Good morning and thank you very much for all of you who have joined us so early on the last day of RSNA. In the next 17 minutes or so, I would like to talk about the acute chest pain in the emergency room. So the importance of the diagnosis of cardiac causes of acute chest pain cannot be overemphasized. It's important to now understand the role of cardiac CT in the emergency room, which not only has been there already for a long period of time, but now has been also validated by the recent American Heart Association and the similar societies recently, approximately a year ago. So if we think about the coronary CT and the role of coronary CT in assessment of the acute chest pain in the emergency room or in the inpatient setting, for that matter, we probably understand that the role of it is not only to diagnose, but also to exclude patients who do not have acute coronary syndrome. In my talk, I will primarily focus on the acute coronary syndrome and its assessment and I will touch base a little bit on the acute myocarditis and acute pericarditis as two other very important causes of acute chest pain. So if we think about the historical approach to acute coronary syndrome, it's really a triad that we are basing our diagnosis on. History, ECG changes, cardiac enzymes. Now, the cardiac CT had a very, very modest role originally in diagnosis of acute chest pain. So if we think about it, only patients with intermediate risk and sometimes patients with low risk who were very stable, they were assessed with CT and we'll talk about the calcium score in this setting, and the rest of it really did not benefit from this modality. But then the pile of evidence continued to grow and there are literally hundreds of papers and dozens of randomized trials and registries who essentially brought cardiac CT, coronary CT in particular, to the first line imaging strategy for rapid triage of the patients in the emergency room, the ones who present with acute chest pain. Those are the guidelines I was referring to. They were published last fall and those are the joint guidelines for the evaluation and diagnosis of the chest pain. So what do those guidelines tell us? They tell us that in acute chest pain, in patients with suspected coronary artery disease, coronary CT is important to exclude, pluck, and obstructive coronary artery disease. And in patients with known coronary artery disease, the ones that we know has coronary artery disease, the coronary CT has an important role to determine progression of the pluck and progression of obstructive coronary artery disease. Just to touch briefly on CTFFR, which is an adjunct and additional information that we get from coronary CT, in patients with suspected CAD, it's important for the diagnosis of vessel-specific ischemia and for guiding decision-making regarding the use of coronary revascularization. And in patients with known CAD, it could be useful for diagnosis, again, of a vessel-specific ischemia and to guide decision-making. So similar approach because in addition to the anatomical information, it gives us a functional information, which is vessel-specific. So if we look at the level where the coronary CT was placed in those guidelines, it's pretty much the highest level any of the imaging modalities has received so far, which is 1A, the highest level of recommendation, most evidence-based, and with the presence of the information gathered by the randomized trials. So as we said, coronary CT is offering us rapid evaluation of the degree of coronary stenosis and atherosclerosis, reduces the time to discharge and resource utilization in the patients in the emergency room. It also helps us to ensure that high-risk patients are appropriately triaged to cardiac catheterization. We know that the patients who have severe stenosis, we see it, they can go directly to revascularization. We obviously can use the fact that this is a CT, as any CT that includes other parts of our body. It shows us other important findings such as PE, pneumonia, pneumothorax, aortic involvement, you name it, everything that comes in the package of acute chest pain, and what was also very important recently and hopefully a little bit less important nowadays, that we also can do it rapidly and it really helped in the aspects of COVID-19 infection to diminish infection. So what are the current indications for use of the coronary CTA in the emergency room? Patients with low ACS risk, patients with intermediate ACS risk, and intermediate to high ACS risk, patients with end-STEMI, believe it or not, when non-invasive strategy is preferred. Why non-invasive strategy? They are in a high risk of bleeding, they have issues with vascular access, or patient prefers it, and I see not once and not twice patients who are high risk and they say, no, I don't want to get my cath until I get a coronary CT and I am sure I have a disease that needs treatment. So how do we triage those patients? There are several ways to triage patients clinically. This is usually the job of our partners, our clinical colleagues. They use several systems to triage the patients into low, intermediate, and high risk, and this includes the results of the troponin testing, and based on this triage, they would indicate if the patient does or does not go into the coronary CT pathway. So if we look at the updated algorithm, the one that we looked at originally, now you can see, and by the green circle, I mean all the risk categories that would benefit from coronary CT, it's essentially all the patients except the patients that have STEMI or unstable and STEMI, and they all could be appropriate candidates for coronary CT. So what is coronary CT? I know many of you are doing it, so for you, this information is really not that new, but I would like to just briefly say that when we are doing the assessment of coronary CT with acute chest pain, we are talking about a dedicated imaging of 12 to 14 centimeters, usually with a small field of view and excellent spatial resolution, with relatively low radiation, less than 3 millisieverts if we are using the contemporary scanners, and in some instances, it could be less than 1 millisievert, which is important in reassurance of our colleagues that we are not delivering high radiation, and we use relatively small amount of contrast, 70 to 80 cc, and sometimes even less than that. So what can we see? We can see a variety of pathology. We can see the atheroscleric disease, the classic atheroscleric disease, and assess the percentage of stenosis. We can appreciate the plaque not only as existing or non-existing, but also if there are high-risk features, for example, the positive remodeling or low-density nature of the plaque. We can see coronary artery dissection, also a known cause of acute chest pain. We can also appreciate myocardial hyperperfusion as a byproduct or a sort of a