For a long time the 12-lead electrocardiogram [ECG] was considered an essential part of the diagnosis and initial evaluation of patients with chest pain. Patients with ST elevation or new left bundle branch block are usually referred for immediate reperfusion therapy, whereas those without ST deviation or those with predominately ST depression are usually treated conservatively initially.1,2 Patients are diagnosed as having anterior, inferior-posterior, or lateral myocardial infarction based on the patterns of ST deviation and assessment of risk is usually based on simple crude measurements of the absolute magnitude of ST segment deviation or the width of the QRS complexes.3
However, there is much more information concerning the exact site of the infarct related lesion, prediction of final infarct size, and estimation of prognosis that can be obtained from the initial ECG without extra costs or time. Although some clinicians feel that with the increased use of primary coronary interventions in patients with ST elevation acute myocardial infarction this information is no longer needed, there are many instances in which even with immediate coronary angiography, identification of the infarct related site and estimation of the myocardial area supplied by each of the branches distal to the infarct related coronary artery occlusion is difficult. In some patients, more than one lesion may be found and identification of the acutely thrombosed lesion may not always be apparent. Figure 1 is an example of a patient with inferior acute myocardial infarction who underwent primary coronary intervention. Coronary angiography revealed complete obstruction of all three major coronary arteries. The culprit lesion was determined to be the left circumflex artery using both the angiographic and ECG criteria. In other cases, complete occlusion of side branches at bifurcation of coronary arteries may be completely missed during coronary angiography.
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Figure 1
A 54 year old man with two hours of chest pain. [A] The ECG shows ST elevation in the inferior leads and V6 and ST depression in I, aVL, and V1–V4. [B] Angiography of the left coronary artery revealed total occlusion of the left anterior descending [black arrow] and the left circumflex [white arrow] arteries. [C] Angiography of the right coronary artery showed complete occlusion of the artery.
It is important to appreciate that the ECG provides information about a totally different aspect of pathophysiology in acute myocardial infarction than does the coronary angiogram. Coronary angiography identifies vessel anatomy whereas the ECG reflects the physiology of the myocardium during acute ischaemia. For this reason, it is possible to observe severe coronary stenoses upon angiography without ECG evidence of acute ischaemia. Moreover, it is possible to observe restored vessel patency upon angiography with ECG evidence of ongoing ischaemia due to “no-reflow”, reperfusion injury, or myocardial damage that has already developed before reperfusion occurs. Thus, while coronary angiography remains the “gold standard” for identifying the infarct related artery, the ECG remains the gold standard for identifying the presence and location of acute myocardial ischaemia. Moreover, with current imaging techniques, including contrast ventriculography, echocardiography and radionuclide perfusion scans, differentiation of ischaemic but still viable from necrotic myocardium during the acute stage of myocardial infarction is impossible.
This review will concentrate on the information that can be obtained from the admission ECG in patients with ST elevation acute myocardial infarction. In particular, we shall discuss the association of various ECG patterns of the acute phase of myocardial infarction with estimation of infarct size and prognosis and the correlation of various ECG patterns and the underlying coronary anatomy. We shall concentrate mainly on the acute phase of myocardial infarction [ST segment elevation with upright T waves] in patients without intraventricular conduction defects.
FACTORS THAT DETERMINE PROGNOSIS IN ACUTE MYOCARDIAL INFARCTION [BOX 1]
The immediate prognosis in patients with acute myocardial infarction is inversely related to the amount of myocardial reserves [total myocardial mass less the myocardium involved in the present myocardial infarction [ischaemic area at risk], zones with scars due to previous myocardial infarction or fibrosis, and remote ischaemic myocardial segments supplied by critically narrowed coronary arteries]. Among patients without prior myocardial infarction and without major pre-existing stenotic lesions in the coronary arteries, prognosis is related to the size of the ischaemic myocardium supplied by the culprit coronary artery distal to the occlusion. However, among patients with low myocardial reserves due to previous myocardial infarctions or diffuse fibrosis, even relatively small infarction may be detrimental. Moreover, among patients with diffuse severe coronary artery disease, a small myocardial infarction may interfere with the delicate balance, and induce ischaemia in remote segments due to obliteration of collateral flow or due to the need for [compensatory] augmentation of contractility in the remote non-infarcted segments. Therefore, in addition to accurate diagnosis, there is a need for early estimation of the size of the ischaemic myocardium at risk and myocardial reserves.
