So, the topic is how to perform and interpret an effigy path CT study for cardiac inflammation and infection. I have no disclosure. So here, when we talk about cardiac inflammation, we specifically refer to cardiac sarcoidosis. And what's the role of effigy path CT in cardiac sarcoidosis evaluation? Basically, it can provide metabolic evidence of the granulomatous status, meaning whether it's ongoing active inflammation or actually the advanced stage with scar tissue formation. And when we say cardiac device infection, we specifically talk about infection of the CID, like pacemaker and defibrillator, and also prosthetic valve, and also left ventricular assistant device infection. And as we know, there are increasing installation of this type of path to a cardiac device. The infection is a major complication. It's very important to diagnose it early stage to treat these patients. And PET has its unique role, unique methods over other anatomical imaging tools, like TEE and CT. So we will talk about that. Okay, so here are the three major learning objectives. First, we will describe how to prepare patients for this study, as the dietary preparation is the key to have a successful evaluation of the infection. And then we will talk about how to acquire and process the effigy path CT images. And then finally, we will talk about how to interpret the effigy path CT findings for cardiac inflammation and infection evaluation. So first, how to prepare patients. And the goal of the dietary preparation for patients is to suppress the physiologic myocardial effigy uptake, like here. As we know, it's not uncommon to see diffuse physiologic myocardial effigy uptake during our routine effigy path CT scan. And as we know, because myocardium sites can also use glucose, although it may preferentially use fatty acid. So how to suppress this physiologic effigy uptake? The goal is we try to provide this body with a lot of fatty acid, and let the myocardium myocardium sites to use the fatty acid and decrease the glucose utilization. So how to achieve that? One way is just to do prolonged fasting. Prolonged fasting will increase the fatty acid and provide fatty acid for the body. And we say prolonged fasting usually will take 18 hours or 24 hours. And the issue with the prolonged fasting is about patients' composure. Most patients probably cannot do that fasting in a day, right? And also, some studies show that this actually is not sufficient to completely suppress myocardial effigy uptake. About 38% of cases would still show some level of effigy uptake. So it's not a perfect preparation. And the second way is we ask the patient to eat a high-fat, low-carbon, hydrate diet. And with this way, we provide a lot of fatty acid to the body with limited sugar. And some studies show if a patient just eats one high-fat, low-carbon, hydrate diet, you will still see about 20% of cases showing effigy uptake in the heart. So you need more. And we will talk about how many meals later, okay? And just one meal is not enough. Maybe two meals or more. And another, you can give two or three times meals, longer preparation. So it can show much better effect. Some study also shows you can actually treat a patient, give patients some heparin before the study, because heparin can dissociate fatty acid from the lipoprotein particles and increase the blood circulation fatty acid level. A study also shows this actually, the effect of heparin treatment is inconclusive. Some can say it's good. Some say no effect. So it's not widely used. In our lab, we don't use heparin to treat patients. Another way, just combine this method. But the most important way is actually to give high-fat and low-carbon hydrate diet. So let's see what's the expert panel recommendations to high-fat, low-carbon diet preparation. It says you need at least two meals before the day of study. And after two meals, you can ask the patient to fast for at least four to 12 hours. And if some patients say, you know, I cannot eat high-fat, low-carbon diet, or it's a vegetarian, or don't want to eat high-fat food, then there's no choice. You can only do long fasting, like 18 hours or one day, 24 hours fasting before the study, if the patient couldn't follow that. Here is a table saying what specific food you can tell the patient to eat, or specific to avoid this kind of food. Definitely, you can ask the patient to avoid bread, or all these things, or all this, you know, food with high carbon hydrate. But mainly ask the patient to just eat meat, or butter, right? Egg, oil, like this. And some other foods are acceptable. Or if a patient, you know, I bet they just say, you just fast 18 hours or longer before a patient comes in. This is a specific food, and also the ways to look at the patient. If you are interested in that, you can refer to this paper in JNN 2017, about specific recommendations. But this is specific for non-diabetic patients, but we know there are some diabetic patients that also need this kind of study. So how to prepare diabetic patients for FDG-PET scan? Well, it's the same. You also use high-fat, low-carbon hydrate diet. But just tell the patient, diabetic patient, if he's using, or he or she's using insulin pump, just use the insulin pump based on their usual measurement. Or just use their pre-meal insulin. How many units he's using, just use this. Just follow patient's usual insulin dose. And this is for type 1 or type 2 with insulin dependent. Or other, you know, regular