international recommendations for electrocardiographic...

International recommendations for

electrocardiographic interpretation in athletes

Sanjay Sharma1dagger Jonathan A Drezner2dagger Aaron Baggish3 Michael Papadakis1

Mathew G Wilson4 Jordan M Prutkin5 Andre La Gerche6 Michael J Ackerman7

Mats Borjesson8 Jack C Salerno9 Irfan M Asif10 David S Owens5

Eugene H Chung11 Michael S Emery12 Victor F Froelicher13 Hein Heidbuchel1415

Carmen Adamuz4 Chad A Asplund16 Gordon Cohen17 Kimberly G Harmon2

Joseph C Marek18 Silvana Molossi19 Josef Niebauer20 Hank F Pelto2

Marco V Perez21 Nathan R Riding4 Tess Saarel22 Christian M Schmied23

David M Shipon24 Ricardo Stein25 Victoria L Vetter26 Antonio Pelliccia27 and

Domenico Corrado28

1Cardiology Clinical Academic Group St Georgersquos University of London UK 2Department of Family Medicine University of Washington Seattle WA USA 3Division of CardiologyMassachusettes General Hospital MA USA 4Department of Sports Medicine ASPETAR Qatar Orthopaedic and Sports Medicine Hospital Qatar 5Division of Cardiology Universityof Washington Seattle WA USA 6Department of Cardiology Baker IDI Heart and Diabetes Institute Melbourne Australia 7Department of Cardiovascular Diseases Pediatric and AdolescentMedicine and Molecular Pharmacology and Experimental Therapeutics Mayo Clinic MN USA 8Department of Neuroscience and Physiology Sahlgrenska University HospitalOstraSahlgrenska Academy Goteborg Sweden 9Department of Pediatrics University of Washington Seattle WA USA 10Department of Family Medicine University of South Carolina GreenvilleSC USA 11Division of Cardiology University of North Carolina School of Medicine NC USA 12Center of Cardiovascular Care in Athletics Indiana University School of Medicine IN USA13Department of Medicine Stanford University CA USA 14Department of Cardiology Arrhythmology Hasselt University Hasselt Belgium 15Department of Cardiology Antwerp Belgium16Georgia Southern University GA USA 17Division of Pediatric Cardiothoracic Surgery University of California San Francisco School of Medicine CA USA 18Advocate Heart InstituteIllinois USA 19Division of Pediatric Cardiology Baylor College of Medicine TX USA 20University Institute of Sports Medicine Paracelsus Medical University Austria 21Center for InheritedCardiovascular Disease Stanford University CA USA 22Pediatric Cardiology Cleveland Clinic OH USA 23University of Herzzentrum Zurich Switzerland 24Heart Center ofPhiladelphia Jefferson University Hospitals PA USA 25Department of Cardiology Hospital de Clinicas de Porte Allegre Brazil 26The Childrenrsquos Hospital of Philadelphia PAUSA 27Institute of Sports Medicine and Science Rome Italy and 28Department of Cardiac Thoracic and Vascular Sciences University of Padua Medical School Italy

Received 17 May 2016 revised 11 July 2016 editorial decision 16 November 2016 accepted 8 December 2016

Sudden cardiac death (SCD) is the leading cause of mortality in athletes during sport A variety of mostly hereditary structural or electrical cardiacdisorders are associated with SCD in young athletes the majority of which can be identified or suggested by abnormalities on a resting 12-lead elec-trocardiogram (ECG) Whether used for diagnostic or screening purposes physicians responsible for the cardiovascular care of athletes should beknowledgeable and competent in ECG interpretation in athletes However in most countries a shortage of physician expertise limits wider applica-tion of the ECG in the care of the athlete A critical need exists for physician education in modern ECG interpretation that distinguishes normalphysiological adaptations in athletes from distinctly abnormal findings suggestive of underlying pathology Since the original 2010 European Society ofCardiology recommendations for ECG interpretation in athletes ECG standards have evolved quickly over the last decade pushed by a growingbody of scientific data that both tests proposed criteria sets and establishes new evidence to guide refinements On 26ndash27 February 2015 an inter-national group of experts in sports cardiology inherited cardiac disease and sports medicine convened in Seattle Washington to update contempo-rary standards for ECG interpretation in athletes The objective of the meeting was to define and revise ECG interpretation standards based on newand emerging research and to develop a clear guide to the proper evaluation of ECG abnormalities in athletes This statement represents an interna-tional consensus for ECG interpretation in athletes and provides expert opinion-based recommendations linking specific ECG abnormalities and thesecondary evaluation for conditions associated with SCD

The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology

Corresponding author Tel 00447930407772 Fax 00442082979100 Email sasharmasgulacukdaggerThe first two authors contributed equally to the study

VC The Author 2017 This article has been co-published in the European Heart Journal and the Journal of the American College of Cardiology An extended version of this articlehas also been jointly published in the British Journal of Sports Medicine

European Heart Journal (2017) 00 1ndash19 CURRENT OPINIONdoi101093eurheartjehw631

Introduction

Cardiovascular-related sudden death is the leading cause of mortality inathletes during sport and exercise1ndash3 The majority of disorders associ-ated with an increased risk of sudden cardiac death (SCD) are sug-gested or identified by abnormalities on a resting 12-lead ECGWhether used for the evaluation of cardiovascular-related symptomsa family history of inheritable cardiac disease or premature SCD or forscreening of asymptomatic athletes ECG interpretation is an essentialskill for all physicians involved in the cardiovascular care of athletes

The 2015 summit on ECG interpretationin athletesOver the last decade ECG interpretation standards have undergoneseveral modifications to improve the accuracy of detecting potentiallylife threatening cardiac conditions in young athletes while also limitingfalse positive results4ndash15 In February 2015 an international group ofexperts convened in Seattle Washington to update contemporaryrecommendations for ECG interpretation in asymptomatic athletesaged 12ndash35 years The goals of the summit meeting were to (i)update ECG interpretation standards based on new and emergingresearch and (ii) develop a clear guide to the appropriate evaluationof ECG abnormalities for conditions associated with SCD in athletesIn the presence of cardiac symptoms or a family history of inheritedcardiovascular disease or premature SCD a normal ECG should notpreclude further assessment

This document provides the most updated evidence-based recom-mendations developed with thoughtful attention to balance sensitivityand specificity while maintaining a clear and practical checklist of find-ings to guide ECG interpretation for physicians and the appropriateevaluation of ECG abnormalities A summary of the consensus rec-ommendations is presented in Figure 1 Tables 1 and 2

LimitationsWhile ECG increases the ability to detect underlying cardiovascularconditions associated with SCD ECG as a diagnostic tool has limitationsin both sensitivity and specificity Specifically ECG is unable to detectanomalous coronary arteries premature coronary atherosclerosis andaortopathies In some instances patients with cardiomyopathies particu-larly arrhythmogenic right ventricular cardiomyopathy (ARVC) mayalso reveal a normal ECG Thus an ECG will not detect all conditionspredisposing to SCD Furthermore inter-observer variability amongphysicians remains a major concern16ndash18 despite studies demonstratingthat using standardized criteria improves interpretation accuracy1920

Normal ECG findings in athletes

Physiological cardiac adaptations toregular exerciseRegular and long-term participation in intensive exercise (minimumof 4 h per week) is associated with unique electrical manifestations

Figure 1 International consensus standards for electrocardiographic interpretation in athletes AV atrioventriular block LBBB left bundle branchblock LVH left ventricular hypertrophy RBBB right bundle branch block RVH right ventricular hypertrophy PVC premature ventricular contrac-tion SCD sudden cardiac death

2 S Sharma et al

Table 1 International consensus standards for electrocardiographic interpretation in athletes definitions of ECGcriteria

Abnormal ECG findings in athletes

These ECG findings are unrelated to regular training or expected physiologic adaptation to exercise may suggest the presence of pathologic

cardiovascular disease and require further diagnostic investigation

ECG abnormality Definition

T wave inversionbull Anterior

bull Lateralbull Inferolateralbull Inferior

gt_ 1 mm in depth in two or more contiguous leads excludes leads aVR III and V1bull V2ndashV4

ndash excludes black athletes with J-point elevation and convex ST segment elevation followed by TWI

in V2ndashV4 athletes lt age 16 with TWI in V1-V3 and biphasic T waves in only V3bull I and AVL V5 andor V6 (only one lead of TWI required in V5 or V6)bull II and aVF V5-V6 I and AVLbull II and aVF

ST segment depression gt_ 05 mm in depth in two or more contiguous leads

Pathologic Q waves QR ratio gt_ 025 or gt_ 40 ms in duration in two or more leads (excluding III and aVR)

Complete left bundle branch block QRS gt_ 120 ms predominantly negative QRS complex in lead V1 (QS or rS) and upright notched or

slurred R wave in leads I and V6

Profound nonspecific intra-ventricular

conduction delay

Any QRS duration gt_ 140 ms

Epsilon wave Distinct low amplitude signal (small positive deflection or notch) between the end of the QRS complex

and onset of the T wave in leads V1-V3

Ventricular pre-excitation PR interval lt 120 ms with a delta wave (slurred upstroke in the QRS complex) and wide QRS (gt_

120 ms)

Prolonged QT intervala QTc gt_ 470 ms (male)

QTc gt_ 480 ms (female)

QTc gt_ 500 ms (marked QT prolongation)

Brugada Type 1 pattern Coved pattern initial ST elevation gt_ 2 mm (high take-off) with downsloping ST segment elevation fol-

lowed by a negative symmetric T wave in gt_ 1 leads in V1ndashV3

Profound sinus bradycardia lt 30 bpm or sinus pauses gt_ 3 sec

Profound 1 atrioventricular block gt_ 400 ms

Mobitz Type II 2 atrioventricular block Intermittently non-conducted P waves with a fixed PR interval

3 atrioventricular block Complete heart block

Atrial tachyarrhythmias Supraventricular tachycardia atrial fibrillation atrial flutter

PVC gt_ 2 PVCs per 10 s tracing

Ventricular arrhythmias Couplets triplets and non-sustained ventricular tachycardia

Borderline ECG findings in athletes

These ECG findings in isolation likely do not represent pathologic cardiovascular disease in athletes but the presence of two or more borderline

findings may warrant additional investigation until further data become available


Left axis deviation -30 to - 90

Left atrial enlargement Prolonged P wave duration of gt 120 ms in leads I or II with negative portion of the P wave gt_ 1 mm in

depth and gt_ 40 ms in duration in lead V1

Right axis deviation gt 120

Right atrial enlargement P wave gt_ 25 mm in II III or aVF

Complete right bundle branch block rSR0 pattern in lead V1 and a S wave wider than R wave in lead V6 with QRS duration gt_ 120 ms


These training-related ECG alterations are physiologic adaptations to regular exercise considered normal variants in athletes and do not require further

evaluation in asymptomatic athletes with no significant family history

Normal ECG finding Definition

Increased QRS voltage Isolated QRS voltage criteria for left (SV1 thorn RV5 or RV6 gt 35 mV) or right ventricular hypertrophy

(RV1 thorn SV5 or SV6 gt 11 mV)

Incomplete RBBB rSR0 pattern in lead V1 and a qRS pattern in lead V6 with QRS duration lt 120 ms

Continued

International recommendations for electrocardiographic interpretation 3

that reflect enlarged cardiac chamber size and increased vagal toneThese ECG findings in athletes are considered normal physiologicaladaptations to regular exercise and do not require further evaluation(Figure 1 Table 1)

Left and right ventricular hypertrophyThe presence of isolated QRS voltage criterion for left ventricularhypertrophy (LVH) (Figure 2) does not correlate with pathology inathletes and is present in isolation (without other associated ECGabnormalities) in less than 2 of patients with hypertrophic cardio-myopathy (HCM)21ndash27 Conversely pathological LVH is commonlyassociated with additional ECG features such as T-wave inversion(TWI) in the inferior and lateral leads ST segment depression andpathological Q waves2829 Therefore the isolated presence of highQRS voltages fulfilling voltage criterion for LVH in the absence ofother ECG or clinical markers suggestive of pathology are consideredpart of normal and training-related ECG changes in athletes and doesnot require further evaluation

Voltage criterion for right ventricular hypertrophy (RVH) is alsocommon in athletes with up to 13 of athletes fulfilling the SokolowndashLyon index3031 QRS voltages for RVH when present in isolation donot correlate with underlying pathology in athletes31 Similar to volt-age criteria for LVH isolated QRS voltage for RVH is part of the nor-mal spectrum of ECG findings in athletes and does not requirefurther evaluation

Early repolarizationEarly repolarization is defined as elevation of the QRS-ST junction (J-point) by gt_ 01 mV often associated with a late QRS slurring or notching(J wave) affecting the inferior andor lateral leads32ndash34 Early repolariza-tion is common in healthy populations (2ndash44) and is more prevalent inathletes young individuals males and black ethnicity3235ndash39 Early repo-larization consisting of J-point elevation with concave ST-segment eleva-tion and a peaked TWI (Figure 2) is present in up to 45 of Caucasian

athletes and 63ndash91 of black athletes of African-Caribbean descent(hereto referred to as lsquoblackrsquo athletes)2230

Some studies on survivors of cardiac arrest and patients with pri-mary ventricular fibrillation (VF) have suggested an associationbetween early repolarization and the risk of VF3340 Although furtherstudies are warranted to fully elucidate the mechanisms and prognos-tic implications of early repolarization in competitive athletes to datethere are no data to support an association between inferior earlyrepolarization and SCD in athletes Based on current evidence allpatterns of early repolarization when present in isolation and with-out clinical markers of pathology should be considered benign var-iants in athletes41

