Good afternoon, and thank you for attending. I suspect that most radiologists who read chest CTs are fairly comfortable with evaluating the size of the aorta, the pulmonary arteries, and left atrium. I also suspect that the left ventricle and right ventricle are not usually evaluated because we know that these studies are not gated, but there's still a lot of information that can be gleaned even on a non-gated study, and I'd like to go through some of the more common things you might see over the next few minutes. So to that end, we'll be looking at ventricular chamber size, abnormalities of the ventricular walls, filling defects, and a few confounders and miscellaneous items. In doing chamber analysis, we need to look at the size, the shape, and the wall thickness of the ventricles. The obvious problem is that we don't know the phase of the cardiac cycle on ungated studies, and also standard imaging planes are not ideal for evaluating either chamber size or wall thickness. The result is that we may underestimate chamber size or overestimate wall thickness. So if you gate your aortic CTs as we do, then your scans will be obtained in diastole, and with the proper views, you can accurately measure the end-diastolic chamber dimension and wall thickness as shown here by the orange line for the chamber dimension and the blue line for wall thickness in a standard short-axis view. The non-gated chest CTs, again, you won't know where in the cardiac cycle a slice was obtained. It's probably during partial contraction at least. And so if a chamber looks too big, then it is too big, and it could be even larger. And if the wall looks too thin, then it's at least that thin and could be even thinner. But if the chamber looks normal size, you don't know, and if the wall looks too thick, you don't know. Normal left ventricle has an elliptical shape. Normal echoed short-axis dimension at end-diastole is 5.4 centimeters. And normal wall thickness, 11 millimeters except in the upper portion of the septum where it's normally slightly more. Here's two examples of left ventricle enlargement. On the left, more of a global or spherical-shaped LV, and on the right, more of a bulge toward the apex. The right-hand study also shows pretty obvious left atrial enlargement. The right ventricle has a triangular shape, and normal echo mid-cavity diameter in the four-chamber view is 3.5 centimeters. And as you all know, the RV should be smaller than the LV. The wall is thin and may be difficult to distinguish from the subepicardial fat. And importantly, the ventricular septum should be convex toward the right ventricular side as it is here. Here are two examples of right-sided heart enlargement with large right atrium and right ventricle in normal left-sided cardiac chambers. Importantly notice that the ventricular septum is either straightened or slightly bowed toward the left side. And when that occurs, you should think about high right-sided pressures. Now, a word of caution, if you're using the RV-LV ratio of greater than 1 as an indicator of RV strain in cases of pulmonary emboli, you're assuming that the right ventricle was not enlarged before the pulmonary embolic event. Ask yourself the following questions, I think. First, what is the embolic load? If it's a couple of small emboli, that's not likely to cause RV strain. Is the pulmonary trunk significantly enlarged? In my experience, this would be unusual in the acute setting and suggests that the patient may have chronic PA hypertension. And then look for other causes of pulmonary hypertension that could cause right heart enlargement or strain, including lung disease, morbid obesity, mitral valve stenosis. And remember that if the LV is already enlarged, then the LV-to-RV ratio could be normal even though the right ventricle is abnormal. Here's a nice example of biventricular enlargement in the three standard planes. Moving on to calcium in the left ventricle wall is an important finding because it's almost always indicative of prior myocardial infarction. It's usually curvilinear in shape, occasionally amorphous. There's a misconception out there that if you see calcium in the LV wall, it means there's an aneurysm or a clot, and it's not necessarily true. So this is an example of an apical infarct in the LAD distribution. You can see, marked by the orange arrow, extensive calcification in the distal portion of the septum and around the LV apex. This patient, you probably already noticed, has a lung cancer on the right. Here's an example of a posterior infarct in the circumflex distribution at the base of the heart in the mid-cavity level. Here's an example of a posterior infarct in the right coronary artery distribution, showing calcium in the inferior portion of the septum and along the bottom of the heart as marked by the orange arrows. And this is another example of a posterior infarct involving the RCA territory, where you see the orange arrows mark calcium in the LV wall, and the blue arrow marks calcium in the papillary muscle, and that can also occur with myocardial infarction. You can also see degenerative calcification in the papillary muscle, I think, and it may be difficult to distinguish the papillary muscle from the chordae tendineae. So if there's no other signs of ischemia, such as coronary artery calcium, then you may be dealing with chordal or degenerative calcification rather than an infarct in the papillary muscle. Some