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SANJEEV KAKAR: This is Mayo Clinic Talks, a weekly curated podcast for physicians and health care providers. I'm your host, Dr. Sanj Kakar, an orthopedic surgeon with a specialist interest in hand and wrist disorders at Mayo Clinic's Rochester campus. With the recent onfield cardiac arrest during a sporting event, much attention has been focused on why does this occur, and what can be done to prevent this from happening again?

Did you know the likelihood of sudden cardiac death in high school athletes is between 1 and 50,000 to 1 in 80,000. And for collegiate athletes, the risk is estimated to be over 1 in 13,000. Among NCAA athletes, there is an increased risk in those who are male, of Black race, and play basketball.

Joining us to discuss this topic are Dr. Thomas Munger, Associate Professor of Medicine and head of Mayo Clinic's Electrophysiology Division, and Dr. Michael Ackerman, Professor of Medicine and the Director of the Windland Smith Rice Genetic Heart Rhythm Clinic and Sudden Death Genomics Laboratory at Mayo Clinic Rochester in Minnesota. Welcome to the program, Tom and Mike.

THOMAS MUNGER: Thanks, Sanj, very much for inviting us.

MICHAEL ACKERMAN: Yeah. Great to be with you, Sanj and Tom. Looking forward to our conversation.

SANJEEV KAKAR: Well, as you've seen in the media, a lot of attention has come on about sudden cardiac death. And just to give an outline to our audience, why does this occur, especially in the athlete, the elite person who's really at their prime of physical fitness?

MICHAEL ACKERMAN: One is really to set perspective correctly. Because I'm not sure that it occurs more in elite. It's just that when it occurs in elite, it's on prime time. And then it's on the newsreel.

So, for example, Monday night's awful scene-- that scene plays out 5 to 10 times a day in young people age 25 and under. Most of those young people who have a sudden cardiac arrest, there's probably 5,000 a year, so 5 to 10 every day, they're not athletes.

They're not on Monday Night Football. They're just ordinary, healthy young people who might have a sudden cardiac arrest episode. Collectively, in the United States, it's really about 100, as in 100 athletes a year die suddenly. And that may not even be during their sport.

It's just that a known, competitive athlete, 100 of them-- junior high, high school, collegiate, professional-- will succumb to that statistic that you gave about of the 1 in 80,000 chance per year. It's just that when it is an athlete, there's incredible attention, energy, focus because it sort of defies our expectations of, how can the fittest among us succumb to something as awful and as tragic as a sudden cardiac death?

THOMAS MUNGER: Yeah. Mike, I would echo your comments about the high profile of athletes, which calls attention to this. Like Reggie Lewis, when I was coming out of training, died at the Boston Celtics. But most of these deaths do occur in the setting of nonathletics, and occur in young and older people. There's over 300,000 of these a year in the United States. Most of these actually occur in the setting of structural heart disease in older patients, but when it occurs in a young patient, there's various different things that we consider.

There was a study, probably within the last 10 years, looking at young US athletes under the age of 40 who had died suddenly-- looking at mechanisms. And while commotio cordis has been discussed recently, hypertrophic cardiomyopathy was at the top of the list. And many of the other genetic diseases that Mike studies actually play a role, as well as Wolff-Parkinson-White, and a host of other causes.

Sudden cardiac deaths defined as unexplained death within 24 hours of symptoms, and most of these deaths occur with no antecedent symptom at all. They just end up having a blackout spell and then go down. And if they're lucky enough to be resuscitated, we can figure out what the cause is. But in other times, we may not get the opportunity to figure out the mechanism, which, I think, Mike, you've actually done some work with understanding mechanisms of deaths in younger patients who haven't really had a diagnosis given.

MICHAEL ACKERMAN: Yeah. I mean, I think Sanj and Tom, like you said, there is a large list of potential whys, as why a previously healthy young person could collapse suddenly because of sudden cardiac arrest, for which that sudden cardiac arrest episode, if it's not short-circuited and corrected back to normal, then we have the tragedy of going from SCA, Sudden Cardiac Arrest, to SCD, Sudden Cardiac Death, and a subsequent funeral.

