Curriculum in Cardiology

Electrocardiographic diagnosis of acute myocardial

infarction: Current concepts for the clinician
Elena B. Sgarbossa, MD,a Yochai Birnbaum, MD,b and Joseph E. Parrillo, MDa Chicago, Ill, and Petah-Tiqva,
Israel

Background Over the past 2 decades, the 12-lead electrocardiogram has attained special significance for the diag-
nosis and triage of patients with chest pain because timely detection of myocardial injury and a rapid assessment of
myocardium at risk proved pivotal to implementing effective reperfusion therapies during acute myocardial infarction. How-
ever, this wealth of information could still be underutilized by clinicians who may restrict their diagnostic quest in patients
with chest pain to the more classic electrocardiographic signs.
Methods The medical literature on electrocardiographic manifestations of acute myocardial infarction was extensively
reviewed.
Results The widespread utilization of both coronary angiography and methods to determine myocardial function and
metabolism in patients with acute myocardial infarction over the last 10 years has provided the means for rigorous compar-
isons with electrocardiographic information. We summarize these electrocardiographic signs and patterns in terms of their
relevance to the clinician to help reduce the incidence of “nondiagnostic electrocardiograms” and improve timely decision-
making.
Conclusions The electrocardiogram continues to be an invaluable tool in the initial evaluation of patients with chest
pain. The plethora of data currently available on electrocardiographic changes correlating with myocardial injury allows
clinicians to make faster and better decisions than ever before. (Am Heart J 2001;141:507-17.)

In comparison with other cardiac noninvasive diagnos-
tic techniques, electrocardiography has evolved rather
slowly over the past 40 to 50 years. Perhaps the most sig-
nificant advance has been the introduction of computer-
ized electrocardiographic interpretation. Although health
professionals have increasingly relied on this feature,
automated reports are not optimal and should always be
overseen by an experienced, well-informed physician
with electrocardiography training.1,2 This is crucial when
expeditious diagnoses may be life-saving, as in acute coro-
nary syndromes. Henry Marriott3 wrote that the electro-
cardiogram is “the single most often used, most cost-
effective, and most diagnostic test in cardiology” and also
“the most frequently misinterpreted.”
Many observations made over the past decade from
both multicenter and small, prospective studies have
systematically correlated the electrocardiographic
changes of myocardial injury to biochemical markers,
early coronary angiographic findings, ventricular con-
From the aSection of Cardiology, Rush-Presbyterian Medical Center, Chicago, Ill;
and the bDepartment of Cardiology, Rabin Medical Center, Beilinson Campus,
Petah-Tiqva, Israel.
Submitted August 16, 2000; accepted December 12, 2000.
Reprint requests: Elena B. Sgarbossa, MD, Cardiology, Rush Presbyterian-St Luke’s
Medical Center, 1750 W Harrison St, Chicago, IL 60612.
E-mail: esgarbos@rush.edu
Copyright © 2001 by Mosby, Inc.
0002-8703/2001/$35.00 + 0 4/1/113571
doi:10.1067/mhj.2001.113571
tractility, and myocardial metabolic state. Such contribu-
tions have considerably improved our ability to diag-
nose acute myocardial infarction (AMI) and are summa-
rized in this article in terms of their relevance to the
clinician reviewing electrocardiograms.
Normal anatomic references
Several anatomic caveats are pertinent to the assess-
ment of new fascicular blocks or axis changes and to
the assessment of infarct location.
The heart lies horizontally with the atria at its base
and the ventricles at its apex.4 Because the heart is
rotated over its long axis, the right atrium and ventricle
are more anterior than the left chambers, and the right
and left sides of the heart are not aligned with the same
sides of the body. Thus the interventricular septum is
almost parallel with the frontal—not the sagittal—plane,
and the left ventricular free wall (usually considered a
lateral structure) includes nearly 300 degrees of the left
ventricular circumference and faces superiorly, posteri-
orly, and inferiorly.2,4 In addition, the heart position rel-
ative to the electrocardiographic electrodes is highly
variable; this results in a wide range of normalcy for the
cardiac long axis.5
The conventional 12-lead system is unfortunately sub-
optimal. Whereas leads V1 through V6 adequately cap-
ture most electrical cardiac phenomena taking place in

508 Sgarbossa, Birnbaum, and Parrillo
Figure 1
Panoramic display of frontal-plane electrocardiographic leads
showing both conventional aVR and a “–aVR” at 30 degrees
(from Reference 34, with permission).
the horizontal plane (and this anatomic area can be
further extended by adding leads V7 through V9 and
V3R through V5R), the cardiac activity that takes place
in the frontal plane is not ideally represented. The rea-
sons are 2-fold. One is that whereas 3 of the frontal
lead pairs are separated between them by 30 degree
angles, a 60 degree gap exists between leads I and II.
This leaves an absent recording point where the lead
“–aVR” should be placed. The conventional lead aVR,
separated from lead III by a 90 degree angle, provides
an inconvenient view from the right shoulder (Figure
1). This results in underdetection of injury currents at
the left ventricular inferior and lateral walls and in a
virtual neglect of lead aVR by physicians during elec-
trocardiographic interpretation.6 The second limita-
tion of the frontal electrocardiographic display is that
it presents the electrical phenomena in the two group-
ings I, II, III, and aVR, aVL, aVF. This sequence is
unlike the true spatial sequence; ventricular activation
starts from the base of the left ventricle with lead aVL
and continues with leads I, II, aVF, III, and aVR7 (Fig-
ure 1). Thus the electrocardiogram interpreter needs
to make a “mental rearrangement” of the spatial lead
distribution.