confounders you run across include calcium in the pericardium, calcium in the mitral annulus, and surgical material, including Teflon pledges and VSD patches. Here are four cases of calcium in the pericardium. The top left and top middle images are non-contrast CTs showing calcium almost the entire pericardium extending up to the origins of the great vessels. The bottom left image shows heavy calcification adjacent to the right atrial wall posterior to the AV groove. The bottom image in the middle shows heavy calcification in both AV grooves, and this is said to be pathognomonic pericardial calcification. The two right-hand images are the same patient coronal and sagittal views, and it looks like the calcium is only adjacent to the LV, and one might wonder whether this was due to a calcified left ventricular infarct. But you see on the top image, it extends beyond the AV groove, and that indicates it's involving the right side of the heart and not just the ventricle. In my experience, I've never seen an RV infarct that calcified. When you see calcium on the right side of the heart, to me that indicates that the patient has pericardial, not myocardial calcification. This case was given to me as a presumed case of right ventricular calcification following an RV infarct, but I doubt that to be the case. The calcium is very heavy, involves both the anterior wall as well as the bottom of the heart. If this were in fact a calcified RV infarct, it would have involved almost the entire right ventricle, and this patient probably wouldn't be alive and certainly wouldn't have a normal-sized ventricle. So I'm completely confident that this is pericardial in origin and not myocardial. Calcium in the mitral annulus is rarely going to cause a problem for anybody. This is kind of your classic appearance on axial and coronal views. But if the patient has caseus necrosis of the mitral annulus, which you see here is a large clump of calcium at the base of the heart, and then more typical mitral annular calcium extending toward the left side of the heart, that could be confused with a pseudo-aneurysm or an aneurysm in the inferior wall of the left ventricle. Ventricular septal defect patches may be radiodense either because they were made of radiodense material or a native material that's calcified. On the left-hand image, you might think that this calcium is in the aortic valve leaflets, but as you scan for the caudate, you can see it extends onto the upper portion of the septum. You'll also notice there are tiny metal wire sternal sutures. This patient had VSD repair as a child. Fat can occur either in the RV free wall or the LV free wall. On the right side, it's most usually a normal variant. Arrhythmogenic RV dysplasia also has had a replacement of the free wall, although this is no longer considered a major criterion for diagnosis of that disease. It can be difficult to distinguish sub-epicardial fat from fat in the RV wall because of the thinness of the wall. Left ventricular wall can have fat as a normal variant, but it sometimes indicates a myocardial infarction. So on the left-hand side, you'll see some normal RV wall fat, a little more obvious in the top image than the bottom image where it's thinner, but both marked by the yellow or orange arrows, I should say. And on the right-hand side, there's two cases of arrhythmogenic RV dysplasia with extensive fatty deposition in the RV free wall in the upper study. Bottom study, not quite as much. The blue arrows mark the normal pericardium, and the white arrows the extent of the RV chamber. In the top set of images, we have three examples of fatty-replaced left ventricular infarcts. The upper left one shows replacement of most of the LV apical wall by fat, as indicated by the orange arrows. The next image over shows subendocardial fatty replacement of the posterior wall in a circumflex or RCA distribution infarct. The top two images are non-contrast studies showing very thin subendocardial fatty replacement of the LV apex and distal portion of the LV free wall. Contrast that with normal fat replacement of the LV on the bottom two images. The blue arrows are fatty replacement in the free wall of the LV. The white arrow shows fatty replacement of the inferior portion of the septum. The diagnosis of normal variant here as opposed to infarct hangs on two things. One is there's also fat in the RV free wall, as you can see with the yellow arrow. But more importantly, the distribution of fat here does not follow any vascular territory. So we've got both circumflex and LAD distribution fat. The LV is normal in size. If the patient in particular has no coronary calcium, you can be confident that this is a normal variant. LV aneurysms come in two flavors, as you're aware. True and false. And true aneurysms come from infarctions. And contrary to what some think, they can involve any part of the ventricle they want to. And they're much more common than pseudoaneurysms. So almost all aneurysms you see will be true aneurysms, regardless of where they live. With rare exceptions, pseudoaneurysms are inferior or posterior, and they result from a contained rupture. So here's a path example of a large aneurysm at the LV apex. And it causes a focal bulge in the LV wall on imaging. It's characterized by a wide mouth or wide neck, if you prefer. And again, can be located anywhere. Here's three examples of LV infarcts on the top left in illustration A. There's a