Hello everyone, thank you to RSNA and the moderator for the opportunity to present. I will be covering valves in my proverbial 15 minutes. This is a tricky subject, there are moving structures, there are a lot of movies, so I'm going to jump right in in the interest of time. First case, we have a male in his 80s, and I have some cases that are cases one and two, more than one, to show you some valve pathology in multiple places on the same patient. In this patient, we see nicely on this reformat short axis through the aortic valve, we can see a little bit of calcific sclerosis of the aortic valve on the right coronary cusp. We can always tell the non-coronary cusp because it's closest to the atrial septum, and then the left coronary cusp is near the left main coronary artery and the left atrium, the right coronary cusp is near the right atrium and the right ventricular outflow tract as well. We see that there is slightly poor motion of the right and left coronary cusps, they are not opening as they should, that is near the area of calcification, the degenerative process of aortic calcific sclerosis. One advantage of CTA is that we can do very nice planimetry. We are able to take a region of interest freehand over the open orifice, this can be tricky to find the correct plane to make sure that you are capturing the true orifice, so it's nice to correlate that with coronal images, and we can get a valve area of 1.97 centimeters squared. It's important to note here that echocardiography finds aortic valve area in a different way. Most commonly, although they can use planimetry, they use the continuity equation. That continuity equation assumes a circular diameter of the left ventricular outflow tract, A1 in the diagram, and then A2 is the area we're looking for. In order to develop A2, the echocardiographer places either VTI or velocity sampling in the left ventricular outflow tract and at the aortic jet, and the ratio of the velocities multiplied by the LVOT cross-sectional area gives you the effective area of the aortic valve. This will be reported as an aortic valve area. Note, it is not quite an anatomic aortic valve area, it's more of an effective aortic valve area. You can see that this is a geometric assumption, and quite often, this doesn't match perfectly with what we see in real life on planimetry, for example. And even the AST guidelines say, of course, valve area calculations are dependable only when there is careful attention to technical aspects of acquisition, and there are some theoretical concerns about continuity equation valve areas. Using the valve area or planimetry, you can come up with your valve area of 2.0 centimeters squared, as we saw in this example. That places this patient in the mild aortic stenosis category. 1.5 and larger is mild, 1.0 to 1.5 is moderate, and below 1.0 centimeters squared is severe. That is what will trigger, potentially, the need to replace the aortic valve. Nowadays, we have several options, surgical AVR, detried and true, very durable, and also transcatheter approaches with CAVI slash TAVR. And here are some of the factors that might favor one or the other. CAVI is increasing indication to lower risk populations. It had been previously reserved for higher risk patients who would not survive a surgery, perhaps, but now it is more and more available to patients with aortic stenosis, and potentially soon available to patients with bicuspid aortic stenosis, traditionally only done in other countries, but not yet in the United States. This same patient had interesting anatomy of the mitral valve, and the arrow is pointing out a fibrous band connecting the papillary muscle to the midpoint of that mitral valve leaflet. That anterior leaflet of the mitral valve that's in continuity with the aortic valve is attached to the papillary in an inappropriate way. And we can see that on the short axis image in the center as a straight band obliquely coursing through the left ventricular outflow tract. How to call this is sometimes difficult. Papillary muscle anatomy and attachments can be quite variable, ranging from true congenital anomalies, like parachute mitral valves and mitral arcade, to subtler differences, like varying attachment points on the leaflet, varying lengths of the papillary muscle, and varying positions of the papillary muscle. Often, hypertrophic cardiomyopathy is associated with papillary muscle and chordate tendon attachment abnormalities and variations. And so you should keep a close eye on the septum. You can see it is somewhat enlarged in this case when you see mitral valve abnormalities because they often go hand in hand. So the second valve abnormality in this case one and two, in addition to the mild aortic stenosis, is variation in papillary muscle and mitral leaflet attachment anatomy. Case three is a 70-year-old male. We see several images here that have been labeled. You see valve written on highlighted calcifications in the center of the image at the aortic valve. For those who haven't seen this before, this is an agatston score, not applied to the coronary arteries, but applied to the aortic valve. You can see in this image how agatston scoring is performed. The calcified lesions are selected, their area is considered, and then that is multiplied by a weighting factor according to how dense the calcium is. That calcium falls in different bins from 130 pounds field units to above 400. All of the lesions are summed and that's the agatston score. Well, we can apply that same approach to the aortic valve and get a total valve score. That valve score in this case was 590, which would be below the limit of severe aortic valve calcification as per the largest study to look at mortality in aortic valve calcification, showing that mortality increased with aortic valve calcification. And that is independent to other factors that might correlate with mortality, like the hemodynamic significance of the valve, the amount of stenosis and peak gradient and velocity. So this was an interesting result. It can be seen as a tiebreaker in patients for whom an aortic valve intervention is considered and might push a patient into getting a procedure to treat the aortic valve because of the severity of the aortic valve calcification. The limits that were set by that study were gender specific norms and 1274 in women and 2065 in men. Here's case four and five, 60 plus year old male. We have an echocardiographic image. And I think part of this is to demystify the echocardiography. We see the probe is at the top of the image. The triangle is emerging. The triangle of the image is emerging from that probe. That probe is near the left atrium. The left ventricle is pointing away from the probe with the apex near the bottom of the image. That means that the probe must be in the esophagus near the left atrium. This is a transesophageal echocardiography showing the left atrium, the mitral valve with a very large vegetation flopping into the left atrium and the left ventricle. We can see the same thing on CT angiography. This patient has a bit of calcific cirrhosis of the aortic valve, but also has a very large nodular mitral valve vegetation on the anterior leaflet of the mitral valve. And that nodular vegetated area is climbing up the aortomitral curtain towards the aortic root, which is an important finding in this patient. Infective endoparditis can not just only affect the valve, but the adjacent structures. So here again, we see that vegetation bouncing on the mitral valve into the left atrium. And now we'll pace through a coronary CTA at the aortic level. And we're seeing a couple more findings. We'll run that for again. We see, first of all, that the aortic valve is a bicuspid aortic valve without much of a rafi. This is a CBERS type zero bicuspid aortic valve with a lot of calcification on it. We then see that there's a little too much contrast extending towards the left ventricular outflow tract where that vegetation