ESC Report Recommendations for interpretation of 12-lead electrocardiogram in the athlete

17 Pages·0.999 MB·English

ESC REPORT
EuropeanHeartJournal(2010)31,243–259
doi:10.1093/eurheartj/ehp473
Recommendations for interpretation of 12-lead
electrocardiogram in the athlete
Domenico Corrado1*, Antonio Pelliccia2, Hein Heidbuchel3, Sanjay Sharma4,
Mark Link5, Cristina Basso6, Alessandro Biffi2, Gianfranco Buja1, Pietro Delise7,
Ihor Gussac8, Aris Anastasakis9, Mats Borjesson10, Hans Halvor Bjørnstad11,
Franc¸ois Carre`12, Asterios Deligiannis13, Dorian Dugmore14, Robert Fagard3,
Jan Hoogsteen15, Klaus P. Mellwig16, Nicole Panhuyzen-Goedkoop17, Erik Solberg18,
Luc Vanhees3, Jonathan Drezner19, N.A. Mark Estes, III5, Sabino Iliceto1,
Barry J. Maron20, Roberto Peidro21, Peter J. Schwartz22, Ricardo Stein23, Do
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Gaetano Thiene6, Paolo Zeppilli24, and William J. McKenna25 on behalf of the nlo
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Sections of Sports Cardiology of the European Association of Cardiovascular ed
Prevention and Rehabilitation; and the Working Group of Myocardial and Pericardial from
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Disease of the European Society of Cardiology ttp
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1DepartmentofCardiac,ThoracicandVascularSciences,UniversityofPaduaMedicalSchool,ViaGiustiniani,2,Padova35121,Italy;2InstituteforSportsSciences,Rome,Italy; rh
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D3CiaagrndoiosvtiacscSucliaernRceesh,aUbinliitvaetriosintyUonfitP,aKdUuaL,ePuavdeuna,,LIetaulvye;n7C,BiveillgHiuoms;p4iKtailn,gC’soCneogllleiagneoH,Iotasplyi;ta8lU,Lnoivnedrosinty,UoKf;M5NedeicwinEenagnladndDMenetdisictrayl,CReWntJerM,BedoisctaolnS,cMhoAo,lU,NSAe;w6DBerupnarstwmicekn,tNoJf,MUeSdAic;al- artj.o
9DivisionofInheritedCardiovascularDiseases,UniversityofAthens,Greece;10DepartmentofMedicine,SahlgrensUniversityHospital/O¨stra,Gothenburg,Sweden;11Department xfo
HeartDisease,HaukelandUniversityHospital,Bergen,Norway;12SportMedicine,UniversityofRennes,Rennes,France;13SportsMedicine,AristotleUniversity,Thessaloniki, rd
Greece;14WellnessMedicalCenter,Stockport,UK;15DepartmentofCardiology,MaximaMedicalCentre,Veldhoven,Netherlands;16HeartCenterNRW,UniversityHospital,Bad jou
Oeynhausen,Germany;17DepartmentCardiology,Nijmegen,TheNetherlands;18DepartmentofMedicine,DiakonhjemmetHospital,Oslo,Norway;19DepartmentofFamily rn
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Medicine,UniversityofWashington,Seattle,WA,USA;20HypertrophicCardiomyopathyCenter,MinneapolisHeartInstituteFoundation,Minneapolis,MN,USA;21Favaloro ls
Foundation,BuenosAires,Argentina;22DepartmentofCardiology,FondazioneIRCCSPoliclinico,SanMatteo,Pavia;23ExercisePathophysiologyResearchLaboratory,Hospitalde .org
ClinicasPortoAlegre,PortoAlegre,Brazil;24SportsMedicineDepartment,InstituteofInternalMedicineandGeriatrics,CatholicUniversityofSacredHeart,Rome,Italy;and25The b/
HeartHospital,UniversityCollegeofLondon,London,UK y g
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Received20July2009;revised22September2009;accepted4October2009;onlinepublish-ahead-of-print20November2009 st o
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CardiovascularremodellingintheconditionedathleteisfrequentlyassociatedwithphysiologicalECGchanges.Abnormalities,however,may 2
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bedetectedwhichrepresentexpressionofanunderlyingheartdiseasethatputstheathleteatriskofarrhythmiccardiacarrestduringsports. , 2
0
It is mandatory that ECG changes resulting from intensive physical training are distinguished from abnormalities which reflect a potential 13
cardiacpathology.Thepresentarticlerepresentstheconsensusstatementofaninternationalpanelofcardiologistsandsportsmedicalphys-
icians with expertise in the fields of electrocardiography, imaging, inherited cardiovascular disease, cardiovascular pathology, and manage-
ment of young competitive athletes. The document provides cardiologists and sports medical physicians with a modern approach to
correct interpretation of 12-lead ECG in the athlete and emerging understanding of incomplete penetrance of inherited cardiovascular
disease. When the ECG of an athlete is examined, the main objective is to distinguish between physiological patterns that should cause
noalarmandthosethatrequireactionand/oradditionaltestingtoexclude(orconfirm)thesuspicionofanunderlyingcardiovascularcon-
ditioncarryingtheriskofsuddendeathduringsports.Theaimofthepresentpositionpaperistoprovideaframeworkforthisdistinction.
ForeveryECGabnormality,thedocumentfocusesontheensuingclinicalwork-uprequiredfordifferentialdiagnosisandclinicalassessment.
Whenappropriatethereferral optionsforrisk stratification andcardiovascularmanagement oftheathleteare brieflyaddressed.
