Hello everyone, and welcome to this webinar on caring for the Big Heart, an update on K9 DCM. So what are we gonna talk about? Well, we're gonna go through the causes of canine DCM which is of course dilated cardiomyopathy.

How to diagnose pre-clinical DCM, so the patients before they've got outward signs of disease. And this is the part of DCM that is particularly challenging, I think, the diagnosis of these pre-clinical patients. We'll talk about that in quite a bit of detail.

We'll then move on to how we diagnose congestive heart failure in the DCM patient, which is fortunately not the most difficult thing. We'll discuss a little bit about the common arrhythmias associated with DCM and then finally finish up on how we treat DCM in the pre-clinical patients and then in the patients that are in congestive heart failure. So firstly, just a little definition to start with.

So dilated cardiomyopathy is a primary myocardial disease characterised by cardiac enlargement and impaired systolic function of the left or both ventricles in the absence of other cardiac or non-cardiac causes. OK, so that's the dilated cardiomyopathy part. Now, we often use the term dilated cardiomyopathy phenotype in these patients when we're describing the structural changes we see on our echocardiogram.

Why do we use that term and what does it mean? Well, phenotype is simply a description of the structural changes, and those structural changes could be caused by several different diseases. So when we pick up a DCM patient, we often refer to them as a DCM phenotype whilst we investigate the underlying causes, because there are multiple different ones that we'll get to in just a second.

So why are we interested in cardiomyopathies in general in dogs? Well, unfortunately, they're really quite prevalent in certain breeds and within those breeds are a cause of significant mortality and morbidity. So we need to be able to pick up these patients, and inform the owners and put together the most robust treatment plan and, you know, accurate prognostication for these patients as well.

So, another reason as well to be interested in cardiomyopathies, as we'll get to a bit later on, is that overt cardiomyopathiesia are easy to diagnose or easy enough, whereas the pre-clinical patients can be a lot more challenging. And it's these patients, I think that we could be doing more for, in helping treat, their dilated cardiomyopathy in, the attempt to delay congestive heart failure, which we'll get to a bit later on. So what are the other causes of canine DCM phenotype?

So the most common one is of course idiopathic DCM that we'll talk about in a second, which is that form of DCM that is diagnosed typically in Doberman pinches, as a diagnosis of exclusion, once we've ruled out all of the causes. However, there are some other underlying causes of DCM phenotype, and one of them that we'll talk about is nutritional DCM. So this is essentially a nutritional sort of deficiency within the patient that causes a DCM phenotype.

And if we can pick these guys up early, it's really important because, by addressing their nutritional deficiency, we can more than likely improve, if not reverse their DCM phenotype, which is great for these individuals. So we definitely want to be aware of this group of patients and how to screen for them. We've then got the patients with myocarditis.

So this is a much less common cause of canine DCM and to be honest, it can be really quite tricky to diagnose. These are generally patients who have significant inflammation of the myocardium for a period of time that leads to its structural failure. And this inflammation is normally caused by infectious diseases, and, and a lot of these infectious diseases are sort of systemic ones which can affect various different organs within the body.

Unfortunately, these guys, even when we do diagnose, the cause of their myocarditis and, and treat the underlying infection appropriately, they often don't do that well, and a lot of these patients do succumb, to their, structural heart changes, despite an appropriate diagnosis and underlying treatment, but, but often these, you know, guys as well, to be honest, are a diagnosis. Of, of sort of presumption really, because it's very hard to definitively diagnose myocarditis in dogs without a myocardial biopsy, which of course we don't really do, in the live patient clinically. So we'll touch on that a little bit more later on, but not too much.

We've then got patients with tachycardiomyopathy. So these are an interesting group of patients. That essentially have a sustained, markedly elevated heart rate, often above 220 beats per minute, because of, a tachy arrhythmia, say for instance, sustained supraventricular tachycardia.

These patients, if they have a a a a very high heart rate, and that is sustained for a protracted period of time, it will actually cause the myocardium to fail and then so induce a DCM phenotype, secondary to the initial tachy arrhythmia. So these are an interesting group of patients it can be quite hard to diagnose because we see tachy arrhythmias secondary to DCM as well. And yet we also now know that, you know, DCM can occur secondary to tachy arrhythmia, so sometimes we've got a bit of a chicken and the egg scenario.

And what we do with these patients is we say, OK, we've got a tachy err. Me, we've got DCM. I don't know whether the tachy arrhythmia came first or not.

