Activity Transcript

Segment 1: Cardiac MRI Overview

James C. Carr, MD: Hello, I am James Carr, and I am the Chair of the Department of Radiology at Northwestern University Feinberg School of Medicine. Welcome to this program, "Cardiac MRI: Case Studies for Improving Patient Outcomes." I'd like to start with a short overview about contrast-enhanced magnetic resonance imaging (MRI).

So the contrast-enhanced MRI exam has multiple different techniques within the same protocol. You can image the anatomy and morphology of the heart using dark blood imaging. You can do cine imaging to look for wall motion. You can inject contrast to look at perfusion in the left ventricular myocardium. You can image the heart after the contrast has been injected, gadolinium-enhancement imaging, and that's to look for scar within the heart. Of course, anytime you inject contrast you can look at the blood vessels with angiography. All of these techniques can be combined together into a single protocol to provide a very comprehensive assessment of the heart.

In the standard cardiac MRI protocol, we do a combination of cine imaging in a 3-chamber, 2-chamber, and 4-chamber orientation. We do a stack of short axis imaging. We inject the contrast to do delayed enhanced imaging, and we use a number of different techniques for that. Typically, to speed up the protocol, we'll inject the contrast early before the cine MRI. This allows us to really shorten the overall protocol. Then the additional advanced techniques are added into the basic backbone of the protocol. And these can be mapping techniques as mentioned, 4D flow or 2D flow MRI.

We can shorten the overall protocol by adding acceleration strategies into the imaging acquisition techniques. For example, cine MRI can be accelerated using compressed sensing and allows us to do real-time imaging and that can be performed in 5 to 10 minutes. And then we can do delayed-enhanced imaging very rapidly with some newer acceleration strategies applied there, and again, allows us to cover the whole heart looking for scar within a matter of 5 to 10 minutes. The overall protocol can be shortened to 30 minutes, and this can really significantly improve overall workflow.

For the clinical stress protocol, stress perfusion MRI, again, the same backbone exists of cine MRI and delayed-enhanced imaging, and we add in stress perfusion imaging, typically before the cine MRI. This is an acquisition of first pass imaging when contrast has been injected. We always image the heart during stress when a vasodilator such as adenosine has been administered. Then about 15 minutes later, after the cine MRI, we do rest perfusion imaging without the vasodilator being infused. So these are really just an overview of the different techniques that can be used for cardiac MRI.

The major focus for cardiac MRI is really subdivided into these different indications and include congenital heart disease; evaluation of coronary artery disease, such as ischemic heart disease, and you might use perfusion imaging for that purpose; looking for inflammatory diseases of the heart, such as myocarditis or other forms of cardiomyopathy, which would include infiltrative cardiomyopathy, hypertrophic cardiomyopathy, and hypertensive cardiomyopathy.

Cardiac MRI is one of the main indications for evaluating cardiac masses. We can evaluate pericardial disease, valvular disease, and of course since we're imaging the chest, we can also assess acquired vascular diseases, such as aortic dissection or thoracic aortic aneurysms.

Thank you. And please continue to the next segment of this activity.

Segment 2: Assessing for Chest Pain

Dr Carr: In this segment, we are going to review some cases where cardiac MRI (CMR) plays a pivotal role in assessing chest pain.

The first case is a 26-year-old male who presents complaining of new onset chest pain. There's no significant past medical history on clinical assessment. His initial electrocardiogram (ECG) demonstrated non-specific T-wave changes, and on his lab values, his troponin was mildly increased. He was sent for a coronary computed tomography (CT) angiogram, and this showed no evidence of coronary disease and no evidence of any coronary anomalies.

So he then underwent a cardiac MRI. You will see the cine view of the heart, which is in a 3-chamber orientation and demonstrates that the left ventricular function is really completely normal.

You can see the delayed-enhanced imaging orientations in a 3-chamber view, which is the same as the cine view and a short axis view. I will draw your attention to the lateral wall of the heart where you see what would be described as a mottled area of enhancement involving the entire inferolateral wall of the left ventricle (LV).

