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com

Journal of Electrocardiology 45 (2012) 433 – 442

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Current electrocardiographic criteria for diagnosis of Brugada pattern: a

consensus report☆
Antonio Bayés de Luna, MD, PhD, a,⁎ Josep Brugada, MD, PhD, b Adrian Baranchuk, MD, c
Martin Borggrefe, MD, d Guenter Breithardt, MD, e Diego Goldwasser, MD, a
Pier Lambiase, MD, f Andrés Pérez Riera, MD, PhD, g Javier Garcia-Niebla, RN, h
Carlos Pastore, MD, PhD, i Giuseppe Oreto, MD, j William McKenna, MD, f
Wojciech Zareba, MD, PhD, k Ramon Brugada, MD, PhD, l Pedro Brugada, MD, PhD m
a
Institut Català Ciències Cardiovasculars–Hospital Sant Pau, Barcelona, Spain
b
Hospital Clínico, Barcelona, Spain
c
Kingston General Hospital, Kingston, Canada
d
Universitätsmedizin Mannheim-I. Medizinische Klinik, Mannheim, Germany
e
Med.Klinik & Poliklinik, Universität Münster, Münster, Germany
f
Heart Hospital, UCL, London, UK
g
Facultad de Medicina del ABC-Santo André, Sao Paulo, Brasil
h
Cannary Islands, Spain
i
Instituto do Coraçao, Sao Paulo, Brasil
j
Universita de Messina, Messina, Italy
k
University of Rochester Medical Center, Rochester, NY, USA
l
Cardiovascular Genetic Center UdG-IDIBGI, Girona, Spain
m
Free University of Brussels (UZ Brussel) VUB, Brussels, Belgium
Received 20 March 2012

Abstract Brugada syndrome is an inherited heart disease without structural abnormalities that is thought to
arise as a result of accelerated inactivation of Na channels and predominance of transient outward
K current (Ito) to generate a voltage gradient in the right ventricular layers. This gradient triggers
ventricular tachycardia/ventricular fibrillation possibly through a phase 2 reentrant mechanism.
The Brugada electrocardiographic (ECG) pattern, which can be dynamic and is sometimes
concealed, being only recorded in upper precordial leads, is the hallmark of Brugada syndrome.
Because of limitations of previous consensus documents describing the Brugada ECG pattern,
especially in relation to the differences between types 2 and 3, a new consensus report to establish
a set of new ECG criteria with higher accuracy has been considered necessary. In the new ECG
criteria, only 2 ECG patterns are considered: pattern 1 identical to classic type 1 of other
consensus (coved pattern) and pattern 2 that joins patterns 2 and 3 of previous consensus (saddle-
back pattern). This consensus document describes the most important characteristics of 2 patterns
and also the key points of differential diagnosis with different conditions that lead to Brugada-like
pattern in the right precordial leads, especially right bundle-branch block, athletes, pectus
excavatum, and arrhythmogenic right ventricular dysplasia/cardiomyopathy.
Also discussed is the concept of Brugada phenocopies that are ECG patterns characteristic of
Brugada pattern that may appear and disappear in relation with multiple causes but are not related
with Brugada syndrome.
© 2012 Elsevier Inc. All rights reserved.
Keywords: r' in V1; ST elevation; Brugada syndrome

☆
Sponsored by the International Society for Holter and Noninvasive
Electrocardiology (ISHNE). Concept
⁎ Corresponding author. Universidad Autónoma de Brcelona, Institut
Català Ciències Cardiovasculars, S.Antoni M. Claret 167, ES 08025
Brugada syndrome (BrS) 1 is a familial, genetically
Barcelona, Spain. determined syndrome characterized by autosomal dominant
E-mail addresses: abayes@csic-iccc.org, msauri@csic-iccc.org inheritance in about 50% of cases with variable penetrance.
0022-0736/$ – see front matter © 2012 Elsevier Inc. All rights reserved.
doi:10.1016/j.jelectrocard.2012.06.004
434 A. Bayés de Luna et al. / Journal of Electrocardiology 45 (2012) 433–442

More than 70 mutations, most commonly in the cardiac Na +

channel, have been described. In around 20% of cases, there
are SCN5A mutations that explain the accelerated inactiva-
tion of Na channels. 2
The diagnosis of BrS is suggested by the clinical history
in a patient with specific electrocardiographic (ECG) pattern
(Brugada pattern [BrP]) (Table 2). Sometimes, it is necessary
to use other electrocardiological findings and methods
(Table 1B and C).
The number of idiopathic ventricular fibrillation (VF)
cases diagnosed as having BrS depends on the ECG
diagnostic criteria used. In fact, the ECG manifestation
(BrP), although crucial, is only a part of the BrS diagnostic
criteria. The ECG criteria are a key point not only for
diagnosis but also for prognosis and risk stratification.
However, we do not want to discuss all these aspects in this
article as we have stated. We plan only to comment on the
12-lead ECG clues for the diagnosis of BrS and how to
perform the differential diagnosis with other ECG patterns
that present with ST elevation in V1-V2 and/or r' in these
Table 1
Electrocardiogram alterations in Brugada syndrome
A. ECG diagnostic criteria
Changes in precordial leads.
1. Morphology of QRS-T in V1-V3. ST elevation (sometimes only in V1
and exceptionally also in V3) (BrP)
Type 1. Coved pattern: initial ST elevation ≥2 mm, slowly descending and
concave or rectilinear with respect to the isoelectric baseline, with
negative symmetric T wave (see other characteristics in Table 2 and text).
