Hi and welcome to this webinar on atrial fibrillation, dysrhythmias, and their role in poor performance and the pre-purchase exam. So what we're gonna do in this session is we're gonna think about the dysrhythmias that we see in the horse and talk about the myths and facts that sit behind them and really focus on the ones that are going to be a problem to us in terms of performance and safety for for riding. And then we're gonna talk about atrial fibrillation in a bit more detail, and then also the, some of the dysrhythmias that are likely to need further management and then thinking about decision making as to what that further management is.

So I thought I'd start by looking at the relationship between poor performance and where cardiac disease sits. And in fact, there's very little published in the literature on overall causes. Now what we do know from a study that came out of the University of Pennsylvania over 20 years ago now, is that poor performance is often a multi-factorial problem.

And the most common reason for poor performance is lameness, particularly bilateral hind limb lameness. And then lower airway disease, usually in the form of asthma, then upper airway disease, and then cardiac disease. And then actually, in this particular study, there was no discussion of muscle disease, but it probably sits somewhere above or below, cardiac disease, depending upon the population that you work with.

And this study really did identify that around 25% of cases had multiple problems, and one particularly commoner pair of problems with that was upper airway disease and cardiac dysrhythmias. So we're now gonna move on to have a think about dysrhythmias and how we go about diagnosing them and what some of the challenges are with that diagnosis. So we've got, you know, the joys and evils of ECG recording devices and ECGs are, you know, rubbish in, rubbish out.

If you end up with a poor quality ECG it's easy to misdiagnose what the problem might be. And so when we're thinking about ECG recording devices, they come in a variety of forms. Some of them, like the live core work via sound waves that will transmit that ECG to your phone.

But that means if you're trying to utilise them in a noisy environment, you're going to end up getting a lot of artefacts and feedback. We've then got some other devices that will work by Bluetooth, and those devices are a lot less likely to be affected by by sound in the environment. And then we've got the devices such as the televet and the Reynolds system.

That will record onto usually a memory card and or transmit to the cloud, and these will usually, unlike the others we've talked about record over multiple leads utilising 3 or 4 electrodes. Now there are also devices that, create an ECG based on the heart rate that they that they detect. And this is much more common in some of the older devices, but it really is important that you understand how the ECG that you're looking at has been generated so that you can understand whether or not, the diagnosis that you've come up with is likely to be correct.

And then the last thing to note is that we've now got stethoscopes that will both allow you to auscultate and they will allow you to record both a phonogram and an ECG that you can look at on your mobile phone or other device. So, where do where do dysrhythmias relate to morbidity and mortality in performance horses, and I thought we'd start by thinking about what, what sort of dysrhythmias we're most likely to encounter. So obviously the physiologic dysrhythmias are very common.

2nd degree AV block being the most common that we see. We will occasionally see sinus dysrhythmias, which is a much more common physiologic rhythm in the dog. We'll see that post exercise or see it with respiratory disease.

And also, often normal, not always. But often normal, we can see sinoatrial pores and sinus arrest and I'll show some examples of those because when you ask or take them, particularly if the horse doesn't have an audible S4, and they can sound like atrial fibrillation. And then we move on to the pathologic dysrhythmias.

And when we think about challenges in our performance horses, they are a pretty uncommon cause of poor performance, as we've said already, but obviously they're important when they are present. And the pathologic dysrhythmias that could result in poor performance and or in Death include atrial fibrillation, ventricular and superventricular premature depolarizations in terms of poor performance if they occur in a high enough prevalence, and then ventricular tachycardia, which can flip if, in unfortunate circumstances, into ventricular fibrillation, which results in collapse and death. So Moving back to that question of, you know, do, do, does upper airway disease and is there a correlation between upper airway disease and cardiac dysrhythmias?

And myself and Mark Bowen, we looked at a group of our, our poor performance cases, they were eventor and racehorses, that underwent galloping exercise with an overground endoscope and an exercising ECG. And in this population of horses, and they were poor, poor performance cases, cardiac dysrhythmias were pretty rare, about 6% at peak exercise, and we didn't find any association between upper respiratory tract abnormalities and those cardiac dysrhythmias. Kate Allen, had a group of horses where she had a group that, had been evaluated in Newmarket, a group at Bristol, and again, these were usually racehorses where they had got a diagnostic quality ECG where heart rates went above 200.

And they actually found a prevalence of peak exercise of 24% of dysrhythmias. Now, quite a few of these horses, particularly. Particularly those that were evaluated at Bristol at the time, had been exercised on a treadmill, and we'll talk about a little bit more in a minute about whether or not those dysrhythmias are real or whether they're induced by treadmill exercise and potentially foot pain.

But they did find an association with the dysrhythmias and their upper respiratory tract findings. Now this is a paper again going back nearly 20 years now, and this was looking at cardiac dysrhythmias during submaximal and maximal exercise in a group of normal thoroughbred racehorses in training in Newmarket. And what they found in this group of horses was that dysrhythmi has occurred at all stages of exercise, particularly prevalent in the warm up and warm down phases.

