Diagnostics

The evolution of electrocardiographic changes in ST-segment elevation myocardial infarction

Jose Victor Nable BS, William Brady MD?

Department of Emergency Medicine, University of Virginia, Charlottesville, VA 22908, USA

Received 24 May 2008; accepted 25 May 2008

Abstract Acute myocardial infarction (AMI) is a not uncommon diagnosis in the emergency department. During ST-segment elevation AMI (STEMI), the electrocardiogram (ECG) typically follows a progression of abnormality, beginning with Hyperacute T waves and culminating with ST-segment elevation; pathologic Q waves can appear early and/or late in the process. Other findings include T-wave inversion and ST-segment depression which can occur before, during, or after the STEMI event. The evolution of ECG through these changes can occur rapidly after coronary artery occlusion. The emergency physician should be aware of the ECG findings that characterize the evolution of an STEMI with a sound understanding of the associated pathophysiology and clinical implication. This review discusses the changing ECG during an AMI. The pathogenesis of these findings is discussed. Finally, the clinical implications at each stage are reviewed.

(C) 2009

Introduction

ST-segment elevation acute myocardial infarction (STEMI) is a not uncommon diagnosis in the emergency department (ED). Approximately 5% of all ED visits in the United States in 2000 were for chest pain, with a range of 5% to 15% of those patients ultimately found to have an acute myocardial infarction (AMI) [1]. The American College of Cardiology/American Heart Association has published guidelines that state that a 12-lead electrocardiogram should be performed on a patient presenting to the ED with chest pain within 10 minutes of arrival [2]. Obtaining and interpreting the ECG is an important step in determining further diagnostic evaluation and therapeutic plan.

Although the classic presentation of STEMI involves elevation of the ST segment, a STEMI actually exhibits a sequence of temporally evolving ECG changes (Fig. 1A-C).

* Corresponding author.

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

Without therapeutic intervention, the ECG typically pro- gresses, beginning with hyperacute T waves, ST-segment elevation, Abnormal Q waves, T-wave inversion, and finally, normalization of the ST segment [3,4]. These changes begin rapidly after coronary artery occlusion. Conversely, bio- chemical markers such as cardiac troponin or creatine kinase-MB may not be detected for several hours [5].

Changes in the ECG during an evolving STEMI reflect differences in the electrical vectors representing depolari- zation and repolarization when compared to monitoring a normal heart. This difference may be increased due to changes in action potential activity in ischemic tissue adjacent to the infarct, known as stunned myocardium [6]. The electrically silent infarcted areas also affect the electrical vectors [7]. These variations in vectors ultimately lead to ST-segment and T-wave abnormalities during an evolving AMI.

The emergency physician should be aware of the ECG findings that characterize the evolution of an AMI. This review discusses the changing ECG during an AMI. The

0735-6757/$ - see front matter (C) 2009 doi:10.1016/j.ajem.2008.05.025

electrocardiographic findings“>pathogenesis of these findings is discussed. Finally, the clinical implications at each stage are reviewed. Although this review will highlight some of the key features of the classically evolving AMI, the physician should remain aware of the importance of interpreting the ECG within the context of the clinical situation. For example, hyperacute T waves in an elderly patient with Multiple comorbidities should raise a higher level of suspicion for an AMI than the same ECG finding in a 20-year-old patient without any medical history to suggest coronary artery disease. The ECG is an important diagnostic tool, but the physician should not base Clinical impressions solely on its findings.

Hyperacute T waves

Electrocardiographic findings

The T wave signifies ventricular repolarization. A relative increase in the amplitude of the T wave is the earliest stage of an evolving STEMI, occurring within the first few minutes of coronary Arterial occlusion [8]. Studies involving ligation of a coronary artery have shown that hyperacute T waves may develop as soon as 2 minutes after disrupting coronary perfusion [4]. Because of the Rapid progression from the hyperacute T wave to frank ST segment elevation (Fig. 1A and B), patients often present to the ED already with significant abnormality of the ST segment.

