Thanks John. And what could possibly go wrong with a webinar with interactive polling? I'm sure everything will go clockwork smooth.
So first of all, thank you all for tuning in, whether it's in real time or whether it's after the events. Thank you to Nuala for some fantastic lectures. Wow, I've got quite a hard act to follow.
And actually, I, I think some of the questions that I'm asking, will be testing your knowledge from Nuala's lectures. So, if you haven't watched those lectures before, then, you'll be coming with this cold. And, also thank you to the webinar and the BBA for, giving me the honour of, of speaking on this course.
It's a fantastic opportunity. It's very fashionable to have a conflict of interest declaration at the beginning of a presentation. I'm an employee of Langford Vets, and I've done speaking and consultancy work for various companies.
I also am an exam examiner from the RBC and involved in BSAVA education. None of them have had any influence over the content of this presentation. I have no conflicts of interest to declare.
Now, when we're thinking about when to treat heart disease in dogs or cats, we find it helpful really as cardiologists to think about stages of disease. And this staging system that we use, is a four stage system really, . Imaginatively called the ABCD system, and this was actually part of a consensus statement from the American College of Veterinary Internal Medicine back in 2009 on mitral valve disease.
The staging system works very well for mitral valve disease, and that's sort of what the consensus is for. I quite like thinking of this system, this ABC. Being used for other diseases too, such as related cardiomyopathy in dogs, and even hypertrophic cardiomyopathy in cats.
It helps me to, tell people or recommend treatments at particular points during different diseases, and I hope it helps you guys too to think about these different stages of heart disease that can be present. Now if we look at this, stage A is a population of animals at risk. So these are animals who do not have heart disease.
It seems strange to classify them, but actually, if you think about, cavalier puppies, most of us will see those animals coming into the clinic and we think all well and good for now. But one day, my friend, you may develop mitral valve disease, actually in cavaliers over the age. 12, somewhere between 80 and 100% of dogs have got mitral valve disease.
So most cavaliers, when they're born, are somewhere in stage A. Stage B is when they have structural heart disease present. So for the example of degenerative mitral valve disease, these might be dogs who present with a murmur.
So they have structural heart disease caused by the, the valve disease there in particular. They do not have clinical signs of disease, and this is an important concept. They're pre-clinical or occult heart disease.
When they develop clinical signs, they're in stage C. So this is what most of us would call heart failure. So with heart disease, we're often talking about clinical signs of congestive heart failure, which is usually tachynia or dyspnea caused by pulmonary edoema.
Or depending on the heart disease, potentially ascites, or hepatic congestion, or pleural effusion caused by right-sided heart failure. Stage D sadly is the last stage. It's closer to death, and this is bad heart failure.
So these are cases that we call refractory, which means that if we give them a different medical management, . We may be able to control their clinical signs, but unfortunately, once we start intensifying their medical management, generally, the clock is ticking, and for every change we make, it's a law of diminishing returns for the patients. So once they're in stage C, we all feel a little bit sad that things are not going as well as they should.
But despite saying that, we can maintain a good quality of life for some months, usually. Just to review clinical signs of heart failure, as I said, tachypnia is a sign of pulmonary edoema. Exercise intolerance can be a sign of, of heart inadequate perfusion from the heart, but actually when we're thinking about stage C, they really have to have congestive signs of fluid accumulation.
So exercise of intolerance alone wouldn't technically classify an animal as stage C, although it would tell you they've got very bad heart disease. Abdominal distension caused by ascites, or even things like syncope caused by arrhythmias, those will be clinical signs, but again, abdominal distension caused by ascites would make an animal stage C because they've got fluid accumulation. That's the key thing.
Syncope, we couldn't classify them as stage C, but if it's caused by ventricular arrhythmias, again, that may be heart disease that needs treatment. So what I'm going to talk about in terms of staging, there's some blurring of these boundaries in some patients. Let's think about pre-clinical heart disease, to begin with, and we'll break this down and think about different diseases and, and how to classify these.
So stage B, when we think about dilated cardiomyopathy, is when we make a diagnosis of a dilated left ventricle with a reduced systolic function. Now usually that requires an echo to take those measurements, and we have to compare those measurements to, usually breed specific reference intervals, if not weight specific reference intervals. So you can't just take a measurement for a chihuahua and.
Compare it to a measurement for a, I don't know, a Great Dane and expect them to be somewhere similar. You obviously have to look at something that accounts for the difference in body size. When we look at ventricular, dimensions.
And as Nuala said in one of her lectures, some patients have quite large hearts, but are normal. So for example, springer spaniels, they have quite a dilated left ventricle, and some of them, I find very athletic dogs, we echo them in their systolic function looks borderline, but usually those dogs are normal, in the context of their breed and their exercise background. So the diagnosis of DCM is not always clear cut.
Probably 50% or less of these dogs have a murmur. So they're not easy to detect without performing echocardiography. If we think about mitral valve disease, that's far more common and thankfully, it's a little bit easier to diagnose because when we think about clinically significant mitral valve disease in stage B, they have a heart murmur.
Now just to add an extra classification stage here, these dogs are either in stage B1, but they have got mitral valve disease in a typical left apical mitral murmur, but they've got no signs of cardiomegaly. So no left atrial dilation, no left ventricular dilation, and no increase in heart size on radiographs. Stage B2 represents a more advanced form of pre-clinical disease.
These patients have cardiomegaly, and the simplest way to measure that, certainly for me would be looking at looking at left atrial size, because that tells you this is, this dog has got more hemodynamically significant mitral valve disease and therefore may benefit from treatment. We're going to talk a little bit about the evidence for pre-clinical treatment that exists. Pre-clinical heart diseases all around us, do not underestimate this.
Older small breed dogs get mitral valve disease very commonly. You have all seen, or rather, you've all heard these heart murmurs in pre-anesthetic checks, pre-dental, or just as part of their routine physical examination for routine health monitoring. Large breed dogs commonly can have dilated cardiomyopathy.
The problem is that many of these dogs don't show overt signs and don't have a heart murmur until things are pretty bad. So we don't obviously look for for DCM in every single large breed dog we see, but we look for this condition maybe in older dogs or dogs with a family history of the related cardiomyopathy or or heart failure, or sudden death, or potentially patients who, have got. Clinical signs of lethargy and exercise intolerance.
Some people will wish to screen particularly high-risk breeds for dilated cardiomyopathy, and that is a very proactive thing to do, and it's something that we would recommend doing in certain breeds such as the Doberman, the boxer dog, Newfoundland, Irish wolfhound, these typical dilated cardiomyopathy breeds. Clinical signs mean that this, this patient does not have pre-clinical heart disease, OK? So any signs that you see, any tachynia, dyspnea, ascites, they're not pre-clinical, so we can forget about those patients.
