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Ok, good evening everybody. Thank you so much for joining us, over 300 people registered tonight. Um It's great to see so many of you joining already. We're broaching on 100 which is fantastic. Um Welcome to this med primary care network event. It's great to see you all again. Um As you know what med all, we're running these events almost every week. We had a little bit of a hiatus over the over the summer, but we are so excited to be back tonight with Dr Patricia Campbell, um consultant cardiologist and heart failure lead here in Northern Ireland where I am from. Um As usual, we will go through presentation for about 45 minutes or so and then at the end, um we will have some time for Q and A. Um So please interact with us, send us your questions, your thoughts. I'll be monitoring the chat throughout. I'll put things off to the side and then we will chat with Doctor Campbell at the end of her presentation. Um If you haven't already, I'd really recommend having a look into the Med All app. We're really pushing the app at the minute. Because everything is there, it's front and central, you can get your certificates, you can join your events, you can register for your events. Um You can get your catch up content all there in the one place. Um I will pop the link for that into the chat. Um As you know, we have these events running almost every week and I'll give a little rundown at the end of what's coming up next. Um But make sure you're registered so that you're the first to get um slides, catch up content and hear what's coming up next. So I am going to hand over to Doctor Campbell. I have slides on the screen for the interests of everyone to actually see Doctor Campbell. I'm going to turn my camera off and slip into the background but be aware. Doctor Campbell, I'm here. I'm listening. I will be, I will be very close to hand if anything is needed. So, thank you so much and I will see you in a little while. Pleasure, Tim. Thanks a million. Um So never be kind to your medical students. Otherwise they come and ask you to do talks when they're all grown up. That's my learning for tonight. Anyway, Tim, thanks a million for asking me to talk. Um Maybe some of you might have heard me before because I tend to be banging on about heart failure all the time all across the UK. Um So it's very nice to have you all here this evening and thanks a million again for joining in. Yes, I am a consultant cardiologist in the Southern Trust in Northern Ireland. I'm also the heart failure lead for across northern Ireland for heart failure. And uh but I do a lot, quite a lot of work all across the UK and also in the Republic of Ireland with heart failure development. So it is my bread and butter and look, I'm going to give a talk tonight and also one next week and I tend to start off with heart failure with reduced ejection fraction. Um because it's the big one, it's the one that we're all, we all know lots about. Um But actually, we talk about half, relatively little. And so I thought we'd start with that tonight because sometimes it's always forgotten. Um So I thought we'd start with how I diagnose and manage F FF and I've done a case study and a little bit of discussion around the diagnosis and management of it to try and make it easy for the primary care setting. Next slide, please. Tim, these are just disclosures next slide. So I thought I'd start with a case of a 67 year old female. So she's had hypertension for 25 years. She's currently on Lercanidipine and Perindopril. She has obesity with a BMI of 37. She's a type two diabetic but very poorly controlled. And I had never seen a HBA1C as high as this when I met this lady. Um and for that, she was on Met Metformin and linaGLIPtin as an outpatient. And again, forgive me if my discussions about any care of diabetes doesn't sound like it's an expert because I am not a diabetes expert. However, I see a lot of patients with multi morbidity, particularly in the cardiorenal metabolic syndrome, which this lady most definitely is. She also has CKD and her baseline GFR sits around the 45 to 50 mark. Currently 48 when she was, when I first met her and 11 years previous, she had had Guillain Barre, she had had a full neurological recovery as is normal, but didn't really have a good psychological recovery and really never regained independence and was used to kind of being lifted and laid by her family and used a wheelchair and had become extremely deconditioned. Uh Next slide, please. Um So she was admitted to hospital multiple times under the medical teams over the period of four months and I never met her during any of these periods. And each of the times she was admitted, she was admitted with shortness of breath and exertion and swollen legs. Um She was a little hypertensive each time she was in sinus rhythm each time and these things are all important, which we will come to you later. She had a soft pansystolic murmur and evidence of peripheral volume overload. Next slide, please. Tim her lab markers showed she's non anemic with a hemoglobin of 100 and 31. She had no evidence of active inflammation or infection with a normal white cell count and normal inflammatory markers. Her GFR was 41. She was slightly hyponatremic and her potassium was normal. At 4.7 she had normal thyroid function which is always important to check on anybody with volume overload. She is slightly iron deficient with a ferritin of 100 and 30 at sat of 19%. And if you want to know more about why I'm saying that's iron deficient when maybe it doesn't meet the typical criteria for iron deficiency. I'm happy to talk about that at the end and her anti pro B MP was significantly elevated at 1108. Her chest X ray showed signs of volume overload with upper low venous diversion and small bilateral pleural effusions. Next slide, please. So they got an echocardiogram for this lady and the echocardiogram summary, you know, you get a big long report. It's like two pages long and at the very bottom, it just said preserved LV, systolic function, mild left ventricular hypertrophy with diastolic dysfunction, mild to moderate tr and the last line said high probability of pulmonary hypertension with an estimated right ventricular systolic pressure or R VSP of 58 millimeters of mercury. And I'm sorry, I'm just gonna turn off my emails there because otherwise we will be tortured with emails coming through Um And on the basis of this echo report, the medical team said you've got pulmonary hypertension and they sent a referral to a specialist center for her to get investigation as to why she had pulmonary hypertension. And it was based on that last line, high probability of pulmonary hypertension with an estimate, estimated RVSP of 58 I will come back to that next slide, please. Tim. So each admission she was treated with some IV diuretics and as it is quite common in hospital, after patients lose a kilo or two of fluid, they go oh I feel so much better. And of course, hospitals are under huge pressure. So a lot of teams take that as a great away. You go, you're great. You're much better. We've done our job. But each time she come back about a week or so later and then I was asked to see and I have a picture of this apple cart here because what I saw was an apple cart that I was ready to upset. Uh next slide, please, Tim. So let's remember her case, but I am going to get back to heart failure and look, these are some of our local trust data here in northern Ireland. But the message I want to give you is that the heart failure burden is rising. There is an estimated 92% rise in all forms of heart failure by 2040. Now, I'm not sure what you feel like in primary care, but certainly in secondary care, we feel like we are drowning in heart failure and our heart failure, nurses cannot keep up and we cannot get good