In our first case, I'm gonna be reviewing cardiac masses, and as you can see here, there is a quite obvious mass within the right heart. It's a very irregular, lobulated mass. It looks like it's crossing from the right atrium into the right ventricle, also a little bit of enlargement. As we look further down, we can see evidence of increased pressure in the right atrium. We see reflux of contrast into the IVC, coronary sinus. We also see some collateral flow in smaller vessels. And if we continue to follow this, we see that there is enlargement expansion of the mass into the superior SVC, as well as a large mediastinal component. So this is an example of a malignant thymoma with direct extension into the heart. And this first case really illustrates the primary thing that we should all remember, that most cardiac masses are going to be metastatic. If you had to place a bet, think METS first. And then depending upon the mass, depending upon other findings, other features, we can try to be a little bit more specific. Somewhat of a correlative case. This is another lesion, again, in the right atrium. And we follow this down. We see that there is expansion in this case of the IVC. So a large mass extending downward. And we see that there is involvement of the left kidney. So obviously this is a case of renal cell carcinoma with METS invading directly into the right atrium. And this is fairly typical. This extension to the IVC, very common. Obviously whenever you see this type of lesion, mass creeping towards the IVC, you wanna look further down into the abdomen to see the extent of it. All right, let's go with our next case. And let me turn on my timer. Sorry, I just cheated. I gave myself some extra time. So here we have two patients. Patient A, patient B. So what do we see? Well, obviously patient A, we see a pretty well circumscribed lesion in the left atrium. It's kind of on the more medial side. You know, kind of near the interatrial septum. As opposed to patient B, patient B also has a left atrial mass. But this is a little more irregular. Looks kind of more villous. So in this particular case, patient A, patient B, these are both examples of a cardiac myxoma. And this actually highlights some of the variation that these myxomas can have. Most occur, most are benign, obviously. It's the most common benign tumor. Most occur in the left atrium, but you can also see them in the right atrium, even rarely in the ventricles. Incidentally, these myxomas don't invade into the myocardium. In fact, when you talk to the cardiac surgeon, they literally say they just kind of pluck them off of the endothelial of the wall. But again, these are going to be the most common benign tumor that we see in hearts. So remember, first, METS first, then myxomas would be the next most common benign tumor. So let's go on to the next case. So here it's case four. We see on echo, they saw this weird kind of echogenic structure near the apex of the heart. Not quite sure what it was. Worried about a mass. So here we did a cardiac MRI. So this is the steady state prepossession sequence, and we can see the mass right here. We can see this kind of India ink artifact around it. This was actually a lipoma. So this is a cardiac lipoma. This is kind of the characteristic appearance here we see on T1, the more characteristic appearance that we see with increased signal. Cardiac lipomas are the next most common benign cardiac mass that we can see. And the features, fortunately, are very characteristic, on cross-sectional imaging, whether it's CT, MR, usually we can characterize it pretty well. And again, whenever I hear, oh, I see an echogenic structure on echo, one of the first things I think about is like, hmm, I wonder if there's a fatty-type lesion. Now moving on to our next case. So here we have, this is a scout from the patient's CT, and we can see that there's an enlargement of the cardiac silhouette. No real appreciable increase in the vascularity on this study. And clearly, when we look on the cross-sectional image on the CT, we can clearly see this kind of well-circumscribed lesion along the left aspect of the heart giving the cardiac silhouette the contour that we see here. Now certainly, this looks low-density. When we look at the histogram, the profile of attenuation across this lesion, we see it's in the low range. This is a pericardial cyst. And certainly a mimic for cardiac mass that we would appreciate on the plain film. And these pericardial cysts are predominantly asymptomatic. Very rarely, these patients can present with symptoms related to compression because of increased size, which less than a quarter of patients. And sometimes there can be enough compression that there's even erosion of adjacent structures. Now as somewhat of a correlate, here's another study. Again, another CT. Again, an enlargement of the cardiac silhouette. And again, we see another lesion, which looks like it's right outside the heart. But I would say when we look at the overall attenuation, certainly looks like there's a different profile. Looks a little more soft tissue. Now certainly, pericardial cysts can be complex. They can bleed. They can have other protonaceous material. But in this particular case, we saw that there was a tremendous amount of cellularity. And this was actually a localized fibrous tumor of the pleura. So a little bit crazy, but they can happen. Most of these do arise from the pleura. But cardiac localized fibrous tumors are possible, but rare. They're still classified in the kind of pericardial category as opposed to being strictly cardiac. But again, another potential lesion that you can see with this enlargement of the cardiac silhouette. All right, let's go back to more characteristic masses. Here again, two patients. Patient A, patient B. So what do you see here? Well, when you look at patient A, we see this kind of a regular mass. It looks kind of intramural in the lateral wall of the left ventricle. We see it seems to cross over the left atrium, left ventricle. We see a spot of calcification in the middle. When we look at patient B, we see a similar lesion. This time more involving the septum. Again, looks somewhat intramural. Maybe a little bit more circumscribed to some degree. So patient A, patient B. Patient A is actually an example of a cardiac fibroma, whereas patient B is a rhabdomyoma. So again, very similar lesions. Some important things to think about when we look at them in contrast. Fibromas are typically solitary. Oftentimes they're very large and sometimes can completely obliterate the ventricular cavity, solitary mass. Where rhabdomyomas oftentimes can be multiple. When we see them in young kids, they can actually even regress. Particularly we'll see multiple lesions. Calcification is very common with fibromas as we see here, whereas we typically do not see calcification in the presence of rhabdomyomas. We see some mild enhancement in fibromas, less so with rhabdomyomas. But important, oftentimes these are gonna be further worked up with cardiac MRI. Fibromas will demonstrate some amount of late enhancement where typically rhabdomyomas have no enhancement. One final thing for both of these lesions to keep in mind is that they both have an association with tuberous sclerosis. So fibromas more so than rhabdomyomas, but both have some. And what's important is that in the presence of these lesions, it's important to also screen the patient for additional findings. Findings that suggest tuberous