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I always wait for this thing to circle on. Sometimes I'm actually live, and I don't realize, Okay, we're live. So hi and welcome everyone, Um, apologies for that little we delay in starting their, um, we just had some tech issues, and that always seems to be some. Um, but before, um, you know just our wonderful speaker today and highlighting what we'll be discussing. I wanted just to welcome everyone back who's been before, um, to the virtual correct journal club. And welcome everyone who's new. The goal of this general club really is a fantastic opportunity to share that expert knowledge driving interest in sciences and allow us all to work that bit closer by collaboratively working and share ing that interest in science and that expertise together online in this free and accessible platform. And that's really the purpose of the journal club. If you're not familiar with it before and if you're not too sure how you can enjoy tonight, well, whilst you won't be able to join any video or audio, you can ask a Q and A so, um, questions at the end. I think Nathan's can I agreed to do a live Q. Now is that correct? Nathan? Can I get a lot of things up? Yeah, sure, if you want. Yeah, Great. Um and so all you need to do there is just like the little Q and a, uh, button that should be on the right hand side of your screen and pop your question in there. Um, and just simply hit. Sent, um, so don't forget to do that. Um, so the time is the Inter just Nathan and Nathan is a senior research associate at the Institute of Sport, Exercise Sport and Exercise and Health in London. He's actually a former colleague of mine at a spot our sports medicine hospital. Um, who are the medical providers for the World Cup? Um, and aspirin are sports medicine hospital, while we were there was a world leader in sports cardiology and still really is with some great research coming out of there, and we're really quite lucky to have Nathan with us today. Um, Nathan has several publications in E c G interpretation. Um, in heart BGs m European Heart journal. If you're not too sure about those journals that really top end journals, especially European Heart journal, you can really get much better in that in karyology. Um, together with that, Nathan is a co offer on international recommendations for E c G interpretation and athletes. Um, so that was international consensus recommendations that was released in 2017, I believe. Nathan. Yeah, um, and Nathan was one of those co offers, so he really is an expert in this space, so Well, it's great to have you on Nathan. Um, so I'm not gonna steal any more of your funder. You take the center stage and fire away. Yeah. No, it's a pleasure. Thank you, govern for having me. And, uh, like I said, um, my experience of, uh, of course, my clicker doesn't work. Looking at that, uh, there's always something. Got it. I haven't got your slides just yet, but I Oh, that's, uh, good. Good, right. We've had way too many technical hiccups here. There we go. Now, is that going to work? Yeah. I'm going to take my video off, but I can keep the limelight on you. All right, there we go. All right? Yeah. So thank you, Gavin. It's a pleasure to, uh, talk today on something like you said, Probably both you and I are very passionate about and that is athlete C. C G interpretation. And like Gavin said, Luckily we've been part of this ASP. It'll program in Qatar where I personally kind of analyzed and evaluated near 20,000 e. C. G. S now in athletes. And now I've moved back to the UK in London. I've continued that work traveling up and down the country, doing cardiac screenings in some of our best athletes and indeed, football players. So what I want to do today is really guide you through where, from where we began in athletes, C C G interpretation and all the way to current thinking in 2022 where we may be moving in that direction. So I guess how far have we come? Well, sadly, this is still the first sentence of any paper you're gonna read an athlete. SCG interpretation. There is still a debate on E. C g interpretation, uh, between North America and Europe, and it's not really that true. We know that in most major sporting organizations in the USA, they do indeed utilize the e c g, the people that don't of the American heart Association and the American College of Cardiology, where they say that the general use of e. C. G within athletes is unfounded and that mainly due to a cost effectiveness point of view and really before I want to get into it before kind of waxing lyrical about E. C. G. We have to understand that there are limitations not gonna identify everybody that harbors pathology. There are cost effectiveness issues, and that really relates to the people and facilities who are interpretative. These findings There's many publications already out there that show that while expert opinion expert cardiology uh, interpretation maybe good, uh, identifying pathology in physicians and search that are not as experienced in sports cardiology. The false positive rates can still be high, and we must also stress that it's okay doing an e c G. But we have to ensure that adequate provisions are there to ensure that if you have an abnormal E c g, you can have an echo, you can have an MRI. You can have a stress test to really either rule out or confirm pathology. So that's really what I want to say before we get into it. But to start we go back to the year 2005. The heady days of when Tony Blair was still prime minister. The E S C guidelines were effectively created, uh, and led by Domenico Karada, one of the legends of sports cardiology. Uh, and what he and the group did was really take with 25 year experience, all the Italians and really kind of document that on paper now, in Italy since 1971 every single athlete that was participating in competitive sport had to undertake pre participation screening with an E C G. And so this was really kind of the the kind of baseline for these guidelines really using that soul Italian interpretation. Um, and really, it kind of spurred the you, uh, kind of documentation