Hi there, thanks for tuning in. We're gonna talk about cardiomyopathy in cats. What is there to think about cardiomyopathy in cats?

Everyone feels like maybe they know about cardiomyopathy. There has been, last year, 2020, a consensus statement on the approach to diagnosis and management of cardiomyopathy. And a consensus statement is where people get a group of specialists into a room, not just specialists, but ones who are super experienced with feline cardiology, and they try and get them to agree on something.

Now you probably know as well as I do that specialists often have quite strong opinions and quite differing opinions, and even within my service where I work, we have a couple of fairly Different approaches to things as specialists and that's OK. But it's nice to have guidelines for particular diseases, especially something as common and important as cardiomyopathy in cats, because then we can make recommendations on what the average opinion amongst specialists is and therefore how best primary care practitioners should proceed. So we're gonna take a walk through that consensus statement.

We're gonna look at some other evidence and we're also gonna look at some some key points on echo these cardiomyopathies, but also how to treat them, when to treat them, and how best to monitor these cases. So we're gonna cover quite a lot in the next 45 or 50 minutes or so. So lecture plan, we're gonna define what we mean by cardiomyopathy.

We're gonna talk about the consensus on how to diagnose and stage that heart disease. And we're gonna talk about HCM particularly, hypertrophic cardiomyopathy, because it's super common and therefore super important as a global problem. What I mean when we say cardiomyopathy, well, the definition is a primary heart muscle disease where the changes detected to the heart on diagnostic imaging cannot be explained by differences in loading conditions or circulating volume.

So as an example of that, hypertrophy, thickening of the heart muscle can be caused by hyperthyroidism, diseases like acromegaly, sometimes referred to as hypersomattotropism, infiltration with, say, lymphoma, or other things too that affect how the the ventricle is working, the loading conditions, but also if there's other things in there apart from normal cardiomyocytes. Diation can be explained by volume loading. So if you give an animal loads of fluid therapy, or create a state where they're moderately to severely anaemic, in cats that will activate the renin angiotensin system, which leads to volume loading.

So anaemia itself in cats can cause cardiac remodelling. So to say an animal had cardiomyopathy, let's say they were an old anaemic cat, I would need to exclude the the fact that the the changes to the heart could be explained by the anaemia. Now that wouldn't explain hypertrophy.

So if they had hypertrophy, I'd be thinking, OK, well they're anaemic, but that's not the cause of the hypertrophy. But if they were hyperthyroid, I couldn't really call them true hypertrophic cardiomyopathy without treating that thyroidism, that hyperthyroidism, and seeing do the changes reverse. So it's quite an important thing because if we're gonna use the term cardiomyopathy, we should probably use it really for primary harmless sort of things.

If we don't know that it's a primary condition, we should use the term HCM phenotype, hypertrophic phenotype or dilated phenotype. So what we're saying with the word phenotype is that it's the appearance of the disease. But there may be something else going on, so just be a little bit careful before making a final diagnosis of HCM in a cat that's eating with weight loss, vocalisation, and changes to thirst, urination, defecation behaviour, because maybe that cat's actually hyperthyroid.

This is an echo of a cat with cardiomyopathy. I'm just gonna use it to orientate you to some of the normal structures. So here we have the left atrium.

The mitral valve And the left ventricle. And in the near field, we have the right heart, right atrium, tricuspid, right ventricle. We see the left heart is much larger than the right, that's normal in itself.

But this left atrium is very large indeed. Most cats have a left atrium round about this size relative to the ventricle. So it's pretty angular looking in most cases, and you can normally fit two of that left atrial area inside the left ventricle.

This is a huge atrium. The other thing we can see here is spontaneous echo contrast, which looks like smoke. In fact, we sometimes use the word smoke to to describe it.

That is commoner as a marker of a hypercoagulable state in cats with cardiomyopathy with significant atrial dilation. We'll talk about this in some more detail later. If you're not familiar with this, you will become familiar with it over the course of this lecture.

The other thing we can see is this wall is slightly thick compared to this wall. The free wall is thicker than the septum, which is probably a normal dimension. And I'm gonna say just eyeballing this heart, probably we have HCM we've probably got hypertrophy with left atrial dilation and a risk of thrombus formation.

Now those descriptive terms are useful because it helps us to define how severe the heart disease is. And as soon as we see left atrial dilation, especially this severe, we say that this cat is in a much higher risk category than a cat who had a normal size left atrium. When we think about cardiology, if someone says to me, well, what's the risk for anaesthesia?

My response is often, well, how big is the left atrium? It's a six word cardiology textbook. So how big is the left atrium?

If we find the left atrium is large, the risk is higher. If the left atriums are normal size, the risk is lower. OK, so this is a very, very important thing to try and stage these cats and, and give them a risk assessment.

The consensus statement is is here, that this is the reference for it, and you can see it was around a year ago that this is is in the process of being published for the ACVIM. It's a really important document. They're not always the easiest to read these consensus statements because they talk a lot about different levels of evidence in the research studies out there.

They can be a little bit dry, and we're going to hopefully distil the most important parts of this really critical document for practitioners during the course of these slides. The consensus describes a number of different classifications for feline cardiomyopathy. And these are diseases which everyone watching is probably familiar with the terms for most of them.

The first one, I've already talked about it, is hypertrophic cardiomyopathy, HCM. So we would define that as a wall thickness of the left ventricle that's 6 millimetres thick or more in a single location. Can be more locations, but at least one location that's measured by 2D or M mode in long axis or short axis.

