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Acute myocardial infarction (MI) is a clinical manife station of coronary artery disease which develops when a blo od vessel is narrowed or occluded leading to irreversible myocardial ischemia [1]. The leading symptom that initiates the diagnostic and treatment cascade in patients with acute coronary syndrome is chest pain. In the United States, 50% of acute coronary syndromes have clinically atypical presentations (e.g. dyspnea, nausea, syncope or pain in the arm, neck or the abdomen) and the 12-lead electrocardiogram (ECG) maintains the gold standard as the first line test [2]. This is the single most important initial clinical test for diagnosing MI and its correct interpretation can be the basis for immediate therapeutic interventions. Based on ECG changes with persistent elevation of ST segment we can distinguish acute MI with ST elevation (STEMI) and non ST elevation MI (NSTEMI). In NSTEMI, the ECG abnormalities may include transient ST segment elevation, persistent or transient ST segment depression, inversion of the T-wave, flat T-waves, pseudo-normalization of the T-wave or it may be completely normal [3]. Sometimes, chest pain with the ECG signs of ischemia and high cardiospecific enzymes can have origins other than coronary, like in myopericarditis [4].



MI--myocardial infarction

STEMI--myocardial infarction with ST segment elevation

NSTEMI--non ST elevation myocardial infarction

pPCI--primary percutaneous coronary intervention

ESC--European Society of Cardiology

Current guidelines [3, 5] do not recommend urgent reperfusion therapy in patients with acute MI with ST depression, except in case of suspected isolated posterior MI. Standard STEMI criteria may overlook patients with atypical and recently described ECG patterns that may indicate risk of transmural MI (STEMI-equivalents) with obstructive coronary disease, who would benefit from primary percutaneous intervention (PCI). The European Society of Cardiology (ESC) Guidelines for the management of acute MI in patients with ST segment elevation [6] recognized atypical ECG presentations in patients with ongoing symptoms consistent with myocardial ischemia that should be performed in pPCI: bundle branch block, ventricular paced rhythm, isolated posterior infarction, and ischemia due to left main coronary artery occlusion in the presence of ST depression [greater than or equal to] 1 mm in eight or more surface leads (inferolateral ST depression), coupled with ST segment elevation in augmented vector right (aVR) and/or V1. These patients have high-risk STEMI equivalent patterns that should be recognized in the emergency department because they have a higher mortality rate compared to other patients with acute MI without ST elevation [7].

Clinical entities that represent the equivalent of acute MI with ST segment elevation described below are:

1. De Winter pattern

2. ST Elevation in aVR

3. Wellens syndrome

4. Isolated posterior MI

5. Presumed new left bundle branch block.

De Winter pattern

In 2008, in their study, Robert J. de Winter and Wellens pointed out the importance of recognizing the equivalents of acute MI with ST elevation and need for emergency reperfusion therapy. After analyzing data obtained from the database of PCIs, ECG on the first contact with the patient, ECG before treatment, findings of coronary angiography, they described ECG pattern found in approximately 2% of patients with angiography proven anterior MI with occlusion of the anterior descending coronary artery [8]. Diagnostic criteria for de Winter pattern are: tall, prominent, symmetrically peaked T-waves in the precordial leads, upsloping ST segment depression > 1 mm at the J-point in the precordial leads, absence of ST elevation in the precordial leads, ST segment elevation (0.5 mm-1 mm) in aVR. Normal STEMI morphology may precede or follow the de Winter pattern. Unlike the hyper-acute T-waves which occur within minutes of coronary artery occlusion and progress rapidly to classical ST elevation MI, STEMI pattern, de Winter T-waves are not transient findings and remain present in subsequent ECGs (Figure 1).

Verounden et al. found de Winter pattern in 35 out of 1890 patients who needed PCI on the proximal left descendent artery (in about 2% of patients). Patients with de Winter pattern were younger, more often male and with a higher incidence of hypercholesterolemia compared to classic MI with ST elevation [9]. The available data suggest that this pattern has a high positive predictive value for acute coronary occlusion [10].

Many case reports confirmed the importance of early recognition of this STEMI equivalent and early reperfusion therapy [11-13].

ST elevation in aVR

Occlusion of the left main coronary artery is a clinical entity that results in the development of acute MI in the anterior or anterolateral region with cardiogenic shock and high mortality rate. Because of the high risk of potential complications and high mortality, early detection of this type of STEMI equivalent and urgent reperfusion is imperative and provides better outcomes [14, 15].

ECG criteria are: ST segment elevation in aVR [greater than or equal to] 1 mm, ST segment elevation in aVR [greater than or equal to] V1, and diffuse ST segment depression in lateral leads (subendocardial ischemia) [16] (Figure 2).

