The electrocardiogram in the ACS patient: high-risk electrocardiographic presentations lacking anatomically oriented ST-segment elevation

a b s t r a c t

ST-segment elevation myocardial infarction \(STEMI\) is defined as pathologic ST-segment elevation occurring in at least 2 anatomically contiguous leads in a patient with a clinical presentation consistent with acute myocardial infarction (AMI); these findings can suggest the need for urgent revascularization. Unfortunately, the electrocar- diogram (ECG) may be nondiagnostic in a large portion of patients who initially present with AMI; furthermore, it is now recognized that ECG patterns that do not meet the traditional diagnostic criteria for STEMI may represent significant AMI–these patterns are generally referred to as the STEMI equivalent patterns in that they are caused by occlusion of an epicardial coronary artery, place significant portions of the left ventricle in jeopardy, and can result in a poor outcome if not recognized and treated appropriately.

(C) 2015


For many years, the electrocardiogram (ECG) has been one of the most useful diagnostic studies for the identification of patients with acute coronary syndrome and myocardial infarction (MI) [1]. Approxi- mately 600000 people experience their first MI annually, with the over- whelming majority of practitioners using the ECG as their initial tool to aid in the diagnosis and selection of therapies [2], illustrating the ECG’s pivotal position and extreme importance in the diagnostic evaluation of these patients.

Classically, ST-segment elevation myocardial infarction has been the most recognizable and well-known ECG pattern indicating sig- nificant myocardial ischemia and infarction [3]. STEMI is defined as a new ST-segment elevation at the J point in at least 2 anatomically contiguous leads of at least 2 mm (0.2 mV) in men or at least 1.5 mm in women in leads V2-V3 and/or of at least 1 mm (0.1 mV) in other contig- uous leads or the limb leads, in the absence of a Left bundle branch block, left ventricular hypertrophy, or other non-acute myocardial infarction (AMI) STE ECG presentation [4]. Unfortunately, the ECG may be nondiagnostic in nearly half of all patients who initially present with AMI [5]. It is now recognized that ECG patterns that do not meet the tra- ditional diagnostic criteria for STEMI may represent significant AMI–in fact, these patterns are generally referred to as the STEMI equivalent patterns in that they are caused by occlusion of an epicardial coronary artery, place significant portions of the left ventricle in jeopardy, and

* Corresponding author at: Department of Emergency Medicine, School of Medicine, University of Virginia, Charlottesville, Virginia 22908.

E-mail address: [email protected] (W.J. Brady).

can result in a poor outcome if not recognized and treated appropriate- ly. Fortunately, if recognized promptly, these high-risk ECG patterns to be discussed may aid clinicians in identifying lesser known presenta- tions of AMI or AMI-equivalent patterns [6].

This review focuses on the 5 of the more common, yet lesser known, high-risk ECG patterns in the ACS patient. These patterns are associated with larger AMI patterns and thus greater risk of poor outcome, including more frequent malignant dysrhythmia, higher rates of cardiogenic shock, stroke, and death, and worsened post-AMI lifestyle due to greater cardiac injury. This review is focused on the patterns most commonly encoun- tered; we sought to review the more common, high-risk patterns, thus alerting the clinician to their existence as well as their significance. Refer to Table 1 for a summary of these 5 high-risk ECG presentations.

First diagonal branch of the left anterior descending artery occlusion

Occlusion of the first diagonal branch of the left anterior descending artery presents with STE in leads aVL and V2, along with upright T waves in these leads and ST-segment depression (STD) with inverted T waves in the inferior leads. This pattern places a large portion of the left ventri- cle in jeopardy.

The left anterior descending artery is the most commonly identified coronary vessel occlusion resulting in AMI [7]. Recent re- search, however, has shown a correlation between characteristic ECG changes and occlusion of branches arising from this artery, which do not meet the classic definition of AMI with STE in 2 anatomically orient- ed leads. The first diagonal branch (D1) of the LAD supplies blood to the anterolateral wall of the left ventricle [8] as it courses diagonally over

0735-6757/(C) 2015

Table 1

Summary of the 5 discussed high-risk ECG presentations, including the entity, ECG findings, graphic ECG depiction, culprit coronary anatomy, and jeopardized cardiac segments

Abbreviation: PDA, posterior descending branch of either LCX or RCA.

these regions [7]. Approximately 90% of individuals have between 1 and 3 diagonal branches arising from the LAD, whereas only 1% have no such branches [8].

