My name is Wael Jaber, I'm from the Cleveland Clinic, and I'll be talking today about non-perfusion PET imaging, namely issues related to assessment of myocardial viability and hibernation. I have no disclosures as related to this subject. My task today is the following. First, try to explain the concepts of ischemia, viability, hibernation, and scar. Explain and describe the role of PET-FTG as a tool, as an imaging tool, in the assessment of myocardial viability. Explain how the PET-FTG imaging data is used in the diagnosis of viable myocardium or hibernating myocardium in clinical practice. Then go over the American Society of Nuclear Cardiology practice points, or protocols, of how to prepare the patient and how to acquire the images. And finally, give you a critical assessment of what components should be in the interpretation, the report that goes back to the referring physician. I will start by this dictum from Tolstoy, Anna Karenina. And in the opening line of this wonderful masterpiece, he talks about happy families being happy in the same way and unhappy families being unhappy in different ways. And to extrapolate this to myocardium, I would say all my happy myocardium, myocardia that are well perfused, are normal in the same way. And when we have underperfusion of the myocardium, these abnormalities can manifest themselves in different ways. I will start with two clinical scenarios, and then we'll see how we can use PET-FTG for assessment of viability. Here's the first patient. It's a 54-year-old female patient with a history of CAD. She had a bypass surgery 10 years prior to presentation with a lemma to the LAD, a vein graft to the RCA, and at that time, the circumflex coronary artery was normal. Now she presents with recurrent chest pain. She had a SPECT at another facility three times over 27 months. And all these SPECTs showed an RCA, territory infarct with no ischemia, basically a fixed defect in the right coronary artery distribution. A cardiac cath followed that, showed a patent left main, patent circumflex, basically normal, and a patent lemma to the LAD. However, the vein graft to a totally occluded RCA had severe disease, and she continued to have angina despite maximum medical therapy. That point, she was referred to our center, and here are the images from her SPECT. You can see here this patient has a fixed perfusion defect, quite severe and extensive involving the entire RCA territory. Now we can argue a little bit about a small defect here that's reversible in the apical inferior wall, but overall, this is a large fixed defect involving the entire right coronary artery distribution. Now, at this point, you will ask yourself, with all the data you have, would you do any further testing? And do believe in a dictum that less than 50% uptake in any territory reflects infarct rather than hibernating or viable myocardium. The second patient is a 70-year-old female patient with total proximal LAD occlusion and an LVEF of 25%. She was referred to our center for surgical revascularization. She has class II heart failure symptoms, but no angina. Here are her resting images showing a severe perfusion defect in the septum, apex, and the anterior wall here. You can see here increased RV uptake. Maybe that's a reflection of the decreased uptake in the septum. Again, this is a resting image. The question now, do we assess for ischemia here knowing that all the rest of the coronaries are patent, the only coronary territory that we're interested in is the LAD territory, or do we leave it alone and say this is a severe perfusion defect, less than 50% uptake from normal, therefore this is scarred? These are the gated images on this patient, and you can see here this is a very dilated ventricle, injection fraction of 20%, and encystotic volume of 171, indicating significant remodeling of this left ventricle. Again, any further testing on this patient, should we open the CTO to the LAD with the data we have? Let's start with some basic concepts. This is a very nice illustration from Vascon Deltizian and his collaborators showing what's the mechanism for a stunned myocardium. We start with a normally functioning myocardium, we have an acute ischemic event as happens with usually ST elevation myocardial infarctions. In this instance here, we have ligation of a vessel in an animal model, and what happens is acutely you have regional wall motion abnormality during this episode. If we restore the blood flow to this area, you will have a persistent regional wall abnormality for a while, and then as this myocardium recovers from this insult, this abrupt but short insult, you have normal recovery and normal wall motion. So this is what we call stunned myocardium. In contrast, a hibernating myocardium functions differently. We start with a normally functioning myocardium that's normally perfused, normal coronary artery blood flow, then we develop slowly atherosclerosis in this vessel, resulting in abnormal blood flow, either at rest or with exertion or with effort. And what we can see here, a downslope or decline in flow or demand, flow demand in this instance, resulting in wall motion abnormality that's gradual and progressive over time, and what happens here is we can end up, instead of having a myocardium that's stunned that recovers abruptly, we have a myocardium that's hibernating and it takes it a longer while if we restore blood flow to recover. Now these are basic concepts and they can sound