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Keywords Athlete’s heart † Cardiomyopathy † Electrocardiogram † Ion-channeldisease † Sudden death † Ventricular
fibrillation † Ventricular tachycardia
*Correspondingauthor.Tel:þ39498212458,Fax:þ39498212309,Email:[email protected]
PublishedonbehalfoftheEuropeanSocietyofCardiology.Allrightsreserved.&TheAuthor2009.Forpermissionspleaseemail:[email protected].
244 D.Corradoetal.
Introduction arrhythmias which usually have ECG changes as their initial
presentation.26,27
Regularsportsparticipationisencouragedbythemedicalcommu- The present document is endorsed by the Sections of Sports
nity as part of cardiovascular prevention measures, because it Cardiology and Exercise Physiology of the European Association
improves fitness and reduces cardiovascular morbidity and mor- of Cardiovascular Prevention and Rehabilitation and by the
tality worldwide.1,2 A large proportion of the young population Working Group on Myocardial and Pericardial diseases of the
participates in competitive or recreational sports activity. The EuropeanSocietyofCardiologyandrepresentsthepositionstate-
12-lead electrocardiogram (ECG) is an established tool in the mentofaninternationalpanelofcardiologistsandsportsmedical
evaluationofathletes,providingimportantdiagnosticandprognos- doctors with expertise in thefield ofcardiovascularevaluation of
tic information on a variety of cardiovascular diseases which are young competitive athletes. The article provides a modern
associated with an increased risk of sudden cardiac death (SCD) approach to interpretation of 12-lead ECG in the athlete based
during sports. Physicians are frequently asked to interpret an on recently published new findings. The target audience are pri-
ECG in the setting of cardiovascular evaluation of athletes. Stan- marilysportsmedicaldoctors,sportscardiologists,andteamphys-
dard criteria for defining the limits of normal (or variation of icians.Themainobjectiveistodifferentiatebetweenphysiological
normal) ECG in the athlete remain to be determined. The adaptive ECG changes and pathological ECG abnormalities, with
interpretationoftheathlete’sECGisoftenlefttopersonalexperi- the aim to prevent adaptive changes in the athlete being erro-
enceandusuallymadeaccordingtotraditionalECGcriteriausedin neouslyattributedtoheartdisease,orsignsoflife-threateningcar-
the general (non-athletic) population. diovascular conditions being dismissed as normal variants of D
Electrocardiogramchanges in athletes are common and usually athlete’s heart. Because only pathological ECG abnormalities ow
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reflectstructuralandelectricalremodellingoftheheartasanadap- cause alarm and require action with additional testing to exclude lo
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tation to regular physical training (athlete’s heart).3–10 However, (or confirm) the suspect of a lethal cardiovascular disorder, de
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abnormalitiesofathlete’sECGmaybeanexpressionofanunder- appropriate interpretation of an athlete’s ECG also results in a fro
lying heart diseasewhich carries a risk of SCD during sport.11–13 considerablecostsavingsinthecontextofapopulation-basedpre- hm
It is important that ECG abnormalities resulting from intensive participationscreeningprogram.17 ttp
physicaltrainingandthosepotentiallyassociatedwithanincreased Thedocumentprovidesguidedclinicalevaluationoftheathletes ://eu
cardiovascular risk are correctly distinguished.14–17 with ECG abnormalities. For every ECG abnormality, the docu- rhe
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Errors in differentiating between physiological and pathological mentfocusesontherecommendedclinicalwork-upfordifferential rtj.o
ECG abnormalities may have serious consequences. Athletes diagnosis and clinical assessment. When indicated the referral xfo
may undergo expensive diagnostic work-up or may be unnecess- options for risk stratification and cardiovascular management are rdjo
arily disqualified fromcompetition forchangesthatfall within the brieflyaddressed, although for moredetailed andelaborated rec- urn
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normal range for athletes. This is of particular relevance for pro- ommendations concerning eligibility for sports participation we ls
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fessional athletes in whom disqualification from competitive refer to other specific guidelines.28–32 The document is also rg
sports has significant financial and psychological consequences. aimed to update general cardiologists and sports medical phys- by/
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Alternatively, signs of potentially lethal cardiovascular disorders icians with the clinically relevant information which can be ue
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may be misinterpreted as normal variants of an athlete’s ECG. obtained from ECGinthe athlete. t o
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A correct evaluation of 12-lead ECG patterns in the athlete M
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and appropriate subsequent action has the potential to increase rc
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efficacy,accuracy,andcost-effectivenessofathlete’scardiovascular 2
Physiological vs. potentially 4
evaluation.17–21 , 2
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malignant electrocardiogram 1
Some consider that physiological ECG changes overlap signifi- 3
cantlywithECGabnormalitiesseeninthecardiovasculardiseases changes
whichcauseSCDintheyoung.14–16TheECGhasthereforebeen
considered a non-specific and non-cost-effective tool for cardio- Theathlete’sECGchangesaredividedintotwogroups:common
vascular evaluation of athletes because of a presumed high level and training-related (Group 1) or uncommon and
of false-positive results. This concept was based on few studies training-unrelated(Group2).Thisclassificationisbasedonpreva-
of small and selected series of highly trained athletes from a lence, relation to exercise training, association with an increased
limitednumberofsportsdisciplines.The25-yearItalianexperience cardiovascular risk, and need for further clinical investigation to
with universal pre-participation screening has offered the unique confirm (or exclude) an underlying cardiovascular disease
opportunity to investigate ECG changes in large cohorts of (Table 1).