come-along data that we receive, acute versus chronic, or we can see other pathologies, such as pericardial effusion in patients with pericarditis, and I purposefully don't touch on pulmonary embolism or acute aortic pathology because they will be discussed later in the session. So how does it work? The first thing that it has to be an established cardiac CT program in the emergency room. I think that's very important. For those of you who do it, you know how important it is to have an algorithm, an established algorithm where both radiology and emergency room participate in according to special steps that start from essentially assessment and the risk determination of the patient and going through all those steps until the interpretation by the radiologist or cardiologist or joint program is done. And the presence of the physician is extremely important. We just spoke about that before the session. You need to have a physician available, ideally on-site, that can really answer all those questions. What protocol should we use? Do we need to do a heart rate control? Do we need to, after the images are done, send this patient immediately to the cath lab? You need to have an involvement of a radiologist, either a high-level trainee or an attendee. Let's look at a couple of cases with certain pathologists that come to us usually through the acute setting. This is a first case of a patient with acute chest pain. What we see is isolated left LAD disease with mixed density plaque, which had less than 70% stenosis, definitely more than 50% stenosis, so moderate disease. In this patient, we also were able to identify type B intramural hematoma. So the patient was then treated for the stenosis. The symptoms persisted, so they were attributed to the type B intramural hematoma, and the patient then underwent observation. So this is the first case and probably the most complex case that I'm going to show you where we can find both pathologists that could be responsible for acute chest pain. As opposite to this case that presented with acute chest pain, where the culprit was another example of isolated LAD disease with mixed density plaque, more than 70% stenosis, patient underwent CAS the same day, and the symptoms have resolved. This is the next case, a patient who was a 72-year-old with acute chest pain. We can see the plaque, and we can also appreciate the high-risk plaque features and the plaque burden. So not only we can see the degree of stenosis, we can also see the high-risk features of the plaque, and we can also appreciate the overall burden of the disease, which has been shown to be related to prognosis. So severity of the plaque, high-risk features, overall burden of atherosclerotic disease comes in one package. We also know that the combination of the high-specificity troponin and coronary CT features, such as high-grade stenosis and high-risk plaque, improve our accuracy for determination of patients with acute coronary syndrome that require treatment. Let's look at two cases here, and those are sort of companion cases. One is a patient that you guys saw. The other is a different patient. Both of them have approximately 50% to 69% stenosis. So what is our next step? So we're talking now about a patient with moderate stenosis. So what would be our next step? And our next step actually could be determined by the CT FFR application, because it will help us to decide if a moderate-degree stenosis is really associated with impairment or functional flow reserve. And we can see in this case that the CT FFR was demonstrated to be above 0.8, which is considered normal, and despite the fact that we said that most likely patient symptoms are not related to the stenosis, the patient was taken to interventional coronary angiography that showed 70% LAD stenosis, but the interventional FFR results confirmed that it's above 0.8 and no intervention was done. As opposite to a different case where also we see 70% stenosis, the CT FFR showed 0.7, which is low, which is abnormal, which was confirmed on the angio and the patient was treated. So our approach when available to patients with moderate stenosis or mild to moderate stenosis might be using the functional information either in the form of CT FFR or in the form of myocardial perfusion. Again, it's based on the local expertise, local availability, but the functional information really helps us to triage those patients even more efficiently. And this is along the same topic, but the patient where different vessels had different degree of stenosis. You can see here this patient had an acute chest pain, had three vessels. One vessel was severe stenosis, the other vessel was mild stenosis, the other vessel was moderate stenosis. So the question was, what are we doing with this patient? How can we get extra information? And then the CT FFR showed that actually the right coronary artery had a substantial drop in the functional flow reserve as opposite to the LED and those results were confirmed on angiography. So if we were to summarize the appropriateness use of Cardiac CT and its applications as a first line imaging in patients with acute chest pain, we do approve coronary CT with either CT FFR or CT perfusion, but there is no role for calcium score in the acute setting of patients with acute chest pain. If we are talking about the patients after vascularization, the major importance is for coronary CT and we don't really have enough data in terms of coronary CT and CT FFR and coronary CT and CT perfusion, although it does bring additional data to the table. So no guidelines as of now, which are being currently developed most likely, will also demonstrate that it does improve the triage of the patients. So what are the contraindications? Really at this point, there are very few, if at all, absolute contraindications. Perhaps anaphylactis to iodine contrast despite appropriate premedication, because everything else essentially could be incorporated and addressed. And currently, in some instances, patients who are pregnant actually are preferred to undergo coronary CT versus invasive intervention because we are looking for potentially coronary artery diseases, atherosclerosis, or dissection. So that was the majority of what I was about to talk to you about, which is coronary CT, and I would like to touch base on acute myocarditis and acute pericarditis. So acute myocarditis in the emergency room setting is really diagnosis of exclusion. We have to rule out acute coronary syndrome, and then we can look for myocarditis where CT really has very limited role, essentially just excluding other causes, and the main questions should be answered by MRI. Do we see the increased T2 that would show us edema and show us that there is an acute process? Will we see early and late gadolinium enhancement associated with hyperemia or necrosis? So we should think