So, good evening everyone, welcome. I want to personally thank the American College of Cardiology for putting these sessions together. We've been doing this now for several years, and these spotlight sessions are really meant to call attention to something clinical that is happening now, it's happening to all of us. I'm in the trenches too, just like you are. And that you have questions about it, you want clarifications, and you want to do the right thing for your patients. And so the ACC has been really ahead of its time doing this, and we pick, as you can see, many other spotlight sessions for different topics that are of concern, and they are in the guidelines. And so this is sort of going down deeper, and pulling this out, so that when you go back home, you can make some good decisions for your patients, and that's the purpose of this. So I'm Ileana Pina, I'm the quality chief for the cardiovascular line at Thomas Jefferson University, and it's my pleasure to be here with a bunch of my friends, which makes it fun. And I'll let you guys start introducing yourselves. Great, good evening everybody, good to see you, thanks for being here. Hope your meeting's going well so far. Rob Ments, a heart failure cardiologist at Duke, where I'm also the section chief there. Good evening, I'm Shelly Zeroth, I am a heart transplant cardiologist from Winnipeg, Canada, and happy to be here. Hi everyone, it's great to see such a full room tonight for our discussion. My name's Nosheen Rees, I'm an advanced heart failure transplant cardiologist and genetic cardiologist at the University of Pennsylvania. Good evening, I'm Susan Gazzara, and I'm Thomas Jefferson. Alright, terrific. Thank you all for saying yes to doing this. The American College of Cardiology also appreciates the grant support from American Regent, particularly for this session that we're having tonight. We're going to have a little fun here, we have a riddle. I did not write the riddle, one of the ACC staff wrote the riddle, and I'm going to read it to you, and I want to know if you can figure out what it is, because I couldn't at the beginning. So within the labyrinth of pathways, I hold a key. In iron's dearth, my role is crucial, you see. A gatekeeper of energy, I orchestrate the dance, but in deficiency's grip, I falter in my stance. I'm a hub of metabolism, a nucleus of might, yet in the heart failure's shadow, I fade from sight. With fatigue as my messenger and weakness as my plea, in this intricate web, I'm a puzzle to decree. What am I? If you didn't notice, it also rhymes. Anybody want to venture a guess? I'm a teacher, so I can call on you. Any table want to confer about it? And have one spokesperson? Well, you're close. A little bit more specific. A little more specific. Come on, this side's winning. Say something. All right. Here it is. It's the pathway, the heme synthesis pathway. Now I want you to look at your QR code and scan your QR code, I was supposed to remind you earlier, so that you can really participate in this session and send us questions. I'll be able to see them up here. And we will try to address as many as we can during the program. So I have some audience response questions here. And we're going to go through them. And they're purely clinical, and they were supplied by our panel. I didn't make them up. They're supplied by our panel. So let's see the first one. A 77-year-old woman with a history of chronic heart failure and reduced ejection fraction, I think I can say HFRF in this audience, presents to the emergency room with worsening heart failure and volume overload. She has elevated jugular venous distension and lower extremity edema. Her labs are notable for an antiprobian P of 2,800, with a normal creatinine, GFR, and a normal hemoglobin level. As indicated in the 2022 guidelines, and these are the HAACC guidelines, and used in prior heart failure trials with iron deficiency, which of the following labs best supports her diagnosis of heart failure with iron deficiency? So select your favorite. Giving you a few minutes to see the numbers and see what you think. I was waiting for music. Where's the music, guys? You forgot the music. Okay, and there are the answers, as everyone here. I can tell if everybody, 22 only? Come on. Get that QR code. Your vote is not counting. All right, second one. Sixty-three-year-old Hispanic woman referred to the heart failure post-discharge clinic for her diagnosis of heart failure. She's diabetic, having been diagnosed in 2015 after chief complaints of fatigue and not being able to do her household activities, and she has a longstanding history of hypertension. After a recent hospitalization in March of 2022, her lab showed an ejection fraction of 25, but her cath showed no coronary disease. Due to a serum creatinine level of 2.1, she was placed on hydralazine and a nitrate instead of brass therapy. The inpatient team also started her on 25 milligrams of metoprolol succinate, but did not start her on spironolactone either because of the concerns of renal function. With her systolic blood pressure at 90, her heart failure team stopped the vasodilator and started her on a small dose of enalapril at 2.5, Spiro at 25, an SGLT2 inhibitor and progressively increased the metoprolol to 150 QD, and that's metoprolol succinate. For the next 90 days, the brass inhibitor was up titrated. The patient continues to complain of fatigue. Her labs show a persistently low hemoglobin, anywhere from 8.5 to 10.5, and this is a table of her iron studies dating back from 2015, which is before she met the heart failure team, and that's what you see in the table below. So you have iron, you have TIBC or iron binding capacity, you have percent saturation, you have periferatin, and you have hemoglobin, so a lot of information on that table. So if you've looked at it well, here are the choices. Which of the following is most likely the cause of the drop in the serum ferritin? This is a little tricky one. This one makes you think. 52% of you thought it was due to iron loss, okay. Question number three. A 70-year-old woman with New York Heart Class Chronic Systolic Heart Failure Class 2, LVEF is 38, seen in the clinic for routine follow-up. She has not been hospitalized for decompensated heart failure in three years. She's on carbidolol-25, VID, sucubitrovalsartan-97 and 103, Spiro-25, and dapagliflozin-10. Routine laboratories checked at this visit demonstrated a sodium of 138, potassium of 4.3, a creatinine of 1.3, a hemoglobin of 11.5, ferritin at 172, transferrin at saturation at 17%, and an NT-proBNP of 243. Get rid of that. Look at those numbers. I'm giving you a chance to look at the numbers. Oops. And there's the possible answers. Which of the following is the most appropriate for the next step in treatment? Do you want to prescribe IV iron? Prescribe an erythropoietin-stimulating agent? Initiate Virisiguat? Or refer the patient for a pulmonary artery monitor? I'm sorry, this screen is showing. Trying to get rid of it. There you go. Refer for an implantable pulmonary artery pressure monitor. So, vote your conscience. And 84% of you want to prescribe intravenous iron. So, now I'm going to introduce Rob Mentz. We have made these talks short. They're about 10 minutes apiece so that we have plenty of time for discussion and questions. Rob, take it away. Great. Thanks so much, Ileana. Thanks to the ACC and Ileana for helping set all this up, and importantly to our sponsor for this, American Region, who have been really important collaborators in evidence generation in this space. So, over the next 10 minutes or so, I'm going to go through some of the epidemiology and key data as we look at incorporation of IV iron into practice to set up some of my colleagues as we think through guideline-directed therapies and how assessment for and treatment of iron deficiency is really critical. These are my disclosures. So, some of the key dilemmas I'm going to talk through are, wait, don't we just need to be thinking about iron deficiency in patients with anemia? Shouldn't we just think about this in anemia? Unfortunately, I think many of us during our training, we were taught this. So, when you see a patient come into the hospital or in a clinic and you see anemia, then you think, oh, what's one of the common causes? Iron deficiency. And I'm going to really make the case that when you see heart failure, you need to think iron deficiency. How common is this? I'll show you some of the key epi data around that, and I'll talk about the right criteria. This is an evolving space, and I think we've been fortunate to develop some evidence in this domain to help better inform clinical practice. And then, how should we treat? We started to touch on this a little bit, but I'll go through briefly some of the key trial data on clinical outcomes. To set this conversation up a little bit, looking through the physiology, this is a really nice scientific statement