The diagnosis of AMI is compounded by the fact
that the electrocardiographic signal integrates the bal-
ance of many competing forces across the
myocardium and that coronary artery occlusions will
result in widely different electrocardiographic mani-
festations, depending on the artery size, length, direc-
tion, and occlusion level; on the presence of collateral
American Heart Journal
April 2001
circulation, previous myocardial necrosis, and intra-
ventricular conduction disorders; and on the position
of the heart in the chest. Thus the 12-lead electrocar-
diogram is only moderately accurate to determine the
anatomic location of AMI, and the correspondence of
some electrocardiographic terms with the pertinent
site of infarction is rather poor.8 The infarction
descriptors “anterior,” “inferior,” and “lateral” have
classically been attributed to occlusions of the left
anterior descending artery (LAD), right coronary
artery (RCA), and left circumflex artery (LCX), respec-
tively. Other terms such as “apical,” “septal,” “high lat-
eral,” and “posterior” are also in use. However, a
detailed review of the anatomic, echocardiographic,
and angiographic correlations has suggested that a cat-
egorization of infarction into anterior, lateral, and pos-
terior (for the LAD, LCX, and RCA territories, respec-
tively) would be more appropriate.9 Other authors
maintain that because the left ventricle has a marked
conal shape, the electrocardiogram can only differenti-
ate between “anterior” and “posterior” and that the
name “inferior” should be included with the latter cat-
egory.8 Yet other investigators believe that the name
“posterior” is misleading, given that this term applies
better to the posterior thoracic wall facing the left
ventricle than to the left ventricle itself.10
Value of ST-segment elevation
The electrocardiograms that give us the most con-
cern in emergency departments are those with a large
amount of ST-segment deviation. The initial ST-segment
sum is the main variable influencing “door to throm-
bolysis” time; the largest ST deviations result in the
shortest times to treatment.11 Although this is usually
justified, many factors such as myocardial mass, dis-
tance between the electrodes and the ischemic zone,
and reciprocal “cancellation” changes may affect the
magnitude of ST elevation. This should be considered
particularly in scenarios of less conspicuous ST shifts
because the choice of electrocardiographic criteria
will determine both the diagnosis and the therapeutic
decisions. A recent controlled study analyzed the ini-
tial electrocardiogram of patients with and those
without chest pain. The optimum electrocardio-
graphic variables for the detection of AMI were ST
elevation ≥1 mm in at least 1 lead, either inferior (II,
III, aVF) or lateral (V5, V6, I, aVL), and ST elevation ≥2
mm in at least 1 anterior lead. Such a model (inter-
nally validated) correctly classified 83% of subjects
with 56% sensitivity and 94% specificity. Changing
the degree of ST elevation greatly modified both sen-
sitivity (45.4% to 68.6%) and specificity (81.2% to
98.1%). The addition of multiple QRST variables
increased specificity but improved overall classifica-
tion only marginally.12
American Heart Journal
Volume 141, Number 4
Electrocardiographic-angiographic
correlations revisited
The most frequent infarct-related artery among
patients admitted with chest pain or discharged from
the hospital after AMI is the LAD (44% to 56% of cases),
followed by the RCA (27% to 39%) and the LCX
(17%).13
Anterior/anteroseptal/anterolateral infarction
(LAD occlusion)
After occlusion of the LAD, ST-segment elevation ≥1
mm is most frequently observed in lead V2 (sensitivity,
91% to 99%) and then—in decreasing order of fre-
quency—in V3, V4, V5, aVL, V1, and V6.14 The maxi-
mum ST elevation is recorded in V2 or V3.
Additional signs (concomitant with precordial ST ele-
vation) were identified over the last decade by Birn-
baum et al15 and others16 as powerful predictors of
proximal LAD occlusion. These include ST elevation in
aVL and ST depression in inferior leads. ST elevation
that extends to leads I and aVL often coexists with infe-
rior ST depression; the magnitude of ST depression in
inferior leads correlates better with that of ST elevation
in leads I and aVL than with the ST elevation of precor-
dial leads.16
Four electrocardiographic signs that had previously
received little attention as indicators of anterior infarc-
tion were recently found to be specific for occlusions
at the level of the first septal perforator. These include
ST elevation in aVR (sensitivity, 43%; specificity, 95%),
disappearance of preexistent septal Q waves in lateral
leads (sensitivity, 30%; specificity, 84%), ST depression
in V5 (sensitivity, 17%; specificity, 98%), and right bun-
dle branch block (RBBB) (sensitivity, 14%; specificity,
100%).17-19
Distal LAD occlusions, on the other hand, usually
have ST elevation of ≤3.2 mm in V2 and slight to moder-
ate ST elevation in V3.19 Also common are new Q
waves in V4 through V6 and augmented R-wave ampli-
tude in V2.19,20 This pattern of acute right septal con-
duction delay results from an ischemic disruption of
the right septal activation pathway and increased septal
anterior vectors and may be indistinguishable from the
changes observed in recent or old posterior infarc-
tion.20 Concomitant ST depression in inferior leads, if
present, is of a lesser magnitude than that seen in proxi-
mal LAD occlusions (0.9 mm vs 1.9 mm in lead III,
respectively).
The significance of ST elevation in lead V1 merits dis-
cussion. Lead V1 captures electrical phenomena from
the right paraseptal area, which is supplied by the sep-
tal branches of the LAD. In some patients, the septum is
additionally protected by a blood supply from a conal
branch of the RCA (double circulation). This explains
why approximately two thirds of patients with anterior
Sgarbossa, Birnbaum, and Parrillo 509
AMI have no ST elevation in V1.19 The presence of ST
elevation in V1 correlates strongly with ST elevation in
V3R and predicts the less common anatomic scenario in
which a small conal branch of the RCA does not reach
the interventricular septum.21 In 7% of the patients
with ST elevation in leads V1 through V4 who undergo
coronary angiography, this ST elevation is secondary to
RCA occlusion.22
Anterior/”high lateral” infarction (occlusion of
first diagonal)
The electrical activity of the anterolateral wall of the
left ventricle (supplied by both the first diagonal and
the first obtuse marginal branches) is well captured by
the contiguous leads aVL and I. During acute anterior
injury, a culprit lesion at the level of the first diagonal
can be suspected when ST elevation is present in both
leads I and aVL (a highly sensitive combination also for
diagonal occlusion) and when precordial ST elevation
is associated with ST elevation in lead aVL (a highly spe-
cific sign).15,23 Occlusion of the first diagonal may pro-
duce unique electrocardiographic changes character-
ized by ST elevation in the noncontiguous leads aVL
and V2, plus ST depression in leads III and aVF or in V4.