about myocarditis when we did exclude already the diagnosis of coronary artery disease. Acute pericarditis is seen more often in the setting of emergency room and acute chest pain, and more often than not, it's seen as an incidental finding on CT because nobody is sending a patient to emergency room to exclude pericarditis. Usually it's dissection or acute coronary syndrome, and then we do see pericarditis as an abnormal appearance of the pericardium on CT, pericardial effusion, pericardial enhancement, and the most accurate parameters for pericarditis are pericardial thickening and pericardial enhancement. Now if we diagnose pericarditis on CT, then we can go to the next step, which is MR imaging, and be very specific on MR, looking into specific findings such as the MR tagging, seen MRI, delayed gadolinium, and do the whole assessment of the pericarditis, again, usually done as a second step. So in summary, coronary CT in emergency room in patients with acute chest pain currently has been shown as a first-line test. Functional assessment, very helpful whenever available, either as the CT adjunct, as CT FFR, or CT perfusion. The acute myocarditis and pericarditis should be remembered in the setting of acute chest pain in patients in the emergency room, and they're usually either incidental finding as with pericarditis or diagnosis of exclusion as with myocarditis. And successful cardiac CT program in the emergency room is extremely important. We really need to have a program to have this modality successfully implemented. But we have to also remember that coronary CT in the emergency room is here to come and to stay. Thank you very much. I have the pleasure of giving the next talk, and we're going to move from the heart out to the aorta and talk about acute aortic syndromes. Our key objectives will be to recognize the common as well as the differentiating features of acute aortic syndromes, to understand and confidently use other terms, many, many acronyms associated with aortic disease, and review some of the prognostic imaging findings. Now these talks are all sort of centered on the vascular side of things, right? Coronary CTA, the aorta, and pulmonary embolus. And as we all know, chest pain is really the most common reason that adults present to the emergency department in the United States. And that's across age groups from 15 all the way up to above 65. And of course, as soon as we've moved out of the realm of trivial chest pain to non-trivial chest pain, then we often move into these differentials of PE or dissection or acute coronary syndrome. In the case of acute aortic syndromes, we're really talking about three main diagnoses. Aortic dissection, intramural hematoma, and penetrating atherosclerotic ulcer. Now the challenge with these things is that the clinical presentation is essentially indistinguishable. The patients present with acute, intense chest or back pain. They not uncommonly use terms very befitting of that pain, such as tearing, ripping, searing. One of the other hallmarks of it is that the worst chest pain is usually at onset. And of course, if the dissection or IMH stops, then the pain can actually regress or even abate for a period of time. This is almost always in the setting of hypertension. And if you look across these diagnoses, the common inciting event is disruption of the media and usually hematoma within it. So our typical CT imaging protocol of this involves multiple phases and of course includes both chest and abdomen. So it's usually either a non-contrast chest CT, which can be acquired or if you have dual energy, a virtual non-con, followed by arterial phase of the chest with or without gating. And then a contrast enhanced CT of the abdomen, again in the arterial phase and perhaps even a portal venous phase to follow up. Now this is quite a bit of imaging, particularly for some younger patients who may be getting screened for aortic dissection. And I think, I don't know what it's like at your institution, but generally speaking, I would say the yield on these studies at our institution, the positive rate is probably, it's certainly under 10% and probably closer to around 5%. So we really try to take, when we're able to, a little bit more of a bifurcated approach where patients who come and have a high pretest probability, either their clinical presentation is very, very dramatic, it's clear that something very significant is going on. If they're a little bit older, not that 50 is that old, I'm over that bracket there, but roughly around 50, and certainly if they've had prior surgery, then we will essentially do the full tilt protocol that I just described. However, in those somewhat low pretest probability patients who are really sort of screening, they have non-trivial chest pain, they're younger, no prior surgery, not likely to have atherosclerosis at their age, we tend to take a little bit more judicious approach and start with just a chest CT with contrast, where if we quickly see an alternate diagnosis and a very normal aorta, then of course we can stop. If there happens to be something that is considered a little bit indeterminate, I mean clearly we have aortic wall thickening here, the surgeon may be reluctant to take this patient to the OR just based on this alone, and we can say fine, we can bring them back, do a delayed scan and show that there's IMH there. If for whatever reason there's something about streak artifact or pulsation artifact that's concerning us, then we can gait it. And if it is positive for dissection, then we will continue it through the abdomen. And so that's just something to consider if you happen to be on site and you're able to screen these patients, particularly in a lower risk, younger population. Once of course we image them and we look at dissection, we classify it into Stanford A, Stanford type A or Stanford type B. About 60% of dissections involve the ascending aorta and about 40% occur after the subclavian and are classified as type B. Now there's somewhat variable appearance of dissections based on what happens once there is that intimal breach. And this is why you see that variable appearance and you have to be aware of it as well as the potential complications of an aortic dissection. So those three scenarios are that once you break through the intima, you can either, once it gets into the media, the media is thrombogenic and so the blood can clot and the dissection can essentially stop. And that's often what leads to what you see on the left, which is more of a, where there is enhancement of the true lumen, but that chrysantic clot within the wall that does not enhance. If the dissection breaks back through from the false lumen into the true lumen, then you get your true double barrel aorta where you have the true lumen that often enhances brighter than, of course, the false lumen as we see