Good morning everyone. Wow the lights come up and you really cannot see. So my name is Debbie Wolf. I am one of the accreditation review specialists for the college. I am one of the heart failure reviewers. So many of you are attending today that I've worked with and I'm so excited to have been able to meet you face-to-face. So again welcome. Welcome everyone. So this morning we are going to talk about heart failure. We are so excited. You know it's been 10 years since the launch of the study for what we now know as Entresto. But prior to that you know we really did not have anything. Anything new for heart failure for a couple decades. So and once we launch that now we have so much to talk about. So I don't want to steal any thunder but we've got some great information that's coming at you. So today's session we're going to answer Q&A's on your mobile app. If you have not downloaded that please take a moment and download the app. Questions will come in through the app. It's very easy to find that that Q&A button at the bottom of the session. Log in to the session that we're in today and the Q&A question button is at the bottom of the screen. You'll see that. So I know that we are standing between you and lunch but I promise we're gonna feed your heart failure hunger from the stage here today. So I want to introduce our speaker. We're thrilled to have Dr. Paul Heidenreich. He is chief of medicine at the VA Palo Alto Health Care System and is a professor and vice chair for quality in the Department of Medicine at Stanford University School of Medicine. He received his medical degree from the University of Chicago and completed his internal medicine and clinical cardiology training at the University of California San Francisco. He completed a master's in health sciences research from Stanford University. He's a practicing non-invasive cardiologist at Stanford Health Care at the VA Palo Alto Health Care System. His clinical interests include cardiac imaging, heart failure, and performance measures. Dr. Heidenreich has an extensive background in outcomes and health services research in the areas of technology assessment, epidemiology, and quality of care. He has conducted several randomized trials of health services interventions to improve heart failure care. He has served as chief of the American College of Cardiology and American Heart Association's task force on performance measurement and chair of the American Heart Association's Council on Quality of Care and Outcomes Research. He has chaired writing committees for the American College of Cardiology and American Heart Association's performance measures and for heart failure and AFib. He recently chaired the writing committee for the 2022 American College of Cardiology Heart Failure Association Heart Failure Society of America guidelines, which I'm very proud to introduce him and I now welcome him to the stage. Thank you. Well, thank you so much. On behalf of the American Heart Association, American College of Cardiology, and the Heart Failure Society of America's writing committee for the guidelines, I'm proud to present some of the highlights from that document that came out earlier this year in 2022. And we'll get our slides going in a moment here. Okay, I'll go back I think one slide. Well, I just want to emphasize you didn't get a chance to see disclosures. I actually have no industry relationships, which is a requirement to be chair of these guideline documents. So we list here 10 of the top heart failure guideline takeaways. And I'll go be going through some of these. I think some of the big ones we've somewhat revised the heart, our heart failure definitions by ejection fraction. We now have four pillars of therapy with SGLT2 inhibitors. We actually consider cost in these guidelines and I'll go discuss those when we talk about the value statements. There's also exciting developments on amyloid heart disease in addition to prevention. So let's talk about the heart failure definition. So typically we would think about ejection fraction and there's multiple ways one could classify this. Right now we're sticking with that ejection fraction of less than 40, less than or equal to 40 percent for what would be considered HFREF or a heart failure with reduced ejection fraction. And then the preserved is 50 percent or above. So in between we now call that mildly reduced. And importantly if someone has a low EF that then improves, we want to recommend that they be treated as if they still had the low EF, that we don't drop the therapy just because they improved on therapy. And that's the what we call heart failure improved EF. We sort of got rid of the recovered EF term because in many ways it's not very rarely it is a true recovery. It's an improvement due to treatment. And this is a nice I think algorithm here that shows how one will approach heart failure. You start with your typical assessment and if the ejection fraction is not low we want some other measure to be sure that we think the symptoms are related to the heart function. So typically you can get that from a BNP or possibly echocardiography and diastolic function. Something to give you additional evidence that the symptoms are related to the heart. Once we then have that heart failure diagnosis we will then determine the ejection fraction. Again we mentioned if it's less than 40 percent over time it can either stay there or that it can improve. If you have mildly reduced EF obviously it could go in all different directions. It could get worse, it could remain the same, it could improve. We don't really know