fairly large bulge at the LV apex with thinning of the wall. In the example B, which are two levels of the same patient, almost seems to protrude beyond the confines of the heart, although you know there's a small amount of scarred myocardium surrounding it. And then the bottom left in example C is a heavily calcified infarct at the LV apex. Now if the infarct is along the bottom of the heart, this can be more difficult to detect. If you look at the top picture, it looks pretty normal. The top right one, you see there's a little bit of contrast down there, a little further inferior than it should be at the base of the heart. In the bottom left picture, you can see that where the orange arrow is, there's some thinning of the LV wall, but it's not really until you get to the sagittal reconstruction on the bottom right that you can see there's a small aneurysm in the posterior LV wall. Left ventricular pseudoaneurysms result from contained rupture and are characterized by a narrow mouth or neck, and almost without exception will be located posteriorly or inferiorly as shown in this path example and in the cartoon above from Becker and Anderson's book. Here are three examples of left ventricular pseudoaneurysms. Illustration on the top left shows a focal pseudoaneurysm at the base of the left ventricle, and I think you can see how that might be mistaken for caseus necrosis of the mitral annulus, although the latter will be heavily calcified and this is not. The bottom left shows a fairly narrow neck to this very large aneurysm. The neck was, in fact, smaller than what the arrows indicate here, but difficult to show on a static picture. Now on the right is an example of an apical pseudoaneurysm, and like the other two that I've seen, both of which were given to me by other people, these were all post-op patients. This patient had a left ventricular aneurysm resection. The very dense material is teflon pledges. There was a leak at one of the anastomoses, and you can see contrast and clot in this large pseudoaneurysm extending over toward the left side of the chest. Now cardiac thrombi are more commonly seen in the LV than the RV. These can be mural or protrude into the chamber, and the ones that protrude are more likely to embolize. Right ventricular and atrial clots are usually from lower extremities or from tumor thrombus rather than occurring in situ. Here's a huge LV aneurysm, and you see it extends all the way down into the abdomen where there's a large amount of clot in a very heavily calcified apical wall. There's a large filling defect in the apex of the left ventricle that I don't think anybody would mistake for anything outside the chamber. I guess it could be a tumor, but clots are certainly a lot more common than tumors, and this was a large clot in the apex of a patient who had an aneurysm. Some RV thrombus that came from somewhere down below. Now the problem is, how do you distinguish an apical thrombus from a fatty-replaced apical infarct? It can be difficult. On the left-hand side, you can see contrast surrounding the filling defect, and if you put an ROI on that, it was soft tissue. On the right-hand picture, the ROI showed fatty deposition, but it can be really difficult to tell the difference between the two. Now two things to know about because they mean nothing and you don't want to say that they mean something and start a big investigation. One are LV sinusoids, which are these protrusions into the septum, and LV diverticulum, which usually goes into the inferior wall of the LV, and both of those are not normal, but they're not of any consequence. In summary, we've looked at ventricular enlargement. We've looked at some evidence of hypertrophy and right ventricular strain. We've talked about findings in myocardial infarction, including fat and calcium deposition, as well as the two types of aneurysm. Looked at normal myocardial fat deposition and a few confounders. I'd like to now turn the podium over to Dr. Jill Jacobs, who will speak to you about CT of coronary artery anomalies. Thank you very much. It's a pleasure to speak to you today on CT of coronary artery anomalies. I have no disclosures. Traditionally, coronary artery anomalies have been classified into four types. Anomalies of origin, anomalies of course, anomalies of termination, and anomalies of intrinsic anatomy. But when I actually start to look at a new case, I typically start by just doing an axial scroll to give me the lay of the land. And I can quickly see the coronary arteries, their sizes, whether they're coming off of the appropriate cusps, I can see the chamber sizes. So I thought it would be useful to be able to group anomalies into typical patterns that we may see. So I came up with five broad categories of patterns that we can recognize. The first being normal caliber vessels. The second being focal vessel narrowing, either solitary or multiple. The third being focal vessel dilatation, either solitary or multiple. The fourth being diffuse single vessel dilatation. And the fifth being diffuse multi-vessel dilatation. So let's start to look at these. So the first category is normal caliber vessels, and these include things like a high takeoff of a vessel, as we can see in this case, where the right coronary artery is coming off above the level of the sino-tubular junction. We can have multiple ostea, as we see in this case, where the left circumflex and the LAD both have separate