We're going to talk about ECG interpretation in athletes, and I think we should just get right to it. So why is this important? Well, as we know, you know, sudden cardiac death represents about 75% of all fatalities during sports and exercise. And effective prevention requires early detection of cardiac disorders predisposing to sudden cardiac death. So why ECG? You know, ECG can be used in clinical practice for two different reasons. We can use it for diagnostic reasons, for further evaluation of symptoms, or an abnormal physical exam, or perhaps abnormal family history, or we can use it as a screening tool to look for cardiac disorders at risk for sudden death, like cardiomyopathy, ion channel disorders, or pre-exhalation. ECG, accurate ECG interpretation requires several things. We have to understand the physiologic adaptations in athlete's heart. We have to understand the pathological disorders that we're looking for and how they might present on ECG. We have to understand the appropriate secondary investigation of abnormal ECG findings. We need lots of training and experience to do this well. And we have to have cardiology resources, just like everything in sports. I would say sports cardiology and sports medicine is also a good team approach. So for this lecture, we're first going to start with just a little bit of history on the evolution of ECG interpretation standards and why this is so important. We'll spend most of our time looking at the international criteria. And I'm going to present my approach to looking at an ECG, what I call six steps to ECG interpretation in athletes. Of course, we'll go through a lot of different examples. And then lastly, we'll spend a few slides talking about sort of the current events and cardiac considerations in COVID-19. So we all have heard the term athlete's heart, and this really refers to physiologic cardiac adaptations related to regular intense exercise, and they can take two primary forms, either increased vagal tone, which leads on an ECG to several things like sinus bradycardia, sinus arrhythmia, early repolarization, first degree AV block, or even MOVITS type 1, second degree AV block. Can also lead to enlarged chamber size, both wall thickness and cavity dimension. And this can lead on an ECG to increased voltage criteria for LVH, or even incomplete right bundle branch block. And some of these are related to the type of sport, your age, sex, body size, and even race and genetics. And the evolution of ECG interpretation standards, the first to really come out was in 2010 by the European Society of Cardiology, and they were the first to recognize that there are common physiologic changes on ECG that can otherwise be confused for abnormal findings. And they classified ECG findings into two groups. Group one was common in training related, and then group two was uncommon in training unrelated ECG findings. This was slightly modified in 2011 by a small international group led by associates at Stanford. And then eventually in 2013, we held our first ECG interpretation summit and developed the Seattle criteria. I think the real benefit of the Seattle criteria was a very pragmatic approach, especially for sports medicine physicians, where ECG findings were listed in a simple table, which define normal versus abnormal, and it's the abnormal ECGs that warrant further investigation. Shortly after the Seattle criteria, Sanjay Sharma and several researchers out of the UK published an article defining the refined criteria, creating really three groups of ECG criteria. And then there was more science that came about, and we held a second summit and eventually developed the international recommendations for ECG interpretation methods. This was published in 2017 and also endorsed by 17 sports medicine and cardiology associations around the world. And this remains the current standard when we look at an athlete's ECG. The international criteria did two things. It wanted to update our ECG interpretation standards, and then it also wanted to have a very clear guide to the appropriate evaluation of ECG abnormalities. So for instance, if you see a specific ECG finding, like lateral TWA inversion, there will be a table that links you directly to what the recommended secondary testing should be. This is the international criteria sort of summary, and as you can see, the ECG findings are divided into a few different boxes, sort of the green, yellow, and red light boxes. Green represent normal ECG findings, and red represents abnormal ECG findings where any single finding warrants further investigation. In the middle are the borderline ECG findings, and we didn't feel like there was enough scientific data to put these findings in either the green or the red box, and there was some data suggesting that two or more of these borderline findings would warrant further investigation. So within the borderline group, if they occur in isolation with only one of those findings and no other finding from the red box, we consider it a normal ECG and no further evaluation is required. I think one common question that comes up as new renditions of ECG interpretation standards have emerged is, does modifying the criteria come with a cost? Do we sacrifice sensitivity to improve specificity or lower the false positive rate? As you can see, there's been a number of different articles from independent researchers really around the world, and they've all shown the same thing. Within each of the renditions and evolution of ECG interpretation standards, we've done a very good job to lower the false positive rate without compromising the sensitivity to detect the conditions that we're actually looking for. This was an article that we published in 2019, looking back at about 5,000 college athletes who've had an ECG, and we applied the international criteria to their ECGs, and I just want to draw your attention to the expert overread. With experienced clinicians, the total abnormal rate was only 1.6%, and