) may be the first indication of an underlying electricalor structural cardiac disorder, and may precede symptoms andmacroscopic structural abnormalities by several years [7]. Thefirst manifestation of such disorders may be a malignantarrhythmia or sudden cardiac death (SCD) [3]. Consideringthat physical exertion is a trigger for fatal arrhythmias incardiomyopathies or primary electrical cardiac disorders,differentiating cardiac pathology from physiologicaladaptation in athletes is crucial [3, 8, 9].Athletes of African/Afro-Caribbean (black) ethnicitycomprise a rapidly growing population of athletes in WesternEurope and such individuals frequently develop a greatermagnitude of left ventricular hypertrophy (LVH) comparedwith their Caucasian counterparts (white athletes) and displaya high frequency of repolarisation anomalies that overlap withthe hypertrophic cardiomyopathy phenotype [1, 2, 4, 6, 7].Differentiating between the ‘athlete’s heart’ and potentiallylethal cardiac abnormalities is occasionally challenging,particularly in black athletes.CaseA 20-year-old black athlete engaged in middle-long distancerunning and soccer underwent a cardiovascular assessment,including a health questionnaire and ECG. He wasasymptomatic and had no family history for SCD or inheritedcardiac diseases. He was not taking regular medication orperformance-enhancing drugs. A 12-lead ECG revealedvoltage criteria for LVH and widespread repolarisationabnormalities with convex ST-segment elevation in leadsV2-V4, biphasic T waves in lead II, and T-wave inversion inleads III, aVF, V1-6 (Fig. 1). Subsequent echocardiographydemonstrated normal biventricular systolic function. The leftventricular dimension at end diastole measured 55 mm with amaximum left ventricular wall thickness of 12 mm. Indices ofdiastolic function were normal and there were no otherfeatures to suggest an underlying cardiomyopathy.Considering the distinct repolarisation abnormalities on hisECG, a cardiopulmonary exercise test (CPEx) and cardiacmagnetic resonance imaging (CMRI) were performed. TheCMRI revealed mild biventricular enlargement with normalventricular function and no evidence of late gadoliniumenhancement to indicate myocardial fibrosis. The athletedemonstrated a maximal oxygen consumption of 42.57 ml/min/kg (95 % predicted) with normal blood pressure responseand no ECG changes or arrhythmias. A 24-h Holter monitordid not reveal any arrhythmias.We were unable to confirm or refute the diagnosis of anunderlying cardiomyopathy with these results, but whenreviewed in our outpatient clinic to discuss the test results itappeared that the athlete had been forced to stop exercising for4 weeks because of a lower limb injury. The ECG at this pointdemonstrated complete resolution of the T-wave inversions inall leads except lead III and V1 (Fig. 2). Following recovery heresumed training and an ECG performed 6 weeks afterwardsrevealed recurrence of marked repolarisation changes (Fig. 3).J. K. Jongman (*)Department of Cardiology, Isala Clinics, Zwolle, the Netherlandse-mail: jessejongman@hotmail.comN. Sheikh :A. Zaidi : S. SharmaDepartment of Cardiovascular Sciences, St. George’s University,London, UKNeth Heart J (2014) 22:523–526DOI 10.1007/s12471-013-0493-9DiscussionThe extent of cardiovascular changes induced by regularphysical exercise is influenced by several factors includinggender, sports classification (static, dynamic or combined),age and ethnicity. In highly trained black athletes,repolarisation abnormalities are a common finding, with upto 22.8 % of individuals demonstrating T-wave inversion intwo or more contiguous leads versus 3.7 % of white athletes[4]. These ECG changes overlap with those observed inseveral conditions associated with SCD in athletes, includingarrhythmogenic right ventricular cardiomyopathy (ARVC)and hypertrophic cardiomyopathy (HCM) [1, 2, 4–6, 10].SCD due to HCM is reported to be commoner in black athletesFig. 1 The athlete’s first ECG with voltage criteria for LVH, convex ST-segment elevation in leads V2-V4, biphasic T waves in lead II and T-waveinversion in leads III, aVF, V1-6Fig. 2 The ECG after detraining, with resolution of the T-wave inversion in leads II, aVF, V2-V6524 Neth Heart J (2014) 22:523–526than in white athletes and therefore the combination ofrepolarisation abnormalities and LVH pose a majorconundrum in black athletes [9].From observations and long-term follow-up in largecohorts of black athletes, T-wave inversion in leads V1-V4preceded by a convex ST-segment elevation in an otherwiseasymptomatic black athlete with no family history ofpremature SCD or cardiomyopathy and a