Hello, everyone. I'm Panitia Charantaitui from the Mayo Clinic. I'd like to thank the course directors, Dr. Kalman and Dr. Sakura, for inviting me to participate in this PET curriculum course. It's a great honor and a pleasure to be with you today. So over the next 60 minutes, I'll review cases of cardiac sarcoid PET. These are my disclosures. So we'll cover the following three learning objectives. We'll describe the characteristics of normal and abnormal PET images for cardiac sarcoidosis, identify characteristics of false positive studies, and then show the components of an appropriate report for cardiac sarcoid PET studies. And this is a list of the different types of studies I'll show you during our time together. There are a few considerations to keep in mind before performing PET imaging for cardiac sarcoidosis, and they include the indications and applications of cardiac PET imaging for sarcoidosis preparation prior to the PET study, the PET acquisition protocol, and then image interpretation. These are the four broad clinical scenarios where cardiac PET could be useful for suspected or known cardiac sarcoidosis. The first group are the patients with histologic evidence of extracardiac sarcoidosis and abnormal screening defined as any of the following features listed on the slide. The second group are the young patients with unexplained new conduction system disease, such as complete heart block. The third group are the patients with idiopathic or unexplained VT. And lastly, the patients with proven cardiac sarcoidosis as an adjunct to follow treatment response. Several societies have developed algorithms for the diagnosis of cardiac sarcoidosis. The two most commonly used are the updated Japanese and the Heart Rhythm Societies algorithms. Both have a histologic pathway for the diagnosis of cardiac sarcoidosis, and both require demonstration of non-caseating granulomas on endomyocardial biopsy. Recall, though, that myocardial biopsy has a very low sensitivity of only 20%. So, most patients are diagnosed using the clinical pathway, which are shown on this slide, and are similar between the two societies. Both require a diagnosis of extracardiac sarcoidosis, plus other criteria, which include cardiomyopathy, high-grade AV block, unexplained VT, positive MRI, or positive cardiac PET. The Japanese use a combination of major and minor criteria, and the Heart Rhythm Society requires just one additional clinical criteria that I've highlighted here in the absence of other causes of the cardiac findings to have a diagnosis of probable cardiac sarcoidosis. I do want to emphasize that a real strength of PET here is the ability to easily identify both cardiac and extracardiac sarcoidosis, and also to detect disease activity, which is inflammation. We do know that there's an entity of isolated cardiac sarcoidosis, which is probably more common than we thought, maybe in about 25% of the cases, and the updated Japanese society also includes diagnostic guidelines for isolated cardiac sarcoidosis, which really includes having no extracardiac sarcoidosis, plus either a tissue diagnosis of cardiac sarcoidosis, or a clinical diagnosis using cardiac FDG uptake, plus at least three major criteria as shown on the prior slide. I mentioned the critical importance of patient preparation prior to performing the cardiac PET for sarcoidosis, and this slide shows our approach to patient preparation at Mayo, which is similar to the patient preparation recommended by the ASNIC and SNMI, and this includes the high-fat, low-carbohydrate meals the day before the PET, followed by prolonged fasting, no exercise 24 hours before the PET. We also ask patients to keep a record of the preparation, and we scan that into the chart for serial imaging. Our nurses also call every patient at least a few days before the PET to emphasize the importance of this preparation and to answer any questions. We don't give adjunctive heparin, which promotes lipolysis and increases free fatty acid availability, but many practices do so, and although protocols vary, a single 50 international unit per kilogram IV bolus of unfractionated heparin about 15 minutes before FDG administration is probably the most utilized protocol. Now we've published a 91% success rate of myocardial suppression using this patient preparation protocol, and this is our PET-CT protocol for cardiac sarcoidosis, which is also similar to the protocol recommended by the ASNIC and SNMI. We perform resting myocardial perfusion using N13 ammonia PET in conjunction with the FDG image. Our FDG uptake period is 60 minutes between injection and cardiac PET acquisition. We also perform a limited whole body PET study from orbits to thighs with the same injection of FDG. As for the cardiac acquisition, if there is clinical suspicion of extracardiac sarcoidosis or no recent extracardiac sarcoid PET evaluation. Before the PET images are examined for cardiac sarcoidosis, the following steps should be taken. Unlike interpretation for myocardial perfusion imaging, which is done in a sort of more blinded fashion, at least initially, for these cardiac sarcoid PET studies, it's important to review the medical record and other imaging studies carefully. It's almost like a mini consultation. It's also important to confirm