Not all ST-segment elevations signify an acute myocardial infarction. Indeed, noncoronary ST-segment elevations are common. Many such patients have diagnoses other than acute STEMI, most often left ventricular hypertrophy (LVH), left bundle branch block (LBBB), left ventricular aneurysm, pericarditis or the early repolarization pattern (ERP). These conditions often masquerade as ST-elevation myocardial infarction and are referred to as “pseudo-infarct patterns” or “coronary mimics.” Misdiagnosis, which may lead to unnecessary reperfusion therapy, is common.
In differentiating benign ST-segment elevation from STEMI, the contour of the ST-segment may be helpful. Or the shape of the ST-segment may be misleading. Benign-appearing (that is, smooth and upwardly concave) ST-segment elevations can still represent an acute STEMI.
The early repolarization pattern (formerly called “benign early repolarization”) is common in young, healthy patients. The hallmark of ERP is the presence of diffuse ST-segment elevation, most commonly in the precordial leads. Other features of ERP include preservation of the upward concavity of the elevated ST-segments; a smooth blending of the elevated ST-segment into the ascending limb of a tall, upright (sometimes “hyperacute-appearing”) T-wave; and prominent J-point elevation with a notched, “fish-hook” appearance. ERP can usually be differentiated from acute STEMI because the ST-segment elevations in ERP are not limited to a regional (anatomic) distribution, and they are not accompanied by reciprocal ST-segment depressions. Still, when the ST-elevations are limited to the anterior precordial leads, it can be challenging to differentiate ERP from a subtle, anterior wall STEMI. A small subset of ERP patients may be at higher risk of developing polymorphic ventricular tachycardia and sudden cardiac death.
Acute pericarditis is characterized by even more diffuse ST-segment elevations, almost always involving the precordial and limb leads. The ST-segments are usually smooth and concave upward and seldom exceed 5 mm in amplitude. The T-waves are less prominent (more “humble”) than in ERP. PR-segment depression is common (except in leads aVR and V1, where PR-segment elevation is often seen).
Patients with electrocardiographic signs of LVH often have ST-segment elevations in the right precordial leads; there should also be high-amplitude R-waves and ST-segment depressions accompanied by T-wave inversions in the left-facing leads. Other features of LVH include poor R-wave progression, left axis deviation, QRS widening and left atrial enlargement. The ST-segment elevations in leads V1–V3 must be differentiated from acute coronary syndromes. The elevated ST-segment can mimic ominous patterns of acute LAD occlusion, including Wellens’ sign.
ST-segment elevations in the right precordial leads are also routine in left bundle branch block (LBBB). In some cases, acute anterior wall STEMI may be differentiated from the secondary ST-segment elevations of the LBBB by applying the Sgarbossa criteria (or by obtaining serial ECGs, by performing bedside echocardiography or by comparing the presenting ECG to baseline tracings).
Other causes of noncoronary ST-segment elevations include hypothermia, hyperkalemia, takotsubo cardiomyopathy and the Brugada syndrome. Examples are provided in this chapter.
Prominent T-waves are also a common ECG finding, especially in the precordial leads. The differential diagnosis includes, in addition to the “hyperacute T-waves” of an acute coronary syndrome, ERP, hyperkalemia, LVH, bundle branch block, hypertrophic cardiomyopathy and other conditions.
In earlier chapters of this atlas, we have covered several important electrocardiographic emergencies, including inferior, anterior and posterior wall ST-elevation myocardial infarctions (STEMIs) and various causes of shortness of breath (pulmonary emboli, pericardial effusion, myocarditis and the classic, everyday electrocardiographic appearance of COPD). In Chapter 6, we described a group of “confounding and confusing conditions” – patients with chest pain, shortness of breath or other cardiovascular symptoms whose ECGs demonstrate only ST-segment depressions or T-wave inversions. Some of these patients have “nonspecific ST-T-wave changes” without any acute disease. In other cases, the ST- and T-wave changes represent an acute coronary syndrome (unstable angina or non-STEMI), pulmonary embolus, digitalis effect, an electrolyte disturbance or left ventricular hypertrophy with repolarization abnormalities (the “strain” pattern).