appointment times because we have long waits because our lists are long and it feels like we are already struggling. So if, if that's the case, now, what are we going to be like in the next 1015 years? It does truly feel like we are that this is a medical emergency for our health services. And look, you can see that they are exponentially rising in each of their our trusts, not by huge numbers just because we are quite a small geographical area, but in terms of the staffing to deal with those people and the chronicity and the recurrent visits that they need. It does, it does consume a huge portion of the health care and over 50% of all of the new heart failure that we will see will be he ff next slide please. And why is that? Well, I will come to that in a moment. But if we actually look at how good a job we are doing at the moment in primary care, this is Northern Ireland data again. And from 2020 we had less than 1% of patients being registered as having heart failure. Now, our most recent data were doing slightly better than that at 1.06%. And I know for many places in the UK, the figures are not anywhere close to what they should be. So, what should it be? Well, the most conservative is a paper that was done in the Lancet which is a UK population and it, it states that really about 1.6 of your primary care population should be listed as having heart failure. But if we actually look more specifically at our patient populations in primary care, it's probably closer to 4.2%. And particularly if we screen those that are over the age of 65 it's probably closer to 12%. So we are missing a huge amount of heart failure out there and probably the vast majority of that is he p next slide please and look just to recap, we're talking about, there are lots of different ways to talk about heart failure. You can talk about ischemic heart failure, you can talk about congenital cardiomyopathies. There's lots of different ways that we can talk about it, but the way we're classifying them at the moment is we're basing them on ejection fraction. Now, that's, there's lots of arguments as to why that's a good thing and why? That's not a good thing, but there are different approved and guideline driven treatment strategies for people depending on their ejection fraction. So half ref or reduced ejection fraction is when the EF is less than 40%. And then these two, the half MF and the half PEF are different. Now, the half MF is a mildly reduced ejection fraction. That's when the EF is between 40 50% they tend to behave a little bit more like the refs. But the PS are an entirely different group. And you can see just by looking at that slide, that bright green box at the bottom, right, looks different than the other two box because there is a lot more stuff in it because to get a diagnosis of he is a lot more complicated than a diagnosis of he and half ref all that is, is some symptoms, signs of heart failure and an ef that's low. But to get a half, half diagnosis, you need an ef above 50% and you also need other bits and that's the difficulty. That's what makes a he he diagnosis a little bit more difficult and sometimes a lot more difficult. And we'll come into that in a little minute. Next slide, please. Now, what is Heff if I'm talking about like what causes it? Well, we actually think heff is the downstream effect of any of these conditions that are listed here on, on the slide. So, chronic kidney disease, hypertension, myocardial fibrosis, chronic congestion, left ventricular hypertrophy, pulmonary vascular dysfunction from like primary pulmonary hypertension, right heart dysfunction, which can happen from anything from COPD, sleep apnea, etcetera, etcetera, chronotropic incompetence. When you've got like really poor heart rate response to exercise. Inflammation is a big one. So you can see he PF in patients that have got chronic things like rheumatoid arthritis. But the big drivers of why he PF is like this going up exponentially is the increasing epidemic that's out there of obesity and alongside that type two diabetes. Um and he really is just the effects that happen on the heart because of all these things happening in the body. And if we are to look at an individual patient level, about half of patients have three or more of these comorbidities in their background. It's very rare to have a heart failure patient that does not have a multiplicity of comorbidities. So these are sick people with lots of problems going on. And then this diagnosis isn't that easy to make and that's why it's really worth concentrating some time in this next slide, please. So look, if we are looking at these comorbidities, this is again, just some local Northern Ireland data, if I exclude hypertension from primary care, and I look at all the other cardiovascular conditions like atrial fibrillation, obesity type two diabetes. There has been an increase in the last decade by 20% next slide. And that's also in the setting of a very aging population. And again, I'm harping on about northern Ireland. It is the same for everywhere all across the UK. But northern Ireland happens just to be particularly worse. We've got the most rapidly aging system of any of the four devolved nations with the biggest change ie the number of those over the age of 65 in the next 10 years than there has been in the previous 40. So, you know, an aging population, an increasing multimorbid population living with multiple chronic long term conditions means that he pe is coming our way. So we need to know how to diagnose and to treat it. Next slide, please. So look to make it even more difficult and why it's been historically difficult is that the trials, which is what we tend to base our evidence on. Have you don't need to know the detail of this slide. But it's just to show you that the the even the most recent trials looking at the SGL T twos, they all classify it in slightly different ways. So really, you know, people didn't really know how best to go about diagnosing that. And that's why we've written the article that I've quoted there. And hopefully Tim is able to share these slides with you is um a review paper for primary care so that you are able to more easily understand heart failure with preserved ejection fraction. So if I don't do a good job tonight, hopefully this paper which is written with me and a lot of people much smarter than me helps you do a better job at understanding it next slide. So a simple definition for it is somebody who's got heart failure with an ef of greater than 50%. But the E SE and that's the European Society of Cardiology, you have to have symptoms and signs of heart failure, evidence of structural and or functional cardiac changes. So that's some echo changes and, or a raised BNP note that I say and, or a raised BNP and we'll come back to that with an EF of greater than 50%. So you can see already it's quite complicated. Like I say again, he ref easy symptoms of heart failure, ef below 40% of an echo, done diagnosis, done. This is a lot more complex. Next slide, please. So look in our paper, we've tried, we've tried to break it down into steps and the vast majority of patients can be diagnosed in this one step. Now, there's a lot of text in there, but I'll talk you through it. So basically, if somebody has symptoms of heart failure and you get an echocardiogram and their EF is greater than 50% how do you know is that a normal because my echo, my ef is greater than 50%. I hope I don't have HEP F or is that a he FF echo? So they have to have another defining feature which is either congestion on exam. So pitting edema is a big one. An elevated J BP. Look, I love AJ BP. Tim will remember me as a medical student. My rhymes are just J BPS all over the place. They are difficult to read though, most people don't know how to do it because it is a very tough clinical