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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.
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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.
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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.
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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.
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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.
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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.
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Patient 1: Complete Myocardial Salvage—Aborted Infarction
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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.
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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.
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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.
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- 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
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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.
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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.
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Patient 2: Partial Myocardial Salvage
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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.
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Based on his initial ECG, he had an Anderson-Wilkins Acuteness Score of 2.8 and a Sclarovsky-Birnbaum Ischemia Grade of II.
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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.
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- 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
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Figure 21–4 shows multimodal polar plot representations for this patient. Note the similarities among the different methods.
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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.
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Patient 3: No Myocardial Salvage Because of Low Protection
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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.
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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.
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- 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
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Figure 21–5 shows multimodal polar plot representations for this patient. Note the similarities among the different methods.
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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.
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Patient 4: No Myocardial Salvage Because of Late Presentation and Low Protection
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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.
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Based on his initial ECG, he had an Anderson-Wilkins Acuteness Score of 3.0 and a Sclarovsky-Birnbaum Ischemia Grade of III.
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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.
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- 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
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Figure 21–6 shows multimodal polar plot representations for this patient. Note the similarities among the different methods.
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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.
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Patient 5: Extension of Infarction Because of Interventional Embolization
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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.
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Based on his initial ECG, he had an Anderson-Wilkins Acuteness Score of 3.5 and a Sclarovsky-Birnbaum Ischemia Grade of II.
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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.
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- 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
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Figure 21–7 shows multimodal polar plot representations for this patient. Note the similarities among the different methods.
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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.