Chapter 21. Acute Myocardial Infarction

When a patient is presented at the emergency department or to a mobile emergency system with acute chest pain, the first assessment includes a standard 12-lead electrocardiogram (ECG). When chest pain is caused by an acute coronary occlusion, the initial ECG can show ST-segment elevation, which meets the criteria that indicate an ST-segment elevation myocardial infarction (STEMI). All five patients included in this chapter presented with first-time STEMI due to an occluded left anterior descending coronary artery as documented by emergency coronary angiography (Fig. 21–1).

The ECG is the initial modality used in the evaluation of patients with suspected acute myocardial infarction. It provides general information about presence and location of the acute ischemia/infarction process. Several ECG scoring systems are being used for assessment of the extent of the initially ischemic myocardium and also the extent of the final infarction. There are, however, limitations in using the ECG as a modality for sizing either the ischemic or infarcted region. In its current form, the ECG does not provide an image of the electrical activation or recovery. New methods are currently in development to transform the ECG waveforms into cardiac images, with algorithms to quantify key aspects of the ischemia/infarction process such as extent, acuteness, and severity.1-3

The five patients included in this chapter represent the varied outcomes that can result from acute percutaneous coronary intervention (PCI) that is intended to provide maximal salvage of ischemic myocardium. The ECG was used to assess the Anderson-Wilkins Acuteness Score and the Sclarovsky-Birnbaum Severity Ischemia Grade on the initial ECG to indicate the patient's potential for recovery of the involved region of myocardium.4,5 Cardiovascular magnetic resonance (CMR) imaging was performed on all patients. Two patients received myocardial perfusion single photon emission computed tomography (SPECT) with the radioactive tracer injected prior to opening of the occluded vessel, and the other three patients received SPECT imaging with injection of the radioactive tracer only after the occluded vessel was opened. Positron emission tomography (PET) was performed on these three patients.

In this chapter, the methods used for analysis will be described briefly, followed by description and visualization of the five presented patients. The category of outcome for each of the patients is also considered.

Anderson-Wilkins Acuteness Score

The ECG Anderson-Wilkins Acuteness Score indicates the acuteness of an episode of acute myocardial infarction on a continuous scale from 4.0 to 1.0; 4.0 represents a hyperacute process, while 1.0 indicates a late, subacute process. The score is based on the comparative T wave amplitudes versus abnormal Q wave durations in each of the leads with ST-segment elevation or tall T waves. The acuteness phase is designated for each of these leads based on the presence (A) or absence (B) of a tall T wave and the absence (1) or presence (2) of an abnormal Q wave, with 1A being the most acute (tall T waves without abnormal Q waves) and 2B being the least acute (positive but not tall T waves with abnormal Q waves).4

The Anderson-Wilkins Acuteness Score is then calculated from the following formula:

In Fig. 21–2, representing the example ECG of patient 1, an ST-segment elevation or tall T wave can be seen in leads I and aVL and in leads V1 to V6. All leads except V1 show a tall T wave and no abnormal Q wave. Lead V1 has a Q wave but no tall T wave. The final Anderson-Wilkins Acuteness Score is 3.6, indicating the presence of a highly acute myocardial infarction.

Sclarovsky-Birnbaum Ischemia Grading System

The Sclarovsky-Birnbaum Ischemia grading system is based on assessment of changes in the T wave, ST segment, and terminal part of the QRS complex, as a method for estimating the severity of ischemia as influenced by protection by either collateral vessels or metabolic preconditioning.5 The grading system consists of three grades representing increasing severity: grade I—tall upright T waves without ST-segment elevation; grade II—ST-segment elevation in at least two adjacent leads without terminal QRS distortion; and grade III—ST-segment elevation with terminal QRS distortion in two or more adjacent leads. Figure 21–2 shows an example of grade II ischemia when assessed by the grading system.

Localizing Myocardial Ischemia

The clinical management of patients with acute coronary occlusion involves a complex assessment of the extent and severity of changes of both ischemia and infarction within the left ventricle. Often, the assessed methods are presented in different formats, and within each method, the orientation of the heart, angle selection for cardiac planes, nomenclature for segments, and assignment of segments to coronary arterial territories have evolved independently. This evolution has been based on the inherent strengths and weaknesses of the technique and the practical clinical application of these modalities as they are used for patient management. This independent evolution has resulted in a lack of standardization and has made accurate intra- and cross-modality comparisons difficult. A uniform method for display that allows for side-by-side comparison would therefore simplify data interpretation. Cerquiera et al6 proposed a 17-segment standardized polar plot representation for the left ventricle, where the outer boundaries of the polar plot represent the base of the left ventricle and where the center of the polar plot represents the apex of the left ventricle. The 17-segment model facilitates multimodal imaging approaches.