from the Heart Failure Society of America, and it goes through, why are patients with heart failure iron deficient? At each step of the game, they're actually at a detriment. So, it tends to be actually due to dietary changes or otherwise, less iron is even coming into the system, and if they are in their diet bringing iron in, it's not absorbed as well. And then, even if it is absorbed, it tends to be sequestered due to inflammation, such that even if the iron is there, it's not effectively used. We know so many of these patients are on antiplatelet agents, they're on other anticoagulants, so there's increased blood loss and iron loss in that context. And this scientific statement, I think, nicely goes through the clinical implications of this. This is now an older figure, but I think gives a good framework as we think of the impact on our patients. It's really from the mitochondrial level, the cardiac abnormalities as a result of iron deficiency, but then also the skeletal muscle changes, and I think that's a key element that's often underappreciated, and leads to worse quality of life, functional status, and worse outcomes with iron deficiency. So, this is that key piece, as we talked through in the questions, defining iron deficiency, and these are criteria that were adapted actually from the kidney literature early on with some of the key trials, but it's a ferritin less than 100, or 100 to 300, with a TSAT less than 20. And this is regardless of anemia status. So, if we, I think as a group, are practicing where we see heart failure and check for iron deficiency, you're already acting at really the 99th percentile here, because most individuals are really not doing this in terms of checking for iron deficiency broadly in heart failure. So, how common is this? This is the best figure I've seen of this. It goes on the left are these chronic heart failure studies, as you move to the right, in the hospital, acute heart failure, and what you see is, even in the outpatient, quote unquote, stable setting, it's upwards of a third of your patients, and as you move toward that hospitalized setting, it's 50, 60, 70, sometimes even 80 percent, and we've looked in our data, and our patients with more advanced disease going on to transplant, nearly everyone is iron deficient in this setting of heart failure. And this is just that framework that I went through for those that prefer a visual representation here of reduced intake, reduced absorption, medications that lead to increased loss, and then the chronic inflammation related to hepcidin. These are early data that really reframed our interpretation of this. So, what you can see on the left is one of the first key studies that looked at iron deficiency and the association with increased mortality, and on the right is the best example early on, showing that it's not just anemia associated with worse outcomes, iron deficiency in and of itself, and that highest risk group is actually those that are anemic and iron deficient. So, we've talked through this. Really, when we see heart failure, we need to be thinking iron deficiency. How common is this? Upwards of 50 percent or more of your patients in the criteria here, and I'll come back to this as I contextualize the HEART-FIT trial as well. So, what data do we have for treatment? And this is coming from a place where the studies early on looked at ferricarboxymaltose, or FCM, in heart failure with those iron deficiency criteria, and really definitively showed that FCM improves quality of life and functional status. So, these are the KCCQ, Kansas City Cardiomyopathy Questionnaire, very well validated, improvements in six-minute walk distance, really substantial magnitude of benefit upwards of 30-plus meters. So, that's on the order of magnitude of what you see with biventricular pacing, or CRT. And now, actually, FCM is the first therapy then in heart failure to have a label here in the U.S. and now also in Canada and other regions of the world for heart failure specifically with iron deficiency. So, the data behind this then have led to important updates in guidelines. So, actually, the most recent ESC guidelines give a class one recommendation for iron deficiency evaluation in heart failure and then use of IV iron to improve quality of life functional status. And then, what do we know about in terms of outcomes? And this is really to set up my colleagues here will talk through the guidelines and then set up our case discussions about implementation. So, HF was a landmark study, a firm AHF. This was in the hospital, acute heart failure, EF less than 50. So, this includes that mildly reduced group as well. People often ask, oh, aren't all the data we have just in HF? No. We've got these important data in mildly reduced ejection fraction as well. The primary endpoint here was looking at total events. So, it was total burden of heart failure hospitalizations and cardiovascular death. This was conducted during COVID. So, this really impacted this trial but, importantly, showed a numerical reduction in this primary endpoint, those curves separating. As you can see, 12 months there. Longer term follow-up. Really, I think, demonstrating this nominal reduction but not meeting statistical significance. Importantly, a pre-specified analysis in the context of COVID actually does meet nominal significance. So, that was over 1,000 patients with FCM starting in the hospital. And we'll talk some about implementation. Great opportunity there to improve not only functional status but potentially clinical outcomes. And a follow-up study, different IV iron formulation, ferric derisomaltose. This was open-label in Europe but did show a similar magnitude of reduction in the similar endpoint of cardiovascular death and total heart failure hospitalization. It actually also had this COVID analysis. So, multiple large studies but most of the data to date have been with FCM. Then we were fortunate to present this last summer, the HEARTFED trial. This is the largest trial of heart failure and iron deficiency to date. This was reduced ejection fraction heart failure with those iron deficiency criteria. And our primary endpoint was designed such that each patient could contribute. So, over 3,000 patients giving IV FCM at six-month intervals and looking at all-cause mortality first, heart failure hospitalizations, and then six-minute walk distance. We saw a numerical reduction in mortality, we saw fewer heart failure hospitalizations, 270 fewer heart failure hospitalization days, and just a more modest improvement in six-minute walk distance. And I think that this is related in part to we're doing this at a six-month cadence looking at six-minute walk distance. And this was really not designed to really focus on the functional status component but does incorporate that within the endpoint. Importantly, this was designed to be one pivotal trial. So, what that meant is in conversations with the FDA, our bar was set higher. So, we had to have a p-value less than .05 that we're so commonly used to seeing. So, we actually did not meet statistical significance despite meeting the nominal significance we usually contextualize here. So, we felt it was important to pool these data with the totality of evidence we have with FCM, building upon this rich history of functional status and quality of life benefits, and then looked here. This is now a pre-specified pooled analysis with multiple FCM trials looking at total heart failure hospitalizations and cardiovascular death. And this was a 13% relative risk reduction, just barely missing statistical significance here. That actually did in the co-primary endpoint looking at CV hospitalizations and CV death. It does meet nominal significance. And when you look at, in fact, the totality of evidence now pooling at a trial level with IRONMAN with that other formulation, a larger magnitude of benefit. So, as I put all this together, I think we have a medication in FCM that we need to be testing for iron deficiency. And it's very safe. We really did not see any safety signals in this. And I would squelch any concerns that we used to have about worrying about infection, worrying about anaphylaxis. This is really easy to give in the hospital and in the outpatient setting. There's some additional logistical implications. But if we can add to quad therapy another therapy that helps people feel function better and has a label indication around that and then likely reduces heart failure hospitalizations, I think that's what our patients deserve. And I think the guidelines, specifically now in Europe, also give this a class 2 recommendation. So, with that, I will stop and hand it over to my colleagues for the next talk. Thanks so much. I might have hit the one above. Sorry. There, we're good. We're good. We're good. All right. Sheesh. It's like I'm jet-lagged from coming from Canada. Okay. All right. I'll lower the mic, lower the podium, all