My advice is to look in 2D long axis and short axis. M mode can be challenging and misleading in cats because you're echoing something the size of an egg or smaller, OK, the size of a bantam egg or something, very small indeed, and the walls are 6 millimetres thick at the. You know, in hypertrophy, the chamber is 15 millimetres wide, so we're talking about something very small that we're echoing.

So when you use something like M mode, which is not a particularly accurate way to look at the whole heart, what's happening is is we can get structures that interfere with the M mode and make it very easy to overestimate hypertrophy or to miss hypertrophy if that's focal hypertrophy. So I would two dimensional echo images, long axis and short axis, and we will look at some of those in the in the coming slides. Don't forget, you have to be able to not explain that thickening of the muscle by the presence of hyperthyroidism, hypertension, things like acromegaly, OK, infiltrative disease.

So these are important things to make sure we exclude as best we can. Restrictive cardiomyopathy is a different phenotype, so these cats do not have hypertrophy. If we measure hypertrophy, don't forget we classify that as HCM.

So restrictive cardiomyopathy comes in two forms. First, we've got a band of scar tissue which crosses the left ventricular cavity from septum to freewall. That would be called the endomyocardial form of RCM.

The alternative is when we have normal wall thickness, but very severe dysfunction of the heart, especially in diastole, and both forms of RCM have left atrial or bi atrial dilation. So it can be quite hard to define normal wall thickness, diastolic dysfunction if you're a practitioner using echo in practise to make assessments of these cats. So my advice would be if you see left atrial or biattrial dilation with no evidence of hypertrophy, I would probably call that RCM.

Diated cardiomyopathy is something we're very familiar with in dogs often, and with DCM we expect to see poor systolic function in a non-hypertrophic dilated left ventricle. We may see that with a normal sized atrium. OK, so DCM we can see it with a normal sized atrium, but they do have poor function and an obviously dilated heart compared to reference intervals.

The 4th classification of cardiomyopathy is called arrhythnogenic right ventricular cardiomyopathy. We abbreviate it to ARVC for obvious reasons. And then this is the same disease as in humans they often refer to as ARVD with the D being dysplasia.

OK, so slightly different terminology in people but effectively the same thing. Here we've got a a right ventral. Predominantly affected.

So often we have a large right heart and because the, the ventricle is infiltrated with fibro fatty tissue, that can cause arrhythmias, and often we see ventricular arrhythmias in these cases, but I have seen supraventricular tachycardia and atrial fibrillation as well, and I would still lump those in as enough of an arrhythmia to call it ARVC. The final type is the nonspecific phenotype, which previously over the last 20 years in veterinary medicine has been referred to as unclassified cardiomyopathy. That's a bit of an oxymoron because by calling it unclassified, you are classifying it.

Seems strange. So they've referred to this now as non-specific phenotype. The deal is that you have to describe what you're seeing.

So for example, if I see a non dilated left ventricle with poor function, but a band of scar tissue crossing the left ventricle, those are features of DCM and the endomyocardial form of RCM. So therefore, I might just call it non-specific phenotype with poor function and a band crossing the ventricle, because then everyone knows what I'm talking about. OK, so it's important if you're gonna use that term to actually write down functionally what you're seeing, the most important thing there would be poor systolic function.

Here's an example of an echo loop of a cat with hypertrophic cardiomyopathy. So we can see we've got the left atrium here, the mitral valve and the left ventricle. The left atrium is a fairly normal size, in this case, you can probably fit two of this fairly square looking left atrium inside the ventricle.

The right heart looks pretty normal, but when we measure the septum here, you can see it looks a little bit bumpy in this region, and there are no papillary muscles on the septum. So in this free wall, the papillary muscle will arise and connect to the mitral valve in this region here, so I wouldn't measure this area to say whether it's hypertrophic or not, because we've got normal structures there that may influence that measurement. I'd measure quite high or below the papillary muscle.

On the septum, looking at the the the the thickening and the bumpiness here, that isn't normal because there's no normal structures there. So we'd measure the thickness there, and in this case it did exceed 6 millimetres and therefore it's classified as hypertrophic cardiomyopathy. You have to be a little careful in the measurement because you have to make sure you don't include these papillary muscles and don't include parts of the mitral valve apparatus or cali tendon, which is surprisingly easy to do in a cat's heart that is only the size of an egg.

Here we've got a cat with HCM. So we've got thickening of the septum. This did measure thick.

We also have a large left atrium, so you can see how we've got this non-square, sort of trapezium looking or rounded looking left atrium, and we've got the mitral apparatus here. We can't fit two of that left atrium inside the ventricles so, that's definitely a big atrium. We also have a free wall of the ventricle which looks abnormal for two reasons.

First of all, it's thin here and it's hardly moving well. And secondly, we've got this white fibrous tissue appearance. This is probably a cat who's had a myocardial infarction caused by HCM we do see that.

The final thing to notice here is there's a small pericardial effusion surrounding the heart, which tells us this cat was actually in the early throes of congestive heart failure, although at the time of the echo there were no outward clinical signs. So this cat would still fall under HCM, but the poor function, you know, some people may classify that as non-specific, there will be a difference in how people classify things. I would say this is probably HCM gone bad.

One way of looking at the left atrial size is in long axis, like we've discussed, but here we compare the size of the left atrium to the size of the aorta with the aortic valve in the middle here. So this is a short axis view at the heart base. We can see the three leaf clover or Mercedes-Benz appearance of the aortic valve and the left atrium below that.