Box 1: Variables that affect the immediate prognosis in acute myocardial infarction
Size of the ischaemic myocardium at risk.
The percent of the ischaemic myocardium at risk that has already undergone irreversible necrosis.
The “severity” of ischaemia [the expected rate of progression of myocardial necrosis].
Presence of old myocardial infarction or fibrosis [myocardial reserves].
Presence of “ischaemia at a distance” due to existence of stenotic lesions in other coronary arteries.
The ECG may help in assessing the size of the myocardial ischaemic area at risk, may help in differentiation between subendocardial and transmural ischaemia, and may assist in identifying the presence of previous infarctions [abnormal Q waves in leads not involved in the present infarction. For example, abnormal Q waves in the precordial leads in patient with inferior ST elevation].4 Furthermore, some ECG patterns may indicate presence of diffuse coronary artery disease and remote ischaemia.5–7
On admission, part of the myocardial area at risk [supplied by the culprit coronary artery lesion] usually has already undergone irreversible damage. The proportion of the ischaemic area at risk that has undergone irreversible necrosis depends on the total ischaemic time, and on the rate of progression of the wavefront of necrosis. The rate of progression of necrosis is highly variable and is dependent on the presence of residual perfusion via collateral circulation8 or incomplete or intermittent occlusion of the infarct related lesion,9 and various metabolic factors including “ischaemic preconditioning”.10 The severity of ischaemia, or the expected rate of progression of necrosis [if no reperfusion occurs immediately] should be assessed. It is plausible that immediate reperfusion will benefit especially patients with large ischaemic myocardium at risk that is still viable upon admission, but have “severe ischaemia” with relatively rapid rate of progression of myocardial necrosis.
ELECTROCARDIOGRAPHIC CHANGES DURING THE ACUTE STAGE OF ST SEGMENT ELEVATION MYOCARDIAL INFARCTION
Shortly after occlusion of a coronary artery, serial ECG changes are detected by leads facing the ischaemic zone [fig 2]: first, the T waves become tall, symmetrical, and peaked [grade I ischaemia]; second, there is ST elevation [grade II ischaemia], without distortion of the terminal portion of the QRS; and third, changes in the terminal portion of the QRS complex appear [grade III ischaemia].11–13 These changes include an increase in the amplitude of the R waves and disappearance of the S waves. These changes in the terminal portion of the QRS are explained by prolongation of the electrical conduction in the Purkinje fibres in the ischaemic region.14,15 The delayed conduction decreases the degree of cancellation, resulting in an increase in R wave amplitude in leads with terminal R wave and decrease in the S wave amplitude in leads with terminal S wave on the surface ECG.14–18 The Purkinje fibres are less sensitive to ischaemia than the contracting myocytes.19,20 Hence, for an alteration in the terminal portion of the QRS to occur, there should probably be a severe and prolonged ischaemia that would affect the Purkinje fibres.14,21 In patients with collateral circulation no changes were detected in the QRS complex during balloon angioplasty.16 Thus, absence of distortion of the terminal portion of the QRS, despite prolonged ischaemia, may be a sign for myocardial protection [probably by persistent myocardial flow due to subtotal occlusion or collateral circulation, or due to myocardial preconditioning]. Disappearance of the S waves in leads with terminal S [Rs configuration] [mainly leads V1–3] can be easily recognised [fig 3].
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Figure 2
The grades of ischaemia. In leads with usual Rs configuration [leads V1–V3]: grade I, tall symmetrical T wave without ST elevation; grade II, ST elevation without distortion of the terminal portion of the QRS complex; grade III, ST elevation with distortion of the terminal portion of the QRS [no S waves in leads V1–V3] [arrow]. In leads with usual qR configuration: grade I, tall symmetrical T wave without ST elevation; grade II, ST elevation with J point/R wave ratio 0.5 in leads III and aVF [see text].
