Our understanding of what constitute the athlete's heart is really paralleled advances in diagnostic techniques with chest radiography in the 40s and 50s, ECG in the 60s and 70s, and most recently non-invasive imaging. This is an example of one of the classic chest film studies from the 1950s in which a five-year marathon champion in the New York marathon was studied by a group of doctors and he was labeled as having the athletic heart syndrome, which is just simply having a big heart by chest x-ray. And in this report, these investigators again raised the question about whether athletic adaptation, which causes big hearts, is a good thing or a bad thing. As most of you are well aware, the ECGs in athletes can look very different than those in otherwise healthy sedentary people. This is the Sentinel report of the WankyBot phenomenon, which is a benign form of heart block, and this is something that if you admit your athletic patients to the hospital and put them on telemetry overnight, invariably you'll see this prolonging of the PR interval and finally a drop of the QRS complex. This was something, again, that was raised as a question of pathology, but we now know is just a normal adaptation to athletic training. The advent of echocardiography was where things really started to crystallize. This is a really important historical study from the mid-1970s that was done by Joel Morgan Roth, Barry Marin, Walter Henry, and Steven Epstein, who were working at the NIH at that point. And they used two-dimensional echocardiography to measure heart size in different types of athletes. And what they found is that in swimmers and runners, the diameter of the ventricle, so the size of the ventricular chamber, was larger than it was in wrestlers, and wrestlers actually looked very similar to normal people who didn't do any sport. This concept of athletes having big hearts has been reproduced in other kind of larger cross-sectional databases. These have emerged from the Italians, who have done a lot of work in the imaging field. And what you can see here is that if you look at these charts where wall thickness of the ventricle and chamber sizes of the ventricle are plotted as a function of gender in different types of athletes, you can see that in general, athletes, like all populations, follow a bell-shaped distribution, but that importantly, on the tails, a significant percent of them exceed what we would consider to be normal. So again, we're seeing a significant minority of athletes that have big hearts, and again, the question is, why is that, and should we care about it? So all of the data I've showed you so far are cross-sectional, and I want to just make a point about the limitations of cross-sectional data. And to do so, I'll show you guys a clip of the University of Connecticut basketball team. This is my med school alma mater, and I'm still a big fan. They had a number of really good years back when I was a trainee, won some national championships. They're not doing so well these days, but that's a different story. But the reason to show you that is just to make the simple observation that basketball players are tall. I don't think that's an observation that anyone would refute. Where it gets more interesting is when you try to explain that observation. So to the majority of us that grew up in a culture where we understand basketball, you realize that the explanation for this is that tall people self-select for basketball. By the time you get to the fifth or sixth grade, if you're tall, your gym teacher might tap you on the shoulder and say, you know what, you're tall, you should think about playing hoops. And that's fine. We know that because we've watched the natural history, we've seen the longitudinal evolution of this theory. But if you ask someone that's never seen basketball before, that has no idea what this phenomenon is, why basketball players are tall, they're just as likely to tell you that basketball makes people grow tall. And so I did this experiment with my kids when they were young, asked them why the basketball players are tall, and my son and daughter said, oh, I'm going to play basketball because I want to grow tall. So this really highlights the importance of understanding the limitation of a cross-sectional observation. And so I think, you know, a question that was very important to me early in my career was this chicken and the egg question, and that is, does exercise cause heart enlargement? Or do people born with bigger than normal hearts simply self-select for sport? Maybe just being genetically endowed with a big heart makes you more likely to be a good runner or a good soccer player, who knows? It really, without repeated measures, longitudinal data is a question and a hypothesis rather than a conclusion. So let's assume for a minute that there is something to be said for the heart getting bigger because of athletic training. Why would that happen? And is there anything that would lead us to believe that this is the case? And the answer is yes, and that is the paradigm of valvular heart disease teaches us an important lesson. As you guys are all well aware, the aortic valve is the last valve that the blood sees when it leaves the heart, and the aortic valve can get sick in one of two ways. It can leak, which we call aortic regurgitation, which presents a volume challenge to the ventricle, or it can get tight. And this is aortic stenosis, and here the ventricle feels pressure. And when the valve gets sick in one of these two ways, the ventricle changes in two very different geometric patterns. The volume stress of aortic regurgitation causes the chamber to dilate and mildly thicken, and we call this eccentric hypertrophy, whereas the pressure stress of aortic stenosis causes the walls to thicken and actually the chamber to get smaller, and we call this concentric hypertrophy. So how might this apply to sport? Well, it actually applies quite nicely. If you