Available online at www.sciencedirect.

com

ScienceDirect
Journal of Electrocardiology 47 (2014) 448 458
www.jecgonline.com
Review
Difficult ECGs in STEMI:
Lessons learned from serial sampling of pre- and in-hospital ECGs
Antoine Ayer, MD, Christian Juhl Terkelsen, MD, DmSc, PhD
Department of cardiology, Aarhus University Hospital, Skejby, DK-8200 Aarhus N, Denmark

Abstract Prehospital interpretation of electrocardiograms (ECGs) is crucial to ensure early diagnosis and
optimal treatment of patients with ST elevation myocardial infarction (STEMI). Recognition of ST-
segment elevations (STE) by qualified personnel in the prehospital phase has successfully reduced
the delay from the first medical contact to reperfusion. A few other ECG patterns without true STE,
referred to as STEMI equivalents, bear the same prognostic significance, reflect imminent or
ongoing transmural ischemia, but are less easily identified. Hyperacute T waves, de Winter ST-T
complex, Wellens' syndrome, and posterior STEMI, as well as myocardial infarction in the presence
of left bundle branch block, paced rhythm or left ventricular hypertrophy, among others are
diagnostic challenges. This article reviews some critical examples of ischemic ECG patterns that may
be ephemeral, misinterpreted by medical staff or not identified by automated ECG algorithms, and it
emphasizes the importance of serial ECG acquisition.
2014 Elsevier Inc. All rights reserved.
Keywords: Electrocardiogram; STEMI; Prehospital ECG; In-hospital ECG; STEMI equivalent; serial ECGs

Introduction T waves
In patients with ST elevation myocardial infarction Hyperacute T waves
(STEMI), electrocardiogram (ECG) pattern recognition in
Hyperacute T waves (HATW) are characterized by tall,
the prehospital phase shortens the delay between the first
often asymmetrical, broad-based T waves (TW) in the
medical contact and reperfusion [1] which improves clinical
anterior leads. HATW are also often associated with
outcome [2]. Several other ECG patterns without ST
reciprocal ST segment depressions (STD) and J-point
elevations (STE) are more difficult to identify, but they
elevation [35] (Fig. 1). They are a transient pattern found
also reflect coronary sub-occlusion or occlusion with
in the early stage of coronary occlusion which usually
imminent or ongoing transmural ischemia. Recognition of
evolves to overt STE. HATW are most often described as
those patterns is a challenge. The ideal of prehospital ECG
normal by the automated ECG interpretation (AEI), and they
acquisition is therefore to identify all the patients who need
are also easily overseen or misdiagnosed by healthcare
emergent reperfusion with a high level of sensitivity and
professionals. Serial ECGs ensure a proper diagnosis in this
specificity. We expose examples of ECG patterns that may
situation because overt STE often develop rapidly although
be ephemeral, misinterpreted or not identified by automated
prominent T waves can occasionally persist [6]. Differential
ECG algorithms. This article also underlines the importance
diagnoses are mainly hyperkalemia (narrow, peaked,
of serial ECG acquisition, especially in cases where
symmetrical TW, frequently preceded by a wide QRS),
symptoms are consistent with acute myocardial infarction
benign early repolarization (diffuse STE, notched distal
(AMI), but the initial ECG is non-diagnostic.
QRS, symmetric TW), and left ventricular hypertrophy
(LVH) (strain pattern, voltage criteria, QS complexes with
STE and prominent T waves in the right precordial leads
(V1V2) [7]), and de Winter ST-T complex (DWSTTC).