origins from the left coronary cusp. We can have origin from the opposite or non-coronary sinus in an anomalous course. Dual coronary artery or duplicated coronary artery. So I want to really focus in on this category, origin from the opposite or non-coronary sinus and anomalous course. The right coronary artery arising from the left coronary sinus occurs four times more commonly than the left coronary artery arising from the right coronary sinus. When the right coronary artery arises from the left sinus, the most common course that it takes is interarterial, and this is associated with sudden cardiac death in up to 30% of patients. The left coronary artery arises from the right coronary sinus in up to 0.11% of patients, and when it does, the most common course is a septal or sub-pulmonic course. And what's important is when the left coronary artery takes an interarterial course, it does have a higher sudden death risk than when the right coronary artery takes an interarterial course. And this is thought to be because the left coronary artery supplies more of the myocardium than the right coronary artery. So when you know you have an anomalous course, the next important thing to look at is what course the coronary is actually taking to reach the proper side of the heart. And there are four different types of courses, the most important being the interarterial course because it is higher risk. That's when the artery crosses between the aorta and the pulmonary artery. In this case, it's the left main to reach the left side of the heart. There is a septal or sub-pulmonic course where the coronary artery actually crosses under the pulmonary outflow tract, an anterior or pre-pulmonic course where the coronary artery crosses anterior to the pulmonary artery, and a retro-aortic course where the coronary artery actually courses posterior behind the aorta, crossing between the aorta and the left atrium, which would reside here to reach the left side of the heart. And the septal, anterior, and retro-aortic courses are all benign courses. Now the interarterial course used to be called malignant configuration, and that's because it has a higher risk of sudden death, but it's probably more appropriate to call it an unfavorable or a higher risk configuration. And in fact, coronary artery anomalies are the second most common cause of sudden death in competitive athletes after hypertrophic cardiomyopathy. This is a right coronary artery coming from the left coronary cusp. You can see it's narrowed at its origin on this axial view and then becomes more normal in caliber as it reaches the right side of the heart. On a parasagittal view, you can see that it's narrowed and ovoid in shape, which implies that there may be an intramural course of this vessel. And that's important because in symptomatic patients, when there is an intramural course, it can be treated with unroofing. The other important thing to determine when you have an anomalous vessel is whether it's a dominant vessel. In this case, it was an anomalous right coronary artery, but it was actually non-dominant. You can see here on the cinematic rendering that the right coronary artery as an interarterial course is coursing between the pulmonary artery and the aorta. But when it reaches the right side of the heart, you can see that it gently tapers. It's a very small vessel. And in fact, when we look at the posterior aspect of the heart, we can see that it's actually the circumflex artery, which is supplying the posterior descending artery. So this is a non-dominant right coronary artery. In this case, the patient was actually not treated because it was felt that the right coronary artery wasn't supplying much of the myocardium. So that's why it's so important to determine dominance. This is an example of a retro-aortic course. The left main was coming from the right coronary cusp and taking a retro-aortic course, crossing between the aorta and the left atrium to reach the left side of the heart. And you can see that there's no compression of the vessel as it's crossing between the aorta and the left atrium. And this is an example of a pre-pulmonic course. In this case, we have an aberrant left main coming from the right coronary cusp. You can see it's crossing anterior to the pulmonary artery to reach the left side of the heart where it's bifurcating into the LAD and left circumflex. And when you look at the left circumflex, you can see that there's actually an area of severe stenosis in the circumflex. If we look at that a little bit more closely on our curve reformat, we can see that there's a large amount of non-calcified plaque there that's causing that stenosis. This is just a short axis view down that vessel. You can see right there is that area of stenosis. So I like this case because it reminds me that when you have a coronary anomaly, you still have to look at the vessel like you would any other coronary artery. They do develop coronary disease and stenosis. This is an example of a septal or sub-pulmonic course. This is a 17-year-old who had chest pain. You can see the left main coming from the right coronary cusp. You can see that it's coursing towards the left side of the heart. And when it does, it's completely surrounded by myocardium. That's because it's coursing under the pulmonary outflow tract. You can see it actually slopes downward as it's coursing towards the left side of the heart. And that's called the