lives at that anterior leaflet of the mitral valve. That is a small area of paravalvular abscess. That extra contrast outside the lumen is called a paravalvular abscess in the cardiology world. We don't call it an abscess because it is a walled off cystic structure as we might in other parts of the body. So it's important to understand these infected paravalvular abscesses are in effect mycotic aneurysms of the affected structure. On the catheterization to the right, you can see with the arrow that there is a relative sail-like triangular defect in the aortic, just above the aortic root in the ascending aorta. That's the area of paravalvular abscess, excluding some of the contrast. One large study experiencing 35 years of infected endocarditis showed that in over 200 patients, the most common findings were that, number one, bioprosthetic valves were increasing in use over time and were a durable prosthesis to place in these patients who had infected endocarditis. And second, that streptococcus feces were the most aggressive, the most likely to extend into adjacent structures. The bioprosthetic valve you see here, the resilia, is what was implanted in this patient. There are other stentless aortic valve prosthetics that can be used without the metal scaffolding. It's also important to discuss the bicuspid aortic valve. I mentioned the CBRSS Type 0, the CBRSS 4, was developed in the late 2000s to help categorize aortic valve morphology in bicuspid patients. A more recent 2021 international consensus statement is coming out to help classify aortic valves in a way that is more in keeping with the surgical approaches. The most common bicuspid aortic valve is a fused bicuspid aortic valve. Partial RAFI or partial commissure is visible, attaching two of the cusps, though they are fused. The angle of fusion can also be something you comment on, whether it's relatively straight angle across the two fused or more of an acute angle. The CBRSS Type 0 is the two sinus bicuspid aortic valve. That is much less common and can be oriented anteroposteriorly or lateral side-by-side. Finally, you can have something in between where you have a form-first condition. Here's a companion case with echocardiography where the aortic valve is in the middle with bright calcification on the aortic valve. So we see at the top, right ventricular blood flow track, at the back, the left atrium, since the left atrium is away from the transducer, this is a surface or transthoracic echocardiography, and we see the aortic valve in the center. The corresponding CT shows nicely that the valve has no stenosis, but does have nodularity along the, again, non-coronary cusp is attached to the atrial septum and the right coronary cusp. We see some nodular thickening of that area. In this case, this was a vegetation on top of a preexisting calcified aortic valve. We have another companion case with a bicuspid aortic valve. We have a young patient. Whenever you see ascending aortic enlargement in a young patient, you see aortic calcification at the aortic valve, you see thickening of the aortic valve, please think about bicuspid aortic valve. Typical calcific spores, this is a senescent process, and you'll start to see it in the 50s, 60s, 70s. You should not see it in a patient in their 30s. If you do, try to get a short access view of the aorta. As in this case, we see a non-stenotic bicuspid aortic valve with fusion of the non-coronary and right coronary cusps. Case eight, we have a 70 plus year old female with a calcium score showing this finding at the mitral valve. We see two different densities of potential calcium, a much denser area, and then a much lighter area of calcium. It almost looks like contrast, and we see that on multiple images. On echocardiography, this area is heterogeneous as well. So we see a regurgitant aliasing jet of mitral regurgitation extending from the left ventricle into the left atrium. Again, left atrium near the transducer at the top of the image. This is a transesophageal echocardiogram with the area of mitral annular calcification just lateral to the mitral valve. That area has almost a yin-yang effect where there's an area that is continuity with the cavity and an area that is slightly different in echo texture. This is caseus necrosis of the mitral annulus or caseus mitral annular calcification. Instead of being dense, hard, rock-like calcium, there's a liquefied interior of caseus material. That explains the echolucency on echocardiography and has been called a toothpaste-like tumor. It's more common with chronic kidney disease, with increasing age, and with female gender. And because of its inflammatory nature, this caseus material can be hot on PET, in fact. It can also embolize and produce left-sided effects by embolizing into the coronary arteries or the carotids. So as it becomes caseus, it becomes more dangerous to the patient. And it's actually at an increased, it's increasingly acknowledged that this is a relatively prevalent finding, previously believed to be less than 1% of patients, but an autopsy in the 3% to 5% range. Here we see a case from literature where from 2011 to 2016, an area that was calcified became more and more liquefied and therefore potentially more dangerous to the patient if that were to embolize. Case number nine, we have a patient with a prosthesis. This prosthesis in the center of the image is a transcatheter valve. And within that valve, we see a lot of dark material in accompaniment with the contrast. On cinematic images, we see that instead of a nice, thin, pencil-like valve plane, we see thickened, nodular, irregular valve. On echocardiography, we see the same finding. And we also see some increased flow, an increased gradient at the center of the image. That aliasing at the very center of that image is the increased flow at the area of this nodular thickening of the valve leaflets of the TAVR. This is an example of HALT in TAVR, hypoattenuating leaflet thrombosis. This has been recognized as a different entity from vegetation and from PANAS, where thrombus begins to line the valve. It's quite common, particularly at 30 days. It can increase the gradient across the valve, which may generate the need for anticoagulation, although it's controversial whether this is a self-limited condition that could potentially be left alone. And with conservative features, patients without large gradients, could they be left alone and then return to no HALT at one year? The higher the degree of HALT, as shown by these images, the higher the likelihood of a gradient, and therefore, potentially much more likely for the patient to need anticoagulation. Case 10, we have a 90-year-old male. This patient, we have echocardiographic images, again, TEE, transesophageal. On the left, we see torrential mitral regurgitation in the center of the valve. We see this jet of aliasing returning back into the left atrium. The right image is post-procedure. So the central ridge of the mitral valve is this bright echo-textured structure, on either side of which there are two smaller mitral regurgitation jets. This is a mitral clipping or a mitral regurgitation. This is a procedure where, through a transephal puncture, access to the mitral valve allows placement under echocardiographic guidance interprocedurally of a clip to cinch the center of the valve shut. As you can see in the bottom right image, we see that the orifices have become almost like an infinity symbol. On either side of the clip, there are some areas that are ovoid. This is the orifice. These are the new valve orifices that reduce the mitral regurgitation from plus four to plus one. Generically, this has been called transcatheter edge-to-edge repair and is increasing in use, potentially with use of these exact clips on the right side of the heart at the tricuspid valve. There are very, very many ways that the mitral valve can become dysfunctional. Probably more common is secondary mitral