that sort of stuff. Okay. So, I'm going to, you know, talk to you about the urgency to diagnose iron deficiency. And I think, you know, one thing that I think we really need to wrap our heads around is that it's not necessarily anemia is going to be present. And in fact, it may be in a minority of patients in which the combination of iron deficiency and anemia are present. Iron deficiency can exist on its own. I just want to take a quick survey of the room here. For those of you in clinical practice or running heart function clinics, how many of you actually check iron parameters on patients for routine blood work for an initial consultation? How many do this? So certainly not the majority, and definitely a minority. I'm going to estimate that at about 15% of attendees screen for iron abnormalities. And this is, if you don't measure it, you don't know. And based on the clinical trial evidence and the clinical guidelines, there really is an urgency to diagnose and recognize iron deficiency anemia. You can see here the common definition here that you may or may not have been quizzed about. And when I reflect back on what these levels are that you have to remember, I also wanted to just refresh for those of you who have not taken the LMCC for a long time or whatever your exams are called here, ours are slightly different in Canada, remembering what the TSAT actually is as well, because that is part of the definition of iron deficiency. It's iron over transfer and times 100 is your TSAT. And that is an important component of the definition you see at the bottom of the screen. Now several groups have looked at or redefined iron deficiency in different ways. Some of them get fairly complicated. For instance, we're not going to do a bone marrow on all of our patients. And the bottom one, I don't even really understand. So I think our traditional definition is very practical and pragmatic for real world clinicians to use and be able to identify iron deficiency. And looking at that top definition, ferritin less than 100 or 100 to 299 with a TSAT of less than 20, if you move to the right-hand panel, you can see that not just across clinical trials, as Rob showed you, for outpatients and for inpatients, but across the continuum of ejection fraction, iron deficiency is present in our heart failure patients. Everything from the left-hand side from HEF-REF, middle is mildly reduced, and of course, PEF having the higher numbers as well. Now they say it takes about 15 years to change the guidelines and or to implement them in real life. And so I looked back to see when we really started talking about iron deficiency in heart failure, there's some papers back from 2008, 2009 as well. I think this one was really one of the first big synopsis on it. And there's a flaw with this author panel as well in that there appears to be no women in it. But a decade later, they found many female French cardiologists to add on to future manuscripts. So very happy for them. But we've been talking about this for well over a decade now. And it's time to implement this into our clinical practice. So these were in 2007, the original American guidelines. And these are based on the early clinical trial data looking at the role of IV iron in patients with predominantly reduced or mildly reduced ejection fraction and improvements in functional status. And so originally, fairly low recommendations. But as Rob alluded to, we have clinical trial data now, which has influenced on the last version of the ACC guidelines, a 2A recommendation in patients with HFREF to improve functional status and quality of life. And I believe it was Rob's HEARTFED trial that really influenced the ESC 2023 guidelines, where with the totality of evidence, we now have a class one recommendation to alleviate heart failure symptoms and improve quality of life and IV iron supplementation to reduce the risk of heart failure hospitalization as well. And that in part is also due to that pooled analysis, which he showed you. So our clinical practice evolves with experience, identifying the underlying problem, recognizing iron deficiency, and recognizing the important changes in clinical trial guidelines that have been influenced by these trials. Now iron deficiency isn't just present in the setting of heart failure. Many of you have broader clinical practices as well. And so I thought that this recent review paper by John Cleland published in the European Heart Journal gives a really pragmatic guideline for the use of a liberal strategy to improve iron levels in patients with overall cardiovascular disease. And then on the right hand side, I know clearly a recommendation for IV iron if the patient has symptomatic HFREF and other factors, including a TSAT of less than 20%. And in fact, this figure highlights the fact that in patients with heart failure with reduced ejection fraction, a mildly reduced ejection fraction with an EF of less than 50%, there are in fact guideline recommendations for the use of FCM in order to improve symptoms, functional status, and quality of life. And so my final slide here is a nod to my distinguished panel. All three of them, Susan, you are not on here on this one, are actually authors of this Heart Failure Society of America scientific statement, which was published in the Journal of Cardiac Failure, which Rob is also the editor of as well. And I think these are really important take home points for us that iron deficiency is a common problem in people with heart failure. We've seen some really impressive percentages. There are adverse outcomes in terms of symptoms, but also increasing mortality and hospitalization when iron deficiency is present. Rob nicely reviewed the pathophysiology of iron deficiency. And the use of IV iron for the treatment of iron deficiency is now a recommendation at the class one level within international guidelines. And there are some interesting trials coming in the pipeline as well to potentially even expand IV ferric carboxymaltose across the spectrum of ejection fraction and other modes or modalities of IV iron as well. So with that, we'll stop. And I think we're going to transition to some really interesting cases. So we've heard about the guidelines now from a couple of our speakers. And so what I'm going to try to do is to bring the guidelines to practice and see what it is that we need to do for that. There you go. I did that right? Here we go. Thank you. So what I find so interesting about the latest edition of the ACCHA guidelines on chronic heart failure is that they're asking us to take a more holistic view of the patient. We've been focused so much on guideline directed medical therapy. And we have panels at every hospital trying to figure out how many patients are actually getting GDMT. GDMT now is pretty common in our epic charts. And we're looking for all these things. But there's a lot more going on with these patients than just the GDMT. And a lot of other items that actually affect how they feel and how they function and how they live. And so these sets of guidelines really are asking us to stop and look at all the other comorbidities that live in the same world as the heart failure of these patients. And as I showed you here in this slide, here is IV iron replacement in patients with HFREF, which is what you heard from Dr. Zeroth, where the evidence is more powerful in HFREF. But that those patients should at least be thought about for iron deficiency. And then among the others are things like CPAP. Are the patients, if they're asymptomatic, what are they on? Do they have hypertension? We have another session going on out here at the same time that we're here on hypertension. We can't ignore blood pressure. We still need to treat blood pressure. And we need to do it with a conscience that we need to get those numbers now. It is not OK to not have a good blood pressure. It is not OK to say, oh, this is white coat hypertension, or check it at home and then come back and tell me what it was. It's not OK. So we need to look at the patients in their totality. And I always ask myself in clinic, what else can I do? What am I missing? How else can I help this patient live better, feel better, and have a better health status and a quality of life? But if you look at chronic conditions, anemia is incredibly common. Whether the patients are over 65 or below 65 with Medicare, these are Medicare data, CMS data in the United States, almost 50% of the patients, whether younger or older than 65, have anemia. So it is so common that we just can't keep ignoring it. And the new US AHA and ACC guidelines talk about a two-way recommendation and a level of evidence BR, stands for randomized. And they also tell us to be really careful about erythropoietin. There was a big trial done in the US called RED that showed negative effects of erythropoietin. And so all the new guidelines have this warning in there. And everybody thought, oh, god, if