Cain et al7 used the polar plot representation for comparing myocardial perfusion SPECT, regional function by CMR, and viability by CMR. More recently, Ubachs et al3 and Bacharova et al1 developed ECG methods to visualize the ST-segment deviation on a polar plot representation (see Chapters 7 and 11). Ubachs et al3 used the presence of ST-segment elevation on the standard 12-lead ECG to locate the ischemic myocardium based on the infarct distribution method described by Strauss and Selvester.8 Bacharova et al1 used the dipolar electrocardiotopography (DECARTO) method, where the center of the location is provided by the spatial orientation of the resultant ST vector.

Perfusion defect size by myocardial perfusion SPECT has been shown to correlate well with ex vivo measures of myocardial ischemia when the perfusion tracer is injected prior to PCI.9 Its evolution and use over the last decades has made myocardial perfusion SPECT the gold standard for quantification of myocardial ischemia (see Chapter 3). However, it has been shown that the perfusion defect size has a strong correlation with the myocardial infarct size when the myocardial perfusion SPECT is performed a few days after opening of the coronary artery.10

Along with recent technical advances, CMR imaging has become a powerful tool for the evaluation of irreversible myocardial injury. During acute myocardial infarction, cell membranes lose integrity and rupture, which increases the extracellular volume. By using an extracellular contrast medium, this region of irreversibly damaged myocardium can be accurately identified.11 CMR imaging is usually undertaken 10 to 30 minutes after injection of an extracellular contrast medium.

Therefore, CMR imaging can be considered the reference method for in vivo visualization of myocardial infarction (see Chapter 6).

More recently, CMR has been introduced as a method for quantification of the myocardium at risk by using a T2-weighted sequence that visualizes myocardial edema. This method has been validated in both animals12 and humans.13 In the patients presented in this chapter, there is a difference in imaging parameters. Patients 1 and 2 were imaged using an 8-mm slice thickness, whereas patients 3, 4, and 5 were imaged using a 15-mm slice thickness. This probably results in a slight overestimation of the myocardium at risk in patients 3, 4, and 5 due to partial volume effect in the most basal slices.

Unlike myocardial perfusion SPECT imaging, which detects single photons, PET imaging detects paired simultaneous annihilation photons. This coincidence detection leads to least an increase in the sensitivity of PET compared with myocardial perfusion SPECT, with improved image quality.

Flow reserve (hyperemic flow/baseline flow) and absolute quantification of regional, baseline, and maximal myocardial perfusion (in mL/min/g tissue) are feasible and well validated using dynamic PET image acquisition. These quantitative data can support visual and semiquantitative image interpretation and improve detection of preclinical and multivessel coronary artery disease. PET provides a sensitivity of 91% and a specificity of 89% for the diagnosis of obstructive coronary artery disease.14 Just as in myocardial perfusion SPECT, PET imaging uses ionizing radiation that can result in late adverse biologic effects. But positron-emitting tracers typically provide less radiation burden when compared with myocardial perfusion SPECT tracers due to their short half-lives.

The most widely used tracers for evaluating myocardial perfusion with PET in clinical practice are generator produced rubidum-82, cyclotron produced nitrogen-13 ammonia, and to some degree oxygen-15 water. Another commonly used PET tracer is fluorine-18 fluoro-2-deoxy-D-glucose (18F-FDG). The uptake and retention of 18F-FDG reflects the activity of the various glucose transporters and hexokinase-mediated phosphorylation in a matter similar to unlabeled glucose. In the setting of ischemic heart disease, viable myocardium often exhibits a shift in substrate utilization from aerobic to anaerobic metabolism. Therefore, 18F-FDG imaging can be used to assess glycolytic activity of the myocardium during ischemia.

More information on positron emission tomography can be found in Chapter 3.

