the early repolarization variant—an electrocardiographic enigma
TRANSCRIPT
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The early repolarization variantan electrocardiographic enigma
with both QRS and J-STT anomaliesB
John P. Boineau, MD4
Division of Cardiology, Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA
Division of Cardiothoracic Surgery, Department of Surgery, Washington University School of Medicine, St. Louis, MO, USA
Department of Biomedical Engineering, Washington University School of Medicine, St. Louis, MO, USA
Abstract A detailed description of the electrocardiogram of the early repolarization variant, including its most
common morphological variations is presented. Included is a recently identified anomaly of the QRS
complex, which has not previously been reported. Ventricular activation data is presented to explain
the unique QRS changes. A comparison with Wolff-Parkinson-White (preexcitation) reveals certain
similarities related to a premature completion of depolarization in early repolarization variant.
D 2007 Elsevier Inc. All rights reserved.
Keywords: Electrocardiogram; Early repolarizationvariant; Left ventricularhypertrophy (bAthlete heartQ); Early depolarization
Introduction
The electrocardiogram (ECG) of early repolarization
variant (ERPV) is familiar to all cardiologists and consid-
ered to be a benign condition (Fig. 1). The most notable
characteristic of the ECG is ST-segment elevation. If thesubject is young, healthy, and in no distress, it is usually
interpreted as benign early repolarization. However, if a
patient presents with chest pain, he is often admitted to rule
out acute myocardial infarction or pericarditis.
Early repolarization is initiated by and, thus, immediately
follows early depolarization. In addition, early repolariza-
tion and late depolarization are occurring simultaneously in
the heart and their separate effects are superimposed near
the end of QRS in the ECG. Because of this superimposi-
tion, ST elevation is only noticeable after the end of QRS
with termination of the dominant activation wavefronts.
Thus, there is usually some bnormalQ early repolarization in
most ECGs, and perhaps, bexaggerated repolarizationQ
would be a more appropriate designation for ERPV. Reports
have described the features of ERPV in young adults and a
predominance in blacks and other melanotic subjects.1-8
Early repolarization variant consists of different ECG
anomalies involving both QRS and ST-T. Although the
unusual repolarization features are well recognized, except
for the frequently observed increases in voltage, the atypical
QRS features have received no attention.
In a subsequent report, the theory is advanced that several
previously unrelated cardiac findings, including athletesheart, sudden death in active and apparently normal young
individuals, cardiomyopathy, and some sudden death related
to inappropriate adrenergic stimulation or drugs (cocaine,
etc) may be related to a common mechanism which is
expressed as ERPV in the ECG. Although there is no
established link between ERPV and either sudden death or
cardiomyopathy, one study reported an association between
hypertrophic obstructive cardiomyopathy and ERPV.9
The purpose of the present report is to (1) describe the
different morphological types of the early repolarization
pattern which are quite variable, (2) point out previously
unreported anomalies of the QRS complex in subjectswith early repolarization ST elevation and J waves, and (3)
demonstrate ventricular activation mechanisms of the
unique QRS pattern, which have some similarities to those
in the preexcitation syndrome.
Electrocardiographic description of the ERPV
Because of individualvariability, poor resolutionof standard
gain and speed ECGs, and foremost, the lengthening effect of
left ventricular hypertrophy (LVH) on the QRS and QT
intervals, which is often associated with ERPV, quantitative
0022-0736/$ see front matterD 2007 Elsevier Inc. All rights reserved.doi:10.1016/j.jelectrocard.2006.05.001
B Supported in part by National Institutes of Health grant numbers 5
R01 HL33277 and 5 R01 HL33722 and Veterans Administration
grant 1013.
4 Washington University School of Medicine, Box 8234, St. Louis,
MO 63110, USA. Tel.: +1 314 362 8311; fax: +1 314 361 8706.
E-mail address: [email protected]
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comparisons between depolarization and repolarization dura-
tions in normal and ERPV subjects did not prove to be useful.
