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Interpreting and Reporting F-18 PET MPI: A Focus o ...
Interpreting and Reporting F-18 PET MPI: A Focus o ...
Interpreting and Reporting F-18 PET MPI: A Focus on Flurpiridaz Cases
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Hello, good afternoon or good evening, everyone, and welcome to this American Society of Nuclear Cardiology webinar on Interpreting and Reporting F18 PET and PI with focus on Flopridaz cases. I am Moaz Al-Mallah from Houston, Methodist, and I will be serving as this program co-chair along with Dr. Panetia Shirintuwati, who is the current ASNIC President and Director of Nuclear Cardiology and Mayo Clinic. We have an esteemed list of speakers. Many of them are known to you, including Dr. Marcella DeCarli from Brigham and Women's Hospital, Dr. Shamshid Medahi from UCLA Medical School in LA, Dr. Peter Slomka from Cedars-Sinai Medical Center, and Dr. Jennifer Renaud from Ottawa and currently with NVM. We have a program that has been developed for you to primarily describe acquisition protocols, interpretation, and reporting of F18 cardiac PET tracers. We also would like to cover some physiologic uptake patterns, incidental findings, and normal variants for F18 tracers, talk about methodologic approaches to review these images, and then finally demonstrate some skills on how to look at these and help you identify abnormalities on these F18 studies. These are the disclosures of all the faculty, including myself, and would ask you if you can be in a quiet area without background noise so we can enhance the learning environment for everyone. Please, you're on mute, your personal phone and computer audio, the microphone. You can send questions using the Zoom chat button at the bottom of your computer. So there is, in the bottom of the screen you'll see the question, you'll see the chat button where you can put in your questions, and our faculty will be looking at them and will try to answer as many as we can during this session. This program is accredited with CME, and you will be able to claim CME by clocking on this link, and this one will be re-emailed to everyone at the end of this program. Also please be sure to follow the hashtag CVNuke and tag MyASNIC on different social media platforms, including Axe, and follow our virtual moderator, Dr. Philip Mora, who will be tweeting about this webinar. And I want to thank our sponsor for tonight, GE Healthcare, who actually, this program was made possible by an educational grant from GE Healthcare, but the program was primarily developed by ASNIC staff, including myself and Dr. Chirin Tiwati. I want to also thank ASNIC staff, and I want to also thank the faculty for their help in putting this program and preparing this educational material for you. This is one of the few programs that will start today, there will be another one in April 15 to review for that one, and if anyone misses one, then they can tell your colleagues about the April 15 webinar, and would like to welcome you to this additional activity. At this time, I'm going to stop, and we'll start with about a few-minute presentation by Dr. Panethia, who will be covering the basics of protocols and image acquisition related to F-18 imaging, and then after that, the entire remaining time will be dedicated towards interpreting cases and looking at cases throughout. So Panethia, please take it from there. I hope I mentioned your name correctly. You're doing great. Thank you so much, Dr. Amalah, and thank you, Mawaz, and hello, everyone. Thank you to everyone for joining us again. Thank you to the faculty. I think I know many of you on the webinar here, but it's really an honor for me to co-host it and to welcome you, and this is such an exciting moment in nuclear cardiology. After nearly three decades without any new FDA-approved perfusion tracers, we now have the approval of F-18 floperidase, and so I think this represents a major step forward in the evolution of cardiac PET imaging, and there's great potential to expand the use of PET to more patients and enhance our diagnostic capabilities. And I'm especially proud that ASNIC is playing a leading role in bringing this innovation to you, to our clinicians, and to healthcare teams worldwide and helping our patients. So today's session focuses on image interpretation, but look for more sessions and documents led by ASNIC on practical insights into the implementation and impact of floperidase on patient care. So we've assembled this fantastic panel of experts to guide us through this discussion, and I'm confident you'll find their insights very valuable. And so before we dive into the images and cases, I'd like to take about seven minutes to provide you with an overview of the unique properties of F-18 floperidase and the protocols associated with its use. So this is the structure of F-18 floperidase. It's derived from the pesticide paraben. It works by binding to mitochondrial complex 1 in the heart, and it has several favorable characteristics. First, it has very high first-pass extraction fraction at about 94%, and this has various benefits, including the ability to identify milder perfusion defects and greater accuracy in reflecting the true extent of perfusion defects as compared to thallium, as well as technetium-labeled tracers or rubidium-82. It also has a linear relationship between tracer uptake and myocardial blood flow, resulting in more accurate myocardial blood flow quantification. Floperidase also has a strong correlation with radioactive microspheres in determining absolute quantification of regional flow over a broad range of flows from 0.1 to 3 mL in pig models, and there is very little, if any, roll-off phenomenon as compared to, for example, technetium-labeled sestamib. So this promotes accurate quantification of blood flow and less underestimation of ischemia. Floperidase also has the shortest post-tran range among the commonly used PET perfusion tracers at 0.1 mm in tissue, and the longest physical half-life at 110 minutes among the commonly used PET perfusion tracers. So these favorable characteristics shown here, the high extraction fraction, linearity with flow, short positron range, and long physical half-life, these all contribute to many advantages, particularly the superior image quality with higher count statistics, high contrast resolution, and greater defect resolution as compared to SPECT MPI. And operationally, the longer physical half-life of F18 floperidase of 110 minutes has the advantage of facilitating floperidase's availability for unit dose distribution from regional radio pharmacies. So this means that practices don't need the higher cardiac PET volumes to be economically viable, which is the case with rubidium generators, and we also do not need an on-site cyclotron. There's also the advantage that floperidase can be combined with exercise stress. But we must also acknowledge that there are some opportunities that we have to consider with floperidase. We have less clinical experience with it, and there are new patterns to recognize with images from the thinner-appearing myocardium, visible papillary muscles, to apical thinning as normal variants, and we will be showing you all of these findings. Floperidase is also associated with higher radiation dose symmetry as compared to other PET myocardial perfusion tracers, perhaps some higher costs per dose, and longer protocols. So speaking of protocols, here is the pharmacologic floperidase PET-CT protocol that was used in the second Phase III, or Aurora, trial. So this is what the FDA approved for the pharmacologic stress protocol. And for PET-CT, following the CT scout and transmission acquisitions in the resting state, we inject 2.5 to 3 millicuries of floperidase, and then a single ECG-gated 15-minute dynamic LISMOD acquisition is performed. After the resting acquisition is completed, we can get ready for the stress, but need to wait at least 30 minutes between rest and stress injections. This is what was approved. Then once the appropriate time has passed, we can administer the vasodilator stress agent, and then inject 6 to 6.5 millicuries of floperidase, and then perform another 15-minute ECG-gated dynamic LISMOD acquisition. So the total time is less than one hour, maybe closer to 45 minutes. There are several additional key points. The total activity should not exceed 14 millicuries for an individual subject, and the minimum of rest to stress ratio 1 to 2. Floperidase and adenosine must be administered through separate lines or separate ports of the same IV line, and the rest I've