And they found in these normal horses that had no clinical signs of poor performance, they found ventricular dysrhythmias. At a prevalence of 3% at peak exercise. And superventricular dysrhythmias at a range of prevalences and 17% in one phase of exercise, 4% in two phases, and 1% in 3 out of 5 phases.

But what they found in this study was that 45% again of these normal horses had one premature depolarization. And 8% had both super ventricular and ventricular premature depolarizations. And then this was another study that came out of Newmarket around the same time that looked at cardiac dysrhythmias during and after treadmill exercise in a group of horses in a group of thoroughbred racehorses that were poorly performing.

And of these, 88 had got some form of upper airway or other respiratory abnormality, and there were 27 that they didn't obtain a diagnosis. But here you can see ventricular dysrhythmias, 4.5% at peak exercise.

Remember, it was 3% in those normal horses that had been exercised on the, on the gallops. And then again, they had a prevalence of 17% of super ventricular dysrhythmias overall and 10% at peak exercise. Again, When you looked at the group overall, 63% had one premature beat primarily in the recovery phase, and 2.3% were classified as having severe dysrhythmias.

So if we put that onto. A graph. The y axis is percentages and the X-axis is showing horses that were normal, horses that had ventricular, superventricular, or both ventricular and superventricular dysrhythmias, from these, both of these studies from Newmarket, the green one was the, study of the normal horses that were exercised.

On the gallops and blue was the number of poor performance horses that had been evaluated on the treadmill. And you can see when you look at these, there's absolutely no difference in prevalence, except perhaps if both ventricular and superventricular depolarizations were present, where that prevalence looks to have been higher in the poor performance group. So that then brings me to the next question, which is somewhat controversial, but what exactly is normal or abnormal on an exercising ECG?

Because I've just told you that we know we see ventricular and super ventricular premature depolarizations in both normally performing and poorly performing horses. And actually there's no real agreement amongst equine cardiologists about how many abnormal beats is too many. And that same, and that same, observation applies to human electrophysiologists as well.

And we don't have a lot of evidence-based medicine, and part of the problem is we've just said, poor performance is multifactorial, but also. We know that poor performance, that the prevalence of these rhythm abnormalities between normal and abnormal horses is pretty similar, so that would end up needing a very, very large population size to study. And then when we think about, well, why do we see this reasonably high prevalence in normal horses of premature depolarizations and we think it's because there's this change in balance between sympathetic and parasympathetic tone during acceleration and deceleration.

And so where we find abnormalities at peak exercise, there's probably a bit more agreement, particularly if there are multiple ventricular ectopics. Whereas when you're in that acceleration or deceleration phase and you find these abnormalities, some people allow and some people think that they're unacceptable and you know, we're very much in that . Very much in that opinion based space.

So, what is significant? This was some data based on expert opinion from one group out of the University of Pennsylvania. And their definition of significance was more than 2 isolated premature depolarizations at peak exercise or multiple pairs or paroxysms or premature depolarizations immediately after exercise.

Now, whether that's correct or not, no one knows that's an opinion that's been based, and I think that. Most people would be happy to say that, you know, multiple ventricular depolarizations at peak exercise probably increases the risk of those horses collapsing. But whether they happen before or after exercise, I think is very controversial.

So, What we know is that sometimes the odd. Monomorphic, ventricular premature depolarization, overridden with exercise or only detected in that immediate post exercise period, probably isn't a cause for poor performance. The consensus statement that came out in 2014 suggested that ventricular premature depolarizations can occur during exercise in normal and abnormal horses and probably are a cause for concern, although the number wasn't specified.

And that one of the really key things that came out of this consensus statement was that importance of these dysrhythmias and the risk of sudden cardiac death requires further investigation, which I couldn't agree with more and I think we still are watching that space. We don't know the relationship with poor performance and premature depolarizations and again requires further investigation. But again, this was all based on expert opinion rather than evidence.

And until we collect that evidence, there's always going to be differing opinions. So then what about sudden death? So what we know is we have a good handle on sudden death in performance horses based in racehorses, and we do know, have that data as well for for some of the sports horses as well.

But what we know about death on UK racetracks is it's pretty rare. And Katlile did some really great work looking at the risk factors for death at racetracks, and what she found was it was usually older horses. It was more common in steeplechase horses than in flat horses, and they were more likely to die during the summer.

In this particular cohort study they looked at postmortem examinations in the horses that died, and the causes of death varied. They only found an absolute cause in 53% of cases, and some of those were associated or described as being associated with cardiac failure. But there were 47% that they didn't identify a cause at all.

And it could be that those horses had a cardiac dysrhythmia, which would obviously not show up at a postmortem examination. So, I now want to move on and go through some ECGs. So this was, two sections that were taken from the same horse over a time period.

And as you can see that the, this CCG demonstrates an irregularly irregular rhythm. And as we move along this CCG you can see that we start off with a nice regular rhythm and You've got a nice regular rhythm that we've got here and you can see there's a P for every QRS and obviously every QRS always has to be followed by a T wave. And that that's those QRS complexes are looking pretty normal, you know, they're fairly narrow and it all looks OK.

