Ecg in athletes limits of normal-samir rafla . cardio egypt 2015
ECG in athletes:
limits of normal
Prof. Samir M. Rafla, FACC, FESC,
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
Group 1: common
Group 2: uncommon and
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
Classification of abnormalities of the athlete's ECG
Group 1: common
Group 2: uncommon and
training-unrelated ECG changes
Right-axis deviation/left posterior
Right ventricular hypertrophy
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
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-
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.
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-
pattern in a
preceded by ST-
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
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
Clues which distinguish a normal “athlete’s heart”
- 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,
- Decrease in wall thickness with cessation of
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.
Demonstration 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
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- Recommendation
It 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
After 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
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: 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.