Clin. Cardiol.
22, 59-65 (1999)
Early Repolarization
MAHAVEER MEHTA,M.D., ABNASHc.JAM,M.D., ANURAG
MEHTA, M.D.
Section of Cardiology,Department of Medicine, West Virginia University,School of Medicine, Morgantown,West Virginia. USA
Summary: Early repolarization (ER) is an enigma. The pur-
pose of this review is to reemphasizethe overallelectrocardio-
graphic (ECG) pattern of this normal ST variant which con-
tinues to challenge the clinician because of its similarity to the
current of injury potential to myocardium or an acute peri-
carditis. The data were provided from the studies identified
through computerized searches of Medline, Toxline, Oxford,
Agricola, and Bios Afterdark, Cumulativeindex, and a review
of bibliographies of relevant articles on the related subjects.
Early repolarization has elevated, upward, concave ST seg-
ments, located commonly in precordial leads, with reciprocal
depression in aVR, tall, peaked and slightly asymmetricalT
waves with notch, and slur on the R wave. The other accom-
panying features in the ECG are vertical axis, shorter and
depressed P-R interval, abrupt transition, counterclockwise
rotation, presence of U waves, and sinus bradycardia. Males
dominate and patients are often younger than 50 years of age.
The incidence of 1 to 2% is found equally common in all
races. Degree and incidence of ST elevation decrease as age
advances.Exercise or isoproterenoladministrationmay nor-
malize the ST segment.Early repolarization is a benign condi-
tion. If the ECG conforms to a classical pattern of ER on seri-
al ECGs, it would exclude the unnecessary hazards of present
day revascularization therapy for myocardial infarction such
as primary angioplasty or thrombolytic therapy, or aggressive
management of acute pericarditis, and so forth. This review
concludes with a discussion of comparative ECG features of
ER, pericarditis, and myocardial infarction, and provides an
Address for reprints:
Mahaveer C. Mehta, M.D.
West Virginia University
Section of Cardiology
2203 Robert C. Byrd Health Sciences Center South
P.O. Box 9157
Morgantown, WV 26506-9157, USA
Received: June 12, 1998
Accepted with revision: August 7, 1998
algorithm for diagnostic management of patients suffering
from these conditions.
Key words: ST segment in early repolarization, race and ear-
ly repolarization, early repolarizationand myocardial infarc-
tion, early repolarization and pericarditis,arrhythmia in early
repolarization, PR interval and early repolarization. early re-
polarization and gender
Introduction
The features of early repolarization (ER) on scalar electro-
cardiogram (ECG)' have to be differentiated from coininon
pathologic causes such as acute myocardial infarction, peri-
carditis, and coronary artery spasm, where ST-segment eleva-
tion is of diagnostic help.2The benign nature of early repolar-
ization is well established. Thus, distinguishing this ECG
entity from other causes of ST elevation is important,particu-
larly in the case of acute myocardial infarction in the era of
primary angioplasty and thrombolytic therapy. The purpose
of this review is to reemphasize the variations, overall ECG
features with long-term natural history, effects of exercise
testing, and hyperventilation of this normal ST variant which
continues to challenge the clinician because of the similarity
to the injury potential of an acute pericarditis or myocardial
disease leading to ECG mimicry.
ElectrocardiographicConsiderationsand Definition
ST segmentis the interval between depolarizationand repo-
larization of the ventricles, that is, from the end of QRS to the
beginning of the T wave on the ECG, and is normally isoelec-
tic. The common pathologic cardiovascular causes of acute
ST elevation are myocardial infarction, pericarditis, and coro-
nary artery spasm.* Persistent ST elevation usually denotes
ventricular asynergy particularly in ventricular aneurysm."
The other cardiac causes of ST elevation described are cardiac
tumors, acute cor pulmonale, left ventricular (LV) hypertro-
phy, hypertrophic cardiomyopathy,left bundle-branch block,
cardiac transplantation,and penetrating cardiac injuries2Var-
ious extracardiac causes that can also cause a variable degree
of ST elevation in the ECG are summarized in Table I.