Repolarization J-STT waveforms
This interval begins with the end of the S wave of the
QRS complex or at the J junction and is introduced by the
positive J wave. It is assumed that the J wave represents a
repolarization event, and mapping data will be presented
later to confirm this.
The pattern of the ST elevation varies in morphology,
degree, and location. It can also be dynamic, the pattern
changing in degree from one recording to the next. In
addition, with sinus tachycardia, exercise, or dobutamine
stress testing, much or all of the ST elevation disappears. In
the most frequently observed pattern (Fig. 2, panels 1A-C),
the elevated ST segment is introduced by a small positive
knoblike deflection at the end of QRS, referred to as a Jwave, resembling the Osborn wave of hypothermia.10 The J
is followed by a cuplike ST-segment elevation and a terminal
positive T wave. This pattern resembles a bwestern saddleQ
with horn, seat, and back rest corresponding to the J wave,
ST segment, and T wave, respectively. The T wave can be tall
and peaked (panel 1C). In panel 1D, the ST is bdomedQ and
associated with a terminally negative T wave; this type is
most often confused with acute myocardial infarction. Less
frequently observed is the type (panel 1E) where there is no
obvious J wave, a domed ST elevation, and a small or
indistinct T wave.
The location of the maximal ST elevation is also variable.The most common pattern is for the maximal ST elevation
and most obvious J wave to be located in chest leads V3 and
V4, referred to here as apical early repolarization (Fig. 2,
panel 1). Maximal ERPV can also occur more laterally (leads
I, aVL, V5, and V6), inferiorly (leads II, III, and aVF; Fig. 2,panel 3), and anteriorly (leads V1 and V2; Fig. 2, panel 2).
The ST segment can be reciprocally depressed in lead aVR
which bviewsQ the basal left ventricular (LV) opening and the
negative side of the repolarization field projecting toward the
apex. These patterns suggest variation in the regional
distribution of the early repolarization. Certain ECGs with
anterior ERPV resemble Brugada syndrome.
QRS waveforms
QRS is also anomalous in many ECGs of subjects with
ERPV, exhibiting increased amplitude and a unique
morphologic asymmetry. An increased amplitude of QRS
is often present and has been described. The QRS voltageis greatest in young subjects with ERPV and can persist
into late adult life. Initial QRS is also atypical in many
subjects with ERPV. In many subjects with ERPV, there is
an initial slurring (slowing), which is subtly similar to the
delta wave in Wolff-Parkinson-White (WPW). This deflec-
tion can be followed by an ascending R wave with a
reduced slope angle. The slower ascending R contrasts with
the more rapid descent of the intrinsicoid deflection (Fig. 2,
panel 1B [arrow]). This results in a QRS complex which
resembles a bleaning tower.Q The ID is so fast that the QRS
appears to end prematurely. In some subjects, this is
associated with apparent QRS brevity (b70 milliseconds).In other subjects, the upward sloping part of QRS can take
Fig. 1. An example of ERPV with marked ST elevation in an apparently healthy 26-year-old black man. Only the chest leads (V 1-V6) are shown. Note that the
maximum ST elevation is in leads V3 and V4, has the typical bwestern saddleQ pattern, and is introduced by a prominent J wave.
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longer to reach its maximum peak, and even the fast ID
cannot abbreviate the total interval. In certain subjects, theshort QRS duration and fast descent of the intrinsicoid
deflection are more prominent than the ST elevation, which
may be minimal. These individuals might not be identified
with the ERPV group except for a prominent J wave and
atypical QRS features.
Variations in ERPV
Variations in the ECG patterns of ERPV are shown for
8 subjects in Fig. 3. Only the chest leads are displayed.
Fig. 3A represents the most frequently observed pattern with
the western saddle J wave, STE, and positive T wave, all
maximal in leads V3, V4, and V5. Electrocardiograms Athrough E exhibit a short QRS duration and rapid
intrinsicoid deflection. Initial QRS slurring with sloping
ascending R wave (leaning tower) is shown in 3B. TheST segment in 3C is domelike, and the T wave is inverted.