already mentioned. For exercise floperidase, the protocol takes slightly longer, because with exercise, the image acquisition will start 15 to 25 minutes after injection of the radiopharmaceutical, and we currently do not really have a way to measure myocardial blood flow with exercise treadmill PET. And also remember that during exercise, the patient should continue to exercise for an additional 1 to 2 minutes after the floperidase injection, pretty much like what we do, for example, with sestamibi, and this is as much as possible. And so now I'm going to turn it back over to Moaz to show us some floperidase images. Please enter questions in the chat box, which I and other faculty members will try to monitor. Let me stop sharing now. Thank you very much. We're going to start with the first case, and our panelists are going to start to help us look at these cases. So the first case is for the history. She is... So the patient is a 51-year-old lady with a BMI of 27, and she's coming in with chest pain, non-diabetic, hypertensive, and dyslipidemic. And maybe we can ask Dr. DeCarli to start with, in terms of quality assurances, once we start with the images, what is like your favorite screen looking at? And this is like in PET in general. What do you look first at? Do you start with the fusion? What quality assurance measures do you want to look at? Well, thank you, Moaz and Panithia, for the invitation to be part of this session. And we're equally excited about this opportunity with new radiopharmaceuticals. So when we read PET-CT, we'd like to start with some quality control, and I guess the basic quality control measure that we want to perform is to ensure that the PET perfusion study is well aligned with the corresponding CT to ensure that the attenuation correction will be done properly and that there will not be any artifacts on the images. And so what you do is you scroll through the images and make sure that essentially the color picture fits well within the gray picture of the cardiac silhouette like you see on this particular scan. You want to do this for the rest and also for the stress images. In this case, I guess we have the stress images. You want to do the same exercise then for the rest images. And you see it here, perhaps a little bit of a misalignment there in the apical portion of the heart. You can see the lung shadow overlapping a little bit on the myocardium, suggesting that there may be some misregistration. Not all misregistrations will lead to artifacts or to defects. So minor misregistration will likely not cause any problems. But you want to be aware of this because you definitely don't want to over call defects that are in fact artifacts. If you do see gross misregistration, you will not be able to fix it at the computer where you're reviewing the images. The images have to be manually or automatically realigned at the console of the scanner and reconstructed again to make sure that they're properly aligned. Thanks, Marcelo. Yeah, so maybe a question to Dr. Slumka, is there a limit to how much misregistration would you accept and not accept? Ideally, we don't want any, but do you think this is going to be concerning, not concerning? Thank you. There is some echo right now. That was not before. I don't know whether to type it before you fix it. OK, maybe until we fix this issue. Jennifer, if you want to take this one, like how much I know Marcelo alluded to it a little bit. Yeah, so here the misregistration is only on a few frames and it's not too far out. So it's I would say it's affecting the image somewhat. But I wouldn't say that now it's become a non-usable image. I mean, rule of thumb is that you want to have the PET CT activity at the 50 percent level within the CT threshold. So obviously this falls somewhat outside of that. But we would have to look at, you know, if you look at the perfusion images to see if there's an actual misregistration artifact. Sometimes it could also be just an issue on the display if the transformation coordinates are not correct. Potentially, we're getting just a problem in the display with the alignment. All right, thank you. All right, Dr. Madahi, what do you how can you we look together at this image and help interpret it? You're muted, Jamshid. Yeah, right off the bat for those people who have been doing SPECT imaging or doing rubidium PET, you will see that what is striking is that the myocardium is thinner. The cavity is much better defined. We often, I would say most of the cases we do see right ventricular activity, which is not an abnormal finding because of a higher resolution visualization of the right ventricle is quite normal with fluoroperidase. The second feature that we notice is that the myocardium activity is quite uniform throughout the left ventricular myocardium. Again, as opposed to SPECT, you can see that the pattern of inferior wall attenuation is not seen as a result of routine attenuation correction with this tracer. Another feature that you notice is that in some of the cases you can actually see the papillary muscle. Here you can see on the resting study the papillary muscle and also on the stress study. We were quite excited when we saw our first few cases that we could see papillary muscle. We were quite excited that if you don't see on the stress but we see it on the rest, that would be an index of ischemia. But after more experience, we realized that we cannot rely on that. So I would not interpret anything into the visualization or lack of visualization of the papillary muscle in these cases. Then when you look at the vertical long axis and horizontal long axis slices, you will see that as we approach the apex, the myocardium gets thinner and there is less activity. This is not evident generally with SPECT or with rubidium PET because of the differences in the image characteristics and in the spatial resolution. Here we have the best spatial resolution and this type of a pattern is apical thinning. The way we can confirm that is that we see often no change from stress to rest. Also we can look at two other ways of differentiating it from scar tissue. One is to look at the gated study that you will see that the apex actually is thickening normally. Or you can compare the end-diastolic and end-systolic images and you can see again evidence of thickening and increased counts in the apex. So that would be very important. Now I would like to, I think that Dr. Al-Malai is going to go to the gated studies. I will wait until we take a look at that and come back. I want to make a few more comments on the quality of the images. So here you can see that this apical thinning on the short horizontal long axis and vertical long axis slices, you can clearly see thickening of the apex or increased counts in the region of the apex. That is indication of normal apical thinning in this individual. Now going back on the non-gated images, I wanted to point out the characteristics of the background. That is a very important feature of Leuropyridas that we often see what you see here is a pretty characteristic. I would say that like probably 80-85% of patients will show some background activity that does not interfere with the myocardium. So in general, we have a high myocardial to background ratio and this ratio is the best on exercise images. On the exercise images that we will be seeing later, you will see that actually you have virtually no background activity and that actually is a very important feature of this tracer with a high myocardial to background ratio. I think that aside from these comments, I would also point out that we have to be very sensitive to not calling the ventricle dilated. We are sort of used to seeing when we see the cavity of the ventricle to the extent that we see here, we tend to interpret it on SPECT images as LV enlargement, but this is not LV enlargement. It is purely related to the higher resolution of this tracer. So Jamshid, are there any numbers that you have been using at least in your prior studies to call or we're just going to extrapolate from our rubidium numbers? We haven't established a normal limit for the ventricular cavity or the ventricular volume. In one publication, the number that I think that part of the problem is that as you know, the size of the left ventricle or the volume of the ventricle depends on the patient's body surface area and therefore the numbers have to be established based on the patient's size. In one publication by Dr. Packer from our group, we looked at what differentiates large versus small ventricle, and we used a cutoff of 130 ml of LV as the median number. But