60 Clin. Cardiol. Vol. 22, February 1999

TABLEI Extracardiacetiology of ST elevation

Cerebral disease Abdominal disease Drugs Metabolic Others
Vascular accidents Acute peritonitis Quinidine Hypothermia Anxiety
TIntracraniaipressure Pancreatitis Procainamide Hyperventilation Cold water drink
Intracranial hemorrhage Acute cholecystitis Digitalis Hyperkalemia Suspended herut
Hemorrhage Hiatus hernia Isoproterenol Excess smoking

ElectrocardiographicCharacteristicsand Features Several publications on ECG peculiarities of African

In 1936, Shipley and Hallarad analyzed the ECGs of 200
normal persons, aged 20 to 35, and noted first of all that a nor-
mal variant of ST elevation occurred quite frequently. They
observed this in lead 11 in 25% of the men and 16% of the
women. With the advent of the 12-lead ECG, Myers et a1.:
Oscher and W ~ l f f as , ~ well as Goldman and Goldman M
pointed out its location in more precordial leads. In 1951,
Grant et ul.’ studied the clinical characteristicsof ST-Tvectors
and coined the term “early repolarization”for this normal vari-
ant. Most publications that concern ST elevation describe its
isolated aspects in case reports5, or as clinical features of
patients’, l7-I9rather than as detailed ECG findings of ER.
Fenichel*()followed patients of unchanged ST elevation for 9
years. Harlan et aL2’ reported minor serial changes in QRS
and T vectors in navy pilots with ST elevation. Parisi et ~ 1 . : ~
while describing ST elevation in Air Force flying personnel,
said “the subjects studied herein cannot be assumed to be
representative of general population.” The cases these authors
included in their studies had ST elevation of 0.05 mV. Ac-
cording to Macfarlane and L a ~ r i e ?ST ~ elevations up to 0.1
mV are normal. We interpreted the ECGs from 60,000 files of
adult patients over a 5-year period and kept ST elevationof 0.1
mV as a mandatory feature for diagnosing ER (Fig. l).l
Americanszu0 and African black^^^-^^ included ST eleva-
tion with or without tall T waves. Grusin’s pattern 2 was that
of early repolarization. He and some of the workers already
cited attributed these abnormalities to race and malnutri-
t i ~ n . * & ~They
l found ER common in blacks probably be-
cause their study population included blacks only. A few
studies on ECG differences between Caucasians and blacks
regarded them as normal variant^;^, l 7 still others were skepti-
cal that valid differences do, in fact, Further-
more, in contrast to the above mentioned data, the frequency
of ER was reported equally commonly between Caucasians
and More recently, ER was described as occur-
ring in other races as frequently as in blacks. Epstein rt
in Peruvians, Shrikantia et ~ 1 . “ )in Asian Indians, Burns-
Coxs1in Chinese and Malaysians, Mizunos2 in Japanese, and
Dharmadasa and N a d a ~ - a j a hin~the
~ Ceylonese population
described this variation as Grusin’s abnonnality. When the
population chosen was mainly Caucasian, ERi was found to
have the same incidence of 1-2% as in all other studies cited
above. One can easily conclude that the incidence of ER is
1-2% in all races.’
Most of the studies cited above agree that ER commonly
occurs in the younger age group. We had a broad spectrum of
age, ranging between 16 and 80 years. Based on decadewise

FIG.I Electrocardiogram showing features of early repolarization: (a) ST elevation at J; (b) concave upward; (c) notch/slur at end of QRS; (d)
tall, peaked, positive, precordial, mildly asymmetrical T waves; (e) sinus bradycardia; (f)depressed PR interval; (g) abrupt transition: (h) tall R
waves; (i) counterclockwise rotation; (i)U waves. (Reprinted from original, appeared in Ref. No. 1, with pelmission from Lippincott-Raven
hbl i shers.)
 M. Mehta et al.: Early repolarization
analysis, there was a high incidence of ER in those younger
than 50 years. The incidence of epicardial injury as a result of
acute myocardial infarction increases from the 5th decade on,
whereas the incidence of ER decreases after SO years.13 Early
repolarization occurred in only 3.5% beyond the age of 70
years. The evidence of decreased incidence of ER with ad-
vancing age was found in a 10-year follow-up. Here, ST ele-
vation lessened in degree in 20% and disappeared at the
end point of the 10-year period in 30%. This tendency to a
decrease in ST elevation with age may be due to the normal
aging process, myocardial ischemia, vectorial changes, elec-
trolyte imbalance, or hormonal changes.
Early repolarization is significantly more common in men
than in women.' Chelton and Burchell13and F e n i ~ h efoundI~~
it predominantly prevalent in men. Burchell et ~ 1attributed
. ~ ~
this to anxiety tension states in men and explained that such
records may partly show the effects of nerve impulses to the
heart; it may also be amibuted to hormonal change. However,
the real reason for this male predominance is far from clear
and needs further investigation.]
In 1961, Wasserburger Pf ~ 1described. ~ (1) ~ ST elevation,
(2) upward concavity, (3) notch and/or slur on QRS, and (4)
symmetrical T waves of large amplitudes as criteria for ER.