the false positive rate was only 1.3%, which is a better false positive rate in statistical performance than most screening tools that we use in medicine. Also, the positive predictive value was very important. One in six athletes who had an abnormal ECG actually had a cardiac condition associated with sudden death. Let's think about when we look at an ECG, the questions we should be thinking about. The first question that you have to answer is, is the ECG classified as normal or abnormal? Normal, no further evaluation is needed, and if the ECG is abnormal, further evaluation is needed. One thing to understand is there are borderline findings, but there's no such thing as a borderline ECG. In the end, you have to make a decision based on the findings you see, are you going to classify this as normal, or are you going to classify it as abnormal and get more testing? If the ECG is abnormal, I think you want to understand specifically why and what the next step in that evaluation is, and then there is some relevant clinical information that can impact how you interpret the ECG, for instance, race, age, or even sex. These are my six steps to looking at an ECG, and after looking at thousands and thousands of ECGs in this setting, I really try to teach people how my eyes flow on an ECG. It starts with the assumption that when I'm looking at a young athlete's ECG, that the ECG is normal until proven otherwise. The way my eyes scan is looking specifically for the things that would flag the ECG as abnormal. We're going to walk through this. Step one is looking, I always start with the pericordial leads, and we go through V1 through V6, and then we'll move over to the limb leads, and we're looking for the big things, pathologic T waves, ST depression, and T wave inversion. I'll run through that again, from the pericordial leads over to the limb leads, looking at QRS morphology, looking for things like WPW, bundle branch blocks. I'll then look for axis and atrial enlargement. We'll look at the rhythm strip at the bottom, and then the last thing that I do is get a rough estimate of what the QT interval is, and that this correlates with the computer calculation of the QTC. How does this look when I look at an ECG? I start in V1, and my eyes go down. I start in V1, and I go down to V3. My eyes will go up to V4. My eyes then go down from V4 to V6, again, sort of looking for Q waves, ST depression, or T wave inversion. My eyes will come across the screen to AVF, up to AVL, over to lead 2, and then up to lead 1, and that's sort of step 1, and I repeat that again for step 2. We don't include AVR. This is sort of a backwards lead where there's often T wave inversion and other abnormalities, and we typically don't look at V3, at least for some things like T wave inversion. We'll look at axis, and if it's up in 1 and up in 2, you'll have a normal axis. We'll look at the P wave for atrial enlargement. We'll run through the rhythm strip at the bottom, step 5, and then the last thing I do is look at the QT and QTC. It's important that when you look at an ECG, you have to understand the definition, so at the bottom right of your screen is that summary slide with the green box, but you have to really understand specifically what the definitions are, so it's important to go back to the resources like those international criteria documents and make sure you've read the tables or have this available as a resource if you need to and you're not familiar. So let's look at this ECG and run through what we look at in step 1, and so again, I'll start at V1 and move my way down to into V2, V3. So far it looks good, no Q waves, no SC segment depression, no T wave inversion. I'll come over to AVF, same thing. This looks good, no Q waves, SC depression, or T wave inversion, and up to V1, and this is a very normal looking ECG, and what it does show is some striking voltage criteria for LVH. Voltage criteria for LVH is met in over 50% of well-trained athletes, and it just is not a good distinguisher for disease, so normal finding. So here's another ECG, and again, as I come down looking for Q waves, SC segment depression, or T wave inversion, I don't see that. It looks good. I come over here, same thing. This ECG doesn't have those specific abnormal findings. It does have some things that are normal findings that are also pretty striking. So for instance, it has pretty widespread SC segment elevation, or early repolarization. This also is present in up to 80% of young athletes who are well-trained, and is not a great distinguisher for disease. This complicates our ability to look for myopericarditis in the COVID-19 era, and we're going to talk a little bit about that later. Also on this ECG are some very large peak T waves, but overall, this is a normal ECG, does not warrant additional investigation. Incomplete right bundle branch block, you can see right away in lead B1 with an RR prime and a QRS width or duration that is less than 120 milliseconds, and again, just looking at the rest of the ECG, having my eyes flow in that same direction, this is a normal ECG. Let's talk about the black athlete repolarization variant. This was characterized in athletes of Afro-Caribbean descent, and it's been characterized for really over a decade. The black athlete repolarization variant is demonstrated in leads B1 through B4 with J-point SC elevation, followed by convex or domed SC segment elevation into a negative T wave. You see this pattern of domed SC segment elevation into a negative T wave. If I was running through my normal process, I immediately see some T wave inversion, but then also recognize that this looks like the black athlete repolarization variant. And importantly, that repolarization variant never advances past B4, it is always confined to the anterior precordial leads, B1 through B4 and not into the lateral leads B5 and B6. This is a normal repolarization variant in black athletes. Here's another example of it that begins in B1, again, a