This pattern has been termed “mid-anterior” infarction
because the akinetic region in the left ventricle
excludes the apex and the septum.24 When ST eleva-
tion in leads I and aVL is accompanied by ST depres-
sion in lead V2, the culprit artery is usually the first mar-
ginal branch of the LCX.25
Inferior infarction (right coronary or circumflex
occlusion)
The typical electrocardiographic pattern of inferior
infarction consists of ST-segment elevation in leads II,
III, and aVF. The occlusion is in the RCA in 80% to 90%
of cases and is in the LCX in the remaining patients.26
Higher ST elevation in lead III than in lead II strongly
suggests compromise of the RCA (Figure 2).27,28
A bedside differential diagnosis between culprit arter-
ies can also be attempted by examining additional elec-
trocardiographic leads. Because the only lead that faces
the superior part of the left ventricle and directly
opposes the inferior wall is aVL, ST depression in lead
aVL is almost always determined by RCA occlusion
(sensitivity, 94%; specificity, 71%), without indicating
concomitant involvement of the posterior wall or the
right ventricle (Figure 2). Injury in leads II, III, and aVF
without ST depression in aVL indicates proximal LCX
occlusion.29
Several studies in the 1980s concluded that ST eleva-
tion in leads V5 through V6 during inferior injury sig-
naled LCX occlusion. However, because most inferior
infarctions are caused by RCA occlusion, the positive
predictive value of this sign is poor. The arteries that
supply the posterolateral region of the left ventricle are
 American Heart Journal
510 Sgarbossa, Birnbaum, and Parrillo April 2001

Figure 2

Twelve-lead electrocardiogram showing sinus tachycardia and inferior wall injury. Presence of ST elevation in lead III > lead II, a V3/III
ratio approximately 0.3 mm, plus ST depression in aVL all suggest proximal RCA occlusion.

Figure 3

Inferior infarction including recording of lead “–aVR” (from Reference 34, with permission).

the obtuse marginal branch of the LCX, the posterolat-
eral, and the LAD branches. Thus ST changes in leads
V5 and V6 indicate rather posterolateral ischemia trig-
gered by either RCA or LCX occlusion.30 When this ST
elevation is significant (>2 mm), it is probably a sign of
“mega-artery-related” (either the RCA or LCX) infarction
with a large ischemic burden.30
Precordial ST depression accompanying inferior
injury is more likely to develop from LCX than RCA
occlusion. Horizontal ST depression with initially nega-
tive, then upright T waves in leads V1 through V3/V4 is
associated with posterior wall motion abnormalities.31
The degree of ST depression in lead V3 compared with
the degree of ST elevation in lead III (“V3/III ratio”) is
highest (1.2 mm) when the occlusion is in the LCX and
lowest (<0.5 mm) when it is in the proximal RCA (Fig-
ure 2). Occlusions of the mid RCA produce V3/III inter-
mediate ratios.32 The absence of ST depression in leads
V1 to V2 rules out LCX occlusion, with a predictive
value of >90%.
Some electrocardiographic leads underutilized in clin-
ical practice can be very helpful in discriminating
infarct-related arteries during inferior injury. ST eleva-
tion in leads V7 through V9 and ST depression in V4R
probably are related to LCX occlusion.26,33 ST elevation
in leads I to aVL or V5 to V6 is frequently accompanied
by ST depression in lead aVR (or ST elevation in “–aVR”
at 30 degrees) (Figure 3).34 This sign is independent of
ST depression in V1, and it indicates a larger infarct
size. However, during routine electrocardiographic
interpretation, most physicians—even electrocardio-
graphic experts—seem to ignore lead aVR6; medical
teaching should probably emphasize its value.
Lateral and posterior infarctions (LCX occlusion)
The vascular beds of the LCX have broad anatomic vari-
ability and supply a rather small ventricular area. This is
why the standard 12-lead electrocardiogram shows ST ele-
vation in less than half of cases of LCX occlusion. When
present, ST elevation is more often seen in leads II, III,
and aVF, followed by leads V5, V6, and aVL.35
One third of patients with chest pain secondary to
American Heart Journal
Volume 141, Number 4
Figure 4
Electrocardiogram from patient with chest pain and left main disease. ST depression is present in leads I, II, and
V4 through V6 (from Reference 41, with permission from Excerpta Medica Inc).
spontaneous LCX occlusion have isolated ST depres-
sion in the electrocardiogram; ST depression in leads
V1 to V2 is a sensitive sign.29,35 Another third of
patients will not have any changes in the 12-lead elec-
trocardiogram. In a study of 33 such consecutive
patients, however, ST elevation in V7 through V9 was
always detected and was associated with posterior
wall motion abnormalities.36 Leads V7 through V9 are
more specific than precordial leads for posterior
infarction (84% vs 57%), with similar sensitivity
(approximately 80%).33
Special electrocardiographic injury
patterns
Anterior plus inferior injury
The combination of anterior and inferior ST eleva-
tion in the electrocardiogram may give the impression
of a critical mass of myocardial injury. However, it
often results from distal occlusion of a long LAD,
which “wraps around” the cardiac apex and results in
wall motion abnormalities circumscribed to the car-
diac apex.37 When injury in leads II, III, and aVF is
accompanied by ST elevation in V1 but ST depression
in V2, right ventricular—rather than apical—infarction
is likely.38
Sgarbossa, Birnbaum, and Parrillo 511
Septal infarction
The ST elevation in leads V1 through V3 encountered
in most patients with LAD occlusion is usually assumed
to represent septal infarction; however, it is signifi-
cantly associated with apical wall motion
abnormalities.39 Instead, the most frequent electrocar-
diographic correlate of echocardiographic septal
hypokinesia is ST elevation in leads V3 to V4. Septal
asynergy is also present in 58% of patients with both
transmural inferior injury and precordial ST
depression.40
Left main disease
The electrocardiograms of patients with rest angina
from occlusion or subocclusion of the left main coro-
nary artery frequently show a combination of ST eleva-
tion in aVR and ST depression in leads I, II, and V4
through V6. A sum of ST changes ≥18 mm is 90% sensi-
tive for left main disease41 (Figure 4).