appropriate patient metabolic preparation before reviewing the images. Proper alignment and co-registration between the transmission and emission data should also be ensured for a high quality study. Other routine QC steps should also be performed. For cardiac sarcoid PET studies, it's very important to use both the normalized cardiac display and the hybrid nuclear medicine display for viewing images because normalization can actually lead to artifactual accentuation of areas of mild FDG uptake. It's also important to review both attenuation and non-attenuation corrected images when there are cardiac devices such as CT attenuation can lead to overcorrection of data and cause artifactual FDG uptake around an ICD lead as an example. So using the normalized approach, the PET perfusion and FDG images are interpreted simultaneously for cardiac sarcoidosis as shown here. And a normal cardiac sarcoid PET examination shows complete suppression of FDG from the myocardium with normal resting myocardium uptake myocardial perfusion as in the first column. Incomplete suppression of FDG from normal myocardium as might occur because of inadequate patient preparation may be accompanied by a pattern of diffuse homogeneous FDG uptake with normal perfusion as in the second row. Cases of possible inflammation may also demonstrate patchy non-homogeneous uptake of FDG or focal undiffused FDG uptake. But unlike homogeneous FDG uptake due to failure to suppress FDG from the normal myocardium, pathological FDG uptake is more likely to be associated with perfusion defects as in the third row. In the presence of active inflammation, focal areas of FDG uptake may be present with an associated perfusion defect sometimes in the same location as in the fourth row, but not always. The perfusion defect may be due to microvascular compression of granulomas or inflammation and may improve with treatment. If there is a prior PET examination, it's very important to review the images because what appears to be a negative study could be treated cardiac sarcoidosis. And in cases of scarring or fibrosis, a resting perfusion defect without FDG uptake may be present as in the second to last row. And lastly, focal and homogeneous FDG uptake along the lateral wall without a perfusion defect or any wall motion abnormality or any other imaging abnormalities is often a nonspecific finding. Now let's look at some cases. So this first case is a 78-year-old man with a remote history of right lung and left eye sarcoidosis that's been quiescent, and he's not on any treatment. He has hyperlipidemia OSA and a history of unprovoked PE. He came to our emergency department with a viral prodrome, presyncope, and monomorphic VT, which was stabilized with amiodarone. His echo showed mild LV enlargement and EF of 61%, grade one of four diastolic dysfunction and mild mitral regurgitation. Cardiac MRI showed upper normal LV size and borderline LVEF, but no findings to suggest myocarditis or cardiac sarcoidosis. He was referred for a cardiac sarcoid PET study because there were still some lingering concerns about an inflammatory cardiomyopathy. So the fused PET-CT images here show good quality data, and I've scrolled through them. I'm just providing a screen capture here. There was satisfactory alignment of the PET and CT data. It's important to check these borders here and here in all the views on both of them. I scrolled through these images and did not see any concerning findings. So here are the reconstructed images in grayscale, short axis from apex to the mid left ventricle on top here, HLA in the middle and VLA on the bottom. For each pair of images, perfusion with N13 ammonia is on top and FDG on the bottom. So far, I can appreciate just blood pool activity on the FDG image, and I'm not seeing any perfusion abnormalities in any of the views. And here are the reconstructed images in color, same orientation as before. Again, normal perfusion and only blood pool FDG activity is appreciated. Now we move from the mid left ventricle in the short axis towards the base. And again, I'm only seeing blood pool FDG activity as I scroll through these and no perfusion abnormalities from the mid LV to the base of the left ventricle. Same in color. Because these viewing software tend to be quite LV centric and RV FDG uptake is very important prognostically. I make the image smaller as shown here, and I can better evaluate the right ventricle in all views. And here I do not see evidence of any RV FDG uptake on these images in all of the views. Same again with the color scale, make the image smaller to look for RV FDG uptake if the software tends to focus on the LV. And again, we do not see evidence of any RV FDG uptake. Again, moving towards the base in gray scale and in color scale. And here we have the gated data, which also looks to be within normal limits with a normal calculated LVEF and no regional wall motion abnormalities, volumes were also within normal limits. Most software also offer this type of quantification that may be helpful, especially as an adjunct for assessing the response to therapy and quantitative techniques for this purpose often use the SUV max. The SUV is the concentration of radioactive tracer in a region corrected by the injected dose and the patient's weight. The