ECG in athletes:

limits of normal

Prof. Samir M. Rafla, FACC, FESC,

FHRS

Cardiology Dept.

Alexandria University

When the ECG of an athlete is examined,

the main objective is to distinguish

between physiological patterns that should

cause no alarm and those that require

action and/or additional testing to exclude

(or confirm) the suspicion of an underlying

cardiovascular condition carrying the risk

of sudden death during sports.

ECG changes in athletes are common and

usually reflect structural and electrical

remodelling of the heart as an adaptation

to regular physical training (athlete's

heart).

Group 1: common

and training-related

ECG changes

Group 2: uncommon and

training-unrelated ECG

changes

Sinus bradycardia T-wave inversion

First-degree AV block ST-segment depression

Incomplete RBBB Pathological Q-waves

Early repolarization Left atrial enlargement

Isolated QRS voltage

criteria for LV

hypertrophy

Left-axis deviation/left

anterior hemiblock

Classification of abnormalities of the athlete's ECG

Group 1: common

and training-related

ECG changes

Group 2: uncommon and

training-unrelated ECG changes

Right-axis deviation/left posterior

hemiblock

Right ventricular hypertrophy

Ventricular pre-excitation

Complete LBBB or RBBB

Long- or short-QT interval

Brugada-like early repolarization

Classification of abnormalities of the athlete's ECG

ECG demonstrates sinus bradycardia with a heart

rate of 40 bpm. P wave before every QRS complex,

normal P wave axis (frontal plane 0–90°s).

ECG demonstrates sinus arrhythmia. Note the

irregular heart rate that varies with respiration.

The P waves are upright in leads I and aVF

(frontal plane) suggesting a sinus origin.

ECG of a 28-year-old asymptomatic handball player

demonstrating a junctional escape rhythm. Note the

constant RR interval between beats.

ECG shows an ectopic atrial rhythm. The atrial rate

is 63 beats/min and the P wave morphology is

negative in leads II, III and aVF (arrows), also known

as a low atrial rhythm.

ECG shows first-degree AV block (PR interval

>200 ms).

A 18 y college basketball player is noted to have an irregular

pulse. Voltage suggesting LVH is present (S in V2 > 30 mV).

Sinus brad., 1st A-V block, and even Mobitz I 2nd A-V block.

No specific treat. is necessary in asymptomatic pts.

ECG shows Mobitz type I (Wenckebach)

second-degree AV block

IRBBB is defined by a QRS duration <120 ms with an RBBB

pattern: terminal R wave in lead V1 (rsR') and wide terminal S

wave in leads I and V6 . IRBBB is seen in less than 10% of the

general population but is observed in up to 40% of highly

trained athletes, particularly those engaged in endurance

training and mixed sport disciplines that include both aerobic

and anaerobic components

Incomplete RBBB should be

differentiated from a Brugada-ECG which

is characterized by a slow, positive

deflection at the R-ST junction (‘J-wave’),

which is evident in leads V1 and V2, with

minimal or no reciprocal changes in other

leads. Unlike the R′-wave seen in RBBB,

the J-wave seen in Brugada syndrome

does not indicate delayed RV activation,

but reflects early repolarization with J-

point elevation and a high take-off ST-

segment.

ECG from a patient with arrhythmogenic right ventricular

cardiomyopathy showing delayed S wave upstroke in V1

(arrow), low voltages in limb leads < 5 mm (circles) and

inverted T waves in anterior precordial leads (V1–V4) and

inferior leads (III and aVF).

(A) Brugada- mimicking IRBBB. The 'J wave’ of Brugada-ECG

is confined to right precordial leads (V1 and V2) without

reciprocal 's wave' (of comparable voltage and duration) in

leads I and V6 (arrowheads). (B) IRBBB in a trained athlete.

The RV conduction interval is mildly prolonged (QRS

duration=115 ms) with a typical rSR' pattern in V1 (arrow).

