Chameleons

Electrocardiogram Imitators of STSegment Elevation Myocardial Infarction

Jose V. Nable,

MD, NRP

a,

*, Benjamin J. Lawner,

b
DO, EMT-P

KEYWORDS
 Electrocardiography  STEMI  Myocardial infarction  Electrocardiogram
KEY POINTS
 Rapid recognition of ST-segment elevation myocardial infarction (STEMI) is imperative;
however, the characteristic electrocardiographic (ECG) pattern of ST-segment elevation
may be seen in other diagnoses.
 An understanding of these other diagnoses, and an awareness of how to distinguish them
from STEMI, often requires obtaining a satisfactory history, comparing with previous
ECGs, assessing serial tests, and uncovering subtle clues in the ECG pattern.
 The morphology of ST-segment elevation may provide a valuable clue at determining if the
evaluated pattern is concerning for either STEMI or one of its imitators.
 Specifically, ST-segment elevation may be seen in patients with left ventricular hypertrophy, early repolarization, left bundle branch block, myopericarditis, Brugada syndrome,
hyperkalemia, Takotsubo cardiomyopathy, and ventricular aneurysm.

INTRODUCTION

The need for timely reperfusion is critical to improving outcomes following STsegment elevation myocardial infarction (STEMI). Indeed, the most recent iteration
of the guideline from the American College of Cardiology Foundation (ACCF) and
American Heart Association (AHA) continues to emphasize rapid recognition and
reperfusion for patients with STEMI.1 Clinicians must recognize electrocardiographic
(ECG) patterns diagnostic of STEMI and rapidly coordinate the delivery of definitive
care in the form of percutaneous coronary intervention or fibrinolysis. Importantly,

Disclosures: The authors have no commercial associations or sources of support that might
pose a conflict of interest.
a
Department of Emergency Medicine, MedStar Georgetown University Hospital, Georgetown
University School of Medicine, 3800 Reservoir Rd NW, G-CCC, Washington, DC 20007, USA;
b
Department of Emergency Medicine, University of Maryland School of Medicine, 6th floor,
Suite 200110 South Pace Street, Baltimore, MD 21201, USA
* Corresponding author.
E-mail address: JoseVictor.L.Nable@medstar.net
Emerg Med Clin N Am 33 (2015) 529537
http://dx.doi.org/10.1016/j.emc.2015.04.004
0733-8627/15/$ see front matter 2015 Elsevier Inc. All rights reserved.

emed.theclinics.com

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the 2013 ACCF/AHA guideline clarified the definition of STEMI to include elevations, as
measured from the J point, of at least 1 mm in two or more anatomically contiguous
leads (with allowance of up to 1.5 mm in leads V2V3 for women and 2 mm in the
same leads in men).1
Unfortunately, ECG features seen in association with STEMI also appear in other
benign, nonischemic presentations. Although a certain amount of overtriage is
accepted, it is desirable to minimize patient risk. Patients with evidence of left ventricular hypertrophy (LVH) without actual acute infarction, for example, will likely not
benefit from emergent reperfusion. Risks associated with inappropriate coronary
revascularization include radiation exposure, dye administration, and medicationinduced bleeding. A thorough understanding of conditions that have the potential to
mimic or confound the diagnosis of STEMI is essential to the provision of timely and
safe patient care. This article focuses on ECG findings, specifically ST-segment elevation, occurring in the absence of ischemia.
LEFT VENTRICULAR HYPERTROPHY