Right ventricular infarction
Timely recognition of right ventricular injury is
important because of both the high risk of complete
atrioventricular block and the need to provide
intravascular volume expansion.42 Transmural injury
of the right ventricle translates into ST elevation ≥1

512 Sgarbossa, Birnbaum, and Parrillo
Figure 5
Anterior wall AMI in patient with RBBB. Precordial and lateral ST elevation as well as inferior ST depression are not obscured by con-
duction defect.
mm in precordial leads; ST elevation in V1 is highly
specific for proximal RCA occlusion.28 In approxi-
mately 7% of patients, ST elevation extends to lead V5,
suggesting anterior infarction. However, this ST eleva-
tion decreases toward V4, whereas in anterior injury
the ST segment is more elevated in V2 to V3 than in
V1.43
Right ventricular infarction is usually concurrent with
infarcts of the inferior wall. Fifty-four percent of
patients with inferior injury have ST elevation in lead
V4R (sensitivity and predictive accuracy for right ven-
tricular infarction are both 93%).43,44 Isolated right ven-
tricular infarction is rare and occurs mainly in patients
with right ventricular hypertrophy.45
ST-segment depression
Many patients with acute chest pain have “reciprocal”
ST-segment depression, that is, ST-segment depression
concomitant with ST-segment elevation in a lead group
different than the one showing ST elevation. The mecha-
nism underlying this ST depression is usually mirroring, a
phenomenon of electrical reflection of the transmural
injury onto the opposite ventricular wall. The ST depres-
sion is captured by a lead placed at 180 degrees of the
lead recording the ST elevation, although the terms “reci-
procal” and “mirror” are loosely applied to recording
points in the complementary electrocardiographic spa-
tial plane as well.46 Another possible mechanism for ST
depression is regional subendocardial ischemia or infarc-
tion. Although, strictly speaking, mirroring is also
involved in the ST depression of subendocardial
ischemia because the ST elevation in the subendocardial
layer is reflected onto the epicardial layer, most clini-
cians consider this ST depression “nonmirror” because it
is a primary manifestation of artery occlusion not associ-
ated with ST elevation in a different territory.47
American Heart Journal
April 2001
ST-segment depression concomitant with ST elevation
In patients with chest pain and predominant ST
depression in any lead except aVR, ST depression of ≥4
mm is 97% specific (and 20% sensitive) for AMI.48 More
than 85% of patients with ST depression in lead aVF
have a culprit lesion in the LAD proximal to the first
diagonal branch. Through assessments by perfusion
imaging, several investigators have found that inferior
ST depression during anterior injury does not represent
inferior injury, suggesting that mirroring—rather than
inferior subendocardial ischemia—is the cause of ST
depression.46,47
The significance of anterior ST depression accompa-
nying inferior transmural injury, on the other hand, may
depend on the leads involved. ST depression in leads V1
through V3 or I to aVL appears to correspond to mere
mirroring, often from LCX occlusion (Figure 2).31 ST
depression circumscribed to V1 through V3 during infe-
rior injury is not accompanied by septal or anterior wall
motion abnormalities.31 In a study of more than 1000
patients with inferior infarction, the presence of maxi-
mum ST depression in leads V1 through V3 indicated a
much lower probability of proximal RCA occlusion
than its absence or than a maximum ST depression in
leads V4 through V6.49 On the other hand, a maximum
ST depression in leads V4 through V6 is associated with
septal asynergy and most likely corresponds to antero-
lateral or septal subendocardial injury from a severe
lesion in the LAD or in the left main coronary artery, or
it is associated with triple-vessel disease.31,41,49
The fact that patients with ST depression in leads V1
through V3 often have a greater magnitude of ST eleva-
tion in inferior leads than patients with ST depression
in leads V4 through V6 may be due to a “canceling
effect” from the concomitant LAD lesion in the latter
group.
American Heart Journal
Volume 141, Number 4
Isolated ST depression
Isolated ST depression ≥1 mm measured at 80 ms
of the J point in ≥6 leads is 96.5% specific for AMI.12
A maximum ST depression in leads V2 to V3 indicates
LCX occlusion (specificity, 96%; sensitivity, 70%).
This is important because patients with isolated ST
depression from LCX occlusion benefit from throm-
bolysis.50
Diffuse precordial (and often inferior or lateral) ST
depression with a peak in leads V4 through V6, on the
other hand, may be caused by subendocardial
ischemia from a subtotal obstruction of the LAD—
particularly if the ST depression is accompanied by
upright T waves not preceded by negative T waves.
The maximum ST depression is observed in the lead
with the highest R wave, either V4 or V5. Patients with
counterclockwise rotation of the heart may have a
maximum ST depression in V3, whereas patients with
clockwise rotation will show maximum ST depression
in V6.51 The subsequent evolution of subendocardial
infarction may include left bundle branch block
(LBBB) secondary to increased ventricular diastolic
pressure; Q waves; and a decrease in R-wave ampli-
tude.51 As discussed above, diffuse ST depression
often signals left main or triple-vessel disease (Figure
4), and in autopsy series, it has been associated with
large subendocardial infarctions.52 ST depression in
leads V4 through V6 accompanied by negative T waves
manifests either the subacute stage of posterior injury
from LCX occlusion or an increased myocardial oxy-
gen demand (eg, tachycardia).51,53
An autopsy study found that ST-segment depression
≥1 mm in the initial electrocardiogram was a sensitive
sign for infarction of a papillary muscle; for half of the
patients, ST depression was not accompanied by ST ele-
vation at admission. Inferior ST depression was seen
exclusively in infarctions of the anterolateral papillary
muscle, whereas ST depression in leads I, aVL, or both
occurred only after infarction of the posteromedial pap-
illary muscle.54
Several prospective studies have shown that patients
with chest pain and isolated ST depression did not have
a survival benefit from timely thrombolysis. A subgroup
analysis in the LATE study (which compared tissue plas-
minogen activator with placebo administered 6 to 24
hours after admission) did find a survival benefit in
patients who had ST depression ≥2 mm.55 This finding
is difficult to interpret. It is possible that the post hoc
nature of the analysis introduced some bias. Or, if
patients with ST depression in leads V1 through V3
were included, perhaps posterior AMI caused by LCX
occlusion accounted for the survival benefit.
Nonischemic ST depression
The most important differential diagnosis in patients
with chest pain and ST depression is aortic dissection.
Sgarbossa, Birnbaum, and Parrillo 513
As many as 50% of patients with dissection of the tho-
racic aorta (some with abnormal levels of creatine
kinase) will have electrocardiographic abnormalities,
mainly ST-segment depression.56 True ischemia may
also develop if the origin of a coronary artery is
involved in the dissection.
Confounding factors
Bundle branch block/ventricular pacing
Inclusion criteria for patients with chest pain in many
clinical studies and registries require grouping patients
with either RBBB or LBBB into a common category of
“difficult” or “impossible” early diagnoses.57 However,
the diagnosis of AMI in patients with RBBB is rarely
obscured by the conduction defect. Myocardial injury
should not be missed more often in these patients than
in those with normal conduction because ST-segment
elevation in both anterior and inferior injury (as well as
reciprocal ST depression) are all recognizable (Figure
5).2,58 Anterior injury can also be suspected when sec-
ondary T waves (ie, with opposite polarity to that of
the QRS complex) in leads V1 through V3 to V4 are
replaced by T waves of concordant polarity with the
QRS (“pseudonormalization”).