The myocardium at risk, defined as the hypoperfused myocardium during acute coronary occlusion, is an important measure because a variable amount of this area will become infarcted. Therefore, to assess the efficacy of reperfusion therapy, it is necessary to determine how much myocardium is salvaged by measuring the final infarct size in relation to the initial myocardium at risk. The initial myocardium at risk is determined by myocardial perfusion SPECT and the finally infarcted myocardium is determined by CMR for the two patients in whom the radioactive tracer was injected prior to reperfusion. For the other three patients, T2-weighted CMR was used to assess myocardium at risk.

Myocardial salvage is defined as:

The five patients included in this chapter are from two study sites; patients 1 and 2 are from Skåne University Hospital in Lund, Sweden; and patients 3, 4, and 5 are from Copenhagen University Hospital in Copenhagen, Denmark. All five patients received standard and DECARTO ECG studies to estimate the location of the ischemic myocardium and CMR imaging with late gadolinium enhancement to measure infarct size. All patients also received CMR imaging with a T2-weighted sequence to measure the myocardium at risk. The three patients from Copenhagen University Hospital received 18F-FDG PET imaging to estimate the infarcted myocardium and the potentially viable myocardium with sufficient metabolic abnormality to appear abnormal by this method.

In patients with acute coronary occlusion, reperfusion before loss of myocardial viability can potentially salvage some portion of the ischemic cells so that they return to their normal contractile function. However, because there is a limited amount of time that non-blood-perfused myocardial cells can rely on anaerobic metabolism for preservation of their anatomy and physiology, the time to reperfusion is critical.15 This can also be called the salvagability time window.

There are several specific etiologies for failure to achieve salvage. One is an excessive delay between time of acute coronary occlusion and time of reperfusion, as illustrated by patient 2.

There is also the variable level of "ischemic protection" provided by preexisting collateral vessels and/or ischemic preconditioning. Prior episodes of ischemia facilitate both of these protective mechanisms. Patients without prior ischemia may have a much shorter salvagability time window, as illustrated by patient 3.

Even when the patient receives reperfusion within their salvagability time window, the therapeutic intervention could be complicated by distal embolization of a portion of the thrombus. The embolic material could occlude native or collateral vessels, producing ischemia and potentially infarction of additional myocardium. An example is presented by patient 5.

Even when the ischemic myocardium is salvaged, there is physiologic delay in its resumption of contractile function by the metabolic process termed stunning.16 The oxygen and glucose provided by the reperfusing blood is used to restore both cellular physiologic function and biochemical substrate. There may be further delay in resumption of contractile function caused my many pathologic processes, and this has been termed hibernation. For patient 2, significant myocardial salvage has been achieved, and for patient 1, total salvage has been achieved. However, this salvaged myocardium requires time before providing its contribution to the global left ventricular contractile function.

Patient 1: Complete Myocardial Salvage—Aborted Infarction

A 71-year-old man with no history of myocardial infarction was admitted to the emergency department with a complaint of increasing chest pain while warming up for a game of tennis. Since then, approximately 90 minutes had passed. The admitting ECG showed sinus rhythm and ST-segment elevation in leads I, aVL, and V1 to V3. The patient's initial serum levels of creatine kinase-MB (CK-MB) and troponin T were within the normal range (5 μg/L and <0.05 μg/L, respectively). The angiography revealed an occlusion of the left anterior descending coronary artery.

Based on his initial ECG, the patient had an Anderson-Wilkins Acuteness Score of 3.6 suggesting a hyperacute stage of myocardial infarction. His Sclarovsky-Birnbaum Ischemia Grade was II.

The patient received myocardial perfusion SPECT with a perfusion tracer injected prior to opening of the coronary artery. Furthermore, the patient received CMR imaging approximately 1 week after acute coronary occlusion with addition of a T2-weighted sequence.

• Ischemic myocardium:
  • By myocardial perfusion SPECT: 37% of the left ventricle
  • By T2-weighted CMR: 36% of the left ventricle
• Infarct size:
  • By CMR imaging: 0% of left ventricle
• Myocardial salvage:
  • By myocardial perfusion SPECT and CMR imaging: 100% of the initial ischemic area is salvaged

Figure 21–3 shows multimodal polar plot representations of the different methods assessed in this patient. Note that no myocardial infarction was seen on the late gadolinium-enhanced CMR images.