athletes, engaged in a broad variety of sports activities with Trained athletes commonly (up to 80%) show ECG changes
differentandwell-characterizedlevelsoftrainingandfitness.22–25 such as sinus bradycardia, first-degree atrioventricular (AV)
The currently available data allow an accurate redefinition of block, and early repolarization, which result from physiological
the spectrum of athlete’s ECG patterns and raise the need for adaptation of the cardiac autonomic nervous system to athletic
a revision of accuracy, utility, and cost–benefit analysis of the conditioning, e.g. increased vagal tone and/or withdrawal of sym-
use of ECG in the cardiovascular evaluation of the athlete. pathetic activity. The ECGs of trained athletes often exhibit pure
In addition, there is growing experience of early and incomplete voltagecriteria(i.e.basedonlyonQRSamplitudemeasurements)
disease expression of the inherited cardiomyopathies and for left ventricular (LV) hypertrophy thatreflect the physiological
Interpretationof12-leadECGintheathlete 245
regard,genotypeanddifferentpolymorphismsoftheangiotensin-
Table1 Classificationofabnormalitiesoftheathlete’s
converting enzymeorangiotensinogengenes have been reported
electrocardiogram
to result in different phenotypic expression in athletes’
hearts.36,37Unlikemaleathleteswhomostcommonlyshowabnor-
Group1:commonand Group2:uncommonand
training-relatedECG training-unrelatedECG malECGpatterns,femaleathletesusuallyhavenormalorvirtually
changes changes normalECGs.24
................................................................................
The higher prevalence of normal ECG patterns in female ath-
Sinusbradycardia T-waveinversion
letesislikelyduetoseveralfactors,includingthemildmorphologi-
First-degreeAVblock ST-segmentdepression
cal LV changes induced by training in women and their lower
IncompleteRBBB PathologicalQ-waves
participation rates in certain disciplines (such as rowing/canoeing)
Earlyrepolarization Leftatrialenlargement that have a substantial impact on ECG pattern.24 Black athletes
IsolatedQRSvoltagecriteriafor Left-axisdeviation/leftanterior
have more prevalent and pronounced ECG changes, including
leftventricularhypertrophy hemiblock
voltage criteria for LV hypertrophy and early repolarization
Right-axisdeviation/leftposterior
changes which reflect the race-related greater magnitude of LV
hemiblock
hypertrophy and/or increased vagal sensitivity.34,35 Basavarajaiah
Rightventricularhypertrophy
et al. reported that approximately one-fifth of black athletes
Ventricularpre-excitation
exhibit LV wall thickness .12mm (compared with just 4% of
CompleteLBBBorRBBB
Long-orshort-QTinterval white athletes) and 3% of black athletes have substantial increase D
ofLV thickness (.15mm).35 ow
Brugada-likeearlyrepolarization n
Level and duration of training or competition, aerobic capacity lo
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RBBB,rightbundlebranchblock;LBBB,leftbundlebranchblock. and type of sports activity play a significant role as well. Partici- ed
pation in sports that require high endurance, such as cycling, fro
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cross-country skiing, and rowing/canoeing has been shown to be h
LsiVze.r7e–m9,1o4d–e1l7li,n24g,25w,3i3th increased LV wall thickness and chamber spihgnysifiioclaongtilcyalaEssCoGciactheadngweisthsuachhiagshesrinurastberaadnydcagrrdeiaatearndexintcernetasoef ttp://eu
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These physiological ECG changes should be clearly separated ofQRSvoltagescomparedwithparticipationinsportsthatrequire e
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from uncommon (,5%) and training-unrelated ECG patterns more strength and speed and relatively less endurance.24 This rtj.o
such as ST-T repolarization abnormalities, pathological Q-waves, seems to be related to the large cardiac output acquired during xfo
left-axis deviation, intraventricular conduction defects, ventricular endurance training, resulting in considerable cardiac remodelling rdjo
pre-excitation, longandshortQTinterval andBrugada-like repo- including increase in LV cardiac dimension and wall thickness.38 urn
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larizationchangeswhichmaybetheexpressionofunderlyingcar- As a corollary, to be considered as a physiological expression of ls
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diovascular disorders, notably inherited cardiomyopathies or the athlete’s heart, ECG changes such as sinus bradycardia, early rg
ion-channeldiseases whichmaypredisposeto SCD.14–17 repolarization pattern or increased QRS voltages should be con- by/
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ThisclassificationofECGabnormalitieshaspotentialfavourable sistent with the gender, age, and race as well as appropriate to ue
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effectsontheathlete’scardiovascularmanagementincludingclini- the level of training and type of sports. Moreover, these ECG t o
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cal diagnosis, risk stratification, and cost savings. Common ECG abnormalities should be interpreted in light of family background, M
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changes due to cardiac adaptation to physical exertion (Group 1) personal history with review of symptoms, and physical examin- rc
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should not cause alarm and the athlete should be allowed to ation of the athlete. In the presence of a positive family history, 24
participate in competitive sports without additional evaluation. symptoms or abnormal physical findings, otherwise physiological , 20
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Hence, in the absence of positive family history, symptoms or ECG changes may become clinically relevant and require clinical 3
abnormal physical findings further diagnostic work-up is only work-upto exclude a pathological basis.
needed for the subset of athletes with uncommon and not
Sinus bradycardia/arrhythmia
sports-related ECG changes, which potentially reflect an under-
lyingheartdiseasewith anincreasedriskof SCD(Group2). Resting sinus bradycardia, as defined by a heart rate less than
60b.p.m., is common in athletes, depending on the type of sport
and the level of training/competition.39–41 Heart rate is generally
Common and training-related
lowerinendurancesportssuchaslong-distancerunning,andinver-
electrocardiogram changes sely correlatewith the level-of-fitness of the individual athlete. In
highly trained athletes, marked bradycardia less than 30b.p.m.