hammock sign, that kind of vertical sloping. Again, you can see the myocardium on both sides of it. In the parasagittal view, you can see that it maintains a round configuration, even though it's surrounded by myocardium. And importantly, it's below the level of the pulmonary valve. It's very important to be able to differentiate septal from interarterial course, because as we know, the interarterial course has a higher risk for sudden death. So the important things to recognize are that a septal course, the artery maintains its rounded shape. It's surrounded by myocardium. It's below the level of the pulmonary valve, whereas the interarterial course often assumes this ovoid shape and it's slightly compressed. It can be very slit-like in some cases, and that often implies an intramural course, and it's at or above the level of the pulmonary valve. You can have other anomalies of origin. In this case, we have the left main coming from the non-coronary cusp, the posterior cusp, and then it courses anterior to the left atrium to reach the left side of the heart. And this is a single coronary artery. You can see the single coronary artery coming from the right cusp, then bifurcating into the right coronary artery and the left main. The left main took a sub-pulmonic course. You can see that hammock sign, that downward sloping, again, of that vessel as it courses towards the left side of the heart where it bifurcated into the LAD and left circumflex. Our second category is focal vessel narrowing, either solitary or multiple, and that includes things like myocardial bridges, congenital atresia, and congenital stenosis. This is an example of a myocardial bridge. You can see the tunneled segment here burrowed down within the myocardium. This is a cross-sectional view of it, short axis view showing the vessel, which is completely surrounded by myocardium rather than the typical epicardial fat. So myocardial bridges are very commonly seen with coronary CT angiography. Most occur in the proximal or mid-LAD, but they can occur in any coronary artery. And the important thing to realize is that plaque is rare in the tunneled segment of the artery, and that's thought to be because the high shear stress within the tunneled arterial segment actually protects the segment from plaque formation. Myocardial bridges are generally regarded to be a benign condition, but they can cause myocardial ischemia and infarction, conduction abnormalities, and sudden death. And it's thought to be the long and deep bridges that are the ones that are more typical to develop myocardial ischemia and symptoms along with sudden death. This is an example of congenital atresia. This woman had atresia of the left main coronary artery and a bicuspid aortic valve. And you can see this little tiny bit of atretic tissue here where the left main should be taking off. Here's another view of it. And this is a cinematic rendering, again, showing that atretic tissue. You can see the collateral vessel formation, which happened before treatment. And this woman was eventually treated with a Lima bypass graft. Category three, focal vessel dilatation, either solitary or multiple. These are a result of anomalies of intrinsic anatomy and include coronary artery aneurysms. And the most common worldwide cause of coronary aneurysms is Kawasaki's disease. In the United States, it's actually coronary artery disease. And coronary ectasia is also a cause. This is a 51-year-old. You can see there's fusiform dilatation of the mid-right coronary artery. And this is a 12-year-old with Kawasaki's disease. You can see that there's diffused fusiform dilatation of the proximal right coronary artery. And you can see that on the curved reformat also. Category four is diffused single vessel dilatation. And this is dilatation due to termination into a lower pressure system and includes coronary artery fistulas and extracardiac termination. A coronary artery fistula is a communication between the coronary artery and either a cardiac chamber, in which case it's called a coronary chameral fistula. It can be connected to the pulmonary artery or to a venous structure, such as the coronary sinus or the SVC. Most coronary fistulas actually involve the right coronary artery. And what you see is that the feeding artery is typically dilated and tortuous because it's draining into a lower pressure system. And the problem is that this can cause myocardial ischemia due to a steel phenomenon. This is a case of a coronary artery fistula from the SA nodal branch of the right coronary artery. You can see how huge that branch is. If we follow it down, we can see that it's very, very enlarged. You can see it's coursing posteriorly towards the left atrium. There's this aneurysmal segment here. And then if we follow that, it actually connects right there to the left atrium right there. And this is a cinematic rendering of it. You can see the huge size of the SA nodal branch of the right coronary artery. Notice that in comparison, the remainder of the more distal right coronary artery is normal in caliber. We can see that aneurysmal segment there that we saw on the axial scroll and the connection to the left atrium. And the last category, diffuse multivessel dilatation. This includes coronary origins from the pulmonary artery. And in this case, diffuse dilatation typically results from collateral flow. This is an example of alkappa, which is anomalous left coronary artery