Thank you all for coming to watch the session, . This is a session that's a little bit niche, I appreciate, but hopefully it is going to give you a bit of perspective on interventional cardiology. We don't really call what we do heart surgery, that implies we're really, you know, like cutting into things and it's it's a bit brutal for us doing that.

What we like to do is access the heart through the blood vessels, through, you know, peripheral vasculature, so it's a very small surgical wound. And that fits with our sort of, slightly anal, very artistic tendencies of, of making a small incision and accessing the heart to do something. Hopefully quite impressive and helpful for the dog.

Along the way we're gonna talk about congenital heart disease, and that is something that you will be seeing in your clinics wherever you are in the world, whatever case load you see, you'll be seeing dogs with congenital heart disease. You will see cats too, but I'm going to steer away from talking about cats because congenital heart disease is just super rare in cats, and if you do have a loud heart murmur in a kitten, it's most likely to be a ventricular septal defect, and in a one year old cat, it's more likely to be something like HCM, so actually, You know, that covers all the, the heart murmurs and young cats, I think that they're relevant. And we're going to talk now about about common congenital heart diseases in dogs and how we can treat them.

Just so you know about what's out there, and, and what you can help your patients with by referring them. So our plan, we're going to define what I mean by interventional cardiology in a bit more detail. We're gonna talk about congenital heart disease and what interventions are available for congenital heart disease in dogs.

We're gonna talk about pacemaker implantation, because these are not young dogs, these are older dogs who can benefit from pacemakers, and we're also. Going to talk about what we can do to help cardiac neoplasia. I'm just going to share one case example, but we do a couple of neoplastic interventions a year for older patients.

So it's not just the puppies that can benefit from the sorts of procedures we do, but you know, the older dogs too. So interventional cardiology is surgical treatments for heart disease approached by access through peripheral blood vessels, and generally we're approaching through the jugular vein, the femoral artery, or sometimes the carotid artery, although because it's quite deep, that's a little bit surgical for me. So we like to go through vessels that we can, we can palpate.

That we can see effectively. We can perform hybrid procedures and occasionally we'll do this where I'll ask one of my colleagues who, is a proper surgeon to open the chest at a thoracotomy, and then we can access either the atrium or ventricle directly with the same kit we'd use to, to access, a blood vessel. So Needle and a modified celldinger approach, or a pulmonary artery maybe, and we'll access that and do procedures that way.

It's not very often we do them, but they're out there and, and, and we can, we can do that in very small patients maybe where we can't get a peripheral vessel or for large implants, again, which we can't fit through a peripheral vessel. Not very often we see cases like that, but it's possible. Here we have an indication of what the jugular vein looks like when we approach it from one of our surgical cases.

So here we can see we've got the the jugular vein being raised, we can identify that and we can access the heart and great vessels through that very easily. And then we take them to the operating room and we access through that vessel to . The large vessels in the chest or the heart, and obviously we can't see once we get inside the chest, we can't see what we're doing.

So we have to use fluoroscopy to do that. So you can see there where I'm operating, we've got the C arm of the fluoroscope, which is getting images, moving X-ray images which allow us to see where catheters and guide wires are. And if we want to see chambers or vessels we In contrast to highlight those on that moving X-ray within the chest.

You can use ultrasound for some things, and we do often place transesophageal ultrasound. And you can do things like close a PDA, for example, entirely using transesophageal ultrasound now. We don't always need to use fluoroscopy to do that.

In humans, when they're doing this, they'll perform some procedures actually using, the patient within a, a magnetic field and. The magnetic field is then used to identify where the metal catheters are moving around in the vessels and in the heart, and it'll generate a 3D model on a computer to see where they are. So they actually will sometimes use that to just virtually image the whole thing, and they won't use any X-ray or any ultrasound at all.

We're not there yet, although it has been done in veterinary patients. I saw that sort of thing done in a horse recently, so it is possible to happen. So we get into the vessel using a vascular access sheath.

This effectively is like a fancy intravenous cannula. So we place that often we'll place a needle first or an IV catheter first into the vessel, and then we'll exchange that over a small wire for this access sheath. And this access sheath has a couple of important things.

First of all, it's got a hemostatic valve, at the end of it. So of course, unlike an IV cannula, it won't just leak blood when you take the, the, the central part out. There is a valve on the end of that and we can push equipment through that valve in order to get in and out.

And when we pull it out, it automatically seals. The other thing is there's a side port, and that side port is where we can use that to, to flush, saline through. We can also take pressures, so if we're in an artery or or something, we can take a pressure from the artery using that without having to place a separate arterial catheter.

Guide wires are used to get through the blood vessels, and they come in all shapes and sizes. You can get these very, very fine wires like the one in the centre here, which we sometimes refer to as a mosquito wire. You can get straight tipped, you can get curve tipped, and you can get things that are actually hydrophilic, which means unless they're.

Wet, they're really hard to handle and really sticky, but when they're wet, they slide through the blood vessels super easily. There's one wire we call the weasel wire, which just weasels its way through little valves and and and hard to reach places. So we have a range of different guide wires available, and we also have a range of different catheters available.

So here we've just got 3 catheters. Which we often use for vascular procedures. One is just a straight tip catheter.

You can see there are little 1 centimetre marks on this catheter. They come out as black dots on fluoroscopy and therefore we can use that to calibrate measurements of vascular size. So if we're choosing the size of a device for a PDA or the size of a balloon to dilate a stenotic valve, which we'll talk about in some detail in a few minutes, then we can use that to calibrate our measurements to account for any magnification that you might see using the X-ray technology.

Here we have a catheter called a cobra catheter because it looks like a cobra snake rearing up, and the cobra catheter will get you into very tight corners. And here we have one called the Bernstein. I presume after after Doctor Bernstein, who first produced this catheter or first used it, it's just like a small hockey stick, which allows us to get round corners into side branches of vessels.

Sometimes we use stents, and we'll talk a little later about using stents for pulmonic stenosis and also neoplastic compression. If we've got a big tumour compressing a blood vessel, we can stent that open. One of the most common times that I use a stent is actually non-cardic interventions where we will place a stent in order to perform a procedure and close off an intrahepatic portosystemic shunt.

Those procedures are non-cariac as I say, but they're still intravascular, which is why I've got a, a lot of experience with doing those. We'll sometimes use coils, and these coils are not just sort of funny looking hairy devices. This is actually a metallic coil, probably stainless steel, but coming up here are synthetic fibres of a material called Dacron, and Dacron is thrombogenic.

So if you place coils in a blood vessel or in an orifice, that will generate thrombosis which will hopefully close that vessel or or orifice. A little bit of a neater way to close vessels is using something called er a a a closure plug, or a closure device. So this one here that I, I've got a picture of, is a sort of uneven dumbbell, so you have a small disc.

And a larger cup And this is actually an AMplatz canine ductal occluder ACDO and ACDO devices are used for closing a PDA in a dog. It's designed specifically for the canine PDA. They're often quite a predictable shape, and this has a very, very high success rate because it's designed for that.