exactly what it means to go from 41 to 49 to greater than 50. We haven't done trials in that group. We have done the trials in those with less than ejection fraction 40 percent. If you stop treatment patients deteriorate. We think that's probably true for the 41 to 49 percent as well but it's not clear. And then finally obviously if your heart failure and preserved ejection fraction you could remain the same or get lower. Now as opposed to the ejection fraction classification there's also the stages I think many of you heard about. And originally many years ago we came up with the stage A to emphasize that there is the prevention stage. There's the at risk being at risk for heart failure. I don't actually tell patients they're at stage A for heart failure when they just have high blood pressure but we do want I think this is to emphasize with the clinicians that it is a continuum and there is an opportunity for prevention at stage A. Stage B is when you have something wrong with the heart itself but it's not yet causing symptoms and you can find that potentially through imaging although biomarkers such as BNP or troponin may also be an indication. Stage C is your classic heart failure with symptoms and then stage D is when this is now advanced marked symptoms interfering with daily life multiple hospitalizations. For those with stage C again we talk about whether it's new whether they've resolved symptoms or the symptoms have persisted or whether they're worsening. So think so not only would we think about the person has stage C or symptomatic heart failure we want to say is this are they stable are they the resolved symptoms are they worsening heart failure. Now this is a very busy slide. This is just meant to show you how we color code our guideline recommendations. So green is a class one. These are things that should be done. We have strong evidence for our very strong opinions that it should be done. And I'll say now the ACCHA has really gone away from expert opinion and really tried to only make recommendations for the most part if we clearly have evidence randomized trial evidence then there are slightly less strong recommendations a moderate recommendation would be the yellow to a and a week would be the orange to B and then the darker color class three is something you should not do either because there is no benefit it's tested there's no benefit or it's potentially even harmful. And so as we go through some of these slides these color look for these colors those will show you which recommendation class we're talking about. So as an example this is just the initial evaluation of heart failure. We have several class one recommendations things that we should do in everyone. And this is obviously looking for symptoms exam but also now we recommend a three generation family history if you are the person who who is first known to have heart failure to screen for inherited disease for laboratories these are particular laboratories that we've gone for a long time particularly iron studies we know now we're getting improved treatment for iron and having iron deficiency and that is even I think more in addition to potentially being a cause of heart failure there's potential treatment as well biomarkers are increasingly used and we have strong recommendations if you want to figure out the cause of dyspnea BNP is very helpful. It's also useful for hospitalized patients at the time of admission to look at the prognosis and those with established heart failure as an outpatient also useful for risk gratification. We have somewhat weaker recommendations to determine at discharge you know to use that data potentially determine their trajectory. We also have a two way classification moderate classification for screening for heart failure. So this would be a patient population at risk. There is actually a trial done. You do a BNP if that was abnormal. We then refer them to a team to examine that potentially get an echocardiogram and that was found to improve outcome if done in high risk patients our imaging strategies chest x-ray echo have been around for a long time. Those are strong recommendations. If your echo is not good or you just can't get it you shouldn't stop there. And that's why we have CT CMR and spect as potential alternatives to get that injection fraction data because it's so important to determine what type of treatment you're going to have. Beyond that there is moderate to weaker recommendations for some of these more advanced imaging. There are things that can be useful but it's not something that is routinely recommended. And finally in patients there is a class three you can see all the way on the right. We recommend that you just don't routinely get echo say every six months if there's no change in the person's status. We're really looking for so either it's been a significant long period of time or there has been some change or you're now considering a procedure for which you need that data to determine their eligibility. Some other items used in the past we use a lot less frequently now would be invasive hemodynamics. You know unless someone is acutely ill and in a myocardial biopsy. They are useful in very select patients but we would say it's a class three to just routinely consider these for your average patient diagnosed with heart failure. So again we have multiple recommendations for preventing heart failure and that's listed on the left on stage A. And then as well for those with what we call pre heart failure or there's something wrong but they're still asymptomatic. So what are those things. So we and