Dr. Manik Veer describes cardiac PET advantages for delivering a higher diagnostic accuracy than alternative tests, changing patient management, and providing quantitative, functional data that guides optimal treatment decisions.
So, first of all, thank you for joining me on a Friday morning. It's 7:00 a.m. and I really appreciate everybody who showed up because um it's an undertaking. So, thank you so much. Um, we're gonna talk about stress perfusion, viability, and sarcoidosis imaging using PET scan today. These are the three tests that the initial rollout is going to be offering. And each of them is very specific and there's a very uh important reason why we decided to offer these three tests first. I've kept this simple, uh, in the sense that I'm not gonna be talking too much about the tracer in detail, nor am I gonna be talking much about the. Techniques involved in image acquisition or things like that. I'm going to try to keep it very focused on the clinical relevance of the test. Uh, but if anybody needs details regarding, uh, image acquisition, radiation, and things like that, please don't hesitate to reach out because that's a separate conversation. So why did we build a cardiac PET program? I think everybody who works with cardiology knows that. Our patients benefit from accuracy and high sensitivity and specificity. What do those three words inherently mean? Well, accuracy is, uh, ability to reproduce the results of a test. How many times am I gonna get one test and it's gonna give me the same results? Sensitivity is how, how much of a disease are we able to pick up, meaning how many positives can we get during a test. Specificity is how many of those positives are truly positive, whereas compared to a test that may be positive but may be a false positive. A very anecdotal example I use in the clinic frequently is. If we start testing a cohort of um penguins in Antarctica with a new HIV test and 80% of them come back positive. Well, the test may be accurate because it's going to be right every single time. It's going to be true every single time, but it's not really sensitive or specific because it's just wrong. So what we need is a test that identifies the right results in the right patient with reproducibility. So cardiac PET is a very, very good tool. It's 90% accuracy. It's one of the best noninvasive perfusion tests. The radiation doses are pretty low or comparable to specks, and it's a one visit test. We can break it up into two visits, but most of the time we're using one visit. The image quality is superior because we have true attenuation correction. The quantificate, there's a qualitative part to it, as well as a quantitative part to it. Um, the quantitative part identifies myocardial blood flow reserve, and then FDG metabolic uh imaging activity can unlock another piece of the equation, uh, which is the viability and inflammation. So let's get right down to it. We have 3 different studies, and we have 3 different questions, and each deserves its own answer. First is stress perfusion testing. Um, in stress perfusion, we're very well aware that we can do multiple different modalities for stress. We have stress spect, we have stress echo, we have, um, exercise treadmill stress. So, there's different kinds of, uh, stress modalities. Um, along with that, uh, we have to choose the right test for the right patient. Then there's the viability component for which we currently commonly use, um, MRI, which is a great test, uh, one of the gold standards, but it has its limitation. And for sarcoidosis, currently we're using MRI. So, uh, once again, all of us who've ordered sarcoid or viability assessments know there is, uh, limitations to what the MRI scanner can do. In my opinion, there are none, but practically speaking, there definitely are. So, let's get down to it. So, why did we need this and what's the benefit of having a PET scanner versus doing it the other way? So how does a PET stress work? First of all, there's um many, many radio tracers that we can use out there. There's rubidium, then there's fluperidise, there's ammonia tracers, there's other research tracers. So why did Sanctura choose fluperidise and why did we decide to go with it? Well, the good thing about Fluperid as is, is that, first of all, it's one of the newest ones. Um, secondly, it has a very long half-life. Rubidium itself has a very short half-life, which ranges to within minutes. So, you can really do a lot of things that we want to do with the stress testing. Effectively, treadmill tests would be out of the question with a Rubidium scan, whereas treadmill testing is appropriate and possible with the use of fluperidas or Flecardio. So that's one of the strongest benefits of using the tracer that we're doing. So, um, Uh, the protocols are pretty similar to the SPECT. We give an injection for rest. We give an injection for stress. Uh, after we give rigadenosin, uh, at maximal hyperemia, we go ahead and, um, um, check for perfusion imaging and we compare rest versus stress to determine whether there's