One topic is left: ST-segment elevations that do not represent myocardial infarctions. Some patients will have acute pericarditis. In other cases, the ST-segment elevations represent a stable pattern of early repolarization (early repolarization pattern, or ERP). Noncoronary ST-segment elevations may also be caused by hypothermia, myocarditis, left ventricular aneurysm, left ventricular hypertrophy, left bundle branch block, hyperkalemia, Brugada syndrome, myocarditis, takotsubo cardiomyopathy or other cardiomyopathies (Huang, and Birnbaum 2011; Goldberger, 1980; Birnbaum, Nikus et al., 2014; Birnbaum, Wilson et al., 2014; Nable and Lawner, 2015; Pollak and Brady, 2012). These conditions often masquerade as ST-elevation myocardial infarction and are referred to as “pseudo-infarct patterns” or “coronary mimics” (Pollak and Brady, 2012; Nable and Lawner, 2015; Wang et al., 2003). In one recent review, these STEMI imitators were called “chameleons” (Nable and Lawner, 2015).
We should emphasize that ST-segment elevations in the right precordial leads are extraordinarily common, even on routine ECGs, in patients without any symptoms or “syndrome” (Huang and Birnbaum, 2011; Tran et al., 2011). ST-segment elevations can be seen in leads V1, V2 and V3 in young and old patients and in health as well as in disease. In one study of 6,014 healthy men ages 16–58 years of age, 91 percent had ST-elevations of 1–3 mm in at least one precordial lead (most commonly in lead V2) (Wang et al., 2003; His et al., 1960; Huang and Birnbaum, 2011; Tran et al., 2011). For this reason (as emphasized in Chapter 6), even minor ST-segment depressions in precordial leads V1–V3 must be considered abnormal and taken seriously.
As noted in Chapter 6, the literature also includes large numbers of case reports where the ST-segment elevations are “caused” by a pneumothorax, cholecystitis, intestinal ischemia, food impaction or even drinking cold (or hot) water. For the most part, these are anecdotal case reports, and no serious attempt is made to demonstrate causality.
Coronary Mimics: ST-Segment Elevations That Are Not Myocardial Infarction
In large series of patients presenting to emergency departments with chest pain, noncoronary ST-segment elevations (pseudo-infarct patterns) are common. Many such patients have diagnoses other than acute STEMI, most often left ventricular hypertrophy, left bundle branch block, left ventricular aneurysm, pericarditis or ERP (Wang et al., 2003; Brady et al., 2001; Nable and Lawner, 2015; Pollak and Brady, 2012). Misdiagnosis is common, even among experienced electrocardiographers; unnecessary thrombolytic therapy or percutaneous angioplasty is often administered (Tran et al., 2011; Jayroe et al., 2009; Huang and Birnbaum, 2011).
The following table summarizes the most common noncoronary causes of ST-segment elevations.
Early repolarization pattern
Hypothermia (Osborn J-waves)
Left ventricular hypertrophy (limited to V1–V3, reciprocal to the lateral wall ST-segment depressions)
Left bundle branch block
Left ventricular aneurysm
Hyperkalemia (“dialyzable injury current;” typically V1–V3)
In differentiating benign ST-segment elevation from STEMI, the contour of the ST-segment may be helpful. For example, in many patients with ERP, acute pericarditis or left ventricular hypertrophy, the normal, concave-upward contour of the ST-segment is usually preserved. And in the majority of STEMIs, the ST-segment becomes abnormally straight or acquires a downwardly concave or dome-shaped pattern (Brady et al., 2001).
However, upward concavity does not rule out a STEMI (Brady et al., 2001; Smith, 2006; Birnbaum, Wilson et al., 2014; Huang and Birnbaum, 2011; Chung et al., 2013; Tran et al., 2011). ST-segments that are straight or dome-shaped (concave downward) may be very specific for STEMI, but this pattern is not at all sensitive, and its absence cannot be used to exclude the diagnosis of STEMI. Furthermore, saying that the ECG shows only J-point elevation (and is, therefore, benign) is a false argument. Most acute STEMIs also have J-point elevation, and sometimes, STEMIs have concave upward (“smiley face”) ST-segments. These patterns are “overlapping, not distinct” (Brady et al., 2001; Birnbaum, Wilson et al., 2014; Chung et al., 2013).