I would say that it is something that we have to provide for every, perhaps it could become part of the automated program that could actually compare to the patient's body surface area and indicate whether it is outside the limit. Excellent. Anyone else would like to add anything? Can we see my echo now is better? No echo? There is no echo. Okay. So sorry about that. I don't know what happened. About these volumes, I wanted to add a comment because we actually tested it a little bit and we found that the filtering affects tremendously the volume size. So I think we have to pay particular attention to the reconstruction parameters as we establish those normal thresholds for volumes, for example, the Gaussian grouping and so forth. An important point. Panethia, do you want to add anything? So far, I've been trying to summarize a few things, but I just want to make some important points that have been said already. One, the left ventricular myocardium looks very well defined, appears thinner. So the LV cavity looks bigger. It's normal. Two, the count distribution is more homogeneous. Three, papillary muscles are often visible and more so at rest than with stress. We don't make too much of that. It doesn't mean there's ischemia or anything. And then four, a very important point, anatomical apical thinning is present in almost all cases. And we must be very careful not to call this as abnormal. RV uptake, five, RV uptake is often present. Six, subdiaphragmatic activity may be present as you can see here, but it rarely interferes with interpretation. So those, I just wanted to emphasize what was discussed already. Yeah. And I would like to highlight in one second, just one thing about the apical thinning. So yes, I mean, the apex will look thinner if I zoom on it a little bit. You can see it there, but if you put your gated, you should not see this kind of, you'll see abnormal contraction. So this is, as we were looking at many of these studies, we found that this is pretty common and we don't want like, want everyone to ensure that they've managed to see it well. So I'm going to zoom on it. One comment was on this. If you see a reversibility in the apex, you cannot assume that is a normal variant of apical thinning because apical thinning will typically be similar on both the stress and the rest images. So be alert to whether there is reversibility in the apex to see if it's truly a perfusion defect or it's just a partial volume effect. Right. And I cannot help it, Marcel. I saw a comment in the chat about splenic switch off. Yes, you can see the spleen here. It looks well switched off and I don't know what kind of, I think this was adenosine, so less controversial, but yeah, this appears to be adequate response. Anyone else want to add anything about this? So we looked at static and gated. We're going to move on to the dynamics and let me make sure I grab the correct one. So these are the dynamics of this patient and Marcelo, again, as you've done in the first one, can you walk us through the quality assurances in general for blood flow and then we can like talk about nuances for flupididase. Well, thank you, Moaz. Okay. So there are a few things that we want to do. Number one is try to ensure that we have a good handle on patient motion, particularly in the early frames when patients are a little more restless because of the pharmacological stress. So you can do this using what Moaz is doing now, which is viewing a SINA display of the various frames across time, or you can stop the gating, you can stop the SINA loop and you can do it frame by frame, whatever you prefer, but you need to ensure that there's proper alignment or proper correction of patient motion. One typical thing that we do in this particular software, you can use a visual display, which is here, it's called the LV spillover map, which will essentially tell you visually whether there was significant patient motion, particularly in the early frames where the blood pool activity may be contaminating the myocardium and you will see it particularly in the septum or the inferior wall, depending on the motion, and you will see high activity. In this particular spillover map, you see that the spillover is very low, it's almost dark and dark blue, which is very, very low here, but this is something that you want to be aware because it will affect your blood flows. And then you want to ensure that your input function, which is the green box that you see in the interface between the LV and the left atrium. One thing that is always helpful is to, or I found helpful, is to unzoom the images a little bit so you can see the entire part of the left atrium. Moaz, if you could unzoom, if you could stop the gating and do a little bit of a frame by frame so that people can appreciate. In this particular case, the frames are too long, so it flies through the left atrium, but this will allow you to see the entire left atrium, perhaps reposition the green box, which is your input function, if necessary. What you want to see is that the input function should be this green curve that should be a very sharp upstroke and a very sharp decline. This is critical because the area under the green curve will be the denominator of the calculation of your flow. So if you miss the peak somehow because the ROI is mispositioned or misplaced, you might actually not get a very accurate input function. The second part of this is that you see the color curves correspond to the tissue and the different parts of the heart. But what you see is that at the beginning of the stress curves, you see that the beginning is not set to zero. You can see, Moaz, if you could point to the stress tissue curve, you can see that this is not set to zero, and this is because there is residual activity from the rest injection that was done. So when you compute the flows, this residual activity has to be subtracted. All of the commercial softwares have a way to do these background subtraction, which will, if you click there, you will reset that curve to zero. Can you do the background? Yeah, I'll do it. I just want to point out. You can see here, the flows are 3.7 before we do the background subtraction, the residual activity subtraction. And now when we correct that, you will see that those flows will actually come down substantially. And you can see that the flows are actually 30% lower on the residual subtracted images. So it is very important to be aware of that. So this is the uncorrected curve, so you see the start is higher. And once we corrected, the software managed to lower the number down here. So uncorrected and corrected. So again, this is the residual activity from the resting that spills into the stress. There's a lot of questions about this. So maybe there's a question about repeating the part about the peak activity. So maybe summarize a little bit on this part. Maybe people didn't quite catch it all. OK. So what you want is ideally the input curve, which is the green line, should have a very sharp upstroke, which as you see here, and then should have a sharp decline, which is essentially as the activity in the blood pool comes down, you see that the tissue begins to take up the tracer. And this is the shape, this is a pattern that you should see on those images. So I think, and it is very important to understand that the peak, you should be able to capture the peak because the peak contains most of the area for the input function. You see that as the blood pool counts come down, there's not much of an area under that green curve. So the entire area is captured by the peak of the input function, which again, is going to be pretty much the denominator of your flow calculation. So if you underestimate your input function, you will overestimate your flow because your denominator will be low. And I think you want to be keenly aware of that. So the shape that you see here is the kind of pattern that will define a normal time activity curve. So it's very important to make sure that that rectangular sampling, the ROI, is where it's not abutting against the myocardium. It's kind of centered in the arterial blood pool, right where MOAS is pointing. And then that you follow the shape that you see here of the curve. In general, we recommend not to place the arterial input function ROI inside the LV. While this may not be a problem in relatively large hearts, it will definitely be a problem in small hearts because you will have contamination of the counts in the myocardium spilling over to the LV blood pool activity. So most software allows for you to, or the automatic placement is typically