many of you are all already aware obviously we want to control the blood pressure but now anyone with diabetes and CVD or high risk for CVD we would recommend SGLT2 inhibitors as a preventive for heart to prevent heart failure. Obviously optimize any management of other conditions and genetic screening and counseling for first generations of relatives with known genetic or inherited cardiomyopathies. Again we mentioned potential screening POP patients at risk as a 2A recommendation. For those with abnormal hearts but without symptoms we have several treatments recommended ACE inhibitors and beta blockers are class one recommendations to prevent heart failure. And as we mentioned before SGLT2 inhibitors obviously would since we use them in a stage A we would continue to use them in stage B. ICDs if the ejection fraction is low enough and then genetic counseling and testing for those with ischemic cardiomyopathy gets a moderate recommendation. Again please be putting in your questions as we go along. I think we'll definitely have time for treatment time for address some of those treatment questions are the meat I think of the guidelines is that shown here. We now have four what we would consider for life prolonging therapies. Those are listed in green and the last one diuretics while not life prolonging is clearly symptom improving. So those life prolonging are Arnie beta blocker MRA and SGLT2 inhibitors. That's how we should be thinking about it. We want to get the patients on those four medications. One thing we don't do I'll try to address this right at the end. We we did feel there was not data to tell you how to get them on. So of course that's one question everyone wants to know which drug first which one second. Should I do them all at once. What dose. And we really don't have a lot of data to to guide you. But people have come out with opinions and there's reasons to believe some may be better than others. And I'll address that at the very end. After you've treated we should then reassess the ejection fraction. If it remains low we would proceed with additional therapies. If it improves and you're an improved EF we don't want to stop those meds. We continue those on indefinitely. Now what is in that step three. We want to consider their symptoms particularly through the NYHA class. And then if they are self-identified as African-American hydrolyzing nitrates are recommended. If their ejection fraction is significantly low they an ICD is recommended and depending on their EKG potentially a CRT as well. Finally one would reassess symptoms if one actually became refractory. We would then consider more end stage therapies such as transplant mechanical devices or palliative care. Now one new thing we've done and I say the ACCHA has has plan has intended to do this for six to seven years. We didn't really have a guideline where we had a lot of data on cost but heart failure is one where you actually have a lot of cost data a lot of well done cost effectiveness studies. And so what we've done is looked at that published data and say well does this meet our society's standards for a good value. Is the cost justified by the benefit. And there are some standards put out there. We could talk about that later about what those would be. But the good news is all of our record treatments for heart failure reduced ejection fraction those forming therapies they're all considered highly cost effective high value. And so that's Ace Arnie MRI beta blockers SGLT2 inhibitors. Maybe you're saying well wait I thought those SGLT2 inhibitors and Arnie were really expensive. They they are while they are expensive the benefits are there. It also shows you what a good deal the beta blockers and aces because they're so cheap and they also provide a benefit. But so even though those drugs are expensive for it from the society's perspective we consider them to be very high value. The same goes for hydralazine and isosorbide dinitrates. What about device therapies. We also looked at the value statements there. And yes these are expensive therapies but they given the strong benefit they provide both ICDs and CRTs are considered to be a good value. One of the things I've always pushed for is all these things. Clearly we should be providing as a society anything that has good value and particularly if it's class one. You know many of us strongly feel there should be no patient copays. There should be no patient barrier in between getting your class one recommendations particularly if to society these are considered high value. Now what about something that's not potentially high value. Here's an example. And this is our wearables for remote monitoring. As you know patients you know with symptoms a few we've tested out putting a pressure monitor into the pulmonary artery and then that that data can be sent out and patients can have their drugs managed. There was one trial that was very promising. A second trial is debatable about how promising it was in the end. Both the treatment got a class 2b recommendation because of conflicting evidence for this wireless pulmonary monitoring or cardiomyems and the value we considered uncertain for that reason. Now there are new therapies you've probably heard about verisigwatt potassium binders in addition to some of our more standard therapies that we've had around for a while digoxin I've evaporated also have polyunsaturated fatty acids have some evidence. They're all you can see either 2a or 2b recommendations because the data just we feel is not strong enough yet to really recommend them. Now CRT the when to