Fig. 3D illustrates another example in which the J wave is
not as obvious. Panels E through H represent patterns of
anterior ERPV where the principal features, including the
J wave and STE, are maximal in leads V1 and V2. Fig. 3E
illustrates anterior ERPV, where ST elevation and J wave are
maximal and associated with early R-wave progression in
chest leads V1 and V2. Panels F and G are examples of
anterior ERPV in association with an rsrV complex in V1and V2. Note the fusion of separate late QRS forces and
the J wave. Panel H represents anterior ERPV with a broad
rV
complex merging gradually with a down sloping STE inthe anterior chest leads (Brugada-like).
Fig. 2. Different ECG patterns of early repolarization. Panels numbered 1, 2, 3 designate three different spatial locations of maximal ST elevation and J-waves.
A, B, C, etc, refer to morphologic variations in the pattern of early repolarization within each group.
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Summarizing, the ECG in ERPV is characterized by
(1) increased QRS voltage, (2) an asymmetric QRS complex
with slurring and a reduced slope angle of the ascending
positive R wave, (3) an extremely rapid intrinsicoid deflec-
tion, (4) a prominent J wave, and (5) different morphologic
forms and spatial distributions of ST elevation.
Short and nonuniform QT interval in ERPV
The J-STT interval appears atypically short in some
subjects with ERPVand can become exceedingly short with
sinus tachycardia (Fig. 4). In Fig. 4, note that in addition to
the uniformly shortened QT in panel A, there are bifed T
waves in the ECGs of subjects shown in panels C and D.
This bifed morphology can be interpreted as a form of
repolarization heterogeneity in which the first T peak (T1)
represents a greater degree of Q-T shortening in one area
and less shortening in other areas (T2). In addition, it is not
rare to observe a third peak in certain subjects. Whether this
represents a third region of latest repolarization or a
nonrepolarizaton U wave event is unclear. As mentioned,
the repolarization duration is difficult to assess usingstandard QT interval rate correcting algorithms. There is a
tendency for LVH to prolong the QT electromechanical
interval which further complicates comparative QT assess-
ment in ERPV. Although the J-STT can be short, the QT
may be normal due to the effect of LVH, which tends to
prolong QRS. Thus, if both QRS and J-STT intervals are
short, the QT is short. However, if J-STT is short and QRS
is long, then QT will be normal or prolonged. In spite of this
ambiguity, nonuniform repolarization shortening may be
detected as T-wave asymmetry.
Left ventricular hypertrophy with ERPV
Unlike other subjects with typical LVH with secondary
ST depression and T-wave inversion (typical LV strain
pattern; Fig. 5A), the ECG in patients with combined LVH
and ERPV can exhibit ST elevation in association with
T-wave inversion. Instead of the usual degree of ST
elevation of ERPV, the J junction can be depressed, but
ST demonstrates a domelike upward convexity (Fig. 5B) in
contrast to the typical LV strain pattern (Fig. 5A). This
represents the combined and opposed interaction of
repolarization changes due to LVH and the ERPV. InERPV with LVH, the ECG can exhibit marked anterior
Fig. 3. Different ECG examples of early repolarization. Panels A through D demonstrate morphologic variations in QRS and ST-T in four subjects. Panels E
through H are four other subjects in which the ST elevation and J-wave are expressed maximally in the anterior chest leads, VI and V2.
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Fig. 4. Short and nonuniform QT in ERPV. Note the ST elevation with short QT in A and B and with nonuniform short QT in C and D, which demonstrate
two T-peaks.
Fig. 5. Left ventricular hypertrophy and early repolarization. Classical LVH QRS and ST-T patterns are shown in A to compare with LVH plus earlyrepolarization in B and C.