any, Stress induced perfusion defects. So we compare stress images to rest images and find out if there's a qualitative difference between um uh stress perfusion versus rest perfusion. And if stress perfusion looks worse, then our um Stress test was positive for ischemia. Um, this, uh, Flecao has the sharpest perfusion images in nuclear cardiology. Um, there's no site generator or cyclotron needed. That means, um, uh, the doses can be brought over by messenger pigeons, uh, from various sites. Currently, we, our site of, uh, requesting the doses is about 4 hours away. So I think we're looking at feasibility of this. Another great thing about this is that these kind of stress tests are safe with left bundle branch block patients, paced rhythms, inability to exercise, and Unlike MRI, we have, we have significant artifact from ICDs, these will be, um, OK to do, great to do in patients who have ICDs because there just won't be those device related artifacts that we see with MRI. So it's a great test. Who should get a pet instead of a speck? So now that we have a better test, does that mean that everybody should get a speck or everybody should get a pet or nobody should get a speck? Um, should we just, um, put a lock on the speck scanner and say down for business? Well, the answer is no, because there's only so many, um, pets that we can do every day, and there's a role for each of these, and the most important thing is patient selection. So let's, who is an ideal patient for a SPECT? So an ideal patient for a SECT is somebody who's skinny, can hold their breath, has ischemia or uh uh a scar from before, um, is able to exercise and uh can lay on the scanner very still for about 20 to 30 minutes because um those are the patients who get the best images. Who's a candidate who's really good for a PET stress? A patient who has a higher BMI. Because we won't have to increase the radiation dose when we have suspected multi-vessel or balanced ischemia, when we suspect microvascular disease, and we'll get into a little bit into that, who has had prior equivocal or artifact laden SPECT, uh, meaning, um, you have a lady who's who has large, uh, and dense anterior, uh, chest wall tissue. And you don't know, does she have, uh, LAD perfusion defect or does she just have attenuation artifact? The spec couldn't answer that question. Um, she's ineligible for other testing, so, In those patients, a PET would be very, very appropriate. Uh, patients who have known CAD, uh, and you want to assess for ischemia burden for revascularization versus medical therapy. And basically, anyone you would send for a SPECT, whom you think, uh, by prior, um, evaluations, has had an, uh, inconclusive SPECT or a poor quality SPECT would benefit from a PET stress test. And so that covers a little bit about stress perfusion. I'm going to pause here. Does anybody have any questions so far? OK. One of my mentors used to say quickly move on before someone can ask questions. So, I'm going to do that, OK? Um, So the patient prep, caffeine is the enemy. Now, caffeine is, uh, there's a lot of uh information and misinformation about caffeine. So when is caffeine the enemy and when is it OK? So for most testing, caffeine is the enemy when we are going to do a vasodilatory test. So every time you plan on using rigadenosine or adenosine for hyperemia or stress induction, caffeine is the enemy, and they should effectively hold caffeine for 24 hours. I know. A lot of people say I only drank decaf. Well, please put the decaf out the window as well for those 24 hours. Chocolate is a very big one. Doc, I had a headache. I didn't drink any coffee. I had two small pieces of Hershey's Kisses. Well, unfortunately, that also counts. Energy drinks, sodas, everything, please put it away for 24 hours, because if we don't get a good vasodilatory response, then the test is just going to be bad in the sense we're not really stressing the patient. So you're getting two resting perfusion images instead of a rest and a stress. Um Exercise studies, which are possible with Flucardo, are really good. However, once again, it's the same situation of, um, treadmill exercise. If patients are ineligible for a treadmill echo, a treadmill spec, then they won't be able to do a treadmill PET because the protocols don't really change from a treadmill standpoint. Uh, diabetics need to hold their rapid acting insulin. We'll go a little bit more into that. Um, and rigadenosin cautions just as before, uh, with your typical spect, uh, active bronchospasm, severe asthma, prior, um, uh, side effects from rigadenosin, systolic BP low or AV, uh, complete heart block without presence of a pacemaker. Those are regular protocol, um, um, Uh, contraindications also apply to our PET stress perfusion imaging. OK? So what is this? Now, this is another number that we are going to be reporting in the, uh, stress protocol. And what is myocardial flow reserve? Myocardial flow reserve is basically a measurement of the difference between absolute flow of blood in the myocardium or the heart at rest