Type 2. Saddle back pattern: The high take-off (r`) is ≥2 mm with respect to
the isoelectric line and is followed by ST elevation; convex with respect to
the isoelectric baseline with elevation ≥ 0.05 mV with positive/flat T
wave in V2 and T wave variable in V1. If there is some doubt (ie, r' b2
mm), it is necessary to record the ECG in 2nd, 3rd ICS. Other
characteristics may be seen in Table 2 and text.
2. New ECG criteria:
a. Corrado index (2010): Ratio high take-off of QRS-ST/height of ST at 80
ms later is in V1-V2 N1 because the ST is downsloping. In athletes, the ST
especially in V2 is upsloping; and the index is b1. The end of QRS (J
point) often does not coincide with the high take-off of QRS-ST as was
suggested by Corrado.36 However, using the high take-off of QRS-ST for
the application of the Corrado index is valid for discriminating BrP and
other conditions mimicking BrP.
b. The β angle formed by ascending S and descending r' is N58º in type 2
BrP (in athletes, it is much lower) (Chevalier et al. 2011) (SE 79%
SP:84%).
c. Duration of the base triangle of r' at 5 mm from the high take-off is more
than 3.5 mm in BrP 2 (SE, 81%; SP, 82%).31
B. Other ECG findings
1. QT generally is normal. May be prolonged in right precordial leads.43
2. Conduction disorders: Sometimes, prolonged PR interval (long HV interval).
The conduction delay located in RV explains the r' and longer QRS duration
in right precordial leads compared with mid/left precordial leads.
3. Supraventricular arrhythmias. Mostly atrial fibrillation.
4. Some other ECG findings may be seen: the presence of r' wave in aVR N3
mm,44 early repolarization pattern in inferior leads,45 fractioned QRS,46
alternans of T wave after ajmaline injection,47 etc.
C. Other electrocardiological techniques: In some occasions, it is necessary
or convenient to find some new diagnostic clues with exercise testing,48
late potentials, 49 and impaired QT dynamics studied by Holter.
Electrophysiological studies remains controversial for diagnosis and for
risk stratification50–52
Fig. 1. In BrS, the heterogeneous dispersion of repolarization takes places
between the endocardium and the epicardium of the RV at the beginning of
phase 2 (voltage gradient [VG]) because of the transient predominance of
outward Ito current. Epi indicates epicardium; Endo, endocardium.
leads. In the presence of the ECG criteria of BrP, BrS is
diagnosed if one/more of the following clinical factors are
present: (a) survivors of cardiac arrest, (b) presence of
polymorphic ventricular tachycardia (VT), (c) history of
nonvagal syncope, (d) familial antecedents of sudden death
in patients younger than 45 years without acute coronary
syndrome, and (e) or type 1 ST pattern in relatives.
The prevalence of the symptoms is estimated to be 5 per
10 000 inhabitants in Southeast Asia; and apart from
accidents, it is the leading cause of death in men younger
than 40 years in this part of the world. 3
The incidence is higher in young men without apparent
structural heart disease, but this concept of the structurally
normal heart in BrS has been challenged. 4 Syncope or
sudden death usually occurs during rest or sleep, sometimes
without any isolated, preceding premature ventricular
contractions. Most often, polymorphic ventricular tachycar-
dia triggers ventricular fibrillation possibly because of a
phase 2 reentrant mechanism due to a voltage gradient
between the different action potential duration of layers of
the right ventricle (Fig. 1).
There are currently 2 pathophysiologic hypotheses used
to explain the ECG changes in BrS 5: (a) the repolarization
hypothesis, 6 involving the presence of a voltage gradient due
to transmural or transregional dispersion of the action
potential of different layers of the right ventricle at the
beginning of repolarization, as a consequence of a loss of Na
current combined with a dominant transient outward K
current (Ito) (Fig. 1) and (ii) the depolarization hypothesis,
involving right ventricular conduction delay at the end of
depolarization 7 combined probably with subtle structural
right ventricular anomalies. 8 This latter mechanism is
indirectly supported by the presence of late potentials, 9
fragmented potentials on the anterior aspect of right
ventricular outflow tract (RVOT), 10 and delayed right
ventricle free wall contraction after ajmaline infusion. 11
Borggrefe and Schimpf 12 commented that both mecha-
nisms may play a role in the genesis of the ECG pattern and
that both may coexist. Elizari et al 13 published the
speculative but fascinating theory encompassing the 2
 A. Bayés de Luna et al. / Journal of Electrocardiology 45 (2012) 433–442
previous ones proposing that abnormal neural crest cells in
the RVOT cause conduction delay, resulting in the typical
ST changes of ECG BrP. The repolarization gradients may
occur not only between epicardium and endocardium but
also between RVOT and normal surrounding myocardium.
In fact, the evidence of right ventricular conduction delay
and abnormal repolarization, which are already seen in the
ECG (at least part of the QRS end and symmetric T wave),
are also demonstrated by VCG (delay of final part of QRS
loop and rounded T loop). 14 Also Hoogendijk et al, 15 based
on the theory that explains ST-segment elevation due to
excitation failure by current-to-load mismatch, proposed a
unifying mechanism for the Brugada pattern. Although both
these unifying theories are scientifically attractive, we need
further studies to definitively establish the underlying
mechanism of BrS. 16 It is likely that both mechanisms, the
RVOT conduction delay and the voltage gradient during
phase 2 of repolarization, play a role in the explanation of
ECG pattern and in the triggering of VT/VF.
