Thank you so much, Ruth, for this kind introduction. And even though I usually, choose to talk about arrhythmias, because that's close to my heart, I figured we'll twitch it up a little bit. And so tonight or this afternoon, I decided to talk a little bit of some about something that is fairly rare.

So I assume the people who've decided to listen to this talk, either do some cardiology or see maybe a lot of puppies or are interested in trying to help pick up these congenital defects that we're recognising and recommending the proper treatment can make a big difference in the life of dogs and cats affected with such conditions. It's actually a fairly small percentage of dogs and cats that present to us with congenital defects. This is an old paper out of UPenn that looked at the clinic population overall, and they found that it was under 1%.

Cats even like maybe even less than 0.2%. But we do think That we're underestimating the prevalence because as we all know, any litter of kittens and puppies where there's a couple that are poor doers or that died right around birth, we don't do postmortems on these, and so we may not pick up on some of the very severe defects.

Or a dog or a cat doesn't present with a murmur, which is then really difficult to know whether it needs to have a cardiac workup. So maybe we have a higher incidence, but let's just real reality is that it's a relatively small population, but as I said before, if we can pick up on those few, we may make a big difference in in the animals' lives. It's definitely of the heart diseases, it's the most common that we pick up in young animals.

And I listed here just sort of for us as a reference, what are the most common ones that we see. In red I highlighted the ones that I'm going to touch on today as they, those are the most important ones and there's some debate whether prolonic stenosis or subbiortic stenosis are most commonly seen a little bit variation between Europe and the USA where most of the data came out of. PDA, a left to right shunting PDA, is the 3rd most commonly seen defect, and, and then it gets a little bit more rare fairly quickly with ventricular septal defects and atrial septal defects even less common.

And occasionally a malformation of the AV valves. Cats have similar defects, but luckily much less common because it's even harder to help the cats with these. So I'll touch a little bit upon cats, but mostly we'll talk about what we can do in dogs.

A quick step back to the pathop phase because it helps us decide and understand what is the appropriate management strategy. So when we think of congenital defects, we think of sort of two major groups of of pathophys, and one is what we call a volume overload physiology, which is due to the atriovenous shunts, AV shunts, and the other group is the pressure overload conditions which are the pulmonic and aortic stenosis, namely, we will discuss these in the second half of the, the lecture. So volume overload, what is volume overload?

Well, when we think of this, graph here that shows the stroke volume on this axis and the filling here, we have a curve where more filling typically improves stroke volume. It's a nice linear relationship until we get to a point where the optimal stretching, if you want, of the ventricles to contract optimally has been met and after that, too much volume actually results in decreased cardiac output, and ultimately will result in congestive heart failure. The congenital defects that we can see this occur with are namely the left to right PDA causes massive volume volume overload, occasionally a ventricular septal defect or an atrial septal defect, and then a rare defect, the AD canal, which I won't go into today, it's a very complex and very poor prognostic, poor life expectancy, but massive ASD and VSD combined basically.

If we have a dysplasia of the AV valves, the mitral and tricuspid valve, we can also get volume overload because we have so much insufficiency, but that's a different, major group. I'm gonna talk about left to right PDA and the ventricular atrial septal defects next. So what is an AV shunt and what do we need to pay attention to?

There's 3 sort of factors that go into the pathophys. We said volume overload because the blood that shunts from the left side, the part of the circulation back to the right side causes overloading of the structures that are seeing that extra volume. And so when we follow the direction or the the path of the the shunted blood, we can then decide or we can know already which structures are likely gonna see that.

Because of that over circulation or recirculation of oxygenated blood from the aortic side, arterial side, we can see over circulation in the lungs, meaning that there's too much volume going through the pulmonary circulation, causing problems in itself. And the blood is actually already oversaturated and we can sometimes pick up where the shunt occurs by looking at where the so-called step up occurs, where all of a sudden the oxygen concentration increases at the point right after the shunt. An important factor to remember is that how much shunting occurs and therefore how much volume overload is a function of two things.

One, the size of the hole that connects the arterial to the venous size, and the difference between the blood pressure on the arterial side at that site and the blood pressure on the venous side at that side, because shunting wants to flow from high pressure to low pressure. That's where the direction of the shunting occurs. Back to the PDA.

When we look at this schematic up here, we can see right atrium, right ventricle, interventricle septum separating to the right from the left side, left ventricle left atrium. But instead of having a nice separated blue bloods. Circulating from the right ventricle out in the pulmonary artery into the lungs and the aortic blood out here, out the aorta, there is a residual vessel that connects the aorta to the pulmonary artery.

Note that this is an extra cardiac structure. It's an extra cardiac vessel, but it allows red blood that come fracs that came back from the lungs to the left atrium, left ventricle and the aorta. To then flow through this little ductus back into the pulmonary artery and into the venous circulation.

We talked about the following the shunt determines what chambers are abnormal. When we follow the shunted blood here, we see it goes in the PA, goes through the lungs, through the pulmonary arterial vasculature, and the pulmonary venous bed back into the left atrium, left ventricle, out the aorta. These are the structures that are seeing limb overload.

The right atrium and right men don't know anything is going rogue up here, so they're not affected and behind the shunt, the descending aorta and the periphery is not seeing extra volume either. This is purely the structures in here that are involved. Why does the duct occur?

In simple terms, it's a lack of the smooth muscle in the ductal wall to result in functional closure after birth. And I'll have a little explanation about this. We see this in a number of breeds, but certainly some breeds we see overrepresented.

Bicon is one of them. A lot of the other small dogs we see Pomeranians, Chihuahuas, Maltese, Yorkshires, a lot of these tiny dogs which cause a challenge to us because it's harder to get to the right place in a tiny dog to fix it. The other extreme is the German shepherd, who has a very large dice, and it's also sometimes a challenge to close that one.

The poodle is well described in the literature and the occurrence of this lack of closure or this failure of closure has been actually well studied in the poodles who had multiple steps in the embryonic development looked at under the under the histologic . With histology. This is something we see more in the female dogs.

So when we evaluate young dogs in our clinic that are females, make, pay special attention to, trying to pick up on anything that would indicate a dog has a PDA. So how does the doctors, what is the role of the doctors? Why does it even exist and then potentially cause so much complication.

So for this, we can go back to a little schematic that describes the foetal circulation. In in utero, there's no purpose in having blood flow get circulating through the lungs. There's no oxygen exchange, so this is a sort of a, a waste of effort to flow out here.

So all of the blood is sort of trying to get straight out to the, through the aortic side back into the umbilical direction so we can focus on that and then the foetal circulation. In order to allow blood from the right side to not have to go through the lungs, there are multiple paths for blood to cross into that systemic circulation. One is the foramen valet, which is an opening in the in atrial septum, and one is ductus.