little bit of J-point elevation, domed SC segment elevation into symmetric inverted T wave. Same thing here, into T wave inversion, convex SC segment elevation into T wave inversion, again, confined only to leads B1 through B4. This is a normal black athlete repolarization variant. This variant has actually been characterized in Caucasian athletes in a study out of Italy and needs to be reproduced. And in my experience, even when we do further investigation in white athletes who have this type of pattern on the ECG, I'm yet to find pathology. So at some point in the future, it could be that we just recognize this as a athlete or exercise variant of repolarization. Let's talk about juvenile T wave inversion. For the pediatricians on the line, you'll be well aware of this. Juvenile T wave inversion refers to some remnants of right-sided heart issues and yawn. That might be present in B1 through B3 in individuals under 16 years old. This is independent of race. So if we follow our usual program starting in B1, I see T wave inversion. I see T wave inversion again. B3, I see T wave inversion. I don't see it in B4. This is a 12-year-old Caucasian female. This is a normal ECG. So juvenile T wave inversion, again, you have to understand those definitions, B1 through B3 is normal. Here are two other examples of juvenile T wave inversion. On the left, 13-year-old Caucasian female. On the right, 15-year-old Asian female. It's important that in any athlete under 16 years old, independent of race, if you have T wave inversion in B1 through B3 that does not extend to B4, this is a normal pattern. So let's move to some of the abnormal ECGs. And again, very important to understand the definitions. And we're going to focus on some of the big ones here at first. T wave inversion, ST segment depression, QAs. So I think as we follow this ECG, starting again in B1 with our eyes coming down, so far it looks normal. I get to B3 and there's ST depression and a big negative T wave inversion. B4, continued ST depression and a big negative T wave all the way through the lateral leads. Also present in the inferior leads, AVF, again, an AVL, again, another inferior lead, 2 and 1. Now, this is infralateral ST segment depression and T wave inversion. This is a markedly abnormal ECG and requires more investigation. Here's another example of infralateral T wave inversion and ST segment depression. Again, as my eyes get to B4, I see that ST depression and T wave inversion. I come across maybe some T wave inversion in AVF, again, AVL, and B2. This is a markedly abnormal ECG and requires more investigation. The workup of this ECG begins with an echo, but as we'll talk about, a cardiac MRI is definitely indicated. Here's another example of lateral T wave inversion, just showing on the side here. I think these patterns, when you see T wave inversion in B5, it immediately makes the ECG. So I'm going to go ahead and show you the T wave inversion in B5. As you see, T wave inversion in B5, it immediately makes the ECG abnormal. So this is table 2 in the international criteria, and if you have determined that the ECG is abnormal and you understand the specific finding, table 2 will be your guide in terms of what that workup should entail. So just draw our attention to T wave inversion, the lateral or infralateral leads. The table talks about the potential disorders that you're looking for. What the recommended evaluation is and some of the considerations for that. So why do we get cardiac MRIs in lateral or infralateral T wave inversion? And the reason we do that is that by ultrasound, by echocardiogram, it's hard to get a very accurate assessment of the apex of the heart. So it's hard to get the ultrasound being exactly perpendicular to measure the thickness of the apex of the heart, where cardiac MRI is going to be much more accurate. Cardiac MRI can also look for more specific etiologies, such as apical variant hypertrophic cardiomyopathy or rhythmogenic cardiomyopathy with LV involvement or something called non ischemic LV scar. This is important, there was a really good study again by Sanjay Sharma and his group looking at the clinical profile of athletes with HCM and really differences in where the hypertrophy was in athletes with HCM versus sedentary patients with hypertrophic cardiomyopathy. And I'll just draw your attention to the red slice of the pie graph. And on the left for athletes, apical HCM, which is hard to detect consistently on echo represented over one third of HCM in our athletes and only about 12% in sedentary patients. If the ECG is markedly abnormal and your imaging including echo and MRI are normal, you know that athlete probably can return to play with close follow-up. The story is not over and this was well shown by Antonio Pulizza in a New England Journal paper in 2008. They followed 81 athletes with that type of pattern, a nine-year follow-up with continued surveillance and repeat imaging and 6% went on to develop a cardiomyopathy over a nine-year follow-up period. Excuse me, five athletes and 6%. And so very important that if your initial imaging is normal and they have a really abnormal ECG, you have to do some annual surveillance. I learned this back in 2008 with one of my own patients. So you'll see this is a 19-year-old African-American male college basketball player, pretty much our highest risk group for sudden death. And you can see on their ECG in panel A that he had some T wave inversion in B4 and certainly into B5, but it wasn't all that impressive, but going into B5 still made it that normal. He had an echo and a cardiac MRI, both of which were non-diagnostic and we continue to follow him with serial surveillance. Panel B is his ECG two years later in September of 2010. You can see what has developed, which is pretty extensive deep T wave inversion and some ST segment depression in the lateral leads. He had a repeat cardiac MRI with clear apical hypertrophy of 20 millimeters and some late dilated