Thank you very much. The pressure's on there, eh? Thanks for the introduction, it's very kind.

And, I wanted to say, although I, I work in a university, I'm predominantly a clinician, so I'm 85% clinical, and 15% of the time I catch up on paperwork and do administration, and occasionally get to do a little bit of research, . So I have total sympathy with those of you out there who've who've rushed around today and had to skip lunch or whatever because we've had a similar day where we are. The other thing just to say about myself is that I was a proper vet for 6 years, so I, I graduated, went to first practise and worked worked in first practise, in the UK.

And then did my cardiology certificate, whilst in practise, and then was still pretty interested in cardiology and wanted to do more. So I went on and did a residency and, and, and my diploma. So, you know, I, I'm trying to be realistic about heart disease and about compliance and things like that.

And I think treating cats with heart disease is something you've got to be realistic about. We haven't got much evidence published to tell us what to do. And we'll, we will cover what little we have.

We'll also talk a little bit about opinion and consensus and theory, because these things are things we have to use in our decision making for, for what to treat cats with, and when to, to begin treatment. For some reason, my slides are not advancing. OK, there we go.

So the aims, we want to think about how to stage heart disease. There are different stages of heart disease in cats, not all of the disease requires treatment, and it's so important to do this staging to decide if and what treatment is needed. Nobody wants to give a cat medicine unless it needs medicine, least of all, the cat.

We're gonna discuss the theory in the evidence. And along the way we're gonna think about compliance. Now compliance is super important because of cats like this.

This is Boris, Boris is my cat. Boris has chronic rhinitis. Because it's not the heart, I don't know anything about it.

But what I do know is that he requires treatment, and he is on doxycycline daily. Now, if someone said to me, prescribe a pill once a day for a cat, you're a vet, give the pill yourself. Sounds easy.

And I could medicate the cat, no worries. Got the pill in, got a 100% success rate getting the pill in. The cat hated me.

I had to give it before foods, it's doxycycline, so I wanted him to swallow it completely, and I'd always give it before I fed him. He then after a couple of weeks would come and ask me for food like he always did, wanted food, I'd go near his bowl, he'd run away and hide. It was very stressful.

Now, I love the cat. The cat doesn't love me so much, but he loved me even less. And it was very difficult for me, it ruined our relationship.

Did he get medicated? Yes. Did any of us like it?

No. And I began to miss doses here and there, stop for a few days. I became a non-compliant client.

Did I tell the people at work that I worked with who prescribed it? No, I kept it a secret that I was doing this because I'm human. So I'd wait till he got clinical signs back and then I'd start treatment again, which is not good for him.

So this, if I'm doing this, or was doing this, this is an issue. Thankfully, a palatable version of doxycycline came along. Now the cat eats it on the food, there is no stress, no hassle, everything is good.

So compliance and palatability are really important if we want to successfully manage our patients. Let's take a step back from treatment. We're gonna think about heart disease in cats, we're gonna think about how to classify heart disease in cats.

I hate this system of classification. I don't think it should apply anymore. I think we should move on from it, but I'm going to acknowledge it because it's something that you may have come across, either back in vet school when you were lectured about heart disease in cats, if you were, and also, in textbooks or in online articles.

Some people stick by this classification system, but I have a few issues and that I'll explain why along the way. So first of all we have the hypertrophic cardiomyopathy, we diagnose that on echo, thick left ventricular walls, function is variable. Some, for poor function in the disease later on, the left atrial size is variable, some have a small atrium, some have a big atrium, more advanced disease, but the thick walls is key.

With dilated cardiomyopathy, DCM, just like in dogs, you've got poor left ventricular function, systole, a dilated left ventricle, with variable left atrial size depending on when you catch the disease, whether it's early or late. You've got restrictive cardiomyopathy. Here, the walls are a normal thickness.

There's no dilation of the ventricle, but there is atrial dilation, you have to have atrial dilation according to the traditional classification system to diagnose this, and you also have to have restrictive flow. What I mean by that is you have to have evidence of high pressure in the atrium. Now you can get restrictive flow in dilated or in hypertrophic cardiomyopathy as well, so these terms are are not straightforward, they're not simple.

You can have obstructive forms of hypertrophic cardiomyopathy, so some people will call a cat HCM or HOCM hypertrophic obstructive cardiomyopathy, if you've got left ventricular outflow tract obstruction. Other people will, will not use that terminology. You can have like box of dogs, a rhythmogenic right ventricular cardiomyopathy, ABC.

We diagnose that when you've got large right heart and arrhythmias, technically it's histopathology, the way you diagnose it, but nobody wants to to do that in cats to get a diagnosis. An unclassified cardiomyopathy. It's just because you can't make your mind up which box it fits into.

I don't know, it's a Thursday, you miss lunch. I, I can't, I, I can't decide what it is. I'm gonna call it unclassified cardiomyopathy.

So these are are cases that just don't fit in those boxes. Now, in terms of how common things are, HCM makes up the vast majority of heart disease in cats. There's a few restrictive, a few dilated, a few erythmogenic cardiomyopathies out there, and depending on how decisive or not you might be feeling, how much you've caffeine you've had in the day, you might have a few more unclassified cardiomyopaths.

Now, here's a thing. If you follow a cat over time, so let's imagine this visually on a graph, if you look at the X axis, you've got time in years, because many of these diseases take a long time to progress. And on the left hand, the Y axis there, you've got wall thickness in millimetres.

So if we follow this cat over time initially, we'll watch the cat's myocardium become thick and 6 millimetres is our cutoff for hypertrophic. So once the cat goes over 6 millimetres here, you can see this becomes tently HCM they'll increase a little bit, plateau, increase rapidly. Cats, cats with HCM can change.

No. Over time, the myocardium becomes too thick for the coronary blood supply. We have a heart that has outgrown its blood supply, the cells are hypoxic.

They are not coping very well, the myocardium becomes fibrotic, sometimes those cells will die, and it will, the walls can get thinner. So we see that actually if you continue following that cat in some cases, they become thinner again. And since wall thickness is really important in our diagnosis, you can see that as we get myocardial ischemia.

If we happen to scan the cat early, we might call this cat HCM. If we happen to scan the cat here, you might find in later disease, you'd call it restrictive cardiomyopathy. And over time as this myocardial ischemia becomes more of an issue, the contractile function can go and you might call it DCM.

So My thoughts are, who cares what you call it? Think about the disease functionally. If they've got systolic dysfunction, maybe we want to give something to improve the function.

So you can see, we now have more like a Venn diagram, where actually, although we're diagnosing HCM in lots of cases, RCM DCM UCM might also be HCM that's gone bad, might be more advanced cases of HCM with wall, ischemia, and wall thinning and infarction, and we end up with something that doesn't look hypertrophic anymore. The arrhythmogenic cases tend to have a big right heart. They're often quite different.

So you see we have some problems in this classification system. There is a study out there performed by the team at the RVC who've done some excellent research in feline cardiomyopathy, and one study that they've performed suggests that cardiologists don't agree with one another when they classify hearts. So this was where many cardiologists took a test.

It was an online test, and I was one of the, the guinea pigs. I filled in the the the answers here, and we had 20 cases, and they were just echo loops. We were given some basic data like wall fitness measurements, clinical signs, things like this, and we were asked to classify it.

Simple question, does it fit into one of these boxes, which one does it fit into? And the sneaky thing they did was they put in some cases, twice. So not only did cardiologists fail to agree with one another on some of those cases.

They also didn't agree with themselves. So just because it's a Wednesday, you might call it HCM the following Tuesday, you might call it something different, OK, with the same echo loops. So this is a problem, and this means, you know, maybe we should move on from this whole classification system.

As I've illustrated, this is a dynamic disease, and cats can change classification again, proven by the team at the RBC and some research that they were involved with, where some cats will just totally change classification from hypertrophic to restrictive cardiomyopathy and sometimes even back again. Classification doesn't matter. All of that stuff I talked about, forget about it.

What you need to do is identify the problems on the echo, the functional problems, and then treat those. We don't treat the diagnosis, we treat the cat. So what I mean is, look for risk of thromboembolism.