In patients with LBBB, electrocardiographic inter-
pretation is indeed more difficult because the normal
sequence of ventricular activation and recovery can
be similarly altered by both LBBB and acute myocar-
dial injury. However, it has been shown that further
distinct ST-segment elevation does occur in LBBB dur-
ing coronary artery occlusion.59 Yet physicians do not
always inspect the electrocardiogram in search of this
ST elevation; one consequence is that patients with
cardiac chest pain and LBBB are as unlikely to receive
reperfusion as those without chest pain and less likely
to receive thrombolysis than patients with previous
stroke or with cardiac arrest at arrival.60,61 This is in
part explained because these patients are elderly; the
median age of patients with chest pain and LBBB in
the United States is 74 years. On the other hand, the
approach “thrombolysis to all [patients with chest
pain and LBBB]” (still strongly supported by some
physicians62) would seem an overcompensation in
light of the recently reported high mortality rates
among patients with LBBB receiving thromboly-
sis.63,64
Thus, identifying patients with LBBB and specific
electrocardiographic signs of infarction may allow for
more effective, individualized therapies, taking into
consideration the patient’s age. In a large population of
patients with chest pain and LBBB undergoing throm-
bolysis (compared with patients without chest pain), 3
independent signs of AMI during LBBB were identified:
ST elevation ≥1 mm in leads with a positive QRS, ST
depression ≥1 mm in leads V1 through V3, and ST eleva-

514 Sgarbossa, Birnbaum, and Parrillo
Figure 6
Unipolar VVI pacing in patient with AMI. ST elevation ≥5 mm is visible in leads V2 through V4.
tion ≥5 mm in leads with a negative QRS. As a clinical
prediction rule, the score value of each sign was 5, 3,
and 2, respectively. A score ≥3 made a diagnosis of AMI
with a 90% specificity and a score of 2 with >80%.65,66
These criteria have shown high interobserver agree-
ment among both cardiologists and emergency physi-
cians67 and have recently been validated in two inde-
pendent populations.68,69
In persons with permanent ventricular pacing, the
presence of ST elevation ≥0.5 mV in leads with negative
QRS complexes in the admission electrocardiogram had
a specificity of 88% and a sensitivity of 53% for the diag-
nosis of AMI (Figure 6).70
Wolff-Parkinson-White syndrome
From the few cases reported in the literature of
patients with both Wolff-Parkinson-White syndrome
(WPW) and AMI, it appears that the diagnosis of AMI
can be made with reasonable specificity. Among 6
patients with WPW enrolled in the GUSTO-I study (3
with left posteroseptal accessory pathways and 3
with accessory pathways in other locations), ST eleva-
tion (∑ST, 7 to 18 mm) was recognizable in all. Five
patients had abnormal creatine kinase-MB; one
patient with a left posteroseptal accessory pathway
was misdiagnosed with AMI from the presence of a 3-
mm ST elevation in leads V2 and V3. In the predis-
charge electrocardiogram of 4 of the 5 patients with
confirmed AMI (all of whom had inferior wall AMIs),
preexcitation was still present but less evident, sug-
gesting ischemic damage of the accessory pathway.
The delta wave disappeared in a patient with a left
posteroseptal accessory pathway and extensive ante-
rior wall AMI.71 Because radiofrequency ablation of
accessory pathways is now a widespread curative
treatment for WPW, fewer patients are expected to
have both WPW and AMI.
American Heart Journal
April 2001
Pseudoinfarction patterns
Several conditions mimic AMI and may pose a diag-
nostic challenge.
Normal variants
Some persons have baseline ST-segment elevation in
precordial leads; normal young men may show ST-seg-
ment elevation of up to 4 mm in leads V1 through V3.72
This pattern appears to result from the onset of ventricu-
lar repolarization in a nonhomogeneous fashion, and it is
known as early repolarization.73 Early repolarization has
been reported in 1% to 2% of the general population and
in as many as 48% of patients seen in the emergency
department with chest pain; these patients are at risk of
receiving erroneous treatment for acute infarction.
Acute pericarditis
Pericarditis may complicate both AMI and myocardi-
tis. Early electrocardiographic abnormalities during
acute pericarditis include diffuse ST-segment elevation
and upright T waves. The myocardial area underneath
the inflammatory process depolarizes only partially.
Newly developed ST vectors point toward the apical
epicardium. Thus ST-segment elevation may be seen in
all leads except aVR, which shows ST depression as
well as lead V1 (which faces the right atrium). Although
the P wave is usually not affected, PR (STa) segment
depression may develop, except in lead aVR or lead
V1.74 Acute pericarditis persists for 3 or 4 weeks. After
the ST segment normalizes, the T-wave changes
become conspicuous. In postinfarction pericarditis,
these changes may consist of persistently positive
deflections after 48 to 72 hours or of gradual reversal of
initially inverted T waves. Premature restoration of the
concordance of the ST segment with the T wave after
infarction is deceptive because it renders the electro-
cardiographic appearance more “normal”; yet it is a piv-
American Heart Journal
Volume 141, Number 4
otal manifestation of pericarditis (sensitivity, 100%;
specificity, 77%).75
Miscellaneous
Other conditions that may mimic AMI are severe
hyperkalemia, primary and secondary cardiac tumors,
acute pulmonary embolism, ventricular aneurysm, left
ventricular hypertrophy, hypothermia with J waves,
and exercise-induced ST elevation in patients with pre-
vious AMI.2 In vagotonic persons, marked negative T
waves—like those observed after AMI—may be nor-
mally present in leads V6R through V2.
Nondiagnostic electrocardiograms
Fifteen percent to 18% of patients with AMI do not
show changes in the initial electrocardiogram, and an
additional 25% show nonspecific changes.2 Although
nondiagnostic electrocardiograms in patients with
chest pain are often associated with lesions in branch
vessels, the probability of detecting AMI does increase
by recording serial electrocardiograms.76 However,
because reperfusion therapies are more effective when
administered early, it is ideal to maximize the informa-
tion provided by the admission electrocardiogram. Non-
diagnostic electrocardiograms are usually 12-lead
recordings; approximately 8% of patients with cardiac
chest pain will display ST elevation only in posterior
(V7 through V9) or right precordial (V3R through V6R)
leads.77 These patients may not be offered reperfusion
if only the 12-lead electrocardiogram is used for deci-
sion-making. Systematically recording leads V4R, V8,
and V9 (ie, a 15-lead electrocardiogram) increases the
probability of detecting ST elevation from 47% to 59%,
with no decrease in specificity.77 It is also reasonable to
assume that a systematic examination of lead aVR may
increase sensitivity for acute infarction.34
Conclusions and recommendations
Relative to other diagnostic methods in cardiology,
electrocardiographic technology has lagged behind.
