All right, I'll kick it off. My name is Murad Fudim. I am a heart failure cardiologist at Duke University. I'm very excited to, you know, moderate this inaugural HFC heart failure seminar on device and heart failure. This is an extension of the annual scientific meeting, which was supposed to be preceded by the device and heart failure day, but the same title was supposed to be device and heart failure from mechanism to implementation. It was unfortunately canceled due to the hurricane, as you all well know, but stay tuned for a repeat at the upcoming annual scientific meeting in Minneapolis. Next slide, please. So our esteemed panel of speakers today will be in alphabetical order here. Dan Benzamone from Cone Health Medical Group here in North Carolina, neighbor, then Shelley Hall from Dallas. We have Lilu Klein from UCSF in California, and Andrew Sauer from MidAmerica Heart. So if you go to the next slide, we actually have the learning objectives that this is really the topics that we'll be discussing. We have about 15 minutes per talk, five minutes for Q&A. You can leave your questions in the chat. I'll try to direct them towards each speaker in five minutes after each talk. We'll kick it off by talking about the landscape will be done by Andrew Sauer and just give a broad overview where we're staying and where we're heading, what might be some challenges along the way. And again, the focus will always be around implementations, really less about introducing new toys and new devices, but more so how do you actually get them to practice because that's where it often lacks. Then we'll talk about the actual implementation of device-based strategies in the clinic. And Dan Benzamone has done second to none, has built a very big device-based clinic both in remote monitoring and in device-based solutions for treatment. And then Leroy Klein will talk about actually setting up a remote monitoring clinic specifically. He runs a very large remote monitoring clinic out in California and will share some tips and tricks. And then last but not least, Dr. Hall will kick it off or finish the actual seminar by talking about what's actually in the pipeline and what the clinical trials coming our way because in many cases, clinical trials is how we get in touch with device-based solutions these days. Next slide. This is an agenda. We'll just hop through it. Next slide again. This is, again, 50-minute talk, five-minute discussions. One more slide. This is when you registered in the HFSA Learning Center, you will be able to A, review the recording and B, actually get your credit, the CME credit. So please don't forget about that. And next slide. And we should be able to kick it off. Thank you very much. We're going to start off with Andrew Sauer. Thank you, Murat and my colleagues for inviting me and for the HFSA for inviting me. I'm going to share my screen and go to slide presentation mode. And I think I need to switch. All right. Let me know if this is not the correct view, but I think this is my title slide. So thanks again for having me. My goal is to really talk about the overview of devices in heart failure and really kind of hopefully encourage folks to think about this as a revolution to really change the status quo. Those are my disclosures. I serve on a number of steering committees related to heart failure and cardiometabolic therapies. So my presentation goal really is quite straightforward. I really am just trying to focus on how to convince you that devices really truly do deserve a place in the toolbox that we have for our patients suffering from heart failure. And that device-based therapy and device-based technology is truly not a zero-sum either-or, but it's truly complementary to our best medical therapies. And really just to hopefully get you excited about where this space is going. And you're going to hear a lot more detail about a lot of these devices that I'll provide teasers for in the subsequent presentations. So the status quo in heart failure, I would argue, is terrifying. I really am concerned about where the epidemic is going, and I think we all should be. When you think about the challenges that we have with access and disparities, this is only going to get worse as the burden of the epidemic grows and becomes more costly. And it's growing really quickly. And when we think about all these bricks-and-mortar challenges where we have with ER beds, hospital beds, and clinic visits, and many of our rural hospitals in particular are closing down and losing beds, this is really a major looming problem. The number one diagnosis for a Medicare beneficiary in the hospital today remains heart failure. And a CEO of any health system will tell you that a Medicare patient occupying a hospital bed is really a venture in, it's an economic challenge. In other words, hospitals really have a hard time covering the bills when Medicare patients take up large volumes of beds in the emergency department of the hospital. So we really need to think differently about how we're going to tackle this disease. And inertia is really a big problem. The number one reason why patients, this is really teased out by Larry Allen's data in EPIC and other cohorts, but the patient is stable. It remains today the most common reason why patients don't have heart failure therapies initiated or up titrated. Now there's a lot of contributors to inertia as I kind of outlined here. And a lot of these problems are real. And we don't have enough time in our clinics. There's a lot of apathy that's coming out of the burnout epidemic. Our formularies are not always updated. Our incentives are misaligned. We have to fight with prior authorization for Medicare Advantage, for example. Our patients are burdened financially. And there's a lot of polypharmacy. The disparities are very real, race, sex, economics, geography. I mentioned the rural challenge is something that's really important to me because that's one of the biggest disparities that we see is some of the disparities that we're seeing between rural and urban or academic and community hospitals. So the opportunity to build is really here. And I literally took those words and put it in chat GPT and this image spit out within 0.2 seconds. And I say that to just point out this is an exciting era that we're in, where open AI and AI is being applied to almost everything we do. Also to point out that if you look at the image, there's some imperfections that obviously would not be there if a human would be there. So there's a need for the human touch. But I do believe that technology is coming to hopefully make our jobs easier and create efficiencies and improve the quality of care. Program building has been really near and dear to my heart for a long time. When I left Boston for residency, I went to Chicago because of the LVAD revolution. I trained and kind of cut my teeth in advanced heart failure, particularly related to the growth and advent of the sort of rise of machines, whether that be a temporary or durable MCS, ECMO. All this was happening when I was in training in the Chicago years from 2010 to 2015 and on faculty there. But I left to come to Kansas and Kansas City because there was no transplant program, no LVAD program to serve the state of Kansas. And so Jimmy Hill here is our first HeartMate II patient, which was a HeartMate II because we weren't able to participate in Momentum because we were building a brand new program. And here you have the first 10 heart transplant patients who were done completely free of charge to them and completely covered by the hospital. They all remain alive today. And I say this because we learned a lot of lessons in program building in those years. Lessons like reducing variations in care and creating standards and checklists, recognizing that there's market opportunities when you talk to folks in the community, they're frustrated with the existing status quo and the other health systems. And so if you're a program builder and you like to build programs, you can learn what those opportunities are to step into those gaps, learning how to build brand, learning how to leverage social media to get attention for what you're doing in your region and to allow you to begin to get access to innovation through clinical trials and delivering high enrollments with good quality, and then recognizing that building teams to care for patients means taking care of those teams. You know, I want to be clear that as a disclaimer, that I'm not against GDMT. As people know, I talk about that often. So when we talk about devices, again, we talk about, we still need to champion good guideline directed medical therapies. In fact, I was fortunate to participate in the American Heart Association's Implement HF initiative and co-champion our city and Kansas City as one of the major regions. And we were able to take implementation of GDMT from 0 to 10% at discharge to over 60% for quadruple defect-free therapy, including SGLT2 inhibitor, beta blocker, MRA, and sacubitril valsartan. And for 30-day follow-up, which was a novel intervention on top of the Get With The Guidelines movement, we went from 0% quadruple therapy to 40% in all seven regions. We have a paper coming out about this soon. The problem is with medical therapies, there's still a lot of challenges and a lot left to be desired. You know, we say the patient is stable after we get them on this initiation stage and residual risk is high. This classic figure that Steve Green has featured in many papers and presentations. And I really like Jane Wilcox's article here talking about the various forms of reverse remodeling and sort of recovery that you can get. And really that the medical therapy and the device therapies can be truly complementary. And why aren't we talking about them as being complementary? Why is it medications versus devices? Why are we waiting for medications to be fully optimized before we think or talk about some of the device therapies that we have out there? In other constructs, we know that this is really not, people are not against being complementary. For example, potassium binders are becoming really important tools that we have to help improve our up titration of GDMT. We're under utilizing these in the US, especially compared to Europe. Our colleagues and our patients actually want more than just living longer and staying out of the hospital. And if you look at a lot of the therapies that we have offered for cardiovascular service lines today, septal reduction, cardiac myosin inhibitors, left atrial appendage ligation, PCI for angina, or even for hopes for improvement in reverse remodeling, atrial fibrillation, ablation, these are not considered so controversial by our colleagues, yet they don't have sort of the hard outcomes that we typically expect for heart failure therapies. Let's keep in mind that tricuspid edge to repair was baked into a wind ratio, which was predominantly driven by KCCQ improvements in a non-blinded fashion. Cardiac resynchronization therapy was originally focused on improving functional capacity in very sick patients. It wasn't until Made at CRT came along that we saw some hard outcomes. And even when we did after four years of follow-up in less symptomatic patients, we didn't really see the needle move much on survival. It was really driven by hospitalization reduction until we had longer follow-up. Our patients do care about quality of life, and when surveyed over and over again, patients will tell you