And then when we move on to the second line, you can see that we get a PQRST and then we just get this really long gap or pause. And then after the pause, it starts up again and then again we see PQRST PQRST. And then when we move to this bottom section, if you look at that middle line, you can see that actually we get a 2nd degree AV block.

So we've got two PQRSTs and then we get a P wave that is not conducted, and then again we get this long pause. Now, depending on how long the pauses are, depends on whether we call this a sinoatrial pause or sinoatrial arrest. And but if you were listening to this horse, it's gonna have an irregular, irregular rhythm.

Now, if the horse has got an audible S4, that will help you decipher that it probably isn't, atrial fibrillation, but if it hasn't got an audible S4, then that's gonna be really tricky. The other thing to note is, in this top ECG on the bottom row, you can see that actually the QRS complexes get wider and closer together. And that is also true on this top line too, and that's gonna be an example probably to us of a.

Dysrhythmia, because the horse's heart rate, the respiratory rate's very slow, we would probably need a longer stretch of ECG in order to be able to confirm that. But your guess would be this animal's got sinoatrial pores and sinoatrial arrest with a sinus dysrhythmia. Now, in most cases, as long as these, this, pause or arrest is overridden by exercise, then, this is not gonna be a problem and it's gonna be physiological.

All the cases I've ever seen of this condition have Always gone away with exercise, but there are an odd number reported in the literature that don't. And obviously, if your heart rate doesn't increase appropriately at exercise, then you have a higher risk of collapse. And then this is an ECG actually taken from a donkey, and we'll come back to talk about this when we're thinking about treatment.

But here, hopefully you can see that we've got pee waves and they are really very regular, coming along at a, at a rate that's, you know, pretty steady. All the way along. And then we've got these QRS complexes which, Always difficult to tell on equine ECGs but look like they're quite wide and bizarre, and they're very irregular, and they are not related to those P waves.

And then we have this period of time where the atria contracts, we've got lots of pee waves, the ventricle doesn't contract, and then actually at this point, right at the end on the second line, the donkey fell over and collapsed, and this is an example of a. Third degree AV block where we've got these probably these are escape beats in order to keep this animal alive. And then we move on to this ECG that we've got here, and the questions always are, so what, what's this abnormal premature beat that we've got in the centre of the screen so that you can see before or after that premature beat, we've got pretty regular R to R intervals.

And then we've got this premature beat. Now, what we want to know is, is that premature beat? Ventricular or super ventricular when we're trying to think about, risk of collapse.

So you look at this ECG and you say, well, the QRS complex looks pretty narrow and it looks quite like the other QRS complexes. The T wave looks different, but sometimes the T waves do look different when we have premature super ventricular complexes. And then we've got this compensatory pause after it, and we normally associate that with.

A ventricular, we normally associate that with a, with a, with a, a, a ventricular premature depolarization. So you look at this and it's actually quite tricky to work out what's going on. And, you know, while we're, we're having to utilise surface ECGs, which we are, it can just be trickier.

Now, this is one of those cases where If you evaluated this in more leads, and we do now have 12 lead ECG systems available in horses, we might be able to work out if that was super ventricular or ventricular. But if you took that recording from, And a live core or a similar device that's recording resting ECGs, and you've got that, it would be pretty difficult to work out which one of those it is. And the reason we care is that one premature super ventricular premature depolarization is not a drama, but a ventricular one, we might be more concerned and might want to evaluate that animal further.

And then this was from an, an interesting case. This was a, this was a young course that had a, a . That had an atrial tachycardia.

And the reason that this ECG looks really weird and funky is that depending on how fast the rate was, depended upon whether the T wave and the P wave fused together. And so when they're fused together, they have one shape and when they're separate and the heart rate slows a little bit, you can see that they separate. And then even though this horse has got a resting heart rate between.

70 and 80, actually it is doing something slightly inappropriate to control its heart rate by having an AV block. So it's got a few second degree AV blocks here. Now interestingly, when you exercise this horse.

He did in fact have an entirely appropriate rate and rhythm at exercise, and went on to compete very successfully for several years, until, until he developed atrial fibrillation, and he continued his career as a dressage horse, but his rhythm, his resting rhythms switched from this atrial tachycardia to having atrial fibrillation. And then this ECG is an exercise in ECG. So, and you can see here that the time stamp down the side is 9:43, and if we look at the graph on the bottom, you can see that at that point, the horse's heart rate was probably around 110 beats per minute and was likely doing trot or maybe a slow canter.

And what you can see when you look at this ECG is everything looks pretty regular. This is a very nice recording for an. And exercising ECG, but then what you can see on the second line just after halfway along is this wide and bizarre QRS complex and it's much wider than the others, it's larger, it's T wave has got a different polarity, and again, it's got that compensatory pause after it.

