SummaryIn patients with suspected myocardial ischemia or myocardial infarction, cardiac MRI (CMR) provides a comprehensive, multi-angle view of the heart. Multiple CMR techniques provide rich information such as myocardial edema (risk myocardium), location of transmural infarcts, quantification of infarct size, microvascular occlusion, assessment of total ventricular volume and function, and assessment of infarcts post refactoring. Multiple CMR techniques are currently used to diagnose myocardial infarction (MI), and studies have shown that delayed enhancement with gadolinium (LGE) imaging is the most reliable method for detecting small or subendocardial infarcts, This method is highly accurate and is the best imaging technique for the diagnosis and evaluation of acute myocardial infarction. At present, reperfusion is widely used in clinical practice. This article focuses on the CMR manifestations of the pathophysiological features of acute myocardial infarction, as well as its clinical application value and guidance for the formulation of individualized treatment plans. Definition of acute myocardial infarction (AMI)
☆ The peak value of cardiac troponin (cTn) exceeds the normal control value 99% have diagnostic value.
☆ At least one of the following symptoms:
• Ischemic symptoms.
• New-onset myocardial ischemia causes electrocardiographic (ECG) changes.
• Pathological Q waves in ECG.
• Imaging data confirmed the loss of new viable myocardium.
• New-onset regional wall motion abnormalities. ☆ Currently new serum biomarkers (such as troponin) or new imaging techniques (such as echocardiography, SPECT, and coronary CT angiography) are currently used for the diagnosis of AMI, but their value is still limited. Sure. Application of CMR in acute myocardial infarction
☆ Cardiac magnetic resonance imaging (CMR) ) is a non-invasive imaging technique that is increasingly used in AMI, and can analyze cardiac function, myocardial perfusion, and histological manifestations in a single examination, even for patients with limited acoustic windows. ☆ CMR can provide a variety of information about the heart, such as myocardial edema (risk myocardium), location of transmural myocardial infarction, measurement of infarct size, and intramyocardial hemorrhage due to microvascular occlusion (MVO). In addition, CMR can comprehensively assess whole ventricular volume and cardiac function as well as post-infarct remodeling. ☆ Although a variety of CMR techniques are available for the diagnosis of MI disease, delayed enhancement with gadolinium (LGE) imaging is the most accurate and effective method. AMI imaging method – CMR technology
1. Delayed gadolinium enhancement (LGE) on the heart The basic principle of evaluation☆ LGE adopts T1WI inversion recovery sequence, and scans after intravenous injection of gadolinium agent for 10-30 minutes. time monitoring method” or “perspective method” to determine. ☆ Gadolinium is an extracellular contrast agent, and under certain conditions, such as myocardial necrosis or fibrosis, it shows markedly high signal, whereas viable myocardium is low signal. ☆ The enhancement type of LGE is useful for distinguishing post-infarct necrosis (subendocardial or transmural delayed enhancement), fibrosis in nonischemic dilated cardiomyopathy (medial, epicardial delayed enhancement) or Myocarditis (epicardial or focal delayed enhancement) (Figure 11.1) is helpful. 
Figure 11.1 Basic schematic of delayed gadolinium enhancement (LGE). Time-intensity curves (arrows) of normal and pathological myocardium after contrast injection. 2. Comparison between LGE and other methods☆ LGE has high spatial resolution, and can even display the microscopic features of 1g myocardium. infarction. ☆ Compared with SPECT imaging, the main advantage of LGE is the high spatial resolution and the slice thickness is 1~2mm, while the slice thickness of SPECT is 10mm. Therefore, CMR can reveal subendocardial myocardial infarction that SPECT perfusion imaging cannot. Compared with PET, LGE can show inactive myocardium more clearly. ☆ LGE can clearly display the inactive myocardium in any part of the cardiac chamber, and is especially useful for displaying left and right ventricular subendocardial myocardial infarctions that are often missed by SPECT and PET (Figure 11.2 to Figure 11.4). havestrongsignalcontrast,andtheinfarctareaiseasytodisplay.</span><imgclass=)
Figure 11.3 Comparison of LGE and SPECT showing subendocardial myocardial infarction. MRI (a) shows anterior septal subendocardial myocardial infarction, while SPECT (b, c) shows reversible perfusion defect. 
Figure 11.4 Comparison of LGE and SPECT showing right ventricular myocardial infarction. LGE (top) clearly shows right ventricular myocardial infarction (arrow) and left ventricular inferior wall myocardial infarction. However, SPECT showed only myocardial perfusion defects in the inferior wall of the left ventricle. Cardiac MRI manifestations of acute myocardial infarction
1. T2WI showing myocardial edema of the risk myocardium☆ In acute myocardial infarction, myocardial edema manifests as a markedly high signal on T2WI, that is, “risk myocardium”. ☆ The determination of myocardial extent of ischemic myocardial injury risk by T2WI is still controversial.