The typical way that we see this is incidental heart murmurs, at vaccination or pre-anesthetic. I have to apologise because I've inherited a cough from my children, so I have intermittent breaks for drinks. We'll talk a little bit about pre-clinical treatment now.
Why might preclinical treatment help these patients? Because they don't have signs, so they're not currently feeling unwell because of their heart disease. Well, if we think about heart failure, we're very black and white about this.
We say if the animal has pulmonary edoema, they've got left sided heart failure. If they have a very big heart and very bad mitral valve disease, but no pulmonary edoema, or they don't have heart failure. The reality is it's more of a continuum.
There are many neurohormonal mechanisms that are activated prior to the onset of those clinical signs, often over months or years before the clinical signs develop. The key things to think about here are sympathetic nervous system stimulation, and this increases circulating noradrenaline. Noradrenaline is one of the bad guys here, and can, can contribute to cardiac remodelling, volume retention, and increases myocardial work.
If you increase the work of the heart, when the heart is sick, you are not going to help the heart, and that contributes to progression of disease. The other side of this, neurohormonal activation is the renin angiotensin aldosterone system. The big bad guys, as part of this system, angiotensin 2, which I've abbreviated at 82 here, aldosterone, these, these molecules are, are key in terms of reabsorbing sodium and water and increasing your circulating volume, increasing myocardial remodelling, fibrosis.
These are all negative things for the heart. The third one I've listed there is vasopressin, or ADH or AVP depending on which side of the Atlantic you're, you're listening from. And, vasopressin or ADH, is actually a potent stimulant for, water reabsorption, but also a potent stimulant for thirst, and, also triggers other parts of this cascade to be amplified as well.
So maybe we can do something to interrupt these, these, mechanisms that are activated to try and improve cardiac output. A quick name check for for Nuala Summerfield, who presented prior to me this morning, and she was the lead author on a key clinical trial called the Protect trial. And this is a very high standard trial which looked at the efficacy of Perveen to prevent congestive heart failure or sudden death in Dobermans.
Why Dobermans? Well, we know the disease is common, so therefore, it's relatively easy as scientific investigators to recruit a group of dogs with early stage DCM. Now, when they were looking at these Dobermans on the ProTE trial, they were screening many Dobermans across Europe and the US and elsewhere, looking for early stage related cardiomyopathy.
They had to have no signs of heart failure on radiographs, they really had to be stage B. And this was what we call a double blind placebo control trial. So because of of a process here of randomising the dogs who had early DCM to receive either piendin or placebo, nobody knew which dogs were receiving which drug, which meant there was no bias in the investigators or the owner's feedback on things.
So that's, that's the double blind part. Placebo controlled the placebo was a very good placebo. It looked and tasted exactly like Hima Bean, in its, its form, made by boring a vetting, but it didn't have the active drugging, so it was a proper placebo.
There was no sort of fancy packaging in one group that made the owners think the dogs were doing better and worse packaging in the other group that mean the other people knew it was not the real thing. And they followed these dogs over time, to an end point of the study, where the dogs either developed signs of heart failure, confirmed on radiography as well as clinical signs, or whether they died. We have to look at both of these things in veterinary clinical trials of drugs, because maybe it looks like the drug really works fantastically well, and they live a long time before they go into heart failure, but they're more likely to drop dead if they're on the drug.
That would not be a good drug. And thankfully, that wasn't the case here, because they looked at both outcomes. As you can see from this curve, this is a type of curve called a survival curve, and you can see we've got two groups represented there, we've got the dogs who are on immobendum and the dogs who are on placebo.
What we tend to do statistically, and it's quite useful from a clinical point of view, is look at the, the median survival times, the average survival time for dogs in each of these two groups. If you follow the curves from the left to the right, you can see the curves drop down, and each time the curve drops down, that's either a dog developing signs of heart failure or dying. I think if I was a Doberman in the Prote trial, I would have wanted to be in the Peerendon group, because you can see the dogs in the Peerendon group have a significantly longer time to the onset of clinical signs or heart failure, death.
So here we've got a group of dogs who live significantly longer in the asymptomatic phase. So this prolonged stage B. It's good to prolong the asymptomatic phase.
Because once you're in stage C and you've got signs of pulmonary edoema, you're never quite right, you're never quite comfortable. Even with the best management in the world, your exercise tolerance probably isn't as good. You may not have the best sleep, that's a common thing in humans with pulmonary edoema, is their sleep is interrupted, because they can't get comfortable.
So it's really good if we can prolong the asymptomatic phase, which pimaendin does in dogs with DCM. Now how does a drug which improves contractility, improves cardiac output and cardiac efficiency, how does that help? Well, one of the key things they found in this trial was actually that the hearts got smaller in dogs who were on yabendin versus placebo.
So you can see from these two box plots that the left ventricular diameter in cystole, which is the plot on the left, and the diameter in diastole, which is the plot on the right, both reduced in the dogs on Pyerendin versus placebo. And if you reduce the heart's size, you improve the cardiac efficiency, you reduce the oxygen demand of the heart, and you should help the heart cope for longer. So it might be purely a mechanical effect of this drug in reducing heart size that actually improves outcome in these patients.
So, in summary for the Protek trial, from this data, this very, very important data, we know that Dobermans with echo evidence of DCM, so who are in, sorry, B of dilated cardiomyopathy should be prescribed hemobendin. They don't have clinical signs, but we can still help them live a better quality of life for longer. One of the things about Dobermans, and you can see these two Dobermans here in the image, they're wearing these very smart halter jackets.
A halter is a 24 hour ECG. So part of our standard diagnostic investigation in, in Dobermans and in other breeds with DCM, is, is an ambulatory ECG recording because ventricular arrhythmias are common, and there are some dogs who will measure normal on echo. Who have got a significant number of VPCs which could pose a risk potentially for them and might need treatment separately, but actually in Dobermans, if they've got enough BPCs over 24 hours, you can diagnose them with DCM irrespective of what the echo looks like.
So for DCM screening, there's a little bit more than echo, although the vast majority of dogs who come into your clinic from other breeds, non-D Dobermans, they may just require an echo for screening. I should say, this trial proves that Dobermans live longer on Pumabendan in stage B. Now that means the drug has a licence, that has a licence just for Dobermans in DCM.
I don't know any cardiologist who just uses it in Domans, because if we think, if we believe that making the heart smaller is the key thing in helping them to live longer, then actually that should be true for any breed of dog. So we extrapolate this evidence to other breeds. Domans just happen to be a convenient population to study.
