 Okay, so far as far as I can see, we actually just have one question from the live chat and this is from Sanjay Shankar, and I'm sorry if I hope I'm saying a question correctly. Question is, how can you figure out the vague, not so clear cut screening test like MGUS when you do the live gene assay? Sorry, no worries. So how can you figure out the vague, not so clear cut screening test? The example they gave is the monoclonal gamopathy of unclear significance. When you do the live gene assay? So we are coming actually on the second phase for that. We only supposed to receive patients where they have negative, negative update. We don't even supposed to get to our to our nuclear medicine practice anyone that has any positive. So this is the first step of the guideline set. I believe the data shows that because there is overlapping between TTR and AL, predominantly the AL, but you have some subpopulation that will have the TTR, that will definitely going to decrease the sensitivity. But the PYP goal, and that is something that I don't think is well spoken. The PYP goal is to skip essentially the biopsy. You don't need the biopsy if you are going through the criteria that I mentioned. Everything else that is outside of those three criteria, negative monoclonal, basically positive, grade two, grade three, and now we adding to that the quantitation should go through a different chain of work up. So this is much before us and that would be probably discussed when Heman will give the talk and then we can discuss the monoclonal. Yeah, I think that as a clinical cardiologist when you have the suspicion of monoclonal hematopathy, you are leading automatically down the hematology side. And then the question there is really working with hematology where they are comfortable navigating that hematopathy and saying yes, no. And do we have enough information here that we are going to do anything? Now by definition, if it's muggus, you are generally going to be watching that patient. Now that does not exclude ATTR. So you still may need to have an evaluation in that regard because you can have, as we have already seen with our presenters, that you can have coexistent problems and coexistent pathology. So then you really have to go back and say look, everything fits for amyloid. Muggus may not explain it and I will defer again to hematology for the final word on that one in the afternoon. But you still have to pay attention to that and this still could be ATTR and again approach it as I don't yet have my answer and we are really not off the hook. If you got an infiltrative cardiopathy appearance on ECHO, you got restricted filling patterns, you got a pericardial effusion, you got all of those other things, you owe it to your patient to pay more attention and not just say, well, it's muggus. We're okay. We'll just take care of it from now. I think I totally agree. One does not exclude the other. I think they can be present concomitantly. So I think we just need to be aware of that. So yeah. Yeah, thank you. Good reminder for the person who asked this question, Sanjay Shankar. We do have a speaker on workup of monoclonal comopathy later in the next panel. Stay tuned. I would like to add one more thing to that. As we saw in one of the cases here, even someone that not related to the muggus, that comes with a negative, complete negative workup and then the bone scan was negative. Again, it's not off the hook because it may be so early that we just don't know that it's there or the deposit didn't even start. So again, I used to call it the new zebra because the newer I'm coming from the oncology as well, so the newer endocrine, I like the elephant in the room because if there are too many clinical areas, it doesn't mean that at some point that bone scan will become positive. So again, it's all about the amount of damage that was done to the myocardium for the calcium to aggregate enough to attract the PYP. So that's sort of the mechanism of action. Do we have any questions from or comments from the? Amyloid is to send a carpal tunnel. How is it related to like, does the amyloid plague deposits in the carpal tunnel or? He finally separated them. Amyloid deposits the costs for the carpal tunnel. Yes. Yes. Yeah. So the amyloid can be deposited in so many different organs, right? So when somebody has, say, a hypothyroid and then they have carpal tunnel syndrome, you want to attribute that carpal tunnel, perhaps, is associated with hypothyroidism. And now your carpal tunnel and you also have somebody who has her failure with preserved ejection traction and they are hospitalized and then you start asking the question, oh, is there something else that I'm missing out here? Is the deposition, you know, inside the nerve neurovascular bundle and the nerve trappings around the bones for the carpal tunnel where the median nerve is going through, whether there is deposition of amyloid in those areas and whether that is the cause of the heart failure as well. How is it related? So I think you need to be just open-minded about thinking that this is carpal tunnel can be isolated and may not be related to anything else at all, even the absence of, you know, hypothyroid or, you know, any other, you know, conditions that can cause carpal tunnel syndrome. But when you have confluence of something else, suddenly, you know, the light bulb goes on and you ask the question, oh, could this be? Could this be? Is the question that you need to be? So that's why we are here because early detection, because it is, you know, clear-cut evidence that you start them on therapy where Julie Rosenthal will talk about that there is opportunity to actually quickly, you know, change the