and stress. The, Ratio is a powerful risk number, and effectively, this is where most of our testing, even in the cath lab or FFR IFR, uh, the FAME trials, this was the gold standard. This is where it all began. So, for myocardial flow reserve, basically what we do is after inducing hyperemia with a stress agent, we calculate the amount of contrast getting into the myocardium and we, uh, assess how much got in at rest and we calculate a ratio. If the ratio is less than 1.5, that means the myocardial flow reserve was, Low and there's something going on like ischemia or multi-vessel disease, microvascular disease, 1.5 to 2 we interpret with perfusion images, and more than 2 is normal. So why does it matter? How many of us have had those patients, those young women or older diabetics who come in, they complain of chest pain, we do a cath or we do a Coronary CTA and we look at it and we're like, hm, there's 20%, 30% lumpy bumpies all over, but it doesn't really explain why they're having chest pain. In those patients is basically where myocardial flow assessment comes into play because. One thing we have to remember is that the coronary tree is very, very complex. I very commonly liken it to three large rivers with a lot of tributaries feeding the forest. So when we look for epicardial stenosis, we're basically flying a helicopter along the main river, but we're not really looking at the small twigs or branches that are supplying the forest on each side of the river. With myocardial flow reserve, what we can do is, since we are testing at the muscular level or, uh, flow at the muscle, we are also not only able to test, uh, those main epicardial branches, but also those small tributaries and micro vessels at the same time. So, if you have normal epicardial arteries, which would be your LAD, left main, RCA or circumflex, But you have a low myocardial flow reserve. That could just imply that the patient has microvascular disease. Now, does it change management? I don't think even Doctor Alamard could stent a micro vessel. Like, I'm just going out on a limb here. I don't think he has the tools. So, we just don't have the tools to deal with very, very small vessels. And that's OK. Because sometimes giving the patient, And answer is much more important than being able to say that, hey, I can fix this. Yes, if we could fix everything, that would be great. But if you do diagnose microvascular disease, number one, your patient has an answer. Number two, you can start them on antianginal therapy. And number 3, if it's, there is also an indication for transplant in patients who have persistent angina, despite maximum medical therapy, who can't be stented or who can't be revascularized. So it really can change management and the trajectory of patients. So this is a really, really good test and in answering a lot of questions for our patients. So foundation for studies 2 and 3 is FDG. This is fluorodeoxyglucose. Now, that's a mouthful, OK? It's just a fancy way of saying we've taken some glucose, attached some isotopes to it, and effectively we want to assess where the glucose goes and where it doesn't go. So, the two viability and sarcoidosis, they're basically the opposite ends of the same spectrum. In one, we want to make the heart eat glucose so that we can assess, are those myocytes alive? Are they able to metabolize? Are they lighting up when we give this, um, uh, Fluorinated glucose. In sarcoidosis, we don't want to actively assess the metabolic function of the myocytes. We want to assess the metabolic function of the granulomas. So what we want to do is force the granulomas to take The glucose up and suppress the glucose uptake in the heart. So in both cases we are meddling around with the glucose uptake of the heart, but for a different purpose and a different function. So for viability, there will be a glucose and insulin load. For sarcoidosis, basically eat everything that's yummy, but really unhealthy for coronary artery disease. Bacon, eggs, fatty stuff. Don't eat carbs for, 24 to 48 hours, so where. Now, the guidelines are a little separate in how long uh the fat diet should go. Japanese studies uh say that the longer the better. For Americans, it's very tough uh to go that long without loading up on carbs because, hey, Coca-Cola is really yummy. So, For our patients, 24 to 48 hours in the US, Japanese who are very, very well adherent to instructions, they can go 48 to 72 hours. But nonetheless, the better the diet prep, the better the testing results. The principle is the same. One is make the heart eat glucose. The other is make the heart eat fat and burn fat. OK. Any questions so far? OK, either I've really confused everyone or I'm really good, so I'm just gonna assume I'm good. I'm gonna move on. So FDG in viability, scar or hibernating muscle. So what we want to do is look at the two for mismatch. What does mismatch mean? So match means there's scar and it's metabolically inactive, meaning there's a matched defect. You don't see FDG in that area, you don't see, you don't see perfusion in that