The outside portion of this shows a linear area of enhancement just outside the abnormal left ventricular myocardium. This area of abnormality is outlined with arrows. Again, you see this mottled, patchy, ill-defined enhancement in the inferolateral wall of the left ventricle, extending from the base of the heart all the way to the apex, and that is nicely visible on the long axis 3-chamber view. Another arrow points to the enhancement of the structure overlying the left ventricular myocardium. On the short axis view you see this linear midmyocardial or mesocardial enhancement, again, within the infralateral wall of the left ventricular myocardium with relative sparing of the subendocardium. There's also enhancement of the linear structure overlapping in the left ventricular myocardium. What is the most likely diagnosis in this particular patient who is young, presents with chest pain, has a mild troponin rise, and very non subendocardial pattern of enhancement within the left ventricular myocardium?

The diagnosis here is myopericarditis. The summary of the findings are mid and subepicardial myocardial enhancement within the left ventricular myocardium and the overlapping line of enhancement illustrates overlapping pericardial enhancement. The combination of myocardial enhancement together with enhancement to the pericardium can only occur in inflammatory conditions such as myopericarditis. In fact, the presence of pericarditis points much more likely toward inflammatory phenomenon.

Myocarditis has been well described in the literature. In a number of different disease states in the left ventricular myocardium. But for myocardium, myocarditis, it is usually caused by a viral infection. It will be associated with interstitial edema, which may be evident on T2-weighted imaging. It typically is depicted as focal or patchy diffuse hyper enhancement of the left ventricular myocardium. Typically, it involves the subepicardial layer, or the mid-myocardial layer, also called the mesocardium, and the lateral wall is most frequently infected. In fact the lateral wall is most commonly affected by viral infections caused by parvovirus. However, for infections caused, for example, by the herpes virus more likely affect the septal wall of the left ventricular myocardium.

Here's another example of myocarditis now from a different patient, where we used a mapping technique to show edema. And again, the image shows this abnormal enhancement within the septum of the heart. You can again see the mesocardial, mid-myocardial enhancement within the interventricular septum. The color image is a T2-mapping image, where the color intensity depicts the T2 value. T2 values above about 55 ms are considered abnormal and are considered indicative of edema. So you can see that the high T2 value of 76 ms also corresponds to the abnormal enhancement within the interventricular myocardium. T2-mapping or T2-weighted imaging can be very helpful as an adjunct image or an adjunct finding in making the diagnosis of myocarditis.

Here's a different case, again showing myocarditis, but this is now giant cell myocarditis, so not an infective viral form of myocarditis. This typically may occur as an autoimmune phenomenon. In this case, there is diffuse enhancement throughout the left ventricular myocardium. When we look at the T2 mapping, all segments of the left ventricular myocardium measure approximately 75 ms, which indicates myocardial edema. So this is diffuse gadolinium or contrast uptake throughout the left ventricular myocardium with diffuse edema in a severe case of giant cell myocarditis. The pattern of involvement of the entire heart does point more likely to a non-infective type of myocarditis, which carries a worse prognosis compared to if it is just more localized.

There are criteria which have been described in the literature, called the Lake Louise criteria to help diagnose myocarditis on cardiac MRI. These are divided into main criteria and supportive criteria. For the main criteria, you need to demonstrate myocardial edema within the left ventricular myocardium, and this can be done with either T2 mapping to measure the T2 value as a surrogate for edema, or you can also do T2-weighted imaging, such as STIR (short tau inversion recovery) imaging, to show bright signal within the edematous segments of the left ventricular myocardium.

You can also look for areas of myocardial injury, and this will most classically be demonstrated by abnormal uptake of gadolinium on late gadolinium-enhanced imaging but can also be demonstrated by abnormally high T1 or an abnormally high extracellular volume measurement within an abnormally damaged area of left ventricular myocardium.

For the supportive criteria, we try to demonstrate the presence of pericarditis, either pericardial inflammation as was shown in our first case or a pericardial effusion, which indicates that there's some type of inflammation going on, plus or minus left ventricular systolic dysfunction. We always measure left ventricular function when we do cardiac MRI.