So, you know, there's no doubt that that is a ventricular ectopic. Now the more difficult decision to make is, Is that significant or not? Is this horse at an increased risk of collapse and sudden death at exercise?

And we'd have to put that into the whole context of what the case was and who was riding it and the, and, and have that conversation with the, with the rider about what those relative risks were. We also might want to Multiple ECGs because today it might have one at peak exercise, and tomorrow it might have 20. And obviously, the risks of, if it has 20 during a, you know, 5 or 10 minute peak exercise phase, it, it, it's gonna be at much higher risk than if it just has one or that, you know, most of the time it might not have any at all.

So, we're now gonna move on and talk about atrial fibrillation. So, obviously, most common and significant dysrhythmia regarding performance, and we know that the atria in the horse really is only required to have function during. Sustained exercise.

And that's when that extra 25% of cardiac output that's provided by atrial contraction is needed because we always have to remember the horse has got a very large cardiorespiratory reserve. So the times when atrial fibrillation is going to affect performance, it's usually gonna be in racehorses, particularly national hunt, but for all racehorses, hunting horses and inventors. Now there are certain, clinical signs that we can sometimes See with atrial fibrillation, that can mean we can see significant, performance effects even at, at lower, at, at lower levels of exercise in, in show jumpers and, and in dressage horses or general purpose horses as well.

So why do horses get atrial fibrillation? Well, they have this pretty poor triple combination of bad things that predispose them. They have a large atrial mass that can be big just because they're a horse, or can be big secondary to training, or obviously can be enlarged secondary to mitral or tricuspid regurgitation.

They have a low heart rate and they have high vagal tone. And that large atrial mass, which means that electrical conduction between the sinoatrial and the AV node has got a long distance to go. But also if that high vagal tone and low heart rate happens, it means that the.

It should go from A to B, like down a motorway. But if you start to get repolarization of that atrial tissue, it means that that, that electrical current can go backwards in the wrong direction and set up these little circuit rhythms, which is then, when we start to get, get fibrillation waves and atrial fibrillation develops. We also know that hypoxemia and electrolyte arrangements and potentially myocardial inflammation can all predispose to the development of atrial fib because again, they will have impacts upon upon the speed and, and way that that conduction occurs through the atria.

So, we always say, you know, you put up this slide and you say diagnosis of atrial fibrillation is really easy, and you know sometimes it just isn't. So the one thing to always look out for when you're auscultating a horse with an irregular rhythm is can you hear an S4? So that's that sound that sits immediately before S1.

And if you can hear an S4, then it has, I'm sure, got a dysrhythmia, if it's irregularly irregular, but it's very, much not gonna be atrial fibrillation because S4 corresponds to active atrial contraction, which, by definition can't occur during atrial fib. So, what we usually find on auscultation is that they have a really, really loud S1 and they will Often have an audible S3 and because of their very irregularly irregular rhythm, you'll see variable heights of jugular fill. Also on auscultation, you usually find that they have a normal to low heart rate, which is obviously in contrast to what we would find in dogs and people.

And we'll talk about, you know, why we do exercising ECGs and why they're recommended in atrial fibrillation cases in more detail in a minute. But we do sometimes see other abnormal rhythms. Now the one thing to note is that this number got bandied around that, you know, if their heart rate at exercise was inappropriately high, above 2.

120 beats per minute, then they were probably at increased risk of, of collapse. Now, again, that's, there is no evidence that that is the case. But also, if you're calculating heart rates of these horses that exercise, it's really, really important that you get an average heart rate over a period of time, which with a lot of the softwares that we use, It's often very easy to get heart rates based on and beat to beat information, but not necessarily, you know, over a strip.

So that's just something to bear in mind because, you know, atrial fibrillation by definition is irregular. So if you measure an hour to hour interval where they're very close together, obviously that heart rate's going to be quite high and equally, if you measure it over a period where there's a gap, then it might be inappropriately low. So that's just something to, to look out for.

And then most of the time we're probably going to want to investigate these animals with echocardiography to make sure they've got no underlying structural change. But fundamentally, if they've not got a cardiac murmur, you know, sometimes, not always, but sometimes the information that we get from the From the echocardiogram, it doesn't necessarily help us with decision making. And I mean, it might do if the, if the animal's got very poor cardiac contractility because it might make some rarer conditions or, myocarditis a little bit more likely on our list.

And then the other form of atrial fibrillation, which is actually incredibly frustrating to manage, is paroxysmal atrial fib. And normally these horses will have a history of sudden reduction in speed. That might resolve very quickly or and.

You may or may not be able to diagnose it, but if you are going to diagnose it, you normally need to be able to ask or take them after exercise. And that can be challenging too, because the faster the heart rate is, the more regular that heart is going to sound. So if these horses, you know, pull up after a race and they've got a heart rate of 250 beats per minute, which is not normal, when you auscultate them, it can sound pretty regular.

And hopefully I'll show you an ECG that really can, can bring that home. The other thing is, obviously we can use exercising ECGs to try and diagnose them, but some horses only develop paroxysmal atrial fib when they're competing, which for most of the time, you know, recording ECGs during competitions is not going to be permitted. So, you know.