We can also see the left oracle alongside the atrium here. The normal left atrial size should be less than 1.5 times that aortic root diameter.

Here we can clearly see we've got the aorta in the middle, opening and closing. We've got this very large left atrium here which is way more than 1.5 times the aortic diameter.

The aortic diameter should come to about there in a normal cat. Maybe here, but in this cat it goes all the way out to this hypoechoic wall here. You can see the oracle is also prominent.

So this is a cat with left atrial dilation. Here we've got the restrictive cardiomyopathy phenotype. So we have the left ventricle here and because we've got this band of tissue crossing from the septum to the free wall, we would call that endomyocardial RCM or ERCMs.

This is definitely a restrictive cardiomyopathy. The left atrium is also rotund and you can't fit two inside the ventricle, so therefore that is left atrial dilation. Again, a little bit of pericardial pleural fluid here, so this cat is in heart failure.

Here's another example of restrictive cardiomyopathy, big atrium. The right heart looks prominent too, so I'd say it's probably bi atrial dilation here. We've got the left ventricle in this region with a band of tissue crossing the ventricle.

We don't know why this occurs. It's an interesting disease because there's some suggestion there might be an association with Bartonella infection, but that's not proven at the moment. It's it's very interesting cos some of these cats do have bartonella in the walls of the heart.

OK, so that's fascinating. Perhaps this suggests previous exposure to. Disease, which is a systemic disorder which has caused myocardial inflammation and scar tissue.

It may be that the changes don't reverse by treating that, we just have to deal with it like it's a primary cardiomyopathy. We're not quite sure about that yet, but that's interesting developments in the last couple of years based on some studies in veterinary pathology journals. The other thing to note, pleural fluid here, again, suggesting this cat is already in heart failure.

And with this particular case, this cat had a fairly prominent heart murmur, and we can see using colour flow Doppler, this green mosaic, that's turbulent blood flow which causes murmurs, and you can see there's turbulence crossing that fibrous band of tissue there, which is a mid-ventricular obstruction. This is the same cap we were looking at with the the RCM we can see we've got left atrial dilation in this short axis for you compared to that aorta. Another thing we we saw on one of our very early slides was smoke spontaneous echo contrast.

We often see that in the left oracle of cats. It's very common in restrictive cardiomyopathy. And we can see the oracle, this is the body of the atrium here, the mitral valve, the oracle falls down over the side of the heart, over the cranial aspect of the left heart, and we can see there's quite thick.

Contrast here, which is swirling around like smoke there but in this region is really aggregating in this blind ending oracle, and we believe that the risk of this happening is associated with the risk of thrombus formation. As you'd imagine we've got little micro platelets here, little microaggregates of red blood cells and platelets and fibrin. Which is here is organising potentially into a thrombus.

One of the reasons this happens, there are probably several contributing factors, but one of the big reasons is this atrium is not contractile. OK, so you can see how the atrium's twitching, it's not contracting very well, and in this blind ending oracle, the blood's just swirling around and around and not going anywhere. Finally we have a cat affected by ARVC arithmogenic right ventricular cardiomyopathy.

This is the left heart over here, left atrium, mitral valve, left ventricle. Look at the huge right heart. The right heart should be 1/3 the size of the left, or even less if the left heart is large, and here they.

Right heart dwarfs the left, you can probably fit two or three of these left parts into the right side. It's huge right atrial dilation, tricuspid valve here, right ventricle. So we would call that arrhythmogenic right ventricular cardiomyopathy if the cat is also affected by arrhythmias, which many of them are.

And here's a similar case in short axis, we've got the left ventricle here, papillary muscles, it's sort of a mushroom view of the left ventricle. And then we've got a very large right ventricle alongside that, which is hugely dilated. Sometimes we see very extreme versions of the phenotype, and I tried to show this image as a cat with HCM.

The septum is here, the left atrium is here, the mitral valve apparatus there, and the free wall is here. Yes, there's some papillary muscle there, but this is a hugely hypertrophic left heart. And actually we know that one of the negative prognostic indicators for cats with HCM is severe hypertrophy, where the wall thickness measures greater than 9 millimetres, and that is certainly true in this case.

This was measuring 11 or 12 millimetres. It's a very rare and extreme form of hypertrophic. And you can see the same thing, very messy, isn't it?

We've got the the ventricle and short axis here, this side of the heart measures normal. This side's very thick indeed around that papillary muscle. So we do see very sort of messy focal, asymmetric hypertrophy.

It's not commonly global and symmetrical. When I see global symmetrical hypertrophy, I'm thinking, could there be something systemic causing it that's affecting the whole ventricle equally? Is the cat hypertensive?

Is the cat hyperthyroid? You know, thinking these things is, is is reasonable when you see very symmetric hypertrophy. So from the consensus statement, they've drawn this quite complicated Venn diagram here to try and describe all of the different things we think about when we think about cardioma in cats.

And the size of these circles in the diagram indicates how common a disease is. So here we have the largest circle as HCM, it's very common. Some cats within the hypertrophic sphere, if you like, of cardiomyopathy will have dysfunction.

We call those end stage HCM like that one with the infarct that I showed. Sometimes when you've got really bad hypertrophy, actually in time the wall can become ischemic and fibrotic and the myocardium can actually die and thin down. So you might end up with normal wall thickness measurements that previously were hypertrophic, so some of these cats will change classification from HCM to RCM or even DCM over time, which is what accounts for this overlap in this Venn diagram.