think about your endurance athletes, these are your Nordic skiers, your rowers, your runners, your track athletes. They ask their bodies to generate very high cardiac outputs, oftentimes four to five-fold what they experience at rest. They do this by increasing their heart rate and their stroke volume, and these are dilating in the periphery. But for the left ventricle, this is a really profound volume challenge. If you contrast that with strength athletes, so these are your football linemen, your power lifters, your throwers, their physiology is totally different. Here we're talking about repetitive surges in blood pressure with systolic blood pressures, oftentimes two, three, 400 millimeters of mercury. This happens because of intense skeletal muscle contraction and some vasoconstriction. But for the left side of the heart, this is a pressure challenge. So this concept of whether or not these two different types of physiology actually cause cardiac adaptation was one of the reasons back in the day that we formed the Harvard Athlete Initiative, which is still an ongoing attempt to work with our student-athletes to study how the heart responds to sports. And I'll just kind of go through the typical model that we use to look at remodeling, and we focus largely on our freshmen who come in having been good high school athletes, but really never having seen the level of training that they get hit with when they come to college. And so what we'll typically do is we'll get some sort of baseline assessment before they come to school or just after arrival, we'll allow them to go through the acute training intensification as part of their fall sport period, and then we'll remeasure them in some way, shape, or form. And depending on what study question it is we're asking on any given year, we might use anything from a simple ECG all the way up through fancy things that we're doing now with PET scanning and MR to look at things like metabolism. And then ultimately, we're now working at multi-year cycles and trying to understand the extended training experience. But the very basic study design, which is just simply capturing this 90-day period of intensification, was one in which we asked one of the very first questions, and that is if you look at strength athletes, and this study defined as football linemen, and compare them to endurance athletes, which in this study was defined as the rowers that were preparing for the Head of the Charles, which is a local five-kilometer rowing event that we have here in Boston every year, we simply wanted to know if these young men experienced cardiac enlargement. And the answer was they did. The hearts in both types of athletes got bigger, and they got bigger by the same magnitude. So again, surprising, but in as short as a 90-day period of training, we saw increases in heart mass by as much as 10 or 15 percent, and again, both types of sports did it. But where it got interesting was with respect to what these hearts looked like after the remodeling. Among the endurance athletes, all of the increase in mass was dictated by dilation of the ventricle, whereas with the strength athletes, all of the increase in mass was explained by thickening in the walls. So this was proof of concept for the first time, I think, in a longitudinal model that indeed it is exercise that causes this heart enlargement, and that the type of sport you do dictates what the enlargement looks like. So life is not as simple as just looking at the two ends of the spectrum. Football linemen and rowers have pretty simple, clear physiology. We now know, and you guys know this as well as I do, that sports can be categorized as a function of how much static, which is another word for pressure stress there is, versus how much dynamic, which is another word for volume stress there is, and in doing so, you can get a sense of what the predominant physiologic knee view of a different sport looks like. And we use this clinically, because when we meet an athlete and we're asked, is this heart enlargement physiologic versus pathologic, the very first question we ask is, what type of sport does this athlete do? And by using schemas like this three-by-three grid, and by understanding which athlete type we're working with, we can predict what the heart should look like. And if the enlargement is commensurate with the type of athlete we're looking at, then it's almost always physiology. If there's a disconnect, meaning thick walls in an endurance athlete or lots of dilation in the strength athlete, then we know that our pre-test probability of pathology is actually quite high. And this is something, as you continue to practice in sports medicine, you'll encounter invariably and hopefully have cardiologists you can partner with to work through these interesting questions. So physiology is one thing, but as practitioners, although physiology is interesting, it's really pathology that we care about. And there's no topic in which physiology and pathology overlap more commonly than that of the athlete's heart. So let's talk a little bit about this. This is a complicated diagram that comes out of our most recent imaging guidelines, and I won't walk you through it in full detail, but I'll just kind of remind you of the fact that as cardiologists, there are basically four things that we typically see that raise the question of physiology versus disease. And those are thick walls, dilated chambers, both on the right and the left, as well as hypertrabeculation, which are these small fronds of tissue that exist in the apex of the heart, which we know in certain types of athletes can actually be stimulated by athletic remodeling, but also have overlap with a form of cardiomyopathy called non-compaction. So we've developed strategies when we find one of these four principal questions to think through and help us try to differentiate whether these are normal versus abnormal findings. Why does this matter? Well, it