We've looked at the large dogs, let's think about the small guys now. Let's think about those with degenerative mitral valve disease. I think a much more common disease than DCM and and certainly one that's easier to detect in your clinics, because these dogs tend to be older, small breed dogs with a left apical systolic heart murmur.
This study is called the EPI study. I think they conceived the name before EPI became a really trendy thing to say if you were in your teens. It's not just an epic study, it's the evaluation of Pima Bendin in cardiomegaly.
It is pretty epic, this trial, because they have a large number of dogs. You can see the large number of authors here. This was a study performed in 36 centres internationally.
So to be eligible for the EPIC study, you have to be a small breed dog, so they have to be less than 15 kg, and they could be any breed, they weren't just cabbies, for example. They had to be over 6 years old. They had to have an echocardiographic diagnosis of mitral valve disease.
And they had to have imaging evidence of stage B2 mitral valve disease. The reason for this is, many dogs with B1 live a long time and many of them die of something else. So actually stage B2 are the dogs who've got the worst mitral valve disease, they're starting to get cardiac remodelling, a big left atrium, big left ventricle.
These are the dogs who we want to help the most. Now, they have to be otherwise healthy and not have a life limiting condition. So as I said, the reason they didn't look at stage B1 m of our disease is that survival in this population of dogs can be really long.
Sometimes they outlive the disease, if you like, or, or, they die of something else. Now, these dogs have a normal size. The time to heart failure on average based on various studies, is about 5 or 6 years.
That's the average time. So more than half of the dogs don't die of their mitral bowel disease. So, is it worth treating them and making the owner tablet that patient every day and spending the money on the drug, it may not be.
It's also harder to study because they live such a long time. If you've got dogs with left atrial dilation in stage B2, the time to heart failure on average is 2 to 3 years. These are a better group, to study, first of all, because they've got a shorter time to either developing heart failure or dying.
But also they, are a better group to try and help in the clinic because they're ones that will benefit more from our treatment. So dogs that were enrolled into the EI trial were randomised to either Ppimoendin or placebo. Once again, they looked the same.
They had the same fancy foil packaging and reassuring orange colour. And they were followed over time, during which time they had repeat imaging, radiographs, and echo. They had repeat blood pressure measurements, blood tests to look at their renal function and haematology and things, and they had that every 4 months.
They were followed to an endpoint of either death or congestive heart failure signs, and that had to be confirmed radiographically. So 360 dogs were recruited from 36 centres, that was the aim. One dog failed to complete enrollment, I think they decided that they didn't want to do it after they got halfway through the the imaging and things, and 5 of them were disenrolled after finding out they weren't appropriate cases to join the study anyway.
So actually it's not a full 360 dogs. It's a mere 354, which is still a pretty good number for a veterinary study, and actually it's the largest veterinary cardiology trial to date. So 178 were randomised, 176 to placebo, that's an example of good randomization, it's around about 50/50.
And they followed them over time and generated this curve again, as with the Prote curve that I showed you. Each drop down here, is an animal who goes into heart failure or dies. Once again, I would rather be in the Pumaendin group if I was a dog in this trial.
You can see that the dogs in the Puma Bendon group lived on average 15 months longer before going into heart failure. So this is a really clinically significant proportion of time. If you have a 10 year old dog, you're giving them more than an extra 10% of their life symptom free.
That is a good thing to do. It helps animal welfare, it helps patients under our care. So the main conclusion of the API trial was that treatment with pendin in dogs with stage B2 mitral valve disease, the big hearts, that prolonged a good quality life for longer than 1 year in the average dog.
That's the sort of thing I will say to an owner to justify why we might want to investigate a heart murmur, even though the dog has no clinical signs. I genuinely believe that the EPIC and Protect trials should affect how we all work. This should affect how we work in first opinion practise at referral level 2.
So What should we do differently? Well, I think we should consider screening for dilated cardiomyopathy in those high risk breeds, the older dogs. Maybe the family history will help us to select the dogs who will benefit the most because they're more likely to have it because we believe that these diseases are inherited.
The other thing that is really crucial is that in the past, we were listening to murmurs in older small breed dogs and saying, I think your dog has mitral valve disease. Why should we bother investigating? Well, it'll help us to confirm the diagnosis.
I would say that many of those diagnoses are confirmed based on auscultation, physical exam and signalment. So actually now, we do have a very strong reason to image the heart in these older patients with mitral valve disease, because we can decide whether or not we can help them. This is the bottom line of our job as a vet.
Now what about cats? We haven't talked about cats so far. Feline heart disease, very common.
Hypertrophic cardiomyopathy, affects around 1 in 7 cats, if you look at all ages of cats across their lifetime. That's about 15%, that's the number published by my colleague Rosie Payne. And, this is really important data.
This is much more common than HCM in humans, it's much more common than many vets think. Some of the cases progress to clinical signs. Now in cats, we've all seen heart failure, we've all seen arterial thromboembolism or ATE.
There are cases of sudden cardiac death. They don't tend to see the vet. They tend to be taken in to the vet's, maybe dead, and a common reason the owners thought the cat had died in a recently published study from the Royal Vet College was actually poisoning.
They thought the neighbours had poisoned the cat, and these cats often had HCM and presumably died because of an arrhythmic death, which is a common, sad cause of death in young people with HCM. Now, there are no published clinical trials, trials of treatment in the pre-clinical phase of HCM. We don't have that data.
The closest thing we have is, evidence of a treatment benefit in cats who've had an arterial thromboembolism. This is a cat who's had an arterial thromboembolism. It's a memorable picture.
We've all seen them. They don't use their back legs very well. This cat is vocalising.
They are painful. OK. And that's the big thing with ATE.
Cats are painful. You can recognise that it had a thrombus to to one of their limb vessels because of paresis or paralysis to that limb. They usually have pulselessness in that limb.
It's rare to get a non-limb ATE, but it is possible. I've seen some cerebellar and some mesenteric ones, the mesenteric one was diagnosed postmortem. The cerebellar went to see neurology for an abnormal gait.
So often these cats have got no previous history or clinical signs, they are asymptomatic, but most of them have got very bad heart disease, so that would put them, up until this point in stage B. They haven't had heart failure, but they have got pre-clinical heart disease. It's very emotional for owners to see a cat develop an arterial thromboembolism because of the pain and the stress, and it may cause stress to the vet as well as the owner.
We've all had that conversation where we say, your cat's got very bad heart disease, and they say, but he was fine this morning. The fat cat trial, which is the feline aortic thromboembolism, clopidogrel versus aspirin trial, was published in 2015, and this is where they're looking at, at, cats who've had an arterial thromboembolism. So they're sort of not pre-clinical.