skill. But if you can see an elevated GBP, that's a sign of volume overload or an elevated BNP. Now, the cut offs and this is anti pro BNP. Um If you're in sinus rhythm of above 100 and 25 if you are in atrial fibrillation, it's above 100 and 365. OK. BNP is also measured in here, but we don't typically use the use B MP. It's NT PRO B MP. Now again note that that's slightly different than the nice guidelines. And again, we can come to that in the Q and A but the official international guidelines states an NT PRO B MP of greater than 100 and 25 sinus R 365 atrial fibrillation and what you are looking for on the echo. So you are looking for these structural and or functional changes on the echo I have listed here. Now, you do not need to memorize these, but these are required on an echocardiogram to make the diagnosis and they include how thick or big the walls are, how fat the walls are on an echocardiogram. And normal left ventricular wall thickness is less than 11 millimeters for the average person. So if you've got somebody who's got very significant left ventricular hypertrophy, it leads to an increased LV mass or an increased LV wall thickness Now, those are things that you should see in an echo report. Now, when you've got a heart that's chronically elevated, under elevated pressure, the left atrium gets big. So you probably all know that the left atrial gets big in the setting of atrial fibrillation. But it also gets big in the setting of heart failure with preserved ejection fraction because the intracardiac filling pressures are really high. So if you've got a left atrium that's dilated, and again, you have a bigger cut off for atrial fibrillation to allow for that development with AFIB. So it's greater than 34 M per meter squared in sinus rhythm and greater than 40 for AFIB. And again, this will be in your echo report. Now, e to E prime is a measure of diastolic function and normal people that will be way less than five or you know, less than nine is very reassuring if it's greater than nine at rest, that's an indicator of elevated um intracardiac filling pressures. And then the last one which we can go back and talk about our lady is this increased tricuspid regurgitant velocity. Now, the reason why that relates to our lady is, that's what gives you an estimated right ventricular or pulmonary systolic pressure. And that's where they I think picked up on this lady, but we'll come back to that. Now, like I say, that is a lot of very, very technical echocardiographic detail that you do not have to know, in primary care. And that's why we wrote this report so that it's there for you, even in our echo room or in our heart failure clinic here in secondary care, there are some of us that know it off the top of our head. Hopefully I do because we've written a paper about it, but a lot of our nurses don't know it and we have it stick out and stuck out and laminated. They've got little cards in their wallets just to try and remember it because it's complicated and there's no need for you to remember all these figures. But if you're trying to make the diagnosis, that's what you're looking for. And so that's step one, about 80% of people will get a heart failure diagnosis at that stage. But what if they don't really fit those criteria or they are not on the echo report or you're not sure. So, next slide, please. Well, if you are really suspicious and perhaps it's because the N TBM PE level isn't greater than 125 in sinus or greater than 365 in atrial fibrillation. Well, then there are these scores out there which you can just Google the fa pe score or the H two F pe score. The first one is the European one. The second one is the American one. Don't tell the Europeans, but I actually prefer the American one because it's much easier. And when you've got a very low score in those zero or one, you do not have heart failure with preserved ejection fraction. If you got a very high score, either greater than five or six, depending on which score you use, you have HEPA, right? So it can be really helpful and we will come on to those in a little moment. And so if step one doesn't get you there and like I say, it should get you there for 80% of people, you go to step two and you try to do these little online scores. Next slide, please. And if, despite that, you're still not sure. So if they get an intermediate score, if their score is three or four, but like they've got really loads of symptoms, well, then that's when they do need something different. Now there something different is a very specialized test, either an exercise echocardiogram where we can get people to exercise on a bike and do an echocardiogram while they're exercising to see what happens. All those parameters that we talked about before or we actually do invasive hemodynamics and measure their intracardiac filling pressures at rest. And ideally by exercising while they're on the calf table, you can get a little stationary bike that we put on the tables and then if you get high filling pressures, either at rest or on exertion, then you get a diagnosis of HFA. But as you can imagine, step three, since I have moved back home to Northern Ireland six years ago. I have never done it. So it is going to be exquisitely rare than in a primary care setting. You're ever going to need to think about sending somebody for that. So step one and step two can be done so long as you have an echocardiogram and a history and that will get you the diagnosis for over 95% of your patients or it will refute a diagnosis next slide, please. So like I say, let's refer it back to our lady. So if I think about the defining features, so she had symptoms of heart failure, right? She kept coming in short of breath with like really swollen legs. So she had the symptoms of heart failure. Did she have any of the defining features? Well, she had chest X ray findings, right? She had evidence of pulmonary vascular um enlargement and then she had small bilateral pleural effusions. So tick for chest X ray. Did she have the anti Pro BNP findings? Yes, she did. Now this lady remember I told you she was in sinus rhythm but still in all her BP was significantly elevated at 1108. And again, maybe are gonna have questions about what causes the B MP. What, what causes the B MP to be falsely reassuring and we can talk about that at the end. But she met the anti Pro BNP criteria. She did meet these echo criteria for significant left ventricular hypertrophy. And again, if you're interested, we calculate the relative wall thickness by adding the intraventricular septum to the posterior wall and dividing it by the diameter of the left ventricle. And hers was elevated at 0.44 that we want it to be less than 0.42. Her left atrial volume index was 45 and again, she's sinus. So it's meant to be less than 34 and her E to E prime which remember I said shows elevated intracardiac filling pressures when it's greater than nine was 21. So exquisitely high intracardiac filling pressures on her exam and she had this tr gradient of 3.3 m per second and a right atrial pressure of 15, there's an echo equation that we use. It's for our squared plus right atrial pressure to get the right ventricular systolic pressure. Again, just for anybody who's nerdy and wants to know and that's how she was given a pulmonary arterial systolic pressure or an estimated right ventricular systolic pressure. They're interchangeable those terms of 58 millimeters of mercury. And that is why this lady because of the 58 millimeters of mercury got this diagnosis of pulmonary hypertension and it was wrong because they saw pulmonary hypertension and went straight there because they did not know about H PF its existence or its diagnosis. Uh Next slide please. But let's imagine that this lady's NT PRO BNP was 100 and 10, right? Instead of 100 and 1108. And that can happen because