They can vary very much from how challenging they are to diagnose and obviously also to treat because if they're only there when the horse is competing but are normal in the interim periods, then it's what we do with those cases in order to you know, keep them in, in competition. So this was an interesting paper, came out about 10 years ago now, and it was looking at the ventricular response during lunging exercise in horses with atrial fibrillation. And they found an incredibly high proportion of horses in this study that developed, we'll call them idioventricular beats, but they developed these sort of wide and bizarre complexes, during an exercise phase.

So they found them in 80% of horses, 16% at rest, 69% during exercise, and a few in the recovery period. And this seemed quite surprising to me where I had done a lot of exercises in ECGs in horses with atrial fibrillation and certainly the prevalence that I found of these idioventricular responses was nowhere near as high. And it's quite tricky because again, we're recording surface ECGs.

All we can say is that they've got these wide QRS complexes, but knowing where the source or where they trigger from is really difficult. They might well come from the ventricle, or alternatively, they could come from some of these bundle branches, and any of you that do small animals as well will know, bundle branch blocks are not an uncommon finding in, in dogs. So after this study, we went and had a look at the at the cases that we've had.

We've got 156 horses that had got lone atrial fibrillation at rest, sustained lone atrial fibrillation at rest. The population was primarily general purpose riding horses, hunters and events. And whereas the study that came out of Ghent looked at horses in a hospital, we were looking at horses that were being exercised at home, and depending what they did, depended what our exercise test was.

The hunters and inventors, we usually put them on gallops, whereas the general purpose riding ponies, we would probably have done walk trot and cantering and a rema. We didn't detect any abnormalities at rest, and we had a prevalence of abnormal rhythms at peak exercise of around 2%, which was pretty different to the nearly 70% in the in that study out of Belgium. Now, is that a breed?

Is that something to do with breeds? Is that something to do with where they were exercising them? I don't, don't know.

But it caused a reasonable amount of excitement, this paper, it was a very interesting paper that was published, and then probably one of the best known equine electrophysiologists wrote a, a really, really nice editorial that went with this paper. And what he talked about was that, you know, there were, there were comments made in the paper regarding. Weakness in coordination and collapse being reported with atrial fib, and yet actually there's very, very, there's very little evidence for that when we look in the literature.

And again, there have been concerns in the racing press regarding safety of horses with atrial fib, but there's never been any evidence of a practical impact on that. And then his assumption that he made was that he thought that these idioventricular beats that had been diagnosed so frequently in this study might well be a reflection of autonomic instability and nothing to do with the atrial fibrillation. I did, I, and that really was aimed at them being a reflection of the experimental protocol.

The study wasn't controlled. There were brief episodes of excitement at rest, or walk, and none of these horses, although they had these idioventricular responses, demonstrated any clinical signs. So, we don't know what abnormal findings on an exercising ECG mean.

In, certainly in my case population, it's pretty uncommon, but I do think because there's a potential that it could cause a problem, we probably should recommend our clients to have exercise in ECGs, particularly if they decide they don't want to treat the atrial fibrillation. And so that then brings me on to whether we should treat or not treat the atrial fibrillation. So obviously, the first question is, make sure the horse actually has atrial fibrillation, and then think about how old the horse is and whether it's likely to change careers.

And then think about, is it affecting performance, you know, did you find it as a vaccination and the owner had no idea, or actually, did the horse have a nosebleed every time it walked out of the stable and the owner was unable to ride it or it was performing poorly, in a performance animal. You then want to know is there any underlying cardiac disease, because if these animals do have mitral or severe tricuspid regurgitation and they've got enlarged atria, that's gonna make it much more difficult to treat or that if they do respond to treatment, make it more likely for those animals to fibrillate again. And then think about, you know, what, what's the likelihood that the treatment's gonna, gonna work and improve performance.

And we know, whichever treatment we recommend, and we'll talk about the treatments in a second, you know, the quicker we treat them, the more, the more likely we're going to have a positive outcome. So, you know, when we think about is it limiting performance, it's likely to be limiting performance in the performance athlete, particularly the athlete that's doing a significant amount of its work at Cantor or or Gallup. Does the horse have exercise induced pulmonary haemorrhage or even worse epistaxis?

We certainly don't see it in all cases, but we do know that it often is secondary to increased left atrial pressure, which can result in pulmonary hypertension. Is the horse collapsing, which is very, very uncommon, except perhaps some of those paroxysmal atrial fib cases that develop that condition at peak exercise. And then as we've said, quite common in pleasure horses that the owner's got absolutely no idea, and the horse has no clinical signs.

And You know, is the horse with atrial fib safe to be ridden, and although, like I've said, that prevalence of these idioventricular responses or these R&T type, complexes like you can see sort of in the middle of this ECG here are rare. It is nice to know whether they are occurring or not. But the other thing I just wanted to show you on this ECG, this is an ECG taken from a horse with atrial fibrillation.