ST segment elevation in aVR is not always specific for the occlusion of the left main coronary artery. It can be indicative for: left main equivalent disease (significant disease of the left anterior descending and left circumflex artery), occlusion of the anterior descending artery, severe three vessel disease and diffuse transmural ischemia [17, 18]. The absence of ST segment elevation in aVR excludes a significant lesion in the left main coronary artery. American Heart Association/American College of Cardiology recommended this pattern to be read as "ischemia due to multivessel or left main coronary artery obstruction".When the resting ECG reveals ST segment depression greater than 0.1 mV (1 mm) in 8 or more body surface leads coupled with ST segment elevation in aVR and/or V1, but is otherwise unremarkable, the automated interpretation should suggest ischemia due to multivessel or left main coronary artery obstruction [3].

Some authors argue that the term "occlusion of the left main coronary artery" is incorrect, firstly because most patients with criteria for this clinical entity have at least slight flow through the main trunk of the left coronary artery, and secondly, occlusion quickly leads to acute MI with ST segment elevation, cardiogenic shock and death [19]. The lack of specificity of this pattern is documented by Knotts et al. because only 43% patients with subendocardial ischemia (ST elevation in aVR and diffuse ST depression) who underwent angiography had significant left main stenosis or a triple vessel disease [20]. Nevertheless, current guidelines recommend early reperfusion strategy for patients presenting with this pattern [3, 6].

Wellens syndrome

Wellens syndrome was first described in the 1980s by de Zwaan, Wellens, et al, who identified specific T-wave changes in precordial leads in 14% to 18% of patients with unstable angina who, subsequently, developed a large anterior wall MI [21]. Some of risk factors for this syndrome are diabetes mellitus, family history of premature heart disease, hypertension, hypercholesterolemia and metabolic syndrome. Wellens syndrome describes ECG changes in T-wave, particularly deeply inverted or biphasic T-waves in leads V2-V3 that is highly specific for significant proximal stenosis of the left anterior descending artery. Patients with these ECG patterns can be without subjective symptoms at the time of recording ECG and have normal or slightly elevated cardiac enzymes. They are at high risk for developing acute large anterior MI in the next few days or weeks if they are on medical treatment only. As soon as the diagnosis is made or suspected, due to possible critical stenosis of the anterior descending artery, definitive treatment is cardiac catheterization with PCI [22].

Reinhardt et al. [23] described the following diagnostic criteria for Wellens syndrome:

1. ECG: deeply inverted T-waves in leads V2-V3 (may also be seen in leads V1, V4-V6) or biphasic T-waves (with initial positivity and terminal negativity) in V2 and V3; isoelectric or minimally elevated ST segment < 1 mm; preservation of precordial R wave progression and no precordial Q waves;

2. Clinical: recent history of angina, ECG pattern present in a pain-free state, normal or slightly elevated cardiac markers.

Wellens syndrome has two patterns of T-waves. In type A, T-waves are biphasic, with initial positivity and terminal negativity, present in approximately 25% of cases. Type B T-waves are deeply and symmetrically negative and are present in approximately 75% of cases. The T-wave abnormalities may be persistent for hours to weeks, even when the patient is pain-free [24] (Figures 3 and 4).

The mechanism of Wellens syndrome remains unclear. It is believed that the changes in T-wave are caused by ischemic changes of anterior myocardial wall after sudden occlusion or subocclusion of the anterior descending artery. Reperfusion of the anterior descending artery relieves the pain and identified T-wave changes as a reflection of reperfusion, form biphasic or negative T-waves. If the coronary artery remains occluded, acute anterior wall with ST elevation develops [25]. These ECG changes are not characteristic and limited to anterior MI, but can be seen in MI of the inferior or lateral wall, with occlusion of the right or circumflex coronary artery or in the vasospasm, and it is described as cocaine-induced vasospasm coronary artery [26].

Differential diagnosis of Wellens syndrome includes: pulmonary thromboembolism, right bundle branch block, left ventricular hypertrophy, right ventricular hypertrophy, hypertrophic cardiomyopathy, Brugada syndrome and hypokalemia [27].

Isolated posterior MI

Posterior MI is a clinical entity that occurs in 15 - 20% of cases of acute MI with ST segment elevation, usually in combination with inferior or lateral MI, while isolated posterior infarction is only found in about 5% of all ST elevation MIs [28], and it is an indication for urgent coronary reperfusion. The ECG findings of a posterior wall MI are different than the typical ST segment elevation seen in other MIs [29]. However, the absence of ST elevation in the standard ECG can lead to missed diagnosis and these patients do not receive reperfusion therapy, the only proper treatment in the acute phase of infarction. About 90% of these patients have critical stenosis or occlusion of the right coronary artery, and 10% of the left coronary artery [30].

There is a high degree of suspicion for posterior MI when the following findings are persisting in the standard ECG: ST segment depression (horizontal, upsloping, downsloping) and prominent upright R wave (> 30 ms) in V1-V3 leads (can be equal voltage of R and S wave in V1), the R/S ratio > 1.0 in V2 lead, combination of horizontal ST segment depression with a prominent R-waves in leads V1-V3. Usually, coexistence of acute inferior and/or lateral MI can be seen [31]. To confirm the diagnosis, extra posterior leads can be used (V7-V9) [32]. Lead V7 is on the left posterior axillary line in the fifth intercostal space, lead V8 on the left side of the back at the tip of the scapula and V9 on the left paraspinal line in the fifth intercostal space) [33]. The use of additional posterior chest wall leads (V7-V9) in patients with high suspicion of posterior MI (with circumflex occlusion) should be considered, in order to increase the number of diagnosed MIs, leading to better risk assessment, prognosis and survival, due to reperfusion therapy.