Its purpose is to let blood flow from the pulmonary or right side back up across the ductus into the peripheral circulation. This is supposed to stay open. However, in the last trimester, there is a slight thickening in the wall that can be seen if you do transactions and you can see that the smooth muscle layers develop that are later on responsible for this to close properly.

In the last trimester, there's a thick smooth muscle layer that is ready to take action during this, during birth or what we call the transitional circulation. During birth now, we have oxygenated blood available after birth and we don't want shunting from right to left anymore. The pressure, the pressure in the left side rises, so we have a higher pressure here than on the right side.

So we have 70 millimetres mercury versus 50. So instead of the the shunt going through a duct as if it were to be open from the right to the left, it now actually would flow left to right. During the transition.

There is a teen amount still going across. But as the oxygen tension rises through the through respiration and the prostaglandins levels decrease, functionally this this smooth muscle starts to constrict and closes within minutes to hours postpartum. And that's the goal with the normal smooth muscle development, and that's what's supposed to happen.

However, because of this smooth muscle misdevelopment, these ductal cysts can stay open and therefore cause shunting in this direction. That's what's the typical development for a PDA if it stays open. In our clinic, you, you might find that these dogs are typically completely asymptomatic.

So they will come bouncing up and down like any other, other puppy. And if you put your stethoscope on and you pick up this really loud, continuous murmur, a murmur that has, you can't tell when the. It's really the S1 and S2, but a little, signal throughout.

I'm gonna play the sound, the way I was imitate and don't laugh, but it would sound a bit like this. Wow, wow, wow. It's a, it's a loud, continuous.

I kind of think of it as a beach sound, a wave in the background, but it doesn't stop. Like there's, never a time of quiet. So you'll hear a loud murmur, and you would expect the dog to have clinical signs, but the owner will look at you with big eyes when you say that there's a really serious cardiac defect present, because at the time when this is still not causing congestive heart failure, the dogs do not experience clinical signs.

They're shunting perfectly nicely oxygenated blood back into the right and into the pulmonary arteries, and they have normal exercise capacity and no signs. However, that's when it's important for us to recognise what this is on our physical exam. So to know what this continuous murmur sounds like and to look for it really hard, loud, it's loudest over the left heart base.

We have to push the stethoscope all the way up under the armpit and under the triceps to really a scalp cranial, so we don't miss this murmur when a puppy is small and fairly easy to a scalp. If we miss it and the dog goes on to develop congestive heart failure, it is a lot harder to turn things around. If we pick up on this murmur in the pre-clinical stage, and we recommend a workup and a diagnosis is made that this is a DAPDA, we can have an excellent prognosis if it's closed appropriately.

So it's one of the most gratifying defects to find. If a procedure can be pursued that, that closes this doctors because it really can then be compatible with the normal life expectancy for this dog. One other important things besides the murmur to help us identify this important defect.

Here's a sheltie. I tell you that a lot of collies, this is probably a collie or it's a puppy, collie shelties is a breeder we see this a lot. An important clinical finding involves palpating femoral pulses.

The femoral pulse will have what we call a bounding, a bounding quality, and what we, what it means is basically it's a super strong pulse. You've all felt a strong pulse. This is even stronger and strong because we have a large difference.

Bounding basically means a widening of the difference between peak systolic and and the trough diastolic pressure. This happens because this duct is being open continuously in cystole and diastole allows blood to run off into the pulmonary circulation during all of diastole and therefore, the, the lowest the diastolic pressure drops is going to be much lower than in a normal dog. So we will have, instead of what we would maybe think is a normal 120 or.

80 millimetres mercury pulse width, we now will see 120/40 millimetre mercury, so enormous pulse width and therefore a very strong pulse. So a continuous murmur, bounding pulse, you've got a PDA until proven otherwise, and you refer it to, or you do an echocardiogram or refer to a cardiologist to be confirmed and then correct it. Quickly, what this looks like anatomically, and I'll show you some angiograms afterwards.

I'm showing this because we make these schematics that show, OK, here's a pulmonary artery, here's the aorta, here's the pulmonary artery, and there's this connection. It does not look like that really, on a, on, when you open up the doctors. And this, this is sort of just to, to understand that it has a connection, but the connection consists of an actual vessel that's somewhat halfway in the.

Aorta. Here we see the out the outer side of this, and it's like a lip that separates it coming off the aorta. And it, it's, it's more like we call it a the aula of the doctors.

I also, it, try to think of it as like it's a, it's in a teeth of a cow, or this is the teeth, and then it has a little opening, the minimal ductal diameter that determines how much something actually occurs that ends and that opens into the pulmonary artery. So, in reality, it's, and often this is very much in the aorta and very difficult to dissect surgically to get some sort of, you know, room to get around a ligature around this. So that's why we have much better success now that we use non-surgical approaches or we have a good success and a low mortality rate, that I should say.

How will you recognise this if you, if you took X-rays? Before we wanna look at X-rays, I'll just refresh ourselves on what we expect to see in our PDA. Remember we said it's a volume overload.

The structures that are seeing that extra volume will be enlarged on an X-ray or on an echo. And those are the left atrium and left ventricle, the pulmonary artery, and then the vasculature, not the right side. So what I'm showing you here is this, this black dash line would be a normal size left atrium.

With a PDA, it stretches and then in stretching or enlargement of the left atrium will lead to a pushing up of the dorsal dorsal caudal angle of the heart. Or a loss of this caudal waste. So normally it's a nice round shape down here.

The PDA will be bigger and the overall quality of silhouette will be enlarged. In a dorsoventral view, this would be the dash line is the left atrium if it's normal. Here we get an enlarged left atrium, this will be like this double density, and the left ventricle can get massively prolonged in this view and be like a like a massively enlarged left ventricular chamber.

So I'm gonna overlay that with some real x-rays of dogs with PDAs. This is a dog that had a fairly small doctors. What we can see is overall an enlarged cardiac silhouette.

I don't see much left atrial enlargement and not much over circulation, but this is definitely enlarged compared to normal, but only by a small amount. Overcirculation, not that evidence. We see veins and arteries here.

However, a dog that has been subjected to that left to right chunting PDA for a long time will now start to develop massive cardiomegaly, a big left atrium, very prominent pulmonary veins and arteries indicating pulmonary overcirculation. And a dog that was not corrected, and then finally came in with congestive heart failure with a PDA will look like this. You see the cardiomegaly is even more pronounced.

This is still a very young dog, but depending on how big that hole is at the at the bottom of that teeth in the ampula, they can go in congestive heart failure at 8 weeks of age. This dog has now pulmon edoema and a massively enlarged left atrium left ventricle. Large cardiac silhouette on the DV view, pulmon edoema, and big, big, big vessels.