Although the transition between the grades of ischaemia is gradual and continuous, for practical clinical purposes we found it convenient to define grade II of ischaemia as ST elevation ⩾0.1 mV without distortion of the terminal portion of the QRS, and grade III as ST elevation with distortion of the terminal portion of the QRS [emergence of the J point ⩾50% of the R wave in leads with qR configuration, or disappearance of the S wave in leads with an Rs configuration [figs 2–4].11,22–26 Only later, the T waves become negative, the amplitude of the R waves decreases, and additional Q waves may appear. However, only the minority of patients with acute myocardial infarction shows grade III ischaemia upon admission. While the underlying mechanism for this difference is still unclear, grade III ischaemia has large implications concerning prognosis, as will be discussed later.
DIAGNOSIS OF ACUTE MYOCARDIAL INFARCTION
In a patient with typical symptoms, presence of ST elevation, especially when accompanied with reciprocal changes, is highly predictive for evolving acute myocardial infarction. However, several investigators reported that the sensitivity of the ECG for acute myocardial infarction may be as low as 50%.27–30 In most of these studies only one admission ECG was analysed. Hedges et al used the admission and a second ECG performed 3–4 hours after admission and found serial ECG changes in 15% of the patients.31 However, continuous or multiple ECGs over time or during fluctuations in the intensity of symptoms were not performed. Such repeated recording may improve the ability to detect subtle ischaemic changes. Furthermore, as determined by independent reviewers, 49% of the missed acute myocardial infarctions could have been diagnosed through improved ECG reading skills or by comparing the ECG to an old, baseline recording.29 It should be remembered that acute myocardial infarction detected by raised creatine kinase MB levels or troponin I or T without ST elevation is not an indication for urgent reperfusion therapy. The only exception is new left bundle branch block. Menown et al studied the sensitivity and specificity of the admission ECG for diagnosing acute myocardial infarction by studying patients with [n=1041] and without [n=149] chest pain. The best ECG variables for the diagnosis of acute myocardial infarction were ST elevation ⩾0.1 mV in ⩾1 lateral or inferior lead or ST elevation ⩾0.2 mV in ⩾1 anteroseptal precordial lead. These criteria correctly classified 83% of subjects with a sensitivity of 56% and a specificity of 94%. Changing the degree of ST elevation greatly modified both the sensitivity [45%–69%] and the specificity [81%–98%]. The addition of multiple QRST variables [Q waves, ST depression, T wave inversion, bundle branch block, axes deviations, and left ventricular hypertrophy] increased specificity but improved overall classification only marginally.32
ESTIMATION OF THE SIZE OF THE ISCHAEMIC MYOCARDIUM AT RISK
The extent of regional wall motion abnormalities can be easily appreciated soon after admission by two dimensional echocardiography or left ventriculography. However, in both methods differentiation between old scars and the acutely ischaemic but viable zones is not always possible. Due to the effect of “stunning”, regional wall motion may persist for long periods of times after reperfusion occurred.33 Moreover, differentiation of transmural from subendocardial ischaemia/infarction is not always possible since akinesis may occur when only the inner myocardial layers are ischaemic.34
Several studies have tried to estimate the ischaemic area at risk or final infarct size with the admission ECG. In these studies, either the number of leads with ST deviation [elevation and/or depression]35–38 or the absolute amplitude of ST deviation3,35,38–40 were used. However, the results were conflicting. Aldrich et al studied patients with acute myocardial infarction who did not receive thrombolytic therapy.35 The best correlation between the final ECG Selvester QRS scoring system [an estimation of infarct size] and the admission ECG was found using the magnitude of ST elevation in leads II, III, and aVF in inferior myocardial infarction and the number of leads with ST elevation in anterior myocardial infarction.35 However, in patients who received reperfusion therapy there was only week correlation between the Aldrich score and either the ischaemic area at risk or final infarct size, as measured by pretreatment and predischarge technetium 99m [99mTc] sestamibi scans, respectively.37 The Aldrich formula was related more to the collateral score than to the ischaemic area at risk or final infarct size.37 Clemmensen et al reported a good correlation between the final Selvester score and the number of leads with ST elevation [r=0.70] in anterior myocardial infarction. However there was only a weak correlation in inferior myocardial infarction.36 Neither the magnitude of ST segment elevation in all leads nor the number of leads with ST elevation correlated with the final Selvester score in inferior myocardial infarction.36 Clements et al also reported only a weak correlation between myocardial area at risk [as assessed by 