We can use other types of plugs which have different, more even shapes, more even dumbbells if you like. Or two discs rather than two dumbbells, and these things can be used for for different blood vessels to be closed or even things like ventricular septal defects and atrial septal defects in dogs. It's pretty amazing what's out there for humans and we can use that in our canine patients too.

Finally, this is a a a a balloon. Now we can see this looks like a long catheter, but at the very end you can just see there is a balloon that's inflated there. Now this is a very, very tiny balloon, and here we've got a main port to get into the balloon with a guide wire and flush and things like that, and a side port which is to inflate and deflate the balloon.

So what we can do is we can cross a stenotic valve or an area of scar tissue maybe in a blood vessel that needs opening up, and we can open that balloon which is built to tolerate high pressure and it will tear open that stenotic valve or that area of fibrosis. Why bother with all this faffing about? Why not just get our hands dirty and go in there and do proper surgery?

Well, there's much lower levels of perio-operative pain if we can go in through a small incision or even just a stab incision in the skin versus opening the thorax. Thoracotomies are painful, especially median stenotomies, but also intercostal approaches. Because with these approaches, we tend to have to transect or operate on the limb muscle as well.

And if we operate on the the muscle for the foreleg, of course, that patient is moving that, that increases risk of wound breakdown, it increases post-operative pain for for days or even weeks afterwards. A small incision or a stabbing incision doesn't give you the same problem. It's much lower risk, of course, because we're not opening the chest and and accidentally lacerating the vena cava.

You know, if you have haemorrhage at the thoracotomy, I suppose it's easy enough to control because you can put your fingers on it, but equally, it's bad and it can be fatal. We're accessing very small peripheral vessels. If we do something wrong there and we get haemorrhage, well, you know what, you put some pressure on it for 5 minutes or 20 minutes even and it stops, OK?

So it's very, very different to accessing the major vessels in the chest. And also there's much lower risk associated with wound infection or wound breakdown with the procedures we do. If we do experience that, and it is rare, but if we do experience that, it's peripheral and it's much easier to deal with than somewhere that's much more central on the chest.

And, and these things are, are, are real concerns for the patients. There's a much shorter hospitalisation period, as you'd imagine, because of the lower perioperative pain and lower risks associated with these procedures. The hospitalisation period for a cardiac intervention tends to be 24 hours or less.

We have them come in on the morning of the procedure, often they have the procedure, and often by the time we leave them that evening, they probably could go home. We keep them in till the following morning just to monitor them and be sure. But if we have a very stressed patient, we'll just get them out of the hospital the same day.

That is not true for a thoropotomy, they're in for 3 to 5 days. And because it's a shorter hospitalisation period, lower risk, lower pain, the costs are more predictable. Yes, they are more expensive, because one of these plugs that you can see in the radiograph here, this is in a dog's PDA.

This is immediately post-operative, but this dog still has some heart failure after closure, but within a day this heart failure was gone. OK. So closing the PDA here costs us, just for this plug, 1150 pounds.

But now we don't put a mark up on that. So we don't double the price of that and charge it out to the client because that seems a little crazy. Fair enough if you're spending 50 quid on a plate for orthopaedics.

Yeah, people will mark that up. But we don't mark this up in the same way that we mark up those implants for or or or drugs, because the costs are so high. However, because the cost is very high to us, that means, of course, that client is gonna have to pay.

For that device. So when we close the PDA, we're going to charge about 3500 pounds. And, over 1000 pounds of that is just buying the plug.

OK. So these, the costs that we charge for them, they are not high, yield procedures, but they are, expensive to the owner. So because of that, not everyone can afford.

However, because of the more predictable costs, the more predictable hospitalisation, everything else, actually, it's a bit easier for some people to say, you know what, I'm gonna spend 3500 because I'm not happy that an estimate of 3 to 5000 is OK, because maybe it'll come out at 3, maybe it'll come out at 5, and I can't afford the latter. So that's an advantage to people too. Let's think about what congenital heart diseases we see.

I think this paper from Pedro Oliveira, who currently works at Virtual Vet Specialists, he's an excellent cardiologist, and this was published back in 2011 when he was still in training in his residency, looking at the prevalence of different congenital heart diseases in a referral centre. So this was a centre that had 976 dogs presented over a number of years looking at what heart diseases were common. So I'm not talking about prevalence in the background population.

You won't see 35% of dogs you see affected by pulmonic stenosis. Of course that's unrealistic. However, of the dogs with congenital heart disease we see, this paper tells us what's common in Europe.

It's different to the US and some of the older publications are all about the USA. So here we see that the big three diseases in this population of European dogs, it's pulmonic stenosis, which is 35%, subbiotic stenosis at 24%, and PDA at 23%. In some of the papers out of the US it seems to be PDA is the most common congenital heart disease in dogs, but it's still those big three, they're just a different order.

Much lower levels were ventricular septal defect, that was more like 8%. Aortic valve stenosis, which is much less common, tricuspi dysplasia and other diseases. Other diseases, I mean things like complex diseases like tetralogyophaow, atrial septal defects, things like that.

It's less than 1% of all these dogs, so they are uncommon. I see them, but they won't cross your path very frequently. Let's think about those big 3, and we're gonna start with pulmonic stenosis because this is the most common disease that we see through our congenital heart disease screening clinics.

And we see many, many bulldog type breeds affected by this, and also we see a huge number of French bulldogs affected by pulmonic stenosis. So what is pulmonic stenosis? Well, most cases have a valvular stenosis.

So this, you could call this pulmonic dysplasia, if you like. So we have a dysplastic or malformed pulmonic valve where the valve has never opened properly. The valve leaflets don't open normally, they're fused.

OK, so they're like a membrane that instead of having a large orifice for flow, have a much smaller orifice for blood flow to pass through. This means the heart has to pump harder to eject blood to the lungs. And if the heart pumps harder, the heart will hypertrophy.

So the heart muscle will thicken in order to do that. And that's because of the pressure overload. Just like any muscle having to work harder and put more pressure, that muscle will increase in size.

Of course, if we're reducing flower out of the right heart, that means we've got reduced flow through the lungs and also reduced flow through the left heart, because the, the cardiac output from the right and the left side of the heart is matched. So if you reduce the the output from the right, you will also reduce the output from the left. So these dogs have systemic effects of something that you could imagine was just confined to the right side of the heart and the lungs, but, but it's not.

It's a systemic effect. They have low cardiac output. Over time, any hypertrophy of the heart muscle will lead to hypoxia because the muscle mass increases, but the coronary blood flow does not keep up.

You do not get a a a proportionate increase in coronary flow and therefore you've got a heart muscle that's working harder and is relatively hypoxic. So that can cause fibrosis of the ventricle, dysfunction of the ventricle. And eventually these patients can develop signs of heart failure, right-sided heart failure, or potentially with fibrosis and hypoxia ischemia.

Sometimes they can develop arrhythmias. So we do identify that some dogs with pulmonic stenosis will sadly just drop dead because presumably are ventricular arrhythmias. Which breeds get pulmonic stenosis?