So what other cardiac possibilities would we want to consider in this younger patient who presents with chest pain? The image shows a classic example of pericarditis. The cine image shows relatively normal function, although the septal motion is abnormal, and then there's diffuse pericardial enhancement, almost like this eggshell of bright signals surrounding the entire left ventricular myocardium. This is the pericardium enhancing and encasing the left ventricular myocardium. This really diagnoses and confirms pericarditis. In this case, the abnormal septal motion may suggest a constrictive physiology, which can be caused generally by chronically thickened pericardium or chronic pericarditis.

The image is a case of apical ballooning syndrome. This is where you get a transient occlusion of, in this case, the left anterior descending artery, which causes an abnormal motion of the left ventricular myocardium, so called ballooning of the left ventricular apex. It looks dyskinetic, but without any enhancement at all on the delayed-enhanced imaging. So the myocardium itself is viable. So there's no permanent damage to the myocardium. However, there's a significant wall motion abnormality. This has been associated with periods of increased catecholamine increase, such as would occur in us with a severely stressful event and typically resolves over time as the vessel reopens.

There are some other non-cardiac causes of chest pain. There's the whole category of acute aortic syndromes, which may mimic chest pain due to cardiac causes. So acute aortic syndrome can either be a dissection, which can be a type A dissection or a type B dissection. You can perform an MR angiogram as part of this protocol to show the dissection or the extent of the dissection. In this case, this is a type B thoracic aortic dissection extending into the abdominal aorta. Or you can get an intramural hematoma, which is bleeding within the wall of the aorta as illustrated by bright T1 within the wall, indicating that there's been hemorrhage into the wall. This is also called a non-communicating dissection because it's very similar to the dissection, it's just that there isn't active flow within the area of hemorrhage.

The is a classic example of a pulmonary embolus. You can see the filling defect in a pulmonary artery. The image shows a filling defect in the pulmonary artery. Typically, we would do CT to diagnose this phenomenon, but you may also see this on an MRI, and as I showed you earlier, the cardiac MRI may be ordered to diagnose a cardiac abnormality, and you may incidentally pick up a pulmonary embolism (PE).

What are the key points with this case? CMR is a quick and easy protocol and easy to run. In a case of chest pain, consider the alternative causes of chest pain besides coronary artery disease. T2 mapping or other mapping techniques may be useful adjuncts, in this case for detecting edema, or T1 mapping for detecting permanent myocardial damage. You can also add an MR angiogram to assess for vascular causes.

Thank you, and please continue to the next segment of this activity.

Segment 3: Incidental Findings

Kate Hanneman, MD, MPH, FRCPC: Hi, I'm Kate Hanneman, an Associate Professor of Radiology at the University of Toronto. I'm also a cardiac radiologist at University Medical Imaging Toronto at University Health Network in Toronto General Hospital. Today, I'm going to review 3 cardiac MI cases of incidental or unexpected findings. Let's get started with our first case.

This is a patient who presented with heart block and a cardiac MRI was ordered to look for cardiac sarcoid. We know that heart block is one of the potential presenting symptoms for cardiac sarcoid and so we performed this cardiac MRI using our standard cardiomyopathy type of protocol. So very early on, it became clear that there was something else happening or going on in this patient's heart.

So we're going to start by looking at the 4-chamber cine steady-state free precession (SSFP), and we can see that both the right and the left ventricles are contracting normally. This patient has normal ejection fraction (EF) for both ventricles, but there's some abnormal thickening in the region of the interatrial septum, which almost has a nodular appearance, and on a short axis stack, near the base of the heart, we can see that this appears to be a mass right in the region of the atrioventricular (AV) node.