☆ The main advantages of T2WI:
• Distinguish acute and chronic infarction.
• The proportion of reversible myocardium can be quantified by comparing the size of the edematous area on T2WI with delayed enhancement images.
• The main characteristic of acute myocardial injury is edema, whereas the main characteristic of chronic myocardial injury is fibrosis. ☆ In the early stage of coronary occlusion, the difference between myocardial oxygen supply and demand can lead to myocardial ischemia. ☆ If the ischemia persists, the myocardium will be irreversibly damaged, and necrosis will extend from the endocardium to the epicardium, that is, the “wave crack phenomenon”. ☆ The final infarct size depends on the extent of the risk myocardium, that is, the ischemic area of the myocardium with complete occlusion of the coronary arteries and no blood supply. ☆ CMR is often used to visualize and quantify the extent of the myocardium at risk, which is hyperintense on T2WI and sensitive to increased local water content (active myocarditis and tissue edema) (Figure 11.5 to Figure 11.9). 
Figure 11.5 Schematic illustration of the “wavefront phenomenon of necrotic myocardium” in the context of acute myocardial infarction. 
Figure 11.11 Termination of myocardial infarction. Coronary CT angiography (a, b) and conventional angiography (c) show severe stenosis in the mid-segment of the left anterior descending artery (arrow). The occluded left anterior descending artery is reopened after percutaneous coronary intervention (c). However, the LGE image did not show significant enhancement (e). T2WI images show only mild hyperintensity in the apical septal wall, mid-anterior wall, and mid-proximal septal wall (d). 3. Reperfusion injuryNo-reflow phenomenon:☆ Arterial recanalization is successful, and prolonged ischemia results in loss of reperfusion in the distal myocardium. ☆ Second, vascular lumen obstruction (eg, neutrophil emboli, platelets, atherosclerotic emboli) and extravascular edema and hemorrhage compress the blood vessels. ☆ After long-term ischemia, the necrotic area will develop into transmural infarction, and the microvessels in the infarcted area will be destroyed. LGE shows microvascular occlusion (MVO):☆ CMR is also currently used to assess persistent microvascular dysfunction in the context of LGE hyperintense areas (infarcted myocardium), where MVO manifests as low signal. ☆ Definition: In the area with significant enhancement of LGE, the delay period still shows low signal. ☆ Persistent microvascular occlusion is an independent predictor of left ventricular remodeling, implying poor myocardial function and an increased probability of subsequent major adverse cardiac events. ☆ In the experimental model, the early changes after reperfusion injury were microvascular injury, followed by intramyocardial hemorrhage. The extent of bleeding is related to the “low signal area” of LGE. ☆ In most patients, the LGE “low signal area” showed low signal on T2WI, suggesting intramyocardial hemorrhage, and was closely related to the markers of infarct size and function (Figure 11.12). 
Figure 11.12 The first perfusion (a) and cine imaging (b) showed low subendocardial signal near the anterior septal wall 3 minutes after contrast injection, Microvascular occlusion is suggested (arrow). Hypo-enhancement in the corresponding area is also shown on the DE-CMR (c) image. 4. Low-dose dobutamine stress MRI☆ Low-dose dobutamine stress MR ( DSMR) can be used to detect myocardial contractility reserve, which is a marker of myocardial survival. ☆ The advantage of DSMR is that it can fully display the myocardium, while the image quality of dobutamine stress echocardiography is poor in patients with poor acoustic window. ☆ Low-dose DSMR is superior to LGE in assessing myocardial function recovery, and it does not depend on the transmurality of scar tissue. Therefore, LGE and DSMR can provide complementary information. 5. Cardiac function☆ Cine MRI is a reference for showing the overall systolic function of the heart and the motion of the cardiac chamber wall region standard. CMR is particularly useful in the study of aneurysm expansion due to large infarcts. 6. Complications of infarction
☆ With the accumulation of CMR experience, CMR is relevant to the diagnosis of MI. A new approach to adverse sequelae, including right ventricular involvement, acute pericarditis, and left ventricular thrombus.
• Interventricular septal perforation due to MI.
• Dressler syndrome (pericarditis after myocardial infarction): secondary pericarditis, occurring in the heart or pericardiumdamage.
• Post-infarct mitral regurgitation.
• Left ventricular thrombosis (Figure 11.13). 