De Winter ST-T complex

Corresponding author at: Department of cardiology, Aarhus Univer-
sity Hospital, Skejby, DK-8200 Aarhus N, Denmark. De Winter ST-T complex should be differentiated from the
E-mail address: antoine.ayer@bluewin.ch classic HATW. In 2008, de Winter et al. described an ECG
http://dx.doi.org/10.1016/j.jelectrocard.2014.03.010
0022-0736/ 2014 Elsevier Inc. All rights reserved.
 A. Ayer, C.J. Terkelsen / Journal of Electrocardiology 47 (2014) 448458
Fig. 1. Hyperacute T waves (same ECG as ECG 4 in Fig. 2).
pattern without STE in anterior ECG leads that occurs in 2% of
left anterior descending artery (LAD) occlusions, consisting of
a 1- to 3-mm upsloping depression of ST at the J point in leads
V1V6 that continues into tall, positive symmetrical T waves,
often combined with a 12 mm elevation the ST-segment in
aVR [8,9]. The authors describe DWSTTC as a static
phenomenon with a J point depression which persists until
coronary patency is established that does not progress into STE
in the anterior ECG leads; the DWSTTC is a STEMI
equivalent. However, based on continuous ECG monitoring
before, during, and after primary percutaneous coronary
intervention (primary PCI), the DWSTTC has also been
observed as a temporary phenomenon that occurs at the
time of reperfusion and precedes the development of typical
STE (Fig. 2). The fact that the DWSTTC can evolve into a true
STEMI within hours of presentation has also recently been
described by Goebel et al [10].
Fig. 2 shows multiple ECG tracings from a patient with
LAD occlusion. In addition to continuous ST-monitoring, a
total of 18 ECGs were acquired before, during, and two
hours after primary PCI. A selection of these ECGs is
presented. ECG-6 demonstrates the DWSTTC occurring at
the time of PCI, but this is a temporary phenomenon
in which classic STE is evident both before reperfusion
449
(ECG-2) and after reperfusion (ST-peak phenomenon: ECG-
7 and 8). The panel below the ECG tracings shows ST
monitoring data. ECG-1 and 3 show HATW, which appear
both before and after the STE. The diagnosis of suspected
LAD occlusion was not made after the first ECG. This set of
ECGs also underlines the importance of serial ECGs.
More T waves
In addition, we present two ECGs which show a pattern
that resembles but is different from both the DWSTTC and
the classic HATW morphology. Fig. 3 is an ECG taken after
a successful 3-minute resuscitation in a patient with
ventricular fibrillation. It shows tall TW in the inferior
leads. This patient had an occluded right coronary artery
(RCA), presumably caused by embolism from the left atrial
appendage due to atrial fibrillation. There is also a down-
sloping STD in V2 suggestive of posterior-wall involvement
as well as an upsloping STD in V3V6, which can represent
reciprocal changes or subendocardial ischemia.
The ST-T wave pattern represented in this Figure was not
static, but transient. It had a slight J-point depression and a
much more convex ST segment than in the examples
provided by de Winter. On the other hand, the ST segment in
HATW is usually flattened or slightly concave or, when
convex, then associated with STE. Fig. 4 shows serial ECGs
where an overt STEMI evolves into a similar T wave
morphology without STE, which confirms the brevity of this
phenomenon. The STE recurred shortly after.
These two examples emphasize the utility of serial ECGs,
the continuous monitoring of ST segment deviation and the
recognition of transient patterns that evolve into overt STEMI
or represent a STEMI equivalent. This specific ST-T pattern
with a transition of a convex upsloping ST segment with a
slightly depressed J point into broad, quite symmetric
T waves has not previously been described unequivocally
to our knowledge. It very likely represents a subtype of
HATW, but it differs significantly from the classic descrip-
tion of this pattern [7]. It is not described in the evolution of
the ECG modifications in AMI [11] although the author does
mention that the morphological characteristics of hyperacute
T waves vary greatly. Dressler et al. reported that the ST
segment rarely can be depressed and that the T wave can be
doming, but none of the provided examples resemble the
pattern illustrated in Figs. 3 and 4. Nor do they look like the
upwardly concave ST segment described by Smith et al.,
which is also slightly elevated [12]. Note that HATW
descriptions differ slightly among authors and also, surpris-
ingly, among articles from the same authors. Alternatively, this
pattern could be described as a STEMI because the very steep
ST segment precludes the detection of a small S wave. We
think that these illustrations are of interest because they may
improve one's pattern recognition in case of suspected AMI.
Wellens' syndrome
Wellens' syndrome (Fig. 5) consists of inverted or
biphasic T waves in V2 and V3. This pattern is highly
specific for LAD disease [13] and it is a quite specific sign of
imminent AMI. Half of the patients in Wellens' study
450 A. Ayer, C.J. Terkelsen / Journal of Electrocardiology 47 (2014) 448458

Fig. 2. Serial ECGs of a patient with left anterior descending artery occlusion who had 18 ECGs acquired before, during, and after primary PCI. Presented are
selected ECGs documenting hyperacute T waves (ECG 1 and 3), ST elevation (ECG 2, 7, 8, 9), and De Winter ST-T complex (ECG 6).

developed the pattern within 24 hours after admission. This
further highlights the importance of obtaining serial ECGs in
patients with chest pain [14].
Left bundle branch block
Two percent of patients with suspected AMI have left
bundle branch block (LBBB) [15]. LBBB impairs the correct
interpretation of the ECG when AMI is suspected in a patient
known to have this conduction disorder because the ST
segment is displaced in the opposite direction to the main
vector of the QRS complex in all the ECG leads. The
presence of an LBBB on the initial ECG is a diagnostic
challenge because only a limited number of patients with
LBBB and chest pain actually have transmural infarction
[16]. Because of this diagnostic uncertainty, patients with
AMI and LBBB are less likely to receive optimal therapy,
and their mortality is therefore increased [17].
Several tools can improve immediate risk stratification.
The Sgarbossa criteria [18] have proven effective in
identifying patients with LBBB who bear the same mortality
risk as STEMI patients [15,19]
1. Concordant elevation of ST 0.1 mV in leads with a
positive QRS complex (5 points)
(sensitivity 73%, specificity 92%)
2. Concordant depression of ST 0.1 mV in V1V3 (3 points)
(sensitivity 25%, specificity 96%)
 A. Ayer, C.J. Terkelsen / Journal of Electrocardiology 47 (2014) 448458 451

Smith's modification of the third criterion from absolute to

relative discordance, as defined by a ratio of ST to S wave of
25%, was reported to be 91% sensitive and 90% specific
[21]. This revised rule is unweighted, and it requires that just
one of three criteria be met. Other algorithms have been
developed in an effort to improve the third criterion. These
algorithms include the Selvester 10% RS criteria (ST
elevation 10% of [S minus R wave] plus STEMI limits)

Fig. 3. This patient is a former smoker known to have hypertension and atrial
fibrillation. He had a cardiac arrest with ventricular fibrillation. Cardiopul-
monary resuscitation was performed during 3 minutes. This ECG was taken
shortly after a direct current cardioversion. The tall T waves are indicated by
the arrows.