enhancement. On the left is his initial cardiac MRI at the outer ends of normal range, less than 13 millimeters in a black athlete. And on the right is his cardiac MRI two years later, now measuring almost 20 millimeters. And again, this overlaying the ECG findings with that. So very important to continue your surveillance with ECG and echo at a minimum, but if the ECG gets worse, I would repeat that cardiac MRI. Let's move now to anterior T wave inversion. Let's move to anterior T wave inversion. So again, starting at V1 and coming down, I see T wave inversion in V1, I see it in V2 and I see it in V3 and I see it in V4. Now what's different about this T wave inversion than what I showed previously? Well, first of all, there's no J point elevation. There's no dome SD segment elevation. They're basically a flat SD segment into a negative T wave. This, if it was someone who's young, who's 12 to 16 years old, maybe this could be juvenile T wave inversion, but it extends into V4, so that wouldn't fit. This is actually a 21 year old Caucasian male. So it's definitely not juvenile T wave inversion. And it certainly doesn't look like a black athlete in polarization variant. This is abnormal anterior T wave inversion in a person who had a rhythmogenic right ventricular cardiomyopathy. Here's another example of anterior T wave inversion. Again, that flat SD segment into a negative T wave, flat SD segment into a negative T wave, into a negative T wave. There's also several premature ventricular contractions on this ECG, also making it abnormal. There's a hint of low limbly voltage in AVL and one as well, which is another hint towards pathology such as rhythmogenic right ventricular cardiomyopathy. Inferior T wave inversion is worth mentioning as well. And let's just move our eyes over to the inferior leads. The inferior leads are 2, 3, and AVF. As I mentioned, lead 3 often has T wave inversion. So in the criteria to have abnormal T wave inversion, you need two continuous leads. So to have inferior T wave inversion, it's lead 2 and lead AVF that you see here. This is an abnormal ECG, the workup of which would be an echo. So is this ECG normal or abnormal? So let's walk through it here. So V1, we come down. I don't see T waves, secondary depression or T wave inversion, V4, V5, V6. I'm over to AVF. I do see a small, maybe inverted T wave, hard to say. Come up to AVL, it's okay. I don't see T wave inversion, but I do see some flattening. Flattening is really not part of the criteria. I come up here and I do see again that T wave inversion lead 3, but we don't include lead 3. So this is a normal ECG. This is one of the common reasons people will call a normal ECG a false positive. And this was read by a cardiologist with good experience who described T wave flattening as a reason for calling this ECG abnormal. T wave flattening is not part of the international criteria. Let's move on now to pathologic T waves. And if you were familiar with the Seattle criteria, this was defined as greater than three millimeters of depth. This was not a great definition with all of the voltage abnormalities in athletes. We often found large, skinny, deep Q waves. And this is an example of it. If we come out into V5 and V6, and this would have been a false positive ECG. The definition changed in the international criteria. The new definition is a QR ratio more than 25% or a Q wave greater than 40 milliseconds in duration. This is an example of large, deep Q waves in a swimmer who had hypertrophic cardiomyopathy in V4, V5, and V6. Here's another example of some pathologic Q waves, and I'll just draw your attention to what they look like in lead 2 and also in EVF, where you have a wide Q wave, more than 40 milliseconds. And it also is greater than 25% of the ensuing R wave. This is a abnormal ECG. There's several other abnormalities on this ECG as well, including PVC. So we learn a lot just from one step, looking at pathologic Q waves, SC segment depression, and interior of inversion. My eyes will run through the ECG again, and this time we're going to look at the morphology of the ECG, and again, I'll go from V1 down to V3, up to V4, down to V6, and then across to the limb leads. So let's look at this ECG, and let's start in V1. In the middle of the screen, we come down. We look here. This starts to look a little funny in V3, V4, short PR, slurred upstroke, or delta wave. This is an example of WPW, or pre-excitation. The classic findings of Wolff-Parkinson-White is a short PR, less than 120 milliseconds, a delta wave, or a slurred upstroke, to the QRS complex that you can see pretty clearly in V4, V5, V6, as well as on the other side of the ECG and AVL and lead one. And you can, in a wide QRS, more than 120 milliseconds. Those are the classic findings of pre-excitation or Wolff-Parkinson-White. If I draw your attention up to lead V1, you can see that the P wave, essentially, as the P wave ends, it goes right up into the QRS complex. This is another ECG depicting Wolff-Parkinson-White, and again, if we just follow down V1, V2, V3, it looks okay. I come up to V4, this starts to look like a slurred or a delta wave, not quite as obvious as the last one. Again, a little slurred upstroke in V5 and V6. This is another example of Wolff-Parkinson-White. We talked about the classic findings in WPW. There are also some additional findings that can support your interpretation of this as pre-excitation. One of them is having a very large P wave in lead three. The other is the absence of a Q wave in lead V6. Both of these suggest that this is pre-excitation. Here's another example of pre-excitation, and again, where we see a short PR and a little bit of a slurred upstroke in V3, also in V4. This is not as obvious, but if I look at some of the additional criteria that might support it, it does have a large Q wave in V3 and no Q wave in V6. This ECG shows complete right bundle branch block. I think everyone could identify that, RR prime in V1 and a QRS complex