The available literature is silent on heart rate, but we consis-
tently found significantly slower heart rate in our series,l and
sinus bradycardia was the only arrhythmia present in the
ECGs of ER. The PR interval was of shorter duration and
was depressed in significant numbers in the precordial leads
of these ECGs compared with those of the control subjects.
Spodick s6 differentiated between ER and pericarditis. He
found PR interval depressed only in precordial or limb leads
in ER, compared with pericarditis where it is depressed in
precordial as well as limb leads. However, Ginzman and
Lakss7 found that PR segment depression did not reliably
distinguish between pericarditis and ER.
We observed some additional features in the ECGs of ER.
Increased QRS duration, abrupt transition, and counterclock-
wise rotation were significantly present in patients with ER.
Increased QRS voltage was detected, which could be ex-
plained as notindl varkdtion because of younger age. Voltage
in pericardits/myocardial infarction is usually not high and
may show low voltage graphs. Notching and slurring at the
end of QRS was a significantly frequent feature in ER and was
seen statistically more in precordial leads than in limb leads.
This finding is also not afeature of pericarditis.'
A persistent ST elevation occurring for a long time in
healthy young individuals with upward concavity is a consis-
tent finding described by all authors dealing with the subject
of ER. Reciprocal ST depression of 1 mm minimum was no-
ticed in aVR in 50% of ECGs.' Consensus on the distribution
of ST elevation showed that, out of 12 ECG leads, it occurred
most frequently in leads VI-V~.Most of the contributors re-
port ER to be located more commonly in precordial than in
limb leads.l.22~s8 In our large series of hospital population, the
location of ER pattern according to frequency of occurrence
was in right-sided precordial leads (74%), followed by transi-
tional zone (V3-V4; 73%) and inferior limb leads (LI, L11,
61
LIII, and a V F 37%) and the degree of elevation of ST seg-
ments in precordial leads was greater than in the limb leads of
the same ECG tracings.' Based on our data, ER usually oc-
curred simultaneously in both precordial and limb leads, but
not in a preferential geographic pattern of association. Alone,
ER was noted 25% in precordial and rarely (S%) in limb leads.
Elevation of ST segment in aVR was not seen at all. I
Many earlier workers4-y. 21 described ST elevation of 0.5.-
1.SmV above the isoelectric line, and Myers ct u I . found
~ an
elevation of 2.0 mV in only one case of ER. However, Gold-
man7 had 25 patients observed over a period of 3 years who
had ST elevation of 2-4 mV. Data compiled in our ECG labo-
ratory had ST elevation of I mV in 57.3% 2 mV in 24% 3
mV in 9.7%, 4 mV in 7%, and 5 mV in 2% of 600 ECGs of
ER. ST segment had a reduction in number and degree of ele-
vation as age advanced, and it occurred in 78.3% of ECGs of
those 50 years oryounger, but only 3.5% in those older than 70
years.
Tall peaked, positive, precordial T waves was the domi-
nant feature described by the majority of the contributors.
Symmetrically limbed T waves were described by W
burger et ~ 1and. other ~ researchers.J,
~ ' A3 i We found the T
waves to be slightly asymmetrical, as was also reported by
Parisi eful.22Negative precordial T waves were absent in this
study. The findings in ER are usually constant and stable. un-
like those in acute myocardial infarction and pericarditis,
where ST may return back to the isoelectric line. negative T
waves evolve, or Q waves appear. Ginzmitn and L a I d 7 con-
cluded that ST/T ratio in v6 is the best method of discrim-
ination between ER and pericarditis.
U waves were seldom noted by Parisi ef a/." in the ECGs
of ER in young Air Force fliers, but we found U waves sig-
nificantly more common in ER than in the control group in
our ECG laboratory.' U waves were present in 50%. of ECGs
with ER and 10.3% of ECGs of the control group (p<
0.00022). Of these 50% ECGs with U waves. they were up-
right in 94% and they were inverted or downward in 6%. U
waves were located 80% and 10% in precordial and limb
leads, respectively, and present in both in the remaining 10%.
W a t a r ~ a b eand
~ ~ Chelton and Burchelli3 measurcd various
electrocardiographic periods and found PR, QRS, QT inter-
vals, and QTc within normal limits. The QT interval was pro-
longed (390 f 40 ms vs. 369 It 27 ms; p < 0.22) in ER but was
not significant, and QTc in those with ER was practically the
same (408 f28; p < 0.15345) as that in control subjects. Thus,
this type of ST-segment displacement is
ma1 Q-T interval.1.60
The effect of various drugs on the pattern of ER was studied
by Chelton and Burchell" and Morace pt ~ r l . ~ Acetylcholine
"
accelerates repolarization of myocardial tissue?'. 63 They
were unable to note any change on ST elevation following ;id-
ministration of atropine, methacholine, and hydergine.