The non-specific cardiomyopathies don't fit neatly into any of these other classifications, and there's a little bit of an overlap between diagnosing a large right heart and a large hypofunctional left heart, because they obviously can theoretically affect both sides of the heart. Some important stuff to think about. The HCM phenotype bubble is much larger than the one representing primary idiopathic HCM.

And that features these cats with hypertension, infiltration, acromegaly, hyperthyroidism that can cause left ventricular hypertrophy and really should be excluded to say that a cat definitely has HCM. Now, in a 3 year old cat. Things like hyperthyroidism, acromegaly, systemic hypertension are incredibly, incredibly unlikely.

So in most 3 year old cats, I don't bother testing for them. I just say the cats probably has HCM. If the cat's age is unknown or it's 3 on the records but it's come from a rehoming centre, maybe that cat's much older, maybe it's 10, in which case we need to think about hyperthyroidism, acromegaly, hypertension.

Take a look at some of these other markers here, we've got reduced preload. That means the cat's hypovolemic. In a hypovolemic patient or very dehydrated patient, the chamber size will reduce cos there's a low circulating volume.

That can make the walls look relatively thick. So sometimes we see this in cats who are clearly systemically unwell, maybe they have vomiting, diarrhoea, abdominal pain, or maybe they have a linear foreign body or something we're aware of that's localising clearly away from the heart. They look as if they have HCM, but the left atrium's often small.

In these cases, we will fluid challenge them. So the left atrium's small, they're low risk, we give them fluids and we reassess what the heart looks like. And oftentimes we would call that when it normalises in those cases, we would say that was a reduced preload, reduced filling, which is causing something called pseudo hypertrophy.

The last thing to mention here is transient myocardial thickening. Transient myocardial thickening is a fairly recently described condition in cats, which many cardiologists, including myself and colleagues, have seen this on and off, you know, for, for decades. It's, it's obviously a long term disease, it's not a new disease, it's just we've recognised it recently.

And we believe that this is a temporary, quite severe cause of myocardial thickening, because when the myocardium thickens, the left atrium can enlarge because the heart can't deal with the normal blood volume. And the function can reduce as the heart thickens, and this can cause very severe signs of congested heart failure. Often this is quite young cats, and it's very commonly associated with a previous stressful event, especially anaesthesia.

So sometimes these are cats who've been into neutering. There may be a young cat they've been neutered, they come back in 2 or 3 days later in severe heart failure. I think there are cats out there where the owners will say, oh, I can't believe he had terrible heart disease.

We want to put him to sleep. You know, he's only young, he's got it really badly, we want to put him to sleep. And many of these cats have been euthanized.

The difficulty that I have with that, and that that is the right decision for those people at the time, but the difficulty I have knowing that is that many of these cats result and they have a good prognosis long term without the need for long-term medication. So in a young cat with very severe sudden signs of heart failure, especially if they've had a recent stressful event or anaesthetic, my advice would be to try and treat heart failure as best you can to see if you can get them stabilised. Because oftentimes if you see them at 1 month or 3 months post diagnosis, their myocardium looks a lot happier, it looks a lot thinner.

We think it's some sort of edoema, we're not quite sure on what happens with these cases. But it's important to know about, and there are case theories described out there in the literature. Left ventricular outflow tract obstruction is a very common cause of heart murmurs in cats.

We see it because of a dynamic obstruction, a dynamic narrowing of outflow from the left ventricle. So this causes a heart murmur that intensifies with an increase in heart rate. So that means the greater the murmur increases as the heart rate increases and reduces as the heart rate reduces.

So you may notice this changeable, this dynamic heart murmur on auscultation. There are two main causes, and they're both associated with hypertrophic cardiomyopathy. So first of all, you can have abnormal mitral valve motion, where the valve fails to close properly and is actually pushed or sucked into the outflow tract to narrow the path through which blood can flow before it gets into the aorta.

The same pathophysiology happens with hypertrophy of the interventricular septum, if it's in that subbiotic region, that can again, as the as the septum contracts and thickens, that hypertrophy can narrow the outflow tract and cause an acceleration of blood flow that leads to turbulence and leads to murmurs. There's no known association with clinical signs or outcome in cats. Humans with these things that cause outflow tract obstruction can develop lightheadedness, chest pain, and even syncope.

So we don't know if this happens in cats. How many cats can you identify that have got chest pain caused by an outflow tract obstruction? I, I have no idea.

I'm pretty sure I've seen two cases that had episodes consistent with chest pain, but it's very difficult to define. As I said, it's commonly a feature of HCM. So if I see this with equivocal wall thickness, so somewhere in the region of 6 millimetres but not quite thick enough called HCM, I'm strongly tempted to think this cat's gonna get hypertrophy in the next 6 months.

Here are some echo images of systolic anterior motion, the mitral valve. I'll just orientate we have the left atrium, left ventricle, aorta. That's the aortic valve here right there.

Look at the mitral valve, especially this image on the left first. The valve closes, then insiststole it flips into the sub aortic region, so watch now, there. Looks like it's high fiving the septum, and you can see that that narrows the cross sectional area of this outflow tract for blood to leave the heart.

And here, if we look on the colour flow Doppler, we can see there's a leak in the mitral valve, turbulent green flow, and also turbulent green flow in that region of obstruction. This is classic because the mitral valve is actually, As well as obstructing flow, it's also partially opening during cystole. So we classically get this turbulence in the airflow tract and in the left atrium associated with systolic anterior motion.