Chronic and uncontrolled hypertension results in remodeling of the hearts left

ventricle. The increase in muscle mass also alters the manner in which cardiac repolarization occurs. Characteristic ECG changes associated with LVH may mimic the
ST-segment elevation seen in the setting of acute myocardial infarction (AMI).2 Other
changes attributed to LVH include prominent septal q waves, T-wave inversion, and
ST-segment depression.3 Several features unique to LVH assist the emergency clinician in differentiating it from the STEMI-related ECG changes. First, ECG changes in
the setting of LVH are static. Unlike an evolving ischemic event, the ST-segment
morphology of the ECG in LVH remains constant. Serial ECGs are therefore of value
when considering the diagnosis of LVH. The ST-segment changes are appropriately
discordant with respect to hypertrophy (Figs. 13). Deep QS waves appear in the
septal precordial leads. The resultant repolarization is upright and occurs on the opposite side of the baseline.
Similarly, high-amplitude R waves occur in the lateral precordial leads. ST-segment
changes, including strain-associated ST-segment depression, occur below the isoelectric line.3 ECG strain seen in LVH does not typically manifest as ST-segment
elevation. A characteristic strain pattern reveals a downsloping ST segment ending

Fig. 1. Left ventricular hypertrophy appropriate discordance. Appropriately discordant ST

segment changes in the setting of left ventricular hypertrophy. The ST segment is below
baseline when the QRS complex is positively deflected (1), whereas the ST segment is above
baseline when the QRS complex is negatively deflected (2).

STEMI Chameleons

Fig. 2. Strain pattern. A characteristic strain pattern reveals a downsloping ST segment

ending in a terminally negative, and asymmetric T wave.

in a terminally negative and asymmetric T wave. Finally, the ECG usually reveals a
rapid return to the baseline. Strain patterns are thought to result from hypertensive
heart disease.
The emergency physician should be keenly aware of the possibility of LVH
confounding the ability to recognize true STEMI. The presence of LVH, and its
concomitant perturbing of the ST segment, has been demonstrated as a risk factor
for false-positive STEMI diagnosis, not uncommonly leading to unnecessary reperfusion therapy.4,5
EARLY REPOLARIZATION

Early repolarization occurs in approximately 1% of the population.6 Patients with early

repolarization may present to the emergency department complaining of chest pain
with an ECG potentially mimicking STEMI. There are several clues, however, that
may assist the physician in correctly distinguishing early repolarization from an AMI.
The ST-segment elevation typically found in early repolarization is less than 2 mm in
the precordial leads and less than 0.5 mm in the limb leads.7 Additionally, the
morphology of the ST segment in early repolarization is generally upsloping in concavity
(Fig. 4).7,8 Although a nonconcave morphology is often worrisome for MI,9 morphology
is not completely sensitive for detecting ongoing infarction.7 Other clues, such as
notching of the terminal QRS complex, prominent T waves that are concordant with
the ST segment, and the persistent nature of early repolarization, should also be

Fig. 3. Strain pattern. Lead V6 shows a downsloping and depressed ST segment.

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Fig. 4. Early repolarization. Typical early repolarization pattern with ST-segment elevation,
prominent T waves that are concordant with the ST segment, and not uncommonly a
notched terminal QRS complex.

considered.7 The importance of assessing for dynamic ECGs to assist in differentiating

early repolarization from STEMI underscores the necessity of frequently obtaining serial
tests.
LEFT BUNDLE BRANCH BLOCK

The left bundle branch block (LBBB) pattern complicates the physicians ability to
assess for STEMI because the pattern by definition includes ST-segment elevation.10
Additionally, the presence of LBBB during an AMI has previously been associated with
increased risk for mortality.11 For many years, it was recommended that patients with
new or presumably new LBBB in the setting of chest pain or other ischemic symptoms
should undergo emergent reperfusion therapy.12
More recent literature, however, has caused a dramatic shift in the approach to
management of patients with LBBB. Although LBBB may identify a high-risk population, only a small proportion of these patients are ultimately diagnosed with AMI.13 The
presence of LBBB also has been shown to be a poor predictor for infarction.14 The
most recent ACCF/AHA guideline on STEMI management notes that LBBB may interfere with the ability to detect STEMI and should not be used in isolation to diagnose
AMI.1 Because patients with LBBB, however, not uncommonly do present with acute
coronary syndrome, the clinician must remain vigilant.
Criteria developed by Sgarbossa and colleagues15 may potentially be useful in identifying those with LBBB who require emergent reperfusion.16 This score-based criteria
system includes the presence of (1) ST-segment elevation of at least 1 mm concordant
with the QRS complex in any lead (5 points); (2) ST-segment depression of at least
1 mm in leads V1, V2, or V3 (3 points); or (3) ST-segment elevation of at least 5 mm
discordant with the QRS complex in any lead (2 points).15 A composite score of 3
or greater has been shown to have an estimated sensitivity of 20% and specificity
of 98% to predict AMI.17 A score of 0, however, does not reliably exclude MI.17 In light
of the recent ACCF/AHA guideline changes regarding LBBB, and the relatively low
sensitivity of Sgarbossas criteria, the development of more versatile clinical criteria
may be necessary.15
MYOPERICARDITIS