Repolarization findings in black athletesEthnicity is a major determinant of cardiac adaptation to exercisewith more than two-thirds of black athletes exhibiting repolarizationchanges29304243 Black athletes also commonly demonstrate a repo-larization variant consisting of J-point elevation and convex ST seg-ment elevation in the anterior leads (V1ndashV4) followed by TWI(Figure 3 and Figure 4B and C) which is regarded as a normal variantand should not result in further investigation in the absence of otherclinical or ECG features of cardiomyopathy3042ndash44

Considerations in athletes age 12ndash16years the lsquojuvenilersquo electrocardiogrampatternTWI confined to the anterior precordial leads may be considered anormal age-related pattern in adolescent athletes up to the age of 16years old The term lsquojuvenilersquo ECG pattern is used to denote TWI ora biphasic T wave beyond lead V2 in adolescents who have notreached physical maturity and is present in 10ndash15 of white adoles-cent athletes aged 12 years old but only in 25 of white athletesaged 14ndash15 years (Figure 4A)224546 Anterior TWI that extendsbeyond lead V2 is rare (01) in white athletes aged gt_ 16 years or

Early repolarization J point elevation ST elevation J waves or terminal QRS slurring in the inferior andor lateral leads

Black athlete repolarization variant J-point elevation and convex (lsquodomedrsquo) ST segment elevation followed by T wave inversion in leads V1-

V4 in black athletes

Juvenile T wave pattern T-wave inversion V1ndashV3 in athletes lt age 16

Sinus bradycardia gt_ 30 bpm

Sinus arrhythmia Heart rate variation with respiration rate increases during inspiration and decreases during expiration

Ectopic atrial rhythm P waves are a different morphology compared with the sinus P wave such as negative P waves in the

inferior leads (lsquolow atrial rhythmrsquo)

Junctional escape rhythm QRS rate is faster than the resting P wave or sinus rate and typically less than 100 beatsminute with nar-

row QRS complex unless the baseline QRS is conducted with aberrancy

1 atrioventricular block PR interval 200ndash400 ms

Mobitz Type I 2 atrioventricular block PR interval progressively lengthens until there is a non-conducted P wave with no QRS complex the

first PR interval after the dropped beat is shorter than the last conducted PR interval

ECG electrocardiogram PVC premature ventricular contraction RBBB right bundle branch blockaThe QT interval corrected for heart rate is ideally measured using Bazettrsquos formula with heart rates between 60 and 90 bpm preferably performed manually in lead II or V5using the teach-the-tangent method1 to avoid inclusion of a U wave (please see text for more details) Consider repeating the ECG after mild aerobic activity for a heart rate-lt 50 bpm or repeating the ECG after a longer resting period for a heart rate gt 100 bpm if the QTc value is borderline or abnormal

4 S Sharma et al

Table 2 Evaluation of electrocardiographic abnormalities

ECG abnormality Potential cardiac

diseasea

Recommended evaluationb Considerations

T wave inversion in the lat-

eral or inferolateral leads

HCM

DCM

LVNC

ARVC (with predominant LV

involvement)

Myocarditis

Echocardiography

CMR

Exercise ECG test

Minimum 24 h ECG monitor

Lateral or inferolateral T wave inversion is com-

mon in primary myocardial disease CMR

should be a routine diagnostic test for this

ECG phenotype and is superior to echocar-

diography for detecting apical HCM LVH

localized to the free lateral wall ARVC with

predominant left ventricular involvement and

myocarditis

If CMR is not available echocardiography with

contrast should be considered as an alternative

investigation for apical HCM in patients with

deep T wave inversion in leads V5ndashV6

Consider family evaluation if available and

genetic screening

Annual follow-up testing is recommended

throughout athletic career in athletes with

normal results

T wave inversion isolated to

the inferior leads

HCM

DCM

LVNC

Myocarditis

Echocardiography Consider CMR based on echo findings or clini-

cal suspicion

T wave inversion in the ante-

rior leadsc

ARVC

DCM

Echocardiography

CMR

Exercise ECG test


SAECG

The extent of investigations may vary based on

clinical suspicion for ARVC and results from

initial testing

ST segment depression HCM

DCM

LVNC

ARVC

Myocarditis

Echocardiography Consider CMR and additional testing based on

echo findings or clinical suspicion

Pathologic Q waves HCM

DCM

LVNC

Myocarditis

Prior MI

Echocardiography

CAD risk factor assessment

Repeat ECG for septal (V1ndashV2)

QS pattern above investiga-

tions recommended if septal Q

waves are persistent

Consider CMR (with perfusion study if available)

based on echo findings or clinical suspicion

In the absence of CMR consider exercise stress

testing dobutamine stress echocardiogram or

a myocardial perfusion scan for evaluation of

coronary artery disease in athletes with suspi-

cion of prior MI or multiple risk factors for

CAD

Complete left bundle branch

block

DCM

HCM

LVNC

Sarcoidosis

Myocarditis

Echocardiography

CMR (with stress perfusion

study)d

A comprehensive cardiac evaluation to rule out

myocardial disease should be considered

Profound nonspecific intra-

ventricular conduction

delay gt_ 140 ms

DCM

HCM

LVNC

Echocardiography Consider additional testing based on echo find-

ings or clinical suspicion

Epsilon wave ARVC Echocardiography

CMR

Exercise ECG test


SAECG

An epsilon wave in leads V1-V3 is a highly spe-

cific ECG maker and a major diagnostic crite-

rion for ARVC

Continued


Table 2 Continued


diseasea


Multiple premature ventricu-

lar contractions

HCM

DCM

LVNC

ARVC

Myocarditis

Sarcoidosis

Echocardiography

24 h ECG monitor

Exercise ECG test

If gt 2000 PVCrsquos or non-sustained ventricular

tachycardia are present on initial testing com-

prehensive cardiac testing inclusive of CMR is

warranted to investigate for myocardial

disease

Consider signal averaged ECG (SAECG)

Ventricular pre-excitation WPW Exercise ECG test

Echocardiography

Abrupt cessation of the delta wave (pre-excita-

tion) on exercise ECG denotes a low risk

pathway

EP study for risk assessment should be

considered if a low risk accessory pathway

cannot be confirmed by non-invasive testing

Consider EP study for moderate to high intensity

sports

Prolonged QTc LQTS Repeat resting ECG on separate

day

Review for QT prolonging

medication

Acquire ECG of 1st degree rela-

tives if possible

Consider exercise ECG test laboratory (elec-

trolyte) screening family screening and genetic

testing when clinical suspicion is high

Consider direct referral to a heart rhythm spe-

cialist or sports cardiologist for a QTc gt_

500 ms

Brugada Type 1 pattern Brugada syndrome Referral to cardiologist or heart

rhythm specialist

Consider high precordial lead ECG with leads

V1 and V2 in 2nd and 3rd intercostal space

or sodium channel blockade if Brugada pat-

tern is indeterminateConsider genetic test-

ing and family screening

Profound sinus bradycardia

lt 30 BPM

Myocardial or electrical

disease

Repeat ECG after mild aerobic

activity

Consider additional testing based on clinical

suspicion

Profound 1 AV block gt_

400 ms


disease


activity

Exercise ECG test


suspicion

Advanced 2 or 3 atrioven-

tricular block


disease

Echocardiography


Exercise ECG test

Consider laboratory screening and CMR based

on echo findings

Atrial tachyarrhythmias Myocardial or electrical

disease

Echocardiography


Exercise ECG test

Consider CMR or EP study based on clinical

suspicion

Ventricular arrhythmiase Myocardial or electrical

disease

Echocardiography

CMR


Exercise ECG test


myocardial disease and primary electrical dis-

ease should be considered

Two or more borderline

ECG findings

Myocardial disease Echocardiography Consider additional testing based on clinical

suspicion

ARVC arrhythmogenic right ventricular cardiomyopathy CAD coronary artery disease CMR cardiovascular magnetic resonance DCM dilated cardiomyopathy ECG electro-cardiogram EP electrophysiologial HCM hypertrophic cardiomyopathy LQTS long QT syndrome LVNC left ventricular noncompaction PVC premature ventricular com-plexe SAECG signal averaged ECG WPW Wolff-Parkinson-White syndromeaThis list of disorders for each ECG abnormality represents the primary cardiac disorders of concern and is not intended to be exhaustivebInitial evaluation of ECG abnormalities should be performed under the direction of a cardiologist Additional testing will be guided by initial findings and clinical suspicion basedon the presence of symptoms or a family history of inherited cardiac disease or SCDcExcludes black athlete repolarization variant and juvenile pattern in adolescents lt 16 yearsdCT coronary angiography if stress perfusion with CMR is unavailableeIncludes couplets triplets accelerated ventricular rhythm and non-sustained ventricular tachycardia

6 S Sharma et al

Figure 2 Electrocardiogram of a 29-year-old male asymptomatic soccer player showing sinus bradycardia (44 bpm) early repolarization in I II aVFV5ndashV6 (arrows) voltage criterion for left ventricular hypertrophy (S-V1thornR-V5 gt 35 mm) and tall peaked T waves (circles) These are commontraining related findings in athletes and do not require more evaluation

Figure 3 Electrocardiogram from a black athlete demonstrating voltage criterion for left ventricular hypertrophy J point elevation and convex(lsquodomedrsquo) ST segment elevation followed by T-wave inversion in V1ndashV4 (circles) This is a normal repolarization pattern in black athletes


younger athletes who have completed puberty2245 Based on currentevidence TWI in the anterior leads (V1ndashV3) in adolescentathletes lt 16 years of age should not prompt further evaluation in theabsence of symptoms signs or a family history of cardiac disease

Physiological arrhythmias in athletesCommon consequences of increased vagal tone include sinus brady-cardia and sinus arrhythmia2247ndash49 Other less common markers ofincreased vagal tone are junctional or ectopic atrial rhythms firstdegree atrioventricular (AV) block and Mobitz Type I second degreeAV block (Wenckebach phenomenon)224750 In the absence of

symptoms heart rates gt_ 30 bpm are considered normal in highlytrained athletes Sinus rhythm should resume and bradycardia shouldresolve with the onset of physical activity

Borderline electrocardiogramfindings in athletes

Recent data suggest that some ECG findings previously categorizedas abnormal may represent normal variants or the result of physiolog-ical cardiac remodelling in athletes and do not usually represent

E

F

DA

B

C

Figure 4 Normal and abnormal patterns of T-wave inversion (A) Anterior T-wave inversion in V1ndashV3 in a 12-year-old asymptomatic athlete with-out a family history of sudden cardiac death considered a normal lsquojuvenilersquo pattern (B) T-wave inversion in V1ndashV4 in a 17-year-old asymptomaticmixed race (Middle-Easternblack) athlete without a family history of sudden cardiac death This is a normal repolarization pattern in black athletes(C) Biphasic T-wave inversion in V3 in a 31-year-old asymptomatic black athlete without a family history of sudden cardiac death Anterior biphasic Twaves are considered normal in adolescents lt 16 years old and in adults when found in a single lead most commonly V3 (D) Abnormal T-wave inver-sion in V1ndashV6 in an adult symptomatic former soccer player with genetically confirmed arrhythmogenic right ventricular cardiomyopathy and a posi-tive family history of sudden cardiac death (brother died at 26 years of age) (E) Inferolateral T-wave inversion in leads I II III aVF V2ndashV6 and STsegment depression in leads II aVF V4ndashV6 in a 31-year-old asymptomatic professional soccer referee These markedly abnormal findings require acomprehensive evaluation to exclude cardiomyopathy (F) An electrocardiogram demonstrating the Type 1 Brugada pattern with high take-off ST ele-vation gt_ 2 mm with downsloping ST segment elevation followed by a negative symmetric T wave in V1ndashV2

8 S Sharma et al

pathological cardiac disease These ECG findings have been catego-rized as lsquoborderlinersquo findings in athletes (Figure 1 Table 1)

Axis deviation and voltage criteria foratrial enlargementAxis deviation and voltage criteria for atrial enlargement account for-gt 40 of abnormal ECG patterns in athletes but do not correlatewith cardiac pathology51 In a large study of 2533 athletes aged 14ndash35years old and 9997 controls of similar age echocardiographic evalua-tion of the 579 athletes and controls with isolated axis deviation orvoltage criteria for atrial enlargement failed to identify any majorstructural or functional abnormalities51

Complete right bundle branch blockAlthough incomplete right bundle branch block (RBBB) is common inyoung athletes the significance of complete RBBB is less certainComplete RBBB is detected in approximately 1 of the general popu-lation and large datasets in young adult athletes reveal a prevalence of05ndash251252ndash54 In a study of 510 US collegiate athletes RBBB wasreported in 25 and compared with athletes with normal QRS com-plexes or incomplete RBBB athletes with complete RBBB exhibitedlarger right ventricular dimensions and a lower right ventricular ejectionfraction but preserved fractional area change55 None of the athleteswith complete RBBB or incomplete RBBB was found to have pathologi-cal structural cardiac disease These patterns among trained athletescould represent a spectrum of structural and physiological cardiacremodelling characterized by RV dilation with resultant QRS prolonga-tion and a relative reduction in the RV systolic function at rest55

Based on the aforementioned considerations left axis deviation leftatrial enlargement right axis deviation and right atrial enlargement andcomplete RBBB are considered borderline variants in athletes Thepresence of any one of these findings in isolation or with other recog-nized physiological electrical patterns of athletic training does not war-rant further assessment in asymptomatic athletes without a familyhistory of premature cardiac disease or SCD Conversely the pres-ence of more than one of these borderline findings places the athletein the abnormal category warranting additional investigation

Abnormal electrocardiogramfindings in athletes

The abnormal findings defined in this section are not recognized fea-tures of athletic training and always require further assessment toexclude the presence of intrinsic cardiac disease (Figure 1 Tables 1and 2) Temporary restriction from athletic activity should be consid-ered for athletes with abnormal ECGs of uncertain clinical significanceuntil secondary investigations are completed