According to Wiener et u1.,12atropine caused further elevation
of the ST segment, and digitalis after intravenous potassium
chloride produced no change; however, inhalation ofamyl ni-
trate brought down the ST segment to a normal level and nor-
malized the terminal T-wave negativity. Morace rt d.(" re-
62 Clin. Cardiol. Vol. 22, February 1999

ported that isoproterenol administration brought ST segments
to an isoelectric level and the T waves decreased in amplitude
or became slurred or negative; propranolol given after isopro-
terenol restored concave ST elevation. A case of propranolol
toxicity presenting as ER was reported by Gwinup.@
Alimurung et a1.65correlated the ER responses to exercise
test and coronary cineangiography and, like other authors,
concluded that performance of an exercise stress test makes
the ST-segment become isoelectric, makes upward con-
cavity disappear, and shortens the QT interval due to exer-
cise.', 13,55,5x,61,6547 During recovery, these parameters re-
turned to preexercise level in 83% of patients. In no patients
did resting ST-segment elevation increase with exercise.', 65
Hyperventilation produced a transitory increase in heart rate
and no changes in ST segment or T wave.'. 12-67,
The benign nature of ER has been well established.'. 7 ,9, 20,
22,31,69
Long-term chronological follow-up of patients of ER
(1983-1993) showed no consistent pattern.' The ER pattern
transiently disappeared and reappeared. The degree of ST-seg-
ment elevation decreased with age and varied from ECG to
ECG even in the same patient. In 30% patients. an ER pattern
was absent in the last ECG recorded.
Differential Diagnosis
Although ST elevation is found in many cardiac and extrac-
ardiac conditions (Table I, II), ECG manifestations of ER,
pericarditis, and acute myocardial ischemia may remain in-
distinguishable (Fig. 2).17ECG manifestations of acute peri-
carditis (stage l ) or ischemia evolve in a matter of hours or
while ECG changes in ER remain stable over an ex-
tended p e r i 0 d . ' 3 ~ ~ In acute myocardial infarction, the evolving
ECG changes (Q wave, ST-T segment) are confined to the
leads reflecting the m a of myocardium involved with recipro-
cal changes in the opposite leads. In pericarditis, the ST-T
changes are almost always found in precordial as well as limb
leads, but in ER mostly precordial leads or, rarely, limb leads
are involved.' No consistentreciprocal changes of significance

TABLEIf Comparison of the electrocardiographicfeatures of early repolarization, pericarditis, and myocardial infarction

Early repolarization Epicardial injury(pericarditis) Myocardial injury (infarction)

Below 5 0 <with aging Any age >Above 5 0 > with aging
>Males No differentiation >Males but incidence same after
menopause in females
Site Precordial leads All leads Involved area leads
Clinical exam No finding Pericardial rub /knock S3/?murmur
Arrhythmia Sinus bradycardia Electrical altemance; sinus
tachycardia: atrial fibrillation ? Atrial /ventricular
Axis Vertical Horizontal
PR interval Short / depressed in limb or
precordial leads Depressed in all the leads
Q wave Absent Absent Abnormal present
QRS morphology Abrupt transition at V2 ; Low voltage; S persists even Descending limb of QRS
notch/slur at the end of QRS ; with raised S-T,T merges halfway with convex
Counter clockwise rotation; raised ST segment
ST segment Concave upward; 2-5 mm Elevated in1st stage: Convex bowing upward;
convex upward can be >5 mm, not unusual
Reciprocal changes Reciprocal depression- aVR No reciprocal changes Reciprocal changes present
T waves Tall, peaked, high and slightly Positive initially become Tall, peaked in earlier stages
asymmetrical negative in later stage become negative late stages
FOIIOW-UP Constant pattern Changes in four stages Serial changes of Q,ST,T
go back toward normal
Exercise Reverted to normal only to return Not done because possibly Not done in acute stage.
back to pre-exerciselevel associated with myocarditis Later ST depressionand
negative T waves result
 M. Mehta et d.:
Early repolarization 63

are to be relied upon in the latter two conditions. In ER, the

axis is usually vertical and in pericarditis it is horizontal. Early
repolarization shows tall, slightly asymmetrical T waves.'.h0
In myocardial mfarction, they are tall and symmetrical. In peri-
carditis, the T waves are not usually tall, and in disputable GIS-
es an ST/T ratio >0.25 in Vg helps in settling a diagnosis.
However, to establish the diagnosis of ER in patients with
chest pain, all other conditions should be carefully excluded.