sclerosis. Okay, moving on. Next case. What do you see? You see some kind of infiltrative lesion surrounding the right heart. Looks like there's a little bit of pericardial effusion, maybe some oculated pleural effusion as well. Here on MR, we see again this kind of circumferential infiltrative mass. It looks a little aggressive. Further imaging on late enhancement, we see that there is definite enhancement of this lesion. Incidentally, when we also look down into the kidneys, we see this significant perinephric stranding. And on PATH, I know all of you are saying, oh, that's quite obvious. We see a lot of foamy cells. This is a case of Erdon-Chester disease with involvement of the heart. And involvement of the heart is actually quite rare. It's more common that you'll see it involving the kidneys. Most commonly you'll see involvement of the bones, kidneys, pulmonary involvement is also common. The heart, involvement of the heart is actually quite rare and is characterized by these non-Langerhans cell foamy histiocytes that the pathologists see as very characteristic. So Erdon-Chester involvement of the heart, very rare. But you saw it here. Next case, another, so this time we see plane radiograph. Again, marked enlargement of the cardiac silhouette. A lot of reticular nodular opacity throughout the lungs. On CT, we see again a very heterogeneous lesion infiltrating into the right heart. We see some other kind of consolidation in the right lung. When we look on the lung windows, again we see multiple areas of nodularity, pleural thickening, as well as this right pleural fusion. This is actually a case of angiosarcoma with pulmonary metastases. Now angiosarcomas, they're the largest group of differentiated cardiac sarcomas that we can see. And they typically involve the right heart, so it's not hard to imagine. Involvement with right heart, cellular debris entering into the pulmonic system and then embolizing into the lung itself. And more than 80% of cases will have some form of metastases at the time of diagnosis. So angiosarcomas are again quite, most common differentiated sarcoma that we see. Now that, as opposed to this, which looks far more benign, we see patient A, patient B. Patient A, we see this kind of well circumscribed small lesion on the aortic valve leaflets. Patient B, we see a similar well circumscribed lesion, this time in the left atrium, kind of along the ligament of marshal. This particular case, both cases are examples of papillary fibroblastomas. So again, very small, well circumscribed lesions. Classically they involve the, they occur on the valve, the aortic valve being the most common. But they can really originate on any endothelial surface. 10% can present on other surfaces. Again, aortic valve, mitral valve most common. Again, classically very small, very circumscribed structures. As opposed to, let's say, valvular vegetations, usually in that setting we'll see some amount of valvular damage because of the inflammation. Okay, next case. So here again, patient A, patient B. What do we see? Well, patient A, again, very heterogeneous, aggressive looking lesion with multiple areas of signal on MR, infiltrating the right heart. Patient B, again, infiltrating mass involving the right heart. We see a little bit of pericardial effusion on the CT. So both of these look very similar. You could argue which one looks more aggressive or if they look equally aggressive. But patient A, in this case, is an example of an angiosarcoma. Patient B is an example of cardiac lymphoma. And again, looking at the contrast between these two abnormalities, angiosarcomas, as we mentioned before, is the most common differentiated sarcoma, has aggressive activity, and as a result of its vascularity, has robust enhancement, as well as late gadolinium enhancement on MR. Cardiac lymphomas are actually quite rare. Now, this is separate from a mediastinal lymphoma, which then secondarily invades the heart. A primary cardiac lymphoma only involves the heart and no other structures. So we see that primarily in immunosuppressed patients. These patients often present with pericardial effusion, sometimes even large pericardial effusion. And the pericardial effusion itself can be, the cytology can be positive for the diagnosis in about two-thirds of cases. And as opposed to angiosarcs, which have robust enhancement, lymphomas tend to have a very mild heterogeneous enhancement. So that's another kind of distinguishing feature. But both of these lesions have a predilection for the right side of the heart, particularly the right atrium crossing over to the right ventricle. So whenever you see a lesion like that, angiosarc and lymphoma can be part of your differential. Now, this is another interesting case. This is actually a relatively recent case. This is a patient with history of hepatocellular carcinoma. And the patient was having increasing signs of, you know, increasing difficulty, incontinence. So a chest was done, and we see that there's a pericardial effusion, a little bit of irregularity of the heart. The resident read this, prelimed it, said, you know, no other findings. Of course, there was a separate abdomen and pelvis, which, of course, we don't go below the diaphragm. But with that delay, we see that there are multiple masses. So there was direct extension of hepatocellular carcinoma directly into the inferior aspect of the myocardium, and again, seeded other aspects of the myocardium that you can only really see, really appreciate well on the delayed image. Subsequently, we brought the patient back for MR, and here we can more clearly see these kind of well-circumscribed lesions, as well as the pericardial effusion. This was part of a T1 mapping, one of the MOLLE sequences. We see multiple areas of abnormality, as well as the T2. So this was metastatic hepatocellular carcinoma to the myocardium. And typically, myocardial metastases is not really common for hepatocellular carcinoma. Usually, we see lung, lymph nodes, the bone. Now, certainly, we can see direct extension into the IVC, but this is a case where we have kind of a direct invasion into the myocardium across the diaphragm. All right, next case. So here we have the CT, well-circumscribed lesion, a little bit of enhancement. Looks somewhat low density in overall signal, but maybe you can say, oh, here we go. Maybe there's a little dot or something there. So we had suspicions that this was not a simple cyst, maybe also a little bit of thickening of the wall here. Patient underwent MRI, and we can see, again, on post-GAD, we see enhancement. We see some internal, well-circumscribed internal material, as well as the lesion on T2. So this was an example of a cardiac teratoma. And as we all remember from our training, cardiac teratomas, they have embryonic origin comprising of all three germinal layers. They can occur anywhere in the body, but they can occur around the heart. About 90% usually occur near the pericardium. And with that, these are among the other benign tumors that we can see of the heart. But again, looking for that kind of multiple areas of attenuation, sometimes even classically seeing bone, is really the key driver for this particular abnormality. All right, I got five minutes. So here's another interesting case. So this was a gated CT. And scrolling down, we started to see this abnormal mass kind of near the atrioventricular groove, kind of involving the tricuspid valve. When we scroll down a little bit more, we actually see that this is