normalcardiovascular examination may be considered an ethnicvariant in response to training and does not require furthertesting [1, 4, 10]. In contrast, we have noted aborted suddencardiac death and development of cardiomyopathy in a smallminority of black athletes with inferolateral T-wave inversion.Given the high prevalence of T-wave inversion in theinferolateral leads in patients with HCM (>80 %), werecommend that this particular pattern of repolarisationchanges should be viewed with caution and triggercomprehensive evaluation [4, 11].The differentiation between physiological cardiacadaptation and a cardiomyopathy requires a combination ofseveral imaging modalities, exercise stress test withsimultaneous gas exchange measurements and heart rhythmmonitoring as well as evaluation of first-degree relatives [2]. Ifthe echocardiogram is inconclusive a cardiac MRI isrecommended, considering its superior spatial resolution andthe possibility of demonstrating late gadolinium enhancement,which is associated with exercise-related ventriculararrhythmias [1, 12]. A period of physical inactivity(detraining) to demonstrate a regression of training-relatedchanges in order to exclude an underlying cardiomyopathyis often regarded as the last resort [13, 14]. In our athlete anaccidental detraining period of just 4 weeks resulted in thecomplete resolution of the repolarisation abnormalities and theevaluation failed to show any of the broader phenotypicfeatures of hypertrophic cardiomyopathy. Our case illustratesthat T-wave inversion in the inferolateral leads, althoughcommon in black patients with HCM, does not necessarilyimplicate underlying pathology in a black athlete. A relativelyshort period of deconditioning could be used to resolve thisclinical dilemma.Open Access This article is distributed under the terms of the CreativeCommons Attribution License which permits any use, distribution, andreproduction in any medium, provided the original author(s) and thesource are credited.References1. Drezner JA, Ashley E, Baggish AL, et al. Abnormalelectrocardiographic findings in athletes: recognising changessuggestive of cardiomyopathy. Br J Sports Med. 2013;47:137–52.2. Chandra N, Papadakis M, Sharma S. Cardiac adaptation in athletes ofblack ethnicity: differentiating pathology from physiology. Heart.2012;98:1194–200.3. Corrado D, Pelliccia A, Heidbuchel H, et al. Recommendations forinterpretation of 12-lead electrocardiogram in the athlete. Eur Heart J.2010;31:243–59.4. Papadakis M, Carre F, Kervio G, et al. The prevalence, distribution,and clinical outcomes of electrocardiographic repolarization patternsin male athletes of African/Afro-Caribbean origin. Eur Heart J.2011;32:2304–13.5. Sharma S, Whyte G, Elliott P, et al. Electrocardiographic changes in1000 highly trained junior elite athletes. Br J Sports Med. 1999;33:319–24.Fig. 3 The athlete’s ECG 6weeks after resuming his training, with reappearance of the biphasic Twaves in lead II and inverted Twaves in leads aVF and V2-6Neth Heart J (2014) 22:523–526 5256. Basavarajaiah S, Boraita A, Whyte G, et al. Ethnic differences in leftventricular remodelling in highly-trained athletes: relevance todifferentiating physiologic left ventricular hypertrophy fromhypertrophic cardiomyopathy. J Am Coll Cardiol. 2008;51:2256–62.7. Pelliccia A, Di Paolo FM, Quattrini FM, et al. Outcomes in athleteswith marked ECG repolarization abnormalities. N Engl J Med.2008;358:152–61.8. Burke AP, Farb A, Virmani R, Goodin J, Smialek JE. Sports-relatedand non-sports-related sudden cardiac death in young adults. AmHeart J. 1991;121:568–75.9. Maron BJ, Doerer JJ, Haas TS, Tierney DM, Mueller FO. Suddendeaths in young competitive athletes. Analysis of 1866 deaths in theUnited States, 1980–2006. Circulation. 2009;119:1085–92.10. Drezner JA, Fischbach P, Froelicher V, et al. Normalelectrocardiographic findings: recognising physiological adaptationsin athletes. Br J Sports Med. 2013;47:125–36.11. Madias JE. Electrocardiogram in apical hypertrophiccardiomyopathy with a speculation as to the mechanism of itsfeatures. Neth Heart J. 2013;21:268–71.12. Van Rijsingen IA, Bekkers SC, Schalla S, et al. Exercise relatedventricular arrhythmias are related to cardiac fibrosis in hypertrophiccardiomyopathy mutation carriers. Neth Heart J. 2011;19:168–74.13. Whyte G, Somauroo J, Wilson M, Sharma S. T-wave inversions andthe role of de-training in the differentiation of athlete's heart frompathology: is 6 months too long? BMJ Case Rep. 2012.14. Ghani S, Sharma S. Electrocardiographic changes in an athlete beforeand after detraining. BMJ Case Rep. 2012.526 Neth Heart J (2014) 22:523–526