do CRT is a little complicated. So we just want to go over this to be thinking about it. So the first step is just obviously look at their health status. If they're expected to survive less than a year we're not going to do recommend anything. We should just continue with medical therapy. However if they're expected to survive at least a year we then look at the ejection fraction. If it's less than 35 percent and and they're asymptomatic or basic NYHA class 1 and they have a wide QRS with a left bundle pattern with ischemia then potentially will give you a 2b a very weak recommendation. It's much stronger if we have symptoms. So symptoms with the low EF the left bundle branch block and a wide QRS. That's a strong that's where the almost most of the data is. That's a very strong recommendation for using the CRT. Then the more narrow the QRS becomes the weaker the recommendation and then the less it looks like left bundle branch block the weaker recommendation. You can see it's only a 2b if it was say a right bundle branch block and only in less than 149 milliseconds not very wide. There are a few other special circumstances where you would use the CRT. For example if you need to do frequent RV pacing which itself can be harmful or if the ejection fraction is good but there's a clearly high degree or complete heart block and they're going to be permanently paced. It's probably better to be paced with a CRT. Another really exciting area I think is the treatment of the mitral regurgitation that we all see with heart failure. Again this is not mitral regurg due to say mitral valve prolapse or something wrong with the valve. It's that the heart failure itself has dilated the ventricle contributed to deformation of the valve structure in that way causing the mitral regurg. If patients are undergoing bypass surgery they should have that valve dealt with at the time. However for the most people we would look at their ejection fraction and if it's high we would consider surgery. But the best data is if it is a low ejection fraction symptoms despite being on guideline medical therapy and I think the important thing is here is if you do have someone who comes in with significant MR but they're not yet on therapy I would not be referring them to a procedure yet. You want to get them on the best this is where you want to wait get them on the best medical therapy you can and then reassess that mitral regurgitation. Sometimes you get some incredible results but if you don't and there are certain mitral anatomies that are more that are good for or not for this if they are good we should this transcatheter edge edge repair that's the mitral clipping we give them a moderate recommendation of 2A. If it's not good for clipping then surgery is even a weaker recommendation. It's a 2A recommendation because as opposed to a 1 while we had one trial that was incredibly positive we had another trial that was so so. So for that reason, it doesn't get the Class 1 recommendation. So that's for those with reduced ejection fraction, less than 40%. Most of us, most of our patients probably have an ejection fraction higher than that. And now, fortunately, we have growing information and data about what to do if that ejection fraction is, say, in this case, 41 to 49%. Mostly diuretics, as we've always done, but now the new thing is SGLT2 inhibitors should be your go-to drug for these patients. That should be the first drug. It's reasonable to do the ACE, ARB, or ARNI, MRA, or beta blockers as well, but that's a weaker recommendation. In general, SGLT2 inhibitors for all of these with mildly reduced ejection fraction. And again, many of you know, we'll talk about this at the end. That was all based on just one trial. A couple weeks ago we had another trial confirming that data. So everything we see here for SGLT2 inhibitors, it's even stronger now. How about for preserved ejection fraction? Very similar. The one difference, no beta blockers. We're not recommending beta blockers for preserved ejection fraction. The data really are just not there. So start with the SGLT2 inhibitor and then consider the ARNI, MRA, or ARB. Another I think surprising to many of us and also very exciting is that we now have life-prolonging therapy for amyloid heart disease. Many of you have seen commercials on television regarding this. The problem is there's a lot of diagnosis you need to do up front to get to that. One of the first things we need to do is make sure that it's not another cause of amyloid, such as monoclonal light chains, because they have completely different treatment pathway. So the first thing, if we're suspecting amyloid, is to check for those monoclonal light chains. If we do see it, then we go down that path, probably includes a potential heart biopsy at some point, and would then get them into treatment by a hematologist oncologist if confirmed. However, if we don't see that, or if they never had light chains to begin with, we would do a pyrophosphate scan. And if this is abnormal, we then actually do our genetic testing for the transluritin cardiomyopathy, transluritin mutations. And this actually helps us then determine how hereditary it is and how you should talk to the family members. Either way, the patient is eligible for treatment. You can see we have a green for tefamidus. It was one trial, but it was very strong. For those with class I to class III symptoms, tefamidus is recommended as a life-prolonging therapy. There's also a weaker recommendation for using anticoagulation. For those, again, for those with the hereditary form, which should be