regurgitation, where enlargement and dilation of the left ventricle leads to incomplete coaptation of the mitral valve leaflets and therefore regurgitation. Primary MR is where the mitral valve itself has an abnormality. Either it is disturbed by vegetation, rheumatic thickening, or mitral valve prolapse leading to mitral regurgitation. This can cause significant symptoms and lead for the patient to need definitive repair or replacement of the valve. Case number 11. We have a teenage boy and we see two MR images where the right ventricle has lost some of its normal morphology. Instead of seeing trabeculations throughout the right ventricle as we are used to, the sepal side of the right ventricle seems to lack them. In fact, the right atrium seems to extend into the right ventricle, so-called atrialization of the ventricle. This is a case of Epstein's anomaly. In a different patient, you can see the wall-to-wall heart phenomenon where if untreated, this leads to extensive tricuspid regurgitation and the progressive enlargement of the right ventricle and right atrium, which then worsens the tricuspid regurgitation in a vicious circle. The approach is to restore the leaflets. In Epstein anomaly, the core embryological issue is that the sepal leaflet of the tricuspid valve has not delaminated itself from the ventricular wall. It stays stuck there, leaving the wall smooth and atrialized and leaving the tricuspid valve plain without much of a tricuspid valve because the sepal leaflet is not there. The goal in surgery is to mobilize some fibrous tissue from that area and then attach it to what is at the tricuspid valve level to create a new monoleaflet or bileaflet valve to prevent regurgitation across into the atrium. Cases 12 and 13 are the same 70-plus-year-old female. We'll pace through a CTA of the heart. And there are a couple of things that we see. The first thing we see is a little fine line between the coronary sinus and the right atrium, and then a larger line between the IVC and the right atrium as well. These aren't atrioventricular or semilunar valves, but anatomically named valves within the heart that are variable. The first is the eustachian valve where the IVC meets the right atrium. And that can be well demarcated. This can be confused for lipormatous hypertrophy of the interatrial septum, potentially a mass lesion, but it is simply a variable normal remnant of a ridge that previously directed flow into the fosso ovalis for fetal circulation, and then in the belt can be somewhat hypertrophied and produce this appearance. The second is the thebesian valve where the coronary sinus meets the right atrium. There can be a thin, sometimes incomplete valve that creates this difference in contrast column appearance. Case 14 is a 60-plus-year-old female. And what we see is striking enlargement of the distal portion of the main pulmonary artery and the left pulmonary artery with respect to the right. The first image shows that left pulmonary artery enlargement. The middle image shows that the right pulmonary artery is relatively normal in size, and both the center and the rightmost images show that the pulmonic valve is somewhat thick. The pulmonic valve should not be this visible on a non-gated CT. You should barely be able to see the valve in most circumstances. The fact you can see it suggests that there is abnormality, and this was a patient who had a history of mixed pulmonic valve disease with some stenosis and some sclerosis. This small red jet in the center was pulmonic regurgitation at the pulmonic valve. This area can be difficult to see in echocardiography, so you're finding it on CTA, maybe the first time someone mentions it, even if a previous echocardiography has been performed, as was the case in this patient. The classic finding is unilateral pulmonary artery enlargement. This enlargement can persist despite therapy or even surgery of the condition, and often it is mixed valve disease, although classically it has been called a finding of pulmonic stenosis from the stenotic jet. The last case is somewhat of a companion case. This is a child, and we see that the pulmonary artery is quite small. Then we get to the level of the aorta, and we see it's overriding a ventricular septal defect. This is a patient who has tetralogy FLO, the classic finding of small pulmonary artery stenosis of the right ventricular aorta tract, ventricular septal defect, overriding aorta. The aorta is sitting straight on top and straddling on that defect, and then as a result of the right ventricular aorta tract, we have right ventricular hypertrophy, thickening of the right ventricle, similar to that of the left ventricle, and those are the four classic findings. RVOT obstruction and RV hypertrophy, those are less seen in the pink FLO situation, ventricular septal defects, and overriding aorta. Classic findings of tetralogy of FLO. Often to operate on this, they will sacrifice the pulmonic valve, so post-operatively, we can have another valve condition. We can have pre-pulmonic regurgitation that can cause right ventricular dilatation and failure, and may require subsequent revision with a percutaneous or surgical valve. Thank you very much for your attention. Enjoy the rest of the conference. Oh, okay. That's good. All right. Let's get going. The first case is 37-year-old male with pulmonary hypertension, and the CT was done for evaluation for shortness of breath, and you can see the pulmonary as well as both branches are very, very dilated. The aorta is normal. This is a left atrial appendage. This is a left atrium. Right side is not well pacified, but you can see a membrane within the left atrium with small calcification. This is a case of cotriatrium, and if the fenestration is not large enough, it can lead to back pressure changes, venous pulmonary hypertension, and longstanding pulmonary arterial hypertension. The presentation depends on the size of the fenestration, and the only differential for this condition is a supravalvular mitral ring, where the ring is present on top of the mitral valve itself. So distinguishing between the cotriatrium and mitral valve ring is the cotriatrium is always behind the left atrial appendage junction with the left atrium, whereas the ring will be on the mitral valve. This is a 36-year-old female with headache and blurred vision. Head CT was normal, and chest radiographs show clearly the right lung is much more smaller as compared to the left, and you have a large vessel which is coursing downward immediately, which is abnormal. Most of you have already recognized what is this. This is a scimitar syndrome, where the anomalous pulmonary venous drainage of the right lung into the IVC, and this patient underwent catheterization, which clearly show the pulmonary arteries here, and on the delay phase, the vein is draining into the IVC. If the shunting is large, these can be symptomatic, but majority of these cases are detected incidentally, and they are often associated with lung abnormalities, such as hypogenetic lung, scimitar syndrome, and sometimes with ASD. This patient has only one lobe instead of three lobes, and also he had anomalous arterial systemic drainage or supply to the right lower lobe, which is better seen on the selective angiography. This is a branch which is coming from the abdominal aorta and supplying the lung without any sequestration per se. This is called Pierce type I sequestration anomaly, and this needs to be occluded because there is a good chance the patient may develop hemoptysis or secondary infection. This is a 46-year-old male who was a nurse who developed shortness of breath in Colorado. It was diagnosed at high-altitude pulmonary edema, and subsequently, he had an abnormal echo, which led to the evaluation with CT. The CT showed mildly dilated pulmonary arteries. There is some hypertrophy of the right ventricle. The chambers are also dilated. How do I go back? And if you look at the SVC, the right upper