Abnormal T-wave inversionTWI gt_ 1 mm in depth in two or more contiguous leads (excludingleads aVR III and V1) in an anterior lateral inferolateral or inferiorterritory is abnormal and should prompt further evaluation forunderlying structural heart disease (Tables 1 and 2) Normal excep-tions include TWI confined to leads V1ndashV4 in black athletes whenpreceded by J point andor ST segment elevation and TWI in leadsV1ndashV3 in athletes aged lt 16 years

Clinical considerations

The relationship between abnormal TWI and several forms of struc-tural heart disease is well documented56 TWI in the inferior or lateralleads is common in HCM56ndash59 Whereas TWI in the right precordialleads (V1ndashV3) or beyond in the absence of a complete RBBB is com-mon in ARVC (Figure 4D)6061

There are no data relating to the significance of flat or biphasic Twaves in athletes but similar to TWI this panel would recommendfurther evaluation of biphasic T waves where the negative portionis gt_ 1 mm in depth in gt_ 2 leads

Evaluation

Lateral or inferolateral T-wave inversionThere is mounting evidence that TWI in the lateral or inferolateralleads is associated with the presence of quiescent cardiomyopathy ina considerable proportion of athletes3062ndash64 Recommendations forthe evaluation of abnormal TWI and other clinical considerations arepresented in Table 2

TWI affecting the lateral leads (V5ndashV6 I and aVL) (Figure 4E)should prompt a comprehensive investigation to exclude cardiomy-opathy If echocardiography is not diagnostic cardiac magnetic reso-nance imaging (MRI) with gadolinium should be utilized Cardiac MRIprovides superior assessment of myocardial hypertrophy especiallythe left ventricular apex and the lateral free wall and may also demon-strate late gadolinium enhancement (LGE) a non-specific marker sug-gesting myocardial fibrosis If cardiac MRI is not availableechocardiography with contrast should be considered Exercise ECGtesting and Holter monitoring also should be considered in the evalu-ation of lateral or inferolateral TWI especially for athletes with lsquogreyzonersquo hypertrophy (males with maximal LV wall thickness 13ndash16 mm)without LGE where the diagnosis of HCM remains uncertain In suchcases the presence of ventricular tachycardia during exercise orHolter may support HCM and is also useful in risk stratification65

For athletes with lateral or inferolateral TWI regular follow-upwith serial cardiac imaging is necessary even when the initial evalua-tion is normal in order to monitor for the development of a cardio-myopathy phenotype6263

Anterior T-wave inversionAnterior TWI is a normal variant in asymptomatic adolescent athletesage lt 16 years in black athletes when preceded by J-point elevationand convex ST segment elevation and in some endurance ath-letes6667 However anterior TWI in leads V1ndashV2V3 also is a recog-nized pattern in patients with ARVC and rarely HCM

There are discrepancies among existing guidelines relating to theextent of anterior TWI inversion before considering further investiga-tions561429 A large study of over 14 000 white adults aged 16ndash35years old including over 2500 athletes showed that anterior TWI hada prevalence of 2368 Anterior TWI was more common in femalesand athletes and was confined to leads V1ndashV2 in almost all individualsand only exceeded beyond V2 in 1 of females and 02 of males68

None of the individuals with anterior TWI were diagnosed with a car-diomyopathy following comprehensive investigation indicating thatthis particular ECG pattern is non-specific in low-risk populationsBased on this report it is justifiable to only investigate non-black ath-letes with anterior TWI beyond V2 in the absence of other clinical orelectrical features of ARVC


Specific information about the J-point and preceding ST segmentmay help differentiate between physiological adaptation and cardio-myopathy in athletes with anterior TWI affecting leads V3 andor V4A recent study comparing anterior TWI in a series of black and whitehealthy athletes and patients with HCM and ARVC showed that inathletes with anterior TWI the combination of J-point eleva-tion gt_ 1 mm and TWI confined to leads V1ndashV4 excluded either cardi-omyopathy with 100 negative predictive value regardless ofethnicity66 Conversely anterior TWI associated with minimal orabsent J-point elevation (lt 1 mm) could reflect a cardiomyopathy66

These data require duplication in larger studies but may prove usefulin the assessment of a small proportion of white endurance athleteswho exhibit anterior TWI and in athletes of blackmixed ethnicity69

In most non-black athletes age gt_ 16 years anterior TWI beyondlead V2 should prompt further evaluation given the potential overlapwith ARVC In these athletes concurrent findings of J-point elevationST segment elevation or biphasic T waves more likely represents ath-letersquos heart while the absence of J-point elevation or a coexistentdepressed ST segment is more concerning for ARVC (Figure 5)66

Other ECG findings suggestive of ARVC include low limb lead vol-tages prolonged S wave upstroke ventricular ectopy with LBBB mor-phology and epsilon waves61 A combination of tests is needed todiagnose ARVC including echocardiography cardiac MRI Holtermonitoring exercise ECG test and signal averaged ECG

Inferior T-wave inversionThe significance of TWI confined to the inferior leads is unknownHowever this finding cannot be attributed to physiological remodel-ling and thus warrants further investigation with at minimum anechocardiogram Cardiac MRI should be considered based on theechocardiographic findings or clinical suspicion

ST segment depressionWhile ST segment depression is common among patients with cardi-omyopathy it is not a feature of athletic training28597071 ST segmentdepression (relative to the isoelectric PR segment) in excess of005 mV (05 mm) in two or more leads should be considered anabnormal finding requiring definitive evaluation for underlying struc-tural heart disease

Evaluation

Echocardiography is the minimum evaluation for athletes with ST seg-ment depression to investigate for underlying cardiomyopathyCardiac MRI should be considered based on the echocardiographicfindings or clinical suspicion

Pathological Q wavesSeveral pathological disorders including HCM ARVC infiltrative myo-cardial diseases accessory pathways and transmural myocardial

A B

Figure 5 Examples of physiological (A) and pathological T-wave inversion (B) Panel A demonstrates T-wave inversion in V1ndashV4 preceded byJ-point elevations and convex lsquodomedrsquo ST segment elevation (green circles) This should not be confused with pathological T-wave inversion(Panel B) which demonstrates T-wave inversion in V1ndashV6 with absent J-point elevation and a downsloping ST segment (red circles)

10 S Sharma et al

infarction can lead to the development of exaggerated (deep or wide)Q waves or unexpected Q waves in atypical leads2856 Pathological Qwaves also may be a result of lead misplacement In particular a pseudo-septal infarct pattern with pathological Q waves in leads V1ndashV2 is com-monly due to high-lead placement relative to cardiac position72

Pathological Q waves have been reported in approximately 1ndash2of all athletes and may be higher in males and black athletes2973 Forasymptomatic athletes pathological Q waves were previously definedas gt 3 mm in depth or gt 40 ms in duration in two or more leads(except III and aVR)610 In practice however this criterion is a com-mon source of false positive ECG results as trained athletes withphysiological LVH and thin adolescent athletes may have increasedprecordial voltages and deep lateral or inferior Q waves

The use of a QR ratio overcomes some of these issues by normal-izing Q wave depth to the degree of proceeding R wave voltage Casecontrol analyses of athletes and HCM patients suggest that this willdecrease the false positive rate without compromising sensitivity forthe detection of cardiomyopathy2974 Thus this consensus panel hasmodified the definition for pathological Q waves in athletes as a QRratio gt_ 025 or gt_ 40 ms in duration in two or more contiguous leads(except III and aVR)

Evaluation

An ECG with abnormal Q waves should be carefully examined for thepossibility of an accessory pathway If the pathological Q waves are iso-lated to leads V1ndashV2 the ECG should be repeated including re-placingthe ECG leads to ensure proper positioning Persistence of pathologicalQ waves in two or more contiguous leads warrants further investiga-tion with echocardiography to exclude cardiomyopathy If the echocar-diogram is normal and there are no other concerning clinical findingsor ECG abnormalities no additional testing is generally necessaryHowever if there is a high index of clinical suspicion additional evalua-tion with cardiac MRI should be considered In athletersquos age gt_ 30 yearswith suspicion of prior myocardial infarction or risk factors for coro-nary artery disease (CAD) stress testing may be warranted

Complete left bundle branch blockLBBB is found in less than 1 in 1000 athletes but is common inpatients with cardiomyopathy and ischaemic heart disease928597576

Thus complete LBBB always should be considered an abnormal find-ing and requires a comprehensive evaluation to rule out a pathologi-cal cardiac disorder

Evaluation

Athletes with complete LBBB require a thorough investigation formyocardial disease including echocardiography and a cardiac MRIwith perfusion study

Profound non-specific intra-ventricularconduction delayEpidemiological studies of nonspecific intra-ventricular conductiondelay (IVCD) in the general population have shown an increased riskof cardiovascular death and have been documented among patientswith cardiomyopathy7778 The significance of non-specific IVCD withnormal QRS morphology in healthy asymptomatic athletes is uncer-tain79 The physiology underlying IVCD in athletes remains

incompletely understood but likely includes some combination ofneurally mediated conduction fibre slowing and increased myocardialmass In patients with LVH left ventricular mass seems to be closelyrelated to QRS duration80

While the exact cut-off to trigger more investigation in athleteswith a nonspecific IVCD remains unclear this panel recommendsthat marked nonspecific IVCD gt_ 140 ms in athletes regardless ofQRS morphology is abnormal and should prompt further evaluation

Evaluation

In asymptomatic athletes with profound non-specific IVCD an echo-cardiogram is recommended to evaluate for myocardial diseaseOther testing may be indicated depending on echocardiographic find-ings or clinical suspicion

Ventricular pre-excitationVentricular pre-excitation occurs when an accessory pathwaybypasses the AV node resulting in abnormal conduction to the ven-tricle (pre-excitation) with shortening of the PR interval and wideningof the QRS This is evident on the ECG as the WolfndashParkinsonndashWhite (WPW) pattern defined as a PR interval lt 120 ms the pres-ence of a delta wave (slurring of the initial QRS) and a QRSduration gt 120 ms81 The WPW pattern occurs in up to 1 in 250 ath-letes9125282 The presence of an accessory pathway can predisposean athlete to sudden death because rapid conduction of atrial fibrilla-tion across the accessory pathway can result in VF

Evaluation

A short PR interval in isolation without a widened QRS or delta wavein an asymptomatic athlete should not be considered for furtherassessment The WPW pattern warrants further assessment of therefractory period of the accessory pathway Non-invasive risk stratifi-cation begins with an exercise stress test where abrupt completeloss of pre-excitation at higher heart rates suggests a low-risk acces-sory pathway8384 An echocardiogram also should be considered dueto the association of WPW with Ebsteinrsquos anomaly and cardiomyop-athy Intermittent pre-excitation during sinus rhythm on a restingECG is also consistent with a low-risk pathway and may obviate theneed for an exercise test85 If non-invasive testing cannot confirm alow-risk pathway or is inconclusive an electrophysiological studyshould be considered to determine the shortest pre-excited RRinterval during atrial fibrillation83 If the shortest pre-excited RR inter-val is lt_ 250 ms (240 bpm) then the accessory pathway is deemedhigh risk and transcatheter ablation is recommended8386 Somephysicians may choose to subject all competitive athletes involved inmoderate or high-intensity sport to electrophysiological studies irre-spective of the results of the exercise test or 24 h ECG on the prem-ise that high catecholamine concentrations during very intensiveexercise may modify the refractory period of an accessory pathwayin a fashion that cannot be reproduced during laboratory tests

Prolonged QT intervalCongenital Long QT syndrome (LQTS) is a potentially lethal geneti-cally mediated ventricular arrhythmia syndrome with the hallmarkelectrocardiographic feature of QT prolongation LQTS is estimatedto affect 1 in 2000 individuals and this may be underestimated giventhe subpopulation of so-called lsquonormal QT intervalrsquo or lsquoconcealedrsquo


LQTS87 Autopsy negative sudden unexplained death represents 25ndash40 of sudden unexpected deaths in persons under age 40 years388ndash

90 In such cases cardiac ion channelopathies have been implicated bypost-mortem genetic testing as the probable cause in up to 25ndash40of cases91ndash94

Calculating the corrected QT interval

Accurate measurement and manual confirmation of the computerderived QT interval corrected for heart rate (QTc) is critical as theaccuracy of computer generated QTc values is about 90ndash95Studies have suggested the ability of cardiologists to accurately meas-ure the QTc is suboptimal95 However accurate assessment of theQTc can be achieved by adhering to the following six principles96

(1) Use Bazettrsquos heart rate correction formula (QTc = QTRR notethe RR interval is measured in seconds) as population-based QTcdistributions most frequently use Bazett-derived QTc values97

(2) Bazettrsquos formula underestimates the QTc at heart rates lt 50 bpmand overestimates the QTc at heart rates gt 90 bpm Accordinglyfor a heart rate lt 50 bpm a repeat ECG after mild aerobic activity isrecommended to achieve a heart rate closer to 60 bpm For heartrates gt 90 bpm a repeat ECG after additional resting time may helpachieve a lower heart rate

(3) If sinus arrhythmia is present with beat to beat variation in heart ratean average QT interval and average RR interval should be used

(4) Leads II and V5 usually provide the best delineation of the T wave(5) Low amplitude U waves which are common in the anterior precor-

dial leads should not be included in the QT calculation The lsquoTeach-the-Tangentrsquo or lsquoAvoid-the-Tailrsquo method to delineate the end of theT wave should be followed (Figure 6)96

(6) The morphology of the T wave not just the length of the QT inter-val also can suggest the presence of LQTS98 For instance anotched T wave in the lateral precordial leads where the amplitudeof the second portion of the T wave following the notch is greaterthan the first portion of the T wave may represent LQT-2 even inthe absence of overt QT prolongation

The easiest and most efficient way to confirm the computer-derived QTc is to examine lead II andor V5 and determine if themanually measured QT interval matches the computerrsquos QT meas-urement If there is concordance within about 10 ms one can trustthat the computer can derive accurately an average RR interval andcomplete the Bazettrsquos calculation If however the manually measuredQT interval is gt 10 ms different than the computerrsquos QT measure-ment an average RR interval should be determined and the QTcrecalculated using the Bazettrsquos formula

