Epidemiology, Trends and Precipitating Factors

Thanks Thank You mr. chairman and thanks again for inviting me to talk I was given this task to talk about acute heart failure and the epidemiology precipitating factors and management so I do my best because it’s a slightly vague subject actually we’ve it’s the two main types of heart failure we’re talking about one is what the chordae know that ie is the first time it comes out of the blue and other and yet more common actually is is probably people who are relaxing it known to have heart failure and then something happens and they get worse and they get admitted again with heart failure and that’s called a cute decompensated heart failure but usually we just talk about people with acute heart failure or acute on chronic was the old term and by acuteness it’s we mean short basically and not severe and that can vary from a few weeks to a few hours or minutes and you do see occasionally people who do go to Cooper edema incredibly fast also called flash Pamir Dima and basically anything wrong with your heart can cause it to go into acute heart failure so there lots of causes and often there is a clear precipitating factor or trigger which I’ll talk about in a minute and the presentation again can vary as I say from life-threatening Palma Dima which can really kill somebody remarkably quickly to a more slow onset with the progression to cardiogenic shock and some people just come in with worsening severe peripheral edema and palmy edema as well it varies a lot in the balance between how much is left and how much is right heart failure some people with severe right heart Fedder just present mainly with / if Redeemer and ascites and not very much pommie edema so now this is some day services from the US but she’s kind of semi relevant but it gives some idea of the rise and possible discharges for heart failure over the last 20 years was 30 30 years and you can see that it’s been steadily rising but it looks like there may be a little bit of a plateau beginning around about 2:05 it’s not quite sure why that is but it may be that the treatment of chronic heart fed has got better so that the fewer patients are getting readmitted and but you can compare that to coronary artery disease which actually showed quite a mark fall so perhaps more these patients as we have mentioned many times before with coronary disease surviving now but with damaged hearts and therefore go on to develop heart failure and this is as some data about the age distribution which all well aware of that is predominate Alder patients but that varies where you live which I’ll talk about in a minute recently there’s been this published this quite nice big review was a particularly relevant to a har society about half fare in the low and middle income countries and they’ve basically looked at every single publication they could find from these countries on half a day and I’ll just review a few points about what they what they found they let these the pace of the countries which they looked at the papers these are what are labeled as middle and low income countries those some are changing quite quickly for instance China as we know getting rich very quickly so that may be in a different category soon this is quite interesting really it shows the age of onset of heart failure against what’s called the human development index which is an index which the United Nations have about was as a measure of wealth basically of a country and education levels and I think this has been apparent at over the last few days many presentations have noted the lower age of presentation in certain countries from this area and other areas of Africa particulars of paper from presented by African Hartford a much lower age about sort of 10 or 15 years younger interesting data from career patients were much older and most patients in sort of more wealthy

countries or in their 70s to 80s this is looking at etiology and we can see here this is the main causes is considered to be ischemic heart disease and I hope you can see this it’s not easy here’s Africa this is the country of myself actually America’s eastern Mediterranean Europe is his best Eastern Europe Southeast Asia and Western Pacific countries which is basically they called China is China yes anyway you can see here what we already know really that ischemic heart disease is not such a big problem yet in in Africa it is in most of the Americas it’s a kind of big problem in what we call eastern Mediterranean Egypt etc and I think that’s obviously apparent in this community that Coriolis ease is on the rise and in Eastern Europe Canarsie is a big problem so of course that the opposite of that is hypertension where we know that hypertension is the main cause in African countries there are some American countries here where hypertension seems to be quite a big problem and you can see it’s less of a problem in these Asian countries and Eastern European countries cardiomyopathy is something which is at a quart cause of acute and chronic heart failure something which we don’t often mentioned very often in in would certainly not in this meeting but it’s actually around and many patients with dilated cardiomyopathy present quite acutely and I can tell you an anecdote when I was working in Birmingham we had a patient transferred berming was a liver and a cardiac transplant center that a patient transferred when a peripheral hospital for a liver transplant and he had severe liver failure but no one had actually bothered to examine his heart or in particular look at his jvp and they did a liver ultrasound it showed a congested liver and then somebody decided to do a colleague out son and it showed a really severe cardiomyopathy and when you talk to the patient it was quite clear his symptoms were originally breathlessness but she’s been having for that previous three or four weeks and he turned out basically had and presuming an acute myocardial and a severe dilated cardiomyopathy with severe right heart failure followed