matters because abnormalities, as you know well, as we're going to talk about in some detail now, can, in the worst case scenario, cause people to have adverse outcomes during sports. And I can show you lots of examples. This is one that's personally very meaningful to me. Ryan Shea was a friend of mine and a guy I had a chance to train with back in the day when I was running competitively. He was one of the best runners in our country back in the early 2000s and was seen here on the start line of the Olympic marathon qualifiers in Central Park in 2007. He had had some medical condition beforehand, but really a lot of uncertainty was left around that. And unfortunately, at mile five in the race, he collapsed to the side of the street and had a cardiac arrest and couldn't be resuscitated. And so this is the type of thing that we, as an athletic care team, whether we're talking about those that engage as sports medicine docs or cardiologists, are trying to prevent. And an important part of preventing this is understanding the key conditions that can cause it. So this is a list of the common and some uncommon causes of why people die from heart disease during exercise. And they can be broken down into the principal anatomic portions of the heart. So problems with the heart muscle, problems with the conduction system, problem with the coronary arteries, problems with heart valves, and then some diseases of the central aorta. And all of these are important common causes of death, but I'm going to review probably the top four or five that I think you should be most familiar with and try to leave you with some clinical pearls around how to think about these things. So a couple of examples. This is a screening ECG in an 18-year-old soccer player. And although the ECG in healthy athletes can sometimes be different than what it looks like in sedentary people, this is by no means a normal ECG. This is markedly pathologic, as you can see, deep symmetric T-wave inversions across many of the leads. And this is the ECG that's typical of this disease, which is hypertrophic cardiomyopathy. HCM is a genetic cardiomyopathy that is relatively common in the general population. It occurs in roughly 1 in 500 people and has on numerous autopsy series been identified as one of the most common causes of sudden death. It used to be thought that it was definitively the most common, but I think we're realizing now that it's just one on a longer list of things that can get athletes into trouble. The image I'm showing you here is an echocardiogram in which the hypertrophy is confined to the intraventricular septum. This is one of the common variants, but this is a highly heterogeneous disease. You can see here from some MR images just how different flavors this disease comes in. The one on our left is the thickening of the ventricular septum, which I showed you by echo. A very common variant that's much different is when the apex of the heart here is thickened. You see this spade-shaped ventricular cavity surrounded by these two almost bulbous enlargements of the heart muscle. And so this is a diagnosis to be well aware of, as we'll talk about what we do with this diagnosis is slowly changing, but it is indeed probably the most notorious killer of young athletes. Moving on, this is a 21-year-old collegiate cross-country runner who had a long history of med refractory asthma, who eventually made it to the cardiology clinic after an episode of syncope. ECG, fairly typical for an endurance athlete, sinus bradycardia, right bundle branch block, a little bit of early repolarization. This by definition is not an abnormal ECG, but I will tell you in the sports cardiology world, when we hear med refractory asthma, there's one diagnosis that pops up to the top of the list always, and that's anomalous coronary arteries. And that's because anomalous coronary arteries can often produce exertional dyspnea that sounds and feels and looks a lot like asthma. And if asthma doesn't respond to medications, this is something we need to be thinking about. This is the CT scan from this individual, and you can see the yellow arrows there showing the left coronary artery that's coming off of the right side and coursing in between the aorta and the pulmonary artery. Just by way of reminder, normal coronary anatomy, we have two main coronaries, one that comes off the right side and one that comes off the left side, and they supply the right and left sides of the heart, respectively. When this goes wrong, when there's anomalous circulation, it looks something like this where you have both arteries coming off of the same side. And without question, the one that is more malignant is when the left coronary artery comes off the right side. And we look not only at where the artery starts, but also at several other high-risk features, things like does it course between the aorta and the pulmonary artery? This is a so-called intragrate vessel course. We look carefully with imaging at the morphology of the ostium of the artery, with slit-like ostia being high risk. We look to see how much of the artery is inside the wall of the aorta, and then we look at the caliber of the artery once it gets to the heart to see if there is enough artery to supply the heart muscle. And this, again, has been identified as a common, sometimes clinically challenging way to find a cause of sudden death in young athletes. So we don't have a ton of really good instructive data on coronary anomalies, but one old study I think is very instructive, and this is a study that comes out of a clinical autopsy series from Italy. We know that coronary anomalies are pretty common, like HCM. They're probably roughly one in 500 in the general population, but not all of them are created equal. So anatomy dictates risk, with anomalous lefts being more dangerous than anomalous rights. And certainly if they're running between the aorta and the pulmonary artery, that confers significant