Myopericarditis is classically associated with diffuse elevations of the ST segment,

usually with upward concavity, along with PR-segment depressions.18 These elevations may be confused with STEMI. Furthermore, similar to MI, patients may present
with chest pain radiating to the arms or neck.18 Cardiac biomarkers are generally
elevated in patients with myocarditis10 and in up to 50% of patients with pericarditis.18
Inflammation of the pericardium and heart muscle is typically idiopathic, although
most often presumed to be caused by a viral infection.19 It is believed that
PR-segment depressions are a manifestation of inflammation of the pericardial

STEMI Chameleons

sac.20 PR-segment changes, however, are dynamic in the course of acute myopericarditis, typically seen in the early phases of the disease process.20
Myopericarditis is an example of the importance of obtaining serial ECGs to help the
clinician distinguish STEMI from other ECG-mimicking processes. As opposed to
myopericarditis, the evolution of STEMI is typically much more rapid, with changes
to the ST-segment and T-wave morphology often occurring over the course of only
several minutes.10 Furthermore, although patients with multiple coronary artery occlusions may present with diffuse ST-segment elevations, such patients tend to have a
much sicker and more dramatic presentation than those with myopericarditis, often
in cardiogenic shock.21 A sicker patient presentation may thus be more worrisome
for the need for rapid reperfusion therapy.
BRUGADA SYNDROME

Brugada syndrome is described as a right bundle branch block with ST-segment

elevation in leads V1 through V3.22 Three types of this pattern have been described
(Fig. 5). In type 1, a coved-appearing ST-segment elevation of at least 2 mm is proceeded by a negative T wave; type 2 contains an ST segment that remains above
baseline followed by an upright or biphasic T wave, giving rise to a saddle-back
appearance; type 3 is typified by ST-segment elevation of less than 1 mm, with either
a coved or saddle-back appearance.23
Patients with this particular ECG pattern have been observed to be at risk for
sudden ventricular arrhythmias leading to death.24 A genetic mutation linked to a
sodium channelopathy has been attributed to this process.25 Although some patients
with the Brugada pattern may have significant ST-segment elevation, chest pain is not
considered part of the syndrome.10 These patients are, however, at risk for sudden
death.
PROMINENT T WAVES

Hyperacute T waves, as manifested by increased T-wave amplitudes, is considered to

be one of the earliest ECG signs of AMI.26 Indeed, the early temporal nature of large T
waves in the evolution of ST-segment elevation has been described since the early
half of the twentieth century.27 The astute clinician, however, should note that large
T waves may be found in a variety of other conditions.

Fig. 5. Brugada syndrome. Type I demonstrates a coved-appearing ST segment with elevation of at least 2 mm followed by a negatively deflected T wave. Type II contains an ST
segment that remains above baseline followed by an upright or biphasic T wave with a
saddle-back appearance. Type III has ST-segment elevation of less than 1 mm with either
a coved or saddle-back appearance. (Data from Wilde AA, Antzelevitch C, Borggrefe M,
et al. Proposed diagnostic criteria for the Brugada syndrome: consensus report. Circulation
2002;106:25149.)