program identifies those and the patient's weight. The program identifies a maximum SUV in the myocardium and also the SUV in the blood pool. So here are the numbers for the myocardium and then here for the blood pool. And I'll show you some positive cases and serial studies later on where this might have added value. But I did want to mention that to date, quantitative measures have not really been correlated with clinical outcomes in large scale studies. In addition, there's really no SUV threshold that can distinguish cardiac sarcoid from normal myocardium. This patient did not have the limited whole body PET acquisition given the lower suspicion for sarcoid doses. And so we go on to our report. And this slide shows the salient portions of the report for the case. We usually mention if myocardial suppression is satisfactory, then we provide also the diagrammatic representation of the images. And here, everything is normal. So everything is white. And we also describe the findings and provide a statement about whether there's active inflammation or fibrosis, or if the findings are compatible with cardiac sarcoid doses. We also provide an assessment of the LV size, the calculated left ventricular ejection fraction, and if there are any regional wall motion abnormalities. Then we review the study and report any CT and extracardiac PET findings. And lastly, we make a comparison statement if there's been a prior study. So this is a nice normal study. Because of his prodrome of viral illness, our electrophysiologist considered the possibility of some type of focal viral myocardium focal viral myocarditis not apparent on the MRI or the PET. And they recommended continuing amiodarone for two months, and then bringing the patient back for follow up. And at two months, the Holter showed rare PVCs and his amiodarone was discontinued. Three months later, he returned again and had less than 1% PVC burden. And now one and a half years later, he's doing well and has very rare PVCs. So this first case was a nice negative case and is illustrative in this regard. So let's contrast the first negative case with the second case of a 41 year old man. And about one year before coming to us, he began to experience dyspnea and exertion. He first had medical attention elsewhere. And his symptoms progressed such that he was admitted to an outside hospital. And by report, a CT showed mediastinal adenopathy, which he had biopsied, and he he was told he had evidence of pulmonary sarcoid. Because his PFTs were normal, and he seemed to stabilize, no specific treatment was recommended. And he seemed to do well initially. But six months later, he had more dyspnea and exertion, dizziness, lightheadedness, and presyncope. An ECG showed complete heart block, and his ventricular escape rate was only 30 beats per minute. ECHO was reported to be normal, and a cardiac MRI was attempted, but he couldn't undergo the study because of severe claustrophobia. A permanent pacemaker was implanted, and he had no further workup or specific treatment. His symptoms initially improved, but then just a few months later, he had really bothersome palpitations. And at this point, he came to Mayo for a second opinion. The Lyme's titer was negative. An ECG showed PVCs. ECHO showed preserved EF overall, but septal and apical wall motion abnormalities. He had very frequent PVCs, mostly singles and couplets, and also some bigeminy. Chest x-ray and PFTs were normal. So, he was referred for a cardiac sarcoid PET with limited whole body acquisition as well. Again, I went through these images, and the PET-CT fusion images showed satisfactory alignment of the data. Scrolling through these, I did not identify any issues for quality control, and I also reviewed the patient preparation, and the study quality was also overall very satisfactory. So, here I'm sharing the reconstructed views in grayscale. The orientation is as previous. There appears to be overall really good myocardial suppression, and on the short axis images, there are actually two perfusion abnormalities. One in the apical, in the inferior wall from apex to the mid-left ventricle, where I'm pointing, and this perfusion defect is associated with focal FTG uptake, also where I'm pointing, and we can confirm that also in the other views as well here. And here in the color scale, we can again appreciate the inferior perfusion defect here all the way to the mid-left ventricle, and then the associated FTG uptake where I'm pointing. And as we move from the mid to the base of the left ventricle, in the short axis, there is actually a second perfusion defect in the anterior and the anteroceptin as we move towards the base, and this area also has associated intense focal FTG uptake here in the anterior anteroceptin. The same defect can be appreciated again in the color scale, anterior anteroceptin, and associated FTG uptake. So, these findings are highly compatible with cardiac sarcoidosis with active inflammation, especially in light of the biopsy-proven extracardiac sarcoidosis. The perfusion defects, as I mentioned, are presumably due to compression of the arterioles from edema, inflammation, and possibly granulomas, and the FTG uptake is due to active inflammation. We look for RV FTG uptake, which I talked about before, and