3. Discordant elevation of ST 0.5 mV (2 points, less useful)

(sensitivity 31%, specificity 92%)

A meta-analysis of 2100 patients documented that a score

of 3 has a specificity of 98%, but a sensitivity of only 20% Fig. 4. Serial ECGs showing a transition from ST elevations in V3V5
for the diagnosis of AMI [20]. The first two criteria could be (ECG 1 and 2) to tall T waves in V3V6 (ECG 3) and then recurrence of ST
summarized as a QRS-concordant ST deviation of 0.1 mV. elevations (ECG 4) as well as poor R wave progression.
452 A. Ayer, C.J. Terkelsen / Journal of Electrocardiology 47 (2014) 448458

LBBB [25], but this needs further investigation. Moreover,

the clinical findings are important. Recent studies have found
that the presence of LBBB itself, whether new or old, does
NOT predict AMI [16,26].

Paced rhythm
Ventricular pacing induces secondary repolarization ab-
normalities due to modifications in the sequence of ventricular
depolarization and repolarization [27] and ventricular pacing
therefore significantly alters the ECG waveforms.
Sgarbossa et al. suggested that the criteria cited above
could be used in patients with ventricular pacing and
symptoms suggestive of coronary occlusion [28]. The first
two criteria have a low sensitivity (18% and 29%,
respectively) and a high specificity (94% and 82%,
respectively). The third criterion had a relatively high
specificity (88%) and a moderate sensitivity (53%) for

Fig. 5. Wellens type B.

and a QRS area-based ST threshold with sensitivities and

specificities comparable to the Smith 25% S-wave criteria
(30% and 93% for the Selvester 10% RS criteria, 24% and
96% for the QRS area criteria, versus 20% and 95% for the
Smith 25% S-wave criteria, respectively) [22]. However,
those rules may be more difficult to remember and apply in
daily clinical practice. Fig. 6 is provided as an example of
LBBB with STE fulfilling the Sgarbossa criteria.
Point-of-care measurement of serum troponin levels is a
promising, yet still not widely used technology that has the
potential to refine the risk stratification in the case of LBBB.
Bedside echocardiography is a rapid and inexpensive
method that has proven useful in the identification of acute
coronary occlusions in patients with non-STEMI (NSTEMI).
It is a good method for identifying very early alterations in Fig. 6. Patient who has a thrombotic occlusion of the second segment of the
left anterior descending coronary artery. ECG showing a left bundle branch
regional myocardial contractility suggestive of coronary block which meets Sgarbossa criteria 1 and 3 as well as Smith-modified
occlusion [23,24]. It may be applicable to patients who have criterion 3 (concordant ST elevation, excessive discordant ST elevation, ST/S
LBBB in spite of the classic abnormal septal motion in ratio less than 0.25).
 A. Ayer, C.J. Terkelsen / Journal of Electrocardiology 47 (2014) 448458
Fig. 7. ECG showing concordant ST elevations in the inferior leads under
ventricular pacing. This is strongly suggestive of an inferior ST elevation
myocardial infarction. This patient had previously undergone CABG. The
coronary angiography showed an occluded vein graft to the circumflex artery.
detecting biochemically confirmed AMI. See Fig. 7 for an
example of positive concordance in the inferior leads.
Interestingly, Kilic et al. [29] discovered that QRS
duration under temporary pacing was significantly pro-
longed during intracoronary balloon inflation. This needs
further investigation in chronically paced patients.
Serial ECGs can help confirm the diagnosis of STEMI
because dynamic STE amplitude variations are strongly
suggestive of ongoing ischemia in ventricular paced rhythms
[30]. Moreover, serial ECGs raise the chance of catching a
period when the ventricles are not paced. This will help
unmask the patient's own complexes and allow a more
accurate diagnosis. Temporary inactivation of ventricular
pacing can help diagnose a true STEMI in patients who do not
have a 3rd degree AV block with broad QRS and no escape
rhythm. One must, of course, be aware of the potential cardiac
memory-related T wave inversions and STD. This phenom-
enon can occur already shortly after pacing starts [31], and it
can persist for months in patients who are chronically paced
[32]. Memory T waves can also occur in the presence of
intermittent LBBB, post-tachycardia, and following periods
453
of pre-excitation [33]; and they can be misleading in the
diagnosis of ischemia. Memory T waves can be identified and
differentiated from precordial ischemic T wave inversion
with 92% sensitivity and 100% specificity if the T waves are
both (1) positive in aVL, (2) positive or isoelectric in I, and (3)
deeper in the precordial leads than in III [34].
Storage of a paced 12-lead ECG in cardiac devices
memory immediately after implantation could also help
detect more subtle ST deviations [35]. Furthermore,
intracardiac ECG monitoring has been proposed as an
effective method for detecting acute coronary occlusion in
patients with pacemakers; a method that ensures a very short
delay to treatment [36].
Biventricular pacing is another challenge. Two recent
case reports underline the usefulness of serial ECGs in
diagnosing STEMI in that particular setting and emphasize
the need for further investigation. [37,38].
Like in LBBB, in the absence of specific criteria for
ongoing transmural ischemia, patients with symptoms
suggestive of AMI and paced ventricles need further risk
stratification in an invasive center that may perform cardiac
biochemical marker analysis, bedside echocardiography or
possibly immediate coronary catheterization. We would like
to point out that in the modern era, diagnostic coronary
angiography does not bear the same risk as blind
thrombolysis administration.
Posterior STEMI
The next example (Fig. 8) shows that the opportunity to
diagnose STEMI can be fugitive. A 68-year-old woman called
the ambulance because of classic central chest pain radiating to
the left arm. ECG-1 shows a posterior STEMI with
pronounced STD in V1V3 (+ V4 V5). The STD are
markedly reduced on ECG-2. Discrete STE are present in the
inferior leads on ECG-3. Dynamic T wave fluctuations in the
inferior leads are suggestive of inferior wall involvement
before the apparition of the STE. The coronary angiography
demonstrated a thrombotic, occluded left circumflex artery and
a chronically occluded RCA. A posterior ECG taken initially
with recording of the leads V7V9 would have shown STE
suggestive of posterior STEMI. However, this is not done
routinely by most paramedics.
Posterior AMI should be suspected when there is mirror
STD in leads V1V3 (V4) 0.05 mV [39,40] (consider
0.1 mV in men b 40 years old [41]), especially if there is a
concurrent, tall R wave in V1 or V2 with an R/S ratio N 1 in
V2 [42]. The suspicion is even stronger if the STD are
horizontal or downsloping [41] and concave [43]. T waves in
these leads are usually positive in posterior wall infarction
and negative in diffuse anterior subendocardial ischemia, but
they can also be negative in the very early stages of posterior
STEMI, whereby they mirror the posterior hyperacute
T waves [44]. The appearance of tall R waves is the
posterior equivalent of Q waves.
Posterior STEMIs are actually situated laterally, as
demonstrated by imaging studies. They are caused by
occlusion of a nondominant left circumflex coronary artery,
454 A. Ayer, C.J. Terkelsen / Journal of Electrocardiology 47 (2014) 448458