That list is a very long list. And it ranges from a genetically mediated heart muscle diseases; genetically mediated heart electrical diseases; nothing to do with genetics at all; inflammatory diseases of the heart muscle; in the old, coronary artery disease that then causes an myocardial infarction, a heart attack, then secondarily causes an electrical attack of SCA.

And so when somebody young and healthy goes down, there's an incredible amount of detective work that needs to take place, Sanj. And one of the issues is when somebody locks in on the why too quickly, as we saw Monday night within 10 minutes of the collapse, it was already declared the why being commotio cordis, I think there can be real, real danger of that because then you fail to discover what may have been the ultimate truth.

So when we deal with a sudden cardiac arrest survivor, it's a significant amount of detective work that Tom and I and our team would place that patient and his or her family through to look at any and all clues and all information to try to triangulate the why behind, why did that collapse and cardiac arrest happen in the first place?

SANJEEV KAKAR: So Mike and Tom, you both mentioned commotio cordis. Can you just explain exactly what that is? And when you went through a myriad of different causes, be that structural or nonstructural causes of sudden cardiac death, but you both mentioned this. Can you just go over that a little bit for us?

MICHAEL ACKERMAN: Sure. It's gotten a lot of attention in the last four days for an entity that is incredibly uncommon. Typically, it is a perfectly healthy host, no underlying cardiac vulnerability, for which there is a collision blow, a contact blow, an impact right over the chest with the missile projectile source, if you will, typically being a baseball, a hockey puck, a lacrosse ball, rarely, a soccer ball, almost never tackle football. Because the energy of a hit is dispersed across the shoulder pads, and just the physics don't work to upset the apple cart.

But when there is that collision impact that hits the heart's electrical system at exactly the wrong time, it trips the heart electrically up into a potentially life-threatening danger rhythm that we call VF, or Ventricular Fibrillation. And if order is not restored soon with rapid chest compressions and external defibrillation, then the heart ultimately cannot be electrically resuscitated, and then we end up with the tragedy of sudden death.

SANJEEV KAKAR: So obviously, you've explain why that occurs. And that's something that's probably hard to recapitulate in a clinical setting. Because many of these athletes go through pretty strenuous medical examinations ahead of time before they are allowed to play. So why does this still occur, given the number of causes that can relate to sudden cardiac death?

MICHAEL ACKERMAN: It's like the lottery ball odd ticket of a freak accident. There's no way to screen for somebody-- if somebody's healthy-- for a vulnerability to that. That's why people have countered it with different ways of the gear to cover that region. So that if there was a hit, that energy would get dispersed across the chest, and not mechanically, physically be able to do it.

There was actually fascinating study back in the same time frame that, Tom, you were talking about with Reggie Lewis. A colleague down in-- now in Southwestern, a good friend of mine, Dr. Mark Link, they did this projectile study of having the timing and the blow and the collision delivered to a nonhuman, and showed in that animal species the necessary amount of force, where it needed to strike, at what velocity it needed to strike, when in the electrical system did it need to strike to have that opportunity to trip up the system.

But one of the things that's happened, Sanj, is so much focus has been put on this entity that almost never happened, that cause football players and others to be worried that are they next, when it almost never ever happens, for which at this point in time, that entity or diagnosis is the thing that Tom and I would conclude two weeks after the episode, after every other stone is turned over, not five minutes after the observation of a collision.

In other words, I don't even know or think whether that tackle or that hit itself may necessarily have had anything to do with his subsequent collapse in cardiac arrest. And if it did, it almost for sure has to mean that that individual, whoever he or she is, had some sort of fragility or vulnerability in the heart substrate-- the different entities that Tom and I search for-- such that what should not have ever upset the apple cart with that kind of activity, with that kind of force, with that kind of distribution, nevertheless, did so. And it did so because that host wasn't a completely normal heart-healthy host in the first place.