type 2 patient, he's not on insulin, just on all the anti-immune sugar agents. Then you have to stop metformin, start one dose before, I mean, during the fasting period. Okay. And some patients may have, may take the long-acting insulin, like lentils, before the night. That's actually okay. Patients still can take a night insulin, because this usually provides as a base level of insulin. It wouldn't change the next day's FDG, HCT scan. But key is to help patient to avoid short-acting insulin four to six hours before the study. No matter type 1 or type 2 patient, cannot take insulin, short-acting insulin, for two hours before the study. But keep in mind, for diabetic patient preparation, there's no optical or uniformed preparation for everybody. It's more like individualized, based on the individual patient's insulin dose. Okay. So this is about patient preparation. And then let's see next step, how to acquire and process the imaging to do this study. It's just like routine oncology and FDG scan. We, you know, before you inject FDG, you have to check patient's sugar level, glucose level. If it's more than 220 milligram per deciliter, you have to reschedule patient. And then if patient's sugar level is below that, you can give IV injection of 10 to 15 millicurie of FDG. And then let patient rest in a quiet room to let the body or tissue to take up the FDG. And usually this uptake time is one hour, same like oncology type CT. But some study show that, you know, you can do three hours, which can increase the signal or decrease the background activity. So the contrast of FDG uptake will be higher, it's better. That's for infection or inflammation evaluation. However, data are not very conclusive. So most of the labs are still using one hour uptake time. So three hour circulation time, you can do that, but it's not in oncology. Especially you want to compare your result with others, or even compare your own result, you have to keep it consistent. So usually we still suggest to use one hour circulation time. So after that, you put the patient under the camera, on the table, and do imaging patient. But key is when imaging patient, you shouldn't just limit your imaging to the chest, the heart region. You may think I'm only interested in the cardiac portion, right? And why I have to imaging actually the whole body from the skull vertex to the feet. The key is because no matter what we are talking about, cardiac sarcoidosis, or talking about cardiac device infection, because you have to take a look at the area outside the heart, because like cardiac sarcoidosis, right? Isolated cardiac sarcoidosis is not so common, because sarcoidosis is a systemic disease. So you want to also evaluate, you know, extra cardiac sarcoidosis, you know, because the whole body. But for cardiac device infection, especially for endocarditis, you want to evaluate whether there is septic embryo effect, like in the brain, right? Or in the spleen, there is an embryo effect. Or actually you want to find out where is the original potential infection source for the cardiac device infection. So you use the PET CT as over the scan to evaluate the extra cardiac portion. So it's very important when you do the study, you have to take a picture to scan from the top of the head to the bottom of the feet. And then each bed is just three to five minutes per position based on your camera performance. And usually we ask patients' arms up to decrease potential attenuation. And before the PET scan, as usual, you do localized CT for attenuation correction. Or sometimes you can do diagnostic CT or even diagnose the CTA based on the physician's request. And then after finishing imaging, you just process the data. And your technology will process the data as opposed to PET and CT data. And you can present this data in your workstation and view the three views, axial, coronal, and the sagittal views, right? You can also take a look at the MIPS. We will show you the image later. The key is when you use FDG PET CT for cardiac device evaluation, you have to also take a look at both the attenuation correct imaging and the non-attenuation corrected PET imaging. What does that mean? We will show you specific images so you will understand why we have to evaluate non-attenuation corrected PET imaging. Okay, very good. So let's now come to our major questions, how to interpret the results. So first, let's see how to interpret FDG PET CT result for cardiac sarcoidosis. Okay, so when we use FDG PET CT for cardiac sarcoidosis evaluation, we actually need also myocardial perfusion scan. Either you use a specter is also fine, but ideally you also do PET myocardial perfusion scan. The purpose of this is, first of all, you want to rule out coronary artery disease in this patient, ischemia or not. But more importantly, you want to evaluate whether there's a sarcoidosis area has corresponding perfusion defect or not. And sometimes in the advanced stage of the sarcoidosis, this area becomes fibroid tissue, scar tissue, scar formation. So this area will have a perfusion defect and that will also help us to make the final diagnosis. So for everybody, you need myocardial perfusion scan also. And then you can display the myocardial perfusion scan along with FDG PET CT scan in a cardiac view panel, and then look them side by side. And after that, then you evaluate the whole body PET scan, not just cardiac, not go outside the actual cardiac region to evaluate systemic