they'll trade life expectancy for improvement in quality of life, and you can see patients are quite disabled by heart failure. The other thing we have to remember is patients are just more congested than we appreciate. In GUIDE-HF, patients came into the implant of CardioMEMS with mean PA pressures over 30, PA diastolic pressures over 20, and a lot of these patients were not that symptomatic. As you can see here, class 2 symptoms, KCCQ score is really not on the floor, 68 on average. So they weren't all that symptomatic, they weren't all that deranged in terms of what you would expect, yet they were very congested. And so we don't really do a great job, I would say, in the clinic or in the ER, or even in the hospital, really assessing and understanding the level of congestion our patients are living with. We have to be honest about medications. They aren't that great at improving symptoms. You know, Preserved-HF, just giving you one example, we were very involved with that here, obviously, that had a very high BMI cohort, the highest of all of the HF-PEF populations studied with SGLT2 inhibitors, and it had some of the most impactful improvements in health status measured by KCCQ and 6-minute walk. In fact, there's only been a few studies that have shown improvement in 6-minute walk with a heart flare therapy. But as you can see from this responder analysis, and I recognize responder analyses are getting some hate these days, but albeit, the reality is there's a number of patients that improve with SGLT2 inhibitors, but it's modest gains. You know, we're talking about a KCCQ of about five points, a 6-minute walk improvement of 15 meters. This is very modest, and there's a number of patients that don't respond and maybe just don't have a diminishment of response. When we look at device-based therapies, on the other hand, there's a long history of device-based therapies like CRT having significant impact on exercise capacity, on health status as measured here by Minnesota Living with Heart Flare, 6-minute walk, as well as improvements in NYJ class. And cardiac contractility modulation, for example, is a novel therapy that's emerging. You'll hear a little bit more about it later. Essentially, it's giving a 7-volt electricity during the absolute refractory period of essentially using a lead in the RV involving two leads, but it can potentially even be done with one, with some pretty dramatic improvements in walking distance and health status. And with some safety data from the FIX-HF5C study showing, at least from a safety standpoint, reduction in heart failure hospitalization and cardiovascular death, but it was underpowered to really be a true outcome study. We're seeing similar improvements in functional capacity and quality of life when we look at Barostim, which is really a technology designed to sort of trick the brain and the heart into basically doing the opposite of what it does in the pathophysiology maladaptive pattern. So it reduces sympathetic tone, increases sympathetic tone through stimulation of the baroreceptor signaling. And this has been shown to improve walking distance, reduce NYJ functional severity, as well as improving health status and walking distance. Disparities are important to us as well, and in GUIDE-HF, it was really interesting and kind of encouraging to see that if you look at this forest plot from the original paper, the patients with less symptoms, the patients who are preserved ejection fraction heart failure, women, black patients, they did at least as well and maybe even better, certainly no heterogeneity here. And so it's encouraging to see that populations that traditionally have struggled to do as well are actually doing as good or better. And perhaps we've argued some of this blinding to the patient has allowed us to reduce some of the implicit bias and treat patients based on their objective markers of disease rather than treating patients and having an implicit bias that sometimes sets in. Device technology really is giving us an opportunity to address problems. I mentioned the problem with congestion. You're going to hear about a lot of different technologies. Levy was very, very involved in presenting cardio sense data, for example. We have other seismic cardiography oriented technologies that can be used at the point of care. It can also be used potentially to detect and diagnose heart failure. This is a really interesting technology that was featured last year in Jack Heart Flare using seismic cardiography technology just baked into Android or iPhone like devices using the accelerometer based technology to be able to actually diagnose and detect incident heart failure progression. So I think that we need to start looking at how we can embrace these as opportunities to innovate and to help reduce care team burden and improve risk stratification and diagnostic technologies. You're going to hear about a number of emerging technologies. I think Shelly's going to talk about a number of these categorically. I just am featuring a couple here, but I think that there's a really exciting space that we can consider with left atrial to right atrial shunts. Also reverser modeling devices, also preload devices that are showing encouraging results. A lot of these technologies are showing us how we can reduce left-sided pressures or right-sided pressures without using medications, which of course, as Murad has taught us convincingly, pressure and volume are not the same. And so a lot of these patients, if you follow them, for example, after remote PA pressure monitoring technologies are implanted, whether that be a Cordella or a CardioMEMS device, they have a lot of refractory pressure elevation that we need to think about different ways to sort of decongest those patients without being dependent on loop diuretics, which have their own toxicities. Heart failure diagnostics today versus the future is really exciting to think about. We're going to start looking at IVC dimensions. We're going to be looking at technology that can simultaneously measure left atrial pressure and right atrial pressure, technology that allows us to have waveform detection, the ability to program technology after it's implanted to monitor the way we want to monitor, the ability to monitor with implantables during activity, during exercise, during sleep, being able to have the essentially going from just monitoring to true management and even turning it into closed loop patient self-management, I think is really where we're going to be in the not too distant future. We do have to work on how to make this better for systems and better for teams, increasing the ease of access. So the NCD for remote PA pressure monitoring, which applies to both CardioMEMS and Cordella technologies is actually very encouraging because we now can expect that there will be less fighting and prior authorizations with Medicare Advantage plans. And that's going to be really a potential game changer for being able to improve access for patients, integrating data into the EMR, automating workflows and also automating billing, I think is really about how we take care of the teams of people who take care of these patients. It's really a wide open space and you're going to hear from my colleagues about many more deeper dives into the emerging technology. But we've talked about remote monitoring, how that's really here and coming and growing. Electrophysiologic modulation, autonomic or neuromodulation technologies, structural inventions are really coming out everywhere you turn. Preload reduction devices, I just mentioned one or two, but you're going to hear about some more and respiratory modulation as well. And we shouldn't forget about the fact that we still have the durable LVAD and the temporary LVAD, which are devices that we already have and have had for many years. And as I mentioned, sort of how I got my start as a fellow. And the reality is there's a lot of opportunities to innovate remaining. We need to improve hemocompatibility. It was really encouraging to see Finn Gustafson take over as the global CMO for Abbott. I think he's been a champion of this and I think that we're going to continue to see work done there. We need to make these lower profile devices. We need to untether our patients from drive lines, which have a number of Achilles heels. Remote management needs to become part of the technology. And my friend Bill Cornwell did a great study showing how speed modulation during exercise, unfortunately, does not improve VO2 significantly or cardiac output. So we need to figure out ways to actually augment exercise capacity and cardiac output without depending on some rudimentary speed adjustments, which is probably not going to cut it. The careers of heart failure oriented specialists need to think outside of the traditional transplant MCS model. We've been talking about this fellowship spots are going unfilled. We don't have a lot of interest in going into advanced heart failure anymore. I think because a lot of our younger colleagues are focused so much on the transplant and LVAD part of the career. But there's so much opportunity that folks like Murat and Liviu and Shelly and I would tell you, you know, there is so much opportunity beyond transplant and MCS. And especially in the device based therapies, if you want to serve a leadership role, if you want to be a program builder, if you want to get into the intersection zones with EP and structural, so much opportunity. So in summary, devices are complimentary alternatives, not just alternatives to guideline directed medical therapy, device based therapies, for example, available technologies today like CCM and Barostim and others actually can improve quality of life probably and arguably better than we can see with guideline directed medical therapies. Devices help reduce residual risk, help improve reverse remodeling in complimentary fashion. Devices and device based therapies can improve access and address equity. And it's a great opportunity for career differentiation and innovation. So it's really never been more of an exciting time to participate in the revolution to really disrupt the status quo by embracing device and technology for our patients. So thank you again to the Heart Failure Society and to my colleagues for inviting me and thank you Murat for preparing some really gentle questions for me next. Thanks, Andrew. So let me fire off this question. There's no specific one in the group chat yet for you. But what do you see as the major barrier to people picking up the ropes and just running with starting device clinics? What do you see as the biggest problem with that? I mean, I really feel like it's intimidating. I think that's a big reason. I think there's just a propensity to just maintain the status quo. So if you have a mindset that you want to be kind of a perpetual disruptor in a constructive way, you know, talk to people who are doing that and they can help really make the experience less intimidating. Right. I mean, it was definitely intimidating to me going out into a state and building a brand new LVAD program. But this taught us, you know, that you can build a remote monitoring program. You can build other device. We do. I think we've done about 50 plus implants of CCM in Kansas City over the years. So I think it's like anything, entrepreneurism, for example, when you when you open up one kind of concept or one business, it's a lot easier to open up more. And so I think that you