Dr Rafal Francikiewicz: Good evening everybody. Welcome to this evening's Identifying and Managing Heart Failure WA Webinar. My name is Dr Raf Francikiewicz and I'll be your host for this evening. Before we get started, I'd like to acknowledge the traditional owners of the land from where each of us is joining this webinar today. I wish to pay my respects to the elders, past, present and emerging. Just a few housekeeping notes. This webinar is being recorded and you'll receive a copy in the coming week. If you cannot see this control panel on your screen, move your cursor over the bottom of your screen and the panel should appear. The control panel provides you with the audio tools for adjustment and is where you can ask questions via the Q&A module.
Dr Rafal Francikiewicz: We have put everyone on mute at the moment to ensure learning will not be disrupted by background noise. If you need assistance, please use the Q&A feature to raise any technical issues and to submit your questions throughout the presentation. We will be addressing your questions throughout and after the presentation in the dedicated question and answer time. You can upload questions by selecting the tick icon on a question. This will assist us in reducing the amount of same or similar questions being submitted.
Dr Rafal Francikiewicz: Tonight's webinar is proudly supported by Medtronic and our presenter this evening is Prof Gerry O'Driscoll, internationally recognized as an expert in heart failure, cardiomyopathy and mechanical heart support. Prof O'Driscoll has served as the medical head of The Western Australia Advanced Heart Failure and Cardiac Transplant Service from its inception in 1994 until 2010. He holds fellowships and high degrees from leading institutions in Australia, Europe and the USA and teaches specialist cardiologists, other doctors, and students in Australia and internationally. Prof O'Driscoll is a reviewer for international journals in medicine and science and has been involved in the development for mechanical heart support devices internationally. His local and international research has resulted in hundreds of conference presentations and journal publications, as well as academic university appointments. We'll get started now and I'll handover to Gerry to commence his presentation.
Prof Gerry O'Driscoll: Thank you very much for the very nice introduction. Now, hopefully, you can see me and hopefully you won't see me for very long, so I'll switch my ugly face off shortly and just put the slides on. Thank you very much for the invitation from the college and for Medtronic for supporting this evening. I have spent an awful lot of time dealing with heart failure and talking about it, etc., and normally I'd like things to be as interactive as possible, not as easy as usual, with the current sort of format, but all the same, you should be able to throw up some questions, disagree with things whatever you like along the way, I may not be able to deal with them in real time, but we'll stick to that as closely as possible and deal with whatever is left at the end. Now, I will just try to share the screen and hopefully that's worked.
Prof Gerry O'Driscoll: There goes the share button.
Prof Gerry O'Driscoll: So, if you can't see a slide, somebody please let me know now because otherwise I'm off the screen and talking to myself for quite a while and I'll just shut down my video feed just to make sure the sound quality and everything is okay.
Prof Gerry O'Driscoll: We've all learned about heart failure in medical school and beyond, and usually people start by defining what it is and tell you how terrible it is. I'm not going to do that. I will tell you some of the terrible stuff later, but one of the things we've realized over the years is that heart failure is not easy and it's difficult to diagnose, people come in short of breath with a little bit of non-specific swelling. Many, many things can cause that.
Prof Gerry O'Driscoll: And sometimes it takes quite a while to arrive at the right diagnosis. It is not always heart failure. It's not always venous insufficiency either and we need to have a structure to diagnose people and decide what tests are required to support our putative diagnosis, based on symptoms and signs.
Prof Gerry O'Driscoll: It is a very complex disease, and it doesn't travel alone. It comes with many other comorbidities which interfere with what we would like to do with the heart failure drugs. Because of that, sometimes you can't up titrate the medications as much as we would like to prognostic levels for the patients' benefit.
Prof Gerry O'Driscoll: And secondary to that, people are not managed as well as they should be. They have been in and out of hospital a lot and cost us a fortune. About 65% of patient costs relate to inpatient care. I've worked in public hospitals across Australia and elsewhere for like 30 years and it is now my insight that even in the private system and I'm all too familiar about how poor the communication is both ways, we get referrals for people which say no more than "please see and advise". Or people go into hospital, stay there for a couple of weeks. There's no discharge summary comes out on the other side. You don't know what medications have been changed. You don't know what diagnoses have been accrued along the way, so communication in and outside of the hospital results in fragmented care, which is siloed inside and outside of the walls of various institutions.
Prof Gerry O'Driscoll: Once people get heart failure, the occasional one is lucky. It's an acute illness that comes and goes, but in general it's not. It tends to be a chronic lifelong disease and when people are confronted with something that takes a long time, just like the rest of us with COVID and lockdown and all the rest, they tend to get a bit sick of all that and noncompliance is a major problem.
Prof Gerry O'Driscoll: The pathways for patients' management inside and outside of the institutions are unclear and disconnected. Patients often come in and go out of hospitals very rapidly these days, and don't receive the sort of opportunity for education that they would have had years ago when they spent maybe 5 to 10 days in the hospital, whereas now it is 2 or 3.
Prof Gerry O'Driscoll: And patients' relatives are usually peripheral to the conversations and many of our patients, particularly in Australia are non-English speaking, which contributes to the problem.
Prof Gerry O'Driscoll: You have all seen different definitions of heart failure. Here's another one. They are not that important at the end of day, but heart failure is a clinical syndrome. It's not a diagnosis based on an echocardiogram or a BNP level, so people have to have some signs and symptoms that correlate with our usual thought process about what heart failure is, which we usually think is the heart is not able to supply enough blood and oxygen to the body when it requires it, for whatever reason.
Prof Gerry O'Driscoll: Over the years, we used to think about heart failure as systolic and diastolic heart failure and there's lots of other terms that we used to use, but now the common terms and it keep evolving is heart failure with reduced ejection fraction or heart failure with preserved ejection fraction. Depending on which guidelines you read, the definitions are a little different, but the Australian ones are probably are the most sensible ones.
Prof Gerry O'Driscoll: Now, a normal ejection fraction and an ejection fraction, by the way, is where we take a picture of the left ventricle when it's full and then we take a picture when it's empty, then what it's going to and we calculate what the difference is, and the normal ejection fraction is around 55% to 65%. Lower than that is abnormal and also higher than that is abnormal and that's sometimes not quite realized, but for now, we've decided that heart failure was preserved. Ejection fraction is 50%. Realizing though that some people who have an EF of 50%, that's actually abnormally low for them. So, it's in the preserved category, but it's actually not normal and the reference ranges for women and men are different and that's really not reflected in the guidelines either, so the ejection fraction while we use a cut-off of 50%. It is kind of crazy to think that somebody whose EF is 50% has got preserved ejection fraction and somebody with an EF of 49% is something different, and that will come up in the conversation a little bit later _____ so it's not a binary discriminator.