that is greater than 120 milliseconds. If we follow through the rest of the ECG, there's nothing else abnormal on this. Right bundle branch block, besides having RR prime and a wide QRS, you usually have a wide S wave in V6 as depicted here. Right bundle branch block is one of the borderline criteria when found in isolation with no other borderline or abnormal findings. This is a normal ECG in an athlete, does not warrant additional investigation. Here's an example of a right bundle branch block that does warrant more investigation. And the reason that you warrant more investigation is because the QRS complex is more than 140 milliseconds, which is part of the red box. So again, this pattern here, very wide QRS, even in a right bundle branch pattern, any QRS duration greater than 140 milliseconds is part of the red box. So step three, just quickly is looking at the access. And I'm not gonna go through this in depth. I think everyone can refer to the hexaxial reference system and figure out the access on an ECG. Step four is looking at for left or right atrial enlargement. So we look at the height and the width of the P wave. And if the P wave is larger than the P wave, is more than 120 milliseconds, that might suggest left atrial enlargement. We'll also look at the P wave before V1 for a negative component. Again, not gonna go into this in great detail, but I think everyone is familiar with this. Let's look at the borderline ECG findings together. So two or more borderline findings equals an abnormal ECG. This is an example of an ECG that has right bundle branch block, the RR prime and a wide S wave in V6. ECG has left access deviation. So it's up in one, but it's down in ABF and down in V2. So an access that is more than negative 30. And it also has evidence of right atrial enlargement with a tall peak P wave, more than two and a half boxes. So this is an abnormal ECG that does require more investigation. Step five is the rhythm strip looking at the bottom, making sure that there's a QRS after every P wave. I don't have time to go into some of the examples, but these are within the ECG international criteria document and the modules that we'll talk about. Step six is looking at the QT interval and really important to understand how to calculate this. So let's look at this ECG. Does this ECG represent long QT syndrome? And so if you're coming down, starting with our pattern V1, V2, V3, if you were going to calculate the QT interval in lead V3, you might get hung up by including a U wave. You never ever want to include the U wave in your calculation of the QT interval. And so you want to make sure that you find an appropriate place to calculate the QT interval. That is typically lead two or V5. And the reason is there is because you usually have a very sharp end of the T wave to calculate. At the bottom here, I will find a QRS complex that starts essentially on a big line, like over here. The big box is 200 milliseconds. So this QT interval is about 400, which is obviously a normal ECG. Again, don't want to include the U wave. And I will find, again, that sort of big box for the QRS starts 200 milliseconds, maybe 440 milliseconds for this ECG in this normal. This is how you don't include the U waves, called teach the tangent or avoid the tail. So if everything has a U wave, you would draw a tangent line down the backside of your T wave. And where that intersects with the isoelectric line is basically the end of your QT interval. This is one of our patients, a 14-year-old very elite female soccer player who was trying out for the national team and required an ECG. Is this ECG normal or abnormal? As we come down and look here, especially if we're looking specifically at the QT interval, you know, we don't have a good view in lead two. You know, in V5, this looks a little bit long and extended. Let's blow this up a little bit. In lead V4, it has a notch. And in lead V5, when we calculate the QT interval, which was essentially the QTC, its heart rate was around 60, it was 500 milliseconds, which is well above the threshold for a female athlete where we define 480 or less milliseconds as normal. Also, the T-wave morphology may give a little clue that this is an abnormal ECG. Notched T-waves in lead V4, V5 can represent morphology from, or suggest long QT type two. So again, lots of nuances and details to look at when you're looking at the ECG. I want to switch gears for a second to talk about why this might be so important. And I think we're all familiar with part of the actual screening. We do it a lot. We do it in all our athletes at different levels. So why is it so important? And is using the PP monograph or the AHA 14 point enough? We first gained experience this at the University of Washington back in 2008, when we started doing ECG. And then in 2010, we were doing ECG in all our athletes. This was our first cohort of athletes where we actually analyzed what we were finding. We were using the PP4 monograph. And almost 800 athletes. And in the middle of the screen represents our positive screen. So in our history, using the PP4 monograph in Division I college athletes, 37% were checking one of the boxes on the PPE questionnaire as something, a positive response. Chest pain, history of syncope, family history, et cetera. Our exam was abnormal at three and a half percent. ECG was abnormal at 2.8% using much older criteria. In this cohort, we had five individuals diagnosed with a condition at risk for sudden death. All five of those individuals were diagnosed by ECG. If we were only doing history and physical, we would have missed all of them. This is more recent data that we published out of working with the Nick of Time Foundation, screening high school students and student athletes using the American Heart Association 14 point versus ECG. Again, with the American Heart Association 14 point, 45% checked one of the boxes as a positive. If we talked to the young athlete, we could probably get rid of half