Hello guys, welcome to this webinar on Caiomyopathies, an update on feline heart disease with myself, James McMurra. So this webinar is aimed at primary care practitioners and nurses. And my hope is to give you a bit of a.

A sort of all encompassing overview really of feline heart disease. I'm gonna focus on a few sort of specific points, however, that I think really are applicable to primary care practise, and really are areas that can be more, difficult, when we're thinking about the management of cats with feline cardiomyopathies. The first thing that we're gonna do is just briefly go over the different types of cardiomyopathies, just to explain what we're gonna see in general practise.

How are we gonna diagnose those various forms of feline heart disease, how they appear sort of structurally, and what's gone wrong pathophysiologically. And then, you know, sort of how frequent they are and, and how we diagnose them. And we're gonna also touch on the screening of occult cardiomyopathies.

So, these are the patients who have pre-clinical heart disease, OK? So this is quite a big, number of patients, that are walking around, as far as the owners are aware, they seem completely normal cats, but they have a brewing cardiomyopathy. And they're an important group of patients because whilst the majority of those, their cardiomyopathy might never become clinically, significant.

There's also a decent proportion of those patients that will progress to a more advanced form of cardiomyopathy, and could develop. Congestive heart failure or a thromboembolic complication of their disease or even sometimes unfortunately the cats, the very first sign of heart disease that a client is aware of is sudden death, because the cat, you know, dies of a massive myocardial infarction or something of that nature. So they're an important group of patients, to be aware of.

And it can be quite sort of, difficult really to screen for. So we're gonna go through how we can do that a bit more, later on. We're then gonna to discuss how we diagnose feline congestive heart failure.

So these again, they can be tricky. So we're talking about patients, who present dyspneic. And the sort of age old problem that we have with cats that present with dyspnea is, is this a primary heart or a primary lung and airway problem, and they're not as good at giving us clues as dogs are.

They don't always have a history of, of, pre-clinical heart disease before they, you know, go into congestive heart failure. And they don't always have classic auscultatory abnormalities, such as a murmur, an arrhythmia or a gallop. So we'll sort of discuss how we can, diagnose those patients, more easily in primary care practise with the tools that are available to you.

We'll then discuss the treatment of congestive heart failure in cats, firstly, focusing in on the really poor acute dyspneic cat that presents, open mouth breathing. Really severely decompensated, what we're gonna do for that patient there and then to get them through the next 12 to 24 hours, and then discuss in more detail the treatment. Of congestive heart failure on an outpatient basis with oral medications and when we need to follow them up and what we're gonna monitor, etc.

Etc. At the end we'll also touch a little bit on the use of antithrombotics in feline heart disease. Essentially because of the potential risks of really severe thromboembolic events.

So we're particularly talking about aortic thromboembolism in cats, which the vast majority of the time is a complication of an underlying cardiomyopathy. And when that occurs, it can be really disastrous for our patients and their owners. So it's a really important aspect of feline heart disease to be aware of how we can screen for and diagnose those patients that are at risk of thromboembolic disease and how we're going to treat them with what medications and how effective they're gonna be at reducing, the time to the next event or, or the possibility of having an event at all.

And for all of this, as I say, we're gonna be focusing on, primary care practise, and I'm just gonna hopefully highlight and dot a few paper references here, there and everywhere, just to let you know what's the sort of latest, that's been published on each of these sort of areas as well. So, cardiomyopathy, phenotypes, so with cats and heart disease, we are talking about heart muscle disease, cardiomyopathies. They really don't get primary valvular disease like, Cavaliers do, like a lot of older terriers do, you know, these guys have primary disease of the heart muscle.

Not primary valvular disease, and it can come in lots of different flavours or types which we'll touch on in a second. So they're a very, very heterogeneous group of cardiomyopathies. Cardiomyopathies in cats as we're talking about are acquired, heart diseases, so we're not talking about congenital heart disease at all, but just those that develop with age.

Now, unfortunately, with cats, their acquired heart disease can really occur at any age, and certainly cats can present with congestive heart failure because of acquired cardiomyopathy at the age of one. Which is again pretty dissimilar really, from dogs with heart disease, where we think about the mitral valve patients being middle to older age, at the time of presentation with their congestive failure, and obviously DCM dogs being a bit younger than that, but nonetheless, certainly not, not as young as some cats can present with cardiomyopathies. So again, it should be on our radar, you know, all the time in cats because it can really strike it at any age.

So a cardiomyopathy can be defined as a myocardial disorder in which the heart muscle is structurally and functionally abnormal, in the absence of any other cardiovascular disease sufficient to cause the observed myocardial abnormality. So we're basically saying it's a primary disease of the heart muscle itself. And that the changes that we're observing in the heart muscle aren't secondary to another disease process in the body.

So, that's important to be aware of and we talk about it in a second when we talk about HCM because it is a good example of this. So that's what we think about as being a primary, cardiomyopathy. So as I briefly mentioned already, cardiomyopathies unfortunately are really quite common in cats.

We'll touch on sort of the incidences of different heart diseases, in a second. But they really are quite common, and particularly there is a large number of cats who'll be walking around, you know, right now with a cult or or pre-clinical heart disease. And a significant proportion of those will progress to congestive failure.

So cardioopathies in cats really are a significant cause of morbidity, and mortality. In our feline friends, so it is something we have to be sort of acutely aware of really, and be able to give very sound advice to, to owners on the, on the best way to investigate or treat their patients, their pets. As you mentioned, it's a very heterogeneous group of phenotypes.

So phenotype, is a word used to define the structural attributes of that disease process. So the thickness of the heart muscle, the size of the chambers. Etc.

Etc. And we'll use the term phenotypes as we talk through, the different, forms of cardiomy cats in a second, but it is a very heterogeneous group of patients, lots of different types of cardioopathies, and some individuals, you know, don't fit really nicely into one disease category, or the next. Some patients even over a period of time, can actually move from one form of cardiomyopathy, such as hypertrophic cardiomyopathy, to a different form of cardiomyopathy, such as restrictive cardiomyopathy as their disease progresses and changes.

And some patients, as I say, will have attributes to their cardiomyopathy that really seem to sort of cover both or several different types of of the primary cardiomyopathies. So it can be quite complicated to think about as a group of patients with lots of different types of cardiomyopathies within individuals. However, one of the interesting things is that, the treatment options are often very similar between the different forms of cardiomyopathies.

So whilst we can get quite caught up on correctly identifying and describing, The changes in every feline cardiomyopathy as accurately as we can do, it often doesn't change the treatment options that much, or at least there are just a few parameters that we look at, when we're performing these investigations, to guide us on our treatment options, sort of regardless of the underlying cardiomyopathy. So that's important to be aware of. There is, however, quite varied, outcome for patients with different types of cardiomyopathies, and some forms of feline heart disease confer a poorer prognosis than others.

So again, I suppose that does highlight the importance of sometimes investigating these patients and getting a definitive diagnosis, so that we can more accurately prognosticate for the clients what's likely to happen, what the outcome's gonna be for their pets. So this is a diagram that I've borrowed from the recent ACVIM consensus statement, on the guidelines for classification, diagnosis and management of cardiomyopathies in cats, published in 2020 in the Journal of Veterinary Internal Medicine. And this diagram really quite nicely highlights the phenotypic nature.

Of this disease and how there are lots of different flavours of cardiomyopathies, and that actually there's quite a lot of crossover as well between the different types of feline heart disease. So the largest group of patients that we'll encounter in practise are the HCM or hypertrophic cardiomyopathy patients, and within HCM, And we break it down into sort of two groups really. The HCM phenotype, so those are patients that have structural changes of hypertrophy or thickening of the heart muscle.