Experts in electrocardiography have called for a con-
certed effort to incorporate modern features to the bed-
side diagnosis such as high-resolution, additional leads
and 3D vectrocardiography imaging.78 These additions
would improve our ability to diagnose AMI.
In the meantime, however, the plethora of data cur-
rently available on electrocardiographic changes
accompanying chest pain should allow clinicians to
make faster and better decisions than ever before. For
example, it is now clear that isolated ST depression in
leads V1 through V3 may indicate LCX occlusion and
potential benefit from thrombolysis. Entirely nondiag-
nostic electrocardiograms may become diagnostic
when serial or previous electrocardiograms are ob-
Sgarbossa, Birnbaum, and Parrillo 515
tained or when posterior and right precordial leads
are recorded. A few hospitals around the world are
already using the 15- or 16-lead electrocardiogram for
routine admission workups. Cardiologists and emer-
gency physicians in the United States should make an
effort to incorporate these leads in both teaching and
clinical practice and should request electrocardio-
graphic machine vendors that electrocardiographers
be set to provide a panoramic display of the frontal
plane leads including a “–aVR.” Finally, electrocardio-
graphic technology would be more helpful if auto-
mated diagnoses were provided along with their prob-
abilities in each case as well as with the clinical value
of the electrocardiographic signs incorporated in
them.
References
1. Willems JL, Amaud P, van Bemmel JH, et al. Assessment of the per-
formance of electrocardiographic computer programs with the use
of a reference database. Circulation 1985;71:523-34.
2. Sgarbossa EB, Wagner GS. Electrocardiography. In: Topol EJ, edi-
tor. Textbook of cardiovascular medicine. Philadelphia (Pa): Lippin-
cott-Raven Publishers; 1997. p. 1545-89.
3. Marriot HL, editor. Practical electrocardiography. Baltimore (Md):
Williams & Wilkins; 1988.
4. Grant RP. The relationship between the anatomic position of the
heart and the electrocardiogram: a criticism of “unipolar” electro-
cardiography. Circulation 1953;7:890-902.
5. Hoekema R, Uijen GJ, van Erning L, et al. Interindividual variability
of multilead electrocardiographic recordings: influence of heart
position. J Electrocardiol 1999;32:137-148.
6. Pahlm US, Pahlm O, Wagner GS. The standard 11-lead ECG:
neglect of lead aVR in the classical limb lead display. J Electrocar-
diol 1996;29:270-4.
7. Anderson ST, Pahlm O, Selvester RH, et al. Panoramic display of
the orderly sequenced 12-lead ECG. J Electrocardiol 1994;27:
347-52.
8. Roberts WC, Gardin JM. Location of myocardial infarcts: a confu-
sion of terms and definitions. Am J Cardiol 1978;42:868-72.
9. Parker AB, Waller BF, Gering LE. Usefulness of the 12-lead ECG in
detection of myocardial infarction: electrocardiographic-anatomic
correlation, part II. Clin Cardiol 1996;19:141-8.
10. Bough EW, Boden WE, Korr KS, et al. Left ventricular asynergy in
electrocardiographic “posterior” myocardial infarction. J Am Coll
Cardiol 1984;4:209-15.
11. Sharkey SW, Berger CR, Brunette DD, et al. Impact of the electro-
cardiogram on the delivery of thrombolytic therapy for acute myo-
cardial infarction. Am J Cardiol 1994;73:550-3.
12. Menown IB, Mackenzie G, Adgey AA. Optimizing the initial 12-
lead electrocardiographic diagnosis of acute myocardial infarction.
Eur Heart J 2000;21:275-83.
13. Blanke H, Cohen M, Schlueter GU, et al. Electrocardiographic and
coronary correlations during acute myocardial infarction. Am J Car-
diol 1984;54:249-55.
14. Aldrich HR, Hindman NB, Hinoara T, et al. Identification of optimal
electrocardiographic leads for detecting acute epicardial injury in
acute myocardial infarction. Am J Cardiol 1987;59:20-3.
15. Birnbaum Y, Sclarovsky S, Solodky A, et al. Prediction of the level
of left anterior descending coronary artery obstruction during ante-

516 Sgarbossa, Birnbaum, and Parrillo
rior wall acute myocardial infarction by the admission electrocar-
diogram. Am J Cardiol 1993;72:823-6.
16. Tamura A, Kataoka H, Mikuriya Y, et al. Inferior ST-segment depres-
sion as a useful marker for identifying proximal left anterior descend-
ing coronary artery occlusion during acute myocardial infarction. Eur
Heart J 1995;16:1795-9.
17. Yotsukura M, Toyofuku M, Tajino K, et al. Clinical significance of
the disappearance of septal Q waves after the onset of myocardial
infarction: correlation with location of responsible coronary lesions.
J Electrocardiol 1999;32:15-20.
18. Tamura A, Kataoka H, Mikuriya Y. Electrocardiographic findings in
a patient with pure septal infarction. Br Heart J 1991;65:166-7.
19. Engelen DJ, Gorgels AP, Cheriex EC, et al. Value of the electrocar-
diogram in localizing the occlusion site in the left anterior descend-
ing coronary artery in acute myocardial infarction. J Am Coll Car-
diol 1999;34:389-95.
20. Selvester RH, Wagner NB, Wagner GS. Ventricular excitation dur-
ing percutaneous transluminal angioplasty of the left anterior
descending coronary artery. Am J Cardiol 1988;62:1116-21.
21. Ben-Gal T, Sclarovsky S, Herz I, et al. Importance of the conal
branch of the right coronary artery in patients with acute anterior
wall myocardial infarction: electrocardiographic and angiographic
correlation. J Am Coll Cardiol 1997;29:506-11.
22. Geft IL, Shah PK, Rodriguez L, et al. ST elevations in leads V1 to V5
may be caused by right coronary artery occlusion and acute right
ventricular infarction. Am J Cardiol 1984;53:991-6.
23. Kim TY, Alturk N, Shaikh N, et al. An electrocardiographic algo-
rithm for the prediction of the culprit lesion site in acute anterior
myocardial infarction. Clin Cardiol 1999;22:77-83.