This dog is gonna be hard to get first out of congestive heart failure and then to undergo the surgery to try to close the doctors. So I said, said this before, but the doctor needs to be closed. There's no good other treatment for this condition because you can give them diuretics until you're dried up to the bone or blew in your face.

It will not correct. The hole allows volume overload, period. And if you don't close the hole, it will, it will never get on top of it.

Another important thing is this 01 here. Even if the dog has no clinical signs, and this is a hard one to to sell to a puppy owner who's just bought a puppy and who's in love with it, but has no money, you have to close it even if they're at this time not clinical, because that's when they're the best candidate for good outcome, and it's the cheapest to do it then rather than wait for congestive heart failure to be in the picture, which can which can actually make it so that the the prognosis is not as good. How do we do this?

This shows the device that we use these days. It's a really neat sort of a double disc device that we put in the duct. And with the advent of this device, we have now made this a fairly simple procedure, takes skill to place it and to measure it for the right size, but it's the the risks of this floating away in the wrong direction, etc.

Have gone down dramatically compared to our initial coral embolization. So this is the procedure we recommend routinely now, the canine ductlacluder. And only if a doctor is exceedingly small because of a small size, like in some of these mini Yorkshires or teacup, whatever, their femoral arteries are tiny, like spaghettini I tell owners where you just can't physically introduce the catheter that has to be able to accommodate this device.

Now this is blown up, this is obviously in a in a shape, but in in a catheter shape when we deliver it. The other issue is if it's too large of a doctor like I mentioned before, and the German shepherd, sometimes this won't stay in the place. So I'm gonna show you a couple of angios of how we just deploy a device.

What we're seeing on the left here is a catheter that is come up through the femoral artery. It goes into the, it's coming up along the descending aorta to the top of the heart. Here's the cardiac silhouette.

And what we see here is the wire end of the deployment catheter basically, and here is the bottom of the mushroom, which sits inside the aula, and here's the top of the mushroom, which sits in the pulmonary artery side. And in this video that I'm gonna start playing here in a second, we are releasing that mushroom in the hope that it's gonna stay right there and then lead to a collusion of the duct. So I'm gonna start playing this, and what you can see.

His heart's beating. Oops, we just unscrewed it and released it and now we're watching and hoping that it's not gonna float away. We're gonna replay this in a second here, we'll see.

So we released it and it stays right where it needs to be. So now, this in itself doesn't include blood 100%, but because it's, it's got this wire mesh structure, it leads to a a blood clot forming here that then will ultimately lead to perfect closure of this doctor. This, this part here is actually a transesophageal ecorobe, and when we do this procedure now, we use very little time with the fluoroscopy because we can see this very well through the TEE probe, which is super advantageous to us because it's less exposure to X-ray.

And then we do watch it both on the floor and with the TEE to see and store the, the, the experience of releasing it in case there is an issue so we can replay this. So after it's been set in in place for a few minutes and the blood clo clot has formed, we now do what's called a post-op angiogram. We inject contrast to see if it's actually resulted in perfect closure.

What we're seeing here is the catheter, a new a different catheter. This is called the pigtail catheter. It has a bunch of little holes to allow us to inject contrast agent that doesn't hurt the wall, the way it comes out through little many little holes.

And again, our TE probe is in place here. What we're gonna do is we inject contrast, and we're gonna see the path of the contrast, showing us that we're not showing continuous flow across the doctor. I'm gonna replay it cause it's a very quick thing.

And I'm gonna freeze here right when, oops, all right. So what we're seeing here, the contrast was injected. It goes in the aortic root out the brachocephalic trunk, and here it fills the ampula.

We saw it on the, on the anatomic picture, but it does not cross into the pulmonary artery. It fills up to here. This is perfect closure and this is how we would like to have every PVA get leave the table.

So this is an accom this has accomplished closure of the doctors. This device sits in there quietly and they go home the next day and the only approach is a, a small nick in the skin and into the femoral artery and they go home the next day as if nothing's happened. It's a really gratifying procedure to do.

I'm gonna move on to Another AV shunt, this is the ventricular septal defect. This is a little bit more common in cats than PDAs are very rare in cats, luckily. They in cats we close them surgically because it's too small to use the catheters, so we send it to the surgeons who sweat a little bit when they have to like dissect around that doctor.

In dogs, it is not so common. Sometimes we see this in English springer spaniels and westies, and basset hounds, bulldogs, kitas, but luckily, because the defect is very small, they these dogs usually have no outward clinical signs. They get referred to us because they have a murmur that's very audible.

In cats, it can be a big enough hole to cause signs of volume overload and thus congestive heart failure, and that could be pretty dramatic. How do we pick this up? It's a, it's a physical exam finding again.

It's usually picked up on a puppy exam because it's there since birth. It's a loud murmur, but this time it's loudest over the right side because if we see this schematic here, we see the left ventricle and the right ventricle here, this little hole between the two chambers, and during systole, only during systole, and the left ventricle pressure is about 100 or 120. Millimetre mercury.

The right is only 25. There's a big gradient of for blood that wants to flow from left to right to the low pressure chamber. In diastole, there's no difference.

They're both down to zero, and even though the hole is open, no blood wants to flow across. Hence, we hear a murmur during systole only, nothing during diastole, so we hear. Very loud, usually very audible, loudest on the right, because it goes from left over to right, and And if they're not clinical, then that's all you will find is an incidental murmur on the right.

What causes a BST? A VST is really basically a failure of the interventricle septum to partition the right and left ventricle properly. And the most important BSTs that we see in small animals occur up here right at the base of the aorta, or we call this the perimembranous septum.

It's actually not a muscular area, but it's a sort of a fascia type tissue there, and if it has small little fenestrations, it can result in left to right chanting BSDs. Muscular defects, which would be down in the in the muscular section of the in the septum, are rare. They are more common in large animals, but those are rare luckily in dogs cause they tend to be much larger and therefore would allow a greater volume to go across.

We said it's volume and pressure difference. Luckily, most of these, the size of the defect is tiny and so even though we hear it very well, it's clinically not gonna cause a lot of volume to go over into the right side. If there is a little volume going over, we could see pulmonary over circulation and eccentric or dilation of the left atrium, which is seeing that blood coming back from the lungs, left ventricle, and then the, the volume goes back over here.

So the pulmonary, the aorta doesn't see it, it just goes right across here and because of the location of the septal defect, it flows right out the pulmonary artery. It doesn't really feel the right ventricle. So usually the right ventricle isn't actually dilated with VSTs.