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T-wave inversion (V1-V3) due to exaggeration of the type
of ERPV shown in Fig. 3C and is incorrectly referred to as
banterior ischemia.Q
QRS duration is often increased in subjects with typical
LVH (90-130 milliseconds). However, in some subjects
with LVH and ERPV, QRS duration may be normal or
appear paradoxically abbreviated. In patients who have
both ERPV and LVH, the slurring/sloping of the initial
QRS limb is even further exaggerated and often associated
with prominent notching (Fig. 5C). Note the slurring and
sloping of the ascending R wave, which contrasts with the
rapid intrinsicoid deflection. Also note the earlier T peak
(T1) and later T (T2 or U wave) in lead V4. Occasionally,
as many as 3 repolarization peaks (T1, T2,and a U ) are
observed in subjects with LVH and ERPV. In Fig. 5C,
although the total durations of QRS and Q-U are
prolonged, the rapid QRS intrinsicoid deflection and earlier
T peak are consistent with local regions of shortened
activation and repolarization.
Methodsactivation mapping
Normal transmural LV activation in canines
Fig. 6 demonstrates activation across the LV wall,
recorded in 2 dogs, and is intended as a normal reference
for comparison with the atypical depolarization in Figs. 7
and 8. The maps of the isochronal depolarization sequence
were constructed from 5 to 6 needle or bplungeQ electrodes
inserted through the LV wall from epicardium to endocar-
dium. Each needle contained from 15 to 20 electrode-
recording terminals with precisely 1-mm spacing. Bipolarpotentials were recorded between adjacent electrode pairs.
The isochrones were constructed by connecting points of
equivalent activation time on each needle. Fig. 6A
demonstrates a typical normal spread of the activation from
the endocardium toward the epicardium. In Fig. 6B, in the
region of the anterior papillary muscle, the depolarization is
slightly more complex. Again, there is outward endocardial-
to-epicardial spread in the LV wall and, simultaneously,
spread in the papillary muscle from its basal attachment
inward toward the cavity.
Mechanism of shortened depolarization in a canine
Fig. 7A illustrates a cross section of the LV in anotherdog. A unique transmural activation pattern of this same
cross section is shown in B. In contrast to the typical
unidirectional endocardial-to-epicardial activation shown in
Fig. 6, the earliest activation in this animal was initiated at
a deep intramural level in the LV midwall. Thereafter, the
wavefronts spread circumferentially (elliptically) in all
directions, both toward the endocardium and epicardium
simultaneously. The mechanism of this unique onset and
spread of activation is indicated by the cross-sectional
anatomy in panel C. This is an immediately adjacent
section of the LV, only a few millimeters distant to the one
mapped in panel A. Note that the endocardium is deeplyinvaginated into the wall, carrying the endocardial Purkinje
fibers intramurally to a mid-LV level (arrows). This effect
of increased trabeculation decreases the transmural distance
that the wavefronts travel at the normal velocity and
shortens the transmural activation time to 25 milliseconds.
This unique type of LV activation results in an approxi-
mately 37% reduction in the transmural activation time.
Note that the axial component is faster than the endo-
cardial-to-epicardial spread, which is related to the
predominant fiber orientation, because activation is faster
in the long axis of parallel fiber bundles than cross-
fiber spread.11
Activation data in a human subject with ERPV
Fig. 8A illustrates lead V4 in a patient with ERPV
before epicardial activation mapping at the time of
coronary artery bypass grafting. Note the short QRS
duration, fast intrinsicoid deflection, and J wave introduc-
ing the elevated ST segment. QRS duration from onset to
peak is 40 milliseconds, and the intrinsicoid deflection
from R peak to J wave is 15 milliseconds. Excluding the Jwave, total QRS duration is only 55 to 60 milliseconds in
this lead. Fig. 8B demonstrates the anterolateral and
posteroinferior aspects of the heart, and epicardial activa-
tion times are indicated for 36 locations recorded
simultaneously. Activation time numbers also represent
Fig. 6. Normal transmural depolarization in 2 dogs is illustrated. Panel A
demonstrates typical activation isochrones representing the wave front
spreading from the endocardial surface outward toward the epicardium.