at the interface between the LV and the left atrium, right around the mitral valve area, as you see in this particular scan. If I may, I would like to add a few points here. I think that what you heard very nicely pointed out by Dr. DeCarli is basically all the steps that is required for quantitation of myocardial blood flow, regardless of the tracer that you're using. This is not what you're talking about here is not all fluoroperidazole specific. These are all points that relate to other tracers, if you're using rubidium or ammonia, you have to pay attention to all the points that Dr. DeCarli mentioned. I would say that the quality of the bolus is very important. We have to make sure that the bolus is tight enough and we start imaging before the injection. So we give a few frames so that you don't cut off the uptake of the blood flow activity. And one thing that is different slightly between rubidium and fluoroperidazole is the sensitivity of the measurement to patient motion. Dr. DeCarli pointed out that you do see often in the beginning of the flow measurement that a patient may be a bit agitated and might move. But we have also noticed, since we started doing fluoroperidazole studies and looking at the gutting into the habit of looking at frame by frame, that another phenomenon that may be responsible for motion. And that is what we had earlier, many, many years ago, described that upward creep of the heart. This is a situation that in the beginning, with the deep breathing of the patient, the diaphragm is in a lower location, the heart is in a lower location, and then it gradually creeps up to a different location, a higher location. And this kind of an upward creep is more evident or would influence the image quality more with fluoroperidazole because of the high image quality or the highest spatial resolution of the image. And the good news is that all the three major software that are available for interpretation do have now provision for correcting for motion, this type of motion. And also, all three software packages allow the residual subtraction that was pointed out that is important to remove activity from the first injection to the second injection. Okay, well, thanks Jamshid and Marcello for all of these important QA steps. As you know, once we've done this, now we can see that the resting flow is 0.72 with little heterogeneity in the resting flow, and we have a nice peak flow, which is 2.73, and also very reassuring in this patient where the flow reserve was almost 3.81. So whichever way you look at it, we have very nice resting flow, we have very nice peak flow, and this is very assuring normal study. I don't know if Jennifer or Pyotr, you want to add something about this from a technical standpoint, otherwise we'll move on. I think you've covered most of the technical aspects. Just one thing I wanted to point out here is that typically there's also a normal perfusion database that matches to your perfusion studies, so you will get a polar map in that IMFR section as well. And I won't go too much into that feature since it's not the focus of this discussion, but that IMFR map allows us to differentiate between areas of focal and diffuse disease as well as normal territories, so it can also be used in your interpretation of these flow studies. Dr. Amalah, if you want to just quickly choose the database in your top two perfusion sets, just to give the viewers an example. Yeah, I mean, I think, because I don't see Flopridas here. Okay. Okay, I think for this case we'll skip that for now, yeah. Anything, Piotr, you want to add? Otherwise we're going to move on to the... I think you've covered it really well. Just one thing about the, pay attention to this peak size and it is also related to the, you know, how long the frame is. If the frame is 10 seconds, it's sometimes maybe a little bit too low, it's because of the... So, I think this protocols that will be established, you know, how long this frame should be, because if it's too, as Dr. De Cali pointed out, if the peak is too low, if it's not capturing, it will underestimate, you know, the input activity of the curve and that will result in overestimation of the flow. All right, so I'm going to move on to another software package. So we give you, you'll see me looking on another monitor, so I may look odd on the screen. Okay. So this is Cedar software and I opened the study and you can see here a similar kind of representation of the fusion images and Piotr, anything you want to mention about the registration here? How does it look for you? So looking at this case here, you know, it looks reasonable, I think. Yeah, looks pretty good, I totally agree. And I wanted to mention, like we said, that when we quantitatively check this, anything above five millimeters is a problematic number, like half of the myocardium. If it's, you know, then anything, you know, in that range will cause some problems. So this should always be the first step in the hybrid imaging to look at this. So maybe I'll move on to the images. I'll show it first in color and then I'll show it in gray later on. Anyone would like to comment on this? Well, I can just start by pointing out that, again, in this case, we can see low activity in the apex that appears to be the same size. And by looking at the gated, we'll see whether that actually moves, which I'm pretty sure that it does. And also you can see the, yeah, let's just take a look at that. So there is proper apical thinning, counts are increasing in the apex, there is thickening of that area, you can see it very nicely here. So this represents apical thinning. And also look at the, please follow the papillary muscle here that you can see it very nicely in the diastolic images and that point that is actually very, very quite prominent. And that prominence of the papillary muscle is not an indication of left ventricular hypertrophy. This is a normal visualization. And also please pay attention to the contraction of the right ventricle, you can see how nicely the right ventricle is visible and you can see the contraction, as opposed to SPECT imaging that when we see the right ventricle, we worry about right ventricular strain or pulmonary hypertension or all kinds of other right-sided disease, visualization of the right ventricle is a quite normal phenomenon. And you can actually pay attention, close attention, you can see even the left atrium behind the left ventricle in many cases, even though it is a very, very tiny and very thin structure. Okay. So, yeah, I agree, I'm just going to go back to show it on color so everyone has the chance to look at it again, apical thinning. And we're going to move now to the kinetic model, so I'm going to go back to, it's there. And again, I'm going to run automatic motion correction for the important things that have already been discussed here. So you can see also the display of the software and here. So Marcelo, anything or Piotr, anyone would like to comment on this in terms of flows? This is a normal flow and you can see the nice peak here. And you could see the motion correction that will affect the flow, so you can kind of see, this motion correction should be performed on every case. It's not an optional step because we find this is happening in many cases and pretty much every case should be done with motion correction. Yeah, I would like to add that the normal values for myocardial flow reserve and stress flow are different that we see with fluoropyridazole as compared to rubidium. The number of stress flow and the MFR are slightly higher because of the higher extraction fraction. Now the normal limits for what constitutes the division between normal and abnormal has been well established with all three software packages and all of these have been published in the literature and I encourage you to look up these. The three software packages that have extensively looked at fluoropyridazole are the NVIDIA that you just saw with the CEDARS package and also the MRE toolbox package that they all have been quite well validated. One of the points that we were curious about was that what is the correlation between these three different ways of quantifying images on the same patient and that actually is a subject of a manuscript that hopefully will come out soon. The message of that manuscript is that when you compare the three different software there is a very close correlation between the numbers. So I think that all of these numbers are available in publication and you can refer to them as a cutoff for abnormal flow in different areas. One other point that I want to make as