From the last ESC guide for acute MI with ST elevation, posterior infarction is confirmed with the presence of ST segment depression [greater than or equal to] 0.5 mm in leads V1-V3 and ST segment elevation [greater than or equal to] 0.5 mm in posterior leads (V7-V9), and prompt primary percutaneous coronary intervention strategy is recommended in patients with ongoing symptoms consistent with myocardial ischemia [6] (Figure 5).

New or presumed new left bundle branch block

ST segment criteria for the diagnosis of acute ischemia are affected by the presence of the left bundle branch block, because of the presented secondary ST changes that occur in this pattern. Left bundle branch block presents a dilemma in the evaluation of chest pain [34]. ECG diagnosis of MI in this pattern is difficult, but possible. The third universal definition of MI [35] gives diagnostic criteria for MI: rise and/or fall of cardiac biomarker values plus symptoms of ischemia, or new or presumed new significant ST segment T-wave changes, or new left bundle branch block. So, new or presumed new left bundle branch block in symptomatic patients is recognized as a STEMI equivalent. Neeland et al. [36] found that only about 40% of patients with presumed new left bundle branch block had a culprit lesion on angiography, and new or presumed new left bundle branch block cannot be a diagnostic criteria "per se", especially not for prompt percutaneous coronary intervention strategy.The American Heart Association/American College of Cardiology/Heart Rhythm Society Guide [3] recommends to think about the possibility of acute infarction in patients with left bundle branch block who have some of ST segment changes: ST segment elevation [greater than or equal to] 0.1 mV (1 mm) in leads with a positive ventricular depolarization (QRS), or ST depression [greater than or equal to] 0.1 mV (1 mm) in leads V1-V3 (concordant ST segment changes), ST segment elevation [greater than or equal to] 0.5 mV (5 mm) in leads with negative QRS complex (discordant ST segment changes). The same criteria are used in ESC guidelines for the management of acute MI in patients presenting with ST segment elevation, with a suggestion for patients with a clinical suspicion of ongoing myocardial ischemia and left bundle branch block to be managed in a way similar to STEMI patients [6] (Figure 6).

Sgarbossa criteria [37] are a set of ECG findings generally used to identify MI in the presence of a left bundle branch block or a ventricular paced rhythm, in order to increase the number of early diagnosed MIs and perform prompt reperfusion. Three included criteria are: ST elevation [greater than or equal to] 1 mm in a lead with positive QRS complex (concordance) - 5 points, concordant ST depression [greater than or equal to] 1 mm in leads V1, V2, or V3-3 points, and ST elevation [greater than or equal to] 5 mm in a lead with negative (discordant) QRS complex - 2 points: [greater than or equal to] 3 points = 90% specificity of STEMI. In the original Sgarbossa criteria, a score < 3 is typically not considered diagnostic of acute MI, but it also does not rule it out. In a review of ventricular-paced ECGs, the most clinically useful Sgarbossa criterion in identifying acute MI was ST segment elevation > 5 mm discordant with the QRS complex and it is helpful in identifying patients who may ultimately benefit from early aggressive treatment strategies [38].

Smith et al. modified Sgarbossa original criteria replacing the ST elevation measurement [greater than or equal to] 5 mm in the third component with a ST/S ratio less than -0.25, greatly improving the diagnostic utility of the rule. Using these criteria resulted in good prediction for acute coronary occlusion: at least one lead with concordant ST elevation [greater than or equal to] 1 (Sgarbossa criterion 1) or at least one lead of V1-V3 with concordant ST depression [greater than or equal to] 1 (Sgarbossa criterion 2) or ST/S ratio [less than or equal to] - 0.25 and at least 2 mm of ST elevation (replaces Sgarbossa criterion 3) [39].


In everyday clinical practice, especially in emergency room settings, it is very important to think about the possibility of having patients with chest pain and atypical electrocardiographic presentations of myocardial infarction with ST elevation and with coronary artery occlusion. In these patients, with clinical presentation of ongoing myocardial ischemia, a primary percutaneous coronary intervention strategy should be indicated to prevent complications and mortality, because these patients are at higher risk than others with uncomplicated myocardial infarction with ST elevation.


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Jadranka DEJANOVIC (1, 2), Anastazija STOJSIC MILOSAVLJEVIC (1, 2), Milos TRAJKOVIC (1), Tanja POPOV (1, 2) and Aleksandra ILIC (1, 2)

Institute of Cardiovascular Diseases of Vojvodina, Sremska Kamenica (1)

University of Novi Sad, Faculty of Medicine Novi Sad (2)

Review article

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Author:Dejanovic, Jadranka; Milosavljevic, Anastazija Stojsic; Trajkovic, Milos; Popov, Tanja; Ilic, Aleksa
Publication:Medicinski Pregled
Date:Jul 1, 2018

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