risk. But what's interesting is in the clinical evaluation of these people, we have challenges. So we do know that most of them, at least in this series, and I think this has been our clinical experience here in Boston as well, is we find these people, we find them because they have symptoms. And again, there's only one thing you remember from my talk, and that is med refractory asthma needs to be evaluated for coronary anomalies. It's the single most common presentation we see. So many of these people have symptoms. It looks like asthma. The resting 12 with ECG will almost never show this condition. So this is one of the pitfalls of ECG screening. This is the diagnosis you're most likely to miss. And somewhat more surprisingly, exercise testing, even when athletes are pushed hard, oftentimes doesn't show ischemia. So the take home with this is that if you're suspecting an anomalous coronary, and again, our adage is any exertional symptoms between the nose and the belly button, this needs to be considered in a young person. And if you're thinking about it, you need to image them. In imaging, we have choices. We can use echo, we can use CT scanning, and we can use MR. That's a local institutional preference thing. But as sports med docs and a sports cardiologist, we're not done with young athletes with exertional symptoms until we rule this condition out. Moving on, this is a screening 12 with ECG in a 16 year old runner. And you can see here a fairly atypical looking right bundle branch block with a tall R prime and this funny deflection at the terminal portion of the right bundle. This is a so-called epsilon wave, which is diagnostic for a condition called arrhythmogenic right ventricular cardiomyopathy. ARVC is a genetic condition which involves the desmosome proteins in the heart, which are the proteins which hold the heart muscle cells together. And when someone has this genetic condition, these links between muscle cells break down over time and the healthy muscle gets replaced by fat and scar tissue. This is an important cause of sudden death in young people. There's some geographic variability to this, but it's alive and well in the U.S. for sure. This is what it looks like on a cardiac MRI. You'll often see a right ventricle that has sacculations or aneurysms. It looks very thin, it's dilated. And this is an important condition for us to find because not only does it cause sudden death, but in people that have it that continue to exercise, even if they just have the gene, we know over time that their likelihood of getting sick, either from malignant arrhythmia or from heart failure, goes up and it does so in a dose-dependent fashion. So the more exercise they do, particularly endurance-based exercise, at least according to this Hopkins-based series, the more likely they are to have adverse outcomes as they get older. Finally, a 19-year-old lacrosse player who had a cardiac arrest on the field and was successfully resuscitated comes in with this ECG. And this is the ECG of long QT syndrome. You can see here, sinus bradycardia, borderline first degree AV block, but a markedly prolonged QT interval with a QT segment that spans more than half of the RR interval. This is one of several manifestations of genetic long QT syndrome. As I think most of you know, long QT is a disease of the ion channels, which prolongs the duration it takes for the heart muscle cells to repolarize after every beat. And in doing so, delayed repolarization makes the heart more susceptible to malignant arrhythmias. And this is something that we find not infrequently on screening ECGs when athletes present with symptoms, but it's probably as importantly because long QT was the first disease that began to teach us that we have the ability to change risk. So what do I mean by that? Well, Mike Ackerman is a close colleague of mine, runs a pediatric sports cardiology program out of the Mayo Clinic and has a really nifty registry of long QT patients, which he has followed, treated, and in many cases, supported in returning to play. And he put together a report of his experience with this type of patient population now about a decade ago, in which he makes the important point that when these patients are treated effectively with beta blockade, in some cases, left cardiac sympathetic denervation, and in some cases, an ICD, that the overall rate of adverse events is really quite low, and that perhaps these athletes, even though they have genetic heart disease, should be considered as being eligible to play sports. So looking at the numbers more closely in his registry, I have about 350 kids. 130 of them went back to playing sports or followed for five or so years. So this would get them through high school and a college career. And there was only one patient event, which was in a really young kid with a very prolonged QT interval who had an ICD in place and got two shocks, but probably most importantly, got these shocks because as a young kid, for numerous reasons, he wasn't able to be beta blocker compliant. And so the take home here was that in this patient population in this experience, and again, this has yet to be repeated. So I would say it's still preliminary. These athletes with genetic heart disease look like they did pretty well if they were allowed to play sports. So from Mike's paper, I think there are some things we can start to talk about and that not all cardiovascular conditions carry the same amount of risk and that phenotype dictates severity. There's no doubt that we can treat many of these people and doing so reduce risk. That being said, risk is very difficult to quantify for any individual patient. And at the end of the day, when we're dealing with these people, we're left with the need to apply some sort of shared decision-making process, which I'll talk a little bit more about in a few minutes. It's not just long QT, we're learning the same lesson with hypertrophic cardiomyopathy. This