Figure 11.13 Poor left ventricular remodeling after myocardial infarction. Cardiac MRI showed apical thinning, dilation of the LV aneurysm, and LGE images showed thrombosis within the LV aneurysm. 7. Assessing left ventricular remodeling☆ LV remodeling and large infarcts and infarcts revealed by MVO and LEG Posterior transmural extent was significantly correlated.
☆ Post-infarction remodeling is divided into early stage (within 72 hours) and late stage (over 72 hours):
• Early stage involves infarction Dilatation of the area may lead to early ventricular rupture or aneurysm formation.
• Late remodeling can manifest as time-dependent left ventricular dilatation, ventricular deformation, and wall hypertrophy.
• After MI, under the action of intraventricular pressure, the ventricular wall gradually expands, the necrotic myocardial tissue turns into scar tissue, and the systolic function decreases.
• Delayed reperfusion therapy increases infarct size, as well as post-infarct dilation-induced poor LV remodeling, progressive thinning of necrotic areas, and compensatory hypertrophy of the distal myocardium. ☆ The assessment of LV volume and mass is independent of geometric assumptions, so MRI is particularly suitable for the assessment of aneurysm expansion due to large infarcts. ☆ Infarct size, transmural infarction, and persistent microvascular injury displayed by LGE can predict poor post-infarction remodeling, better than other clinical indicators (Figure 11.14). 
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Figure 11.1. Left ventricular remodeling and persistent microvascular damage. T2WI (a) of this case showed low signal in the center and high signal in the periphery of the blood supply area of the left anterior descending artery. LGE (b) shows delayed enhancement around the central PMVO in the corresponding region. Cine MRI (c) shows severe hypokinesia and loss of motion in the anterior wall and the septal wall near the anterior wall. However, F/U MRI (d) showed myocardial thinning with loss of motion in the corresponding area, suggesting left ventricular remodeling. 8. Complications after PCI: microinfarction after coronary microembolization☆ atherosclerotic plaque Coronary embolization by ruptured microemboli causes acute coronary syndrome and reperfusion-induced microinfarction after percutaneous coronary intervention, and release of myocardial infarction-related factors. It is difficult to differentiate from reperfusion injury effects. ☆ After coronary intervention, the first perfusion MRI showed acute and subacute hypoperfusion caused by coronary microembolism. LGE-MRI is helpful for quantitative assessment of subacute microinfarction. ☆ Microinfarction after coronary microembolization, LGE-MRI showed streak-like high signal from the endocardium to the epicardium (Figure 11.15). 
Figure 11.15 Microinfarction after coronary microembolization. LGE images showed multiple irregular and patchy enhancements from the endocardium to the epicardium in the mid-basal, apical, and basal parts of the interventricular septum. Differential Diagnosis: Noncoronary Disease
☆ Although some patients have typical features of acute myocardial infarction, coronary Arterial angiography showed no abnormality.
☆ Cardiac MRI can be used in patients with chest pain and elevated myocardial enzymes but with normal or mildly abnormal coronary arteries.
• The type of significant LGE enhancement (whether or not enhancement is present or the degree of enhancement) is important and is useful in the etiological diagnosis of myocardial injury (eg, myocarditis).
• Cardiac MRI studies show that the most common conditions are myocarditis (31%), stress cardiomyopathy (31%), and ST-segment elevation myocardial infarction with spontaneous thrombolysis (29%) (Figure 11.16). 
Myocarditis. A 36-year-old female patient with acute chest pain and elevated myocardial enzymes. Apical anterior, lateral, mid-anterior septal, proximal-inferior septal, and basal proximal-inferior septal and inferior walls (arrows) Median to epicardial layers show multifocal perfusion defect (left row) and enhancement of LGE hypoperfusion zone (right row).
Summary600″>
☆ In conventional CMR, clinicians can obtain the following information:
• T2WI Shows risk of myocardial edema;
• LGE to assess myocardial activity and low-dose DSMR to assess myocardial contractile reserve;
• re- perfusion injury;
• cardiac function;
• infarct complications.
☆ CMR Additional Information:
• Assess left ventricular remodeling;
• LGE assesses infarct size.
☆ Differential diagnosis of MI:
• Myocarditis, pericarditis, stress cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, etc.Content of this article Excerpt from Cardiac CT and MRI Practical Tutorial” (published by Tianjin Publishing and Media Group/Tianjin Science and Technology Translation Publishing Co., Ltd.). Yimaitong has been authorized by the publisher. For more, read the original book.
●HD Map Series< strong> ●
● How CT and MRI look at normal and abnormal heart structures
● How CT and MRI look at normal and abnormal coronary arteries
● How CT looks at coronary stenosis
● Practical application of MR coronary angiography