Prof Gerry O'Driscoll: Now, we've all learned how to spot people who've got heart failure, they don’t come in saying, "I've got heart failure". They usually come in, being a bit short of breath, which you can grade from just a bit short of breath on doing something, to being a "bit short of breath when I lie down" or "I'm gasping for air", "I'm drowning in the middle of the night".
Prof Gerry O'Driscoll: Separate to that, people may not complain of shortness of breath at all. They might complain of reduced exercise tolerance. "I can't take the rubbish bins up the hill anymore from my house". "I can't make it to the mailbox with fatigue or tiredness" and also, they might have some signs of fluid overload which is usually ankle swelling.
Prof Gerry O'Driscoll: Then, we've been taught to examine people to see do they have signs of congestion. The JVP, if it's elevated is great, but most of us and I include myself in this are wrong about 50% of the time. The JVP is really difficult to assess. You have to be at 45 degrees. You have not to be particularly fat, because if you are, your neck is too fat to see what the JVP is doing anyway. So, a lot of time you get it wrong. If you're not sure if somebody is really overloaded while they are sitting at 45 degrees, you can push on the liver and see if you can find an elevated venous pulsation in their neck. Again, it's not that useful. If the ventricle is dilated, it slaps up against the chest wall and you might have a third heart sound. If you're really good at listening to heart sounds, you might pick that up, but again when people are tachycardic, you're probably going to miss it and when you are feeling for the apex beat, you might find it's displaced laterally, you might not and particularly in people who have got bad lung disease or who are obese, you'll probably miss that too.
Prof Gerry O'Driscoll: Wheezing, feeling bloated, loss of appetite, palpitations, dizziness and a new sort of term is bendopnea where people who bend down feel short of breath when they are tying their shoelaces.
Prof Gerry O'Driscoll: They're less specific for the diagnosis of heart failure, but it tends to be what a reasonable amount of people complain of when they come in, so they don't always come in with the top two blue boxes.
Prof Gerry O'Driscoll: You can have weight gain if you're collecting fluid, but if you're really, really sick with heart failure, you get cachexia and those people lose muscle. They might still have lots of fluid on board, but their weight will be going down because the TNF causes their muscles to rot away. You might have crackles in the lungs, you might not.
Prof Gerry O'Driscoll: People who are acutely unwell tend to be tachycardic. They might have atrial fibrillation given a regular pulse. They might be breathing fast, you might find that the liver is big or you might not.
Prof Gerry O'Driscoll: I've seen over the years that all of these signs and symptoms are great in all people who will fit into the usual sort of categories that we’re used to looking for.
Prof Gerry O'Driscoll: They're not that relevant to young people, so you can see young people who come in with cardiogenic shock because of myocarditis. They don't have any of these signs at all. They just won't lie down for you, because every time they try to, they are short of breath, which is orthopnoea. Their blood pressures will look okay. They will not have an elevated JVP. They will not have oedema and they tend to be sent off to the medical wards in hospital with a dental inhaler and not infrequently, they end up dying with cardiogenic shock from a cardiac arrest in the middle of the night, so the absence of these signs and symptoms doesn't really mean a whole lot for young people.
Prof Gerry O'Driscoll: Now to diagnose heart failure, you can't do it with a stethoscope and history on its own. Plus, you need to decide whether the patients have got preserved ejection fraction or reduced ejection fraction heart failure because the treatments are different and the prognosis is different, so for people who have got signs and symptoms of heart failure, you do an ECHO, and their ejection fraction is less than normal. It's very, very likely that you're right that they've got heart failure as a cause for their symptoms.
Prof Gerry O'Driscoll: On the other hand, if you got the same signs and symptoms, so lower limb oedema, perhaps a bit short of breath, exercise tolerance has reduced, you do an ECHO and the ejection fraction is 50% or above, you're not really sure whether that's heart failure or not.
Prof Gerry O'Driscoll: The ejection fraction is a very elastic number. It'll vary about plus or minus 10% from one day to the other when people measure it. The way it is measured excludes about a third of the left ventricle, so it's not a number you can really rely on, but all the same, if it's over 50% you need something else to tell you that the patient really does have heart failure.
Prof Gerry O'Driscoll: We are talking about somebody whose diastolic function is abnormal. Diastolic function is something that changes over time and it's again pretty rubbery, but the real things are that if you've got somebody where their ECHO report is saying that they've got some diastolic dysfunction, usually it relates to hypertension or ischemic heart disease.
Prof Gerry O'Driscoll: Have a look and see if the left atrium is enlarged. Have a look and see if they have got left ventricular hypertrophy. If they don't have those, it's more likely that not a lot is going on, except that they've gotten old. So, some objective measure of something going wrong with the heart is required when the ejection fraction is over 50% , plus you usually need a biomarker which says there's tend to be one of the brain natriuretic peptides, preferably the NT-proBNP. I'll talk about that a little bit later, so if they got a normal NT-proBNP, the EF is 50% and above, there's nothing else going on that you can see on the ECHO, it makes it unlikely that heart failure is not the issue.
Prof Gerry O'Driscoll: What tests do you throw at patient when they've got heart failure. So you've done your history, you've done your examination, you think perhaps they've got heart failure and to confirm that, then the next thing you do for everybody is an echocardiogram. The reason for the ECHO is it'll tell you why they've got heart failure hopefully. It might be a problem with the heart muscle, it could be a problem with the valves, it could be ischemic heart disease.
Prof Gerry O'Driscoll: And also it dichotomises people into preserved or reduced ejection fraction heart failure above or below 50%. After that, you can decide if further help is needed with specialist investigations, etc. And then you can think about moving on to treatment.
Prof Gerry O'Driscoll: Everybody should have a full blood count and nowadays iron studies. Everybody needs to check on the kidney function, because the heart failure itself causes kidney dysfunction, but so do many of the drugs that we use.
Prof Gerry O'Driscoll: Liver problems might indicate that there is congestion, or perhaps that somebody has got hemochromatosis. An ECG is somewhat helpful, mainly to exclude things like atrial fibrillation, heart block or maybe a previous myocardial infarction. It's also useful to look to see if they've got a wide QRS complex because of the left bundle branch block because that might lead to pacemaker type of therapy and we'll get to that a bit later too. Chest x-ray is often misleading. It's usually in obese people, it says the heart is enlarged when it's not when you look with an ECHO. You may or may not find that there is congestion there, so a normal chest x-ray does not exclude the diagnosis of heart failure.