(A) Borderline Brugada-ECG pattern mimicking incomplete RBBB. Unlike the ‘R-wave’ of RBBB, the ‘J-wave’ (arrows) of

Brugada-ECG is confined to right precordial leads (V1 and V2) without reciprocal ‘S-wave’ (of comparable voltage and

duration) in the leads L1 and V6 (arrowhead). (B) In this case,

definitive diagnosis of Brugada ECG was achieved by a drug

challenge with sodium channel blockers which unmasked

diagnostic ‘coved type’ (arrows) pattern (V1 and V2).

Different patterns of precordial early repolarization

in two healthy athletes. (A) ST-segment elevation

with upward concavity (arrows), followed by a

positive T-wave (arrowheads). (B) ST-segment

elevation with upward convexity (arrows), followed

by a negative T-wave (arrowheads)

ECG from a 29-year-old asymptomatic soccer player

demonstrating early repolarisation (J-point and ST elevation)

in I, II, aVF, V2–V6 (arrows) and tall, peaked T waves (circles).

These are common, training-related findings in athletes and

do not require more evaluation

(A and B) Classic definition of early repolarisation based on ST elevation

at QRS end (J-point). Examples without (A) and with (B) a J wave. (C and

D) New definitions of early repolarisation showing slurred QRS

downstroke (C) and J-wave (D) without ST elevation

ECG from a 19-year-old asymptomatic soccer player

demonstrating voltage criteria for LV hypertrophy (S-V1+R-

V5>35 mm). Note the absence of left atrial enlargement, left

axis deviation, ST depression, T wave inversion, or

pathological Q waves.

A patient with hypertrophic cardiomyopathy

ECG from a 24-year-old asymptomatic black/African soccer

player demonstrating 'domed' ST elevation followed by T wave

inversion in leads V1–V4 (circles). This is a normal

repolarisation pattern in black/African athletes.

(A) Normal variant repolarisation changes in a black/African athlete

characterised by domed ST segment elevation and T wave inversion in

V1–V4. (B) Pathological T wave inversion in V1–V3. Note the isoelectric ST

segment. The absence of ST segment elevation prior to T wave inversion

makes this ECG abnormal. Additional testing is required to rule out

arrhythmogenic right ventricular cardiomyopathy.

(A) Normal variant repolarisation changes in a black/African

athlete characterised by domed ST segment elevation and T

wave inversion in V1–V4. (B) A downsloping ST segment

elevation followed by T wave inversion in V1–V2 suggestive

of a Brugada-pattern ECG.

Right precordial T-wave inversion in a patient with ARVC. Note

that unlike early repolarization, in the ARVC the right

precordial leads do not demonstrate any elevation of the ST-

segment.

A- Early

repolarization

pattern in a

healthy black

athlete

characterized by

right precordial

T-wave

inversion

(arrowhead)

preceded by ST-

segment

elevation

(arrow).

Twelve-lead ECG of an asymptomatic athlete with HCM. The

disease was suspected at pre-participation evaluation thanks

to ECG abnormalities consisting of increased QRS voltages

and inverted T-waves in lateral leads. HCM was diagnosed by

echocardiography afterwards.

Twelve-lead ECG in an asymptomatic athlete with ARVC.

The athlete was referred for further echocardiographic

examination and cardiac magnetic resonance because of

ECG abnormalities found at pre-participation evaluation

which consisted of inverted T-waves in the inferior and

anteroseptal leads and low QRS voltages in the peripheral

leads.

Clues which distinguish a normal “athlete’s heart” include :- LV wall thickness generally 13 mm; upper limit physiologic hypertrophy approximately 16 mm.

•LV systolic function is normal, even if mild LV dilatation is present. - Absence of a systolic murmur consist with LV outflow tract obstr. - No personal symptoms suggesting HCM (eg, syncope); no family hist. of S. cardiac death, HCM, etc. - Decrease in wall thickness with cessation of athletic training.

ST-segment depression

Although ST-segment elevation due to early

repolarization is a common finding in the

basal ECG of trained athletes, resting ST-

segment depression is rarely seen.