Morphological characteristics of hyperacute T waves vary greatly (Fig. 2A and B). While the amplitude may be large in typical hyperacute T waves, some T waves may simply appear “domed” when compared to previous ECG tracings [9]. The hyperacute T wave, a short-lived structure which evolves rapidly on to ST-segment elevation, is often asymmetric with a broad base (Fig. 2A and B); these T- waves are also associated not infrequently with reciprocal ST segment depression in other electrocardiographic leads. Such a finding on the ECG is transient in the AMI patient; progressive ST-segment elevation is usually the typical pattern encountered. As the infarction progresses, the hyperacute T-wave evolves further into the giant R wave, yet another transient structure (Fig. 1A and B).

If the patient has had previous myocardial damage resulting in T-wave inversion, the first sign of an evolving STEMI may in fact be paradoxical normalization of the T wave [10]. These patients may appear to have a normal ECG when first presenting with chest pain. It is, therefore, the relative increase in positive amplitude-rather than absolute height-that signifies hyperacute T waves.

Pathogenesis

The exact mechanism for hyperacute T waves has yet to be elucidated [11]. One theory is that the repolarization time

of ischemic tissue is prolonged due to a delay in recovery [4]. Ischemia during an evolving AMI first occurs in the endocardium. Because repolarization progresses from the epicardium to the endocardium, prolonged repolarization of the epicardium causes an increased repolarization vector in the same direction as a normal heart, resulting in an increase in the amplitude of the T wave.

Investigators have found that delayed repolarization due to ischemia has been attributed to stunned myocardium [6]. In stunned myocardium, adenosine triphosphate stores have been depleted and concentrations of electrolytes such as calcium are abnormal [12]. These changes within ischemic cells ultimately prolong repolarization time.

Clinical implications

Earlier diagnosis of a STEMI has been found to be one of the most significant modifiable factors in determining the amount of benefit from reperfusion therapy [13]. With the presence of hyperacute T waves often being the earliest ECG change found in an evolving STEMI, it is a significant diagnostic finding because it can indicate an approximate timing of the onset of coronary occlusion. Because hyperacute T waves represent ischemia without necrosis, intervention at this earliest stage of the STEMI may prevent infarction, resulting in improved outcome than therapy begun in later stages of the evolving AMI [4].

The finding of hyperacute T waves without other abnormalities on ECG likely will have no associated increase in cardiac serum markers such as troponin or creatine kinase-MB [14]. By the time ST-segment elevation is seen on the ECG, injury to myocardium has already begun. Therapy initiated early enough to prevent the progression from hyperacute T waves to ST-segment elevation may therefore prevent morbidity associated with an AMI. Furthermore, because ECG changes occur before increases in cardiac enzymes, the ECG is an important diagnostic and risk stratifying tool in the ED.

The differential diagnosis of hyperacute T waves include an early STEMI, hyperkalemia, benign early repolarization, and left ventricular hypertrophy. Along with clinical features that should raise suspicion for an AMI, such as chest pain, age, and comorbidities, the ECG findings can often be used to focus this differential. For example, the narrow T waves in hyperkalemia are more likely to have a peaked and symmetric appearance compared to STEMI [11]. Benign early repolarization tends to have characteristic findings in addition to the heightened T waves, such as ST-segment elevation with an initial upward concavity as well as notching or slurring at the end of the QRS complex[15]. Left ventricular hypertrophy, however, should be considered if the ECG demonstrates a strain pattern with ST-segment depression and T-wave inversion in the lateral leads; a QS pattern with ST-segment elevation in leads V₁, V₂, or V₃; and voltage criteria with a total amplitude of 35 mm between the S wave in V₁ and the R wave in V₅ or V₆ [11,16].

ST-segment elevation

Electrocardiographic findings

The ST segment represents the intervening period between ventricular depolarization and repolarization. There are various criteria used to classify abnormally

elevated ST segments indicating significant myocardial ischemia. One study examined the accuracy of the Minnesota code 9-2, which defines ST-segment elevation as 1-mm elevation in at least 1 inferior or lateral lead, or 2-mm elevation in at least 1 anterior chest lead. Investigators found that such criteria was 94% specific for an AMI, with a sensitivity of only 56% [17].

Fig. 2 A, Prominent, or hyperacute, T waves of early STEMI. Note the large amplitude, broad base, and asymmetric configuration. B, Prominent, or hyper-acute, T waves of early STEMI. Note the large amplitude, broad base, and asymmetric configuration. Also note the initial ST-segment elevation in leads V₂ and V₃.