we didn't find any, and the non-attenuation corrected images also show the same findings. Here are the gated N13 ammonia PET images showing borderline LV size, a calculated LVEF of 60%, and slight basal septal wall motion where I'm pointing here. And then here are the quantitative inflammatory data provided by the software, which again includes the SUVs in the myocardium and SUV in the blood pool. And the maximum SUV in the myocardium is 4.5, in the blood pool 2.3, giving a ratio of about 2. Now, when the ratio of myocardial to blood pool is greater than 1.5, it may suggest more significant inflammation, but this does not always hold true because it depends also on the pattern and the location. One could have diffuse physiologic myocardial FTG uptake that is quite intense and that gives a high ratio as well. We also perform the limited whole body FTG scan in this patient with the same injection of FTG as for the cardiac scan, and here is the MIP image. And with the limitations of the normalized cardiac display for hotspot imaging, it's important to confirm cardiac findings on the non-normalized general nuclear medicine hybrid display as shown here. And we see again the septal myocardial FTG uptake on this MIP image. And if we look carefully, we can also see the uptake in the inferior wall that I showed you on the short axis images. And again, can appreciate this in the screen capture, the interseptal myocardial FTG uptake on the PET-CT. There's also fairly symmetric lower cervical FTG uptake in the lymph nodes, as well as pretracheal and subcarinal FTG avid lymphadenopathy, superior mediastinal and bilateral hyler, again, FTG avid lymphadenopathy. He also has innumerable bilateral pulmonary nodules, the largest of which had an SUV max of 5.3. And these findings are compatible with the outside biopsy diagnosis of pulmonary sarcoidosis. There's also heterogeneous nodular FTG uptake throughout the spleen and also multifocal FTG uptake in the liver. So this is the cardiac report first, depicting the perfusion abnormalities on the diagram, the multifocal FTG uptake. And we make the diagrammatic representation perfusion on top here, just like on our images, and then FTG images on the bottom here. We talk about the excellent patient preparation, the description of the perfusion defects, the FTG uptake, the SUVs in the myocardium and blood pool. And then I think the rest is quite self-explanatory. We do give an overall impression that findings are compatible with cardiac sarcoidosis with active inflammation. So the PET findings in this study were really classic for active cardiac sarcoidosis, showing both the perfusion and FTG abnormalities, especially involving the basal septum and the inferior walls, which are really the most commonly affected left ventricular regions, as shown by the autopsy series of patients who died suddenly with sarcoidosis. The septum in the red bar was the most involved in almost a third of the cases, followed closely by the inferior left ventricle, then the anterior wall, the RV, and lastly the lateral wall, where only 14% of the cases had evidence of sarcoid. And this is the separate, limited whole body report that is issued by our radiologist, summarizing the findings with the impressions up top here of extensive metabolic activity in the chest, spleen, and possibly the right lobe of the liver. So with the cardiac and extracardiac PET findings of active inflammation, immunosuppressive therapy was commenced with prednisone, as shown on the slide, was slowly tapered down to 20 milligrams daily, which is what he was on when he came back three months later to see us. He underwent a repeat PET using the exact same preparation and exact same protocol. And I've done all the QC already, and everything was technically satisfactory. And I also confirmed that he followed the exact same preparation. And here are his follow-up images in grayscale. I think what's most striking on first viewing these follow-up images as compared to the pretreatment images is the blood pool activity on these FDG images. And this suggests satisfactory suppression of physiologic myocardial FDG uptake, but also that there may be a different level of FDG uptake compared to previous. And careful review shows that there is still here an inferior perfusion defect where I'm pointing. And there is also that's probably a little bit less severe and less extensive. And again, there might also be some focal FDG uptake in the same inferior segments. A little bit hard to know when there's all that blood pool activity, but it may be less intense and perhaps less extensive. And again, this can be appreciated on the color scale images. We see the perfusion abnormality, and then we see the FDG uptake, perhaps a little bit less extensive and less severe or less intense. As we move towards the base, we see the second perfusion defect in the anterior and interseptal segments. And perhaps this is also slightly milder and less extensive, but there is still this focal FDG uptake that is milder and less extensive, but tougher to evaluate because of all the blood pool. So, whenever we see low-level uptake that we're not sure about, it's really good to ask the question of if there's been a prior study and if the patient's on treatment, because if you know