remember I told you at the very start, her BMI was 37. Now BNP can be falsely low in patients living with obesity and it's for reasons that are very poorly understood. But we, we do know that you are much more likely to have insulin resistance when you're living with obesity. And there's something about that even in the absence of type two diabetes that makes your um bioavailability of BNP or your production of BNP, much less. But it doesn't mean that you don't have elevated into cardiac filling pressures. So BNP can be falsely low in people living with obesity. Um So if it was 100 and 10, so I still have a high index of suspicion because this lady has lots of ec a criteria but just doesn't have the anti pro B MP. So what do I do next? Then I go to these scores, this fa pe score or the H two FP EP score next, please. Tim. So if I go to the first one, which is the European one, I don't like this one, even though I know the guy that wrote it and it's very good, but it's written by a, like the main author is a German guy who has got access to everything, right? We don't, I live in northern Ireland. I barely have access to a hospital bed. Um But if you look at, if you kind of ignore the stuff in the bottom two, they are all very difficult stress tests to get and invasive hemodynamics and CT S and pets and all sorts of things that I don't have access to. She actually had a score of six. Even just by going on her symptoms, her comorbidities, her anti pro BNP and her echocardiogram and she got a score of six and that's very high. So even if I had to go to step two, because her BNP was normal, she still got a diagnosis of H PF by the end of it next slide. And this is the one that I prefer. This is the American one, the H two F PF score where you get a score for heavy hypertension, hypertension, fibrillation, pulmonary hypertension. And you see the pulmonary hypertension is in there, which is indeed itself a help to remind you that the pulmonary hypertension is probably just a sign that they've got he pef elder greater than 60 elevated filling pressures on the echocardiogram. And again, she got a score of six in this. So you do need an echo for these scores, but they're very helpful. And again, she went to step two if her BNP had been normal and we still were able to make a half path diagnosis next slide. So, what did I do? Yes, I upturned the Apple Cart and I tell you this was probably one of the more difficult cases in my life because this lady has been in the hospital a huge amount. She has a beautifully devoted family who were obviously going well. Hold on. We were just told we are going to see some super duper specialist in the center. And now you're telling me we don't need to go. So they were really, really upset with me because they had been told over the course of many, many weeks that this was happening. And then suddenly I'm going, actually, I don't think you've got that at all. Trust me. I am a doctor and, you know, they were really upset at me. In fact, actually, there was one really difficult period where they kind of came into my office and closed the door behind me and got really cross with me. But anyway, I managed to convince them that I had the skills to be able to diagnose it and to treat her. And if they trusted me, I would get her much better than she had been in a long time. And again, that makes me sound like I'm really big headed, but I just knew what I was looking at. Um, so I kept her into the hospital for much longer than she had ever been in before, but she did really well. So next slide pleased him. So he pef is different than the rest, you know, and we will talk about, he ref next week and we'll touch on heart failure with mildly reduced ejection fraction next week. Um, but there are really three central tenets of care for. He pef and the first is, and I suppose what we used to just do was diuretics. So, if you've got symptoms, you need to give diuretics to manage the symptoms. Now, this lady, every time she came in was markedly volume overload. But in the primary care setting, you might just get somebody who is short of breath on exertion. And if that's the case, you institute diuretic therapy or you escalate diuretic therapy. But in the last 18 months, we've had two huge trials to tell us about the use of SGLT two inhibitors which you again in primary care have been using way longer than I have. And indeed, it probably took me a year or two after the trials came out in 2018 to actually get into the way of using them. But flows and 10 or flows and 10 are both now class one indications for somebody with a diagnosis of he pf now they probably work as a slight potentiator for a diuretic. But there is other properties involving antiinflammatory properties and decongestant properties with synergistic effects on other medicines that we don't really fully understand. But we do know that they definitely reduce heart failure, hospitalizations and maybe have an impact on cardiovascular death as well. So again, these are not patients with diabetes, although our patients often have diabetes, but we're not using it for a diabetes indication. The third central tenet that's really important is that you must screen for and treat the other comorbidities. So, if somebody has got hypertension, it needs to be under good control. If somebody's got atrial fibrillation, you don't want them bl at 100 beats a minute, they want to be around 80 or 90 beats a minute. If somebody's got obesity, you really want to think about a GLP one receptor agist, you really want to think about an exercise program, caloric restriction, et cetera, et cetera. If somebody's got sleep apnea and you haven't looked for it, you need to send them for sleep studies, etcetera, etcetera. So you need to be looking at any of the other chronic conditions that can be contributing to the development and acceleration of he PF and again, that's a central tenet because we only have one class one indication medicine. That's an SGLT two diuretics don't save lives. They just make people feel a bit better and help keep them out of hospital, but they do not save lives. Um But treating these comorbidities often uses lots of the other medicines that we use in cardiology and, and heart failure like ace inhibitors, sometimes beta blockers, sometimes Mra and we'll touch on that a lot more next week. Um But you know, they are not a class one indication. They're not the primary reason I'm not using them is to treat the he pf I'm using them to treat the comorbidities. So that's the three central tenet SGLT two diuretics for decongestion and then treat everything else that's going alongside to cause this half pf next slide, please. So what did I do for this lady? So this was back in 20 I was just back from maternity leave. So 2021. So Dapagliflozin 10, she had previously been sent home on frusemide 20 each time. And I rapidly escalated that to now she got lots of intravenous diuretics. I had her on a diuretic infusion while she was in the hospital and she stayed in the hospital for 10 days, but I sent her home on a much higher maintenance dose. So she sent home on bumetanide two M GBI D. She'd come in on Lisinopril and we had to put her up to max dose of her ace inhibitor to control her BP. And because she started to develop hypokalemia with her diuretics and also because her BP wasn't under excellent control. We added spironolactone 25 mg once a day. Now I can talk a bit about why else I might use an MRA in this setting. But um we might have a little bit more um time at the end to, to, to query that um we also sent for cardiac rehab because every single person who has a diagnosis of heart failure deserves to get a cardiac rehab. We know that cardiac rehab helps keep people out of hospital. It's not a medicine but it definitely does as good a job as many medicines in keeping people with