just have to kind of figure out how to make it less intimidating and realize that we do need disruption. And the status quo, as I've hopefully outlined, is really kind of terrifying and we shouldn't accept it. You know, Maria Rosa just posted, you know, that ABIM should call a specialty heart failure, not advanced heart failure transplant. So I agree. Some of that is actually nomenclature. Some of that is training. What would you say about training and how much training do or does the young generation get, you know, about the topics we're going to be discussing? yeah, I've been pretty vocal about that. I think that we really have to refocus how we think about training. I think there's a lot that's been written about that appropriately. I referenced a really great working group article that was assembled by HFSA. I think a lot of the ideas there are really solid. I think we need to think about how not everybody that wants to get into the heart failure space necessarily wants to or needs to be focused on transplant or durable LVAD. As I've pointed out, and as you pointed out, Murat, there's just so many other intersection zones that we can be getting excited about and getting involved with. So I think the training has to change at the general fellowship level, and a lot of people have talked about that. We need to have an earlier exposure to heart failure and intersection device spaces. And we also need to, I think, create pathways where people can get more specialized training in some of these niche zones without having to go down the transplant LVAD path. Not everybody needs to focus on that, but I know not everybody agrees, and it's a controversy right now, but we can't just stand back and watch this advanced heart failure transplant specialty continue to have ACGME spots that go increasingly unfilled, and that model is not going to work in the future. We obviously need to change. I agree with that. So thank you very much. We have time. We will transition to Dan Benzamon for his second talk. He will bring up the slides. And Andrew, stay with us for maybe later discussion, so we'll get you, okay? Thank you. Let's see if you can see these. Am I right? Yeah. Good. Can we see this? Dan, present them out. Great. I think they are. No, no, no. Yes, we see your comments. Oh, we see the next slide. Oh, can you? Let's see here. Let me. How about that? Disclosures? Can you see those slides? Yeah, I still see the next slide on top of it. Okay. Present them out. I am looking. I am. Here we go. All right. Good? Perfect. Good. Okay. Sorry about that. We're only how many years into telepresentations? Thanks, everybody, for having me. Marat, thanks for asking me to participate here. Certainly a tour de force by Dr. Sauer, really introducing the field and what the opportunities here are and what the challenges are. My task today is really to drill down a little bit on some of the devices used for management of patients with chronic heart failure and try to, how do we build these into our day-to-day program? So I'm going to spend a little bit of time, 10 or 15 minutes here, drilling down on some of the topics that Dr. Sauer already introduced. So here are my disclosures. I think this was well pointed out previously, right? We know that GDMT is really what our focus is on. And not only GDMT for people with systolic heart failure, but GDMT for people with diastolic heart failure now is really gaining momentum and really what we need to focus on. Unfortunately, we still have big gaps here and many patients are woefully undertreated. And we can see from our guidelines and our growing guidelines that through these therapies, we have a big opportunity to improve mortality and improve symptoms. If you look at patients who are no therapies and you get them on four-drug therapy in the setting of HFREF, we're talking a 70% relative risk reduction in mortality and heart failure, heart endpoints. But a lot of these patients, as was referred to before, there's still a lot of residual risk, right? If you look at the event rates in the treatment arms of these studies, especially in the most recent SGLT2 studies where patients are on quadruple therapy, we still see significant residual risk when you look at cardiovascular death and hospitalization, as well as these patients also tend to have a significant symptom burden. So what we look for is how can we do better for our patients? How can we say, look, you've maximized your drug therapy. You're not yet ready for advanced therapies, VAD, transplant, and other things. Can we do more for you? And how do we do that? And that's where I think the intersection of thinking about these devices for these patients who you've been very aggressive with their drug therapy, you've got them to where you think you can get them on maximally tolerated drug therapy, but yet you're still worried about the patient. You're still having symptoms. What do you do? So I'll drill down a little bit on some of the specifics. We'll focus on three devices here, starting with CRT. I think one of the things with all of these therapies is that they require partnerships, right? With drug therapy and GDMT, we can do these a lot in our heart failure clinics. We use our pharmacists, we use our nurse practitioners, and we get people on good guideline directed medical therapy. When it comes to device therapies, it's really important that you identify partners, whether it be an EP or in the case of some of these therapies, vascular surgeons who have been a big part of our program and bringing them into the program. And it's really been our experience, particularly with our vascular surgeon here, who's really been taking a part of the heart failure program and has really enjoyed seeing these patients and participating in improving their outcomes. So I'll start with CRT. I think we're all very familiar with resynchronization therapy in patients with systolic heart failure and ejection fraction at 35% or less and a left bundle branch block, right? There's clear evidence that when you resynchronize these patients, not only do you improve their mortality, you also improve their symptoms. So I think there's a very nice algorithm. I suspect most people are familiar with this in this space, where these devices for resynchronization fit into this patient population. But once again, we're thinking mainly about people who are class EF less than 35%, class two and class three symptoms with a wide QRS, and the patients who have a high degree heart block and have low EF and have the need for chronic pacing. You don't want to set these people up for RV pacing. You want to make sure that they're biventricular paced, so they don't develop an RV pacing cardiomyopathy. So I think we're all familiar with CRT. It's well built into our algorithms for these patient populations. And most clinics, I think, are up and running with this. I want to talk now about a couple of new devices, or newer devices, I should say, that Dr. Sauer mentioned upon. And when I think about these devices, I think about these devices as filling the gap between medications and VADs and advanced therapies, right? Either prolonging the time course for people to get to advanced therapies, or using them for people who are not candidates for advanced therapies. One thing I do want to emphasize here, these are not a replacement for advanced therapies, right? If somebody's truly end-stage heart failure, class four symptoms, these devices aren't indicated in that patient population. What you need to think about is my patient is progressing, they have progressive symptoms or residual symptoms, but it's, as I tell our trainees here, you're not pulling people back over the cliff. You want to prevent them before they get to the cliff. So I think, you know, if you think about the gap in heart failure therapies, you know, we have our stage B heart failure things where people are asymptomatic and they have asymptomatic LV dysfunction, and then we get stage C where they're symptomatic or titrating medications, which we know can often be a progressive course of their heart failure, and then obviously a class four and stage D heart failure. So as patients are progressing through their stage, their symptomatic stage three heart failure, we get them on the meds and they still have symptoms, what can you do? And so there's GDMT optimization, followed by device therapy. So focus a little bit on Barostim here, Barostim is, as was pointed out before, is a neuromodulation therapy. It, you know, as patients develop heart failure, they often get signals from the brain, which actually make the heart failure symptoms worse, they increase sympathetic tone, decrease parasympathetic tone, and patients often end up with worsening heart failure symptoms. So this is a way in order, in essence, to fool the brain and to change that signaling pattern and create impulses where we get a system where there's less sympathetic tone, more parasympathetic tone, and reduced heart failure symptoms. You know, it's much like reducing afterload, where you get increased afterload to preserve blood pressure hemodynamically, this is sort of the electrical or neuroequivalent of that. The implant does require partnership with a vascular surgeon to implant the device around the carotid artery where the Barostim reflex, in a sense, goes. And so there needs to be some partnership here. If you look at the, so if you look at the outcomes, some of these outcomes were already presented, very promising outcomes in this patient population. So the current indication is for patients who have an ejection fraction of 35 percent or less, NYH class 2 who are recently class 3 or NYHA class 3, despite treatment with GDMT and an NT-proBNP of less than 1,600. So you can see with regards to biomarkers, significant reduction in N-terminal proBNP levels, followed by significant improvement in functional capacity and exercise capacity. So you see in this patient population a 60-meter improvement in six-minute walk distance, 14-point reduction in the Minnesota Living with Heart Failure questionnaire, and a significant improvement in heart failure class. And I think I was just pointing out earlier, this is really important stuff to our heart failure patients, right? This can be the difference often of being independent or having to rely on someone else to do a lot of their ADLs, right? And if you look at NYHA class, you see almost 15 percent of these patients improved to NYHA classes from baseline, and none of these patients actually got worse. We've been very aggressive about implanting this device in our clinic. And really, two-thirds, one-half to two-thirds of the patients come back and say, wow, this has really changed my ability to do what I need to do. And these were patients who are already maximized on guideline-directed therapy, and we're still struggling to get them to a point where they felt better. So a very important addition to our therapy for that patient population. Switching now to CCM, or cardiac contractility modulation, we have the device here. As pointed out earlier, this is a seven-volt signal. Usually it comes through two electrodes through a pulse generator that's usually implanted on the right side of the chest, much like a pacemaker with a pacemaker pocket, and delivers electrical signals to the RV septum. Typically, patients receive five hours of therapy a day in one-hour intervals. And it does a couple of things here. So you get additional calcium secretion, but there