Corrected QT cut-offs

Given the overlap between QTc distributions in population-derivedcohorts of healthy individuals compared with patients with geneticallyconfirmed LQTS the QTc cut-off value compelling further evaluationmust be chosen carefully to balance the frequency of abnormalresults and the positive predictive value for LQTS

Recent consensus statements on ECG interpretation in athleteshave recommended that male athletes with a QTc gt_ 470 ms andfemale athletes with a QTc gt_ 480 ms undergo further evaluation forLQTS to better balance false positive and false negative findings610

These cut-off values are around the 99th percentile and consistentwith thresholds defined by the American Heart Association and

Figure 6 This figure illustrates the lsquoTeach-the-Tangentrsquo or lsquoAvoid-the-Tailrsquo method for manual measurement of the QT interval A straight line isdrawn 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

12 S Sharma et al

American College of Cardiology99 This consensus group also recom-mends QTc values of gt_ 470 ms in males and gt_ 480 ms in females todefine the threshold of QT prolongation that warrants further assess-ment in asymptomatic athletes

Short QT IntervalThe precise cut-off and clinical significance of a short QT interval inathletes is unknown Data from over 18 000 asymptomatic youngBritish individuals found that the prevalence of a QTc lt 320 ms is01 suggesting an abnormal cut-off value of lt 320 ms is prag-matic100 However over a mean follow up period of 53 years noneof the individuals with a short QT lt 320 ms experienced any adverseevents syncope or sudden death100 Based on the rarity of this find-ing and absence of data to suggest long-term morbidity in asympto-matic athletes this panel recommends that a short QT interval onlybe investigated in the context of concerning clinical markers

Evaluation

It is critical that an athlete with a single prolonged QTc reading not beobligated a diagnosis of LQTS but rather that these cut-off valuestrigger the need for additional evaluation The importance of addi-tional evaluation but not a premature diagnosis of LQTS was demon-strated in a study of 2000 elite athletes in which 7 (04) had aprolonged QTc (range 460ndash570 ms)101 A QTc of lt 500 ms in theabsence of symptoms or familial disease was unlikely to representLQTS In contrast a QTc gt_ 500 ms was highly suggestive of LQTS asall three athletes with a QTc value of gt 500 ms exhibited one of para-doxical prolongation of the QTc during exercise a confirmatorygenetic mutation or prolonged QTc in a first-degree relative101

A personal history of syncope or seizures and a family history ofexertional syncope lsquoepilepsyrsquo postpartum-timed syncopeseizureunexplained motor vehicle accidents unexplained drowning and pre-mature unexplained sudden death lt 50 years of age should bereviewed If the personalfamily history is positive the athlete shouldbe referred to an electrophysiologist for further evaluation If the per-sonalfamily history is negative a repeat ECG should be obtained(ideally on a different day) If the follow-up ECG is below the QTccut-off values then no additional evaluation is needed and the athleteshould be reassured

If the repeat ECG still exceeds the QTc cut-off values then ascreening ECG of the athletersquos first degree relatives (parents and sib-lings) should be considered and the athlete should be referred to anelectrophysiologist for the possibility of newly discovered LQTSReversible extrinsic factors such as electrolyte abnormalities(hypokalaemia) or the presence of QT prolonging medications mustalso be evaluated If an athletersquos ECG shows a QTc gt_ 500 ms and noreversible causes are identified then the athlete should be referredimmediately to an electrophysiologist as the probability of LQTS andfuture adverse events has increased102 The Schwartz-Moss scoringsystem electrocardiographic features stress ECG provocative test-ing and genetic testing may be needed to clarify the diagnosis andshould be performed and interpreted by a cardiologist familiar withthe disease103ndash106

Brugada Type 1 patternBrugada syndrome (BrS) is an inherited primary electrical diseasewhich predisposes to ventricular tachyarrhythmias and sudden death

during states of enhanced vagal tone It is characterized by the distinc-tive Brugada ECG pattern which consists of a coved rSrrsquo pattern ST-segment elevation gt_ 2 mm and inversion of the terminal portion ofthe T wave in leads V1 V2 and V3 (Figure 4F) Although three typeswere described only the Type 1 Brugada pattern is now considereddiagnostic107ndash109

The coved ST segment elevation in Type 1 Brugada pattern resultsin a broad rrsquo and should be distinguishable from the upsloping ST seg-ment elevation of early repolarization in an athlete In this regard thelsquoCorrado indexrsquo measures the ST elevation at the start of the STsegmentJ-point (STJ) and 80 ms after the start of the ST segment(ST80)110 In Type 1 Brugada pattern the downsloping ST segmentwill have a STJST80 ratio gt 1 while the initial upsloping of the ST seg-ment found in early repolarization patterns in an athlete will producean STJST80 ratio lt 1 (Figure 7)

Evaluation

The Type 1 Brugada ECG pattern should be investigated regardlessof symptoms If the pattern is unclear confirm correct lead place-ment repeat the ECG if necessary and perform a high precordiallead ECG with V1 and V2 placed in the 2nd or 3rd intercostal spaceIf the Type 1 pattern is seen on a high-precordial lead ECG thenreferral to an electrophysiologist is indicated Consideration shouldbe given to potential accentuating factors for a Brugada-like ECG pat-tern such as hyperkalaemia fever medications with sodium ion chan-nel blocking properties and lead placement

Profound sinus bradycardia or firstdegree atrioventricular blockSinus bradycardia and moderate prolongation of the PR interval(200ndash399 ms) are recognized features of athletic conditioningAlthough a resting heart rate lt_ 30 bpm or a PR interval gt_ 400 ms maybe normal in a well-trained athlete it should prompt further evalua-tion for cardiac conduction disease

Evaluation

Evaluation of profound sinus bradycardia or a markedly increased PRinterval should include assessing the chronotropic response to mildaerobic activity such as running on the spot or climbing stairsExercise testing is useful in this situation to provide an objectivemeasure of the PR interval and heart rate response to aerobic activityIf the heart rate increases appropriately and the PR interval normal-izes and the athlete is asymptomatic no further testing is necessaryConversely further evaluation should be performed if the heart ratedoes not increase or the PR interval does not shorten appropriatelyon exertion the athlete experiences pre-syncopesyncope or in ath-letes with a family history of cardiac disease or sudden deathDepending on the clinical scenario an echocardiogram or ambulatoryECG monitor may be indicated

High grade atrioventricular blockMobitz Type II second degree AV block and third degree (complete)AV block are abnormal findings in athletes Complete heart block canbe confused with AV dissociation without block a situation wherethe junctional pacemaker is faster than the sinus node leading tomore 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 theexpression of autonomic mismatch between AV and sinus nodalmodulation but is not pathological Like all other functional distur-bances a small exercise load with repeat ECG recording will showresolution of the ECG findings in AV dissociation

Evaluation

If Mobitz II AV block or complete AV block is detected further evalu-ation includes an echocardiogram ambulatory ECG monitor andexercise ECG test Based on these results laboratory testing and car-diac MRI may be considered Referral to an electrophysiologist isessential

Multiple premature ventricularcontractionsMultiple (gt_ 2) premature ventricular contractions (PVCs) are uncom-mon and present in lt 1 of 12-lead ECGs in athletes912 Althoughmultiple PVCs are usually benign their presence may be the hallmarkof underlying heart disease111112 PVCs originating from the right ven-tricular outflow tract (LBBB and inferior axis origin) are consideredparticularly benign when associated with a normal ECG however thisPVC morphology can also be present in patients with early ARVCparticularly when the QRS exceeds 160 ms113 Therefore the findingof gt_ 2 PVCs on an ECG should prompt more extensive evaluation toexclude underlying structural heart disease

Evaluation

The extent of evaluation for gt_ 2 PVCs is controversial and excludingpathology may be difficult At a minimum an ambulatory Holter mon-itor echocardiogram and exercise stress test should be performedThe availability of modern small leadless ambulatory recordersallows for longer electrocardiographic monitoring including duringtraining and competition to exclude complex ventricular arrhyth-mias If the Holter and echocardiogram are normal and the PVCs

suppress with exercise no further evaluation is recommended for anasymptomatic athlete A previous study has shown that among ath-letes with gt_ 2000 PVCs per 24 h up to 30 were found to haveunderlying structural heart disease compared with 3 and 0 inthose with lt 2000 and lt 100 PVCs per day respectively112

Therefore in athletes with gt_ 2000 PVCs per 24 h or with episodes ofnon-sustained ventricular tachycardia or with an increasing burden ofectopy during an incremental exercise test additional evaluation mayinclude contrast-enhanced cardiac MRI and more invasive electro-physiology study114115 Although some studies have suggested thatregression of the PVC burden with detraining indicates a good prog-nosis other studies have not confirmed this116ndash118 Thus detrainingas a diagnostic or therapeutic measure is not recommended

Atrial tachyarrhythmiasSinus tachycardia is the most common atrial tachyarrhythmia but isvery rarely due to intrinsic cardiac disease Supraventricular tachycar-dia (SVT) atrial fibrillation and atrial flutter are rarely seen on a rest-ing ECG in athletes and require investigation Atrial tachyarrhythmiasare rarely life threatening but can be associated with other conditionsthat can lead to SCD including LQTS WPW BrS myocarditis con-genital heart disease and the cardiomyopathies

Evaluation

If resting sinus tachycardia gt 120 bpm is seen a repeat ECG shouldbe considered after a period of rest as recent exercise or anxiety maybe the cause Other underlying aetiologies may be sought includingfever infection dehydration stimulant use anaemia hyperthyroidismor rarely underlying cardiac or pulmonary disease

For paroxysmal SVT a repeat ECG when not in SVT should beobtained if possible If the Valsalva maneuver carotid sinus massageor the diving reflex is used to terminate the arrhythmia a rhythm stripshould be obtained which can help elucidate the mechanism of the SVTAn echocardiogram ambulatory ECG monitor and exercise treadmill

Figure 7 Brugada Type 1 electrocardiogram (left) should be distinguished from early repolarization with lsquoconvexrsquo ST segment elevation in a trainedathlete (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 arecalculated The lsquodownslopingrsquo ST segment elevation in Brugada pattern is characterized by a STJST80 ratio gt 1 Early repolarization patterns in an ath-lete show an initial lsquoupslopingrsquo ST segment elevation with STJST80 ratio lt 1

14 S Sharma et al

test should be completed Referral to an electrophysiologist may beindicated for consideration of electrophysiology study and ablation

If atrial fibrillation or flutter is found an echocardiogram should becompleted to assess for structural heart disease and anti-coagulationconsidered based on standard guidelines119 An ambulatory ECG moni-tor should be used to assess if the rhythm is paroxysmal or persistentand what the ventricular rate is throughout the day A thorough familyhistory may elucidate an underlying genetic cause Depending on whatthese results show cardiac MRI electrophysiology study with possibleablation andor genetic testing may be considered

Ventricular arrhythmiasVentricular couplets triplets and non-sustained ventricular tachycar-dia always require investigation as they can be a marker for underlyingcardiac pathology or lead to sustained ventricular tachycardia whichmay cause SCD

Evaluation

If ventricular arrhythmias are seen the evaluation should include athorough family history an echocardiogram to evaluate for structuralheart disease cardiac MRI to assess for ARVC or other cardiomyopa-thies ambulatory ECG monitor and exercise ECG test Dependingon these results further evaluation may be needed including electro-physiology study or genetic testing

Considerations in athletes 30 years ofageIn athletes gt_ 30 years of age CAD is the most common cause ofSCD8990 In addition older athletes may be less fit compared with20ndash30 years ago increasing the possibility of underlying CAD120121

While resting ECGs have a low sensitivity for CAD some ECG pat-terns may suggest underlying CAD such as TWI pathological Qwaves ST segment depression left or RBBB abnormal R wave pro-gression left anterior hemiblock and atrial fibrillation122ndash124

Evaluation

The main role of a resting ECG in older athletes is to identify thoseathletes who may potentially be at high risk for CAD and warrant fur-ther testing123125126 Initial testing should include an exercise stresstest resting echocardiogram and assessment of traditional risk fac-tors for CAD When indicated this evaluation may be complementedby coronary CT angiography or a functional stress test

Electrocardiogram patterns requiringserial evaluationSeveral common heritable cardiomyopathies may present with ECGabnormalities prior to the onset of overt heart muscle pathology6263

Therefore athletes with abnormal ECGs suggestive of cardiomyopathyand initially normal clinical evaluations should be followed with serial eval-uation during and after their competitive athletic careers Evaluationsmay be conducted annually or more frequently depending on individualcircumstances These athletes may be permitted to participate in com-petitive athletics without restriction contingent on longitudinal follow-up

Conclusion

Accurate ECG interpretation in athletes requires adequate trainingand an attention to detail to distinguish physiological ECG findingsfrom abnormal ECG findings that might indicate the presence of car-diac pathology The international consensus standards presented onECG interpretation and the evaluation of ECG abnormalities serve asan important foundation for improving the quality of cardiovascularcare of athletes As new scientific data become available revision ofthese recommendations may be necessary to further advance theaccuracy of ECG interpretation in the athletic population