To see this, you're gonna have to slow down the echo images. These are on about 25% speed because the echo machine will generate more images per second than you can see, and if you don't slow it down with a cat's heart rate, you're never going to identify this reliably. What causes systolic anterior motion?

Well, this figure is taken from a paper, published more than a decade ago now, but it still really is the authority on why we get obstruction in this region. If you look at the diagram at the top, this is a diagram of normal left ventricular outflow, open aortic valve, closed mitral valve, cordi tendons and papillary muscles. Some cats have a long anterior mitral leaflet.

This doesn't appear to be a congenital feature of dysplasia, but it seems to be the leaf that actually elongates early on in the disease course of HCM. The same thing happens in people, they get mitral valve anterior leaflet elongation before they get hypertrophy with some particular genetic mutations. You may have long or slack cordi tendi, and that may be the cordi tendons do the same thing, they elongate because of changes to connective tissue that are associated with hypertrophy, or hypertrophy of the papillary muscles actually slackens the cordi tendon.

And then what happens is as the heart contracts, the cordi tendon gets sucked or pushed into the outflow tract, causing obstruction. And the final thing is we know that cats with HCM seem to get abnormal cordi, these things called false tendons that don't attach to the mitral valve or necessarily papillary muscles, and they seem to get more of these on the interior aspect of the left ventricle, and some of these can be placed in the outflow tract as a contributing factor towards surgence. As I said, the other factor that can cause outflow tract obstruction is sex or hypertrophy, as illustrated in these images on the left here we have normal outflow through a normal heart, and on the right we have a hypertrophic septum, which, as you see, narrows the path available through which blood can flow.

So therefore it causes acceleration of blood across that increase in turbulence and an increase in in velocity which lead to murmur generation. So what happens with cardiomyopathy, what, what occurs that makes this an important problem? Well, first of all, it's heart failure.

If we reduce contractility in DCM if we reduce filling of the heart with HCM or or restrictive cardiomyopathy, or reduce output by affecting the right side of the heart with ARVC, then this will cause activation of the renin angiotensin allosterone system. That causes sodium and water retention, vasoconstriction, and increases cardiac work. So the heart works harder, has to deal with a higher volume of blood, and therefore becomes relatively hypoxic and doesn't cope very well.

Also, the disease progresses, the hypertrophy gets worse, the systolic dysfunction gets worse over time. So eventually the heart fails, and the manifestation of that is an increase in pulmonary capillary pressure behind the left atrium, which drives transiational fluid, causing pulmonary edoema or pleural effusion in cats. Arterial thromboembolism, we've mentioned about spontaneous echo contrast and this sort of hypercoagulable situation because of poor atrial function.

And arterial thromboembolism occurs probably in 1 in 10 cats with HCM. It is a bad condition. We know that there's a very high morbidity and mortality associated with it.

And in a study that I published 8 or 9 years ago now looking at first opinion practises, many vets euthanized cats in the 1st 24 hours. I think 61% were dead because of spontaneous death or euthanasia in the 1st 24 hours. So it's a very, very bad disease indeed.

We may see clinical signs of outflow tract obstruction, we know humans get that. Perhaps cats do too. Put a question mark by that because I'm not so sure.

Arrhythmias occur because we have a hypoxic heart working very hard, which can promote ventricular arrhythmias, which can lead potentially to sudden cardiac death. Myocardial infarction definitely occurs because we, again we have a hypoxic myocardium working super hard, and eventually we can get myocardial imparts caused by the the pathophysiology of HCM. However, many cats live a normal lifespan with little or no progression.

So you'll see in a minute from some statistics I give you that actually more than half of cats HCM don't seem to experience clinical signs. And therefore, in most cats who get cardiomyopathy, it's quite a benign disease. That's important because it means we need to find out which ones are gonna progress and therefore which ones we need to monitor or treat.

And which ones actually are totally fine and can just undergo their normal routine dental work, anaesthesia, whatever, just carry on with life as normal. We certainly don't want to be treating all cats with cardiomyopathy with drugs if we don't need to because everyone knows what cats are like with compliance. We don't want to make the cat's life miserable by abating them.

Twice a day when we don't need to. I have a geriatric cat who I tablet once a day in the morning and I give a liquid to once a day in the evening, and frankly, that's enough for me. I see cats in the clinic and I can prescribe 2 meds that are twice a day and 1 med that's once a day, very easily for heart failure.

I certainly don't want to be prescribing that where it's not necessary. So why is HCM important? There's a study here by Rosie Payne, as part of her PhD a few years back, looking at cardiomyopathy prevalence in apparently healthy cats.

This is not a biassed population. This is not cats presenting to vets with heart murmurs. It's not.

Who are breeding cats who have a pedigree that's full of HCM. This is just mostly domestic shorthaired cats or domestic long haired cats presented for rehoming. OK, so there's 780 cats in this study and all these cats underwent auscultation, blood work, and echo.

1 in 7 cats had HCM. That's a massively high prevalence, OK. That means 15% of all the cats that are walking around today, or all the cats that you see in your clinics have HCM.

They don't all die from it, but they do have it. It's out there. This figure of 15% has come from a couple of other studies too, OK, so this is not the only one, it's just the largest one, the most important one to share with you.

In humans, the prevalence of HCM, and it's considered a fairly common heart disease, the prevalence of HCM is 1 in 500. So it's massively different, cats are really afflicted by this disease. The other cardiomyopathies that Rosie reported in this study made up less than 1%.