They've had clinical signs, although they're not heart failure. This is the closest to the evidence, in dogs that we have in cats. Now here, these cats had to have heart disease causing arterial thromboembolism.
I've seen a few cats with AT who have not had heart disease, not many, but they're out there. They had to have survived 3 months after the initial event. So these are guys that have got over the initial event, the initial electrolyte disturbances and everything else are out of the way, so they don't affect survival.
It's not a pure pre-clinical population, but it's the best we've got. It is high quality evidence. That there is a treatment benefit to giving clopidogrel over aspirin.
So if you look at this curve here, we can see that cats who were on clopidogrel lived after a thrombus more than 400 days on average. Now if that doesn't cause a sharp intake of breath or a raised eyebrow, I don't know what will, because many vets will euthanize these cats on presentation saying this cat has got hopeless disease and needs to be put to sleep. Here.
Admittedly they are the survivors of the initial event, but if they survive on clopidogrel, they can have more than a year of good quality life. OK, so this is a really important factor and a really important number I think to remember. Aspirin people often give every 2nd day or every 3rd day.
Clopidogrel is once a day, that's the, the only compromise really. So clopidogrel has a key benefit over aspirin in that it doubles survival time at least. Now, treatment before heart failure, just to summarise what we've said of those few studies, it's mostly based on the echo assessment of cardiac size, although sometimes you might be able to make a radiographic assessment, especially in a dog who's got a very big left atrium, and that may be much more obvious on on radiographs than if they have mild or moderate.
Left atrial brillation. So dilated cardiomyopathy is when you diagnose the disease, they don't have to have a big atrium with DCM, OK, that's really important. So if you're looking on radiographs alone, you're gonna miss the early, the early guys, and and you need to have an echo to diagnose those early stages.
With mitral valve disease, well, we want FH brillation to know they're in stage B2, and therefore they'll benefit from hemoendin. With HCM, we believe, or, or we know really that that one of the major risk factors for thrombus formation. I left atrial donation or poor left atrial function.
So actually we would use that as a criterion for for prescribing clopidogrel to cats. We don't wait for them to have an ATE because the mortality rate is so high. So, cats and dogs at risk of heart disease, or who you think may have some crinkling for heart disease, require imaging.
This is the logical conclusion of this data to identify the ones that we can help, we need to decide who's got the heart disease. So this is where we come to some cases to think about. So I'm going to look for some interaction from you and some voting.
It's very sim simple, this first case here, we just have the poll. Of does this patient have pre-clinical heart disease that requires treatment or not? OK, so it's a simple poll, the answer is a yes or no.
If you select option A, you are saying the patient does have pre-clinical heart disease, the answer is yes, and if you're going for option B, it's they don't have pre-clinical heart disease requiring treatment. OK. So this is your first radiograph, if we can open polling please John, that'd be great.
Up and running. Fantastic. So here we've got a radiograph of a dog, a lateral radiograph.
I'm afraid I'm not giving you the orthogonal view. I'm a bad cardiologist. You're just getting this view.
Here, to look at the heart. So the question is, does this patient have pre-clinical heart disease which requires treatment or not? OK.
Let's, let me give you the breed to contextualise it. This is a cavalier King Charles Spaniel. We all know what disease it might have, but does it need some treatment?
I'll just leave it running a few more seconds and then I'll give you the results. Thank you very much. So I think we're almost there on the voting.
So any last minute voters? So we have a result that 56% of our delegates are saying, excuse me, are saying yes, and 44% are saying no. I love interactive polling.
I think this is maybe my favourite part of my, my job at, you know, presenting and lecturing. I hope everyone else enjoys it as much as I do. This is a normal, lateral thoracic radiograph.
There is no evidence of left atrial glation here. So, a really crucial thing, I hope you can. See my mouse pointer moving now.
identifying the left atrium and the lateral radiograph, we all know about vertebral heart scale. Sure, we can all, you know, measure that. We take the long axis of the heart and the short axis of the heart, and we add it up, and we go from T4 backwards and measure that in vertebrae.
Actually, a better way for looking for the left atrium for me is look where the cord vena cava intersects the cardiac silhouette. If you draw an imaginary line between that point where my mouse pointer is, up to the carina, which is here, that's the bifurcation of the trachea, there should be none of the cardiac silhouette above that line. In this case, there is none of the cardiac soar above that line.
This little bit of fluffiness here, that's probably some pulmonary arteries, maybe a pulmonary vein coming back into the left atrium, which sits below that imaginary line. Now if there's anything above that line, that is the left atrium, it's the only thing it can be. And actually, that's diagnostic for left atrial diation.
So it's really interesting we had such a split on that radiograph. I think thoracic radiographs pose a genuine challenge, you know, I, I, I, I think I found them difficult when I was a proper vet, when I was in practise, I think the only way to, to simplify them is to get lots of experience looking. So our students, two of whom are actually in my office with me now just watching this webinar, so, hello to Hannah and Hannah.
The, . They find it very difficult, you know, initially looking at radiographs, and I fully sympathise. I've been through that phase two.
Let's have a look at some more. So if we can open polling for number 2, so the question just to reiterate, is, does this patient have pre-clinical heart disease that requires treatment? OK, so, this patient, let's say is a cock spaniel, and again, just one natural radiographic view.
If you answer, yes, then that means this is a dog you would prescribe some treatment to, and if you answer no, then it means this is a dog he would not prescribe treatment. And just remember this is totally anonymous, we can't possibly trace who's voted what. There's no.
So just another 556 seconds. And we will close the polling. No.
So we have 90% answering yes, 10% answering no. It's a bit of a difference to the previous radiographs. I think it's always hard to be confident about normal, and I'm sure you'd all agree with that.
When we see a patient like this, where we draw that line between the cordal in a cava here, it hits the cardiac silhouette, draw the line up to the bifurcation of the trachea, which is just here, you can see one bronchus coming this way, another one going this way. Cardiac silhouette tends above the line. Therefore, this dog has got left atrial elation, and actually it's also got venous distention, if you compare this vein to the size of the artery.
That's a wide cranial lobar vein. So this is a patient who would be at risk of heart failure, if not on the turn into heart failure actually. So I would say that dog probably should be treated with pendin if we suspect it's got mitral valve disease or or DCM if it's a cocker spaniel they can get both.
So I'd agree with the majority there. OK, let's have a look at this, bit, bit tougher maybe because it's an echo image. If we can open poli again, John, that's fantastic.
So this is a cat, and this is an echo of a cat, looking at the short axis for at the heart base. For anyone who missed N's lectures, you can see this is the aorta here. Mercedes Benz sign is somewhere here, and then we can see this is the left atrium.