lobe pulmonary vein is draining into the SVC, and below, as we go downward, there's a junction of the SVC with the left atrium where the right middle lobe is growing. This is the superior sinus venosus ASD, which is more commoner than the inferior sinus venosus ASD. It's always associated with partial anomalous pulmonary venous drainage of the right upper lobe. The inferior sinus venosus SVC PAPVR is more difficult to diagnose. It can be actually missed, but it is not that common, where the IVC, as well as the inferior pulmonary veins have communication with both right and left atria. MR can be done in these cases to quantify the shunt in this patient who had a right middle and right lower lobe pulmonary veins connected to the right atrium. The blood flow from the main pulmonary artery was 190 as compared to 55 in the aorta with QPQS ratio of 3.5 to one. This is a 38-year-old male with progressive shortness of breath. We had presented to ED, and the radiograph shows heart is enlarged. The main pulmonary artery is very dilated. The main, both right and left pulmonary artery is dilated, and there is a pruning of the vessel, suggesting the patient has pulmonary artery hypertension. A CT was done for further evaluation. You can see there is a big connection between the aorta and the left pulmonary artery with a huge main pulmonary artery corresponding to what you see on the CT. This is a case of patent ductus arteriosus, undiagnosed till patient presented with shortness of breath. And this stage, he has developed Isominger physiology because of the longstanding nature. At cath, you can see the ductus is very large, and these cases can be difficult to manage percutaneously, so they will need a surgery. As we know, ductus closure functionally occur between 18 to 24 hours, but anatomically, it can persist up to one month. PDA is a asynodic left-to-right shunting. Shunt volume is determined by the size of the communication as well as the pulmonary vascular resistance. As I said before, the treatment depend on the size of the PDA, degree of calcification, any distortion or any additional dilatation. This is a 45-year-old female with increasing shortness of breath. Cine MR alleviated shows a moderate aortic insufficiency, and there is a big outpouching from one of the sinuses, better seen on the short axis view. This is a large sinus of Valsalva aneurysm from the right sinus, which is protruding into the RVOT, causing right ventricular alpha tract obstruction, hence causing the symptoms. Very clearly, you can see it is the tricuspid aortic valve on the right sinus. Valsalva is aneurysmal. These are all congenital cases. It's similar to Marfan etiology, weakness of the elastic lamina or deficiency of the normal elastic tissue. They are often associated with other anomalies such as bicuspid aortic valve, VSD, or coronary artery anomalies. Clinical features depend. Most of them are actually asymptomatic, and symptoms only occur when there is a mass effect or the sinus ruptures into one of the right cardiac chamber, which are commonly right ventricular or right atria. The last case I showed, this patient has both right and left coronary artery sinus aneurysm, which were causing compression of the both coronary arteries itself. A 17-year-old male found to have murmur at the well child visit, which led to abnormal echo, and the CT was done. Right away, you can see all the coronary arteries are very dilated. That suggests that there is some kind of shunting going on, and as you see on both coronal and axial, the right coronary artery is arising from the pulmonary artery itself. The right coronary artery arising from the pulmonary artery. The left is coming from the aorta. So this is a case of anomalous right pulmonary artery from the right coronary artery from the pulmonary or r-kappa. It is usually not diagnosed in the early childhood and may remain asymptomatic till adulthood in comparison to the r-kappa, which is often diagnosed early in life. This is a 28-year-old female with postpartum shortness of breath. She didn't have any previous cardiac diagnosis, and here you can see the right coronary artery is arising from the right cusp, but we did not see the left coronary artery arising from the left cusp, but actually the left coronary artery is arising from the pulmonary artery. So this is a case of r-kappa, which is usually symptomatic in the early infancy or early childhood, but sometimes they can survive to adulthood. Most common form is the left coronary artery arising from the pulmonary artery, and they often lead to coronary steel phenomena, which was seen here. This is a patient who had a CTA done for coronary artery disease, but what we found, this is a prospective CT, there is an anomalous origin of the left main coronary artery from the pulmonary artery, and you can actually see the jets suggesting there is a left-to-right shunting going on in this patient, which was causing his symptoms. 38, 34-year-old female with shortness of breath. Right away you can see there is abnormal contrast blush in the pulmonary artery, and there are several squiggly vessels around it, which are communicating with the LAD, and this was confirmed, this is a coronary artery to pulmonary artery fistula, which is causing the symptoms. These fistulas are often congenital, they can be communication with the chamber or with a vein when it is called AV malformation. Drainage is more commonly to the right ventricle, right atrium, or pulmonary artery. In our practice I have seen more cases draining to the pulmonary artery itself. Smaller fistula, if you're detecting childhood, they tend to grow, so these need to be properly screened and followed closely. This is a 47-year-old patient with syncope, an exercise-induced transient ventricular tachycardia. He had a cath, but they could not cannulate the right coronary artery. Subsequently he had an MR. You can see part of the right coronary artery, but do not see where exactly it's coming from. That led to the CT examination, and you can clearly see the right coronary artery is abnormal course. It's going more medially and to the left in between the pulmonary artery and the aorta, and it's arising from the left coronary cusp. Shown nicely here, this is the right cusp, this is the left cusp, right coronary artery is coursing in between the pulmonary artery and the aorta. In these cases, there is a high risk for sudden cardiac death, which can be due to slit-like opening, acute angulation of the ostium, the stretch of the intramural component, and the compression of this intramural component between the commissures of right and left coronary cusp. And if you do the coronal CT, you will see the oblong, elongated configuration of the anomalous vessels showing there is a compression of this vessel. This is a four-day-old baby with abnormal echo, and you can see there are two vessels which are coming from this vessel. The subclavian artery is separate. The one big vessel arising from the heart, there's no second vessel. Better seen on the coronal, very large, abnormal-looking annulus, give rise to two vessels, brachycephalic left common carotid. There's a pulmonary artery, left pulmonary artery, this is PDA, which is connecting to the descending thoracic aorta, and subclavian is arising from that. So this patient has a truncus arteriosus, which is giving rise to the aorta, which is giving rise to right two branches, and then giving rise to two right and left pulmonary artery, and then through a patent ductus arteriosus communicated to the descending aorta, which is giving rise to subclavian artery. Truncus is a cyanotic congenital anomaly. In these patients, VSD is almost always present, and there is a single trunk, and that variation can be described by different methods. The valve, which is abnormal, often it is either bileaflet, or just in case, there are four leaflets. This patient also has interrupted aortic arch. There are three types of interrupted