by liver failure and there was a lot of debate about whether he then also went into renal failure so we were trying to tear him up for a joint cardiac and renal transplant but unfortunately he he died before we could get it so the the the cauda marthy patients are still around and I don’t know interest know whether in this community you find many patients with dilated cardiomyopathy it’s partly genetic as we know there’s very strong genetic influence and that may vary between different communities Bovril heart disease is still around causes rheumatic back mitral and aortic valve disease is particularly it’s disappearing everywhere in the world but it’s still present in in in Africa a bit but I’m sure it’s going down there but coming through a course is all the more chronic bowel disease they auto stenosis particularly often presents with acute heart failure and diagnose aortic stenosis is very common in in eighty Rhodes that present with heart failure and I think that’s one of the main reasons for doing echo on every single patient that comes in with acute heart failure because you cannot diagnose acute a very severe aortic stenosis that someone in Hartford is so great difficult diagnosis because the pulse is very small volume which could be due to the heart failure and the murmur is very short it’s not a particularly loud nervous um when the left ventricle is failing so a oldest noses should not be missed because whatever state the left ventricle is in it’s nearly always worth replacing aortic valve and now you can even do that you know trans arterial replacements rather than cardiac surgery but I’ve seen patients with terrible left ventricles with aortic stenosis the bowels been replaced and they do very well so it’s a very good reason for always doing an echocardiogram on anybody with acute heart failure now there is some local this was paper it was referred to a couple of days ago which is a registry which has started in South Saudi Arabia and just to give you a quick summary of what they found they hid this in locally here as a fan over a thousand patients who were admitted into hospital the majority sixty-six percent were admitted acute heart failure and this this is chronic heart failure h CHF the agency’s is younger at sixty years how those Saudi Arabia’s in Krabi rich country so I don’t know maybe this is a sunny anomaly but over half were completely new heart failures very high

level of diabetes which I think probably is a problem in this community the high level of diabetes it’s also increasing problem in in Asia 70 percent had severe 11 to historic function which is slightly different from other as the world and over half had coronary artery disease and mostly were treated according to guidelines they Lisa got beta blockers and a CIS and the patients with chronic heart failure had a similar profile in hospital mortality was 5.3 percent and 7.5 percent after discharge so gradually high mortality but not unusual now one of the things you saw that studying that locally it’s in be mainly patients with systolic heart failure but this is actually some data from the US and their data shows that half the patients actually have what we call heart failure with a preserved or normal ejection fraction and here’s some data the acute heart failure of the big trials which have been published and the adhere trial is here as well which is the the one which is basically acute heart failure registry and you can see here that the age of course as I says about 70s in the US but younger here about a very variation on on gender between the different types of preserved ejection fraction and is a slight proponent more of women in the preserved hypertension again it comes up as more common in the preserved than the reduce but is not highly significant and coronary disease is getting more common with reduced and preserved diabetes is about 30 40 percent in this community compared to 60 percent in Saudi Arabia and proof edema of course is quite common so it’s not a huge difference is clinically really but this is quite an interesting that a point they make about the difference in response to treatment up not covering treatment today but I thought there’s just a little vignette of the pathophysiology of heav heav and the real thing I think we should think about have Peppers as a disease of circulatory stiffness okay the arteries are stiff the heart stiff and actually probably the veins are stiff as well but not people not maybe have looked into the veins so this they have very high end systolic elastin so the left ventricle actually stiff in systole and they also have high arterial stiffness and when you treat them with vasodilators they get a much bigger drop in blood pressure because the arteries and everything are very stiff so when you dilate those arteries a blood pressure drops a lot for any given for change in in arterial elastance the same and change anterior it’s almost but a much bigger drop in blood pressure so basically if you’re giving betadine ages for people with a heavy F you want to be a bit more careful about the blood pressure because it may drop surprisingly quickly much more quickly than you might anticipate so that’s some basic epidemiology which I think a lot of it is pretty well known to all of you now the initial assessment monitoring the patient’s three things you have to do really when you get a patient in is firstly does the patient have heart failure now often that’s completely obvious and they have all the typical signs acute primary edema crepitations and they look sick and but you must be wary of other possible causes particularly chronic lung disease sometimes people present with a lung cancer with a huge palm area fusion pleural effusion with right heart failure which looks like heart failure people with kidney failure often look like heart failure and actually the problem is compounded by the fact that heart Fedder with Norma Jetson fraction is actually common in people with renal failure independent of the fact they may be born I’m overloaded because they have hypertension they have had diabetes they have the risk factors for hef peph and we’ve written a few paper and in collaboration with her and the foragers called angela wang we wrote quite a lot of papers on this subject upon lambda is the one which often myths they present sometimes just with a cute what looks like a cute right heart fado and they have a history of increasing breathlessness and but the characteristic thing as a chest x-ray is clear there’s no signs of palmy edema so that’s something always to look out for I’ve seen patients admitted with cute so-called heart failure breathless on exert and they die two days later with massive saddle