No one likes a cat who develops an arterial thromboembolism. They're horrible for the cat, horrible for the owner, very stressful for vets, there's a high mortality rate. If we can reduce the risk, that would be a positive thing.

Cats who've got reduced ventricular function, so contractile function of the ventricle, very importantly for you, they reduce their cardiac output, they progress faster. These are cats who will benefit from some treatment. And if they have clinical signs of congestive heart failure, the cornerstone of that is diuretics, but there are other things we can think about too.

If they have arrhythmias, we won't talk about antiarrhythmics in this this presentation really, cos that's a whole can of worms, but antiarrhythmics can be used to treat arrhythmias, and that is classified as a separate problem. Let's think about the epidemiology of feline heart disease. So this is a paper that was published as part of her PhD by my colleague Rosie Payne, and it's a fantastic paper because this.

Paper tells us what normal looks like and what common it is. So this is a paper looking at the prevalence of heart disease on 780 cats who are apparently healthy in rehoming centres. As cardiologists like to give names to papers, sometimes they make sense, sometimes they don't.

Here, this is the CAT scan study, it makes sense, because all these cats were scanned. They also have blood pressure taken, thyroid profile, measured. They had renal markers on cardiac biomarkers, so they had some blood work as well as part of their general health screening.

These cats were not selected. They were any cat who would tolerate auscultation, bleeding, blood pressure, and echo. OK.

So this is really important stuff, because these are cats that are normal, not cats that come into silly little referral hospitals like mine, where we see a very small population, of very strange animals. What this is is is the normal background. I've just altered a figure here from the paper, that basically shows HCM prevalence increases with age.

This is an important thing. You can see on the left here, you've got cats with hypertrophic cardiomyopathy in the red segment of the pie chart, and they are a minority of patients, but you can see probably 3 to 4% of cats at that age were classified as having HCM. That doesn't mean they're in heart failure, it doesn't mean it was bad, but it just means they have thick walls.

If we think about 1 to 3 years of age, that prevalence of HCM increased, as the cats got older, it increased up to the older age group over 9 years category, where it was actually around about 30%, 3, 29 to 30% who had. HCM. So that means roughly 1 in 3 cats over 9 years, which is not that old, coming into your clinic will have HCM and that prevalence, we believe, increases as they get even older.

So the 14-year-old cat coming in for a dental, maybe half of them have got HCM, OK, whether or not they have a heart murmur. So you can see the prevalence increases as they age, and that's an important concept because it means that the cat's risk of having a disease, how serious we take heart murmurs and things, increases as they get older. So if we just look at the background population of cats, 1 in 7 cats over all age groups, both sexes will have HCM.

So that's 15%. What can happen to these cats, well, they might get congestive heart failure, we know that they might get pulmonary edoema or pleural fluid. They could develop an arterial thromboembolism.

They might experience sudden cardiac death. Now interestingly, if you talk to vets about cats who drop dead with heart disease, especially if you talk to cardiologists, they say, nah, we don't see much sudden death in HCM. Well, no one takes a dead cat into the vet for diagnostic tests.

They go to the pathologists. And if you talk to the pathologists, they say that HCM is the most common cause of sudden cardiac death. And one paper suggested that actually.

The cats who presented with sudden cardiac death, a large number had HCM and the commonest reason they were taken to the pathologist is the vet, the owner thought a neighbour had poisoned the cat. So if you see that whole suspicious poisoning case, think about heart disease unless there's some obvious other signs. What's very important is that many cats with HCM never experience clinical signs of their disease.

So when we diagnose HCM we do not write a cat off. We don't say, oh, the cat has a loud murmur, therefore it can't have a dental, or therefore we can't treat its disease that we need to treat to improve its well-being. Many cats with heart murmurs, many cats with HCM, they go on to live a normal lifespan, they die of something else.

For example, kidney failure. So HCM is not always a lethal disease, and that's a very important concept. I know of a cat who was diagnosed at 6 months old, Bengal cat.

The breeder was going to put the cat to sleep, so very kind cardiologist took the cat on. The cat did die of its HCM, but it died at 14.5.

So that cat had what I would call a normal lifespan and actually lived for 14 years post diagnosis with no clinical signs until very close to the end. And so it's very important to think of this as potentially a benign, slowly progressive disease. The difficulty can be identifying which cats will progress.

This is another wonderful study. It's a large study published last year, no sorry, 2017 looking at the outcome of cats with HCM. So I said cardiologists like to give something a title, a study, a sort of name.

This was the reveal study. I don't know where reveal comes from, but it was a study to assess cardiovascular risk and look at long-term health in cats with HCM without clinical signs and compare them to apparently healthy cats. You can see there are a lot of authors here, huge number of authors, this means it's a lot of cats in the study contributed by different sentences.

So the reveal study is very important. 1730 cats involved, that's a good solid number for a veterinary paper. Around about half of them had HCM around about half of them were apparently healthy cats.

What we know from this, the facts about HCM, it occurred in middle to older age on average, we know that from the CAT scan paper. About 1/3 of cats developed heart failure or a thromboembolism, sometimes both, because of their HCM. So that's about 70% of cats with HCM who didn't get those signs.

And about a third of cats with HCM die of their disease, so not all the cats who got heart failure at AT died from it, but most of them did, that's predictable. Let's look at a larger population of cats now, so we have, imagine all the cats in the world. What I've done is I've put together some figures from various studies.

And try to estimate the risk. How many cats are at risk of clinical signs of HCM? They're highlighted in the green.

That's 8% of all cats worldwide could be at risk of heart failure or ATE. That's a huge number of animals. This is a very important disease.

If any of your colleagues think it's not, ask them to watch this webinar. This is an important situation. OK, and it's something we need to think about.

So how can we identify which cats go on to develop signs of heart failure or arterial thromboembolism, or in this paper, we tried to look at sudden death as well. So we identified some risk factors. I'm gonna warn you something here, sorry, hashtag spoiler alert to speak in modern parlance, and this is not that revealing, OK, but there are some things we can take from this paper that will help us.

So, the independent risk factors for heart failure were reduced left ventricular function, so reduced systolic function. I said it was important, here it's here it's proven. Also, previous heart failure, well, we kind of knew that anyway, so previous heart failure is not a great risk factor to take on to predict a cat getting heart failure, but reduced systolic function is.

Arterial thromboembolism, reduced left atrial functions, so contractile function of the left atrium is an important risk factor for arterial thromboembolism. Again, disappointingly, the other independent risk factor was previously having had an ATE. Now, a bit useless if the first one's fatal, to use that one to predict the next one, it's not gonna happen.

So reduced atrial function is important in predicting ATE and reduced ventricular function is important in predicting heart failure. Predictions of sudden death. A history of syncope.

So if you have a cat with cardiomyopathy who's presented with clinical signs of syncope, that cat is immediately in a higher risk category for developing a sudden death event. So that's a little bit more useful. You don't have to echo to do that, you just have to take a good history.

The difficulty with syncope in cats is many cats are alone all day. They might be experiencing events daily, but the owner may not realise. So let's think about staging HCM, different stages of disease.

You may have come across the consensus statement or the idea of staging mitral valve disease, where we have an ABCD system, and that's just been revised. You should look at the new system, it's a little bit different to the old one, in terms of how we classify those dogs and what treatment we give them. Let's think about 3 stages of HCM.

We have pre-clinical HCM. We know that 70% of cats with HCM will remain in pre-clinical HCM lifelong. These cats have left ventricular hypertrophy, that's the diagnosis.

Normal left atrial size and normal left ventricular function. The next stage will be at risk. So these guys don't yet have clinical signs, I suppose they're still pre-clinical, but they are different because they are at risk.

They have left atrial dilation and or poor function of the left atrium. As well as potentially left ventricular dysfunction. So we look at left atrial size and function, we look at left ventricular function really.

So we might have cats who are at risk of heart failure, cats who are at risk of ATE but have never had signs. Then we have the group that are clinical. So these are the cats with congestive heart failure, CHF or arterial thromboembolism.