aortic arch. Type A when the disruption is beyond the origin of the left subclavian artery. Type 2 is between the left common carotid and subclavian artery. This is our case. And type 3 is between the right inominate artery and left subclavian artery. This is a 17-year-old female without any known diagnosis with tachypnea and tachycardia and history of syncopal attack. An MR was done for further evaluation. You can see the chambers are dilated. The right ventricle is very hypertrophied. And as we go down, better seen on here, there's a VSD and overriding of the aorta, and the main pulmonary artery is very small. Seen on the face contrast imaging, the main pulmonary artery is small. Here's a static image showing the main pulmonary artery and the right pulmonary artery small. There's a large PDA, which is communicating with the left pulmonary artery. So this is a patient with Tetralogy of Fallot, which was undiagnosed since birth, but presented with these symptoms and diagnosed ultimately with MR. Majority of the cases of Tetralogy are treated in a childhood. Then we do imaging to detect any kind of complication. This is one such patient, 5-year-old, who had undergone Tetralogy repair, now presenting with shortness of breath. And MR face contrast images show that there is a significant jet coming back in the diastole into the RVOT. That suggests that significant pulmonary regurgitation. Also in the delayed imaging, you can see there is a date enhancement of the right ventricular outflow tract, which has thickened. And the regurgitant fraction was almost 46%, which is very significant, although the right ventricle function was normal. Now there are replacement of the pulmonary valves in these patients. There are certain indications. These are two criterias among several. When the indexed RV and diastolic volume is more than 150 mL per meter square, or the end systolic RV and systolic volume is more than 80 mL per meter square, this is where we should consider replacing the pulmonary valve. At 57-year-old patient with the known congenital heart disease presented with chest pain, clearly you can see the abnormal connection of the vessels. The aorta is to the left and anteriorly. The coronary artery is behind. The coronary artery is the normal in origin. They face the pulmonary artery. This aorta, which is anterior to the left, is connected to this very hypertrophied ventricle, which shows trabeculation along the interventricle septum, as well as a very large, thickened myocardial band right here. So this is the right ventricle, which is connected to the aorta, and the pulmonary artery is connected to the right-sided morphologic left ventricle. So you know this is an altered anatomy. And also look, this is a big dilated atria with a triangular aortic atrial appendage, which is connected to the right ventricle. So morphologic left atrium connected to right ventricle, morphologic right atrium connected to left ventricle, and that leads to a systemic series communication, which is not causing end septum. So most of the systemic circulation come back to the venous, to the right atrium, which goes to the left ventricle, then to the pulmonary artery, goes to the lung, oxygenated blood come back to the left atrium, right ventricle, aorta. So a patient may remain asymptomatic, not diagnosed till a later age when the systemic right ventricle start to fail. This is a congenitally corrected transposition of great artery, or LTGA. This is a good diagram to remember how to differentiate different types of anomalies. In normal patients, the pulmonary artery is anterior and to the left. Aorta is back and posterior. If you cross these opposite of this is aorta anterior to the left, pulmonary artery behind. This is the LTGA or congenitally corrected. In cases of situs inverses, the pulmonary artery is medial and aorta is posterior to the left. And if you alter these, reverse phenomena here will be aorta in the anterior, pulmonary artery behind. So this is a DTGA. So this example will help you relationship between the relationship of the arteries. This is a nine-year-old TGA patient, which we had as arterial switch operation. In these cases, we do follow-up series to look for complications such as pulmonary artery diagnosis of stenosis of the pulmonary artery. This is a supravalvular diagnosis. Also, the neo-aorta is often dilated in these cases and can lead to regurgitation. So this is a JATIN procedure, Leigh-Comptey-Manure. And the information needed on follow-up is the anatomy of the pulmonary artery, coronary artery evaluation, because these are detached and they can lead to stenosis and ischemia and evaluation of the right ventricle. In patients with TGA, arterial switch operation is also done. In these cases, we do imaging to look for baffle stenosis or leak. In this case, the SVC is the baffle, superior baffle is very significantly narrowed. And these patients may or may not present with SVC syndrome because there is an azygous vein which can decompress the SVC. So the superior baffle stenosis may be asymptomatic, whereas inferior baffle stenosis can lead to ascites and hepatomegaly. The pulmonary venous obstruction is less common. It usually occurs at the junction of the left baffle, inferior baffle and the left atrium junction. The last case, 38-year-old presented to ED with chest pain and he had a known heart surgery, but we do not know the details. This is one of the clinical presentation of these cases. What we see here is multiple collaterals. There's only one big ventricle with a large VSD and it is connected to one un-opacified structure, which on delayed imaging is very clearly opacified. This is the case of a Fontan shunt in a patient with a univentricular heart. In the initial phase, it is un-opacified and can be confused with thrombosis, where in the delayed phase it is completely opacified. So univentricular heart can be due to hypoplastic left ventricle, hypoplastic single ventricle or tricuspid atresia and that leads to Fontan procedure. And I will stop here. Thank you so much. So my name is Gene Judy from the University of Maryland and we're going to go over a bunch of cardiac masses. Let's go. Now the challenge with many cardiac masses is, well, they all tend to look the same. Here we have a large intracavitary mass. We see that there is marked enlargement of the right ventricle and atrium. Incidentally, when we take a closer look, we see that there isn't any involvement of the IVC. This is largely an intracavitary mass and when we look more superiorly, we see that the mass is actually, it's a mediastinal mass extending into the SVC. Incidentally, we see all these collateral vessels also kind of periodic around the trachea mediastinum as a result of compression and obstruction due to this mass. This was actually a malignant thymoma with direct extension into the SVC and extending into the heart. And this is probably one of the most important things to recall is that most cardiac masses are going to be metastatic. So if you had to place a bet, think metastatic first. Then, you know, we're going to look for kind of specific features that help us distinguish whether or not it is truly a primary cardiac mass. So now moving on to the next case, we have patient A and patient B. So both intracavitary masses look at patient A, a largely well-circumscribed lesion in the left atrium. We see it has this kind of pathognomonic attachment to the intraatrial septum. Patient B, a similar type lesion, but of course this time much less defined as we see in patient A. It looks more villous. This is also, both of these cases are examples of cardiac myxomas. And again, it's that presence within the left atrium, the attachment to the intraatrial septum, which are the pathognomonic features of myxomas. Now myxomas are the most common benign cardiac neoplasm. So if you're going to think of a primary neoplasm, myxomas are going to be the most common. And most occur in the left