When we looked at some more detailed tissue characterization sequences, here I'm showing you a still image of a cine SSFP, again, in short axis and the corresponding post-contrast, or late gadolinium-enhancement (LGE) image, we can again see that there's this ovoid mass in the region of the AV node, and which enhances homogeneously on post-contrast imaging. Importantly, there was no other myocardial LGE that would be in a typical pattern for cardiac sarcoidosis. There also wasn't any myocardial edema on our T2-weighted imaging, and we did not see any lymphadenopathy or pulmonary findings to suggest extracardiac sarcoidosis. So again, no findings to suggest cardiac sarcoidosis, but we have this unexpected finding of a mass in the region of the AV node. And importantly, of course, the AV node is important for conduction, and so this got us thinking, "Well, perhaps this is actually related to the patient's presenting symptom," which was heart block. We also did some more tissue characterization sequences on MRI, native T1 mapping and native T2, and we can see that on the T1 map, this ovoid mass has a very low T1 and a very high T2 compared to myocardium.

And again, here are some multiplanar sequences, post-contrast. Again, showing us that this is an enhancing mass. So we know this is a mass that is taking up contrast, and it's actually taking it up homogeneously, and it's located in the region of the AV node. Importantly, again, there were no findings to suggest cardiac sarcoidosis, which was the reason we did the cardiac MRI in the first place, but we have this incidental finding of a mass.

In this patient, we performed a cardiac MRI due to heart block. We were looking for cardiac sarcoid, which we did not find, but we found another finding, which was this tumor of the AV node, which would explain the patient's presenting symptoms. This was surgically resected, and on histopathology was consistent with a cystic tumor of the AV node. And this was a really important, unexpected finding, of course, because the treatment and prognosis is completely different than cardiac sarcoid. And really important to keep in mind potential differential diagnostic considerations that, again, might explain the patient's presenting signs and symptoms.

It's important that we target our cardiac MRI protocols so that they're appropriately short, so we can ensure patients have timely access to cardiac MRI and patients are comfortable in the scanner, that the scans are not too long. That being said, we also need to be sure as imagers that we evaluate all of the images and keep differential diagnostic considerations in mind that might be alternative explanations for the presenting signs and symptoms, other than the top differential that was being considered, as in this case, when the patient was initially referred for cardiac MRI.

Here, the key strengths of cardiac MRI really shine, and that is the tissue characterization. Not only were we able to identify tumor in the heart, but we were able to confidently say that this was a solid enhancing mass and had a very high index of suspicion that this would be a cystic tumor of the AV node even before the patient went to surgery.

Our next case is somewhat related. This is the patient who was undergoing chemotherapy for a known cancer and was referred for cardiac MRI for evaluation and assessment of the left ventricular ejection fraction. Here in 4-chamber cine SSFP, you can see, again, both left and right ventricles are contracting normally. So we have normal left and right ventricular ejection fraction. So we answered the clinical question that was provided to us in the indication, but you can see that there is a large filling defect in the right atrium. This appears to be attached to the right atrial wall, somewhat irregular and has low signal intensity. This was recognized at the time of the scan, so further imaging was performed at the time.

Here's the corresponding short axis cine SSFP and we can see to better advantage that this filling defect or mass is somewhat mobile. It does appear to be attached or adherent to the posterior inferior right atrial wall near the inferior vena cava (IVC) inflowing Eustachian valve but doesn't appear to be causing obstruction of the IVC. Again, it's somewhat irregular with margins and has low signal intensity.

On T1-weighted imaging, you can see that this is relatively isointense to myocardium and does not saturate on fat saturation imaging, telling us that there's not a significant component of fat.

On first-pass perfusion imaging, again, in a short axis orientation, we can see that there is no uptake of contrast. And on our delayed post-contrast imaging, we can see that the mass is homogeneously very low in signal intensity, again, suggesting that there is no cellularity, no uptake of contrast, and this is consistent with a thrombus. And so this is a potentially important incidental or unexpected finding in this patient who is undergoing cancer therapy.

And when this patient had subsequent CT, we can see that this thrombus is actually associated with a tip of an indwelling catheter that had been placed for chemotherapy. And this is likely related to that device tip in the right atrium, and this is a really important finding. This patient was subsequently started on anticoagulation therapy and really important to identify, of course, particularly when they're this large as this could embolize into the pulmonary artery circulation.