heart failure out of hospital. Now, I don't know what it's like for lots of places in the UK. I often hear stories from lots of my lovely friends in England about the great services that we have. We have really restricted services here in northern Ireland and not many places have cardiac rehab. And if we do have cardiac rehab for heart failure, we have usually restricted to he or post M I or something similar. But we're trying to expand ours out and we have a really amazing dedicated um rehab team who are really interested in it. So we're trying whether this lady, this lady had to wait quite a long time before she got on it. But for her, I thought it was particularly important because she had had a huge amount of deconditioning after her about 11 years ago. No more recently when I had seen her. Now, this lady hasn't been in the hospital since 2021. So that that difficult period that I had with her family behind my office door when I was a bit scared because they were so cross, you know, was worth it. And the tough conversation to try and convince them to follow my treatment plan was worth it because this lady has never been back in the hospital with her heart failure. Um So it really was something that was critically important for us to do to get the diagnosis right, to treat her adequately when she was in hospital so that she could maintain um a better quality of life, life and health status as an eye patient. Um So more recently, we talked with her primary care physician and um we have changed her linaGLIPtin for a GLP one receptor agist for a multiplicity of reasons, but particularly for her, her obesity. And there's huge amounts of emerging data for semaglutide in particular for patients with he pe now, we don't have a huge trial and it's not at the point yet where we're going to be recommending it as a class one or two agent any time soon. But certainly looking at meta analysis of data for some agli in cardiorenal populations and diabetes populations that have subsets of he pef within them. And then there have been tiny small trials um about 100 patients in the E HE PF program and the Step HEF Diabetes program. Um it certainly looks like it has an impact on heart failure, hospitalizations and quality of life for these patients. It certainly improves quality of life, but it does look like it has heart failure implications too. So, um maybe, you know, if I give this talk in four or five years time, perhaps we'll be recommending some IDE as a class one agent but not yet. But certainly we know that it has good cardiovascular outcomes for patients living with obesity and type two diabetes. Um, we also sent this lady for sleep studies, not only just because she has a BMI of 37 but patients with he PF often have sleep apnea that isn't hugely recognized because a lot of the symptoms overlap, you know, fatigue, exercise, intolerance, quite sleepy, exhaustion. Um, but especially in the setting of very high BMI sleep studies are critically important to try and identify sleep apnea. Not surprisingly, she had sleep apnea and has since been initiated on CPAP. Uh Next slide, please. Now, what might future care look like for HF Pef? Might there be another pillar? Well, there might, so I've talked to you about some Aglietti but that's quite a ways away. Next slide, please. Tim, but just hot off the press. I was at the EE that's the European Society for Cardiology just last week. And the Fine Arts heart failure trial was the big trial that all us heart failure nerds. We're very excited to see. And that's with Fenin, which is a nonsteroid lame right now. Maybe you have seen Fenin being used. It is licensed for patients with CKD and type two diabetes because it reduces the renal comps outcome. So, worsening renal failure or sorry, worsening renal function with a decline in GFR greater than 50% development of endstage renal disease requirement of dialysis or transplant, right. So it, it is licensed for ad population, but this was looking in a hef pef population. So next slide please, Tim. And it definitely showed a significant reduction in cardiovascular death and total heart failure events of about 16%. And that's not insignificant for these people. You know, you might hear a lot of people saying, well, what about he? It's nowhere near as severe as he actually. So in the trials initially done in he, these patients weren't, didn't tend to have as many events as a he ref population. But actually real world data shows that they are in equally as much. They have often got huge diuretic resistance. They are often really burdened with many more comorbidities than a half ref population. And they are very difficult to treat and have a much worse or if not worse than equal, equally bad quality of life as a half ref patient. So a 16% improvement in hard endpoints of heart failure, hospitalization and cardiovascular death is very impressive. So look, it is not in our Armamentarium at the moment, but it's very likely at the next iteration of the guidelines that there's going to be a change. And I certainly know that I've had been thinking about and waiting on this trial date to come out for months now and was very happy to see this. And, and certainly I'm already aggressively looking at my CD populations to see if any of them could be benefiting from Fone So hopefully we'll be using it a lot more uh next slide, please. So, conclusion A he pe diagnosis is definitely more complicated than LV systolic dysfunction. So once you got an ef that's low, it's very easy. But he pf there are much more bits to it. And therefore, that's why we tried to write that paper for the lancet to use these simple steps, giving you a step wise approach to the diagnosis. ST LT twos are our only class one medicine diuretics to treat congestion effectively is really, really important. And the treating comorbidities are the three central tenets. But if you are not sure, please call your friendly heart failure cardiologist. And hopefully we will help you either diagnose and or manage these patients. And so Tim, I think I have enough time to open it up for questions. Absolutely fantastic. And your friendly heart failure, cardiologist couldn't ask for a more, more friendly local helper here for me. Certainly. Um Folks, I hope you agree with me if we can maybe get some reaction in the chat. That was absolutely fantastic. Um mesmerized. He, he f always confused me as a medical student. I always struggled so much more with it. He ref made so much more sense. It just was logical functions down much more difficult or easy to manage what we do. Four pillars, Bang Bang Bang He Pef was always that kind of one that you hope didn't come up on an exam question because you were like, oh, it's going to be confusing. It's going to be awkward. It's not going to know what to do. But no, that was absolutely fantastic. Some new emerging stuff there towards the end as well, which was really interesting to hear about. Um I picked up on a couple of things, um, Doctor Campbell that you had mentioned yourself that I just wanted to circle back to. So the first was the BNP cut off being higher in AF is that just because of a physiological thing where or what, what's the reasoning there? Yes. So um there are loads of things that cause your BNP to go up. So you may, you may see discharges coming out of hospitals and in the discharge summary, it will say, oh, you know, the BNP was 600 but there's no mention of heart failure mentioned in it and because there are a multiplicity of cardiac and non cardiac causes that cause your BNP to go very high. Um And CKD atrial fibrillation and hypertension are some of the big ones. But also if somebody comes in with a really bad COPD exacerbation, your BMP is going to come up because you've got significant back pressure to the right heart from high pulmonary pressures. When during