seems to be two or three mechanisms at work. So you get improvement of calcium handling within the myocyte. You get remodeling the ventricular myocardium. And there's some evidence also to see normalization of abnormal gene expression that can be seen in heart failure. So you get some immediate effects over time from improved calcium handling, and you get longer-term biological and genetic effects through changes in gene expression. If you see initial data, as was pointed out earlier, you see improved functional capacity. And I'll show you in the last slide where some registries now are showing potentially improvements in harder outcomes. So if you look at the landmark trials comparing CRT and CCM, you can see significant improvements in multiple parameters, whereas CRT being the gray, CCM being with a reduced ejection fraction being the light green, and CCM with ejection fraction 35% to 40% being the dark green. And I think that's one of the important differentiators here. So the indication is for patients with heart failure class III symptoms. But the EF is a little broader. There's an opportunity to enroll patients or implant patients with an ejection fraction of 25% to 45%. So if you have a patient who has an EF of 40%, they may not be a candidate for other therapies such as barostim. You now have a therapy that can treat a broader range of patients with significant benefits. So once again, significant improvements in peak VO2, significant reductions in Minnesota living with heart failure questionnaires, 25-meter improvement overall in six-minute walk where you can see in the patients with a higher ejection fraction of 57-meter improvement in six-minute walk and significant improvements in NYHA class. So a very robust therapy and growing. If you look at some of the European registry data, we're looking at heart failure hospitalizations here you see significant reductions, at least a trend of significant reductions in heart failure hospitalizations. And interestingly, those reductions were similar in patients who are in normal sinus rhythm as well as patients who had atrial fibrillation. So significant improvements on top of GDM, GDMT. So I'll stop there. I'll wind it up there. Murad, I'll turn it back over to you. If there's any questions about therapy and how we implement this in the clinic, I'm happy to discuss that. Well, I'll ask the same question as I asked Andrew. What do you see as the biggest barriers in clinical practice to scale that up with you just presented, the actual sort of hardcore device clinic? Yeah, I just think, you know, as heart failure docs, we just can't talk to a patient and run up to the lab and put the device in for our patient, right? I think you really need buy-in and someone at your center who's not only willing to do the implant, but also to think about, is this patient the appropriate patient for the device and to sit with the patient and explain to the patient how the procedure goes and really have buy-in. And in both cases, we have one vascular surgeon who has really bought into this as part of what he sees as his workflow and really likes to be part of it and comes to the heart failure meetings. And, you know, we have five EP docs here and in particular, one person has really taken an interest in the heart failure devices as well and has really become part of the heart failure clinic. So when a patient needs adjustment in their therapies and we want them to perhaps adjust their therapies, giving them a little bit more stimulation, it's really helpful to have someone who's bought into the program from EP and vascular surgeons. So developing that buy-in was the biggest challenge for us to get this done. So it sounds to me, just to repeat what you say, is you really need champions and you need to identify champions, maybe across silos before you, you know, jump into this, because if there's no champion, I like GDMT where everybody tends to be a champion, you know, this is a little bit more specialized, it appears. Right. I think, you know, if you, if someone should say, hey, I'll put the device in, but you take it from here, that's not the person you want, right? You want someone who's really willing to think about it, troubleshoot it and say, you know, sometimes it's not the right patient and say, well, listen, I don't think this is really going to, this is difficult, the anatomy is not going to work, but really you need a champion. And I would also add, you need a champion and a partner to help do this. Okay. Any, you know, any other barriers you see? So, I mean, having a champion, what else do you anticipate as barriers for newcomers? You know, I think part of it is people just don't think about it, right? I think the second part is, you know, we, there's all this talk about GDMT and what we have to do with GDMT and it's top of mind and you spend a lot of time in your visit thinking about that and you have a 10 or 15 minute visit thing and you say, okay, you forget that we have something else to offer a patient. Instead of jumping from medicines to a VAD workout, workup, you forget that there's something else in between that. So I think the second challenge is to build it in your mind, your algorithm that there are now devices that are coming through that can actually make patients feel better and maybe stall this process of getting to advanced therapy. So I think the second part, if I say any barrier, is kind of rewiring our brains to think about filling this gap with these devices and learning more about these devices. So you know, from a personal experience, the way things run in our institution is that if you do have a champion, we often then are the sole proponent of that intervention, whether it's a remote monitoring tool, a device treatment tool, and then often it doesn't spread beyond that because it stays with the champions. So how do we actually train, educate our partners and trainees to think about this, even though they might not be the champions? What has been your strategy? Because you've done it quite successfully. Right. I think there's two parts to that, though. I think someone should own it. I think someone should understand it. Someone should own it. Someone should really get behind it and really do the groundwork to make your system be able to have the technology there. Someone has to sort of build the program. And then one of the nice things in our clinic is when you share these patients, you know, we have four heart failure docs here, when we share these patients and I see my partners, you know, I probably do more Baristim than CCM. He probably does more CCM than Baristim. To see how we select patients and which patients benefit from which device, I think it's helpful to work together and talk about it. And then quite frankly, you know, in our monthly meetings, we talk about what we're doing, new therapies coming through, and really talking about it. So I think functioning as a group and talking about what you're doing to benefit your patients and move the program forward, I think we have a responsibility to bring not only our partners, but our MPs and our PAs and fellows and residents along with that thinking as well. So it lies on us to educate our team. Okay, so again, people can post questions that they have, but I have another one. So I think the number one question I get when I talk about these devices, when do I think about it's time to refer? So now you can give a probably 20-minute talk about when or recite the FDA cutoffs. But, you know, in your clinical practice, when do you want your partners, your APPs to send patients? I don't think it's that difficult. It just has to be top of mind, right? You have a patient in front of you, you've maximized GDMT, and they're still saying, you know, I'm struggling, you know, with symptoms. I'm class three, and it says all over the place, I'm class three, and I'm struggling. And you're sort of at the end of the road, and maybe you do a cardiopulmonary exercise test, and it's too early for VAD and transplant. And now you say, well, you have two choices. One is to say, well, you know, kind of live with it, maybe go to cardiac rehab and start trying to feel better, which is an important thing. But I think that's the time when you say to yourself, yeah, let's think about referring you or having a discussion with one of our implanters. So I think it's easy. I think it's patients who have persistent NYHA3 symptoms or maybe two to three symptoms who are maximized on therapy and looking to feel better. Yeah, you know, it's interesting that Andrew is making actually a comment about KCCQ embedded into clinic notes as a trigger for you to think, oh, the patient's actually telling me they're quite sick. And not insignificant amount of patients. Just today, a patient that I talked to self-referred himself for one of those two device therapies you just noted. There's about a third of patients that self-refer for these type of therapies. They think ahead of it, ahead of doctors in many cases, self-refer to institutions. Actually quite interesting development. You see that as well? Oh, now I see it, but it's almost embarrassing, right? When a patient comes and says, here, what about this device? And then you put it in, they feel better. And they're like, I'm glad I told you about that device. Right? I think patients, smart patients are going to outpace us. So I think, you know, it's really important that this be just built into our algorithm of patients with refractory symptoms and thinking about where it lands. Andrew, it looks like you have something, you have a comment on that. I'd love to hear your thoughts. Well, yeah, I think that, you know, I want to give a lot of credit to our intersection team. So EP and structural, they actually were the first to come up with the idea that, you know, we should really embed KCCQ into our pre-implant spaces. Because, you know, I mentioned this as another example, you know, tricuspid edge-to-edge repair is really a symptomatic improvement intervention. Right? So if you have a patient with severe TR, for example, but has a KCCQ of 85, it's a pretty strong argument. You're not helping that patient as much as you think you are by making that patient go through a procedure. Now, obviously, there's a lot more evidence generation. But I do think that when you're looking at a KCCQ and you look at the patient, sometimes how the patient looks is not as bad as they actually feel. And so I think we're not the best judge, as I said earlier, of congestion. We're not the best judge of a patient's quality of life. So measuring it with a validated, a psychometrically validated tool like the KCCQ I think is a great way to pick up on patients who might benefit. How often will you do those routinely in clinic? You know, one of the things is, you know, we see, you know, an average clinic day, we probably see 18 to 24 patients here. And it's hard to get the KCCQ. We're building it in like a vital sign. So it's done before we see the patient. And it's not 100%. It's a brand new rollout. But we started doing that in the last year, and it's been really helpful for a lot of these technologies, devices, even medical therapies where we're saying the goal is to make them feel better. I mean, I mentioned earlier cardiac myosin inhibitors, you know, really are functional improvement, health status improvement interventions. So we should be thinking about this a lot more than I think we are historically doing. Great, good points. I