The extent of cardiac morphological and electrical changes in andasymptomaticsinuspausesgreaterthan2sarenotuncommon
trained athletes varies with the athlete’s gender, race, during24hECG,particularlyduringsleep.Escapejunctionalbeats
level-of-fitness, and type of sport.24,25,34–37 Physiological ECG orrhythmsarerecordedinathleteswithmarkedbradycardiaand
abnormalities are more prevalent and significant in male athletes resultinfunctionalAVdissociation.Sinusbradycardiaiseasilyover-
and athletes of African/Caribbean descent, in whom genetic/ comewithexercise,suggestingthathighvagaltonecausesslowing
ethnicpredisposingfactorsaccountforamoreprominentcardio- ofthesino-atrialnode.However,itisnoteworthythatchemically
vascular remodelling, either structural or neuroautonomic, in denervatedheartsinathleteshavesignificantlylowerintrinsicheart
response to physical training and competition.24,34,35 In this rates than those of sedentary controls: this suggests that sinus
246 D.Corradoetal.
pacemaker cells are influenced by athletic conditioning indepen- LV hypertrophy differed with respect to the type of sports disci-
dent ofneural input.42 plineandwasmorefrequentinathletesengagedinendurancedis-
Sinusarrhythmiaisalsoreportedwithwidelyvaryingfrequency, ciplines,suchascycling,cross-countryskiing,androwing/canoeing.
from13to69%.39–41,43Suchvariationsareexplainedbytheindi- Increased QRS voltagewas also associated with male gender and
vidual athlete’s autonomic state and level-of-fitness, as well as by increased cardiac dimensions and wall thickness. No athletes
the definition of sinus arrhythmia used by the various authors. with isolated increase of QRS voltages had evidence of structural
Like bradycardia, sinus arrhythmia is believed to reflect an heart diseasesincluding hypertrophiccardiomyopathy(HCM).
increasedvagaltone. Non-voltage ECG criteria for LV hypertrophy such as atrial
enlargement,left-axisdeviation,a‘strain’patternofrepolarization,
Recommendation and delayed intrinsicoid deflection (which are incorporated into
Bradycardia isthe resultof a physiological adaptive change of the the Romhilt-Estes point score system) are not usually seen in
autonomic nervous system and reflects the level of athletic con- athletes.24,25,33TheseECGabnormalitiesraisesuspicionforunder-
ditioning. Only profound sinus bradycardia and/or marked sinus lying cardiac pathology e.g. HCM, aortic valve disease, hyperten-
arrhythmia (heart rate less than 30b.p.m. and/or pauses (cid:2)3s sion. On the other hand, an isolated increase of QRS voltages
during wake hours) need to be distinguished from sinus node (Sokolow–Lyon or Cornell criteria) is a very uncommon finding
disease. Sino-atrial node dysfunction can be reasonably excluded in HCM patients (see Non-voltage criteria for LV hypertrophy
by demonstrating that: (i) symptoms such as dizziness or section).
syncopeareabsent;(ii)heartratenormalizesduringexercise,sym-
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patheticmanoeuvresordrugs,withpreservationofmaximalheart Recommendation ow
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rate, and (iii) bradycardia reverses with training reduction or AthleteswhoshowpureQRSvoltagecriteriaforLVhypertrophy lo
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discontinuation. on 12-lead ECG do not require systematic echocardiographic e
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evaluation, unless they have relevant symptoms, a family history fro
Atrioventricular block m
of cardiovascular diseases, and/or SCD or non-voltage ECG cri- h
Fdiergstr-edeegArVeebAloVckblaorcekcaonmdmMoonbiintztrTayinpeedIa(tWhleetnekse,bbaecihn)gsperceosnednt- teriasuggestingpathological LV hypertrophy. ttp://eu
in (cid:2)35 and 10% of athlete’s ECGs, respectively.43–45 As with Incomplete right bundle branch block rhe
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sinusbradycardia,AVconductionslowingandblockaremediated The prevalence of incomplete right bundle branch block (RBBB) rtj.o
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by increasedparasympathetictoneand/or decreasedrestingsym- (QRS duration ,120ms) has been estimated to range from 35 fo
pathetic tone. Second-degree Mobitz Type II and third-degree to 50% in athletes compared with less than 10% in young, rdjo
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heart block are rare in the athlete and caution should be used in healthy controls.24,47,49–52 The ECG pattern is moreoften noted rn
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acceptingthesefindingsasnormaladaptivechangestotraining.30,43 in athletes engaged in endurance sports, with a striking male pre- ls.o
Recommendation pcoonndduecratinocne.dIetlahyasisbneoetnwsuitghginesttheedstpheactiathlizeerdigchotnvdeuncttriiocnulasrys(tRemV), byrg/
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Resolution of (asymptomatic) first- or second-degree AV block but is caused by the enlarged RV cavity size/increased cardiac ue
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with hyperventilation or exercise confirms its functional origin muscle mass and the resultant increased conduction time.49 The t o
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and excludes any pathological significance. In athletes with Type RBBB morphology has been shown to be reversible with M
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II second-degree (Mobitz Type II) and third-degree AV block, a deconditioning.52 rch
carefuldiagnostic evaluation is mandatoryand pacemaker implan- 2
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tationmaybe indicated. Recommendation , 20
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IncompleteRBBBdoesnotrequirefurtherevaluationinthepres- 3
Isolated increase of QRS voltages
enceofanegativefamily/personalhistoryandphysicalexamination.