we go forward is because of the higher image resolution that we have with fluoropyridazole, we are now able to do flow analysis on a segmental level, meaning that instead of regions, as you see that we have three regions here, we can go to a 17-segment model and measure flow at each one of these 17 segments and that has been shown by our group, Dr. Packard, that this actually provides superior information as compared to the regional flow in patients and that is something that as we go along you will probably see some cases that if you rely on the entire territory flow we may not see an abnormal number because it gets diluted by the normal portions of that territory, but if you go to segmental flow you will clearly see the abnormality in that segment. So as we go forward I'd like you to take a look at these segmental versus territorial flow numbers and how they can help. So I think, Dr. Malak, if you can see there are great groups here on the top and in the blue you could show this just a little lower. Sorry, you can do that segmental processing here, but we don't show the curves for each segment because it would make it very complicated. If you see groups here in the last, like in the blue, you were right, almost there, like at the bottom of the blue, like go to the bottom of this blue, lower, lower, lower, just switch to segments here. So you can get segments in each. I need to change the font on my computer to show it well. Okay, but yeah, I mean all packages allow you to do this and this is, it's reassuring to hear that almost all of them are very correlated, very closely based on your work, Dr. Madahim. Okay, so another normal case we wanted to show with this software, Marcelo or Jennifer, anything else you want to add here? No, no, the only clarification is that you can actually look at segmental flows with all the tracers, not just for data, okay. So I think that's something that it's important to remember. And like Dr. Madahim mentioned, you know, when you have small branches that can lead to artifacts, you know, if you look at the entire territory, you might actually miss a flow abnormality. So you have to look for the homogeneity around those areas in the entire territory. Okay, so for the sake of time, I'm going to try to, so that we show our audience as many cases as we can. So we're going to try to limit the time we look at each case. So points that we've already made, we'll try not to kind of hammer. So this is the third case on our list that we have for the faculty. So looking at this, Dr. Madahim, anything you want to add here? Like I'm not starting with the usual one that I showed you. Right, yeah, this is a case that we see that the counts are decreased on the rest and more so, I mean, on the stress and more so on the rest in the lateral wall. When I see any defect in the 12 to 3 or 4 o'clock location, before I call it an abnormality, I want to go back and check for misregistration, because this is a very common area for misregistration that you see defects in the 12 to 4 o'clock location. So let's see what we have here. So here we can clearly see that the myocardial activity is actually outside the area that is misregistered, clear-cut misregistration that affects the lateral wall. That is the same area that shows abnormality. And as it was pointed out, in order to correct this, you know, you need to go to the main module and adjust this. What we have required of our technologists is that they routinely do this and correct for it, so that they don't wait until we call their attention to a problem. So this is one of the quality control steps that all techs should pay attention to, not only for fluorocutas, but for any other tracer using PET. Okay, and anything about this uptake in the lung here? Is this part of the misregistration process? It could be. I think if we register it completely and still there is uptake, then we have to worry about perhaps some pleural effusion. Yeah, so the hint here is that misregistration can happen. It's a common finding and, like, looking at how does it affect your assessment of ejection fraction in this case? Probably the effect on ejection fraction is not as pronounced, because still we can see the endocardial level, but I wouldn't rely on that. I would think that a case like this should not be interpreted or guesswork until we go back and correct for misregistration. Okay, and what about flow there? I mean, would you rely on flow? And again, Jennifer or Pyotr, if you want to add there? Like, with this degree of misregistration, would you utilize flow data? I think the short answer is that, I think, Jennifer, I don't know. This is a significant amount of misregistration, so I wouldn't find this dataset reliable. Okay, yeah. One note I would make is that when we do calculate the flow, at least at INSIDERS, we use only the first one and a half minute of the data. So, if you see some misregistration, it's possible that there can be, you know, there will be misregistration also on the flow, but it could be different. So, I think it depends on the model that you're using and how much data goes into it. And I think it would be useful to look at the flow, but it may help you, but it's not going to save you. I think the flow will be affected by the misregistration. There's data to show that, so it will be affected, but maybe a little differently. So, the key message is to sites that will be starting with flow periods and they have not done that, you need to train your techs, as Dr. Madahi mentioned. When they see something like this, they're not going to wait for you to tell them. The tech have to go correct the misregistration and not only correct the static images, but they need to correct the static gated and dynamic, because otherwise the flow may not be that accurate in this case. All right. So, again, I'm jumping between multiple computers, so bear with me. And here we are with this case. And for the faculty, this case is labeled as 012-017. So, this is a 66-year-old male with a BMI of 27, hypertension, diabetes, dyslipidemia, and the patient is coming in with chest pain. And anything that you would like to add on the QA here, Dr. Slomka? This looks... There is a lot of epicardial fat in this case. So, you know, you see the, you know, the heart is where the heart should be, I think, but there is epicardial fat, you see. So, I think... Yeah. I think one very important thing on this case to plug in for assessment of calcium, you can see this is the LAD for... This is the left main, the LAD, and the left circumflex, and all of them are heavily calcified. So, clearly heavily calcified vessels, and the right also. So, patient has multiple calcified territories, as we see here. And here's the splash images, and I'll let you comment on that. Or, Marcelo, if you want to look at this, let me zoom out a little bit. Yeah. Can you zoom out? Is this good, or do you want to zoom more? No, I think it's good. Okay. So, in this particular case, we have... Okay. So, the images are well aligned. Can you move the short axis images on the top two rows a little bit? Just scroll through to make sure that you fit them on the... It's easier to visualize. If you can... No, no, no. Just move them to the left, I guess. So, with the arrows, I think... With the arrows on the right side. No, no, no. The arrows. Yeah. The arrows, the vertical arrows there. Okay. It doesn't matter. All right. I'll figure it out. Okay. So, what we see in this case are very... The cavity looks normal, perhaps. I don't see, really, TID. Perhaps, if there is, it must be very mild. But starting from the vertical long axis views, you changed the case here? No, no. These are both stress. It has to go back to the... Yeah. Okay. All right. So, starting from the vertical long axis views, you could see that there is a defect involving the apex. Unlike the previous cases that we saw, in this case, we see reversibility in the apex. So, in a case like this, we wouldn't call the stress defect as apical thinning, because you can see clearly reversibility in this particular case. If you then move to the short axis images, you see that in the apical short axis, there is reversibility. Okay. Can you align? Yeah. I'm aligning them. Yeah. Is this good? Yeah. You could see that the... If you look, for example, at slice number 17, you see that there is a perfusion abnormality that involves all the apical segments. And how do I know that? Because my reference is more to the base of the heart. And if you see the base of the heart, the base of the anterior wall and the septum in the stress images, you would see that the