appreciate everybody's time. Let's move on to Levi Klein from UCSF to talk about how to set up a remote monitoring clinic. Thanks, Dan. Thank you. Thanks, Marat, and let me pull up my slides. So talking about the other devices, which are really for monitoring, start my disclosures. We used to think of, or we are still thinking of remote monitoring technology as technology to prevent readmissions. And that's really just, you know, not the right way to think about that. We know that in a heart failure patient, the course of disease is progressive. We know about these decompensations where something happens, patients end up in the hospital, and every time they get out, they're really not going back to the same state as they were before. Unfortunately, we only meet these patients here. A lot of the heart failure specialists don't get involved in patient care in many places, both outpatient and inpatient setting. The patients are cared for in telemedicine physicians or general cardiologists, and we don't get involved. Usually we get involved when the patient is decompensated, oftentimes several times, several hospitalizations before we get involved. And really our goal should be to get involved earlier, to try to get the patients earlier, because I think we need to not only prevent the hospitalization, but we really need to stabilize the disease trajectory. And we can do that with medical therapy, device therapy. And I would argue that remote monitoring is probably the perfect tool to actually do that, to really catch these patients early and stabilize their disease trajectory. Unfortunately, as it has been alluded several times, we treat patients because they are congested, right? And we treat patients who have clinical congestion. We're always used to tell our patients, watch your signs and symptoms. If you gain weight or leg swelling, or become short of breath, call us, tell us your blood pressure, tell us your weight. And by the time they provide this information to us, it's too late, and a lot of these patients decompensate, end up in the hospital. We've been trained for decades to treat the clinical congestion, but now we actually have devices that can help identify the hemodynamic congestion, the subclinical congestion. A lot of these devices, again, can be used for long-term monitoring. So we have sort of bystander products from the cardiac implantable devices, CRTs, ICDs, that can provide different features, neurohemodynamic features, that can tell us about the patient status. We have wearable devices, some that are approved, some in development, that tell us about autonomic adaptation and congestion. And then we have implantable hemodynamic sensors that tell us about hemodynamic congestion. The more proximal you go in the disease process, you can get better data and much earlier data to prevent the disease from progressing. So how do you set up a remote monitoring clinic? And this is really meant to be a sort of practical approach and some approach that we took at our site. When I think about remote monitoring, really I think about four different features. One, it has to be a comprehensive approach. You cannot just say that for patients who decompensate or patients who have recently discharged because your hospital wants to prevent readmission. You really need to think about all patients and also not just HF-REF patients, but also HF-REF patients. You really have to have a dynamic, differential approach or monitoring. Someone that's stable, there's one way to monitor those patients with a different goal, titrate medical therapy, ensure that they are getting the optimal medical and device therapy versus patients who are high risk or post-discharge patients, right? Those are in need of more comprehensive and more acute monitoring. But really the goal of the program should be to integrate your device monitoring clinic into a HF-REF program strategy to optimize patients on their best medical and device therapy. It has to be intentional. It cannot just start with whatever device you have and see what you do and how to add things. You really have to plan this before you start. You know, what device I'm gonna use? Am I gonna use three, four, five different devices? Am I gonna use a single device? You know, are we gonna use that for all patients or are we gonna use some devices for unstable high-risk patients, some devices for stable patients? And more importantly, once you get these devices and you start getting data, how do you systematically manage the data? How do you interrogate it? How do you use it? What treatments do you apply for this data? You have to have appropriate resources in clinic. Who's gonna get the data? Are you gonna be your medical assistants? You have a device stack. You have different companies that provide, you know, aggregators that provide this data to your system. Are you gonna integrate them into your EHR or are you gonna go to five, six different websites to get the data? You have nurses. Do you have APPs? Who does what? You know, oftentimes I've seen people doing the same work and you really should have a very clear workflow so people don't duplicate. Try to establish automated protocols, right? If you have your nurses calling you or texting you or MyCharting you for every single patient on how to change medical therapy, you're quickly gonna put an end to that remote monitoring program because you just don't have the time to be responding to all these questions all the time. And of course, it has to be financially viable. You have to, you know, make sure that you're getting reimbursed and your clinic gets reimbursed for all the activities that you perform. Otherwise, you're not gonna be able to be in business for too long. And very importantly, we're not really taught very well as physicians. You really need to go to the hospitals and to insurance companies and try to argue with them to actually get financial incentives because you're making their life better economically. So some of that wealth should be start up on you as a physician or a clinic to be able to function. So as I mentioned, you know, you really have to think about having comprehensive approach, all your patients and try to get the patients to do maximum medical therapy. I think it's really important because you can get this data to help titrate GDMT and not only titrate GDMT because some people will argue, well, I'm gonna titrate my GDMT regardless of what the data says, but you use the data to make sure that you're not, you know, preventing GDMT titration because you think the blood pressure is too low or maybe, you know, the heart rate is too low or the patient is doing well. Integrate your KCQ, as Andrew mentioned, integrate it into your remote monitoring strategies. We actually built, we use Epic, so we build a KCQ-12 questionnaire in Epic that we can push through MyChart to our patients. Usually they do it every clinic visit. If we see a patient every three or four months, they do it every clinic visit, but we can push it more often if we need to. So then we have a numeric data point where we can see if the patient is doing better or getting better on GDMT. And as Dan has mentioned, once you titrate somebody on GDMT, how do you know if they're still symptomatic? You can have some objective data from the KCQ. You know, we use a lot of labs, you know, for our patients, chem panels, anti-probe BMP, and so forth. Right now they have to go to Quest or LabCorp or different labs. There are actually patches in development that will measure transcutaneously potassium reacting in anti-probe BMP. So in the future, you can have an app at home with a patch that can tell your patients your potassium level. And again, you can titrate your ARNIs or your MRAs without having to delay that. You know, if you have a patient and you know you've maximized their therapy, their KCQ is still low, those are the patients, and you don't have to wait for the next clinic visit. Those are the patients where you think about the device therapy that can improve their quality of life. Of course, we have, you know, CRT for patients who have conduction delays. We have a mitral tear for patients with mitral regurgitation. But there's a lot of patients that are still symptomatic that don't have significant MR or left bundle branch block. So those patients should be thought about getting devices, as I call them, devices for quality of life, right? So Varisteam, CCM, and possibly in the future, Shuntz. So those devices can be identified, again, but based on your monitoring for your patients. You have a lot of patients who have reduced ejection fraction, who have CRT device or ICD devices. We're fortunate to have all this wealth of bystander heart failure data. And there are now several products that have different scores that one can use, a triage HF, the HeartLogic, the CoreView. So those are very useful to predict the compensation, but you can also use them to titrate cardiomedical therapy in stable patients. And of course, you have the implantable monitoring devices, Cardiomedicine Cordella. We can really do an enhanced hemodynamic management. We've shown in ProActive, for instance, in Cordella and ProActive, that adding vital signs to PA pressure management leads to further decrease in hospitalization. And we had probably about half of hospitalization rate compared to guide HF in the ProActive study. And to answer Dr. Costanzo's question about patient self-management, we're launching ProActive 2, where we have one group of Class III heart failure patients that will be randomized to self-management versus clinical management. So we will hopefully show that self-management is simple, patients can do it, and it's safe. So that will allow us to integrate algorithms to allow patients to self-manage. We did it in the laptop trial a decade ago, and we actually had very good results. Unfortunately, it never went anywhere because the product didn't go anywhere. Hopefully, we'll be able to show that with ProActive 2 that we can do this for our patients. And it's really important to have a differential approach or monitoring based on the patient needs. Someone that's completely stable, again, using the Type III GMT, someone that's been recently discharged, maybe use another technology. For instance, you have wearable technology such as the Zoll heart failure management, where you can use in a post-discharge setting that has been shown in the BMAP trial to decrease subsequent hospitalizations within 90 days of discharge. So maybe temporarily for some patients, you need to use that. You really have to have an intentional setup of your clinic to really devise to have a strategy, which device or monitoring strategy will you use for which type of patients. Very simple, blood pressure, weights, and symptoms, KCQ are very easy, relatively inexpensive to implement. They're not really good to predict the compensations as we've seen for many, many trials. However, you can use them to titrate medical therapy. And it's really easy to set up. Very easy ability to integrate in EHR. Either you can use from the devices, and I gave a couple of examples, like Amron or Cardio, that a lot of patients are using and buying them online. And all those have apps that can be installed, and then you can get data from FHIR integrated into your EMR. Or you can use an aggregator like Acellis or ActiCare, Best Buy Health, and so forth, to get this data for you. They'll charge you a fee, but get this data for you from your