Let's treat the tachy arrhythmia, of course, we'll treat the structural DCM as well. But if we treat the tachy arrhythmia, get that heart rate under control and re-evaluate that patient in a later period, with the significant structural improvement in their DCM phenotype, then it is possible that their tachy arrhythmia came first and caused Their heart structural heart disease in the first instance, you know, and those patients potentially can have a degree of, of reverse remodelling of their, DCM phenotype, so quite, quite a tough group, of patients, but interesting nonetheless. We've then got the hypothyroidism, patients.

So what we sort of know is that hypothyroidism itself does not cause, structural DCM, OK? It does, however, Reduce systolic function in patients with DCM and can cause increased chamber sizes and by treating their hypothyroid state, it can improve some of these parameters that we will identify on echocardiogram. However, it will not cure their DCM phenotype, and it won't tend to affect their outcome.

So it's something to be aware of and I think probably screen for it in, You know, most patients with DCM, particularly because, you know, some of these breeds such as Doberman pinschers are overrepresented for both hypothyroidism and idiopathic DCM. So I think it's worth screening for and treating, but I wouldn't sort of, hang my hat on the fact that a hypothyroid DCM dog will have significant improvements in their structural heart disease if you treat their, their thyroid. So a bit more about idiopathic or primary DCM.

So this is essentially a diagnosis of exclusion once we've ruled out the other causes that we've just listed of a DCM phenotype. And this disease of course is strongly familial, with a suspected genetic basis, seen in, in certain, large and giant breed dogs. Within which mutations have been identified in Doberman pinches, Irish wolfhounds, and Great Danes.

But it certainly is much more prevalent in these, pedigrees, and in some pedigree breeds such as the Doberman pinscher, the incidence can be as high as 58%, in some studies, which is incredible to think that every other, Doberman pinscher will be affected by this heart disease at some point. It's really quite scary to think of. .

So in these at-risk breeds, we kind of need to be really aware of how we're gonna screen these guys for pre-clinical DCM and you know, be aware of, of the fact that they could present for the first time at your clinic in full blown clinical DCM. We've said this is particularly common in large to giant breeds, but, we do also see this in cocker spaniels and Dalmatians in the UK as well, so, so don't forget those guys. But otherwise, generally, smaller breeds of dog tend to, develop mitral valve disease as as their most common, acquired heart disease, whereas in general, you know, large to giant breed dogs are more likely to develop DCM than than mitral valve disease, so.

We know that the prevalence increases with age, kind of makes sense, and most commonly affects sort of middle, to older age dogs. And that males are particularly overrepresented for DCM and unfortunately progress more rapidly to congestive heart failure than females, and therefore sort of have a poorer prognosis. Females, however, have Their own nuances and certainly in dopamine pinches, it appears that females have a higher incidence of ventricularectomy.

So, you know, we would treat potentially females a little bit differently to males, or at least approach the investigation a little bit differently, but we'll touch on that a bit more later on. So we've said that DCM is myocardial eccentric hypertrophy of the left and and commonly the right ventricles, but generally this comes in two distinct histopathological forms. Now the differentiation of these isn't really important, clinically in that the diagnosis of these patients will still be the same, the treatment plan, you know, will still be the same, but it is important to be aware of that there are a couple of, you know, different sort of histopathological causes, of idiopathic DCM.

And the first of which is the attenuated wavy fibre type, where patients develop really thin wavy myocytes, with large areas of edoema between their myocytes. And this really significantly affects the function, the the systolic function of the myocardium leading to this eccentric hypertrophy. And for those that don't know, eccentric hypertrophy is an outward dilation of that heart chamber, so essentially causing marked increases in in the internal diameter of that ventricle in both cystole and diastole.

Rather than concentric hypertrophy that a lot of HCM cats get where it's a thickening of the heart muscle itself, causing a decrease in the ventricular, luminal diameters. So these guys essentially developed, as I'll show you in the grammes later, large, round, thin walled ventricles. So the attenuated wavy fibre type is seen in medium, to giant breed dogs, and particularly in the Doberman pinschers.

We then have the fatty infiltration type, where we get large areas of fat infiltrating within, the heart muscle, and that can be associated with varying degrees of fibrosis, myofiber degeneration, atrophy and vascularization. And was initially described in boxes, with their box of heart disease or rhythmogenic right ventricular cardiomyopathy, but has also been found, at postmortem as well in, in many other breeds of dog with, DCM phenotype, including some Doberman pinschers no less. So these images were taken from, the DCM, taskforce paper that I'll, I'll show you a little bit later on, which describes, the guidelines on the diagnosis of DCM.