And within that, there are the patients who have HCM due to secondary diseases, which are these ones sort of listed around the edge, it'll go over in a second. And then those patients that have primary HCM, which are the patients in this inner darker blue circle. So with HCM phenotype, if your disease is secondary, to process elsewhere in the body, that's not classed as a primary HCM but a secondary, and there's quite a few different causes that in cats.

So hypertension is an important one. We know as cats get older, the prevalence of hypertension increases, whether it's, primary arterial hyper systemic hypertension. Or whether it's hypertension associated with the disease states such as chronic kidney disease, but chronic hypertension.

Increases the afterload on the heart, OK, it increases the pressure within the systemic arterial system that the heart has to pump into, and therefore the heart undergoes concentric hypertrophy. To be able to, augment its cardiac output. So hypertension, when severe enough for long enough, certainly over, something like 180 millimetres of mercury, will induce hypertrophy of the heart muscle in cats.

So when we are investigating. Patients with heart disease, if we stumble across a HCM phenotype, one of the things we'll always want to do is just check that patient's systemic, arterial blood pressure, just to make sure that that might not be the cause of their HCM and that the treatment of that hypertension, you know, might, reverse a lot of the cardiac changes if it is secondary to the hypertension alone. We've then got pseudo hypertrophy.

So this is something that's seen in patients that are really quite dehydrated or hypovolemic. As there is less blood or sort of pre-load filling the heart, the heart, its walls, the heart itself is less stretched, and as a result of that, the walls of the heart actually appear thicker than they normally would do. So these patients don't have genuine thickening of the heart muscle, but when they're really hypovolemic, the heart muscle appears thickened on ultrasound because they're essentially underfilling their heart with blood.

So this is not infrequently seen, to be honest, in patients, that are presented in congestive heart failure, had a whole heap of diuretic therapy and the breathing has improved, and at a point when they're then stable enough to undergo echocardiography, and we scan these patients and say, oh, actually, this patient's got really thickened heart muscle, however, they're very dehydrated, and what we need to do is really scan patients ideally that are nor bulimic. So, A recommendation here is to always check PCB and total solids, as well as physical examination parameters at the time of doing echocardiography, to see how dehydrated the patient is and whether or not that could be contributing to some erroneous measurements. If we're at all in doubt by the measurements that we Taken and that patient is already presented to us dehydrated, we can always get them back at a later date, as a normal volemic patient, just repeat a couple of those parameters on the echo, because these patients, when they become normally hydrated, have normal heart muscle thickness.

TMT is transient myocardial thickening, which is a quite uncommon disease process that's sometimes seen in younger cats, where the heart muscle becomes thickened transiently, we're unable to sort of ascertain a reason why, but over time as we follow this patient up with serial echocardiograms, that heart muscle thins out and gets back to a normal thickness, and essentially that disease state of a HCM phenotype is reversed. And these patients can present in congestive failure, but actually over time can be weaned off of medications and in the long term, have a good prognosis. So they're a very uncommon group of patients, but an important one to sort of be aware of nonetheless.

So then down the bottom, we also have patients who've got acromegaly, so acromegaly, Is due to a functional tumour of the pituitary, in which growth factor is secreted in excess, and growth factor stimulates organomegaly or organ growth within the body, and a lot of these cats can develop HCM phenotype, renal enlargement, growth of the, the bones of the skull. And unfortunately, as their, kidneys and hearts, undergo this sort of hypertrophy, it does actually quite significantly affect their function, and quite a lot of acromegalic cats will develop not only heart and kidney disease, but progress to heart failure, and then kidney failure as well. So again, in a patient that we suspect acromegaly, we may screen for that with some blood work.

Hyperthyroidism as well drives concentric hypertrophy of the heart and can induce a HCM phenotype. So any patient you think could be potentially presenting as a HCM phenotype with hyperthyroidism, which you screen for the total T4. So we'll do that, and again, the treatment of hyperthyroidism in these patients is very beneficial that reversing.

Or the HCM that that has developed in these patients, it's really important that we do screen patients for these secondary diseases because the treatment of them can often significantly improve the underlying heart problem. We then have, some of the other sort of less common but kind of equally important forms of cardiomyopathy. So we've got end stage HCM.

So this is really the point at which patients with HCM have progressed over time. They've got marked cardiomegaly, and often they develop quite bad systolic dysfunction, and that's most frequently associated with little regions of, myocardial infarctions, or heart attacks within the heart muscle. That after the heart attack has occurred, they undergo replacement fibrosis, and we end up with, little regions of very much thinned heart muscle in these patients, that's just fibrous tissue that has very little systolic function.

So these patients, often appear really quite differently, from the regular HCM patients, and are an end stage of that HCM disease. We've then got restrictive cardiomyopathy phenotype. So these patients have a normal left ventricular wall thickness.

It's not thickened like in HCM, but they have much more marked diastolic dysfunction. Because of generalised fibrosis of the ventricles, so these patients often present incongestive heart failure or really very much on the cusp of congestive heart failure with quite profound left atrial dilation. We've then got the DCM phenotype, so DCM is a dilated cardiomyopathy, where we get really marked for chamber enlargement, and it's an eccentric hypertrophy, rather than a concentric and is seen in association with really marked systolic dysfunction.

So this can be a primary disease process, but very, very, very infrequently in cats compared to dogs, and in fact it is much more commonly. Secondary, to either dietary taurine deficiency, which fortunately we don't see very much of these days is, commercially enabled diets are, appropriately supplemented with taurine, but we may see it in cats that are fed home prepared diets. So again, it's always important when we've got a cat that we're taking a history from that could or does have a cardiomyopathy to check the dietary history.

But you can also get a DCM phenotype from what we call a tachycardia mediated cardiomyopathy. So this is a patient who will have had an uncontrolled, tachy arrhythmia, with a high heart rate for a protracted period of time. So .

For instance, if you've got an SVT with a really high heart rate, over sort of 220 beats per minute, and that's persisting for a protracted period of time, it really wears out or burns out the heart muscle, and you can develop a DCM phenotype secondary to those sustained very high heart rates. We've then got ARVC, which is a rhythmogenic right ventricular, cardiomyopathy, which is essentially a disease of the right side of the heart. There's an echo of that in a second.

And then we have this, category of patients, the non-specific group. So, these are patients that we were diagnose as having a cardiomyopathy of a non-specific phenotype, as they don't neatly fit into one of these other, categories of disease. So, for instance, you know, they may have significant changes of .

Their, right side of their heart, but also might have changes of the left side of the heart as well with profound, left ventricular, hypertrophy, for instance. So these patients are those that just don't neatly fit into any other disease category. So just to quickly touch on each of them in a bit more detail, so here's a a 2D image from a patient with HCM, and this is the left atrium of the heart, the right atrium, the right ventricle here, and the, sorry, the right ventricle here, and this is the left ventricle here.

And what we can see is really profound thickening of the myocardium of the left ventricular free wall here and the interventricular septum here. And this really profound thickening is causing almost complete luminal obliteration in these patients. And this thickening causes really pronounced diastolic dysfunction, of the left ventricle and puts this patient at really increased risk.

Developing a myocardial infarction, because they've only got a set amount of coronary arteries to supply blood to the myocardium with. And then when that myocardial markedly increases in thickness, those coronary arteries then having to provide blood flow to much larger sort of volume of heart muscle, and therefore areas are likely to get under perfused and undergo myocardial infarction. So this is a really profound Case of HCM, but any patient who has myocardial thickness of more than 6 millimetres in diastole, would be described as having concentric hypertrophy of the left ventricle, and it really is primarily a disease of the left ventricle, in cats, although it can lead to right-sided congestive heart failure as well.