Wow, look at this graph, this is something. We think as cardiologists that cocker spaniels have a predisposition to pulmonic stenosis. Now, in this paper, this is Pedro's paper, they classified cocker spaniels as having a risk level of one, cos they're fairly commonly affected by pulmonic stenosis through the clinic of the cardiologist.

Non-pedigree dogs had a third of the risk. I very rarely see non-pedigree dogs come through my clinic with pulmonic stenosis. There's a few breeds, some other terrier breeds, English bulldog, Chihuahua had a 3 times risk.

The boxer dog had a 5 times risk. The French bulldog had a massive increase in risk, 19-fold increase in risk compared to cockers, who I think are predisposed. So Frenchies, we all know they have issues.

We love them dearly. They're beautiful natured dogs, but the poor souls are really afflicted and certainly cardiologists see that as much as the surgeons and the ophthalmologists do as well, and the neurosurgeons. I could go on.

But we see Frenchies a lot through my clinic at the moment, and that doesn't seem to be a trend that's reducing it. A couple of years ago in the UK that the Kennel Club registered more French bulldogs than Labrador Retrievers, which is really something, and that's the ones who are registered as pedigrees, you know, which probably is not the the majority of the dogs that are bred and sold and imported into the United Kingdom. So this is a huge thing that we see.

So what clinical signs do we see with pulmonic stenosis? We hear a heart murmur, and mostly with the stenotic lesions, the louder the murmur, the worse the disease. So if you have a young bulldog come into your clinic that has a grade 1 or 2 heart murmur.

It may have pulmonary stenosis, it may not. The chances are that dog does not have bad enough stenosis for you to need to worry about. So amplitude of heart murmur in a young dog is important because the quieter the murmur, the more able you are to actually shelve that and and not worry unless the dog develops sight.

That does rely upon you having a good auscultation and sometimes with these breeds. The brachycephalic nature of them means you don't get a good auscultation. So do bear that in mind.

If you have a fidgety dog, a chatty owner, and the brachycephalic upper airway noise that's referred, your grade 2 murmur may be a grade 4. OK, so just bear that in mind. If you, if you're confident you've got a good auscultation and it's a quiet murmur, you probably don't need to worry unless it's an animal who's intended for breeding.

We would say a grade 345 murmurs certainly should be investigated. So as loud as the heart sounds or louder, we would certainly recommend investing that investigating that in a puppet. So it tends to to be localised to the left heart base, tends to radiate dorsally up the chest, by which I mean if you listen up in the same room space, it's as loud or louder.

If you listen cranial to the heart base, it gets quieter. So that's typical homonic stenosis, the opposite is true for aortic stenosis. Often these dogs are reported to be asymptomatic, so no overt clinical signs.

The problem with that is if they've had this from, you know, the day they were born, the owner may not notice signs developing. It's only if they have another dog without heart disease that they may say, oh, you know what, actually he's not as active as the other cocker spaniel. He often will exercise, then come and sit by me and the other dog will carry on running.

Another difficulty with the brachycephalic dogs is sometimes people expect they don't exercise so well because of airway confirmation, and that's very difficult because it implies they're accepting a slightly substandard quality of life for those individuals. So exercise intolerance is difficult to assess and I think after a procedure. Over 90% of patients where the owner said there were no signs at all.

Over 90% come back 4 weeks later and they say this dog is crazy, they're a different dog. So I think they are symptomatic, but we just don't know it. Some doctors who are badly affected may have syncope episodes, so episodic weakness or fainting, associated with poor cardiac output.

They may have ventricular arrhythmias, as I said, because of hypoxia, fibrosis of the myocardium. They may even develop right sided congestive heart failure, so jugular distention, pulsation and ascites. There are 2 different types of hormonic stasis that we see.

There are, in the literature listed this, type A and Type B pulmonic stenosis, and Type A is classified as fused valve leaflets. This is the most common that we see in the non-French bulldogs or non bulldog breeds. Type B pulmonic stenosis is common in bulldogs, English bulldogs and French bulldogs.

Subvalvular stenosis is rare. I maybe see one case a year. And that's in a tertiary referral centre, so that's super rare.

Supravalvular stenosis is almost exclusively the preserve of the French bulldog. There was a paper from last year from France reporting 60 or so French bulldogs. The vast majority had supravalvular stenosis, and that fits with our experience in this breed.

We have one that we're doing a procedure on on Monday, which is largely supravalvular stenosis, and the valve looks fine, but it's a very severe case. So what does this look like on Echo? I'm gonna orientate you here because you may not be very familiar with looking at echo images.

Here we have the right atrium, trachus, a bit of valve of the right ventricle. In the middle we have the aorta. And then from the right ventricle, coming up here we have a valve, which is a bit funky looking, and we have the main pulmonary artery, and the pulmonary artery then bifurcates into two.

OK? Now, first thing to notice, the aorta in the middle looks about the same diameter as that pulmonary artery. Therefore, that's a normal pulmonary artery.

It should be about the same size as the aorta. When we look at this valve, this valve is not opening normally, it's like a sort of ridge or a membrane of tissue moving backwards and forwards. So this is a valvular stenosis, this would be a type A pulmonic stenosis.

If we use colour flow Doppler, we can look for the source of the murmur and colour flow Doppler tends to show a green mosaic pattern where turbulent blood flow is, and turbulent flow is generally where the murmur is is localised to. So here we have a green mosaic in cytoly at the pulmonic valve. We also have a leak in the valve in diastole, can you see that, that sort of red leak in the valve.

So this, this is definitely an abnormal valve, we've got stenosis and insufficiency or regurgitation. We don't worry too much about regurgitation, but the the the stenosis is a problem. This is an angiogram, and this shows more globally what we're talking about with pulmonic stenosis.

I'm gonna orientate you here. Imagine it's like a lateral thoracic radiograph. OK, so we've got the spine at the top, the ribs coming in vertically, the sternum at the bottom, and the diaphragm here.

So here we have the cardiac silhouette. That's the vena cava you can see. And this catheter is coming down the cranial vena cava.

Curving ran through the right atrium into the right ventricle where a little balloon is at the tip. And you can see we're injecting dye, we're injecting contrast into this dog's right ventricle. And what we're seeing is the contrast flows forward.

Up to the pulmonic valve, which is here, and then off into the pulmonary artery. There's two things to notice. First of all, watch the valve in the region of the laser pointer.

You can see the valve opens and closes. Almost like a winds sock. You can see how the tips of the valve leaflet are fused up here.

The second thing is that this pulmonary artery should be a tube that runs up here. About the same diameter all the way along to where it bifurcates. And what we can see is it looks like it's wearing a baseball cap.

OK, there's a big dilation of that pulmonary artery before the bifurcation, and that is classic for post stenotic dilation. So this is a dog who's got severe enough stenosis of the valve to have remodelling of the pulmonary artery. It's very unfamiliar looking at angiograms for most people, I, I appreciate that, but hopefully we're gonna look at a few today and you'll get your eye into this.