simplistic, especially when I show you this kind of information. So these are a regular microscope, light microscope of a normal myocardial cell here, hibernating myocardium. And you can see here, we've lost a lot of myocardial cells. What we have here is abnormal function, mismatch on a PET study, meaning we have perfusion defect, but there is FDG uptake. So there is preservation of the myocytes with accumulation of glycogen here between the cells. If this is not resolved or the blood flow is not restored to this myocardium over time, what you will see is scarring developing here, where we have abnormal function, a PET match, meaning the perfusion defect is matched by an FDG defect, loss of myocytes and extensive connective tissue replacement, replacing the myocytes. So this is without magnification. If we go to electron microscopy, the picture becomes more complex. We have here over time from a normal myocardium all the way to scarred myocardium and increased loss of contractile material elements of the myocardium. So you can have here in the extreme right, you can have preservation of FDG uptake, but we can see here that all these beautiful, nice lined contractile elements of the myocardium are gone now, and we are left with cells that are viable, but don't have the ability to contract even with restored blood flow. But the picture even is more complex. So this is instead of focusing on contractile elements, now we're going to focus on gap junctions. These are the junctions between different myocardial cells that allows them to contract in synchrony. In normal cells here, you can see extensive and white gap junctions between these normal cells. As it becomes ischemic, these junctions become patchy. And then finally, as the cell goes into hibernation, you can see now we have very few gap junctions left for the cells to interact, and therefore contractility will go down. So it's an interaction between getting blood flow, getting enough blood supply or glucose supply, fatty acid supply to the cell, contractile elements of the cell being preserved, loss of gap junctions, and finally death of the cell. Now at the cellular level, we are trying to target usually when we do flow imaging or we do perfusion imaging, we're targeting this sodium potassium ATPase. So this is rubidium and thallium here, as you can see here. When we're trying to image fatty acids, usually we're using carbon-11 acetate. And finally, when we're trying to image metabolic activity of the cell, we're targeting this area here, the glucose cycle of the cell or the glycolysis cycle of the cell. So this is where F18 deoxyglucose will mimic glucose uptake in the cell, penetrates the cell, and we use this path to detect cell viability. So again, just to remind or recap everything, a cell that's hibernating is a cell that switches its metabolism from predominantly fatty acid metabolism to predominantly glucose metabolism for efficiency. And therefore, it preserves its viability at the expense of, of course, losing contractile ability and contractile elements. Having said that, now we move to the viability part and what patients and what methods do we use to assess viability. Now as everything we do in imaging, it's very important with imaging the right patient, using the right test, and using the right test and methodology. What we have here is imaging the right patient and image guidance, specifically that ASNIC has led this, American Society of Cardiology has led this effort to image the appropriate patient. They always tell us when not to image patients. So when not to image patients with FDG PET for viability assessment is patients who have normal left ventricular ejection fraction. These are patients who have normal contractile walls, therefore all the walls are viable, all the walls are normal at rest. Therefore these walls or these segments of the myocardium do not require viability assessment. The essential element of viability, which is contractility, is preserved, therefore you don't need PET FDG. Now the second patients that wouldn't, usually I don't recommend imaging, is patients who have CAD, severe CAD, but have no targets for revascularization. Imaging these patients becomes an academic exercise to determine extensive ischemia, extensive viability, but really has no clinical endpoint in terms of helping these patients with revascularization. Now the next group of patients is patients you have done a cardiac catheterization on and you found they have normal coronary arteries and normal LVF. These are patients you're not going to target revascularization, therefore there is no point in imaging these patients for viability. Now you might want to image these patients for evaluation of inflammation, such as sarcoidosis or myocarditis, but not for hibernation. And finally, patients with prior PET FDG scans showing no viability. Now we try to dream about resurrecting the dead here, but if you have a viability scan from a year, two years, three years earlier, showing let's say an LAD territory that's dead, that's done and enough, unless you're assessing viability in a different territory, you should not reassess viability in these patients. So this is the concept of imaging the right patient and one not to image patients, one is futile to image them. Another group of patients where we do not recommend imaging with PET FDG, unless you're looking for inflammation, is patients who have normal perfusion at rest. So for every patient who walks into