its marginal branch or distal to the right ventricular branches

of an RCA with predominant posterolateral distal branches
[45]. Posterior STEMIs represent 1520% of all AMIs, the
vast majority occurring with acute infarction of the inferior
or lateral wall of the left ventricle [42]. The incidence of
isolated posterior STEMI lies in the range of 5-10% [14].
Subjects with posterior STEMI have a longer door-to-
balloon time than subjects with classic STEMI and only 30%
are revascularized within 90 minutes [46]. In a study of 215
patients with a discharge diagnosis of NSTEMI, 12% had a
posterior STEMI. Among those, 50% were treated with PCI
and 50% with CABG [47]. Further research is warranted to
define the consequences of overlooked posterior STEMIs on
morbidity and mortality.
Although not described as a STEMI equivalent, STD in
V4V6 have even higher mortality than posterior infarcts
[48]. A study in which 155 patients admitted with chest pain
underwent contrast-enhanced cardiac magnetic resonance
imaging demonstrated that consideration of STE and STD
significantly increased the electrocardiographic sensitivity
for the detection of AMI from 50% to 84% with only a slight
decrease in specificity from 97% to 93% [49]. The clinical
outcome of patients with STD (independently of their
location on the ECG) treated in the same way as patients
with STEMI is currently under investigation [50].

Left ventricular hypertrophy

ECG with left ventricular hypertrophy (LVH) is the most
significant predictor of false-positive STEMI activations [51].
ECG with LVH may represent up to 18% of all STEMI alarms.
A small retrospective study by Armstrong et al. analyzed the
correlation between specific features of ECG with LVH and the
presence of a culprit lesion on coronary angiography in patients
presenting with chest pain where STEMI alarm was activated
[52]. Among ECG with hypertrophy (Cornell or Sokolow-
Lyon criteria or R-wave amplitude N 11 mm in lead aVL):

- STE of more than 25% of QRS peak to nadir

amplitude AND
- STE in three contiguous leads or T-wave inversions in
the anterior leads

had the same sensitivity as classic STEMI criteria, but had a

much higher specificity (91% versus 58%). This algorithm
reduced the occurrence of false positive diagnoses by 35%,
which spared unnecessary catheterization laboratory (cath
lab) activation. Reciprocal STD was also a strong predictor
of an angiographic culprit lesion in this study. Future
research should test these criteria in diverse patient
populations and in a prospective manner.

Fig. 8. Infero-posterior myocardial infarction (see the text for details).
Difficult ECGs missed by the automatic ECG algorithms
It has been claimed that a prehospital, purely automated
STEMI diagnosis with non-physician cath lab activation is safe
and effective [53]. However, this interesting study did not
assess the incidence of false negative AEIs, which have more
 A. Ayer, C.J. Terkelsen / Journal of Electrocardiology 47 (2014) 448458 455