Intensive athletic conditioning is associated with morphological BecauseincompleteRBBBisatypicalECGfindinginpatientswith
cardiac changes, including increased cavity dimensions, wall thick- an ‘ostium secundum’ atrial septal defect, symptoms and a fixed
ness, and ventricular mass, which are reflected on the 12-lead split of the second heart sound on auscultation should be
ECG.3–6 Physiological LV hypertrophy in trained athletes usually excluded.
manifests as an isolated increase of QRS amplitude, with normal ‘Typical’ incomplete RBBB is uncommon in patients with
QRS axis, normal atrial and ventricular activation patterns, and arrhythmogenic RV cardiomyopathy (ARVC).53 Arrhythmogenic
normal ST-segment T-wave repolarization.14,24,33,41,43,46–48 A RV cardiomyopathy should be suspected when the pattern of
highprevalenceofECGsthatfulfilSokolow–Lyonvoltagecriteria incomplete RBBB is associated with T-wave inversion extending
forLVhypertrophyhasbeenconsistentlyreportedintrainedath- beyondV2toincludeleadsV3andV4orinthepresenceofpre-
letes.24,33,45 Pelliccia et al.24 assessed the prevalence and type of mature ventricular beats with a left bundle branch block (LBBB)
ECG abnormalities in 1005 elite Italian athletes, aged 24+6 morphology.
years, 75% male who participated in 38 sporting disciplines. They Insomecases,incompleteRBBBshouldbedifferentiatedfroma
correlated ECG changes with cardiac morphology assessed by Brugada-ECGwhichischaracterizedbyaslow,positivedeflection
echocardiography.TheECGwaslabelledas‘abnormal’in402ath- at the R-ST junction (‘J-wave’), which is most evident in leads V1
letes (40%), however, an isolated increase of QRS voltage and V2, with minimal or no reciprocal changes in other leads54
accounted for (cid:2)60% of such changes. The prevalence of voltage (Figure 1). Unlike the R0-wave seen in RBBB, the J-wave seen in
Interpretationof12-leadECGintheathlete 247
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Figure 1 (A) Borderline Brugada-ECG pattern mimicking incomplete RBBB. Unlike the ‘R-wave’ of RBBB, the ‘J-wave’ (arrows) of n
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Brugada-ECG is confined to right precordial leads (V1 and V2) without reciprocal ‘S-wave’ (of comparable voltage and duration) in the a
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leads L1 and V6 (arrowhead). (B) In this case, definitive diagnosis of Brugada ECG was achieved by a drug challenge with sodium channel ed
blockerswhichunmaskeddiagnostic‘covedtype’(arrows)pattern(V1andV2). fro
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Brugada syndrome does not indicate delayed RV activation, but differentiation from the Brugada-ECG (see Brugada-like ECG ://e
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reflects early repolarization with J-point elevation and a high abnormalities section).61,62 rhe
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take-off ST-segment. The downsloping ST-segment is followed The magnitude of ST-segment elevation is characteristically rtj.o
by a negative (‘coved’ type) or a positive (‘saddle-back’ type) modulatedbyautonomicinfluencesandheartratechangeswhich xfo
T-wave. In typical RBBB, the R0-wave recorded in V1 and V2 is explainthedynamicnatureoftheECGabnormalitieswithwaxing rd
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associated with a reciprocal S-wave in leads I and V6, and there andwaningoftheST-segmentandT-waveovertime.56–59Slowing urn
isnoST-segmentelevationintherightprecordialleads.55Differen- ofheartrateexaggeratesST-segmentelevation,whereassinustachy- als
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tial diagnosis may require a drug challenge with sodium channel cardiaoccurringduringexerciseorafterisoproterenolreducesand rg
blockers(Figure 1). ofteneliminatesearlyrepolarizationchanges.Earlyrepolarizationin by/
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athletesreflectsthedevelopmentofatraining-relatedhypervagoto- u
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nia, and ECG abnormalities are a reversible phenomenon which t o
Early repolarization reducesordisappearswithdeconditioning. n M
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Earlyrepolarizationhastraditionallybeenregardedasanidiopathic Recently,isolatedchangesofearlyrepolarizationininferiorand/ rc
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and benign ECG phenomenon, with an estimated prevalence in or lateral leads with terminal QRS slurring has been reported in 24
healthy young individuals of 1–2%, and a clear male preponder- patients with idiopathic ventricular fibrillation.63 The study was a , 20
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ance.56–59 The early repolarization ECG pattern is the rule retrospective analysis of a selected cohort with episodes of 3
rather than the exception among highly trained athletes, in shortcoupledrapid/polymorphicventriculartachycardiaorventri-
whom it is observed in 50–80% of resting ECGs.,60,61 The early cularfibrillationleadingtosyncopeorcardiacarrest.Theavailable
repolarization ECG shows elevation of the QRS–ST junction data do not support the view that in the general population of
(J-point)ofatleast0.1mVfrombaseline,associatedwithnotching asymptomatic young individuals or athletes this ECG pattern is
or slurring of the terminal QRS complex which may vary in predictiveofanincreasedriskofmalignantventriculararrhythmias.
location, morphology, and degree.58,59 These changes often are
localized in precordial leads, with the greatest ST-segment Recommendation
elevationinmid-to-lateralleads(V3–V4),butmaximalST-segment Early repolarization is a physiological and benign ECG pattern in
displacementmayalsobeseeninlateralleads(V5,V6,I,andaVL), the general population of young people and athletes and does
inferiorly (II, III, andaVF), oranteriorly (V2–V3).59,61,62 The most notrequirefurtherclinicalevaluation.
commonmorphologicalpatternseen inCaucasiansisanelevated InathletesofAfrican/CaribbeanoriginthepresenceofST-segment
ST-segment with an upward concavity, ending in a positive elevationfollowedbyT-waveinversionconfinedtoleadsV2–V4iscon-
(‘peaked and tall’) T-wave (Figure 2A). In athletes of African- sistentwithaphysiologicalearlyrepolarizationECGpattern(Figure3A).