OK. So the question is, does this patient require treatment or not? Yes or no.
And if you're scratching your heads, that's OK. Echo's tough if you're not doing it quite a lot. OK, so we'll close the polling now.
And we have 19% saying yes and 81% saying no. So it's a bit more of a consensus towards no, and I would agree the left atrial size is normal in this case, and you know, certainly not a patient, we would, we would think about prescribing, treatment to or clopidogrel to, because of poor left atrial functional left atrial fibrillation. Echo is tough if you're not looking at it frequently.
So, we'll have a look at the next case. This is a cat again. It's not a perfect image of that aortic valve there, so any purists out there will go, this cardiologist can't echo.
It just happens to be a good example of something on our table what there is in a minute that would give the game away, but this is the aorta in the centre here, and the left atriums to the bottom there. So the question is, does this have, is this a cat who would benefit from clopidogrel? Does this patient require pre-thercal treatment or not?
OK, so here we have 100% saying yes and no one saying no. You are good people. This is a cat who has a huge left atrial dilation.
I mean, cats do not do things by halves, you know, when they get upset, they, they really go for it, and when they're happy, they really go for it. And when they've got heart disease, they really go for it sometimes as well. And this is a huge left atrialbrillation.
You can see the spontaneous echo contrast swirling around here. In the left atrium, this cat is at risk of thrombus formation, absolutely. Not just because of left atrial size, but it's not moving very much.
We can see that there that the spontaneous echo contrast or smoke is caused by aggregates of platelets in their blood cells that the ultrasound machine picks up. This cat's aiming for a thrombus at some point, so definitely clopidogrel would be a strong move. So I would say in that case, I, I agree with the 100%, treatment is definitely required.
It's another cat. So this is a standing echo, it's not, again, not perfect, these are all real cases, you know, and this is a cat who presented with, . Abnormal auscultation.
Wouldn't tolerate a lying down echo, so we do them standing. So the question again is, does this cat have anything that requires treatment on the echo or not? And I think we're really putting the pressure on by making you answer so quickly, but it's in the interest of time.
Task very harsh, I think, yeah. Just a few more seconds. OK, we'll finish there.
And we have 78% answering yes and 22% saying no. It's a tough one. If you're not used to looking at cat echoes, this is the left atrium here.
You should be able to fit two of this small normal left atria inside the left ventricle of the cap. You probably can't fit one of these. So this is a big left atrium.
I bet if you measure it, it measures more than 16.5 millimetres, which is what Nuala was saying is a cutoff, which we all use, I think, as cardiologists. The other thing to note here, it's a bit of a naughty question, really, because I said, does the cat have pre-clinical disease?
There's no overt clinical signs. The cat presented with a gallop sound, which is suggestive of high filling pressures. Look here, where my mouse pointer is.
It's a little pericardial and a little pleural diffusion. So actually, this cat is in in congestive heart failure, but it's not showing signs. So really it is pre-clinical, but it's very close to developing signs in the coming weeks.
So in that case, I would absolutely recommend treatment. I'd probably treating the clopidogrel in that case. Given the fluid accumulation, I might start some rozamide as well, although it wasn't really overtly clinical, but the cat's heading that way pretty soon.
Let's have a look at this one. This is a dog. This is an echo you can see in the middle you've got the aortic valve, the Mercedes Benz sign there opening and closing.
You can see we've got the left atrium to the bottom left here of that. So I hope to be nice and quick with this one. Does this patient have pre-clinical heart disease that you think requires treatment?
Let's say it's a dog with a mitral murmur. Do you need to give it to them or not? And I was wondering what's around this side of the heart here if you look at the mouse point.
This is the right atrium, tricuspid valve, right ventricle. If we were to follow that up, we'd see the pulmonary artery. OK, so here we have 38% saying yes and 62% saying no.
So this is a case of normal left atrial size. One thing that may be confusing people slightly, if you look at the the pointer is, we can see we've got the pulmonary veins are entering here into the left atrium. So it's really important not to include that pulmonary vein in your assessment of left atrial size.
So I would probably measure the aorta as they described inner edge to inner edge. And I might measure just to that little mark there, I might extrapolate that round and take an estimate, but the ratio here is less than 1.5.
The ratio between the left atrial diameter and the aortic diameter is less than 1.5, and therefore this is a normal left atrial size. So irrespective of what the mitral valve looked like or how loud the murmur was, we wouldn't treat this case.
OK. Very good, we're coming up to the end of this, this initial challenge, there is another one later, this is a boxer dog presented for for vaccination. 8 years old, and the vet was pretty switched on and said, you know what, older boxers sometimes get heart disease, and the owner said, Oh, my last boxer dropped dead.
I want to know what's happening. I want to be able to treat if I can. So this is a dog who presented for assessment to see if he had dilated cardiomyopathy or not.
So if you think he does have dilated cardiomyopathy, then we would prescribe him a bein treatment, so select yes. If you think he looks like a more normal boxer, you can select no. So remember, don't be shy, we cannot trace what your vote was.
There's no points system here. No points, unfortunately I'm not allowed to vote, so I'm in a very strong position. John, I'd love to know what your, your votes were actually.
I'd prefer not to share that with the very distinguished delegates we have today. If you asked me to vote on cattle health, I wouldn't be able to hold them together in that one. OK, so we'll finish there, and 93% have voted yes and 7% have voted no.
I agree with the majority, again, this dog's got a very poor systolic function. Look at the left ventricle. You can see the apex of the ventricle here, the, the sort of what remains of the pointy bit of the ventricle is moving.
These walls, they're really just along for the ride. They're not moving very well at all. Actually, there's also left atrial dilation.
So this is, this is a dog with dilated cardiomyopathy and quite advanced dilated cardiomy, the left atrium is so big. You should be able to fit two left atrial areas into a left ventricle, and this one again, you might just squeeze one. Just trying back to my slides failing.
OK, there we go. So again I vote for the, for treating that dog, absolutely. This is another case.
This is a a patient who, this is a Doberman, again, family history of heart disease. Dogs presented for for screening, and this is the right paraeral long axis echo. So we've got left atrium over here, mitral valve, left ventral corner.
If we can open polling again, the question is, do we think we want to treat this dog, because we've got a diagnosis of DCM or not? So I'm conscious some of you have commented that the polling box is getting in the way of the image, so I'm trying to make sure that stops being the case, but if it's out of the way done, yes, my apologies for that. I think, I think every, every individual will have to drag it out of the way.
I'm having to do it myself as well. If you just drag it like a normal window to the right of your screen, you can look at the image again and then you can select yes or no. OK, so on that one, we have a result of 90% yes and 10% no.