atrium, 70-80%, although a smaller percentage can occur in the right atrium or even in the ventricles. Usually they're solitary, but certainly when in conjunction with other genetic disorders, we can see multiple myxomas as well. All right, moving on. This was a patient who had a echo for preoperative planning. On echo, we see there is a large echogenic structure in the left ventricle. As a consequence, the patient was referred to us for MRI. And on MRI, we see a similar lesion kind of revolving the infralateral aspect of the left ventricle. Incidentally, we see that it's largely high in attenuation. It's bright. On the SSP image, we see that there is this kind of chemical shift artifact on the edges of it. When we look at the same image on classic T1, we see that it's uniformly increased in signal. And this was an example of a cardiac lipoma. And lipomas themselves are considered the second most common benign cardiac mass that we see in adults. And fortunately, you know, the features are very characteristic. Bright on T1, low on T2, no evidence of enhancement. Whether it's CT or MR, it's usually not difficult to make the diagnosis of cardiac lipoma. Next case. Here we see, first we see a scout image from a CT. We see that there's marked enlargement of the cardiac silhouette. Subsequently, we look at this coronal reconstruction. And again, we see a large kind of homogeneous mass. Looks like there's more mass effect on the heart itself. But based on its location, it looks like it's within the pericardium. When we look on the axial image, again, we see that this large mass, largely within the pericardium, causing significant mass effect on the adjacent heart. So this was actually a case of a fibrous tumor of the pleura. Again, arising not within the pleura, but actually within the pericardial space, leading to the mass effect that we see here. This is just a histology just showing the multiple lymphocytes and classic appearance. Now, when we think of localized fibrous tumors, obviously, yes, most arise from the pleura. But very rarely, you can have cardiac localized fibrous tumors. And in that situation, they are considered pericardial tumors. OK. All right, onward. So patient A, patient B. So we have two different lesions, both of them kind of intramural masses. Patient A, we see the large intramural mass. We see a focus of calcification in the center of it. Certainly, mass effect on adjacent structures. Patient B, this time, intramural mass involving more of the interventricular septum. We don't see any evidence of calcification. Looks slightly, maybe a little bit lower in density compared to the rest of the myocardium. So these two cases are two different cases. Patient A has a cardiac fibroma. Patient B has a rhabdomyoma. And as we see, they both have a very similar appearance. When you think of an intramural lesion, these are really the two primary diagnoses that we consider. When we consider the differences between them, fibromas are typically solitary, whereas rhabdomyomas are often multiple. We usually also see them in younger patients. So multiple lesions, and they may often spontaneously regress as well. Fibromas frequently calcify. So calcification is very common when we see a fibroma, whereas rhabdomyomas typically do not calcify. So another distinguishing feature. Fibromas will have some amount of enhancement and even late enhancement on MRI, whereas rhabdomyomas typically have very low enhancement and typically do not have any evidence of late enhancement. The most important thing is both of these lesions, fibromas and rhabdomyomas, are associated with tuberous sclerosis. So the presence of either of these you should also screen for other abnormalities. Okay, next case. Here we see clear abnormality in the right atrium. We see kind of an irregular mass. And as we follow it down, we see that there is extension into the IVC. So obviously any mass that involves the right atrium extension to IVC, we should get further into the abdomen. This was a renal cell carcinoma with direct extension across in the IVC and extending into the right atrium. And you know, for renal cell tumor extension into the IVC is very common. Again, whenever you have a mass that has IVC involvement, you want to make sure that you continue that survey into the abdomen to look for the primary lesion. Next case. So this is an interesting case. Patient presented with, you know, kind of progressive shortness of breath. We see this mass-like density that's encasing the right atrium and also into the atrioventricular groove. Incidentally, we can see that it looks like there are also some loculated effusions as well. This is what we have on CT and MR and SSFP. Again, we see this kind of large encasing lesion around the right heart. Now subsequently on delayed enhancement, we see again that there is enhancement of this abnormality. Incidentally, there was also this kind of hazy involvement enhancement involving the kidneys. So this was actually a patient with Erdemchester disease, a very rare disorder. Basically, you get this systemic xanthomatous infiltration and it can occur in the lungs involving the heart, the kidneys. It's characterized by these foamy histiocyte infiltrations. And again, the actual mass itself doesn't really have distinctive features, but the distribution of findings, the distribution of abnormality can clue you in on the diagnosis. Moving on to the next case. So chest X-ray shows innumerable nodular densities throughout the lung parenchyma, enlargement of the cardiac silhouette. On CT, we see that there's a large enhancing mass involving the right atrium and right ventricle. We get the sense that there is some invasion into the heart itself. Subsequently, we see in the lungs, we see again areas of consolidation. We see some oculated effusion. And on further imaging, we see multiple modules throughout the lung itself. So in this particular case, one could argue is this from the lungs going into the heart or the heart to the lungs. This was actually a patient with an angiosarcoma, primary angiosarcoma of the heart, with metastasis to the lung itself. And angiosarcomas are the largest group of differentiated cardiac sarcomas that we can see. And more than 80% of them will have some form of metastasis at the diagnosis. So we have invasion into the right heart. Those cells then progress into the lung parenchyma where they metastasize. So now that being said, lung cancer is the most common pulmonary abnormality to metastasize to the heart. So lung cancer is always on the differential. But here clearly we have an abnormality where the primary mass is in the heart and what we see is distributed metastasis throughout the lungs. All right, next case, patient A, patient B. We see a well-rounded density, small density on the aortic valve in patient A. Patient B, a similar lesion, this time more this is kind of at the junction of the atrial appendage and the pulmonary vein, the kind of ligament of Marshall. So these two cases are actually the same. These are both of papillary fibroblastomas. And classically, when we think of papillary fibroblastomas, we think of them involving a lot of the valves. Most occur on the valve itself. The aortic valve and the microvalve are the most common locations. But 10% can occur on other locations. Endothelial surfaces can occur on the papillaries, even within the ventricles themselves. But again, classically, well-circumscribed small lesions on endothelial surfaces think of a papillary fibroblastoma. Next case, again, patient A, patient B. In both cases, we see an infiltrative mass that's invading into the right heart, particularly the right atrium and right ventricle. Patient A, we see multiple areas of signal within the lesion, so very heterogeneous and again, a very aggressive-looking lesion. Patient B, again, another aggressive-appearing lesion, ill-defined. We do see that there is somewhat of a modest pericardial effusion associated with