The morphology of ST-segment elevation may also provide a clue to the diagnosis of AMI (Fig. 3A). A study by Brady et al [18] found that a majority of STEMI patients presented with ST segments demonstrating convex, or nonconcave, morphology. Convex morphology was found to be 97% specific for STEMI [18]. The morphology of the ST segment during a STEMI may also evolve from concave, to straight, and finally to convex [4]. Patients who continue to have a convex morphology after reperfu- sion therapy have worse morbidity in terms of left ventricular ejection fraction [19]. Although morphology is an important diagnostic indicator, the clinician should be aware that physicians often disagree when analyzing the morphology of the ST segment. One study in which

3 emergency physicians were asked to describe the morphology of the ST segment of patients with ST segment elevation found disagreement in 8% of patients [20].

Furthermore, the ST-segment elevation may be more subtle for infarctions involving the inferior and lateral walls

(Fig. 3B). Circumflex artery occlusion in one study produced ST-segment elevation in only 32% of patients, with left anterior descending and Right coronary artery stenosis causing ST-segment elevation in 84% and 92%, respectively [21]. In patients with circumflex arterial occlusion, subtle or absent changes in ST-segment eleva- tion may result in a missed diagnosis. In other situations, the ST-segment elevation can be very obvious (Fig. 3C and D). Refer to Fig. 3E to H for various examples of STEMI of the inferior, lateral, anterior, and posterior walls of the left ventricle.

Pathogenesis

There are several theories proposed to explain ST- segment elevation in AMI. The diastolic current theory suggests that incomplete repolarization of ischemic myocardium results in a more negatively charged surface of cells when compared with normal tissue [22]. Because

Fig. 1 A, Progression of electrocardiographic abnormalities in the STEMI patient. At 12 and 18 minutes in this scenario, the T wave enlarges with development of the hyperacute, or prominent, T wave. At 18 and 24 min, the ST segment elevates and, along with the prominent T wave, assumes a progressively larger complex, ultimately forming the giant R wave (a combination of the prominent T wave along with significant ST segment elevation) at 28 min. Here at 50 min, obvious ST-segment elevation is seen and is the most frequently encountered finding in the STEMI patient with diagnostic ECG on presentation. In certain patients, the Q wave can develop. Persistent ST-segment elevation after the STEMI can indicate LVA. Note that these times listed here are not absolute; significant patient variation is seen in the clinical arena. B, Electrocardiographic findings in the STEMI patient, ranging from the early presentation with either normal or prominent T wave to obvious ST segment elevation. C, The ECG can rapidly evolve in patients with acute coronary syndrome progressing to STEMI. Here, a middle-aged male presents to emergency medical service with chest pain; the initial ECG demonstrates nonspecific abnormalities; within 15 minutes time during transport, the ECG demonstrates significant inferior ST segment elevation, consistent with inferior wall STEMI.

Fig. 3 A, Different morphologies of ST-segment elevation in STEMI. a, Convex morphology. b, Obliquely straight morphology. c, Concave morphology. B, Subtle anterolateral STEMI. Note the minimal ST segment elevation in leads V₃ to V₆. The magnitude of the elevation is minimal yet the morphology of this elevated ST segment is concerning - it is obliquely straight in shape. C, Obvious extensive STEMI of the anterior, inferior, lateral, and posterior regions. The degree of ST segment elevation is extreme in the inferior leads. D, Lead III in an inferior wall STEMI with R-on-T event producing ventricular tachycardia. E, Inferior wall STEMI. F, Inferoposterolateral STEMI. G, anterior STEMI. H, Extensive anterolateral STEMI. I, Electrocardiographic differential diagnosis of ST-segment elevation. J, Pathologic Q waves with persistent ST segment elevation 3 weeks after anterior wall STEMI, indicative of LVA.

Fig. 3 (continued).

the normal myocardium has completely repolarized during diastole, an electrical gradient develops, and current flows from ischemic areas towards normal areas. This current causes a negative electrical potential surrounding the heart during diastole, thus depressing the TQ segment. When the ventricular myocardial cells completely depolarize during systole, no electrical

potential is detected, and the ECG records a relatively more positive voltage than baseline. This theory then supposes that ST-segment elevation is actually a mani- festation of a downward shift of the baseline voltage. Because the ECG records relative changes in voltage, however, the TQ segment remains at normal baseline while the ST segment elevates [23].

Fig. 3 (continued).