I genuinely think early DCM is very difficult. I expected people to vote no, because this actually is a dog who does have early dilated cardiomyopathy. But it is very early, so you've come down on the right side of things there, absolutely.
But this is one that, you know, personally, I'd have to measure this to say that this dog had dilated cardinal. I'm gonna skip the last one there, just in the interest of time. So I think generally people are performing pretty well on their assessments there of, of whether these patients have preclinical heart disease.
So very well done. You're obviously either paying close attention to Nuna's lecture or you've got quite a lot of experience in assessing heart size themselves. So, let's get back to our staging system, just to summarise what we've talked about there, the ABCD system.
We think about pre-clinical heart disease. If they've got pumabendin or stage B2 mitral valve disease, sorry, if they've got DCM or stage B2 mitral valve disease, they will benefit from pumabendin. If they're a cat with HCM and left atrial dilation or any, any sort of the of the cardiomyopathy, left atrial dilation, they will benefit from clopidogrel, and we hope.
It's quite different to stage C because stage C, we start adding more drugs in, we start thinking about polypharmacy. The the cornerstone of therapy once they're in, congestive heart failure is furozamide, as a first line diuretic. Other loop diuretics are available.
But generally we, we, treat with furozamide, in addition to the other drugs. So heart failure is a clinical syndrome of fluid accumulation secondary to advanced heart disease. Left sided heart failure is most common.
That's the, that's the most common thing we see, pulmonary edoema causing tachypnea, or sometimes pleural diffusion in cats, and that's because cats often, develop bilateral failure. They have a very low threshold for developing right-sided heart failure, and if they're in left-sided heart failure, some patients will then develop secondary right sided heart failure very easily, very similar to humans and horses, actually, probably cattle as well, John, you can tell me if that's the case or not. But, right-sided heart failure.
Less common, but we do see it, certainly in very bad heart disease, and we often see ascites, we can see pleural diffusion as, as a sole entity, in patients with right-sided heart failure, dogs or cats. Now, imaging confirmation of heart failure is important. Now that can be radiographs, but the last thing you want to do is is radiograph a dyne.
It can't just confirm a pleural effusion, this large volume. Small volumes, well, OK, I mean, we may miss those on physical exam, but large volume pleural fluid, really is best diagnosed by ultrasonography. So it almost makes me a little bit sad if I detect pleural fluid first on a radiograph.
I'd like to know about it in advance of that, because I've performed a thoracic ultrasound. You can also use ultrasound to confirm a SciTS. The other thing to to look for is bee lines, which is beyond the scope of this presentation, but bee lines and lung ultrasound confirm an air fluid interface, which suggests the lung is wetter than it should be, and therefore you've got pulmonary edoema.
So let's think about these cases. The question this time is, does this patient have heart failure or not? So the first answer would be yes, second answer would be no.
Just come down on that. If you're not sure, well, I mean, toss a coin and choose. So here we've got a lateral radiograph of a cat, with congestive heart failure, again, just drag the pole window out of the way, and you should be able to, to see the image.
Lateral radiograph of the cat, sorry, with, with, suspected heart disease. The radiograph was taken to confirm whether it has got heart failure or not. I think cat chest X-rays are difficult.
More difficult than dogs even. OK, so we'll wrap it up now. And we have 55% saying yes, 45% saying no.
I think if I surveyed a million vets, I have a similar proportion saying yes and no to any cat radiograph of the chest, because they are pretty difficult. There's a lot going on in a small space. Here, we've got cardiomegaly, the, the, thoracic, sorry, the, the cardiac silhouette width should be no more than 2 rib spaces.
And here you can see if we extrapolate that, it's probably 3. So this cat's got cardiogaly. What's interesting is if you look for the vessels like we do in dogs, these vessels are quite The inquests ready, except for the vena cava, it's got a huge vena cave.
So this cat has probably got right-sided heart disease, causing vena caval distention. There's no evidence of pulmonary edoema in this picture. I can't see any evidence of a cis radiographically either.
You can still see abdominal definition of the liver and the pylori food in the stomach there as well. And you can see this falciform fat pad under the liver, differentiating it from the liver parenchyma. So, there's no evidence of plural fluid either.
This little. Here is the psoas muscle that's, that's seen in cats. It's normal to get a little bit of retraction of these lung lobes in the cordo dorsal margins.
So if you see that, look elsewhere for pleural fluid, look and see if you've got any fissure lines, any rounding of the cranial lung lobes, which we don't have here. So this radiograph does not have evidence of heart failure per se, although I bet this cat's got bad heart disease, and I can't exclude that there being a small amount of ascis. So I would vote no for that, but I can see why people might have voted yes because the cardiac ccelerator is so large and there might be a small volum with CITES.
OK, this is a lateral radiograph of a Doberman. I'm just giving the game away here. Has this, has this patient got evidence of of heart failure caused by the related cardiomyopathy or not, obviously we'd be expecting left-sided heart failure in this patient.
OK, so I'll bring that to a close, and we seem to have a very clear cut result there with 97% yes. And 5%, no, that doesn't add up to me, so there's clearly some error. But that's what the, that's what the computer is telling me, but 90%, 97% yes, 5% no.
It's because it's because people are giving 102% their answers. So the, this is, this is a dense alveola pattern, you can see here we've got this. White out.
I always ask myself, can I see the vena cava? If I can't see the vena cava, there's something in front of that, which is probably fluid density. OK, I can't see the vena cava here.
Actually, what you can see is a very white, density with air bronchograms. You see the branching bronchi, as a sort of grey, more air-filled space in amongst this dense alveola pattern. And the same is true once you start looking for airbron.
Programmes you see them cranially too, cordially, dorsally. This is a radiograph that should not be taken. This dog was in extremists.
One of my ex-interns took it. I forgave them. We shook hands, because the dog was still alive, and they, they made a diagnosis and saved the dog by giving it furozamide and piendin.
And, the dog did very well, actually, and it's the only radiograph I have that I think is so severe. Let's think about the next case. So I would vote yes, absolutely, supporting the majority there, we've got congestive heart failure.
Let's have a look at this patient. Do we have evidence of congestive heart failure in this dog? This is a Cavalier King Charles' family.
I would say if you're, if you think the patient is on the turn or somewhere in the middle, this is true for all the radiographs, vote yes. I was mean enough not to give you a third option. OK, so we'll wrap that one up.
And the result is 69% yes, 31% says no. At least it adds up to 100. It does, it does.
We're back down to sort of mathematics aren't we, which is good. This is a tough one. I think there is, I think there's an interstitial pattern here, .