the lesion. We were kind of cutting the top of it, and this is the lesion here. And subsequently, on delays, we see that this filled in. So this was actually a giant RCA aneurysm that was simulating a mass. And again, we were happy to see, we happen to have delays, so we can appreciate this. You can also see that there is some decreased attenuation involving the inferior aspect of the right heart also kind of pointing towards abnormalities in the RCA territory. Moving on, another patient. This is a patient who came in. Significant history, history of strokes, Factor V Leiden, a lot of issues. We can see that there is a, and I'm already kind of driving you in the direction of what this is. We see this kind of layering lesion in the left atrium. And on echo, they were worried, could this potentially be some kind of additional mass that was causing some infiltrative mass in the left atrium causing abnormal atrial motion? We can see that clearly the left atrium is enlarged. Left atrium is not moving very well. And again, it looks very layered, it looks organized. On subsequent delay, we see that this is an avascular tissue. This was enlarged left atrial thrombus. And when we think about thrombus, obviously we want to see patients, typically we see in patients with AFib, underlying mitral valve disease, including mitral stenosis. Usually they're avascular, adherent to the wall. And there's always a controversy, anticoagulation versus surgery. Obviously the risk for embolic events is significant with particularly large thrombi. But some studies have shown that anticoagulation actually works very well for the right patient. This particular patient, unfortunately, did have another stroke on top of it and unfortunately had passed and didn't make it to surgery. Moving forward, last few cases. So here we kind of see, we have a CT. We see this kind of salt and peppery mass in between the aorta and pulmonary artery. Here we have this coronal reconstruction. Again, showing this mass kind of interspersed between the two. So any thoughts, any thoughts? Exactly, this is a paraganglioma. And this is the classic appearance that we see. This kind of, again, very vascular, kind of salt and peppery appearance, both on CT and MR. 20% of patients who have cardiac paragangliomas will likely have a paraganglioma somewhere elsewhere in the body. So it's an important thing to screen the patients for other abnormalities, other paragangliomas throughout the body. And classically, hypertension is one of the features that these patients have. So two interesting cases, two different patients. Patient A, we see this mass within the left atrium. We see that there's involvement of the right inferior pulmonary vein. Patient B, a similar mass within the left atrium. Again, also looks like there's involvement of the pulmonary veins. In this case, it looks like there's more encasement in the vein and narrowing as opposed to going inside the vein and making it larger. We also see some speckled calcification. Interesting enough, this rare disorder, both of these cases are examples of a left atrial osteosarcoma. Now, left atrial osteosarcomas are very rare, but they do tend to have this characteristic appearance of arising within the left atrium. And that makes them primary lesions. Now, this is in contrast to when we see osteosarcomas involving the right heart. Osteosarcomas in the right heart are more likely to be metastatic. So there's a distal osteosarcoma with mets to the heart. Whereas those which arise in the left atrium, there are a lot of potential cells in the left atrium, and that's where the primary left atrial osteosarcomas can develop. So again, a rarity, but if you see a lesion, looks like it starts within the left atrium. And particularly if you see areas of calcification, think about that rare left atrial osteosarcoma. And finally, this is our last case. We see, again, another heterogeneous lesion involving the right heart. We see, again, areas of low attenuation, necrosis on delay. Again, we see, again, significant heterogeneity. There's also pericardial effusion, right pleural effusion. Now, this was actually quite baffling case. You know, we had a host of different ideas. Obviously, mets, we have to think about mets. Could this be an angiosarcoma? Could be. I mean, typically angiosarcomas look a little bit more aggressive, but could be. Lymphoma, patient didn't really have any history. So this ended up being a pericardial mesothelioma. Again, these are very rare. Caught us all by surprise. And as other mesotheliomas, there are different subtypes. There's epithelial, spindle cell, and certainly mixed. And unfortunately, these patients have a very poor prognosis. This patient, unfortunately, came to their disease within a month after this initial study. But with that, you know, my mouth is dry. We've gone through a lot, but this is still only the beginning. So I wanna thank you all for your attention. So let's jump in. I'm trying to pick some cases that, I tried to pick some that were non-gated, just to kind of simulate what you might see crossing across your workstation. So in this case, we wanna think about a couple of things. We may not always see the valve lesion itself. So that's one thing to keep in mind. But on this image, you can see clearly the right heart is enlarged compared to the left. The right ventricle should be smaller than the left ventricle. Here, it's clearly much larger on the abdomen. We see ascites and liver disease. And when you think about this, you might go through your typical core pulmonale and right heart and pulmonary hypertension and intracardiac shunts, but don't forget about carcinoid. So in patients who have abdominal disease, tricuspid carcinoid syndrome comes from metastatic carcinoid tumors. There are neuroendocrine tumors that secrete serotonin. That serotonin goes to the right heart, but then is inactivated by the pulmonary arterial bed. So it doesn't affect the left heart valves like it affects the right heart valves. It causes a fibrosis, and then this is a study from a friend, Carlos Rojas, showing tricuspid here, marked thickening of the tricuspid valve that really should be thin and imperceptible, and then also marked thickening of the pulmonic valve. This is another case from the literature showing echocardiographic thickening of the tricuspid leaflets. Because it's a neuroendocrine tumor, you can do an octoris scan, a somatostatin type scan, but the heart is not affected by tumor at the valve, so it won't be positive. You'll see the metastatic disease, but the heart thickening won't take up the octoris scan. So here's a lady in her female, a female in her 60s. Again, non-gated scan. This is a P protocol CT. There's a fairly obvious finding here that's got the calipers, and Dr. Judy already went through what this could be. Let's see more images. So now we have MR, balanced steady state free procession, bright blood on top, delayed enhancement, bottom left, and then an echocardiographic image. And we see a large lesion with a small stalk. So it's actually somewhat rare to see the stalk itself, a pedunculation of a left atrial myxoma. It's a classic appearance, ball valve effect across the mitral valve. You are looking for a quote unquote pedunculated lesion, but you may not always see the stalk. So what you're trying to say is that the maximum width of the overall tumor is much larger than the base of attachment. That base of attachment may not actually be long and elongated, so