patients. And again, with HLA-7 integration into your EHR. You have the data from implantable devices, you know, 3-HHF from Metronin, for instance, gives you a score in either low, medium, or high, which is the patient's risk of hospitalization in the subsequent 30 days. And it's composed of seven different parameters, depending on atrial fibrillation burden, CRT percent pacing, ventricular tachycardia, activity level, thoracic impedance, nighttime ventricular rate, and heart rate variability. And then you get this risk, and you can get a sense of, you know, does this patient need immediate intervention to prevent an event? You also have data from HeartLogic, where, you know, you have a multitude of parameters, S1, S3, respiration, nighttime heart rate activity, where you can get a score, a score over 16 correlates with a hospitalization. So again, this is very helpful to titrate in the immediate period where the score rises, to titrate medications in asymptomatic patients to prevent a hospitalization. We actually showed in MENA-JHF that this is really powerful, and titrating in asymptomatic patients leads to a hospitalization decrease, and it's safe with really no adverse events in these patients. So we can use this strategy for patients who have a rising level. Of course, implanted with humanoid monitors, with cardiomyosin and cordella, you get PA pressure waveforms, and you can titrate to improve the PA pressure. Again, not just for decompensation, but we know now that long-term exposure to high PA pressure is associated with increased mortality and morbidity. Mike Zile has published in the journal, really superb papers looking at this patient population, and we've seen, you know, from data from cardiomyosin data, for instance, that a two millimeter change in PA pressure over six months can mean a 40% change in mortality. So really, really important to try to keep these PA pressures, you know, as low as possible, the area under the curve as low as possible. A lot of us probably are involved in the TMHF study where the hypothesis is that if you have a HF-REF patient who has a sustained PA pressure over 30, despite optimal medical therapy, maybe that patient is defined as an advanced heart failure patient, and we'll do a trial to see if implanting a Harmony-3 L-VAD in that patient will actually lead to improved quality of life and improved survival compared to just general medical, continued medical management. So it'll be very interesting over the next five years to see where this goes. Now, as I said, for patients post-discharge, maybe you do need to use a wearable device, the Heart Failure System Monitor from Zolforyst that gives you this data, and you can use it for a short period of time to decrease the immediate risk of hospitalization. And there's many, many devices, and I borrowed this slide from Ben. Thank you, Ben, for the slide. And you can see all these devices, and new devices coming out every day, you know, with technologies that can help us monitor patients. But very important, once you have this strategy, you really have to set up a systematic management based on data. You can't just have data coming through, and then everybody gets flooded, everybody gets frustrated, and, you know, they don't want to see data anymore. You really have to figure out what data to look at. Are you going to look at arrhythmias, which oftentimes can decompensate patients? How can you get data on patient medication compliance or dietary changes that may have influenced some of these findings? And you really need to empower your nurses to really act on the data rather than asking a physician all the time. What we've done, we've sat down with our nurses and pharmacy committees, and we came up with protocols that were approved by our hospital nursing committee and pharmacy committee, where nurses can actually drive these medication changes based on pre-specified criteria. So if you have a high peer pressure or heart logic increase, for instance, or even an increase during certain parameters, they are prescribing, you know, increasing amounts of diuretics, you know, let's say three days doubling your loop diuretics, checking a chemistry panel afterwards. If the signal has not returned to normal, they are allowed to add a thiazide diuretic, and again, in another three days, check for changes. And all this is done without the physicians or the APP to be involved. Then if things don't go according to the plan, then they will involve the APP and then the physician. So again, an escalation, stepwise escalation, so everybody can practice on top of their license. We also have nurses-driven protocol for GDMT. We don't wait for clinic-type GDMT. We do complete asynchronous titration of GDMT, and we get our patients within, you know, three to four months to be maximal tolerated dose. You can also, you know, use the signal from your more milder antiviruses to push GDMT again, if you have a good blood pressure, for instance, and to deescalate diuretics, if you have a thoracic impedance that's increasing, or if you have a S3 that's decreasing, for instance, or if you have a weight that's decreasing. So you can use the data to empower your nurses to do the titration. You really have to make sure that you have the appropriate resources, right? Who gets the data, right? Do you have a medical assistant? Do you have a device that gets the data? Do you have outside vendors that feed the data into your system and integrate it with your EHR? That's how you reduce personnel time. That's how you reduce, you know, waste. It's really integrated data. And then use device features, for instance. You know, cardamoms, you can ping the patients from the Merlin to tell them that they are not compliant and they forgot to send their data or automatically downloads from devices. And who are the treating providers, right? You have nurses, you have NPs, you have MDs. Really, everyone should treat the patients based on protocols, and then everybody should really practice on top of their license. So how many FTs do you need? Well, it depends. You don't need that many if you use technology. In our clinic, we have 1,600 heart failure patients. We have three nurses and two nurse practitioners managing all these patients because we use technology to make life easier. And what we found that 80% of the patients are actually stable. They only need GDMT titration. And we use, again, technology to break the inertia. And the nurses and NPs spend less time per patient. And we have about 20% of patients who are unstable and need a lot of titration. When we actually did a time study, we saw that, you know, 80% of the patients take about 15 minutes a month, you know, for nurses to spend with them. The 20% take about 75 to 80 minutes. However, these patients used to be in the ER or hospice all the time. So now we shifted that cost from the out-inpatient center to the outpatient world. And we're minimizing, you know, patient admissions. And please document everything that you're doing because everything is billable. And then if it's billable, you get reimbursed. That's how you get your money to pay for your FTE. So you have to feel financially viable. And there's many, many things you can, you know, you can do. You can set up codes for monitoring data, for retrieving data, and for chronic care management because what we do, it's really chronic care management. And if you do it appropriately, you can charge anywhere between $150 to $400 per patient per month for the work that you're doing. And that actually pays, again, for your nurse's salary, pays for your APPs, pays for the IT to be able to implement this data. And then you go back to the hospital and you point out that they're actually making money for them so they should, you know, financially help your clinic out as well because you're decreasing their readmissions, you're decreasing bed utilization. As Andrew pointed out, any heart failure admission, it's a chronic mind loss for the hospital. So you're making money, you know, you're saving hospital money so they should actually, you know, help you out. They can hire APPs, right? They can hire the staff. They can pay for devices. They can, you know, give your physician bonuses. And then you go back to the insurance companies and they negotiate better rates, Medicare Advantage or private insurances. And, you know, when you do that, again, all that makes the program financially viable. So I'm going to end up here. But in conclusion, you know, I think it's really important when you start a remote monitoring clinic to plan before you start. Really have a comprehensive approach to break the heart failure treatment inertia, both, you know, devices and medications. And it's really important to be intentional when you set it up rather than just, you know, build it as you go and kind of shooting from the hip. Use technology. I cannot emphasize this enough. Use technology because it saves you time and money and frustrations. And plan appropriately for your resources. You know, planning steps, like how many patients can you take? I'm going to take everybody with a year less than 20, then 40 and 50 and so forth. And then make sure that you document what you do and you track what you do to stay financially viable and profitable. And I think in the end, the goal is to really improve patient care. Really, we need to be doing better to keep patients at home in an optimal state of health and improve the disease progression or slow down the disease progression. Thank you, Lebo. You see, I have a question on this. You know, I think you made a compelling point that, you know, there's a lot of value to remote patient care. What of an upfront investment does one have to count in when you want to start that type of clinic? Because obviously this doesn't start overnight and you made the case, you can actually make money to sustain the clinic, to pay for the clinic, but what is the upfront investment? That's a great question. So the upfront investment that we made is in technology. Is because, you know, if you look at these clinics, people say, well, I can't do more than a hundred patients because I need to hire more nurses, right? Why do you need to hire more nurses? You have to break down the cycle. Like what do the nurses actually do? We did a time, before we started, we did a time study. And when we looked at the time card, we were horrified. 