So this patient did have treatment. And here just showing you some follow-up axial CT images, the thrombus was followed with CT because it was obviously clearly seen. So on the baseline image, around the time of the cardiac MRI on the left, we can see, again, a large mass in the right atrium, and it did decrease with anticoagulation therapy over time, but didn't completely resolve and you can see on the follow-up that it's actually partially calcified. And so this became a partially calcified chronic thrombus, despite anticoagulation therapy. But again, a completely unexpected finding in this patient who had a cardiac MRI for another indication altered this patient's treatment at that time.

Our third and final case is a patient who also had a known malignancy and was referred for cardiac MRI for a different indication. This is the patient who was on immune checkpoint inhibitor therapy and had presented with some new cardiac symptoms, shortness of breath and had a slight troponin elevation. And the clinicians were concerned that they may have had myocarditis or immune checkpoint inhibitor therapy-related cardiac injury.

So we performed a cardiac MRI, and we'll start with our cine images. You can see by the way on the 4-chamber cine SSFP, that this heart looks very different than the ones we've seen before. So unlike the prior cases, the left ventricle is not contracting normally, we have impaired biventricular function. The left ventricular wall also appears diffusely thickened, which we can see on better advantage on our short-axis cine SSFP. So the wall is very thick, the ventricle is not contracting normally, and we can also see important extracardiac findings. There are bilateral pleural effusions and a circumferential pericardial effusion. So right away, even on the cine SSFP images alone, we can start to see that these are not findings that we would typically expect in a myocarditis or myocardial inflammation, but these are findings that we might think about in the setting of cardiac amyloid or infiltrative disease.

Of course, we went on and we performed further evaluation with our tissue characterization sequences. We can see on our black blood T2-weighted imaging and short axis orientation, there's some patchy areas of higher signal intensity, perhaps some edema, but not in a typical pattern that we might expect from myocarditis. And on our late gadolinium-enhanced image, again, in short axis, we can see that this is very abnormal. There's a dark blood pool, there's difficulty knowing the myocardium with diffuse high signal intensity, not only in the left ventricle but also in the right ventricle. And again, we can see that pericardial effusion. So again, if you showed this case to anyone without any clinical context, likely the first diagnosis that would come to mind would be infiltrative disease, including cardiac amyloidosis.

We also did some quantitative assessment with parametric mapping. Native T1 values were extremely elevated, well above the normal reference range, and those were diffusely elevated not only in the LV, but you can also see the part of the right ventricle (RV) that we see also has elevated T1.

We calculated extracellular volumes (ECVs), we had post-contrast native T1 in addition to hematocrit, and the ECV was also extremely elevated, almost 50%. The T2 map has some artifact, the patient was having difficulty with breath holding, and it's quite inhomogeneous, but you can see that there are perhaps some areas of high T2 signal, or high T2 mapping values rather, suggestive that there could also be some edema in this patient.

So to bring all of our findings together, we have a patient who has impaired biventricular function. They have diffusely thickened ventricular walls, and the atrial walls were also thick, difficulty knowing the myocardium, very high native T1 and ECV. All of those, again are classic findings that we would often think about in the setting of cardiac amyloidosis.

For a reminder, this patient had a known diagnosis of malignancy. In this case it was melanoma, and they were being treated with cancer therapy. In this case, the patient did go on to have a biopsy because these findings were unexpected and certainly we didn't find what the clinician was asking us to for, which was myocarditis. In this case, the histopathology was consistent with diffuse infiltrative melanoma.

So just a reminder here that this was an unexpected finding and a reminder that not all infiltrative disease in heart in amyloidosis, although of course that would be much more common than diffuse malignancy or diffuse infiltrative melanoma, in this case, which is quite rare. But really the clinical context is very important.