sarcoidosis. Okay, so here is more like a protocol, right? And based on the perfusion scan and also FDG scan, you determine whether this sarcoidosis is ongoing active or actually it's delayed phase. For example, if you see focal, very focal, or focal in a mild diffuse background, you can see optic. This is more like ongoing active inflammation in that area. But when disease is advanced, this sarcoidosis area becomes scar or fibrotic changes, then you wouldn't see any activity. For some time, you still will see activity with the immune cells, the myocytes are already fibrotic changes. So you wouldn't see significant FDG uptake. But combining with corresponding perfusion scan, you will make a decision. If perfusion is normal, like here, perfusion is totally normal without perfusion defect, and although you don't see FDG uptake, this is totally normal scan, very easy. But occasionally, if you don't prepare patient well, you may actually see diffuse FDG uptake in the heart. Even perfusion normal, and because you still see FDG uptake diffuse, and this is non-diagnostic, you have to repeat the study. But if you see a normal perfusion, myocardial perfusion, but you see focal area of FDG uptake, that means that area has ongoing active inflammation, sarcoidosis formation. There are a lot of immune cells there. So our FDG uptake actually represent immune cells uptake, not the myocytes. Myocytes uptake has been already suppressed by high-fat, low-carbon diet. And the later stage of the disease is, you may actually now you see perfusion defect, but this perfusion defect is usually very focal, doesn't like ischemic or myocardial infarction, which go along the vascular territory. But in the sarcoidosis, advanced sarcoidosis, this data is usually focal. And this focal perfusion defect area also could show FDG uptake, which means it still has residual ongoing inflammation, or actually totally there's no FDG uptake, which means it's completely scarred. So this is a different combination of perfusion funding and FDG funding. You can tell whether this is ongoing, early inflammatory disease or late disease. And that's the advantage of ICD compared to CARDIG-MR. MR wouldn't tell you this is ongoing or late. So you can go to this paper again to see they show a table right here to show the different combinations, okay? Perfusion, FDG, and show the different stages of disease. But I don't like this image, it's poor quality. So I'm going to show you some of our own data, which I think is better than the published one. So first of all, you can see here, you see normal perfusion. I don't see any area of defect, right? This is a rubidium pattern for myocardial perfusion. And the corresponding FDG pattern doesn't show any myocardial uptake. Here is just cavity, blood pool, background, but the surrounding myocardial cavity doesn't show any uptake. So this is a totally normal scan without evidence of CARDIG-SAR for those disease. Then how about this one? Here I see totally normal myocardial perfusion. Meanwhile, I also see diffuse myocardial uptake of FDG. Okay, some areas lower, some areas higher. This is just due to poor dietary preparation. It's not diagnostic. So if you see this kind of pattern, you have to repeat your FDG PET portion after dietary preparation. Hopefully in the practice, you wouldn't see this kind of image a lot. How about this one? Yeah, you see totally normal perfusion without any perfusion defect. But on the FDG PET CT, you see a very focal uptake here, right? Like in the inferior septal region, okay? Very focal. And the rest of the myocardium actually has suppressed FDG uptake. That's a typical ongoing early phase of sarcoidosis in the inferior lateral portion of the heart. Okay, normal perfusion, but focal increased FDG uptake. And then you have the late phase of disease. Late phase of disease, usually you will see focal perfusion defect, very small, okay? Like here, perfusion defect, also in the inferior septal region. And corresponding area also shows FDG uptake. So which usually means that the underlying pathology is that this sarcoid, the sarcoidosis, sarcoidosis inflammation there, like the immune cells shows up there. And also this sarcoid granulomatosis changes also affect the local small vessels. And that's why you see perfusion defect. And that's why this area is also very focal. It doesn't follow the vascular territory. So it's different from a vascular disease. So which, if you see this pattern with perfusion defect, focal perfusion, that means the granulomatosis inflammation change has already affected the small vessels. That's why perfusion defect. But there are still immune cells in this area. So that's why you see FDG uptake. And on the other hand, you can see this pattern. So you see perfusion defect focal uptake, which means the vessel is also involved, affected. But you don't see any FDG uptake in that area, corresponding area. That means it's totally scar tissue, okay? All fiber, all the tissues is scar tissue. So if you see this pattern. And then you actually would see a mixed pattern in the same patient, same heart, just like this case, okay? And so this area, all this area is perfusion is normal, but you see perfusion defect in the inferior portion. But the perfusion defect area actually shows if dejected, which means they are still ongoing, the immune cells, they are inflammation there, okay? But this area has been also linked to cardiovascular is also affected. And, but the normal perfusion