our lab, before we inject FDG for imaging, for viability assessment, we look at the resting perfusion PET images. And if these PET images are completely normal, and the clinical question is hibernation, usually we stop there and we say, okay, well maybe we should stress these patients and not do a stress PET perfusion imaging versus proceeding with viability assessment. There is no point in doing viability assessment when the resting images have normal perfusion. Now also patients who have large areas of ischemia on rest stress PET images, these are patients who have by definition viable myocardium, ischemic myocardium is viable myocardium and therefore they do not require PET FDG, unless you're trying to image ischemic memory, but again, this becomes an academic exercise rather than a clinical exercise. Now, this is a pathway that has never been clinically tested, but I thought about a few years ago. This is, and if you're evaluating a patient with an LVEF under 40% and you can create your own cutoffs, about 50%, probably we all agree these patients should not have a viability assessment, but let's say under 40%, you go for a cardiac cath or CT, angio if you wish in the modern era, and if it's not suitable for revascularization because of diffuse disease, bad disease that will have no targets, you continue with medical therapy or you assess these patients for transplant is suitable. If they're suitable for revascularization, this is when viability testing is ultimately the best at guiding therapy, and these patients with viable myocardium can go for bypass or percutaneous intervention, and patients without viability can be treated medically again or be referred for transplant. Now let's talk about some clinical data on the use of viability. Why do we assess myocardial viability and what the literature say about that? This is one of the earliest studies by Marcello De Carli in 1994, which seems to be now ancient, but still very relevant. It took 73 patients with injection fraction of 25%, and you can see here survival with PET viable versus no viability as it interacts with revascularization. If you have patients who have viability on PET and in orange here, they went for revascularization, you can see that these patients did very well versus patients who had viable myocardium but did not go for revascularization were treated medically. You can see here the outcomes were not good. However, patients who have no viable myocardium, you can see here there is no difference between the medically treated group versus surgical group. So this created one of the concepts, at least in a series of patients rather than individual patients, that if you go and assess patients for hibernation and use that data from the PET images to guide your therapy, patients who have large area of hibernation might benefit from revascularization beyond the basic concept that we think of as intuitive. Followed by the series of basically mostly single center studies with different variable definitions of viability showing improvement in LVEF post-revascularization in patients who have viable myocardium. So you can see here the problem with this kind of data is the definitions were variable, were not standardized. They were single center studies mostly. The endpoint was improvement in LVEF in most of these studies versus the study from DeCarli showing having a mortality as an endpoint. In a landmark paper by Allman that we've all seen, he did a meta-analysis of all these studies and now we have over 3,000 patients, almost two-thirds of them are men, in 24 viability studies reporting variable types of assessment using thallium, PET-FTG, or even dobitamine echo. And in this meta-analysis, he showed similar data to what Marcelo DeCarli showed in his paper in 1994, showing here that if you revascularize on top, patients who have viable myocardium, you can cut the event rate down to 3.2% versus 16% in patients who were treated medically. However, you cannot change the outcomes in patients who have no viability in revascularization versus medical therapy. So the outcome was similar. Now if you look down here at this panel B, these are revascularized patients who were viable. Again, event rates were very low. Down here, you can see non-viable myocardium that was revascularized. We exposed these patients to the risk of revascularization, but now we did not derive the benefits. So the top one is the dependent variable is viability. The bottom panel is the dependent variable is revascularization. So we can harm patients who have no viability, but we expose them to the risk of revascularization. Again, we can harm patients who have viability by treating them medically alone and not revascularize them. Now, not all these methods of assessing viability perform the same way. You can see here, reduction in death and event rate is probably best with thallium and echo, given the high specificity, and least with FDG, given the high sensitivity. So what do I mean by that? When you look at, let's say, echocardiography here with dobutamine echo, you're looking at almost the endpoint, which is the contractile element of the myocardium is still preserved. So therefore, this cell has traveled less down that pathway from normal all the way to scar. So it's probably half the way down that pathway. So it lost its resting wall motion, but it did not lose its contractile element. Similarly with thallium, the cell now, because of the low sensitivity of thallium in