60% of the time that the nurses were spending were collecting data. That's insane, right? This is not nursing care. They're collecting data. So then we automated, we tried to automate as much as possible and eliminated that. And then the second time is, you know, we need to treat the patients. We don't have a protocol. Creating protocol and, you know, paying IT to embed those protocols in your EHR. So the biggest financial resource was really convincing the hospital to give us money for IT. And then we have our own IT person that, you know, works with us, you know, with our own EPIC to do that. And the second was, you know, to really get FTEs enough to get a critical mass of patients. So we got approval. Then, you know, we hired a couple of nurses at 1NP and we grew, you know, to close to 900 patients within six months. And then we started to make money. And then we went back to the hospital to get more FTEs. They're like, oh yeah, you're making money. Sure, you can hire whoever you want. And then continue to do that and, you know, accumulate more patients. All right, thank you very much. Let's move on to our last talk. And it's going to be Dr. Hall from Texas talking about heart failure devices in the pipeline. Too bad we don't even have more time for discussions. I could be at it all day. Thanks Livu. Great, thank you so much. Sorry for the glare. I'm in the ICU working. so my favorite place to be. So these are my disclosures. I think the most important thing is that I have minimal to no experience with any of the devices. These are all experimental, none are commercially available. And so it's to whet the appetite. And I broke these into three categories, chronic heart failure, acute support, and durable devices if we have time. We obviously get tight timelines. So moving to the chronic heart failure space, we'll start with shunts. And this has been our shunt history, these kind of scary looking metal spiders that are put into the heart. And the concept of putting those inside your patient is a little scary, and you're like, walking around with that, and what's the thrombobolic risk? But what is even more important is that the structural heart failure space has advanced so much in the past decade that they really need that real estate to do some of their procedures now. And when you look at the pictorial on the right, you can see that we can make it very difficult for them to do these interventions. And so the thought is bypass those space-occupying leases and just cut the hole. And these are some scary looking devices that basically cut a hole out of the atrial septum and it lasts. There are two of them. The first is the alleviate, it's a seven millimeter shunt, just got FDA breakthrough designation, and they've done their feasibility studies. They were safe and effective with shunt patency at 12 months. So the allay heart failure trial is underway for further data. The other is the inter-shunt percutaneous atrial, and that's called the ease heart failure trial. And that is similar concept, different appearance. Both of these are just gonna cut a hole in the heart. Well, if that scares you and you don't really wanna give your patient an ASD, there's another way to get blood from the left to the right and that's through the coronary sinus. And so this little device, basically threading it through the coronary sinus, puncturing into the left atrium, and then allows blood to shunt that way through the service road, so to speak. Moving on to neuromodulation, obviously we're talking about a neuroendocrine disease. Looking first in the abdomen, you're like, why would we look in the abdomen? Well, the reality is the splanchnic circulation carries a lot of blood volume and has very dense autonomic innervation. In heart failure, you've got high sympathetic tone, low vascular compliance. And if you could find a way to decrease that sympathetic tone and the splanchnic vascular tone, you could redistribute volume appropriately. And so the reality is that, let me just move everybody out of the way, is that this was looked at with the rebalanced heart failure trial, permanent splanchnic nerve ablation. They looked at 90 HFPEF patients. Overall, it was a negative trial. However, like most of this, it's patient selection. They did identify a responder group. And the responder group had the ability to preserve their cardiac output. When they exercise, they could augment their heart rate when needed. And they didn't have very advanced structural disease. And those patients did improve their heart failure symptomatology with a drop in their exercise wedge, an improvement in their six minute walk and their quality of life, as well as an improvement in biomarkers. So further trials are being designed that will focus on this responder group. Well, you've heard a lot about barostim and external stimulation. Well, now let's make it simple. Forget a little can on the outside with a wire, use this nitinol cage, band it in the coronary sinus, the carotid sinus, and essentially it reshapes the arterial wall, increases vessel stretch, and produces a reduction in sympathetic nervous activity. This has been demonstrated in preliminary trials to improve all the parameters that we look at for heart failure, including quality of life, six minute walk, EF, and biomarkers. And this trial is the MOBIUS HD trial. Well, if you're into decorative jewelry and you don't want anything invasive in your patients, then you might want to go low-level tragus stimulation. And I learned about the tragus with my daughter going to get her tragus pierced. And it's a very strong source of being able to stimulate the vagal nervous system. Those are various types of devices being trialed, two that are active right now. They obviously would have a sham arm, but they may be wearing the decorative jewelry without any nervous effect. Let's not forget about the importance of the diaphragm, which deteriorates during heart failure. The muscles atrophy and fibers change and their metabolism changes. So let's paste the diaphragm. This device is implanted with a simple scope and then leads to the two diaphragms. And preliminary results are encouraging with an improvement in quality of life, functional class, biomarkers, and EF. All of these have very similar end, which was mentioned at the beginning, is this is all about quality of life for patients, improving how they feel. We don't have anything long enough yet for these kinds of devices to study mortality. This continues to be studied in HEPRA and we'll see where it goes. This is an interesting new device from Berlin Heal called the C-MIC system. It's got an LV and RV lead. And if you can't get down the coronary sinus, you can use an LV patch. And what happens with this device is there's just this low level of direct current continuously, not pulsatile. It doesn't affect the cardiac excitation cycle. And what they found is that with this continuous low level, they had some pretty dramatic results. This is an X-ray of cardiac silhouette after four weeks. And they showed an improvement in EF and an improvement in the six minute walk. The other thing that's interesting about this device is after six months of it being on, they turned it off and followed for 30 months. And they found that the improvements were sustained. The EF remained elevated and the six minute walk remained improved and the functional class remained improved. So these are patients that are continuing being followed and further trials are being designed. Moving to structural remodeling in the chronic heart failure space. We know about this, it's been happening for a long time. Lots of big surgeries that have come and gone, but they all had similar goals. Reduce LV wall stress, try to minimize how invasive they were. And today, especially talking about all the things we do, preserve the ability for future interventions. And so things like wraps and nets and big open heart surgeries really have died away. But to no worries, there is plenty of less invasive options happening in the research space, showing some of them, AccuCinch, which this picture looks very benign and sweet. But when you look at the actual cinch, it does look a little scary with all of its hooks that are grabbing into the endocardium. This has shown some excellent outcomes, very seems to be safe with a 90% freedom from all cause of death, decreased hospitalizations, improved functional capacity and improvement in LV size. The trial is called CoreCinch and this is ongoing. Well, if that whole thing scares you, then you only feel like you should do a cinch up a side of your pan instead of a whole elastic waistband. You could go to the Clarion device, which goes from the coronary sinus to the greater cardiac vein, less invasive, shorter procedure time. And it allows you to intervene on the valve in the future with TIR or MVR. Below is the series of trials that have been going on with this device. And we are now into the full randomized controlled trial. Well, if you don't wanna be inside where the blood flow is and you don't wanna be outside where the coronary arteries, how about inside the left ventricular walls? This device essentially thread this wire through the wall. I'll show you the device. It's pretty interesting accessing through the right side. And you basically are going to thread this shoelace implant through the muscle and then cinch it up. So we'll see where that goes. Well, the door procedure, and Batiste is not dead. We're trying to find a less invasive way to do it. And this is a hybrid thoracotomy and catheter-based way to go and isolate an anterior apical scar. And the video is kind of showing you the concept of it. The preliminary results completed a couple of years ago with a two-to-one randomization, it was safe. As far as the mortality morbidity was lower than TAVR or TIER. But while the safety endpoints were met, the primary composite efficacy endpoints were not. And it appears from a sub-study analysis that if that cinching involves the right ventricle, those are the patients who don't do well. So it's being re-evaluated to find methodologies to not involve the RV. Contraband, this is, I still don't quite understand how this works, but you place these wraps around the two PAs and in half-breath patients. And to me, you would think that you're causing RV afterload increase, but at least in their preliminary works, the hemodynamics did not change on the right, certainly did not worsen. And there was a improvement in LV volume and functional capacity. So the pivotal trial will be starting with this device this year. Moving on to sensors in heart failure, you heard allusion to some of them. One is the fire system, which is in the IVC. Again, when we talk about pressure in the pulmonary arteries, it takes a while for pressures to translate from volume. The bulk of our blood volume is in the abdomen and the bulk of that volume, as far as a single vessel is in the IVC. So it's a big capacitance vessel. And we know that the larger the IVC, the worse the prognosis in heart failure. Looking at this, you can kind of see how easy it can be to put in. And it demonstrates that there's a long, wide range where the IVC can expand with volume and it won't produce any pressure changes. So by the time we see pressure changes in the pulmonary system, you've got significant volume. So if you could intervene earlier in the volume problem before you have pulmonary hypertension develop, then you could potentially intervene quickly, easily with responsive kidneys. And so that is the concept behind this device. The trial happening in the US is Future HF2. You heard about this briefly, and that's if you don't want anything invasive and you want your little pocket device that you lay over yourself that provides information. This got a FDA breakthrough device designation for potential wedge surrogate called CardioTag. If you don't want to be touched at all, then you can walk up to your little monitor here, stand in front of it, and this will contactlessly assess your body fluid. This is in development through a Notre Dame think tank. And so we can get patients to get on their scale and then move over and stand on this. Moving to the hospitalizations and acute support devices. The first is managing volume. This is the cardiac pulmonary stimulator. There's just like in the abdomen and the splenctic bed, there's also a very robust autonomic cluster of nerves around the PA. This is put in similar to right heart cath, and then you expand this cage with all of the electrodes and deliver the stimulation. And what