don't require that. Because of the ball valve effect on the mitral valve, that can cause hemodynamic consequences and leads the patient to surgery. That surgery can have a three to 5% in-hospital mortality. Usually they do not recur. Most of the series show that when they have recurred, it's because there were multiple lesions in the heart or because the resection was incomplete. It is the most common primary tumor in adults. METs are the most common tumor, but the most common primary cardiac tumor is the myxoma. So 70s male, I haven't given you a whole lot of information, but we see a valve here where there maybe is some thickening of the leaflets. This is the aortic valve. And it's better to look at a moving image. With your MR protocols, we often hyper focus on the left ventricle for cardiac MRI. I would recommend and suggest that you add a short axis image of the aortic valve. Aortic valve disease is very common. And it's very easy to miss if you focus on the left ventricle. You'd be surprised how many bicuspid valves and stenotic valves you won't see if you don't go out of your way to try to image it. So two different patients on the top, we see an open valve that is bicuspid. So we see fusion of two of the cusps. The cusp that is pointing to the atrial septum is the non-coronary cusp. So you can think of this atrial septum pointing at the non-coronary, and then you can orient yourself, then right is anterior near the sternum, and then left is posterior near the left atrium. So left and right are fused, no stenosis. So we can see quite easily with MRI that by planimetry, that is measuring the opening of the valve, that there is not significant aortic stenosis. We can also use phase contrast imaging to measure the velocity of flow across that to see if there's elevation of velocity as in the case for aortic stenosis. You can see on the bottom that quite often aortic valve disease is mixed. So we see not only a stenotic jet heading into the ascending aorta, but we also see a regurgitant jet. And again, we can use short axis imaging to do planimetry of the valve. You can see some aliasing of flow through that valve. So what we want to tell our technologists is to try to set the venk. The venk is an encoding factor on your MRI that tells the MRI what speed to expect the moving blood to be. If you set it at near the right level, you won't get aliasing. If you set it too low, you will get aliasing and your tech will have to recognize that and set the venk a little higher so as not to get this kind of black and white mosaic image in the point of flow. If you do get a black and white mosaic, you won't get accurate velocity measurements. Aortic stenosis, again, very common disease. These are the echocardiographic factors. So if we do planimetry, we are looking for one centimeter as kind of a cutoff, one centimeter squared as a cutoff for severe aortic stenosis. And this is an example of how you can do contouring in your PACS or your post-processing system, whatever you'd like to use. So now we have a mid-40s female. This is an axial stack. I'll let it run a couple of times. This is how you would see it. And we see just this little finding here, this little nodule on the back wall of the aorta. Hard to tell where that is without some short axis views. And one of the teaching points of this case is that valves are hard to biopsy. You're not going to biopsy that percutaneously. It requires an open heart surgery to get at the valve lesions. You may not always get the answer, and you're going to have to kind of do your best and characterize what you think it is based on the pathology. This case was actually last month, very recent, but it hasn't gotten a pathological result. But what we can tell is that this was a bicuspid aortic valve, so we know there's some baseline aortic abnormality. And then this nodule, which has a little fleck of calcification, we'd have to give a differential diagnosis, as mentioned by Dr. Judy. Papillary fibroblastoma, very common. Myxoma can happen anywhere in the heart. Maybe it's a strange variant of calcific sclerosis with some asymmetry because it's a bicuspid valve. But sometimes you're just going to have to be happy with this and go along with following it up with echocardiography or CTA because you may not get the answer. Here's another patient that shows a different valve disease. We just went through several examples of the aorta. This does have some aortic stenosis, so we see restriction of the valve leaflets. But that's not the main reason I showed this. Here we have, this is a so-called three-chamber view, left atrium, left ventricle, aorta, and then a little bit of the right ventricular outflow tract simulates the first view they get in echocardiography, the parasternal long axis view. And looking at the mitral valve, we see a little funny activity of the anterior leaflet. So the anterior leaflet is in continuity with the aorta. That's this one here. And then we can see it curls up. And as it curls up, there's a little white line in the left ventricular outflow tract that heads toward the aortic valve. This is a classic finding for systolic anterior motion of the mitral valve. So this is a typical finding for hypertrophic cardiomyopathy where thickening of the septum causes pulling over by pressure effect of this valve leaflet. And so you see it very nicely. That's about as nice as you're going to see it. Other times you're just going to get a glimpse of it. You're just going to get an idea that the leaflet is moving towards the septum. And it's essentially, as I mentioned, the pressure effect called the Venturi effect where the thickened septum narrows the space between the valve leaflet and the septum because it's thicker. And just like putting your finger on top of a garden hose and accelerating the flow, it accelerates the velocity in that space. Increased velocity lowers pressure, which then creates a partial vacuum that pulls over the valve leaflet. That valve leaflet comes over and therefore further narrows that area, increasing the velocity and lowering the pressure into a vicious cycle. And that's how these patients get into dynamic obstruction. They're fine in their daily life. They go to exercise on a basketball court. They get their heart rate up. They get their muscle working. They get their muscle to thicken even more in systole. And you can have a disastrous sudden death type event from this kind of systolic anterior motion. Hypertrophic cardiomyopathy is the most common genetic disease that affects the heart. It's estimated in one in 1,000 people roughly. And what we're doing as imagers, we're going to try to quantitate a few things. Often these patients will be known because they have echocardiographic findings already. We are going to measure accurately the septal width. They may already have that on echo. We're going to look for the physiologic effects of that enlargement, systolic anterior motion, and the acceleration of flow across the outflow tract. When you get delayed enhancement images, we're going to try to quantify how much of the myocardium is affected by fibrosis. So the gadolinium collects in areas of fibrosis, which is in the most hypertrophied segments of the heart. And the threshold is typically 15%, where an asymptomatic patient with more than 15% delayed enhancement is going to get a prophylactic ICD to prevent sudden cardiac death. Similarly, if the septum is larger than three centimeters, again, prophylactic. Now, these are for