and, um, publication of research within the field. This is a quick pub med search of looking at the trend of e c G papers in E. C G, uh, interpretation in athletes papers from that 1971 part, uh, start and you see, from around 2005, there's a massive increase in the literature, so they really kinda were a catalyst in sports cardiology research that must be commended in itself. What are your things worth? However, the citations used for these guidelines consisted of these These two, the Dominican Corado paper looking at hydropic card um opera. See, uh, screening for high profit card, um, opposition, I say in young athletes. And then this textbook, which was diagnostic electoral choreography from this HCM paper. They only really used three citations kind of governing the e c G interpretation in athletes. And this is it's quite, you know, not a lot of papers kind of governing that whole principle, the ones that they were were the s s, uh the wrong pill s s paper looking at LVH. So they developed this criteria. There's one with p wave analysis in valvular heart disease and thirdly, e c G findings in HCM. So really, these were mainly, uh, pathological cohorts that we used and ultimately developed our guidelines to athletes. And this is what effectively they were doing. It was based around the identification of feed men pathologies, but what they did was take any e c g finding that was associated or found within these pathologies and considerate abnormal. Even in highly trained athletes. This led to this whole list of abnormal findings being part of this initial 2005 criteria. However, when we look at papers from as early as 1985 this great New England Journal of Medicine paper highlighted that some of the abnormalities, such as Sinus bradycardia in in the first degree AVB block, were present in up to 85% of our athletes. Indeed, with left ventricular hypertrophy on FEG up again, 85% of athletes of Olympic athlete so highly trained athletes had this finding. And so despite this paper been in 1985 in the whole 20 years before these criteria, they were not addressed within this athlete recommendations. So I'm not really sure why that was the case, but ultimately it led to quite a significant false positive rate or abnormal e c g. Read in these athletes. The three cities you see at the bottom there the bag ish wean of Malhotra are all from the U. S. A. R. Now actually quite low When we look at it, this Adam Package city, for example, they identified nobody with a Q t C prolongation PR, interval shortening or, indeed, PR interval prolongation. Nobody with silence, bradycardia and nobody with PVCs. That's quite unusual when we think about that 1985 study. In the 85% up to 85% have bradycardia. Then there's something unusual going on here. Similarly, with this weakness study, they identified that there were quite a significant portion of athletes with LBH and right bundle branch block, but again, very infrequent presentation of other findings. The best Um, study, however, which identified 47% of athletes that would have had to undergo on the every evaluation due to the finding of an abnormal E c G feature. Well, they kind of looked at it a bit differently and identified that 27% of their athletes had this prolongation of the QT QT interval and that 27% and that 15% sorry, 27% had LB age and 15% had long Q T presentation. And that's probably more reflective of the general kind of standing as it is. Indeed, when I looked at our data from Qatar when you were sitting around 35% here, so what? This did well, Domenico Corado lead the next rendition. Five years later, it was quite a way. But five years later they developed the recommendations for interpretation of the 12 lead, E. C. G in the athlete. And again, it was a consensus. So a group of leading cardiologists and physicians gathered around the table to decide what was abnormal and what would not? Well, thankfully, they identified five factors that were considered physiological. They were the first to kind of, uh, dichotomies these findings into training related such as these and training unrelated findings Sinus bradycardia, for example, as we know the rule rather than the exception in our unsolicited cobalt. Of about 19,000 screenings, about 65% had Sinus bradycardia, and 24% had a heart rate lower than 40 beats a minute, which would have been flagged by those previous findings and lead to further investigations. Now this is all related, potentially to an increase in the vagal tone, effectively decreasing this phase four slope of the action potential in the sinoatrial node. And this is done by a kind of, um, what is it, a shooting of the the sodium channels, kind of, um, a kind of less frequent kind of, uh, conduction through the sodium channels or decreased kind of trans mule action potential. Um, but then is it vagal completely vagal related? Or the study from Ricardo Stein in Brazil showed that potentially, it may also be due to intrinsic adaptation in the S a node in the a V node. And so they suggested that vagal tone was only potentially related to 25% of the decrease in heart rate, the rest of it potentially being related to structural adaptation. Again, When we think about athletes heart, we think about the structural adaptation and potentially there's something going on there when we move on to first degree AVB block. Then again, it's we see it in 12% of athletes and up to 33% in the athletic cohort, compared to just 10% in, um, Oprah max of 10% and kind of general population. And again, in our data, 7% would have had to undergo further investigation. We move on to probably the biggest, um, kind of hindrance in our, uh, progression through e c G. Interpretation at this point which was isolated. Curious voltage, the LBH In our data, 40% of our athletes would have had to undergo echocardiography because of the finding of increased voltage. But here you can see the correlation between maximal war think Mathon, echo and supposed criteria to LVH on E. C. G. Is incredibly, incredibly weak. I can't remember the exact correlation, but it's like 0.1 something or other, but very weak and finally just to