posteriorly in this patient's descending aorta. And the other possibility, of course, is that it breaks into the media and that the dissection continues and eventually bakes out through the adventitia so that you have the aortic rupture. And that, of course, can happen in the mediastinum and the retroperitoneum, or it can happen back into the pericardial space where you have hemopericardium. Now, it's also important to understand and to recognize the findings on enhanced CT, not only because it's often done when we're ruling out dissection, but sometimes, of course, the patient may not be able to get contrast or the patient may be getting screened for something else without contrast. And so it's important to recognize these three major findings that we see on enhanced CT. One is, of course, the positive entomal flap sign, which we see in the upper left image where it is aided often if you narrow the window to help you see better. The next one is intramural hematoma, which not infrequently accompanies aortic dissection. And of course, displaced entomal calcification. And so on non-contrast CT alone, you might be surprised. I mean, of course, we have to do contrast-enhanced CT to exclude dissection and to evaluate whether or not there is the morphology of the aorta. But it's important to recognize that, actually, unenhanced CT alone is actually quite powerful in seeing aortic dissection. In one study that looked at only the non-contrast CT, the readers were blinded to seeing anything on the contrast CT. They were able, when they said there was a positive entomal flap sign, aortic dissection was present in 87% of those cases. Deviated calcification, if they said that that was present in 78, nearly 79% of cases, aortic dissection was present. And high-density aorta, or intramural hematoma, was identified. And when that was identified, aortic dissection was present in 57% of cases. And you can see when aortic dissection was absent, when the contrast study was negative, that there were almost no false positive cases. And so it's actually quite powerful. Okay, now after we sort of transition away from aortic dissection, it's sort of the other AAS, which is sort of our aortic alphabet soup, right? We have IMH and PAU, IBP, sometimes also called IMBP, BAP, ULP. And so it's important to sort of understand this terminology and to recognize it. It helps that really that these two things are really the same thing. An intramural blood pool and a branch artery pseudoaneurysm are the same thing. So let's begin to take a closer look at this. So, a little bit later in the talk, we're going to look at this slide again. I'm going to ask you if you can identify the diagnoses that we just looked at, that aortic alphabet soup, on these images. So I'm going to give you just another minute here to begin thinking about it. And then we'll quickly talk through the other diagnoses. Okay, let's start with intramural hematoma. Like all of these diagnoses, they're almost always in elderly hypertensive patients. And when we talk about it in its purest form, we're talking about spontaneous IMH, which is where there is rupture of the vasovasorum, which is that small network of vessels that are along the adventitia, penetrate that and go down into the media to supply oxygen to the outer aortic wall. But more and more, we're recognizing that IMH may just simply be thrombosis of a dissection lumen. And if it's fully thrombosed and we don't see the intimal disruption, then of course it looks exactly the same as spontaneous IMH. We're also recognizing that there are microscopic intimal tears that we can't really see well on imaging. But when patients have surgery and the aorta is excised, those are seen at pathology. And then of course, you can have progression of penetrating atherosclerotic ulcers. As with all acute aortic syndrome, it's classified into Stanford A and Stanford B because that has some prognostic value. And the appearance at imaging is the smooth precintic aortic wall thickening, where there's high attenuation on the non-contrast CT, usually around 60 to 70 Hounsville units. And on IV contrast-enhanced CT, there is enhancement only in the true lumen. This is really sort of the classic appearance. And I think you can appreciate on the image on the right with contrast enhancement how subtle sometimes it can be on contrast-enhanced imaging alone, which is why non-contrast imaging has come to play such a central role when we are asked to rule out dissection. Treatment and prognosis. Type A is, again, for IMH, is managed surgically. And this is, of course, to prevent progression to dissection or rupture. If these are managed medically, about a third of these will progress, and there's about a 40% mortality rate. When it involves type B, it's usually just antihypertensive medical management, and those patients often do fine, and the hematoma can regress. But what are the risk factors for progression? Well, one is the presence of an ulcer-like projection, a ULP. The thicker the IMH, particularly over 10 millimeters, is a risk factor for progression. If there's an associated aortic aneurysm, it increases risk of progression. And of course, if you do follow-up imaging, if there's increasing thickness, then that is demonstrative of progression. So since we said ULP matters in the setting of IMH, let's take a look at that. What is it? Well, it's a small, broad-based protrusion of contrast enhancement from the true lumen into the IMH. It looks just like a little projection that of contrast into the IMH. By virtue of that, it reflects intimal disruption. And if you look closely, it's present in about 40% of IMH. And again, this is where it gets a little bit gray in terms of the overlap between IMH and, of course, a dissection. These usually occur in the descending thoracic aorta, and they do adversely affect prognosis. If you see them and they're present, there is a greater likelihood of progression of the IMH. They frequently enlarge. And of course, progression means that it can lead to dissection, aneurysm, or rupture. Let's contrast that with the IBP or BAP, where you have a small focus of contrast enhancement. It's, again, it's within the IMH, within that precintic hematoma, but there's no visible connection with the true lumen. These are also more common when the IMH has a thickness of greater than 10 millimeters, because that's what allows the little tear in the branch artery. So these are associated with the intercostal and lumbar arteries, which is, of course, why they're most commonly seen in the descending aorta. And importantly, unlike ULP, an IBP or BAP do not adversely affect the prognosis. These often regress spontaneously and require no dedicated treatment. If treatment is needed, it can be an endovascular coronabilization if they're enlarging or if the patient is having lots of symptoms. And