Figure 7.1 The shape of the ST-segment elevation.
The ST-segment elevations in Panel A appear reassuring; indeed, this smooth, upwardly concave morphology is classically associated with more benign, nonacute coronary syndrome etiologies such as early repolarization pattern, left ventricular hypertrophy or pericarditis. The patterns in Panel B are usually more sinister, with ST-segments that are straighter, have lost their upward concavity or are concave downward. However, as highlighted in this section, a reassuring, concave-upward ST-segment does not exclude acute STEMI.
As highlighted throughout this atlas, the key to recognizing an acute STEMI, even if the ST-segments have a benign shape, is the presence of a regional (anatomic) pattern to the ST-segment elevations and reciprocal ST-segment depressions. These two features make a STEMI much more likely (although focal myocarditis may also represent with regional ST-segment elevations).
So, does the shape of the ST-segment matter? Yes, sometimes – but not as much as previously thought. If there is a regional pattern to the ST-segment elevations, this matters more. Regional ST-segment elevations with reciprocal ST-segment depressions signify a STEMI and trump “shapeliness” every time.
“Looking Backward”: Reviewing the Patient’s Old ECGs
When patients present with ST-segment elevations, the first step is always to rule out (or rule in) an acute STEMI. When the clinical or electrocardiographic diagnosis is less clear, we also know to search for old ECG tracings to ascertain whether the ST-segment elevations are new or are more pronounced.
However, while critical, this approach is not foolproof. Changes in lead placement can cause variability in the position of the ST-segments. And some nonischemic patterns of ST-segment elevations may also fluctuate over time, depending on the patient’s heart rate, body position, autonomic tone or other factors. For example, the ST-segment elevations of ERP tend to be less dramatic at higher heart rates, and the features of ERP may even disappear over time (Adhikarla et al., 2011; Birnbaum, Wilson et al., 2014). The patterns of the Brugada syndrome have a tendency to show spontaneous variability in addition to fluctuations caused by multiple different medications and changes in sympathetic-parasympathetic balance (Huang and Birnbaum, 2011; Birnbaum, 2014; Pollak and Brady, 2012).
This is only a cautionary note; reviewing baseline ECGs remains a vital step in patients with chest pain, dyspnea, abdominal pain, dizziness or other suggestive symptoms, if the diagnosis of STEMI is not clear.
The early repolarization pattern (ERP) has, for many decades, been referred to as “benign early repolarization.” ERP is a common ECG pattern that can be recognized, in most cases, by a constellation of electrocardiographic findings (Huang and Birnbaum, 2011; Nable and Lawner, 2015; Pollak and Brady, 2012):
Diffuse precordial ST-elevations with preservation of the normal upward concavity.
ST-segment elevations that are more common and more dominant in the anterior or lateral precordial leads (especially V4); often (30–50 percent of cases) there are concurrent ST-segment elevations in the inferior leads.
An upwardly concave, rising ST-segment that blends into the ascending limb of a tall, upright (and sometimes peaked) T-wave.
Prominent J-point elevation with a notched, “fish-hook” pattern – especially in leads V3 and V4.
ST-elevations that typically do not exceed 3 mm in the precordial leads or 0.5–1 mm in the limb leads.
Absence of a regional (anatomic) pattern to the ST-elevations – and absence of reciprocal ST-segment depressions.
PR-segment depression may occur, although less frequently than in pericarditis.
Some ECG features of ERP may overlap with the “athletic heart syndrome,” including sinus bradycardia, heart block (first or second degree), junctional rhythms and pronounced sinus arrhythmia.
ERP may be present in more than 10 percent of the population. ERP is much more common in young individuals, and it is more common in males (Huang and Birnbaum, 2011; Pollak and Brady, 2012; Klatsky et al., 2003). We should be cautious in suggesting the diagnosis of ERP in patients older than age 50.