area, meaning there's reduced perfusion, reduced metabolic activity, that means it's scar, it's dead tissue. Hibernating myocardium is basically, you will see a little bit of FDG activity and, but the perfusion is reduced as compared to the rest of the heart. So there's a mismatch pattern. That means the muscle is alive, metabolizing glucose and it just needs a blood flow supply to come back to life. In the scar, revascularization won't help. Uh, in hibernating muscle, the revascularization will probably help. Um, so who do we refer for viability and when do we refer, how do we prep? Cardio, I think all of us do this very well, right? Like we have all these patients in the heart hospital, pre-bypass, uh, pre-PCI, complex PCI, low EF. I think we do a very good job. And, uh, uh, we know who to refer for viability. It's just the glucose loading that we need to be cognizant of and the stress lab will help you along with this, how to prepare them for this, OK? Uh, sarcoidosis, why PET? So, cardiac involvement occurs in up to 25% of patients and can be the first manifestation. Inflammatory cells, Are very glucose hungry. So there's active granulomas, um, I think if I remember pathology right, it was non-caseating granulomas, but don't quote me on that, um, are very, very hungry for glucose and they take up glucose very actively. So PET is the test for detecting active inflammation, active glucose uptake, and the only practical way to track response to immunosuppressants, Over serial scans. Cardiac MRI is also a great tool because it can show scar, it can show edema, but it can't really separate burned out disease. So the two tests are basically complementary. Some centers, and this is really expensive way of doing it, but some centers also do PET plus MRI on the same day. So, um, those, uh, those, that would be like 200%, uh, proof for sarcoid testing. I doubt we're going to roll that out here, but just, uh, putting it out there. That's something that happens in some centers as well. Plus, you can do a whole body FDG imaging, um, The benefit is that. As you've probably observed, and a lot of EP uh uh team members know this, when patients have sarcoid, a lot of them get ICDs. And by the time they have ICDs and you send them to us for MRI, my report is probably gonna say there's an anterior uh Anterior septum, anterior lateral, and anterior wall. Uh, defect secondary to the ICD and, um, Enhancement images cannot be interpreted in this region. Presence or absence of scar noted in the basal to mid inferior, inferior lateral or inferior septal segments. And that's just because of where the ICD sits and how it sits. Now, those issues are very easily circumvented by the use of PET because the ICDs don't cause an artifact because we are inherently imaging two different things. In MRI, we're inherently imaging the, uh, we, um, Tissue changes the, Properties of magnetism. Over here, we're directly giving a, a tracer that affects perfusion. So, we're imaging two different things. So, that's why we don't get those artifacts that we get with MRI and PET, uh, testing. But effectively, the prep makes or breaks the study. So like I said, all the yummy stuff, eggs, bacon, sausage, steak, chicken, fish, cheese. And, um, uh, once again, no caffeine. Strictly avoid any carbs. Bread, pasta, rice, fruit juice, milk, yogurt, gums, mints, cough drops. The cough drops and the mints and whatnot, those are usual culprit that just goes unnoticed, but you really have to be very, very carb shy for about 24 to 48 hours. So, who to refer, uh, uh, and what the patterns mean. So, uh, so patients are basically with unexplained, uh, AV block, young patients, unexplained VT, patients who have extra cardiac sarcoid, um, noted on, uh, CT scans, uh, bilateral, like hilar lymphadenopathy, Or prior diagnosis of sarcoid, so uh we can have normal perfusion and no FDG, meaning the study is normal. We can have focal FDG uptake plus minus normal perfusion defect, plus minus perfusion defect. So if there's FDG uptake, that means there's active inflammation. If perfusion is normal, that means that tissue is not scarred yet. Treat escalate. If there is FDG but absent perfusion. That means it's actively inflamed, may have a scar, but still, because of the active inflammation, we treat and we escalate. There's a perfusion defect and no FDG, that means there's a scar in that region, and that's probably that. Now, someone may come and ask, hm, how do you know if this is sarcoid or something else? We really won't, because if you think about it, an absent perfusion and no FDG is also noted in viability. When it's scar tissue. So those patterns are going to be similar, just that in this, it's going to be in a non-coronary artery distribution, whereas in, uh, uh, in a viability case, when you have a perfusion defect and no FDG, it's going to be in a coronary artery, uh, distribution. So, if something like this comes up and there's a confusion, hey, was this a scar from CAD or sarcoid, reach out to us and we'd be more than happy to have a look and um uh