Prof Gerry O'Driscoll: Heart failure is a syndrome. It's not an end diagnosis and if you have diagnosed somebody with heart failure, the next question is why? What's wrong with the heart? Is it the heart at all? If it is the heart, ischemic heart disease is common, so you need to have some assessment to see whether it's there or not. If they are really short of breath, doing an exercise stress test tends not to be that useful because they peg out before they can exercise sufficiently.
Prof Gerry O'Driscoll: A stress ECHO gives you more information than stress ECG, particularly if there are resting ECG abnormalities.
Prof Gerry O'Driscoll: If somebody has got aortic stenosis or mitral incompetence, fixing that might fix the heart failure and you're done, so doing an ECHO again is useful for that. Hypertension accounts for about 50% of people who have got heart failure.
Prof Gerry O'Driscoll: It tends to cause diastolic heart failure but also systolic heart failure, and treating that might make the heart failure go away.
Prof Gerry O'Driscoll: If you've diagnosed them with hypertension, have a look and see if the secondary causes of heart failure that might be correctable.
Prof Gerry O'Driscoll: Thyroid dysfunction is particularly common, it could be either overactive or underactive. Particularly, in elderly people who might be on amiodarone because of atrial fibrillation, so that always needs to be looked for and asymptomatic arrhythmias are really common causes of heart failure to begin with, but also a cause for precipitous decline in the airways. This could be either fast or slow. Again, atrial fibrillation tends to be one of the common ones.
Prof Gerry O'Driscoll: BNP and pro-BNP. I use them sparingly. I see people with heart failure every day of the week and I probably order a BNP level or NT-proBNP level a couple of times a year. They're not reimbursed. There's an out-of-pocket cost. Most of the time you can make the diagnosis without having a BNP level and there is no magic level.
Prof Gerry O'Driscoll: Nowadays, we're using sacubitril/valsartan or Entresto, it's currently called, that will increase BNP levels in the lab, so to avoid confusion I just use NT-proBNP. Again, where it fits in is it's designed to either rule in or rule out heart failure.
Prof Gerry O'Driscoll: And it depends on your age, so forgetting about BNP, NT-proBNP. If your NT-proBNP is really low, it makes it less likely, but not zero probability that you've got heart failure. Then again, if you're trying to diagnose heart failure, if you've got somebody who is short of breath, who is pretty old, if their NT-proBNP is 500 that probably does not mean anything, so over the age of 75, the NT-proBNP needs to be up closer to 2000 to rule in somebody with heart failure.
Prof Gerry O'Driscoll: And there's lots of other things that impact BNP level, so there is no above a number or below a number that you've got heart failure.
Prof Gerry O'Driscoll: Natriuretic peptide levels can be elevated for non-heart failure problems. They go up with age, they go up with renal dysfunction, they go up if you have a heart attack, they go up if you've got bad lung disease, pulmonary embolus, septicaemia, cirrhosis, thyroid overactivity and atrial fibrillation. So just having a BNP level that's up doesn't mean you've got heart failure, you need to put it in the context of signs and symptoms.
Prof Gerry O'Driscoll: Conversely, you can have somebody who's got really bad heart failure and BNP levels will be in the normal range. That can happen if they've got a pericardial effusion with tamponade or they got pericardial constriction, reason being that BNP, NT-proBNP levels are a measure of stress, strain stretch on the myocardium. You can have heart failure without anything happening to your myocardium, so a normal BNP level does not exclude the possibility.
Prof Gerry O'Driscoll: So now we've arrived at somebody whom you think has got heart failure, we’ve supported that diagnosis with some tests, next thing is, why has it happened?
Prof Gerry O'Driscoll: Ischemic heart disease is really common. Hypertension is really common, but other things are relatively common too, so toxic damage from anthracyclines and various other chemotherapeutic things administered in childhood can end up with a dilated cardiomyopathy later in life. SLE, rheumatoid arthritis and various other inflammatory conditions can do that too, so can influence trait of things like hemochromatosis, amyloidosis and other things that migrate into myocardium and make the muscle stiff.
Prof Gerry O'Driscoll: Genetic abnormalities, some of them are cardiomyopathies but some of them are just shunts, so somebody who has got an ASD, VSD or whatever has got a shunt that hasn't been picked up before or congenital bicuspid aortic valve disease can also result in heart failure. Again, an ECHO will help you with some of that.
Prof Gerry O'Driscoll: Arrhythmias, as I mentioned before, but in children, particularly, they tend not to notice palpitations and in a young child who is not able to speak.
Prof Gerry O'Driscoll: They might crouch down because they're feeling very short of breath because they've got an intracardiac shunt. Some of them have incessant tachycardias that can be atrial flutter or supraventricular tachycardia or something.
Prof Gerry O'Driscoll: And if you take a heart and expose it to fast pacing for a long time, you will end up with a dilated cardiomyopathy which is indistinguishable from any other cardiomyopathy except when you stop the tachyarrhythmia happening. It usually goes back to normal, so it is really important to see if they've got an arrhythmia.
Prof Gerry O'Driscoll: In the elderly people, they can end up with heart failure because they go very slow. They might have a left bundle branch block and then occasionally go into a second or third degree heart block, so that's the common stuff.
Prof Gerry O'Driscoll: Less common but tends to run in families. There are things like hypertrophic cardiomyopathy. If you do have somebody who's got hypertrophy diagnosed on the echocardiogram and they are not hypertensive, it might be because of hypertrophic cardiomyopathy which runs in families. It might be amyloidosis, it might be Fabry's disease, it might be a bunch of other things. So, if you've got somebody where the ECHO says there is hypertrophy, but the blood pressure is normal, you need to dig deeper, and if you do diagnose cardiomyopathy, particularly hypertrophic cardiomyopathy, you should be screening all of the first-degree relatives with echocardiography.
Prof Gerry O'Driscoll: Lots of the newer biological agents, the mabs and mibs, as well as the various therapeutic drugs and radiotherapy can damage the heart many, many years after they've been inflicted and some of them are reversible. A lot of them responds to ACE inhibitors and beta blockers given after the event or prophylactically.
Prof Gerry O'Driscoll: You won't see this much, but I've seen it a lot. Myocarditis, particularly parvovirus b19 and other things can cause acute inflammation in the heart.
Prof Gerry O'Driscoll: They might present with pain like pericarditis which you can pick up and give non-steroidals, etc. Sometimes that moves ahead and causes damage to the heart muscle, which can be progressive, so not particularly rare but uncommonly seen in general practice.
Prof Gerry O'Driscoll: Okay, so next moving to the pathophysiology and there's only two or three slides here to explain why we use the drugs we do. In general, what happens with the body and heart failure is people have constrictors and dilators, so constrictors make the blood vessels tighten up, increase the heart rate and increase the blood pressure and in heart failure, you get overactivity of the sympathetic nervous system, the renin angiotensin system and you get increased vasopressin and endothelin.