The mechanism of ERP is, surprisingly, unclear. The ST-segment elevations may represent “nonhomogeneous repolarization of the ventricles,” with an imbalance in repolarization between the epicardium and endocardium or among different anatomic regions of the heart (Huston et al., 1985; Eastaugh, 1985). Increased parasympathetic tone probably plays a causative role. “Early repolarization” has never been proven, but the name persists (Huang and Birnbaum, 2011).
The ST-segment elevations of ERP most commonly appear in the anterior precordial leads, especially leads V3 and V4. In 30–50 percent of cases, similar ST-segment elevations may be present in the inferior limb leads. However, ST-segment elevations restricted to the inferior leads alone is not common in ERP and must be considered suspicious of an acute coronary syndrome or another etiology. Most importantly, ERP causes prominent ST-elevations but does not cause reciprocal ST-segment depressions.
The traditional name “benign early repolarization” implied that the condition has no prognostic significance. Indeed, ERP is more common in young persons, overlaps with the “athletic heart syndrome” and has always been considered a sign of good health (Adler et al., 2013). ERP is more common in individuals younger than age 40 who are physically active (Klatsky et al., 2003).
In recent years, the view that “early repolarization” is always “benign” has changed (Patton et al., 2016; Antzelevitch et al., 2017). Large epidemiologic studies (as well as case reports) have suggested that some patients with this pattern – especially those with ST-segment elevations involving the inferior, as well as the anterior, leads – carry a higher risk of sudden cardiac death due to ventricular fibrillation (VF), even in the absence of other structural heart disease (Wu et al., 2013; Tikkanen, 2009; Adler et al., 2013). Patients with more “horizontal” or “descending” (as opposed to “ascending”) ST-segment elevations and patients with greater J-point elevation (≥ 2 mm), especially in multiple leads, may also be at higher risk of sudden VF (Rosso et al., 2008; Wu et al., 2013; Huang and Birnbaum, 2011; Tikkanen et al., 2009; Antzelevitch et al., 2011; Antzelevitch et al., 2017; Patton et al., 2016; Benito et al., 2010).
Whether the association between the ERP pattern and malignant ventricular arrhythmias is causal, and whether this observation should affect clinical decision-making, is unclear (Adler et al., 2013). The overall risk of a malignant ventricular arrhythmia in asymptomatic, healthy patients with the incidental finding of ERP is low. Possibly, the finding of early repolarization changes involving both the anterior and inferior leads has greater significance in patients who present with syncope, those with a family history of sudden cardiac death, those with coronary or other structural heart disease, those with a prolonged QT interval, or those resuscitated from out-of-hospital cardiac arrest. Patients who present with syncope should always be asked whether there is a family history of SCD, and this certainly applies to patients whose ECG demonstrates early repolarization.
Some investigators have proposed the term “J-wave syndrome” in view of the higher risk associated when the early repolarization pattern is present in multiple leads. When the ECG demonstrates marked J-point elevation, and especially if the elevated ST-segments are horizontal or downsloping (rather than steeply upsloping), it may even represent a variation of the Brugada syndrome and carry similar arrhythmogenic risks (Benito et al., 2010; Antzelevitch et al., 2011; Antzelevitch et al., 2017; Patton et al., 2016). Indeed, there is a growing consensus that the J-wave syndromes (including Brugada as well as some high-risk early repolarization patterns) have similar ECG patterns, genetic substrates and arrhythmogenicity.
The early repolarization pattern probably overlaps with other normal juvenile patterns (Huang and Birnbaum, 2011). In particular, young athletes often have anterior precordial ST-elevations that are indistinguishable from ERP. The ERP pattern in healthy athletes likely represents a state of increased parasympathetic tone. The common features of the athletic heart syndrome, including resting sinus bradycardia, sinus arrhythmia, first- or second-degree AV block and, of course, diffuse ST-segment elevations (with J-point elevations and tall T-waves), are also features of ERP. Classically in these patients, the J-point and ST-segment elevations, and the prolonged PR-segment, revert to normal during exercise (Somers et al., 2002; Goldberger, 1980).
Review ECG 7.1, which illustrates classic features of ERP.
ECG 7.1 A 25-year-old man was transported from the airport after a syncopal episode. He had no chest pain or dyspnea. A “cardiac alert” was called by the paramedics because of the ST-elevations on the prehospital ECG.