Similar to the PDA, if it's a large defect, we may say, we may see left-sided chamber enlargement on X-rays and pulmonary over circulation. All of that depends on how large the defect is. I'm gonna show you some echoes in a second, what that looks like, and because when it's a small defect, not much goes across, there's not much volume overload.

They have a good prognosis and we don't have to do anything about it. It would be difficult for us, for most of us, to help a dog with a big BSD because it requires cutting open the heart to fix it surgically. This is something that we in veterinary medicine have not really mastered yet because it requires to have an animal go on bypass.

So, I would say most dogs luckily don't require any intervention because we don't have a good way to offer that. There are similar devices to what I showed in the PBA that people are now trying to place trans catheter wise that would not need the the chamber to be open, that may be the future of doing interventions for big BSDs. What, what does the VST look like?

This is an example of a big VST I have to say. This is the rare ones, but I want to show you one that really would demonstrate what we're looking at. So here's the left ventricle cut open, that's the left ventricular wall, and we're looking at the left ventricular chamber here, and here's the aortic outflow, and right below the aortic outflow is this large hole.

It's not supposed to be there. So these are the aortic valves. This is the mitral valve and this is the left ventricle.

When we look at the right side. From the right side, this this defect is actually sort of right below where the tricuspid valve sits, and then the blood flows right out to the pulmonary artery. In this case, I would say that right ventricle looks dilated, so because it's so large, this did result in both the left and right ventricle volume overload.

Obviously this dog didn't do well with it because it was too big of a defect to fix, to tolerate with no intervention. So for those of you who do echo here, I'm gonna show you some echoes of a BST. It's a kind of acute, finding.

You, you look at the left ventricle here, a little bit the left atrium, and here's the aortic outflow and these permembranous BSTs are very high up and right below the aortic outflow and this is gonna this little echo dropout is the BSD. Sometimes we can't even see it on the two-dimensional echo, and we'll have to look at it on colour echo, colour Doppler, which will show us sometimes even though we don't see the hole where there's blood something in the in the in an inappropriate place or blood flowing. So I'm gonna play this, so, oopsie.

This is not looping. So, but what we're seeing here is that little echo drop out during during cystline. This here shows us where there's colour flow, so this isn't looping, no, it's not looping either.

We see that there's flow here going from a high pressure below the aorta to a low pressure chamber, so the flow is going from here to here. This is the VSD flow. It's gonna be a high velocity flow and it's very beautiful to pick up on an echocardiogram.

Moving on to a septal defects, the third defect that causes an AV shunt and can cause volume overload depending on how large the defect is. So the primary lesion is a defect in the angio septum. This is a structure that has multiple ways where it could be remain open.

Maybe first we should talk about the foramen of valley. If the foramen valley doesn't close postop postpartum and remains open a little bit, we call it a patent frame in a valley, and that will allow blood to flow basically in the middle of the septum from the left side to the right. The frame in the valley is basically a a kind of a flop that is supposed to allow blood to flow from right to left, so it's like a door hanging out here, and then after birth when the pressure in this side rises higher to this, it sort of slams the door shut and the frame in a valley flop sort of heals over and closes.

Every once in a while it's not big enough or it doesn't heal over until we have a patent forever. The osteum primumseum, and venosis are three forms of atrial septal defects that are either a primum very low in the atrial septum, adom the most common in the middle of the atrial septum, and then very rarely a sinus venosis, ASD. Again, following the shun pathway, what change, what structures will see this extra shunt volume will also be dilated.

So if we jump from the left atrium to the right, we, we have a small increase in pressure, a small gradient. The left atrium is a little bit higher on the right. So we'll see volume or below to the right atrium.

It flows down into the right ventricle, out into the pulmonary artery, back into the left atrium, across the AST and down here. So the only chamber that's gonna be not enlarged with an ASD is a left ventricle in the aorta. So this is unique in that it causes a big right side.

And this is the one defect that causes a big right side as a congenital defect, the right atrium and right ventricle. Because we have a low difference between the two chambers in pressure, we do not often hear a murmur. And so that is a bummer because no murmur, how are we supposed to diagnose this.

So these get missed until they cause often so much right side overload that they cause right heart failure. And this is to no one's fault. Again, they're not showing clinical signs when they're compensated, and they have no murmur.

So unless you incidentally do an echo or you do an X-ray before the clinical signs have caused congestive heart failure, you can't pick this one up. It's a real problem. What does it look like?

Similar to the VST, so now we were down here in the interventricular septum. Now we're looking at the in atrial septum. We can see there's a big hole here and this would allow a lot of shunting to flow across.

Luckily, in this case, the pressure differential is low. So even though it's a big hole, a low pressure differential will not be as significant in terms of volume overload. Also, for this defect, you can use these devices because otherwise you'd have to open the heart.

Opening just the atria is a little bit less tricky and so that has been done and I have had cases that had surgical closure of big ASDs, but we're hoping that these devices will allow us to use non-invasive ways to close these that are maybe better tolerated and less risky. If they're small, we don't do anything about them, and we hope that they're not causing enough volume overload to ever result in congestive failure. OK, moving on from the volume overload to the pressure overload cases.

So now we have two important ones to know about is pulmonic stenosis and aortic stenosis. And basically, in terms of reviewing the physiology, the pressure has to go up if you have an out obstruction. I, I think of it as a hose being kinked when I try to spray the roses further away, I kink the hose and it sprays fast or further away.

But I have the same amount of volume of flow that has to go out because all the blood that comes into the heart has to leave the heart. So if the resistance is high and the flow is the same, then the pressure has to go up. That leads to secondary pressure overload, secondary ventricular hypertrophy.

Many of these dogs are also clinically stable or are asymptomatic at rest, but when they try to run or to go, for a walk or go upstairs, they have weakness or sometimes even fainting because during a faster heart rate, they cannot provide the amount of flow that's needed to have normal oxygen supplementation. So they have exercise intolerance, and sometimes they can have fainting because they get secondary arrhythmias because the heart muscle is ischemic during exercise and high heart rate, and sometimes even they can have sudden death from arrhythmias because their heart is so hypertrophied and poorly profused. This is a very common defect, and we also see it sometimes in cats.

We see it in a lot of the terrier breeds, English bulldogs, they have everything including PS. The most common type is the valvular type. We could also see a stenosis if there is a ridge below the valve.

This is what we mostly see on the aortic side, or rarely supravalvular stenosis, which is difficult to treat actually. Luckily, most of them have the valvular type which we can treat with the blue valveloplasty and I'll show you what that looks like in a second. Anatomically speaking, it's a valvular malformation that, in fact, the valves normally nicely separating and open during systole, can't, if they are not separated properly at the hinge levels here, they remain fused, then.