black ethnicity: differentiating pathology from physiology.

Electrocardiogram in apical hypertrophic cardiomyopathy with a speculation as to the mechanism of its features.

Electrocardiographic changes in 1000 highly trained junior elite athletes.

Electrocardiographic changes in an athlete before and after detraining. BMJ Case Rep.

Ethnic differences in left ventricular remodelling in highly-trained athletes: relevance to differentiating physiologic left ventricular hypertrophy from hypertrophic cardiomyopathy.

Exercise related ventricular arrhythmias are related to cardiac fibrosis in hypertrophic cardiomyopathy mutation carriers.

Normal electrocardiographic findings: recognising physiological adaptations in athletes.

Outcomes in athletes with marked ECG repolarization abnormalities.

Recommendations for interpretation of 12-lead electrocardiogram in the athlete.

Sports-related and non-sports-related sudden cardiac death in young adults. Am Heart J.

Sudden deaths in young competitive athletes. Analysis of 1866 deaths in the United States,

T-wave inversions and the role of de-training in the differentiation of athlete's heart from pathology: is 6 months too long? BMJ Case Rep.

The prevalence, distribution, and clinical outcomes of electrocardiographic repolarization patterns in male athletes of African/Afro-Caribbean origin.

Recurrent repolarisation abnormalities in an athlete.