They have signs of CHF and or ATE. And obviously, as you know, with arterial thromboembolism, a good proportion of those cats will be euthanized or or die in the 1st 24 hours. So, this is our staging system for HCM.

If you like, compare it to the dogs with mitral valve disease. We've got stage B1, stage B2, and stage C or D, I guess. Now, the important thing is that the at risk group benefit from treatment, and the heart failure group or AT group benefit from treatment.

The pre-clinical group, those cats could live a normal lifespan, they may never benefit from treatment. The at-risk cases and the heart failure cases are. So, the evidence base for treatment.

Let's think about our treatment point associated with the at-risk group. This is the left atrial brillation, left ventricular dysfunction. So if we have left atrial fibrillation and poor function, we'll see that on echo.

This is echo shows a normal left atrial size. We can see it's a short axis image at the level of the aortic valve. So in the centre there is the aortic valve opening and closing.

So they're little fast. It's a cat, and at the bottom there between 6 and 8 o'clock, we've got the left atrium. The left atrium and the aorta are roughly the same size, that is absolutely normal.

Contrast with this, we have the aortic valve in the middle, looks a lot smaller, but it's not the same size as the previous one. Here, we've got a huge left atrial dilation, we don't need to measure that. We can see that the left atrium is more than our cutoff value of 1.5 times the aortic root diameter.

If you look carefully, that left atrial function is also poor, it's not changing size much. So if we looked at left atrial function using an M mode, we don't have to do an M mode, but it illustrates quite nicely that the change in atrial size as the atrium contracts. So here we can see we've got an M mode cursor across the left atrium, the aorta.

The aorta is the sort of black space in the middle, the left atrium is black space below that, if you like. If we measure just maximum to minimum atrial size there, atrial diameter there, we see we've got a contraction. It's probably 25 to 30% of the original diameter.

That's a normal left atrial function. Look at this kitty cat. Not only is it a big atrium compared to the aorta, but the contractile, state of the atrium is reduced.

So you can see that the actual dimension of the atrium at its smallest is probably 10%, that, sorry, 10% lower than the atrium at its largest. That's poor function. This cat's definitely a risk of thromboembolism.

So our aim is to reduce the ATE risk in these cats. So we can use an antiplatelet drug. Now the antiplatelet drug is of choice is clopidogrel, and we give that a dose of 18.75 milligrammes once daily per us.

We base that on this paper, the acronym here was fat cats, but I can see where this comes from. This is the feline arterial thromboembolism, clopidogrel versus aspirin trial. So here, cats were randomised clopidogrel or aspirin if they were, if they were cats who'd survived the previous ATE and they were at risk of developing.

Other ones. So to, to fulfil the criteria of this particular trial, these cats had to have had a previous ATE, so it's not quite the same population we're talking about as the at-risk of the first one, but it's just the way the study was conducted to make sure they were, they were likely to find a, a, a, a, a decent result from, these, these cats on the trial. So.

We can see these cats were recruited 3 months after the ATE event, between 1 and 3 months they had to have survived. So already, you know, it's not quite the guys we're looking at. They were randomised to aspirin for a bit of growth followed over time to an end point of either death or heart failure or a repeat thrombus.

So this is a what's called a survival curve, and you can see if you follow my pointer here, we've got a group in red, dark red, which is the clopidogrel cats. And we've got a group in blue, which is the cats on aspirin. Each step down on these curves represents a cat who's either gone into heart failure, died or developed another arterial thromboembolism.

So you can see here, if you were one of these cats, you would want to be in the clopidograd group because it on average it takes them longer to develop. A recurrence of their signs. So we know that clopidogrel is a better drug for capsulating than aspirin.

When I talk to the students, sometimes we have to try and modernise our terminology. So for the students, we have the happy emoji group, and we have the sad emoji group. So, you know, if that works for you, that's absolutely fine.

We definitely want to be in the top of the graph group here. So our recommendation based on that evidence is we prescribe clopidograph for cats who have a large left atrium. My cut off, a little bit arbitrary, but my cut off that I would recommend is a left atriotic ratio of greater than 2.

And or a fractional shortening of the left atrium, less than 15, so that M mode measurement of maximum to minimum, if the difference is less than 15%, that cat has poor function. So I'm not only looking at size, I'm looking at function as well. The function trumps the size.

If the size looks 1.8 maybe ratio, then the and then the fractional shorting is 10%, but leave the fractional shortening and go with that. That's the stronger recommendation, but we do look at both.

This is another risk factor. Here's a cap. We've got a left atriumum, off to the left of that image there, we've got a left ventricle in the mitral valve.

This structure here is the left oracle. In the left oracle, you can see spontaneous echo contrast, also called smoke. One of my students last week said it was a snow globe effect, which is very romantic, isn't it?

But, this, this smoke suggests we've got a risk of arterial thromboembolism. We believe these are microthrombi that are forming within the blood, and we're seeing them on the echo. So, the second group in the at-risk category that we talked about were cats with left ventricular dysfunction.

Now that can be global dysfunction, so we can have like a DCM appearance where the walls just generally look a little bit lazy, they're struggling, they're having difficulty. Or we can have regional dysfunction. I saw a cat yesterday with regional dysfunction, and we suspect in these cases they've had a previous infarction.

So they've actually had a heart attack, although many vets say to owners, oh, cats and dogs don't really get heart attacks. We do see them, and especially we see them in cats with HCM. Here's a cat who has had just that.

So if we look here, we've got the septum, the left ventricle is here, this is the septum, looks pretty thick to me. This is hypertrophic. Follow the wall round.

Suddenly we've got a very thin bit. Looks like someone's taken a bite out of this wall. This wall might be measuring thick again.

But look here, we've got a white area. This tissue's damaged, this tissue's dead. OK, it's infarcted.

If you cover up the septum with your hand, you can see that free wall's not moving much. It's got regional dysfunction. Look at the atrium, it's large.

The atrium should be a little square atrium that fits inside the ventricle twice, but here it's a big sort of trapezium or circle of an atrium won't fit in there once. So definitely this is a cat who's not only at risk of, heart failure because of the dysfunction of the left ventricle, but is also at risk of, arterial thromboembolism. There's also a little bit of pleural fluid, a little bit of pericardial fluid too.

So our aim in cats who've got left ventricular dysfunction is we give a positive inotrope. Now we give pymobendum. And this is a, a sort of hot topic really in cardiology is pyendin in cats.

The reason it's very controversial is that in the package insert for Pimendin and in the NOA directory, in the UK for looking at, drugs and their use, it specifically says pumerendan is contraindicated in hypertrophic cardiomyopathy. And that's a very important thing, we'll have to think about why in a second, but the dose that we use is 1.25 milligrammes per o for 12 hours, so twice a day.

There are some studies out on out there on the internet, out there in publication about using in cats. There are no prospective, blinded, placebo controlled trials. That's the sort of thing we need if we're going to make a decision about whether or not this is a drug that's first choice to use.

We need not only retrospective data, which is what this is, or anecdotal evidence, we need proper drug trials, we don't have that yet. Here is the closest thing we have. This is a retrospective study.

Now we shouldn't use retrospective studies to define proof of treatment benefit. That's not what they do. What they do is generate a hypothesis that maybe we should do further research.

So this is a publication from a few years back now in Jama, and again this is a survival curve. So what these investigators did is they looked back at their hospital data, or a couple of hospitals data on cats with HCM. They looked at cats who were given him aendum and followed them over time till the point they died.

They then took a control group of twice the number of cats who were not given abundant, but were also diagnosed with HCM and treated exactly the same way otherwise. I think these cats were also matched for age and and other diseases, things like this. So this is quite a nice retrospective study, but I will re-emphasize it's not conclusive proof of treatment benefits.

However, Look what happens here. This is the Pima Bean group. We want to get the happy emoji again because look how long it takes for some of these cats to die.

If you look at the X axis here, the average survival time is around about 2 years in these cats, or is approaching 2 years. Compare that to the cats who are not on Pima Bin, it's short. That suggests there might be a real benefit of using Pendant in these cases.