It can't open fully during cystole. The Type A is the most commonly seen where these valve leaflets aren't separated properly and so we can put a catheter with a balloon in here and sort of burst it open and therefore maybe relieve the stenosis. Bulldogs in particular can have an aberran coronary artery that wraps around the outflow tract and therefore makes it narrow.

And those dogs have to be treated very carefully because we don't wanna tear the a coronary and cause sudden death during the valveloplasty. These are examples of what we see in the dog. These are massively stenotic valves.

We're looking on from the top, we cut away the pulmonary artery, so we're seeing the pulmonic valve, malformed, sometimes the osteum is tiny, tiny, and obviously these four dogs didn't make it, but the valvular form is the one that we think has the best prognosis in terms of being able to make a difference with the valvloplasty. The hypoplastic ones or the ones from a coronary artery, sometimes we really can't provide a a good treatment at all. Secondary to that obstruction, we said we see ventricular hypertrophy thickening of the wall.

This looks almost like a left ventricle, but it's a right ventricle. It's so thick because of the outer obstruction. And behind the obstruction, we see what's called a posttenotic dilation or a bulge, and you may see that on an X-ray.

I'll show you an example. And together with the auscultation and the and the maybe the clinical signs on X-ray and the physical exam, you may be able to make this diagnosis and decide this needs to be referred and potentially can be treated with the bayloplasty. Now I've said this many times, but I just want to make this a very important take home message.

Again, these dogs may not be symptomatic at all, yet it's up to us as veterinarians to pick up a significant murmur and say, hey, this is not a puppy murmur. Anything over a grade 1 to maximum grade 2 out of 6 murmur, especially if it persists beyond 1612 to 16 weeks of age, this is Not something benign. This needs to be worked up because then maybe it's gonna be amenable to an intervention that's gonna make a huge difference in the life expectancy.

So no clinical signs or exercise intolerance or syncope in worst case scenario, that's when it's obvious to, to pursue an intervention as soon as sooner than later. The murmur has similar to the BSD murmur, a systolic component only, and otherwise, these dogs will have a fairly normal physical exam, a normal femoral pulse strength. So it's other than picking up on that murmur, it may be very difficult to diagnose this if we don't use our stethoscope at the right time.

The very advanced case where we see secondary dilation, a secondary tricuspid insufficiency and right heart failure due to severe long standing outflow tract obstruction, we may see right side of heart failure or ascites in that case. So how's it gonna look like on X-rays? We may see evidence of right ventricular hypertrophy here, the A, which would be maybe increased sternal contact on the X-ray or the bulge of the pulmonary artery that post-stenotic dilation we talked about.

On the DV and this is a very helpful X-ray, I think for recognising, potentially a pulmonic stenosis. We could see that the right lapertrophy results in this nice what's called a reverse D. So it makes this really rounded shape which is totally not.

Normal. And again, we might see a bulging of the pulmonary artery here. We can see where that, where that bulging is seen.

It's because here's the stenosis that's sort of inside the cardiac shadow, but then the pulmonary artery sticks out here, which it shouldn't normally do. So that's what we see on X-rays. On echo, it's by examining the pulmonary outflow tract.

So here we're looking at a short axis of the heart, and here's the pulmonic valve, and we see this narrowing here and on the colour flow. We see this spectral broadening of the colour jet and acceleration of flow, and then we would call, we would put a Doppler in there it has to be a continuous way to diagnose the severity of the stenosis. In this case, we measured the peak velocity to be over 6 metres per second.

That's considered a very severe stenosis. In the interest of time, even though I don't, I know, I know I did start a little bit late, I'm gonna go fairly fast through the Bernoulli. But for those of you who do echoes, maybe just worth quickly remembering the equation.

How do we know how severe this is by looking at the flow velocity? Well, we know that a 6 metres per second velocity using the Binouli equation can be translated into a pressure difference or gradient between the right ventricle and the pulmonary artery, and that then in turn could tell us if the stenosis is mild, moderate, or severe. What what our echo machine can compute or we can do in our head is the Bernoulli equation says we we square the velocity that we measure and then multiply it by 4.

So 4 times the 6.5 times square we end up with a pressure gradient of 170 millimetres of mercury. That's a severe pulmonic stenosis that goes with that image we saw, but we can give you some, some, just hallmarks.

A mild pulmonic stenosis will have a gradient that's under 50, moderate is 50 to 85, and anything over 85 is considered severe. And in cases of severe pulmon stenosis, we recommend the valbuloplasty. We also recommend that we put these dogs on a beta blocker.

This will a little bit diminish them having these bursts of fast heart rates during activity that then sometimes cause fainting. And it also may decrease the myocardial oxygen demand on a daily basis or especially again during tachycardia and therefore spare the heart and we preserve it better to deal with this outflow obstruction. How do we do a valvoloplasty?

So here's some catheters to show you what we do. We inflate these catheters. Here's sort of still frames I'll show you an angio in a second, but we have a catheter come up the femoral vein now into the right ventricle, and then we place the balloon across the pulmonic valve, and we inflate it and we hope that we can make this waste, this little ring here which where the stenosis is pop open and then the whole balloon looks like a big sausage in the heart.

How would that look like? So here's, this is the head of the dog, and here's the tail, and here's the catheter, sorry, the catheter came actually down the jugular vein. I'm gonna replay that in a second.

This, this time we came, we approached from the jugular vein. There's 22 ways to approach it. Let me just didn't mean to do that.

I'm just gonna replay that for one second. I'll try to stop it at the moment. So we had this.

We stop right here, so every place. So the balloon is here in the outlow track and you can see how we're inflating it, and then the waste goes away. And so unlike the previous picture where it looks like, oh nice, you see the, it's obviously a beating part and it's a beating object.

You have to be quick, you have to inflate very quickly and deflate very quick. It's very dynamic and the balloon wants to float out with the blood. So it can be tricky to keep it in place and we usually inflate it a couple 3 times before we say this is as good as it's gonna get.

Our goal is to reduce the gradient by 50%, so, even if a dog has a gradient of 170, we may not drop into the normal range, but we will have made a significant difference in that dog's outflow obstruction, and sometimes the dog goes from fainting every day when he tries to go upstairs to being able to have a normal walk, etc. So, but our goal is to go, of course, below 50 to make it mild, but if we have a severe stenosis, we don't often manage to achieve that. OK, now moving on to SAS, which is the other of the big four that we see, this is a condition we see mostly in goldens.

A lot of the big dogs breeds get this Newfoundland, shepherds, boxers, different, a little bit different manifestations. Most of them are subbalar and a few of them are baler and very rarely do we see a super vallar stenosis. What does it look like?

Here's on the schematic to show this is actually a fibrous ring that forms below the aortic in the aortic outflow tract area. And we look at the valve and it looks nice and normal. So stenosis can make like almost a tunnel of fibrous tissue.