intensity should be higher. And so, what that tells me is that all apical segments are involved in the defect. And you can see that at rest, there is complete reversibility of all apical segments. When you move to the mid part of the heart, maybe slices 20 or 21, you can see that there is a second perfusion defect involving the inferior wall, which is also showing reversibility at rest. And that extends even far into the base that involves the inferior and the inferior septal walls. So, in this particular case, I think there's evidence of stress-induced ischemia in the mid to distal LAD involving apex and apical LV segments. And then a second area of abnormality seems to involve the mid and basal portions of the inferior and inferior septal walls. So, I would say that this is consistent with ischemia in the mid to distal LAD and right coronary territory. There were some questions previously on TID. This might be a good time to make some comments on that. Yeah. So, I honestly don't know what the normal value of TID would be for fluorpyridas. I think we need to know more. You know, what I typically like to see for TID is I need to see it visually before I rely on a number. The number is more to corroborate what I see visually. In this case, you know, there seem to be a mild difference between the stress and the rest images. And that seemed to correlate with that 1.14 that you see here on the images. I'm not sure if this is truly an abnormal ratio for fluorpyridas. I think maybe, Jamshid, do you know what a normal ratio should be? Yeah, well, I think that these numbers have to be verified, again, formally. But from my experience, looking at a lot of these studies, the numbers are like, you know, what we use a 1.2 as the cutoff for being abnormal, very similar to what we had seen on SPECT and on petruvidium. But I think that, but it has to be clarified. I would say for the time being, a cutoff of 1.2 is a reasonable number for TID. Okay. All right. We actually use 1.13 for pet ammonia. And I kind of feel like there's some similarities with respect to fluorpyridas and ammonia. But I mean, this is just anecdotal. Yeah. You know, the ratios depend on the doses that you're injecting. For example, if you do ammonia rest and stress with the same dose, you would expect that the ratio will be close to 1, 1.05. If you're injecting a low dose for ammonia and a high dose for the stress ammonia, then the ratio will be slightly different. And I suspect what Panithia is saying, you know, will be similar here with fluorpyridas where we're injecting low dose and then a high dose for stress. So, but more to be determined. I think more important than just to get hung up on the number is it needs to be obvious to you visually. If it isn't visually obvious, don't believe in the number. That would be my rule. I agree 100% on that. I think if you don't see it, don't. Because there are so many things that can go wrong in measuring this. Depends on the outline of the ventricle and how far into the base your regions of interest go. So it has to be visually visible to believe it. The number is often a technical issue, but this one does look like maybe there's a hint of it, you know? Yeah. And actually, I just want to say, and I think Moa has read my mind, put the contours on because you can see then because sometimes the algorithm, when you read this TID blindly, you don't really know what the program is doing. And in this case, you can see the base. And if anything to my eye, maybe it's a little undercalling it on stress, like in terms of the contour on the base. So that will just mean that the TID would be actually a little bit larger, but slightly. That's just what I see here, but I think it's okay in this case. In any event, when you see multiple perfusion defects, you will typically see a little bit of TID because the counts are reduced, the wall gets thinner, and then the cavity looks larger. Yeah, you don't see the wall. Yeah. There are several questions about the hot septum in this case, but I think it is that the other walls are reduced, but... Yeah. So I think the hot septum in part may relate to spillover counts from the RV free wall because they get hotter as you go distally, and then they sort of gets more normal when you go farther into the base where the RV is farther away from the septum. So sometimes you need to be aware of that. Now, but can we go to the gated images in this case and see... People have asked, does the EF drops? So in this case, our ejection fraction... Okay. 67 to 64. 67 is the rest? 67 is the rest drop down to 64. Okay. So what we see is just a little bit of a drop. You could see that in end-systole, the volume particularly, you would see it more obvious at the base of the heart. The end-systolic volume seems to be larger on the stress images than what you see at rest. And so this would be an abnormal response, but not unexpected because we saw ischemia in two different territories. So what we generally say, not just for flurbidas, but for any tracer is that if the EF doesn't change, it's probably an okay response. But if the EF drops is when you begin to worry about significant stress-induced ischemia. Of course, you need to make sure that the segmentation was done properly. Maybe you can put the contours to make sure that we didn't misplace the valvular plane and overestimate the end-diastolic or the end-systolic volumes. And in that case... Is that the gated? Yeah, this is the gated, yeah. Okay. All right. So in this case, there is a slight drop in ejection fraction. And to me, that would be somewhat consistent with what we saw visually on the perfusion images. Okay. So, so far we have a patient... Are we calling the flows? Yeah. So, so far to sum the case, we have a patient with heavy calcification, at least two vessel perfusion defect, three percent drop in ejection fraction. And now these are the flows. So we have the background correction already. I'm just going to do the motion correction. Yeah. So many people wrote in that it may be three vessel. Yeah. Yeah. I think that's the hot spot that Pernithia was pointing out. Actually, when you look at the splash images, you see that the lateral wall seems to reverse. So I think that I kind of agree that this may be beyond the two vessel disease. Maybe a complex lateral wall is involved also. So the question to you is that, what do you think, first of all, of the absolute numbers? Again, Jamshid, you were making a good point before about the segmental versus territorial. If I go like here by segment, and you can see some segments look okay. Some segments are like really severely reduced, like 1.03. So how do you kind of walk through this? Yeah, I think that we look at both. I think that when we see that the global or the territorial flow is low, that is sufficient. That gives you the answer. But if it is normal, and it is different than what we saw visually, then I will go to segmental to see whether they correlate better with what I saw. So here in this case, I think that if you look at MFR in the inferior wall in the RCA territory, I'm pretty sure that you will see that there are, some of them that are 1.2, maybe 1.3, and some are a little bit higher. So the average is 1.1, 1.95, but there could be, I wouldn't be surprised that there are lower numbers in that territory. So if we're gonna look at the numbers, I just wanna make that kind of, so, I mean, we put a lot of emphasis on my cardioblood flow reserve, and here, if I'm just gonna take a superficial kind of assessment of this, I will say flow reserve of 2.2, but I saw two defects, what I call the study normal, abnormal. Do we need to just look at the flow reserve global, or we need to go beyond that to look at the peak flow, resting flow, and as you were mentioning, segmental or territorial? You are more senior. Yeah, I think that we need to go beyond, I think that the work that Dr. DiCarli and his group have pioneered in terms of global is still valid. I look at it as sort of an ejection fraction, that you can have regional wall motion abnormalities that help you with regional disease, but when the ejection fraction is okay, prognostically, it is a good study. So I have always assumed that if I see a global flow for the myocardium that is normal, but I have segmental flow abnormalities, the segmental abnormalities are helping me with identification of individual disease vessels, but the global flow helps me with perhaps prognosis. This is an idea, this is a concept that hasn't been validated. I wanna hear Marcelo's opinion on this. So I'm separating diagnosis from prognosis, basically. Exactly, exactly. So