of those responses that may be not clinically relevant, but still at least 20% had some finding on their questionnaire that warrants some more investigation. Our abnormal ECG rate was only 3%. And we look at the cardiac conditions that we found, using the AHA 14 point, more than half of the detected conditions would have been missed if that's all we were doing. Whereas if ECG only missed one of the 16 conditions. I wanna emphasize this a little bit further. And this is a table from that article and just draw your attention again to the total positive response rate for the AHA 14 point. It's really high and you have to go through each one of these responses in great detail to understand if it's clinically relevant. I find it much easier to interpret some of these symptoms or reported positive responses in the setting of a normal ECG can be quite reassuring. If we compare the AHA 14 point versus ECG, ECG outperforms the AHA 14 point in every statistical measure of performance, sensitivity, specificity, positive and negative predictive value. I just wanna draw your attention to positive predictive value. What does this mean? If we're using the AHA 14 point, you need over 300 athletes to check one of those boxes and have a positive response, followed by appropriate investigation to find one athlete with a cardiac disorder at risk for sudden death. In contrast, for ECG, the positive predictive value was 13%, or you need seven athletes with an abnormally ECG to find one that has a condition at risk for sudden death. So ECG interpretation, in my mind, is a required skill for a sports medicine physician. Since you guys are all in fellowship, if you wanna be a team physician, this is absolutely an essential skill. I say this is as important as doing a good knee exam and a lock-in test. Spend your time in your fellowship learning how to do this. It's hard in the US. We don't have a big infrastructure. We need a lot more training to bridge this gap, to provide better screening at all levels of sports participation. Let's look for a moment at this ECG and ask you, test yourself here. Is this ECG normal or abnormal? As we walk through it here, this is clearly an abnormal ECG. It has T-wave inversion in V5, V6, as well as the V2 and EVF. So, implateral T-wave inversion requires a pretty comprehensive workup to exclude the pathology. But don't get confused that it also has some black athlete repolarization pattern in V3 and V4, and they can be on the same ECG. But this is an abnormal ECG that requires more investigation. This lecture will not be enough. Hopefully, this is a start, but I encourage all of you, if you haven't done it already, to take the ECG interpretation modules. There are six of them, and they walk through all of the international criteria. There's a pretest and a post-test, normal findings, findings in cardiomyopathy, findings in electrical disease, common pitfalls. I would estimate it'd probably take you four hours to do all six modules, and I think this is well worth your time. I wanna switch gears just for a few minutes to talk about COVID-19 and some cardiac implications and what to look for on an ECG. Unfortunately, this is raging really around the globe, and in the US alone, over 6 million cases already. We've known for a long time that COVID has an affinity for the heart, and 28% of the sick patients, patients who are hospitalized, had some form of myocardial injury. There was also some information that came in patients who had been hospitalized, but had ongoing symptoms of potential cardiovascular involvement, and 54% of them had abnormal findings on cardiac MRI. I think we're all aware of this paper that came out of Germany looking at cardiac MRI in a spectrum of patients, middle-aged, with different levels of symptoms. Some of them were asymptomatic, some had mild infection, about a third were hospitalized, 22% had abnormal T2 on an MRI, and 32% had late gadolinium enhancement. We don't have the details. We don't know how extensive these findings were. We don't know if they crossed a threshold to truly diagnose myocarditis, but it definitely raises the caution flag that we need to know more about how COVID affects the hearts, especially the hearts of young athletes. We've started to hear cases of myocarditis in athletes, and even athletes who have died after a recent bout of COVID. Early on in the pandemic, we published basically an editorial with some suggestions on how to evaluate individuals who have been afflicted by COVID-19. I still believe that the likelihood of myocardial involvement is related to the severity of disease. That doesn't mean that mild infections can't have heart problems. I just think it's more common if you've really had a bad flu-like syndrome or truly were in the hospital. And I encourage you to look at these sort of tiered recommendations that we have within BGSM. There's also recommendations for college athletes as posted on the AMSSM website in collaboration with the NCA. So what are those EECD manifestations of myocarditis? You know, diffuse ST segment elevation, ST segment depression, Q wave inversion, pathologic Q waves, and PR segment depression. And I'll just show you a few EECDs. In regards to diffuse ST segment elevation, you know, this is a common finding in our athletes at a baseline. If you have a prior EECD, it's really important to compare to a prior EECD. Here's your Wikipedia, myocarditis, sort of classic that shows ST segment elevation, V4, V5, V6, also AVF and lead II. You can see it across the board. In a setting, you know, clinical setting of chest pain or palpitations or recent fever, this would be concerning. This EECD also could be found in a lot of our athletes as well. So again, having that baseline would be important. Here's another EECD showing some findings of myocarditis. Again, ST segment elevation in V3, V4, V5, and V6. ST segment depression up here in V1, something called PR depression. And so let's look a little bit at lead II just