Caribbean descent, however, the morphology is often different SuchadaptiveST-segmentandT-waverepolarizationchangescharac-
with anelevated ST-segment with anupward convexity, followed teristicallynormalizeduringexerciseoradrenergicstimulation.
by a negative T-wave (Figure 2B) in V2–V4. This pattern, with Intrainedathletes,rightprecordialST-Tchangesofearlyrepo-
the ‘domed’ morphology of the elevated ST-segment requires larization show typical features which permit differentiation from
248 D.Corradoetal.
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Figure 2 Different patterns of precordial early repolarization in two healthy athletes. (A) ST-segment elevation with upward concavity gu
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(arrows), followed by a positive T-wave (arrowheads). (B) ST-segment elevation with upward convexity (arrows), followed by a negative st o
T-wave(arrowheads). n M
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ARVC (Figure 3B) and Brugada syndrome (Figure 1).61,62,64,65 25-year Italian screening experience has demonstrated that , 20
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Rarely, athletes may require pharmacological testing with sodium 12-lead ECG has a substantial incremental value over and above 3
channel blocking agents, electrophysiological study, or cardiac historyandphysicalexaminationforidentifyingasymptomaticath-
imaging to exclude orconfirmunderlyingpathologyandrisk. letes who have potentially lethal heart disorders.17–23,66–69
Inathletespresentingwithsyncopeorcardiacarrest,whichremain Electrocardiogram-detectable cardiovascular diseases include car-
unexplainedafteradetailedclinicalwork-upaimedtoexcludecardiac diomyopathies,suchasHCM,ARVC,anddilatedcardiomyopathy;
causes and neuromediated mechanisms, the ECG pattern of early aorticvalvestenosis;cardiacion-channeldiseasessuchaslong-QT
repolarization in inferior and/or lateral leads, particularly when syndrome(LQTS),Brugadasyndrome,short-QTsyndrome(SQTS),
associatedwithaprominentterminalQRSslurring,shouldraisethe and Lene`gre disease; and Wolff–Parkinson–White (WPW) syn-
suspectofanunderlyingidiopathicventricularfibrillation.63 drome. On the basis of published series from the USA and Italy,
these conditions account for approximately two-thirds of SCD in
young competitive athletes.26,27 Electrocardiogram abnormalities
Uncommon and
associatedwiththesecardiovasculardiseasesincluderepolarization
training-unrelated
abnormalitiessuchasinvertedT-wavesandST-segmentdepression,
electrocardiogram changes pathological Q-waves, conduction disease including left-axis devi-
ation, ventricular pre-excitation, long- and short-QT interval, and
MostcardiovascularconditionsresponsibleforSCDinyoungcom- Brugada-likerepolarizationchanges(Table1).
petitiveathletesareclinicallysilentandunlikelytobesuspectedor Unlike the ECG changes characteristic of athlete’s heart,
diagnosed on the basis of spontaneous symptoms.11–13 The such ECG abnormalities are relatively uncommon (,5%) and
Interpretationof12-leadECGintheathlete 249
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4
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Figure3 (A)EarlyrepolarizationpatterninahealthyblackathletecharacterizedbyrightprecordialT-waveinversion(arrowhead)preceded 3
byST-segmentelevation(arrow).(B)RightprecordialT-waveinversioninapatientwithARVC.Notethatunlikeearlyrepolarization,inthe
ARVCtherightprecordialleadsdonotdemonstrateanyelevationoftheST-segment.
training-unrelated. Further diagnostic work-up is mandatory for is often in the differential diagnosis with adaptive changes of ath-
those athletes who exhibit such ECG changes in order to lete’sheart.AnisolatedQRSvoltagecriterionforLVhypertrophy
confirm(orexclude) anunderlyingcardiovascular disease. (Sokolow–Lyon or Cornell criteria) is a very unusual pattern
(1.9%) in HCM patients in whom pathological LV hypertrophy is
characteristically associated with one or more additional non-
Non-voltage criteria for left ventricular
voltage criteria such as left atrial enlargement, left-axis deviation,
hypertrophy
delayedintrinsicoiddeflection,ST-segmentandT-waveabnormal-
Electrocardiogram offers the potential to distinguish between ities, andpathological Q-waves (Figure4).70–72
pathological and physiological hypertrophy, given that ECG
abnormalities of structural heart diseases manifesting with LV Recommendation
hypertrophy, such as cardiomyopathies, valve diseases, or hyper- Regardlessoffamilyandpersonalhistory,athleteswithnon-voltage
tensive heart disease overlap only marginally with training-related criteria for LV hypertrophy require an echocardiographic evalu-
ECG changes. HCM is the leading cause of SCD in apparently ation in order to exclude underlying structural heart disease and
healthycompetitiveathletesagelessthan35years.Thiscondition pathological LV hypertrophy.
250 D.Corradoetal.
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Figure4 Twelve-leadECGofanasymptomaticathletewithHCM.Thediseasewassuspectedatpre-participationevaluationthankstoECG ls.o
abnormalitiesconsistingofincreasedQRSvoltagesandinvertedT-wavesinlateralleads.HCMwasdiagnosedbyechocardiographyafterwards. brg/
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ST-segment depression the Sokolow voltage criterion for RV hypertrophy was reported t o
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by Sharma et al.33 among junior elite athletes (12%), although M
Although ST-segment elevation due to early repolarization is a
a
common finding in the basal ECG of trained athletes, resting therewasnoadifferencewithcontrols(10%).Indeed,asignificant rch
ST-segment depression is rarely observed.14–16 In the literature, proportionofathletesandnon-athletesinthisstudywereyounger 24
than 16 years, and in such age-group a voltage criterion for RV , 2
ST-segment depression is usually lumped together with T-wave 0
1
hypertrophyis more common. 3
inversion, making the real incidence of isolated ST-segment
depressionunknown.14
Recommendation
Though uncommon, if present the ECG pattern of atrial enlarge-
Recommendation
mentand/orRVhypertrophyshouldnotbeinterpretedasamani-
Demonstration of ST-segment depression on resting ECG, either
festationofexercise-inducedcardiacremodelling.Thepresenceof
isolated or associated with T-wave inversion, should prompt
either congenital or acquired heart diseases associated with an
further investigationstoexclude heart disease.
increased right atrial size and/or pathological RV dilatation/
hypertrophyshouldbe excluded.