So when we talk about HCM RCM DCM, yes, the other phenotypes are important, but HCM is the most important that you will see because it's the commonest out there. We know from a study called the Reveal Study looking at a very large population of about 1000 cats, but half of those had HCM, half of them didn't have HCM. One third of those with HCM go on to develop clinical science.

So if we flip that around, it means that more than 60% of cats with HCM live a normal life with no requirement for treatment. So what are the risk factors that we can look for that suggest a patient with HCM is going to progress? Well, we know that dilation of the left atrium is associated with progression to heart failure or arterial thromboembolism.

We know that poor atrial function is associated with the future risk of heart failure or ATE. This is poor contractile function. And we know that poor left ventricular function is associated with the risk of heart failure.

In addition, very severe hypertrophy is also associated with an increased risk of developing signs and dying because of heart disease. Let's just take these figures that we know about from the reveal study and from the CAT scan study, and we're just gonna try and apply those more globally. So we know that 1 in 7 cats overall have HCM.

It's higher prevalence in older age, but let's just take that 1 in 7 cats. And we know that 30% of cats have risk factors for heart failure or ATE. So, in Europe, there's around about 103 million cats.

In the USA 96 million. China burgeoning cat ownership of 90 million. 60 million cats are owned in Brazil.

Around 10 million in Japan. 4 million in Australia, 3 million in South Africa. There's a lot of cats in the world.

Around about 500 million cats are estimated to be owned as pets worldwide. 1 in 7 has HCM. Which means that there are around about 75 million cats in the world have HCM today.

And if 1 in 3 are at risk, that means 25 million cats are currently at risk of heart failure or ATE. This is a massive animal welfare problem. So it's a really important disease to understand and to be able to diagnose and treat effectively.

So what affects the prevalence of HCM? I mentioned that older cats have a higher prevalence of HCM. We know that to be true.

We also know that males are overrepresented, around about 60% of cats with HCM are male. The prevalence does increase with age, so the prevalence of HCM in cats at a year of age is less than 5%. OK, it's much lower than that.

Prevalence in cats over 9 is about 1 in 3. We don't know the exact prevalence for cats at age 12 or 14 or 1520. We're seeing old cats now fairly frequently.

The prevalence is likely to continue increasing with age. We do know that younger cats at the time of diagnosis have a shorter survival. So it seems to be that that's a more aggressive form, which is why it's manifests young, it's more progressive.

Cats in older age group tend to be slowly progressive, so cats diagnosed at 14 or 15 are likely to progress fairly slowly if they do not have clinical signs at that time. The same is true in older people. HCM diagnosed in people in their 90s, often is a fairly benign disease, but 9nosed in their 20s is really problematic.

There's also evidence that higher body condition score is associated with increased wall thickness, so cats who are obese are likely to have secondary factors which increase wall thickness and can promote the development of HCM. That's also true in humans, so it seems to be not a statistical quirk but part of the disease. We think of cardiomyopathies in stages.

Any of you who are familiar with the consensus on mitral valve disease treatment in dogs, it's been around now for more than a decade and was reviewed again last year, and we know there's an ABCD system, and the consensus statement from last year on cardiomyopathies in cats. Applied the ABCD system to cats with cardiomyopathy, it's a very useful thing to think about which stage a cat is in and therefore what the general recommendation is. It isn't gonna fit every single case that you see out there.

It's a very useful guide for us to make recommendations to practitioners, but also for practitioners to make decisions about treatments. So this ABCD system is in place. Stage B is subdivided into B1 and B2, just like in the dogs with mitral vowel disease.

Stage A is defined as at risk. These cats do not currently have heart disease, but they're at risk. Maybe have a family history or or there's history in the pedigree of cardiomy being a problem.

Stage B is defined as pre-clinical, so no overt signs of heart failure or ATE. But we split the pre-clinical stage into a high risk and a low risk stage. So B1 and B2.

So but they progress from being at risk stage A to developing HCM, but with a normal or very mild increase in left atrial size, that's defined as stage B1. Stage B2 is defined as having cardiomyopathy, hypertrophic, or otherwise. With a large left atrium.

They are at risk of clinical signs, they don't have signs at the moment that are overtly detectable, but they do have an increased risk because of moderate or severe left atrial dilection. Stage C is clinical signs, so overt clinical signs of heart failure or arterial thromboembolism. And stage D are the refractory group.

These are often patients who have been on treatment before and they're not responding. So we classify them as stage D. They may be diuretic resistant, they may have other factors like arrhythmias, or of course they may have a recurrence of an ATD even if it was successfully treated first time round.

So the stage B1 and B2 are about risk, low risk and high risk, and that is important because it does have bearing on our decision making for treatment. And how often to monitor these patients and how to think about things like anaesthesia or or routine dental work or medication, you know, it's important we're thinking about how much of a risk there is to the cat of giving fluid therapy or sedating with a particular protocol. And actually, even though they haven't got out with clinical signs, the left atrial signs can help us to advise on that risk.

Here are some cats in stages C or D. So let's look first at the video. This is a cat who's tachypneic, dyspneic, classic signs of heart failure, pulmonary edoema or pleural fluid.

This cat also had arterial thromboembolism, look at the posture of the tail and the back legs, that's a weird position for a normal cat to sit in, so this cat had ATE. Look at the radiographs now, we can see we've got a lateral view, I think it's a right lateral and the dorsoventral projection of a cat in heart failure. We have cardiomegaly, defined by the heart being greater than 22 rib spaces wide in lateral and also greater than 2/3 the width of the thorax in TV.