The ECG is consistent with early repolarization. There are diffuse precordial and inferior wall ST-segment elevations with preservation of the normal upward concavity and prominent, upright T-waves. A prominent J-point notch (the “fish hook”) is present in several leads, including lead V4. The ST-segment elevations are upsloping. There is no anatomic or regional pattern, and there are no worrisome reciprocal ST-segment depressions. There is slight PR-segment depression, which occurs in ERP, albeit less often than in acute pericarditis.
The patient underwent a thorough evaluation for dizziness and near-syncope and was discharged from the emergency department. What is unknown in a patient with a complaint of syncope and an ECG that demonstrates ERP involving the precordial and limb leads is whether additional evaluation is needed. At the very least, it is prudent to inquire about prior syncopal episodes or a family history of sudden death.
In textbooks, it is easy to recognize the patient with acute pericarditis: he or she is young and healthy and has chest pain that is sharp, pleuritic and positional (improved by sitting up and leaning forward). More often than not, there is a preceding cough or febrile illness. And careful auscultation reveals a one-, two- or three-component pericardial friction rub (LeWinter, 2014; Demangone, 2006).
But in actual clinical practice, acute pericarditis can resemble acute coronary syndromes. The patient may be young or old. Shortness of breath is common. Diaphoresis may be present. The pain of pericarditis may be heavy, pressure-like or squeezing, and occasionally, the pain may radiate to the arms (Spodick, 2003). And in both conditions, the troponin levels may be elevated on presentation. In pericarditis, troponin elevations reflect subepicardial myocarditis (myopericarditis) (Nable and Lawner, 2015; Pollak and Brady, 2012). For these reasons, the ECG plays a critical role in differentiating pericarditis from ACS or other significant cardiorespiratory emergencies.
Here are the most common ECG findings in patients with acute pericarditis (Huang and Birnbaum, 2011; Nable and Lawner, 2015; Demangone, 2006). Because the pericardium is electrically silent, these changes reflect inflammation of the subpericardial myocardium (Pollak and Brady, 2012). Sometimes, pericarditis occurs without significant inflammation of the epicardium; one example is uremic pericarditis. In these cases, there is little if any alteration of the ECG (Rutsky and Rostand, 1989; Huang and Birnbaum, 2011).
Global ST-segment elevations
Without a regional (coronary anatomic) pattern or reciprocal ST-segment depressions (except in aVR and V1).
Typically seen in all leads except aVR and V1 (leads that do not directly face epicardial surfaces).
Often most prominent in leads V5–V6 and limb leads II, III and aVF.
The normal upward concavity of the ST-elevations is usually preserved.
The ST-segment elevations typically do not exceed 5 mm.
These reflect sub-epicardial atrial injury or atrial repolarization abnormalities and are most common in lead II (also common in III, aVF and V4–V6).
Usually, the PR-segment is elevated in aVR and V1.
The T-waves are often small or “humble,” especially when compared to the height of the elevated ST-segments.
In lead V6, an ST-segment amplitude: T-wave amplitude ratio ≥ 0.25 usually indicates pericarditis, not ERP.
The T-waves remain upright while the ST-segments are elevated, helping to distinguish acute pericarditis from a STEMI.
The T-waves often become inverted later, sometimes over hours or days but usually after normalization of the ST-segments.
As many as two-thirds of patients presenting with uncomplicated pericarditis have a small pericardial effusion. Larger effusions are less common (LeWinter, 2014). If there is a large pericardial effusion, other distinctive ECG changes may appear, including low-amplitude QRS complexes and electrical alternans. See Chapter 5 for additional discussion.
Severe myocarditis is often heralded by low-amplitude QRS complexes, sinus tachycardia, conduction system delays and ST-T-wave changes, including regional ST-segment elevations that may mimic an acute STEMI (Pollak and Brady, 2012). These were reviewed in Chapter 5, The Electrocardiography of Shortness of Breath.
PR-segment depression in all leads except aVR and V1 is a common finding in acute pericarditis. The PR-segment is usually elevated in lead aVR. In contrast, PR-segment depression is uncommon in acute STEMI, although it can occur as a reflection of atrial infarction. PR-segment depression also occurs commonly in ERP, although it is usually less marked than in pericarditis. PR-segment depression may also be seen in various tachycardias (for example, sinus tachycardia and ectopic atrial tachycardias) and other high-catecholamine states.