Supplementary material

Supplementary material is available at European Heart Journal online

AcknowledgementsThe 2nd Summit on Electrocardiogram Interpretation in Athletes wassponsored by the American Medical Society for Sports Medicine(AMSSM) the FIFA Medical Assessment and Research Center (F-MARC) and the National Collegiate Athletic Association (NCAA)Participating medical societies included the American College ofCardiology (ACC) Sports amp Exercise Council and the Section onSports Cardiology of the European Association for CardiovascularPrevention and Rehabilitation (EACPR) a registered branch of theEuropean Society of Cardiology (ESC) This statement has beenendorsed by the following societies American Medical Society forSports Medicine (AMSSM) Austrian Society of Sports Medicine andPrevention Brazilian Society of Cardiology - Department of Exerciseand Rehabilitation (SBC - DERC) British Association for Sports andExercise Medicine (BASEM) Canadian Academy of Sport andExercise Medicine (CASEM) European College of Sports andExercise Physicians (ECOSEP) European Society of Cardiology (ESC)Section of Sports Cardiology Federation Internationale de FootballAssociation (FIFA) German Society of Sports Medicine andPrevention International Olympic Committee (IOC) NorwegianAssociation of Sports Medicine and Physical Activity (NIMF) SouthAfrican Sports Medicine Association (SASMA) Spanish Society ofCardiology (SEC) Sports Cardiology Group Sports DoctorsAustralia and the Swedish Society of Exercise and Sports Medicine(SFAIM) The American College of Cardiology (ACC) affirms thevalue of this document (ACC supports the general principles in thedocument and believes it is of general benefit to its membership)

Conflict of interest SS reports grants from Cardiac Risk in theYoung grants from British Heart Foundation outside the submittedwork MP reports grants from Cardiac Risk in the Young outside thesubmitted work MJA reports personal fees from Boston Scientificpersonal fees from Gilead Sciences personal fees from Invitae per-sonal fees from Medtronic personal fees from St Jude Medical otherfrom Transgenomic outside the submitted work In addition MJAhas a patent QT and T Wave Analytics pending VFF reports otherfrom insightinc from null outside the submitted work this is an entitythat manufactures and develops ECG software and devices forscreening purposes HH reports other from Biotronik during theconduct of the study other from Biotronik personal fees fromBiotronik personal fees from PfizerBMS personal fees from Daiichi-


Sankyo personal fees from Bayer personal fees from Boehringer-Ingelheim personal fees from Cardiome outside the submitted work

References1 Harmon KG Asif IM Klossner D Drezner JA Incidence of sudden cardiac death

in national collegiate athletic association athletes Circulation20111231594ndash1600

2 Maron BJ Doerer JJ Haas TS Tierney DM Mueller FO Sudden deaths in youngcompetitive athletes analysis of 1866 deaths in the United States 1980-2006Circulation 20091191085ndash1092

3 Harmon KG Asif IM Maleszewski JJ Owens DS Prutkin JM Salerno JC ZigmanML Ellenbogen R Rao A Ackerman MJ Drezner JA Incidence Etiology andComparative Frequency of Sudden Cardiac Death in NCAA Athletes ADecade in Review Circulation 201513210ndash19

4 Corrado D Biffi A Basso C Pelliccia A Thiene G 12-lead ECG in the athletephysiological versus pathological abnormalities Br J Sports Med 200943669ndash676

5 Corrado D Pelliccia A Heidbuchel H Sharma S Link M Basso C Biffi A BujaG Delise P Gussac I Anastasakis A Borjesson M Bjornstad HH Carre FDeligiannis A Dugmore D Fagard R Hoogsteen J Mellwig KP Panhuyzen-Goedkoop N Solberg E Vanhees L Drezner J Estes NA 3rd Iliceto S MaronBJ Peidro R Schwartz PJ Stein R Thiene G Zeppilli P McKenna WJRecommendations for interpretation of 12-lead electrocardiogram in the ath-lete Eur Heart J 201031243ndash259

6 Uberoi A Stein R Perez MV Freeman J Wheeler M Dewey F Peidro RHadley D Drezner J Sharma S Pelliccia A Corrado D Niebauer J Estes NA3rd Ashley E Froelicher V Interpretation of the electrocardiogram of youngathletes Circulation 2011124746ndash757

7 Williams ES Owens DS Drezner JA Prutkin JM Electrocardiogram interpreta-tion in the athlete Herzschrittmacherther Elektrophysiol 20122365ndash71

8 Drezner J Standardised criteria for ECG interpretation in athletes a practicaltool Br J Sports Med 201246i6ndashi8

9 Marek J Bufalino V Davis J Marek K Gami A Stephan W Zimmerman FFeasibility and findings of large-scale electrocardiographic screening in youngadults data from 32561 subjects Heart Rhythm 201181555ndash1559

10 Drezner JA Ackerman MJ Anderson J Ashley E Asplund CA Baggish ALBorjesson M Cannon BC Corrado D DiFiori JP Fischbach P Froelicher VHarmon KG Heidbuchel H Marek J Owens DS Paul S Pelliccia A Prutkin JMSalerno JC Schmied CM Sharma S Stein R Vetter VL Wilson MGElectrocardiographic interpretation in athletes the 0Seattle criteria0 Br J SportsMed 201347122ndash124

11 Corrado D Pelliccia A Bjornstad HH Vanhees L Biffi A Borjesson MPanhuyzen-Goedkoop N Deligiannis A Solberg E Dugmore D Mellwig KPAssanelli D Delise P van-Buuren F Anastasakis A Heidbuchel H Hoffmann EFagard R Priori SG Basso C Arbustini E Blomstrom-Lundqvist C McKennaWJ Thiene G Cardiovascular pre-participation screening of young competitiveathletes for prevention of sudden death proposal for a common European pro-tocol Consensus Statement of the Study Group of Sport Cardiology of theWorking Group of Cardiac Rehabilitation and Exercise Physiology and theWorking Group of Myocardial and Pericardial Diseases of the European Societyof Cardiology Eur Heart J 200526516ndash524

12 Pelliccia A Culasso F Di Paolo FM Accettura D Cantore R Castagna WCiacciarelli A Costini G Cuffari B Drago E Federici V Gribaudo CG IacovelliG Landolfi L Menichetti G Atzeni UO Parisi A Pizzi AR Rosa M Santelli FSantilio F Vagnini A Casasco M Di Luigi L Prevalence of abnormal electrocar-diograms in a large unselected population undergoing pre-participation cardio-vascular screening Eur Heart J 2007282006ndash2010

13 Drezner JA Fischbach P Froelicher V Marek J Pelliccia A Prutkin JM SchmiedCM Sharma S Wilson MG Ackerman MJ Anderson J Ashley E Asplund CABaggish AL Borjesson M Cannon BC Corrado D DiFiori JP Harmon KGHeidbuchel H Owens DS Paul S Salerno JC Stein R Vetter VL Normal elec-trocardiographic findings recognising physiological adaptations in athletes Br JSports Med 201347125ndash136

14 Drezner JA Ashley E Baggish AL Borjesson M Corrado D Owens DS PatelA Pelliccia A Vetter VL Ackerman MJ Anderson J Asplund CA Cannon BCDiFiori J Fischbach P Froelicher V Harmon KG Heidbuchel H Marek J Paul SPrutkin JM Salerno JC Schmied CM Sharma S Stein R Wilson M Abnormalelectrocardiographic findings in athletes recognising changes suggestive of cardi-omyopathy Br J Sports Med 201347137ndash152

15 Drezner JA Ackerman MJ Cannon BC Corrado D Heidbuchel H Prutkin JMSalerno JC Anderson J Ashley E Asplund CA Baggish AL Borjesson M DiFioriJP Fischbach P Froelicher V Harmon KG Marek J Owens DS Paul S PellicciaA Schmied CM Sharma S Stein R Vetter VL Wilson MG Abnormal

electrocardiographic findings in athletes recognising changes suggestive of pri-mary electrical disease Br J Sports Med 201347153ndash167

16 Brosnan M La Gerche A Kumar S Lo W Kalman J Prior D Modest agreementin ECG interpretation limits the application of ECG screening in young athletesHeart Rhythm 201512130ndash136

17 Magee C Kazman J Haigney M Oriscello R DeZee KJ Deuster P DepenbrockP Orsquoconnor FG Reliability and validity of clinician ECG interpretation for ath-letes Ann Noninvasive Electrocardiol 201419319ndash329

18 Hill AC Miyake CY Grady S Dubin AM Accuracy of interpretation of preparti-cipation screening electrocardiograms J Pediatr 2011159783ndash788

19 Drezner JA Asif IM Owens DS Prutkin JM Salerno JC Fean R Rao AL StoutK Harmon KG Accuracy of ECG interpretation in competitive athletes theimpact of using standised ECG criteria Br J Sports Med 201246335ndash340

20 Exeter DJ Elley CR Fulcher ML Lee AC Drezner JA Asif IM Standardised cri-teria improve accuracy of ECG interpretation in competitive athletes a rando-mised controlled trial Br J Sports Med 2014481167ndash1171

21 Ryan MP Cleland JG French JA Joshi J Choudhury L Chojnowska L MichalakE Al-Mahdawi S Nihoyannopoulos P Oakley CM The standard electrocardio-gram as a screening test for hypertrophic cardiomyopathy Am J Cardiol199576689ndash694

22 Papadakis M Basavarajaiah S Rawlins J Edwards C Makan J Firoozi S Carby LSharma S Prevalence and significance of T-wave inversions in predominantlyCaucasian adolescent athletes Eur Heart J 2009301728ndash1735

23 Pelliccia A Maron BJ Culasso F Di Paolo FM Spataro A Biffi A Caselli GPiovano P Clinical significance of abnormal electrocardiographic patterns intrained athletes Circulation 2000102278ndash284

24 Sohaib SM Payne JR Shukla R World M Pennell DJ Montgomery HEElectrocardiographic (ECG) criteria for determining left ventricular mass inyoung healthy men data from the LARGE Heart study J Cardiovasc MagnReson 2009112

25 Sathanandam S Zimmerman F Davis J Marek J Abstract 2484 ECG screeningcriteria for LVH does not correlate with diagnosis of hypertrophic cardiomyop-athy Circulation 2009120S647

26 Weiner RB Hutter AM Wang F Kim JH Wood MJ Wang TJ Picard MHBaggish AL Performance of the 2010 European Society of Cardiology criteriafor ECG interpretation in the athlete Heart 2011971573ndash1577

27 Calore C Melacini P Pelliccia A Cianfrocca C Schiavon M Di Paolo FMBovolato F Quattrini FM Basso C Thiene G Iliceto S Corrado D Prevalenceand clinical meaning of isolated increase of QRS voltages in hypertrophic cardio-myopathy versus athletersquos heart relevance to athletic screening Int J Cardiol20131684494ndash4497

28 Lakdawala NK Thune JJ Maron BJ Cirino AL Havndrup O Bundgaard HChristiansen M Carlsen CM Dorval JF Kwong RY Colan SD Kober LV HoCY Electrocardiographic features of sarcomere mutation carriers with andwithout clinically overt hypertrophic cardiomyopathy Am J Cardiol20111081606ndash1613

29 Sheikh N Papadakis M Ghani S Zaidi A Gati S Adami PE Carre F Schnell FWilson M Avila P McKenna W Sharma S Comparison of electrocardiographiccriteria for the detection of cardiac abnormalities in elite black and white ath-letes Circulation 20141291637ndash1649

30 Papadakis M Carre F Kervio G Rawlins J Panoulas VF Chandra NBasavarajaiah S Carby L Fonseca T Sharma S The prevalence distribution andclinical outcomes of electrocardiographic repolarization patterns in male ath-letes of AfricanAfro-Caribbean origin Eur Heart J 2011322304ndash2313

31 Zaidi A Ghani S Sheikh N Gati S Bastiaenen R Madden B Papadakis M RajuH Reed M Sharma R Behr ER Sharma S Clinical significance of electrocardio-graphic right ventricular hypertrophy in athletes comparison with arrhythmo-genic right ventricular cardiomyopathy and pulmonary hypertension Eur Heart J2013343649ndash3656

32 Tikkanen JT Anttonen O Junttila MJ Aro AL Kerola T Rissanen HA ReunanenA Huikuri HV Long-term outcome associated with early repolarization onelectrocardiography N Engl J Med 20093612529ndash2537

33 Haissaguerre M Derval N Sacher F Jesel L Deisenhofer I de Roy L Pasquie JLNogami A Babuty D Yli-Mayry S De Chillou C Scanu P Mabo P Matsuo SProbst V Le Scouarnec S Defaye P Schlaepfer J Rostock T Lacroix DLamaison D Lavergne T Aizawa Y Englund A Anselme F Orsquoneill M Hocini MLim KT Knecht S Veenhuyzen GD Bordachar P Chauvin M Jais P Coureau GChene G Klein GJ Clementy J Sudden cardiac arrest associated with earlyrepolarization N Engl J Med 20083582016ndash2023

34 Macfarlane PW Antzelevitch C Haissaguerre M Huikuri HV Potse M Rosso RSacher F Tikkanen JT Wellens H Yan GX The early repolarization pattern aconsensus paper J Am Coll Cardiol 201566470ndash477

35 Tikkanen JT Junttila MJ Anttonen O Aro AL Luttinen S Kerola T Sager SJRissanen HA Myerburg RJ Reunanen A Huikuri HV Early repolarization elec-trocardiographic phenotypes associated with favorable long-term outcomeCirculation 20111232666ndash2673

16 S Sharma et al

36 Uberoi A Jain NA Perez M Weinkopff A Ashley E Hadley D Turakhia MP

Froelicher V Early repolarization in an ambulatory clinical population Circulation20111242208ndash2214

37 Junttila MJ Sager SJ Freiser M McGonagle S Castellanos A Myerburg RJInferolateral early repolarization in athletes J Interv Card Electrophysiol20113133ndash38

38 Noseworthy PA Weiner R Kim J Keelara V Wang F Berkstresser B WoodMJ Wang TJ Picard MH Hutter AM Jr Newton-Cheh C Baggish AL Earlyrepolarization pattern in competitive athletes clinical correlates and the effectsof exercise training Circ Arrhythm Electrophysiol 20114432ndash440