The three things I look for in a radiograph to say whether there's left-sided failure or not. Again, that imaginary line between the caudal caver and the carina, there's a left atrial dilation here. You can just see that.
It's not huge, but it's there. Look at the vessels, we can see vascular distention. So if you compare the vein here.
To the artery in front of it, the vein is wider than the artery, so there's some vascular distention, and there's an interstitial lung pattern. It's not alveolar, it's not dense like the last one, but the last one was extreme, as I said. So this patient is on the turn into heart failure, I think, or maybe has got clinical signs.
So of course, if the patient was tachypneic, I would say this patient was in heart failure. OK, almost there with these, so the agony of voting is nearly over. Tell me what your thoughts are, is this patient in congestive heart failure or not?
If any of you don't have digital X-ray systems, you might be thinking, these animals all have bronchial patterns. That's what I thought when I remember switching from analogue to digital. So it just highlights the the bronchi and the small vessels very well.
OK, we'll bring that one to a close. Less clear cut, yes, it's 37% and no is 63%. Some of these are tough, aren't they?
I, I'm gonna go with no, in this case, because the vessels, are prominent. One of the things here that's difficult actually is if you look, you've got, an artery and a vein, and then the artery in the vein for, for the other lung is actually overlying on the top, so it's a bit difficult, makes this vein look quite wide, but that's actually, oh crikey, I've gone backwards. That's actually vein plus artery there.
So it's a bit difficult to assess the vessels. These are normal lungs. I can't see an alveolar pattern here.
I can see the vessels really clearly. If you have an alveolar pattern, it's because you've got fluid in the alveoli surrounding the vessels, which means that you have a fluid density overlying a fluid density. So you lose the vessels.
I can see the vessels so clearly, this is not an alveolar pattern. So this patient does not have, I don't think, congestive heart failure. Final one to vote on, this is a cat.
That's all I'm gonna tell you. No, I'm gonna tell you it's a cat who was dyspneic, presented as an emergency, also had a history of occasional coughing, that was, that was the story. OK, so I'll bring this one to a close.
Here we have 42% saying yes, and 60% saying no. So again, we've got a mathematical error there. 102% effort.
So this, this is a curveball, and I apologise, it's just me being mean, really. And this is a cat who, who's got TB. It's a miliary pattern.
So the cardiac's a normal size, can't see it really clearly, but it's pretty small. Can't see the cord of in a cava, so, there's probably some alveo density there, but see how it looks speckled, doesn't it? And it looks speckled all over.
My differentials for this. Would be metastatic neoplasia or tuberculosis. Now, I'm based in the southwest of England and have been for some time.
We see a lot of TB in cats. Have a look at the body condition score, look away from the chest, I dare you for a second. Look at the body condition score of the cat.
You can see the spinous process of of the thoracic vertebrae, outside of the body there, look at that bump. This cat is wasting away, OK? That really is the clinical clue that this is a non-cardiac case.
Not to say cardiac, cases don't lose weight, but this cat's really emaciated. So, Just to quickly look at a cat who has got heart failure, we can see here we've got the cardiac cell in the middle. We've got pleural fluid on the sternum, we've got a fissure line between the the lung lobes here, as well as retraction called a dorsi, not just that normal retraction from the saris muscle.
We've got quite prominent vessels. I can't clearly see the vena cava. All these things suggest to me this cat's got a big heart, it's got pleural fluid, it's maybe have alveolar edoema as well, and it's got vascular distention.
Now, there are some cats where we look at a radiograph and we think that's quite hard to call. So sometimes it might be worth repeating a radiograph after giving some frozenide. So let's just have a look.
That's the same radiograph up front, same cat. This is the same cat 24 hours later. It's a dramatic difference, and the difference we see there really highlights the abnormalities we get in cats with heart failure.
Again, look at this image here. This is a cat with heart failure before and after frozenide treatment. I don't routinely repeat radiographs myself.
These are radiographs I've inherited from, colleagues, or interns or or people that I've worked with, where they wanted confidence to know they were improving things by giving diuretics, and they clearly have in these cases. So you can see a dramatic difference. Look at the, the post-treatment radiograph here.
Cinna cava, very obvious. In the pre-treatment radiograph, not obvious at all, and that's because of the alveolar pattern obscuring the vena ca. Right, quickly summarising standard heart failure therapy, if we think about dogs first, we treat them with furozamide.
I tend to start 2 migs per gig twice a day. It's rare that I go 3 times a day, but I do sometimes. And I titrate it to effect by which I mean I ask owners to monitor respiratory rate, and if the respiratory rate is well controlled after this initial dosing, we try and back off to g per gig or a mid.5, and the longer we can keep them on a low dose, the better.
I also treat them on pibendin. The dose rate for that is 0.25 mg per kg twice daily.
It used to say, well, it still does say on the packet must be given one hour before food. In the EPIC trial, they didn't specify. So most of the owners probably gave this drug with food, because that's what people do with tablets.
And actually there was still a significant clinical benefit. So I've stopped recommending that differentiation from food, which makes owners much happier. I mentioned the word earlier, polypharmacy.
We can give ACE inhibitors, I tend to use Benazapril, but other prills are available, and that's used once a day. We can also use spronolactone, which has to be given with food to improve absorption, and that the starting this is that is 2 migs per gig once a day as well. Mhm.
Now, if you're on a budget and you have to prioritise, ruzammide works to control pulmonary edoema, so definitely give that. And Pimabendin seems to have an overwhelming benefit, in these patients to prolonged survivor and improve quality of life. So if you have to choose something, you give risemide and pumabendin.
The other drugs really are optional, according to, to compliance, although they may help in the longer term. In cats, my standard therapy, rozamide, 2 migs per gig, twice a day, titrate of effect, sound like a broken record. Cardiology is easy, hey, we only have a few drugs to think about.
The other thing we use is clopidogrel for the reason that we said earlier, we, we're trying to reduce the risk of arterial thromboembolism, which is bad. Now Pimaendin has been used in cats. It says on the label, contraindicated in cats.
But there are numerous case reports out there and, and small studies, often retrospective, looking at using pyvein in cats with various heart diseases. We know in normal cats it's safe, it doesn't make their head fall off or the liver fall out or anything. And, and it does seem to, work in a similar way to how it works in dogs, in terms of the, the, the, actual effect on the heart.
There's a few metabolic differences, but it seems like it's a fair drug to consider. Now the contraindications to pumendin, one of the big contraindications is do not use pumendin in hypertrophic cardiomopathy. Now, obviously if you're using it in cats, most of them have got HCM, so how can I consider using it really?