complete it. No pun intended but incomplete right bundle branch block. You know, again, quite a common finding in our athletes in our endurance athletes. It is more common Meghan wants to be study from. I think Harvard rowers showed again 40% of their athletes identified showed incomplete right bundle branch block. And the study there from Carville is in, um, football players again showing a high prevalence. And what suggested is that especially in endurance sport, we have this increased right ventricular delectation due to the exertion of sport and the prolonging the prolonged kind of training effect, and that can ultimately cause potentially slight, slight dyssynchrony in, um, in the chambers. But ultimately this kind of RV adaptation. So what did this do we have the first degree? Uh, group one changes, But what about the group to change is Well, you can see there that I've highlighted a few specifics with regards to this. And this is where we are starting to get into more of the specific details of abnormal E c G findings. And this is what it did to the false positive rate. You can see the very end there, Gavin study, uh, being, uh not an outlier, but certainly having the highest prevalence of false positive rate, but similarly followed by this other pediatric study in 2021 suggesting that adolescent athletes may have against, like, different adaptation than adult athletes. But again, up to 40% of fourth positive rate is again unacceptable. In our data, we were looking at 22% of a false positive rate again. When a quarter of athletes are going to have to undergo further evaluation due to a supposedly abnormal finding, it means that screening on a large scale which would not be conducive. But how did this breakdown the best? Um, study again showed that long Q T was the main corporate with Rite Aid to enlargement being found in 10%. The pediatric study I mentioned before again long Q T interval being the most predominant factor for an abnormal E c g. Similarly, with our our data a long peut interval so that over 440 milliseconds in males with bounding over a quarter of our athletes importantly T wave inversions were found in a fixed. So over 20% of our athletes had a T wave inversion, which would have had to again lead to an echocardiogram or potentially even MRI to rule out pathology. So why does our study stand out there? You see the best, um, study showing only 3% of T wave inversion. Well, fortunately, in Qatar, one of the great things we had about our data was that we had athletes from 100 and 51 different countries, which is really quite unparalleled and something we are quite proud of in our data, and that is really quite a worldwide representation. I mean, there's only 100 and 95 countries in the world, so it's pretty widespread there. So could it be that the E. S C criteria, which predominantly used athletes from Europe and the USA, we're ignoring athletes from other countries and even other continents In fact, this criteria mainly looked at studies in Italy and Europe, not even really that much from the USA. But Karada and colleagues identified that there may be limitations with this, but further studies are indeed needed and that we need to understand the Z e G e c G criteria in relation to gender, age, ethnicity and type of sports and training level. So this led to the Seattle criteria only two years later, so hot on the heels of and it was led by John Dresner from the University of Washington and this really kind of tackle some of the nuances of the criteria in the Group. One findings we went from only five E. C. G. Features that were considered a normal finding and representative, a physiological adaptation to 10 in the Seattle criteria, the big one being this. The convinced ST Elevation combined with a T wave inversion in these, the 1 to 4 in black or and or African athletes. And this came from the Sanjay Sharma Group, led by the first author of Michael Papadakis. I'm going to mention this group a lot. They have really shaped our understanding and our thought process on this whole topic of sports cardiology and e c g interpretation. But they found that black athletes had a way, way, way greater presentation of T wave inversions across the board that, particularly within the anterior T wave inversion compared to controls it was still higher. But white athletes have significantly less t wave inversion than the controls, suggesting that there may be some kind of ethnic adaptation here that is going on when they compared it to hypertrophic cardiomyopathy. Patient's The picture starts kind of unraveling Lateral T wave inversions are the predominant presentation in cardiomyopathy Patient's. When we are looking at anterior T wave inversions, we see that the prevalence between black controls and hypertrophic cardiomyopathy patient is pretty much identical. Threefold. Higher is a prevalence in black athletes. So again, could it be that this is an athletic adaptation, an athletic response? We already know that early repolarization is another feature already more commonly found in black athletes, and therefore could it be along the same mechanism that we are seeing this finding? We see inferior T wave inversion showing something similar rich, and we'll get to that a bit later on. But ultimately, irrespective of T wave inversion. There are two factors that really stand out and they are pathological Q waves in ST Depression, which is founding up to 50% of cardio occupations, compared to just 500.4 in our athletes. Therefore, if you find any of these factors, then it is quite a significant thing and we need to undergo further evaluation to try and rule out any pathology left Atrial enlargement seen in 44% of car democracy patient's But typically this is in isolations and seen in 9% of the athletes. So this is the list of abnormal findings. We see that the T wave inversion has been modified to that now, extending not from be one but from B two, so two or more consecutive leads. And we have various other factors on the E c G that have changed in their definition. And so this is where we are getting a lot more nuanced in our understanding