Springer - Publisher Connector

CASE REPORT
Recurrent repolarisation abnormalities in an athlete
J. K. Jongman & N. Sheikh & A. Zaidi & S. Sharma
Published online: 9 November 2013
# The Author(s) 2013. This article is published with open access at Springerlink.com
Introduction
Electrocardiographic changes due to regular physical exercise
are well recognised and result from a combination of structural
cardiac changes and increased vagal tone [1–6]. However,
abnormalities on the athlete’s resting electrocardiogram
(ECG) may be the first indication of an underlying electrical
or structural cardiac disorder, and may precede symptoms and
macroscopic structural abnormalities by several years [7]. The
first manifestation of such disorders may be a malignant
arrhythmia or sudden cardiac death (SCD) [3]. Considering
that physical exertion is a trigger for fatal arrhythmias in
cardiomyopathies or primary electrical cardiac disorders,
differentiating cardiac pathology from physiological
adaptation in athletes is crucial [3, 8, 9].
Athletes of African/Afro-Caribbean (black) ethnicity
comprise a rapidly growing population of athletes in Western
Europe and such individuals frequently develop a greater
magnitude of left ventricular hypertrophy (LVH) compared
with their Caucasian counterparts (white athletes) and display
a high frequency of repolarisation anomalies that overlap with
the hypertrophic cardiomyopathy phenotype [1, 2, 4, 6, 7].
Differentiating between the ‘athlete’s heart’ and potentially
lethal cardiac abnormalities is occasionally challenging,
particularly in black athletes.
Case
A 20-year-old black athlete engaged in middle-long distance
running and soccer underwent a cardiovascular assessment,
including a health questionnaire and ECG. He was
asymptomatic and had no family history for SCD or inherited
cardiac diseases. He was not taking regular medication or
performance-enhancing drugs. A 12-lead ECG revealed
voltage criteria for LVH and widespread repolarisation
abnormalities with convex ST-segment elevation in leads
V2-V4, biphasic T waves in lead II, and T-wave inversion in
leads III, aVF, V1-6 (Fig. 1). Subsequent echocardiography
demonstrated normal biventricular systolic function. The left
ventricular dimension at end diastole measured 55 mm with a
maximum left ventricular wall thickness of 12 mm. Indices of
diastolic function were normal and there were no other
features to suggest an underlying cardiomyopathy.
Considering the distinct repolarisation abnormalities on his
ECG, a cardiopulmonary exercise test (CPEx) and cardiac
magnetic resonance imaging (CMRI) were performed. The
CMRI revealed mild biventricular enlargement with normal
ventricular function and no evidence of late gadolinium
enhancement to indicate myocardial fibrosis. The athlete
demonstrated a maximal oxygen consumption of 42.57 ml/
min/kg (95 % predicted) with normal blood pressure response
and no ECG changes or arrhythmias. A 24-h Holter monitor
did not reveal any arrhythmias.
We were unable to confirm or refute the diagnosis of an
underlying cardiomyopathy with these results, but when
reviewed in our outpatient clinic to discuss the test results it
appeared that the athlete had been forced to stop exercising for
4 weeks because of a lower limb injury. The ECG at this point
demonstrated complete resolution of the T-wave inversions in
all leads except lead III and V1 (Fig. 2). Following recovery he
resumed training and an ECG performed 6 weeks afterwards
revealed recurrence of marked repolarisation changes (Fig. 3).
J. K. Jongman (*)
Department of Cardiology, Isala Clinics, Zwolle, the Netherlands
e-mail: jessejongman@hotmail.com
N. Sheikh :A. Zaidi : S. Sharma
Department of Cardiovascular Sciences, St. George’s University,
London, UK
Neth Heart J (2014) 22:523–526
DOI 10.1007/s12471-013-0493-9
Discussion
The extent of cardiovascular changes induced by regular
physical exercise is influenced by several factors including
gender, sports classification (static, dynamic or combined),
age and ethnicity. In highly trained black athletes,
repolarisation abnormalities are a common finding, with up
to 22.8 % of individuals demonstrating T-wave inversion in
two or more contiguous leads versus 3.7 % of white athletes
[4]. These ECG changes overlap with those observed in
several conditions associated with SCD in athletes, including
arrhythmogenic right ventricular cardiomyopathy (ARVC)
and hypertrophic cardiomyopathy (HCM) [1, 2, 4–6, 10].
SCD due to HCM is reported to be commoner in black athletes
Fig. 1 The athlete’s first ECG with voltage criteria for LVH, convex ST-segment elevation in leads V2-V4, biphasic T waves in lead II and T-wave
inversion in leads III, aVF, V1-6
Fig. 2 The ECG after detraining, with resolution of the T-wave inversion in leads II, aVF, V2-V6
524 Neth Heart J (2014) 22:523–526