Here's the aorta. This is actually dilated because of post-synotic dilation, similar to what we saw on the PS condition before, but this fibrous ring here, you can see how this would be very hard to balloon this open and fix it because it's a big messy, tight sort of cuff that's causing the problem and it is not easily amenable to ballooning. There's some other examples of what this looks like, a fibrous ring and sometimes it involves even the mitral apparatus, and it is like a tunnel that's a narrow tunnel that we, we can't really easily pop open.

Clinically, same thing. I'm repeating myself, but these dogs are usually asymptomatic. They've just picked up during a murmur, a murmur during a well visit.

If it's really severe, they can have clinical signs just like a pulmonic stenosis dog of exercise intolerance because during high heart rates, they cannot necessarily allow enough blood flow up into the brain. This you will pick up again with a murmur over the left side, loudest over the 3rd or sometimes 4th in the across the space, but the, the aortic stenosis because the aortic valve is situated a little bit higher in the middle of the heart, it might radiate over to the right, so and sometimes up into the thoracic inlet. So this radiates more over to the right and Something that sometimes is helpful is that the femoral pulse might be weak in this condition, as opposed to pulmonic stenosis.

Honestly, the location of these murmurs between aortic and pulmonic stenosis is so similar that many times it's hard to know for sure. It helps to remember the breeds, so I have, absolutely if I see a Rottweiler or a golden retriever, I'll first think it's gonna be aortic stenosis until proven otherwise. But it helps to to do the femur pulse and see if it's weakened with, with a severe aortic stenosis, only with severe though.

The femoral pulse will be weak because the blood takes a little bit more time to flow out across the stenosis, and that makes the pulse rise more slowly and therefore appear softer. Another thing, another thing that's different in pulmonic versus aortic stenosis is that this fibrous ring can continue to develop after birth and get progressively worse until a year of age. The dog may have soft murmur that you think is a puppy murmur, that's a grade 1 or 2, that doesn't disappear but actually continues to get a little bit more, then that would sort of point you towards this maybe an aortic stenosis.

Because of this, we can't clear dogs of congenital aortic stenosis until they're one year of age, because they could still maybe become become an audible murmur until one year old. For aortic stenosis, how do we recognise this on X-rays? That can be actually tricky.

This x-ray shows us mostly that this aortic root is dilated, indicating a post-stenotic dilatation. Because it's a pressure overload, it causes what we call concentric hypertrophy. So it doesn't always make a visible enlargement of the cardiac silhouette until a very advanced stage.

Unlike a PDA, which is a volume overload and eccentric hypertrophy, which we see very soon as stretching here, this could be sort of a normal looking silhouette until it's very advanced. So the X-ray isn't the best test. I'll show you what it looks like on an angio.

I don't have a dynamic angio to show you because we don't do an intervention, we don't really angio these dogs these days. Here's a frame of the normal aortic outflow showing a, a nice left ventricle contrast. It's actually left atrium, left ventricle, and then an open outflow into the aorta.

These are the coronary sinuses. So this is how flow is supposed to go unimpeded. This patient has subbiortic stenosis, so you see the left ventricle and then it buckles down to this narrow waist, and then we have this big sausage behind.

This is the ascending aorta with post-synotic dilation. This is really a diagnosis that you have to make on echo these days. What do we see?

We see sometimes a discrete ring below the aorta. This is very, very subtle in most cases nowadays and mild ta stenosis can be very tricky to diagnose, I have to admit. The subbiotic ridge would be a sort of a a definite diagnosis of subbiotic stenosis and what we see with that is acceleration of flow across the stenosis and sometimes a leak during diastole, so aortic insufficiency, turbulent flow and and And the ridge here would be a definitive aortic stenosis.

Sometimes we don't see that ridge. We see turbulent flow, but we do see evidence of left ventricular hypertrophy. These two mountains here are not Swiss mountains.

These are papillary muscles that are too bright and too prominent for this chamber. This, this chamber is pumping very well, but overall the wall thickness is increased as opposed to a normal left ventricle. To diagnose the, the severity, we have to do again the Doppler and we look from the left side and the long axis here, this is the aortic outflow and you can see here actually diastolic aortic sufficiency as well as the aortic outflow.

And on the Doppler, we can do this same. We do a Bernoulli equation, we measure the peak velocity, we translate that into a pressure differential and we say, OK, this is a severe aortic stenosis and this will this will help us prognosticate for the owners. A mild aortic stenosis, again, is well tolerated below 50.

Usually these dogs are completely asymptomatic. We do exclude them from breeding because we know that mildly affected dogs with a congenital defect can throw puppies that have a severe form of it, but we tell them that this dog in themselves will not be impaired in its activity or excess capacity and will have a normal life expectancy. A moderate stenosis, 50 to 80 is most likely also gonna be normal, so that's the good news.

It's the severe ones that are over 80 that we start to worry that it's gonna impact survival, and if they're over 130 millimetres gradient, they have a high risk of sudden death in the 1st 3 years of life. So that is a very bad prognosis. What causes them to die?

One is that they have sudden death because of ventricular arrhythmias. This shows a quick strip of a normal sinus beat here, nice and PRST and then a round of ventricular beats. If we see ventricular arrhythmias, we are even more so recommending to have a dog be treated with an anti arrhythmic including a beta block or sometimes it could be atenolol or it could be a sotalol if we see a lot of ventricular arrhythmias.

But this means that this dog is at high risk of sudden death at any time. A rare complication we see in patients with subbiotic stenosis is they are a little bit more predisposed to infective endocarditis, where we see vegetative lesions build up on these valves. And the theory behind them being more predisposed to it is that the stenosis creates a turbulence, as you can imagine, if you kink the hose, the blood, the water is sort of more turbulent in there, the blood flow turbulence here.

Well probably destroys a little bit the surface, the sheer stress, and makes it maybe more open and amenable to adherence of thromboemboli. And and therefore these these these like to these vegetations like to sit on the aortic valves. If it's a severe stenosis that's gone for a long time and the heart has developed more and more hypertrophy to try to compensate for this, at some point it will go out and get too tired of doing this, basically, and these dogs can also develop all sudden signs of congestive heart failure and dilation even though they had a chronic pressure overload.

How do we manage them? The beta blockers, and this is really the only thing that we can routinely recommend, even though we don't have good evidence that it makes a difference in the life expectancy. We have no studies that prove that survival is prolonged.

But we do think that reducing the heart rate and those surges of high heart rates during activity does limit a little bit the seizure, the fainting episodes or the excess intolerance. And so we hope it protects the myocardium. More recently, we have been starting to use what's called cutting balloons.