So HCM has a prevalence of about 15% in the general population, but is as high as about 30% in all the cats. So that is really big numbers of patients when we think about it, across the whole population. Of these patients, as I say, most will sort of not have progressive forms of the disease, but about a quarter of patients, Will have progressive disease, that will lead to congestive heart failure, aortic thromboembolism or arrhythmias in later life.

HCM is more common in older cats, and certainly more common in males and females at about a 2 to 1 odds ratio. Sometimes we observe, a phenomenon in these patients, which is called, or sort of basically due to a dynamic left ventricular outflow tract obstruction. So this is, something that we see in patients with HCM where as the left ventricle is contracting and pushing blood out of the left ventricular outflow tract up into the aorta.

The mitral valve and certainly the anterior leaflet of the mitral valve moves into the left ventricular outflow tract, causing a dynamic narrowing. In that region. And what this leads to is an increased pressure gradient of blood flowing out of the left ventricle across the left ventricular outflow tract.

So we get increased flow velocities of blood out of the left side of the heart. We get turbulent blood flow within the left ventricular outflow tract. And as the anterior septal leaflet is drawn into the left ventricular outflow tract, It causes it to leak, and actually, these guys can have quite leaky mitral valves, and develop quite large mitral regurgitations, which can be auscultated as heart murmurs.

So that's interesting to be aware of because we've sort of said that feline heart disease is primarily heart muscle disease, not valvular disease. However, in this form of the disease, which we call hypertrophic obstructive cardiomyopathy, we often do hear quite loud heart murmurs because of leaky valves, not because of primary valvular disease, but because of this dynamic movement of the valve into the left ventricular outflow tract. So we call that hypertrophic obstructive cardiomyopathy.

What do we know about hypertrophic obstructive cardiomyopathy and dynamic left ventricular outflow tract obstruction? Well, fortunately, it doesn't appear to affect prognosis. So it's sort of important that we document it and describe it, but fortunately, it doesn't worsen the outcome for these patients.

So HCM is seen really quite frequently in domestic short hairs, but also in certain breeds of pedigree cats as well. So we should have a lot of these guys on our radar when we're screening for HCM and primarily those are the Maine Coon, ragdoll, British shorthair, Persian, Bengal, sphinx, and Norwegian forest cats as well. OK?

So that's HCM where we have this profound thickening of the left ventricular myocardium. We now move on to the second most frequent feline heart disease which is restrictive cardiomyopathy. So these patients can present in two different forms.

The myocardial form, which is essentially a fibrosis of the left ventricular myocardium, which markedly affects. It's ability, to relax and it's, it's diastolic function. And we also see the endocardial form in which there is fibrosis of the endocardium, which is.

The innermost sort of layer of the heart muscle, if you will, on the inside of the ventricular lumen. And these patients can present with scars of tissue bridging the left ventricle, which again could further worsen diastolic dysfunction. So these patients typically on their echocardiograms have normal left ventricular myocardial thickness, as you can see in this 2D image here.

They often do have, eccentric dilation of the left ventricle and often really quite profound left atrial or biattrial, cardiomegaly as well. As I say, these guys often do present for the first time in congested heart failure, or sometimes, with aortic thromboembolisms or, or, you know, arrhythmias, because it really is quite an advanced form of feline heart disease. It is more common in older cats.

It can be seen in association with hyperthyroidism as well as HCM so you have to sort of be aware of that. But unfortunately, patients with restrictive cardiomyopathy do carry a poorer prognosis, than those with hypertrophic cardiomyopathy. As I said, with hypertrophic cardiomyopathy, a lot of those patients, can live with their disease.

Subclinically it never cause a problem when they do go into heart failure, and the median survival times can be sort of up to 12 months, whereas with restrictive cardiomyopathy, once you develop failure, really the median survival times of up to 6 months would be more appropriate in a lot of these patients. We then have the DCM guys, the dilated cardiomyopathy patients. So as I say, it really is quite uncommon, and you're only probably likely to see it in patients that have nutritional deficiencies because of home prepared diets or occasionally, there's an end stage of other cardiomyopathies.

We sometimes refer to it as a burnt out cardiomyopathy, when essentially huge portions of the ventricular myocardium. Have undergone replacement fibrosis and essentially lost a lot of the systolic function, and that chamber has undergone quite profound eccentric hypertrophy. But essentially the the main findings in these patients are that they have normal to thin left ventricular myocardium.

We've really profoundly dilated, chambers and very much rounded left ventricles as well. And when we look at their systolic function, they have very little. So we have really quite profound, reduction in, in the shortening fraction, which is essentially, as this diagram sort of tries to highlight, the difference between the diameter of the left ventricle in diastole and cystole, OK?

So as you can see in this patient here, this left ventricular internal diameter in diastole acquired on this M mode image is really not too dissimilar at all from the left ventricular internal diameter in systole, which should be much, much smaller if that heart is effectively pumping. Patients with DCM unfortunately do have a very poor prognosis, if, unless that patient has, a nutritional deficiency, and that deficiency, can be addressed, with survival times in the order of just a few months. We then move on to patients with a rhythmogenic right ventricular cardiomyopathy.

So as this echo loop shows us, we have a really profound right atrial and right ventricular cardiomegaly. You know, the right atrium is several fold larger than the left atrium in this patient, as is the right ventricle. And this is essentially a disease of the right ventricular myocardium, which leads to profound heart enlargement, right sided congestive heart failure, and quite frequently, arrhythmias as well, that originate from the right side of the heart.

Fab. So before we go on any more about how we're going to screen for and diagnose these different patients, it's just worth highlighting how we can stage them. So this again was from the ACBIM consensus statement on cardiomyopathies in cats.

And it's been very much lifted from the ACBIM consensus statement on mitral valve disease in dogs for a year or two earlier, and it basically allows us to group our cardiomyopathy cats into one of these categories based on their stage of disease. So, we refer to them as A, B, C, and D, and stage A are those patients that are predisposed to a cardiomyopathy. So for instance, Maine Coons of a certain age.

We then, but they currently don't have any heart disease, so those are the ones, that are at risk, but don't have any disease at this that moment in time. And bear in mind you can over the course of time, move from one category to the next if your disease is progressive. We then have patients with, stage B disease, so these are the patients who are pre-clinical or sub-clinical.

So they have disease, but they don't have any clinical signs of it. And then within this we subdivide it into B1 and B2. So B1 is the patient that has no cardiomegaly.

And B2 is the patient who does have cardiomegaly. So as you can imagine, patients who are B1 are the patients who've got subclinical heart disease that are lower risk of progression to failure than the patients who are in stage B2, who are at higher risk of progression to failure and or thromboembolic disease. So we get a bit more excited and interested in the B2 patients.

Stage C patients are those that have clinical signs or in congestive heart failure, so they have current or previous congestive heart failure or aortic thromboembolism. So, these are the patients that we're gonna really concentrate on with our therapy, as we'll get on to a little bit later on. As congestive heart failure, progressively worsens, patients can transition from stage C into stage D.

So stage D patients, are those who have refractory congestive heart failure and essentially aren't responding to traditional. Heart failure therapy at standard doses. So these patients are the by far the most problematic to deal with, and often do benefit from referral to a cardiologist, sort of when, possible.