referred to genetic counseling and potentially screening of other family members, they also may have more neuropathy and there may be treatments for that. So a little bit now about advanced heart failure. I think many of us always wonder, I'm a general cardiologist. The question is, at what point do we need to get them into advanced heart failure clinic? And there's this I NEED HELP acronym that's been around. It's all listed here. That's I for, and if any of these things are going on, you think about, okay, maybe this person now should be with a more advanced team. So that's inotropes, and it's New York heart class III or IV, more than one hospitalization, ejection fraction, shock, edema, hypotension, as well as just intolerance of taking their current medications. Another change is that we're less excited about fluid restriction than we were in the past. When I went to medical school, that was a standard thing, and patients suffered. You say, no, no, you can't have any more to drink. You had your 50 cc's for today. It was torture to watch them, and they're so thirsty. And finally, we've done some trials, and we actually cannot find the benefit of doing that. Why were we doing that? No differences in mortality hospitalization, no differences in sodium levels, no differences in duration of IV diuretics. So we really don't know, and we didn't want to just drop it. So we've made it sort of a to be saying, well, the benefit really is uncertain here, and you should really think strongly, maybe have some other good reason for restricting fluid. Don't restrict fluid just because someone has significant heart failure. When people do deteriorate such that they're in the hospital, there are certain things we want to consider, and these shows the six things potentially when they come into the hospital or in the clinic with severe function. The key is the last one, continue or initiate GDMT. We don't want to say, oh, they're getting worse. Maybe let's pull back on your medications. We try to avoid that wherever possible. And this shows how we recommend, these are all class-run recommendations, during hospitalization, do everything you can to continue the medication. If the person has a drop in renal function that's relatively mild, we don't stop the diuresis, we don't stop the medication. And if for some reason you do have to stop the medication that you really consider reinitiating prior to discharge or whenever clinically stable. We unfortunately know that patients who don't go out on meds, even if it was intended that they get started, they often never are started as an outpatient. And this is our typical decongestion strategy. We would do IV loop diuretics first, and then you have your choice of what to do second if that's not working, whether it's doubling up, whether it's using an infusion or doing some other drug to sequentially block the nephron. And then the important thing is at discharge, make sure the patient knows what the diuretic plan is, what the new dose is, and how you want them to take it. Transitions of care are obviously important. We feel the strongest thing here is referral to a heart failure management program. Potentially, you know, there's this idea of seeing patients early. We don't have a huge amount of data, but seven days seems reasonable. And participating in benchmark programs is also a reasonable thing, but not as strong of a recommendation. A few things about comorbidities. Some of the newer ones. Iron deficiency, we now have data. We're not talking about anemia itself, but iron deficiency alone is a reason to have intravenous iron therapy that gets a moderate recommendation. Of course, we should manage hypertension, SGLT2 inhibitors are relatively new, and sleep disorder breathing. We recommend that for improving symptoms of sleepiness. We do not have the data that's going to improve their heart failure survival or decrease hospitalizations for heart failure, but there's probably enough reasons just for quality of life to treat those with significant sleep disorders. The committee recognized that these guidelines are great, but many vulnerable populations have disparate use of these treatments, and we need to do whatever we can to try to improve that, potentially using multidisciplinary teams with our goals of eliminating disparate health outcomes. And one of the things we should be doing is tracking all of our data and not just, oh, yeah, we did great, we're at 90% beta blocker use, but we should be looking at among all these various subgroups and saying, well, is everybody getting that 90% and if some are clearly falling behind, why? Thinking about patient-reported outcomes, the committee felt this is a reasonable thing to be tracking. For one, it provides independent data from your typical NYHA, which I say is the physician or the nurse practitioner or basically a provider-reported outcome. The patient report, often these are disparate, and they provide unique information, and we're now starting to have trials where a patient fills this out before clinic, the physician or nurse reviews it, and then discusses management based on that. Just anecdotally, we're often finding a lot of times where the patient will say, oh, yeah, I'm doing fine, no problem, and then you look and you say, well, your score here suggests you're pretty symptomatic, you can't even, you know, walk up one flight of stairs. And then they sort of let it come out, yes, actually, it is not going as well. So it does, I think, also help with the history and our interaction with patients. Performance measures, some of these Class 1 