from the pulmonary artery. You can see how enlarged the entire coronary artery system is in this case. We can see the numerous collateral vessels connecting the right coronary system to the left coronary system. And we can see the left coronary artery coming from the pulmonary artery. This is just another reconstruction showing that coronary artery coming from the pulmonary artery. So alkappa is also called bland white garland syndrome. It's very uncommon. Most patients become symptomatic in infancy and early childhood. And in fact, if untreated, 90% of those infants will die in the first year of life. But we do see late presentations in adults like in the case I just showed you. And that's due to the development of collateral flow between the right coronary artery and the left coronary artery. The problem is that these patients can develop a coronary steel into the pulmonary artery because of the lower pressure system. So you get retrograde flow in the left coronary circuit to the pulmonary artery. The blood flow is from the aorta into the right coronary artery through collaterals into the left coronary artery in the pulmonary circuit. And so these patients can develop chronic ischemia, cardiomyopathy, and congestive heart failure. And treatment is typically ligation of the left coronary artery from the pulmonary artery and bypass grafting. This is an example of r-kappa or anomalous right coronary artery from the pulmonary artery. And again, notice the enormous dilatation of the right and left coronary system. You can see the right coronary artery coming off of the left main in this case. And this is just a cinematic rendering view showing the number of collateral vessels, the enormous size of the right coronary artery, and the left system. And again, the collateral is here from r-kappa in a relatively smaller circumflex. So in conclusion, I hope I've shown you that coronary CT angiography enables exquisite depiction of normal cardiac anatomy. And because of that, it has become the gold standard for evaluation of anatomic variants and anomalies. I thank you very much for your attention. And I'm delighted to introduce our final speaker, Dr. Kordopassi. Good evening, everyone. My name is Isabel Kordopassi. I'm going to be talking about performance of cardiac MRI in patients with cardiac nevus. First, I would like to thank Dr. Stroll and the Education Committee for the opportunity. It's always a pleasure and an honor to be involved with RCNA. I have no relevant financial interests to disclose. As we all know, MRI is a great technique, especially because of its high tissue contrast. It can assess myocardial viability, it can characterize cardiac masses, it is also the gold standard for evaluating the right ventricle, and there are several indications when we use cardiac MRI for patients with cardiomyopathy or cardiac diseases. Cardiac implantable electronic devices, it refers to pacemakers and ICDs, defibrillators. Many patients with this cardiac disease, they will need to have cardiac devices implanted. And from these patients, it is estimated that approximately more than half will need an MRI over their lifetime. And this can be a cardiac MRI or a non-cardiac MRI, such as a brain MRI for stroke. These patients usually need a cardiac MRI because they are being evaluated as part of a transplant program or because they have new decline in cardiac function and new mass, new constricted physiology. Also, if you're following, are resizing and functioning in patients with congenital heart disease and pulmonary hypertension. So the main concerns that are raised when imaging these patients are referring to patient safety and image quality. Over the past 20 years, there have been several studies looking at the safety of MRI in patients with cardiac devices, and there's growing evidence supporting that it's safe. The main concerns have been related to device malfunction and heating of the lid with secondary tissue damage. During MRI, there are three types of fields that can, either alone or in combination, adversely affect the cardiac device. The patient or both, you have a static magnetic field, you have gradient magnetic fields, and you have radiofrequency fields. These forces can potentially lead to a device malfunction, excess heating, electric current induction. They can lead to abnormal read-switch behavior or battery depletion. So let's look at each of them separately. The main concern related to the BZ or the static magnetic field is that it may cause motion of the device and its lids due to the presence of ferromagnetic material. The thing is, the lids themselves are mostly composed of non-ferromagnetic material. The generator box has some ferromagnetic material on it, but it's not sufficient to cause significant motion. There have been no documented adverse events related to BZ effects on these devices. And the six-week waiting period that is recommended is related to device stabilization, as we'll see upcoming, rather than motion itself. The magnetic field gradients are time-varying gradients used to encode elements of the image, for example, spatial location. They are turned on and off during the pulse sequence. They are weaker than the BZ, but they change rapidly, and this leads to induced electrical fields and circulating currents in the tissues. And those can affect conductive devices like the cardiac devices. The main concerns associated with this are biological