ECG abnormalities of the BrP
Firstly, we have to say that the abnormal ECG constitutes
the hallmark of BrS; but it is necessary to emphasize that the
ECG changes can be dynamic and sometimes are concealed.
Indeed, the ECG BrP is sometimes intermittent; and it may be
observed only in certain situations, such as fever, intoxication,
vagal stimulation, and electrolyte imbalance (Table 1). 17,18
Furthermore, there are some drugs (sodium channels blockers)
that may unmask a BrP. 19 The ECG pattern characteristic of
BrS that may arise from multiple causes (metabolic disorders,
electrocution, ischemia, etc) and disappear upon resolution of
the injury has been named Brugada phenocopy. 20 Although
Fig. 2. See how the devices with non-linear-phase filters may produce, when using high pass filter of 0.5 Hz, changes in the ECG pattern of V2 in case of left
ventricular hypertrophy, which mimics BrP. Color illustration online.
435
this concept has to be confirmed, it is considered that the
Brugada phenocopies have a negative pharmacological
challenge test result (to Na channel blockade) and a negative
genetic test result for recognized BrS mutations. 20 The
prognosis in these cases is unknown. For more details, consult
www.brugadadrugs.org. 21
It is also important to be sure that the ECG is recorded
correctly and that there are no artifacts due to the use of
inappropriate filters 22 (Fig. 2). However, currently, most
ECG devices use linear-phase digital filters that allow cutoff
points until 0.67 Hz without inducing ST alterations. 22,23
Currently, the most commonly used ECG criteria are the
ones proposed by the 2 consensus documents that were
published in 2002 and 2005 under the auspices of the
European Society of Cardiology. 24,25 However, the limita-
tions of previous reports, especially in relation to the
differences between types 2 and 3 ECG patterns, and the
evidence that it is very important to define ECG criteria
with a high degree of precision because the decision to
implant an ICD depends on it mean that it is necessary to
review the current criteria. More recently, the criteria
proposed by previous consensus documents have also been
used in other articles related to this topic, 26,27 although, in
a Japanese study, it was suggested to combine types 2 and
3 into only 1 type. 28
We will now describe the most useful current ECG
criteria to make this diagnosis and also some other ECG
abnormalities that may be found.
New ECG criteria
Morphology in V1-V2
Only 2 ECG patterns have to be considered (Tables 1 and 2).
Type 1 is identical to the classic type 1 described in the
436 A. Bayés de Luna et al. / Journal of Electrocardiology 45 (2012) 433–442

Table 2
ECG patterns of BrS in V1-V2
Type 1: coved pattern Type 2: saddle-back pattern

This typical coved pattern present in V1-V2 the following:
a. At the end of QRS, an ascending and quick slope with a high
take-off ≥2mm followed by concave or rectilinear downsloping ST.
There are few cases of coved pattern with a high
take-off between 1 and 2 mm.
b. There is no clear r' wave.
c. The high take-off often does not correspond with the J point (Fig. 4 B).
d. At 40 ms of high take-off, the decrease in amplitude of ST is ≤4mm.28
In RBBB and athletes, it is much higher.
e. ST at high take-off N ST at 40 ms N ST at 80 ms.
f. ST is followed by negative and symmetric T wave
g. The duration of QRS is longer than in RBBB, and there is a mismatch
between V1 and V6 (see text).
This typical saddle-back pattern present in V1-V2 the following:
a. High take-off of r' (that often does not coincide with J point) ≥2 mm.
b. Descending arm of r' coincides with beginning of ST (often is not
well seen).
c. Minimum ST ascent ≥ 0.5 mm
d. ST is followed by positive
T wave in V2 (T peak N ST minimum N 0) and of variable morphology
in V1.
e. The characteristics of triangle formed by r' allow to define different
criteria useful for diagnosis (see above and text).
• β angle.26
• Duration of the base of the triangle of r' at 5 mm from the high take-off
greater than 3.5mm31
f. The duration of QRS is longer in BrP type 2 than in other cases with r'
in V1, and there is a mismatch between V1 and V6 (see text).

previous consensus, although we will describe some new there are only small morphological differences between the 2
parameters to identify it. The new type 2 pattern combines of them that do not impact on prognosis and risk stratification.
patterns 2 and 3 of previous consensus. These 2 patterns may Even with drug challenge, 24 conversion of type 3 to type 2 is
be unified in only one that encompasses both patterns. In fact, considered inconclusive.

Fig. 3. A, Typical example of BrP type 1. Note the morphology in V1-V2, with a concave ST down-sloping elevation with respect to the isoelectric baseline,
with no clear evidence of R′. B, Typical example of type 2 BrP (saddle-back pattern). Note the morphology in V1-V2 with final r' of special characteristics
(Table 2).
 A. Bayés de Luna et al. / Journal of Electrocardiology 45 (2012) 433–442
Type 1 (Fig. 3A): This pattern, known as a coved pattern,
presents as ST-segment elevation followed by a symmetric
negative T wave in the right precordial leads. 1,24,25,28
Usually, the pattern is seen only in V1-V2. But in some
cases, it is recorded only in V1 or V2; and, in others, it is
observed from V1 to V3. Usually, a clear r' is not seen. This
typical electrocardiographic pattern that may be considered
diagnostic of BrP presents the following characteristics
(Table 2):
1) The high take-off of QRS-ST that is at least 2 mm in V1
is followed by downsloping ST-segment elevation
concave or rectilinear with respect to the isoelectric
line. There are a few cases of coved pattern with high
take-off less than 2 mm and at least 1 mm. 28 This high
take-off level is higher than ST level after 40 millisec-
onds, and this is higher than ST after 80 milliseconds
(high take-off N ST after 40 milliseconds N ST after 80
milliseconds) (Table 2).