And what you can see if you look in the second half of this ECG is, although this horse does have an irregularly irregular rhythm, if you were listening to this, this would sound pretty regular at this at this heart rate. It would be very hard to say that that those are to R intervals varied. So then what about treatment options for persistent atrial fibrillation?

We've got renadine sulphate given by nasogastric tube and we've got electrocardioversion. And For electrocardioversion, the horses need to be anaesthetized and we place catheters into the right heart. We put one into the right atrium and one into the pulmonary artery, and although not reported in the horse, there's certainly placement of these catheters has been associated with morbidity in other species.

So there's the risk factors that go with the general anaesthetic, but the risk factors with Quinidine, of which we have a large amount of experience and data in the horse, is that it's not licenced and we do require an SDA if we're shipping that into the UK and probably. In 10% of cases, we're going to see moderate to severe side effects. Mar actually presented a good number of her cases a few years ago, and what she found was that actually those moderate to severe side effects significantly increased once she got above administering 3 or more doses of Quiddine.

And those side effects include. Diarrhoea or a particularly nasty form of superventricular tachycardia, certainly has been associated with with death and torsard the plan, which is a a, a very unpleasant form of ventricular tachycardia and then down the line, presumably because of of leakage from the, the GI tract, we can see secondary laminitis and I've certainly lost a case that we successfully converted to sinus rhythm only for its feet to fall off about 5 days later. So it's one of those things where, you know, it used to be, it was the only treatment option we had, so that's what we used.

And now that we've got two treatment options, well, it's certainly still something to consider, particularly for cases that haven't been fibrillating very long, and which are less likely to need, larger doses. And when we're using Quiddine, actually, when we're doing either of these procedures, we need to ensure that we've got really excellent monitoring during conversion. We want to keep an eye on clinical signs where the Quiddine's concerned, and you know, we normally say we won't give another dose of Quiddine if we get prolongation of the QRS complex, more than 25%.

But that monitoring's really important for electrocardioversion as well. We want to make sure that the defibrillation machine is always sinking, in the right place. So we want it to sync on the QRS because if we do shock these animals on the, the T wave, they will, they will normally go into ventricular fibrillation, and they'll be very difficult to, to get back.

There have been a plethora of other drugs that have been evaluated, and some of them don't work, some of them are incredibly dangerous, and some of them are very, very expensive. So, you know, in terms of what's practically available to us, these two methods are, you know, currently. What we would use and there will be times when we might combine or add in drugs like amiodarone or digoxin to help us with specific issues that we encounter when we're using either Quidine or DC electrocardioversion.

So, I wanted to finish up with a few pieces. So this was a 10 year old Irish sports horse mare that presented following a day's hunting with epistaxis. The horse had got an irregularly irregular rhythm, it's got a really loud S1, an obvious S3, no S4, and no cardiac murmur.

On echocardiography, there was no chamber enlargement and the heart had good contractility. We measured cardiac troponin eye concentrations and electrolytes, and they were all normal. And you can see the ECG on the right hand side here is a very classic ECG that we would expect to see, in an atrial fibrillation case.

We've got normal QRS complexes. That are narrow. We've got this irregular irregular rhythm, and then we've got this wobbling baseline which is caused by fibrillation waves, so the sort of those little circuit rhythms that, you know, are causing little mini contractions within the atrial tissue and no obvious pee waves.

So we exercised this horse and this is an ECG taken from a little bit of walk, trot and can on the lunge. And what you can hopefully see here is that, as we talked about before, many of the beats look like this rhythm is pretty regular, not all of it, I'll grant you, but some of it. But then we've got these really nasty sections, particularly this one right in the centre here, where we've got this sort of R and T phenomenon, and we've got this really very fast focal rate.

And where I would regard myself as being, you know, very, pragmatic about management of these cases. I really felt that these types of, complexes in this sort of pattern on an ECG like this, with quite a fast heart rate for the degree of exercise the horse was doing, this horse was at very high risk of developing ventricular fibrillation. And I've just got a sort of close up of that ECG.

This ECG was taken when the heart rate was around sort of 170 beats per minute, but you can see this is really not a very nice looking rhythm. It's got this sort of R&T phenomenon. So, So this was a horse that we opted to treat with DC cardioversion.

She hadn't been fibrillating very long. The owners had had a previous horse that had had atrial fibrillation and in fact had developed laminitis and had to be euthanized after being given quinadine sulphate, so we opted for MDC cardioversion in this case. We knew this horse hadn't been fibrillating very long.

And we knew that there was no, as far as we could tell, no underlying cardiac disease. And this horse converted a relatively low energy, when we when we cardioverted her, and I had to follow up on this case for about 5 years post conversion, and she stayed in sinus rhythm. So when we're thinking about about treatment, you know, is it likely to work?

Well, as we've said, the longer that the horse has been fibrillating, the more likely it's not gonna work, and also, the more likely we're gonna have to either give more doses of Quiddine or give higher energy for DC cardioversion. And obviously, in both those cases it increases risks of adverse events which are gonna be higher for the quinadine group. But if we've got underlying disease, like in this ECG that's shown here on the right hand side, where actually this is an animal that's looks like it's got a, a slight tear and it's got a really, really large jet of mitral regurgitation.