to show what PR depression is. You know, the PR depression between the P wave and the QRS complex is related to the isoelectric line between the end of the T wave and the beginning of the P wave. And so when there's PR depression, sometimes it's quite subtle, but it is somewhat of a unique finding for myocardial injury or myocarditis. And here's another example of myocarditis in the pediatric population. The first thing that jumps out at you, obviously, is the tachycardia, which would be consistent with current infection. Again, ST segment depression that you have to look very closely with, but again, some of this is a nuanced and detailed view. And then again, that PR depression related to the TP segment within V2. So some final take-home points for us. You know, I think we should all follow the international criteria recommendations for ECG interpretation, as well as the secondary evaluation of specific ECG abnormalities. I use the six steps for accurate ECG interpretation in athletes. Lateral and infralateral TUA inversion requires contrast enhanced cardiac MRI, and serial cardiac imaging is required for athletes with remarkably abnormal ECGs and normal cardiac imaging. And then just a word on COVID, you know, past infection with COVID-19 increases the risk of myocarditis, and review of ongoing symptoms and severity of illness should really guide the extent of that cardiac evaluation. So appreciate your time and attention. I'm gonna turn it back over to Irv and see if we have any time for a few questions. Thanks, John. That was an outstanding presentation. Thank you. Again, to remind everyone, if you have questions, feel free to use the chat and we'll begin answering those. And we have about 10 minutes. So if it's all right, John, maybe I'll just start us off with some questions that you might be able to answer. So for the fellows, if they were to start reading ECGs, how many ECGs do you think it might take for them to feel comfortable based on your experience? Certainly if they listened today, did the modules, they would need some practical experience. And so what would you recommend for the fellows to do so that they could do this well? Really good question, Irv. You know, you've sat with me at NIC and Timescreens as well. And I think people learn it pretty fast. If you come in prepared, have read the International Criteria document, done the modules, now you sit down, I think after 10 ECGs, you'll start to get more comfortable with a pattern of how to look at the ECG. To become confident in looking at ECGs, I think you probably want to get about 500. So you need to look at a lot of ECGs in athletes, specifically a lot of normal ECGs. The hardest thing, I think, for physicians to understand is that there are a lot of striking findings on an athlete's ECG like voltage criteria or right bundle branch block that are normal findings and that they don't require more investigation. So I think if you come prepared, you can get comfortable with that pattern pretty quickly, but you need to look at a lot of ECGs to be able to finally pick out the one that stands out at that moment. And when you're using your ECG criteria for talking to the fellows, how young should we be using the criteria? What's your age cutoff? Yeah, so, I mean, I sort of look at this, use this ECG pattern for most ECGs that I look at. The International Criteria specifically was developed for age 12 to 35, but if they're 11 years old or 10 years old, I think that would still apply it. And then certainly in our older athletes, some of the findings become potentially more concerning for cold coronary artery disease, you just have to keep that in mind. We got a question in the chat about HCM. And so the question is, does exercise worsen HCM? So the one patient that you discussed, did exercise worsen the HCM in that case or was it the natural course of disease in your opinion? Yeah, that's an excellent question. I think the answer is both. It was the natural course of the disease to develop more hypertrophy and there was some physiologic hypertrophy on top of that. So in this specific individual, we actually repeated his cardiac MRI after about a year of relative inactivity after he had stopped playing college basketball, but was continuing to do some light exercise like stationary bike. And his hypertrophy decreased almost three millimeters, but was still in a pathologic range. So I think there is the potential that exercise either brings out a predisposition or perhaps you tack on the physiologic hypertrophy on top of the pathologic hypertrophy. I definitely think that's a possibility. And just a couple more follow-up questions about that particular case. Why do you think the ECG showed findings that might have been, I guess, worrisome before the echo or the cardiac MRI based on your experience? Yeah, really important point here. In cardiomyopathy, the electrical manifestations usually come first. So the ECG starts to change before the morphologic changes in the heart. And so for HCM, this is why it's so important. If you have an abnormal ECG that you follow that over time if your initial cardiac imaging is normal. So the electrical manifestations will often come first and this was an example of that. And so for our fellows, you mentioned serial follow-up in that particular player. Based on your experience, what would be the serial follow-up? Would you want it every three months, six months, one year? What do you think? Annual follow-up. So I think one year is fine. When we didn't know what the right answer was back then, we were doing follow-up every six months. But I think annual follow-up is probably adequate, definitely an ECG and an imaging study. And again, there are some additional tests that if they have some gray zone findings of hypertrophy, that's when you're gonna work with your cardiologist, of course, things like an exercise stress test or a 48-hour holter, making sure that those are normal as well. Because if abnormalities start