ECG 7.2 A postoperative patient who developed chest pain and tachycardia.
This patient’s chest pain was due to postoperative pericarditis. While the diagnosis cannot be confirmed solely from this lead II rhythm strip, he has striking PR-segment depression.
Acute pericarditis may be complicated by atrial fibrillation or atrial tachycardias. However, acute pericarditis is seldom complicated by malignant ventricular tachycardias or conduction system delays unless there is underlying cardiac disease or unless myocarditis is also present (Spodick, 1976; Lange and Hillis, 2004).
Troponin elevations are common (occurring in at least 30 percent of cases of acute pericarditis) and usually represent myopericarditis. It is the accompanying myocarditis that presents a risk. Life-threatening arrhythmias and left ventricular dysfunction are the feared complications of myocarditis or myopericarditis, and these are most closely associated with wall motion abnormalities and cardiac enlargement on echocardiography.
High-risk pericarditis patients include those with fever, a subacute onset (over weeks), a large pericardial effusion or signs of pericardial tamponade, trauma, abnormal left ventricular wall motion, use of anticoagulants and those who are immunocompromised (Lange and Hillis, 2004; Imazio et al., 2007; Imazio et al., 2010). Elevated troponin levels and radiographic evidence of cardiac enlargement may also help select high-risk patients who require same-day echocardiography.
When faced with the patient, young or old, with clinical and electrocardiographic signs of pericarditis, the key questions are: Is the heart enlarged? Is left ventricular dysfunction (myocarditis) present? Is there evidence of a pericardial effusion or tamponade? For these reasons, emergent or urgent echocardiogram is recommended in all patients presenting with acute pericarditis (Spodick, 1976; LeWinter, 2014; Klein et al., 2013; Cheitlin et al., 2003). Acute myocarditis can have a fulminant course. (See Chapter 5, The Electrocardiography of Shortness of Breath.)
The most important feature that differentiates acute STEMI versus acute pericarditis in a patient with chest pain and ST-segment elevations is the regional (anatomic) pattern. That is, in patients with STEMI, the ST-segment elevations usually correspond to a single coronary artery distribution, and there are ST-segment depressions in the opposite-facing leads.
In contrast, the ST-segment elevations in pericarditis are generalized and typically involve most of the precordial and limb leads. The only “reciprocal” ECG changes in pericarditis are in leads aVR and V1, where ST-segment depressions and PR-segment elevations are commonly seen. In addition, the ST-segment elevations in acute pericarditis usually do not exceed 5 mm, and they usually maintain their normal smooth, upward concavity.
Emergency clinicians should also examine the T-waves, PR-segments and QT interval:
In patients with acute STEMI, it is common to see ST-segment elevations and T-wave inversions in the same leads on the same tracing. This rarely occurs in acute pericarditis, as the T-waves typically do not become inverted for one or more days. In acute pericarditis, the ST- and PR-segments usually normalize before T-wave inversion is seen.
Tall, broad, bulky or “hyper-acute” T-waves should always raise concern for STEMI rather than acute pericarditis. In pericarditis, the T-waves are relatively “humble” relative to the ST-segment elevations. T-waves that “tower over” the R-waves in multiple precordial leads are likely to be “hyperacute,” signaling an acute STEMI.
PR-segment depressions are much more common in acute pericarditis, although they may occur in patients with acute myocardial infarction in the presence of atrial infarction.
QT-prolongation also favors acute STEMI.
The ST-T wave changes of acute STEMI evolve much more rapidly than the ST-T-wave changes of acute pericarditis.
A caveat: on rare occasions, an acute STEMI may involve the anterior and precordial leads. As discussed in Chapters 2 and 3, occlusion of a long “wraparound” LAD can result in a simultaneous ST-segment elevations in the anterior and inferior leads, which at times may resemble the global ST-segment elevations of pericarditis. As always, serial ECG tracings and echocardiography may be diagnostic.