We can see there's a pulmonary infiltrate. OK, so there's an increased interstitial or alveolar pulmonary infiltrate. I'd call it alveola cos I can't see the caudal vena cava, which means you've got fluid density in the alveoli, which reduce the contrast between the normal lung and the fluid density in the vena cava.

So when you have pulmonary fluid, it means you can't see that cava very clearly. And therefore it means that's an alveolar pattern. Institial is, it means you can still see blood vessels like up here you can still see vessels, but it's increased greyness of the lungs.

So that's probably interstitial alveoli, maybe alveola down here. OK. The third finding that's important is distension of the veins, the pulmonary veins.

We've got quite prominent pulmonary vessels back here and then we can see on the DV we've got the linear densities here, we've got the artery. And then a bronchus in the middle, and then a vein. And the veins are wider than the artery and both vessels are wider than the 9th rib where they cross it.

And that tells us that those vessels are distended. So we've got a big heart with high pressure in the blood vessels in the lungs and a pulmonary infiltrate, and those three things we classify this as heart failure until proven otherwise for me. Now we know that stage C is a bit more obvious because the cats present with signs.

Stage B is more challenging. Maybe they have a murmur, they maybe they have no murmur at all. Most often we'll define stage B as either a patient who has got a family history of something, or a patient with a heart murmur.

So we'll be mostly picking these up on murmur investigations prior to anaesthesia or or or fluid therapy or something else. Radiography unfortunately is unhelpful to define our sexual size. The left atrium often sits over the top of the ventricle so you can't really see if the atrium is big or not.

It's quite different anatomy to dogs. Cardiac biomarkers are very accessible like radiographs are, but they're also pretty unreliable. The cut-offs between stage B1 and stage B2 are not defined for cardiac biomarkers, and they probably will never be defined because there's a 50 to 70% day to day variability reported.

In things like antiro BMP. So that means it's very difficult to know if cardiac biomarkers would be helpful. So I'm afraid the only useful technique is echocardiography, it requires some training and a decent machine to make good functional assessments, but I have used very low specification machines to get a broad assessment of left atrial size in a cat.

So I think that it, it is accessible, it is useful. You just need to overcome if you're not used to doing it, you need to overcome that initial er sort of learning curve. So here I've got a still image of left ventricle, left atrium and a normal cat.

We can see the left atrium's quite square, you can fit two inside the ventricle. Look at the schematic. I think it's pretty accurate, you can fit 2 of those inside that left ventricle.

That's just eyeballing it, we're not measuring anything now. In short axis we have the aortic valve in the middle, the left atrium and the oracle attached to that, and they're roughly the same size in this particular patient. We would say the maximum diameter of the atrium should not be more than 1.5 times the aortic root diameter measured as shown here.

Here's a cat with bad chimay. This cat happened to be stage C cause we've got some fluid. But they're not always stage C when they've got this size heart.

We can see this huge rotund spherical appearing atrium. Can't fit one of those inside the ventricle, let alone two. In the same count in short axis, it's easy to see the ratio is much more than 1.5 times, in fact, probably more than 2.5 times the aortic root diameter.

So you don't necessarily have to perform detailed measurements to look at atrial size, you can eyeball that and judge that subjectively as well. So what are the treatment recommendations for cats with different stages of cardiomyopathy? Well, the guys who are at risk.

It's hard to define them. So therefore we're not gonna treat them because they haven't got disease yet. The stage B1 cases, these cats have cardiomyopathy but no atrial dilation or very mild atrial dilation.

No treatment is indicated. This is the consensus recommendation. The important ones to detect because it might prevent the cat suffering an ATE.

It's the stage B2. So stage B2 cats are higher risk and therefore we recommend treatment with the antiplatelet drug clopidogrel. The dose is 18.75 milligrammes per cat, so that's the total dose, once daily.

OK, clopidogrel generally is very safe. We don't use it in all cats with heart disease, we only use it in ones who are at the highest level of risk because of atrial dilation, or ones that have shown previous signs of heart failure or ATE. Stages C and D, diuretic treatment is indicated, as is clopidogrel, if they're not already receiving it from stage B2.

And there may be other treatments you choose to prescribe as well. So patients who become hypokalemic on diuretic drugs will often benefit from the use of spiralolactone to help conserve the potassium loss. There's some recent data suggesting ACE inhibitors aren't particularly useful in cats with cardiomyopathy, so we don't tend to routinely recommend ACE inhibitors.

And the jury is still out as to how effective Pimabendan is. There are some cats with poor function like DCM or maybe RCM or advanced HCM who will benefit from the use of Pimerendan in their disease. Not all cats with HCM may benefit and potentially sometimes it may pose a risk to cats without flow tract obstruction.

Data out there suggests it is safe in cats without flow tract obstruction, but the licencing on the veterinary licence forms of abundant says it's contraindicated with outflow tract obstruction, so you have to be pretty sure and get client written client consent before you prescribe that. That you're not gonna do any harm and the owner is accepting a level of risk. The last thing you want to do is prescribe pumendin.

The cat died because it has heart disease and arrhythmias and things, and the owner to come back and say, oh well, I googled that drug and you should never have used it, it says it's contraindicated. You really want to have that conversation up front before prescribing immobendam and hopefully, ideally you get signed consent for that drug's use. OK.