But essentially what we really nicely show is, a normal, dog's heart on the right of the image, where these individual sort of lines are the individual, myocytes. So this is what a normal heart looks like on the right. Top left, we then have a patient who's got the wavy attenuated form of DCM and you can see that these myocytes look a lot thinner, a lot more wavy, they're not as straight, and there is a lot of spacing in between them, which is large.

Areas of edoema between the myocytes as well. So you can really look at this image and imagine how this, these microscopic changes, you know, on a macroscopic scale significantly affect myocardial function. We've then on the left the bottom left, got a patient with fatty infiltration, which is, typically, you know, these boxer dogs.

And what we've got here are sort of islands or clusters, of myocytes that are interspersed with really quite large areas of fatty infiltration, and associated fibrosis as well. So again with these guys, you can really appreciate how these changes are really quite marked, compared to what would be considered normal and how that could quite readily cause that patient to develop congestive failure. So moving on to the nutritional DCM patients.

Essentially we are talking about patients that really, classically, if you will, are taurine deficient, OK? So these are patients that have low taurine levels within, their myocardium, which leads to structural failure. So taurine itself is synthesised, from methionine and cysteine within the liver.

And taurine is the most abundant amino acid within the heart, and normal levels are essential to maintain normal myocardial health. Now, taurine deficient DCM is something that we saw back in the 80s with cats, because they were being fed commercially available diets that were deficient in taurine, and we identified this group of patients. We supplemented them with taurine and they got better.

We then looked at their diets, realised they were taurine deficient. And supplemented, you know, the diets appropriately and essentially got rid of this disease. We're now starting to see taurine deficient, DCM in dogs that are fed, some of these newer, commercially available, what we would call, non-traditional, diets.

Which are those that are based on novel proteins or, you know, grain-free, increased legumes within the diet, all patients, of course, that are being fed a home prepared, you know, diet. Now, these diets themselves, some of them are out and out taurine deficient. There's not enough, sorry, the, the, you know, isn't in taurine and.

Other essential amino acids, but actually some of these diets, you know, themselves are not taurine deficient, but actually the levels of, the other constituents within the diet alter the ability of the patient to metabolise and utilise taurine, and then as a result cause a state of taurine deficiency. Via different sort of mechanisms of action really. So what this means is that they are, quite a difficult group of patients, to sort of understand exactly why they are becoming taurine deficient.

But essentially we need to be aware of them in primary care practise, because, these patients are the ones that if we do identify, by changing the diet that they're on, supplementing taurine, we can improve or reverse their DCM phenotype. So there's a few different studies that have looked at this, and found different things really. Essentially the things that have been found are that some dietary related DCM dogs do not appear taurine deficient when we test their blood, yet they respond to dietary manipulation, changing them from a non-traditional to a traditional diet.

Now, this may be based on the fact that when we are screening patients for taurine deficiency, the best that we can do is run blood work because gold standard would be considered to take a myocardial biopsy to assess the myocardial taurine, however, this isn't practically possible in our patients. So instead, we measure the blood taurine levels as sort of a surrogate marker really. .

And they are only so accurate. So when we're doing this, you can run taurine levels on either whole blood or on plasma. Now whole blood has been found to be more reliable than plasma, but it's less, commercially available.

So I think gold standard, when we are screening for taurine deficiency is to run whole blood and plasma taurine. But otherwise, if we're running plasma urine and the levels are low, then that would be indicative of a state of taurine deficiency, you know, and the need to, to treat that. But, we, we also know that that there are some patients as well, who have normal blood taurine levels and, and yet respond to taurine supplementation with improvements of their, their DCM phenotype.

And we also have some dogs as well that are fed traditional diets that, that, you know, . Contain very well normal components that traditionally have not been associated with DCM before, and these patients have improved nonetheless on taurine supplementation. So I think it's, it's, it's an unusual group of patients, but I think the important take home messages are be aware that nutritional DCM is out there as a cause of structural DCM.

Be very thorough in your, history taking to make sure we're screening for any non-traditional or or home prepared diets that could cause taurin deficiency. If we see a breed. That you wouldn't typically expect to have idiopathic DCM, you know, such as a Labrador retriever, do consider the other causes and do consider screening, blood taurine levels.

And really, if in doubt, we should be recommending that any patient with DCM is moved from non-traditional diet onto a traditional diet. And or supplemented with taurine, and then monitor response, because if we do change that patient onto a traditional diet or supplement with taurine, and we reassess them 6 to 8 weeks later and a significant structural improvements, it's likely that that patient did have a nutritional DCM. Carnitine deficiency is something that's been talked about, as well as a potential cause of DCM.