we really push that bone marrow, we're going to get good effects. Well, many of those patients were also iron deficient. You can push all you want. If you have no iron, you're never going to make blood. It's just as simple. And I am sure that many of you see patients who have been on iron tablets, which they usually hate because it either makes them constipated or gives them diarrhea. And that's what they've been on for years and years and years. And who are these? I very commonly see older women who may have had a perimenopausal bleeding, really gross bleeding. And that iron has never been replaced. And they've been put on this iron. And now I see them in their 60s, and this has been going on since their 50s, that they've been taking iron with really not much success. And the iron deficiency in the 2022 HACC guidelines is defined, as we've been hearing today, a ferritin level of less than 100 or 100 to 300 if the transferrin sat is less than 20%. And intravenous repletion of iron has been shown to improve exercise capacity and quality of life. And when I say quality of life, I really mean health status, which includes quality of life. But it's not all that it is. In 2021, and I have to really give credit to our European colleagues, because they started talking about the importance of iron deficiency and of iron replenishment way before we did in the US. And I think Rob knows this. They were already writing position statements even before the guidelines to alert us to look at these numbers and to check the iron in our patients. And when 2021 came around in their guidelines, they had ferric carboxymaltose considered for iron deficiency, and they defined it very similar to what we saw here today. And they called it a two-way with a level of evidence B. But then with the newer studies that came around, particularly in the European Heart Journal, they changed that recommendation to A. And guidelines are really meant to be a movable source. We shouldn't live with the guidelines of 10 years ago, and both the American College and the American Heart Association are moving toward guidelines being much more useful and much more timely when studies come out that really should change practice, issuing a statement, modifying them online, bringing them to reality. And they did that, and they did that pretty quickly. So my talk today is really brief, because what I summarize is that do this on your patients. Check their iron. Do the iron studies. It should be sort of like a regular reflex. You order the chem panels. Heaven knows how many chem panels we order. Heaven knows how many people we make anemic because we're drawing blood on them every day in the hospital when we're not doing anything with them. And we've limited those in our pre-transplant patients already. And the fact that this applies not only to HFREF, but also to MREF, that middle-of-the-road ejection fraction that sits between 41 and 49, which I personally think is really HFREF, and they behave like HFREF, but it's also for that milder HFREF. And consider all the other comorbidities that the guidelines want us to point out to in addition to the guideline-directed medical therapy. If the patient is hospitalized, what a wonderful opportunity to give the IV iron. It makes life so much easier to do it if you're doing it in the hospital with the patient there. And what a good opportunity to check for the iron while they're there. Inflammation with ferricarboxymaltose should be considered. Insymptomatic heart failure patients recently hospitalized. So when they come to the post-discharge clinic, which we're all supposed to have because we're trying to lower readmission rates today still in 2024. And in heart failure with an LVF of less than 50 and iron deficiency defined as we do it, we can reduce the risk of hospitalization. So think about it. NT-ProBMP, getting a 12-lead ECG. We do trans-echoes all the time. We get x-rays. We do routine blood tests. Like I said, your creatinine and the BUN and you know the potassium and you get the potassium 20 more times. Think of adding the iron studies to that. That's how you bring the guidelines into practice. And I thank you. And our next speaker will be Dr. Reza Nosheen, who will give us an interesting case. All right. So now we're going to get into the active learning phase of our session. And I'm going to present a case, which will sound a little bit similar to some of the aspects of the multiple choice questions and cases that you saw earlier. We're going to walk through all of these cases with insight from our expert panelists so you can really see how they think about consolidating all of this knowledge, incorporating what we know about the foundational treatment of heart failure and what we're reviewing today about IV iron, how all of that is additive, and work through some diagnostic and therapeutic dilemmas. So let's get started. So this is Ms. L. She's a 62-year-old woman with chronic systolic heart failure, left ventricular ejection fraction of 30% due to a non-ischemic cardiomyopathy. And you're seeing her in clinic for symptoms of fatigue, exertional dyspnea. Essentially, she has Neurocard association class 3 symptoms. She completed cardiac rehab after a recent prolonged hospitalization, but just hasn't been able to do her daily walk from her home down the driveway to her mailbox. And she would love to go around the block, but she just hasn't been able to do that without feeling exhausted since she got home. Here's her relevant medical history. She has hypertension, and it was untreated for years, and this is thought to be the cause of her heart failure. She has stage 3 CKD. She does not smoke cigarettes and rarely uses alcohol. She went through menopause at age 54 and had menorrhagia for months during that time. And this is her current medical therapy regimen. She's on Zacubitril-Valsartan 49-51 twice a day, long-acting metoprolol 50 milligrams daily, spironolactone 25 daily, dabagliflozin 10 milligrams daily. She takes Torsamide 20 milligrams two to three days a week, depending on her daily weights, which she's religious about doing every morning. She keeps a little diary, a little notebook of all her vital signs and brings them to clinic and she's on iron sulfate oral 325 milligrams daily. So in clinic, she seems fatigued as expected. Her blood pressure is 105 over 76. Her heart rate is 68. She's in sinus rhythm, and her BMI is 32. Her heart exam is regular rhythm, no abnormal heart sounds. She has clear lungs. Her JVP is 7. Her abdomen is non-distended. She has no peripheral edema that you can see, and she has good pulses. You check some routine labs to work up this fatigue, and here's what you get. So you can see there her sodium is 138, her potassium is 5, her creatinine is 1.6, which is around her baseline. Her hemoglobin is 10.1. White count is normal. Her hematocrit is 30. And then like Dr. Pina just taught us, we should be checking iron studies when we see our patients. So you go through her prolonged hospitalization record and you saw that actually nobody checked iron studies during the time she was an inpatient, so you check them when she comes to see you as an outpatient. And you can see that her ferritin is 78. Her transferrin saturation is 16%, and her n-t-propion P at this visit is 189. So I'm going to work through parts of this case by asking our panelists some questions. And I think when I was thinking about putting this together, I was really just thinking like a heart failure clinician. So I'm hoping to see if that translates to you all. I think common questions that may be going through your mind as you're seeing this patient. So let's just sort of start by asking, Dr. Zeroth, what do you think, sort of what's your differential for when you see a patient who's just still fatigued after a long hospitalization? Give us the laundry list. I think that the laundry list is that they want to make sure that they're optimized on their GDLP. They want to make sure that their GDLP is up to date. And I would say noting device optimization. And then you look for other causes of health, which would include IHL. Yeah, exactly. So as you, of course, very expertly picked up, you were talking about congestion, perfusion. This always comes up when we're talking about these therapies in patients with heart failure to make sure that she's completely decongested after this hospitalization for volume overload and decompensated heart failure. And I hope I gave you hints by her physical exam that she's relatively well decongested uvolemic. Blood pressure is adequate. She seems to be perfusing well. She has good pulses. So we've checked those two boxes that Dr. Zeroth just let us know. Subtly had put in there, you know, her heart rate's 68 on this much beta blocker. You are thinking about actually, of course, how much more medical therapy can she tolerate? But based on her hemodynamics, both clinically and what you're