Another hypothesis to explain ST-segment elevation is early repolarization. Injured myocardium has demonstrated accelerated repolarization [24]. This systolic current theory proposes that the faster repolarization of ischemic cells again results in an electrical gradient, causing current to flow towards the ischemic areas of the heart [23]. The injury current is manifested as an elevation of the ST segment.

Clinical implications

ST-segment elevation is the most sensitive ECG marker for AMI [25] and an obvious requirement for the diagnosis of STEMI. The number of leads with ST-segment elevation and the sum of the total deviation in all leads-the ST-segment deviation score-has been shown to predict the eventual size of the myocardial infarction (MI) [26]. Furthermore, patients with larger ST-segment deviation scores benefit most from fibrinolysis in terms of reduction of the size of infarction

[27,28]. The initial 12-lead ECG is therefore clinically useful in determining both the severity of the AMI and an expected degree of benefit from reperfusion therapy.

Continuous ST-segment monitoring may also increase the sensitivity of the ECG to detect STEMI. In a study involving 1000 patients admitted with chest pain undergoing auto- mated serial 12-lead ECG monitoring, the initial ECG was found to be 55.4% sensitive for STEMI, whereas serial ECGs improved the sensitivity to 68.1% [29]. Furthermore, an absence of evolving ECG changes in serial ECG monitoring may help exclude a STEMI diagnosis.

A significant number of chest pain patients presenting with ST elevation have left ventricular hypertrophy, followed by STEMI and Left bundle branch block— among other entities [30]. This rather broad differential diagnosis makes the presence of ST-segment elevation a less specific marker for AMI (Fig. 3I). A recent study found that only 15% patients presenting to the ED with

chest pain and ST-segment elevation ultimately were found to have had AMI-the majority of these patients with ST- segment elevation were experiencing a noninfarction cause of the ST-segment abnormality [30]. The presence of ST- segment elevation should not be used as the sole precondition for providing fibrinolysis [31]. The positive predictive value of ST-segment elevation for an AMI may be increased with clinical features such as clinical presentation, cardiac risk factors, other diagnostic study results, and, most importantly, clinical suspicion.

The morphology patterns of the ST-segment elevation also have important clinical implications. Although concave morphology is less specific for AMI, its presence should not be used to rule out a diagnosis of infarction [32]. Instead, the emergency physician should search for other evidence supporting STEMI such as reciprocal changes, altered T- wave morphology, or evolving changes of the ECG [33]. A convex morphology, being 97% specific, is confirmatory for AMI. A concave morphology, however, can be encountered, particularly early in the course of STEMI.

Persistent ST-segment elevation can indicate left ventri- cular aneurysm (LVA). left ventricular aneurysm is characterized electrocardiographically by persistent ST- segment elevation seen several weeks after STEMI. Because of the frequent anterior location of LVA, ST-segment elevation is most often observed leads V₁ to V₆ (Fig. 3J). There are frequent Q waves and T-wave inversion.

Abnormal Q waves

Electrocardiographic findings

Q waves are often found in normal ECGs. Abnormal Q waves suggesting a MI, however, usually have a greater

negative deflection and a longer duration (Fig. 4A). The presence of any Q waves in leads V₁ through V₃ that are at least 30 milliseconds in duration, or Q waves in at least 2 contiguous leads in leads I, II, aVL, aVF, or V₄ through V₆ that are at least 1 mm in depth, is considered to be worrisome for an MI [34]. Pathologic Q waves typically appear within the first 9 hours of infarction, with a range of only a few minutes to 24 hours [3,24].

Pathogenesis

Abnormal Q waves may be caused by a change in the balance of depolarization vectors [35]. In an anterior infarction, for example, depolarization vectors pointing in the anterior direction are lost because infarcted tissue is electrically silent as it does not propagate an action potential. Electrodes placed on the anterior chest record a negative deflection because of posteriorly directed depolarization vectors originating from the posterior myocardium. The production of pathologic Q waves requires a relatively large amount of infarcted tissue [4]. A small infarction may therefore not develop pathologic Q waves.

Further, infarcted tissue has been hypothesized to act as a “window” into the normally electronegative left ventri- cular cavity [24]. Because of this negative potential within the cavity, electrodes placed directly over an area of infarction record an initial downward deflection during ventricular depolarization.