Right atrial enlargement and right
ventricular hypertrophy T-wave inversion
Electrocardiogramevidence ofright atrial enlargement and/or RV Recent studies on large athletic populations disproved the tra-
hypertrophy are uncommon findings in athletes. Pelliccia et al.24 ditional idea that T-wave inversions are common and
reported a prevalence of 0.08% for right atrial enlargement and training-related ECG changes in the athlete. Pelliccia et al.24
0.6% for a right-axis deviation (.1108) among a large cohort of reported a 2.7% prevalence of T-wave inversion in 1005 highly
highly conditioned athletes. Sokolow–Lyon voltage criteria for trained athletes and 2.3% in a large population of 32652 young
RV hypertrophy (R2VIþS2V5.10.5mm) were seen in one of amateur athletes. Moreover, Sharma et al.33 reported that the
172 (0.6%) professional soccer players.73 A higher prevalence of prevalence of T-wave inversion is similar among elite athletes
Interpretationof12-leadECGintheathlete 251
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Figure5 Twelve-leadECGinanasymptomaticathletewithARVC.Theathletewasreferredforfurtherechocardiographicexaminationand rh
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cinafredriiaocrmanadgnaenttiecrroesseopntaanlcleeadbsecaanudseloowfQECRGSvaoblntoagremsailnitiethsefopuenridphaetrparlele-paadrst.icipationevaluation which consisted ofinverted T-wavesin the artj.o
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andsedentarycontrols(4.4vs.4.0%,respectively).Thepresenceof Inverted T-waves may represent the only sign of an inherited rn
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T-wave inversion (cid:2)2mm in two or more adjacent leads in an heartmusclediseaseevenintheabsenceofanyotherfeaturesor ls
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athleteisa non-specificwarningsignofa potentialcardiovascular beforestructuralchangesintheheartcanbedetected.Hence,the rg
b/
disease at risk of SCD during sports. T-wave inversion in inferior perspective that T-wave inversion is due to cardiovascular adap- y
g
(II,III,aVF)and/orlateral(I,aVL,V5–V6)leadsmustraisethesus- tationtophysicalexerciseshouldonlybeacceptedonceinherited ue
s
picion of ischaemic heart disease, cardiomyopathy, aortic valve formsofcardiovasculardiseasehavebeendefinitivelyexcludedby t o
n
disease, systemic hypertension, and LV non-compaction.24,67,74 a comprehensive clinical work-up, including family evaluation, and M
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The post-pubertal persistence of T-wave inversion beyond V1 mutationanalysiswhenavailable/appropriate.Inthisregard,athletes rc
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may reflect an underlying congenital heart disease leading to a with post-pubertal persistence of T-wave inversion beyond V1 24
RV volume or pressure overload state, ARVC, and uncommonly, require further clinical and echocardiographic evaluation to , 20
1
an inherited ion-channel disease. Recent studies showed that exclude an underlying cardiomyopathy such as ARVC or HCM. 3
T-wave inversion beyond V1 is seen in post-pubertal athletes TherecentobservationthatT-waveinversionmayidentifyathletes
less commonly than previously thought (,1.5%), but deserves at risk for subsequent development of structural heart disease,
special consideration because it may reflect underlying ARVC underscorestheimportanceofcontinuedclinicalsurveillanceand
(Figure5).75,76 follow-up by serial ECG and echocardiography evaluations of
T-wave inversion in young and apparently healthyathletes may trained athletes withT-waverepolarization abnormalities, evenin
representtheinitialphenotypicexpressionofanunderlyingcardi- theabsenceofclinicallydemonstrableheartdisease.74
omyopathy, prior to the development of morphological changes InhealthyathletesofAfrican/Caribbeanorigin,invertedT-waves,
detectable on cardiac imaging.77 Thus, failure to detect structural usuallyprecededbyST-segmentelevation,arecommonlyobserved
abnormalities on imaging does not exclude underlying heart inleadsV2–V4(upto25%ofcases)(Figure3A)andrepresentadap-
muscle disease, as this may only become evident over time, but tiveearlyrepolarizationchangeswhichnormalizeduringexerciseor
may nonetheless be associated with risk of sudden cardiac adrenergic stimulation.35 On the contrary, T-wave inversion in
death.74,77 inferior(L2,L3,aVF)and/orlateralleads(L1,aVL,V5,andV6)are
uncommoneveninblackathletesandwarrantfurtherinvestigation
Recommendation forexcludinganunderlyingheartdisease.
T-wave inversion (cid:2)2mm in two ormoreadjacent leads is rarely The significance of minor T-wave changes such as flat and/or
observedontheECGofhealthyathletes,whereasitisacommon minimally inverted (,2mm) T-waves in two or more leads
findinginpatientswithcardiomyopathyandothercardiacdisease. (mostly inferior and/or lateral) is unclear. These changes usually
252 D.Corradoetal.
reverttonormalwithexerciseandinthissettingmaybeabenign left anterior hemiblock, or RBBB and left posterior hemiblock)
phenomenon resulting from increased vagal tone. Like deep to exclude a genetically determined progressive cardiac conduc-
inverted T-waves, minor T-wave abnormalities are infrequently tion disease (Le`negre disease).84 Le`negre disease is an autosomal
encountered in the athlete heart (,0.5%),33 but are common in dominant condition that has been linked to mutations of the
cardiomyopathy. This indicates that they may have a pathological SCN5Agenewhichencodesforcardiacsodiumionchannels.Clini-
basis and should be investigated and followed-up over time cal phenotype consists of various combinations of conduction
before they are definitively ascribed to physiological defects or AV block which characteristically occur in young
neuro-autonomic remodelling. individuals.