measuring in clinic, seems like this seems like the right recipe for her. And then, as Dr. Zeroth said, then you start thinking about, all right, in addition to decongestion, perfusion, optimization of foundational medical therapy, guideline-directed therapies include device therapies. So I did leave that out on purpose to see if somebody would pick it up. So that's something that we need to work on. And this is real life, right? These are the patients that we see in clinics. You've identified already an evidence-based gap. And then, of course, we move on to thinking about therapies like IV iron, because what I've identified in this patient is that she has poor functional status and poor quality of life. And so you should really be thinking about, what are my therapies that I know that can address those two aspects? Okay. Dr. Pena, you notice that I put in here her gynecologic history. She's 62 years old. Why am I asking about her gynecologic history? And do you think this is actually something that routine heart failure clinicians or any cardiologists do in patients that they're seeing? I always do ask a lot about her gyne history, because we know that problems during pregnancy are a fire shot telling you that this patient's going to have cardiovascular problems early. I ask about that. She doesn't seem to be having any chest pain. My other question is, is she really functional? I want to know. Give me a real essence. I also think she may be able to tolerate a higher methodol. You know, in the merit trial, the mean dose. I'm sorry. Thank you. You mean they didn't hear anything I said? I was saying that she may actually be either depressed, which is existent in 35% of heart failure patients, out of shape, and even though she went through cardiac rehab, what was the response to cardiac rehab? Did she really improve her function? So I'd like to see some numbers on her and get a good GYN history, including her pregnancies, which I think are just a fire signal that something goes wrong. Yeah, absolutely. So with regards to the gynecologic history, I think all of us know in this emerging literature, much of which is being featured here at this meeting, that adverse pregnancy outcomes are an independent risk factor for the future development of heart failure in our female patients. So certainly important to know. I didn't provide you that history here, because I wanted to bring it up as a discussion point, but we should be asking about her pregnancy history and the history of adverse pregnancy outcomes, including preeclampsia, eclampsia, gestational hypertension, gestational diabetes. And then, of course, we talked about menopause here. The average age of menopause is 51. So you can see she had prolonged menopause or late menopause here in menorrhagia for months, so heavy bleeding around the time of menopause for some time. And as Dr. Pini alluded to in her talk, these individuals often get put on, as our patient has, oral iron for years and sort of suffer with the side effects. And as you can tell from her labs, which we'll again review next, really not an adequate therapeutic response for the anemia that they've suffered. And then, of course, always appropriate, Dr. Pini is challenging the notion that she is on optimized guideline-directed medical therapy and wants us to do some objective testing with cardiopulmonary exercise testing, for example. You could consider a right heart catheterization, as well, as we've talked about. And so, really getting objective data surrounding this issue to really see what is the limitation in her functional status, quality of life, and so forth. Okay. So let's skip ahead back to review her laboratory values. And so, in totality, Dr. Mentz, can you just walk us through how you interpret labs? And really, as a heart failure clinician, through and through, when you're checking these labs on patients on GDMT, what are you looking at and how are you thinking through them? Yes. I think I would underscore this potassium, as well. Right? So many of us, I bet in your EHR it pops up, the potassium is five, it's in red, your alarm bells are going off, everybody's wondering, do we need to reduce the ARNI and stop their spira? So I would underscore that. The answer to that is no. We need to carefully monitor. We see that she does have a reduction in her GFR. But I, too, would try to push up the ARNI if we can, as well as beta blockers. So I'd underscore the potassium. We need to monitor it closely, but potassium five should not freak us out. And then, in line with our conversation tonight, is really focused on the iron indices. And we've talked a lot about these numbers, and some of it, it does make me a little worried, just some of the complexity. We've got so many things we're juggling in clinic. So just to have it, like, on hand, that ferritin less than 100, all right, that's a no-brainer. That is iron deficiency. But it can be all the way up to 300 with ferritin if their T-SAT is low. And we have some evolving data, some of which are presented at this meeting, actually, can we be ferritin agnostic? So this is still an evolving space, meaning, can we just look at the T-SAT if the T-SAT is less than 20? So we still have some unanswered questions around that. But I think this is clearly iron deficiency, and oral iron is going to be insufficient. Absolutely. Can I ask one more question there? Yes, please. And how much is ferritin associated with heart failure itself? And so it's strongly prognostic, but it's a little bit of a complicated relationship. Nice data from HeartFit, as well as some data from the Ironman program. Actually, that lower ferritin group, yes, we need to certainly rule out any GI bleeding, any other reason for this. But they tend to actually have lower event rates and may not respond as we'd anticipate if they don't have a T-SAT that's also low. So evolving data there, but I think this is clearly a case of iron deficiency. Great. And I think one thing also our audience would probably love to hear how you think through is, you know, as Dr. Beacon-Boskert has sort of named, foundational guideline-directed medical therapy for our four pillars of heart failure therapy, and then the concept of consolidation therapies or add-on therapies sequentially after we've optimized guideline-directed medical therapy, in which IV iron certainly falls into. But there are a lot more. And as Dr. Men said, you know, we're juggling a lot in clinic. And not only are you trying to figure out, is everything that patient is on, is that appropriate? But then you're also trying to think about, well, what is missing, as Dr. Pena said? And there are so many things out there. How do I keep them all straight, and how do I know what a patient might be eligible for in the world of add-on therapies for heart failure? There's soluble guanyl cyclase stimulators, ivabiridine, IV iron, crazy new devices. We're learning about all of them all the time. So Dr. Mentz, how do you keep all of these things straight? And when you're thinking about seeing a patient in clinic, incorporating the evidence, and thinking about those add-on therapies, what's your sort of framework for that? Yeah, I think Shelly said it nicely, that we want to better understand, how do we get on quad therapy at max tolerated dose? And I think that's where my key message is. Often what we will see in either a discharge summary or a clinic note is like, we'll consider SGLT2 at follow-up. If you consider it, it will never happen. You've got to use these therapies. And I think as we think of the different components here, the volume status sounds, looks good, but actually, do they have worsening of their MR? Do we miss it on exam? Do we need to think about an EKG? Do they have a left bundle as we're optimizing GDMT and probably pushing device out a little bit further than just a three month because you're getting ventricular remodeling with all these therapies? So thinking of all the different components, I ask about depression. I ask about kind of other comorbidities, sleep disorder, breathing, where we know we can help people feel and function better by actually thinking about CPAP therapy and appropriately select the patient. So I try to go through all this laundry list, but that's a lot. You've probably got like 15, 20 minutes tops. It truly takes a team. And actually, nurses are such an important part of the care of patients living with heart failure. And they follow these really important protocols. They have checklists. They can multitask better than most of us physicians, I think. And so I think it's really important to incorporate that in your outpatient clinical practice to have these very important checklists for patients with heart failure to make sure you are ticking all the boxes to reduce residual risk for heart failure hospitalization. You also remind the audience that left bundle branch block is more common in women and that women also do