They have little blades, believe it or not, little razor blades built into the balloon, and you can imagine if you blow them up in this tunnel that I showed you and you kind of manoeuvred them up and down a little bit, which happens anyway because the heart's beating as you inflate this. You might be able to cause a little bit of cutting open of this stenosis with this and allowing a little bit of that about to flow out. We don't have much experience with them.

I'm not one to say, oh, anybody should have this procedure, but if dogs are absolutely clinical and owners want to try something, this is something that some centres now offer. And I'm, I, I'm now so my time may be up, so it's up to the, the webinar, masters whether I should finish up. I have a few more slides about right to left ching, defects and, AV valve dysplasia, but it's up to you.

I'm happy to finish up. Yeah, and I think carry on going if people want to leave, they're welcome to, but let's carry on going. So we talked about PDA a lot and we talked about it at the beginning of the talk when we talked about left to right something or volume overloading conditions.

However, a few of these PDAs go a different direction in that they jumped from the right to the left side. How is that possible? It's only possible if an animal has developed pulmonary hypertension to the degree where the pulmonary pressures supersede the systemic pressures.

So now, the flow can go from the pulmonary side to the arterial side if the ductus remains open. What does that do? It results in deoxygenated blood, so the blood from the right side flowing through the ductus right from the main pulmonary artery into the systemic circulation and therefore it never makes it into the lungs, it never gets reoxygenated.

So it bypasses the lungs. What does that do? It makes cyanosis.

There's a couple of defects that we see this. The one I'm gonna talk about is the right to left PDA, but terology of flow is another one that causes cyanotic heart disease, or if you have some complex defects like a malposition of the great arteries, or we have VSD or ASDs that are associated with pulmonary hypertension. Again, where the pulmonary pressure on the right side, the pressures are actually higher than the left, and so deshanting is reversed.

Overall, they have all the same clinical sign, no matter which defect causes to sign on heart disease. They have exercise intolerance and weakness, and they'll have blue mucous membranes. This little dog had actually shunting ASD a right to left shunting ASD and had severe polycythemia.

This is the, the sort of clinical hallmark of a right to life hunting PDA and even though I show you an exam where example where it's very visible, what we see with this condition, what we look for clinically is called differential or caudal cyanosis. The gums are pink, but the preepuse or the vulva will show cyanosis. How is that possible?

Why would only the one end be blue? Well, it's because if you remember the anatomy of the PDA, the duct is actually shuns blood into the descending aorta or from the descending aorta. So if we have deoxygenated blood go from the lung.

Into the descending aorta, then the rear end of the animal will be blue, whereas the blood that comes out from the left ventricle in the aorta and the brachophic trunk is nice and pink. That causes this differential cyanosis. These dogs will have hind limb weakness when they, when they run, they get weak in the back because that's where the blue blood is, so they will sit down and they can't run.

They also can have seizures. Why can't they seizure? The blood gets so thick because the body will compensate for hypoxemia by increasing the hematocrit.

These dogs will come to us with a PCB over 70, sometimes over 80%. So the blood is like a thick slurp. It's like when you do a phlebotomy, it comes out like black tar.

It's really, it's unbelievable that it even flows, but in the brain when it has that thick, thick. Consistency, it doesn't flow enough and sometimes they get seizures from this, secondary to having this high hematocrit. Because we Can't hear a murmur?

We have to do an echo to diagnosis. Why can't we hear a murmur? It's a PDA should make a loud, continuous murmur.

But the murmur is only in the left to right PDA proceeds, because that's where there is a high pressure in the aorta and a lower pressure in the pulmonary artery, and we have turbulent flow from left to right. In a right to left PDA or any of those right to left jumping situations. The pressure of the right side is typically only just slightly higher than the left, and so the blood, the blood flows sort of in a, in a laminar way from right to left and doesn't create a murmur.

So you cannot diagnose this on physical exam, the, the, the type of heart defect. You can't hear a murmur. So you have to go by either seeing this causal cyanosis.

Having clinical signs or picking up on a high hematocrits during it when you do a CBC and you have to do an echo to diagnosis. Very important. A right to left PDA does not get surgically closed.

It will cause the dog to die from acute right heart failure. This dog, this dog has pulmonary hypertension and by closing off this doctor, you will increase the pulmonary pressure massively acutely, and it's not able to overcome that, and that will not correct the problem. So we're down to very cursory intervention as veterinarians.

We basically phlebotomize these dogs. We pull off, if the PCB gets too high and the dogs show to be clinical from it. We pull off a lot of blood to try to get the hematocrit down, and it's actually surprisingly effective.

You pull off and the PCD drops by just a few percentage points and they're now back to being able to do their little routine. Occasionally we have such severe polycythemia that we recommend the cytoreductive agent, hydroxyrhea, or a combination thereof, which the dog that I showed you before with the ASD, he was on a high doses of hydroxyurea to try to keep that PCV from going too high. Quickly, just to show you what the anatomy would look like, we would have a And this is sort of hard if you're not used to looking at angiograms, but this is the aorta and the pulmonary artery is here, and we see contrast going from the pulmonary artery side into the aorta.

And this is only possible because this here is actually the ductus. That's how large this ductctus is. We don't see the cranial aspect of the aorta at all because it's not filling with contrast.

This is contrast injected into the right ventricle, it flows out into the pulmonary artery and across this massive big duct disconnection into the, into the left descending aorta. You can also see something that's typical with with right to left PDAs that's indicating pulmonary hypertension. That's the presence of these torturous vessels.

You remember, heartworm disease is a condition that makes tortuous vessels, it's also pulmonary hypertension. This is very typical, very abnormal looking pulmonary arteries, tortuous vessels, right to left PDA. Nowadays, we don't do an angio diagnose this.

We really do an, an echocardiogram and you actually have to do what's called a bubble study to show bubbles flowing down the aorta after you inject them in the right side. So it's a little bit tricky to diagnose that defect. OK, I have a couple more here, the tetrology.

This is another dog that had the cyanotic mucous membranes. This is where we have a combination of a ventricular septal defect, pulmonic stenosis, a straddling of the aorta over that open defect, and secondary right ventricular hypertrophy. Luckily this is very rare because we don't have much to offer for these dogs.

These dogs have right to left chunting. Similar to the right to left PDA, you can do phlebotomy, you can, use a beta blocker to slow a little bit, the heart rate and decrease the pulmonic stenosis. Occasionally, we can try to pop open this pulmonic stenosis with the valvulloplasty to see If we can diminish a little bit the pressure in the right ventricle and therefore the, the flow from right to left.

This is a, a difficult condition. This would require a complete repair in a person and we don't do that and so we don't have good outcome with this condition at all. Then I could fly through a couple 3 more slides here with AB valve dysplasia.