they found early on in HF patients, 52 of them, it was overall safe to implant, and they produced more diuresis with no adverse creatinine change than standard of care. The benefits went through about the 30 day follow-up, but then the efficacy decayed. So this is definitely a more acute intervention device, and we'll see where it goes. Well, if you want to try and limit volume getting to the heart so that it can get back on the Frank Starling curve properly, there are two ways to do that. The first is this device, Precardia, which does intermittent occlusion of the SVC, decreasing right-sided filling pressures, and getting that heart back onto the Frank Starling curve. Seems to be safe, and there was definitely an effective reduction in filling pressures. The effects, this was on for 24 hours with a five minute inflate, 10 second deflate, and the effects were sustained for at least three hours after the device was turned off. What's good for the upper body is fine for the lower body, and so the Daria device is looking at intermittent IVC reduction in flow. You can imagine that's gonna have an immediate impact on renal vein congestion and allow better renal kidney function, and it's pretty easy to deploy through the femoral vein. Or maybe it's not a whole volume we manage where it goes, but just that we manage how to tell the kidneys what to do, and the Reprieve device monitors urinary sodium continuously to optimize whether they should have hypertonic saline or what diuretic dosing to use. It is not all automated yet, so you don't have the computer going around and upping things left and right, but it does relay the information for nursing to then adjust, and hopefully this will evolve to be automatic. The FasterPilot study showed that it was effective and safe, and so the Pivotal IDE is about to start. When we move to hospitalized hemodynamic support, we've got some fun devices as well in our arena. The first is a balloon pump for the right ventricle. This is floated out to the PA, and you can see the balloon, and essentially it's just that. It's gated to the rhythm, and it's a balloon pump to unload the right ventricle. Preliminary results showed a significant increase in cardiac output, improvement in PA compliance, and RA pulse pressure. And the AspirePH study is the next study for looking at this. As we go to our LD unloading, which we all understand is the best type of acute support for the LD, the one who gets this to be percutaneous wins the race, and the race seems to be getting closer. This superior device via 20 French percutaneous heath can generate over five and a half liters of flow. It actively unloads the left ventricle and dumps the blood into the ascending aorta. Right now, these devices are being studied for high-risk PCIs because it's a faster methodology to get them approved rather than in a shock or acute and chronic heart failure state. This trial showed on 30 patients no adverse device events, stable blood pressure, and hemodynamics throughout the high-risk procedure. The Magenta device could be the real home run with a 10 French heath developing greater than five liters of flow, and it had similar favorable safety and hemodynamic early data. Now, if we look at things that try and increase flow or decrease afterload from the aorta side of the system, the aortics looks like the good old virus drawings we did in high school. This is implanted in the descending aorta. Make sure you point it the right way. And it has been demonstrated to be easily deployed with a mean support of about five days, a significant improvement in renal function and biomarkers at the end of the therapy of five days with a 30-day sustainment of that effect. And this trial is called the DRAIN-HF trial as it gets into its bigger trial. The Module Heart just released this last year. They did four of these with high-risk PCI with 49 minutes of support, no change in the hemothorbital, so considered well-supported and no hemolysis. And so this will go forward into longer support trials. And then, of course, second and fifth has been around for a bit. And it is this nitinol cage with the little T-motor in the center looking like an airplane propeller. And this can produce afterload reduction as well as improved cardiac output. And it's moving to its next generation where it is deployable or where if you see in that upper right, the clip that basically releases it and it stays in the aorta, this could potentially be a dischargeable type of partial support device. And they would wear that little rubberized water-proof vest that has the module for powering it and recording it. Now, those are all continuous devices, and we know those last longer and are easier to build, but pulse is important. We know that every part of the body would prefer to have a pulse if possible. And so we go back, okay, where there wasn't a pulse. Where there was a pulse, we take it away. Well, where there isn't a pulse, we're going to add one back. This is a pulsatile ECMO called VentraFlow where it unloads the left ventricle instead of increasing the afterload and improves the blood flow to the coronary arteries while oxygenating the blood. To do these devices and trials, they basically have to be cleared for a less than six-hour cardiopulmonary bypass pump or extracorporeal pump. They have to go through that pathway to then be approved for potential ECMO support, which is just longer cardiac bypass. This device is trying to add more pulsatility through a balloon pump type of cannula and diverts the blood into this membrane pump that will then fill and eject back into the aorta producing more pulsatility. So, you know, whatever we have, we tend to want the opposite, and there seems to be trials for everyone. Very briefly in the last minute on durable support, the durable LVADs, the Everhart from Japan, this was an improved in that they didn't have the inflow cannula abutting into the LV, and so there's no growth around it. However, there was a cluster of neural events, and so this trial has been put on pause while they do some redesign. The BrioVAD just started its safety implants. I think we've had two in the U.S. so far. This kind of looks like a younger brother of the HeartMate 3. It's smaller, the driveline's smaller. There's one less battery to carry around. So patient-popular components. This will be the Innovate trial, which should go fully live this summer. The CoreWave LVAD is interesting in that it adapts to the native function of the LV so that during diastole, they'll set the pump support low, and then they'll augment during systole to kind of work with the heart instead of continuously separate from the LV. There are two total artificial hearts, the BivaCore. This is no valves, diaphragms, or barriers, just a single rotor with two sides that control the left and the right, and it's pretty small. The first site to implant this was in Texas. The second one has been implanted, and we'll see where this goes. And then the CARMAT artificial heart device was approved for a BTT device in Europe. The U.S. started with three implants, and then there was a trial halt for modifications, and we're still waiting to hear where that goes. So I know that was drinking through a fire hose, and certainly not meant to make you an expert in any of them, but just to let you know a flavor of what's out there. There's a lot more in the pipeline than I would have ever imagined. This is a fun specialty to be getting into, and hopefully you'll have one or more of these things at your site and get involved in the research. With that, I will stop. Two out of four. Thank you so much. You covered so much. Yeah, you can take a breath now. So let me ask you this. So obviously, I wouldn't go into any individual device, but there's a question that came through from a fellow, you know, thinking, going to a heart fellow. How does somebody who is budding into that space get involved and manages sort of this, the new era of device? Because for every approved device, you present a 20 that are not yet approved in the pipeline. Some of them will make it, some of them don't. If I'm starting out, how do I get involved? Yeah, I think the first is reaching out to mentors that are already involved in that research space. You got to kind of pick what you like. There's so much out there now that you can't do everything. And so, you know, looking at what you're interested in, finding out who's involved in that research and reaching out to them. Hopefully, it's at their institution, but that may be a factor in deciding where they apply for their job as a trainee, if they have the technology that they're interested in. Obviously, the bigger sites tend to have more of these devices, but nowadays, I mean, small sites get access to these, and sometimes private hospitals get access to them even faster. So you don't have to go to a full-blown, giant academic center to be involved in these research trials or get this technology to your patients. Yeah, and I'll maybe just, you know, add how many of us on the call said is that you just have to get involved by enrolling patients, you know, by being somebody who is the helping hand to make this trial a success. I think that's how you put yourself on a map and really get exposure to this technology. Any comments from Andrew, I'll leave you? I just totally agree. I think, you know, we were the largest combined enroller for GuideHF in a system that was relatively brand new, and it was just all coming down to a team effort focused on, you know, making a dent in the space and then trying to grab some attention for it because that turns into more momentum, and then more companies will look to you as a site, for example, for other novel technologies. So a lot of this just comes out of good old-fashioned grit and being willing to sort of outwork, you know, the so-called competition. But I think doing it for the reasons of focusing on doing it together as a team really helps because then you don't feel like alone, and you really kind of create a, you know, a group effort. And I think that's really a key. And as Shelly points out, your mentors really are there to help you. Liviu was my preceptor when I was a first-year fellow and got me hooked on this intersection zone type activities when most people probably know, but maybe some don't, that he actually trained formally in EP and heart failure. And at the time, that was like the sexy, you know, intersection zone that we were all talking about. But I think I got the bug back then. And I think if you catch the bug as a trainee, you know, grab it and continue to look to your mentors to give you connections. All right, we have a couple of minutes over. I would like to thank everybody that stayed late, the speakers, the audience, all the people that are raising questions. Thank you so much. This will be recorded. You can access it to get your CME points to review the recordings. And, you know, stay interested in this field, reach out to the speakers. Our emails will be available online. And hope to see you at the HFSA meeting later in Minneapolis. Please sign up for the device and heart failure day, which will be more of this, more hands-on sessions. And again, there will be no hurricanes. That's why we went to Minneapolis. Have a good day. Thanks everybody.

heart failure

device therapies

HFC seminar

Dr. Murad Fudim

Andrew Sauer

Dan Benzamone

Shelley Hall

Lilu Klein

CRT

Barostim

CCM

remote monitoring

multi-disciplinary collaboration