the range of 50% compared to FDG, we're probably picking up extensive amount of viability, and therefore the chances of recovery of function are high. However, with FDG, we're looking at one of the basic metabolic functions of the cell. So a cell could have traveled way down that, again, normal hibernating scar pathway, and we still can detect some faint signal from that. However, that cell is not going to recover probably contractile function, and probably has traveled far enough, lost all the gap junctions, all these elements, and therefore some of these patients will not benefit from a revascularization, even if FDG has picked up viability. So again, these tests do not perform the same. However, in general, assessment of viability will lead to better outcome if patients are treated according to the results of the PET. What do I come, where did this statement come from? This is, before talking about that, let's talk about the limitations of past literature. This is a nice paper by Benetia from the Mayo Clinic showing the limitations of past literature. Most importantly, no randomized trials, small sample size, reference selection bias, and a long laundry list of limitations. Now what about the modern era, or so-called modern era? We'll talk about two important things. The first I start with is the STITCH trial. I will ignore it completely because it's not a randomized viability trial. FDG or MRI were not used, and it has many, many issues related to unblinding of the physicians, unblinding of the patients, selection bias, small sample size, small experience in centers performing the revascularization, so on and so forth. And I will focus on the PART 2 trial. Probably it's the only randomized clinical trial we have for viability assessment. And this is PET-guided therapy versus standard therapy, and you can see here, despite the fact that the PET arm showed some benefit, especially if followed, or if the clinicians followed the guidance by the PET, there are some limitations of this trial. Overall, the trial was negative when comparing PET arm versus standard arm for the referral of patients for revascularization. But if the PET arm, or if the recommendation of the PET were followed, the patients benefited. What do I mean by that? I mean sometimes in clinical trials, even if you try your best to guide the therapy or to have the samples separated, there is a lot of crossover by the clinicians, and therefore patients will end up crossing from one arm to the next, and that will muddy the waters. These results from the PART 2 trial are more impressive, again, when the physicians or the interventionist or surgeon adhere to the result or adhere to the result or respected the PET results and follow them versus the standard arm, again, with a significant p-value here. Now, importantly, this is a sub-study analysis from PART showing most of the benefit from improvement in LVEF as a function of scar was when the amount of scar was small. So if you have patients who have a very small amount of scar, you can see the LVEF change was or improvement was about 9% versus patients who have a large amount of scar but have viable myocardium, the improvement in LVEF is about 1%. So this is almost like an intermediary step. This is a hypothesis generating or an element that we look at in terms of a surrogate endpoint for improvement in outcomes where patients, let's say, who started at an LVEF of 30% but now have small amount of scar and large amount of viability but were revascularized, they can end up with an EF of almost 40% range. And these patients, hopefully, you have changed their clinical outcome significantly. One of the outcomes we can look at is probably you avoided with an EF of almost 40%. Now you do not need to have these patients have an ICD, for example. So versus patients who start with a large amount of scar and do not improve LVEF, now these patients will probably benefit from ICD and other therapies. So again, you can use this surrogate endpoint for improvement in clinical outcomes. Again, where does this cutoff start? This is, again, a sub-study analysis from the PAR study. And you can see this is about the hazard ratio start showing us a significant improvement once the mismatch, meaning the viability, crosses this 7% point. So at 7% and on, you can see here we are now below 1 for hazard ratio, meaning there is a significant improvement in outcomes and at about 7% viable myocardium. So mismatch here means viable myocardium. So the bigger the mismatch, the more viability you have. So more viability, lower hazard ratio with revascularization. Now we move to another very important topic. Now we have, hopefully I've convinced you that viability assessment is important in changing clinical outcomes and guiding revascularization. I've explained to you the importance of selecting the patients, the right patients, to assess viability and which patients will not benefit from having a PET-FTG for assessment of hibernation and viability. Now we move to patient preparation. We separate our patients when they come to our lab into two categories, diabetics and non-diabetics. This is based on a very nice, again, paper from the American Society of Public Cardiology. I'm not going to go in details here because this is very beautifully illustrated in this guideline statement. We start with the non-diabetic patients. We load these patients with glucose after a fasting period of at least six hours, sometimes eight to 10 