This patient presented at the emergency department approximately 90 minutes after onset of chest pain. The high Anderson-Wilkins Acuteness Score (3.6) indicates that the occlusion had not remained complete for that entire 1.5 hours. The ECG myocardial perfusion SPECT and T2-weighted CMR indicate a moderate-sized ischemic region in the left anterior descending coronary artery distribution. The late gadolinium-enhanced CMR indicated a completely aborted infarction.

Patient 2: Partial Myocardial Salvage

An 84-year-old man was admitted to the emergency department with a complaint of severe chest pain accompanied by dyspnea for approximately 4 hours. The admitting ECG showed sinus rhythm and ST-segment elevation in leads aVL and V1 to V4. The patient's initial serum levels of CK-MB and troponin T were within the normal range (3.5 μg/L and <0.05 μg/L, respectively). The angiography revealed an occlusion of the left anterior descending coronary artery.

Based on his initial ECG, he had an Anderson-Wilkins Acuteness Score of 2.8 and a Sclarovsky-Birnbaum Ischemia Grade of II.

The patient received myocardial perfusion SPECT with a perfusion tracer injected prior to opening of the coronary artery. Furthermore, the patient received CMR imaging approximately 1 week after acute coronary occlusion with addition of a T2-weighted sequence.

• Ischemic myocardium:
  • By myocardial perfusion SPECT: 39% of the left ventricle
  • By T2-weighted CMR: 31% of the left ventricle
• Infarct size:
  • By CMR imaging: 11% of the left ventricle
• Myocardial salvage:
  • By myocardial perfusion SPECT and CMR imaging: 72% of the initial ischemic area is salvaged

Figure 21–4 shows multimodal polar plot representations for this patient. Note the similarities among the different methods.

This patient presented at the emergency department approximately 4 hours after pain onset. The mid-range Anderson-Wilkins Acuteness Score (2.8) indicates that the occlusion had not remained complete for those entire 4 hours. The extent of the ischemic myocardium in the left anterior descending coronary artery distribution was moderate: between 31% and 39% by the clinical modalities. Because the extent of the infarcted myocardium is much less (11%), there is "partial" myocardial salvage.

Patient 3: No Myocardial Salvage Because of Low Protection

A 74-year-old man presented to the emergency department complaining of central chest pain for approximately 2 hours. The admitting ECG showed sinus rhythm and an ST-segment elevation in leads I, aVL, and V1 to V6.

Based on his initial ECG, he had an Anderson-Wilkins Acuteness Score of 4.0 suggesting a hyperacute stage of myocardial ischemia/infarction; however, his Sclarovsky-Birnbaum Ischemia Grade was III, indicating poor myocardial protection. Coronary angiography performed approximately 1 hour later revealed an occlusion of the left anterior descending coronary artery, and catheter-based reperfusion was achieved approximately 90 minutes after the initial ECG. The patient received myocardial perfusion SPECT, CMR with T2-weighted imaging, and 18F-FDG PET imaging during the following days.

• Ischemic myocardium:
  • By T2-weighted CMR: 56% of the left ventricle
• Infarct size:
  • By CMR imaging: 36% of the left ventricle
• Myocardial salvage:
  • By T2-weighted CMR and CMR imaging: 36% of the initial ischemic area is salvaged

Figure 21–5 shows multimodal polar plot representations for this patient. Note the similarities among the different methods.

This patient presented at the emergency department approximately 2 hours after pain onset. On the initial ECG, the Anderson-Wilkins Acuteness Score (4.0) indicated that the ischemia/infarction process was very acute, but the Sclarovsky-Birnbaum Ischemia Grade (III) indicated absence of protection of the ischemic myocardium. The extent of the initially ischemic myocardium in the left anterior descending coronary artery distribution was estimated by T2-weighted CMR at 56% of the left ventricle, and the extent of the finally infarcted myocardium was estimated at 36% of the left ventricle. The ischemic myocardium is probably slightly overestimated due to the previously described partial volume effect, which would result in even a lower percentage of myocardial salvage. This small percentage of myocardial salvage is probably due to the rapid development of infarction in the poorly protected myocardium before reperfusion was established.