effects and acoustic noise. The time-varying gradients in the MARS system provide position-dependent variation in magnetic field strength. These cardiac devices are actually made to respond in the presence of a magnetic field. So when you have these rapidly changing fields, it may cause the possibility of changing the programming and inhibition of basic output. The reason why they are made to respond is so that we can non-invisibly manipulate the device through the REED switch in the generator. In terms of radio-frequency pulses, the main concern is heat deposition, particularly at the interface of the lead and the myocardium. Heating at the tip can cause myocardial damage, pain, changes in pacing and sensing function. So what do we have in the literature regarding heating? Lead-electron heating can be affected by many factors, like patient size, patient position within the scanner, the sequence of the scan, the lead route, and the lead design. In vitro studies, shown temperature changes that ranged from 7 to 68 degrees Celsius. But in vivo studies, shown a much lower range and no heat-induced damage. This is thought to be related to the cooling effect of moving blood, which does not occur in vitro. Handling a cardiac implantable electronic device, MR conditional, entails that there is a modification of the features of the leads, the generator, and the MR scanner itself. So an MR conditional system is going to be composed of both the generator and the leads have to be approved by the FDA and has been specifically tested to be safe for MR under specific conditions. So engineers face two general challenges when designing these leads that are MR conditional. They have to minimize heating at the tip and they have to reduce the unintended effect that has the potential of inducing arrhythmias. Compared to the leads, the generator faces more challenges from magnetic fields and RF energy. Reducing the ferromagnetic content will decrease the magnetic attraction in emerging artifacts. As we talked about the REED switch, it initiates a synchronous operation in the presence of a magnet. So replacing the REED switch with a solid-state Hall-effect sensors, behave more predictable in a magnetic environment, has led to more reliable behavior of these devices in the MR environment. And finally, there is also MR conditional generators that contain a dedicated MR programming pathway that can be turned on and off before and after a scan. It's called MR mode. The features include pre-scan, integrity check, asynchronous pacing, disabling tachycardia defection, increasing the output during the scan, and restoring the pre-scan program states and values. The decision to perform an MRI on a patient with a cardiac implantable device is similar to any other medical decision. There are potential benefits and risks. Factors that influence these risks and benefits should be identified and weighted. Pacing characteristics that could increase the risk of BRADI arrhythmias or tachyarrhythmias should be understood and determine the appropriate pacing program for the scan. So it's very important to have a multidisciplinary group that's going to look at each patient individually. These are the current MR conditional cardiac implantable electronic devices that are available. What we have in the literature, there's some large prospective multicentric randomized control trials. The first two demonstrated an increase in pacing capture threshold and some paresthesia and include warmth, but the others have no significant events. There are also multiple single center retrospective cohort studies that demonstrate as well increasing PCT, but it was very rare and it was not statistically significant. What about MRI in non-conditional devices? So any device that does not fulfill that criteria for MR conditionality is regarded as non-MR conditional. This can include an MR conditional generator combined with a non-conditional component and device systems that combine individual conditional lead and device components from different manufacturers. Conditional labeling also specifies the location of the device generator, some to be pectoral location for transvariant system. So the evidence from retrospective and prospective series and registries, in general, there's no significant adverse effects to the lead, to the generator, or to the patient. However, there have been a few things like Fontaine et al have 53 report cases of abrupt cardiac pacing during a 1.5 Tavla in a patient with dual chamber pacemaker. There are other adverse events that are published in case reports, such as inappropriate shock or power on reset and high impedance, but they're not considered significant. So this is where we're talking about safety. What about image quality? For every imaging test that we perform, we need to be able to provide diagnostic quality images in a diagnostic report, otherwise it makes no sense to perform it. The main component of cardiac devices that degrades image quality is the generator, not the leads, due to its ferromagnetic components. It is important for us to recognize these artifacts in no way to try mitigating. These are the most common artifacts we see when performing cardiac in a patient with cardiac device. So let's go over each of them. Distortion artifact. An object with high susceptibility, such as an electronic cardiac device, will be highly off-resonant from the main magnetic field. So during spatial encoding, the