Unfortunately, we can't run blood taurine levels to assess, the myocardial taurine levels. You really have to perform this on a myocardial biopsy. So as a result of that, it's very hard to sort of speculate as how much carnitine is a con deficiency is a contributing factor to nutritional DCM in dogs.

I think essentially, If in doubt, we do no harm supplementing carnitine in these patients and actually a lot of veterinary approved sort of nutraceuticals that contain taurine also contain carnitine as well, so we'll likely do no harm by supplementing carnitine nonetheless. So we're just gonna talk a little bit now about the difference between the patients with occult or pre-clinical DCM and overt DCM which is of course those that have outward clinical signs. So the occult patients.

Can have a pre-clinical period that can be surprisingly long, that they're living with this, disease before they develop any outward clinical signs, and that pre-clinical period can be as long as 4 years potentially in some of these DCM patients, which is really interesting to think about because that's quite a long period of time that they're pre-clinical, considering that when they develop signs of DCM. Such as congestive failure, they often then have really quite short survival times from that point, in the order of approximately 6 months. So this relatively long pre-clinical period, and very much shorter clinical period in these patients.

The pre-clinical period, as its name are cult, indicates. I A period in which they are actually not showing any outward clinical signs and as a result can be really quite challenging to diagnose. And the diagnosis of these patients has been described and published, most recently for, for dopamine pinches in the Journal of Veterinary Cardiology, referring to what what the sort of gold standard should be, for screening these guys for, for, occult pre-clinical DCM.

And what they did, is they, looked at patients and decided that the gold standard should be considered echocardiography, yearly in patients that are at risk in combination with a 24 hour Holter monitor. Now, on the echocardiogram, what they're looking for are any structural changes of DCM. So reduced systolic function, any evidence of cardiomegaly, increased scleicity of the left ventricle, etc.

Etc. And of course if we see these structural changes that will tell us that this patient has preclinical DCM. However, a lot of dogs who have preclinical DCM will have no structural heart changes that are detectable on an echocardiogram, but simply, the only way to diagnose them is because they will have an increased frequency of ventricular ectopy.

Now what do we mean by that? It is normal for any dog, as they're walking around, to have a certain number of ventricular rectopic beats, VPCs if you will, during a 24 hour period, and often up to 50 can be considered a normal amount for a normal, healthy dog. However, we do know that in pre-clinical DCM patients, they have significantly higher frequency of ventricularectivy than normal dogs.

And as a result, we can use a 24 hour Holter monitor to look for the number of ventricular rectopics that they have within a 24 hour period and see if that puts them, In a category that is consistent with either risk of developing DCM or a diagnosis of pre-clinical DCM and the sort of need to start treatment. So, the gold standard for screening for DCM is yearly echocardiography and Holter monitor. And we do it yearly because, of course, just cause that patient is clear, on one screening test doesn't mean that in the next 12 months they will develop pre-clinical DCM and go on to develop heart failure at a later date.

So we really want to be screening patients yearly who aren't in the highest risk. For this disease, and this paper, that we've got a picture of on the right here recommends doing that in Doberman pinsers from the age of 3 years, OK, to screen them yearly for pre-clinical DCM. Now, you might be asking why are we getting so interested in the pre-clinical period in these patients if they've got no outward clinical signs.

This seems like a lot of screening, you know, of these patients and what for. Well, as we'll get to in the treatment section. Off the back of a study that was done a few years ago called the Protect Study, we do know that in Doberman pins and therefore likely in other large breeds of dog with pre-clinical DCM, if we start them on Pemaendin, we're able to prolong the pre-clinical period by a median of 9 months.

So that's really quite a long period of time when we consider the fact that when they eventually go into heart failure, they'll only live up to 6 months and actually Dober pinches, it's often a lot less than that. So prolonging the pre-clinical period by a median of 9 months. Is really quite a big difference to these patients versus not going onto that drug.

So essentially, we're interested in the pre-clinical periods that we can pick these guys up as early as possible and get them on piabendin if we believe they will benefit. Now, what if we have clients who are unable to afford the gold standard of yearly echocardiography and halter monitoring, because of course, it's not cheap at all. Well, we have some other options as well.

And, other options include the use of cardiac biomarkers. So we're looking at troponin, which is a marker for myocyte damage. It is released when myocytes.

Are damaged and will be at increased levels in patients with called DCM. And we're also looking at the biomarker end terminal Pro BNP. And this is elevated in patients who have cardiomegaly.