2) At 40 milliseconds from the high take-off of QRS-ST, the
decrease in amplitude is less than 0.4 mV. This is much
less than the decrease observed in right bundle-branch
blocks (RBBBs) because the down-slope is slower. 28
3) The index QRS-ST elevation at high take-off/height of ST
at 80 milliseconds later is greater than 1 in BrP and less
than 1 in athletes (Fig. 6). According to Corrado
(Fig. 4A), the high take-off QRS-ST coincides with J
point (end of depolarization). However, although this
phenomenon is not present in all cases 7,29 (Fig. 4B), this
index is still valid (Figs. 4 and 6).
4) The QRS duration is longer in V1-V2 than in mid/left
precordial leads because of evidence of right ventricular
conduction delay. However, in many cases, it is
impossible to measure it in the ECG because we cannot
identify exactly the duration of the terminal QRS.
Although the VCG may measure with more accuracy
Fig. 4. A, According to Corrado et al,36 the J point coincides with high take-off (see text). B, Simultaneous lead ECG recording at baseline and after ajmaline in a
patient with BrS. See how the J point at the end of QRS in lead II after ajmaline occurs later than the high take-off of QRS-ST junction.7
437
the milliseconds of the QRS loop, it is also difficult to
ensure the exact duration of the QRS loop because in the
first and late part, around 30 to 40 milliseconds, it is
slowly inscribed and difficult to measure exactly.
5) The ST segment is followed by an asymmetric T wave.
The ECG BrP type 1 with the above criteria is easily
recognized; and when found in a patient without apparent
structural heart disease, it strongly supports the diagnosis of
BrS (Tables 1 and 2 and later differential diagnosis). The
cases with coved-type pattern that present a high take-off of
QRS-ST between 0.1 and 0.2 mV but with negative T wave
in V1-V2 have been considered suggestive of type 1. 28
These cases are very infrequent; and to confirm the
diagnosis, some of the other ECG findings listed in
Table 1 should be present.
Type 2 (Fig. 3B): It is characterized in V1 and V2 with the
presence of terminal positive wave called r', although in fact,
it is a mixture of final QRS and beginning of repolarization.
This r' presents a high take-off of at least 0.2 mV of
amplitude, followed by elevated ST segment (≥ 0.5 mm)
convex with respect to the isoelectric line (saddle-back
pattern) and by a T wave that is positive in V2 (amplitude of
the peak of the T N minimum amplitude of ST) and of
variable morphology in V1: mildly positive, flat, or mildly
negative (Fig. 3B and Table 2). It has been considered that
the descending limb of the r' terminates when a sudden
change in the slope occurs. However, sometimes, especially
in V1, there is no clear change in the slope direction so that
the T wave onset cannot be determined.
In this scenario, it is important to verify whether
intravenous administration of a drug that blocks the sodium
channels (ajmaline, flecainide, procainamide, pilsicainide)
turns the type 2 pattern into type 1 25,30 (Fig. 5).
The characteristics of the “r'” in BrP are different than in
RBBB and other conditions with r' in V1-V2. In a BrP ECG,
438 A. Bayés de Luna et al. / Journal of Electrocardiology 45 (2012) 433–442
Fig. 5. A, Electrocardiogram of a young man with nonvasovagal syncope. B, The ECG in fourth intercostal space (ICS) is suspicious (V2). A, With the
electrodes located in second ICS, the ECG was BrP type 2. The diagnosis was confirmed by the ajmaline test, where the typical ECG pattern type 1 was
observed. The patient experienced ventricular fibrillation with just one extrastimulus in the electrophysiologic study, and an implantable cardioverter
defibrillator was implanted.
the high take-off of r' is not peaked; and the descending arm
of r', considering the “r'” as a triangle, has a gradual slope.
The r' of BrP type 2 compared with other types of r' has the
following features:
1. The angles between both arms of r´ are wider (α and β
angle). 26 The sensitivity (SE) and specificity (SP) are
higher in β angle (79% and 84%, respectively) with a
threshold of 58º (Table 2).
2. The measurement of the duration of the base of triangle of
r' at 5 mm from the high take-off is more than 3.5 mm in
BrP type 2, with an SE of 81% and an SP of 82%. 31 This
criterion is easier to measure than the α and β angles
(Table 2).
Accuracy of these ECG criteria
The use of these ECG criteria is very helpful for the
diagnosis of BrP that may be undertaken even by
nonexperienced physicians, especially type 1 ECG pattern
that has a high specificity.
Recently, in a Japanese population, a computerized
diagnostic criteria for BrS that demonstrated a high level
of accuracy have been published (type 1 N 90%, type 2
N 85%). 28 This study was based on the comparison with
RBBB in apparently healthy people but not with athletes and
people with pectus excavatum.
Other ECG findings or ECG techniques may be used for
correct diagnosis of BrS
Table 1B and C shows the most important other ECG
findings that may be used for correct diagnosis of BrS.