better with CRT than men. Add an arrow or QRS. So going back to check that EKG again, even though you may get a reading, I would advise go look at it yourself and make sure that that's a narrow QRS. Wonderful. So I hope you all, I'm eating all this up. I'm just, you know, I want to take this all in. I'm learning so much from all of you. I hope our audience is feeling the same way as well. So we've identified, again, in a very real world conversation, opportunities to optimize therapies that she's already on, perhaps opportunities that were missed during a hospitalization that we want to capitalize on now. We have new information that's been provided to us via her labs that you've checked as an outpatient in terms of her iron studies. So this is now new information we need to act on. And so let's do that. And so with our final question, and now we've gone through the guidelines, you've gotten a high level overview of the evidence in this space, and we're just going to do a free response here. How do you improve this patient's exercise capacity and quality of life as we've gone through? So QR code is up, 30 seconds. Just type in what you think. That pulls over, but the music's still going. I'm loving it. Awesome. Okay. So wonderful. So we have, of course, a lot of IV iron, ferric carboxymaltose, FCM. We've got even dosing strategies in there. I love it. And we've been talking about it, like we mentioned earlier, improving the GDMT. Somebody decided to be a little cheeky and say definitely not IV iron. I was going to thank John Rommel for entering definitely not IV iron. Thank you, thank you. We get your point. All right. And so just to transition us to our next case presentation, our next discussion, it's going to be focused on exactly what we just left the finality of this case with in terms of the importance of the multidisciplinary team and how do we actually overcome these barriers of therapeutic inertia and this burden that you may feel as a clinician that there's so many things to accomplish in a 15 to 20 minute visit. How do I do it all? And we're going to learn exactly how to do that next. So thank you all very much. Thank you. Together we will dive into navigating the process of implementing our, implementing your iron infusion action plans. Before we navigate the motion, let's pause to emphasize the importance of this conversation. It does feel redundant to reiterate the similarities of heart failure and iron deficiency. However, to the patient suffering from iron deficiency, it is profound. Iron deficiency alone often makes normal activities of daily living feel impossible and compounds that with heart failure. How can we tell this population to be more active for their heart, for their health? Are we setting them up to fail without iron, without iron deficiency treatment and then witnessing the responses be unfavorably critiqued? Through understanding and exploring the impactful symptoms of iron deficiency, we can grow into our improved future. This is my heart failure nursing perspective summed up. Oral iron is considered to be the first line of therapy for iron deficiency or iron deficient patients. It often fails though due to malabsorption in the gut. IV iron is an option if oral iron should fail, which it typically does. 100% of the IV iron is delivered into the bloodstream. To start the process, the order just needs to be written prescribing the infusion of iron and sent to the infusion center. Once they receive the request, the infusion will then be authorized through the insurance. Your patient will arrive at the designated clinic site where they will be fully evaluated. Pre-medication is no longer given to all patients as it used to be. However, patients with previous reactions or given medications in the past will be given Tylenol and Benadryl as ordered. All infusions require a 30 minute observation period after their infusion is received. IV iron instructions before they go, these are the answers to the most commonly asked questions when you're speaking to your patients. Your patient does not need to fast before an iron infusion. They may take all their normal medications prior to the infusion with the exception of oral iron if they are still taking it. If they are still taking oral iron, please advise them to hold off for seven days prior to the iron infusion. They do not need a ride home and just let them know to rest and hydrate within their limits once they do get home. It may take a couple days to two weeks to start feeling the results of the treatment. For those of us that love a good formula, here is the formula for iron replacement dosing. Or you could use the mdcalc.com. This is the app that our pharmacists recommend and this is what it looks like. You plug in your data and it does the magic. It's advised to discuss follow-up labs at your appointment with your pharmacist. It's advised to discuss follow-up labs at your appointment with your patient when you're discussing the iron infusion. Reason being, if they're forewarned about these labs, it gives them time to process this and plan it out in their schedule. You have a more successful rate of having them actually get it done. Request that they have it done seven to nine days, I say ten days to make it easy for them to remember after their infusion. Also, please remind them that if they need to get it done sooner, that they don't go sooner than 48 hours after their infusion. They could get a false reading. Keynotes discussed with your patients are the side effects. Iron side effects are typically very minimal. If you should have any question of an adverse event, it would be encouraged to share that with the FDA med watch. However, the side effects have been like a two percent and it's been nausea, headache, flushing. Post-site the infusion care instructions include rest and hydrate after the infusion. You may want to let your patient know that their urine may be temporarily darker the following day as five percent is excreted through their kidneys. If an IV infiltrate with IV infusion, which you don't necessarily have to bring up initially in your conversation, but depending on the extent of it, it may take a couple of days to heal depending on the infiltration. The iron may stain the skin a little bit, but the fabulous take home note on this is that IV iron is not a vesicant. So, and just like that, you have activated your IV iron therapy plan. Thank you again for having me. We have, believe it or not, a lot of questions on the, from you guys in the audience. So, since we still have some time, I'm going to go through them. I'm going to try to summarize some of them. One of them, and I'm going to give this one to you, Shell. Once the iron deficiency is treated, how often do you treat it? Once the iron deficiency is treated, how often do you test for iron deficiency afterwards? Well, I come from a slightly different healthcare system, and we're very conservative with blood tests, but I would typically check within three months is what we do in our clinic. I think if you know that there's an obvious cause of the iron deficiency, though, that may be earlier if you know that they have GI blood loss, for example. There could be differences in opinion, though. Rob? Yeah, I think most of the data support looking at three to six months. So, in HeartFit, we did every six months. We would repeat assessment and redose if needed. Yeah, I think three to six months is appropriate. Susan, what are we doing? Are we repeating in three to six months? She puts up with me, so. We typically repeat when we see them again in clinic and then follow up in three to six months. So here's another question. What about screening for iron deficiency in HFPEF? Interesting question. So Shane, do you have any data on HFPEF? I don't think we have those data yet, but they're coming. Yeah, it's a little bit limited, right? So a firm went up to EF of 49, so it was less than 50. There's some smaller studies looking at it now in HFPEF, mostly looking at different function and field surrogate or other endpoints. So it's fairly limited in terms of the data we have. That being said, we commonly assess for many of our patients, especially in the hospital. And we're giving IV iron based on this experience, translating kind of the art of medicine from HFREF to HFPEF. Yeah, absolutely. We actually mentioned this in that HFSA scientific statement. So if you actually go to the end, we have a whole section on future directions in which we actually discuss the upcoming trials planned in the space of HFPEF. So it's a great read, obviously plugging it for selfish reasons, but also for your education as well. And we've talked about what's in the guidelines, right? So if you're a very evidence-based guideline driven clinician, the European guidelines really say HFREF, mid-range ejection fraction. HFPEF is not clearly mentioned in those class one, class two A recommendations. And that's where we