last, let's look at penetrating atherosclerotic ulcers. These are usually seen in elderly male patients, particularly sort of like in the later decades, seventh and eighth decades. If you look at these patients, hypertension is present in 92%. There's usually a smoking history and a high percent as well and nearly half of these patients will have concurrent aortic aneurysms, usually a AAA in the abdomen. Again, these are classified just like dissection and IMH into A and B. And the appearance at imaging is that these most commonly occur in the descending thoracic aorta. They also occur to some extent in the arch and they're actually relatively rare in the ascending aorta. This is going to be a contrast-filled outpouching. And the important thing that you're often trying to differentiate here is, I mean, unless it's really large, when they're smaller is, is this a PAU or is this just a plaque with an ulceration in it? And so one of the things that's very helpful to have that differentiation is when contrast, when that outpouching extends beyond the intimal calcification. And so you're going to be paying attention to the ulcer in relation to the intimal calcification. Also, usually with penetrating atherosclerotic ulcers, intimal calcification is often remote from the ulcer itself. And it's often accompanied by a little bit of intramural hematoma, and that will give it a smoother interface as opposed to the more undulating appearance that we see with plaques. Here's a classic penetrating ulcer. This one's not subtle on the larger side, on the medial side of the descending aorta. And you can see associated with that ulcer that chrysantic smooth thickening that's coming around the aorta, which is accompanying IMH. The treatment and prognosis here, the initial imaging features are limited, actually, in predicting the course of these. There's no clear consensus on when to treat these. That tends to sort of be somewhat variable across institutions. But we do know that these can progress to dissection, aneurysm, or rupture. And the way that they're treated, if treated, is with endovascular stenting. So then, what maybe are some of the risk factors for progression? Well, definitely type A involvement of the ascending aorta. These will very frequently progress, and so just like IMH and just like dissection, these are usually treated. Makes sense that the larger the ulcer, the more likely it is to progress or to have complications, such as being the lead point for a dissection or rupture. So ulcer depth greater than 10 millimeters or a diameter greater than 20 millimeters. And again, on follow-up imaging, because these patients, if they are managed conservatively, are often monitored by repeat CT. And so if we see increasing size of the ulcer on follow-up CT. All right, so there is our alphabet soup. As we wrap up here, I just want to see if now when you look at these, you have a good sense of how you would parse out the different diagnoses here. So take another look. And I'll share with you one thing that I find helpful, which is it often is really useful to sort of, in your mind, draw a circle, what you think the outer wall of the normal aorta is. Because that will often help you tremendously in the differential. And here are the answers. So in the upper left, here is the outer wall of the aorta. We have a penetrating ulcer that's actually large enough that there's actually a contained pseudoaneurysm. If you compare that to the case immediately to the right, that's an ulcerated plaque, notice that the intimal calcification is beneath the plaque and the ulceration is just within that plaque. And of course, it's not extending beyond the wall of the native aorta. In the case over here, hopefully you recognize that the native aorta is back here and that this patient's had a graft. And so this is just a pseudoaneurysm at the site of graft anastomosis. This, of course, I'm sure everyone recognized is a dissection. And this is the classic appearance of the cobwebbing that we can see in chronic dissection, particularly in type Bs that are managed medically. And then differentiating our IBP from a ULP, notice the little contrast blush that we see in that smooth crescentic hematoma. There's no communication with the aortic lumen. And so this is in the thorax, so this is a little branch artery pseudoaneurysm of a intercostal artery. And then on the bottom right, we have again that smooth crescentic thickening of the anterior aortic wall consistent with IMH. And that little ulceration, that is a ULP, which makes it more likely that this particular IMH will progress. Finally, in terms of the acute aortic syndromes then, what are our imaging features that we want to report? In every case, of course, the Stanford classification. We're going to also be sure to report the maximum aortic diameter, particularly again if aneurysm involves the abnormality. We want to report that maximum IH thickness because if it's more than 10 millimeters, it probably has prognostic value or indicates that there could be worsening. The presence of a ULP or an IBP, but only a ULP has a negative prognostic value. The depth and diameter of our ulcers. Of course, if there's any periodic fat stranding that may indicate impending rupture or actual hematoma where there is rupture. And even though pleural and pericardial fluid, not necessarily blood, but just fluid, are fairly nonspecific, these also, when these diagnoses are present, have been found to be negative prognosticators. Okay, thank you very much for your attention. Good morning, everyone. I hope you're all awake after these two wonderful speakers in front of me. So today I'll be talking about pulmonary embolism in AD settings and predominantly concentrating on the acute PE. Oops, I'm sorry. Before I proceed with my talk, I would like to acknowledge the contributions of my wonderful colleagues towards the case for the mimickers. Colleagues from Indiana University, University of Kentucky, Wisconsin, VCU, Mayo Clinic, and Mass General. I really appreciate your help in the presentation. So my objectives today is just to show you the vascular changes that are relevant to the acute pulmonary embolism and talk to you about the importance of right heart dysfunction. And present to you some additional features that could be judged from multi-detector CTA in regards to the assessment for the mortality in the acute phase. I will also hopefully will have enough of time to show you the causes and imaging features of some of the non-thrombotic mimickers. Multi-detector CTA, the standard one, still remains the main working horse in the assessment of the acute PE, but the diagnostic power depends on the pretest probability as well as the location of pulmonary embolism in the sense that if the patient presents with the clinical picture that fits the acute PE and then there is a significant