Prof Gerry O'Driscoll: So, there's a lot of constriction going on, which makes it harder for the heart to pump against resistance.
Prof Gerry O'Driscoll: On the flipside, there's not enough vasodilators around so nitric oxide and related compounds are not as prevalent as they are supposed to be.
Prof Gerry O'Driscoll: The sympathetic nervous system, adrenaline causes to increase your heart rate, increase your blood pressure, increase fluid retention, assuming that you're bleeding to death. In the short term great, but over time, the increased heart rate increases oxygen demand and supply can't keep up with it. It also causes vasoconstriction and it's also directly toxic to myocytes, so you kill myocytes the more overactive your sympathetic nervous system is.
Prof Gerry O'Driscoll: Another system we look at it is the renin angiotensin system. Don't focus too much on the slide here. The angiotensinogen goes to angiotensin I and the business end of it tends to be angiotensin II, so angiotensin II you can reduce the production of that by blocking it's pathway from angiotensin I by using an ACE inhibitor and that's what we've been using for decades. If it's already produced, you can block the effect of it like giving angiotensin receptor blockers or ARBs and doing that blocks the effects of angiotensin II. Angiotensin II causes vasoconstriction, fluid retention, hypertension and damage to the heart muscle.
Prof Gerry O'Driscoll: The next bit that's not recognized as much as angiotensin II is after angiotensin II was formed, then you increase the amount of aldosterone that's around and aldosterone causes myocardial fibrosis, inflammation in the heart muscle and vessels, _____ it makes your blood pressure go up and all sorts of other things that contribute to the pathophysiology of heart failure.
Prof Gerry O'Driscoll: On the other side, your body makes natriuretic peptides to try to protect it from the effects of the renin-angiotensin system.
Prof Gerry O'Driscoll: So, while angiotensin II causes fluid retention, BNP is like your endogenous ______, it makes you lose fluid and salt. It tends to cause a bit of a vasodilatation and improve your renal profusion, so having BNP around is a good thing, but if your BNP levels are really high, it means that your heart is really struggling, so it's not that it's a bad thing in itself. It is just a prognostically bad thing to have BNP levels that are high.
Prof Gerry O'Driscoll: Alright, so next just the structure of what we use for medical therapy.
Prof Gerry O'Driscoll: In general, we got a few things that we give to most people and some other things that are a bit more selective. For people who have got symptoms, so people who've got short of breath, swelling in the legs, increase in weight gain, diuretics are great. They shift the fluid, but they don't do anything to alter the pathophysiology of blocking the overactivity of the renin-angiotensin system by ACE inhibitors or angiotensin receptor blockers, ARBs comes in there. It improves symptoms it improved death rates, but it doesn't improve sudden death.
Prof Gerry O'Driscoll: Beta blockers on top of that do all of the foregoing. They also decrease the potential for arrhythmias and reduce the sudden death potential.
Prof Gerry O'Driscoll: And blocking the effects of aldosterone with mineralocorticoid inhibitors, so spironolactone, eplerenone and similar things comes in there too. So, in general, what we try to do is put people on RAS blockers, renin-angiotensin system blockers that's an ACE, ARB, MRA and also then a beta blocker plus or minus sparing use of diuretics.
Prof Gerry O'Driscoll: Other drugs that you can use, we will come to that in the next slide, which you probably haven't used at all, ivabradine, digoxin _____ are the favourites back in again. Some people who can't use ARBs or ACE inhibitors because they got terrible kidneys can have hydralazine and nitrates as vasodilators to take the pressure off the heart, and more recently we've got sacubitril/valsartan which is the combination drug which is proven to be better than ACE inhibitors and ARBs.
Prof Gerry O'Driscoll: Polyunsaturated fatty acids have a miniscule amount of data to supporting their use so I am not going to talk about them.
Prof Gerry O'Driscoll: This slide is from the European Society of Cardiology and I've just slowed down. I would like to stare at this one for a little bit. Because it summarizes an awful lot.
Prof Gerry O'Driscoll: First thing is, and this is relating to people have got reduced ejection fraction. In the ESC Guidelines, it was less than 40%. In the Australian Guidelines, it is less than 50% for the EF.
Prof Gerry O'Driscoll: The same message, though, that if people have got no symptoms of heart failure, so they are in NYHA (New York Heart Association) Class 1, there's something wrong with the heart, but they don't have any symptoms and these guidelines relate to people who do have symptoms, so they can be class 2 which is only very minimal symptoms all the way up to class 4, which are symptoms at rest. Regardless, whether Class 1 or all the way up to Class 4, if they got a dilated left ventricle with reduced ejection fraction, everybody should have an ACE inhibitor as first consideration and also a beta blocker. If, for some reason they can't have an ACE inhibitor, an angiotensin receptor blocker is a reasonable choice, but the vast majority of the evidence favours ACE inhibitors above ARBs.
Prof Gerry O'Driscoll: So, everyone who comes to you, something wrong with the ventricle, they have got some symptoms, give an ACE inhibitor, give them a beta blocker. And if they've got signs of congestion looking down the left-hand side of the thing, you can give them a diuretic for a while to get rid of the congestion and then get rid of it because diuretics don't increase people's lifespan and they just make them feel better. They do increase the risk of sudden death from arrhythmias and increase the risk of renal impairment as well.
Prof Gerry O'Driscoll: Having done your ACE inhibitor and beta blocker, if they're still symptomatic, then that's where you add in spironolactone or eplerenone and if you're doing that, you usually need to think about reassessing the kidney function within a couple of weeks for a deterioration in their eGFR and creatinine.
Prof Gerry O'Driscoll: Hyperkalaemia is a possibility. It's really not that common, but it needs to be looked for and if people are really sick, it's not really an indication to get rid of the spironolactone. You might need to give them a resin binding thing such as ______ so you can persist with prognostically important drugs.
Prof Gerry O'Driscoll: Despite doing that, if they're still symptomatic, nowadays we would bail out of the ACE inhibitor and ARB and move to the sacubitril/valsartan or ______ tablet.
Prof Gerry O'Driscoll: One practice point there is if they've been on an ARB, you can move across to the sacubitril/valsartan tomorrow. If they're on an ACE inhibitor though, you need to give them a gap of at least 36 hours because, otherwise, when you start the new drug, there's a chance that they might develop angioedema.