about the findings of the prior study, it's actually easier to identify some of these areas, and the interpretation could change tremendously. So, keep that in mind as you look at these So, keep that in mind as you look at these images. We always pull up the old study if that's available to us. It's really hard to make comparisons when the blood pool looks so different between the two studies, and here's where the SUVs might help us and serve as an adjunct to our interpretation. So, the SUV max in the myocardium now is 2.5, and it's also close to 2.3 in the blood pool. So the ratio is close to one. Recall that it was 4.5 in the myocardium and 2.3 in the blood pool with a ratio of two. So this suggests a lower intensity of uptake and also we recognize that it's also less extensive. And here are the gated images calculated EF 60%, again, with the same kind of basal, anterior and septal wall motion abnormalities. And here again are the salient portions of the report on the follow-up study. We again mentioned the patient preparation, described the perfusion defects diagrammatically and the associated FDG uptake, provide the SUVs and describe volumes and function. And then we also make a comparison statement. And here we say perfusion abnormalities are less severe, less extensive, focal FDG uptake also less prominent and less extensive. We provide the myocardial SUV and blood pool SUV values for comparison as well. And sometimes we'll also make a comment about that as well. It can be challenging to appreciate sometimes the changes on the FDG image before and after treatment on those smaller images. So I've screen captured just the FDG images here to show them side-by-side so we can actually compare baseline versus follow-up and see the difference in the two. I think again, it's really helpful to have the SUVs for follow-up and in this situation, very helpful to have the prior study for side-by-side comparison. I want to emphasize again, the importance of viewing the images on the non-normalized hybrid nuclear medicine display in addition to the cardiac display. And on this display, we can appreciate the septal uptake on the baseline image and three months after therapy, we see quite complete metabolic response and interval resolution of a lot of the previously seen increased FDG uptake in the neck, chest, spleen, and liver, and also that there is far less uptake in the heart as well. And so with the findings of the PET, the patient was maintained on the same dose of prednisone, 20 milligrams daily for another three months when it was tapered. And at that point, it was tapered down to zero and he's been doing well for the past few years. Pacemaker interrogations have not shown any significant ventricular ectopy and his dyspnoeic exertion is also markedly improved. So in addition to having diagnostic value and serving as an adjunct tool for a following therapeutic response, cardiac PET may also have prognostic value in cardiac sarcoidosis. And this patient had both perfusion and FDG abnormalities and was really at increased risk of BT and death as shown by the red line based on this small study and a few other observational studies. And so I think the question of the questions is whether his pacemaker should have been upgraded to an ICD. And in this case, it was not, his EF was normal. And after treatment, the inflammation was markedly reduced. And so he did not have any further BT or PVCs and so he was just continued with the pacemaker only. So although there are no randomized control trials and no consensus on how to treat the patient with cardiac sarcoidosis, many would treat the symptomatic patient with active inflammation by PET. And this was the case with our patient. I think there's a lot more debate regarding treatment for the asymptomatic patient with active inflammation by imaging. Some will try, will treat to try to prevent damage to the heart structures. But again, there's no consensus and no definitive data. PET is currently though the best non-invasive tool we have for identifying inflammation and that's really needed to help guide management. The case also illustrates that for serial FDG PET imaging, it's very important to do everything the same way as outlined on the slide. And a change is more likely to be significant when both intensity and volume change in the same direction and by at least 20%. The potential ability to follow disease activity is a real strength of PET for cardiac sarcoidosis. So here's some take home points from this case and the first case. Remember to incorporate all available data including other imaging findings when interpreting the cardiac sarcoid PET studies and use both normalized cardiac display and hybrid nuclear medicine display for viewing images. Always look for prior images and know whether the patient's been treated. PET provides additional diagnostic and prognostic value in cardiac sarcoidosis. And two unique strengths of PET are the ability to obtain information on extracardiac disease activity which is important for diagnosis, patient management and potential biopsy sites. And then it also allows us the ability to follow disease activity with serial imaging. So let's go now to case three, which is a 56 year old woman with a history of complete heart block at age 50 and