number of the risk factors that are associated with PE, then the positive multi-detector CTA, positive predictive value is up to 95%. And vice versa, if the patient clinical picture doesn't really fit the classic PE and there are no risk factors, then the normal multi-detector CTA has a negative predictive power of 96%. The diagnostic yield, however, of the detection of PE depends on the proximity of the thrombotic materials. It's very good for the proximal PE and it decreases, unfortunately, towards the distal branches. And in the case of the acute sub-segmental isolated vessel, PE, the discrepancy call could be as high as 67%. So what do we see in regards to the vascular findings in acute PE? So there are a couple of things that we should account when we're trying to decide if this is acute PE or if it's more of the chronic PE. It's just the caliber of the vessels involved and the location of the thrombus. So in the acute PE, the thrombus is usually located in the center of the vessel, in the non-thrombotic, not completely thrombotic PE. And if you cut the vessel on the short axis, then you will see something which is called the polar mean sign, with the thrombus in the center and the range of the contrast around. If you see this vessel in more of the longitudinal plane, then this is what it looks like. So again, the thrombus is gonna be in the center and the contrast is gonna be on both sides, creating so-called the railway sign. And noticeably, the size of the vessel is preserved, but in the case of the completely thrombotic PE, it's gonna be increased. And if it's a partially thrombotic or neocompletely occlusive, just pay attention to your borders between the thrombus itself and the pacified lumen. So the angles are usually acute, as opposed to the chronic PE, where it's more of the blunt. So as we go by, and when the thrombus starts to disappear, hopefully with the treatment or by just the natural evolution we have, decreasing or melting sign of the thrombus in the vessel and the vessel assumes more of the normal position. And about two months of later or so, a small number of the patients still have a little bit of thrombotic material within the vessels left. So these are usually more of the eccentric and the size of the vessels, of the involved vessels is normal. In about one third of the patients, about three months, completely asymptomatic patients to note, you would still see a little bit of the residual thrombi in the case where they presented with the web-like feeling defects. And detection of this web-like feeling defects are much better for the segmental branches rather than for sub-segmental branches. Contrast this to the cases of a chronic PE where the thrombus, most of the time, assuming the eccentric position and forms the obtuse angles with the pacified lumen. In the cases of chronic thromboembolic pulmonary hypertension, you would frequently encounter some of the distal branches that will be completely occluded, as in this example, but they're usually beaded or irregular. And in severe cases, you will be presenting with the evidence of collateralization. Most of the time, it's just the bronchial arteries that are significantly dilated. In about 1% of the time, chronic PE will present with small calcifications in addition to the chronic thrombi, but obviously, those calcifications are very seen on the non-contrast phase. In 90% of the time, acute PE, they resolve. And the ED-related incidental 30-day mortality decreases from the subtle location of PE at 43% to less than 6% with the sub-segmental location of PE. And in regards to the chronic thromboembolic pulmonary hypertension, this one is not that frequent. It's about 4% of the time, but the survival is not that great, especially if pulmonary artery pressure is about 50. The risk factors do include the large perfusion defects, especially if it's more than three of them, younger age with significant initial abstraction to the vascular bed, and presence of antiphospholipid syndrome. And clinically, those are suspected to develop chronic thromboembolic pulmonary hypertension if the patient presents with a persistent dyspnea at three months after the acute PE, despite the full anticoagulation. Prognosis and clinical decision depends on the pre-test and post-test probability, and the patients are usually stratified into several groups. Significant number of the patients with acute PE, about 95%, will fall into the category of low-risk mortality group, with the chance of death of about 1% to 2%. So in this group, the patients will be normotensive. There will be no signs of the right heart dysfunction, and the location of PE is rather distal than proximal. Intermediate group comprises about 2% to 3% of all the patients with PE, and the chance of death is about 3% to 15%. So as opposed to the normal low-risk mortality group, so those patients also will be normotensive, but there will be signs of the right heart dysfunction, either by the imaging or by the lab assessment. And for the lab assessment, there are two factors that seem to be playing the most of the sensitivity, so it's a pro-BNP factor, which represents the shear stress to the right ventricle, or the cardiospecific troponin that gets elevated when there is a necrosis of the right ventricle. So if the patient shows those signs, so that will be categorized into the submassive PE group, and usually more aggressive treatment is instituted for this group. So there is only a small number of the patients that will fall into the high-risk category, but the mortality here is very, very high, 25% to 65%, and even higher, up to 80% if the patient requires the mechanical ventilation presentation. So those patients present with a significant hemodynamic instability with the systolic blood pressure less than 90 millimeters that is not correctable for at least 15 millimeters, or signs of shock with pulselessness or profound bradycardia that would require an atrophic support. So those patients are categorized into the group of the massive PE, and usually require significant measures in terms of the thrombolysis, or even the mechanical thrombectomy, but even then, the mortality is still very high in this group. So what are the imaging prognostic factors that we can provide from our multi-detector CT? The one that has been established and shown on multiple papers and guidelines is the size of the right ventricle, and even more so, the ratio between the right ventricle and the left ventricle. If RV to LV ratio is one, then the risk of death is about 5%, and then this ratio, the higher the ratio gets, the more mortality we get. And if the ratio of RV to LV is 1.7, then mortality is at least 20%. So how about the other features? So septal deviation has been shown to be one of the most specific predictors of significant right heart dysfunction, but it is seen in