Prof Gerry O'Driscoll: After that, if they remain tachycardic and we're looking down the right-hand side of the slide over here. If they are in sinus rhythm, not atrial fibrillation, they have to be in sinus rhythm, you can give them ivabradine on top of the other drugs. Ivabradine slows down the sinus node rate and doing that in a reasonable amount of people improves their heart failure too, but again, not for somebody who is in AF.
Prof Gerry O'Driscoll: It's not all about drugs, though, if they've got a wide QRS like a left bundle-branch block, that usually means that the heart wobbles and causes a reasonable amount of mitral regurgitation and you can fix that by giving them biventricular pacing which we call a cardiac resynchronization therapy.
Prof Gerry O'Driscoll: If the patient's symptoms are reasonably controlled after all that, they're still at risk of dying and you might want to think about a defibrillator and I'll come to that in a little bit.
Prof Gerry O'Driscoll: After all of that, you can think about adding in digoxin or if they're really going down the gurgler, it's time to send them to your local heart transparent service for consideration of more advanced therapies or palliative care.
Prof Gerry O'Driscoll: Now, the trouble with heart failure is it's not like respiratory disease, where you can find that you can plug people's decline reliably. It tends to be a disease that comes and goes. And sometimes they are well, they have a deterioration, they come back up. Sometimes they go down again and might come back up again, and it might not balance as much as before, so it's very hard to give a prognostication of how well people do.
Prof Gerry O'Driscoll: And we underestimate that, so if you look at people, this is a three-year span, looking at people from less than 40 years of age to elderly people, sure the elderly people do much worse and around 60% of them are dead within three years, but even if you look at people who have an age less than 40. About 60% and 70% of them will be dead in three years anyway, so a pretty lethal disease.
Prof Gerry O'Driscoll: I mentioned this earlier. You already know, so I won’t dwell on it, but NYHA Class is just short-term for saying how sick somebody is and how limited they are by their symptoms.
Prof Gerry O'Driscoll: If you look at people who are really sick, say NYHA Class IV, so they've got symptoms at rest, they feel terrible, they are short of breath all the time. Sure, they go off and die pretty readily and around 60%-70% of them will be gone in six months.
Prof Gerry O'Driscoll: All the same, if you look at people who are in NYHA Class II, so these are the guys that you would see every 3, 6, 12 months, whatever it happens to be and you think, "Oh! My patient has got stable heart failure". When you're looking at them, there's still a significant proportion of them who will be dying every year, something like 7% to 10% of them.
Prof Gerry O'Driscoll: When you're looking at people who die with heart failure, how did they die? They either die from pump failure or they can die suddenly. People with NYHA Class I have got an impaired left ventricular function, but no symptoms. People with Class II heart failure have gotten very mild symptoms, but about 34% of them, a third of them die in a three-year followup.
Prof Gerry O'Driscoll: And people who have got more advanced symptoms die a bit more, but not that much. So, 34% versus 42%, so the concept of having a stable heart failure patient really doesn't hold because a third of them die over a three-year followup.
Prof Gerry O'Driscoll: And just under half of them who die, tend to die suddenly usually because of an arrhythmia. It's not always progressive pump failure resulting in terrible oedema, shortness of breath, progressive renal failure. They just don't show up because they are dead.
Dr Rafal Francikiewicz: Sorry, Gerry for stopping here for a second. We have a few questions and I think it's a good opportunity to put them in here because it's very relevant to your last few slides.
Dr Rafal Francikiewicz: So, a recent question that came up, how long can we use diuretics in congestive heart failure and what if the symptoms reoccur every time we stop the diuretics? Any thoughts on that?
Prof Gerry O'Driscoll: Yeah look, you can use them indefinitely, but it's just for symptomatic relief and use them as sparingly as you can.
Prof Gerry O'Driscoll: So, we've got patients I’ve never been able to stop diuretics on. I tend to find in the summertime. They dry out, you have to back off on it to allow you to continue with the ACE inhibitors and beta blockers.
Prof Gerry O'Driscoll: So, you can safely use them forever, but I think the new message is to not rely on them that much and try to increase the prognostically important medications which are beta-blockers, ACE, ARBs and spiro, and yeah, if you need to use a loop diuretic on top, that's fine.
Dr Rafal Francikiewicz: What about patients with chronic kidney disease with an eGFR of less than 30? The concerns obviously with the limitations of ACE, spironolactone and so on, if you're unable to give those, what other options are there?
Prof Gerry O'Driscoll: One of the recent plagues I think is the acute medical units in the emergency department, so invariably patients who've been stable on life-saving therapy for years go into ED with diarrhea and something they label as having an acute kidney injury and then, they stop everything.
Prof Gerry O'Driscoll: So, people with heart failure die and they're gonna die from that much more quickly than renal failure. If they've got a very low eGFR, they are going to need more diuretic to get into the tubules to give them diuresis. It will not save their lives, but it will improve their symptoms, so there isn't a cut-off for the eGFR. It just means you need to use more and you can get by with combination diuretic therapy and I've got a slide a bit later for this.
Prof Gerry O'Driscoll: Where if you block the nephrons at different spots, you can get a better diuresis without given nephrotoxic doses of frusemide. If you give massive doses of frusemide, you kill nephrons and people go deaf. You don't need to be doing that, if you lose lower doses of a thiazide plus a loop plus spiro plus you know, whatever other diuretic.
Prof Gerry O'Driscoll: That answers that or not, I'm not sure.
Dr Rafal Francikiewicz: I hope it did. You definitely answered my concerns.
Prof Gerry O'Driscoll: Just on that too, if you've got who somebody because of hypertension, hyperkalaemia etc., you really can't give ACE or ARBs and they do exist.
Prof Gerry O'Driscoll: You give a combination of hydralazine and nitrates. You can't just give nitrates on their own, you have to give hydralazine with them.
Prof Gerry O'Driscoll: Otherwise, you get tachyphylaxis and that's something that was harking back to like 40 years ago. It's not as good as giving the other stuff, but it's better than nothing. Yeah.
Dr Rafal Francikiewicz: Perfect. Thank you very much. I'll let you continue with the presentation.
Prof Gerry O'Driscoll: Okay. Now heart failure, I mentioned that it doesn't travel on its own and all of us are confronted with people, I am a heart failure guy, so I'd like to see people with heart failure and nothing else, but unfortunately they all come in with hypertension, AF, angina, myocardial infarction, strokes and lots of other stuff or cardiovascular disease, but a substantial proportion of them had lung disease, they had cancer which has been treated before, they got anaemia and other things, so you have to be cognizant of treating those other conditions without adversely impacting how you're managing the heart failure, and many of them have four or five comorbidities at the same time.
Prof Gerry O'Driscoll: I have just picked out a few, and this is from the ESC guidelines, but the same thing pertains to the Australian and American Guidelines.