areas, they also shows scattered vocal activity, which means there's ongoing early stage vocal inflammation. So this area's early sarcoid is all late sarcoid also. Okay, that's different stages. And you will see that. Now, after you finish evaluating this sarcoid, I mean cardiac sarcoid images, and then you have now go outside, like in this case, the typical media standard lymph node involvement, the different portion, different stations of the media standard. And sure, most common actually, you will see lung sarcoidosis change, okay? Vocal uptake in the lung corresponding to a different type of lung pancreatic disease, okay? Can be nodule, can be atyloidosis, consolidation, and even fibrological change. So you have also, you have to evaluate media standard nodes, lung, and even bring other organs, spleen, okay, in the body, go to whole body to evaluate actual cardiac sarcoidosis involvement. And the same study, you can actually use FDG-PASID not for diagnosis. You can also use FDG-PASID for evaluation of treatment response. The same case, right? We saw heart uptake of a big heart and also media standard node involvement. And after steroid, this is patient, uptake is totally gone. This shows the treatment response, okay? So this is the role of FDG-PASID-T for cardiac sarcoidosis evaluation of what's the different patterns of, with the combination of the perfusion and FDG-PASID. Now let's switch to the cardiac ear virus infection. First, we will see what's the role of FDG-PASID-T for CRED infection. And then we will talk about prosthetic bulb, endocarditis, and AOF-F later. For specific for CRED infection, the role of FDG-PASID-T is actually to provide additional information or contributory effect to difficult cases, which means these cases have not equivocal TEE findings, whether they're vegetation or not, or broader culture is negative, positive, and clinically it's unclear. It's truly infected or not. Then FDG-PASID-T can add additional information, okay? And how to evaluate this infection is still mainly based on visual evaluation. If it's focal, intense, it's usually associated with infection. And, but if you see a homogenous, homogenous uptake, very mild homogenous, it's usually like inflammation. And because inflammation area can also show the FDG uptake in immune cells, right? Infection definitely would show uptake because WBC, all the cells, neutral fields, where it shows significantly increased FDG uptake. And then we will talk about how to differentiate between infection and inflammation, right? If we don't know that, and we may take inflammation area as infection, and of course false positive diagnosis. Again, when you evaluate CID infection, we have to review both the attenuation-corrected and non-attenuation-corrected images, very important. Let's take specific examples. Here, and you can see very focal heterogeneous increased uptake around the device pocket in the left upper chest wall, it's a pacemaker pocket. And everybody will know this is infected, right? And here is corresponding CT area. And in this kind of case, actually you have to, I said you have to take a look at the non-attenuation-corrected images. Why? Because the device is a high-density metal device. CT will detect, oh, there is a very high-density material there. And this material, because high-density material, it can block the X-ray photon for CT, right? Block the signal. Attenuate the signal. And then the CT will, because there's so intense uptake, the software will, if you're, then this device would also block or attenuate the signal from the PET, 511KB photons for the PET. And then, you see, because it's attenuated by the device, so I have to add back, add the counts back to this area to correct the attenuation based on the percentage of the attenuation rate. Let's say block 80% of the counts. Then we add 80% counts back to this area. So it can potentially force the increase, the counts in this area. That's called attenuation correction. To avoid that, you have to take a look at the non-attenuation-corrected images. Take a look at the original counts, whether it's truly increased or not. So if you still see increased uptake in the non-attenuation-corrected images, that means this activity is true. It really is due to the WPC uptake there. And if the activity, this amount of counts is gone on the non-attenuation-corrected images, that means it's truly artifact, okay? But in this case, I don't show here, still see very intense uptake on the non-attenuation-corrected images. That means this activity is true counts, true activity. So it means infection. So this is a part of the infection. This, another example is the device-lead infection in the left lateral chest wall. Is the lead go to the subcutaneous region? It's a very intense uptake here. So in this kind of case, you have to completely extract the device, okay? And this is a normal or non-infection case. You don't see anything in this area, right? So totally no infection area. Then how to really differentiate infection from inflammation? Actually, visually, it's easy to differentiate, as we just said. Infection usually is very focal heterogeneous, very intense. Inflammation usually diffuse around the device. And sometimes you can tell if it's just a very short time, within two to three months after installation, then it's usually more common with inflammation. But keep in mind, there's no ACUV value, okay? The data you measure the ACUV of the uptake, right? And