Why do we worry about it? Well, it might worsen outflow tract obstruction. So if we increase systolic function, increase contractility against an obstruction, we make the obstruction worse, and we don't.

The Prese cardiac output, all we do is make the that it's having difficulties, and this is not a good situation for these cats. So theoretically, Pyin could make them worse. However, this is hot off the press.

I've come across this this week, apparently it was published back in February, but it's not a journal I read frequently, maybe I'll have to start. This is the cardiac effects of Pybinin capital HCM. It was a single dose.

It's a nice prospective, placebo controlled trial. This is the beginnings of the sort of data we need to make decisions about safety of pyvelin in cats. So this is looking at the outflow tract obstruction in these cats, you can see in this graph, these are the cats who were given placebo, these are the cats who were given Pybin, and these are the same cats because they actually were given placebo first, given Pybendin later.

There is no difference in the vast majority of cats between the first and the second drug. So the first tablet, i, no drug, and the pumendam. You see there's one cat who increases quite a lot.

Maybe 1 more increases a little bit or 2 more increase a little bit, but some cats will just increase because their heart rate changes, their sympathetic tone changes. This may not be a drug effect, and that's one of the weaknesses of this study. However, it doesn't seem to be a big repeatable worsening of the problem in these cats.

So maybe we're missing a trick here. I don't know, the studies are pending, but in cats who've got dysfunction, I will consider using pyendam. So, my advice for when to use pyribendin in cats, and remember this is all off label, OK, so I can't recommend it based on, on data, as I say, this is all recommendation theory.

So we prescribe pyribendin for cats who've got regional or global dysfunction, maybe if they've got poor atrial function in that same paper that I reported just now, that very recent one, with the prospective trial, they they report that it increases atrial function as well. And these cats that I prescribe himendin to should have no significant outflow tract obstruction. So unless the cat's not doing well, I still don't use it in outflow tract obstruction if it's bad.

If it's mild, we might do to help signs. If it's absent, if they've got normal flow patterns, we definitely will. Now this is best done by Doctor Echo because we can have a good look at that region, we can measure the, the, the pressure across the aortic region, and that helps us to make a decision about whether the outflow tract is obstructed or not.

However, if you don't have access to Dopp or Echo in your clinic, if you're not performing it yourself, then that's absolutely fine. I would suggest go on an echo course because it's easier than we make it out. So if you learn to do it, it can help you make some big decisions.

However, auscultation is useful because if you find that a cat has no murmur. On Echo has a big atrium, poor function and has signs of heart failure. The absence of a murmur, if you've had a good auscultation on the sternal region, tells you that cat doesn't have significant outflow tract obstruction.

One very important thing I will say is that you should get an off label consent form for this drug signed by the owner. To have the conversation with them. I don't think your cat has outflow tract obstruction.

If it did, then that would be a potential risk. This is not a licenced drug for cats because we haven't got the research, but I think it'll benefit. Get a signed consent form.

The reason for that is. It says it's contraindicated, so there's something in writing saying vets don't use it. Now, there's also lots of stuff online like the website Himendan Kills Cats.com.

I think it does exist. I'm pretty sure there's definitely websites on this topic. Owners, of course, if they go and Google Himendum, they're gonna find these things.

And if their cat happens to be a cat who unfortunately has got bad heart disease and happens to drop dead that week after you start the drug. They might blame the drug, OK, they might blame you. So have this conversation, be open, be honest, but make sure you get a signed consent form about it because you want to make sure you, you really, clarify these things with these owners just to make sure there's no misunderstanding if things do get worse, OK.

Right, we'll move on from the at-risk group. We'll think about the cats who've got signs of heart failure, and this is probably the majority of the cats with with cardiomyopathy that you're seeing your Phoenix, unless you're routinely screening or doing echo in these patients. So these are the cats with signs of heart failure and or an ATE.

This is a wonderful video I have of a cat called Fred. Fred's in the foreground. These owners, have two cats, obviously, and, Fred, was so stressed coming into the vet that he went into heart failure every time he got in the car.

It was really not good for his health to come and see a vet. And so everything was done via home visits, vaccination, routine prophylaxis, everything else, medication checks. But the owners would send me videos and you can see very handily they have an internal control.

So look at the cat in the background, he's a normal cat, can't remember what he's called, but look at his breathing. Now compare that to poor Fred at the front. So these owners could make some pretty useful decisions about how Fred was doing before he developed overt signs that were bad enough to be rushed to the vet.

They could compare him to their other cat, they could monitor his respiratory rate, and keep track of that. And if they saw worsening of the effort, increases in the rate, then they would call us and they'd talk to us about increasing medication. So Fred's showing a classic clinical sign of heart failure here.

He's got tachypnia. He's also got some abdominal effort as well, so he's got dyspnea. We sometimes see cats with ascites causing abdominal distention.

And we often see lethargy, weight loss. I guess we see exercise intolerance, but you know what, cats don't really exercise, so it's really hard to identify that. I find lethargy difficult to assess as well, because many owners will say, oh well, he goes out, I don't know what he does.

So the cat goes outside, sits under a bush all day. They might presume he's running around like he used to climbing fences, hunting, but actually the cat might be going outside and just lying in the sunshine. So really lethargy might be there.

Weight loss is often more obvious. Signs of heart failure, we, you know, congestive heart failure, I'm defining this not as poor output exercise intolerance, I'm defining it as fluid accumulation. So here we've got pulmonary edoema or alveolar edoema.

We've got pleural fluid. These are the biggies for HCM. You sometimes will see ascites as well, associated with it.

Now, diagnosing pulmonary edoema or pleural effusion can be done on ultrasound, which is much better than doing it on radiographs. Because radiographs, you're relying on the cat to maybe Sedated, line lateral recumbency to get a lateral image. Cats who are dyspneic, you don't want to do those things really.

Maybe sedation to get rid of the anxiety, but not position them in lateral, in radiography. Use ultrasound. You see on the left here we've got the bee lines.

These are vertical lines. Extending from the pleura down is a classic for lung water. So this is pulmonary edoema.

OK, if you find this on both sides of the chest, cranial and caudal, it's highly suggestive of cardiogenic edoema, as good a sensitivity and specificity as radiographs in cats. On the right here you can see an image of pleural fluids. We've got the heart beating in the middle, it's actually quite bradycardia for a cat, this cat presented with, with an arrhythmia.

But you can see here you've got a classic, appearance of this hypoechoic fluid, which is, is pleural fluid. Radiographs can be helpful if you can't get the ultrasound images, or if you stabilise the patient sufficiently to make them safe. See here, see here we've got a lateral radiograph, what I can see in this image is, I can't see huge cardiomegaly.

I can see a fissure line caused by pleural fluid. I can see prominent, tortuous looking vessels, and I can see an alveolar interstitial pattern. You may not feel so confident making those decisions, but look at this cat when he's been treated for his heart failure, look at the difference.

The vessels here, you see are much smaller, quite thready. Before they were very thick, bendy looking, very obvious even cordially. You can see we have a fissure line here with a small volume of pleural fluid.

And you can also see pleural fluid in this region here, around the heart. The other thing is, you can't really see his corral vena cava very well. So look on the, the post treatment image, you've got a nice clear cadal vena cava from the diaphragm to the cardiac shouette.

I can't really see it clearly, maybe it's here, but the fact we're we're having trouble with that means this cat's got a dense alveolar infiltrate, and that is highly suggestive of, of pulmonary edoema when you've got vascular distention as well. So stabilising the acute heart failure cats, we, we really all know this, I think, so we want to give them oxygen therapy. Axiolytic sedation.

I really like butorphnil. I'm not on any commission at all from drug, companies who sell butorphannil, but I use 0.2 to 0.4 makes per kick, 0.4 if I'm going IM, 0.2 if I'm going IV, and you can top up the 0.2 if you need to.

I don't fight them to get an IV, you know, I'd much rather reduce their stress levels. So we also give them a dose of rosemide, 2 mes per gig IM, and repeat it in 1 to 2 hours depending on the response. If they've got pleural fluid that you find on ultrasound, remember, not on radiographs, we perform thoracocentesis.