Just think of it as a radiograph and I'll guide you through. So, There is some data out there suggesting that if we do a balloon procedure to dilate that pulmonic valve, these dogs will live longer than if dogs do not have an interventional procedure. This is a survival curve.

So on the Y axis we have survival. 100% are alive at the start of the study, that's a good thing cos we're looking at survival. And on the, on the X axis we have days.

So just look at this for a second. Some of these dogs are living 8, 10 years. OK, so not all dogs with coronary stenosis have a short survival time.

That's quite important. What's important is quality of life too, and we don't know about quality of life based on this. We just know about when dogs die.

So in these curves here, there's two different groups of dogs, and each step down is when a dog dies. So, the group at the top in green, these dogs have a balloon procedure to dilate that stenotic valve. The group at the bottom have no balloon procedure.

So you can see which group you'd rather be in. Fewer deaths in the balloon group, and when they do die, when they do step down, they step down much later in life than. The nobling group So look at these guys here, they really survival really drops off in the first year or two of these dogs' lives.

There are some who do die from their heart disease like this guy, probably at age 10 here. I don't know what his quality of life was. So I'm not saying that not having a balloon is good cos they survive longer.

Clearly it's not. Have a balloon valvularplasty or recommend a balloon valvularplasty, you're doing the best thing for your patient to promote longevity. But if the owner can't afford it or they don't want to go down that road, it's not the end of the world.

These dogs will survive, however, we've got to think about their quality of life. So quality of life is very important and it's probably improved with a balloon valvular plasty. That's my experience certainly.

So here's what we do. I'll orientate you again. Similar thing, imagine it's like a radiograph.

Spine, sternum, diaphragm. This is the cardiac silhouette. Follow the wire from the cranial cava through the right heart, across the synotic valve and into a pulmonary artery.

And we inflate a balloon. So you can see at this point in the pulmonary artery, there is a stenosis. This is the same dog as I showed you before on the angiogram, so we know there's a stenosis at the valve.

And you can see when the balloon inflates it looks like an hourglass, just here. And then pop. The stenosis opens.

That's the effect of the balloon valvularplasty, and that generally yields positive results for these patients. It reduces stenosis severity and improves outcome. There are procedures that can help called pulmonic stents, and this is something we've been pioneering really in the UK.

There are 8 cases reported from the USA. Ah probably more have been done than have been reported. We've just got a case series of 15 dogs in press looking at outcome, and we've found this is a well tolerated procedure.

For dogs who have type B pulmonic stenosis, or have weird things like coronary artery malformations which prevent normal balloon procedures. I'm not going to go into any detail just to say that this is something that's out there, this is what they look like. We inflate the balloon in the same way.

This strange alien thing here is our transesophageal echo probe. So we inflate the balloon in the same way, but when the balloon deflates, if you watch what happens when we deflate. You can see on the outside of the balloon is a scaffold, that's the stent, OK.

So you can just see it emerging there as the balloon deflates. And we're leaving the stent in position. And here is what it looks like after the stent is deployed.

Nice open pulmonary artery. So stents are possible, and I think they that you need quite an experienced team to do them because they're a little bit challenging, but these dogs tend to do fairly well. Aortic stenosis is the next most common congenital heart disease in dogs.

This is a very sleepy looking dog to Bordeaux. I promise it's definitely a sleeper and er alive. Most cases of aortic stenosis, subaortic stenosis.

So here, if we look at the diagram, we have a ridge of fibromuscular tissue below the aortic valve in this case. This is an interesting disease because it isn't always there at birth. Often what seems to happen is it gets worse over the first year of life.

Now we still believe it's congenital, we, we believe that there's something in the outflow tract of these dogs that promotes the growth at birth, so we call it a congenital heart disease. The narrowing forms around the the outflow from the left ventricle, between the mitral valve and the septum, and it thickens and becomes fibrous in this particular area which narrows flow. So the aortic valve is normal in these dogs.

It's this ridge below the valve. Has the same pathophysiology as palmystenosis. We get a pressure overload on the ventricle, we get hypertrophy of the ventricle hypoxia of the ventricle, fibrosis, arrhythmias, heart failure signs, and all of this caused by reduced cardiac output.

Breed predispositions to aortic stenosis. Well, there was a reason that I put a dog to Bordeaux on there, because the risk is 11 compared to the lower risk dogs. Now I think of German shepherds as being predisposed, golden retrievers, Newfoundlands.

These are all breeds we see in our clinic. See how uncommon it is to see this in a non-pedigree dog. Again, I don't often see this in non-pedigree dogs or cross breeds.

What clinical signs? Well, they have a left sided heart murmur again, we see very mild cases of aortic stenosis that live into old age, they often have a low grade murmur, grades 12. Again, grade 3 murmurs in young dogs are things to investigate.

And don't forget with aortic stenosis, it may not be there at first vaccination, or it may be quiet at first vaccination, and then it may be present when you see them at 1 year old, you may have a much louder murmur, OK, because the stenosis gets worse over the first year of life. This tends to be at the left heart base again. So if you palpate the thorax, the apex is where you feel the apical impulse, and you just go a couple of those spaces cranial to that, and that's the heart base.

OK. So it's the more cranial point of auscultation on the left. These often radiate cranially.

So with pulmonic stenosis, I said move your stethoscope dorsally up the thoracic wall and it's as loud or louder. That's not true with pulmonics with the aortic stenosis, sorry, with pulmonic stenosis, you move up the chest and it's the same, but you go. Cranial and it gets quieter.

Aortic stenosis is the reverse. You go cranial, it gets louder. So this will often radiate cranially.

Sometimes it's even loudest at the right side because of the course of the aorta wrapping around towards the cranial right thorax. OK, so these murmurs can be a little bit different to where you'd expect them to be sometimes. Left base and right base is almost certainly aortic stenosis.

Left base only, getting louder as you go up the chest, is probably pulmonic. Again, murmur intensity is associated with worse disease. Quiet murmurs are less likely to be important in these patients.

So when you come up against owners who don't want to investigate further, or you haven't got access to see a cardiologist easily, or there are financial restrictions, quiet murmurs should provide you with some reassurance for the vast majority of these cases. They have exercise intolerance, they have syncope, they have arrhythmias, and heart failure, as I said, it's the same pathophysiology but on the other side of the heart. We can see subvalvular stenosis and valvular, but the subvalvular stenosis is most common.

So here is a dog with a subvalvular aortic stenosis. I'm just gonna see if I can get that video to run. Here we go.

So we can see this is the region of the aorta, that's the aortic valve, and there's this horrible, thick ridge below the valve. And look at how white the heart muscle looks here and how white this is, very fibrous in this region. So you can see that the diameter of of the the outflow should be about the same as the ascending aorta.

So if we look here, you can see the diameter there. It should be the same down here, but it's not. It's much, much smaller indeed.