embolism so it’s something not to be missed particularly obese patients middle-aged obese women are very prone to this in my experience so if the patient does have heart failure what is what’s caused it what’s precipitated it and does this require immediate treatment I in a rhythm or is it is there a queue coronary syndrome and wear of diabetics they get acute quarantine drove without any chest pain they often just present with breathlessness and that’s another trap sometimes to miss the acute ischemia and then the next big question does this patient need to be in an is this an ITU title situation do they need ventilation or particularly ventilation either as CPAP on a ward or do they need to go to an ITU to be ventilated properly are they a person who’s ending heading for an LVAD or even transplants so that’s the clinical decisions you have to make these are some kind of data or presenting profiles in emergency departments people with acute heart failure that’s about a quarter were actually due to hypertension so their pedometer just hypertensive heart failure in others it’s the blood pressures a bit elevated now of course as a heart fails the blood pressure tends to come down so you can be mislead someone may have hypertensive heart failure present with heart failure but the blood pressure would be particularly normal and I saw a lot of this in Nigeria when I worked when I was much younger and we found a lot of patients presented quite severe heart failure who were normal Tennessee but while you treated the blood pressure once you treated the heart fair that brought pressured man to creep back up as a heart recovered and then you’ve then you realized these actually were hypertensive patients so a low or normal blood pressure doesn’t rule out the fact that the main this may all be hypertension actually a very low blood pressure less than 90 is quite uncommon karna genic shock is also uncommon usually less than 1% flash balm edema is also quite uncommon 3 percent and acute coronary syndrome is about 25% and a sorry 25% of patients are killed qhorin syndrome have heart failure symptoms and signs and as I said if they’re diabetic there may have no complaints of chest pain at all so it’s something to think about in a diabetic patient this is some more data on an acute heart failure mergency presentations this is some mortality figures here in is mainly from North America and see in Hospitality’s three to four percent and two days is acute coronary syndrome sorry and you can see here acute heart failure is much the same but has a much higher mortality at ninety days sixty to ninety days so this is a problem with a lot of these patients they get treated acutely but then they don’t really get looked after very well prior to discharge or after discharge because they they people they get into a different department and or under general physicians are not followed up and we know a lot of death how to treat ACS but as you’ll hear later I’m sure there’s really very little data on how to treat acute heart failure you would think by now acute heart failure is sudden as being with us for centuries and we still actually are still using the same tree which is diuretics because it works but we have no data and there’s very little other useful treatment it seems so mostly the guideline data is is what’s called CIE anecdotal really so precipitating factors I think any clinician and working in wards are well aware of all these things particularly a rhythm atrial fibrillation very common as the pressures rise in the ventricle the atrium works harder and then eventually get atrial fader and finally atrial fibrillation which then pushes a patient into heart failure as I said a cute corny tsukimiya marcona schema is often there and may be made worse by the heart failure because the rising wall stress increases a demand and increases the chances of getting of inducing ischemia post coronary syndrome were all well aware of this a ruptured septum much of are called a rupture and right trigger infarction are very common we know the difference Parmalee diamond doesn’t occur with it usually with a VSD you get right heart fader much of our quarter option you get screen stream breathless with pearl Madeira and right trick infarctions alright heart failure the clear lungs so these are other things that keep our embryos and I mentioned cardiac tamponade is another one that’s often missed looks like a big again always do an echo they audit deception that’s a very misleading one severe chest pain it does sex back down into the aortic root and you get a pay car effusion and they often present with breathlessness as well as chest pain and peripartum cardiomyopathy is a very