are now. But of course, like we discussed, the science is very quickly evolving. So we expect updates in the future. But if any sponsors or independently wealthy folks wanna fund the trial, we work for that. We'd be happy to do it. It's also interesting because it's an intersection, isn't it? You've got more women having HFPEF than men, right? And you have more women having iron deficiency from whatever reason or the menorrhagia, et cetera. So you have an intersection of, and symptomatic. The HFPEF is very symptomatic in these people. And trying to decipher whether it's iron or whether it's the HFPEF itself. That's where putting them on the treadmill, I keep doing that, would obviously help. Here's a question. If the patient gets the IV iron in series and is still iron deficient, do you go ahead and give it to them again? Yeah, so we presented this meeting important data from HeartFit where actually, so it's six months when we give IV iron at baseline. At six months, 82% of people were still replete. So you still got about 20% at six months that were needing more iron. And then we've characterized and we'll present, I don't know exactly when they're coming out. So I don't want to steal Greg Lewis's thunder. But it really is, we repeat levels of assessment at three and six months and then re-dose. So Susan, there's a question here about after you've done the IV iron replenishment and the patient appears to be doing well, do you give them any dietary recommendations? Whatever they can eat. I see there's another one here. Would it be correct to say that ICM is indicated for systolic heart failure? I think that means FCM? Yeah. So it is indicated in patients with symptomatic heart failure with an ejection fraction less than 50%. So I think it's, you know, systolic heart failure is not really a term that we use anymore. We really specify reduced ejection fraction and mid-range ejection fraction. So I think it is appropriate to say it's indicated for reduction in hospitalization for heart failure and improvement in symptoms and functional status. Susan, another one for you. How long does the IV infusion last if your patient says to you, how long do I have to be there? I typically tell them to be there for about two hours just so that they're not watching the proxies and the ashes, but typically once they go in, they're assessed, the vital signs are taken, the infusion can go in over a half hour at the longest and they're watched for a half hour. Yeah, so we learned a lot in HeartFit about this and some of it's how we frame it with our patients. So early on, we were saying, you know, this is gonna involve an infusion and then there's this framing of like, oh my gosh, this is like a cancer therapy. So we've reframed it, it's really an injection, it's super easy, so it takes seven and a half minutes. Some of this I actually worry on the implementation side as a carryover from some of the early formulations where we saw anaphylaxis. I suspect many of you may have, that you can give IV diuretics in clinic. This is actually just logistically about that easy, but it's taken a million steps to get our institution to say, hey, we don't have to do this in infusion clinic, but rather we can safely give this in clinic and it requires sometimes a little room shuffling if we, it's like the flow through clinic, but it's super easy, seven and a half minutes in clinic, my gosh. Some more questions here. I'm really happy to see that there's many questions. Should we consider inpatient infusion after optimizing for an acute heart failure? There's a couple of questions about, should we be doing this in an acute heart failure admission, a decompensated admission, should we be doing this? Michelle, what do you think? Yeah, well, the affirmed trial actually showed that it was safe to do so in patients prior to discharge with their first dose, followed up by infusions at six weeks, 12 weeks, and then 24, depending on their iron status parameters, hemoglobin as well, so definitely in hospital. I mean, we know that's a key component of implementation of any therapy, including heart failure therapies. Some people don't check for iron deficiency in their outpatient clinics, so if it's recognized, there is a need to treat. Yeah, I was hearing some kind of key pearls. So we actually put it in our admission order set. When you're getting the BMP or CMP, if you're worried, check iron studies, and it's very easy to give on the inpatient side. And then some of it's just the logistics on the outpatient side, still. What we've found is actually engaging, like you were describing, with this multidisciplinary team. Now we have it set up, we've got this great pharmacist support where I just say, hey, sending iron studies, if iron deficient, will you set up an infusion clinic? And then realizing that requires that you've got that support, but that we really use that to advocate for pharmacist support by actually lowering our readmission rate related to use of IV iron. Do you worry about the volume? Amount of fluid they're actually getting? No. Yeah, yeah. The volume of patients. No, the volume of fluid that they're getting. Susan, another one for you. What other nutritional deficiencies do you talk about to the patients who maybe iron deficient? What do you do in the clinic? We talk about low sodium diet, part healthy diet, high protein, how they can eat a smaller meal, do you talk about eating healthy nutrition and... Thank you. So dietary-wise, that would be the way that we go. What about potassium? Depending on what their potassium level is to begin with and what dose boron lactone they're on. So if they're low on potassium, and they can consume more foods that are higher in potassium, or if they need to restrict it. And we find that every time we approach one element, there's another question about something else in their diet. I also recommend that they go to a diet and I also recommend that some of the best spent money is a visit to a good nutritionist, to put it all together. Because we're telling them, you know, watch your potassium, I don't want you to eat more sodium, now eat iron-containing foods. And it makes life pretty difficult for these patients because we're really trying to restrict them. Now Sheen, how do you address the dietary issues? Yeah, I think very similar. Again, I think realistically, which is what we're talking about here, what can a really busy clinician accomplish in a 15 to 20 minute visit? This is what we struggle with, all of us struggle with, and this is a lot of the lines of the questions that we have. I like to use a lot of asynchronous teaching materials, just want to bring that out. And the ACC honestly has the best resources for this in terms of the patient-facing information with CardioSmart. And so I talk about, I save what I talk about in the visit for things like IV iron and medication changes, you know, things that really need my explanation. And then the things that I know that we have time and tested peer-reviewed strategies and information, like the CardioSmart nutrition handouts, for example, that's where I use those asynchronous teaching strategies. And I think patients really do appreciate having something in their hands that they can also go home and share with the family or whoever's doing the cooking. I've been through all the questions, now I want to ask the audience here questions, please. I have two questions. Yes, sir. Patients with hemochromatosis, heart failure, now they're being detected, they can die and die. What do you do with those patients? I don't have much experience with hemochromatosis. Do any of you? As a source, obviously, of liver disease. No, no. And cardiac disease. They don't have liver disease, just have iron, but have iron in the heart failure. I have not had anybody like that. Okay, I've got two patients. The other question is, I always check my patient for vitamin B12. B12. Because many patients have got diabetes and glucophage for many years. It's amazing how many patients are B12 deficient. And B12 deficient is obviously a big risk factor for many things. So I check them all routinely, at least once. That's a great point. And if their levels are low, I'll leave them alone, but if they're low, I treat them appropriately. How do you treat them with B12? Well, there's a protocol. Protocol is if, for example- Injectable or oral? No, it depends. Usually, if they have got, for example, gastric bypass surgery, got a number of those. Those are gonna be intramuscular injections, and there's a protocol of one injection a day for seven days, one injection every four weeks, followed by one injection per month for life. You check all those again. I also check intrinsic factor antibodies. And if they're abnormal, I refer those to upper GI endoscopy, because there's a small number of those, maybe the gastritis, and I find a few patients, because obviously they are now diagnosed as pernicious anemia. Now, the