a COPD exacerbation, somebody septic, you know, they're going to put the heart. There's lots of things, anything that causes your heart to be under pressure causes your BNP to be raised. But those conditions that are chronic hypertension, CKD and atrial fibrillation all raise your BNP. Um atrial fibrillation. We just, we know a lot more about atrial fibrillation and we know kind of the cut offs between when are normal intracardiac filling pressures related to BNP and when they're not. And that's why we're able to give very specific cutoffs for that. We tend to kind of look at CKD much the same way as we do um for atrial fibrillation. But if you've got somebody who's got really well controlled BP on their antihypertensive medicines with a history of hypertension, they shouldn't have an elevated BNP to be put down to their hypertension alone. So it depends on the setting, do you know? But atrial fibrillation will certainly make your BNP go up. The only thing that can make your BNP falsely low is obesity and not. So that's why I, that's why I gave the two scenarios for that lady. So that if her BNP had only been 100 and 10, but she had everything else going for her for a half pack diagnosis, then you just look at the one of those scores that we talked about and then you were able to say actually, yes, she does have half pack despite a normal BNP. I know scoring systems was something else to pick up on and something that I genuinely hadn't recognized before that existed. It was really interesting. I was, I was frantically med Kin here to actually look at the, at the parameters for things just before you brought the slide up. Um The other question I had picked up on and hopefully there'll be a couple more maybe pop into the chat was with regards to the MRA S, the alternative indications for those. Um, apart from the low potassium caused by diuretic use, you'd mentioned you sort of alluded to other comorbidities that that can be useful for. Right. Well, it was more that I kind of knew fine arts was coming. So I, and the reason trials are done is because people really believe in the hypothesis behind them. You know, and the hypothesis was that we think MRA S are good for heart failure with preserved ejection fraction. So if you look historically at he ref right? And we are going to talk about that next week, about all the pillars of care that we use for. He fr we've also done all of those trials for HPE. They've just never been positive before the SGL T two, right. So we did an Mra trial a long time ago for he pe and it was a negative trial, but there's lots of bots. So it was called the top cat trial. And it looked at spironolactone. We all know spironolactone. It looked at spironolactone in heart failure with preserved ejection fraction. Then while the trial was negative, actually, when you look at the trial and how it was done. And again, II used to sit, I was working in Boston at the time and I was part of the Endpoints Committee and the people in the trial who were in the Americas all definitely had heart failure. They had very high BNP S. They had admissions to heart failure to hospital with heart failure. They needed to go and get intravenous diuretics as an outpatient, they needed escalation of their diuretics as an outpatient. So we knew they definitely had heart failure. Whereas the people from Russia and Georgia, which was the other population in, in the big trial, they had very low BNP S and they never or very rarely had a heart failure event needing intervention. So they probably didn't really actually have heart failure with preserved ejection fraction. And again, we had, it was a lot, it was quite a while ago. So we didn't really have clear echo criteria for what he was. But if you took just the Americas people who we knew definitely had heart failure, it was a strongly positive trial. Now, sadly, you can't just take bits of a trial that you like and ignore the rest of it and apply that as science because that's not how science works, right? But I think many of us have believed that Mra S actually were really, really helpful and anecdotally, we've used them for many, I've been doing this a long time as you know, for many patients over the years, particularly in the setting of hypertension as an add on. And as you know, in primary care, we use spiractin way down the line as, as an added agent for people with resistant hypertension. But we might use it a little further up the line for these patients. And we definitely find an again, but again, universally, a lot of people would say this is that we find that it actually really has helped patients and patients who would frequently be in and out of hospitals when you institute that suddenly they're a little bit easier to manage. But it also does help the hypokalemia that these patients tend to get when they because they do require quite high doses of diuretics frequently. Um and it does help the hypokalemia there. And as you all know, hypokalemia as well as hyperkalemia both increase your cardiovascular risk. So anything that you can do to mitigate hypokalemic event, then I think is important. Now, a lot of people don't use MRA S because of this, worry about hyperkalemia. And again, that's all I sound like a historian, I'm that old. But that all came from the ra trial back in the day. And that was looking at lactone in the setting of dysfunction post M I and everybody started using it in everybody. And lots of people, a Canadian group had a big paper in the New England Journal of Medicine in 1993 showing we are killing people with hyperkalemia, but it's because people were instituting Mra and not checking e within about two weeks and then not doing 3 to 6 months, depending on the baseline e to keep an eye on the potassium. So you do have to keep an eye on the potassium on an MRA, but they weren't doing that. And so the world got afraid of Mra. And actually, again, we'll talk about them next week in half ref you need, you need to treat only eight people to prevent a heart failure or cardiovascular death in half ref So it's one of our most effective medicines. Um So look, II think historically we have been under using them. Um but I think if you look and treat, try and treat the hyperkalemia or you know, look for hyperkalemia and try to offset it by doing other things like increase diuretics or whatever it is, you can really help prevent it. And these are now lifesaving medicines and then fine arts come out last week. So we kind of hoped fine arts would be positive and it is overwhelmingly positive. So it does look like fine arts or fone is going to be the next pillar to the care for these people. The fifth pillar, all those teaching about the four pillars is going to have to be updated. The four pillars is half ref right? And that's why I hate pillar here because then it gets confusing. Four pillars is half ref which we'll talk about next week is SGLT two. That's the only medicine that really, we've got as a pillar with two other central tenets of care. You know, it's decongestion with diuretics and treat comorbidities. They are not, you know, they are not exactly a, I can write prescription for those but, you know, they are kind of, they are a way that you must care for these patients, but there's only one medicine at the moment and SGL T two. But I think you'll start to see us using for even before it gets to the guidelines. Sure, sure. There are a couple of questions coming in. I think the creative juices are flowing. Um Carla has asked, can BNP be used to monitor treatment? Great question, Carla. So do we use it? We don't typically use it again because we are a cash dropped poor third world place in Northern Ireland. Um We sometimes do, there is a quick answer. So here is where we definitely know BNP is really useful diagnosis. You cannot make a heart failure diagnosis without a