24. Sclarovsky S, Birnbaum Y, Solodky A, et al. Isolated midanterior
myocardial infarction: a special electrocardiographic sub-type of
acute myocardial infarction consisting of ST-elevation in non-
consecutive leads and two different morphologic types of ST-
depression. Int J Cardiol 1994;46:37-47.
25. Birnbaum Y, Hasdai D, Sclarovsky S, et al. Acute myocardial infarc-
tion entailing ST segment elevation in lead aVL: electrocardio-
graphic differentiation among occlusion of the left anterior descend-
ing, first diagonal, and first obtuse marginal coronary arteries. Am
Heart J 1996;131:38-42.
26. Braat SH, Brugada P, Den Dulk K, et al. Value of lead V4R for
recognition of the infarct coronary in acute inferior myocardial
infarction. Am J Cardiol 1984;53:1538-41.
27. Herz I, Assali AR, Adler Y, et al. New electrocardiographic criteria
for predicting either the right or left circumflex artery as the culprit
coronary artery in inferior wall acute myocardial infarction. Am J
Cardiol 1997;80:1343-5.
28. Zimetbaum PJ, Krishnan S, Gold A, et al. Usefulness of ST-segment
elevation in lead III exceeding that of lead II for identifying the loca-
tion of the totally occluded coronary artery in inferior wall myocar-
dial infarction. Am J Cardiol 1998;81:918-9.
29. Hasdai D, Birnbaum Y, Herz I, et al. ST segment depression in lat-
eral limb leads in inferior wall acute myocardial infarction: implica-
tions regarding the culprit artery and the site of obstruction. Eur
Heart J 1995;16:1549-53.
30. Assali AR, Sclarovsky S, Herz I, et al. Comparison of patients with
inferior wall acute myocardial infarction with versus without ST-
segment elevation in leads V5 and V6. Am J Cardiol 1998;81:81-3.
31. Porter A, Vaturi M, Adler Y, et al. Are there differences among
patients with inferior acute myocardial infarction with ST depression
in leads V2 and V3 and positive versus negative T waves in these
leads on admission? Cardiology 1998;90:295-8.
American Heart Journal
April 2001
32. Kosuge M, Kimura K, Ishikawa T, et al. New electrocardiographic
criteria for predicting the site of coronary artery occlusion in inferior
wall acute myocardial infarction. Am J Cardiol 1998;82:1318-22.
33. Matetzky S, Freimark D, Chouraqui P, et al. Significance of ST seg-
ment elevations in posterior chest leads (V7 to V9) in patients with
acute inferior myocardial infarction: application for thrombolytic
therapy. J Am Coll Cardiol 1998;31:506-11.
34. Menown IBA, Adgey AAJ. Improving the ECG classification of infe-
rior and lateral myocardial infarction by inversion of lead aVR.
Heart 2000;83:657-60.
35. Huey BL, Beller GA, Kaiser DL, et al. A comprehensive analysis of
myocardial infarction due to left circumflex artery occlusion: compari-
son with infarction due to right coronary artery and left posterior
descending artery occlusion. J Am Coll Cardiol 1988;12:1156-66.
36. Boden WE, Kleiger RE, Gibson RS, et al, and the Diltiazem Reinfarc-
tion Study Group. Electrocardiographic evolution of posterior myo-
cardial infarction: importance of early precordial ST-depression. Am
J Cardiol 1987;59:782-7.
37. Sapin PM, Musselman DR, Dehmer GJ, et al. Implications of inferior
ST-segment elevation accompanying anterior wall acute myocardial
infarction for the angiographic morphology of the left anterior de-
scending coronary artery morphology and site of occlusion. Am J
Cardiol 1992;69:860-5.
38. Mak KH, Chia BL, Tan AT, et al. Simultaneous ST-segment elevation in
lead V1 and depression in lead V2: a discordant ECG pattern indicat-
ing right ventricular infarction. J Electrocardiol 1994;27:203-7.
39. Shalev Y, Fogelman R, Oettinger M, et al. Does the electrocardio-
graphic pattern of “anteroseptal” myocardial infarction correlate
with the anatomic location of myocardial injury? Am J Cardiol
1995;75:763-6.
40. Boden WE, Bough EW, Korr KS, et al. Inferoseptal myocardial
infarction: another cause of precordial ST-segment depression in
transmural inferior wall myocardial infarction? Am J Cardiol 1984;
54:1216-23.
41. Gorgels APM, Vos MA, Mulleneers R, et al. Value of the electrocar-
diogram in diagnosing the number of severely narrowed coronary
arteries in rest angina pectoris. Am J Cardiol 1993;72:999-1003.
42. Braat SH, de Zwaan C, Brugada P, et al. Right ventricular involve-
ment with acute inferior wall myocardial infarction identifies high
risk of developing atrioventricular nodal conduction disturbances.
Am Heart J 1984;107:1183-7.
43. López-Sendon J, Coma-Canella I, Alcasena S, et al. Electrocardio-
graphic findings in acute right ventricular infarction: sensitivity and
specificity of electrocardiographic alterations in right precordial
leads V4R, V3R, Vl, V2, and V3. J Am Coll Cardiol 1985;6:1273-9.
44. Zehender M, Kasper W, Kauder E, et al. Right ventricular infarction
as an independent predictor of prognosis after acute inferior
myocardial infarction. N Engl J Med 1993;328:981-8.
45. Kopelman HA, Forman MB, Wilson H, et al. Right ventricular
myocardial infarction in patients with chronic lung disease: possible
role of right ventricular hypertrophy. J Am Coll Cardiol 1985;5:
1302-7.
46. Camara EJN, Chandra N, Ouyang P, et al. Reciprocal ST change
in acute myocardial infarction: assessment by electrocardiography
and echocardiography. J Am Coll Cardiol 1983;2:251-7.
47. Tabbalat RA, Haft JI. Are reciprocal changes a consequence of
“ischemia at a distance” or merely a benign electric phenomenon?
A PTCA study. Am Heart J 1993;126:95-103.
48. Lee HS, Cross SJ, Rawles JM, et al. Patients with suspected myo-
cardial infarction who present with ST depression. Lancet 1993;
342:1204-7.
American Heart Journal
Volume 141, Number 4
49. Birnbaum Y, Wagner GS, Barbash GI, et al. Correlation of angio-
graphic findings and right (V1 to V3) versus left (V4 to V6) precor-
dial ST-segment depression in inferior wall acute myocardial infarc-
tion. Am J Cardiol 1999;15:83:143-8.