Panel B demonstrates normal activation in the region of the papillary
muscle. Activation times are in milliseconds, and the positions of the wave
front at each 10-millisecond interval are indicated at the boundary betweenthe different time zones.
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the locations of the electrodes, and the unipolar electro-gram associated with each electrode is displayed to the
right of the recording site. At the time of this early digital
recording (1980), the purpose (then) was to focus only on
activation. The total repolarization interval of the electro-
gram was not digitized and cannot be demonstrated.
However, data relevant to ventricular depolarization,
QRS brevity, and the J wave are present. Several points
are emphasized:
1. A wide area of the LV surface anteriorly and
posteriorly was depolarized between 50 and 60
milliseconds or within 10 milliseconds (gray zone),
and this correlated with the rapid intrinsicoiddeflection in the ECG. Only the lateral LV margin
and basal regions of the posterior LV and right
ventricle (RV) activated later than 60 milliseconds.
This LV epicardial activation brevity with such a
large surface completed within a 10-millisecond
window is atypical.12
2. Note the prominent J waves (arrows) at several, but
not all, epicardial sites. Particularly note the larger J
complexes indicated by the larger arrows in the
anterior LV at sites activating at 51 and 54 milli-
seconds and posteroinferiorly at LV and RV sites.
Smaller arrows indicate less prominent J waves atadditional epicardial sites in LV and RV.
3. Observe t hat all of t he J waves occur aft er completion of epicardial depolarization at each site,
that is, after the rapid (negative) intrinsic deflections.
These data indicate that the J wave is a postactiva-
tion complex and represents an anomaly of early
repolarization.
The circles on the anterior and posterior LV in panel B
indicate the locations of two 20-point bplungeQ electrodes
such as those used in the canines. The encircled values
represent the activation times of the electrode points closest
to the epicardium. Fig. 8C is a representative cross section
approximately midway between apex and base, and super-
imposed is transmural activation recorded from these2 locations. Although activation in the anterior wall began
at the endocardium and spread unidirectionally and outward
toward the epicardium, depolarization in the postero-
inferior wall began deep intramurally at the midventricular
level and spread bidirectionally toward epicardium and
endocardium simultaneously. As a result, posterior wall
activation terminated earlier (42 milliseconds), compared
with 59 milliseconds in the anterior wall (D = 17 milli-
seconds). Although it cannot be demonstrated from this one
electrode, it is assumed that the posterior depolarization
spread circumferentially (elliptically) from this midwall
site, forming a highly canceling electromotive field as in thedog in Fig. 7.
Fig. 7. Bidirectional transmural activation from the mid-LV wall toward the endocardium and epicardium due to deep penetration (invagination) of the
endocardium containing the Purkinje system in a dog in panel B, recorded from the LV cross section shown in panel A. Panel C illustrates the adjacent LV cross
section demonstrating the marked endocardial invagination carrying the Purkinje fibers (arrows) deeply into the midmyocardium.
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Discussion
Comparison of early repolarization and
preexcitation (WPW)
To emphasize and explain certain features of the ERPV
ECG, it is compared with the ECG in WPW for which
mechanisms have been established.13,14 Fig. 9 compares the
ECG of a subject with ERPV (panel A) with that of a patient
with ventricular preexcitation (panel B). Only the lateral
chest leads (V4-V6) are illustrated for this comparison. Note
the subtle similarity of the initial QRS slurring and sloping
in ERPV (panel A) to the delta wave and more exaggerated
sloping in the patient with preexcitation (panel B). Thus,
initial QRS in ERPV can resemble a mini delta wave.
However, in contrast to WPW, the PR segment is not
abolished, and the QRS is not wide.
Slurring and reduced sloping of QRS is typically absent
when there is normal rapid expansion and abrupt extin-
guishing of multiple opposing wavefronts. This action
results in fast swings in the deflections. In contrast, slurringor exaggerated sloping of QRS occurs in conditions where
focal, noncompeting activation is occurring, as in WPW.