OK, so we're now gonna discuss the importance of and how to screen for pre-clinical cardiomyopathy in cats. So these are the stage B1 and B2 patients. So as you mentioned just before, they don't have any clinical signs, so they have a normal history.

The patients that we're gonna think about being at risk of are called cardiomyopathy, are gonna be patients who are sort of older, particularly male cats, those that are of certain breeds, such as Maine Coons, and rag dolls. And those patients as well, that might have one of those comorbidities, that can cause us to develop a a cardiomyopathy phenotype, such as hyperthyroidism or hypertension. So these are the patients that as they walk in the door we're gonna start thinking, OK, could this guy or gal, have a pre-clinical cardiomyopathy?

How likely is it? How much should we push for investigation of these patients? So these patients, as they say, aren't gonna have clinical signs of heart disease, but they do have heart disease.

So these individuals are really gonna focus hard on our auscultation to try and identify any features that might tell us that that patient has got heart disease. So we're gonna listen for a murmur. Now, as I said earlier, murmurs are really common in patients who have obstructive, hypertrophic obstructive cardiomyopathy, but actually not that frequent in other forms of heart disease.

Because it's not primary valvular disease. So we don't get a lot of leakage. However, those that do have murmurs, they can be evident, but they're often quite quiet, a lot quieter than you'd expect to hear in, say, a dog with mitral valve disease.

So often cats with quiet heart disease, their murmurs don't get any louder than grade 3, and often You can just be a grade 1 or 2. So you have to be very focused with your auscultation in a really quiet room. Have a good listen all the way along the sternum, on both sides, because it's the sternum in cats, where you often hear these murmurs, the loudest.

And if you do hear a murmur in a cat, It is suggestive of feline heart disease for the things in the picture fit, but it doesn't mean the patient has got feline heart disease because about 30% of all murmurs in cats, in young cats at least, are physiological murmurs and are not because of heart disease. So if you hear a murmur, it means we need to investigate further. If we don't hear a murmur, it does not mean that patients does not have heart disease.

Gallop sounds are a good one to listen out for as well. Gallop sounds are a third heart sound, which can be the S3 or and or the S4 heart sound, which we don't normally hear. And these are able to be auscultated in patients who have more advanced diastolic dysfunction of the heart.

And diastolic dysfunction really is the main problem that cats have with their cardiomyopathies. And it causes, a sound of galloping hooves like a triplet effect of the heart sounds instead of the regular lubed up lubed up lubed up. So if you do hear a gallop sound, this is highly suggestive of feline heart disease and quite often advanced preclinical heart disease because they're very, very, very rarely heard in any other situation.

Arrhythmias are also one to be aware of because cats as their cardiomyopathy worsen, can develop ectopy of the heart, so they can develop supraventricular ectopy, so beats, that originate from ectopic foci within the atria or ectopic fosite within the ventricles. So sometimes they may be individual beats that come a little bit early or a little bit late, or you may hear runs of an arrhythmia or a persistent arrhythmia if, for instance, the cat's in atrial fibrillation. Any patient that you hear an arrhythmia in that's a cat, you should definitely suspect that the patient's got feline heart disease, and perform an ECG and consider further investigation, for, for an underlying cardiomyopathy.

So these are 3 really useful things to listen out for in our cats that have occult cardiomyopathies. We can then look at, some blood work in these individuals. Genetic testing can be of use, in breeds in which the genetic tests are available, to see if they are significantly increased, at increased risk of developing cardiomyopathy in later life and or whether or not they should be bred from.

But I think the, the genetic testing is kind of beyond the scope of what we're gonna talk about today, and actually we're gonna focus a lot more on the utility of the NTR BMP, which we'll get on to in a second. In patients who have pre-clinical heart disease, the gold standard really for investigation is echocardiography. And that is the best way to diagnose pre-clinical heart disease.

I mean, it's the only way to definitively diagnose pre-clinical heart disease and allow us to make decisions about therapy. But often echocardiography isn't affordable for, for every patient, so that's why we're gonna use some of these other tests first, such as auscultation and maybe antiro BMP testing to really narrow down the group of patients we think will benefit the most from echocardiography and try and persuade the clients to, you know, spare some cash to pay for it. Bear in mind radiography is of no use in these patients, as they don't have any congestive heart failure changes, and a lot of these patients, even with stage B2 disease that have, cardiomegaly, it's often not that easy to identify.

On thoracic radiographs. So just a little bit about the quantitative NTro BMP and how we can use it, successfully in general practise. Well, antiro BNP is a, natural atic peptide that's produced by the body, when the heart muscle is stretched, OK?

So essentially, this marker is used to diagnose, cardiomegaly, OK, or at least increase our index of suspicion of significant, cardioomegaly. And can therefore be useful in determining which patients are best to undergo echocardiography, i.e.

Those with the largest hearts. So what we use this test for is to, screen patients, we get a number back from the lab that tells us exactly how high that cat's NT pro BNP level is, and we can use that to sort of approximately correlate. With one of four, categories of either normal, mildly increased, moderately increased, or markedly increased, and based on that, makes some sort of recommendations, for our patients.

Essentially, if the quantitative antiro BMP level is very high, we're going to push more strongly for echocardiography in those patients because they likely have more advanced cardiogaly and likely have more advanced heart disease, which is likely or more likely to progress to failure. Patients who have normal levels. Of N Tro B and P, or very mildly elevated levels, those are the patients that either don't have heart disease or have very mild heart disease.

You know, probably at that point, there might not be a huge amount of benefit to echocardiography, because, as we'll talk about a bit later on, there are very few treatment options for cats with pre-clinical heart disease, currently, and as a result, we may be pushing a client for an echocardiogram that then doesn't really change what we do with that individual. . So the best way to sort of use this test is, in, in a patient you think is at risk of having pre-clinical cardiomyopathy, we can run a quantitative NTR BNP, and if that level is normal, at that point, we can say this cat likely doesn't have significant cardiomyopathy and doesn't need echocardiography, but it doesn't tell us about what's gonna happen in the future and we will need to repeat that test yearly at the follow-up vaccinations or whatever physicals that are being performed.

But if that patient does have a significant elevation of the NT pro B&P, then they probably would benefit from, detailed echocardiography, to diagnose their probable underlying, heart disease and make treatment recommendations based on that. We're now gonna go over the diagnosis of congestive heart failure. And then at the end, as I say, we talk about, the treatment of congestive heart failure and and preclinical heart disease as well.

So congestive heart failure, typically presents in cats, as tachypne and laboured breathing. This is often seen in association with, inhabitants, lethargy, altered behaviour. But really infrequently coughing, OK?

So if we do have a patient who presents with dyspnea and a cough, it's much more likely that they have primary airway or lung disease than they do congestive heart failure if they're a cat, OK? The physical examination really is paramount in a dyspneic can in allowing us to sort of quantify the severity of their breathing problem, but also help point us in the right direction as to whether or not it's a primary heart or airway lung problem. And there's a few really important things to listen out for and look for in these patients that I'm just gonna highlight now for you.

So, a lot of this information, has been identified in, the Rapid CAT study from a few years ago, where they basically looked at physical examinations in cats presenting dyspneia for the first time with either heart, congestive heart failure, or primary, airway and lung disease. And what they found is that there are certain things you can look for that would really increase the index of suspicion of it being a primary heart problem. And these were an arrhythmia.

A gallop sound, a murmur. Tachycardia at over 200 beats per minute. Tachy near at over 80 beats per minute, and the one that I find sort of the most interesting and and has honestly, I think the most utility is the rectal temperature.