Because it's got a big left atrium, we know it's got a pathologically, pathological reason why it's got atrial fib and therefore, it's likely either the treatment's not gonna work or there will be early recurrence of that atrial fib, particularly as in the case of a, of a, a severe mitral regurgitation like this, the only thing that's gonna happen is that that left atrium is gonna continue to get larger. And then, as we've said, is that murmur significant? So, really, really important that we, you know, if we do hear murmurs, we make sure that those, that those underlying cardiac abnormalities are evaluated before we go too far down the line as to what sort of treatment, or if any treatment, we should be recommending for the atrial fib.

And what about the success with Quinidine? Well, we know that with careful case selection. With duration of atrial fib of less than 3 months and no underlying cardiac disease, we can get success rates of around 85%.

You know, some studies going back a while now, but they showed actually recurrence rates were pretty low. You can see this is a this is a picture of a Cleveland Bay that's had, that's had quinadine sulphate and you can see he looks a bit sorry for himself and he's, he's got this sort of quite classic nasal edoema that we'll often see following administration of a few doses of quinadine. And then, so we had, that was all we'd got for a very long time.

And then in the early 2000s, the group in Gwelth looked at performing transvenous electrocardioversion. We can't use paddles on the outside of adult horses because we just can't and we just can't generate the energy that's required to try and stop the heart and put these animals back into, into sinus rhythm. So this is an image here of a horse under anaesthesia.

This is taken at Rossdale's where you can see he's he's anaesthetized collected to a breathing system and has got catheters going down into his heart, and that we then shock him and eventually we did shock that horse back into, into sinus rhythm. And then these are just some these are just some printouts that we will often get during this cardioversion procedure and you can see the ECG at the top where we've got the, The horse has got atrial fibrillation. The little black arrow at the top is where we give the shock, and you can see this is 175 joules.

We then often get this pause and then the horse goes into sinus rhythm, and something similar is shown on that second ECG down except this time you can see we've had to take the energy all the way up to 360 joules. The two ECGs at the bottom are actually intraattrial, sorry, intracardiac ECGs, and that what you can see here is you can actually see the, you can actually see if you like what you would see on an ECG, the P wave, but you can see the, atria contracting, whereas the ECG at the bottom is what happens, what's going on inside the atria when we've got atrial fibrillation, and you can see it's just fibrillating, it's just bobbing along, and fibrillating. So, some of the early results that came out of wealth was that they had a 90, almost a 99% success rate.

They were dealing with, standardbred racehorses, so they were diagnosed very quickly. They were quite small animals, they'll be about 450 kg, and, but they did have really, really good results. We looked at some data that we collected as a group at Rossdales and most of the horses here had been treated with quinadine, either at Rossdale or somewhere else.

And we found that those horses, many of whom had failed to convert with Quinnadine, we got a 65% success rate on the first shocking attempt, and then 82% success rate if a second cardio cardioversion attempt was included. Now, 10 years on, probably if we relooked at that data, and those numbers would be much higher because we're much better at selecting those patients. And in the early days, we did horses that had got moderate, sometimes severe mitral regurgitation.

So we were almost setting ourselves up to fail. So the recommendations are for atrial fib that has been happening for less than 3 months, probably either treatment is suitable, but for atrial fib that's perhaps more long standing, better success might be had with DC cardioversion, plus or minus combination with some other drugs. When we've got underlying cardiac disease, probably you have to consider that that increased, that likelihood of recurrence is gonna be higher.

But if you've got mild to moderate disease, valvular disease, we perhaps think success would be better with DCC cardioversion. And if you've got a fast atrial fib because the horse is in heart failure, then neither treatment is appropriate. So, In the last section here, we're just going to move on to a few other rhythm abnormalities.

So I thought we'd start with the superventricular dysrhythmias. So they're quite common in normal horses, and you will only see performance problems if they're present in large numbers, and they're likely to be affecting cardiac output. The big downside to superventricular dysrhythmias is that they are likely to predispose to or have similar underlying causes to atrial fibrillation.

And so it's always thinking about, you know, should you treat these or try and treat these superventricular dysrhythmias in order to prevent them developing atrial fib. And probably, you know, everyone's got an idea about how we might manage these, there's almost no evidence for any of the things that we do, probably rest in case there is an. In underlying inflammatory cause, other, other drugs that have been proposed include Sotalol, and I do sometimes try Sotalol steroids.

I don't use steroids unless there's an increase in cardiac troponin I and then other things proposed include things like phenytoin, but we really don't have that much evidence for their, for their use. And then as we, we started off this talk thinking about the ventricular dysrhythmias, and we know they occur in normal horses. We don't know how many is too many, and what you always have to think when you're evaluating these patients is riding courses is dangerous and therefore, whatever you find is that likely to increase the risk of the dangerousness of the sport.