interesting condition presents usually within six weeks of delivering the baby it’s no one quite knows what the cause is but it’s maybe an autoimmune disease it may be ready to prolapse in and it is very severe disease it actually has quite a high mortality when I my research project in northern Nigeria the reason I went there was a study postpartum heart failure because in northern Nigeria is very common and I met a professor of medicine there and he said oh we got this problem with heart failure why didn’t you come out for a year or so and it was terrific experience I really enjoyed northern Nigeria in those days and it turned out actually it was related much more to related special postpartum procedures where they feed the mother a lot of salt and also keep her very hot and it induces a kind of water fluid overload and they get better very quickly but that’s different from true peripartum cardiomyopathy which is worldwide so less in fetch less rapid deterioration is particularly infection and most one which is often missing and most winery’s infective endocarditis in the best centers in the world infective endocarditis has a mortality of about 25 percent so it’s a disease it’s a killing disease and is one of those things in medicine should never be missed like meningitis or cerebral abscess because they’re treatable so always think about encode itis murmur plus fear as endocarditis exacerbation of COPD I’ve mentioned one sees and the other other port was a charger intragenic people given a nonsteroidals for their arthritis and the fashion standard nonsteroidals a very powerful sodium and water retention and they block the action of ACE inhibitors so that’s a very common cause of inducing heart failure or making a heart failure relapse a number of arrhythmias again another one which is often in more subtle as atrial flutter two to one block the heart rates 150 you think it’s just heart failure the second P wave is not easy to see and but it’s very easy treated you just give them a twenty five joules they go back into sinus rhythm but if you don’t spot the atrial flutter they’ll stay in heart failure and it would be difficult to treat so atrial flutter you’ve got a heart rate of 150 and it’s not varying always suspect atrial flutter and thyroid disease of course usually these days Bloods taken for thyroid but thyrotoxicosis or hyperthyroidism often induce particular thyrotoxicosis induce heart failure and in the elderly the thyroid that’s classical steroid signs are not very obvious okay they don’t always have the high signs and the shakes and all that or even the weight loss t3 tucks lots of cases you know it can be very alcohol is another one and drug abuse alcohol is in his widespread in some communities in the world not this one but in certain parts of Europe people drink very heavily and when I was an Oxford we did a quest nice study I was interested in the relationship because in Africa I was suspected a lot of hypertensives going to heart failure because they drink of our homebrew alcohol I mean we took it spontaneous hypertensive rats not a lot of not a great and I study this but he put spontaneously a hypertensive rats we fed them alcohol in their water we put 5 percent or 10 percent or 15 percent in their water and we they drank that all day and they were hypertensive and after and with LVH and we then after one pirate and then another but I mean we kept it going actually for about six months and they develop a Aarthi the blood pressure comes down and the heart dilates and the LV function goes right off so that’s chronic alcohol a lot of people drink 10% of their water intake as alcohol as I said not here but they do if you go to Scotland or Sweden particularly maybe they drink a lot so it’s something which is at the in the background and a lot of middle-class people drink a lot now there’s a big problem in UK about actually middle class people like doctors who like to have a bottle of wine every night and it gradually they get into the habit of having a bottle of wine every night and they actually was drinking too much so the middle class alcoholic is a problem because they won’t tell you their drinking they just so I just have a glass of wine every now and then but actually they’re having a bottle every

night so that if you’ve got hypertension and you’re drinking alcohol like that you would may well develop heart failure so a cute poem oedema yeah I think everybody knows all this is kind of medical school stuff okay that the pressures go up PA pressure goes up etc and but I just want to make the point it’s very complex all this it’s that looks quite simple but a lot of these things start in systole even in Heffner VII as we discussed yesterday that it’s delayed and reduce early diastolic filling there’s reduce RB systolic function and RB suction the same reasons and so the return into the right ventricle is reduced atrial systolic function atrial fitting may be affected and reduces we just know the increased heart rate shortens diastasis so reduces a time for filling in the heart the palm Raveena’s tone is very important and we know that the sympathetic nervous system causes venous constriction which will increase of Pama venous pressure and I once had a patient who had had a sympathectomy done on one side for some reason I forget now I know that sweaty hands or something anyway only worked on one side the patient name got half Vader and they had unilateral Pamir demo the hapana edema in the lungs where the sympathetic nerves were working but they didn’t have it in the lungs whether synthetic nerves had been cut so that’s a it’s illustration of the importance the sympathetic nervous system and the venous tone and this is just illustrative our actual function we know it it’s impaired in these patients prior to admission to heart failure and this is just a quick thing about congestion because actually the main reason for meeting patients is congestion rather than low cardiac output patients complain of of breathlessness or peripheral edema but actually it’s very difficult to actually quantify because we just put our fingers on the on the legs and say oh there’s a bit of a team or not and it’s also not done systematically before discharge and I think as a rule of thumb I may be only probably well well aware this I was like to say the patient when the patient sitting at 45 degrees the jvp should be just visible above the clavicle they should be just you could just see it when they breathe in okay that’s when they can go home you don’t if the J BP is up halfway up their neck or they still got preferred Eva they should they need more diuretics now this is a data I