As a result of acquired heart disease, and in patients with preclinical DCM this can be elevated, and we can use some cut-offs to screen patients, to see if their NT Pro BMP is high enough, to be consistent with, pre-clinical heart disease. We can also do a 5 minute lead to ECG as well. So instead of a 24 hour Holter ECG at home, if you pop that patient on a multi-parameter for 5 minutes and observe them, if you see a single ventricular ectopic, so a VPC, that is abnormal, potentially, and one, VPC on a 5 minute ECG is likely consistent with more than 50 BPCs, on a 24 hour Holter monitor.

So essentially what we can do is use these cardiac biomarkers and a 5 minute ECG to test a patient, and if they're all normal, we can say, look, this isn't the gold standard, but it's certainly an acceptable standard to say your dog probably doesn't need a halter or an echo at this stage. Come back in a year's time. If, however, these tests are abnormal, then these are the patients that we should then push .

Towards having a detailed echocardiogram, and a Holter monitor for, for sort of definitive diagnosis for their pre-clinical heart disease. If the owners really are strapped for cash, and you can only do one of these three things, probably the NTR BMP is the most useful, certainly, in Doberman pinches, as we do have a cutoff for these guys, which we'll get to a little bit later on. What we sort of also, you know, know, as this, as I sort of said earlier, is that, patients who've got preclinical DCM will inevitably progress to clinical DCM and and therefore, these are the patients, you know, that want to try and get on immobendin as early as possible.

And here's a little screen grab, of the PE study, over on the right, which is open access through the Journal of Veterinary Internal Medicine. So what about the patients with overt or clinical DCM? So these are the guys that are easier to diagnose, and they can present with, various different things in their history that can help point us in the right direction.

They've got congestive failure. So they may have dyspnea and coughing, lethargy, weakness. Exercise intolerance quite commonly, potentially in appetences, maybe syncope, cardiac eexia or weight loss can be seen, and ascites as well if, if they've got, right-sided congestive failure.

So, these clinical signs, you know, could be caused by primary respiratory tract disease as well, but, but also, you know, very commonly, seen with, with congestive heart failure. So it's the physical examination really which should point us in the right direction, as to the fact that this large breed dog that's presenting to us with these clinical signs above likely has congestive heart failure, you know, rather than primary, lung or airway disease. So the things that we're gonna really look for.

Would be, firstly, pulmonary crackles, which can be indicative of pulmonary edoema. Now these are often really quite fine, in my opinion, when you're trying to listen for them, and can be missed unless that patient, you know, is is sort of swimming in pulmonary edoema. So I would say that, you know, if you hear them, that's great.

Certainly can be consistent with fluid in the lungs, but a lack of crackles on ausipation shouldn't really be used to exclude significant pulmonary edoema. What we may hear though, that's more specific for DCM would be muffled heart sounds. So they can be muffled because either there is a pleural effusion, if the patient's got right-sided heart failure, or simply because of their degree of myocardial systolic failure.

So that lack of pump function, which is really characteristic of structural DCM causes often a reduction in the lub dub or S1 and S2 sounds of the heart when the auscultate them. Although this can also be quite subtle. Tachycardia is frequently seen in patients that present with heart failure.

If they're not tachycardic, they'll often have at least, high normal heart rates, and if that patient is in congestive heart failure, they should really not present with a sinus arrhythmia. So sinus arrhythmia in a dyspneic patient will really be inconsistent with congestive heart failure. However, other arrhythmias are really quite frequently seen in clinical DCM patients either because of supraventricular or ventricular ectopy.

So with these guys who want to listen out for whether they have an irregular heart rhythm, whether they have any pulse deficits, and whether or not, their pulse quality is varied, because if they do, that would be, you know, highly consistent with a cardiac cause of their dyspnea rather than primary, respiratory. So with regards to murmurs, we should be very careful and consistent when we're auscultating our large breed dogs for murmurs. And the reason for that is that actually a lot of DCM dogs don't have heart murmurs, OK?

And those that do often only have really quite low grade ones, grades, really 1 through 3, and no higher. And the reason for this is that we've got to remember that DCM is a myocardial disease, a heart muscle disease, it's not a primary disease of the valves. And as a result of that, a lot of these patients either don't have any valvular regurgitation, or if they do, it's very mild.