recommendations, the strongest ones we turn into performance measures. And we recommend that these be used, tracked. A lot of our accreditation programs will take these to determine accreditation. There's a moderate recommendation for participating in those QI programs, registries, similar things that the ACC does to help you reach these performance levels. So that was a very brief overview of some of the highlights. I think many of you say, well, what about some recent studies, just in the last four, you know, since those guidelines were used four months ago, things have changed. For example, DELIVER trial came out, dapagliflozin, reduced composite heart failure, hospitalization and death for those with preserved ejection fraction. It will be interesting, you know, I would guess we were heading toward a Class 1 recommendation for people with injection fraction over 40%. That remains to be seen. And the ACCHA and HFSA are going to try to update these in a much more timely manner. We don't want to be waiting every six or seven years. So I'll end on this. So this is not in the guidelines. So I'll put that out there. How should we start these drugs? And this is from Dr. Packer and McMurray, who published their recommendations last year, which I intend to agree with. You have the conventional sequencing on the left, where we sort of go in the order of the trials. Well, ACE inhibitors were the first drug. And then let's add on a beta blocker, MRA. Then let's switch out the ACE for ARNI. And finally, we'll get to the SGLT2. And you could say, well, that makes sense based on how the data evolved. But there's many reasons. First, this takes forever to do. And probably people won't end up on all four. And there's reason now to start with the SGLT2 inhibitor, which has a little diuretic effect, and the beta blocker at the same time. Together, you will actually tolerate the beta blocker probably than if you just started with a beta blocker alone. At least that's the theory. And that's anecdotal experience of many. And then after that, quickly add on an ARNI and MRA. The thought is you could do this all within four weeks. Some say you could even do it faster than that. And so that's one on the right. The rapid sequencing is my preference. And then you maybe adjust these based on the patient. But we don't want to do the sequential thing every couple of months. It'll just take too long. So I want to thank you for your attention. Thank the American Heart Association, who helped put this together in the group. I think they've done an outstanding job. And thank you to the committee for helping us put this guideline together. And I'm happy to take your questions. All right, thank you for that information. And we do have some great questions that's coming through the queue. So first question, Maria asks, have you seen ejection fraction decrease after COVID vaccination is given? I haven't seen that myself. I don't think we think that is a significant concern. And we definitely don't recommend that ejection fraction has to be done after the vaccine. Having said that, we know that in general with vaccines, there's incredibly rare but small complications from vaccines. But we don't think that the COVID vaccine would be any different, say, from some of the other vaccines. Multiple people are asking, in HFREF, should a reassessment of guideline-directed medical therapy occur with each hospitalization, if previously contraindicated? Is the standard to address all four therapies with each hospitalization? Yeah, so I think the first one was, should we get an ejection fraction with each hospitalization? Usually, you could say, yes, there's a reason to do that, because supposedly they deteriorated, right? They were fine. They've gotten worse. We should look, is something going on? Maybe there's worsening mitral regurgitation. Something else is going on. So the fact that they deteriorated is a reason to get it. And I think we should always be considering, for every patient comes in, are they on the best doses of those four medications? Is there something I can do this admission to get closer to that? We should always be reassessing and just not assume, oh, well, they figured it out the last admission, and so we're just going to maintain the status quo. I would not do that. I think take each admission as an opportunity to try to improve the medications. Excellent. And then for those patients that are known illicit drug users and have severe heart failure, what are treatment recommendations for that patient population? Yes. Well, I think it'll depend on what drugs are being used. I think it is important to do various screens, tox screens, things like that, to know what's going on. We know, say, methamphetamines are associated with increased heart failure. So I think one is finding out what is going on and then seeing what can be done to get them into therapy to stop that thing that may be hurting them. I think that's the main thing we can do for them. And then talking about family history, as you mentioned in the beginning, and evaluating for family, for patients where family history is unknown, is genetic testing for heart failure risk available, or is it recommended? We wouldn't normally just recommend it if you didn't have a family history as a strong recommendation. There's a weaker recommendation if you have a very dilated cardiomyopathy not due to coronary artery disease or some other cause. That's sort of a moderate recommendation. I will say there are definitely tests out there that one could do. I think the problem is our ability to test is really