guide forward therapies. So, where does uh MRI versus PET come in? What's the uh what's the um comparison and how does it differ? So, Because we have flucardo, we can do an exercise PET stress. Uh, however, for MRI there's no such option. We have to do a vasodilatory perfusion scan. We can do a dobutamine scan, but over here we're currently doing adenosine or rigadenosine. Um, both of them have a very high spatial resolution. MRI has no radiation. MRI adds function, scar, and anatomy in one exam. PET on the other hand, adds myocardial blood flow reserve. Uh, it's very good in high BMI patients, patients who have devices like ICDs or CRTs and patients who are claustrophobic. So talk to your patient, get to know them and figure out. Um, these issues and it will help guide you along the tree of which test would be the most appropriate. Should I do a stress spec? Should I do a stress echo? Should I do a stress PET? Should I do a stress MRI? So, it really depends on what you're looking at. Let's take a couple of cases just anecdotally, OK? Uh, 38-year-old patient comes in, non-diabetic, fairly healthy his whole life, comes in, suddenly has chest pain. You go to the ER and they have mildly elevated troponins, no real ECG changes. You do a coronary CTA because the probability is low. Um, the coronary, uh, CTA is clean, clean epicardial arteries, no anomalies. So, in this situation, What's the suspicion and which test are we going to offer? The highest suspicion in this patient is going to be, uh, myocarditis or pericarditis. So, even though we have clean coronaries, we could also have something like microvascular disease or something else, especially if there were risk factors like smoking or, uh, hyperlipidemia. So in this young patient who has no epicardial disease but has chest pain and mildly elevated troponin, I would prefer doing an MRI because it would help me understand if there's any myocarditis involvement, any pericarditis involvement, or whether, um, It's microvascular disease. Let's take another case. Uh, you have a 73 year old patient who has prior PCI. Um, somebody did a SPECT stress test somewhere. Everything lit up. Everything is, uh, normal on the SPECT, uh, meaning the myocardium shows good perfusion everywhere. They didn't report any infarcts on the specks, but the patient keeps having, uh, chest pain and you're just not sure what's going on. In that patient, a stress PET would be appropriate. Uh, it can be exercise or pharmacological because not only can we get absolute myocardial blood flow, um, we can also get better perfusion data as well as we can assess viability at some point as well. So I hope those two cases highlight the case utility of one versus the other. Uh, both of them are really good for viability assessment. Sarcoidosis assessment, um, In MRI, we're able to see edema plus enhancement. And that shows us if a patient has edema and enhancement, probably active sarcoid, only enhancement, once again, maybe quiet sarcoid or burnt out sarcoid. Um, PET shows us active inflammation, it's the tool for serial treatment monitoring. You can also do whole body surveys with PET. So 5 ways for a PET study gets ruined. Uh, one is, oh, doc, I fasted for 36 hours, but I had to have my coffee at 5 a.m. because I needed to wake up. Well, that's a bummer. I ate an energy bar on the way or drive to the hospital because I was fasting and really hungry. Insulin just before the sarcoid scan, uncontrolled sugar at viability, or vague or, uh, missing details. This is completely on us. We can definitely fix this and prevent any of this from happening. If there's any confusion in what order to place, please just call us and we'd be more than happy to help. Uh, one slide, uh, cheat sheet. Pet stress ischemia, how much viability, scar or hibernating, sarcoidosis, active inflammation or no. Um, for pet stress, fluperidide exercise regadenosin, viability rest perfusion plus FDG, uh, sarcoidosis perfusion plus FDG, Key prep, uh, for pet stress, no caffeine, NPO 4 to 6 hours, viability fast, then glucose load, and sarcoidosis, really high fat. Uh, pet stress, obese patients, equivocal spec, prior known CAD, prior multiple PCI, uh, evaluations, uh, viability, we know this, uh, sarcoidosis, clinical suspicion of sarcoid on the basis of symptoms, um, and basically things to look at, look out for, um, FDG, viability, and myocardial flow reserve. Basically, all of you. are the gatekeepers in cardiology. Without any of you, our clinical practice would suffer and We really want this program to be a success, and all of you are going to be the gatekeepers, not only from a standpoint of ordering the right test, but also helping the patients prep appropriately, answering their questions and making Making sure that um they show up appropriately prepared mentally as well as metabolically. So you guys are going to be the stars of success of this program, and I cannot stress how important the role of the whole team is in all of this. So that's the end of my slides. Does anybody have any questions?
BROADCASTMED