39 Noseworthy PA Tikkanen JT Porthan K Oikarinen L Pietila A Harald KPeloso GM Merchant FM Jula A Vaananen H Hwang SJ Orsquodonnell CJ SalomaaV Newton-Cheh C Huikuri HV The early repolarization pattern in the generalpopulation clinical correlates and heritability J Am Coll Cardiol2011572284ndash2289

40 Rosso R Kogan E Belhassen B Rozovski U Scheinman MM Zeltser D HalkinA Steinvil A Heller K Glikson M Katz A Viskin S J-point elevation in survivorsof primary ventricular fibrillation and matched control subjects incidence andclinical significance J Am Coll Cardiol 2008521231ndash1238

41 Quattrini FM Pelliccia A Assorgi R DiPaolo FM Squeo MR Culasso F CastelliV Link MS Maron BJ Benign clinical significance of J-wave pattern (early repola-rization) in highly trained athletes Heart Rhythm 2014111974ndash1982

42 Sheikh N Papadakis M Carre F Kervio G Panoulas VF Ghani S Zaidi A Gati SRawlins J Wilson MG Sharma S Cardiac adaptation to exercise in adolescentathletes of African ethnicity an emergent elite athletic population Br J SportsMed 201347585ndash592

43 Di Paolo FM Schmied C Zerguini YA Junge A Quattrini F Culasso F Dvorak JPelliccia A The athletersquos heart in adolescent Africans an electrocardiographicand echocardiographic study J Am Coll Cardiol 2012591029ndash1036

44 Rawlins J Carre F Kervio G Papadakis M Chandra N Edwards C Whyte GPSharma S Ethnic differences in physiological cardiac adaptation to intense physi-cal exercise in highly trained female athletes Circulation 20101211078ndash1085

45 Migliore F Zorzi A Michieli P Perazzolo Marra M Siciliano M Rigato I Bauce BBasso C Toazza D Schiavon M Iliceto S Thiene G Corrado D Prevalence ofcardiomyopathy in Italian asymptomatic children with electrocardiographic T-wave inversion at preparticipation screening Circulation 2012125529ndash538

46 Calo L Sperandii F Martino A Guerra E Cavarretta E Quaranta F Ruvo ESciarra L Parisi A Nigro A Spataro A Pigozzi F Echocardiographic findings in2261 peri-pubertal athletes with or without inverted T waves at electrocardio-gram Heart 2015101193ndash200

47 Sharma S Whyte G Elliott P Padula M Kaushal R Mahon N McKenna WJElectrocardiographic changes in 1000 highly trained junior elite athletes Br JSports Med 199933319ndash324

48 Stein R Medeiros CM Rosito GA Zimerman LI Ribeiro JP Intrinsic sinus andatrioventricular node electrophysiologic adaptations in endurance athletes J AmColl Cardiol 2002391033ndash1038

49 Northcote RJ Canning GP Ballantyne D Electrocardiographic findings in maleveteran endurance athletes Br Heart J 198961155ndash160

50 Meytes I Kaplinsky E Yahini JH Hanne-Paparo N Neufeld HN WenckebachA-V block a frequent feature following heavy physical training Am Heart J197590426ndash430

51 Gati S Sheikh N Ghani S Zaidi A Wilson M Raju H Cox A Reed MPapadakis M Sharma S Should axis deviation or atrial enlargement be categor-ised as abnormal in young athletes The athletersquos electrocardiogram time forre-appraisal of markers of pathology Eur Heart J 2013343641ndash3648

52 Fudge J Harmon KG Owens DS Prutkin JM Salerno JC Asif IM Haruta A PeltoH Rao AL Toresdahl BG Drezner JA Cardiovascular screening in adolescentsand young adults a prospective study comparing the Pre-participation PhysicalEvaluation Monograph 4th Edition and ECG Br J Sports Med 2014481172ndash1178

53 Magalski A McCoy M Zabel M Magee LM Goeke J Main ML Bunten L ReidKJ Ramza BM Cardiovascular screening with electrocardiography and echocar-diography in collegiate athletes Am J Med 2011124511ndash518

54 Baggish AL Hutter AM Jr Wang F Yared K Weiner RB Kupperman E PicardMH Wood MJ Cardiovascular screening in college athletes with and withoutelectrocardiography A cross-sectional study Ann Intern Med 2010152269ndash275

55 Kim JH Noseworthy PA McCarty D Yared K Weiner R Wang F Wood MJHutter AM Picard MH Baggish AL Significance of electrocardiographic rightbundle branch block in trained athletes Am J Cardiol 20111071083ndash1089

56 Rowin EJ Maron BJ Appelbaum E Link MS Gibson CM Lesser JR Haas TSUdelson JE Manning WJ Maron MS Significance of false negative electrocardio-grams in preparticipation screening of athletes for hypertrophic cardiomyop-athy Am J Cardiol 20121101027ndash1032

57 Chen X Zhao T Lu M Yin G Xiangli W Jiang S Prasad S Zhao S The relation-ship between electrocardiographic changes and CMR features in asymptomaticor mildly symptomatic patients with hypertrophic cardiomyopathy Int JCardiovasc Imaging 201430 Suppl 155ndash63

58 Sheikh N Papadakis M Schnell F Panoulas V Malhotra A Wilson M Carre FSharma S Clinical profile of athletes with hypertrophic cardiomyopathy CircCardiovasc Imaging 20158e003454

59 Bent RE Wheeler MT Hadley D Knowles JW Pavlovic A Finocchiaro GHaddad F Salisbury H Race S Shmargad Y Matheson GO Kumar N Saini DFroelicher V Ashley E Perez MV Systematic comparison of digital electrocar-diograms from healthy athletes and patients with hypertrophic cardiomyopathyJ Am Coll Cardiol 2015652462ndash2463

60 Nasir K Bomma C Tandri H Roguin A Dalal D Prakasa K Tichnell C JamesC Spevak PJ Marcus F Calkins H Electrocardiographic features of arrhythmo-genic right ventricular dysplasiacardiomyopathy according to disease severity aneed to broaden diagnostic criteria Circulation 20041101527ndash1534

61 Marcus FI McKenna WJ Sherrill D Basso C Bauce B Bluemke DA Calkins HCorrado D Cox MG Daubert JP Fontaine G Gear K Hauer R Nava A PicardMH Protonotarios N Saffitz JE Sanborn DM Steinberg JS Tandri H Thiene GTowbin JA Tsatsopoulou A Wichter T Zareba W Diagnosis of arrhythmo-genic right ventricular cardiomyopathydysplasia proposed modification of thetask force criteria Circulation 20101211533ndash1541

62 Pelliccia A Di Paolo FM Quattrini FM Basso C Culasso F Popoli G De LucaR Spataro A Biffi A Thiene G Maron BJ Outcomes in athletes with markedECG repolarization abnormalities N Engl J Med 2008358152ndash161

63 Schnell F Riding N Orsquohanlon R Axel Lentz P Donal E Kervio G Matelot DLeurent G Doutreleau S Chevalier L Guerard S Wilson MG Carre FRecognition and significance of pathological T-wave inversions in athletesCirculation 2015131165ndash173

64 Chandra N Bastiaenen R Papadakis M Panoulas VF Ghani S Duschl J FoldesD Raju H Osborne R Sharma S Prevalence of electrocardiographic anomaliesin young individuals relevance to a nationwide cardiac screening program J AmColl Cardiol 2014632028ndash2034

65 Elliott PM Anastasakis A Borger MA Borggrefe M Cecchi F Charron PHagege AA Lafont A Limongelli G Mahrholdt H McKenna WJ Mogensen JNihoyannopoulos P Nistri S Pieper PG Pieske B Rapezzi C Rutten FHTillmanns C Watkins H 2014 ESC Guidelines on diagnosis and management ofhypertrophic cardiomyopathy the Task Force for the Diagnosis andManagement of Hypertrophic Cardiomyopathy of the European Society ofCardiology (ESC) Eur Heart J 2014352733ndash2779

66 Calore C Zorzi A Sheikh N Nese A Facci M Malhotra A Zaidi A Schiavon MPelliccia A Sharma S Corrado D Electrocardiographic anterior T-wave inver-sion in athletes of different ethnicities differential diagnosis between athletersquosheart and cardiomyopathy Eur Heart J 2015372515ndash2527

67 Brosnan M La Gerche A Kalman J Lo W Fallon K MacIsaac A Prior DLComparison of frequency of significant electrocardiographic abnormalities inendurance versus nonendurance athletes Am J Cardiol 20141131567ndash1573

68 Malhotra A Dhutia H Gati S Yeo T-J Dores H Bastiaenen R Merghani RNAFinocchiaro G Sheikh N Steriotis A Zaidi A Millar L Behr E Tome1 MPapadakis1 M Sharma S Prevalence and significance of anterior T wave inver-sion in young white athletes and non athletes JACC 2016691ndash9

69 Riding NR Salah O Sharma S Carre F George KP Farooq A Hamilton BChalabi H Whyte GP Wilson MG ECG and morphologic adaptations in Arabicathletes are the European Society of Cardiologyrsquos recommendations for theinterpretation of the 12-lead ECG appropriate for this ethnicity Br J Sports Med2014481138ndash1143

70 Maron BJ Wolfson JK Ciro E Spirito P Relation of electrocardiographic abnor-malities and patterns of left ventricular hypertrophy identified by 2-dimensionalechocardiography in patients with hypertrophic cardiomyopathy Am J Cardiol198351189ndash194

71 Haghjoo M Mohammadzadeh S Taherpour M Faghfurian B Fazelifar AFAlizadeh A Rad MA Sadr-Ameli MA ST-segment depression as a risk factor inhypertrophic cardiomyopathy Europace 200911643ndash649

72 MacAlpin RN Clinical significance of QS complexes in V1 and V2 without otherelectrocardiographic abnormality Ann Noninvasive Electrocardiol 2004939ndash47

73 Bent RE Wheeler MT Hadley D Froelicher V Ashley E Perez MVComputerized Q wave dimensions in athletes and hypertrophic cardiomyop-athy patients J Electrocardiol 201548362ndash367

74 Riding NR Sheikh N Adamuz C Watt V Farooq A Whyte GP George KPDrezner JA Sharma S Wilson MG Comparison of three current sets of elec-trocardiographic interpretation criteria for use in screening athletes Heart2014101384ndash390

75 Kim JH Baggish AL Electrocardiographic right and left bundle branch block pat-terns in athletes prevalence pathology and clinical significance J Electrocardiol201548380ndash384

76 Le VV Wheeler MT Mandic S Dewey F Fonda H Perez M Sungar G GarzaD Ashley EA Matheson G Froelicher V Addition of the electrocardiogram tothe preparticipation examination of college athletes Clin J Sport Med20102098ndash105


77 Aro AL Anttonen O Tikkanen JT Junttila MJ Kerola T Rissanen HA Reunanen

A Huikuri HV Intraventricular conduction delay in a standard 12-lead electro-cardiogram as a predictor of mortality in the general population Circ ArrhythmElectrophysiol 20114704ndash710

78 Desai AD Yaw TS Yamazaki T Kaykha A Chun S Froelicher VF Prognosticsignificance of quantitative QRS duration Am J Med 2006119600ndash606

79 Dunn T Abdelfattah R Aggarwal S Pickham D Hadley D Froelicher V Are theQRS duration and ST depression cut-points from the Seattle criteria too con-servative J Electrocardiol 201548395ndash398

80 Xiao HB Brecker SJ Gibson DG Relative effects of left ventricular mass andconduction disturbance on activation in patients with pathological left ventricu-lar hypertrophy Br Heart J 199471548ndash553

81 Surawicz B Childers R Deal BJ Gettes LS Bailey JJ Gorgels A Hancock EWJosephson M Kligfield P Kors JA Macfarlane P Mason JW Mirvis DM Okin PPahlm O Rautaharju PM van Herpen G Wagner GS Wellens H AHAACCFHRS recommendations for the standardization and interpretation of the elec-trocardiogram part III intraventricular conduction disturbances a scientificstatement from the American Heart Association Electrocardiography andArrhythmias Committee Council on Clinical Cardiology the American Collegeof Cardiology Foundation and the Heart Rhythm Society endorsed by theInternational Society for Computerized Electrocardiology Circulation2009119e235ndashe240

82 Drezner JA Prutkin JM Harmon KG Orsquokane JW Pelto HF Rao AL HassebrockJD Petek BJ Teteak C Timonen M Zigman M Owens DS Cardiovascularscreening in college athletes J Am Coll Cardiol 2015652353ndash2355

83 Cohen MI Triedman JK Cannon BC Davis AM Drago F Janousek J Klein GJLaw IH Morady FJ Paul T Perry JC Sanatani S Tanel RE PACESHRS expertconsensus statement on the management of the asymptomatic young patientwith a Wolff-Parkinson-White (WPW ventricular preexcitation) electrocardio-graphic pattern developed in partnership between the Pediatric and CongenitalElectrophysiology Society (PACES) and the Heart Rhythm Society (HRS)Endorsed by the governing bodies of PACES HRS the American College ofCardiology Foundation (ACCF) the American Heart Association (AHA) theAmerican Academy of Pediatrics (AAP) and the Canadian Heart RhythmSociety (CHRS) Heart Rhythm 201291006ndash1024

84 Daubert C Ollitrault J Descaves C Mabo P Ritter P Gouffault J Failure of theexercise test to predict the anterograde refractory period of the accessorypathway in Wolff Parkinson White syndrome Pacing Clin Electrophysiol1988111130ndash1138

85 Klein GJ Gulamhusein SS Intermittent preexcitation in the Wolff-Parkinson-White syndrome Am J Cardiol 198352292ndash296

86 Klein GJ Bashore TM Sellers TD Pritchett EL Smith WM Gallagher JJVentricular fibrillation in the Wolff-Parkinson-White syndrome N Engl J Med19793011080ndash1085