and our interpretation of the athletes. E c G. So what did this due to our false positive rate, what it was massive, a really big decrease in the false positive rate and the C abnormal e c G findings in our study, it was halved in Gavin Study again halved. So when we are having the rate of the number of athletes needing to undergo further evaluation, this is a massive, uh plus for our progression in our understanding of e. C. G interpretation in athletes, and also for the factors such as cost effectiveness in our cohort. What govern this would, particularly this long QT syndrome you can see in red. The short beauty and long beauty was really quite prevalent using with 95% cut off when we use a 99% cut off, those being flagged are a lot more rare. As you can see here. I mean, the short PR has basically been kind of completely wiped out. Similarly, with the T Wave inversion, we see a lot of other athletes with anterior t reading version. By utilizing the new Seattle criteria, it would spare about 7% of our athletes from undergoing further evaluation. Now we still must be careful with the anterior T wave inversion, and I guess always have it in our mind about the clinical context of which, with patient's are coming, there's been work suggesting that the ST Elevation is very crucial in differentiating between benign T wave inversion well, more normal and the more abnormal state of this T wave inversion. But again, clinical context is key. When we look at it, we are still seeing seeing studies where fourth positive rates are booked, 10% myelin Gavin's included. And so what the ST George's Group did were look at this and identified further areas. Improvement 16% had right ventricular hypertrophy on the E C G again, Is that something that could be considered well, They suggested that again, this was not necessarily related in isolations to pathological findings. And again, 43% of athletes having an abnormal e C G were flagged because of entering enlargement and axis deviation. So 43% in our study was about 55% of abnormally CGs were due to these findings. In the study of up there from Gatti, they identified that none of their athletes with hypertrophic cardiomyopathy had these findings in isolations in the nonathletic cardio pretty patient's. I think it's about 4% but ultimately, when we are looking at a sensitivity of our screening and our e c G sensitivity, it decreased from. I think it was 91% to 89.5% in terms of sensitivity, so really not much lost in terms of sensitivity. But a whole lot gained with regard to, uh, Gavin's data in adolescent athletes again. Most of this that we saw with atrial enlargement, axis deviation and this complete wrap on the branch block were predominately due to write here to an enlargement to up to 12% of athletes were having to go further investigations due to these findings. So what? The ST George's Group again, led by Sanjay Sharma, the first author was, uh, nubile chic. And this was a great paper that set in stone something that was coined. The refined criteria introduced this concept of the borderline finding whereby should you have two or more at these findings, it will be considered abnormal in isolations. It will be considered a normal finding. What did this Due to the fourth positive rate well again, we have decreased significantly again our data from 2014 again half that false positive rate to just 5% in the UK studies from ST George's, we are down to 4 to 7% of this fourth positive rate and just 3% in adolescent athletes. So this is really making strides in our understanding here all the while sensitivity and our ability to detect pathology, it maintained, because the refined criteria we're not a consensus group. They were not an official process. The international recommendations, again led by John Dresner and Sanjay Sharma, were created and, like Gavin mentioned Start. I was looking enough to be part of this collaboration, and it's really honored to be part of this, and hopefully, you know, going forward, we can make more adaptations to this. But ultimately what the international guidelines stated was this borderline findings should be integrated into the criteria. So should you have access deviation or a tree in acknowledgment or complete right under branch block? If you haven't been isolations, consider it normal in combination with one or the other. It should be considered a pathological finding, requiring further evaluation. So what did this? Due to just recap are false positive rate and our progression throughout 2025 to 2017. Well, as you can see, we have come a long, long way going from 47% false positive rate to now. The studies in the US A. Such as hides in 2019, shown a false, positive or abnormal e c G rate of just 1.3%. And, of course, that is well within the realms of clinical acceptability. And if we are able to identify all those with pathology while kind of not losing any anybody mixed from a finding, then again, cost effectiveness is coming, always improving, and the feasibility of E. C. G lead screening is again being reinforced. So going into more nuance of these latest criteria, one of the other things they did was look at the T wave inversion and realize that in and actually under the age of 16, the juvenile pattern is still very much present, so typically again, due to right ventricular predominance in well in in in from birth, this kind of have a prolonged effect, kind of showing more right ventricular kind of, um, presence again being reflected on T wave inversion in the high anterior leads. But what we must consider is maturation. Girls peek at velocity make peak and around average of 12 years old and boys around 14. But this may start as early as 9.5 years in girls and up to 16 in boys, where a skeletal fluctuation may not peak until 18 1920 years of age. And it's important because of the physiological, pathological gray zone that we have in our e C G interpretation, particularly when we understand that some pathological features of conditions such as hypertrophic cardiomyopathy or, Regardless, syndrome, for example, just to pick, too our only sometimes present after puberty. So