asymptomatic patients. If patients have an event, have an arrhythmia, have a sudden cardiac type death event that is averted, then those patients would get an ICD as well. But these are for asymptomatic patients who have otherwise no reason to have an ICD. And those ICDs end up with a pretty appropriately high fire rate for that condition. So it is important to identify these patients. So now we're looking at a mid-60s male. We have a couple of cardiac valve issues going on, both of the aortic and the mitral valve. So we can see that the upper image is a balanced steady state three-percession image. The lower one is a gradient recalled echo image. And what we can see on the gradient recalled echo image is that the flow jets are accentuated. So one teaching point here is that you can make the regurgitant flow into the left ventricle from the aorta look worse just by changing your parameters. Obviously, you've not made it worse in the patient. So try not to use visual estimates of regurgitation as this is severe because this jet is huge. Well, you may make it worse by just changing your TR and TE. So try to use quantitative measurements, which we can do on MRI. And the way to do that is with phase contrast imaging. So we get phase contrast images like the ones we showed before. You will get a magnitude image down here. And at the same time, you'll get a phase encoded image. And then we can draw contours, usually 20 frames. So you'll get a movie with 20 images. And you'll put a red circle around that. And then you'll get a cross-section of the flow at that point. And anything that goes below zero is the regurgitant volume. And then you can divide that by the total flow to get the regurgitant fraction and come up with severity. So please try to use this kind of approach. If you'd like to say something visually qualitative rather than quantitative, say a small jet or a large jet, try not to say severe regurgitation because you'll only conflict with the echo that was done, say, three days before or three days after. So now we're looking at a 50-year-old female. We have a stack of three-chamber view going through the heart, balanced steady state through procession. And we see abnormality centered at the mitral valve. And there's a couple of things we're seeing. First, we're seeing a dephasing jet into the left atrium, right there and there. That is mitral regurgitation. There's an eccentric jet there. And it's caused mostly by the abnormal motion of the posterior mitral valve leaflet. So anterior is connected to the aorta. Posterior valve leaflet is here. And we can see that it is prolapsing. So it is prolapsing into the left atrium because it is bowing backwards. So the valve is supposed to be tethered into the left ventricle by the chordae tendineae and the papillary muscles. It's supposed to keep it, kind of ventricular side. But when there's laxity in that system, you have bowing of that posterior or anterior mitral valve leaflet into the atrium. That bowing causes lack of coaptation and then you get regurgitation. You can also see how abrupt the motion is. That's what leads to that audible click you might hear on a stethoscope exam and auscultation. Mitral valve prolapse, they're not clear really what causes it. But you can get any kind of degenerative process in the valve can predispose you to it or accelerate the process. MVP has a spectrum of disorder. The most recently described and more dangerous version of MVP is MAD, mitral annular disjunction. And what they're looking at here is that essentially you should have the muscle of the left ventricle abut the valve leaflet, right? The annulus should be basically inseparable from the muscle. But in MAD, there is a disjunction here because there is non-muscular tissue at the AV groove between the valve leaflet and this muscle. And that puts abnormal wall stress on this segment, can cause fibrosis in this segment, which you can see on delayed enhancement images here shown by the arrows. And that fibrosis can predispose to malignant arrhythmias. So now there are malignant arrhythmias associated with MVP and MRI is seen as one of the primary ways to get at that. Here's an example of that mitral annular disjunction. You see that the arrow is showing where that segment of the muscle is disjointed from the valve plane. You can see the valve bulging into the atrium. You can see the jet of mitral regurgitation, this black plume into the left atrium. And the valve leaflet's bowing, almost like a seagull look into the atrium. This case had some delayed enhancement right adjacent to it. I tried to tilt this image to be similar in terms of where the left ventricle was positioned in space. And it should be no surprise that patients who had more delayed enhancement or had some delayed enhancement had a much worse prognosis compared to those who don't. We'll look at a case. This should be familiar to you all based on the previous presentation. We see on the post-contrast scan, we see a small nodular lesion here affixed to the aortic valve. Very common lesion, papillary fibroblastoma. Here's a pathological image. On post-contrast image, if you're lucky enough to have the valve finding stay somewhat still, right? This valve is moving and it can get blurred out, particularly smaller lesions. So at about, say, four to five millimeters, you can start to get some resolution there. But don't be surprised if you don't see the delayed enhancement. If you do see it, that can help confirm the fibrous nature of this lesion like a fibroblastoma does. And they can be quite high intensity on MRI images. Here we have a companion case, non-gated study. Much harder to see. You kind of have to make sure the arrow helps a lot, right? This nodular filling defect at the level of the aorta, not even that obvious on the echocardiogram. This was also a papillary fibroblastoma. So 70s male. There's a couple of things to kind of digest from this radiograph. We see that it's post-operative. And we see, if you look down here, there's kind of a valve, prosthetic valve, hanging out way down farther than you would expect. And we're trying to figure out what's going on at the right lung base. Is this elevation of the diaphragm, atelectasis, lung disease, or is it something that's heart-related? Well, it turns out this was heart-related. This is that prosthetic valve kind of pushed south because of this massive enlargement of the left atrium. Surprising there's not any thrombus on that image. And this is kind of a typical appearance of post-rheumatic mitral stenosis. So rheumatic mitral stenosis is not endemic in this country. This is a map, relatively recent, of endemic areas where children have rheumatic heart disease as a result of group A strep. That leads to an immune-related rheumatic heart disease. That rheumatic, sorry, the rheumatic fever leads to rheumatic heart disease, which is immune-mediated, thickens, and tethers the leaflets, causes stenosis eventually. Although in the young, the first presentation is typically mitral regurgitation when it presents. Mitral stenosis is kind of the end stage. So keep that in mind in the back of your head. Like the tricuspid carcinoid case, this is the left-side version that you should keep in mind. 50s male, again, non-gated, CTA, PE study. And what we're seeing here, typical type Bord's case, we're comparing the sizes of the right and the left pulmonary arteries, and we see that the left is significantly larger than the right. So this was kind of a classic