And what they noted in this study is that if your rectal temperature presentation was lower than 37.5 degrees C, then that was highly consistent with congestive heart failure, rather than primary airway and lung disease. And I think that's really, really, really, important to know about, because anybody can check a temperature in a cat, and just that one parameter alone can give us a lot of information about what the, the probability is of that cat being in congestive.

Failure. And it's one of the things we kind of forget to do in a dyspneic patient, because we just think, oh, out of all the other things that I can check on the physical, it's probably the least important. Now, I do bear in mind that some cats who are very dyspneic and extremely fractious, a rectal temperature might be enough to actually kill that cat.

So, I'm not saying every patient has to have this performed. You know, no ifs, buts, or maybes, but if you can perform the temperature, absolutely do, OK? And you can certainly use that in combination with some or all of the other findings to increase your index of suspicion that that patient has congestive failure, .

We may also have muffled heart and lung sounds if that patient has a pleural effusion, although obviously there's lots of different causes of pleural space disease such as pyothorax and hemothorax, which are not our primary heart problems. We may, or quite frequently, to be honest, see paradoxical breathing, with pleural space disease or really advanced parental disease, where you get the chest wall and abdominal wall. Moving in opposite directions to each other as the patient breathes in and out.

We may hear pulmonary crackles in cats that have got quite significant pulmonary edoema, but certainly the absence of crackles does not rule out pulmonary edoema. So I think if there's literally one thing that I'd like you to remember from this talk, and you go home and do in practise, it's check rectal temperatures in dyspne in cats. If you forget everything else, I'll still be a happy man, OK?

So we've performed our physical examination on a cat that's dyspneic, and we've taken history from the client and we're slowly increasing our index of suspicion this patient has got heart failure. How are we going to definitively diagnose it? Well, ultimately, congestive heart failure is a diagnosis that's made on imaging.

So we can use radiography to document pulmonary edoema, pleural effusion, sometimes cardiomegaly. However, what we're gonna concentrate on and talk about more today is the use of ultrasound. For the diagnosis of fluid within the lungs or alveolar and interstitial lung disease, which we see with pulmonary edoema, for the diagnosis of pleural effusions, but also to allow us to quickly look at the heart itself and assess the heart for any evidence of enlargement or heart muscle thickening that might point us towards a specific feline cardiomyopathy.

Of course, in the investigation of these patients, once they're fully stabilised, a detailed echocardiogram is, always recommended, but that has to be at the point in which they are safe enough to be performed. There's no point rushing an echocardiogram on these patients, and putting them at risk. A couple of the other things that we're gonna touch on as well are the use of the NT Pro BNP snap.

So this is a, a qualitative test, different from the quantitative test we mentioned a couple of slides ago, but very useful. In practises that don't have access to ultrasonography, for the diagnosis of, of congestive failure, in, in, in these patients presenting with dyspnea. Troponin I is not the most useful thing in the world.

Essentially this can be used to screen for cardiomyopathy in cats. And it can be used to help us prognosticate because the higher troponin I, the poorer the prognosis. However, it really doesn't allow us, in general practise.

To do a huge amount of the information, so wouldn't recommend performing that routinely. Electrocardiography is going to be essential in any patient that's got, an arrhythmia, particularly low, particularly high heart rates, and blood pressure assessment really in all of our patients, as mentioned earlier to screen for hypertension in patients that we think could have a secondary cardiomyopathy, or to screen for hypotension in patients that we think of presenting the cardiogenic shock. And then thyroxine measurement in patients that we think are in the at-risk group of cats for hyperthyroidism.

So with regards to the NT Pro BMP snap, this is a really useful test that I'm sure many of you are aware of and maybe are using in clinic already, but it's a qualitative, Test that can be performed on plasma from a blood sample on a cat, or pleural effusion, which is quite a useful thing to be able to do because some of our cats that present dyspneic are so dyspneic that even getting a jugular blood sample could be too stressful for them and push them over the edge, because of a large volume pleural effusion. In instead, actually just Therapeutically draining that pleural effusion. To improve their ventilation and running the test on that pleural effusion will save the stress of having to handle that cat for a jugular blood sample.

So the test is most useful for discriminating cats with cardiac versus non-cariac causes of respiratory distress where a point of care ultrasound is not available. So what does this mean? Well, basically, if you've got a dyspneic cat and you run one of these tests and the test is positive, If everything else on the physical examination fits with congestive failure, then that is highly indicative that that patient has congestive failure and requires frozenide.

If, however, you've got a dyspneic cat and the test is negative, then that is highly inconsistent with the diagnosis of congestive failure, and that patient probably doesn't need rosemide at that point. Now bear in mind this test is not 100% sensitive or specific, so you will get caught out every now and again. But that is where it is most useful in practises that don't have, ultrasonography, to be able to rapidly, assess the heart, and the lungs, for, for, for sort of cardiogaly or, or fluid within the lungs.

And it can be very, you know, useful in those clinics to help differentiate cardiac from non-cardiac causes of dyspnea. So just moving on to point of care ultrasound, so this has gained a lot of momentum over the last few years, in the emergency and critical care, scenario, particularly in dyspneic patients, so. Why is it so useful?

Well, point of care ultrasound, certainly, at our clinic has really superseded, radiography in a lot of situations, because one, it is very, safe and rapid to perform. So we perform point of care ultrasonography, on our cats, fully conscious, with no physical restraint. Set up internal recumbency whilst receiving the flow by oxygen.

So it really doesn't cause them any distress. We don't need any physical or chemical restraint to cause it, and we actually don't even clip the fur from the chest. We simply spray spirits on the side of the chest wall, and apply copious amounts of ultrasound gel.

And we're able to then just pop the probe against the chest wall and get a really nice image of the lungs and the heart without any stress being caused to the cat. And secondly, it gives us actually a lot more information than radiographs. And the studies in humans that have identified that ultrasound will detect pulmonary edoema, earlier in its development than radiographs will.

And also as we've said with cats, they often don't have profound radiographic cardiogaly, so actually when we're looking for cardiomegaly, ultrasound is by far the best way of doing that. We simply do a rapid assessment of the lungs, the pleural space, the heart itself, and as I said, we can use this to diagnose pulmonary edoema, pleural effusion, pericardial effusion. And cardiomegaly, in cats with relative ease.

And there's a couple of studies sort of looking at this, in, patients in, sorry, clinicians that have a very basic level of training, and actually the amount of information that can be gained, from a point of care or even very basic levels of training is very, very high, and of a large amount of diagnostic utility. So just to briefly show you what bee lines are, . Beelines are produced when a patient has significant alveolar interstitial lung disease, and most frequently we're talking about wet lung or pulmonary edoema, fluid within the lungs.

And after we popped the ultrasound probe on the chest wall, we get an image that looks something like this, where we have a rib here, a rib here. This is our intercostal space, and this is the interface between, the pleura, of the inside of the chest wall, and the pleura on the outside of the lungs, and this all here is lung tissue. And what we're seeing.

Are multiple alternating black and white vertical lines, sometimes referred to as rockets, and these are produced in patients who have pulmonary edoema or wet lung. So if we see beelines in a cat with . Dyspnea, it certainly tells us that that patient has quite bad alveolar or interstitial lung disease, and if that fits with cardiogaly on its point of care ultrasound or an abnormal NTro BMP or an arrhythmia, that can really help reinforce the diagnosis.

Of congestive heart failure and pulmonary edoema. This is a very easy thing to be able to do in practise, and if you're not doing it already, I'd highly recommend you get a textbook or go on another webinar about point of care ultrasonography and get some practise in doing this, because it is something that we perform on a daily basis on our clinic. Then, we can use ultrasonography to very easily diagnose pleural effusion.