Intraventricular conduction
Non-specific intraventricular conduction
abnormalities
defects
Complete bundle branch block (QRS duration (cid:2)120ms), and
hemiblocks are uncommon in athletes (,2% of athlete’s ECGs) AprolongedQRS (.110ms)notsatisfying thecriteriaforeither
andrepresenta potentialmarkerofseriousunderlyingcardiovas- LBBB or RBBB is referred to as non-specific intraventricular con-
culardisease.78–81TheprevalenceofcompleteRBBBandLBBBis duction disturbance.85 Because the conduction delay occurs in
low in the general population, particularly in the younger age theventricularmyocardiumratherthaninthespecializedconduc-
groups, occurring in (cid:2)0.6% of males and 0.3% of females, age tion system, this conduction defect is a particular indicator of a
less than 40 years. A comparable incidence of either complete possible heart muscle disease and requires further cardiovascular D
o
LBBB or RBBB has been reported by Pelliccia et al.24 in large investigation. For instance, localized prolongation of the QRS w
n
athletic population of highly trained competitors (0.4%) and complex (.110ms) in the right precorial leads (V1–V3), often loa
d
amateurathletes ((cid:3)1%). associated with an ‘epsilon wave’ (i.e. a terminal notch in the ed
Bundlebranchblockmaydevelopasaconsequenceofaprimary QRS complex) and/or delayed S-wave upstroke, is an ECG fro
m
degenerativelesionofthespecializedconductingtissueorfroma markerfor ARVC(Figure 6). h
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variety of cardiac pathologies, e.g. ischaemic and hypertensive ://e
heart disease, cardiomyopathies, myocarditis, channelopathies, u
Ventricular pre-excitation (Wolff– rh
cardiac tumours, sarcoidosis, Chagas’ disease, and unoperated ea
and operated congenital heart disease.78–81 Complete RBBB is Parkinson–White) rtj.o
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uncommon in healthy individuals/athletes and may represent an The prevalence of ventricular pre-excitation in the general popu- fo
idiopathic, isolated and clinically benign conduction interruption/ lationvariesfrom0.1to0.3%andissimilarinathletes.86Mostindi- rdjo
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delay through the right bundle branch, whereas LBBB is very vidualswithWPWpre-excitationsyndromeremainasymptomatic rn
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rare in otherwise healthy individuals.82,83 This latter conduction throughouttheirlives.Whensymptomsdooccur,theyareusually ls.o
disturbanceisastrongECGmarkerofanunderlyingstructuralcar- secondary to reciprocating supraventricular tachycardia which brg/
diovasculardisorderandmayoccurasanearlyandisolatedmani- causes disabling symptoms. The WPW patients, however, may y g
festationofischaemicheartdiseaseorcardiomyopathy,manyyears also develop other arrhythmias such as atrial fibrillation, which ue
s
beforestructuralchangesintheLVcanbedetected.Intermittent, could degenerate intoventricular fibrillation and SCD, as a result t on
rate-dependentLBBBmayoccurasaprecursorand,thus,havethe of rapid conduction over an AV accessory pathway with a short- M
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same clinicalandprognosticsignificance ofstableLBBB. anterograderefractory period.87 Theriskof SCD associated with rch
Leftanteriorhemiblockismorecommoninmenandincreases ventricular pre-excitation is (cid:2)0.15% per year in asymptomatic 24
in frequency with advancing age. The estimated prevalence in the individuals and 0.25% per year in symptomatic patients.88–90 It , 20
1
general population (age less than 40 years) is 0.5–1.0%, a figure has been estimated that one-third of patients with WPW syn- 3
similar to that reported in the athletic population.24,81 Although drome may develop atrial fibrillation. Exercise has been reported
isolated left anterior hemiblock is usually an incidental ECG to be associated with an increased risk of developing ventricular
finding in subjects without evidence of structural heart disease, fibrillation.84 Moreover, athletes may have an increased risk of
the association with a variety of cardiovascular disorders has AF even after they have ceased high-level sports competition.
been reported. Isolated left posterior hemiblock is a very rare Therefore, sports activity may expose an athlete with ventricular
finding, being usually associated with RBBB. Combinations of pre-excitationtoincreasedriskofSCD.13,30
bundlebranchblockandhemiblockreflectamoreextensiveinvol- Recent studies have indicated that WPW syndrome rarely is
vement of the specialized conduction system and carry an genetically determined. Pathogeneticmutations arelocatedin the
increasedriskofclinicallysignificantAV block.81 gene encoding for the regulatory g2-subunit (PRKAG2) of the
AMP-activatedproteinkinase.91FamilialWPWsyndromeisinher-
Recommendation itedasanautosomaldominanttractwithvariableclinicalexpressiv-
Demonstration of complete bundle branch block and/or hemi- ity. The clinical phenotype is characterized by the association
blockinanathleteshouldleadtoacardiologicalwork-upincluding between ventricular pre-excitation and progressive ventricular
exercise testing, 24h ECG, and imaging for the evaluation of hypertrophy. Supraventricular tachyarrhythmias, progressive AV
underlying pathologicalcauses. conduction disease and heart failure are common and there are
An ECG should be obtained in the siblings of a young athlete reports of associated skeletal muscle involvement.92 Clinical fea-
with an ECG pattern of bifascicular block (i.e. LBBB, RBBB and tures, biochemical studies, and experimental animal model