And normally when they do develop the valvular regurgitation, it's not because the valve itself has changed and has degenerated like in mitral valve disease, but it's actually because of the enlargement of the left ventricle, stretches the mitral annulus, causing a failure of coaptation and a little bit of regurgitation in those patients. So, . It certainly is very different from small breed dogs with mitral valve disease, where they often have a grade 4 or above murmur to be in heart failure, you know, and a lack of heart murmur would really exclude the patient, the likelihood that the patient has mitral valve disease.

So it's very different from DCM. So don't get caught out. By missing low grade murmurs in these patients, because even a low grade murmur in a large breed dog is significant and warrants further investigation.

And a lack of a murmur in a large breed dog does not exclude significant DCM. We may auscultate a, gallop sound, which is, it's not that frequent, but it's an additional heart sound, an S3 or S4 because of diastolic dysfunction. We may detect signs of, forward failure, so, reduced femoral pulse quality, pale mucous membranes, capillary, prolonged capillary refill times, and hypothermia, .

As I said earlier, we might see ascites as well with right-sided congestive heart failure, as well as jugular venous distention. So don't forget to, you know, check, the jugular vein to see if it is, distended and, or if there's any jugular pulsation, which would be indicative of what it's added failure. So we've got a, a patient that is presented with a history consistent with clinical DCM.

And our physical examination points towards that as well. How can we make our diagnosis? Well, We'll talk about laboratory findings initially and then move on to how we're going to image the patient.

So NT Pro B&P is not so useful, unfortunately, in the patient that presents some congestive heart failure, because that has to be sent away to the lab, it takes a few days to come back. We kind of need to know there and then whether or not that patient is in congestive heart failure or not. So Pro B&P is not so useful in this stage.

It's much more useful, of course, for screening those pre-clinical patients. And as I mentioned earlier, there's a nice cutoff that's been published for Doberm and pinches. So if their, NT Pro BMP is over 735 picamoles per litre, that is, indicative of the need for further investigation of that patient with an echocardiogram and or Holter monitor, because, Their increased risk of occult DCM and troponin, so this is running patients with clinical DCM simply to screen for myocarditis.

So, we said that could be a cause of phenotypic DCM a bit earlier on, and if you've got myocarditis, what that tends to do is increase your troponin really quite high, several fold. The top end of normal. So if you do have a patient, that has structural DCM which should pretty much always screen for myocarditis by sending off a troponin, if that is markedly elevated, and that patient has other, clinical, sort of clinical pathological or clinical signs referable to myocarditis, then those patients often will be started on treatment for that myocarditis or, sort of undergo further screening for infectious causes with the extended blood work and things.

Renal values and electrolytes are always pretty important at baseline in patients with congestive failure, because of course they could have concurrent, kidney disease, and these patients are likely to be started on diuretic therapy, which of course can cause elevations in your ear and creatinine, even precipitating in azotemia in some individuals, and of course, will often cause a reduction in all of your electrolytes as well. As we mentioned earlier, we might run a taurine essay if we're suspicious of, nutritional DCM and we might run a T4 and a TSH in these patients as well, to screen for hypothyroidism as mentioned earlier. ECGs are gonna be quite commonly performed as well in the clinical DCM patients, certainly if there is any evidence of an arrhythmia on the physical examination.

And the most common arrhythmias that we're gonna see in these patients are atrial fibrillation, which causes a tacky arrhythmia, that's supraventricular in origin, that causes really very irregularly, irregular heart rhythms, and warrants specific therapy, with digoxin and diltiazem. In order to rate control these patients, but then of course we have a large amount of ventricular ectopy as well, which may come in the form of, Sort of individual ventricular premature complexes or more complex ectopy, which may involve runs or salvos of VPCs as we can see in this ECG on the right, where we have a period at the beginning of the ECG of a thing called ventricular bigemony, where we have a sinus complex, followed by a ventricular ectopic, followed by a sinus, a ventricularectopic, and then we have this run. A ventricular tachycardia here.

So, one thing to bear in mind is that, patients who do have complex or malignant ventricularectomy need to be identified because they also will likely warrant specific therapy. Of their, arrhythmia, as both significant ventricular ectopy, and much more recently atrial fibrillation have been shown to increase the risk, of sudden death in these patients, and, and therefore will likely require therapy. Holter monitors as we used, we mentioned, sorry, earlier on, are commonly used, for a 24 hour period to screen for DCM, to diagnose preclinical DCM.

But we also quite commonly use them when we are treating and monitoring patients with clinical DCM. So any patients such as this patient here on the right who's diagnosed with, a significant arrhythmia and he started in on anti-arrhythmic therapy, might well be followed up with a Holter monitor, to be able to monitor their treatment response for, evidence of reduction of their ventricular ectopy, as well as to be sure that we are not causing any other. Arrhythmias as well, because we've got to remember that every anti-arrhythmic drug that we use is potentially also pro-arrhythmic.