signal will be mismatched with erroneous spatial frequencies. Is this going to cause a shift in the signal and create this warped image? We see this type of artifact on the HASTE inversion recovery sequence that we call black blot technique. And you can see here, the distortion artifact here and here. Fielding artifacts are artifacts predominantly at off-resonance points in the magnetic field or in areas with significant distortion of the homogeneity of the field. So cardiac devices are going to cause field inhomogeneity, so that's going to be an area where this is going to happen. And multiple dark bins are caused by dephasing of these bins that result in loss of the steady state signal during a single TOR. We see this type of artifact on the balanced static state free precession sequence, which is a gradient echo sequence that utilizes a train of radiofrequency excitation pulses with alternating large flip angles. We can see the bending artifact here, here, and here. What we can do when we see this kind of artifact is, because SSFP or the static state free precession is typically used because of the high contrast-to-noise ratio and compared to the spoiled gradient echo, we can go back and revert to the spoiled gradient echo. SSFP bending artifact extends beyond the ferromagnetic objects themselves. When we use a spoiled gradient echo sequence, these artifacts can be minimized. As you can see here on the axial images, the same patients here, first image using a balanced static state free precession, have significant bending artifact, limiting the evaluation of the left ventricle and right ventricle as well, but in the same patient, when you repeat the image using spoiled gradient echo, most of the left ventricle now can be seen. Dephasing artifact. The presence of metal causes regions of extreme inhomogeneity in the magnetic field, and it's going to shorten T to a star. Patients are not refocusing using the RF pulse, so gradient echo is subject to signal voice to this uncompensated T to a star dephase. We see this type of artifact in the spoiled gradient echo images, you see here, here. We also see this with stenotomy wires or metal device in the spine on all of these images. And there isn't much you can do to eliminate the artifact, but patient selection plays an important role here. The physical proximity of the cardiac device in relation to the heart is an important factor when discussing artifacts, so device position plays a very important role. This is a patient with a left chest wall device, demonstrating significant dephasing artifact and discouraging the heart, and here you have a patient with the right chest wall device, where the artifact is not projecting with the heart. Same patients on a short axis view, you have the left-sided phase generator and the right sided one, and you can actually see pretty well and have a diagnostic MR. So appropriate patient selection in regards to cardiac device location can drastically impact the diagnostic quality of the exam. So susceptibility artifact, so metallic materials such as a cardiac device are classified as paramagnetic. These substances are going to have unpaired electrons, and they concentrate low magnetic forces, leading to this field inhomogeneity, and therefore, distortion of the images. The susceptibility artifact appears as a falsely increased signal, making the identification of true delayed enhancement very difficult. So we see this type of artifact on the delayed enhancement images, and it can cause the study to be non-diagnostic. Since we do these MRIs in patients with new onset of cardiomyopathy or looking for a new MR, this is really going to be a problem. You can see this band of bright tissue here over the heart and the anterior wall, and you can't tell if there's a delayed enhancement there. There have been some early success with the use of motion correction GRA sequence, which is called MoCo, on Siemens, and compared to the single shot through FISP. However, its clinical utility is still under research, but you can see here, this patient without the MoCo and with the MoCo, you can see a little bit better, but you still have limited visualization. Other strategies that can be used for protocol optimization is, like I said, using spot gradient echo sequence, tuning, doing a frequency scout, increased spatial resolution or decreased slice thickness, increasing the bandwidth, decreased TR and TE, you can swap the phase and frequency encoding directions, increase the average to boost the signal to noise ratio, and you also have to limit the specific observation rate. So in summary, literature shows that MRI can be safely performed under specific monitoring and scanning conditions and after device reprogramming, if it's crucial for the management of the patient. Institutional multidisciplinary approach is required to assure these patients are appropriately selected for the test, you need proper monitoring before, during, and after the test is also pivotal, and protocol selection and optimization is unallowed from diagnostic images. This concludes our session on cardiac imaging. On behalf of the RSNA and our speakers, we thank you for your participation and we look forward for your feedback. Thank you.

advanced cardiac imaging

CT and MRI

ventricular chamber sizes

coronary CT angiography

coronary artery anomalies

sudden cardiac death

cardiac implantable electronic devices

diagnostic accuracy