so if ACUV is above certain level, three, five, then it's more likely to be infection. Below that is inflammation. There's no such kind of magic if it's activity, value ACUV value for the differentiation, okay? So ACUV wouldn't happen. It's more like the pattern of the uptake, whether it's a focal heterogeneous or diffuse. Here is like what we call diffuse. My mind, if it's around the device, okay? Very mild, but it's entire curvilinear activity. This kind of thing is not true. Infection is more inflammation, okay? So good. This is for the cardiac device. I mean, for the CID, pacemaker, defibrillator, pocket and lead infection. Now let's see what's the role of FDG-PCD for prosthetic valve endocarditis evaluation. Now these days, we install more and more prosthetic valves and this can, if there's an infection, then it cause endocarditis and it's very important to diagnose it early, right? So what's the role? And make a, you know, very straightforward about FDG-PCD for valve endocarditis evaluation is that if you add FDG findings as also as a major criteria, okay? To then modify the two criteria, it can actually increase the sensitivity of the two criteria for the diagnosis of endocarditis, but it doesn't compromise specificity. We'll show you later why it can increase intensity, I mean, sensitivity, but without compromise specificity. And also in addition to that, FDG-PCD can diagnose this disease for infection endocarditis much earlier than morphological changes you've seen on TEE or even sometimes use CTA, okay? Before the morphological changes, FDG-PCD can diagnose this early. And then another point of FDG-PCD is that you can detect extracardiac infection source. What causes this? Which area, which bacteria? And the bacteria, where does the bacteria come from? They have to treat the primary infection source. Otherwise, the endocarditis will come back. And also sometimes you can detect the septic emboli. If the patient has endocarditis, where it causes septic emboli, it's very important to treat this septic emboli. So we'll show some data. As this case, this patient has aortic valve replacement. You see very intense heteronegious activity, right? Around the device, around the valve device. Since the CT is fused in different views. So this is the endocarditis. So you detect some, maybe to correspond to this soft tissue here, right? So it doesn't really detect the vegetation. Sometimes there's vegetation formation. Yes, FDG-PCD can detect vegetation if it's large enough or, you know, shows very intense activity. But usually TEE actually is better to detect the vegetation formation. PET is more like detect this peripheral complication, like abscess formation or others, okay, like this. And how does it increase the sensitivity of the Duke criteria? As shown in this study, if you just use Duke criteria, like vegetation formation on TEE, right, culture positive, and others as major criteria. And they showed there are 70% of cases were diagnosed as definitely TEE. TEE, prosthetic valve endocarditis, 70%. And 50% of cases were ruled out, rejected. But this same patient, if you do FDG-PCD, and if you found abnormal activity on PET, and add this as a major criteria to the Duke criteria, which mean Duke plus PET-CT, now you actually identify 97% of the cases as positive. But meanwhile, this specific or rejected cases is still 50%, okay, rejected cases. And I'm sorry, this actually wrong here, because this move down here is 40%, okay, not 50. But from 50 to 40 is not a very significant change. But the key is the sensitivity increased a lot. So this means adding FDG-PCD finding to the Duke criteria can increase the sensitivity of the diagnosis without compromising specificity. Here's the example, typical example to show how FDG-PCD can diagnose the disease much earlier than morphological changes. Okay, this patient also has aortic valve replacement, and the CT didn't show any complications, like abscess or aneurysm or any morphological change, no. But FDG-PCD showed full co-active around the valve. So they opened, and the aortic surgeon opened and said, oh, there's no abscess, nothing, no infection. So they saw that FDG-PCD is too sensitive. It's a false positive study. So they closed it, right? So this is not good, it's false positive. However, eight days late, the patient continued to have symptoms, right? Eight days, now they repeated the CTA. Now they show aneurysm formation, and the TE also shows abscess formation, and they reopened, and now you see a lot of abscess. So this means, in this case, FDG-PCD at least can diagnose disease eight days earlier than morphological change. It's simply because FDG-PCD is a metabolic imaging. It doesn't show the morphological change. It only targeted the early immune cells, so WEC migration, accumulation in area. So it definitely can diagnose disease much earlier. This is one of the advantages for diagnosis of infection. And this just shows how FDG-PCD can detect the septic embolite event. This case, the patient has the right side, and tricuspid valve infection, endocarditis, so the bacteria can be sent to the lung, right? So in this case, actually you see lung septic embolite. Okay, this is the primary side. So this is lung septic embolite event. But sometimes if you see aortic valve endocarditis, you may see brain septic embolite. You see spleen septic embolite. So you have to evaluate the FDG-PCD from the top of the brain to the bottom of the feet. That's the