if we were screening prior to puberty, we may mix these athletes if they were not screened before. Therefore, having an understanding and appreciation of maturation is vital now. This study, from uh, led again by Sanjay Sharma and the Normal Ultra, showed that sensitivity using the international guidelines was maintained in adolescent athletes, whereas specificity all the while improved again, improving uh, the ability to interpret, uh, the athletes E C G. However, they looked at adolescent athletes. But what does this mean? Well, the entire cohort, just comprised of athletes for 15 to 17 years of age, importantly, 74% of academy football player in this age rate are early insurance, so Actually, this could just be reflective of these athletes actually being muscularly and cardiac well, cardiac leat. That's not the right word. But you know what I mean? From a musculature and cardiac point of view, they are already developed into an adult athlete and therefore not representing the true general cohort of other license. Especially now when we are thinking that athletes are being screened from early as young as 12 years old in the official guidelines. But this may be done from the earliest five years old in some cohorts again thinking about maturation two athletes here that have a chronological age of nine years old. They have two very different biological ages, and Gavin, very eloquent study again show the importance of this, whereby chronological age was a poor predictor of, um, the anterior T wave inversion, but also the the diagnostic accuracy of having a T wave inversion biological age being a much better predictor of whether an anterior tear of inversion was considered or actually physiological or pathological. And this has not been considered in the international criteria, but I do feel like it's an important point for further renditions. Next, we've got female athletes Currently, there has been no discussion in any of the guidelines about the differentiation between the female and male athletes heart, yet we know it exists. The prevalence or the kind of the presence of female representation in the Olympics has soared from 2.2% in 1900 to now almost been equal at 49%. So thankfully, female participation and representation is increasing. Sadly within the athlete, e, c, G and research world, we are still lagging behind, so more research definitely needs to be done in the female athlete. Currently, it has been long understood that that the Q T C interval can be governed by sex, so over 99% confidence into 99 percentile for long. Q. T threshold is longer in females than it is in males again in pre puberty, the Q T CS are often very similar between boys and girls, and it is post puberty where this differentiation occurs. There are other factors on the C G that do differ between female and male. Well, many of these look like males have have, uh, more, uh, percentage of curious over 100 milliseconds or sock off criteria for LVH the stand out there is, of course, the interior T within version, and this again eloquently studied by a near Mon Holter Sanjay Sharma group, where they found that 4% of female athletes had t wave inversions in the these leads, compared to just 3% in males. And this prevalence can range from 4.4 but up to 9% of female athletes having to wave inversions in the leaves. So can we consider it a normal finding? Well, one of the things I think it's always important to understand and consider is ucg electoral position, particularly with the female athlete where where, of course, there is breast tissue. And so what often happens is that the E. C G electrodes are placed lower than where they should be. So that's a key consideration when doing the CGs, but also kind of trying to understand why we have these differentiations. But this is one for further research, for sure. Again, the pattern of the tea with the version is also different in female athletes. One crucial aspect for me anyway, a big one to my research has been taking this concept of the T wave inversion in black athletes and applying it to our cohort. Currently, the term black athlete is used. But what does that mean? Can we really use this term black athlete? When we think about Africa, we see there is such a massive, you know, kind of ethno linguistic differentiation between the areas. You know, even from a geographical point of view, you've got the Sahara Compared to the Rift Valley, Africa is massive. You can fit. Uh, I did have a slide on how many countries you could fit into Africa, but it's huge, you know, like I said before 2000 different ethno linguistic groups within Africa alone. So it seems implausible that we are kind of collectively terming, terming these athletes as black athletes can we do better? Well, I think I think we can when we look at our data. East African athletes have a prevalence of anterior tea with a version of 2%. Compared to North African parodic athletes, it's higher. But compare this to West African and Middle African athletes, where the prevalence of tea wedding versions oh, surpasses that you start to feel athlete and this is the also in the kind of normal T wedding version in the anterior right whereby just 1.5% of these African athletes have it. So can we really consider this in normal finding in the East African athlete? I really do think more research needs to be done in having this blanket approach whereby athletes are considered normal just by this kind of black African term again with abnormal e. C g. Very, very different findings. East African athletes having a similar prevalence of abnormal E c G T wave inversions to that of the Arabic North African athletes and again way lower than the East Western medal African athletes. So again, I feel like more consideration needs to be put into here as well. Also, trying to understand what is behind next you know, um, are factors such as socioeconomic status at play. Also here, ultimately, most different research to date has been in these continents and countries. We must acknowledge that our world is not that small and that we need greater representation in our international