The mechanism of the early QRS changes in ERPV is
explained by the activation data obtained in that subject
(Fig. 8). This initial slurring is related to the local
depolarization of the anterior wall and septum in which
the opposing effects of posterior wall activation have been
minimized. Because of the deep midwall onset of activation
in the posterolateral wall, with wavefronts spreading in all
directions, that is, midwall to both epicardium and
endocardium and axially, the spherical or closed electro-
motive surface of this wavefront results in maximal local
cancellation effects. Thus, the outward, endocardial-to-
epicardial activation in the opposite anteroapical wall has
minimal competition. Although not preexcited as in WPW,
the local anterolateral activation in ERPV is, nevertheless,
relatively unopposed early in QRS and dominates and
produces the sloping and slurring. Thus, it is the
unbalanced activation of the anterior LV succeeded by
the rapid and premature termination of the remaining LV
depolarization that coincides sequentially with the initial
sloping of QRS, followed by the fast intrinsicoid deflection
in ERPV.The initial QRS sloping is further enhanced by LVH
because of the larger and longer-lasting wavefronts moving
outward in the thickened septal and anterior walls. In some
Fig. 8. Ventricular activation in a patient with ERPV. Panel A illustrates the ECG recorded from lead V 4. Panel B demonstrates the epicardial activation
sequence and unipolar electrograms recorded from the anterior and inferoposterior aspects of the ventricles. Transmural activation in the same subject is shownin panel C. The data were recorded from two 20-point needle electrodes inserted into the anterior and posteroinferior LV. See text.
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subjects with ERPV and LVH, a longer activation time of
the anterior LV results in a wider QRS and later ID, which
can overlap and mask the J-wave and the early ST elevation.
In those subjects, the early J is obscured and its terminal
component is merged with late QRS and appears as a
terminal QRS notch or slope.Questions relating to what anatomic mechanisms
underlie the atypical midwall activation process must also
be addressed. It is postulated that this is due to
exaggerated LV endocardial trabeculation. Both the canine
and human activation data implicate an increased trabe-
culation with greater depths of endocardial invagination,
carrying the Purkinje system deeper into the midmyocar-
dium. Studies in various animal species demonstrate an
increased trabeculation and endocardial invagination as a
basis for a more rapid activation of a thicker LV wall.15
Diffusely distributed LV trabeculation should even further
narrow the total QRS duration. Another feature sometimesobserved in subjects with ERPV and short QRS duration
is high-frequency notching of QRS complexes in some
leads. These fine, fast notches are usually best visualized
in low-voltage transitional leads where major activation
events do not compete. This type of notching may result
from changing discontinuities in wavefronts propagating
through a highly trabeculated subendocardium.
In addition to the similarities in QRS, note that there is
also a pattern of ERPV ST elevation introduced by a J
wave in the subject with WPW. This is due in part to the
premature completion of depolarization which, by its
advancement, exposes the J and early ST, which might
otherwise be obscured by late QRS in both ERPV and
WPW. In addition, because of the earlier termination and
reordering of activation and, secondarily, repolarization
in the posterior LV walls, there are diminished outward
posterior repolarization forces to counterbalance those of
the anterior LV, and this exaggerates the anteroapical
J-STE deflections in both conditions. Thus, at least some
part of the J-STT anomaly is contributed or exaggerated by
alterations in the phase and distribution of activation and,secondarily, repolarization. An issue in ERPV is whether
the QRS and ST-T anomalies are separate and unrelated
but linked by some common genetic polymorphism or
whether the ST-T changes are all secondary to the QRS
changes. That the J-STE morphology can be seen in
subjects with longer QRS duration and also that subjects
with very narrow QRS can have minimal ST elevation
implicate separate primary alterations in both depolariza-
tion and repolarization phases.
As in most natural systems, different morphological
features are usually associated with certain specific func-
tions or effects, bnothing exists for no reason.Q In the
following publication, a two-part theory involving both the
electrophysiologic and electromechanical systems in ERPV,
as well as possible consequences of these anomalies, is
presented along with certain supporting clinical evidence for
the concepts.
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