This is the same dog. And we can see that in short axis we've got the left ventricle here, the right ventricle here, and you see this bright white ridge of tissue around the heart, around the endocardium. That is ischemic fibrous tissue.

So this is a ventricle that's really struggling and unhappy, and this is a very high risk patient. So here's an angiogram of aorticcaflate. So what we've got.

We've got a catheter coming down the carotid artery now. This is a marker catheter. You see the dots telling you 1 centimetre?

They're coming down the carotid artery through the ascending aorta, through the valve, and this subvalulars is into the left ventricle. So you've got the left ventricle outline here, this is where the mitral valve is. You can see a little whiff of mitral regurgitation if you look carefully, sometimes these are very beautiful images for me.

And then here below the aortic valve is a very big ridge of tissue. I think this is the same patient as we saw on that echo, OK? Again, the aorta seems to get wider here than I'd expect.

I'd expect it to say about this diameter all the way around, but it gets wider. So that's a post stenotic dilatation, just like in the pulmonary artery. And we can see the normal anatomy here, brachycephalic trunk, left subclavian artery, arch and descending aorta.

So you can also see, so these vessels curving around, these are the coronaries. So this dog's got coronary anatomy that you can see very, very clearly here. So what can we do for these guys with sub aortic stenosis?

Well, we can do a balloon procedure, it's a bit different to a pulmonic stenosis procedure where we just want to pop open a valve that's fused. This is a ridge of fibromuscular tissue below the aortic valve. So we actually use two balloons in sequence.

First is called a cutting balloon. Second is a high pressure balloon. The cutting balloon is very specially made so that when it inflates, some sharp wires or razor blades are exposed on the outside of the of the balloon.

Now when the balloon deflates, the balloon itself folds over those sharp areas. So therefore you can insert it and remove it very, very carefully without damaging the blood vessels as you go. But when you inflate it, there's these sharp wires, these razors exposed, and that scores the tissue, scores that scar tissue in the outflow tract.

Then we deflate it and remove that. This, this is the cutting balloon, it's very small. Then we place a high pressure balloon, much larger, and if you watch the high pressure balloon here, you'll see it fill up, and it actually just stretched the outflow track there.

I could just see it go, but it's very subtle compared to the pulmonic balloon that we saw before. So if you watched on the inflation, you'll see a little dent in the balloon about here. That just disappears, OK, and when you're in doing this, you can actually feel that go, you can feel suddenly the pressure increases, and then it moves again because you relieve the pressure in the outflow tract.

Hormonic balloons are much more well established. Aortic balloons are are much less commonly performed. They're quite a recent procedure, and the difficulty with that is we don't have great long-term outcome data for these dogs.

What I can say from my experience of doing maybe 20 balloons over the last 5 years is that these dogs have a huge improvement in clinical signs. Aortic stenosis patients can often live into middle age or old age without any treatment. And I don't know if these balloons improve longevity, but they sure as heck improve clinical signs.

So if you've got a dog who's very exercise intolerant, that dog will be running like a puppy after one of these procedures if you've sized the balloon right and, and, and, you know, done it carefully enough. I don't know what happens 23 years down the line. Sometimes these stenosis will reform, not all cases, but some of these stenosis.

Reform after this procedure, and some dogs do develop aortic insufficiency and therefore can be compromised because of that in the future. That's not so common, but they are possible. So this is not a procedure where we have all that data I could show you for pulmonic stenosis.

It's quite new and therefore, you know, we don't use it in dogs who are who are really very well or borderline cases of stenosis. We use it in the most severe stenosis or the very overtly symptomatic patients. Payton darteriosis, they're often quite cute, these guys, bit cuter, than most of the other dogs we've talked about so far.

We've got Pembroke Welsh corgi here called Violet, but, we, we do commonly see this in in terrier breeds, toy breeds, spaniels, and we don't see it so much in the bracky breeds like the stenosis lesions. So very different now, what's happening with the PDA, a pain ductus arteriosis, compared to the stenosis lesions? Well, here we've got a vessel, the ductus arteriosis, which connects the descending aorta to the main pulmonary artery.

Now in the foetus, that's really important because it blood flows through it from the pulmonary artery into the descending aorta, and that allows blood to bypass the developing lungs because it's pointless perfusing them, because we're not breathing air at this point. And it, it helps with the, the normal foetal circulation and priority of oxygenation. In a proportion of dogs, it doesn't close, and that's because there's not enough smooth muscle present in the artery.

It is hereditary, it is familial, and we, we know there's genetic defects behind this, although that must be very complex. But what happens, it tends to partially close at one end and be open at the other, which gives this funnel-like shape. So on the diagram here, it's deliberately shaped like a cow's teat or a funnel or a finger, and that's exactly what they look like.

You'll see the angiograms that we we use. Now, it flows from the Aorta to the pulmonary artery after birth because of the changes in pressure. So this doesn't actually protect the lungs like it does in the foetus, it over perfuses the lungs.

And if we over perfuse the lungs, the blood's going from the aorta into the pulmonary artery, into the lungs, back to the left heart. The left heart is what fails, OK, so the right heart, we might call it left to right flow, but the right heart never sees this, and the left heart becomes overloaded and they develop heart failure because of that. So the left heart becomes overloaded and we see these dogs with pulmonary edoema sometimes in very young, at very young ages.

Some important statistics about this, the one year survival is around about 50%. So if you find a heart murmur that's super loud in a young puppy, that could be consistent with the PDA, you need to investigate that. Don't just wait and see because they might be dead by the time you get around to investigating, OK?

If they're left untreated, almost 100% of them go into left-sided congestive heart failure to develop pulmonary edoema. And females have a a sex predisposition to this, so there's a 3 to 1 ratio, girls versus boys that are affected. That obviously comes down into the genetics of it.

We often see with things like pulmonic stenosis, aortic stenosis, a mild male predisposition. So the breeds that are predisposed to PDAs, this is one where we do see crossbreds represented, and I especially see this in particular crossbreds that I'll mention in just a second. So poodles are historically called predisposed.

Irish setters that has a ratio of 1. The non-pedigree's only got a 30% risk reduction compared to these dogs we consider predisposed. So I see it in crossbreds and non-pedigree dogs all the time.

I've seen it in staffies and you know what staffies are like, there could be any, any, combination of dogs. We do see them in small breeds in large breeds, we see them in toy breeds like Pomeranians, Maltese, Chihuahua. We see them in spaniels like the, cocker spaniel, the cavalier.

We also see them in big dogs like Newfoundlands, shepherds, Dobermans. So it seems fairly indiscriminate. In the last 5 years, I have commonly seen them in cockapoos.

Don't forget, it's a cocker spaniel that get PDA cross with the poodle, that get PDA. So we see them in cockapoos. We see them in, in Kaappos, and we see them in these bichon crosses.

As well. So these are dogs that we, we, you know, by crossing them, we do get some hybrid vigour. That is true.

There are advantages in crossing those breeds. But I think we see quite a lot of heart disease in those dogs. That's just my personal feeling, so don't really call that science, but it's just something to to remember.