trajectory of the disease and, you know, the prognosis is actually changed. So that's why thinking about it is very important. Thanks to the panel for a good way to start the morning. Eric Stelly from Mayo Clinic. So Chris, you said in your talk that, you know, that epiphany occurs and you make the diagnosis, but as I go on, you know, epiphanies get farther and farther apart. And so, you know, perhaps the imaging folks could give us an idea of how do we push the report or the information out from the lab to the clinician because, like I said, you know, we go through our busy days and we pray for an epiphany, but often it's just patient after patient after patient. So tell me a little more about how you guys would institute a mechanism to spark that. Yeah, great, Eric, great to see you. Thank you for being here. Great question, right? So the minute you start thinking about it and then you say, okay, I want to do some more testing and then you already have the echo and that's where some of the red flags are coming up in your mind. And then now you do the PYP because in your system, the, you know, in our system, the radiologists, we actually put the whole protocol together for them. And so we are one-on-one directly, my nurse practitioner directly is constantly asking, when is the PYP scan? When is it done? And right on that day that it's done, you know, can we quickly connect with that radiologist to give me a call back, give her a call back, or whichever it is. And then now you have the results quickly. I totally agree with you that we need to translate that information quickly to, you know, all of the folks that are involved with that patient's care, including PCP, and then the therapeutic strategy needs to be initiated if it is positive, right? So even if it's negative, we've got to be asking the question of if it's negative, you know, we need to be thinking something else is going on, if the patient truly has, is symptomatic. So we can't just say, oh, it's negatives, it's not I'm allowed, you know, I'm out of the picture, I'm not going to do anything more because the patient is still having symptoms and struggling. So again, patients first, to your point, yeah, we need to be a little bit more proactive clearly. So, Eric, how about this? How about the echo reports have the risk score on them? So we had it calculated. And then the clinician, you say, well, if they have hypertension, please add one point to this score. And this is the sensitivity and specificity associated with this score. This was done with the suggesting beta blockers in patients who had a low ejection fraction that was found to increase beta blocker prescription rate. So I don't know if we could do that as kind of a clinical decision support. What do you think? Well, I think all of this starts actually with our sonographers. So really what it comes down to is that you really do need to have a very solid echo lab. And that begins with your sonographers first and foremost, and maintaining very high quality standards. And without that, we're lost because, again, garbage in, garbage out. If your baseline data that comes into the care of that patient is not accurate, we go down lots of different pathways. Measurement issues with regard to just simple septal thickness, posterior wall thickness, do we actually define concentric LVH well? That's critical. And it's a stupid, simple thing that we've been talking about since we started doing M mode for that matter. So with that being said, having accuracy and fidelity in that measurement is critically important. Along with that, having the ability to do appropriate diastology and making sure that those measurements that we have are accurate and that we really can define, is this a restrictive pattern in any way, shape, or form? Those things are critical. Now, a trivial or small pericardial effusion, yes, being mindful and not just blowing it off, those are simple things that we can do that we need to do. Now, as far as the reporting aspect is concerned, we get into trouble. And where we get into trouble is that a lot of our screening tools, and we talk about the risk scores, if you're 80 years old with any LVH, you're high risk for amyloid, period, by echo criteria. And that's not incredibly specific. It may be sensitive as all get out, but our specificity there really tends to fall off. So we do need to be mindful of that because I get into my world of, oh, gee whiz, everybody can have amyloid. And you start getting into the structural realm and you start talking about TAVR patients. Again, we know that they have a high prevalence. Now, the question is, what are we going to do about it? Okay, so you talk about TAVR patients, they have LVH, they have at least some degree of diastolic dysfunction, they've got conduction problems, and conduction problems occur independently of anything else. You talk about a right bundle, we worry about that all the time. What do we do about it? We get EP involved. We want them to put a pacemaker in before we put a TAVR in so that we don't have to keep them any longer. That tends to be the mindset. Now, when we talk about amyloid, let's go back a little bit. When we got into doing structural heart, and I'll talk about my other world just a tiny bit here, we ended up getting into a multidisciplinary, multi-specialty beast. Now, we have to have that same model for amyloid. On the structural side, we have interventionalists, we have cardiac surgeons, we have imagers, we have radiology, and we have anesthesia. For amyloid, we still have largely the same team, but really, we don't have anesthesia in this one, but we have hematology. We have to build a very similar multi-specialty team. This