The algorithm described herein (Fig. 3) has proven to be of
ready help in our ECG laboratory.
Significance
Alimurung et d5 detected 16 patients with ER of263 pa-
tients studied while undergoing diagnostic cardiac catheteri-
zation. In 13, exercise test made ST elevation return to iso-
electric baseline, and the coronary angiograms were nomial in
14patients. The remaining two patients had significant coro-
nary atherosclerotic occlusive lesions. Thus, ER and coronary
artery disease may coexist, and exercise test may not reveal is-
chemic cardiac disease.
ST-segment elevation as a criterion for the diagnosis of
myocardial infarction has a sensitivity of 46%)and a speciiici-
ty of 91%.'l In the setting of chest pain with ST elevation,
thrombolytic therapy or percutaneous transluminal coronary
angioplasty to preserve left ventricular function may i n'I( 1ver-
tently be given. However, this may happen in the case of pa-
tients who do not have coronary artery occlusion without rec-
ognition of the presence of ER.
(A) (B) (C) (D) Mechanism of Genesis of Early Repolarization
FIG.2 Electrocardiograms showing (A) early repolarization, (B)
pericarditis-stage 1, (C) myocardial infarction, and (D) ventricu- The mechanism of genesis of ER is unknown. Vagal stim-
1;~aneurysm. ulation caused accelerated repolarization of myocardial fi-

Chest pain
I
I
No clinical finding Pericardialfriction / knock Triple rhythm
I I I
CPK-MB-normal CPK-MB k CPK-MB - high
I I I
ECG ECG ECG
Elevated concave ST in precordial Stage 1-raised, convex ST in all ST raised convex peaked
leads; isoelectric in V;, vertical axis; the leads; depressed in V,; horizontal positive waves; abnormal
PR deviation only in precordial or axis; PR deviation in precordial as well Q waves; reciprocal changes;
limb leads abrupt transition; as limb leads; findings change with all these findings evolve and
counterclockwise rotation; notch resolution of disease into stage 2-ST get reverted back to normal
or slur at the end of QRS; peaked return to baseline and T-wave amplitude
positive slightly asymmetrical decrease; stage 3-T wave shallow to
T waves; stable constant findings inverted; stage 4-ECG resolution; serial
on serial ECGs ECGs show changes
I I I
Early repolarization Pericarditis Myocardial infarction
I I I
Echocardiogram Echocardiogram Echocardiogram
I I I
Normal Pericardialfluid Asynergy
FIG.3 Algorithm for diagnosis. CPK = creatine phosphokinesis, ECG = electrocardiogram.
64 Clin. Cardiol. Vol. 22, February 1999
Slow heart rate and sinus bradycardia are due to
vag~tonia.~ In~experimental
~~’ right sympathet-
ic nerve/stellate ganglion stimulation produced upward con-
cave ST elevation due to ventricular gradient between the site
with faster recovery (apicoanterior wall) and the site with
slower recovery (posterobasalregion). Early repolarization of
the apicoanteriorwall may be related to an optimum enhanced
activity of the right sympatheticnerves, which run into the in-
terventricularseptum and anterior wall of the heart. All ECGs
with ER had upward concave ST elevations.In addition, Zim-
mennann et al.,*I described shorter and depressed PR inter-
vals due to sympathetic overactivity.Short and depressed PR
intervals were observed to occur significantly more often in
ER than in the control subjects.A decrease in ST-segment el-
evation due to exercise suggests sympathetic stimulation.An-
tzelevitch et a1?2 described the appearance of a prominent
spike and dome in ventricular epicardium but not in endo-
cardium while describing the ECG sequels due to the differ-
ence in monophasic action potential observed in the endo-
cardium and epicardium.Early repolarizationmay be one of
the patterns representing this difference, because it has ST el-
evation frequently initiated by a small deflection at junction J.
This may also be one of the mechanisms to explain the phe-
nomenon of ER. Early repolarization in the subepicardium
may occur before depolarization of the whole myocardium.
This results from nonsynchronous repolarization in all my-
ocardial fibers at any moment. There is a normal biological
range for the time delay following depolarizationof the ven-
tricular myocytes before their repolarization begins. This re-
polarization process begins at the extreme early end of the
range of the time delay in patients with ER.6O Large R waves,
abrupt transition, counterclockwiserotation, and large T and
U waves present in ECGs with ER suggest such a phenom-
enon. Early repolarizationmay be explained by more than one
mechanism, which may operate alone or coexist in the same
subject at the same time.l
Conclusion
Strict protocols must guide the management of patients
with chest pain and ST elevation. Careful history recording,
age, duration, onset, character, and radiation of pain, associat-
ed symptoms, and response to nitrates, all risk factors for
coronary artery disease, should result in correct diagnosis of
myocardial disease. Previous and serial ECGs can provide
comparison. The presence of characteristic, consistent, and
stable patterns of ER (concave ST elevation from the J point )
should deter the clinician from managing the patients with
reperfusion therapy of any type. The normal appearances of
these indications on ECGs of ER deserve wider recognition
to prevent confusion in the interpretation of the ECG.