this lesion. Patient A is in angiosarcoma, whereas patient B has a primary cardiac lymphoma. Now both of these lesions have a predilection for the right heart. Again, angiosarcomas are the most common differentiated cardiac sarcoma that we can see and can be very aggressive. The prognosis is quite poor. And they have robust enhancement as well as late enhancement. Now lymphomas, primary cardiac lymphomas, are actually fairly rare. Typically when you see a lymphoma involving the heart, it's going to be secondary, a media-style lymphoma that extends into the heart. But a true primary cardiac lymphoma typically is going to be seen more often in immunosuppressed patients, patients with HIV or immunosuppression of other things. Typically it's a B-cell lymphoma. Pericardial effusions are actually quite common with cardiac lymphomas, and often in about two-thirds of cases, the effusion, the cytologic evaluation of the effusion can be diagnostic. And as opposed to angiosarcomas, which tend to have very robust enhancement, lymphomas tend to have very mild enhancement. And again, both lesions tend to have a predilection for the right side of the heart as far as involvement. Okay, next case. This is a patient who came in, again, some atypical chest findings. We see here this kind of soft tissue density. Looks like it's kind of bordering both the right atrium and ventricle, kind of near the valve plane. When we look a little bit more inferiorly, we also see this other structure. It looks like there may be some enhancement, in fact, and it may actually extend out into the epicardial space. So on delayed imaging, we actually see that this does, in fact, enhance. This was a giant RCA aneurysm. We can see its connection to the right coronary artery. Very subtly, you can actually see that there is some relative decreased attenuation of the inferior aspect of the left ventricle as well, likely related to it. So this was, again, just a large RCA aneurysm mimicking a cardiac mass. Okay, rounding out cases, we have another case, patient A and patient B, both cases of an intracardiac mass involving the left atrium. In patient A, we see that this mass, it's really kind of at the junction of left atrium and pulmonary vein, extending into the pulmonary vein. One might even question, is this from the lung coming in as opposed from the atrium coming out? Here on patient B, we see a more definitive left atrial mass, extensive calcification, and again, very aggressive-looking lesion. Both of these are examples of a left atrial osteostarcoma. And interestingly enough, when we have these lesions involving the left atrium, these are more likely primary osteostarcomas, not metastatic. Metastatic lesions tend to occur on the right side, whereas the left atrium, the left atrium contains many potential cells that can differentiate into osteostarcomas. These are highly invasive and they frequently invade much of the mediastinum as well as into the pulmonary veins. Okay, again, with our rapid fire here, we have another case. We have a large mass, again, invading the right atrium, right ventricle. We see that there is some peripheral enhancement. So if we had to put money, we would say that this is what? Exactly, a metastasis, more than likely. But are there any primary disorders that we think? Well, right heart, angiosarcoma, we do see some evidence of enhancement. Lymphoma, well, there is a pericardial effusion. Well, in fact, this particular case, a very unique case, this was actually a pericardial mesothelioma. This is a person who actually had abdominal mesothelioma and was then found to have pericardial involvement as well. And this is extremely rare. And like mesotheliomas, it's made up of abundance of subtypes, epithelial, spindle cell, and there can be mixed subtypes as well. As one can imagine, the presence of a pericardial mesothelioma, the prognosis is quite poor, and it's unfortunately quite resistant to therapy. But again, a mix of chemotherapy and surgery are often the case with this. And with that, my mouth is dry. We've gone through 15 cases, and I'll stop here. Thank you. Hello. My name is Diana Palacio from the University of Texas Medical Branch, and here are the pericardial cases. Case 1, the normal pericardium. Most of us are able to recognize the pericardium on CT as a fine layer of tissue that encases the heart but also travels superiorly to cover the proximal aspect of the gray vessels, as you can see here on chronal and sagittal planes. The appearance of the pericardium on MR is such that it follows the signal characteristics of muscle in all sequences. And also, the lack of enhancement is characteristic in normal conditions, whether it's early or delayed phases, as you can see here. What we see on cross-sectional imaging is the combination of the visceral and the parietal pericardium, as well as a small amount of fluid. The pericardium protects, lubricates, and anchors the heart to the posterior medial stannum. The abnormal pericardium is considered thick when it's above 3 millimeters. Case 2 is a patient undergoing surveillance for prostate cancer and presumably a lymph node in the right lower paratracheal station. Upon further review, these images demonstrate that this is a structure that continues on posteriorly along the wall of the area. So this is a prominent pericardial recess, a pitfall for potential infiltrative disease or lymphadenopathy. It is composed of two major sinuses, the transverse and oblique sinus. The transverse sinus encompasses the layers along the PA, the aorta, and the SVC, whereas the oblique sinuses, in case the pulmonary veins, they do not communicate with each other. Case 3, patient evaluated for radiography. We see an enlarged heart silhouette on chest radiograph, perhaps little deviated left. The CT images demonstrate that there is actually significant displacement of the heart to the left with clockwise rotation, and you can see there is absence of the pericardium as we know it. This is congenital complete absence of the pericardium, which can be asymptomatic, but it can also cause angina. In most cases, it's partial absence of the pericardium, actually more often seen on the left side. Patients that are symptomatic may require surgical reconstruction. On chest X-ray, notching between the aorta and the pulmonary artery is due to the lack of the reflection of the pericardium in that area, which is absent, and leftward deviation of the heart. The MR characteristics are the same as on CT, but you can see also hypermobility on CT images in some cases. Case 4, patient with abdominal pain, palpitations at night, and shortness of breath, and the X-ray revealed abnormal contour of the left lower medial stynum. CT abdomen demonstrated a structure that was homogeneous in the posterior aspect of the heart that was displacing the esophagus anteriorly and to the right on upper guy series. The signal characteristics on MR were classic of a cystic attenuation lesion with no enhancement after gadolinium injection and bright signal on T2 images. So this was presumed either a neuroenteric cyst or a pericardial cyst, and the final diagnosis was a pericardial cyst. On CT, the pericardial cysts are usually homogeneous, well-defined, and there may be some cases with intermediate attenuation due to complexity of the fluid. On occasion, they can bleed or they can get infected, and MR is the best modality to identify the signal characteristics. Some pericardial cysts may, quote unquote, disappear, and this is because they might just be diverticula that communicate with the pericardial sac. Pericardial cysts, by definition, do not communicate with the pericardial sac. There is a variety of differential diagnosis for this location. Case 5 and 5A are related. One is an obese 39-year-old female patient with shortness of breath, and the other one is a 71-year-old female with history of breast cancer and a shortness of breath. Both cases demonstrate abnormal cardiophrenic