she received a permanent pacemaker at that time. She then developed left ventricular systolic dysfunction with heart failure and frequent non-sustained VT and her device was upgraded to an ICD. There's also a history of atrial flutter, status post ablation. She was referred for a cardiac sarcoid PET study with limited whole body imaging using the same injection of FDG. And she confirmed following the metabolic preparation. The fused images show highly satisfactory alignment of the PET and CT data. And as I scroll through these images and the processing everything looked highly satisfactory. So here are the reconstructed views and there is a very large moderate to severe perfusion abnormality in the apex, anterior, the septum, inferior and lateral segments really not following any coronary distribution. We see FDG uptake in some areas, but in other areas we don't see FDG uptake. So for example, in the septum we have a severe perfusion defect with focal FDG uptake. So this area is likely compatible with active inflammation. On the other hand, in the mid lateral wall and inferior wall, we have a severe perfusion defects but no FDG uptake. And so they are potentially scarred and fibrotic with perhaps more burnt out cardiac sarcoidosis. There is also evidence in this case of RV FDG uptake which can be appreciated in the horizontal long axis as well as the short axis views. And here are the images in color again showing the very large moderate to severe perfusion defects with some with associated FDG uptake in some areas but not in all areas. And we move towards the base in the short axis. We also see the severe perfusion defect in the septum, no FDG uptake in some areas there that could be compatible with scar, for example here and also other areas in the inferior wall that has a kind of perfusion defect here with FDG uptake. So that could be active inflammation. And so kind of a combination of both active inflammation and perhaps scar tissue in the same patient in the same heart. And again, the images in the color scale. And recall though that this patient has an ICD and we see the effects of the ICD, the device on the CT images with a lot of artifacts. So here I like to bring in the non-attenuation corrected FDG images to be sure that I'm not seeing the FDG uptake due to over-correction of an ICD lead or some other device, for example. And here the non-attenuation corrected images are added to the third row of each set of images. And they don't really change my interpretation. They look pretty much the same as the attenuation corrected images. So I can confirm that most likely this is not due to artifact from over-correction. And here I'm moving up towards the base and still seeing the same findings in both gray scale and in color. The inflammatory data by the program showed a maximum SUV in the myocardium of 6.1 with a blood pool of 2.8, so a ratio of 2.2. And so there are definitely some areas that are compatible with active inflammation. The gated ammonia images showed an EF of 33%, similar to echo with akinesis of the apex, the septum and inferior wall, in addition to hypokinesis of the remaining segments. So here are the salient findings of the report, very colorful on both perfusion here and uptake on the FDG. And there's a large perfusion defect with the associated FDG uptake and in a somewhat patchy distribution involving many areas of the left ventricle. And some areas we did code as scar. And we also provide the SUV values and the description. We state that the combination of findings is compatible with cardiac sarcoidosis with mostly active inflammation, but that there may be areas of fibrosis or scar. We also point out the focal RV FDG uptake. I think the rest is quite self-explanatory. And the RV FDG uptake, we like to point out because in the same study that I showed you before by our colleagues at the Brigham, RV FDG uptake was associated with a five-fold increased risk of BT or death compared to patients without focal RV FDG uptake. A limitation of the study was a small sample size, but this is something that we do keep in mind. So the patient also had the limited whole body FDG acquisition using the same dose of FDG as for the cardiac acquisition. And here are the images. And this shows a lot of tracer avid lymph nodes above the diaphragm and also below the diaphragm and likely secondary to sarcoidosis with upper abdominal, mediastinal, bilateral pulmonary and hilar lymph nodes, as well as small lymph node involvement in the intraparotid and external iliac areas and a focus of uptake in the medial left clavicle all likely related to sarcoidosis. She has diffused splenic hypermetabolism also likely related to sarcoidosis and diffused marrow hypermetabolism, again, probably likely secondary to sarcoidosis. And then a lot of tracer avid lymph nodes above and below the diaphragm here shown in this image. So the take-home points from this case are shown on this slide. Inflammation, edema, fibrosis and scar may coexist in the same heart. Always look for RV FDG uptake and use the non-attenuation corrected FDG image to look for evidence of ICD-Lead artifact. So let's go on to case four, which is a 64-year-old man with known systemic sarcoidosis. He has a history of complete heart block and unstable VT and he's