hours is better. This is to induce some endogenous insulin response. So when you inject patients with glucose, the pancreas is stimulated, and now you have insulin, endogenous insulin secretion. So this will lead to reduce plasma fatty acid levels. And now we have a normal steady glucose level in the plasma. So then what we do is we load these patients usually either with load of 25 to 50 grams, but at our center to standardize this, we load most of these patients with IV glucose. We found this to be more standard and less prone to absorption and bad taste and stuff like that. Some patients don't like to drink sugar and that's important. So the simplicity of this loading approach will help us in the next step, which is checking the fasting blood sugar. So these patients will come in, we'll check their blood sugar. We load them with the glucose. Then we monitor the blood sugar again, as you can see here. If the blood sugar is acceptable, we can right away go and image them. Otherwise, we will actually do a glucose clamp and start to give them insulin to force the glucose or the FTG to enter the myocardium. So for diabetic patients, diabetic patients have no endogenous insulin or they have insulin resistance. So the cells cannot utilize insulin the right way. So the simple fasting glucose or a glucose loading is not effective in this population. So what we do is we use insulin along with the close monitoring of blood sugar. And that will help us in obtaining very good images. Sometimes these are very difficult patients to manage just because you have to wait long hours or long time between the injection of FTG and acquisition of the images to get the appropriate blood sugar. So these are some guidance depending on the blood sugar administration for diabetics. So if your blood sugar is between 130 and 140, we give you one unit of regular insulin. If your blood sugar is 140 to 160, we'll give you two units of regular insulin and so on and so forth. We have also cutoffs where if the blood sugar is above 200, we notify the physician. Usually when it's there, I usually give anywhere between six and eight units of insulin. These are not, there is no risk here, almost no risk because after you give the insulin, these patients stay in the lab here, we keep monitoring it. So this is a very labor intensive test. You cannot just set it and forget it. So these patients will go on to have repeat insulin measurements. Again, this is some of the guidelines. You can find these guidelines again at ASNIC website in the practice points. Actually, the practice points, this is a plug here for the practice points, is probably my go-to to ask many questions that I usually are, you know, I'm faced with by fellows, residents, technologists. What do I do with this? How do I acquire this image? These are beautifully illustrated, simple, user-friendly, and easily accessible on the ASNIC website. So if you don't have them, you might save them as PDFs on your desktop or laptop to refer to. So I'm not going to go into details here because these are available for everybody. Now, as far as the tracer dose, we use at our center 3D mode, so we can cut down on the millicuries injected. We use anywhere between five and 10 millicuries for the purpose of FTG images. Often I see seven, eight. For non-diabetics, we wait anywhere between 45 and 60 minutes. For diabetics, we wait an hour to an hour and a half. This is supine position as in most of our studies. We use list gate, list mode acquisition for the image mode. All these images are CT attenuation corrected, so we have a CT scanner with these images, and then we reconstruct these images with a pixel size of two to five millimeters. So how do we display these images once we acquire them? It is extremely important that you display these images simultaneously with the perfusion images. Otherwise, you will be completely lost, even if you have a lot of experience. So here are the three easy steps in display. So this is a patient coming to PET imaging at our lab. We start with the rest and stress perfusion images. You can see here rest and stress images. We have a moderate size, moderate insensitivity perfusion defect in the infralateral and lateral wall right here. You can see it very well in the horizontal long axis. Not much change from rest to stress, so this is a fixed perfusion defect. Haven't seen the rest images to decide whether we should do the FTG images. Now we have gone on to do FTG images. So now the next display is to put the rest images on top, the FTG images on the bottom, as you can see right here. And you can see here this perfusion defect that's present on the rubidium images now is again present on the FTG metabolic images, and therefore we are dealing with a fixed perfusion defect, or a matched perfusion defect indicating a scar in the lateral wall. This is how it is displayed on a polar map. We have the rest images in the middle, stress images on the left, and the FTG images right here. Now you can see some patchy uptake here on the polar maps in the inferior infralateral wall, but this reflects probably GI activity that's commonly seen in rubidium images and not true myocardial uptake. Then we have to decide is it matched, mismatched, what about glucose uptake in normal tissues, and recommendations from finding. So this is a matched defect. Now we have rest, stress on top, and what's says here is delayed images. These are the FTG images. So rest, stress, and delayed images. This