Changes of morphology according the location of
the electrodes
In some cases, the ECG pattern is only evident or is more
evident in the upper precordial V1-V2 leads recorded at the
third or second intercostal space. This occurs because the
abnormal electrical activity leading to BrP arises from a
limited zone located in the RVOT. Accordingly, only an
electrode located exactly over the affected zone is able to
record the BrP. Recently, it has been published 32 that, in BrP
type 1, lead positioning according to RVOT location by
using CV magnetic resonance imaging correlations may
improve the diagnosis of BrP. The ECG pseudonormaliza-
tion observed when the electrodes are located in the correct
position does not constitute any guarantee that the diagnosis
is incorrect, especially if some ST elevation persists, albeit
less markedly (Fig. 5). Therefore, it is very important to
position the electrodes in the same location when serial
recordings are performed to allow comparative assessments,
and to perform ECG recordings in upper precordial leads if
some suggestion of BrP exists in V1-2 in the ECG recorded
at the fourth intercostal space, such as minimal ST elevation
and/or positive terminal forces of the QRS.
Variability of BrP over time
In most patients, BrP is not evident at any time, changing
from the most obvious type 1 to a barely recognizable type 2.
In a follow-up study based on 90 ICD patients with BrS, one
third of analyzed tracings showed type 1 BrP and one third
showed perfectly normal ECG tracings. 33 This is not
surprising because the sodium channel dysfunction under-
lying BrP is variable, being influenced by different factors
(drugs, fever, autonomic imbalance, etc).
 A. Bayés de Luna et al. / Journal of Electrocardiology 45 (2012) 433–442 439

3. Differential diagnosis The distinction between the 2 conditions is straightforward

because, usually, in advanced RBBB, the ST segment is
We have to distinguish (a) the cases of spontaneous
not elevated in the right precordial leads, the terminal
typical BrP type 1 in case of BrS; (b) the typical BrP type 1
wave (r' or R') is synchronous with the broad S wave
induced by some drugs (sodium channel blockers) or other
observed in leads I and V6, and the QRS is wider (≥ 120
circumstances (fever, etc) that unmask a BrS; (c) the cases
milliseconds). In type 1 BrP, however, usually no wide S
of ECG BrP especially type 1 induced by many
wave is present in the left leads because the terminal
circumstances that disappear upon resolution of the injury
forces of the ventricular complex in V1-V2 can be
and that do not present BrS (named phenocopies) (These
recorded only by electrodes placed in proximity of the site
include acute ischemia, pericarditis, myocarditis, pulmonary
where the abnormal electrical activity occurs (the outflow
embolism, metabolic disorders, ionic disorders, administra-
tract of the right ventricle) and not from further away
tion of some drugs, electrocution, and a miscellaneous
leads. Therefore the QRS in left leads is usually is less
group [consult www.brugada.org and Baranchuk et al 20].);
than 120 milliseconds.
and (d) the cases of similar BrP (Brugada-like) that are
Type 2 BrP and incomplete RBBB raise more problems:
permanent patterns and may be confused with a BrP type 1
whenever a small positive terminal QRS deflection (r') is
or 2. These include RBBB, septal hypertrophy, arrhythmo-
present in V1-V2, it is possible to distinguish the r' wave of
genic right ventricular dysplasia/cardiomiopathy, athletes,
incomplete RBBB from the terminal positive r' wave of type
pectus excavatum, and a long number of processes (consult
2 BrP on the basis of the following: (1) the positive terminal
www.brugada.org) (Fig. 6).
r' wave is peaked in RBBB, whereas, in BrP, type 2 is
Sometimes, the differential diagnosis of BrP from other
rounded, wide, and usually of relatively low voltage; (2) in
conditions associated with ST elevation by ECG alone may be
incomplete RBBB, the QRS complex duration in leads V1-
quite difficult, even for the more experienced cardiologist. 34
V2 is identical to that observed in lead V6. In type 2 BrP, in
The clinical setting is very important, bearing in mind that, in
contrast, the QRS duration is longer in the right precordial
many cases, the patient with this problematic pattern presents
leads than in V6 because the terminal deflection observed in
with acute symptoms. Patients with acute coronary syndromes
V1 (the r' wave) cannot be recorded by the V6 electrode. In
with ST elevation may present in some cases a similar pattern
other words, in BrP, the QRS complex end is earlier in V6
but obviously in a very different clinical setting. In some
than in V1-V2. 35
doubtful cases of type 2 pattern, to determine the correct
diagnosis, we may check if there are changes after the
intravenous administration of Na channel blockers (ajmaline)
(already discussed). There are however frequent cases of Athletes
Brugada-like pattern, especially type 2, in which the ECG is
Type 1 BrP compared with athletes (Fig. 6) depicts an ST
usually seen in asymptomatic patients that require a detailed
segment clearly elevated and down-sloping, usually with no
ECG analysis to obtain the correct interpretation. We will
visible r'. This pattern is difficult to be mistaken with the
comment on the most challenging cases (Fig. 6).
ECG pattern seen in V1-V2 in athletes.
In type 2 BrP, the high take-off is an r' usually rounded
Isolated RBBBs
(see characteristics of r' before), which is followed by a
Type 1 BrP and advanced RBBB are both characterized down-sloping ST elevation with a final T wave of variable
by a terminal positive wave and a negative T wave in V1-V2. morphologies in V1 and positive in V2 (Table 2).

Fig. 6. Comparison between type 1 and 2 BrP, arrhythmogenic right ventricular dysplasia, pectus excavatum, athletes, and partial RBBB to view the presence of
mismatch in the QRS duration in V1-V2 and mid/left precordial leads. There is clear mismatch in type 1 and 2 of BrP, and there is none in the other cases. The
second vertical line is located at 80 milliseconds of the J point (first line) to check the Corrado index. Color illustration online.