Clinical implications

In the evolution of an AMI which does not reperfuse, Q waves usually appear within 9 hours of occlusion of the affected coronary artery [36]. Because Q waves are

Fig. 4 A, Pathologic Q waves indicative of past MI. B, Anterolateral STEMI with Q waves in leads V₁ to V₄. This patient noted the onset of chest discomfort approximately 2.5 hours before presentation. Despite the presence of fully formed Q waves in leads V₁ to V₄, the ECG should be interpreted within the context of the patient’s history, that is, the recent onset of chest pain. It should be noted that Q waves can appear very early in the setting of STEMI, a time point at which reperfusion benefit can still be obtained.

classically thought to be a late finding, many patients may not receive reperfusion therapy. However, Q waves can commonly appear early in the course of an AMI (Fig. 4B). One study found that 53% of patients presenting with an AMI had pathologic Q waves in their initial ECG taken within 1 hour of the onset of chest pain [37]. Abnormal Q waves may in fact be due to ischemia of the Conduction system as opposed to irreversible infarction [38]. Q waves should not be used exclusively as a marker of late presentation of Acute coronary occlusion, denying a patient potentially beneficial reperfusion therapy. Once again, the ECG must be interpreted within the Clinical context-in this instance, considering the time course of the chest discomfort.

Since pathologic a Q waves often persist following an MI, their presence may suggest the presence of preexisting coronary disease, an important issue in risk stratification at future chest pain presentations. Up to 85% of patients who do not receive reperfusion therapy will have a persisting Q wave after MI [4]. The clinician should therefore be more suspicious for a new AMI in patients presenting with chest pain who have old pathologic Q waves on ECG.

The Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) trial found that patients who did not develop Q waves after fibrinolysis for STEMI had a lower mortality rate when compared to those who did develop Q waves at 30 days post infarction and 1 year post infarction [39]. The absence of Q waves post fibrinolysis may then serve as a favorable prognostic indicator.

T-wave inversion

Electrocardiographic findings

In healthy patients, T waves are normally upright in the left-sided leads (I, II, V₃-V₆). Within hours to days, an evolving AMI will typically demonstrate T-wave inversion [24]. This temporal development tends to make T-wave inversion a fairly late finding in the evolving AMI. The inverted T waves appear generally in the same leads that demonstrated ST-segment elevation [40]. The morphology of inverted T waves of an AMI tends to be symmetric [7].

Pathogenesis

In the course of an evolving AMI, T-wave inversion occurs when ischemia involves the epicardium. T-wave inversion is hypothesized by Mandel et al [41] to occur because of delayed repolarization in ischemic tissue. In normal hearts, the epicardium is the first to repolarize, whereas the endocardium is the last. Delayed repolarization of the epicardium during ischemia reverses the direction of

the progression of ventricular repolarization. With repolar- ization now moving in the direction of endocardium to epicardium, the repolarization vector also reverses, causing a downward deflection of the T wave [4].

Clinical implications

Because T-wave inversion reflects epicardial ischemia, transmural infarction is generally involved; this delayed appearance makes T-wave inversion a relatively late sign of an evolving AMI. Patients presenting with T-wave inversion with symptoms suggestive of coronary artery disease should be considered at high risk for having had an AMI. However, T-wave inversions are not specific to AMI and, therefore, without other clinical correlation, are not necessarily diagnostic of a MI [4].

The morphology of the T-wave inversion may help differentiate between these other causes of T-wave inversion (Fig. 5A and B). Pacemaker T waves, in other words T wave inversion related to permanent ventricular pacemakers, tend to be broader than the narrower infarction T waves [24]. A prolonged QTc distinguishes long QT syndrome. In mitral valve prolapse, T waves may be flattened or even inverted in inferior or lateral leads [24]. In stroke, T waves tend to be very wide and the QT interval prolonged [42].

T-wave inversion occurs in approximately 3 quarters of all patients with a completed AMI [40]. Other investigators found that the presence of T-wave inversion in anterior chest leads of at least 2 mm has a positive predictive value of 86% for left anterior descending artery stenosis [43].