So again, pop that probe on the chest wall, and in this patient here we have a large volume of anechoic fluid here surrounding this lung tissue. Bingo, we know why this patient's dyspneic, let's. And get a sample of that drain as much of it as we can to stabilise this patient, you know, prior to further investigations.

So again, this is a much better way of diagnosing pleural effusion than thoracic radiographs, is the patient does not have to have any form of chemical or physical restraint. It's also, a nice way to help us, you know, perform thoracentesis via ultrasound guidance, as well. And, of course, if you don't have ultrasound and the patient isn't stable enough for radiographs but you highly suspect plural space disease, it is.

Safe and appropriate to perform a blind thoracentesis and just pop that needle into the chest cavity, the 7th to 8th intercostal space and draw back and see what you get if you're highly suspicious of pleural space disease based on your physical examination. And if you don't get anything back, the patient probably hasn't got pleural space disease and you're wrong, but it's quite unlikely, that you're going to cause any problems such as pneumothorax for that patient. So thoracic radiographs we will perform in the investigation of our patients, but often a lot later on once they've been stabilised and it's safe to undergo radiography.

And what you might tend to see are such things as you can in this patient, where we've got quite a diffuse, alveolar pulmonary parental pattern which is suggestive of pulmonary edoema. Quite a small, but evident, . Pleural effusion, as we've got scalloping of these lung lobes cordially, and this cat fortunately is making our job quite easy and showing pretty pronounced cardiomegaly.

As we can see on both this lateral and DV view here as well, but do bear in mind that actually a lot of cats with advanced, cardiomyopathy and congestive heart failure do not have any radiographic cardiogalase. If you don't see it, it does not mean it's not there, OK? So just a little bit about the echocardiogram.

So a detailed echocardiogram is recommended in all these patients to diagnose the primary heart disease and allow us to, to be guided with the treatment options, but it's highly user dependent. So, you know, it is something that takes, a lot of time and skill to be able to sort of become proficient at, so do bear in mind, that when, when you are performing these in-house yourself. They should only be performed once the patient is stable enough, and as I say, it is the only way to definitively diagnose feline cardiomyopathies.

It also gives us much more information about prognostication as well. And it also can help guide us with our therapeutic choices. And as I mentioned earlier, hydration status can affect the measurements, so we should always bear this in mind when when performing a detailed echocardiogram.

OK, so we've talked about the diagnosis of feline heart problems. What about the treatment? OK, well, firstly, let's start with occult or pre-clinical cardiomyopathies and essentially say, there's not a lot to them.

Unfortunately, there are no drugs that have been proven to delay congestive heart failure in cats of cardiomyopathy, unfortunately, compared to, you know, dogs with DCM or mitral valve disease, where Pendin has been, you know, used successfully. So, a pre-clinical cardiomyopathy in CAT is really a lot about just monitoring and actually not doing a huge amount with therapy because we don't seem to be able to delay progression to heart failure in these patients. Now you might say, well, what about atenolol?

Because over the years we've sort of intermittently used atenolol, for hypertrophic cardiomyopathy and hypertrophic obstructive cardiomyopathy. So essentially what we know from a few different studies is that if we have a cat with hypertrophic obstructive cardiomyopathy, where they have that increased pressure gradient across the left ventricular outflow tract because of systolic anterior motion of the mitral valve, well, atenolol. Can reduce that pressure gradient and the velocity of blood flow.

And it can reduce, the volume of their murmurs. So you think, well, brilliant. Is that not doing the job that we want it to?

Well, it is, but it doesn't seem to translate, to a difference in outcome for these patients. So essentially, What we know is that we can use atenolol in patients with dynamic left ventricular outflow tract obstruction, but it doesn't seem to actually affect the outcome in these individuals whatsoever. So it's quite infrequently used, now in these patients unless they've got particularly severe left ventricular outflow tract obstruction, in which case we may have a conversation with the client and say, look, we know this drug can reduce the pressure gradient in this patient, we know it can reduce the murmur intensity, but what we don't know is that it will actually improve outcome.

Now, these studies are. You know, have inherent flaws depending on the nature of of the the study. And of course, it doesn't always, these studies, you know, don't always tell us about what exactly will happen in the individual.

So I think occasionally there are case by case discussions that we have with the clients and and some of those patients will go on a Tenolol long term, but the vast majority won't. Do bear in mind as well that tenolol is a beta blocker and whilst it's great at reducing pressure gradients in an obstructed left ventricular outflow tract, it is not great for patients that have congestive heart failure. So what we recommend is that a patient who's on chronic atenolol therapy, should have that therapy discontinued as soon as they develop congestive failure, and that any patient who has existing congestive failure should not go on atenolol treatment.

Antithrombotics, we'll get onto, on the last slide of the talk. These are the only drugs that actually have been, of use in preclinical heart disease in cats, and that's in their ability to reduce, the likelihood of an aortic thromboembolic event. We'll touch on that a little bit later on.

But essentially, most cats who diagnosed with they called cardiomyopathy, either go on antithrombotics or no drugs whatsoever, and all we do is yearly or six monthly, monitor them with serial echocardiograms. So on to the treatment of congestive failure, so firstly, the emergent patient. So, any patient presents with dyspnea because of congestive heart failure needs immediate oxygen supplementation.

That can be done via flow by, via mask, or preferentially, probably an oxygen, tent or cage to achieve the highest levels of inspired oxygen percentage. We should often consider the use of an anxiolytic in these patients as well. Often the stress of these cats, being in an unfamiliar environment, being unsure of what's wrong with them, it actually worsens, their level of dyspnea.

And sometimes just 0.2, to 0.3 Migs per kick of butorphenol, IV if we have an IV, in place, or IM if not, can be really useful at just reducing, The anxiety in these patients, which helps improve actually their ventilation and oxygenation.

So sometimes the best thing you can do for a dyspneic cat, before you do anything else, physical examination, ultrasound, IV is just jab them with some bornol, pop them in an oxygen cage and just observe them from a distance before you get too hands on. As we mentioned earlier, thrachicentesis should be performed as an emergency, if we believe they have, plural space disease. And if based on everything that we've done up to this point, our history, our physical examination, any point of care ultrasonography, we're suspicious enough that they have congestive failure, we're gonna start with some furosemide.

Good old rosemide, 1 to 4 mic the k IV. So, We tend to give it IV because it has a faster onset of action. We don't have to tablet cats that are dyspneic and also it causes a degree of vasodilation, which can be beneficial as well at reducing preload in these patients.

And what we tend to do is little and often, OK? So 1 to 4, migs per gig every 1 to 6 hours, . And often my initial bolus is, is somewhere in the order of 2 to 4 mgs per gig, and then I'll just use 1 mg per gig every hour or every other hour until their resting respiratory rate has started to improve.

Once their respiratory rate has started to improve, we know that what we're doing is working and that respiratory rate should only continue to improve. So at that point I start to drop. The sort of frequency of rosemide bolus.

I don't wait for the resting respiratory rate to necessarily get below a certain value, because we kind of might overshoot our patient with rosemide and do bear in mind that cats are highly sensitive, to ruzamide, and it's not uncommon to give a cat so much rosemide in the 1st 12 to 24 hours of treatment of their dyspnea, that you can actually push them into an acute kidney injury or acute renal failure. Which will just then confound our problems and give us yet another thing that we have to treat and monitor on top of everything else. So to help screen for an AKI and assess hydration status, we tend to recommend repeating renal values, electrolytes, PCV and total solids every 12 to 24 hours in our patients.