dramatic consequences than false positive AEIs. Nor did it

compare AEI alone with AEI plus physician interpretation.
Whilst AEI is probably an acceptable method where
transmission for or direct interpretation of the ECG by trained
personnel is not feasible, our experience suggests that some
overt STEMI can be missed by AEI. Fig. 9 shows an example
where the AEI did not detect the presence of ST elevation in the
anterior leads, probably because the J point has a very obtuse
angle. Interestingly, this patient had a thrombotic occlusion of
the first segment of the RCA. Some useful criteria to help
differentiate RCA occlusions from LAD occlusions in case of
STE in the anterior leads have been proposed based on a small
case series: RCA occlusion is suggested in the presence of
doming STE, STE N 1 mm in V1, absence of STE in V6,
maximal STE in V1V3 with a tendency to subside and
disappear toward leads V5-V6, STE in V4R, frontal ST axis N
90, and unaffected initial part of the QRS [54].
In the second example (Fig. 10), the AEI concluded to a
simple right bundle branch block (RBBB) despite evident STE
in aVL and V2V4. The diagnosis was initially also missed by
the physician on call, but an immediate secondary evaluation
by a supervisor ensured triaging to primary PCI with a small
delay, and a subocclusion of LAD was treated. Like LBBB,
RBBB accompanying AMI carries a high mortality risk [17].
Authors historically advocate that RBBB does not
hamper interpretation of the ST segment, but minor STE in
leads V1V4 can be missed because of the ST-T abnormalities
associated with RBBB [55]. Some authors recommend that
patients suspected of having AMI and who have RBBB should
be treated in the same way as patients with LBBB. [56].
Although cath lab activation is adequate when STEMI is
detected, a large number of STEMIs are missed by the current
algorithms and error rates exceed 40% [57]. Clark et al.
demonstrated that two different AEI systems had a 7% lower
sensitivity for the diagnosis of STEMI than human interpre-
tation [58]. Furthermore, actual diagnostic algorithms are Fig. 9. ST elevation myocardial infarction missed from the automated
unable to detect STEMI equivalents (HATW, DWSTTC, ECG interpretation.
posterior STEMI, left main artery occlusion, Sgarbossa
criteria, Wellens' syndrome). Albeit a very promising
technology and a useful diagnostic help, AEI should only be identifying classic STEMI as physician reviewers blinded to
used in conjunction with the advice of a trained professional. the clinical data [60]. However, they were not challenged on
Although AEI speeds up STEMI diagnosis, the system delay STEMI equivalents, and this clinical investigation excluded
caused by human interpretation is shorter than 5 minutes in our patients with bundle branch block, which is a typical
center where ECGs are sent via GSM for interpretation. But confounder for non-experts. Another recent study included
given the rapid increase in mortality with time to intervention, 472 paramedics trained to interpret ECGs. In a standardized
we recognize that further optimization is desirable. 10-ECG test where the paramedics were blinded to the AEI,
Prehospital activation of cath lab by joint AEI and they recognized only 78% of the anterior and 51% of the lateral
primary paramedics with basic ECG training (4 hours) has STEMIs [61]. An older study reported that cardiologists
also been documented to be safe and effective in a study with detected anterior and inferior STEMI with 84.9% and 71.7%
134 stable patients because only one adverse event that sensitivity, respectively [62]. In a very small British study,
necessitated advanced care occurred during transport and paramedics demonstrated astonishing abilities to interpret
because in hospital outcomes were acceptable [59], but that ECGs without AEI 12 month after a 2-day training course
study did not assess the number of false negative events. [63], but these results may not be applicable to the general
Furthermore, among the patients brought to the cath lab paramedical population. In a review article, Salerno et al.
for primary PCI, two died of a non-cardiac cause, which reported that both computer software and physicians of every
questions the consequences of the higher rate of false medical specialty and any level of training make frequent
positives compared with ECG interpretation by experts. errors compared with expert electrocardiographers [64].
A promising study demonstrated that highly trained The disadvantage of the AEIs' lower sensitivity has to be
paramedics (6 hours) helped by AEI had a similar accuracy in weighed against the benefit of very rapid cath lab activation
456 A. Ayer, C.J. Terkelsen / Journal of Electrocardiology 47 (2014) 448458
Fig. 10. Right bundle branch block with ST elevation myocardial infarction
missed from the automated ECG interpretation.
by additional investigation. Further optimization of AEI is
expected. Insufficient data exist about paramedics' sensitivity
in the presence of confounding ECGs (pericarditis, LBBB,
early repolarization, left ventricular hypertrophy or aneu-
rysm) and STEMI equivalents. Local population densities,
available human and technological resources, and time to the
nearest cath lab may further influence the choice of strategy.
Discussion
Prehospital ECG recording and their interpretation have
paved the way for a new era in the management of patients