87 Schwartz PJ Stramba-Badiale M Crotti L Pedrazzini M Besana A Bosi GGabbarini F Goulene K Insolia R Mannarino S Mosca F Nespoli L Rimini ARosati E Salice P Spazzolini C Prevalence of the congenital long-QT syndromeCirculation 20091201761ndash1767

88 Tester DJ Ackerman MJ Cardiomyopathic and channelopathic causes of suddenunexplained death in infants and children Annu Rev Med 20096069ndash84

89 Eckart RE Shry EA Burke AP McNear JA Appel DA Castillo-Rojas LMAvedissian L Pearse LA Potter RN Tremaine L Gentlesk PJ Huffer L ReichSS Stevenson WG Sudden death in young adults an autopsy-based series ofa population undergoing active surveillance J Am Coll Cardiol2011581254ndash1261

90 Meyer L Stubbs B Fahrenbruch C Maeda C Harmon K Eisenberg M DreznerJ Incidence causes and survival trends from cardiovascular-related sudden car-diac arrest in children and young adults 0 to 35 years of age a 30-year reviewCirculation 20121261363ndash1372

91 Behr E Wood DA Wright M Syrris P Sheppard MN Casey A Davies MJMcKenna W Cardiological assessment of first-degree relatives in suddenarrhythmic death syndrome Lancet 20033621457ndash1459

92 Tester DJ Spoon DB Valdivia HH Makielski JC Ackerman MJ Targeted muta-tional analysis of the RyR2-encoded cardiac ryanodine receptor in sudden unex-plained death a molecular autopsy of 49 medical examinercoronerrsquos casesMayo Clin Proc 2004791380ndash1384

93 Tan HL Hofman N van Langen IM van der Wal AC Wilde AA Sudden unex-plained death heritability and diagnostic yield of cardiological and genetic exami-nation in surviving relatives Circulation 2005112207ndash213

94 Finocchiaro G Papadakis M Robertus JL Dhutia H Steriotis AK Tome MMellor G Merghani A Malhotra A Behr E Sharma S Sheppard MN Etiology ofsudden death in sports insights from a United Kingdom Regional Registry J AmColl Cardiol 2016672108ndash2115

95 Viskin S Rosovski U Sands AJ Chen E Kistler PM Kalman JM RodriguezChavez L Iturralde Torres P Cruz FF Centurion OA Fujiki A Maury P ChenX Krahn AD Roithinger F Zhang L Vincent GM Zeltser D Inaccurate

electrocardiographic interpretation of long QT the majority of physicians can-not recognize a long QT when they see one Heart Rhythm 20052569ndash574

96 Postema PG De Jong JS Van der Bilt IA Wilde AA Accurate electrocardio-graphic assessment of the QT interval teach the tangent Heart Rhythm200851015ndash1018

97 Bazett HC An analysis of the time-relations of electrocardiograms Heart1920353ndash370

98 Malfatto G Beria G Sala S Bonazzi O Schwartz PJ Quantitative analysis of Twave abnormalities and their prognostic implications in the idiopathic long QTsyndrome J Am Coll Cardiol 199423296ndash301

99 Ackerman MJ Zipes DP Kovacs RJ Maron BJ Eligibility and disqualification rec-ommendations for competitive athletes with cardiovascular abnormalities TaskForce 10 The cardiac channelopathies a scientific statement from theAmerican Heart Association and American College of Cardiology J Am CollCardiol 2015662424ndash2428

100 Dhutia H Malhotra A Parpia S Gabus V Finocchiaro G Mellor G Merghani AMillar L Narain R Sheikh N Behr ER Papadakis M Sharma S The prevalenceand significance of a short QT interval in 18 825 low-risk individuals includingathletes Br J Sports Med 201650124ndash129

101 Basavarajaiah S Wilson M Whyte G Shah A Behr E Sharma S Prevalence andsignificance of an isolated long QT interval in elite athletes Eur Heart J2007282944ndash2949

102 Goldenberg I Moss AJ Peterson DR McNitt S Zareba W Andrews MLRobinson JL Locati EH Ackerman MJ Benhorin J Kaufman ES Napolitano CPriori SG Qi M Schwartz PJ Towbin JA Vincent GM Zhang L Risk factors foraborted cardiac arrest and sudden cardiac death in children with the congenitallong-QT syndrome Circulation 20081172184ndash2191

103 Gollob MH Redpath CJ Roberts JD The short QT syndrome proposed diag-nostic criteria J Am Coll Cardiol 201157802ndash812

104 Schwartz PJ Moss AJ Vincent GM Crampton RS Diagnostic criteria for thelong QT syndrome An update Circulation 199388782ndash784

105 Schwartz PJ Crotti L QTc behavior during exercise and genetic testing for thelong-QT syndrome Circulation 20111242181ndash2184

106 Ackerman MJ Priori SG Willems S Berul C Brugada R Calkins H Camm AJEllinor PT Gollob M Hamilton R Hershberger RE Judge DP Le Marec HMcKenna WJ Schulze-Bahr E Semsarian C Towbin JA Watkins H Wilde AWolpert C Zipes DP HRSEHRA expert consensus statement on the state ofgenetic testing for the channelopathies and cardiomyopathies this documentwas developed as a partnership between the Heart Rhythm Society (HRS) andthe European Heart Rhythm Association (EHRA) Heart Rhythm201181308ndash1339

107 Wilde AA Antzelevitch C Borggrefe M Brugada J Brugada R Brugada PCorrado D Hauer RN Kass RS Nademanee K Priori SG Towbin JA Proposeddiagnostic criteria for the Brugada syndrome consensus report Circulation20021062514ndash2519

108 Bayes de Luna A Brugada J Baranchuk A Borggrefe M Breithardt GGoldwasser D Lambiase P Riera AP Garcia-Niebla J Pastore C Oreto GMcKenna W Zareba W Brugada R Brugada P Current electrocardiographiccriteria for diagnosis of Brugada pattern a consensus report J Electrocardiol201245433ndash442

109 Priori SG Wilde AA Horie M Cho Y Behr ER Berul C Blom N Brugada JChiang CE Huikuri H Kannankeril P Krahn A Leenhardt A Moss A SchwartzPJ Shimizu W Tomaselli G Tracy C HRSEHRAAPHRS expert consensusstatement on the diagnosis and management of patients with inherited primaryarrhythmia syndromes document endorsed by HRS EHRA and APHRS in May2013 and by ACCF AHA PACES and AEPC in June 2013 Heart Rhythm2013101932ndash1963

110 Zorzi A Leoni L Di Paolo FM Rigato I Migliore F Bauce B Pelliccia A CorradoD Differential diagnosis between early repolarization of athletersquos heart and coved-type Brugada electrocardiogram Am J Cardiol 2015115529ndash532

111 Verdile L Maron BJ Pelliccia A Spataro A Santini M Biffi A Clinical significanceof exercise-induced ventricular tachyarrhythmias in trained athletes without car-diovascular abnormalities Heart Rhythm 20151278ndash85

112 Biffi A Pelliccia A Verdile L Fernando F Spataro A Caselli S Santini M MaronBJ Long-term clinical significance of frequent and complex ventricular tachyar-rhythmias in trained athletes J Am Coll Cardiol 200240446ndash452

113 Novak J Zorzi A Castelletti S Pantasis A Rigato I Corrado D McKenna WLambiase PD Electrocardiographic differentiation of idiopathic right ventricularoutflow tract ectopy from early arrhythmogenic right ventricular cardiomyop-athy Europace 2016 doi 101093europaceeuw018

114 Corrado D Basso C Leoni L Tokajuk B Turrini P Bauce B Migliore F Pavei ATarantini G Napodano M Ramondo A Buja G Iliceto S Thiene G Three-dimensional electroanatomical voltage mapping and histologic evaluation ofmyocardial substrate in right ventricular outflow tract tachycardia J Am CollCardiol 200851731ndash739

18 S Sharma et al

115 Heidbuchel H Hoogsteen J Fagard R Vanhees L Ector H Willems R VanLierde J High prevalence of right ventricular involvement in endurance athleteswith ventricular arrhythmias Role of an electrophysiologic study in risk stratifi-cation Eur Heart J 2003241473ndash1480

116 Biffi A Maron BJ Verdile L Fernando F Spataro A Marcello G Ciardo RAmmirati F Colivicchi F Pelliccia A Impact of physical deconditioning on ven-tricular tachyarrhythmias in trained athletes J Am Coll Cardiol2004441053ndash1058

117 Delise P Lanari E Sitta N Centa M Allocca G Biffi A Influence of training onthe number and complexity of frequent VPBs in healthy athletes J CardiovascMed (Hagerstown) 201112157ndash161

118 Delise P Sitta N Lanari E Berton G Centa M Allocca G Cati A Biffi A Long-term effect of continuing sports activity in competitive athletes with frequentventricular premature complexes and apparently normal heart Am J Cardiol20131121396ndash1402

119 Anderson JL Halperin JL Albert NM Bozkurt B Brindis RG Curtis LH DeMetsD Guyton RA Hochman JS Kovacs RJ Ohman EM Pressler SJ Sellke FWShen WK Wann LS Curtis AB Ellenbogen KA Estes NA 3rd Ezekowitz MDJackman WM January CT Lowe JE Page RL Slotwiner DJ Stevenson WGTracy CM Fuster V Ryden LE Cannom DS Crijns HJ Curtis AB EllenbogenKA Le Heuzey JY Kay GN Olsson SB Prystowsky EN Tamargo JL Wann SManagement of patients with atrial fibrillation (compilation of 2006 ACCFAHAESC and 2011 ACCFAHAHRS recommendations) a report of theAmerican College of CardiologyAmerican Heart Association Task Force onPractice Guidelines J Am Coll Cardiol 2013611935ndash1944

120 Aagaard P Sahlen A Braunschweig F Performance trends and cardiac bio-markers in a 30-km cross-country race 1993-2007 Med Sci Sports Exerc201244894ndash899

121 Sahlen A Gustafsson TP Svensson JE Marklund T Winter R Linde CBraunschweig F Predisposing factors and consequences of elevated biomarker lev-els in long-distance runners aged gtor=55 years Am J Cardiol 20091041434ndash1440

122 Rose G Baxter PJ Reid DD McCartney P Prevalence and prognosis of electro-cardiographic findings in middle-aged men Br Heart J 197840636ndash643

123 Chou R Arora B Dana T Fu R Walker M Humphrey L Screening asymptomaticadults with resting or exercise electrocardiography a review of the evidence forthe US Preventive Services Task Force Ann Intern Med 2011155375ndash385

124 Daviglus ML Liao Y Greenland P Dyer AR Liu K Xie X Huang CF Prineas RJStamler J Association of nonspecific minor ST-T abnormalities with cardiovas-cular mortality the Chicago Western Electric Study Jama 1999281530ndash536

125 Borjesson M Urhausen A Kouidi E Dugmore D Sharma S Halle M HeidbuchelH Bjornstad HH Gielen S Mezzani A Corrado D Pelliccia A Vanhees LCardiovascular evaluation of middle-agedsenior individuals engaged in leisure-timesport activities position stand from the sections of exercise physiology and sportscardiology of the European Association of Cardiovascular Prevention andRehabilitation Eur J Cardiovasc Prev Rehabil 201118446ndash458

126 Maron BJ Araujo CG Thompson PD Fletcher GF de Luna AB Fleg JL Pelliccia ABalady GJ Furlanello F Van Camp SP Elosua R Chaitman BR Bazzarre TLRecommendations for preparticipation screening and the assessment of cardiovas-cular disease in masters athletes an advisory for healthcare professionals from theworking groups of the World Heart Federation the International Federation ofSports Medicine and the American Heart Association Committee on ExerciseCardiac Rehabilitation and Prevention Circulation 2001103327ndash334


ehw631-TF1

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Introduction

Cardiovascular-related sudden death is the leading cause of mortality inathletes during sport and exercise1ndash3 The majority of disorders associ-ated with an increased risk of sudden cardiac death (SCD) are sug-gested or identified by abnormalities on a resting 12-lead ECGWhether used for the evaluation of cardiovascular-related symptomsa family history of inheritable cardiac disease or premature SCD or forscreening of asymptomatic athletes ECG interpretation is an essentialskill for all physicians involved in the cardiovascular care of athletes

The 2015 summit on ECG interpretationin athletesOver the last decade ECG interpretation standards have undergoneseveral modifications to improve the accuracy of detecting potentiallylife threatening cardiac conditions in young athletes while also limitingfalse positive results4ndash15 In February 2015 an international group ofexperts convened in Seattle Washington to update contemporaryrecommendations for ECG interpretation in asymptomatic athletesaged 12ndash35 years The goals of the summit meeting were to (i)update ECG interpretation standards based on new and emergingresearch and (ii) develop a clear guide to the appropriate evaluationof ECG abnormalities for conditions associated with SCD in athletesIn the presence of cardiac symptoms or a family history of inheritedcardiovascular disease or premature SCD a normal ECG should notpreclude further assessment

This document provides the most updated evidence-based recom-mendations developed with thoughtful attention to balance sensitivityand specificity while maintaining a clear and practical checklist of find-ings to guide ECG interpretation for physicians and the appropriateevaluation of ECG abnormalities A summary of the consensus rec-ommendations is presented in Figure 1 Tables 1 and 2

LimitationsWhile ECG increases the ability to detect underlying cardiovascularconditions associated with SCD ECG as a diagnostic tool has limitationsin both sensitivity and specificity Specifically ECG is unable to detectanomalous coronary arteries premature coronary atherosclerosis andaortopathies In some instances patients with cardiomyopathies particu-larly arrhythmogenic right ventricular cardiomyopathy (ARVC) mayalso reveal a normal ECG Thus an ECG will not detect all conditionspredisposing to SCD Furthermore inter-observer variability amongphysicians remains a major concern16ndash18 despite studies demonstratingthat using standardized criteria improves interpretation accuracy1920