References
I. Mehta MC, Jain AC: Early repolarizationon scalar electrocardio-
gram. Am JMedSc 1995;309:305-3 1 1
2. Braunwald E: Heart Diseuse, 3rd ed., p.2 12. Philadelphia: W.B.
Saunders, 1988
3. Shipley RA, Hallaran WR: The four lead electrocardiogramin 200
normal men and women. Am HeartJ 1936 1 1 :32.5-34.5
4. Myers GB, Klein HA, Stofer BE, HiratzkaT Normal variations in
multiple precordial leads. Am HeurfJ 1947;34:785-808
5. Oscher HL, Wolff L Electrocardiographicpattern simulatingacute
myocardial injury.Am JMedSci 1953;226:541-546
6. Goldman MJ: RS-T segment elevation in mid- and left precordial
leads as normal variant.Am Heart J I9S3:46:X 17-820
7. Goldman MF: Nomal variants in the electrocardiogramleading to
cardiac invalidism.Am Heart J 1959:59:71-77
8. Goldman MJ: Principles of clinical electrocardiography,p. 83.84.
Los Altos: Lange Medical Publications, 1964
9. Grant RP, Estes EH, Doyle JT:Spacial vector electrocardiography.
The clinicalcharacteristicsof S-T and T vectors. Cir-c,rt/atiorr195I ;
3: 182-1 97
10. Morace G, Padeletti L, Porciani MC, Fantini F: Effects of isopro-
terenol on the “early repolarization” syndrome. Am H w r t J 1979:
97343-347
1 I. Edeiken J: Elevation of the RS-T segment, apparent or real. in the
right precordial leads as a probable normal variant. Ani H e w / J
1954;48:331-339
12. Wiener L, Rios JC, Massumi RA: T wave inventions with elevated
RS-T segment simulating myocardial injury. Am I-feurf.I 196467:
684-688
13. Chelton LG, Burchell HB: Unusual RT segment deviation in elec-
trocardiograms of normal persons. Am JMedSci IY.55;230:54-h0
14. Bedford DE, Thomas SG: The sickle-shapedR-T plateau. A com-
mon RS-T pattem in health. ProcBr Curdiuc Soc, p. 469, 1954
1.5. Graybiel A, White PD: E1ectroeurdii)~~ruph~ irr P r u c t k . 2nd ed.
Philadelphia: W.B. Saunders, 1946
16. WasserburgerRH: Riddle of the labile T wave. Am .I Curdiol i 958:
2~179-183
17. Spodick DH: Differential characteristicsof the electrocardiogram
in early repolarization and acute pericarditis. N Eiig1.I Mvd 1976:
295523-526
18. Santos-Campo DC: Diaphoresis and ST-segment elevation.
Choices Curdiol 1992;7:62-70
19. Sokolow N, Friedlander RD: The normal unipolar precordial and
limb lead electrocardiogram.Am Heu1.t J 1949;38:6654,87
20. Fenichel NN: A long term study of concave RS-T elevation,a nor-
mal variant of the electrocardiogram.A r z g i o b g ~1962; 13:36@366
21. Harlan WR, Graybiel A, Mitchell RE, Oberman A, Osbome RK:
Serial electrocardiograms:Their reliability and prognostic validity
during a 24-year period. JChron Dis 1967;20:853-859
22. Parisi AF, Beckmann CH, Lancaster MC: The spectrum of ST seg-
ment elevation in the electrocardiograms of healthy adult men.