So it's just to make people aware that Holter monitors are sort of not only used to diagnose but also to, to sort of monitor patients as well with DCM. So moving on to imaging of these patients, and this is how we're really gonna make a diagnosis of structural DCM. You know, an echocardiogram is the only way you can definitively diagnose DCM in these patients.

And whilst a full echo should be recommended in all patients, there are a few sort of simple, structural changes that we can look out for, on a basic echocardiogram, or even a thoracic point of care ultrasound, which we refer to as a pocus, to help us diagnose DCM in these clinical patients, or at least increase our index of suspicion. And again, this all comes out of this paper that's on the left, which is the, Proposed guidelines for the diagnosis of DCM in dogs are published in 2003 through the Journal of Veterinary Cardiology, and this is also open access as well. So the things that we're gonna look out for, as I'll show you, in some sort of videos in a second, are increased sphericity of the left ventricle.

So that's increased roundness of that chamber. Eccentric left ventricular hypertrophy, so that is, enlargement of the left ventricle with thinning of the walls. Significant left ventricular systolic dysfunction, which is really one of the hallmarks of canine DCM.

And of course if they've got clinical disease, they will also have enlargement of their left atrium. They will have beelines within their lungs if they have pulmonary edoema on a thoracic point of care ultrasound, and or pleural effusion if they also have, right-sided heart failure. So this is a cine loop of a patient with clinical DCM and what you can see is that this chamber here.

The left ventricle is really quite rounded in its shape, so it should look much more rectangular than this, with much more parallel, walls, whereas this is very much rounded, and the walls also appear. Sort of subjectively thinned, and when we're looking at the pumping of that chamber, it doesn't look like there's a huge amount of excursion of either of the myocardial walls. So this is a really very basic, view, the, the four chamber, right parasternal long axis view.

Which is something that if you are interested in echocardiography or point of care thoracic ultrasonography, is, is one of the first views that you learn. And from this view alone, you can really get a very good idea about whether or not this patient like. He has structural DCM and simply this, this, this single view alone without necessarily even having to take any measurements whatsoever.

And this patient as well has a really subjectively enlarged left atrium and was in congestive heart failure. At presentation. So we can then move on to probably the second most useful view, if you're starting to learn basic echocardiography for diagnosing canine DCM and this is the short axis view from the right parasternal approach at the level of the papillary muscles, and this is an M mode, where basically you drop a cursor through the middle of the left ventricle.

And we measure over time what happens with the interventricular septum, which is this here. This is the left ventricular lumen, and this is the left ventricular free wall. And what we can see is that over time we have a period, for instance, here, of left ventricular, diastole, and here's left ventricular end diastole at the beginning of the QRS complex, and then we have ventricular systole.

And what you can sort of subjectively see in this patient is that there's really not a huge amount of movement of that interventricular septum, and almost no movement of the left ventricular freewall, which is highly suggestive of left ventricular systolic dysfunction. So we can do specific measurements from this view and calculate shortening fraction and use other views, to calculate other indices of systolic function, but I think that's gonna go way beyond, what we need to be talking about today. These are a couple of radiographs of a patient that presented with congestive heart failure and DCM.

And the things that we're gonna look out for here are of course left ventricular and also right ventricular cardiogaly. So, the two most useful views are the right lateral and dorsoventral. And what we see on this right lateral view here is that the back of the heart has a very straight appearance to it.

So it should curve forward gently, the back of the heart and have a much more sort of curved, appearance to the, the left side of the heart. Whereas here it's very straight, and that's because of left sided cardiomegaly, and here, In this region, we have a large bulge from the heart cardiac silhouette, which is the left atrium itself, so highly suggestive of left-sided cardiogaly. And we also see this patient have quite a degree of right-sided carddiomegaly as well, with all this increased sternal contact down here from the enlargement of the right side of the heart.

So we can of course measure vertebral heart scores in these patients. Which is a tried and tested way of screening for cardiogaly, and of course remember that certain breeds have published breeds specific reference ranges to account for, but if you have marked cardiomegaly, in a patient who has clinical signs that are referable to to congestive heart failure, you know, in combination with pulmonary edoema on their radiographs, or pleural effusion, then it's highly likely. That that patient has congestive heart failure, you know, and if they're a large breed dog, it is highly likely that cause of heart failure is DCM.