It is not always possible to differentiate ERP from pericarditis, absent a clear and compelling history or a pericardial friction rub. However, clues are often present:
The ECG pattern of ERP tends to remain stable over time (although, as noted earlier, the ST-elevations and J-point elevation may fluctuate with the patient’s heart rate and autonomic nervous system balance, and the entire ERP pattern may disappear over a period of years).
Acute pericarditis almost always causes “global” ST-segment elevations, involving the precordial and limb leads equally. As noted earlier, the ST-segment elevations of ERP are usually widespread in the precordial leads, while they spare the limb leads in more than half of all cases.
The T-waves in ERP are unusually tall, and they may even appear peaked. In pericarditis, the T-waves are not so prominent; as noted earlier, they often appear “humble” relative to the elevated ST-segments. Later in the evolution of acute pericarditis (over a variable period of hours to days), the T-waves typically become inverted. In 1982, a paper was published in Circulation suggesting that the ratio of the ST-segment amplitude to the T-wave amplitude in lead V6 may help distinguish ERP from pericarditis. If the ST:T-wave ratio is ≥ 0.25, the diagnosis of pericarditis is virtually certain (with a positive and negative predictive value both, reportedly, of 100 percent (Ginzton and Laks, 1982)).
ERP is also more likely when there is sinus bradycardia or even AV block, reflecting heightened vagal tone (which may have a causal role).
The following ECG tracing has abnormal ST-segment elevations. Which is more likely – acute STEMI, pericarditis or ERP?
ECG 7.3 A 33-year-old man presented with chest pain and shortness of breath.
The ECG shows classic findings of acute pericarditis. There are global, concave-upward ST-segment elevations involving the precordial and limb leads. The T-wave is upright but is relatively small in lead V6 (the ratio of the ST-segment height:T-wave amplitude is greater than 0.25); this makes the diagnosis of pericarditis much more likely than ERP. And there is marked PR-segment depression in lead II and in other leads, accompanied by the expected PR-segment elevation in leads aVR and V1.
There is no localized, regional pattern to the ST-segment elevations, and there are no reciprocal ST-segment depressions (except for aVR and V1). Thus, acute STEMI is highly unlikely.
ST-segment elevations in the anterior precordial leads are characteristic of BER. But they are also characteristic of acute anterior wall STEMI. How do we tell one from the other?
In a widely cited article, Smith et al. described 171 emergency department chest pain patients with ERP and 143 patients with subtle, nonobvious anterior wall STEMI (Smith et al., 2012). When the ECGs were compared, a single (albeit complex) equation was derived that accurately predicted an anterior wall STEMI: [1.196 × ST-segment elevation 60 msec after the J-point in lead V3 in mm] + [0.059 × QTc in msec] – [0.326 × R-wave amplitude in lead V4 in mm]. If the value of this equation was ≥ 23.4, it predicted anterior wall STEMI with strong test characteristics. Importantly, J-point elevation, notching, T-wave amplitude and upward concavity of the ST-segments did not help in distinguishing ERP from STEMI.
Online calculators are now available to help clinicians diagnose subtle anterior STEMI and differentiate STEMI from ERP. These electrocardiographic predictors could also be incorporated into the ECG computer algorithms. However, the bottom line is that, in patients with anterior wall ST-segment elevations, an acute STEMI is more likely if the R-wave amplitude is lower, the ST-segment elevation is higher, and the QTc is longer.
As always, diagnostic accuracy is aided by comparing the presenting to ECG to baseline tracings, obtaining serial ECGs and performing echocardiography.
Here is an example. Does this patient have ERP, acute pericarditis or an acute anterior STEMI?
ECG 7.4 A 43-year-old woman with a history of hypertension and hyperlipidemia presented with substernal chest pain, nausea and shortness of breath over the prior 2–3 days. Her blood pressure in the emergency department was 108/78.
The patient presented with a compelling history, accompanied by hypotension. Her 12-lead ECG is compelling as well. There is sinus tachycardia. Also, the ECG demonstrates obvious ST-segment elevations in the anterior precordial leads (V2, V3 and V4), consistent with acute anteroseptal STEMI.