Prof Gerry O'Driscoll: Hypertension is really common as a cause of heart failure and there's lots of drugs you can use to treat it. Again, because ACE and ARBs are prognostically good as are MRAs for heart failure treatment. Managing blood pressure with that is a good thing to do.
Prof Gerry O'Driscoll: If they're already on a thiazide which is good for hypertension, that's great and it might reduce the need for a loop diuretic such as frusemide and it can be given in combination.
Prof Gerry O'Driscoll: If you're going to use a calcium antagonist, basically you shouldn't, because calcium antagonist confuses a lot.
Prof Gerry O'Driscoll: Amlodipine is probably the one to go for, but even then, it tends to cause lower limb oedema when you're using doses of 5mg or above, then you start using more diuretics to deal with the oedema, then the kidneys go off. So, in general, I try not to use amlodipine or any other calcium antagonists, but of the ones that are available, amlodipine is the least toxic for the heart when you've got heart failure. Hydralazine is not a bad idea, instead of an ACE inhibitor if you got really resistant hypertension.
Prof Gerry O'Driscoll: Felodipine, I am not a great fan of really but it's there. Moxonidine, you shouldn't use; it's been shown to increase death rates in people who got heart failure and also people around prazosin, it causes an increased activity of the sympathetic nervous system, tachycardia, fluid retention and so on. So, for people who have got prostate issues, using something different to that would be preferable. If you have to use it, it is kind of okay, but best not to if you can and you shouldn't really be using diltiazem or verapamil in people who have got heart failure even if they have got atrial fibrillation. Digoxin, amiodarone and a beta blocker are preferable.
Prof Gerry O'Driscoll: Many of our patients are anaemic, but a lot of them are not anaemic and they've got low iron and we've learned in the last few years that even if they don't have anaemia, if their ferritin is less than 100 or if the transferrin saturation is less than 20, they do much better if they give them iron.
Prof Gerry O'Driscoll: How you give them iron seems to be important. Giving it orally doesn't seem to do the job and given intravenous iron in the form of carboxymaltose stuff now like Ferinject has got little if any side effects related to it. It can be given as an outpatient quickly and reduces hospital admission rates and symptoms.
Prof Gerry O'Driscoll: Moving on to diabetes, we were told for years that people with heart failure it's a terrible thing to do, to give them metformin because of lactic acidosis. That's actually not real. It's definitely the first line drug to give them but nowadays if people are on metformin and are diabetic, you should really be thinking about giving them an SGLT2 inhibitor. This is a trial with one of them called empagliflozin.
Prof Gerry O'Driscoll: And in diabetics who had heart failure, the various endpoints in the trial were improved dramatically, so death from cardiovascular causes, death from any cause, need to be admitted to hospital were reduced with that drug in diabetics.
Prof Gerry O'Driscoll: More recently, that's been extended to people who don't have diabetes, but do have heart failure. One of the drugs is _________ and now that's been shown in DAPA-heart failure and DAPA-CKD to reduce the progression of kidney disease in diabetics but also to reduce death rates, admission and other things in people who have got heart failure, but who do not have diabetes at all.
Prof Gerry O'Driscoll: That's not listed on the TGA for this at the moment, but it is available under a patient familiarization program.
Prof Gerry O'Driscoll: So, it's kind of moved from being a diabetic drug into being a cardiovascular drug and as cardiologists now, we're darling to SLT2 inhibitors to a substantial amount of people who have got heart failure but don't have diabetes.
Prof Gerry O'Driscoll: Atrial fibrillation, really common, not going to spend a great deal of time on this. There's a debate about rate versus rhythm control.
Prof Gerry O'Driscoll: It kind of comes down to how symptomatic the patient is. If they are not that symptomatic, rate control does as well as rhythm control, so you don't have to send everybody for an ablation or a cardioversion. The drugs we use to control the AF in heart failure should be a beta blocker. If it's paroxysmal, the beta blocker to use is usually sotalol or alternatively amiodarone which tends to be better tolerated than sotalol. Not a great deal of use for verapamil or diltiazem in heart failure.
Prof Gerry O'Driscoll: And for rate control, digoxin in the recent trials have been shown to be tolerated better than any of the foregoing and it's back in favour for AF again.
Prof Gerry O'Driscoll: Diuretics we use for symptom control, not for prolonging life, but using combinations of ACE, thiazide and loop diuretics work better than giving a massive dose of any other diuretic. You can give them orally, IV, or if you can't get IV access, subcutaneously works fine. So, using frusemide 80 to 160mg a day plus maybe 25mg of hydrochlorothiazide on top tends to give you more bang for your buck than 250mg or 500mg of frusemide.
Prof Gerry O'Driscoll: We all have patients who've been stable for a while and then they're not. Common things are common. So, a lot of them stopped taking tablets or they start taking things that they shouldn't or they developed a new disease along the way, so just because they had cardiomyopathy before, doesn't mean they haven't developed a new valvular lesion.
Prof Gerry O'Driscoll: They might become pregnant. They might be having arrythmias which you haven't picked up on. Sleep apnoea is not often thought of, but it is a common reason for people to deteriorate and people who have got a lot of congestion and sit around a lot can have recurrent pulmonary emboli which results in right heart failure. And, as I mentioned, iron deficiency is a problem. Here's a list of some medicines which you already know, but it is just in the slide pack so you can look at it later. I guess the tick out things are the steroids, whether they are oral or intra-articular, tend to cause hypertension and fluid retention. Diabetic medicines like the gliptins tend to cause fluid retention and heart failure too.
Prof Gerry O'Driscoll: And some of the old fashioned antidepressants and most of the calcium antagonists and all of the non-steroidal anti-inflammatories can cause a problem.
Prof Gerry O'Driscoll: We focus as doctors on dolling out medicine, but it's not the whole deal. They also need to eat properly, reduce salt content. There's not a great deal of evidence for a fluid restriction in heart failure. It actually tends to be something that we tell people to do. I don't think it's practical in Australia to tell somebody to stay on a 1200 mL fluid restriction. 1500mL per day is tight enough and it actually doesn't seem to make a great deal of difference. If they are drinking 5 to 6 litres sure, but somewhere between 1500 and 2 litres a day for most people is fine. Reducing alcohol, exercising a bit more, and getting immunized is good.
Prof Gerry O'Driscoll: _________ inhibitors tend to improve symptoms in heart failure. There was no real contra-indication for them to be used.
Prof Gerry O'Driscoll: People with heart failure bounce in and out of hospital a lot, here, if you look at the left side panel.