Electrocurdiogruphy 1971;4:137-144
23. Macfarlane PW, Lawrie TDV Comprehensive Electrocardiogr~i-
phy, Vol. 1 , l st ed. New York: Pergamon Press, 1989
24. Ashman R: An electrocardiographic study of Caucasians and
Negroes. Pi-State M J 194I ;13:2686-2704
25. Littman D: Persistenceof the juvenile pattern in precordial leads of
healthy adult Negroes with a report of electrocardiographicsurvey
on 300 Negro and 200 white subjects. Am Hecrrt .I 194632:
370-382
26. Keller DH, Johnson IB: TheT wave of the unipolar precordial elec-
trocardiogram in normal adult Negro subjects. Am Hcurt J 19.52;
44:494-498
27. Greene CE, Kelly JJ: Electrocardiograms of the healthy adult
Negro. Circukution 195Y;2OYO~909
28. Wasserburger RH: Observation of the “juvenile pattern” of adult
Negro males. Am JMed 1955; 18:428-437
29. Gottschalk CW, Craige E A comparison of the precordial ST and T
waves in the electrocardiogramsof 600 healthy young Negro and
white adults. South MedJ 1956;49:453-457
30. Thomas J, Harris E, LassiterG: Observation on the Twave and S-T
segment changes in the precordial electrocardiogramof320 young
Negro adults.Am .I Cardiol1960:5:468472
 M. Mehta er al.: Early repolarization
3 I . Grusin H: Peculiaritiesof the African's electrocardiogramand the
changes observed in serial studies.Circulation 1954;9:860-867
32. Woods JD, Laurie W The electrocardiogramof the South African
Bantu. Circulation 1959; 19:251-256
33. Powell SJ: Unexplained electrocardiogram in the Africans. Br
HeartJ 1965;21:263-268
34. Seriki0, Smith AJ:The electrocardiogramof young Nigerians.Am
HeartJ 1966;72:153-157
35. Rees P H The ST segment in the electrocardiograms of young
adults. EustAfrMedJ 1971;2(suppl48):622-630
36. Walker ARP, Walker B F The bearing of race, sex, age and nutri-
tional state on the precordial electrocardiograms of young South
African Bantu and Caucasian subjects. Am Heart J 1969;77:
441-459
37. Somers K, Rankin AM: The electrocardiogram in healthy East
African (Bantu and Nilotic) men. Br Heart J 1962;24:542-548
38. Blackburn H, Keys A, Simonson E, Rautaharju P, Punsar S: The
electrocardiogram in population studies. A classification system.
Circulation 1960;21:1 1-1 175
39. Brink AJ: An investigation of factors influencingrepolarization in
the human heart. SAfrJClinSc 1951;2:288-295
40. Fleishman SJ: Observations of the electrocardiogramof the appar-
ently healthy African. M. D. Thesis, 1962, University of the Wit-
watersrand,Johannesburg, South Africa
41. FIeishman SJ: The normal electrocardiogramin the African. S A P
MedJ 1965;39:177-1 84
42. Blackman NS, Kuskin L InvertedT wave in the precordial electro-
cardiogram of normal adolescents.Am Heart J 1964;67:304-3 12
43. Simonson E: Dczerentiation between Normal and Abnormal in
Electrocardiography. St. Louis: The C. V. Mosby Company, 1961
44. Philips JH, Burch GE: Cardiovascular diseases in the white and
Negro races. Am J Med Sc 1959;238:97-104
45. Schwartz MB, Schamroth L, Seftel HC: The pattern of heart dis-
ease in the urbanized (Johannesburg) African. Med Proc 1958;4:
275-278
46, Sutin GJ, Schrire V: Inter-racial study of the electrocardiogram in
first two days of life. Am Heart J 1964$7:749-754
47. Turner P P The electrocardiogram of fifty normal young adult
Kikuya males. East Afr Med 1959;36:555-560
48. Mann GV, Shaffer RD, Anderson RS, Sandstead HH: Cardio-
vasculardisease in the Masai. J Atheroscl Res 1964,4289-3 12
49. Epstein FH, Pollack AA, Ostrander LD: An electrocardiographic
survey in Peru. Am JMed Sci 1964;247:687493
SO. Srikantia SG, Padmavati S, Gopalan C: The electrocardiogram in
some Indian population groups. Circulation 1964,29:118-123
5 1. Bums-Cox CJ: The electrocardiogramof healthier young Chinese
and Malay men. JElectrocardiol1971;4:211-219
52. Mizuno Y: Normal limits and variability of electrocardiographic
items in the Japanese.Jpn Circ J 1966;30357-367
53. Dharmadasa K, Nadarajah M: Electrocardiograms in young
Ceylonese. Br Heart J 1968;30:765-768
54. Burchell HB, Barnes AR, Mann FC: The electrocardiographic
picture of experimental localized pericarditis.Am Heart J 1939;18:
133-144
5 5 . Wdsserburger RH, Alt WJ. Lloyd C: The normal RS-T segment el-
evationvariant.AmJCurdiol 1961;8:184-192
56. Spodick DH: Differential characteristicsof the electrocardiogram
in early repolarization and acute pericarditis. NEngl J Med 1976;
295 523-526
57. Ginzman LE, Laks MM: The differential diagnosis of acute pen-
carditisfrom the normal variant: New electrocardiographiccriteria.