But if you look at the detail there on the contraindications, it says, or diseases or the diseases, I suppose, in which an improvement in cardiac cat cannot be achieved for functional or anatomic reasons. What they're talking about is obstruction to outflow. Aortic stenosis is a typical example of dogs.
You have obstructed outflow. If you look at this echo at the bottom left, you can see this cat has got something called systolic anterior motion of the mitral valve. The mitral valve closes and it opens.
If you look just here where the pointer is, I'll move the pointer so you can see it. It's sort of like the mitral valve is high fiving the septum. It hits the septum during systole.
Now what that's doing is narrowing the outflow tract and putting pressure on the left ventricle. If we use a drug like yendum. Which is a positive ionotrope, theoretically, we increase the pressure in the left ventricle and put the cat at risk of things like, increased myocardial oxygen demand, infarction, ischemia.
These are bad things if you are a cat with heart disease. However, One study, retrospective study, looking at him abandoning cats, was looking at cats who, who were given it for their heart failure management. This is not a clinical trial, it's a retrospective study.
It generates a hypothesis rather than proves evidence. OK. Now, here they had 22 cats with non-obstructive HCM, 5 cats where the vets were brave enough or the cats were sick enough for them to consider using it in HCM with obstruction.
And they compared this group of cats to a group of cats who were given no pyendum, but had heart disease and heart failure. If you look at these survival curves, the median survival time shows us that cats on Pumerendan lived much longer than cats not given pumendin. So maybe in the right cases, Pervendan has a positive effect in cats.
We do not have clinical trial data, and currently the licence still says that it should not be used. Why might it help? Well, If we think about cats with HCM, we know from various studies that systolic function does deteriorate in more advanced HCM.
And actually, in my colleague Rosie's, study, the prognostic indicators in Casle HCM study there, from 2013, you can see, that, if you read it, the, the. Paper which is open access, you can see that cats who had poor left ventricular function, poor fractional shortening, actually did worse. They had a reduced survival time.
So the systemic function is important in HCM, although we think of it as largely a hypertrophic disease rather than a disease of weakness. As they advance, hemovendum might be beneficial. So I have very set criteria forumend and use in cats.
They have to have had a history of clinical signs. I never use it pre-clinically in cats. Those signs of heart failure, syncope maybe if they've got reduced output and a and a deleted phenotype on the echo.
If they had a poor or diminishing response to other drugs. So if you have, increased your frozamide and you're increasing it and you're increasing it, and the respirator is out of control, and the owners are thinking, is it time to put the cat to sleep? You know what?
Maybe try giving it herendum, because maybe it pulls the cat back from the brink and buys it a, a better quality life. They have to have no significant airflow obstruction on echo. It's easy for a cardiologist to say, just look at this on echo and do some Doppler measurements, but actually, if you can't perform Doppler echo, ask yourself, does this cat have a loud murmur?
If it does not have a loud murmur, it probably doesn't have significant outflow tract obstruction on echo. So just think about that, if you've got a count with heart failure, no murmur, but definite heart failure. Think about using cuerendam.
You must get signed consent forms specifying off label use in these patients because it is on the contraindication. So to protect yourself from an owner who might be upset if the cat dies because maybe it was going to die anyway, but you've given it Penden, then you need to make sure that they're fully consenting, that it says contraindicated, but you can say, based on my clinical opinion and the evidence and a fantastic lecture I saw on the webinar there, then maybe Puma Bendon would be a useful thing in your particular cat. If the owner's in doubt, don't push them, OK, because if something goes wrong, you could be in trouble.
Really quickly just totting up other drugs that are out there. Diltiazem, but it's the only licenced drug for feline heart disease, which is hilarious because we don't think there's a benefit in HCM unless they've got arrhythmias. Most cardiologists don't use it, plus, who wants to tablet a cat 3 times a day.
Beta blockers, there's some evidence to say there's no identifiable benefit over 5 years in pre-clinical HCM and actually if they're in heart failure, giving them beta blockers could worsen heart failure signs. So if you're not sure about the heart failure status, don't give them. ACE inhibitors, well, many of you might be thinking, well, why doesn't he give ACE inhibitors with frozenide?
Well, actually there's no proven benefit in pre-clinical or in heart failure cases, in cats. So I, I use ACE inhibitors in dogs, sure, in cats, they're not part of my standard of care. So just to summarise, I think identifying the stage of heart disease is really important because we know that certain patients with pre-clinical disease do benefit from treatment.
Not all of them. So don't just treat every murmur with pumabendin because you might just be wasting the drug, wasting the money, wasting the client's time and the dog's stress levels, OK? So definitely try and image the heart.
And if we can prolong the pre-clinical phase, this leads to a better quality of life for a longer period of time. Identify heart failure, because that's when you start your intensification of treatment, has a big prognostic implication too, but this is when we definitely need to start diuretics. Remember to use imaging findings and clinical signs.
You did well in, in, in, in the polls there, and I think that, you know, it's really important to try and integrate that imaging knowledge you've got with the clinical signs of the patient, because the imaging can look whatever it looks like, whatever it likes, but if there's no tach near, then it's not heart failure. And do learn to perform basic echo. Any of you who aren't doing it out there, pick up the probe, switch on the machine, push the buttons, turn the knobs.
If it all looks very strange, turn it off again and start again. Go on some courses and do learn some basic Echo because looking for left atrial dilation is invaluable, I think, in this group of patients. So sincere apologies for overrunning a little bit.
I know Nuna did too, but, I hope everyone's OK with that and, has enjoyed the, the interactive elements of this talk, and I'm sure have. Thanks again to, webinar and the B the honour of speaking. This photograph is the wonderful town, the wonderful city I live in of Bristol, and this is the harbour.
So, anyone who wants to visit Bristol, you know, it's fantastic. Kieran, thank you very much indeed, and I'm afraid we really are out of time, as you say. Just one question I'm gonna pass on, please, cause more than one person's asked us, asked it.
Clopigero, what is the dose, please? Several people said they didn't actually catch it. Yeah, no, that's important.
So it's 18.75 milligrammes per cat, so irrespective of cat size, once daily. That's derived, that's derived from a quarter of the old big human pill.
So it was derived for convenience, but actually now in the UK Summit Pharmaceuticals have made a tablet that is just 18.75 megs for cats, which is quite, seems to be quite palatable. So 18.75 is our is our go to do.
Thank you for that. So, we've had 3 hours of the most amazing. Information on cardiology, going through some very basic and important stuff that so many of us fail to understand properly because we're not working as specialists.
Can't thank our speakers enough for what they've done today, and in terms of being highly informative, very, very clear and very, very thorough in what they've been teaching us. So thank you very much indeed, and I thank you both on behalf of all our delegates for what you've done.