Prof Gerry O'Driscoll: About one of five people who are discharged come back within a month, half of them come back within six months and
00:58:42.150 --> 00:58:56.250
Prof Gerry O'Driscoll: And if you look at the death rates 1:8 would be dead in a month and about 50% of them will be dead in a year. A lot of that is because that when they're in a hospital they get discharged before they've been optimized. There's no follow-up care plan or patient education, which is why we need to move to a different model with multidisciplinary care, which was a question somebody asked earlier.
Prof Gerry O'Driscoll: So doing that, which was something we set up at Royal Perth many years ago when you've got exercise physiologist, dietitians and psychologists, specialist nurses, pharmacists and things involved, which is great, and it all works really well inside the walls of one unit.
Prof Gerry O'Driscoll: Definitely it does reduce mortality and morbidity, reduces hospitalization and stops the revolving door, but it's very difficult to translate it into an outpatient setting.
Prof Gerry O'Driscoll: The people you need to be involved in that is the patient in the middle, plus their carers, family who are educated and provide support.
Prof Gerry O'Driscoll: Outside of that, I guess the next primary person is the GP and from time to time a cardiologist, whether it's a heart failure cardiologist who can be involved or not.
Prof Gerry O'Driscoll: And as they get older, they may need the help of a diabetologist, geriatrician, social workers and other things, and that will vary from time to time for each patient. We've tried to put together a program to streamline that in the outpatient environment. I will allude to that at the end, but it's not easy to do.
Prof Gerry O'Driscoll: I don't have enough time in my life to see every heart failure patient that is there, neither do you and you need some resources to point patients towards.
So, they can educate themselves and be a bit more proactive. The Hart Foundation has a bunch of materials available. It gives patients an idea about what to expect every day and what's abnormal, when to look for care, what signs that they should note down and when to pick up the telephone. So that's a good resource and it comes in a bunch of different languages. There's another one.
Prof Gerry O'Driscoll: Here from the heartfailurematters.org which comes in a whole bunch of languages as well, it gives patients a diary so they can keep track of their symptoms, their weight, their blood pressure and medications and that's something you can download yourself or give to them, so just circling back to the medications and I've only got another few slides here.
Prof Gerry O'Driscoll: It's not all about medications. It has to be about the overall management of the patient's psychological and social interaction with the family and trying to negotiate the various healthcare systems that they interact with.
Prof Gerry O'Driscoll: But, in general, everybody should be on an ACE inhibitor in preference to an ARB. If they continue to decline despite that, the next thing these days is sacubitril/valsartan, the ARNI drug. Everybody who's got systolic heart failure which is reduced ejection fraction should be on a beta blocker as well and most of them, in fact, nearly all of them should be on spironolactone, eplerenone or something similar.
Prof Gerry O'Driscoll: Having achieved that, if they still remain symptomatic and they are in sinus rhythm, giving them ivabradine is useful, but the criteria to access that under the PBS and the heart rate based on ECG has to be 70 beats per minute and the ejection fraction has to be less than 25%. So, even though I've seen heart failure patients all the time, I've got a handful of people who are on ivabradine.
Prof Gerry O'Driscoll: Pacemaker treatment, and this is not for heart block. This is for people who've got a left bundle-branch block with a wide QRS is worth considering. That's where you put the wire into the right and left ventricles and pace both of them at the same time, and that improves symptoms and death rates.
Prof Gerry O'Driscoll: A defibrillator is worth considering for people who've got a low ejection fraction but are doing okay, you don't want to put a defibrillator into somebody who's just about to die or who has got uncontrollable symptoms. It's a real bad thing to do.
Prof Gerry O'Driscoll: Mechanical support, which is ventricular assist devices and transplantation are available for selected people, but it resides at Fiona Stanley Hospital in this state and that's where people who might be young enough to benefit from transplantation should be referred.
Prof Gerry O'Driscoll: And for symptoms, a few things you can do. If they are iron deficient, top that up; if they're congested, deal with that with diuretics for as little time as you can get away with and exercise training improves things a lot, so a lot of the functional abnormalities that people get with heart failure are peripherally located. So, you can show that you can make them feel better, move more, walk longer distances without showing any difference in the cardiac function and that's because of hormonal changes in their muscles and blood vessels and we've done quite a bit of research on that over the years. So, these people should not be told to not exercise, or to stay in bed. They should exercise and as an example for people who are waiting for a heart transplant, they go to the gym three times a week for about a half an hour at a time and we have never had an adverse event or a death in 25 years of doing that.
Prof Gerry O'Driscoll: When do you refer to people, well clearly if they got orthopnoea or PND, they probably need to be in a hospital. If they remain tachycardic or hypertensive, not necessarily you need to go to hospital, but you might need some assistance from your cardiologist to help out there and if they've got elevated troponins. Now, the elevated troponin, I don't think you should check ever as a GP actually because if its elevated, it means the patient needs to be put into a hospital in a monitored environment and, if you think you should be checking a BNP, you should not and send somebody to ED instead.
Prof Gerry O'Driscoll: I'll skip that one.
Prof Gerry O'Driscoll: There's some recommendations now about referring people to multidisciplinary team, which is all well and good, but they don't exist. There is one at Fiona Stanley. We've set up one through PCI recently but there isn't capacity for people to be sent to a multidisciplinary team, even though it gives you better outcomes than a single cardiologist or a single GP doing things. They exist and the people who are accepted into those programs are getting a little more restrictive, purely because of the capacity, but they do exist, and it definitely helps on top of usual care.
Prof Gerry O'Driscoll: Kind of things that you see in a heart failure service is a bunch of people who can give dietary advice, exercise, rehab, might be able to fix a valve or blocked artery or whatever or deal with arrhythmias and it's complex, so sending to your local private cardiologist or physician is fine as long as things are working. If things are not working, think about sending them to one of the specialist heart failure services.
Prof Gerry O'Driscoll: This is not a plug for us, but we do have one which exists. We can't deal with everybody, happy to help where we can. But it's an area that needs to be grown in public health in Australia.
Prof Gerry O'Driscoll: Now, these are the last couple of slides just to tell you what I've been talking about.
Prof Gerry O'Driscoll: Most of it's coming from the 2016 Guidelines for the ESC. The rest of it is coming from the Australia, New Zealand guidelines for 2018 and it's a bit of a work in progress, but that's pretty much where it is. So, I'll stop with the slides now and I am happy to take any questions and see if I can get.
Dr Rafal Francikiewicz: Thanks Gerry, for that great presentation. Very, very insightful. There are a couple of questions, one which is always close to my heart, I like throwing that question out at educational sessions is, what can we do as GPs differently or is there anything you would like us GPs to change in our approach to heart failure?