is a matched defect inferior infralateral wall. Again, this is the best way to display these images, always simultaneously with the perfusion images, image preferably the rest image to decide on what's matched and what's mismatched. This is a patient presenting to our lab for viability assessment. We have looked at the rest images. They're completely normal as seen here in the bottom row here, short axis, horizontal long axis, and vertical long axis. You can see in the stress images you have ischemia in the inferior wall, moderate intensity, moderate size perfusion defect in the inferior wall indicating ischemia. This patient does not need FTG assessment. This patient has ischemia in inferior wall. We can go on these data presented here or these images to decide on revascularizing the RCA in this instance. What about mismatch? So we have a patient here. This is the patient I showed you, patient one, earlier in the presentation today. Perfusion defect at rest and stress matched fixed defect. This patient who was having angina has had three specs, rest and stress showing no ischemia, a fixed defect. Now you can see here on top are the resting images. On the bottom are the FTG images. And you can see these FTG images completely filling in for the perfusion defect in the rest images. So what you see here, a mismatch, meaning decreased uptake, tracer uptake on the perfusion images at rest, and the increased FTG uptake. This is the hallmark of myocardial viability. This is what you're looking for when you're looking for hibernating myocardium. This is the image that shows that. This is the patient that I showed you, second patient, who had a totally occluded LAD. Now this patient comes here. We did not stress this patient. The LVEF was 20%. We have the cath already. We know that all we're interested in is the LAD territory here. On top, you can see the perfusion images showing a large LAD perfusion defect. On the bottom, you can see the FTG images showing filling of this perfusion defect right here. The entire septum, apex, anterior wall are filled with FTG, again indicating LAD hibernation. So now I've showed you an example of a match defect, meaning scar, normal with ischemia, meaning ischemia, mismatch in the RCA, and mismatch in the LAD. And this is an example here of mismatch in the circumflex. You have a patient presenting with rest images here showing a moderate size perfusion defect in the lateral wall. When we do FTG images here on the patient, the metabolic images indicate increased FTG uptake or switch of metabolism from fatty acids to glucose in the lateral wall, indicating again hibernating myocardium. Again, this is a patient with a CTO of the circumflex coronary artery, and now you have images that tell you this territory is hibernating and probably opening that CTO is worth your while and worth it for the patient. Now we often talk about glucose or FTG as non-specific agent. This is a patient who has normal coronaries presenting for a test. He slipped through the cracks. You have rest and stress images are completely normal, and probably I was out doing something and they went on and did the FTG images on this patient, and you can see this heterogeneous uptake of FTG in different parts of the myocardium. This is normal. This is not abnormal. FTG, if you image patients, normal individuals with FTG, you will see this kind of heterogeneous patchy uptake, and this should not be confused with either inflammatory myocardium or hibernating myocardium, unless you have something else to go by. In general, this is a normal FTG uptake that is heterogeneous in normal tissue. Now, doing all the images, understanding all the philosophy behind it, reading the practice guidelines, the practice points and the guidelines from American Society of Cardiology, arriving at all these conclusions is meaningless unless you can communicate them well to the referring physicians. So we try to communicate things in a way that's clear. This is a slide from a recent published paper from our center, and how we categorize our scans starting by the LVEF and then going down by the size of the perfusion defect, TID, drop in EF, and so on and so forth to decide between a low-risk scan, high-risk scan, or an intermediate risk scan. So we not only report defects, we report the totality of the clinical implications of the scan to the patient. These are the implications of such an algorithm where patients who we reported as low-risk, very few of them end up going for coronary angiography, and patients where we report intermediate and high-risk, we have significant number of these patients going for subsequent angiography after the test. Not only that, the test results when reported as low, intermediate, and high-risk were respected, where patients now with low-risk scans, very few of them underwent revascularization versus patients who have intermediate and high-risk scan, significantly 7 to 10-folds higher odds ratio of undergoing revascularization. Now, when we follow this hypothetical assessment from our lab about low, intermediate, and high-risk over 1,400 days, you can see that the way we categorize these patients was not just, again, a hypothetical scenario. This had clinical implications and actually was associated with significant guidance as far as survival for these patients. You can see prognostically, patients with high-risk scan did the worst, and patients with low-risk scan did the best. So, we use this as our