The biopsy was performed as it's possible that the patient could have had 2 different diagnoses, their underlying malignancy as well as amyloidosis. But here there was actually unifying diagnosis. So again, the tissue characterization findings here were very helpful in helping us to think about what might be going on, that might be causing the patient shortness of breath and that elevated troponin levels here because there was so much infiltrative diseases in the heart and the myocardium itself. There was, of course, myocyte injury as a result of that. So another unexpected or incidental finding that cardiac MRI has to not only detect, but characterize, and try to understand what was going on based on some of our multiparametric imaging.

Thank you very much and please continue on to the next segment of this activity.

Segment 4: Evaluating Dyspnea

Raymond Y. Kwong, MD, MPH: Hello, I'm Raymond Kwong, Professor of Medicine at the Harvard Medical School and the Director of Cardiac Magnetic Resonance Imaging at the Brigham and Women's Hospital. Today I'm going to review a case of a female patient presenting with dyspnea.

So this is the patient who presented at age 50. She has a history of hypertension, diabetes, not well controlled, and has chronic atrial fibrillation over the last few years. She presented to the emergency room in April of this year with severe shortness of breath. She has a hemoglobin A1C presenting at 13% confirming that her diabetes has not been well controlled. Interestingly, because of atypical chest discomfort, that she has experienced over the past year, she had a normal pharmacological stress MIBI-SPECT scans 2 years ago. When she presented this time, she had a high-sensitivity troponin T, which was minimally elevated at 26 ng/L. The upper limit of normal at our hospital was 9 ng/L.

A chest CT was performed in the emergency room to rule out a pulmonary embolism. And that was the case that PE was ruled out. A CTA was performed several months ago when the patient presented with atypical chest discomfort, and it confirmed that the patient had no significant coronary obstruction based on these images.

You can see the left anterior descending coronary artery (LAD) on the top panel, showing mild proximal narrowing and the right coronary artery (RCA) was also showed mild proximal narrowing. The circumflex had evidence of narrowing reported to be moderate. However, all 3 vessels were reported to not have any flow-limiting significance based on CT-FFR (fractional flow reserve – computed tomography).

Given her symptoms and her presentation of troponin elevation and her dyspnea, she was referred to a stress cardiac MRI for further characterization of her risk and also diagnosis of her symptoms. The first thing that was performed was a quick scan showing no evidence of myocardial edema using T2 imaging. Now, T2 is a way to look for myocardial edema, so it is an effective way to rule out any region of the myocardium that is an edematous due to an acute myocardial injury from acute coronary syndrome. And in her case, the T2-weighted images on the top panel show what was negative and it demonstrated no evidence of swollen myocardium or area at risk from a coronary event. This negative scan was confirmed by a negative T2 mapping, indicating no area of myocardial edema confirmed on the right side of the polar plot, demonstrating that the T2 value of all 16 segments were less than 50, which is the upper limit of normal. And you can see that the T2 is negative based on the diffusely blue color, indicating low T2 values.

The myocardial structures and fibrosis also confirmed that there is no wall motion abnormality, which also suggest that there's no acute injury. However, on the top panel, you can see that the patient has significant increased wall thickness in the presence of a normal systolic ventricular function, EF of 65%. The LV wall thicknesses are diffusely increased, and not only that the LV mass is increased at 65 g/m², indicating that she has concentric left ventricular hypertrophy. This pattern was matched by the pattern of late gadolinium enhancement, or LGE, as shown below that there is myocardial fibrosis in this thickened ventricle. You can see the mid level on the center, the basal level on the left, and the apical level or distal level to the right, that between 12 o'clock to 3 o'clock, there is mid-myocardial late enhancement that demonstrated increased signal in the myocardium consistent with fibrosis. Now, this pattern of diffuse fibrosis is suggestive of diseases such as hypertension or diabetes that affect the myocardium. It is not of the pattern of myocardial infiltration.

Now, such finding again in CMR, not only we can see it by weighted imaging scan but also it can be confirmed by tissue mapping. So what I'm showing on top here is the late enhancement on top. On the bottom panel is the ECV mapping, which is a method to map the degree of fibrosis in a continuous scale. You can see that in the matching region in the anterior wall, the green area indicating mid myocardial enhancement, which is indicating the area of increased fibrosis, matching the late LGE. On the polar map, the similar pattern that show you that the extracellular volume is expanded from fibrosis. The degree of expansion of ECV is noted on the polar map showing the ECV is of the value between 37 to 39, which is increased compared to a normal value of about 30. So this indicates a degree of fibrosis from likely hypertension or diabetes. This is not the pattern seen in amyloid.