RecommendationDemonstration of ST-segment depression on

resting ECG, either isolated or associated

with T-wave inversion, should prompt further

investigations to exclude heart disease

Right atrial enlargement and right ventricular

hypertrophy

ECG evidence of RA enlargement and/or RV

hypertrophy are uncommon findings in athletes. Sokolow–Lyon voltage criteria for RV hypertrophy

(R−VI+S−V5 >10.5 mm) were seen in one of 172

(0.6%) professional soccer players.

Recommendation: Though uncommon, if present

the ECG pattern of atrial enlargement and/or RV

hypertrophy should not be interpreted as a

manifestation of exercise-induced cardiac

remodelling. The presence of either congenital or

acquired heart diseases associated with an

increased RA size and/or pathological RV

dilatation/hypertrophy should be excluded.

F6 ECG recording of a patient with ARVC showing non-specific RV conduction

defect, which is characterized by an increase of QRS duration (115 ms) in the right

precordial leads, associated with an epsilon wave (arrow) in V1 (i.e. a low

amplitude, low-frequency wave occurring after the end of the QRS) and a

prolonged S-wave upstroke in V1 and V2 (arrowhead).

Ventricular pre-excitation (Wolff–Parkinson–White) Athletes with a diagnosis of ventricular

pre-excitation should be referred to a specialist

for evaluation by electrophysiological study

(either transesophageal or intracardiac) for the

inducibility of AV re-entrant tachycardia and

refractoriness of the accessory pathway

(shortest pre-excited RR interval at rest and

during exercise or adrenergic drug stimulation),

which may influence eligibility to athletic

competition, risk stratification, and therapy,

including catheter ablation.

Long-QT interval- RecommendationIt has been suggested that the demonstration of

a QTc value of ≥500 ms, otherwise unexplained,

is indicative of unequivocal LQTS, regardless of

family history and symptoms. Athletes with QTc

intervals >440 ms (males)/460 (females) and <500

ms represent a ‘grey zone’ which requires

detailed assessment to achieve a definitive

diagnosis. A careful family and personal history

is important for the assessment of the genetic

nature and the presence of relevant symptoms,

such as syncopal episodes, which increase the

probability of LQTS

Short-QT interval

RecommendationAfter identification of an abnormally short-QTc

interval in an athlete (QTc <360-380 ms), causes of

transient QT shortening, such as hypercalcaemia,

hyperkalemia, hyperthermia, acidosis, and some

drugs (e.g. digitalis), must be ruled out. It has

been recently reported that a QTc interval ≤380 ms

in strength trained athletes may be a marker of

abuse of anabolic androgenic steroids. In the

absence of acquired causes of short-QT interval,

the athlete should be referred for familial ECG-

clinical screening and molecular genetic

evaluation.

Fig. 7: Patterns of Brugada ECG. Type 1 Brugada ECG is

characterized by a ‘coved’ ST-segment elevation ≥2 mm

(0.2 mV) followed by a negative T wave (A). The Type 2

Brugada ECG shows a ‘saddleback’ morphology with a

high takeoff (≥2 mm) ST-segment elevation, remaining ≥1

mm above the baseline, followed by a biphasic (B) or

positive (C) T-wave. Type 3 has either a coved or

saddleback morphology with J point elevation ≥2 mm but

the terminal portion of ST-segment <1 mm (D).

Fig 8

Fig 8: Differential diagnosis between

representative right precordial ECG patterns from

(A) a Brugada patient and (B) two trained athletes.

Vertical lines mark the J-point (STJ) and the point

80 ms after the J-point (ST80) where the amplitudes

of ST-segment elevation are calculated. ‘Coved’

type ST-segment elevation in the patient with

Brugada syndrome is characterized by a

‘downsloping’ elevated ST-segment with a

STJ/ST80 ratio of 1.9. Right precordial early

repolarization patterns in both athletes show an

‘upsloping’ ST-segment elevation with

STJ/ST80 ratio <1; 0.7 for the ‘concave’ toward the

top (B, top) and 0.68 for the ‘convex’ toward the top

(B, bottom) ST-segment elevation.

F9