50. O’Keefe JH, Sayed-Taha K, Gibson W, et al. Do patients with left
circumflex coronary artery-related acute myocardial infarction with-
out ST-segment elevation benefit from reperfusion therapy? Am J
Cardiol 1995;75:718-20.
51. Sclarovsky S. Angina at rest and acute myocardial ischemia. In:
Electrocardiography of acute myocardial ischemic syndromes. Lon-
don (England): Marlin Dunitz Ltd; 1999. p. 1-30.
52. Cook RW, Edwards JE, Pruitt RD. Electrocardiographic changes in
acute subendocardial infarction, I: large subendocardial and large
nontransmural infarcts. Circulation 1958;18:603-12.
53. Shah A, Wagner GS, Green CL, et al. Electrocardiographic dif-
ferentiation of the ST-segment depression of acute myocardial
injury due to the left circumflex artery occlusion from that of myo-
cardial ischemia of nonocclusive etiologies. Am J Cardiol 1997;
80:512-3.
54. Dabrowska B, Walczak E, Preis R, et al. Acute infarction of the left
ventricular papillary muscle: electrocardiographic pattern and
recognition of its location. Clin Cardiol 1996;19:404-7.
55. Langer A, Goodman SG, Topol EJ, et al. Late assessment of throm-
bolytic efficacy (LATE) study: prognosis in patients with non-Q wave
myocardial infarction. J Am Coll Cardiol 1996;27:1327-32.
56. Weiss P, Weiss I, Zuber M, et al. How many patients with acute dis-
section of the thoracic aorta would erroneously receive thrombolytic
therapy based on the electrocardiographic findings on admission?
Am J Cardiol 1993;72:1329-30.
57. Rogers WJ, Bowlby LJ, Chandra NC, et al. Treatment of myocardial
infarction in the United States (1990 to 1993): observations from
the National Registry of Myocardial Infarction. Circulation 1994;
90:2103-14.
58. Eriksson P, Gunnarsson G, Dellborg M. Diagnosis of acute myocar-
dial infarction in patients with chronic right bundle-branch block
using standard 12-lead electrocardiogram compared with dynamic
vectorcardiography. Cardiology 1998;90:58-62.
59. Cannon A, Freedman B, Bailey BP, et al. ST-segment changes dur-
ing transmural myocardial ischemia in chronic left bundle branch
block. Am J Cardiol 1989;64:1216-7.
60. Barron HV, Bowlby LJ, Breen T, et al. Use of reperfusion therapy for
acute myocardial infarction in the United States: data from the
National Registry of Myocardial Infarction 2. Circulation 1998;97:
1150-6.
61. Berger AK, Radford MJ, Krumholz HM. Factors associated with
delay in reperfusion therapy in elderly patients with acute myocar-
dial infarction: analysis of the cooperative cardiovascular project.
Am Heart J 2000;139:985-92.
62. Shlipak MG, Lyons WL, Go AS, et al. Should the electrocardiogram
be used to guide therapy for patients with left bundle-branch block
and suspected myocardial infarction? JAMA 1999;281:714-9.
63. Thiemann DR, Coresh J, Schulman SP, et al. Lack of benefit for intra-
Sgarbossa, Birnbaum, and Parrillo 517
venous thrombolysis in patients with myocardial infarction who are
older than 75 years. Circulation 2000;101:2239-46.
64. Berger AK, Radford MJ, Wang Y, et al. Thrombolytic therapy in
older patients. J Am Coll Cardiol 2000;36:366-74.
65. Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic
diagnosis of evolving acute myocardial infarction in the presence of
left bundle branch block. N Engl J Med 1996;334:481-7.
66. Sgarbossa EB. Value of the ECG in suspected acute myocardial
infarction with left bundle branch block. J Electrocardiol 2000;
33(Suppl):87-92.
67. Sokolove PE, Sgarbossa EB, Amsterdam EA, et al. Interobserver
agreement in the ECG diagnosis of acute myocardial infarction in
the presence of left bundle branch block. Ann Emerg Med 2000;
36:566-71.
68. Edhouse JA, Sakr M, Angus J, et al. Suspected myocardial infarc-
tion and left bundle branch block: electrocardiographic indicators
of acute ischaemia. J Accid Emerg Med 1999;16:331-5.
69. Kontos MC, McQueen RH, Jesse RL, et al. Can the ECG diagnose
acute myocardial infarction in emergency department patients with
chest pain and left bundle branch block [abstract]? J Am Coll Car-
diol 1999;33:347A.
70. Sgarbossa EB, Pinski SL, Gates KB, et al, for the GUSTO-I Investiga-
tors. Electrocardiographic diagnosis of acute myocardial infarction
in the presence of ventricular paced rhythm. Am J Cardiol 1996;
77:423-4.
71. Pinski SL, Sgarbossa EB, Wagner GS, for the GUSTO Investigators.
Electrocardiographic manifestations of acute myocardial infarction
in patients with Wolff-Parkinson-White syndrome. PACE Pacing Clin
Electrophysiol 1995;18:1739.
72. Spodick DH. Differential characteristics of the electrocardiogram in
early repolarization and acute pericarditis. N Engl J Med 1976;
295:523-6.
73. Kambara H, Phillips J. Long-term evaluation of early repolarization
syndrome (normal variant RS-T segment elevation). Am J Cardiol
1976;38:157-61.
74. Spodick DH. Differential characteristics of the electrocardiogram in
early repolarization and acute pericarditis. N Engl J Med 1976;
295:523-6.
75. Oliva PB, Hammill SC, Edwards WD. Electrocardiographic diagno-
sis of postinfarction regional pericarditis: ancillary observations
regarding the effect of reperfusion on the rapidity and amplitude of
T-wave inversion after acute myocardial infarction. Circulation
1993;88:896-904.
76. Gibler WB, Sayre MR, Levy RC, et al. Serial 12-lead electrocardio-
graphic monitoring in patients presenting to the emergency depart-
ment with chest pain. J Electrocardiol 1993;26(suppl):238-43.
77. Zalenski RI, Rydman RI, Sloan EP, et al. Value of posterior and right
ventricular leads in comparison to the standard 12-lead electrocar-
diogram in evaluation of ST-segment elevation in suspected acute
myocardial infarction. Am J Cardiol 1997;79:1579-85.
78. Selvester RHS. A call to concerted action for change. J Electrocar-
diol 1998;31:367-70.