The first published study regarding identification of AMI resulting from D1 occlusion, considering the ECG findings, was published by Sclarovsky et al [9]. They identified 8 patients with occlusion of D1, all with ECGs showing STE 1 mm or more and an upright T wave in aVL and V2, STD and inverted T waves in leads III and aVF, and STD with up- right T waves in V4 and V5. In addition, 6 of these patients demonstrated STE and an upright T wave in lead I. During the same year, Iwasaki et al

[10] published a study with similar results. STE in lead I was demon- strated in all patients with D1 occlusions, compared to 50% to 80% of pa- tients with LAD lesions. This study also reported the presence of STE in lead aVL in all patients with D1 occlusions, compared to just 55% of pa- tients with LAD occlusions. Importantly, it must be stressed that this ECG presentation does not include 2 anatomically oriented leads with STE; rather, single leads with STE are seen in 2 nonanatomically (classi- ECG sign“–anterior wal”>cally, nonanatomic) oriented distributions.

A comparison of patients who demonstrated STE in aVL by Birnbaum et al [11] sought ECG features that could be used to identify patients with D1 lesions. In this study, patients with D1 lesions confirmed by cor- onary angiography demonstrated STE in leads aVL and V2, lacking STE in other leads. In addition, only 2 of 8 patients with confirmed D1 lesions demonstrated STE in other precordial leads, specifically lead V1. The

investigators also concluded that in the presence of STE in lead aVL and V2, a lack of STE in the other precordial leads results in an 89% pos- itive predictive value for MI of the anterior wall caused by a D1 lesion. Thus, STE in leads aVL and V2 can be the sole STE manifestations of a high-risk ECG presentation; such presentations can involve large amounts of myocardium in jeopardy situated in the anterior wall region of the left ventricle. Recognition and altered management of these le- sions in a more aggressive fashion can be indicated in certain situations. A representative example such a presentation is found in Fig. 1. This adult male patient presented with severe chest pain and significant di- aphoresis. The ECG revealed concerning STE in leads aVL and V2 as well as inferior STD. The “nonanatomical ECG presentation” did not meet traditional diagnostic criteria for STEMI. Yet, the emergency physi- cian interpreted the ECG within the context of a high-risk presentation, initiating care appropriate for ACS and urgently consulting cardiology.

At percutaneous coronary intervention (PCI), a 100% D1 lesion was noted and stented.

The “de Winter ECG sign”–anterior wall ACS event

The de Winter ECG sign includes upsloping STD in leads V1-V4 with tall, prominent T waves in the same distribution; Lead aVR demonstrates STE. This constellation of ECG findings is associated with proximal LAD occlusion and significant risk for anterior wall STEMI.

Fig. 1. Normal sinus rhythm with STE in leads aVL and V2 and STD in leads III and aVF. This ECG pattern is consistent with a first diagonal, or D1, lesion.

In 2008, de Winter and colleagues reported a case series describing a novel ECG pattern that was present in 2% of patients with acute LAD ar- tery occlusion [1]. A year later, Verouden et al [12] demonstrated this pat- tern with remarkably similar results (present in 2% of patients with acute LAD occlusion). This ECG pattern consisted of 3 defining features:

(1) upsloping STD greater than 1 mm at the J point in the precordial

(V1-V6) leads in the absence of STE; (2) the continuation of the STDs into tall, symmetric T waves; (3) STE (0.5-2 mm) [1,12] in lead aVR. Also of note, the latter study did reveal that the selected patients were more likely to be young males with coexisting hypercholesterolemia [12].

Although tall, symmetric T waves have previously been recognized as a transient feature indicative of impending STEMI and preceding STE in leads V1-V6 [13], the previously mentioned studies showed this novel ECG pattern to be present from the initial ECG until angiographic confirmation of the occluded LAD artery was obtained [1,12]. Immedi- ate resolution of this pattern was subsequently observed after PCI as well. This study is in contrast to a case report by Goebel et al [14], which documents a similar ECG pattern rapidly progressing to an overt anterior wall STEMI caused by a total mid-LAD occlusion. de Win- ter ECG sign also shares features of LAD lesions, which were reported in work done by Engelen et al [15]. In this study, STE in lead aVR was shown to be due to the presence of a proximal LAD occlusion in most of the cases present.

Although anatomic variations of the Purkinje fiber system leading to a conduction delay have been proposed as a possible explanation for the observed ECG pattern, the electrophysiological mechanism of this phe- nomena is still unknown [1]. In addition, studies have shown an absence

of STE during LAD Artery ligation of mice homozygous for a particular cardiac KATP channel, which alters intraventricular conduction [3]. Therefore, the de Winter ECG pattern may occur in part due to acute is- chemia causing inadequate activation of these KATP channels [1].

Regardless of its electrophysiologic basis, its presence in the setting of a patient with typical ACS symptoms and signs should alert the emer- gency physician to a high-risk presentation.