with AMI, an approach that ensures shorter delays to
treatment and improves clinical outcome. This triage system
is, unfortunately, still suboptimal because health care
professionals often fail to recognize AMI on ECGs.
Although considerable effort has been made to improve
automated ECG algorithms, their sensitivity remains insuf-
ficient. The past years have seen the emergence of the
concept of STEMI equivalent. This notion encompasses a
group of ECG patterns that reflect the acute occlusion of a
coronary artery, but without the classic STE. They are often
associated with delayed treatment and poorer outcome.
These patterns include, but are not limited to HATW,
DWSTTC, Wellens' syndrome, and posterior STEMI, as
well as AMI in the presence of LBBB, paced rhythm
or LVH.
As a result of the constant improvement in the delay to
medical contact, the first ECG recorded is not infrequently
normal or inconclusive in patients with acute coronary
occlusions. Furthermore, some STEMI-equivalent ECG
patterns can be evanescent. Serial ECGs taken both routinely
and triggered by continuous ST-segment monitoring are
therefore a decisive asset in the management of patients with
suspected AMI. A growing number of centers have
abandoned thrombolysis in favor of primary PCI. In case
of symptoms suggestive of coronary occlusion but ambig-
uous ECGs, further risk stratification is needed, using cardiac
biochemical marker dosage, bedside echocardiography or
possibly immediate coronary angiography, which has a very
small periprocedural risk. Other functional and anatomical
imaging techniques can be considered, but they may result in
unacceptable delays and do not permit immediate treatment.
We presented a few ECGs which are considered difficult
for the non-specialist. We hope that this article will encourage
the insiders to improve pre- and intra-hospital triage by
broadly teaching such ECGs to their residents. There is little
doubt that adequate training can also equip the paramedical
personnel with the necessary knowledge to quickly and
accurately interpret STEMI and STEMI equivalent ECGs. In
the authors' e-learning website www.ecg-quiz.com, a playful,
case-based method of improving one's ECG interpretation is
proposed. It is freely accessible to everyone.
References
[1] Curtis JP, Portnay EL, Wang Y, McNamara RL, Herrin J, Bradley EH,
et al. The Pre-Hospital Electrocardiogram and Time to Reperfusion in
Patients With Acute Myocardial Infarction, 20002002: Findings
From the National Registry of Myocardial Infarction-4. J Am Coll
Cardiol 2006;47:154452.
[2] De Luca G, Suryapranata H, Ottervanger JP, Antman EM. Time Delay to
Treatment and Mortality in Primary Angioplasty for Acute Myocardial
Infarction: Every Minute of Delay Counts. Circulation 2004;109:1223.
[3] Collins MS, Carter JE, Dougherty JM, Majercik SM, Hodsden JE,
Logue EE. Hyperacute T-wave criteria using computer ECG analysis.
Ann Emerg Med 1990;19:11420.
[4] Dressler W, Hugo R. High T waves in the earliest stage of myocardial
infarction. Am Heart J 1947;34:62745.
[5] Goldberger AL. Hyperacute T, waves revisited. Am Heart J
1982;104:88890.
[6] Birnbaum Y, Bays de Luna A, Fiol M, Nikus K, Macfarlane P,
Gorgels A, et al. Common pitfalls in the interpretation of electrocar-
diograms from patients with acute coronary syndromes with narrow
QRS: a consensus report. J Electrocardiol 2012;45:46375.
[7] Somers MP, Brady WJ, Perron AD, Mattu A. The prominent T wave:
Electrocardiographic differential diagnosis. Am J Emerg Med
2002;20:24351.
[8] de Winter RJ, Verouden NJ, Wellens HJ, Wilde AA. A new ECG sign
of proximal LAD occlusion. N Engl J Med 2008;359:20713.
[9] Verouden NJ, Koch KT, Peters RJ, Henriques JP, Baan J, van der
Schaaf RJ, et al. Persistent precordial hyperacute T-waves signify
 A. Ayer, C.J. Terkelsen / Journal of Electrocardiology 47 (2014) 448458
proximal left anterior descending artery occlusion. Heart 2009;95:
17016.
[10] Goebel M, Bledsoe J, Orford JL, Mattu A, Brady WJ. A new ST-
segment elevation myocardial infarction equivalent pattern? Prominent
T wave and J-point depression in the precordial leads associated with
ST-segment elevation in lead aVr. Am J Emerg Med 2013;32:287.
e2858.
[11] Nable JV, Brady W. The evolution of electrocardiographic changes in
ST-segment elevation myocardial infarction. Am J Emerg Med
2009;27:73446.
[12] Smith SW. Upwardly concave ST segment morphology is common in acute
left anterior descending coronary occlusion. J Emerg Med 2006;31:6977.
[13] de Zwaan C, Bar FW, Wellens HJ. Characteristic electrocardiographic
pattern indicating a critical stenosis high in left anterior descending
coronary artery in patients admitted because of impending myocardial
infarction. Am Heart J 1982;103:7306.
[14] Lawner BJ, Nable JV, Mattu A. Novel patterns of ischemia and STEMI
equivalents. Cardiol Clin 2012;30:5919.
[15] Neeland IJ, Kontos MC, de Lemos JA. Evolving considerations in the
management of patients with left bundle branch block and suspected
myocardial infarction. J Am Coll Cardiol 2012;60:96105.
[16] Chang AM, Shofer FS, Tabas JA, Magid DJ, McCusker CM,
Hollander JE. Lack of association between left bundle-branch block
and acute myocardial infarction in symptomatic ED patients. Am J
Emerg Med 2009;27:91621.
[17] Go AS, Barron HV, Rundle AC, Ornato JP, Avins AL. Bundle-branch