Prof Gerry O'Driscoll: Look, we see a different spectrum of disease, so the guys who end up teaching hospitals and particularly at transplant stuff are not the guys you see. They tend to be young people who have got nothing much else wrong with them. They've had a disastrous MI, they had caught a terrible infection or something. And they are heading down the gurgler, and the only thing you can do is patch them up with transplants. That said, about 30 years ago, everybody who ended up like years ago, before Rob Larbalestier and I set up the transplant unit here.
Prof Gerry O'Driscoll: Everybody who got on the transplant list either died or got transplanted, and they didn't get transplanted in WA. They got transferred to Sydney or Melbourne. Some of them got transplanted and some of them didn't, and then carvedilol came on.
Prof Gerry O'Driscoll: And when we started using beta blockers, suddenly the number of people who are waiting for transplantations fell through the floor because most of them got better.
Prof Gerry O'Driscoll: And that's the way things have gotten, so the number of transplants that are done now is now more than it used to be 20 to 30 years ago, even though there's much more heart failure around the place. So I think we've got confidence now that the neurohormonal blockers that we use, ACE, ARBs and so on, and beta blockers work, but they work at doses that have been proven to work in clinical trials and if there's one thing I'd say that doctors are a bit hesitant to uptitrate the drugs because of the blood pressure reading.
Prof Gerry O'Driscoll: The blood pressure I've got loads of people who are running around the place feeling absolutely fine with systolic blood pressures at 80-85 and in those people, and we've done this several years ago. When they came in sick, we started the ACE or beta blockers or whatever and force titrated them up to as maximum dose as we could, and we got about 85% of people up to the top dose that is available, so 10mg of bisoprolol, 25 bd carvedilol and on it goes. That tends not to happen in GP land. And I can understand why because people are concerned about all people falling over and breaking hips etc., but the doses that have been proven to work in trials and the doses that have been proven to save lives, the one thing I think really is to be less cautious about uptitrating and that's much, much easier if you've got a nurse involved. So, some of you have got practice nurses who can see people or phone them every couple of weeks and see how they're going, somebody coming along to see every three months or six months or something. Nothing ever happens, so that's why some programs have just got nurses in them and they've shown to increase the doses of prognostically important drugs better than before.
Prof Gerry O'Driscoll: Now, there's a question came through. The patient feels unwell and we checked the BNP and the doctor says, "no, I will not uptitrate the dose". There's nothing magical about the blood pressure, so a blood pressure of 120 fine, but if the blood pressure drops down to 90 and the patient is feeling fine and not dizzy, there is no reason now to continue to uptitrating the drugs and usually what it means is you need to back off on the diuretic.
Prof Gerry O'Driscoll: You can't get up to top doses of the drugs with everybody and also, I got to say that the guidelines that we have are based on clinical trials for particular groups of people. If you drill down into the papers that have resulted in the guidelines for anything, you usually find that it's middle-aged white men, 55 to 65, there's no lot of blacks, not a lot of women, not a lot of Asians, they don't have terrible kidneys and diabetes and all the other stuff, so the guidelines are actually relevant to most of the people that we look after.
Prof Gerry O'Driscoll: So you have got to take some inference from the outcomes of the trials and marry it to the patient, you can't get up to top doses with everybody, but you should try.
Dr Rafal Francikiewicz: Okay. Thank you, Gerry and there's another question about HFpEF, so what would be the first line of treatment in heart failure with preserved ejection fraction and one of the attendees says they have a patient with a diastolic dysfunction, only symptom was palpitations, so bisoprolol was given.
Prof Gerry O'Driscoll: Yeah, look HFpEF is really difficult and it's a whole other night's conversation, so the HFpEF in Australia is somebody who has got an ejection fraction above 50%. Normal ejection fraction is around 60% or so. So in that bunch, you've got some guys who really have reduced ejection fraction, but we're calling HFpEF. The clinical trials that have been done have been a total mess, because there were different definitions, sometimes it is above 40%, sometimes 50, sometimes it was 35, sometimes it was whatever. A lot of them were just people who were fat and who were hypertensive and never had heart failure. They were just a bit short of breath and because of that, they had trials that didn't have the right people involved and we didn't show any benefit with any of the drugs.
Prof Gerry O'Driscoll: If you zoom out of that and try to look at the totality of what's available in the clinical trial data, there's a continuum for ejection fraction, so above and below 50% doesn't mean you've got HFpEF and it doesn't mean you got HFrEF. It is on the definition for guidelines, but it makes no sense, women are smaller than men in general, so they’re ejection fractions are different. The guidelines are based on men's ejection fractions again 50-60% men, so out of all that waffle, we don't have a convincing trial of benefit for sure, but in people who have got some reduction in the ejection fraction, we're talking 55-57 and below maybe, using the same kind of drugs, particularly probably spironolactone beyond the rest and again there's no overwhelming benefit there. That seems to be a good thing to do, blocking the renin-angiotensin system seems to be a good thing to do, and then you're stuck with managing the symptoms with a loop diuretic, which is a nightmare because their ventricles are stiff. If you give them too much they go dry, the kidneys go off and if you don't give them enough, they feel short of breath and it's a real juggling match. And to deal with that, sometimes we ended up putting in invasive monitors in people, kind of like a pacemaker that measures your pulmonary artery pressures to help you adjust the diuretics, not a big thing in Australia, but it has been shown to be beneficial. So, the short answer is we tend to treat people with preserved ejection fraction whatever that term means with the same drugs. We haven't been able to show as much benefit with those drugs as people who've got reduced ejection fraction. It seems to be the case that women benefit more than men if they've got preserved ejection fraction with the same drugs. Yeah, so not a simple answer. There's not a trial saying yeah we've got the magic bullet for HFpEF and the other thing is that if you're looking at people who have got diastolic dysfunction which is a different thing. Diastolic dysfunction is a parameter of ______. A lot of them don't have heart failure and actually a lot of them have got nothing wrong with their heart. We're just measuring changes that happen with age.
Dr Rafal Francikiewicz: Fantastic. Thank you very much Gerry. We're running a little bit over time. That was a brilliant presentation, so thank you very much on behalf of all attendees. I must say one noble symptom I'll be looking for now is bendopnea. That is a term, first time I came across that one.
Dr Rafal Francikiewicz: But that was really great. I'm afraid that's all we have time for this evening. Thank you very much to everyone for attending and we hope you enjoyed the webinar.
Dr Rafal Francikiewicz: A big thank you to our presenter, Gerry for sharing his knowledge and time this evening and also thanks to our webinar partner Medtronic and obviously RACGP for allowing this happen tonight. Have a good night everybody and we'll see you next time.
Prof Gerry O'Driscoll: Thank you very much.