440 A. Bayés de Luna et al. / Journal of Electrocardiology 45 (2012) 433–442
Compared with this pattern, the ECG of athletes presents
the following:
1. The end of the QRS in V1 coincides with the end of the
QRS in V5-6, whereas in type 2 BrP, this is not usually
clearly seen because the QRS complex ends later in V1-
V2 than in V6 (see above).
2. In athletes, lead V1 shows an r' usually peaked and sharp
with no ST elevation or only mildly elevated (b 1 mm);
and the ST segment starts after the clear end of QRS and
is often followed by a negative and sometimes deep T
wave in V1. Occasionally, the T wave is positive,
especially in V2; but in these cases, the ST segment is
gradually ascending (Fig. 6). Therefore, the index ratio
ST-segment elevation at high take-off of QRS-ST/ST
elevation after 80 milliseconds in V1-V2 distinguishes
BrP from athletes: in the latter group, the ratio is less than
1, whereas in BrP, it is greater than 1. 36
Pectus excavatum
The ECG diagnosis of this normal variant of the ECG
seen in pectus excavatum 37 is supported by the following:
− A negative P wave in V1 taken in the correct location
(fourth ICS)
− A peaked r' in V1 very well defined, which may be
followed by an elevated ST usually mild. The T wave
is usually negative or plus/minus in V1 and positive in
V2 (Fig. 6).
Arrhythmogenic right ventricular dysplasia/cardiomyopathy
From an electrocardiographic point of view, it is usually
characterized by an ECG pattern in V1-V2 38 different from
BrP by the following:
- Atypical RBBB morphologies have been shown, with
a “plateau” in the R wave in lead V1. The ST segment
is at times somewhat elevated but does not usually
mimic type 2 BrP, although, in some cases, it may be
similar because the ε wave may be confused with the
r' wave of BrP.
- In arrhythmogenic right ventricular dysplasia/cardio-
myopathy, moreover, T waves are more frequently
negative in many precordial leads (V1 to V3-V5).
The ECG pattern is always fixed.
The signal averaging technique may help to differentiate
both processes because although in both of them abnormal
high-frequency components are present (positive late
potentials), wavelet analysis demonstrates that the frequen-
cy level is higher in arrhythmogenic right ventricular
dysplasia/cardiomyopathy. 39
Early repolarization pattern
The early repolarization variant is a well-recognized
common enigmatic idiopathic electrocardiographic phenom-
enon, considered to be present when at least 2 adjacent
precordial leads show ST-segment elevation with values of
at least 1 mm. This pattern, which has recently been
associated to ventricular fibrillation (sudden death), 40 may
be defined as a positive, sharp, and well-defined “hump-like”
deflection immediately following positive QRS complexes
at the onset of the ST segment, recorded especially in the
midleft precordial (not right precordial) and sometimes
inferior leads. The transition from QRS to ST segment is
considered “slurred” and not a clear J point (wave) when the
R wave gradually becomes the ST segment with upright
concavity. 41 The characteristics of this ECG pattern are very
different from BrP, but sometimes both patterns may
coexist. 42
Conclusions
We have exposed the current ECG criteria of BrP,
including the ones described after the last consensus
statement, 24,25 which have very high accuracy and could
used by nonexperienced physicians for a reliable diagnosis
of both types of BrP, especially type 1. The most important
points are the following:
1. Only 2 ECG patterns should be considered: type 1
(coved type) and type 2 (saddle-back type) that
encompass the patterns 2 and 3 of previous consensus
(Table 2).
2. In both types 1 and 2, the end of the QRS in the
mid/left precordial leads (J point) occurs before the
end of the QRS in V1 due to localized RVOT
conduction delay. However, it is impossible to
confirm by surface ECG the exact difference because
of the impossibility of determining exactly the end of
QRS in V1. Furthermore, often, the J point in mid/left
precordial leads does not coincide with the high take-
off of the QRS-ST in V1, 29 as was considered by
Corrado et al. 36
3. Type 1 pattern is very specific; and when it appears in a
patient without apparent heart disease, it strongly suggests
the diagnosis. The small number of cases with no typical
pattern (ST elevation b 2 mm) has to be evaluated with
complementary ECG criteria test to reach a final diagnosis
(Table 1B and C).
4. Electrocardiographic patterns identical to BrP can be seen
in the absence of true BrS (phenocopies).
5. In BrP, the slope of ST in V1-V2 is descending; and in
athletes and other cases with r' in V1, it is usually
ascending at least in V2 (Fig. 6).
6. Type 2 pattern may be confused with several other
situations with r' in V1-V2. The characteristics of r' in
incomplete RBBB, athletes, and pectus excavatum
however are especially different from those observed in
BrS. These differences include (Table 2) (a) the angle of
ascending and descending arms of r'; (b) the duration of
the base triangle of r' at 5 mm from the high take-off; and
(c) the configuration of r' is peaked in RBBB, pectus
excavatum, and athletes and rounded in BrP. The Corrado
index can also be helpful in distinguishing BrP from
athlete's ECG (Table 2 and Fig. 6).
 A. Bayés de Luna et al. / Journal of Electrocardiology 45 (2012) 433–442
References
1. Brugada P, Brugada J. Right bundle branch block, persistent ST
segment elevation and sudden cardiac death: a distinct clinical and
electrocardiographic syndrome. A multicenter report. J Am Coll Cardiol
1992;20:1391.