There's a great article by Luca Ferrison and Theresadi Francesco, who work on either side of the Atlantic and have, have a very nice, discussion in this article about the approach to cats with acute heart failure. That's in the Journal of Veterinary Cardiology, from, from a few years back, you might be able to get this online, and, really is, is a very nice summary of the different approaches to treating acute heart failure in cats. So, longer term, we want to reduce fluid accumulation, don't we?

We talked about a stabilising dose of frozmide, well, oral frozemide is is the the mainstay of treatment, it's the cornerstone of treating heart failure in dogs and cats, in ferrets, and in horses if you want. My starting dose is 2 migs per kg across, twice a day. We adjust that dose of clinical effects, we get owners to monitor respiratory rates, really important, sleeping respiratory rates, not purring, because they always look disne when they purr.

And, get owners to monitor sleeping respiratory rate, track it over time, and actually you can use that to make decisions about increasing diuretic doses, either acutely or increasing doses long term. So this is a really great way of avoiding. Those emergency vet visits when you can have the cat presented, via the telephone, the owner can say, oh, we've had a mild increase in respirators, and you can just titrate the freezingide up a little bit.

Conversely, if cats are doing well, titrate it down, see what's the lowest dose you can get away with. Some cats who present with acute heart failure signs can come off the diuretic for a period of time, which can be incredibly useful. There's a paper looking at sleeping and resting respiratory rate in dogs and cats, and this is basically suggesting that respiratory rates when they're asleep, is an incredibly useful thing to do, and it gives you some cutoff values for what normal is.

So normal should be less than 30 per minute for well-controlled heart failure. Now owners can use an app, I tend to recommend an app called Carvalis. I'm not on any commission, it's made by a drug company, you know, it's free to owners, they don't have to be using the drugs that are in Carvalli, they can just be using the app, which is really neat.

And this can track trends over time, and if you've got a particularly, dedicated owner, they can email you graphs of the trends from the app, which is good. They can give the additional frozenide early and avoid things getting worse, and, they can potentially, you know, subvert those, those distressing emergency out of hours calls. Let's think about what else is going on in heart failure.

So we've got reduced cardiac output with heart failure, that triggers the bar receptors initially, and then the renin angiotensin aldosterone system. So hello kidney, the, the, kidney senses, we've got reduced sodium delivery to the distal tubule. And what happens, that causes renin release.

Renin converts angiotensinogen to angiotensin 1, angiotensin 1 to angiotensin 2 is converted by AAC, which is angiotensin converting enzyme. Angiotensin 2 does a heap of bad things. It's a vasoconstrictor, it triggers sympathetic nervous system activation.

It causes sodium and water resorption. It triggers aldosterone release and it triggers ADH release. So you can see how we've got a trend towards increasing the work of the heart, because the heart's having to pump into a vasoconstricted system, and also you're increasing the work of the heart.

Because you've got more blood to pump because you're absorbing free water. Aldosterone is something that causes cardiac fibrosis. It also triggers sodium, and water retention, and also potassium excretion.

So these are negative things, which can, can complicate the situation for you. So theoretically we've got some therapeutic targets in here. So we could use ACE inhibitors in cats to reduce the effects of antiotensin 2 by blocking that anti-attensin 2 production.

Theoretically, very beneficial. Data in dogs suggests very beneficial. If you've got reduced cardiac output, you've got a RAS activation, and the RAS activation is actually worsened by frozamide.

So we've got a recipe here in cats for ACE inhibitors being particularly good. I don't use them routinely and lots of cardiologists don't. So why, if theoretically they're beneficial, well, there are no studies available that show a benefit.

In fact, there's one trial that's in press, which is years old, and the data has taken a very long time to get published. And as far as I know, I'm not an author on it, but as far as I know, it doesn't show a benefit. I'm waiting for the publication to read that for sure.

So currently we don't have studies available to back up, back it up. We're increasing the number of medications. I've already said these cats are gonna be on clopidogrel, they're gonna be on frozamide, that's 2 drugs.

3 is kind of the most, maybe they're already on Pimabendin if they're suitable candidates for it, in which case, 4 tablets, we're starting to get into real polypharmacy, and as a cat owner who, you know, whose cat is not compliant, even with the best tableting skills, then, you know, this is a difficult situation for many owners. The other thing is that ACE inhibitors will interact with non-steroidals, and also with frozamide that they can reduce renal perfusion, so they couldn't exacerbate pre-existing kidney injury, could potentially trigger kidney injury. The non-steroidals thing is a common issue in geriatric cats, and it's something to consider.

If you have a cat who's very compliant, who will take the medication on some food or with some treats and dreams or something, well, actually, you know what, you might as well use it. If it's no stress for the owner, if costs not a big issue, you can throw it into the mix, but it is not your first choice, OK. So the dose that I would tend to go for, I go for 0.5 milligrammes per kilo benazapril once daily per us.

Don't give it to the hypotensive cat in acute heart failure. Make sure the cat is eating, stable, tolerating oral frozenide. I'll bring them back a week after they've gone home.

We'll check renal markers, or you know what, maybe I didn't pull them back to my clinic because they might have driven 3 hours or something to get there. They go to their local vet, the vet. The hands on them, performs an exam, has a chat about compliance and how the cat's tolerating it, has a chat about appetite, weight, everything else.

If the cat is normotensive, if the renal markers suggests things aren't too bad, down in the kidneys, then you can consider introducing an ACE inhibitor. If you give it in the acute cats, you can really, increase the risk of acute kidney injury. Just check blood pressure.

So there's another nice article here, nice review by Sonia Gordon and Etienne Coia about pharmacotherapy of feline cardiomyopathy. It said chronic management of heart failure, the home management, in that same issue of Journal of Veterinary Cardiology, it's a really neat little article and, you know, can inform quite a lot of thinking. Another clinical sign of HCM, everyone's least favourite, is the arterial thromboembolism.

You can see we've got the classic cat posture at the top right there. This is a cat who presented with a loss of use of both hind legs, and at the bottom, left there, you can see a cat who's lying in lateral recumbency on the left. The back, right leg, you can see, nice and pink pads, beautiful colour.

The front right leg to the right of the image, it's very pale. So that cat had of four limb ATE. And I think clawbed cyanosis, clawbed pallor, colour of the pads is really useful for detect those four limb ATEs and supporting the diagnosis in the hind limb cases.

This is not a very nice video to watch. I find it quite distressing actually. I remember the cat very well.

This is the cat, some years back when I was at the RBC, and you can see the cat's posture, cat's breathing. We've given the cat the medication, to make it as pain-free as we possibly can. We've, we've treating heart failure, he's in oxygen, he's had some anxiolytic sedation.

But look at the cat, it's not having a good time. That posture's very unnatural for cats. See the, the tail's splayed out there at the back, the legs splayed out.

This cat's got an arterial thromboembolism. So he's exhibiting the classic signs, the five Ps, pain, parsis or paralysis, pulselessness, pallor, and poikilothermia.poikilothermia is differences in body temperature on different parts of the body, so he's got cold hind limbs as well.

Their needs, analgesia, I sort of wanna write analgesia, analgesia, analgesia. I can't overemphasise, use full opiate agonists and agonists and get in there soon. They also need comfort, you know, not only minimising stress, but, they need to go to the toilet, you know, they might not be posturing to empty their bladder, so make sure they're they're sitting in a nice position.

If they've got limb swelling, try some basic physiotherapy and massage. Try and reduce their stress level. You need to reduce their platelet activation.

You see how low down that is on the list? My priorities are analgesia, patient comfort and reducing stress, which all go together. Reduce your platelet activation is your next thing.

That's where clopidogrel comes in. And nutrition, these cats need to eat. They might be on diuretics as well, which are making them pee out potassium, you wanna replace that, you wanna get them eating.

So what can we do? Well, as I said, a full opioid agonist, methadone, morphine, those are the things you need, fentanyl, maybe, although it's very rare that I'd reach for something like that. Methadone only works great.