So in my view, and it is an opinion. Increased ventricular premature depolarizations or ventricular tachycardia at peak exercise, I think is likely to increase that risk of weakness, collapse and sudden death. Other findings, I think we just don't know.

What we do know is that there's likely to be an increased predisposition to, to the production or the presence of VPDs and ventricular tachycardia if we have an enlarged left ventricle. And we can see that with training, we can see it with aortic regurgitation. And we can often identify those horses with aortic regurgitation that have got an enlarged left ventricle, because they're the ones that are gonna have those bounding or hyperkinetic pulses, because we know those pulses are a .

Or a an estimate of a stroke volume. And then obviously with severe mitral regurgitation after we've got enlargement of the atria due to starling's laws, we'll then start to get enlargement of the left ventricle as well. And really with these ventricular dysrhythmias, we, we need to look at exercising ECGs under the condition that the horse works to determine risk.

And it might be we need to record more than one of those in order to make a more accurate assessment. And again, I looked at some data a few years ago from, a group of horses that had, that have got aortic regurgitation, and we had got 226 horses and we had an ECG on more than one occasion from 165 of them, and of that 226, 184 had got an enlarged left ventricle based on . Published data for their, for their breed type.

And we had all types of horses, general purpose riding, Juventus, endurance horses, and the prevalence of ventricular premature depolarizations exercise was 3%, which is exactly the same as the number that Professor Ma found in her study of normal racehorses. And when we looked at the prevalence of those VPCs and how they correlated to left ventricular size, 7% of the VPCs were from horses that had normal size left ventricles and 2% were from horses that had got enlarged left ventricles. So who knows the impact that The enlargement of the left ventricle has, maybe there's more to do with, you know, changes in catecholamine because of, abnormal blood flow.

We don't know all that it affects coronary blood flow when you've got, jets. But what we do know is that prevalence certainly in our population was still pretty low. So when we think about ventricular dysrhythmias, we are, when are we gonna treat them?

Well, if at rest, we're only gonna treat them if they clinically affect the patient, which is usually when that heart rate goes above 100 beats per minute or we start to see significant increases in blood lactate concentration. And before treating, we need to make sure that the electrolytes. Or normal, particularly as best we can anyway, potassium, magnesium and calcium, and also to look for underlying disease processes.

If animals have got SERS and sepsis, then it's going to be pretty difficult to treat them until you've got that underlying disease process under control. And then treatments will usually, we normally start with bolus of magnesium sulphate and then if that doesn't work after we've done several bolus, think about administering lidocaine initially as a bolus, and then as an infusion. If we only find ventricular, if we only find ventricular dysrhythmias at exercise, then we have to think about, do we have a reversible underlying disease process, which is gonna be pretty rare.

You know, myocarditis is a relatively rare condition that we diagnose, we can utilise cardiac troponin I from that. And these animals might need rest for potentially months. If they've got an underlying disease process such as aortic regurgitation or a very enlarged heart, then there's going to be safety concerns and thinking about retiring them because that disease is not going to go away and probably that heart is gonna continue to enlarge.

And this is, actually the myocardium taken from a horse that had ventricular tachycardia. He'd presented as a colic and had got, had got ventricular tachycardia but was passing faeces. And we scanned his heart, his heart looked on echo.

A little bit small because it was, his rate was around 100 beats per minute. And, you know, we diagnosed him using an, an ECG that he got ventricular tachycardia. He didn't respond to magnesium, but he did respond to lidocaine.

Right came down to about 48 beats per minute. He went into a sort of sinus tachycardia. I was very pleased.

I went for a coffee. I came back and he was dead. He hadn't killed the, ECG machine, which I was very excited about.

And what we found prior to him going into, into, ventricular, fibrillation was that he developed this sort of torsoon, this sort of sine wave type of ventricular tachycardia, and then he, and then he died. And you can see here he's got significant myocardial fibrosis. We couldn't see that on on echocardiography and it hadn't impacted on his cardiac contractility.

And so it was surprising he ever really responded to the drugs. So, in summary, we know that dysrhythmias are really common in the performance horse and others, but in fact, those pathological ones are going to be pretty uncommon. And, but they could be an important cause of poor performance and in those very rare cases, sudden death.

What's most frustrating is that understanding what's clinically significant really is not based on evidence-based medicine, but sort of centres around expert opinion. We know that atrial fibrillation is the most common pathological dysrhythmia. And that when you do have suitable candidates, they have really good to excellent chances of conversion, but they need early diagnosis and treatment.

You know, the very worst thing you can do with those is, why don't we see whether it's still there in 3 months, because in 3 months' time, it's gonna be much, much harder to treat. And we know that there's pros and cons of using Quinidine or DC cardioversion. And the really key thing is, if you want to identify risk courses which have dysrhythmias, we need to make sure we record really high quality exercising ECGs in order that we can make sure the diagnosis that we make are correct.

And with that, thank you very much. If you have any further questions after this webinar, please feel free to email me at gale. Halliwell@ IVC Evidencia.com.