2. Probst V, Wilde AA, Barc J, et al. SCN5A mutations and the role of
genetic background in the pathophysiology of Brugada syndrome. Circ
Cardiovasc Genet 2009;2:552.
3. Nademanee K. Sudden unexplained death syndrome in Southeast Asia.
Am J Cardiol 1997;79:10.
4. Frustaci A, Priori SG, Pieroni M, et al. Cardiac histological substrate in
patients with clinical phenotype of Brugada syndrome. Circulation
2005;112:3680.
5. Meregalli PG, Tan HL, Probst V, et al. Type of SCN5A mutation
determines clinical severity and degree of con duction slowing in loss-
of-function sodium channelopathies. Heart Rhythm 2009;6:341.
6. Yan GX, Antzelevitch C. Cellular basis for the Brugada syndrome and
other mechanisms of arrhythmogenesis associated with ST-segment
elevation. Circulation 1999;100:1660.
7. Postema PG, van Dessel PF, Kors JA, et al. Local depolarization
abnormalities are the dominant pathophysiologic mechanism for type 1
electrocardiogram in Brugada syndrome: a study of electrocardiograms,
vectorcardiograms, and body surface potential maps during ajmaline
provocation. J Am Coll Cardiol 2010;55:789.
8. Lambiase PD, Ahmed AK, Ciaccio EJ, et al. High-density substrate mapping
in Brugada syndrome: combined role of conduction and repolarization
heterogeneities in arrhythmogenesis. Circulation 2009;120:106.
9. Nagase S, Kusano KF, Morita H, et al. Epicardial electrogram of the
right ventricular outflow tract in patients with the Brugada syndrome:
using the epicardial lead. J Am Coll Cardiol 2002;39:1992.
10. Nademanee K, Veerakul G, Chandanamattha P, et al. Prevention of
ventricular fibrillation episodes in Brugada syndrome by catheter
ablation over the anterior right ventricular outflow tract epicardium.
Circulation 2011;123:1270.
11. Tukkie R, Sogaard P, Vleugels J, et al. Delay in right ventricular activation
contributes to Brugada syndrome. Circulation 2004;109:1272.
12. Borggrefe M, Schimpf R. J-wave syndromes caused by repolarization or
depolarization mechanisms a debated issue among experimental and
clinical electrophysiologists. J Am Coll Cardiol 2010;55:798.
13. Elizari MV, Levi R, Acunzo RS, et al. Abnormal expression of
cardiac neural crest cells in heart development: a different hypothesis
for the etiopathogenesis of Brugada syndrome. Heart Rhythm
2007;4:359.
14. Peréz-Riera AR, Ferreira Filho C, de Abreu LC, ET al; On behalf of the
International VCG Investigators Group. Do patients with electrocar-
diographic Brugada type 1 pattern have associated right bundle branch
block? A comparative vectorcardiographic study. Europace. 2012 Jan
10. [Epub ahead of print]
15. Hoogendijk MG, Potse M, Linnenbank AC, et al. Mechanism of right
precordial ST-segment elevation in structural heart disease: excitation
failure by current-to-load mismatch. Heart Rhythm 2010;7:238.
16. Brugada P. Commentary on the Brugada ECG pattern. Circ Arrhythm
Electrophysiol 2010;3:280.
17. Antzelevitch C, Brugada R. Fever and Brugada syndrome. Pacing Clin
Electrophysiol 2002;25:1537.
18. Samani K, Wu G, Ai T, et al. A novel SCN5A mutation V1340I in
Brugada syndrome augmenting arrhythmias during febrile illness. Heart
Rhythm 2009;6:1318.
19. Yap YG, Behr ER, Camm AJ. Drug-induced Brugada syndrome.
Europace 2009;11:989.
20. Baranchuk A, Nguyen T, Hyung M et al. Brugada phenocopy: new
terminology and proposed classification. Ann NonInvasive Electro-
cardiol 2012 (in press).
21. Postema PG, Wolpert C, Amin AS, et al. Drugs and Brugada syndrome
patients: Review of the literature, recommendations, and an up-to-date
Web site (www.brugadadrugs.org). Heart Rhythm 2009;6:1335.
22. Garcia Niebla J, Llontop-Garcia P, Valle J, et al. Technical mistakes
during the acquisition of the electrocardiogram. Ann Noninvasive
Electrocardiol 2009;14:389.
441
23. Kligfield P, Gettes L, Bailey JJ, et al. Recommendations for the
standardization and the interpretation of the ECG: part 1: the ECG and
its technology. J Am Coll Card 2008;49:1109.
24. Wilde AA, Antzelevitch C, Borggrefe M, et al, Study Group on the
Molecular Basis of Arrhythmias of the European Society of Cardiology.
Proposed diagnostic criteria for the Brugada syndrome: consensus
report. Circulation 2002;106:2514.
25. Antzelevitch C, Brugada P, Borggrefe M, et al. Brugada syndrome:
report of the second consensus conference. Heart Rhythm 2005;2:
429.
26. Chevallier S, Forclaz A, Tenkorang J, et al. New electrocardiographic
criteria for discriminating between Brugada types 2 and 3 patterns and
incomplete right bundle branch block. J Am Coll Cardiol 2011;58:
2290.
27. Ohkubo K, Watanabe I, Okumura Y, et al. A new criteria differentiating
type 2 and 3 Brugada patterns from ordinary incomplete right bundle
branch block. Int Heart J 2011;52:159.
28. Nishizaki M, Sugi K, Izumida N, et al. Classification and assessment of
computerized diagnostic criteria for Brugada-type electrocardiograms.