Methadone also gives me a little bit of sedation, which is useful with the lowering the stress level. They need good nursing care and physio. These are where, where, you know, our, our fantastic nurses really come into their own, and looking after these patients.

We have physiotherapists as well on site. We're very lucky to have that. They will help by contributing plans and and assessing these patients regularly.

Axioistis, so, you know, the, the methadone is good, the opiates are good for axiolysis, and maybe a tiny sage of ACP, think about the environment as well, you know, really, you want a cat only ward. If you don't have a cat only ward, try and make sure the cat's in a sort of quiet area, provide a cardboard box for them to hide, cover the kennel. You've got to balance that with monitoring.

Clopidogrel, as I said, is the treatment of choice. Nutrition, try and tempt them to eat. You can try some appetite stimulant like mirtazapine, warm the food, hand feeding, all those fantastic nursing care things, but also consider a feeding tube if they're not eating for a day or two, really, you know, especially a couple of days.

Try and get a feeding tube in. Nasal esophageal tubes are generally tolerated very well, as you all know. Look at this cat, this is Paul Suki.

Suki's here a couple of days after an ATE. So you see, she's not ambulating well. She's got an IV in, and she's got a buster collar in to stop her pulling out a feeding tube that she's got in.

She needed a high level of care. However, 3 days later, the cat was doing great, walking very well, not normally but very well, and was discharged. Again, a nice review article from 2012, a little bit older this time.

This is from JFMS Journal of feline Medicine and Surgery, written by Virginia Lewis Frontes, who I'm sure many of you will know, who's an excellent cardiologist with feline bias, and, it's a very, very nice review on arterial thrombos managing these guys in some more depth. Additional considerations for ATE cases. They can get ischemia reperfusion injury.

So if they reperfuse their ischemic muscles, they can, they can end up with, free radical release. They can get asidedemia, hyperkalemia, acute kidney injuries. It's a complete disaster.

They can get limb necrosis. How far do you go? I'm still not sure how comfortable I am with amputation, but I have had cases that have gone through it.

Recurrence is common, OK, recurrence happens quite a lot with ATE as does heart failure if they're presented with heart failure. This is Boo, you'll notice Boo is about 4 months post ATE. Boo only has 3 legs.

I wasn't massively comfortable with this case from the get-go. The owners were very committed. The owners are very sensible.

They actually just wanted to do everything for this guy. He did brilliantly, apart from the fact his left hind limb was really not coping very well. So his left hind limb was cold, he had black claw beds, poor function, and really the tissue palpated like wood after a couple of days.

It was really distressing. He was doing fine on his analgesia and supportive care, was really doing great. Owners were very keen to go for amputation.

And this cat 4 months post amputation here just was going from strength to strength, did really, really well, and was having an amazing 4 months, OK. So I was very uncomfortable about this case. I didn't sleep great about it, however, he did well.

So I think sometimes my personal boundaries have been pushed a little bit with these cases, and actually, you know, on this occasion I was, I was proven wrong, the owners were really happy with how he was getting on with that. OK, we'll quickly review some other drugs and some other things. So drugs that we use in very selected cases, Spronolactone, this is an aldoserin antagonist, it therefore it jumps in on the ras on the aldosterone side of things.

Has a very mild diuretic effect, about 1 to 2% diuresis versus frozamide, which is 30%. So frozamide is the big hitter for diuresis, that's why we use it first line. We use fronolactone, not for its diuretic effect, although it may be synergistic with frozamide.

We use it potentially for antifibrotic properties. We said that HCM becomes fibrotic in the myocardium, it may help with that, we're not sure we don't have the data. However, big thing for me, it helps conserve potassium.

So if you're managing a cat who's having high doses of frozenide for a long period of time, you can reduce the hypokalemia by giving spoolactone. It's only once a day. So for me, I use it in hyperkalemic patients or patients where we're having to push the rosamide dose higher and we think they're getting diuretic resistance.

There's a study, I don't know where this name comes from, sizesaca, no idea, but the sizesaca study was a pilot study looking at efficacy and safety of spronolactone in cats with heart failure. Now, in this study, they found that the spronolactone was very well tolerated, and there was a trend towards improved outcome. However, it was quite a small study.

The groups at the baseline weren't evenly matched, so it's very hard to say that trend. An improved outcome as anything, to, to change how we work. So I don't give this drug first line, however, it can be helpful and we believe in certain cases, OK, so I do use it now and again, we've got to factor in compliance as well.

I think I use it more than I use ACE inhibitors. Drugs for selected cases, beta blockers. Many people will think about giving beta blockers to cats with outflow tract obstruction.

Now, they can certainly reduce outflow tract obstruction, but they do it by reducing systolic function, which may not be good. It may precipitate all worse than heart failure signs in cats who are in the at-risk group, so we wouldn't give beta blockers to cats who've got a big atrium unless there's a very good reason. And some cats don't tolerate them, some cats seem to get quite depressed, go off their food, they don't like having the beta blockade.

I use them for arrhythmias, and I use them if they've got very bad systolic anterior motion with clinical signs of either arrhythmias or collapse episodes. There was one study looking at 5 year survival in cats with HDM who were given atenolol or not. That's the survival curve.

You can see there's no difference between cats who were given atenolol and cats who weren't over 5 years. This didn't measure quality of life. Maybe there's a difference, we don't know, but survival, there's no difference.

This is the reveal study, and if we look at the two graphs here, first concentrate on the left. Time to congestive heart failure. The one on the right is time to arterial thromboembolism.

We've got two lines here, we've got the obstructive cats and the non-obstructive cats. So we've got the cats without flow tract obstruction, and the cats without cat flow tract obstruction. They're they're red versus blue respectively.

There is no difference in time to heart failure or no difference in time to arterial thromboembolism. Which means maybe obstruction is not a bad thing. So they had the same survival time, but they were diagnosed younger, so maybe they've got a worse disease causes their overall longevity is lower.

We don't know. This study didn't evaluate that, but what we can say is that it's not our priority to get rid of outflow tractor obstruction, there are other things to worry about. Drugs that are rarely used, terrazamide or torzamide is marketed as UCA, that's very rarely used by us.

It's a loop diuretic, it's similar to frozamide, it's off licence, for cats, potentially has a higher receptor affinity or higher bio bioavailability. There's no studies on that in dogs or. Cats, although it's true in humans, we use it as a rescue protocol.

So if cats are very resistant to furosemide, we'll give terrazamide. It can make a massive difference. You can't go with the label dose.

The label dose in cats who are resistant is too low. You have to speak to a cardiologist and work out an adaptive protocol to switch from frozamide to shinozamide. So I use it if they're resistant.

I don't use it first line, but I do use it fairly frequently, well, frequently. I use it often enough, that it's in my, my toolkit of drugs that I can use, but not all cats get it by any means, and it's not a first line treatment for us. Diltiazem rarely used, very rarely used, it's the only licenced drug for feline HCM.

Amazing that it got licenced based on the studies that were published it. So it's licenced by Decora as a Hypercard, 10 milligramme tablets. The initial trial results have never been repeatable.

It's administered 3 times a day, big compliance issue, especially if we don't think it does very much. We do use it as heart rate control in cats with atrial fibrillation, and that's a very important drug to use for those cats who've got high heart rates with atrial fibrillation, because it can slow down their rate, improve their output, and improve their quality of life. However, that's the only use for it.

It's not the fact they have hypertrophy, or the fact they have heart failure that we would ever give to ias. We rarely use antiarrhythmics in cats, and we have to assess the arrhythmia to, to find out how significant it is. We can use sotalol for ventricular arrhythmias, diltiazem for AF, as I said, and atenolol for ventricular or supraventricular arrhythmias, if they're not at risk of heart failure.

So, to summarise, way back at the start we talked about classifications. I don't care about classifications other than to say they're not important. Think about functional problems and treat the functional problem if it's present.