So the anatomy of a PDA, I drew the picture before, if we look where it is now, we've got the descending aorta, the pulmonary artery, and this is where it comes on a radiograph. So think about that, when we auscultate, we auscultate here over the apex, we auscultate here over the base. So The PDA's up here.

So don't forget to auscultate dorsal in puppies. Auscultate dorsal to the heart base and also push the triceps cranial. Sometimes this murmur radiates really far forward behind the triceps muscle, so you need to really lift that, that left front leg forwards.

What I like to do in puppies is actually, when I examine them, and I recommend all first opinion vets do this. Use the palm of your hands, put it under the dog's armpits, lift them up like that, and the owner can be chatting about what the breeder told them, and the dog can be wriggling and it's not great auscultation conditions. But many of these dogs have such a loud murmur that it's a grade 5 or 6, you can palpate it, and that's where your palpate is under the armpit, not where you might normally auscultate, which maybe, if you're in a rush, just down here on the left, you may hear a little quiet murmur and you'll say, OK, you know what, little murmur.

I'll just chalk this up to this being a puppy, and we'll see them in 6 months. Dog comes back in 4 months in heart failure, you're gonna feel pretty bad about that and wonder what's going on. But actually some of that is avoidable if you palpate or do a more thorough auscultation, which can be challenging.

So we're gonna listen to a PDA murmur. Hopefully you'll be able to hear this OK. I'm gonna change my pointer first before we do.

I apologise for that mobile phone interference. It's actually not my phone. It's on the recording.

What you can hear is a murmur that doesn't stop. You can hear it through sisterly and dastily, and when I first heard these, I imagined wind blowing through a tunnel. Mhm Most hot moments you hear are sounds.

And it's not like that. It's much sort of more hollow than that, it's less coarse. And if you're not expecting that, you might think it's respiratory noise.

I don't know how many PDAs I missed when I was in first opinion practise. Over 6 years, probably a couple. I found a couple too, but I probably missed a couple.

So ausculate cranial, palpate with the palm of your hand up behind the triceps, and listen for that wind blowing through a tunnel. OK, most of them are grade 5 or above. They can be really focal if it's a small PDA and they can be challenging, but if it's a small PDA it's less to worry about and there's more time to assess it later on.

So looking at the anatomy here just to show you again, we've got my schematic. This is an angiogram on the right. We've got the aortic arch.

We've got the pulmonary artery behind it, and we've got the PDA coming from the aortic, the descending aorta, sorry, down to the main pulmonary artery like a finger or a cow's teat. OK. So you can see the anatomy is not that far from my bad schematic I've drawn here.

So, what are we looking at when we see it on an echo? Well, this is a view that, you know, you're probably not hugely familiar. We've got the right heart here, got the pulmonic valve here, so similar to what we we saw before.

Pulmonary artery comes around, you've got one branch. It's actually another branch just here, and then that is the PDA. OK, so the PDA is this conical or finger like vessel that comes down onto the main pulmonary artery.

It's much easier when you put colour on there. I'm sorry this colour box moves halfway through the video, it's a bit distracting, but let's focus on the anatomy. We can see we've got this finger light projection here.

This is laminar flow, this solid colour. OK. And laminar flow is normal within the PDA cos it's coming off the ultra, it's just a vessel, then it hits the small hole.

As the vessel constricts down to where it inserts the pulmonary artery, hits a small hole, sprays out as a big green jet, OK, into the pulmonary artery. So flows going from the bottom to the top in this image, and that green, like I said before, is where the murmur is located and it's continuous flow. It's not just systolic, it's.

Systolic diastolic. And that's what the flow looks like, well that's what the sound looks like. So we've got a peak in cytoly, diastole, systole, diastole, cystole, diastole.

It's one of these old drawings of a factory roof, isn't it? You know, it never goes down to baseline, so this is a continuous flow from your ulster pulmonary artery. How do we treat this?

Why have we got to close the vessel? If you know a really good surgeon, you or, or a good, really good surgeon yourself, you may have closed these. I've closed one, poor boy, I shouldn't have done that.

But that dog back in the day when I was in practise, couldn't be referred. They couldn't afford it. I knew we had to close it.

I knew what was going on. So we did. We opened the chest and we closed it.

It went fine. Everything was really good, and I got lucky because I was never that good a surgeon and I've seen excellent surgeons lose these guys on the table. Overall, the mortality rate's about 1 in 10 for open chest surgery.

Mortality rate for these procedures is less than 0.1%. It's Very, very low indeed compared to surgery.

But if you've got a really good surgeon, and a good surgical team, sometimes something bad can happen, the doctors may rupture and they'll they'll get the dog back. OK, so it's not the end of the world, but in many centres these dogs die, and just a couple of weeks ago, one of my excellent, excellent surgical colleagues lost the dog on the table. One of my cases, and, you know, he was beside himself.

He was gutted. He's a brilliant heart surgeon, a vascular surgeon. He's got huge amounts of experience.

The death of that dog really knocked his confidence. So don't go just trying those out like I did. Learn from my error, and, you know, try, try and, you know, speak to an experienced surgeon about you or get someone to come and help you if you do need to do one because they can't be referred or whatever.

Surgical approaches are necessary for some of these, not all of them are suitable for occlusion using a a device like this. Most of them are because most of them form a cone with a small hole you can put a plug in. Some are just a tube, and these tubular PDAs, very common in German Shepherd dogs, these tubular PDAs, you can't put a device in there and therefore you have to do it via traditional surgical means.

So in most cases we can place this ACDO device that we looked at before. In some cases we use a thrombogenic coil, these hairy Dacron coils, and this is about as good as surgery but with a much lower mortality rate. So with a properly designed plug like the ACDO 98% have an immediate complete occlusion.

Most of them are occluded 100% after a few days. Thrombogenic coils, about 75% of them are completely occluded, but the ones that don't. Completely occlude, often just have a little bit of residual flow and therefore are not clinically important.

So most of them have a resolution clinical signs and and normalisation of the measurements on the echo. So here's a PDA in slow mode. So we can see we've got a marker catheter coming from the femoral artery up the aorta round into the arch.

So the injection of contrast is here. You've got the arches are pacified, and then the pulmonary arteries are pacified and. Between the two is the PDA, the persistent ductsulteriosis, so you can see it coming down here.

Onto the main pulmonary artery, so look again, you can see the jet coming through it, which are pacifies that pulmonary artery. And here's a little summary video of us closing one. And this is a few years ago now, so the video's not the most amazing quality, but it has got all of the elements in it to show you the occlusion.

Watch the device come out, got 2 discs. So that's the distal disc, that's in the pulmonary artery, we're pulling it back. Up against the hole in the ducts, so we're pulling it back up so it contacts there, and then before we put the cup out, the little waste on the device, we want that waste to sit perfectly across the hole.

So now we're releasing the cup. We're pushing that into place just now inside the PDA. So we've got the distal disc in the pulmonary artery, the proximal cup inside the PDA.