Heart Rhythm 2010;7:1660.
29. Bayés de Luna A, Garcia Niebla J, Goldwasser D. The ECG
differential diagnosis of Brugada pattern and athletes. Eur Heart J
2010 [May 14 (E-Public)].
30. Kurita T, Shimizu W, Inagaki M, et al. The electrophysiologic
mechanism of ST segment elevation in Brugada syndrome. J Am Coll
Cardiol 2002;40:330.
31. Serra G, Goldwasser D, Capulzini L, et al. New ECG criteria taken from
r' characteristics for differentiate type 2 Brugada pattern from
incomplete RBBB in athletes. Abstract accepted to European Congress
of Cardiology; 2012.
32. Veltman C, Papavassilu T, Konrad M, et al. Insights into the location of
type 1 ECG in patients into the location of type 1 ECG in patients with
Brugada syndrome: correlations of ECG and CV magnetic resonance
imaging. Heart Rhythm 2012;9:414.
33. Richter S, Sarkozy A, Veltmann C, et al. Variability of the
diagnostic ECG pattern in an ICD patient population with Brugada
syndrome. J Cardiovasc Electrophysiol 2009;20:69.
34. Jayroe JB, Spodick DH, Nikus K, et al. Differentiating ST elevation
myocardial infarction and nonischemic causes of ST elevation by
analyzing the presenting electrocardiogram. Am J Cardiol 2009;103:301.
35. Oreto G, Corrado D, Delise P, et al. Doubts of the cardiologist regarding an
electrocardiogram presenting QRS V1-V2 complexes with positive
terminal wave and ST segment elevation. Consensus Conference promoted
by the Italian Cardiology Society. G Ital Cardiol (Rome) 2010;11:3S.
36. Corrado D, Pelliccia A, Heidbuchel H, et al. Section of Sports
Cardiology, European Association of Cardiovascular Prevention and
Rehabilitation; Working Group of Myocardial and Pericardial Disease,
European Society of Cardiology. Recommendations for interpretation
of 12-lead electrocardiogram in the athlete. Eur Heart J 2010;31:243.
37. Karaoka H. Electrocardiographic patterns of the Brugada syndrome in
two young patients with pectus excavatum. J Electrocardiol
2002;35:169.
38. Marcus FI, McKenna WJ, Sherrill D, et al. Diagnosis of arrhythmogenic
right ventricular cardiomyopathy/dysplasia. Proposed modification of
the Task Force Criteria. Circulation 2010;121:1533.
39. Yodogawa K, Morita N, Kobayashi Y, et al. A new approach for the
comparison of conduction abnormality between arrhythmogenic right
ventricular cardiomyopathy/dysplasia and Brugada syndrome. Ann
Noninvasive Electrocardiol 2011;16:263.
40. Haïssaguerre M, Derval N, Sacher F, et al. Sudden cardiac arrest
associated with early repolarization. N Eng J Med 2008;358:2016.
41. Rosso R, Kogan E, Belhassen B, et al. J-point elevation in survivors of
primary ventricular fibrillation and matched control subjects: incidence
and clinical significance. J Am Coll Cardiol 2008;52:1231.
42. McIntyre W, Perez Riera A, Femenia F, et al. Coexisting early
repolarization pattern and Brugada syndromes recognition of potentially
overlapping entities. J Electrocardiol 2012;45:195.
43. Pitzalis MV, Anaclerio M, Iacoviello M. QT interval prolongation in
right precordial leads in Brugada syndrome. J Am Coll Cardiol
2003;42:1632.
442 A. Bayés de Luna et al. / Journal of Electrocardiology 45 (2012) 433–442
44. Babai Bigi M, Aslani A, Shahrzad S. aVR sign as a risk factor for life-
threatening arrhythmic events in patients with Brugada syndrome. Heart
Rhythm 2007;4:1009.
45. Sarkozy A, Cherchia G, Paparella G, et al. Inferior and lateral ECG
repolarization abnormalities in Brugada syndrome. Circ Arrhythmic
Electrophysiol 2009;2:154.
46. Morita H, Kusano KF, Miura D, et al. Fragmented QRS as a marker of
conduction abnormality and a predictor of prognosis of Brugada
syndrome. Circulation 2008;118:1697.
47. Tada T, Kusano KF, Nagase S. The relationship between the magnitude
of T wave alternans and the amplitude of the T wave in Brugada
syndrome. J Cardiovasc Electrophysiol 2008;19:56.
48. Makimoto H, Nakagawa E, Takaki H, et al. Augmented ST-
segment elevation during recovery from exercise predicts cardiac
events in patients with Brugada syndrome. J Am Coll Cardiol
2010;56:1576.
49. Huang Z, Patel C, Li W, et al. Role of signal-averaged electrocardio-
grams in arrhythmic risk stratification of patients with Brugada
syndrome: a prospective study. Heart Rhythm 2009;8:1156.
50. Brugada P, Brugada R, Mont L, et al. Natural history of Brugada
syndrome: the prognostic value of programmed electrical stimulation of
the heart. J Cardiovasc Electrophysiol 2003;14:455.
51. Priori SG, Napolitano C, Gasparini M, et al. Natural history of Brugada
syndrome: insights for risk stratification and management. Circulation
2002;105:1342.
52. Probst V, Veltmann C, Eckardt L, et al. Long-term prognosis of patients
diagnosed with Brugada syndrome: results from the FINGER Brugada
Syndrome Registry. Circulation 2010;121:635.