is a cardiopulmonary exercise test by a 50-year-old member of our national US rowing team who competed in one of the recent Olympic games. And the red dots here you see are his oxygen consumption. And suffice to say, this athlete is incredibly fit. He's got a peak VO2 of five liters per minute, which places him at an elite level of sport. And this is important because up until the last maybe five, 10 years, the teaching had always been, and this kind of comes out of one old historically important paper, is that HCM patients and athletes look very different. And that is that HCM patients are essentially cardiac cripples that can't generate the amount of VO2 needed to be good at sports, and particularly when you compare them to good endurance athletes. But we now know that's absolutely not the case and that athletes with HCM often have mild forms of disease and are quite capable and their hearts look different. They tend to have bigger heart chambers, they tend to have less wall thickening due to HCM. And in at least one decently evaluated series in Italy, those with HCM who were elected to continue competitive sports actually did as well, if not a little bit better than those that were restricted and decided to adhere to those restrictions. So again, we're starting to see signs that maybe some of these really scary historical heart things that kept athletes out of sport without talking about it should be approached with a little bit more equipoise. So I wanna conclude just by talking a little bit about this document, and this is the so-called update of the Bethesda Conference Proceedings. It's now the AHA ACC Scientific Statement around eligibility and disqualification. And this is the document if you detect heart disease in an athlete and send an athlete to a cardiologist that they will invariably turn to to ask the question, should I give this athlete clearance to get back into training and competition? So what does this document look like? Well, the first thing to remind you of is there's not a single class 1A recommendation in this entire document. There's not a single randomized controlled clinical trial that allows us to say with certainty that something is appropriate versus something is inappropriate. So this is all based on anecdotal experience and in many cases, opinion. Looking at the structure of the document a little more closely, it's actually divided into 15 taskforce documents, which are organized by topics and diseases. This is meant to really focus primarily on disqualification and restriction and not how to manage these people. Those guidelines need to be looked for elsewhere. It's geared toward competitive athletes at either the high school collegiate or the professional levels. There's a statement in this document that these types of athletes are a limited control population and I'll explain why I think that's a mistake. But importantly, we don't really extrapolate these to master's athletes or to just physically recreationally fit people. One of the biggest changes in the most recent update of this document was the addition of class 2A and class 2B recommendations. And I'll give you a list of what those look like in a second, but those are important because those are hard conditions in which this document now says things like, it may be reasonable to play, it may be appropriate to play, so it leaves a lot of wiggle room in terms of what we do with these people. This document has a very specific definition of what the athlete looks like that it should be applied to. These are people that are participating in organized team or individual sports that compete regularly, that place a high premium on excellence and do something with intensity. But one of the things that I took issue with when we were writing this, and unfortunately it was outvoted, was that these athletes should be treated paternalistically, meaning they face unique pressures and they probably should not be trusted to exert individual control. They may lie about warning signs, they may not be forthcoming because they don't wanna be excluded. And so we as doctors maybe should treat them a little more paternalistically than we would non-athletic patients. That has not been my experience taking care of many hundreds of athletes with heart disease. I think people are generally straightforward and if talked to and treated respectfully are honest about what they're experiencing, but this is what the document says. That being said, the document also provides us with flexibility. It says that clinicians may prudently deviate from the recommendation, particularly with fully informed athletes and that we have the opportunity to practice with flexibility and allow for individual responsibility. So this is a list of some of the most common things that now carry class two recommendations. So things like anomalous right coronary arteries, athletes with ICDs, athletes with non-compaction with normal function, athletes with coronary disease, athletes with heart transplants, athletes with genetic heart disease. These are all people in which this document now supports at least going through a process of determining eligibility and not just saying no from the get-go. But this recommendation series really does necessitate a process. So what does the process look like and where are the competing kind of motivations here? Well, on the sudden death prevention perspective side of things, I think we can all agree that life is a precious commodity, that some forms of disease increase the risk of death, that sport is a luxury, not really an essential part of life and that any suspected form of disease should lead to no sports or no exercise. That's one end of the spectrum. On the other end of the spectrum, which is really about enabling people to live their lives the way they want to lead their lives, we know that the risk of death is variable and in many of these conditions quite small, that individuals come to us with