reason for FDG-PCD imaging. Don't just focus on the heart, okay? And this case actually shows typical, the original infection source, okay? This patient had osteomyelitis from the greater toe. So without identifying this, even you replace his valve, the disease will come back, right? Because the bacteria can be sent here. So have to treat this one also. And then you will show this wouldn't have a recurrent endocarditis. That's very important. And this can only be done by FDG-PCD. Now then, finally, let's take a look at the rule of FDG-PCD for left ventricular assistive device infection. As we know, there are different types of AOVs, like a heart-made tool, had a jar of it, but they all have a pump and also a conduit to transfer blood. But also every device has a driveline, which is connected to the battery to provide the power to the pump. So infection can occur at any part of this device, either along the driveline, or the pump, or the conduit area portion. So let's take a look of this case. And we can, everybody can see that very focal, intense up to the excess side of the driveline in the abdomen, right up abdomen here, okay? But there's no activity along the subcutaneous portion of the driveline. So it's only an infection in the excess side. So this case, maybe you can manage this just by deburring here, clean this area. You don't need to replace, remove the device because it's very limited, right? So FDG-PCD can tell you that, and others, you don't know whether there's an infection inside or not. It can only be diagnosed by this kind of study. But this case is different. Now you see diffused activity around the entire driveline in the subcutaneous area. Now you have to remove this line, right? In Taiwan, it's not limited to the excess side. So the entire driveline. So we treat it like a driveline or excess side as a periphery infection of the device. And in contrast, this just shows there's no infection, right? Clearly there's nothing, this negative study. Infection can also occur inside the pump or the conduit around the central portion, we call the central infection. I think in this case, right? It's more like the inflow conduit or canoe like here, okay? Correspond to this area, very heterogeneous intestine. So this infection in the conduit, and in the canoe or inflow. And this is the outflow canoe infection like here in this portion, okay? Diffused here, intense, right? So in another case. And we previous our data from our lab and it shows actually, depending on the different locations of infection, whether it's outside the pump, we call periphery, that driveline or excess side, or whether it's inside the device like central portion in the pump or the inflow or outflow canoe. Then they actually, the prognosis is different. Like this, if there's no infection, totally negative on FDGPC, this survival rate is very high, no death. But if a patient has periphery, this periphery infection, which means the driveline or excess side, this is the survival rate. The worst is the central portion, central infection, in the pump or in the inflow, outflow canoe. Then the survival is the worst. So if FDGPC can not only diagnose disease, but also based on the location of the infection, it can predict the patient's survival or clinical prognosis is very important. It's published in JAK Cardiovascular Imaging in 2019. Okay, so now let's make a summary about the role of FDGPC for cardiac inflammation, cardiac infection evaluation. First of all, no matter you use it for cardiac sarcoidosis or diabetic infection, you have to prepare patient to do a dietary preparation with high fat, low carbon diet for at least two meals before the scan, before the day of the scan. And after two meals, you have to fast, ask the patient to fast for four to six hours or longer. And before you do this study, that's very important. And when you imaging patient, you don't just imaging the heart or the chest. You have to go from the top of the brain, to the bottom of the feet, because you want to detect any disease outside the heart. In sarcoid, it detects actual cardiac sarcoidosis. In diabetic infection, you want to detect septic embryo event or to detect, to identify potential infection source. So it's very important from a patient care point of view. But specifically for cardiac sarcoidosis, and it can tell the metabolic information or status of the disease, whether it's ongoing active inflammation or whether it's advanced fibrotic tissue. So differentiate this. And also you can guide the treatment or monitor treatment response by showing the activity change. In terms of the rules of FDG-PEDCT for cardiac diabetes infection, it can diagnose disease at the earliest stage because it's a metabolic imaging, not a pure morphological change. And so it's diagnosed earlier or before morphological damage issues. And especially for valve endocarditis, prosthetic valve endocarditis, it can increase the sensitivity of modified Eukaryoteria for the diagnosis of endocarditis without compromised specificity. And also it can detect actual cardiac infection source or septic embryo event. That's the rule of the FDG-PEDCT for diabetic infection. Okay, so here we have several additional reading literature if you're interested, you can refer to these papers. And thank you very much.

FDG PET-CT

cardiac inflammation

cardiac infection

cardiac sarcoidosis

cardiac device infection

dietary preparation

granulomatous status

prosthetic valve endocarditis