showed the other day because I just wanted to illustrate the rapidity with which so many things happen so here we have people with systolic heart fare and diastolic heart failure and you can see here the this is the estimated parmie aren’t you – with pressure which which corresponds to the left atrial pressure really you can see how it gradually comes up and then shoots up towards the end so there’s something happening here there’s some kind of vicious cycle you know something’s triggering and then everything gets worse very quickly and the patient goes into partly edema very fast so I think one of the things that’s happening is and what is not necessary with it without an increase in body weight and this is just skip this I want to get on to the more interesting stuff now this is interesting because this is a recent paper which I’ve always wondered about this again years ago we tried to look at Venus tone in hypertension but it was very difficult this this is a very interesting study so animal study but they found that when they the if they interrupted the normal arterial of bow reflexes and then they basically infused some fluid and what they found was that here the changes in left atrial pressure in response to infuse volume when when the bow receptors were failing were removed in out of the system and normal arterial baroreceptors and you can see that whenever bear acceptors are removed the pressure rises enormous ly much higher than when the baroreceptors working normally now I know beerus said two functions affected by hypertension arterial disease and in the neck affects reduces bear acept a function that’s been known for 20 years the barycenter function is depressed and hypertensives so what i think is happening here is because if our cells are not buffering the normal rise in pressure by dilating the veins the veins remain very tight so that you pressure will rise much faster the venous tone is much higher and this may be part of the reason why this vicious cycle happens so quickly the splanchnic volume the volume of the of the of our blood is mainly in our

veins and it takes a very small change in venous tone to shift that blood out of spanic reservoir into the IVC and into the cardiac circulation and a bit of tightening can shift a lot of our low volume and very quickly put the patient into Parma edema so it’s something which we pets ought to think about treating somehow I used to think my traits would work quite well for dilating the veins I mean and they certainly do and that may be one reason why nitrous do relieve symptoms although recently there doesn’t seem to be any evidence in nitrates actually affect mortality so this is going to skip all this girl I’ve seen this is all on the program for later so I’m just going to skip all this I just wanted actually this is the esc guidelines alright very difficult very complicated there’s an organization in Britain called nice National Institute clinical essence which tells doctors what they’re allowed are not allowed to use and they do massive cost effective analysis ashes oh no it’s a very very good organization and it stops a lot of waste of useless treatments they don’t want an acute heart failure which has only just come out they do a very very thorough in a nice analysis and they basically just say no it’s pretty straightforward but the BNP is vital now I better I think there’s going to be talked about later in the next thing but they they’re their guideline is very simple and they summary is is basically there’s nothing that there’s no good evidence that anything works apart from diuretics ventilation does work in certain individuals so I just want to skip one thing I want to just skip all this yes this is something you might be interested in because this is good evidence to say that coid ologists have some value we can add value to being other than a general physician okay here’s a standard management this is what happens in many hospitals in the world patient half-acre submit into a general medical ward especially if you’re 80 years old and you come in with heart failure you don’t get the high-tech treatment you know you don’t get a Mayo Clinic treatment or they Brompton treatment you get put in a general ward and somebody comes around who’s some intravenous frozen ID and and then that’s it okay now if you’ve got being standard management plus BNP it’s slightly better you usually get into the right treatment for the diagnosis you’ve got heart failure but if you’ve got a cardiologist plus BMP you’re much better off okay your your outcome is better and it’s very cost effective in more quarries and what we call quarry is a better value so anyway that’s an introduction to acute heart failure you hear more about management and treatment soon say it’s common it causes a lot of burden on healthcare systems particularly in high and middle-income countries and these countries have got to cope with this double burden of communicable diseases and a rising tide of non-communicable disease so actually it’s tough the commerce causes we know our skivvy heart is hypertension but there are some little traps don’t miss cardiomyopathy IOLTA stenosis and constrictive pericarditis another one that lurks around the path of is our is complex but I think they ought to be thinking more about Venus compliance and venous tone as well as arterial and turn and not so much on the harp house and patients for the kid Harper are better treated by a specialist which is nice to know and this sigh has been shown before often showed this one when I’m teaching the medical students in Hong Kong that let remind them of their history of China 2600 BC well I don’t know what was happening in Britain not much at that time but they they had doctors right and this I think you all know this right superior doctors prevent the disease mediocre doctors treat the disease before evident in fear doctors like me treat the full-blown disease okay so obviously prevention is better than then treating to rate okay thank you very much you