had an ICD placed. He comes in now with worsening fatigue and an echo showing an EF of 43%. And his EF had previously been in the 60s. So the presentation raised concerns for cardiac sarcoidosis with active inflammation. And so he was referred for the cardiac sarcoid PET study and he followed all of the instructions. Fused images were satisfactory in terms of alignment and quality. CT showed even more artifact from the ICD-Lead in this patient, so we must keep this in mind. And so for this reason, we brought in the NAC to start. The NAC is the non-attenuation corrected image, FDG image shown here in the third row of the slide. And this is a graph of each set of images. So the perfusion here looks generally satisfactory, maybe a little bit of mild reduction at the apex, which we often see with these PET studies and is usually due to a partial volume effect where I'm pointing. And on the FDG image, we do see blood pool activity, mid left ventricle. We do see a focus of uptake right here that might be more evident as we move up even further. And I'm pointing to the area that's sort of in the inferior septum or maybe just adjacent to it more on the right side, the RV side. And it's a bit streaky and looks like artifact to me. And if we go to the non-attenuation corrected images here in the third row, we don't really see it there. And if we just scroll through, it's not there and yet it's on the attenuation corrected image. And in color, we can appreciate it, this bright spot. And it's also confirmed in the VLA image. And so because we don't see it on the non-attenuation corrected FDG image, in this case, it's most likely over-correction by the presence of the device lead. And this really was a negative study. There was a little bit of potential lateral wall uptake here but we don't really appreciate it very much here on the attenuation corrected image. We had wondered if this was papillary muscle uptake but I think this might've just been some layering within the blood pool. So I think overall, this was a negative study. And these were the salient portions of the report. We didn't code any abnormalities on the perfusion or on the FDG. We mentioned the excellent metabolic preparation, no inflammation, and no evidence of active inflammation or fibrosis. And then the rest is self-explanatory. So the take-home points in this case, case four, is to remember to use the non-attenuation corrected or NAC FDG image to help determine if FDG uptake may be due to artifact, for example, from an ICD lead. So this next case, case five, is a 49-year-old man with presumed isolated cardiac sarcoidosis on the basis of syncope with frequent non-sustained BT and MRI with LGE in the mid-ventricular septum and borderline LV systolic function. An ICD was placed when his EF was lower and he now presents with severe fatigue and palpitations. Good quality data based on the fused images. It was satisfactory alignment of the PET and CT transmission data. And in our practice, we don't get very many inadequate suppression on the FDG image, but here's one where the patient consumed lots of carbs, carbohydrates, before the cardiac sarcoid PET. And there's some LV enlargement and a mildly reduced EF with lateral hypokinesis. But when I first pulled this study up, I thought I was looking at a viability study. So it's really important when you sit down to know the indication for the study, the patient preparation, the clinical history and other imaging findings. And in this case, it's important to note that this was supposed to be a cardiac sarcoid study and myocardial suppression was clearly inadequate. We didn't see any perfusion abnormalities. And here again are the images in color. We see quite diffuse FDG uptake throughout the myocardium, it's quite intense. And as we move up towards the base on the short axis, there is a bit of an abnormality here that we see on both perfusion. We wonder if this is septal dropout or if there is a defect here on both of the perfusion as well as FDG. But it's difficult to know in this case. Here are the gated images showing a calculated EF of 39% and LV enlargement. So this study was non-diagnostic, likely due to suboptimal myocardial suppression of FDG. And we coded this as diffuse, the green here on the FDG. And we weren't sure if we saw a definite perfusion abnormality. And we thought this was likely, most likely physiologic myocardial uptake given the diffuse nature of the uptake, but underlying inflammation can't be excluded when we're seeing this much uptake. And so we did recommend that the FDG portion of the study be repeated with greater emphasis on metabolic preparation. I think this one was a different gated PET. I think the EF was lower actually. In the same autopsy series of patients who died suddenly with sarcoidosis that I showed you earlier, a very small number of the deaths, 25 deaths, I think two of the patients had actually diffused scarring from cardiac sarcoid. So it's possible to have involvement of the entire left ventricle, but I think it's less likely. And I'm not sure whether it would be in the form of active inflammation or more likely scarring where we wouldn't see necessarily FDG uptake. Now, because the patient preparation was reviewed and the patient had consumed a lot of carbohydrates, we