I agree with that, and I think what, you know, we have two parameters that are key. One is the stress flow, which is abnormal everywhere, and then is the flow reserve. In every study that has been published with ammonia, with rubidium, and with flurpididas, I think the stress flow is always most accurate than the flow reserve, because the flow reserve is a ratio, can be up or down depending on the rest flow. But as Dr. Madaki mentioned, here, the stress flow is very abnormal. It is consistent with the visual abnormalities we saw on the scan. So from a diagnostic point of view, the flows at stress are consistent with a visual presence of defects. So this patient clearly has flow-limiting coronary disease. The second question is, is this high risk? And here, you know, again, we need to find out what the normal flow reserve is with flurpididas, but strikes me that 2.2 would not be too bad for these patients. So yes, there is flow-limiting coronary disease. Is this high risk? Well, I guess we'll find out when we have prognostic data with flurpididas about how do we use these data for defining who is at high and low risk. What we learn for ammonia and rubidium is that if the flow reserve is above two, yes, you might have obstructive coronary disease, but if your flow reserve is preserved, your risk may not be as high as someone who would have low flow reserve. So again, diagnosis and prognosis are different. When it comes to diagnosis, I like to use, if the two are discrepant, I rely on the stress flow, which in this case correlates very nicely with the visual abnormalities we saw on the scan. And then for prognosis, you can pay attention to the flow reserve. Okay. Anything else you wanna add, Jennifer or Piotr? So I think it's all true. I think prognosis is like a very different thing than diagnosis. In this case, we actually don't have any prognostic data so far on flurpididas, but we do have diagnostic data. And at least in our testing of this was, we found this MFR was a little higher thresholds, about 2.3 per vessel, while the flow was about the same, 1.8. And I don't know if this is something to do with these different doses of residual subtraction, but in this case, it would be diagnostically abnormal by both, at least in two vessels. And prognostically, as Marcelo said, it may not be that severe. But I think we need to get more data, prognostic data to find out the meaning of this. And I think there are a lot of questions about what normal flow reserve is with flurpididas, obviously. And I think as Piotr and others were saying, there are some technical factors that come into play that may be affecting the flows that we're seeing here. So potentially if there was different sampling of the dynamic images, you might capture that peak a little bit differently and your flow estimates may be slightly different. So those are all factors that still remain to be fully investigated with flurpididas. Okay. So just to give everyone a hint, this patient did go for coronary angiography, has total occlusion of the RCA, total occlusion of the LAD, sorry, of the LCX, and 70% of the metadistal LAD. So severe multi-vessel disease. As we predicted, and yeah, so the distal LAD, the LCX and the RCA, and as we kind of like integrating the peak flow, the flow reserve and everything, kind of give you a sense of where the risk of this patient, but also the diagnostic power of flow. All right, we're gonna move on so that we show more cases. So for the faculty, this is case, where is it now? Case 2086 on your list. So this patient is a patient who has been having chest pain, 71-year-old female, and from a fusion or quality. So for the sake of time, I'm just gonna quickly go over this. This is gated, sorry. So what is the stress? Perfusion form, 3D. Gonna zoom. So we can look at the fusion. Looks very reasonable, much better than the other case we were looking at. And I'm sharing my screen, correct? Yes. Okay. So good quality image, patient on the obese side, but others than that, good quality. And from image standpoint, so we see a defect and we always say, whenever you see lateral wall defect, you would like to confirm this is not misregistration, which we already did. I don't know, Marcelo or Jamshid, do you wanna mention anything about this in terms of defects? I think that I go back to what Marcelo said, that visually strikes you that there is a significant TID. We don't need a number. It is much larger at stress than rest. Now, in terms of where the abnormalities are, clearly the lateral wall is reversible all the way to the distal portion of the ventricle, but we also see reduction of activity in the anterior wall, especially if you use the color format, you can see the anterior wall is reduced and then a distal anterior or mid to distal anterior wall and apex. So we are dealing with a case of a patient with LAD and left circumflex disease. The amount of reduction of activity in the left circumflex is quite a bit. So that has to be over 70% narrowing. By the way, we use the criterion of 50% cutoff for disease in the phase three study, but I think that clearly this is more than a 50 to 70% stenosis, it is much more severe than that. And the LAD also, I would say that that is also about 70%. So I would say that severe LAD and left circumflex disease. Okay, so clearly to vessel disease defect based on this, and you can look at the gated information or I can open up the whole thing. Yeah, to corroborate that defects are real is that we look for wall motion abnormality that is often seen because we are doing, if it is a pharmacologic stress, the images are obtained at peak stress. So we would expect to see in most cases, wall motion abnormality in the same territory of defect. And here you can see clearly in the lateral wall, there is wall motion abnormality. And then in the anterior wall, it seems that wall motion abnormality goes beyond just the distal portion. Even the proximal portion is not contracting as vigorously. Still the diagnosis remains the same, that this is a double vessel disease. Okay, and again, for the sake of time, I'm gonna show the flow data. Hopefully it will come quickly. Okay, so this is a quality screen. So again, there is motion correction applied. So even if the portion moved, so we can look at this. I'll put in the contours. Marcelo, feel free to comment on this. Okay, well, it looks the shape of the curves look generally okay. You've already accounted for the residual activity I see. And can we go to the next page so we can do this in close? So now we see that all the stress flows are reduced and not very surprising because we saw two areas of abnormality in the patient. And not surprisingly, even the right corner is abnormal. And you can see here that the flow reserve is also reduced in all territories. So it has multiple perfusion defects, TID, a drop in ejection fraction, low flows and low flow reserve. All of these are signs of high risk. And in this case, I think consistent with multivessel coronary disease. So Marcelo, like looking at this again, the global flow is 1.7. If I go by vessel, LAD is 1.9. Although we saw distal LAD defect. Should I ignore that LAD defect just because my flow looks okay? No, no. And here what you see is again, what was mentioned before, you have the advantage. You can look at the segments and you can see the polar map, the segmental flows on the stress, which is the top four polar map that you see on that list. You can see that the defects, particularly in the mid to distal LAD territory are much lower than in the rest of the myocardium, consistent with flow limiting coronary disease. In fact, you could even see the gradient between the basal anterior wall and the apex indicating a significant stenosis, you know, obstructing flow there. You could see also in the circumflex, for example, the inferolateral wall has much lower flows than the anterolateral segments. Again, on the polar map, again, indicating that is likely a severe stenosis of one of the obtuse marginal branches there. And then you could see that the inferior wall also has low stress flows. So on this software, I can see like the flow in the area of the perfusion defect that I see, which is 1.43. Is this like something that we should pay more attention to this, like the flow in the area that's affected? Yeah, but not the flow reserve necessarily. I think the stress flow is more important than the flow reserve in this particular case. And you can see that the stress flows are very reduced, you know, so. Okay, so this is another case of multivessel and this patient actually did go for