Bord's case on either plain film or CT that you have pulmonic stenosis. And so here we're looking at the pulmonic valve. The leaflets should be almost imperceptible. You should not see them. This is a companion case also with pulmonic stenosis. So if you are seeing with good definition on either CTA or a non-gated study, the leaflets of one of the right-sided valves, the tricuspid valve, the pulmonary valve, please suspect dysfunction. Pulmonic stenosis is not that uncommon, and you will see it if you look at that space. It's just something that we don't typically look for. It's one association genetic is Noonan syndrome. You get thickened and restricted leaflets. There are percutaneous valve approaches to pulmonic stenosis. Most common is balloon valvuloplasty just to open the pulmonic valve. There are pulmonary valve replacements, of course. And if that pulmonary valve replacement or a similar conduit fails, then there are indications for a percutaneous valve similar to TAVR in the pulmonic position. So now we're looking at 20s female. That should be triggering your brain for some kind of congenital abnormality. We again see marked enlargement of the right atrium and right ventricle. And then we see reflux into the hepatic veins, well into the periphery of the liver. Please keep in mind that on power-injected CTA, particularly like a PE study, you will get some normal, quote-unquote, reflux into the hepatic veins. Don't always call it on a power-injected study because it can happen on those studies. But in this case, I think it's pretty convincing that it's real. And if we're looking for the reason for that, this image is the most convincing in the bottom left. We see that the arrow is showing the attachment point of the septal leaflet of the tricuspid valve. So you have the tricuspid valve leaflet moved apically. That's classic for Epstein's anomaly, where you have apicalization of the septal leaflet most commonly. That leads the ventricle to be more atrialized. It causes tricuspid valve dysfunction, generally open tricuspid regurgitation, eventual failure of the right ventricle. And the more recent approach, Dhirani is a Mayo surgeon who's pioneered this along with Da Silva at Pitt. And what they do is the so-called cone procedure where they take the valve leaflet apparatus that's there, they delaminate the tricuspid valve, and then they attach it into a cone. So this valve leaflet apparatus now post-operative is called the cone after the cone procedure. And then they also cinch up the right ventricular wall so that there isn't as much atrialized ventricle. They kind of pull this up and make the ventricle smaller, restoring tricuspid valve leaflet function and hopefully improving dilation and function. So now much more of an eye test. Again, non-gated study. We see tricuspid valve stuff. So this is blurred out. I think this is hard to see in prospect, but something that was seen in retrospect that this person had a vegetation on the valve leaflet. So don't just think about mass or masses. When you're predisposed by Dr. Judy's talk to think about masses all the time, recognize that thrombi and vegetations are way more common. This was a tricuspid valve vegetation seen only retrospectively on the CT. There is a Duke criteria where you essentially need two major criteria. Those are in bold, blood cultures times two, positive echocardiogram surface or SFGL, or one minor and three major. Small vegetations can be missed by echo. CTA is complementary. We're looking for things like the paravalvular abscess. We might call that a mycotic abscess elsewhere in the body. It's not going to be walled off. It's going to be in communication with the blood and therefore it's going to receive contrast. The companion case for this, we have a small nodular finding here, mitral valve. That's another focus of endocarditis, mitral endocarditis. I think this will be my last case because I'm running out of time. We have a lesion in the center of the heart here. It's low density on echocardiography even after post-contrast. It did not fill with the contrast. You see it here in the center of the heart. As we scroll up and down, this is similar to the RCA aneurysm case that you saw. This is attached to the aortic valve, however, and on coronal it's much easier to appreciate that this is a partially thrombocinus of valsalva aneurysm. So you have enlargement of the sinus of valsalva. When they do rupture, luckily for the patient, they can rupture into the heart as opposed to into the mediastinum, and therefore they just create a shunt rather than exsanguinating the patient. But just something to think about. This was very confusing on both MRI and echocardiography to the imagers involved. So thank you for your time and I hope this was useful. With these 20 cases, we're going to review the value of cardiac MR in the evaluation of primary cardiomyopathies as well as establish the main findings and biomarkers when we are evaluating patients with myocardiopathies. And we all know that cardiomyopathies are a heterogeneous group of diseases involving the myocardium, and ultimately produce an inappropriate response of the myocardium leading to heart failure and death. And cardiac MR is a unique one-stop-shop method for evaluating these patients as a whole because it provides detailed information of volume, global and regional function, but also ventricular hemodynamics and physical characterization. Also, moreover, cardiac MR provides also a vast portfolio of quantitative imaging biomarkers that are robust, and some of them has important prognostic implications. So let's begin with the first three cases. One of the things that we have to take into account when we are facing a patient with possible cardiomyopathy is to evaluate the ventricular geometry. And for doing that, we are going to focus on three parameters, the ventricular end-diastolic volume, the ventricle mass, and the relative wall thickness. The first case has normal ventricular end-diastolic volume, normal mass, and normal thickness. The second one has an increased mass and relative wall thickness. And the third one has increased ventricular end-diastolic volume, increased mass, and increased relative wall thickness. And as you can see, the ventricular geometry is way different. The first case is a patient healthy subject with normal geometry. The second case is a hypertrophic cardiomyopathy. And the third case is a delighted left ventricle with mixed hypertrophy. So changes in left ventricle geometry and structure both after myocardial injury and overload, either pressure or volume. So geometrical patterns are related to systemic hemodynamics, but also to risk factors, adverse events, and mortality. Therefore, first of all, we have to tell if the left ventricle is dilated or not with the left ventricle end-diastolic volume. Secondly, if the ventricle is hypertrophied or not with focusing on the left ventricle mass. And finally, if the hypertrophic or eccentric or remodeling of the left ventricle is either concentric or eccentric or mixed, focusing on the relative wall thickness. This is a 16-year-old female with sudden cardiac death in familiar relatives on positive gene testing. As you could see, this patient had an increased left ventricle mass, increased relative wall thickness. It's a patient with concentric hypertrophy asymmetric involving the anterior septal and inferior walls. And this patient had mid-ventricular late-term enhancement septum, but also increased