criteria in our literature to support our findings, because we have to acknowledge that e. C G screening is implemented and recommended by organizations such as FIFA and the IOC, which are worldwide federations. And so we need to have a better representation of athletes from all around the world to really guide our understanding. The final one for T wave inversion is that inferior leads. Like I said before, the prevalence between black controls and high profit Khatemi opposite Patient's was quite similar. Where again, it was higher in the black athletes not quite as much as the anterior needs. But it makes us question. What is the role of what is the prognosis of an inferior T wave inversion? In our data, we identified seven athletes with hypertrophic cardiomyopathy thinks have lateral T with inversions. One did have solely inferior T weather versions, but importantly, they have pathological Q waves and ST Depression. In all of the cohort, no athlete with inferior teary conversion was diagnosed with cardiomyopathy. This was similarly found in the ST George's Group in the study led by Leo Mahanta. So again, it's something that we need to be considering to flip that the Australian study led by Maria Brosnan showed that in arrhythmogenic cardiomyopathy, inferiority with inversions were found, and so again, could it could be an expression of arrhythmogenic cardiomyopathy. I do feel like more research needs to be done on this topic, and but there's certainly conversation to be had again. This was kind of shown within the international recommendations whereby T wave inversions isolated to the inferior lease, had its own reception, where only Echo was recommended for further evaluation. Of course, clinical suspicion, family history, symptoms governing everything as well. But it's an interesting take as we move on PVCs with one of the other considerations in the international criteria whereby if we see in two or more PVCs percent, 12th e c g. We should consider an abnormal finding. One of the things I note is that sometimes we will see a run of the not run as in, uh, nonsense NBT But we will see several PVCs isolated, but they don't have any. And again, how do we document this in our reports in our in our research? So maybe there's a point here, but ultimately, one of the things this doesn't consider the international criteria is where the PVCs are coming from, because, of course, there are different origins. The right ventricular outflow tract left ventricular outflow tract of are more common but also, of course, we see it in the mitral and tricuspid Aniela food, papillary muscles and the left ventricle. And these have potentially different kind of workups and puts different thinking in our mind because, uh, traditionally PVCs originating from the outflow tracks that are considered more benign. And this is really identified here where if we see PVCS looking like this, then maybe we can consider them of a more benign origin. If we've seen if they're originating from the RVOT, then we have an inferior access with this left of the branch block pot pattern, um, left ventricular outflow tract again. Inferior access with the left bundle branch pattern that the curious transition being a bit further up the left and and to the left posterior and anterior particulars of the left from the branch block again also showing or not showing inferior access, but now showing either inferior or superior, but of the right bundle, branch block pattern, and again here, the crucial partners, if they have a cure, s under 1 30. So maybe future iterations we should be considering the origin of the PBC and whether they are benign or not. The more pathological related PVCs originate in former LB from papillary muscles with even mitral annular, which is this pattern, or indeed, the right ventricular three wall low QRS voltage is another consideration that has recently come to the fore as a potential consideration in the future. E. C G interpretation guidelines. It is typically considered when we have, uh, in the inferior leads the Curis of less than five millimeters in the prick prick or really 10 less than 10 minute ages. Now, typically, this has been due to, um, a well. For example, with obesity, you have this bat layer, so there's an increased layer of, um, tissue between the electrode and the conduction of the heart. Similarly, with new before pericardial effusion. For example, in the Dema, we don't have fat that we have fluid, which is causing this low QRS voltage, but also importantly in things such as myocarditis, all the infiltrative processes such as amyloidosis or sarco doses. And again recently, researchers suggested that low curious voltages may be an indication of arrhythmogenic right ventricular cardiomyopathy, particularly with biventricular involvement. The Brazilian paper showed that 21% of ARVC patient's had low curious voltages compared to just 1% of athletes in this police yesterday they showed that shouldn't athlete have low curious voltages? It's 4% and varicella, but they were much more likely to have PVCs up to 40% who were found to have PVCs, compared to just 7% of PVCs. When the curious voltages were normal or high. And also the origin of these PVCs were considered to be more sinister. Should the athlete have a low QRS voltage? So again, a very important thing to be thinking of when interpreting the athletes. CCGs Uh, the final thing is the borderline finding. Now we talked about the study from Serbia Gotti and Sanjay Sharma group that led to the refined criteria and ultimately the international criteria. But what is a borderline finding? What did it really mean? Well, the hallmark one is, of course, left out of an enlargement, which has been a feature of hypertrophic cardiomyopathy but again rarely found in isolations, particularly in the athlete cobalt. But when we're when we're thinking about borderline findings, we've got to be thinking about what combination are considered pathological. The minute all of them, any combination is considered pathological. But really, if we see biatrial enlargement or kind of atrial anomalies. Is this alone? Um, should