Fig. 2, in a 42-year-old man with chest pain, demonstrates STD with J-point depression in leads V2 to V5; prominent T waves are noted in leads V2 to V4; and last, STE is seen in lead aVR. Again, as seen in the case depicted in Fig. 1, the emergency physician noted the high-risk na- ture of the ECG findings occurring in the setting of a patient with concerning presentation. Appropriate therapy including urgent cardiol- ogy consultation was made with urgent PCI. A proximal LAD lesion was noted and successfully stented.

Widespread STD and STE in lead aVR–left main coronary artery (LMCA) occlusion

ST-segment elevation in lead aVR and/or widespread STD can indicate occlusion of the LMCA, a pattern that is extremely high risk. Sudden cardiac death is seen frequently in this ECG presentation; if the patient does not experience cardiac arrest, large anterolateral STEMI is likely encountered.

In most instances, the LMCA supplies approximately 75% of the left ventricular myocardium as it bifurcates into the LAD and left circumflex (LCx) arteries [16,17]. Although rare, acute occlusion of the LMCA is not

Fig. 2. Normal sinus rhythm with STD with J-point depression in leads V2 to V5; prominent T waves are noted in leads V2 to V4; and last, STE is seen in lead aVR. This ECG pattern is termed the de Winter finding and is consistent with a proximal LAD occlusion.

Fig. 3. Normal sinus rhythm with lead aVR STE and widespread STD in leads II, III, aVF, V4, V5, and V6. This pattern of ECG findings is consistent with LMCA occlusion.

infrequently accompanied by cardiogenic shock, pulmonary edema, life- threatening arrhythmias, and sudden cardiac death [18]. Unfortunately, many of these patients experience sudden cardiac death and do not sur- vive; thus, there is no ability to identify and treat these lesions.

In those patients who do not expire rapidly, prompt identification of LMCA stenosis is crucial for emergency physicians to avoid these possi- ble catastrophic consequences and select appropriate management strategies. Although a large number of patients with LMCA occlusion may present with typical STEMI patterns [17], it is important to recog- nize lesser known ECG patterns indicating the LMCA as the culprit ar- tery [19]. Two such ECG manifestations of LMCA occlusion are diffuse STD and “isolated’ STE in lead aVR, as seen in Figs. 3 and 4.

One of the earlier studies that considered ECG abnormalities associ- ated with LMCA occlusion was published by Dassen et al [20] in 1993. In this retrospective study, the investigators noted that STD in leads I, II, and V4-V6 and STE in lead aVR was present in 90% of patients with great- er than 70% stenosis of the LMCA on coronary angiography; these find- ings correlated with a 90% sensitivity for identification of the LMCA as the culprit artery. This study also revealed a cumulative amount of ST- segment deviation greater than 12 mm to be a sensitive marker for LMCA disease. Another investigation of 310 patients admitted to a cor- onary care unit that subsequently underwent coronary angiography yielded similar results. Kosuge and colleagues [21] found widespread STD 1.0 mm or greater to be present in 82% of individuals with 75% or greater LMCA stenosis, whereas only 49% of patients without significant

LMCA stenosis demonstrated this ECG pattern. The aforementioned study also revealed STE 0.5 mm or greater in lead aVR to be present in 78% and 14% of patients with and without LMCA stenosis respectively. Although the previously discussed studies searched for an ECG pattern to aid in the identification of LMCA occlusion, Taglieri et al [22] expand- ed on these results by investigating patients with ECGs showing wide- spread STD with and without STE in lead aVR for the prevalence of LMCA occlusive disease as confirmed by coronary angiography. The re- sults of this study concluded that widespread STD 0.5 mm or greater plus STE in lead aVR 0.1 mm or greater was present in a significantly larger proportion (P b 0.001) of patients with LMCA disease compared to those with widespread STD alone.

Lead aVR is frequently ignored during ECG interpretation, consid- ered by many physicians to provide only a mirror image of information shown by the left lateral leads [23]. Lead aVR, however, was initially de- veloped to provide further localizing information regarding the right upper portion of the heart, which includes the basal part of the septum [24]. The importance of lead aVR in relation to LMCA occlusion was ini- tially demonstrated after a group of investigators [25] hypothesized that the presence of lead aVR STE in LMCA occlusion may be due to septal is- chemia as was shown in previous studies of proximal LAD occlusion [15]. A retrospective study compared ECGs of patients with 3 different occlusion patterns, including LMCA, LAD, and right coronary artery [25]; this study demonstrated that 88% of patients with LMCA oc- clusion showed STE in lead aVR as compared to only 43% and 8% of

Fig. 4. Normal sinus rhythm with lead aVR STE and widespread STD in leads I, II, III, aVF, and V2 to V6. This pattern of ECG findings is consistent with LMCA occlusion.

