The early repolarization variant—an electrocardiographic enigma

8/2/2019 The early repolarization variantan electrocardiographic enigma

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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]

Journal of Electrocardiology 40 (2007) 3.e13.e10

www.elsevier.com/locate/jelectrocard


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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.

J.P. Boineau / Journal of Electrocardiology 40 (2007) 3.e13.e103.e2


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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.

J.P. Boineau / Journal of Electrocardiology 40 (2007) 3.e13.e10 3.e3


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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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and J, ST-T. See text for explanation.



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The early repolarization variant—an electrocardiographic enigma