reviewed the preparation again with the patient and he returned for another FDG acquisition, another FDG study after a more extended high-fat, low-carbohydrate diet to 72 hours, which we sometimes do. And we emphasize the importance of not exercising for 24 hours also before the cardiac PET. And here are his images. And now I think we can maybe appreciate a different perfusion defect, maybe infralaterally as we move up towards the mid left ventricle. And here we again see it in color. And there is some, as we move towards the base, we see some FDG uptake in the septum at the base of the left ventricle and a little bit in the infralateral portion of the left ventricle as well. So we can see this again in color, infralateral perfusion defect with associated FDG uptake and then mid to basal and triceptal defect with FDG uptake. And so here are the salient portions of the report. We mentioned the satisfactory metabolic preparation now and then code these abnormalities. And there's, as you can see, compared to the prior PET study there's now greater myocardial suppression and there's more focal FDG uptake. And we can also better appreciate the infralateral perfusion defect. And there's findings that are compatible with cardiac sarcoidosis with active inflammation. So with a presentation and the PET findings, a patient was treated with immunosuppressive therapy and has significant improvement in his symptoms and follow-up cardiac PET also showed complete resolution of the FDG uptake. So I think the take-home points from this case are that even with the best preparation protocols, at least 10% of the cases may have inadequate myocardial suppression and physiologic myocardial FDG uptake. The physiologic uptake may be diffuse or it could sometimes be focal. So last case, case six is a 46 year old man with biopsy proven pulmonary sarcoidosis diagnosed four years before seeing us. And he now has atypical chest symptoms, occasional palpitations, and presyncope with prolonged standing. Echo was entirely normal and ECT showed sinus bradycardia. He was referred for a cardiac sarcoid PET study and he followed the diet and I already performed the quality control and we're going straight to the reconstructed images. So on these images, we don't appreciate any perfusion abnormalities at all but there does appear to be FDG uptake in probably the entire lateral wall but it's milder or less intense towards the apex. But as we move towards the base, it's quite intense and you can appreciate that in color. In the vertical long axis, horizontal long axis, we can see how intense the FDG uptake is at the base of the lateral wall. And we can also see this in short axis as we move towards the base and we do not see an associated perfusion abnormality. The papillary muscles appear to be involved in varying degrees. And again, in color, basal lateral wall FDG uptake without any definite perfusion abnormalities. The maximum SUV in the myocardium was 3.8 and in the blood pool was 1.9 giving a ratio of two. So what do we do now? I'm not sure the gated data showed much in the way of abnormalities, EF was 55% and I don't think there was any convincing wall motion abnormalities, especially not laterally. So when we see isolated basal lateral wall FDG uptake without any other findings at all whatsoever, we often think that this is a nonspecific finding. But in this case, this uptake also involved the mid lateral wall and to some extent the apical lateral wall. So in the report, we hedged a bit and said that this could be nonspecific but we couldn't entirely exclude lateral wall inflammation. And we did put in a one segment of blue or turquoise that suggests that the inflammation could be more focal. And this helped the clinician because the clinician will perform extended cardiac monitoring based on these findings to see whether the patient has any additional arrhythmias and we'll bring the patient back sooner for more testing and probably a repeat cardiac PET to see where things are at that point. So our findings look very similar to the highlighted row here. And the interpretation here is that it could be early disease or a normal variant, especially a normal variant if we don't see anything else at all, no perfusion abnormalities, no MRI findings that might suggest cardiac sarcoidosis, no wall motion abnormalities, echo is completely normal. And so this case highlights an important take-home point about FTG uptake, which is that FTG is taken up by any metabolically active tissue, which includes normal myocardium. So it's physiologic uptake, inflammation as in inflammatory cardiomyopathies, cardiac sarcoidosis, infection, hibernating myocardium, cancer, other. And so interpretation of the FTG PET images really requires meticulous and comprehensive review of the history and all of the available data, as well as the metabolic preparation and other imaging findings. So I think I will leave you with that last take-home point and thank you very much for your attention. And this concludes my presentation. Thank you.

cardiac sarcoid PET imaging

normal and abnormal PET images

false positive studies

appropriate report

PET imaging considerations

indications and applications

disease activity detection

interpretation of PET images

treatment response evaluation