different levels of risk tolerance and risk aversion, that for some people, exercise is not a luxury, but really truly a way of life and that no one should be categorically restricted, that we should be thinking about these people as individuals and really allowing them to make some of their own decisions. So the decision-making process, again, it exists on a spectrum. On one end, you have the paternalistic gray-haired doctor who says, I know best, clearing athletes is my job. This is a simple process. If they have a hard problem, they sit on the bench. Why make it complicated? It turns out that athletes don't typically really see things the same way. They kind of tell us that doctors don't always know best, that we're individuals, that there are not just medical reasons that why I should or should not play sports, but there are also non-medical reasons and you shouldn't make it complicated because it actually is complicated. And so the sweet spot here is the concept of shared decision-making, which is not new to the field of medicine, but something, at least in the sports cardiology world, it is quite new over the past couple of years. So we've spent some time thinking about this. This was, I think, the first sports cardiology document calling for a change in the way we think about athletes and emphasizing the need for shared decision-making. This is something I wrote with Mike Ackerman, whose data I showed you earlier, and Rachel Lampert, who's a cardiologist at Yale. And the goal of this paper was really to introduce the concept of working with an athlete with heart disease and not just saying no from the get-go, thinking about the options. And really the document can be summarized as follows, and that is that the shared decision-making model acknowledges that paternalistic medicine is limited while recognizing the fundamental role of the physician in guiding decisions. It's not just letting people do what they want, it's around guiding them through difficult decisions. And in doing so, we need to be careful to explain both what we know about risks and benefits and what we don't know, and at the same time, take into account their personal preferences and values. So how do I do this? First is just starting with the medical facts, and that's ensuring that we're clear what the diagnosis is, and we do as much for stratification as we possibly can. The second step is moving away from medicine and just simply getting to know the athlete. And that is, who are they? How important is sport to them? How risk-averse are they? Do they ride a motorcycle back and forth to the football stadium? Do they go skydiving? If so, their likelihood of dying from one of those things is a heck of a lot lower than them dying from any form of heart disease. After we know the medical facts and we know the person, it's really where we delve into the discussion about the risks and what's known and what's uncertain. And then we're always documenting. And I want to be clear that when we meet athletes with heart diseases that have been associated with sudden death, even if we think the risk is very low, the athlete needs to know that that risk exists and we need to document that as part of the medical record to make clear that we've had that discussion. As most of you know, it's not just about the doc and the athletes sitting in the exam room together. This is part of a system approach. So after we identify the athlete's preference, this is where getting all of the stakeholders involved, which include medical staff, but also coaches, athletic directors, oftentimes deans of colleges, owners of professional teams, because really everyone needs to know what's going on and understand what's at risk and what the athlete wants to do. It's often helpful to know if there's local precedent. So if leagues have done this in the past and what decisions have been made, ultimately we try to reach a consensus in which the athlete, the coaches, the parents, the athletic trainers, the team docs, all feel like the right decision is being made. And if an athlete gets back onto the field, we're clear that there needs to be an emergency action plan and a clear plan for clinical follow-up and individual surveillance. So the paper we wrote was followed by another important paper focusing on this specifically with respect to hypertrophic cardiomyopathy. And again, I think we're seeing a shift in the way we think about this disease. I'm not saying that all people with HCM should be permitted to play sports, but I'm saying that people with mild phenotypic disease should at least be given the opportunity to discuss that as an option. And if you're interested in kind of a how-to guide to do this, this was a document that the ACSM asked a couple of us to put together in which we laid out a stepwise approach to do this, which again here is an eight-step algorithm, confirming diagnostic accuracy, risk stratifying and treating, discussing and educating the family, determining patient preferences and values, synthesizing what the patient and the clinician think is the best decision, working with stakeholders, implementing the decision, and then making certain there's long-term follow-up. So if this is of interest to you and maybe relevant to your practice, I'm happy to send along a slide deck with this reference. I will say in closing that the impact of shared decision-making among competitive athletes with cardiovascular disease is completely untested. We have no idea what the pros and the cons look like. We have no idea how many more people this is going to help versus hurt. And so this is something that a number of us are working hard now to study so that we can bring some science to what this process actually means to the people that we're applying it to.

2nd Edition, CASE 04

2nd Edition

Cardiac

athlete's heart

athletic heart syndrome

cardiac remodeling

endurance athletes

strength athletes

echocardiography

shared decision-making