term pernicious itself is very bad. So I find a few patients who get gastric cancer carcinoma. Interesting. Thank you. Very good point. Yeah, thank you. You've kind of triggered a couple kind of key pearls. One is we talk about this with patients. You know, they'll often ask, like, if you're starting irony, they're like, well, doc, how does this work? Or like, SGLT, you're like, I don't really know. But this concept of your iron is low, we're gonna give you iron, yeah, that's great. And it really resonates that you're gonna likely feel better, right? So as I'm starting an SGLT2 inhibitor, and when I'm talking about IV iron, I say, we have good evidence within a couple weeks you're gonna feel better. They say, that's great. And they really do feel better. That's amazing. They really do. The patients come back and say, thank you, I'm sorry, you didn't give this to me before. And interestingly, for those that haven't given it previously, so it is a brown liquid. And it's interesting, like, many patients are like, this stuff's like going in, this is great. So all these trials were placebo controlled, which I think is an important thing to know. So if they wore actually like a blindfold, or this was covered. So these are really regularly done trials. And I haven't had anyone be like, why are you putting this in? But rather, they're like, this stuff's working. Yeah, yeah. We have a question from the audience. Yes. Hi, thank you so much for the talk. My name is Ian, I'm an inpatient heart failure pharmacist at University of Rochester. Do you want me to hold this? Okay. I have two burning questions, just because I've seen the same issues occur over a cross of three hospitals I've worked at now. My first question is, a lot of the major heart failure iron deficiency trials actually excluded patients with average like hemoglobin over 15, or actually in Ironman, I believe it was women, I think it was hemoglobin over 13 and men over 14. And so in that scenario, like I've seen a couple of patients that still meet the criteria for ferritin and TSAT. And so would you give those patients IV iron? And if so, how do you justify that they would actually benefit if they were not included in the trials? No, Sheena and I were debating this one here. We saw the question on the- Sorry, that was me. Oh yeah, we saw it on the app. I thought it was easier to explain. And we both said that we wouldn't, particularly if they're outside of the clinical trial inclusion criteria. But you always hear about indication creep, but Rob, Eliana, I don't know. Yeah, I mean, it's a great question, right? And so what I, my textbook answer would be, we've got to do what the label says. I think the actual art of clinician is you talk to the patients, you know, we don't really have data around your exact situation. You know, these are the risk benefits. And many patients may actually say, yeah, I'd actually like to try it. I can't get to my mailbox. I'm pretty miserable. So I don't think there's actually per se a safety- Concerns with the higher end ranges of hemoglobin in these clinical trials, so probably. And also that may be the early phase of the iron deficiency really showing up in the hemoglobin. And you may have caught it at an early phase. So that one may merit getting repeat study, you know, getting repeat iron in a few months and see if it changes. Great question. Thank you, that was, I think that was a good explanation. I agree with that. My second burden question is the hospital, there's two hospitals I worked at now where the choice of IV iron on formulary is iron sucrose. And there's a lot of, you know, you can give it higher doses over infusion, but then pharmacy has got to mix it. Those vials are small. So there's a lot of like people involved in making it. So the easiest way that people are doing and not willing to change, even when I bring it up is iron sucrose, 200 milligrams IV daily for five days. Biggest question I get is, you know, the trials actually went off of hemoglobin and weight. And, you know, earlier there was a, I think Susan presented that, you know, Gonzoni's equation. And there's also, you know, there's so many considerations, but, and then like patients may leave, like if they don't, if they get discharged on the second day, what do you do after? So in terms of dosing IV iron, if we were to strictly follow the trials, it would actually be based on that hemoglobin cutoff and the weight, recheck it a couple of weeks and then do it again. But in reality, that's not what's happening in these hospitals. And so I'm curious, like what kinds of things that you've experienced in your practices and what suggestions you have for the, we're not gonna change our practice, iron sucrose for five days. Yeah, I mean, I love these questions. Next time you got to get up here and be with us. Thank you so much. I love it. Yeah, so in our, at our hospital, they were trying to say iron is iron. And I was like, well, you're crazy. That's like, you can't say chemotherapy is chemotherapy. Give this one that we haven't tested in any way. So we pushed on that piece. And then we actually did a pilot study to say, our readmission rate is too high for six months. Let's do IV FCM in the outpatient clinic as well. And as part of a broader comprehensive strategy around readmission, we actually were able to reduce our readmission rate. Now we're able to get that on formulary as well. So I think there are creative ways we can do it because we really have no data on the inpatient side at all with any of these other IV iron formulations. It's pretty crazy. You need to pester, you need to pester your P&T committee. Whenever you want anything, you need to join the P&T committee so you can pester them. Thank you so much. Appreciate it. Thank you. Any other questions? Then I will call, oh, one more question back there. Getting a hematologist, you mean on the case? Yeah. How frequently do you refer to hematology and how pleasant were your interactions with the hematology regarding? Yeah, I do not have unpleasant interactions with our hematologists. They're actually very happy to hear from us that we're paying actually attention to something like IV iron, which they pay attention to. So I have not had that negative, but let's say I don't call one every time. Do you call a nephrologist every time the creatinine goes from 1.8 to two? No, I didn't think so. So we generally don't, but when I have, my interactions have been fine. For ambiguous cases where hemoglobin is 13.5, ferritin is 10, this kind of stuff. Exactly, or that you're worried about something else going on with that patient, I think it's very reasonable to get a consult before you involve the IV iron infusion. That's a great point. Thank you for that question. I will call this, oh, one more. Oh, my goodness, thank you. I have something to talk about. In terms of everything being said, like actually incentivizing people to make the IV iron infusion, where is the effort in terms of making it part of the GDMC, like you mentioned on Epic, where it's a quality measure? Do you have the magic four checked off? Where's the effort to making it like the magic five, if you will? Yeah, I can tell you what I have done since I'm the quality chief. I have asked our heart failure nurses, which Susan is one of them, to feel free to talk to the attendings when they're not paying attention to the iron studies and they're not doing them, getting them to do it. So that's my way of doing it internally because nobody's gonna get upset with them. They say to the doc, hey, did you think about this or did you think, you know, I do the same thing with potassium. So then do you think it has to happen like at a institution by institution level because the magic four came from consensus statement and now everyone adopted it. Is there a way to like centralize and spread it out? I think you can centralize it because every hospital, especially if you can show, because you need to show data, right? Especially if you can show that the patients feel better, that maybe they go from New York Heart Class III to II or to I, if you have decreased readmissions, if that patient isn't getting readmitted, anything that you can show data-wise would convince them, but it really should come from the top down because it's as important as GDMT is as we have seen here tonight. Thank you. This has been wonderful and those of you who stuck with us, much appreciate. And again, I thank the ACC for their willingness. Is there another question? I can't see on this side. Yeah, maybe we want to respect everybody's time. Maybe we'll wrap up. And other questions, please feel free to come up. Come up and talk to us. Thanks. Thank you. Appreciate it.

chronic systolic heart failure

severe fatigue

exertional dyspnea

hypertension

CKD

menorrhagia

iron deficiency

IV iron therapy

hemoglobin levels

nutritional deficiencies

multidisciplinary teams

patient education