Circulation 1982;65:1004-1009
58. Kambara H, Phillips J: Long-term evaluation of early depolariza-
tionsyndrome.AmJCurciid 1976;38:157-16l
59. Watanabe Y Purkinje depolarization as a possible cause of the U
wave in the electrocardiogram. Circulation 197.531:1030-1033
65
60. Hurst JW: Abnormalities of the S-T segment-Part I. Clin Carrliol
1997;20:511-520
61. Morace G, Padeletti L, Porciani MC, Fantini F: Effects of isopro-
terenol on the "early repolarization" syndrome. Am H e w J 1979:
97:343-347
62. Burgen ASV, Terroux KG: On the ionotropic effects in the cat's au-
ricle. JPhysioll953; 120:449-464
63. Hoffman BF, Sucklig EE: Cardiac cellular potentials: Effect ofva-
gal stimulationandacetylcholine.Am J Ph?j.sio/1953;173312-320
64. Gwinup GR: Propranololtoxicity presenting with early depolariza-
tion, ST segment elevation and peaked T waves o n the ECG. Ann
Emerg Med 1988;17:171-174
65. Alimurung BN, Gilbert CA, Felner JM, Schlant RC: The influence
of early depolarizationvariant on the exercise electrocardiogram:
A correlation with coronary arteriograms. Anr Hear/ J IY8O;YY:
739-745
66. Surawicz B, Saito S: Exercise testing for detection of myocardial
ischemia in patients with abnormal electrocardiograms;it rest. Am
J Cardiol 1978;4I :943-948
67. Wasserburger RH, Siebecker KL Jr, Lewis WC: The effect of hy-
perventilationon the normal adult electrocardiogram. Ciwr/ution
1956;13:850-855
68. Thomsen JH, WasserburgerRH: The effect of hyperventilation on
precordial T waves of children and adolescents.Circdation 1967:
36700-707
69. Somers K, Rankin AM: The electrocardiogram in healthv East
African (Bantu and Nilotic) men. Br Hear/ J l962;24:542-548
70. Mabey BE, Wallis RM: Acute pericarditis..I Emt.t:q Mrd IY85:3:
457467
71. Bren CB: The electrocardiogram in patients undergoing throm-
bolysis for myocardial infarction. Ciruuktrion 1987;75(suppl11):
18-24
72. Burchell HB, Barnes AR, Mann FC: The electrocardiographicpic-
ture of experimental localized pericarditis. Am Hearr ,/ 1939;18:
133-144
73. Schamroth L The Electrocardiogruphy of Coronary Artety Dis-
ease. Oxford Blackwell ScientificPublications. 1975
74. Hoffmann BF, Suckling EE: Cardiac cellular potentials: Effects
of vagal stimulation and acetylcholine. Am .I Physiol 1953;173:
3 12-320
75. Yanowitz F, Preston JB, Abildskov JA: Functional distribution of
right and left stellate innervation to the ventricles: Production of
neurogenic electrocardiographicchanges by unilateral alteration of
sympathetictone. Circ Res 1966;18:41W2X
76. Randall WC, Szentivanyi M, Pace JB, Wechsler JS, Kaye MP:
Patterns of sympathetic nerve projections onto canine heart. Circ
Res 1968;22:315-328
77. Randall WC, Armour JA, Geis WP, Lippincott DB: Regional car-
diac distribution of the sympathetic nerves. Fed Pmc. 197231:
1199-1208
78. Ueda H, Yanai Y, Marao S, Harumi K, Mashima S, Kuroiwii A.
SugimotoT, Shimomura K: Electrocardiographicand vector-cwdi-
ographic changes produced by electrical stimulation of the cardiac
nerves.Jpn HrartJ 1964;5:359-372
79. Kralios FA, Martin L, Burgess MF, Millar K: Local ventricular re-
polarization changes due to sympatheticnerve-branch stimulation.
AmJPhyxiol 1975;228:1621-1626
80. Kuo CS, Surawicz B: Ventricular monophasic action potenhl
changes associated with neurogenic T wave abnormalities and iso-
proterenol administration in dogs. Ant JCurdiol 1976;38:i 7G177
8 1. Zimmermann HA, Eduardo B, Carlos D: The Aiirktdar. E/e.cWo-
cardiogram. Springfield:Charles C. Thomas. I968
82. Antzelevitch C, Sicouri S. Lukas A, Nesterenko VV, Liu DW.
Diego JMD: Zipes/Jalife Cardiu Elec.troplr~,sio/[)'~~, 2nd ed. Phil-
adelphia:W. B. Saunders, 1995