I want to show you the tricuspid valve dysplasia cause I see this to a breath that's close to my heart. It's a Labrador. We, screen Labradors for this because they're used in a, in a lot of the seeing eye dog programmes, and we try to avoid them going into right heart failure early because of the tricuspid valve dysplasia.

We see mitral valve dysplasia in bull terriers and in some other breeds. Both of these can either early on or later in life result in congestive heart failure. If it's a mitral valve dysplasia, it would be a left sided heart failure.

Spival dysplasia, right-sided heart failure. This is a puppy that had tricuspival dysplasia. It's a bulldog, and what do we see here?

This big pendulous abdomen. This is a dog that has massive ascites because he has severe tricuspid insufficiency and right heart failure. Again, as a puppy, no clinical signs.

A little murmur over the tricuspid valve which would warrant the referral to a cardiologist, it's too loud to be an innocent murmur. It's loudest on the right. The differential diagnosis would be a VSD.

But this is actually a more severe condition. Most of the dogs that have severe tricuspid dysplasia will develop ascites little in middle age or older. We treat them like any right heart failure dog with sometimes just tapping the belly and drugs for congestive heart failure.

I'm not really sure anybody is doing surgical repair of the tricuspid valve at this point. This was offered and tested at UC Davis, and it's really not taken off. I think a movie of the dog with asci does not play.

So we move on to my last couple slides showing what this actually looks like pathologically in the tricuspid valve dysplasia, we see that instead of having a nice normal valve and chordate tendinna, the valve is thickened and the cordate are shortened and the valve nearly inserts directly into an abnormal papular muscle. And a photo of your doc Doctor Buchanan's collection, which is a beautiful collection of specimens of a normal valve with a nice corda here and a thin leaflet, as opposed to a tricuspid dysplasia, which has gnarled edges, it's thickened, and the valve inserts directly into the papillary muscles. So this is tricuspid valve dysplasia.

And on echo, if you pick up a dog with tarcoplasia, it's a beautiful study, because you can see severely abnormal here's a right left ventricle, left atrium puny and tiny, and he has a severely dilated right atrium and right ventricle, and this arcuspid valve here that's sticking out, very abnormal looking, very insufficient. This is from the left side, which is the view that you should do for a definitive diagnosis for tricuspi dysplasia. This is the right atrium.

Again, look at this tiny left ventricle left atrium and mitral valve. This is a massively enlarged right atrium. The tricuspid valve is tucked down to the septum, and it's redundant long dysplastic leaflet here, but these valve leaflets are supposed to meet in the middle and they're not meeting at all, resulting in severe cuspid regurgitation.

This is over long term typically results in right heart failure and the SciTS, and it is not something we can fix, so it doesn't have a good long term prognosis, but the medium term, these dogs can do sometimes quite well. Last but not least, mitral valve dysplasia. It's the one thing that we see sometimes in cats, so I just wanted to throw that in for the cat lovers.

It's a bad condition. Mitral valve separates a very high pressure left ventricle from a low pressure left atrium, having mitral insufficiency would would create a lot of volume overload to the left atrium. And you put that into a puppy or in a kitten, it means that very early on in life, these animals develop congestive heart failure.

If this the valve is so dysplastic that it not only leaks, but it also causes restriction to inflow or microstenosis, it's a double wham and it's extremely poorly tolerated. These animals die very early in life. We diagnose this by echo, but they may come in on, for congestive heart failure, and you might just see a big heart and and congestive heart failure.

You have a very poor prognosis. The mitral valve repair is just up and coming slowly for degenerative valve disease. There's a group in Japan that, some of you have maybe heard that have successfully, been able to start micro valve repair, but dysplasia.

Cases that I'm not aware of that are really being treated at this time. So this is a very, very bad condition and we see this in little kittens too that succumbed to left heart failure early on. That's what it would look like.

Again, here's a signal. Side of a normal AV valve mitral valve, and here's this really gnarly thickened. This plastic valve, and you can see how this would not be able to provide a nice closure and cooptation.

And this is, I believe my last slide, so. I'm ready for questions. I have to take a drink of water here.

Excellent wet your whistle that was very, very insightful and some beautiful, beautiful pictures there. We do have a couple of questions that have come through. Anna wants, or Ann wants to know, how young would you go ahead and do the closures for the PDA with that balloon you put in or the, the stent you put in.

The device. OK. Very good question.

So it depends on how well the dog is doing. If a, if you diagnose this in a 6 to 8 week old puppy, and the puppy is Completely, well in terms of the heart doesn't show massive cardiac enlargement or an X-ray doesn't show impending congestive heart failure. I may say to this owner, you know, he's 8 weeks old, everything is teeny tiny.

Why don't we see how things are in a month or 2 months, and then he's a better candidate for the procedure and it's easier for us maybe to get access. If that same dog, however, has congestive heart failure then and there, then there's no time to wait. So we do this sometimes in 8 week old dogs.

It's definitely easier to do it in a 4 to 6 months old, if that's how long it can wait, but so I think the, the size matters to us to our ability to advance catheters and everything like that, but we do it when we think it's the time is right for that patient. OK. Alistair wants to know, does sub-aortic stenosis continue to develop past a year old or what they've got at a year is basically what they've got for the rest of their life?

Good question. I think in them for the most part, what they've got at one year is what they've got for the rest of their life. However, what they continue to maybe develop secondary to the stenosis is progressive left ventricular hypertrophy.

So because it's constantly seeing that extra pressure load, the left ventricle might continue to get thicker over time. So even though at one. Age, we can say, OK, your dog has moderate aortic stenosis.

This is the diagnosis. I do advise follow-up echoes to see if there is progressive hypertrophy or potentially a need for a beta-blocker institution if we haven't started it at that point. So I do follow up.

If they are a moderate degree, sometimes I don't scan them every year or maybe every other year. And then once they get a little bit older, I may become a little bit more relaxed about the interval. If they are severe, I definitely recommend to see them frequently enough initially to get a sense of the rate of progression.

OK. And then the last question for tonight, also from Alistair. He says, is there a DNA test for tricuspid valve dysplasia in Labradors?

I don't think at this time, I think I listed here that they were looking for a defect on this chromosome 10, but I don't think that we have a definitive test at this point, unfortunately. There are, there are groups working on that and, and that's my hope for all of these defects that I just showed you that eventually we can pick up on this and say, your dog carries this and don't make this mating again so we don't get more offspring with this defect, but to my knowledge, we don't have a definitive DNA test at this time. OK.

Well, Mark and Anna, it's my great privilege to be able to thank you for spending the time with us and some beautiful presentations and beautiful photography and everything else. So thank you very much for giving up your time to be with the webinar vet and our virtual congress for this year.