block and in-hospital mortality in acute myocardial infarction. National
Registry of Myocardial Infarction 2 Investigators. Ann Intern Med
1998;129:6907.
[18] Sgarbossa EB, Pinski SL, Barbagelata A, Underwood DA, Gates KB,
Topol EJ, et al. Electrocardiographic diagnosis of evolving acute
myocardial infarction in the presence of left bundle-branch block.
GUSTO-1 (Global Utilization of Streptokinase and Tissue Plasmino-
gen Activator for Occluded Coronary Arteries) Investigators. N Engl J
Med 1996;334:4817.
[19] Wong CK, French JK, Aylward PE, Stewart RA, Gao W, Armstrong
PW, et al. Patients with prolonged ischemic chest pain and presumed-
new left bundle branch block have heterogeneous outcomes depending
on the presence of ST-segment changes. J Am Coll Cardiol
2005;46:2938.
[20] Tabas JA, Rodriguez RM, Seligman HK, Goldschlager NF. Electro-
cardiographic criteria for detecting acute myocardial infarction in
patients with left bundle branch block: a meta-analysis. Ann Emerg
Med 2008;52:329336.e321.
[21] Smith SW, Dodd KW, Henry TD, Dvorak DM, Pearce LA. Diagnosis
of ST-elevation myocardial infarction in the presence of left bundle
branch block with the ST-elevation to S-wave ratio in a modified
Sgarbossa rule. Ann Emerg Med 2012;60:76676.
[22] Gregg RE, Helfenbein ED, Babaeizadeh S. New ST-segment elevation
myocardial infarction criteria for left bundle branch block based on
QRS area. J Electrocardiol 2013;46:52834.
[23] Grenne B, Eek C, Sjoli B, Dahlslett T, Uchto M, Hol PK, et al. Acute
coronary occlusion in non-ST-elevation acute coronary syndrome: outcome
and early identification by strain echocardiography. Heart 2010;96:15506.
[24] Kukulski T, Jamal F, Herbots L, D'Hooge J, Bijnens B, Hatle L, et al.
Identification of acutely ischemic myocardium using ultrasonic strain
measurements. A clinical study in patients undergoing coronary
angioplasty. J Am Coll Cardiol 2003;41:8109.
[25] Shan Y, Villarraga HR, Pislaru C, Shah AA, Cha SS, Pellikka PA.
Quantitative assessment of strain and strain rate by velocity vector
imaging during dobutamine stress echocardiography to predict
outcome in patients with left bundle branch block. J Am Soc
Echocardiogr 2009;22:12129.
[26] Mehta N, Huang HD, Bandeali S, Wilson JM, Birnbaum Y. Prevalence
of acute myocardial infarction in patients with presumably new left
bundle-branch block. J Electrocardiol 2012;45:3617.
[27] Rautaharju PM, Surawicz B, Gettes LS, Bailey JJ, Childers R, Deal BJ,
et al. AHA/ACCF/HRS recommendations for the standardization and
interpretation of the electrocardiogram: part IV: the ST segment, T and
U waves, and the QT interval: a scientific statement from the American
457
Heart Association Electrocardiography and Arrhythmias Committee,
Council on Clinical Cardiology; the American College of Cardiology
Foundation; and the Heart Rhythm Society. Endorsed by the
International Society for Computerized Electrocardiology. J Am Coll
Cardiol 2009;53:98291.
[28] Sgarbossa EB, Pinski SL, Gates KB, Wagner GS, The G-I. Early
electrocardiographic diagnosis of acute myocardial infarction
in the presence of ventricular paced rhythm. Am J Cardiol 1996;
77:4234.
[29] Kilic H, Atalar E, Ozer N, Ovunc K, Aksoyek S, Ozmen F, et al. Early
electrocardiographic diagnosis of acute coronary ischemia on the paced
electrocardiogram. Int J Cardiol 2008;130:148.
[30] Rosner MH, Brady WJ. The electrocardiographic diagnosis of acute
myocardial infarction in patients with ventricular paced rhythms. Am
J Emerg Med 1999;17:1825.
[31] Goyal R, Syed ZA, Mukhopadhyay PS, Souza J, Zivin A, Knight BP,
et al. Changes in Cardiac Repolarization Following Short Periods of
Ventricular Pacing. J Cardiovasc Electrophysiol 1998;9:26980.
[32] Chatterjee K, Harris A, Davies G, Leatham A. Electrocardiographic
changes subsequent to artificial ventricular depolarization. Br Heart J
1969;31:7709.
[33] Goldberger JJ, Kadish AH. Cardiac Memory. Pacing Clin Electro-
physiol 1999;22:16729.
[34] Shvilkin A, Ho KKL, Rosen MR, Josephson ME. T-Vector Direction
Differentiates Postpacing From Ischemic T-Wave Inversion in
Precordial Leads. Circulation 2005;111:96974.
[35] Munclinger M. Ventricular paced rhythm and acute coronary
ischaemia. Int J Cardiol 2010;145:778.
[36] Fischell TA, Fischell DR, Avezum A, John MS, Holmes D, Foster 3rd M,
et al. Initial clinical results using intracardiac electrogram monitoring
to detect and alert patients during coronary plaque rupture and ischemia.
J Am Coll Cardiol 2010;56:108998.
[37] Ukena C, Mahfoud F, Buob A, Bhm M, Neuberger H-R. ST-elevation
during biventricular pacing. Europace 2012;14:60911.
[38] Karumbaiah K, Omar B. ST-Elevation Myocardial Infarction
in the Presence of Biventricular Paced Rhythm. J Emerg Med
2013;45:e3540.
[39] Task Force on the management of STseamiotESoC, Steg PG, James SK,
Atar D, Badano LP, Blomstrom-Lundqvist C, et al. ESC Guidelines
for the management of acute myocardial infarction in patients presenting
with ST-segment elevation. Eur Heart J 2012;33:2569619.
[40] American College of Emergency Physicians, Society for Cardiovas-
cular, Angiography and Interventions, O'Gara PT, Kushner FG,
Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of
ST-elevation myocardial infarction: executive summary: a report of the
American College of Cardiology Foundation/American Heart Associ-
ation Task Force on Practice Guidelines. J Am Coll Cardiol 2013;61:
485510.