Patients who have undergone successful reperfusion therapy may first demonstrate an acceleration and deepening (>=3 mm) of T-wave inversion. In a study by Oliva et al. [40], the maximum deepening of the T wave in successfully reperfused patients occurred within 48 hours of occlusion of the affected coronary artery. Patients in whom reperfusion did not occur demonstrated maximum T-wave inversion 72 hours after occlusion. A deepening T wave soon after fibrinolysis may then determine successful reperfusion. Normalization of T waves may also predict lesser morbidity months after the AMI. One study by Tamura et al. [44] found that patients with T-wave normalization within 6 months of infarction had higher left ventricular ejection fractions than those whose T waves remained inverted, indicating that patients with normalization of inverted T waves had improved myocardial recovery.

Normalization of the ST segment

Electrocardiographic findings

Within 12 hours of onset of a STEMI, the ST-segment elevation beings to normalize [3]. Using serial ST-segment mapping recorded every 2 hours in patients after an acute

Fig. 5 A, ACS-related T-wave inversion. Inverted T waves resulting from ischemia or infarction are symmetric in morphology with similar down-and upsloping limbs. a, Minimally inverted T waves. b, Deeply inverted T waves. B, ACS-related T wave inversion. i, Anterior T wave inversion. ii, Anterolateral I wave inversion. iii, Deeply inverted anterolateral T wave inversion. iv, Anterior biphasic T waves consistent with Wellen’s syndrome.

anterior AMI, Essen et al [45] found that the degree of ST-segment elevation rapidly resolved after a peak elevation at approximately 1 hour after the onset of chest pain, reaching a plateau at approximately 12 hours. This plateau is followed by a gradual decline over the next couple weeks. Another study concluded that ST-segment elevation com- pletely resolved within 2 weeks in 95% of patients following an inferior STEMI and 40% of patients following an anterior STEMI [46].

Pathogenesis

Normalization of the ST segment occurs as myocardial cells die, reducing the current of injury that manifested as ST segment elevation [47]. In the diastolic current theory noted earlier, the electrical gradient that caused current to flow from ischemic tissue to normal myocardium during diastole diminishes as ischemic tissue infarcts. Whereas in the systolic current theory, the current that flows from normal tissue to ischemic areas during repolarization likewise fades. This reduction in the injury current results in a gradual lessening of the degree of the ST-segment elevation.

Clinical implications

Normalization of the ST segment is the last ECG change to occur during an AMI. It usually occurs when transmural ischemia has progressed to completed infarction. At this point in the evolving AMI, the role of reperfusion therapy is therefore limited. Resolution of the ST segment without therapy may also occur resulting from spontaneous reperfusion [48].

The timeline of ECG changes following an STEMI has dramatically changed since the introduction of reperfusion therapy. One fibrinolytic study found that at least a 50% reduction in ST segment elevation within 60 minutes of therapy had a 90% positive predictive value for a patent coronary artery which was later confirmed by angiography [49]. Further, patients who have persistent ST-segment elevation tend to have experienced more severe infarctions and have increased mortality post infarction due to congestive heart failure [46]. The normalization of the ST-segment following reperfusion is thus an indicator of improved prognosis and Ultimate success of therapy.

The significance of ST-segment normalization as a marker of reperfusion has led some investigators to suggest that continuous ST segment monitoring be employed as a noninvasive method to determine if fibrinolysis is successful [50]. Continued elevation of the ST segment following reperfusion therapy indicates potential treatment failure. These patients can require more aggressive measures to achieve better outcomes that those with ST-segment normal- ization. A study by Richardson [51] found that, within 30 minutes of reperfusion therapy, ST-segment elevation

decreased by at least 2 mm. Successful fibrinolysis appears to cause an abrupt change in the pattern of repolarization. An abrupt decrease in ST-segment elevation is an indicator of reperfusion. One study examining outcomes after primary angioplasty found that persistent ST-segment elevation is the most important independent determinant predicting a major adverse cardiac event [52]. Another study found that a decrease in ST-segment elevation by at least 50% was associated with 94% positive predictive value for complete reperfusion [50].

Studies have also found that patients with persistent ST- segment elevation even after achieving a patent coronary artery following reperfusion therapy may in fact have continued nonperfusion of the microvasculature [53]. This is known as a No-reflow phenomenon, and these patients have an associated higher morbidity/mortality than those with normalization of the ST segment [54]. Normalization of the ST segment indicates adequate perfusion throughout the myocardial microvasculature and not just the major coronary vessels. Reperfusing the microvasculature is clinically important to improve prognoses of patients following an AMI.

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