guide for our lab for all our scan reads. So, every nuclear stress test, this is our standardized reporting system. I will share it with you. You have the stress images here. We have a 17-segment model for it, rest images down here, and this is, we do myocardial blood flow on all our PET scans unless the patients have an ejection fraction that's low or they've had prior revascularization. That's a subject for another module. And then we find a report viability in a binary way here, 1 or 2. So, viable would be 1, and scarred myocardium would be 2. So, this is reported here in our database, in our standardized report system. And not only we report present or absent for this amount of scar viability or ischemia, we have thresholds where we have mild under 10% in each territory, 10% to 20%, more than 20% as severe, and this applies to all ischemia, scarred, and hibernation. Now, from there on, we go to report the scan risk. Again, we have it here. These are all hard stops in our system, so you cannot finalize the report without clicking on one or choosing one of these scenarios, low, intermediate, and high risk. And finally, we report some findings from the CT scan, basically related to coronary calcification, thoracic aorta. We picked a few things that are low-hanging fruits and should not be missed on the CT scan done for attenuation correction. And we compare all the findings with the prior studies, if available. So, importantly, you have to report the extent, location, and severity of ischemia. So, the location is very important to be reported by vessel. And extent is, within each territory, is it mild, moderate, or severe? And within each territory, is it mild, moderate, or severe ischemia? Similarly, you have to report that for scar and for hibernation. So, the report has to be clinically meaningful, communicate the territory that you are attributing the defects to by vessel and not by segments. So, I cannot stand when I see a report coming from other places where, in the conclusion, they report every single segment, 17 segments. It's impossible to read those for most of the clinicians or most of the cardiologists managing these patients. This becomes a confusing morass of basically counting segments and trying to attribute segments to territories. We should facilitate that. And in the conclusion, you should communicate that as clearly as possible. Now, in the body of the report, you can fill whatever you want as far as the segments. But in the conclusion, this should not be the case. It should be related as territorial more than segmental. And then we communicate the left ventricular function size and the right ventricular function size. These are extremely important elements of prognosis and guiding therapy. And guiding therapy as far as medical therapy, ICD therapy, we should not be shy about reporting these things that are readily available in every nuclear stress test. Now, importantly also, educate your partners about the importance of trying to have some assessment of coronary anatomy and suitability of the vessels for revascularization prior to ordering the PET-FTG. Otherwise, you will end up with a PET-FTG with a lot of findings that have no clinical impact on the patient if the coronary arteries are normal or the coronary arteries are not suitable for revascularization. Try to educate your partners on the importance of not selecting patients for viability assessment or hibernation assessment when the left ventricular ejection fraction is normal or when the resting perfusion is normal. And importantly, if you do not know or you do not standardize your preparation for the patients, you will have garbage. It is extremely one of the most challenging tests we do, I think, in nuclear cardiology is PET-FTG for either hibernation or even more challenging for inflammation. So, standardize your patient preparation. Use the American Society of Cardiology practice points. They're simple, they're standardized, and that way we can in the future compare our data. So, I know a patient that comes to your lab has been followed the same standard that when they come to my lab and we can compare our images side by side. Finally, I will conclude with this was, you know, reinforcing that normally contracting myocardium, you have green light, nothing to be done here. These patients should not have PET-FTG for viability or hibernation assessment. Hopefully, we understand the continuum between normal myocardium to stunning to a hibernation and scar. I've showed you some of the ultrastructural changes that the cell will undergo when it moves from being normal and then start of blood flow all the way down to losing all its contractile elements, gap junctions, and then finally death. How to handle achinitic myocardium with referring these patients for perfusion images and if you have a perfusion defect for PET-FTG. We've showed you some data about improvement in function and survival after revascularization from meta-analysis of various single-center studies and from the Part 2 study, and possibly we will have large studies in the future addressing issues related to improvement in prognosis when using PET guidance for revascularization. Thank you so much, and hopefully you enjoy this module and this kind of format from American Society of Nucleic Cardiology. Thank you.

non-perfusion PET imaging

myocardial viability

hibernation

ischemia

scar

PET-FTG imaging

American Society of Nuclear Cardiology

viability assessment