angle on the right with intermediate attenuation. Case 5 is a case of prominent fatty tissue in the region, which on MRI with T2 without fat saturation follows the signal characteristics of fat and does not enhance on T1 post-contrast. So this is your classic pericardial lipoma, which is mature adipocytes. They tend to be asymptomatic unless they are large enough to cause pressure symptoms. They tend to be encapsulated, although not very well seen. Case 5A was actually a more typical pericardial cyst. Case 6 is a patient who has breast cancer, was noted to have impaired left ventricular relaxation and some echogenic material in the pericardium, and you can see here the echogenic material in the pericardium. On MR, we did not see fluid, but we did see these tissue characteristics of fat on non-fat saturated T2 and fat saturated T2 images, and on STIR images as well. You can see that on this 4-chamber imaging, seen it, there is a little bit of compression of the right ventricle and a little bit of straightening of the interventricular septum. So this was clearly epicardial fat tissue that was causing some hemodynamic effect over the right heart, and characteristically on CT, significant amount of fat surrounding the epicardium, whereas the pericardium looks within normal limits, and on PET-CT, no FDG activity. So this is called massive epicardial lipomatous hypertrophy. Sometimes the accumulation of epicardial fat around the heart may be such that it causes mass effect and some degree of tamponade physiology, requiring decompressive parietal pericardiectomy. It can also be a pitfall for complex pericardial effusion on echo. Case 7, 63-year-old female with chest pain elevated by declining troponins. The rest of the cardiac workup was negative. The images demonstrate supralateral distal high signal on T2-weighted images. That area was hypokinetic or dyskinetic, and the delayed gadolinium enhancement revealed high signal due to enhancement of the pericardium and the myocardium in the vicinity, as you can see on 4-chamber and short-axis images. Focal myopericarditis, myocarditis and myopericarditis always should be considered in the differential diagnosis for elevated troponins, causes viral autoimmune or toxic, and this patient complied with the Leck-Lewis criteria for myocarditis, in which pericarditis is a supportive criterion. Case 8, patient with chest pain where they wanted to rule out PE, but the patient was allergic to iodine, so we ended up doing an MRI of the chest, and in this case we found significant high signal intensity along the pericardium and enhancement after gadolinium injection on T1-weighted imaging, both axial and coronal planes with thickening. There was no fluid whatsoever, so this is a case of dry pericarditis. Dry pericarditis, as with other form of pericarditis, can be viral, other etiologies to be neoplastic disease or systemic disease, and interestingly, the more the pericardium is thick, the more likely the post-inflammatory therapy will work. Some cases will evolve into a more chronic constrictive pericarditis. Case 9 is a patient who was transferred for chest pain, coronary problems in the past, alcohol abuse. In this case, we see a very infiltrated soft tissue around the heart, but also causing a significant amount of pericardial fluid with high attenuation. The MRI demonstrated that this was tissue with low signal on T2 over T1-weighted imaging and slightly low also on T2-weighted imaging. The pre- and post-contrast images revealed no significant enhancement, so this was kind of against the behavior of an aggressive tumor. The pericardium was, however, significantly thickened and enhancing with the complex effusion in between, so this turned out to be a fibrosin mediastinitis case with pericardial involvement. We know this entity in chest diseases, especially within the mediastinum, when it causes compression of all these venous structures, arteries, or bronchi. There are two types. The more diffuse type tends to be due to autoimmune diseases, drugs, and radiation. And the typical appearance is that of low to intermediate T1 and low to intermediate T2 signal due to the high fibrotic or high cellular tissue. And no or variable post-contrast enhancement. Case 10, patient with smoking history, admitted for pericardial effusion with tamponade, pericardiocentesis with body fluid. And you can see the large amount of fluid that is not only large, but it's causing significant effect over the right heart during the cardiac cycle. And the same situation on the CNN-MR images, where there are bridging fibrin bands between the two in both. You can see a little bit of septal bounce and compression of the right heart due to the large amount of fluid. And the signal characteristics, classically complex with thickening and edema, as well as loculated pockets of fluid enhancement. So this is malignant effusive constrictive pericarditis. The causes are usually due to malignancy. All of these malignancies can cause this problem. And there's a combination of exudation, hemorrhagic effusion, and inflammation all together to form effusive constrictive pericarditis. Case 11 and 11A are related. The two patients with fatigue, edema, have some degree of calcification outlining the pericardium. In this case, the CT demonstrated speckles of calcification around the pericardium. And here you can see this one is even larger amounts of pericardial thickening. Throughout after pericardiectomy, this is the result, more expanded ventricles. This is the result after pericardiectomy on this patient where the heart has recovered its shape. There is a little bit of residual stuff there. So chronic constrictive pericarditis is usually manifested with calcification. Most of the patients are not associated with constrictive pericarditis, but about 30% may have constrictive pericarditis. And up to 50% are visible on chest radiograph. Case 12 is a patient who has a pericardial effusion and a pleural effusion and had a pericardial window previously. We have a very hypervascular mass center within the pericardium with pericardial enhancement and pleural effusions. And so this turned out to be a pericardial angiosarcoma. Most of them are in the right atrium or right ventricle, but this one particularly was centered in the pericardium. Case number three, a patient with rectal cancer found to have a mass in the chest, was asthmatic otherwise. And in this case, we found also hypervascular lesion within the pericardial recess in the AP window. This particular case had no significant pericardial thickening. It was just situated in the pericardial sac in this area where these cells tend to live and is a periganglioma. So the difference between periganglioma and angiosarcoma, even though both are hypervascular, one of them tends to be infiltrated and has more commonly pericardial effusion, whereas the other one encases but does not infiltrate the adjacent structures and is usually not associated with pericardial effusion. Hemangiomas are a little bit less common. Case 14 has a patient with a previous cabbage and gunshot wounds to the chest. And this is the chest radiograph, fairly unremarkable with maybe a little bit of distinctness there in retrospect. And we can see that there is pericardial fat stranding and thickening. And this was a case of penetrating trauma to the pericardium without involvement of the myocardium, perhaps because this patient had a cabbage in the past and was somewhat protected that way. And case 15 is a patient with post-MVC with a large amount of air around the heart. This is the normal pericardium, which most of the time is not associated with symptoms, but it can be sometimes presenting as a tension in the pericardium requiring immediate drainage via pericardial window or open subcythoid eye poach.

cardiac abnormalities

pericardial conditions

cardiac masses

imaging techniques

CT

MRI

echocardiography

myxomas

pericarditis

congenital anomalies