showing up on other tests, that might sway you over towards that this is truly pathology and not just athletic modeling. We had another question in the chat. I think COVID has made us think about potential, like you said, affinity for the heart. And so this question is actually outside of COVID. So non-COVID viral URIs or even potentially the flu, what are the typical guidelines for ECG or cardiac evaluation? And do you believe that might be changing now that we're seeing with COVID? Yeah, that's a great question. We clearly have a really bright class of fellows here because the questions are fabulous. I don't think there is a standard in terms of getting ECGs post-viral syndrome from the past. In my own practice, if I had an athlete that was really knocked out with a febrile illness, whether that was influenza or mono, as they recover, I would typically get an ECG because I'm tuned into this and I'm worried. And I wanna make sure that there are no new findings. I don't know how sensitive that is. ECG is not a perfect tool looking for myocardial injury or myocarditis. One thing we don't know, if we got cardiac MRIs after influenza in young athletes, what would they look like? Would some of them have some of this TQ or LGE? We don't have that comparison. So there are a lot of unanswered questions, but I do think that myocarditis is a very important entity. Typically, it can present with symptoms, but often it doesn't. And when we look at myocarditis as a cause of sudden death in college athletes, before COVID pandemic, myocarditis represented 9% of sudden cardiac death in college age athletes. So it's a very important entity. And I think having a heightened concern in individuals who have a significant viral syndrome, I think that makes sense. And I think considering a good symptom evaluation and a repeat ECG would make sense to me. A few more questions. So thinking about the criteria and how they were developed, you mentioned some differences with black athletes. Do you feel comfortable with the criteria involving folks from different ethnic backgrounds and say Hispanics or other populations? Yeah, really good question. I think this is one of the deficiencies in the criteria, especially with mixed racial individuals. And then we don't have a big Latino community and Hispanics that we've studied. And how do you determine that this person is race or you're just looking at the color of their skin to interpret their ECG? So I think honestly, it's fraught with difficulties and some deficiencies. And I leave it up to your best judgment. Again, the black athlete repolarization variant is pretty obvious when you see it. I think it's a very distinct pattern. I think it's probably normal in non-black athletes as well. We just need more data. Another COVID question. So if we get EKG and intraponin post-COVID that are normal, what is the utility of echo post-COVID? I think none of the tools looking for myocarditis post-COVID are perfect. And so troponin in more of the acute phase, I think is probably our most sensitive screen, more so than echo and more so than ECG. The current standard that's emerged for elite athletes in the college setting and in the professional setting is ECG, troponin, and echo, because none of them are perfect. And when we add them all up, maybe that's our best chance of finding something. And then of course, some places are using cardiac MRI as a screening tool. And we don't really have great information about what that means yet. There was a follow-up question about the criteria, thinking about male versus female athletes. It looks like most of the studies may have been done on males. So do you have any expectations or do you use the same criteria on female athletes when you think about adaptations? Correct. That's a really good point. I think T-wave inversion and ST-segment depression are abnormal, regardless of sex. And so most of the criteria I think really do apply. The one area where we use a different cutoff is the QT calculation or QTC, 470 for males and 480 for females. Other things that may not be as prominent, for instance, pure esteration or true bundle branch blocks, but I think the criteria still hold. We need more research and validation in female athletes, but I do think that red box still applies to females. And the last question is just trying to think about the future. You've got things that your Apple Watch can do, your iPhone can do, and we're sort of entering a world of digital health. And so what do you think about all of those devices as it relates to ECG interpretation? Is there anything on the horizon? Good question. I don't know the answer there, Irv. I think that a lot of the wearables tell us about our heart rate or some maybe even heart rate variability. There may be ways to use that to detect illness. I think people are trying to understand that. I think when you're talking about looking for abnormalities on an ECG that hints towards a condition that's at risk for sudden death, I think it's hard to do that with just one lead or two leads like a wearable. And most of the wearables aren't one of the leads that we would want to use. Like if I had to pick one lead, I'd pick B5. And we don't have that on a wearable yet. So maybe in the future there'll be something like that and we'll see technology evolving really fast. Awesome. Well, John, I really want to thank you for an outstanding talk today. I think of all the ones that we've given so far, this might've been the one with the most attendance. So thank you for giving this talk. Thank you for all that you do. It's been an honor and a pleasure and look forward to hearing more from your work soon. Thanks, John. Thanks again, Irv, and thanks everyone for your attention. Have a great day.

2nd Edition, CASE 05

2nd Edition

Cardiac

ECG interpretation

athletes

sudden cardiac death

cardiac disorders

cardiomyopathy

European Society of Cardiology

hypertrophic cardiomyopathy

COVID-19 myocarditis

sports medicine