T1 native and ECV values. This, indeed, is a patient with hypertrophic cardiomyopathy. It's the most common primary cardiomyopathy and it's characterized by hypertrophic myocardial dysphoria and fibrosis. In up to 60% of the patients, this has a familial form with autosomical dominance inheritance. And it's the most common cause of sudden cardiac death due to ventricular arrhythmias in young individuals and at least. In CNA imaging, we're going to see a very thick myocardium, commonly more than 15 millimeters, with increased relative wall thickness and usually is asymmetric, commonly involving the anterior and basal septum. There's, we could see also borderline increased thickness, also what is called a gray zone. And in those patients, with the appropriate clinical setting and familial history, we could also suggest a hypertrophic cardiomyopathy. On late-term enhancement, we're going to see enhancement in the insertion points, also could be patsy, confluent, mid-ventricular involving the hypertrophic segments, and commonly with non-coronary distribution. We're as told, as Dr. Valle said, we have to measure late-term enhancement because if there is an extension of late-term enhancement of more than 15%, there's an increased risk of sudden cardiac death. T1-native and ECV values are going to be increased, and this could be helpful for differentiating hypertrophic cardiomyopathy from other phenocopies like hypertensive cardiomyopathy. In the differential diagnosis, which we have to do with hypertrophic cardiomyopathy, we should include at least heart disease, hypertensive heart disease, or other entities like aortic stenosis. This is an example of 45-year-old male, strength and lead, we could see that there's only a mild alteration in the relative wall thickness. This patient had a concentric remodeling with normal systolic function, no normal diastolic function, no late-term enhancement, and normal T1 values. There's been described one value that has great utility for differentiating at least heart disease from hypertrophic cardiomyopathy that is the volume-to-wall ratio. It's been described an accuracy of 100% for differentiating at least heart disease. Left ventricle hypertrophy has been seen in up to 30% and 52% respectively of patients with hypertensive heart disease or aortic stenosis. Commonly, the hypertrophy in those patients is commonly concentric, whereas it has been described also as symmetric in aortic stenosis. The left vertical hypertrophy in aortic stenosis, it's not correlated with the degree of aortic stenosis. Although uncommon in those patients, late-term enhancement could be seen, typically with mid-ventricular septal pattern in hypertensive heart disease, and in aortic stenosis, we could see a spondocardial diffuse late-term enhancement or otherwise mid-ventricular enhancement. This is another case, 64-year-old female with abnormal repolarization on AKG, and we could see a typical spade-like appearance of the left ventricle hypertrophy of the apical segment with more than 15 millimeters of thickness, and also an apical to vascular ratio of more than 1.5. Indeed, this is a case of apical hypertrophic cardiomyopathy and is more commonly seen in Asian people, and up to 2.3% can be associated with apical aneurysms. The main differential diagnosis we have to make in patients with apical cardiomyopathy is non-compaction cardiomyopathy, but also endomecardial fibrosis. This is an example of a 44-year-old female with Lovelace disease, and we could see there's usually obliteration of both apex with thickening and diffuse subendocardial edema in both ventricles, intracavitary thrombi, and a typical triple-layer pattern on late gallium enhancement with internal non-enhancing thrombi, then subendocardial fibrosis and normal myocardium. We have to remember that endomecardial fibrosis is the most prevalent form of restrictive cardiomyopathy. Another case, 60-year-old female with left ventricle low flow tract obstruction. We could see that this patient has, again, increased left ventricle mass, altered relative wall thickness. This is a patient with concentric asymmetric hypertrophy, mainly of the septum, and we could see also there's an acceleration of the flow in the left ventricle low flow tract with antithrombotic motion of the middle valve. This also could be nicely depicted with in-plane phase contrast, and we could see the secondary mitral regurgitation. Another issue that I want to highlight is that it's important to make a through-plane imaging in the left ventricle low flow tract in order to measure the peak grain and the peak velocity in those patients. This also could be excellent, depicted by for the flow, and it's a very valuable tool, especially for quantifying the secondary mitral regurgitation in those patients. So, I'm not going to stay on the pathophysiology of the left ventricle low flow tract obstruction because Dr. Valle has already explained it, but I want to highlight that left ventricle low flow tract obstructions could be seen in up to 70% of classical hypertrophic cardiomyopathy, and has a risk of five failure-related deaths. Another thing I want to highlight because it's very useful, very useful parameter is that we could see in those patients a red left ventricle low flow tract area in systole of less than 2.7 square centimeters. Another less common form of hypertrophic cardiomyopathy is focal hypertrophic cardiomyopathy, and the main differential diagnosis we have to make is with cardiac tumors, and in this setting, myocardial tagging provides a very helpful approach for differentiating them. In patients with focal hypertrophic cardiomyopathy, we are going to see a distortion of the myocardial tags with tagging, whereas in patients with cardiac tumors, these myocardial tags remain undistorted. This is another case, a two-year-old male with family history of sarcomere, gene protein mutation, and sudden cardiac death. You could see this patient had normal ventricular geometry, normal mass, normal relative wall thickness, apparently normal systolic function, but what we could see is that this patient had several myocardial creeps, and also there's mildly apical displacement of the anteroradial papillary muscle, and what is more concerning is there is alteration in the attachment of the papillary muscles into the mitral valves, and this is what is known as subclinical hypertrophic cardiomyopathy, also known genotype positive, phenotype negative hypertrophic cardiomyopathy. It's defined as patients with gene mutation but without hypertrophy, and the risk of sudden cardiac death in those patients is exceptional. What are we going to see in those patients? Myocardial creeps, elongated anterior mitral leaflets, apical myocardial trabeculations, accessory bundles of accessory papillary muscles, and in those patients, we could see also expanded accessorial space in T1 mapping. So as you could see with these all cases that we have presented is that hypertrophic cardiomyopathy is a spectrum of disease that include from preclinical stage to advanced end-stage that can have or a delayed or a restrictive phenotype. Therefore, adverse remodeling and late stage of disease have been associated with higher degree of late cardiomyopathy enhancement, higher risk of sudden cardiac death, lower ejection fraction, and then also lower left ventricle force tract obstruction. Left factorial enlargement is often multifactorial in these cases, and it's a marker or if each person is at risk of