that alone be kind, kind of considered an abnormal finding again. I think more research needs to be done in looking at these combination of the borderline findings and whether they are true representations of pathology. And finally, the other one is complete wrap on the branch block, which I know some people have reservations about. And really, because it was only really seen and the whole kind of complete right from the branch block being in this borderline finding was governed by one paper. And that was by Kim from the United States, where they found 3% of their athletes having complete wrap under Branch Block, which is quite high. But they attributed it again too, right, ventricular adaptation, particularly endurance athletes again suggesting some kind of ventricular dyssynchrony. But ultimately in these athletes they had a lower heart rate and know pathology. So they suggested that they should be considered a normal finding. Our study, for example, our cohort of 18,000 athletes, we find a prevalence of just 0.3% with complete right under branch block. So I think again, more research needs to be done looking into this of whether it's like a soul kind of physiologic adaptation to really endurance exercise, or is it may indeed be a hallmark of pathology. So to finish while this isn't strictly related to the e c G. I mean, it's a bit of a plug, but this is my latest paper, uh, looking at the quality of the guidelines. This is mainly for, uh, cardiac screening in general, but ultimately that we need to really work on are kind of documentation process of the recommendations, trying to move away from ultimately trying to move away from a consensus based approach. But if we are going to do a consensus, make sure we have people from many different, uh, many different stakeholders, many different professions with different ideas, but also really kind of utilizing the whole literature base and really trying to make it as kind of quality quantitative as possible. So to conclude, uh, both positive rate of BCGs has decreased significantly to the point where they are within the realms of clinical acceptability, and the international criteria really are a useful tool. We need to make sure that physicians, cardiologists, physiologists are all comfortable with these guidelines. Understand that these are the latest guidelines and are able to interpret these and apply them to their own athletes. And ultimately, that there are notable areas for future consideration. But ultimately, again, more robust guideline development is also needed. So thank you for your time. Um, and that's me. Thanks, Stephen, for a great talk. Um, it's always good to talk about athletes art, and I hear from you in regard. Um, uh, if anybody has any questions, please used to pop them in, um, Nathan's more than happy to take them for you. But in the meantime, whilst we might wait for some of those questions to pop in, you really outline a great point in regards to the international recommendations in terms of how it can register false positive rate and how we can really maintain that sensitivity at the same time. And I guess that use you kinda hinted towards. What might be holding back towards the star is that they're like, um, ultimate lay the need for expertise in athlete TCG interpretation. I guess what my question really is, What what sort of things or what sort of barriers do you think will really help allow for that implementation of those recommendations with regards to training for the practitioners attending practitioner. Yeah. So there's that, um, for the Seattle criteria, there was the be GSM modules online E c G. Interpretation. Since then, for the international guidelines, we also have, uh, again a learning course that people can do, which I'm not sure where it is online, but it's somewhere online, Uh, which is a training course to allow you for holding your skills and learning about 80 g interpretation. So I think that's a real important point is that anybody interpreted interpreting an absolute C c g all familiar with the guidelines. Um, because they are our latest understanding and will hopefully reduce that both positive rate and ultimately, the number of athletes having to undergo further evaluation. That maybe unnecessary. Yeah. And I guess, um, one of the great things without their paper international recommendations. Is that really nice figure? Um, so you've got that clear green number red. Um and that really helps in terms of identifying those findings. And, of course, within that paper, I think you outlined if somebody wasn't too sure what they're finding is actually really clear. Define it. And what for? Diagnostics to Yeah, it's good that that's an important point, Gavin. Yeah, that the in the paper highlighted there is if you have an abnormal finding, then what is the recommended further evaluation That you want to go? Yeah. Um, one other question I might I would have is, um I guess where do you see e c. G. Interpretation improve. Uh, where do you see improving? I guess. Do you see it mostly? Do you see the adoption? Like we in that pediatric athlete study? We use biological age, right? But not everybody has readily access to it. You know, you outline the aspect about height, but then I guess from my side the thing of height is that you need that historical deer that makes it really challenging. Um, do you have any thoughts on that there? I know I've given you really difficult question. No, I mean, no, it's a good point. And I I guess that is one of the crucial practice, because all the while when I was going through that presentation, I was highlighting your study whereby you with the kind of the standout in terms of fourth positive, right? I say you, that's quite harsh, isn't it? Uh, the data that we had that you published, um that was the highest kind of prevalence of both positive rates and one of the factors there may be due to the fact that we had, uh, young athletes that these not adult athletes and combined like asset in our day together, we had 100 and 51 different nations represented, which is, you know, math. And so I think, together with