99mTc sestamibi scan] and either the number of leads with ST deviation, total ST deviation, total ST elevation, or total ST depression.38 The myocardial area at risk correlated modestly [r=0.58] with total ST deviation in anterior myocardial infarction, and with total ST depression normalised to the R wave [r=0.70] in inferior myocardial infarction. However, because of large standard errors [9%–15% of the left ventricle], these formulas for estimation of the myocardial area at risk cannot be used in the clinical setting for estimation of infarct size.38 Birnbaum et al showed that among patients with first anterior myocardial infarction, the correlation between either the number of leads with ST elevation or the sum of ST elevation and the extent and severity of regional left ventricular dysfunction [both at 90 minutes after initiation of thrombolytic therapy and at predischarge] was poor.41
All of these studies were based on the hypothesis that each lead represents the same amount of myocardium and that a similar size of ischaemic area in different locations of the left ventricle will result in similar magnitude of ST deviation in the same number of leads. However, the 12-lead ECG does not equally represent all myocardial regions. The inferior and anterior walls of the left ventricle are well represented, but the lateral, posterior, septal, and apical regions are relatively ECG silent.42,43 Moreover, ischaemia in opposed regions may attenuate or augment ST deviation. For example, in patients with ischaemia of the high anterolateral and inferior regions due to proximal occlusion of a dominant left circumflex coronary artery occlusion, attenuation of ST deviation in leads I, aVL, and the inferior leads may occur, whereas subendocardial high anterolateral ischaemia may augment ST segment elevation in the inferior leads. Posterior myocardial infarction is commonly associated with ST depression in the precordial leads V1–V3,44 whereas right ventricular infarction may cause ST elevation in leads V1–V2.45
In concomitant right ventricle and posterior myocardial infarction, the opposing forces may neutralise each other and therefore, no ST deviation may occur in these leads. Because different leads represent different areas of the myocardium, a different coefficient should probably be used for each lead, and even for each type of infarction. To overcome the unequal presentation of the myocardium by the different leads, another technique has been suggested.46,47 In this technique the maximal points of the Selvester score is given to each lead with ST elevation ⩾100 μV. The sum of these initial scores is considered to represent the percentage of the left ventricle that is ischaemic. This method was compared to thallium-201 perfusion defect in 28 patients [10 patients on admission and 18 patients on day 5 after reperfusion therapy].46 A good correlation was found between this potential Selvester score and the extent of thallium-201 perfusion defect [r=0.79, p3 predicted right coronary artery occlusion whereas a S:R ratio ⩽3 predicted left circumflex artery occlusion.122
A summary of the criteria to distinguish the culprit artery in inferior acute myocardial infarction is provided in box 2 and an example of the criteria is shown in fig 6.
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Figure 6
ECG of a patient with acute inferior myocardial infarction. [A] There is ST elevation in leads II, III, aVF, V5, and V6, and ST depression in I, aVL, V1–V3. Several criteria implicate the right coronary artery as the infarct related artery including: [1] greater ST elevation in lead III than in II, [2] greater ST depression in aVL than I, and [3] a S:R ratio >3 in aVL. There is also evidence for a larger than expected inferior infarction with extension to the lateral aspect of the cardiac apex [ST elevation in V5 and V6] and injury to the posterior wall [ST depression in leads V1–V3]. [B] Coronary angiography confirms complete occlusion of the right coronary artery. [C] After primary angioplasty, a dominant right coronary artery with a large posterolateral branch is revealed, which is in agreement with ECG findings of posterior and lateral wall infarct extension.
Diagnosis of inferior infarction extending to contiguous myocardial zones
Right ventricular myocardial zone
When right ventricular infarction occurs, it almost always occurs in the setting of inferior acute myocardial infarction. Although isolated right ventricular infarction has been reported, it is rare and occurs most often in patients with right ventricular hypertrophy.125 Multiple investigators have found that ST elevation in lead V4R is diagnostic of right ventricular infarction with sensitivities and specificities well over 90%.116,126,127 It is important to point out that ST elevation in the right precordial leads [for example, V4R] is most prominent in the early hours of inferior acute myocardial infarction and rapidly dissipates thereafter. Hence, the window of opportunity to diagnose right ventricular infarction using the ECG is limited and right precordial leads should be recorded immediately when a patient with ST elevation in the inferior leads presents to the emergency department.