So ideally, those patients can then be started on failure therapy for their failure, but would be recommended to go on and have a follow-up detailed echocardiogram. Remember that pulmonary edoema can be seen as an interstitial or interstitial alveola or alveola pattern within the pulmonary parenchyma and is most commonly seen in the perihiala region round here. So we've talked about how we diagnose congestive heart failure, what about the treatment of these patients?

Well, it's good old fashioned quad therapy. So there's evidence to support the use of all four of these types of drugs in patients, with structural DCM and congestive failure. And those drugs are the loop diuretic rozamide.

The phosphodiesterase 3 inhibitor Peabendin, an ACE inhibitor such as benazapril, and the aldosterone receptor antagonist spironolactone, and these are the doses, that we traditionally use. So this is very similar. Of course, to how we treat mitral valve disease in congestive heart failure patients.

So I'm not going to talk about it really in any great detail, we'll make a couple of comments. So frozamide, within the emergent setting, we'd always recommend giving it parentialally if possible. If it's given intravenously, it also causes, vasodilation that can help reduce venous congestion in these patients.

So I tend to recommend boluss. I 1 to 2 migs per kg. Every 1 to 4 hours, often after an initial I Ebolus of 2 to 4 Migs per gig if they're informing of congestive heart failure.

And then once we get improvements in their resting respiratory rate, we can start to decrease the frequency of this drug or consider transitioning then onto the oral form, which typically starting dosages would be in the order of 2 migs per gig, twice daily of rozamide. Terazamide is a newer, loop diuretic, which is available, you know, licenced for the treatment of mitral valve disease in dogs, which is something that's not been looked at yet in particular detail in canine DCM, so watch this space. Pemaendin, as we've already mentioned, is one of the cornerstones of treatment of pre-clinical DCM and of course, is, using in clinical DCM as well.

Just do bear in mind that this should be given twice daily, 1 hour before a full meal, to increase its oral, bioavailability. the ACE inhibitors, are given, you know, once daily at standard dosages, and often, you know, in combination with spironolactone, if they can afford, these two drugs as part of their treatment plan. In the pre-clinical guise, really there is just immaendin, that we would tend to use for, the evidence, because of the evidence that it delays, progression to congestive heart failure and doin pincers, and of course we can extrapolate that to other breeds as well.

Of course, if these patients as well have significant ventricular ectopy, they may warrant treatment of that as well. But otherwise, the pimaendin is the drug choice for these patients. With regards to the other treatments, whatever, arrhythmia we diagnose our patients with, that should be treated and monitored appropriately.

As we mentioned earlier, if they do appear to be, taurine deficient, we're gonna supplement, them with taurine, which is, commercially available over the counter at, you know, all pharmacists and, and health food stores, . If we do diagnose myocarditis, then we'll do our best to identify the underlying cause and and treat that appropriately and of course we'll start levothyroxine supplementation for those with hypothyroidism. So just moving on to prognosis, how well do these patients do?

Well, as we mentioned, if we pick them up in the pre-clinical period, they can live potentially for several years before developing congestive failure. However, once they do develop congestive failure, unfortunately, most of these patients will die within 6 months of diagnosis and within DCM Dobermans, it may actually be closer to 3 months from diagnosis, unfortunately. Occasionally though, we will get the odd patient will survive longer than this, which is great, but we have to be very realistic when we're gauging our owner expectations.

And we have to be very clear, in educating clients as well that these guys have, an increased risk of sudden death as well. So, that about wraps it up for this presentation. If you're only gonna sort of remember three things, what should they be?

Well, ideally, remember that there are different causes of DCM other than idiopathic, and that we should be looking for, suspecting and or screening for these types of DCM in our patients. The second would be, an increased awareness of, the sort of prevalence of DCM in its pre-clinical state, and certainly the, the length of the pre-clinical period. And that we can therefore, as primary care veterinarians, maybe increase, our screening, of this, in practise.

In an attempt to try and delay progression to congestive heart failure in some individuals. So an increased awareness of pre-clinical DCM. And then the third thing really is just remembering the importance of a really thorough nose to tail physical examination, in the diagnosis of clinical DCM because really, there are a lot of things on the physical examination that can point us towards a diagnosis of clinical DCM.

And of course we can combine that, with the use of point of care ultrasound these days, which is getting really better and better, with better machines, with wider availability and more training, you know, in, in primary care practise to help, in the detection of DCM in these patients. So many thank you thank you to everybody, for listening. I hope you've got a few top tips to take away from that talk, and I hope to see you again in the future.

All the best.