We've already mentioned why we're gonna monitor the renal values, but also, we're gonna monitor, the electrolytes, in particular the potassium, because often with, the induction of diuresis, these will start to drop, and in particular the high, the potassium level will go low. If we do develop hypokalemia, it can be a bit of an issue because it causes, skeletal muscle weakness, hypoorexia, and both of those things delay, so the patients making it home from the hospital. So we do want to treat it if we come across it, and I tend to do that most frequently, with oral potassium supplementation.

Given twice daily, and also encouraging patients to eat as early as possible to help improve their, potassium levels. And what we really want to do is avoid, potassium CRIs, simply because any fluid we give this patient intravenously is just gonna further worsen, their venous congestion and really negate the effects of our diuretic therapy, so. There are always exceptions to the rule, but really please do avoid intravenous fluid therapy in any congestive heart failure can, it will only worsen the problem, even though you're trying to correct a state of dehydration and or hypokalemia and and trying to do the best for that individual.

We're gonna monitor closely various parameters in hospital, and those include systolic blood pressure. Resting respiratory rate is by far the most useful thing in my opinion, you know, and sometimes, I will say to the other vets that have been working with all the nurses, let's just monitor this cat's resting respiratory rate in its kennel and not do anything else for now. Every time we go into that oxygen cage to do a mucous membrane colour or a capillary refill time, we're just letting all of the oxygen out, we're stressing the patient, and often that information unless we've already identified problems such as cardiogenic shock or something else that sort of changed the way we treat the patient.

It often doesn't alter how we're gonna manage them. So honestly, sometimes the best thing to do is just hands off, monitor the resting respiratory rate, and don't get too giddy about anything else. The temperature obviously can be useful in these patients, as we said, to diagnose congestive heart failure, we want to make sure that temperature's coming back up to normal, or of course in cats that are in oxygen tents, we want to make sure their temperature doesn't go high, and they become hyperthermic as they struggle to cool, and we want to monitor urine output as well.

And body weight in these individuals. We can consider the use of positive ionotropes such as immobendin and dobutamine for low output failure, but really, the cornerstone of treatment for congestive heart failure in cats is frozamide and rosamide alone, and we very, very rarely need much more than that, to stabilise our patients, which is great because everybody has a bottle of dimsum on the shelf. So what about the outpatient treatment of these guys?

And once we've improved their breathing enough for them to be able to be discharged, we're gonna send them home on oral rozamide. So we're looking at doses of 1 to 2 mg per gig orally twice daily. And I often find that rosemide or oral suspensions work great in cats, because what we do is start with this initial dose of 1 to 2 weeks per gig, and what we then can do is 57 days later, start to down titrate the dose to get our lowest effective dose for that patient.

And I find that really easy with our rosemide suspensions, you know, because we can just knock it down by 0.1 of a mil every week or two, you know, to titrate the dose to the effect. Obviously, there are also, oral tablets as well, but none of these are licenced for cats, in the form of rosemide, but they can be, you know, equally as useful.

And do bear in mind that with rosemide, again, cats are more sensitive to it than dogs, so I tend to use lower doses in cats than I do in dogs. So I tend to err on the side of caution, a bit closer to one week per gig twice a day initially, . In cats and a bit closer to 2, in dogs, just because the the effects of the dehydration and the hypokalemia just seem, you know, more prevalent in cats in my opinion, than it does in dogs.

Frozammide, is, you know, a tried and tested favourite for treatment of congestive heart failure as an outpatient, but also there is some evidence, about the use of a newer, loop diuretic, Terazamide. So Terazamide, is a much more potent loop diuretic, somewhere between 13 and 20 times the potency of furosemide, but it also has some other advantages as well. So it has got a longer half-life, and that's one of the problems with furosemide, that it does not last 12 hours, and yet we do tend to use it twice daily in our patients.

So they spend quite a bit of time. When they're on rosemide, outside of the therapeutic range, whereas with terrazamide, these patients, when given it once or twice daily, often spend a lot longer inside the therapeutic range where they have appropriate levels of, of diuretic, therapy on board. So it has a longer half-life, but it also has a better oral bioavailability, meaning that the more of the drug is absorbed and, and gonna be active.

And I think that's particularly useful in patients who have a right-sided congestive heart failure, as they're at risk of having quite significant gut wall edoema. Which unto itself would reduce, the absorption or bioavailability of drugs given orally. So there, there really is no sort of set way of doing it.

I think a lot of patients would tradition, sorry, clinicians would traditionally select rosemide as their first line loop diuretic and only move to terrazamide if there's problems of twice daily medicating or they fail to respond to the rosemide. But certainly there is more and more evidence that terrazamide is as good as, or as we can otherwise say, not inferior. To furosemide, and there is some evidence in dogs and in humans that actually survival times may be improved on or long-term terrazamide therapy overruamide, but it's probably too early to say much about cats.

Otherwise, there's really no strong evidence for any of the medications for feline congestive heart failure. So in dogs, there's evidence about the use of piendin, an ACE inhibitor and spironolactone, in combination with rozamide, which you can refer to as quad therapy for the treatment of canine congestive failure. It's not really the same in cats, with the evidence base that we have got.

So, I think we have to bear in mind that patients with congestive heart failure are not cheap, you know, to medicate and monitor for clients. And these are a lot of drugs, and cats are not the best for tableting, and I think polypharmacy is a major issue in these guys. And I've certainly had clients who we send away with heaps of medication, to be given multiple times a day, and they become so despondent that they're not getting these tablets in that they start to consider euthanasia.

For their patient, just because of the amount of medications that they're having to administer alone. So I think, off the back of polypharmacy, I certainly am using furosemide alone as the sole treatment of congestive heart failure in a lot of my cats, and on a case by case basis, discussing the pros and cons of each of, you know, the, the other three medications, but not routinely prescribing them. But that is very much clinician preference, but there certainly isn't any evidence for the use of any of the other drugs.

So when we send our cat home on its furosemide oral medication, we're going to want to see them back 7 days post discharge for a physical examination and to check their blood tests. So whenever we start a patient on ruzammide or increase the dose, we should really check their renal values and electrolytes 7 days later, just to be sure that there's not been any complications of that dose adjustment. And then we're going to discuss with our clients the utility of monitoring sleeping respiratory rates.

So these are really invaluable for the monitoring of congestive heart failure patients at home. And what we know is that if that cat is fast asleep, they have to be fast asleep, if they look like they're asleep and they've just heard a cat two doors down, meowing, that will stress them out and put their respiratory rate up. But if they are fast asleep, a respiratory rate of less than 30 breaths per minute would be consistent with good control of their congestive failure, and that the client can be reassured that their cat is doing well on the dosage they're on.

If, however, their sleeping respiratory rate is persistently above 30, that would be indicative of, development of pulmonary edoema and the need to phone the clinic for advice and or attend the clinic. And then if a resting respiratory rate is persistently above 40 in one of these guys, that'll be highly consistent with significant pulmonary edoema and to be fair, the need to probably just attend the clinic for an assessment and possibly even emergency treatment, OK? So there's quite a lot of.

Information out there on the web about sleeping respiratory rates that you can share with the clients. There's various apps from some of the drug companies, more veterinary College, that allow clients to count, record and monitor their cats sleeping. Rates and it's something that I highly recommend we teach all of our clients to do because it gives them and then, by proxy so much additional information when they're phoning for advice at 6 p.m.