BNP. And even when the B MP is less than you would expect, then you follow the steps that I showed you. Um So it's critical for diagnosis. It's also really important prognostically at the time of discharge. So if somebody is admitted to hospital with heart failure and say, for example, they come in with ABM P of 16,000, if that person goes home with a BNP of 1000. I am very happy that we have done a great job and that person's outlook is really quite good. If that person goes home with a BNP of 13,000, I know that is a high risk person and I know that there is somebody that we need to keep a much closer eye on. So it's prognostically important at the time of discharge. So, diagnosis and discharge, but the question of whether or not it is useful to monitor treatment is an interesting one. So back when I was living in Canada, yes, I am old and I've lived everywhere. Um we did the guided trial and we were one of the first sites to recruit and actually that trial was negative and that was looking at BNP in the outpatient setting to see if it improved outcomes compared to usual medical care. And it didn't. But what I would say is we were all advanced heart failure, practitioners, transplant consultants, you know, that's our bread and butter looking after these people, but it didn't really, you know, it wasn't done in the primary care setting. For example, there's been a more recent trial called Strong HF, which is patients early post discharge or in hospital and early post discharge started on all the pillars of medicine that they need. And this again is mostly a half population and followed quickly with BNP. And it showed that rapid up titration with BNP resulted in reduced heart failure, hospitalizations and death. So maybe that's the BNP driving it. But most of us think it's probably that we are doing a really good job and we are seeing these people a lot and getting them on the guideline directed medical therapies as quickly as we can. So I think it's a little bit unanswered as of yet if you are not sure that the times when I use it is, you know, it's particularly helpful in the elderly who got a little bit of memory issues, not really able to tell you their symptoms, but they are just a bit off their feet and you're going, is this a heart failure exacerbation? Because I know they've got heart failure is this, you know, are they having a decompensation and just not presenting in a very typical, you know, we all know our apnea is really typical. We all know like loads of peripheral edema is really obvious, but sometimes for the older person, it's just off their feet, nocturnal incontinence, which is brand new, you know, loads of nocturia, which they've never had before. Something different. Um And then that's when I would tend to use it quite a lot. So hard to know it's no harm to do it. We know it's no harm but whether you really need to do it, I don't know. And so we don't because we are a cash strapped environment. Brilliant. Um, Jasmine has asked about diuretic choices I wonder is this just a matter of potency or um how do we decide which diuretic to use? Can I just say all these questions are absolutely brilliant. It's like they have gone and read all the heart failure literature and then come back to me with these really pertinent questions. I love them. Um But it's a great question. So the question is Frusemide Bumetanide, Torsemide or spironolactone. So you've heard what I think about spironolactone? It is and again, next week, it's all about he and it is a central pillar of care. MS are probably going to be used. And again, it's based on data that was just presented last week for he in the future. At the moment, we use spironolactone as an add on agent sometimes, but it's not a, you know, it's not got a class one indication. So for he pf it's just kind of sometimes at the moment. But for heart failure in general, if I'm just using a diuretic, we typically use a loop diuretic. So the first three that Jess mentioned there is Frusemide bumetanide and Torsemide. So those are all loop diuretics and what's the difference between them? Well, when I was in the States in the Brigham holy Smoke, we used torsemide until it was coming out our eyes, but it's like a million times more expensive than Frusemide. And actually Rob Men who was training with me at the same time, just did a paper in a trial in it last year looking at, was there a big difference? And actually there was no difference. You might have lost a bit more weight a bit more quickly with the tour. But it was just exactly the same, really, the outcomes were the same patients didn't stay in the hospital any less time. They didn't get readmitted any less. Um, and it's just really expensive so we don't tend to use it here at all occasionally. You know, we've had one patient, I can think in the last six years since I moved home who had allergies to the others and didn't have an allergy to torsemide and we used it, but that's the single time that I've used it since I've got here. So really the choice then is between Frusemide and Bumetanide. And how I make the decision for that is Frusemide I tend to use in the diuretic naive people. And so if somebody has never been on a diuretic before, I'll start Frusemide 40. Not occasionally, I'll start 20 if they're very old, very frail person with a very high clinical frailty score occasionally. But frusemide 20 is essentially air, you know, so it's typically a frusemide 40 starting dose if that doesn't work. I double it if that doesn't work, I double it. Now, once I'm starting to think about 80 mg BD or flus, then I start thinking this is a lot, quite a lot of diuretic. And frusemide has about a 45 to 50% bioavailability from the gi tract. So you're kind of only absorbing half of that. Whereas Bumetanide has 80% bioavailability. So one mg of bumetanide is equivalent to 40 mg of frumide. But actually, you might be absorbing more of the diuretic because you're getting more of it through your gi tract. So if I'm starting to go up to really high doses of frusemide orally, I'll just change it to bumetanide. So if somebody is on 80 BD or frusemide, you know, if that's working for them fine. But if it's not, then I can go. Ok. Well, three of bumetanide in the morning, two in the afternoon, that's, you know, the equivalent of 100 and 2080. But they're probably getting a little bit more of it or if they're borderline renal function and I just want them to get a touch more diuretic, I'll just go two and two, which is equivalent, but they may get more of the diuretic function from it. So that's how I make my decision. So torsemide, never frumide bumetanide or my two loops, frusemide for the diuretic naive bumetanide for those requiring high dose of frusemide. And spironolactone is a class one pillar for HEF ref and at the moment, an add on for Heff. Amazing. That's actually really interesting. So that actually brings it home because I always knew about the equivalence, but I didn't realize the bioavailability factor as well. That's really interesting actually. Um a great question from a primary care point of view here. Um While I has asked, um are they correct in saying that SGL T two inhibitors can't be initiated in GP? Is that a myth to bust? You guys have been using them way longer than us. Stupid cardiologists have been using them. Definitely not, definitely not. So, you know, we have um for anybody that is living in Northern Ireland in the Southern Trust, we do a virtual outreach clinic to our patients, to our colleagues in primary care for patients out in the community who either have a diagnosis of he fr or he F PF and have never been put in an GLT two. But rather than go on an interminable waiting list to see a heart failure nurse maybe in three years. And we know these medicines are life saving. Actually, these medicines start working, the