We don't always inject contrast, but you can, if you fancy it like that. You can see we've got a little bit of residual flow, but the device looks like it's in a good place. That residual flow is not worrisome to me because normally when we release the device by unscrewing the delivery cable, which is what's gonna happen now.

That residual flow is absent, OK, so when you release it to, to go back to its natural confirmation that where it wants to be, there's not enough residual flow to worry about. You see there's a tiny whiff of residual flow just there, but actually it was occluded very nicely. And that's what it looked like on a post-op radiograph.

This is not the best radiograph that I've ever seen of one, because actually this suggests the device is a little small for any of you aficionados out there, but, but you know, I, I don't like them to look like that. I like them to look slightly more sort of rounded and under pressure because that suggests they're in there, but this dog did absolutely fine. Potential complications, well, have a look at this radiograph first.

Sometimes you can lose a device. This dog is a very valuable dog now because not only have we got one device nicely in position, you've got another one in a pulmonary artery. That's not where we like it to be.

It's better. Being in the aorta, because if you embolize an aorta, that's bad news for, for everybody, especially the dog. But if it drops into the pulmonary artery and you lose it in the pulmonary artery, you know what?

Most dogs are fine. However, it's not going to be great for their lung blood flow. So it's not ideal, but it's a complication that often dogs cope with.

Haemorrhage from the cytovascular access is possible, much more minor complication, a bit of a hematoma on the femoral artery, that's fine. We just like get the vessel, tends not to happen. When you close the PDA, changes to hemodynamics can cause a bradycardia, a vaguely mediated bradycardia.

Again, most of the time it happens, it reassures us that we've closed the PDA. But sometimes those cells can get really bradycardia, heart rates of 20, you know, after closure, in which case we need to give atropine or glycopolate to drop that vagal influence and normalise the heart rate, OK, so it's something to be aware of. There's a very low proportion who will die suddenly post-op.

These dogs are almost exclusively dogs that are adults were in heart failure prior to the procedure, and often these dogs, had things like atrial fibrillation or ventricular arrhythmias prior to the procedure. So we presume they're arrhythmic deaths, we, we don't know. Every cardiologist who does enough of these has seen one.

I've had one. I had one dog crash on an induction that had atrial fibrillation and heart failure for ages before closure. I think most cardiologists have a story of one or two dogs over their career this has happened to.

So together there's a, you know, a fairly large number of dogs it's occurred to, but as a proportion of all the dogs who've had this procedure performed, it's incredibly tiny. Coal embolization is something we can do for very tiny patients. It's much cheaper than the ACDO device, but if you have a big PDA, you need lots of coils.

So the cost can add up. It can be very time consuming to put lots of coils in. And the problem is that often these coils are more slippery, you can drop them in the lungs, you can embolize a lung.

Some dogs, because of this sort of thrombosis causing sheer stress on blood vessels to the PDA if they don't completely occlude, can develop hemolysis, which is bad. Hemoglobinuria, renal failure, that's not a great situation. And sometimes you can put coils in, but it's just not enough.

I tend not to do them in big PDAs. I tend to only do them in very tiny, tiny tiny PDAs where you just put one coil in and it's closed. OK.

You can also use transvenous plugs. We can use these in smaller patients. It's also cheaper than an ACTO.

They're about 850 pounds rather than 11 or 1200 pounds. And you tend to go retrograde through the right heart to do these two approaches. The smallest one we've ever done using a transvenous plug is 1.8 kg.

I think the smallest one I've done with an ACDO is about 3 kg. So here what we've got is we've gone backwards through the PDA if you can see that. We've gone through the right heart from the femoral vein.

Through the vena cava, the right heart, pulmonary artery, into the PDA into the aorta, so there's the PDA. Here we're putting a coil into that PDA. Bit messy this one, but it's real life.

Coil's in And then we unscrew the coil, just like we unscrewed that plug before. And leave it in place. I think you're seeing it unscrew now, it's just a little bit longer video than I anticipated.

Yeah, call's in place now, closing that PDA. That dog was nearly 2 kg, I think, and here's the angiogram posto collusion. You can see that PDA is nicely occluded there.

We're gonna briefly talk about other interventions. We're gonna briefly talk about pacemakers, and also, for neoplastic, compression. So this is a West Island white terrier.

They commonly suffer a condition called sick sinus syndrome, which can make them collapse or appear weak. This poor guy hits his head on the table, poor lad, but he was fine, didn't fracture a tooth or anything. This is a a Brady arrhythmia called 3rd gravy block.

You can see the heart rate's about 30. QRS complex, P, P, P, P, PQRS, P, P, P, P. There's no relationship between the Ps and the QRS's, there's a complete atrioventricular block here, and this is much more.

Common in large breeds of dog. This is 6 sinus syndrome, which is very common in West Highland white terriers or miniature schnauzers. And in six sinus syndrome it's pretty crazy.

You have tachycardias here, you have long pauses in bradycardias, you even have AV blocks. So this is a very weird arrhythmia, it's not just the sinus node that's affected, although the name six sinus syndrome sometimes makes us believe that there's other parts of the conduction system are unhappy too. Both of these are indications for pacemakers because they both cause significant amount of clinical signs.

With the grey block they may experience syncope, but often they experience heart failure if left untreated. They can experience sudden death. 6 sinus syndrome don't tend to experience heart failure or sudden death, but just like that video of the Westie, you saw that it can be really inconvenient to faint 1012 times a day.

So we like to put a pacemaker in. And what's happening here is we're placing a pacemaker wire lead down the jugular vein. Through the vena cava into the right heart and attached into the myocardium of the right ventricle, and then we connect that to the brains of the pacemaker called the pulse generator, which is the battery as well and the little computer that runs it, and that's in a a pocket under the homo transversarus muscle up in front of the scapular spine.

So this is the region we operate on, we isolate the jugular vein. And here we advance the pacing lead down the vena cava, into the heart, into the ventricle. We check the position of that electrically, and then we have a second incision and we turn all this through, so these dogs have a couple of surgical incisions, but the pacemaker then is not in the neck where you might have damage or or or whatever from dogs playing or or exercising, but it's hidden up just on the shoulder.

Not a great image here. My complications slide. I remember this case, this Labrador.

He pulled the pacemaker out because he kept scratching at it and coiled this round in humans, they call it twiddler's syndrome because people will sometimes play with it idly and absentmindedly and rip it out of their myocardium if they do so. And this dog scratched it, scratched it, scratched it, wouldn't leave it alone, pulled it out of the heart. It's not supposed to be in the atrium here or in the cranial vena cava, it's supposed to be down in the ventricle where we saw it.

The lead dislodgement is the biggest complication here, it's awkward, it's annoying, we have to just do the whole thing all over again. Happens very rarely. The last time this this pacemaker I'm looking at here was back in 2014, I remember, and then I had one happen to a case of mine last month.

So, you know, they're not very often. I, I maybe do 15 pacemakers a year, and, I, I think I've seen 2 then over, well, I guess 1 every 5 to 6 years. OK, so they're not particularly common, but that's because we're very, very cautious about managing these patients postoperatively.