outpaced our ability to treat. And so I, myself, if the person doesn't have other family members who I might want to screen, I think it's unclear what the benefit to the patient would be for some of these tests since we don't necessarily have a treatment. We want to test for something for which we think we could benefit the patient or their family. And the guidelines do address devices, additional devices. The audience would like your thoughts on the cardiomems to help manage heart failure. Yeah. So I'll say the cardiomems, we had one trial, the champion trial, that looked very promising. It was a decrease in hospitalization, strong decrease. There were complaints about the study in that they felt people also were getting extra advice. The intervention group was getting, they thought they might be getting extra advice from nurses and others about how to manage themselves that the control group wasn't getting. So I don't know how strong of a, how valid a complaint of the trial that is. But then they did a second trial, unfortunately it happened right as COVID was coming out. So if you looked at the overall results, it weren't very impressive. But they said, oh, well, COVID changed things. Just look at the results right before COVID. Then it looked better. So it's rather confusing. So I would say it's something, and we gave it a 2B recommendation. I think it's not an unreasonable thing to do. But I wouldn't say we can strongly recommend that all patients have it. So a lot depends on if your clinic and others are set up to collect the data, do the management, have the staff available to do it. I think we need another trial. And then a question regarding fluid status. Many interventional cardiologists are holding fluid post-procedure due to heart failure. Oops, hold on, it just jumped. Is there no longer recommendations and does this affect acute kidney injury post-PCI? About holding fluids? I don't think we have strong enough data to say that you should or should not hold the fluids. I think small changes in kidney function we're not that concerned about. There are some data actually looking at saline infusions along with diuresis that might be better than just diuresis alone. I think there's a lot we don't truly understand, I think, about the fluid volume. And we haven't really done the studies. So I don't think we can give a firm recommendation to say, or any concern that that practice is a problem. And then regarding some of the medications, how do you adjust your recommendations for patients with a higher creatinine, especially the SGLT2 inhibitors? Yeah, so we would be looking at the GFR and depending on that glomerular filtration rate based off the creatinine. And in general, though, I'd say we know that we would still use this except for the most extreme patients, the SGLT2 inhibitor actually is the first drug shown to reduce the progression of kidney failure. So we actually want to get it into these patients. If someone does have some kidney failure that I'm even thinking more strongly, I want to use the SGLT2 inhibitors. It's only when we get incredibly low, less than 20, that I think we may have concerns about using them and then they weren't used in the clinical trials. But all the clinical trials used it well down into, well below, say, 40 milliliters per minute for creatinine clearance. Wonderful. So speaking of cardiac rehab and the guidelines that have, or payment structure, let's say, that's been put before us by CMS, any other recommendations within the guidelines that can support, better support the alleviation of that six-month waiting period for optimization and getting our patients in cardiac rehab sooner? Yes. I think it's not clear to me exactly what CMS's concern is about having, you know, paying more for, or making it easier for cardiac rehab. In general, we have a strong, there's a strong recommendation for cardiac rehab in general for heart patients and that, I think, continues for those with heart failure. We also, so I'm not sure what it's going to take for them to move on that issue. They may say, oh, well, you need more trial evidence, you know, your trial evidence is relatively weak, but, you know, I think we've, you know, I think the guidelines have stated we recommend it, you know, I would, I wish they would change their policies. All right, wonderful. And so you definitely addressed the implementation of the medications. So for the, and, you know, so much of the guidelines have been focused on the HF-REF patient. We're super excited. There's some introduction with a little bit more guidance on the HF-PEF patient. For the medication classes, is there recommendations with starting medications as you kind of outlined with the HF-REF patient? Yeah, I think there, in fact, it's even more clear. I think SGLT2 inhibitors should be the first drug used. And then after that, there often are other reasons why you might want to use a medication. If there's coronary disease, if, you know, either the ARNI or ACE are beta blocker, obviously if there's hypertension issues, a beta block, ARNI could be a good medication. I think it's sort of based, you'd then, after you got the SGLT2 inhibitor on place, you sort of look at the other comorbidities and see which one would fit best of these remaining medications. And again, I mentioned beta blocker. That's only for those with mildly reduced. We would not recommend that for the preserved.

2022 ACC Heart Failure Guidelines

heart failure treatment

Entresto

ejection fraction

therapy for heart failure

treatment options

comorbidities

patient-reported outcomes