atrial fibrillation, those patients are at risk of atrial fibrillation. This is an example case of 18-year-old male with familial hypertrophic cardiomyopathy. We could see there is an increased left ventricle mass, again, altered relative wall thickness. It's a concentric hypertrophy, asymmetric, but also there's a severe dilatation of the left ventricle with enlargement of the left atrium. This patient has an extensive enhancement of the ventricular, anterior wall ventricle and ventricle septum, and indeed this patient had adverse remodeling, hypertrophic cardiomyopathy with adverse remodeling. This adverse remodeling occurs in up to 10 to 20% of hypertrophic cardiomyopathy, and those patients are at risk, intermediate risk of sudden cardiac death. What is considered adverse remodeling? It's considered when there is present of diastolic or systolic dysfunction, when there is severed left ventricle enlargement or dilatation, and left vaginal enlargement, reduction of left ventricle fractal obstruction, and extensive flacoid enhancement. Another case, this is a 75-year-old male, left ventricle hypertrophy and ventricular dysfunction. We could see there's concentric hypertrophic, hypertrophy, asymmetric, mainly in the septum, but also mild dilatation and ventricular dysfunction. We could see in left ventricular enhancement a diffusive endocardial enhancement involving both ventricles with areas of transmural enhancement in the left ventricle, and also a very low signal in both cavities. This is known as the severed pattern, and indeed we are in a patient with amyloid heart disease. Amyloid heart disease is a rare entity, and it's secondary to the deposition of low molecular weight proteins in the extracellular space. It could be primary or hereditary, and what we see in those patients in imaging is a severed left ventricle hypertrophy with commonly preserved ejector fraction, and also a small cavity. We are going to see vitreol enlargement. That is a marker of restrictive physiology, and commonly these patients can have normal or mildly reduced contraction, and this is in contrast with what we see in hypertrophic cardiomyopathy where the contraction is often hyperdynamic. On late gallium enhancement, we are going to see a fast washout of the gallium from blood, and therefore, when we are acquiring late gallium enhancement, this acquisition should be earlier than normal, typically less than five minutes. Also, in look-looker sequences, we are going to see that there's an inverse relationship of the signal attenuation, being the signal attenuation of the cavity before the myocardium. On T1 mapping, we are going to see elevation of the T1 native and ECV values, and this could be present even in the absence of late gallium enhancement, such as in this case. Case 17, 75-year-old male with, it was referred for a study of left ventricle hypertrophy, but at the end, what we found is a patient with markedly delayed left ventricle with eccentric remodeling, that is normal left ventricle mass and reduced relative wall thickness, and severely left ventricle ventricular impairment. This patient had a mid-ventricular septal late gallium enhancement, linear, and altered T1 native and ECV values. This patient indeed have delayed cardiomyopathy, and is defined as a left ventricle dilatation as historic dysfunction in the absence of coronary artery disease or impairment of the left ventricular filling. The prevalence of these entities less frequent than in hypertrophic cardiomyopathy, in up to 50% is of unknown etiology, and up to 20 to 30% are familial. We have to take into account this entity because it's the third cause of heart failure, and it's the first cause of heart transplant. In CT imaging, we're going to see a dilated left ventricle with increased volume and normal vein cardial thickness, as well as commonly impaired left ventricular ejection fraction. On late gallium enhancement, we're going to see septal mid-wall enhancement up to 30%, but please remember that in up to 60%, we're not going to see any late gallium enhancement. The presence of late gallium enhancement and transomorality has associated increased risk of sudden cardiac death and arrhythmias, and also is related, has inverse relationship with the improvement of the left ventricular ejection fraction after treatment. On T1 mapping, we're going to see interstitial myocardial fibrosis, that is increased T1 native and ECV values that have associated prognosis, but we have seen patients with hypertrophic cardiomyopathy with dilated cardiomyopathy and restricted cardiomyopathy, and we are focused on all the information that we could extract from the left ventricle wall, but what if instead of doing that, we add the information that we could extract from the cavity? We know that 44 imaging provides an excellent tool, it's an excellent tool for evaluating the patient, the cardiovascular and motor dynamics, not only of great vessels and congenital heart disease, but also in valvular heart disease, or other ventricular situations, like left ventricle obstruction, or dynamic stenosis of the middle valve in patients with arterial fibrillation. And flow component analysis by using particle tracing and kinetic energy allows us to evaluate the quantitative motor dynamics and differentiate four different flows, direct flow, delayed flow, retained flow, and residual flow. And this has been related with how efficiently the blood is transported from the left ventricle towards the aorta. In normal individuals, where there is an efficient blood transportation from the left ventricle towards the aorta, the amount of direct flow is dominant in the inter-cavitory flow. So how we could apply this in cardiomyopathies? We have four cases. The first one, healthy individual. The second one, a left heart disease, normal ventricular geometry. We've already seen it. The third one, apical hypertrophic cardiomyopathy with congenital hypertrophy. And the last one is the idiopathic delayed cardiomyopathy with severe impairment, severe dilatation of the left ventricle and inter-cavitory thrombi. As you could see, when we analyze those patients with interventricular 40 flow, we could see that in a left heart disease, the proportion of the four flow components is similar to the healthy individual. But if we move towards the apical hypertrophic cardiomyopathy we could see that there's mild increase of the residual flow component, and this is related to somewhat an impairment of diastolic function. Moreover, if we focus on dilated cardiomyopathy, we could see that the proportion of these four components is markedly altered. We could see that there's a huge amount of residual volume, and this is associated with an efficient transportation of the fluid flow into the aorta. This indeed has been associated also with an increase of static volume and the risk of inter-cavitory thrombi. So hopefully in this barely 20 minutes, I've been able to show you why it's important to assess left ventricle geometry in patients with cardiomyopathies, and that it should be the first step when analyzing them in order to narrow the differential diagnosis. And there's several biomarkers that we could provide with CARI-MR in order to refine the diagnosis. Thank you very much for your attention.

cardiac masses

cardiomyopathies

medical imaging

metastatic cardiac tumors

cardiac myxomas

CT MRI echocardiography

hypertrophic cardiomyopathy

cardiac MRI

four-dimensional flow imaging

clinical decision-making