I'm not saying it's gonna harm cats. I'm saying that it's not licenced. There are some contraindications that are probably the.

There's a lot of data now supporting its use, but we don't know it improves survival and it's not licenced. It may cause harm. Just be a little wary about using it in all the cardiomyopathy cases out there and certainly be wary in cases with obstruction to outflow.

If you're not confident in your Doppler echo skills, just listen, have a really good auscultation. If there's no murmur or only a really quiet murmur, there's not significant outflow tract obstruction, cos that would be associated with a loud murmur. How do we monitor these cats?

Well, stage A, you're only really gonna monitor them if you're screening them for breeding. So these are generally pedigree cats. They have annual echo in theory.

Many breeders come, they have an echo of one year of age and never come back, and tell everyone that the animal's heart tested, but there are some very, very dedicated breeders out there, and as increasing awareness of cardiomyopathy happens amongst the breeding community, they're more dedicated to knowing that they should do annual scans. In stage B1, we tend to recommend an annual echo. After 2 or 3 years, sometimes the heart looks really static.

We might span that anecdote every 18 months or 2 years for an individual who appears to be slowly progressive. We're looking to see if they progress and get left atrial dilation, and we do see that sometimes we see a cat who's in B1, 1 year and the next year they've got quite prominent atrial dilation and poor atrial function, so we're glad that we've echoed them manually. Once they're in B2, we say we want to scan them every 6 months.

The main objective of that is actually to see if there's a thrombus in the heart. OK, because if we've got a thrombus in the heart or a little bit of pericardial fluid or pleural fluid that tells us that cat's in heart failure, then we've, we've got more information earlier without a cat experiencing horrible negative welfare, we can start diuretics or start clopidogrel earlier. Stage C, well, we monitor them as required.

Now, I've put a question mark on routine follow-up for C and D here because owners can monitor respiratory rate at home. So if respiratory rate is less than 30, the owner's getting a good read on that and the cat's tolerating the monitoring it sometimes. People say if they look at the cat, the cat breathes faster, you know, so some owners find it very hard, but most owners can can sort of train themselves to do it with time.

And in those cases we're only gonna really change things in terms of diuretic dose or treatment protocol if the cat becomes tachynia or dyspneic. So there's not as much of a requirement to come back in stage C. You could argue that we're looking for worsening of heart failure, just like in stage B2.

We're looking for effusions, we're looking for intracardiac thrombus. The reason I question the utility of that in stage C and D is some cats do not cope well with stress. And they can be fine at home and get into the basket.

And get into the car and they get a catecholamine surge. So the catecholamine surge can increase circulating noradrenaline adrenaline. They get a big veno constriction.

All the blood that sits in their capacitance veins will end up coming back to the heart. The heart rate will increase, the cardiac work will increase. This combination of factors can lead to them going back into heart failure.

So I've seen a number of cats, too many, too many who are at home totally fine, owner comes to the console, oh yeah, fantastic, his respirator's 24. Things are looking great, tolerating meds really well. I opened the basket and the cat's a dyspneic mess.

I've had a few of them die because they've come for routine checkups. So you need to try and assess the stress level of that patient. I've got cases in in stage C which are ongoing.

They, they come every 6 months for checkup because the owner's are very concerned, they want to be on the ball and the cat's fine, tolerates travelling in the car very well, it's pretty blase about everything. The cats feel very stressed at coming to the vets. I tend to ask them to stay home and just monitor respiratory rate.

So, in summary, cardiomyopathy in cats is a very important clinical problem. Globally it's a massive problem, but to us as practitioners, it's also an important thing to think about. Not all cats with HCM have murmurs, not all heart murmurs mean they've got HCM, but it's one of the most important things to think about.

Other phenotypes are out there, restrictive cardiomyopathy, dilated cardiomyopathy, these things are out there and also sometimes they have what looks like HCM caused by systemic disease. So classifying them into different phenotypes can be important, not quite as important as ruling out other disease processes which may affect the heart as well. HCM cats commonly have a benign disease course.

Over 2/3 of cats with HCM never develop clinical signs. So I'm not saying ignore it, forget about it. I'm saying we need to identify the cats that are most progressive and therefore the ones who benefit from treatment.

You don't treat every cat with HCM with clopidogrel. It's a waste of a drug, it's a waste of the stress being tableted for the cat, and it potentially could pose a risk giving unnecessary treatment. Staging the cat's heart disease is super important, and monitoring the cat's heart disease is super important.

Echo is the most important tool for doing that to help you give a good prognosis, well, or bad, to help you prognosticate for an owner and let them know what to expect from that cat, but also to help you make treatment decisions as the vet who's responsible for that cat's wellbeing. So if you're not doing echo, try to learn just the basics of assessing atrial sizes because that's a super important tool which will help you a much more refined decision maker and will help you stage these cases according to what they need and therefore recommend the best treatment approach and monitoring approach as decided by an expert panel. So thanks very much for listening.

Normally at this point in the lecture I'd I'd asked to take questions, but obviously this is something that you guys are watching. You know, at variable time points. So I'm more than happy if you've got questions about this lecture for you to contact me through my Instagram handle.

It's at vet_cardo. I don't make any money out of that, so there's no conflict of interest, but I'm more than happy if you ask me some questions on there to, to take those questions and have a chat with you, via that medium. Once again, thanks for tuning in, and I hope you've benefited from this little tour of cardiomyopathy and have got a bit more of a an understanding of how we should approach these cats, as we see them through our clinic.

Thanks very much.