has to be something that is actually taken into account for all of our systems, and not just, well, you're at Mayo Clinic, so you get to do this, and that's great, but it has to be everywhere else because Mayo can't take care of everybody, and our patients are going to multiple areas. Oh, his bandwidth, he's got more business than he wants. Trust me. But that being said, we have to have these multi-disciplinary, multi-specialty teams as a part of our regular conversation, and being able to take care of patients that way. Like I said, structural heart, we've done that, and we do a fair job. We're certainly not there, but at least we have models now, which we didn't have a decade ago, so I think this is very hopeful for all of us. I would like to add one thing, so I'll put the head of the co-chair of the outreach of the outreach committee at the Society of Nuclear Medicine as a sort of what we do. As the imager is one of the biggest problems, and it's not, you know, not only for cardiac amyloidosis, it's everything we do. We come up with so many new tracers, and how do we tell you guys how to correctly use it? And I think your question is really looking at sort of the entire picture, because if everyone here has something that is very good at what it does, but how do we collect that? So one of the things of the Society of Nuclear Medicine, you can all just click ATTR amyloidosis, you'll find being it. That's for patients. So we also got an educational grant from Pfizer to be able to do something like that. Those kind of events are the one that going to bring us into a full practice. Because yes, even if they wanted to take care of everybody, they can't because of also region areas, right? Different population, different geographic. So if we take from the cardiology world what we do for cardiac amyloidosis, there are clinics for that. So maybe less of prevalence with amyloid, again, because I don't think we really know the extent of that disease at this point. But getting in each hospital, help administrators, and that's how we do it from the Society. We help administrators teach the physician, and it's not, you know, it doesn't need to be only oncology, only cardiology, I apologize. They go to see their PCP, and that's what you said. They do not make the connection. I always like to tell the story of a girl that had headaches, and then they gave her ibuprofen, and then she didn't see anything. So they gave her glasses, and then she lost her period. But nobody sent her to a neurologist to look at the P231. So that's exactly the same concept. So we have to educate the primary physician, because it's over the line that we'll see them first. And then in each hospital, even we will see one person a week, we can still call it amyloid clinic. And that's what attract people, because they go to the place where the coffee machine is pretty. So if they see amyloid clinic, they don't care what's going on inside. And that's the key of outreach, and that's what we do. We're making sure the patient is aware. Where is it? Where is searchable? And it's not out there for amyloid. So that's sort of my advice from the upper side of it. Hi, I'm Matt Moore from Columbia. So I wanted to just follow up on Eric's excellent comment, which he always has. And at our center, one of our junior faculty discovered that at the end of an echo report, when individuals who are reading the echo actually write suspect amyloid, the diagnosis is five to seven times more commonly made by providers than when I guess it's not written. So the other thing I just wanted to applaud you guys have been at, you know, hundreds of amyloid programs. But I think this is very forward-looking. The rationale here is very clear. The drugs that we have to treat amyloid prevent new deposits. We're not sure they extract. They're markedly more effective when given earlier. And, you know, there's no doubt that what we want to do is try to identify people as early as possible. Just to highlight one other thing with colleagues at the Cleveland Clinic recently is that 83% of patients with wild type amyloid have an orthopedic manifestation. So it's nearly universal. So everyone in clinic needs to ask when they're seeing anyone who's elderly with the phenotypes we talked about about carpal tunnel syndrome, lumbar spinal stenosis, and any joint replacement, hip, knee, or shoulder. Collectively, like I said, 83% of patients are going to have one of those findings and heightened suspicion is the key. If you don't put amyloid on your differential, you're never going to make the diagnosis. I think that's an excellent point. And the one thing that I failed to mention in, again, echo reporting is with structured reporting having the ability to say, you know, features consistent with infiltrative cardiomyopathy slash amyloid. And that is a common summary statement that we have and we use. We've not tracked that as far as outcomes, but it is something that we routinely do. The biggest challenge that you get, I think, in community practice is that for the most part, you don't have a dedicated group of echocardiographers that are actually reading. So this is an all comers event. So whether you're an interventionalist or noninvasive or an echo guy, you're still reading your own echoes. And so it does create a great deal of heterogeneity, particularly in community practices. And I don't know that we're going to get away from that, except for ongoing educational events, getting people to at least go to grant rounds, conferences like this, and then hopefully maintaining some degree of heightened awareness. But it is, it's a major challenge because, you know, echoes are still a big part of the general