understanding that geographical origin, I think is an important factor for the abnormal T wave inversion. But also that maturation is the important point as well. And that, um, again, going before this kind of more going before you're kind of 16. Based on chronological age, you main it, uh, you know, kind of pathology. If you only scream once. I guess the argument could be made also on this since that if you're the hesitation might be okay with the biological edge on the on the on the basis that will get us another test that could just happen out of that patient can have an echo, but then you probably want to be aware of that patient's maturational state. Um, I know we've got some work coming out in that regard, but with echo. But then it also comes into your C MRI as well. And it just helps that holistic picture, I think, um and then, yeah, totally. In terms of geographical origin aspect is really there's a really interesting findings and it be interesting to see if anyone else can replicate that. But I think they would struggle because it would be so hard to get such a heterogeneous population. But it's really nice to see further studies in there. Yeah, absolutely. You know, I I just hope we kind of unravel why it's happening as well. You know, um, like the studies in the US coming out and and looking at like like I said in the talk about socioeconomic status and things like that. Like, is it access to healthcare in early age? Which is kind of making that some of these athletes you are only coming to a doctor when they go to high school or something. I I don't know. Um, they may have been selected out of sport at a younger age. Um, you know, something like that. It may. It may be a factor, and it's it's, sadly, something that's very difficult to kind of quantify. Yeah, that's a really good point. Um, a good question. That's just come in, is one I think, um, you hear frequent. We get frequently is high. Applicable. Do you think E c G guidelines are 22 recreationally athlete? Um, and it really does it come down to training volume? Does it come down to train intensity? Um, when is that appropriate time to plot to consider this person an athlete? I guess, uh, that's that's a million dollar question. And that's something where hopefully we've got the data for and hopefully we're going to be at answering. You know, I've said soon, but, um, it's one of those, isn't it where, like I said in Italy and Spain now, because the got the EFC guidelines said that you should start screening athletes at the start of competitive activity? Well, when is when? When did you start competitive activity? I started competitive activity when I was like, six years old, and and that's when people are being screened. You know, in some of the Spanish studies, you've got athletes athletes as younger spy that are being part of the, uh, the athlete cohort. There's some great work from, uh, researchers in, uh, I'm gonna say scanned in area because I can't I think it's Norway that looked at cross country skiers, and it was more of an echo paper. But looking at the adaptation, and when the adaptation occurs and it can, it can start to occur in his little three months of, uh, training, even in preadolescent Children. So just three months of, uh, training can elicit adaptation on on Echo. Um, there's probably going to be some delay in kind of e c g features of that, but I I would imagine that it wouldn't take long to show initial e c g features of athletic adaptation, Um, and then with regards to the recreational athlete, um, again, it's identifying that crossover between what is an athlete and what isn't right. Um, the international guidelines, for example, state something like an athlete is anybody. That party participates in physical activity. Well, that can be anybody. And so if that's what the guidelines are staging and actually tells, um, yeah, I guess that's what we've got to go with anybody that is participating, Uh, sciatic activity. But, um, again, Big one, depending on age, particularly over the age of 35. Yeah. Oh, no. I can't hear you. Yeah, we were We were doing so well. Please. So I was muted nave, and that's why you didn't hear me. So, uh, someone kindly outlined that. So an idiot me, uh, suggest while Nathan was answering that I quickly whipped up the international recommendations, and they really they say it ultimately that they can be applied in regular. Somebody who's has regular and long term participation, intense exercise, a minimum of four hours per week. Um, it's associated with those athletes. Um, heart changes. And that makes sense. Because if somebody is doing it over a short period of time being three months and we see that change is an echo, it's just that repetitive volumetric demand. You're gonna see those adaptations. As a result, your heart's going to adapt to that stress. Um, and even a little a really good point. I've just lost this video. Um, to the point of that veteran athletes, someone over 35 we haven't done a great deal of research in that space, and it's somewhere That's really, um, need some research. So we can really be a sure when applying b c g interpretation guidelines in athletes. Um, I was just wondering if we have any other questions there just before we wrap up. Uh, somehow I lost Nathan, um, video, but I can take there we go. Let's go back. Um, if there is any other questions, just far them in now. But otherwise, um, Nathan, it's really good having you on. Um, despite some tech issues we enjoyed pretty and during giving it didn't happen during the talk. But thank you very much for your expertise is really good, uh, to have you on and discuss and give that nice overview of everything right from the start and how much positive impact the research has been has the positive impact research has had on maintaining that sensitivity while increasing that specificity, which is great. Um, thank you. Um, so everyone else enjoy the rest of your night. And, Nathan, you enjoy yours too. Thank you. And I hope to see you in the new year where we'll have some more guest speakers on in different areas on cardiology. So thank you. Cheers. Mhm.