Wellens syndrome–potential LAD occlus”>patients with LAD and RCA occlusions, respectively. Furthermore, this group determined STE in lead aVR >=V1 to have 81% sensitivity, 80% spec- ificity, and 81% accuracy for identifying the LMCA as the culprit artery. Whereas Yamaji and colleagues’ study included a small number of pa- tients, a subsequent study combining data from 3 separate clinical trials demonstrated STE in lead aVR to have 77.6% sensitivity, 82.6% specifici- ty, and 81.5% accuracy for prediction of LMCA occlusion. The high nega- tive predictive value (92.8%) calculated in this study also seems to indicate that an absence of STE in lead aVR may be a useful tool for the exclusion of LMCA occlusion [18].

Figs. 3 and 4 demonstrate widespread STD and STE in lead aVR. This constellation of findings, in the appropriate patient, can suggest LMCA obstruction. In both examples, the patients presented with concerning chest pain and were extremely ill appearing on examination. On the basis of the ECG findings, the patients were taken urgently to PCI with LMCA lesions noted and appropriately managed.

Wellens syndrome–potential LAD occlusion

Deeply inverted or biphasic T waves in leads V1-V4 can indicate proximal LAD occlusion in the patient with suspected ACS; these pa- tients are at extreme risk of progressing to anterior or anterolateral STEMI within a short period. Although many patients with ACS not resulting from MI are managed medically [26], it is important for the emergency physician to recognize certain electrocardiographic patterns that may indicate a preinfarction stage of acute coronary syndrome [27]. One such pattern is known as Wellens syndrome.

Wellens syndrome was first described by de Zwaan et al [26] in 1982 after this group recognized a specific ECG pattern in patients with unsta- ble angina who were found to be at high risk for the development of an- terior wall AMI. The results of this initial study revealed the ECG pattern to be present in 18% of patients admitted for unstable angina, with 75% of those patients who did not undergo a coronary revascularization pro- posterior wall MI”>cedure developing an anterior wall AMI within days to weeks of the ini- tial hospitalization. A larger, prospective study by the same group was then published in 1989, which showed the Wellens syndrome pattern to be present in 14% of patients admitted for unstable angina [28]. In both studies, all patients who underwent coronary angiography showed evidence of significant proximal LAD occlusion, whereas serum analysis revealed minimal, if any, elevation in cardiac biomarkers [26,28]. Thus, the investigators concluded that the ECG pattern of Wellens syndrome indicates a high-risk, preinfarction stage of ACS resulting from signifi- cant LAD stenosis.

The clinical description of Wellens syndrome is as follows [29]:

(1) active (or recent) anginal chest pain; (2) minimal or no cardiac bio- marker elevation; (3) absence of pathologic precordial Q waves;

(4) minimal or lack of STE (b 1 mm); (5) no loss of precordial R-wave progression; and (6) characteristic T-wave abnormalities. The T wave changes, being the most important diagnostic feature of Wellens syn- drome, consist of 2 distinct patterns in leads V2 and V3. The more com- mon abnormality (75% of cases) consists of deeply inverted and symmetric T waves, whereas the second subtype consists of biphasic T waves (25% of cases) [27]. In addition, 25 of 26 patients in the initial study showed these abnormalities in lead V1, with an additional 22 showing evidence of Wellens syndrome in V4-V6 [26].

Although an impending anterior wall AMI makes the identification of ECG abnormalities in Wellens syndrome essential to the emergency physician, the fact that there may be no other clinical signs of LAD dis- ease makes this distinction all the more important. In fact, most patients are pain free when the initial ECG is conducted, with Wellens T waves evolving into precordial STE in those who experience chest pain [29,30]. Another caveat is in order–in that many emergency depart- ment protocols for patients with “nonspecific” T-wave abnormalities culminate in the administration of an exercise or pharmacologic stress test [31], significant caution must be exercised in this type of presenta- tion. provocative testing can prove to have disastrous consequences, as is shown in a case report by Tandy et al [29], where a patient with Wellens syndrome had an AMI shortly after Stress testing was initiated. Therefore, it is important for an emergency physician to recognize the features of Wellens syndrome so patients may be referred for emergent coronary angiography [26,28].

In Fig. 5, a patient with recent chest pain presents with biphasic T- wave abnormalities in the anterior leads. The significance of the ECG findings was noted by the emergency physician resulting in cardiology admission and cardiac catheterization, which demonstrated proximal LAD occlusion and subsequent appropriate stenting.