Infection, any implant can get infected, but here we've got something that's relatively superficial, and if we've got an animal that's got skin disease or something and we're, you know, we're trying to implant a pacemaker through that, that can be a problem. Or an animal with a septic focus elsewhere, of course we've got a long term foreign body, if you like, in the right ventricle. Seroma can happen and seroma is a relatively minor thing, but it may increase the infection risk.

Lead thrombosis, we think happens probably in about, I think 1 in 10 dogs develops a lead thrombus. That figure is something that we've been working on, looking at our own data and the data from other centres featuring about 400 or 500 dogs, to try and get a good prevalence of lead thrombosis because it's not reported anywhere. So we haven't published that yet.

Don't hold me to it, but Feeling is that maybe 1 in 10 dogs gets a lead thrombus. Generally we can treat them with antiplatelet drugs, tip the balance of thrombosis versus breakdown and deal with that problem. It generally isn't a problem for dogs, but the important thing is to identify it.

Otherwise, of course, if it gets large, it can cause problems, or if it embolizes, it can cause a PTE. Finally, another old dog thing, compressive cardiac neoplasia. So we can use vascular stents to relieve obstructions to large vessels and generally I'm thinking about the pulmonary artery or the cava, or you can use it on on the aorta as well.

So we tend to use metal stents like urethral stents or tracheal stents, depending on where the location is. And the corvina cava, there is a specific type of stent for intrahepatic obstructions, but that's not something that we tend to think about with the heart. So here's a good example of cardiac neoplasia.

This is a dog from a long time ago now, look, 2015, who had a heart-based tumour. This is, looks like it's sitting in the left atrium here, but actually what it is is it's coming from the pulmonary artery and it's compressing the left atrium and also compressing the right atrium. That is the right atrium there.

So this dog presented with signs of right-sided heart failure, presented with ascites. You can see why this should be atrium here, there should be a right atrium here, but it's really squished. And this tumor's arising from the aorta, which is classic for a type of tumour called chemodectoma, which tend to be quite benign and slow growing, but really annoyingly positioned and very difficult to operate on.

So here's a CT of the dog. An injection of contrast was given cordially, so let's look at this. This is the spine, sternum, this is like a radiograph again, diaphragm here.

This wide thing is the coralvina cava. And I injected contrast from the saffurous vein, so this should be full of contrast coming back into the right atrium. There's no contrast in there.

Contrasts coming through the azygous vein. Into the cranial cava, and even the vertebral veins here. So this blood from the back half of the body is taking a very circuitous route through the spine to get back into the cranial cava and then the heart.

That's the tumour. And we can see the same phenomenon here, this is looking top down on the heart. Here we've got black lung fields, we've got the heart there, tumour here, corral vena cava snaking off wide and tortuous, no contrast in it.

And this is looking at a transverse slice of the dog's thorax, that's left ventricle left atrium, right ventricle right atrium, and there's the tumour, just like we saw on the echo. So what do we do? Well, we can place a stent to relieve the obstruction in a case like this as well.

So if you watch the video, we've got the diaphragm here. This catheter's going past the tumour, you can just see the caudal margin of the tumour there really obstructing cave or flow. Now what we need to do is a bit strange here, we pass a wire into the heart, then we grab that wire using a snare from the jugular vein.

So we go from the femoral, we grab it from the jugular. And then we pull it. Out of the jugular veins.

This dog is on what's called a through and through wire. So the wire goes from the femoral vein all the way through the body out through the jugular vein. Kind of freaks the nurses out cos they think we're skewering this dog, but actually it's very useful cos then we've got a very steady wire over which to pass a stent.

So here we're balloon dilating, we're passing a balloon and we're stretching all the bits of the tumour that are adhering the blood vessel together, the the caudal cava and the atrium wall. We're stretching that all out to relieve that obstruction. And make it easier to pass the stent.

So we're gonna pass the balloon down here, you can see the tumour goes all the way down here. And up to about here. Based on the balloons, so we're just stretching that out.

Now we're passing the stent along. There's a little nose cone on this stent so you can spot the end. And this is the stent here, so the nose cone is coming through.

This is actually a tracheal stent. So it's designed for the airways, but it works beautifully for neoplasia like this which will curve the stent round cos they're very, very flexible. So you'll see in a second we're gonna withdraw the delivery system, we're gonna start deploying the stent, so you can see the stent opening here.

And I'm just gonna reposition that a little bit as I go and withdraw this through, so you can see we'll end up with a tracheal stent coming through here. And then we'll release that to lift that tumour away and allow blood to re-enter the heart. So we can see the tumor's now being pushed up here somewhere.

I can't see it exactly, but I suspect it's this area here. You see how compressed that stent is there compared to where it's wide open at the end? And we're back here.

And the stent will be released. So now, that stent's in position, we're not holding onto it anymore. And in a second, you'll see we do an angiogram which will show you filling from the caudal aspect here of the heart really nicely.

So the wires coming out now, dog's no longer on a skewer. Stent's in position to relieve that obstruction. If you watch in a second, we'll do an angiogram again.

You see how easily it flows into the heart there and we can really see that tumour mass there and there, can't we? But this is now getting nicely into that heart. I did deliberately mention the date on this before, 2015.

This dog died last year, so it was alive five years postoperatively, having had a cardiac tumour diagnosed. So. That's really good in my view.

And here you can see postoperatively we've got the stent in the same case in position. So we talked about a lot. It's possible to do some pretty major procedures that improve quality of life or even cure the dog in the the case of PDA for example, through the blood vessels.

Minimising pain, minimising risk, maximising quality of life, OK, and longevity. And most dogs do very, very well long term. Who do we choose to investigate for this?

Well, we, with the young dogs, we think about dogs who've got louder heart murmurs, grade 345 heart murmurs, OK. Grade 1 or 2, probably not that important for the common congenital diseases. OK.

Most dogs do very, very well long term, even the dogs who are old, those dogs who need a pacemaker or who need something for for cardiac neoplasia, they can do incredibly well long term. The costs and experience can limit setting up a service somewhere, so there's not many centres that do a full complement of interventional procedures. However, there are people out there with experience and it's worth inquiring to try and find out where the centres who've got lots of experience are so that you can, you know, choose the right cases to go to the right people.

Thank you very much for sticking with it. There's been a lot of grey images, so I thought I'd show a beautiful colourful piece of street art from Bristol near where I live. This is a huge seagull who looks around the corner of the building.

So as you walk on the road, you see his slightly sinister face looking out from the side street. I just think it's a wonderful thing. It's a great experience.

It's part of an annual street art festival in South Bristol. I put my Instagram handle on there. I don't make any money from Instagram.

There's no conflict of interest there, but I do want to say that if any of you have any questions based on this presentation or want to make any further inquiries, that's an easy way to contact me. You can message me on there and we can have a conversation. Thank you very much for paying attention and and for enjoying, hopefully looking at some neat images of cardiac procedures.