Patient 4: No Myocardial Salvage Because of Late Presentation and Low Protection

A 51-year-old man presented to the emergency department with a complaint of increasing chest pain while cycling to his workplace. Since then, approximately 2 hours had passed. The admitting ECG showed sinus rhythm and an ST-segment elevation in leads aVL and V1 to V6. The patient's serum levels of CK-MB and troponin T approximately 6 hours after presenting at the emergency department were 780 μg/L and 14.1 μg/L, respectively. The angiography revealed an occlusion of the left anterior descending coronary artery.

Based on his initial ECG, he had an Anderson-Wilkins Acuteness Score of 3.0 and a Sclarovsky-Birnbaum Ischemia Grade of III.

The patient received myocardial perfusion SPECT, CMR imaging with T2-weighted imaging, and 18F-FDG PET imaging after the coronary artery was opened by PCI.

• Ischemic myocardium:
  • By T2-weighted CMR: 39% of the left ventricle
• Infarct size:
  • By CMR imaging: 39% of the left ventricle
• Myocardial salvage:
  • By T2-weighted CMR and CMR: 0% of the initial ischemic area is salvaged

Figure 21–6 shows multimodal polar plot representations for this patient. Note the similarities among the different methods.

This patient presented at the emergency department approximately 2 hours after pain onset. The mid-range Anderson-Wilkins Acuteness Score (3.0) indicated that the LAD may have remained occluded during the 2 hours following onset of chest pain, and the high Sclarovsky-Birnbaum Grade (III) indicated that the extensive (39%) region of ischemic myocardium was poorly protected. The large infarct size by CMR (39%) indicated the absence of myocardial salvage, probably because the infarction process had progressed rapidly even before the initial ECG was recorded and continued during the time before reperfusion was established.

Patient 5: Extension of Infarction Because of Interventional Embolization

A 60-year-old man presented at the emergency department with a complaint of increasing chest pain radiating to left arm and chin for approximately 60 minutes. The admitting ECG showed sinus rhythm and ST-segment elevation in leads I, aVL, and V2 to V5. The patient's serum levels of CK-MB and troponin T approximately 6 hours after presenting at the emergency department were 432 μg/L and 10.0 μg/L, respectively. The angiography revealed an occlusion of the left anterior descending coronary artery that was rapidly removed by PCI.

Based on his initial ECG, he had an Anderson-Wilkins Acuteness Score of 3.5 and a Sclarovsky-Birnbaum Ischemia Grade of II.

The patient received myocardial perfusion SPECT, CMR imaging with T2-weighted imaging, and 18F-FDG PET imaging after the coronary artery was opened by PCI.

• Ischemic myocardium:
  • By T2-weighted CMR: 59% of the left ventricle
• Infarct size:
  • By CMR imaging: 51% of the left ventricle
• Myocardial salvage:
  • By T2-weighted CMR and CMR: 14% of the initial ischemic area is salvaged

Figure 21–7 shows multimodal polar plot representations for this patient. Note the similarities among the different methods.

This patient presented at the emergency department approximately 1 hour after pain onset, and the acuteness of the process was confirmed by the Anderson-Wilkins Acuteness Score (3.5) on the initial ECG. The Sclarovsky-Birnbaum Grade (II) indicated the presence of protection of the extensive (59%) ischemic myocardium. Despite the early reperfusion therapy, this patient developed a large final infarct size measured by CMR (51%). This final infarct size, despite the presence of protection, can in this case be explained by a complication during the PCI.

Currently, patients presenting with the ST-segment changes typical of acute coronary occlusion receive primary PCI if this is logistically feasible. However, PCI is not always possible in smaller local hospitals, where these patients are treated with intravenous thrombolytic therapy. Indeed, patients with smaller, well-protected infarcts might benefit more from thrombolytic therapy instead of from PCI. The use of the polar plot representation of the ischemic region by ECG might provide support for the decision of which reperfusion treatment should be used. In centers capable of performing diagnostic methods such as myocardial perfusion SPECT and magnetic resonance imaging, the polar plot provides a common format for comparing the location and extent of both the initially ischemic and finally infarcted myocardium. Furthermore, in the current era of data storage, the treating physician often has to review a great amount of files to get a clear understanding of the outcome from all the performed modalities. Polar plot representation of these modalities provides a quick visually comparable image and is therefore a potentially helpful method for patient management.

The authors express their gratitude to Ljuba Bacharova, Peer Grande, Erik Hedström, Marcus Carlsson, and Håkan Arheden for assistance in performing the studies.