angiography has LAD 82%, transmit to the cell most likely LCX 70. The RCA did not have flow limiting disease. It was called only 34%. We can go back and look at the images and we didn't see a perfusion defect in the RCA and the flow looks here, at least the peak flow was probably among the best segments in the RCA. Now, Moaz, I'd like to also address a question that Denny Skalnon brought in about, have a higher extraction tracer and how do we calibrate the severity of the defect and how do we correlate that with the severity of obstructive disease? I think this is a work that still needs to be done. It is likely that, you know, if you have a moderate stenosis, but a high extraction tracer, you might actually see discrepancies or heterogeneity of tracer uptake in the myocardium. And I think this is where I think incorporating the flow data will allow us to define whether this is flow limiting disease or whether there is diffuse atherosclerosis. I think that work still needs to be done in my mind. So I think the flow will be a very important part of the interpretation of the images. If you see a little bit of heterogeneity, but normal flows, it's probably not obstructive coronary disease, but I'm saying that without any data, I think this is the experience that had been done with O15 water. And I think it may apply similarly to flurbiditas here. Okay. For the last few minutes, I cannot help it, but show you an exercise case. I know Dr. Madahi mentioned about the extraction. So Jamshed, do you want to mention anything about the quality and what you were mentioning before about how exercise looks different? With exercise, as you can see the, if you can go back to the slices, you can see that you really are against a dark background. There is very little background activity that that's very good and interesting that we get with exercise. Another thing about exercise is that the uptake by the myocardium with exercise is lower than it is. I'm talking about normal myocardium, is lower than with pharmacologic stress. And that is not unique to flurbiditas. It is true with all tracers that when you inject them at exercise, there is less activity getting to the myocardium because it's also peripheral muscles take up activity. And that's the reason why when we do the protocol with exercise, we have to wait a little bit longer and give a higher dose for the exercise injection. Now, coming back away from kinetic that I just described on the quality of the images, again, very good quality, very high target to background ratio. I wouldn't call this to be apical thinning because I can see that there is reversibility in the apex. And also we can see that very clearly on the horizontal long axis slices. And also on the short axis slices, you can see the last few slices in the short axis towards the apex, there is a reversible defect in the septal region as well as the infra-apical area. So this seems to be a case that has at least LAD disease. The one issue to know is that because we cannot image the patient while we're injecting the patient under, cannot image it under the camera, we have to wait until the stress is over and then move the patient to under the camera. So we miss the sort of input function and what we need for quantitation. So at the present time, there are several groups working on developing methods for coming up with something that is equivalent of coronary flow with exercise patients. I saw recently an abstract that by the Canadian group that are being submitted to the Society of Nuclear Medicine. And I think that I've seen actually more data from that group. And I think that it is a method that will become available that even though we are not doing the imaging right under the camera at the time of injection, we can get some flow data in the future. So again, judging in this case, we'd have a LAD disease patient with defects in the distal, septal, distal anterior and apical regions. And regional wall motion abnormality in the apex. So compared to the apical thinning case that we saw before, this is very different. And I just wanna show the gated one. And you can see here that there is the defect persists compared to the prior case where it improved with systole. So this is a true ischemic defect that's not fixed as we saw before. All right, so then this patient did go for coronary angiography and has a 99% distal LAD territory. I think we have one more minute, so I'll leave it to the faculty. If you wanna mention anything or any recommendation for the colleagues who are considering to use this agent or planning to start cardiac path, any words of wisdom, we'll start with Jamshid. Well, first of all, I would like to thank all the faculty and your leadership for this session. It was very, very educational. And I think that I would encourage people to also attend the second session as well in April. I'm sure that there are quite a few questions. I think that we could probably handle them offline by responding to them somehow. There's not enough time for that. And Marcelo. Not much to add. I think there's so much to learn about this that we're gonna need two, three, five sessions to become comfortable with what we're seeing and how to integrate the flow data into our interpretation. And Jennifer. I think I echo the same things that everyone else has been saying. There's still a lot to learn. There are lots of technical factors that go into quantification, like the flow estimates. So still some more work to be done there. Lots of promise shown, but still some uncertainty around flow estimates. And so I think it's a great work in progress. And Piotr. I'd just like to thank everyone for fantastic questions because it just gives us ideas what to test in the coming months, because you rightly pointed out that the ID, the right ejection fraction, or flow, all those things, we need to test a little more and we'll be back with more and more data. And finally, our president, Dr. Panethia. Thank you, Moaz. I wanna thank you again for helping to put all these cases together and this webinar and thank all the faculty and also all the attendees today. Lots of great questions. We've been a great audience. We've been a great audience. And this is really an exciting time and really a lot of opportunities, but a lot to learn and a lot more to do to understand how to interpret these images and the flow data. But it's really an exciting time for us. Thank you. All right. With this, I wanna thank you all for participating. Thank the faculty for your time and for long hour of preparation. Thank our sponsor, GE. I wanna also thank ASNIC staff who worked with us tirelessly for long hours to put this one together and look forward to seeing everyone on the second session. Thank you.
Video Summary
The webinar hosted by the American Society of Nuclear Cardiology focused on interpreting and reporting F18 PET and PI with an emphasis on Flurpiridaz cases. Co-chaired by Dr. Moaz Al-Mallah and Dr. Panetia Shirintuwati, it featured experts like Dr. Marcella DeCarli, Dr. Shamshid Medahi, Dr. Peter Slomka, and Dr. Jennifer Renaud. The session aimed to educate participants on acquisition protocols, interpretation, and reporting of F18 cardiac PET tracers. It emphasized understanding physiologic uptake patterns, incidental findings, and methodologic approaches to review these images. <br /><br />The webinar highlighted the importance of quality assurance in PET CT imaging and the need to ensure proper alignment to avoid artifacts. Speakers discussed the nuances of different tracers like Flurpiridaz, including its advantages such as high image quality and its potential drawbacks like exposure to higher radiation doses. A significant portion of the session was dedicated to interpreting cases and identifying abnormalities using the new tracer. <br /><br />Key insights included the importance of recognizing normal variants like apical thinning and papillary muscle visibility, understanding the impact of tracer pharmacokinetics, and utilizing flow data for diagnosis and prognosis. The session concluded with a strong emphasis on continuous learning as Flurpiridaz is integrated into clinical practice, noting the need for diligence in technical execution and ongoing professional education to maximize the tracer's potential clinical benefits.
Keywords
American Society of Nuclear Cardiology
F18 PET
Flurpiridaz
cardiac imaging
quality assurance
PET CT imaging
tracer pharmacokinetics
interpretation
acquisition protocols
physiologic uptake patterns
artifacts
clinical practice
professional education
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