only about 25% of the cases. Main pulmonary artery dilatation is a sensitive, but it does not link to significantly to predict the mortality. The predictive power of the main PA delayed is only low to moderate at the most. But on the other hand, the dilatation of the azigous vein, more than 12 or 15 millimeter, or SVC millimeters, or SVC, more than 21 millimeter, or coronary sinus. So these are additional significant features that would help, in addition to the RV, to stratify the patient into a more severe case for the mortality prediction. And even more for the IVC reflux, but it's not just the reflux itself. Like, for instance, if you have reflux into suprahepatic IVC, so this one doesn't seem to have a whole lot of correlation with the mortality, but if the reflux gets deeper into the retrohepatic or infrahepatic IVC, so this is the one that's been linked even better than the septal deviation with significant RV dysfunction, and very little correlation with the biomarkers level as well. One of the other imaging prognostic factors that might be an early predictor of the hemodynamic compromise and further cardiac chamber changes is actually the size of the left atrium in the presence of the DALI, the trite atrium. And if you do volumetric analysis, then the volume of 62 seems to be the cutoff that is linked to the two times increased 30-day mortality. But if you, I'm not the person that likes this significant, and sometimes there's just not time for that. So I just use the short axis diameter of LA at the mid portion. If it's less than 2.5, then to me, it seems to be too small. In the cases of PE, it may have an impact on the stratification. How about the left heart dysfunction and the presence of coronary artery calcifications in the PE settings? Do they matter? They obviously do. And they make our assessment, of course, difficult, especially assessment of the acute right heart dysfunction when your left ventricle is that huge, as in the case here. But overall, if you have any signs of the heart failure, most of the time, it's the left heart failure, then the long-term low-cost mortality will be higher in the settings of PE by at least a factor of two. In the same with the presence of coronary artery calcifications. So moderate to severe coronary artery calcifications, they do increase mortality anywhere between 7% to 10%. And in regards to the significant left ventricular dilatation and even distal subsegmental PE, these patients have a tendency to be more symptomatic, develop more of the pulmonary infarcts just because they have a low cardiopulmonary reserve to start from. Incidental PE, a couple of words on that. So they may be symptomatic, they may be asymptomatic, and they're seen most of the time in the patients after significant trauma or the patients with the cancer. In regards to the cancer, they might be linked with the overall progression of the malignancy. So outside of these groups, about 16% of the ICU patients and about 17% of the patients of advanced age may also present with incidental PE. And most of the time, this is not the CT-APE, it's just a standard CT examinations, contrasted ones. So what do we do with those? So if we see the incidental PE and the patient is not suspected to have one, then the next step will be the duplex of the lower extremities just to look for the signs of DVT. So if the patient has isolated sub-segmental PE and DVT comes back negative, then it may not be unreasonable just to withhold the anticoagulation provided there is no risk factors, and just to watch this patient. On the other hand, if there is a significant amount of incidental PE, even in the case of negative DVT, so these are the ones that should be treated with the full anticoagulation. And also, there is another category of the patients even with sub-segmental PE, but if the patient hospitalized, his mobility is decreased, and there are no reversible risk factors for PE, these are also the ones that should be treated with the full anticoagulation. But overall, if there are no risk factors, there is one single vessel sub-segmental PE, then the recurrence risk for the subsequent PE is very low, less than 1%, but at the same time, with the full anticoagulation, these patients are more in danger of the major bleeds, up to 5%. All right, so let's look at some of the mimickers. So this is increased vascular resistance case, which is a frequent source of debate, especially for my residents. So in these situations, we have decreased, relatively decreased, the pacification of some of the distal branches if you compare them to the contralateral branches. And most of the time, it happens in the cases that looks like that, a significant amount of autolactosis that has been present for a while, most of the time in the presence of chronically thickened pleura plus minus effusion. And the way to overcome that is just to give more contrast at the higher rate and more of the volume, and then the image the patient at the end of the injection. So that way, you can have a better pacification of these vessels under the question. The other one is the in situ thrombosis I have seen. I'm sure you have seen many cases of that over the last two years. So most of the time, these type of cases are seen in the patients with a protracted course, the patients that are hospitalized, that are still with fevers, et cetera, insignificant dyspnea. So what you're gonna be seeing, you're gonna be seeing most of the time just sub-segmental feeling defect. It's usually one or two. It may be complete, as in the case here, or it could be just partially occlusive. And they are just dealing with the whole mediated induced inflammation in the cases of COVID, such as endothelial inflammation and then hypercoagulability in hypoxia. These are the patients that would require more of the full, and that would benefit from the full anticoagulation rather than prophylactic doses of anticoagulants. Other cases of in situ thrombosis are related to the previous surgery for the lung cancer, specifically pneumonectomy. And in small number of the patients, up to 12%, you can see the presence of the thrombus at the stump. It's more of the right pulmonary stump rather than the left. And in about two or three months, the amount of the thrombus is decreasing. But in some situations, you can see the buildup of the thrombus in convex borders, in which situation some of the groups propose the prophylactic anticoagulations just to prevent the PE to the contralateral lung. In addition to the surgery in the cases of treatment for the lung cancer with the radiation treatment to the central forms of the cancer, you can see also thrombus formation, which usually presents with the obtuse margins in regards to the pacified lumen. And similarly to the post-pneumonectomy side, the amount of the thrombus has a tendency to decrease by two, three