than in white athletes and therefore the combination of
repolarisation abnormalities and LVH pose a major
conundrum in black athletes [9].
From observations and long-term follow-up in large
cohorts of black athletes, T-wave inversion in leads V1-V4
preceded by a convex ST-segment elevation in an otherwise
asymptomatic black athlete with no family history of
premature SCD or cardiomyopathy and a normal
cardiovascular examination may be considered an ethnic
variant in response to training and does not require further
testing [1, 4, 10]. In contrast, we have noted aborted sudden
cardiac death and development of cardiomyopathy in a small
minority of black athletes with inferolateral T-wave inversion.
Given the high prevalence of T-wave inversion in the
inferolateral leads in patients with HCM (>80 %), we
recommend that this particular pattern of repolarisation
changes should be viewed with caution and trigger
comprehensive evaluation [4, 11].
The differentiation between physiological cardiac
adaptation and a cardiomyopathy requires a combination of
several imaging modalities, exercise stress test with
simultaneous gas exchange measurements and heart rhythm
monitoring as well as evaluation of first-degree relatives [2]. If
the echocardiogram is inconclusive a cardiac MRI is
recommended, considering its superior spatial resolution and
the possibility of demonstrating late gadolinium enhancement,
which is associated with exercise-related ventricular
arrhythmias [1, 12]. A period of physical inactivity
(detraining) to demonstrate a regression of training-related
changes in order to exclude an underlying cardiomyopathy
is often regarded as the last resort [13, 14]. In our athlete an
accidental detraining period of just 4 weeks resulted in the
complete resolution of the repolarisation abnormalities and the
evaluation failed to show any of the broader phenotypic
features of hypertrophic cardiomyopathy. Our case illustrates
that T-wave inversion in the inferolateral leads, although
common in black patients with HCM, does not necessarily
implicate underlying pathology in a black athlete. A relatively
short period of deconditioning could be used to resolve this
clinical dilemma.
Open Access This article is distributed under the terms of the Creative
Commons Attribution License which permits any use, distribution, and
reproduction in any medium, provided the original author(s) and the
source are credited.
References
1. Drezner JA, Ashley E, Baggish AL, et al. Abnormal
electrocardiographic findings in athletes: recognising changes
suggestive of cardiomyopathy. Br J Sports Med. 2013;47:137–52.
2. Chandra N, Papadakis M, Sharma S. Cardiac adaptation in athletes of
black ethnicity: differentiating pathology from physiology. Heart.
2012;98:1194–200.
3. 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.
4. 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.
5. 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.
Fig. 3 The athlete’s ECG 6weeks after resuming his training, with reappearance of the biphasic Twaves in lead II and inverted Twaves in leads aVF and V2-6
Neth Heart J (2014) 22:523–526 525
6. Basavarajaiah S, Boraita A, Whyte G, et al. Ethnic differences in left
ventricular remodelling in highly-trained athletes: relevance to
differentiating physiologic left ventricular hypertrophy from
hypertrophic cardiomyopathy. J Am Coll Cardiol. 2008;51:
2256–62.
7. 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.
8. Burke AP, Farb A, Virmani R, Goodin J, Smialek JE. Sports-related
and non-sports-related sudden cardiac death in young adults. Am
Heart J. 1991;121:568–75.
9. Maron BJ, Doerer JJ, Haas TS, Tierney DM, Mueller FO. Sudden
deaths in young competitive athletes. Analysis of 1866 deaths in the
United States, 1980–2006. Circulation. 2009;119:1085–92.
10. Drezner JA, Fischbach P, Froelicher V, et al. Normal
electrocardiographic findings: recognising physiological adaptations
in athletes. Br J Sports Med. 2013;47:125–36.
11. Madias JE. Electrocardiogram in apical hypertrophic
cardiomyopathy with a speculation as to the mechanism of its
features. Neth Heart J. 2013;21:268–71.
12. Van Rijsingen IA, Bekkers SC, Schalla S, et al. Exercise related
ventricular arrhythmias are related to cardiac fibrosis in hypertrophic
cardiomyopathy mutation carriers. Neth Heart J. 2011;19:168–74.
13. Whyte G, Somauroo J, Wilson M, Sharma S. T-wave inversions and
the role of de-training in the differentiation of athlete's heart from
pathology: is 6 months too long? BMJ Case Rep. 2012.
14. Ghani S, Sharma S. Electrocardiographic changes in an athlete before
and after detraining. BMJ Case Rep. 2012.
526 Neth Heart J (2014) 22:523–526


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Recurrent repolarisation abnormalities in an athlete.

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