Physiological cardiac adaptations toregular exerciseRegular and long-term participation in intensive exercise (minimumof 4 h per week) is associated with unique electrical manifestations

Figure 1 International consensus standards for electrocardiographic interpretation in athletes AV atrioventriular block LBBB left bundle branchblock LVH left ventricular hypertrophy RBBB right bundle branch block RVH right ventricular hypertrophy PVC premature ventricular contrac-tion SCD sudden cardiac death

2 S Sharma et al
















conduction delay





120 ms)






























Continued
























4 S Sharma et al



diseasea




HCM

DCM

LVNC


involvement)

Myocarditis

Echocardiography

CMR

Exercise ECG test









myocarditis






genetic screening



normal results


the inferior leads

HCM

DCM

LVNC

Myocarditis


cal suspicion


rior leadsc

ARVC

DCM

Echocardiography

CMR

Exercise ECG test


SAECG



initial testing


DCM

LVNC

ARVC

Myocarditis




DCM

LVNC

Myocarditis

Prior MI

Echocardiography













CAD


block

DCM

HCM

LVNC

Sarcoidosis

Myocarditis

Echocardiography


study)d





delay gt_ 140 ms

DCM

HCM

LVNC




CMR

Exercise ECG test


SAECG



rion for ARVC

Continued


Table 2 Continued


diseasea



lar contractions

HCM

DCM

LVNC

ARVC

Myocarditis

Sarcoidosis

Echocardiography

24 h ECG monitor

Exercise ECG test





disease



Echocardiography



pathway





sports


day


medication


tives if possible






500 ms


rhythm specialist







lt 30 BPM


disease


activity


suspicion


400 ms


disease


activity

Exercise ECG test


suspicion


tricular block


disease

Echocardiography


Exercise ECG test


on echo findings


disease

Echocardiography


Exercise ECG test


suspicion


disease

Echocardiography

CMR


Exercise ECG test





ECG findings


suspicion


6 S Sharma et al









E

F

DA

B

C


8 S Sharma et al











Evaluation














Evaluation



A B


10 S Sharma et al




Evaluation




Evaluation





Evaluation



Evaluation




















12 S Sharma et al



Evaluation







Evaluation



Evaluation





Evaluation



Evaluation





Evaluation




14 S Sharma et al




Evaluation




Evaluation




Conclusion













































16 S Sharma et al




















































































18 S Sharma et al














ehw631-TF1

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ehw631-TF6

ehw631-TF7

ehw631-TF8
















conduction delay





120 ms)






























Continued
























4 S Sharma et al



diseasea




HCM

DCM

LVNC


involvement)

Myocarditis

Echocardiography

CMR

Exercise ECG test









myocarditis






genetic screening



normal results


the inferior leads

HCM

DCM

LVNC

Myocarditis


cal suspicion


rior leadsc

ARVC

DCM

Echocardiography

CMR

Exercise ECG test


SAECG



initial testing


DCM

LVNC

ARVC

Myocarditis




DCM

LVNC

Myocarditis

Prior MI

Echocardiography













CAD


block

DCM

HCM

LVNC

Sarcoidosis

Myocarditis

Echocardiography


study)d





delay gt_ 140 ms

DCM

HCM

LVNC




CMR

Exercise ECG test


SAECG



rion for ARVC

Continued


Table 2 Continued


diseasea



lar contractions

HCM

DCM

LVNC

ARVC

Myocarditis

Sarcoidosis

Echocardiography

24 h ECG monitor

Exercise ECG test





disease



Echocardiography



pathway





sports


day


medication


tives if possible






500 ms


rhythm specialist







lt 30 BPM


disease


activity


suspicion


400 ms


disease


activity

Exercise ECG test


suspicion


tricular block


disease

Echocardiography


Exercise ECG test


on echo findings


disease

Echocardiography


Exercise ECG test


suspicion


disease

Echocardiography

CMR


Exercise ECG test





ECG findings


suspicion


6 S Sharma et al









E

F

DA

B

C


8 S Sharma et al











Evaluation














Evaluation



A B


10 S Sharma et al




Evaluation




Evaluation





Evaluation



Evaluation




















12 S Sharma et al



Evaluation







Evaluation



Evaluation





Evaluation



Evaluation





Evaluation




14 S Sharma et al




Evaluation




Evaluation




Conclusion













































16 S Sharma et al




















































































18 S Sharma et al














ehw631-TF1

ehw631-TF2

ehw631-TF3

ehw631-TF4

ehw631-TF5

ehw631-TF6

ehw631-TF7

ehw631-TF8























4 S Sharma et al



diseasea




HCM

DCM

LVNC


involvement)

Myocarditis

Echocardiography

CMR

Exercise ECG test









myocarditis






genetic screening



normal results


the inferior leads

HCM

DCM

LVNC

Myocarditis


cal suspicion


rior leadsc

ARVC

DCM

Echocardiography

CMR

Exercise ECG test


SAECG



initial testing


DCM

LVNC

ARVC

Myocarditis




DCM

LVNC

Myocarditis

Prior MI

Echocardiography













CAD


block

DCM

HCM

LVNC

Sarcoidosis

Myocarditis

Echocardiography


study)d





delay gt_ 140 ms

DCM

HCM

LVNC




CMR

Exercise ECG test


SAECG



rion for ARVC

Continued


Table 2 Continued


diseasea



lar contractions

HCM

DCM

LVNC

ARVC

Myocarditis

Sarcoidosis

Echocardiography

24 h ECG monitor

Exercise ECG test





disease



Echocardiography



pathway





sports


day


medication


tives if possible






500 ms


rhythm specialist







lt 30 BPM


disease


activity


suspicion


400 ms


disease


activity

Exercise ECG test


suspicion


tricular block


disease

Echocardiography


Exercise ECG test


on echo findings


disease

Echocardiography


Exercise ECG test


suspicion


disease

Echocardiography

CMR


Exercise ECG test





ECG findings


suspicion


6 S Sharma et al









E

F

DA

B

C


8 S Sharma et al











Evaluation














Evaluation



A B


10 S Sharma et al




Evaluation




Evaluation





Evaluation



Evaluation




















12 S Sharma et al



Evaluation







Evaluation



Evaluation





Evaluation



Evaluation





Evaluation




14 S Sharma et al




Evaluation




Evaluation




Conclusion













































16 S Sharma et al




















































































18 S Sharma et al














ehw631-TF1

ehw631-TF2

ehw631-TF3

ehw631-TF4

ehw631-TF5

ehw631-TF6

ehw631-TF7

ehw631-TF8



diseasea




HCM

DCM

LVNC


involvement)

Myocarditis

Echocardiography

CMR

Exercise ECG test









myocarditis






genetic screening



normal results


the inferior leads

HCM

DCM

LVNC

Myocarditis


cal suspicion


rior leadsc

ARVC

DCM

Echocardiography

CMR

Exercise ECG test


SAECG



initial testing


DCM

LVNC

ARVC

Myocarditis




DCM

LVNC

Myocarditis

Prior MI

Echocardiography













CAD


block

DCM

HCM

LVNC

Sarcoidosis

Myocarditis

Echocardiography


study)d





delay gt_ 140 ms

DCM

HCM

LVNC




CMR

Exercise ECG test


SAECG



rion for ARVC

Continued


Table 2 Continued


diseasea



lar contractions

HCM

DCM

LVNC

ARVC

Myocarditis

Sarcoidosis

Echocardiography

24 h ECG monitor

Exercise ECG test





disease



Echocardiography



pathway





sports


day


medication


tives if possible






500 ms


rhythm specialist







lt 30 BPM


disease


activity


suspicion


400 ms


disease


activity

Exercise ECG test


suspicion


tricular block


disease

Echocardiography


Exercise ECG test


on echo findings


disease

Echocardiography


Exercise ECG test


suspicion


disease

Echocardiography

CMR


Exercise ECG test





ECG findings


suspicion


6 S Sharma et al









E

F

DA

B

C


8 S Sharma et al











Evaluation














Evaluation



A B


10 S Sharma et al




Evaluation




Evaluation





Evaluation



Evaluation




















12 S Sharma et al



Evaluation







Evaluation



Evaluation





Evaluation



Evaluation





Evaluation




14 S Sharma et al




Evaluation




Evaluation




Conclusion













































16 S Sharma et al




















































































18 S Sharma et al














ehw631-TF1

ehw631-TF2

ehw631-TF3

ehw631-TF4

ehw631-TF5

ehw631-TF6

ehw631-TF7

ehw631-TF8

Table 2 Continued


diseasea



lar contractions

HCM

DCM

LVNC

ARVC

Myocarditis

Sarcoidosis

Echocardiography

24 h ECG monitor

Exercise ECG test





disease



Echocardiography



pathway





sports


day


medication


tives if possible






500 ms


rhythm specialist







lt 30 BPM


disease


activity


suspicion


400 ms


disease


activity

Exercise ECG test


suspicion


tricular block


disease

Echocardiography


Exercise ECG test


on echo findings


disease

Echocardiography


Exercise ECG test


suspicion


disease

Echocardiography

CMR


Exercise ECG test





ECG findings


suspicion


6 S Sharma et al









E

F

DA

B

C


8 S Sharma et al











Evaluation














Evaluation



A B


10 S Sharma et al




Evaluation




Evaluation





Evaluation



Evaluation




















12 S Sharma et al



Evaluation







Evaluation



Evaluation





Evaluation



Evaluation





Evaluation




14 S Sharma et al




Evaluation




Evaluation




Conclusion













































16 S Sharma et al




















































































18 S Sharma et al














ehw631-TF1

ehw631-TF2

ehw631-TF3

ehw631-TF4

ehw631-TF5

ehw631-TF6

ehw631-TF7

ehw631-TF8









E

F

DA

B

C


8 S Sharma et al











Evaluation














Evaluation



A B


10 S Sharma et al




Evaluation




Evaluation





Evaluation



Evaluation




















12 S Sharma et al



Evaluation







Evaluation



Evaluation





Evaluation



Evaluation





Evaluation




14 S Sharma et al




Evaluation




Evaluation




Conclusion













































16 S Sharma et al




















































































18 S Sharma et al














ehw631-TF1

ehw631-TF2

ehw631-TF3

ehw631-TF4

ehw631-TF5

ehw631-TF6

ehw631-TF7

ehw631-TF8











Evaluation














Evaluation



A B


10 S Sharma et al




Evaluation




Evaluation





Evaluation



Evaluation




















12 S Sharma et al



Evaluation







Evaluation



Evaluation





Evaluation



Evaluation





Evaluation




14 S Sharma et al




Evaluation




Evaluation




Conclusion













































16 S Sharma et al




















































































18 S Sharma et al














ehw631-TF1

ehw631-TF2

ehw631-TF3

ehw631-TF4

ehw631-TF5

ehw631-TF6

ehw631-TF7

ehw631-TF8







Evaluation



A B


10 S Sharma et al




Evaluation




Evaluation





Evaluation



Evaluation




















12 S Sharma et al



Evaluation







Evaluation



Evaluation





Evaluation



Evaluation





Evaluation




14 S Sharma et al




Evaluation




Evaluation




Conclusion













































16 S Sharma et al




















































































18 S Sharma et al














ehw631-TF1

ehw631-TF2

ehw631-TF3

ehw631-TF4

ehw631-TF5

ehw631-TF6

ehw631-TF7

ehw631-TF8




Evaluation




Evaluation





Evaluation



Evaluation




















12 S Sharma et al



Evaluation







Evaluation



Evaluation





Evaluation



Evaluation





Evaluation




14 S Sharma et al




Evaluation




Evaluation




Conclusion













































16 S Sharma et al




















































































18 S Sharma et al














ehw631-TF1

ehw631-TF2

ehw631-TF3

ehw631-TF4

ehw631-TF5

ehw631-TF6

ehw631-TF7

ehw631-TF8

















12 S Sharma et al



Evaluation







Evaluation



Evaluation





Evaluation



Evaluation





Evaluation




14 S Sharma et al




Evaluation




Evaluation




Conclusion













































16 S Sharma et al




















































































18 S Sharma et al














ehw631-TF1

ehw631-TF2

ehw631-TF3

ehw631-TF4

ehw631-TF5

ehw631-TF6

ehw631-TF7

ehw631-TF8



Evaluation







Evaluation



Evaluation





Evaluation



Evaluation





Evaluation




14 S Sharma et al




Evaluation




Evaluation




Conclusion













































16 S Sharma et al




















































































18 S Sharma et al














ehw631-TF1

ehw631-TF2

ehw631-TF3

ehw631-TF4

ehw631-TF5

ehw631-TF6

ehw631-TF7

ehw631-TF8


Evaluation



Evaluation





Evaluation




14 S Sharma et al




Evaluation




Evaluation




Conclusion













































16 S Sharma et al




















































































18 S Sharma et al














ehw631-TF1

ehw631-TF2

ehw631-TF3

ehw631-TF4

ehw631-TF5

ehw631-TF6

ehw631-TF7

ehw631-TF8




Evaluation




Evaluation




Conclusion













































16 S Sharma et al




















































































18 S Sharma et al














ehw631-TF1

ehw631-TF2

ehw631-TF3

ehw631-TF4

ehw631-TF5

ehw631-TF6

ehw631-TF7

ehw631-TF8







































16 S Sharma et al




















































































18 S Sharma et al














ehw631-TF1

ehw631-TF2

ehw631-TF3

ehw631-TF4

ehw631-TF5

ehw631-TF6

ehw631-TF7

ehw631-TF8




















































































18 S Sharma et al














ehw631-TF1

ehw631-TF2

ehw631-TF3

ehw631-TF4

ehw631-TF5

ehw631-TF6

ehw631-TF7

ehw631-TF8














ehw631-TF1

ehw631-TF2

ehw631-TF3

ehw631-TF4

ehw631-TF5

ehw631-TF6

ehw631-TF7

ehw631-TF8

international recommendations for electrocardiographic...

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