As aforementioned, ST elevation in leads V1–V3 in a patient with acute inferior myocardial infarction is a manifestation of associated right ventricular infarction due to a proximal right coronary artery occlusion.45,104,105 Lopez-Sendon et al reported that the criterion of ST elevation in lead V4R greater than ST elevation in any of leads V1–V3 was a very specific sign of right ventricular infarction [specificity, 100%].128 However, this criterion was less sensitive [sensitivity, 78.6%] than ST elevation in V4R alone.128
Lateral apical myocardial zone
In patients with acute inferior myocardial infarction, ST elevation in leads V5 and V6 is thought to indicate extension of the infarct to the lateral aspect of the cardiac apex; however, there is as yet no direct evidence for this.129 The cause of such an extension may be occlusion of either the left circumflex or a right coronary artery with a posterior descending or posterolateral branch that extends to the lateral apical zone.129 Tsuka and coworkers found that ST elevation in lead V6 during inferior acute myocardial infarction was associated with a larger infarct size, a greater frequency of major cardiac arrhythmias, and a higher incidence of pericarditis during the patient’s hospital course.64
Posterior myocardial zone
In patients with acute inferior myocardial infarction, ST depression in leads V1–V3 has been shown by numerous investigators to indicate a larger infarction with extension of the injury to the posterolateral and/or the inferoseptal wall.44,50,54,57–59,95,97,130–135 Such ST depression in these “anterior” leads during acute inferior myocardial infarction is a reciprocal change and does not indicate concomitant LAD coronary artery disease.7,99 It is seen in both right coronary artery and left circumflex related inferior infarctions.43,136 However, in inferior myocardial infarction due to proximal right coronary artery occlusion with concomitant right ventricular infarction, posterior wall injury may be masked because the two opposed electrical vectors may cancel each other [that is, ST elevation in leads V1–V3 with right ventricular infarction and reciprocal ST depression in these same leads with concurrent posterior infarction].94
A more direct sign of posterior wall injury is ST elevation in leads V7–V9.65,137–139 However, waveform amplitudes in these posterior leads are lower than in standard precordial leads, presumably because the heart is situated more anteriorly in the chest and thus, is a greater distance from posteriorly placed electrodes. There is preliminary evidence that ST elevation of 0.5 mm should be considered a sign of injury when analysing the posterior leads.140 Isolated ST elevation in leads V7–V9 without ST elevation in the inferior leads occurs in only 4% of patients with acute myocardial infarction,139 and is usually due to left circumflex coronary artery occlusion.137 In patients with acute inferior myocardial infarction, ST elevation in leads V7–V9 is associated with a higher incidence of reinfarction, heart failure, and death.65
“Ischaemia at a distance” in acute inferior wall myocardial infarction
Patients with ST elevation in one myocardial zone often have concurrent ST depression in other myocardial zones. Such ST depression may represent pure “mirror image” reciprocal changes or may be indicative of acute ischaemia due to coronary artery disease in non-infarct related arteries [“ischaemia at a distance”]. Most of the ST depression patterns seen during ST elevation myocardial infarction represent reciprocal changes rather than ischaemia at a distance.82 However, one ECG pattern, ST depression in leads V5 and V6 in acute inferior myocardial infarction, does signify concomitant coronary artery disease of the LAD vessel with acute ischaemia in a myocardial zone remote from the infarct zone.5,7,99,141 Patients with maximal ST depression in leads V4–V6 during acute inferior myocardial infarction have higher morbidity and mortality compared with patients without precordial ST depression or with maximal depression in leads V1–V3.63 Likewise, patients with maximal ST depression in leads V4–V6 undergo multivessel revascularisation [multivessel percutaneous coronary interventions or coronary artery bypass surgery] more often than do patients without such an ECG pattern.141
DISCUSSION
The question might be posed, “Is it necessary for emergency physicians to have in-depth knowledge in assessing the ECG in patients with ST elevation myocardial infarction?” Three ECG assessments presented in this review that are especially relevant to the emergency department setting are the identification of: [1] right ventricular infarction accompanying acute inferior myocardial infarction, [2] a very proximal LAD coronary artery occlusion in anterior myocardial infarction, and [3] patients at higher risk, grade III of ischaemia or ST depression in V4–V6, indicating multivessel disease in inferior acute myocardial infarction. Moreover, it is crucial to recognise cases in which opposing ECG vectors cancel each other and result in attenuation of the ischaemic changes, such as occlusion of a proximal LAD that wraps the cardiac apex or a proximal dominant left circumflex artery. In terms of the first assessment, the opportunity to diagnose right ventricular infarction using the ECG is greatest in the emergency department because ST elevation in the right precordial leads resolves quickly. For example, in patients diagnosed with right ventricular infarction in the emergency department, it is not unusual to see isoelectric ST segments in the right precordial leads, despite continued ST elevation in the inferior leads, II, III, and aVF, by the time the patient is admitted to a hospital unit. Hence, emergency physicians should make certain that all patients with acute inferior myocardial infarction have a second ECG recorded with right ventricular leads. If ST segment elevation of 1 mm is observed in lead V4R, the diagnosis of right ventricular infarction can be made and no further right precordial ECGs need to be recorded. The reason it is important to identify patients with right ventricular infarction is that hypotension in these patients is usually caused by inadequate filling of the left ventricle by the poorly contracting right ventricle. Therefore, treatment should be aimed at augmenting ventricular filling by volume expansion and avoiding diuretics and nitrates. Such treatment is contrary to the treatment of cardiogenic shock due to pump failure, as occurs with large infarctions of the left ventricle.