We also quickly perform a stress myocardial perfusion. We typically use the quantitative stress perfusion method, which is increasingly available across many centers. On the top panel is the stress profusion during regadenoson stress on the bottom are the same slice and the basal, mid, and apical orientation at rest.

So you can see on top, the stress profusion, there's a diffuse endocardial blush or defect circumferentially around the base and also the mid region. Also involved the apex as well. This pattern of diffuse and endocardial and mid myocardial changes or perfusion defect is typical of microvascular coronary disease as seen commonly in hypertension and diabetes. It is not suggestive of diffuse coronary disease or epicardial stenosis-type pattern, which is consistent in this case from the CT scan that she has no significant epicardial coronary stenosis. When we quantify the stress myocardial blood flow, all the segments and the base and mid were reduced to 1.3 to 1.6 range. A normal segmental myocardial profusion typically will go over 2 mL/g of tissue per minute. In this case, it's diffusely reduced, which is again, as I mentioned, is consistent with a small vessel disease.

Interestingly, 10 years ago when the patient was 40 years old, she was diagnosed with hypertension. At the time, she did not have diabetes. Her ventricular function was normal. She had less severe wall thickening, and she did not have any pattern of myocardial fibrosis on her late-enhancement imaging as shown on the bottom panel. Indicating that over the course of 10 years, as she has developed uncontrolled diabetes and also worsening of her other risk factors, she is now presented with a picture of heart failure with preserved ejection fraction (HFpEF) with evidence of increased myocardial fibrosis and microvascular dysfunction as a result.

In this case CMR examination, which took a total of 35 minutes, including the stress CMR component, was able to rule out an acute coronary syndrome (ACS) using T2 imaging cine and LGE. It also excluded a myocardial infiltration due to amyloidosis or sarcoidosis, but it was able to diagnose a pattern of adverse left ventricular remodeling consistent with heart failure with preserved ejection fraction, likely due to hypertension and diabetes. But most importantly, CMR was able to also diagnose microvascular disease by quantitative perfusion method, which explained the patient's longstanding dyspneic symptoms.

Based on her symptoms and the clinical picture and most importantly the CMR results, the patient was treated with intensified diabetic control and other antihypertensives, in addition to her other guideline-directed medical therapy. At 2 months follow-up, the patient reported that she was chest pain-free and her dyspnea has substantially improved on exertion on a follow-up clinic visit.

With that, I hope this case has been effective in demonstrating how CMR can allow us to better understand the presenting symptoms of patients presenting with dyspnea, especially in this middle-aged lady.

Thank you. And please continue to the next segment of this activity.

Segment 5: The Clinical Value of Cardiac MRI

Dr Kwong: In summary, CMR performs high resolution imaging of cardiac structures and soft tissue characteristics, allowing evaluation of myocardial ischemia, infarction or infiltration, inflammation, and myocardial fibrosis.

CMR not only diagnose but also prognosticate common causes of chest pain and dyspnea as in the cases you have seen, such as coronary disease, but also it can assess for microvascular coronary disease and non-coronary pathologies, including acute myocarditis and various causes of cardiomyopathy. A standardized CMR protocol that may include cine imaging, perfusion, T1 and T2 tissue mapping, and late-enhancement imaging, or LGE, can be achieved in as little as 30 minutes, allowing high patient throughput and comfort. CMR imaging often can see incidental or unexpected conditions, therefore it is important to keep an open mind when you approach different cases. Some overlapping patterns can also exist across different diseases, so CMR interpretation should always be aligned with the clinical context of the case in order to provide informed decisions.

With that, I thank you for your participation in this activity. Please continue on to answer the questions that follow and complete the evaluation. Thank you.

This transcript has not been copyedited.