Just before the practise is about to close, OK? So just a little bit on Piemabendin cos it's often a bit of a hot topic in cats with cardiomyopathies. So there's a few papers looking at Piemaendin.

And essentially, what we believe is that there are likely benefits, to the use of emobendin as it improves left atrial function. And left atrial function, as we'll touch on in just a second, when we're talking about, thromborombolic disease, is really important to try and maintain. There have been some studies that basically described in in retrospective studies a benefit in survival for cats that received Pymobendin that had HCM over those that didn't receive Pybendin.

But it's hard to draw some conclusions from these studies because of their inherently retrospective nature. But there has more recently been a prospective and non-pivotal study looking at the use of Pymain in cats, with HCM and what it found is that there was no benefit, in this population of patients with HCM, in receiving Pymobendin versus those that didn't. Now, What that means is that, you know, perhaps the evidence that we had from the earlier retrospective studies isn't as reliable as we would sort of hope it to be, but essentially, further studies are needed, .

There also was a more recent study looking at the use of pemoendin in cats with hypertrophic obstructive cardiomyopathy, or dynamic left ventricular tract obstruction, and traditionally we've always said you shouldn't give pemoendin to these patients becausepimaendin as a positive ionotrope, increases the contractility of the left ventricle. What that can do is worsen the pressure gradient. Across the level of the obstruction in these patients and worsen their heart problems.

So traditionally it was, don't ever give a cat emo, unless you've echoed it, to be sure it's not got hypertrophic obstructive cardiomyopathy. Well, in this recent paper, they looked at the use of emoendin in a population. Of cats with hypertrophic obstructive cardiomyopathy, and essentially it was found to be very, very safe in these guys with the obstructive or non-obstructive forms of the disease.

And actually even in the cats that that had the left ventricular outflow tract obstruction, it didn't seem to cause any complications in these patients. So I think the jury is still out there in Pima Ban. But these more recent studies we'd say there's maybe no strong evidence to say it works, but there's also some evidence to say it's probably quite safe.

So I think, again, on an individual clinicians sort of, Basis, we can make a decision about whether or not we use Pinabendin based on how, I suppose, refractory to other drugs that cat is, or based on the severity of its systolic dysfunction. If it has systolic dysfunction, we need to help improve that with a positive yotrope. But certainly, we're not recommending carte blanche, the prescription of Pymoendin, to all cats with congestive heart failure, as, as we are doing, with dogs, OK.

So just finally, a little bit, about thromboembolic disease, and anti, thrombotic therapy. So as I said right at the beginning of the lecture, thromboembolic disease is a horrendous complication of feline heart disease. And when it does occur, it causes significant morbidity and mortality in our patients.

So we want to do as much as we can to screen for it and then effectively treat it to reduce the likelihood of it occurring. So this is an echocardiogram here showing a left sided cranial view looking at the left aricular appendage here. And the left atrium, and what we can see is a large blood clot forming here in the left aricular appendage, with a small amount of spontaneous echo contrast or smoke in adjacent to that.

And this is what we see in patients who have thrombosis within their heart. And it most commonly occurs in the left ricular appendage or the left atrium of the heart, and it occurs there because of a variety of reasons. But in cats with advanced heart disease, they develop advanced left atrial cardiomegaly.

That left atrial cardiomegaly affects blood flow within the heart. It slows it down and increases the turbulence. This in combination with the damage that's caused to the endothelium of the chamber because of that degree of stretch, in combination with the fact that all cardiomyopathies and cats to some degree are inflammatory diseases, and we get an increased risk of thrombosis development in the left side of their heart.

And then this. Thrombotic material can sit within the left side of the heart and not cause any problems until a large part of the thrombus shears off, and gets loose within the systemic circulatory system, and then lodges or embolizes at a distant site, cutting off blood flow to that area and affecting profusion significantly to that organ or limb. So, this is why ATE occurs in cats because of thrombosis of the left side of the heart, and it really can only be diagnosed on echocardiography, which is why again, earlier we stated that, If we are looking at diagnosing cardiomyopathies in cats.

And using that information to guide us on our treatment options, really echocardiography should always be considered the gold standard for these patients. So if we see thrombosis of the left atrium, or other factors that put the patient at increased risk of having a blood clot, such as marked left atrial cardiogaly, reduced left atrial fracture shortening, or reduced left aricular appendage flow velocities. We'll start about the, think about the use of an anti-thrombotic drug to help reduce the risk of that patient having an event.

So, when we look at anti-thrombotics, and they are blood, they are drugs that. Help reduce the formation of blood clots, as the name suggests, and they generally come in one of two categories. We have the anti-platelet drugs, which directly inhibit platelet aggregation, and these are of most use in patients who have platelet-rich blood clots that are formed in higher shear conditions, and the two drugs that we think about are most frequently are clopidogrel.

And aspirin, OK. We then have the second group of antithrombotics, which are the anticoagulants, which are much more beneficial in the fibrin are rich. Blood clot patients that are formed in low Shia environments, and within this group, we talk about rivaroxaban, as a sort of a newer generation, drug that we're using orally, as an anticoagulant, but also things like heparin and low molecular weight heparins as well.

So, looking at the evidence base for antithrombotics in cats, there is some strong evidence about the use of clopidogrel, and that was from the fat cat study, and clopidogrel. Was, used, in patients with, previous thromboembolic disease, and it was trialled against aspirin, in, in, in a similar group of patients as well, . And essentially what was found is that patients who received clopidogrel in preference to aspirin had prolongation of the period between thrombobolic events.

It was twice that of aspirin, with basically being it being about 12 months in the clopidogrel group versus 6 months in the aspirin group. So as a result of that, I think there's a pretty strong evidence base to say that clopidogrel is likely beneficial in patients at risk of thromboembolic disease and certainly should be used in preference to aspirin. We tend to use it as a dose.

Of 18.75 milligrammes per cat once daily. So that basically equates to a quarter of a Plavix 75 milligrammes, which is the human.

Trade name for the drug, but we can also get, clopidogrel now. In 18.75 milligramme tablets from Summit, the compounding pharmacy, so they can just be administered at one tablet once daily to a cat.

And do bear in mind that they're quite bitter, however, so sometimes it can be beneficial to administer the clopidogrel inside of a gelatin capsule with any other cardiac medications need giving as well. When we're now talking about, the, anticoagulant antithrombotics, rivaroxaban is something that we're starting to use more and more in our patients with feline thromboembolic disease. This is a direct inhibitor of activated factor 10, which is given at 2.5, .

Ms per kg, orally, once daily to cats. And there is a study at the moment that is currently underway, the Supercat study, where it's looking at comparing the efficacy of clopidogrel versus riveroxaban in a population of cats with increased risk of thromboembolic disease, and the results of which may sort of once again change our selection of medications. That we use as antithrombotics for these patients.

But I think in, in summary, I'd say at the moment, a lot of people are using clopidogrel routinely as the antithrombotic of choice in patients that are at risk of thromborombolic disease and probably adding in rivaroxaban as well as that, which does appear to be safe, as a combination therapy in the patients that are the highest risk of a thromboembolic, event. But again, I think these decisions, you know, can be made on a case by case assessment. Other drugs such as aspirin, low more like your weight heparins, and warfarins sort of losing favour and certainly have, their uses, more so perhaps in the really per acute situation, but again, sort of would discuss it with a, with a cardiologist on a case by case basis.

So that's the end. I hope everybody has found that interesting and enjoyable with at least one or two, takeaway tips that'll help you, navigate this, to be honest, minefields that can be feline cardiomyopathies. So once again, thank you very much for listening.