curves start to separate after days of using them. So within 14 days, you've got a benefit from being on an SGL T two and that benefit is can be life saving and by by a month, you are starting to save lives as soon as you use it. So why would you delay? There is absolutely no reason. So the only time we say not to give an DL to is when there is an active contraindication like pregnancy or breastfeeding or a type one diabetic. I never ever, ever, ever given a type one diabetic or somebody who's got a lot of diagnosis, you know, those latent autoimmune diabetes of adulthood and we don't give to those patients. Um, but everybody else can get an SGLT too so long as they're able to follow the sick day rules. You know, most people will never have. What the big thing that we all worry about in the altitude is a euglycemic DKA. It's an extremely rare complication that was really only seen in the patients who are diabetic and typically with CKD. But we always give every patient the sick day rules, meaning if you are, can't eat and drink or you've been vomiting and diarrhea or you're fasting for some reason, probably don't take your SGLT two until a day or two after you're better. Um So that's really the only, the only things that say yes or no to an SGLT two. You know, we do definitely um counsel about very good genital hygiene because thrush can be a problem because you're peeing out sugar. Um But with good genital hygiene, even in the trials, they didn't see an increased risk of severe genital tract infections, simple uncomplicated ones that are easily treated with over the counter creams or fluconazole. Um So, you know, if they are simple, yes, they are recurrent, but you do just advise about genital hygiene and UTI S weren't seen as an increased risk in, in the trials. We've seen a couple in the community that we've had to stop, but we've always rechallenged once they've been treated for the UTI and it's rare that we've had to stop entirely for recurrent UTI S. So, don't think I can't do it because I'm only in primary care. Of course, you can. Why would you not? It's got a heart failure diagnosis. They have a class one indication for an SGL T two. Fantastic myth. Busted my amazing uh I think we maybe touched on this from Richard about being anxious of giving high doses of diuresing the community without frequent blood monitoring. That um is that a concern about potassium dysregulation or? So look um the time to worry about using high dose diuretics is when you have somebody who has previously had very little dose diuretics and now they are in very high dose diuretics. It's the delta. That's the worrying thing. If somebody has been on bumetanide three MGB D for two years, you know, at the start when we initiate very high dose diuretics, yes, you need a and within two weeks and yes, you probably need one within another two weeks. But after that, you can do three monthly or six monthly depending on their. And so typically for the patients with CKD, we would recommend them three monthly or for the patients who have normal renal function, we would recommend them six monthly unless they've had intercurrent event. That means you need to check it again anybody on high dose diuretics. But again, there are lots of people out there in the community who are on high dose of diuretics. But when you change somebody from a relatively low dose to a very high dose in the community, they do need quite frequent monitoring. And that's probably when you need your heart failure and our specialists to be aiding you. You know, if somebody has had a decompensation, they do tend to, you know, if they are really, really unwell, they do tend to benefit from seeing a heart failure nurse specialist. And so look for me, I would always ask for help. And even if you know, you can't, the patient say for example, is a nursing home resident or is just unable to come to the hospital. That's why we do things like our heart failure virtual clinic. So I think it's really helpful to have access to a heart failure specialist, even in the absence of being able to see one face to face. And that's why we do that. So we can say, look, I've done this blood test. Is this ok? And you're able to talk to me like you're looking at me right now on the screen and say, look the GFR has done X the potassium is done. Why is that? OK? What should I do next? Should I adjust the dose of diuretics? And that's why we set up that service because heart failure is difficult and these patients are very complicated. Um But look chronic high dose diuretic use. We see, we see a lot and yes, they need frequent monitoring at the start, but often then thereafter they are very stable. Amazing. I've had a quick scan through the rest of the questions. Quite a few of these are maybe answered earlier in the talk. Um So I'm going to jump to one final one just in from Kerry who's asked about if a diabetes patient, um is newly diagnosed with heart failure already on Can Flosin for, for their diabetes control. Would you consider switching the Flosin for the heart failure benefit? Probably not. So we we've seen patients, patients come into our clinic on Can Flosin. Now, there was never a dedicated heart failure trial for Can Flosin, but there was the cardiovascular outcome trials at the same time that Emre and those came out there were Can Flo Canvas was the name of the cardiovascular outcome trials for that. And look, it does have cardiovascular benefit as well. So I think it's a class effect. We can only recommend A and da because that is the only ones that have been tested in heart failure. So they are the only ones that we can recommend. But I don't typically change. No, you might ask somebody else and they might do something different. But I don't. Amazing. Fantastic. I think in the interest of time we will, we will call it a day on the Q and A there. But can I share a few things with you including um, a couple of upcoming talks um before a massive thank you to um, Doctor Campbell. I'm just going to pop up the QR Code um, while I'm running through these last couple of bits and Bobs, um, just for getting your feedback, um, certificates, please do fill these out. They mean a lot to our speakers. Um They mean a lot to our speakers in terms of um editing their talks and also getting feedback on teaching and things. They really appreciate it. We like to hear your ideas for upcoming events as well, which are which we do look at, we do try and tailor things. Um And with that in mind, with heart failure having been such a common um thing in previous feedback. I'm just going to pop in the link to next week's talk, which is heart failure part two with um Doctor Campbell. We'll be looking more at he fr and also um after that um premature ovarian failure with Dr Vikram Tar, which we have had the joy of having teaching from as well, which is upcoming. Those two links are in the chat now, please register for them so that you don't miss out on those upcoming events. Um without any further blabber on, I think we've had an absolutely fantastic night. I want to say a huge thank you to Doctor Campbell who I know is um frantically busy with other things. Between papers and deadlines and all sorts. So I want to four year old and family commitments too not to forget. Um and say a massive thank you on behalf of the, of the all 100 and 10 people who were here during tonight and 100s more who I am sure will be catching up on the content. I had a look at the statistics you want to see um the worldwide reach of this teaching. Um We are right across the world with registrations. Um I'm not even going to start the name because it's impossible. Um But we really look forward to having you back again next week. Doc Campbell. Thank you so much for your time. Um And folks have a great week and check out our upcoming events and we will see you soon. Bye.