[41] Thygesen K, Alpert JS, Jaffe AS, Simoons ML, Chaitman BR,
White HD, et al. Third Universal Definition of Myocardial Infarction.
J Am Coll Cardiol 2012;60:158198.
[42] Brady WJ, Erling B, Pollack M, Chan TC. Electrocardiographic
manifestations: Acute posterior wall myocardial infarction. J Emerg
Med 2001;20:391401.
[43] Boden WE, Kleiger RE, Gibson RS, Schwartz DJ, Schechtman KB,
Capone RJ, et al. Electrocardiographic evolution of posterior acute
myocardial infarction: importance of early precordial ST-segment
depression. Am J Cardiol 1987;59:7827.
[44] Porter A, Vaturi M, Adler Y, Sclarovsky S, Strasberg B, Herz I, 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;90:2958.
[45] Bays de Luna A, Wagner G, Birnbaum Y, Nikus K, Fiol M, Gorgels A,
et al. A New Terminology for Left Ventricular Walls and Location of
Myocardial Infarcts That Present Q Wave Based on the Standard of
Cardiac Magnetic Resonance Imaging: A Statement for Healthcare
Professionals From a Committee Appointed by the International Society
for Holter and Noninvasive Electrocardiography. Circulation
2006;114:175560.
458 A. Ayer, C.J. Terkelsen / Journal of Electrocardiology 47 (2014) 448458
[46] Waldo SW, Armstrong EJ, Kulkarni A, Hoffmayer KS, Hsue P, Ganz P,
et al. Clinical characteristics and reperfusion times among patients with
an isolated posterior myocardial infarction. J Invasive Cardiol
2013;25:3715.
[47] Wei EY, Hira RS, Huang HD, Wilson JM, Elayda MA, Sherron SR, et al.
Pitfalls in diagnosing ST elevation among patients with acute myocardial
infarction. J Electrocardiol 2013;46:6539.
[48] Birnbaum Y, Herz I, Sclarovsky S, Zlotikamien B, Chetrit A, Olmer L,
et al. Prognostic significance of precordial ST segment depression on
admission electrocardiogram in patients with inferior wall myocardial
infarction. J Am Coll Cardiol 1996;28:3138.
[49] Martin TN, Groenning BA, Murray HM, Steedman T, Foster JE,
Elliot AT, et al. ST-segment deviation analysis of the admission 12-lead
electrocardiogram as an aid to early diagnosis of acute myocardial
infarction with a cardiac magnetic resonance imaging gold standard. J
Am Coll Cardiol 2007;50:10218.
[50] Terkelsen CJ. Acute Versus Subacute Angioplasty in Patients With
NON-ST-Elevation Myocardial Infarction. ClinicalTrials.gov
NCT01638806.
[51] McCabe JM, Armstrong EJ, Kulkarni A, Hoffmayer KS, Bhave PD,
Garg S, et al. Prevalence and factors associated with false-positive ST-
segment elevation myocardial infarction diagnoses at primary
percutaneous coronary intervention-capable centers: a report from
the Activate-SF registry. Arch Intern Med 2012;172:86471.
[52] Armstrong EJ, Kulkarni AR, Bhave PD, Hoffmayer KS, Macgregor
JS, Stein JC, et al. Electrocardiographic criteria for ST-elevation
myocardial infarction in patients with left ventricular hypertrophy. Am
J Cardiol 2012;110:97783.
[53] Potter BJ, Matteau A, Mansour S, Essiambre R, Montigny M, Savoie
S, et al. Performance of a New Physician-Less Automated System of
Prehospital ST-Segment Elevation Myocardial Infarction Diagnosis
and Catheterization Laboratory Activation. Am J Cardiol 2013;112:
15661.
[54] Alzand BS, Gorgels AP. Combined anterior and inferior ST-segment
elevation Electrocardiographic differentiation between right coronary
artery occlusion with predominant right ventricular infarction and
distal left anterior descending branch occlusion. J Electrocardiol
2011;44:3838.
[55] Di Chiara A. Right bundle branch block during the acute phase of
myocardial infarction: modern redefinitions of old concepts. Eur Heart
J 2006;27:12.
[56] Widimsky P, Roh F, tsek J, Kala P, Rokyta R, Kuzmanov B, et al.
Primary angioplasty in acute myocardial infarction with right bundle
branch block: should new onset right bundle branch block be added to
future guidelines as an indication for reperfusion therapy? Eur Heart J
2012;33:8695.
[57] Guglin ME, Thatai D. Common errors in computer electrocardiogram
interpretation. Int J Cardiol 2006;106:2327.
[58] Clark EN, Sejersten M, Clemmensen P, Macfarlane PW. Automated
Electrocardiogram Interpretation Programs Versus Cardiologists'
Triage Decision Making Based on Teletransmitted Data in Patients
With Suspected Acute Coronary Syndrome. Am J Cardiol
2010;106:1696702.
[59] Cantor WJ, Hoogeveen P, Robert A, Elliott K, Goldman LE,
Sanderson E, et al. Prehospital diagnosis and triage of ST-elevation
myocardial infarction by paramedics without advanced care training.
Am Heart J 2012;164:2016.
[60] Feldman JA, Brinsfield K, Bernard S, White D, Maciejko T. Real-time
paramedic compared with blinded physician identification of ST-
segment elevation myocardial infarction: results of an observational
study. Am J Emerg Med 2005;23:4438.
[61] Mencl F, Wilber S, Frey J, Zalewski J, Maiers JF, Bhalla MC. Paramedic
ability to recognize ST-segment elevation myocardial infarction on
prehospital electrocardiograms. Prehosp Emerg Care 2013;17:20310.
[62] Willems JL, Abreu-Lima C, Arnaud P, van Bemmel JH, Brohet C,
Degani R, et al. The Diagnostic Performance of Computer Programs for
the Interpretation of Electrocardiograms. N Engl J Med 1991;325:176773.
[63] Whitbread M, Leah V, Bell T, Coats TJ. Recognition of ST elevation
by paramedics. Emerg Med J 2002;19:667.
[64] Salerno SM, Alguire PC, Waxman HS. Competency in Interpretation
of 12-Lead Electrocardiograms: A Summary and Appraisal of
Published Evidence. Ann Intern Med 2003;138:75160.