cardiologists' livelihood. So we're not changing that anytime too soon. Absolutely. Great point, Matt. And the other thing that many times happens in the echo is that we diagnose hypertrophic cardiomyopathy mistakenly. And so when we see, especially for the echo technicians who are all in the audience, when you see something that's suspicious, it looks like LVH, maybe there is a symmetric septal hypertrophy a little bit more. And you assume, maybe there is a hoax, maybe it's just LVH. But make sure that you do valsalva on every one of those patients to make sure that is it truly hypertrophic? Is there a gradient that significantly increases with valsalva? And if it isn't, then question is, oh, could this be amyloid? So it should be always thinking about that. I come from the world of geriatrics and cardiology as well as medical education. And I agree that vast majority of these patients are seen on the primary care level, but you have a captive audience who doesn't have time necessarily to go to grant rounds of that. But in the state of Arizona, to renew your license, you're required to take a certain quiz every two years on basically the opioid crisis in this country. And that's critical that you take that and pass that before you get re-licensed. Why don't we have an initiative to have at least some basic training about amyloid? Because I think the problem is huge. And having spent the last 15 years in medical education getting these people at the fellowship level in geriatrics and being a cardiologist and a geriatrician myself, they don't know much about amyloid. I mean, it's like, oh, that's really weird. Thank you, Dr. Seymour. But I think that that's a golden opportunity. They have to do this to recertify, get their license again. And even if it's only, if you don't make it your licensure, depending on this, at least have them respond to a CMA program and a quiz. And then you'll have an idea of how big the problem of recognition at the level where most patients are. So thank you so much for our speakers and presenters. We appreciate you. You're now during our coffee break. Please come back at 10, 10. Thank you. Hold on, hold on, hold on, hold on. I'm sorry, one more thing. I forgot to call out to Chris DJ. He wanted to speak briefly about ACS. Thank you. Almost. So just before the break, I just want to kind of update you about something very important. This event is actually endorsed by the American College of Cardiology. And we are truly humbled and really honored to have had that opportunity. And April and the team have really worked hard on getting that together in the ACC, the Zerna chapter, especially with Liana Collins. I want to thank her, who's been the executive director for a number of years. And she made it happen. And so we have ACC endorsement. So I just want to kind of thank Dr. Sue Wilber. Sue is a current governor. We call them governor of Arizona chapter for ACC. There are 60 governors in the country. And we all are part of the Distinguished Committee of the Executive Board actually of ACC at the national level when you become a governor. And I was privileged to and humbled to have been the governor for ACC from 2009 through 2013. I can't believe it. Almost 10 years ago, I finished my tenure. I can't believe that. But it was such an incredible experience. And Wilber Sue, who's an electrophysiologist here at Banner, he's not able to come today. And he was going to say a few words about ACC. And they all can, can I talk about it together as one of the previous governors? And I just want to just briefly tell you about their purpose and what they do. So the purpose is to contribute to the prevention of cardiovascular disease and to ensure optimal quality of care for individuals with such diseases in carrying out this purpose. So the chapter functions in consultation with the leadership of the college at the national level as a source of advice to local and state government and professional organization concerning issues related to cardiovascular. The chapter in the interest of patients, physicians and the public in general maintains a high level of social consciousness and involvement with all of the social economic factors. You heard the term DE and I, the diversity, equity and inclusiveness is the buzzword. It's going all over the place with every society really picking up that tab and also giving access to the highest possible quality of cardiovascular healthcare. So they have core values of patient centered. Centeredness, teamwork, collaboration, again, is very, very apropos to our discussion with amyloidosis with teamwork and collaboration with all of the multi-marbid modality that we see with multiple specialties here. And of course the professional excellence. They do it through conferences and publications and newsletters and social media presence in Twitter, Facebook, lots of resources and the conversations in cardiology, quality outcomes, they do door to balloon, gap, H2H, images in cardiology and also the large registries, right? So one of the largest registries is going on is called the Pinnacle Registry. And I'm part of Pinnacle India on the Australian Committee, which is also part of the extrapolation of the Pinnacle in the U.S. And they got awarded for the FIT fellowship, in training for the local chakra and also for the best women in cardiology for a chapter in the country. So kudos to all of them. Thank you to ACC for endorsing. And again, thank you all for coming. And any questions you have about ACC, just reach out to me. And thanks to Liana Collins who has also done some phenomenal work. Again, thank you all for coming. Let's have a break and then we'll meet up and regroup again. Thank you.