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Hyperkalemia

Elevated serum potassium is known to cause a variety of ECG changes, including

increasing amplitudes of the T wave. Hyperkalemic T waves, however, tend to
maintain a narrow base with a symmetric morphology.26 In contrast, hyperacute T
waves associated with AMI tend to be broad-based and asymmetric. Although STsegment elevation may also be seen in hyperkalemia,28 such elevations are typically
diffuse. Additional historical factors, such as the presence of kidney failure, may
also provide valuable insight.
Finally, the evolution of ECG changes may provide some clues. The typical pattern
of progressing hyperkalemia includes (1) peaked T waves, (2) prolonging PR interval,
(3) widening QRS complex, and (4) sinusoidal pattern (Figs. 6 and 7).
Early Repolarization

Early repolarization can be confused with STEMI. In particular, the large T waves not
uncommonly found with early repolarization may mimic the early stages of AMI. These
enlarged T waves, however, tend to be symmetric and concordant with the ST
segment.10
TAKOTSUBO OR STRESS-RELATED ST-SEGMENT ELEVATION

Takotsubo cardiomyopathy (TTCM) was first recognized in 1990 at Hiroshima City

Hospital. Dr Sato detailed a syndrome of apical wall motion abnormality and ECG
changes occurring in the absence of coronary artery disease.29 TTCM presents with
signs and symptoms similar to those seen in acute coronary syndromes. Patients
may report chest discomfort and shortness of breath. The accompanying ECG may
show ST-segment abnormalities including ST-segment elevation.
A recent review documented the prevalence of ST-segment elevation in cases of
TTCM as high as 90%.30 The magnitude of ST-segment deviation in TTCM tends to
be less than the elevation occurring with STEMI, and TTCM is less likely to present
with reciprocal changes.29,31 Because the left ventricle is most commonly affected
in TTCM, ECG changes may be more likely to occur in the lateral, septal, and anterior leads.30 History may offer additional diagnostic clues because patients often
report a stressful or precipitating event in these cases. Currently, the ECG is not
useful as a stand-alone tool to set TTCM apart from STEMI. Both conditions produce ST-segment elevation and elevated cardiac biomarkers. If available, emergent
transthoracic echocardiography may identify typical wall motion abnormalities that
accompany TTCM. The literature is not clear about the underlying physiology.
Catecholamine release and an upregulation of myocardial b-receptor activity have
been implicated in the disease process.29

Fig. 6. Early hyperkalemia. The typical pattern of progressing hyperkalemia includes (1)
peaked T waves, (2) prolonging PR interval, and (3) widening QRS complex.

STEMI Chameleons

Fig. 7. Severe hyperkalemia. Sinusoidal pattern not uncommonly seen in severe

hyperkalemia.

VENTRICULAR ANEURYSM

The finding of persistent ST-segment elevation following a recent MI has long been
recognized as a possible sign of the development of a ventricular aneurysm.32,33
Although the exact mechanism for its persistence has yet to be elucidated, at least
one study has shown that continued ST-segment elevation may be a further marker
of extensive transmural necrosis and microvascular damage.34 Because of the typical
location of ventricular aneurysm postinfarction, ST-segment elevation in this setting is
most commonly in the anterior leads.35
Historical factors, such as known recent AMI, should help provide the emergency
physician some clues in distinguishing an acute STEMI from ventricular aneurysm.
Additionally, comparison with prior ECGs may be helpful.
SUMMARY

The time-sensitive diagnosis of STEMI demands that emergency clinicians maintain

proficiency in the interpretation of the ECG. In addition to the recognition of potentially life-threatening ECG patterns, emergency clinicians must separate STEMI patterns from mimics, confounders, and other conditions that produce similar
changes. Fortunately, close scrutiny of the ECG in combination with a focused clinical
history assists practitioners with sorting out conditions that likely do not benefit from
urgent percutaneous coronary intervention. ST-segment morphology yields valuable
diagnostic clues and represents another tool useful for the triage of patients with ECG
findings.
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