However, the QRS amplitude is low in the limb and precordial leads; combined with sinus tachycardia, this raises acute myocarditis as a possibility. To add to the confusion, there is PR-segment depression in numerous leads, which could indicate acute pericarditis (although PR-segment depression is also seen in the setting of a STEMI, attributed to atrial infarction).
Furthermore, can we exclude ERP, in light of the precordial lead ST-segment elevations? After all, the upward concavity of the ST-elevations is preserved, and there is marked J-point elevation with a “fish-hook” notch (for example, in V2, V3 and V4).
What is her diagnosis?
She has an acute anterior wall STEMI. The ST-segment elevations are regional, found almost exclusively in the territory of the LAD (precordial leads V2–V4). True, the ST-segment elevations in V2–V4 are concave upward, and there is even notching and J-point elevation; but as emphasized repeatedly, these features do not rule out acute STEMI. In addition, the ST-segment elevations are relatively dramatic when compared with the modest amplitude of the precordial lead QRS complexes.
This particular STEMI is not so subtle, so we may not need to deploy the Smith equation. Nonetheless, if we measure the R-wave amplitude in V4, the QTc and the height of the ST-segment in V3 and deploy the Smith equation, the result is ≥ 29, indicative of a STEMI.
This patient was taken immediately to the catheterization laboratory, where (not surprisingly) the LAD was totally obstructed in the middle segment. Normal flow was restored by percutaneous coronary angioplasty.
The electrocardiographic features of left ventricular hypertrophy (LVH) were discussed extensively in Chapter 6. On the ECG, LVH is likely in the presence of high-amplitude R-waves in the left-facing leads (I, aVL, V5 and V6) and deep S-waves in the right-sided leads. LVH is usually accompanied by repolarization abnormalities (the “strain” pattern): gradually descending ST-segment depressions are present in the left-sided leads, accompanied by asymmetric T-wave inversions. There are several supporting ECG criteria for LVH: (a) poor R-wave progression, (b) QRS widening, (c) left axis deviation and (d) left atrial enlargement (Pollak and Brady, 2012).
Chapter 6 included a detailed discussion of “LVH with repolarization abnormalities” because the ST-T-wave changes in the left-facing leads must be differentiated from other causes of ST-segment depressions and T-wave inversions, especially an acute coronary syndrome. ST-segment depressions may be reciprocal to an acute STEMI, or they may represent subendocardial ischemia (unstable angina or a non-STEMI).
This chapter has focused on ST-segment elevations that are not caused by an acute STEMI. There is a good reason to include LVH. Many patients who have electrocardiographic signs of LVH also have ST-segment elevations in the right precordial leads that can be indistinguishable from the current of injury of an acute anterior wall STEMI (Armstrong et al., 2012). The ST-segment elevations in the right precordial leads are a normal and expected finding in LVH; they likely represent a reciprocal change to the ST-segment depressions in V5 and V6. When the hypertrophied LV rotates leftward and posteriorly, the anterior precordial leads V1–V3 actually become “reciprocal” to V5 and V6 (Huang and Birnbaum, 2011; Pollak and Brady, 2012).
Unlike the ST-elevations of an evolving acute STEMI, the ST-segment and T-wave changes of LVH remain relatively fixed over time (although changes in lead placement and other factors can lead to changes in the 12-lead ECG). Thus, serial ECGs may prove invaluable. Still, the right precordial ST-segment elevations of LVH are a common reason for false-positive STEMI diagnoses, often resulting in unnecessary reperfusion interventions (Nable and Lawner, 2015; McCabe et al., 2012; Armstrong et al., 2012).
In LVH, the elevated ST-segments often retain a smooth, upwardly concave and benign-looking contour. But not always. The ST-segment elevations in leads V2 and V3 can look ominous, exactly like Wellens’ syndrome. Examples were provided in Chapter 6.
LVH with repolarization abnormalities is often so readily apparent on the 12-lead ECG that it prevents us from making other critical diagnoses. For example, Chapter 2, Inferior Wall Myocardial Infarction, included two examples of inferior wall STEMIs that were missed. Inferior wall STEMIs may be missed if the clinicians (and the computer) became so distracted by the diagnosis of LVH with strain that they never examine the rest of the ECG.