Another ECG assessment of importance to emergency physicians is the identification of a very proximal LAD coronary artery occlusion in acute anterior myocardial infarction. If the infarct site is proximal to the first diagonal branch of the LAD artery, a large portion of the left ventricle is at risk for infarction including the anteroseptal, anterosuperior, anterolateral, and apical regions. Such high risk patients may require urgent transfer to the cardiac catheterisation laboratory for primary percutaneous coronary intervention or immediate treatment in the emergency department with a thrombolytic agent. Patients with grade III ischaemia on the admission ECG have a higher mortality22–24,142,143 and reinfarction rate.142,144 Retrospective analysis of the GUSTO IIb trial patients revealed that grade III ischaemia was associated with higher mortality both in the primary angioplasty group and in the thrombolysis group.142 In the grade II group, in-hospital mortality was similar in the thrombolysis and angioplasty subgroups [3.2% and 3.3%, p=0.941]. In patients with grade III, in-hospital mortality was 6.4% and 7.3%, respectively [p=0.762]. The odds ratio for the grade III group for death with thrombolysis was 2.06 [95% confidence interval [CI] 0.82 to 5.19; p = 0.125]; the odds ratio for primary angioplasty was 2.30 [95% CI 0.93 to 5.66; p = 0.07]. In the thrombolysis group, reinfarction occurred in 3.3% and 6.5% of the grade II and grade III subgroups [p=0.137]. In the angioplasty group, reinfarction occurred in 1.3% and 4.4%, respectively [p=0.239]. Thus, primary angioplasty reduced the risk of reinfarction in grade III as well as grade II patients, but did not reduce mortality. Currently we are comparing the clinical outcome of patients with acute myocardial infarction treated with primary angioplasty or thrombolytic therapy both in patients treated in hospitals with and without on site intervention facilities [the DINAMI 2 trial]. The decision to treat patients with early reperfusion therapy is the domain of emergency physicians, who therefore play a critical part in salvaging myocardium in patients with potentially extensive myocardial infarction.
There are two additional reasons for emergency physicians to become more skilled in the ECG assessment of patients with acute coronary syndromes. First, there is a growing trend for 12-lead ECGs to be recorded in the field by paramedics. Cellular telephone transmission of ECGs recorded in the field to the target emergency department is currently feasible. It is conceivable that emergency physicians will be involved in triaging patients in the prehospital phase to hospitals offering primary percutaneous coronary intervention, which is now recognised to be a superior reperfusion strategy, compared to thrombolytic therapy.145 Second, there is a growing trend for patients to be held for long periods of time in the emergency department because of a shortage of acute care hospital beds. Thus, the emergency department is becoming a critical care unit in many hospitals, requiring emergency physicians to be astute in the assessment of serial ECGs in the management of patients with acute coronary syndromes.
CONCLUSION
The admission ECG in patients with ST elevation acute myocardial infarction is valuable not only for determining who should and should not receive early reperfusion treatment, but also for providing information regarding the location and extent of acute myocardial injury. By reflecting the pathophysiology of the myocardium during acute ischaemia, the ECG conveys information unique from that of coronary angiography and provides important information to guide clinical decision-making.