months. And if this is the situation, the patient usually does not require the anticoagulation but rather observation. All right, so let's switch to some mimickers of the pulmonary embolism. So the ones that are significant diagnostic dilemma is obviously tumorous mimickers of pulmonary embolism. Even when you see them, and there is still, it's quite a bit of uncertainty because patients with the cancer overall are hypercoagulable and increased risk of just the blunt PE. So what are the things that would allow you to suggest that you are dealing probably with the tumorous PE rather than the blunt PE? First of all is the presence of advanced malignancy elsewhere. And by elsewhere, most of the time it's gonna be HCC or the RCC, less frequently the pelvic tumors or the breast cancer or sarcoma. And if you look at the source of the malignancy, then it's usually just behind the organ itself. And most of the time you will see the presence of the vascular and venous invasion in the vicinity of the main bulk of the tumor. And then if you look at the PE, which is the result of the tumorous pulmonary embolism, so it's usually the large bulk of the tumor, less frequently it's gonna be just a small amount of the PE to the distal branches. And they're usually heterogeneous in appearance. And by heterogeneous, you can put your ROIs, but sometimes I like to do just a visual assessment and compare the density with the density of the muscle. So if the density of the thrombus matching the density of the muscle, then it's probably more than just the blunt PE. This is another case of tumorous mimickers of pulmonary embolism in a person with the advanced HCC. If you look at this tumor emboli, you will see that they are heterogeneous, especially on this one. So they're alternating areas of the low density with the higher density. And again, if you look at these areas of the higher density, they're matching the density of intercostal muscles. So this is just not just a blunt tumor. And the other one which is almost always missed, there is a bunch of case reports and they always start with like, well, we missed this case for many, many months. But sometimes you can catch it on the first presentation. So what are we looking for? Well, again, we're looking at the density. The density will be higher than just the blunt thrombus. And then if you see the extension of this pseudo-PE beyond the vascular margins, then it's probably not just the blunt PE as in the case here. And if you see something that looks like that, where you have this so-called cauliflower appearance of the pulmonary thrombus, and which regards, which sort of involves and deals with the circumferential growth of the angiosarcoma, then it's one of the other characteristic features of pulmonary angiosarcoma. And then obviously, these are very aggressive tumors with a very low survival rate, only 8% by five years. So if we do a PET-CT, we will see significant metabolic activity, which is with the mean SUV of six or even higher. The other mini-cure is the air embolism. So please be aware that about 20%, 25% of all contrasted CT, we would have a little bit of air in the main pulmonary artery, even sometimes in the right heart. Two, three lacules in a stable patient doesn't mean much, so you shouldn't really worry much. But if you start to see the presence of air beyond the proximal pulmonary arterial circuit, this is the ones that usually require some observation. So the patients, even with that set of scenarios, tend to have a tendency to do well and absorb the air in about 24 hours. They may be symptomatic with dyspnea, with the chest pain. And if they do have symptoms, then you probably need to do more than just the observation. You will have to put the patient in the left lateral D-cube, put the head down, and sometimes even need to supplement with the additional oxygen. So the lethal volume of the air is very, very rare, and there are some case reports which has shown that the lethal volume of air is about half of the liter injected with 100 cc, 100 milliliters per second, which almost never happens in diagnostic presentation. And the final case that I'm gonna show you is the fat embolism. So if you see the fat density in the pulmonary arteries, you are lucky. Most of the time you won't see them because there will be some contrast, the volume averaging with some contrast in the vessels, and you will see something like this. You may see just a slit of something that looks a fat density, but a significant amount of those feeling defects will just look like PE. But the clue for you will be obviously the risk factors for the fat embolism. So those risk factors will be significant fractures of the long bones, usually the lower extremity more than the upper extremity, plus minus the pelvic fractures. And so these feeling defects, they usually have, they absorb with about one week or so, but in a small number of the patients, they may develop the fat embolism syndrome, in which case about 24 to 48 hours after the initial episode, you may see something that looks like this with GGO, ground glass opacities, which could be diffused, as in the case here, or geographic. They may or may not present with septal thickening, and the pleural effusions are usually not the feature of this syndrome. So the patient symptoms may range between little bit of dyspnea, but in small number, they may evolve into the ARDS. And the other one that I'm gonna show you is even more difficult. So this is the one that actually presents with the blunt fat within the vessels, but then this is not because of the trauma, this is because of the tumor. So in the case of the tumor with the fat embolism in the pulmonary artery, it could be just the fat itself from the bone marrow, or it could be the tumors emboli that containing the fat. And similar with the case here from the literature where you can see there is a patient has some mass-like lesion in the liver, which was proven to be HCC with the fat content, and later that has embolized to the pulmonary artery, presenting mainly like a fat embolism, that that was actually the tumors embolism. So in a summary, I would like to provide you with some points, so just when you look at the PE in the acute settings, just don't look only at the vessels. Try to make an attempt to assess the hemodynamics in regards to the cardiac chamber changes and interdependence between them. In the case of isolated sub-segmental PE, do not be hesitant to recommend DVT. And if you are dealing with the potential case of the mimickers, then you can do the follow-up, short-term follow-up, especially in the cases that don't seem to respond to the end-day coagulation. And with that, I would like to thank you for the attention, and this is my email if you have any questions afterwards. Thank you.

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