Consider not only the cats who are showing overt clinical signs, those cats who will present with dyspnea, think about at risk cats as well. And be prepared to adjust your doses, adjust your medication plan based on the individual treatment response and also based on compliance. I've treated a number of cats where we've had to drop out the clopidogrel and just use liquid frozamide once a day, you know, really just, enough to help them cope, but it's amazing how many of those cats at home with minimal stress of intervention can have a very good quality of life, and with owner monitored respirates, it gives additional control over coming into the practise repeatedly.

Home respiratory rate monitoring is crucial. Find an app or even just get them to fill in a spreadsheet or something. It can change how these cats survive.

It can really help preempt those those awful out of hours calls that can end up with a dead patient. So thank you very much for listening. It's, you know, 9:30 UK time, so people are probably beginning to think about a gin and tonic and a bed maybe, but, thank you for coming along and, and joining us for this, and, I'd welcome any questions if anyone has them.

Thank you very much Kieran, absolutely brilliant talk, really, really good. We do have a couple of questions through already. So the first one is from Greg.

He's asking why the microthrombbi develop? And if you have no access to ultrasound, what is your initial treatment for a cast presenting with an ATE? So, good questions, we'll tackle the microthromy one first.

So I would say that the microthrombbi we think, which are the sort of predisposing factor or the initial trigger if you like, for thrombosis in the atrium, are caused because the atrium is enlarged and the atrium contractile function is reduced. Now we believe. That that causes the blood to stagnate in the oracle.

We tend to see thromy form in the oracle of the atrium, which is a blind ending sac, and actually, you'll see the smoke, the spontaneous echo contrast, just swirling around in the oracle, going nowhere in some of these cats. If the blood stagnates there. You don't get the normal mixing of the blood with anti-calculant factors.

You don't get that blood passing over the endothelium out around the body, and the endothelium is a very important thing that that secretes anticoagulant factors. So we believe that these cats are actually are sort of in a prothrombotic state, regionally, that goes on to trigger thrombus formation. That's why they start getting these microaggregations is because of a sort of, dysregulation, if you like, of the, of the sort of balance between prothrombotic and antithrombotic factors.

The second part of the question, if you don't have access to ultrasound, how do you approach a cat with an ATE? Well, you don't need the ultrasound to find the thrombus, for example. If you've got the cat with the 5 P's, so pallor, pain, poikilothermia, so differences in body temperature, paresis or paralysis, and, I've forgotten the fifth one, that's so embarrassing, .

There's 5 P's, you remember them, and then our pulselessness, of course. So you might feel the femoral artery and no pulse, and in those cases, if you're fairly convinced of your diagnosis, analges them, give them antiplatelet drugs, treat them in exactly the same way, you need to monitor respirate to see whether they have a heart failure or not. Initially when they present you often can't tell if they've got heart failure because the rest rate will be high through pain and distress, but analgesia, get them calm, let them settle in.

You can always give them oxygen or freeamide if you're not sure, and then see if they're in heart failure later. So maybe take a radiograph once they've stabilised and see what, what things look like, or consider a referral once they've stabilised for ultrasound. Excellent, thank you very much.

And another one from Greg asking, does pima Benzin reduce cardiac size in cats like it does in dogs? That's a good question. And the answer is we don't know.

We haven't got any data. No one's done the studies. I, I'd love, you know, anyone to fund a good study into pyvedon in cats, but, but we're not there yet.

So we don't know. My presumption is it would, because it does in in dogs with microvive disease in dogs with dilated cardinopathy, but we just don't know in cats. OK.

And do you have experience with turazamide in cats? So yeah, I was expecting a question on Terazamide in cats actually. And I think you may have asked before I, before I put the slide up there on Terazamide.

So I do use it, I tend to give, if I'm using it as a rescue diuretic, which is the only way that I use it, obviously it is off label, it's important for me to say. I calculate the total daily dose of furozamide. And I divide that by 10 to get you terrazam my total daily dose, and I split it into morning and evening doses.

So for example, if you have a cat who's receiving a very high dose of freezide like maybe 20 milligrammes TID so every. 8 hours. So you've got a total daily dose of 60 milligrammes for that cat, you know, it's an obscene dose of rizide for a cat, but there we go.

And, if you, take your total daily dose of 60 divided by 10, that's 6 milligrammes of terrazamide per day, I'd give 3 milligrammes in the morning, 3 milligrammes in the evening. So you do that sort of calculation, always monitor your BP, your renal marks and things around those changes, you know, your creatinine, your potassium, and just make sure. Sure you're not making things worse.

And if you are back off the dose of the terrazamide, because maybe you've been overzealous, in doing that. But that's very rare in my, in my experience of using it in cats. We tend to use that, that switch, it tends to work quite nicely.

But as I say, it's off label. Make sure you get signed consent forms and, and, and do, if you can't remember what I said there, or if you're not sure, do speak to a local cardiologist, contact them for advice, because they'll probably be more than happy to guide you through it. Lovely, thank you.

And would you use cloth and aspirin together? I have used a combination of clopidogrel and aspirin together. In humans, there's there's a belief, or there's some evidence, I think that they're synergistic.

They do work on different receptors on the plate that the aspirin works on. The, arachidonic acid receptor, which, which causes thromboxane, to be released by the platelets, so it reduces thromboxane concentration. Clopidogrel works on the ADP receptor, so it's a different thing entirely.

So you can use both, and they should have synergistic effects. And my approach is if you have a cat on clopidogrel. Who has got smoke still, or quite a lot of smoke, I might add aspirin, or if you get a cat on clopidogrel who develops an ATE and sometimes they will, then I will add aspirin as well.

I don't go with dual therapy first line again for compliance reasons. With the aspirin, my dose is 18.75 milligrammes every other day is how I use that.

Some people use it every third day or use higher doses, but we, we tend to use the lower dose, the 18.75, and every 48 hours, we, we believe that might have a better effect than every third day, but again, we're, we're lacking the data. Lovely.

And the next one's quite an interesting question. So how do you recognise the at-risk cats which have no murmur? That's a toughy, isn't it?

Heart murmurs in cats are are a whole, whole can of worms, and many cats with the worst heart disease don't have a murmur. So my approach, well, I'm going to flip it around first of all and say the cats with murmurs. I'll investigate a grade 3 plus murmur, or, you know, a, a grade 1 or 2 murmur if you've got things like arrhythmias, gallop sounds, signs, of course you've got to take those murmurs seriously.

And what we do with cats who don't have murmurs is we've got to look at the age category. So you've got to say cats over 9 or 10, well, the, the, you know, 1 in 3 of them have got HCM, cats over 12, it might be 1 in 2. So just when they walk in the door, half of cats over 12 have probably got HCM.

So despite your at-risk cats, you're gonna have to echo them. Now, I'm not suggesting you echo every single cat over 12. It might be that you're confident doing a left atrial size check rather than a full echo, that's fair because left atrial size, you know, is, is a very important thing.

So if you can get some experience just looking for left atrial size, then you can really do many more of those scans than than you think you're. To if you're, if you're a novice, and actually that will change how you work, and it will allow you to screen those cats quite accurately for risk. If you're not confident with that, or if it's something where you feel like costs may prohibit people, going for for left a size checks, as I say, we only charge 80 quid for a left atrial size check, so it's not a hugely expensive thing, you know, for inpatients or for our own patients on revisits.

So we, we try and keep the cost down to maximise the utility of that test. The other thing you can do is look at cardiac biomarkers. So, potentially look at pro BMP, there is the SNAP test, the EISA test, available in cats, which will come back as abnormal or normal, and the abnormal, is roughly about 120 pea moles per litre.

And we know that above that level, cats are more likely to have heart disease, . The difficulty with that Snap test is that based on some data that I'm, I'm, in publication with at the moment, of cats in first opinion practise, we think that around about 60% of cats who have got an abnormal Pro BMP have got heart disease on an echo. That means 40% don't.

So it's fairly close, it's getting close to tossing a coin, if you have a positive test or an abnormal pro BMP snap test. It's fairly close to 50/50 as to whether they have changes to their heart or not. However, the ones that are negative seem to be truly normal in the vast majority of cases.

So it's quite a good rule out test to run anti-ProbMP snap tests. It may not be the best rule in, however, it does reduce the number of cats that you might want to echo. So it helps you to select your population and therefore make the echo, a higher yield test, a better, a better test for, for finding the heart disease if it's there.