Left ventricular posterior wall MI

Infarction of the posterior wall of the left ventricle is a significant form of AMI. Unfortunately, its ECG presentation is not infrequently missed. The presentation includes horizontal, or flat, STD in leads V1-V3 with Prominent R waves (V1 and V2) and upright T waves (leads V1 and V3).

In most individuals, the posterior wall of the left ventricle derives its Blood supply from arterial extensions termed the posterior descending artery. These distal arterial branches arise from either the RCA or the LCx

Fig. 5. Normal sinus rhythm with biphasic T wave abnormalities in leads V1 to V4. Biphasic refers to both upright and inverted T wave abnormalities in a single T-wave configuration. These

findings occur in the setting of Wellen syndrome and is consistent with proximal LAD occlusion.

Fig. 6. Normal sinus rhythm with STD in leads V2 to V4. In addition, prominent R waves are noted in leads V2 and V3 along with upright T waves in leads V2 to V4. These findings are con- sistent with acute posterior wall AMI.

artery, and are respectively termed right and left dominant patterns of circulation. In a smaller percentage of people, arterial supply of the posterior wall is shared by smaller branches of the RCA and LCx, a pat- tern known as codominant circulation [32]. Thus, posterior wall infarc- tion arises due to occlusion of either the RCA or the LCx. However, identification of posterior wall myocardial infarction (PMI) from the perspective of the 12-lead ECG often proves to be challenging, as this area of the left ventricle may not be adequately imaged using the tradi- tional approach of seeking STE and using standard leads. For this reason, it is believed that PMI is one of the most frequently missed ECG patterns representing AMI [33].

Although PMI often occurs in conjunction with acute lateral and/or in- ferior infarctions, ECG manifestations of isolated PMI include the follow- ing in leads V1-V4: (1) horizontal STD; (2) upright T waves; (3) a tall, wide R wave; (3) an R-to-S wave ratio of greater than 1.0 in lead V2 [32,33]. When observing this pattern, it is interesting to note the STD, tall R waves, and upright T waves seem to represent STE, Q waves, and inverted T waves seen when the classic STEMI pattern is flipped 180? [33]. Despite this, STD in the precordium is more typically seen in non- ST-segment elevation MI of the anterior wall of the left ventricle [34].

A prospective study by Boden et al [34] consisting of 50 patients with isolated STD greater than 1 mm in 2 or more consecutive precordial leads sought to identify ECG features that could help differentiate be- tween PMI and anterior non-MI ACS. This group noted significantly higher elevations in mean biomarker levels and a greater degree of pre- cordial STD in leads V1-V3 (P b .01) in the 40% of patients who were found to have PMI as compared to the remaining patients who were found to have only anterior non-MI ACS. Furthermore, all 23 patients in the PMI group were noted to have horizontal STD and upright T waves, whereas the remaining 27 patients had downsloping STD and T-wave inversions.

As was previously suggested, the diagnostic challenge posed by the identification of isolated PMI may warrant the use of expanded ECG tech- niques when the diagnosis remains in question. One such modality is the use of the 15-lead ECG, with posterior leads V7-V9 being placed on the fifth intercostal space at the posterior axillary, midscapular, and paraspinal lines of the posterior left thorax, respectively [35]. A study rep- licating posterior wall AMI, using temporary balloon occlusion of the LCx, demonstrated that posterior lead STE of 0.5 mm or greater (74% vs 38%) or 1 mm or greater (62% vs 34%) was very suggestive of acute myocardial infraction [36]. These additional posterior leads can aid in the diagnosis in certain presentation and should be considered by the clinician if the diag- nosis is in doubt based upon the 12-lead ECG [37].

Fig. 6 was obtained from a 54-year-old woman with chest discom- fort. The ECG demonstrates normal sinus rhythm with STD in leads V2 to V4. In addition, prominent R waves are noted in leads V2 and V3 along with upright T waves in leads V2 to V4. These findings are recog- nized as consistent with acute posterior wall AMI. The patient was taken to the catheterization laboratory, with PCI of a distal LCx artery oc- clusion successfully stented.


Although the STEMI pattern is the most widely known and easily identifiable ECG pattern indicating the presence of significant ischemia with impending infarction [3], it is important for the emergency physi- cian to recognize other high-risk ECG markers of ACS. Although these patterns do not always indicate a time-sensitive, high-risk ACS event, these findings can indicate a potentially more serious form of ACS. Through understanding and identification of these 5 discussed ECG pat- terns, practitioners may recognize high-risk patients who would other- wise be diagnostically “missed” or, at least, not managed in a time- and medically appropriate fashion.


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