It's not perfect, but it's the best we've got. Excellent, thank you. We do have some really great questions coming through tonight.

Catherine is asking, have you ever used an epidural catheter to deliver pain relief in cats with some saddle thromboembolism? The answer is no, I haven't, but I think if you're, confident in getting, getting that in, then absolutely, you know, great idea, great idea. You won't get so much of an anx anxiolytic effect, obviously if you're doing that, but, but you know, I think if you're able to provide that in other means, then, then that's a great, a great way of doing it, yeah, yeah.

Lovely, thank you. And would you consider an ACE inhibitor if the cat has an AT and renal issues? So, you know, I mean, my preference for ACE inhibitors is clear in that I don't, you know, really use them very frequently in cats with heart disease.

But, I, you know, using them in a cat with renal issues, and an ATE. I, I don't think ACE inhibitors are massively helpful for ATE per se. They don't have the antiplatelet effect.

The vasoconstriction caused by the thrombus is, is, you know, not really amenable to, to vasodilation using an ACE inhibitor. So, there's not a direct indication for using it in those cats, you know, just because they've got a thrombus. Most cats with a thrombus, you know, 95% or so have got bad heart disease.

And, you know, if they have got bad heart disease, you might be able to use an ATE, but I, again, I wouldn't use it in the acute phase, and it certainly wouldn't be my preference. Lovely. And what is the dose of Paabendin that you use?

So the dose of pumabendin, it's pretty crude, really. It's, it's a tablet per cat twice a day. So it's 1.25 milligrammes per cat twice a day, which is a small tablet size of, of vet mein and Cardiffure.

The thing you could think about, obviously, if you've got a very small cat, or a cat who's very low body condition, you might want to half that dose because the tablets split quite easily. So you could get a 0.625 BID.

The studies that have been done on cats, suggest that 1.25 BID is safe for your average sized cat. Lovely, and just a few more questions.

How long does it take for a cat with an ATE to start to respond to treatment? That's a really important question, because I have known cats to be euthanized when they're not walking in 12 hours, which seems a little bit of a shame, because actually most cats will take, you know, 34 days to, to show a decent response. The average time in, in hospital, in first opinion practise based on some data that I've published on 250 cats with ATE, was between 2 and 7 days.

So I would say if you're getting, you know, progress by day 3. 4, the cat's doing, you know, averagely well. I would say if there's a lack of progress by day 5 to 7, then you're probably in trouble.

So that's my rule of thumb. So if you've got good progress by day 3 or 4, fantastic, or sooner, of course, that's great. but if you've not got a significant improvement by day 5, day 7, you're really, you know, not, not feeling very positive about that case.

What I would say is my point of discharge from the hospital. Is not return of a pulse. Some cats never get their pulse back, but they can walk, they can run, they can jump and climb the fence, because they get collateral circulation to the limbs, so it may not go through the bit of femoral artery that you're feeling, but they can perfuse the limb.

What I, you know, what I use for my marker for discharge is, is the comfortable? Is the cat, if it had heart failure, is that controlled? Is the cat able to posture and use the toilets?

I don't like sending the cats home for, for expressing bladders and things. Owners don't want to do it, and, and I don't think, you know, I don't think I do it very well, so I think most owners probably don't do it very well either. And, and they need to, of course, be pain-free and, and, and eating.

So those are my markers for discharge. They may not be walking totally normally, but if they can use the loo, get around, and they're happy, well, that, that trumps everything else, and they can be discharged. That's really interesting to hear that they may never regain that post back.

So the next question, have you used heparin in an ATE? Yeah, I have, but I've stopped a number of years ago. Heparin, is sort of a wonderful idea, for using these cases, but there, there are two difficulties.

First of all, it requires frequent injections, IV if they're in hospital, subcut if they're at home. The second thing is that, heparin in cats has got a huge range of pharmacodynamics. So if you give, you know, cat A a dose of heparin, then it might last, or sorry, low molecular weight heparins that, you know, like fragment and things, they're supposed to last longer.

And in humans, you can give them 33 times a day or, or twice a day. That's just not true in cats. Sometimes you give a dose of fragment to a cat, and it'll last.

2 hours. Other times you give a dose and it lasts 22 hours, and you just don't know what you're doing with it. So it's so variable in cats, there's just no point in using it, in my opinion, because you're just guessing.

You're going to be overdosing some cats, you're going to be under-dosing others. And if you want to really monitor it, you want to monitor COAGs, so you're going to have to frequently check bloods, in every cat you give it to. It's a whole heap of needles and a whole heap of stress for everybody, .

And there's no proof of benefit. I, I, again, in my study looking at cats in first opinion practise, it's retrospective. So it's it's not a good treatment study, but we did say in that, that actually there there wasn't a significant benefit of heparin.

And actually, at one level, the use of heparin was associated with the worst outcome. But as I say, that's not proof of treatment benefit, but it doesn't swing me either way to using heparin. And because of that complexity and dosing, I just steer clear of it.

Lovely. And just 2 more left. Do you use Carterfe in ATE?

I don't use Cartrafe in ATE. I've been asked that before, and I, I've, I, I don't know what the rationale is, I must look it up. So if you're willing to comment and let me know, or email me or something, I'd love to know.

I, I'm not sure where the basis of that comes from, but, but certainly there's no data and, and, and therefore, you know, I don't use it. Lovely, and finally, what percentage of ATE cases improve and specifically those that have signs of congestive heart failure? That's a good question.

Again, referring back to the, the data that I, I know is the data of my own, and looking at cats in first opinion practise, they're not, you know, managed by specialists, although there's little difference. These cats seem to do the same wherever they're managed. So the cats in first opinion practise managed by vets there.

If, if you look at overall, the mortality rate is really high. But oftentimes that's euthanasia on presentation with no attempt to treat. Now there are some cats that I would recommend euthanasia for with an ATE because they've got negative prognostic signs, like a very low rectal temperature.

Those cats just don't do well, OK? So statistically they're much more likely to die if they've got hypothermia on presentation. So if they're hypothermic, or if you just can't control the pain, you know, then I'll think about euthanasia.

Heart failure, you know, alone doesn't make me want to euthanize them. It, it does reduce survival time, if they've got heart failure, but actually, sometimes they've sort of been tipped into heart failure by the, the, the stress, the pain of the ATE. The travel to the vets, you know, all of that, and actually if you can control a lot of those things, control the pain, get them walking again, reduce their stress, sometimes they come out of heart failure and you don't need diuretics.

So why heart failure is a bad thing, you know, they're not always in persistent heart failure, if you like, . So it might be that, that, you know, by, by using heart failure as a prognostic indicator, you might consign some cats to, to, to, euthanasia when actually they could do well. So, I, I'll treat the heart failure, I guess, because I'm a cardiologist, that's what I do.

And, and I'll treat the ATE and, and if they're both improving, well, fantastic, we'll, we'll, we'll carry on. So, your specific question was, what proportion will, will respond to treatment? If you look at just the cats where treatment was attempted.

Survival rate was just over 50%, so it's between 50 and 60%, survival for 7 days if the vets tried to treat. Many of them didn't try to treat because the owners were, were so shocked and horrified by what was happening that that euthanasia was, was the top of the list of things to do. So although we look at cats with ATE, and many, you know, many emergency vets out there will say, oh, we should put them all to sleep.

I, I, I don't agree with that. I see where they're coming from. I understand that, but I don't agree with that, because if we do try to treat, the response rate is as good as some other conditions.

Lovely, thank you very much. Thank you so much for answering our questions so thoroughly. I think you deserve that gin and tonic now.

Thanks very much. I'll go for a non-alcoholic beer, but you know. Thank you to everybody, all of our attendees for listening.

And please take a few moments just to fill in our feedback form that will have popped up in your browser so that we can give some feedback to. And finally, thank you so much Kieran for all of your time this evening. No problem, it's been a great pleasure.

Thank you. Lovely. I hope you can enjoy the rest of your evening.