And so we have to be way more careful in doing the detective work. And commotio cordis-- yes, it happens. But it's what we back into at the end of a very careful evaluation when we've ruled out basically everything else, and all we have is a healthy person for which right next to the collapse was a particular collision or impact, where you would then invoke and say, I wonder if that rare, rare thing of commotio cordis did it to this person?

SANJEEV KAKAR: Why do you think then, Tom, we've heard so much about commotio cordis, given what Mike mentioned. As he said, there's a long laundry list of other causes before this, which are more common. Why do you think that's gained so much attention?

THOMAS MUNGER: Well, I think part of it is screening. So I mentioned hypertrophic cardiomyopathy is right at the top of most lists. Although, again, I think based on what I've seen in Division I and professional levels now, a lot of patients get echocardiograms. And so that's reasonably good at screening it out-- not completely.

So that does beg the question, is our testing good for screening for some of these things? And it's good, but it's not perfect. And if you even use an electrocardiogram, say, to screen for something like WPW, or Long QT syndrome, or use an echo to screen for HOCM, you will not find all the cases of it out there with initial screening.

Secondly, we assume it's the heart here, too. But it may be other things as well. There's cerebral aneurysms. There are aortic aneurysms, like in that journalist in Doha a few weeks ago who died suddenly covering the World Cup.

There's other things like pulmonary emboli. I've seen several patients in the last couple of years in the setting of COVID who come in and present with syncope as their initial presentation for myocarditis or a pulmonary embolism associated with COVID infection. So we have to keep our minds open with commotio. It's certainly a entity that can cause sudden death. But I must say, again, everything has to be lined up just right to get that.

We induce ventricular fibrillation in the laboratory using low-energy shocks on the T wave for testing ICDs. And the window of doing that is extremely narrow. It's usually somewhere in the 3 to 10 joule range. It has to be timed almost perfectly on the T wave. And, as Mike says, it has to be generally a projectile that provides that amount of force localized onto the chest, not dispersed through pads and such.

So why has it been given so much? I think probably because most people think that these professional athletes probably have been screened for everything else, and it must be that. But that's a drawback to arriving at that conclusion.

MICHAEL ACKERMAN: I think one has to step back and say, in general, though, what did this scene teach us? It teaches us about what is our state of emergency preparedness, readiness for if there's a witness collapse that's deemed to be extraordinarily unordinary, as in SCA that could head to SCD.

What are the steps in preparation to do the call, push, shock, the chain of survival drill? Is the community ready for the witness collapse of somebody? How hard would it be to die suddenly in your community out there? Is there a safety plan?

And some communities, as you know, like ours in Rochester, Minnesota, we may not have a lot going for us, as some would say. But it is hard to die suddenly in this community in a witness way, and that's because of the vision and the preparedness of people like Dr. Roger White and the first response plan that got built into this community decades ago now, equipping all squad cars, ambulances, fire trucks, first responders with an automatic external defibrillator that then made it very hard that if you collapse in a witness way, to die. Because somebody is going to get to you pronto, and is going to start that chain of survival.

And I think that's what people should be looking at this, as a reflection of how safe is that community, and not focus so much on the athlete. I love athletes. But what's so special about the athlete? I mean, we should want to prevent and rescue sudden cardiac arrest victims, whether they're an athlete, an artist, an academic. It really doesn't matter.

It only matters because it got visualized in such a profound way. And it was, and I'm delighted to hear the great news today that was reported out, that it looks like neurologic recovery is very, very good for this young man. And I can't wait to see a full recovery.

I hope to see a full return to his sport, which is a whole nother topic of, can athletes return to their sport when they've had a close encounter like this? And the answer used to be absolutely no. But at Mayo Clinic, it's been absolutely, yes, you can, for the last 20-plus years.

SANJEEV KAKAR: Well, Mike, I'm glad you said that because regarding soccer, there was a soccer player, Christian Eriksen, of the Danish team, who a few years ago went down in a major European tournament and had a defibrillator placed. And is now back playing professional soccer, was at the World Cup this year.

So can you talk a little bit about that? Because obviously, people will be worried. And forget about the athlete. Let's talk about a regular person. If this happens to them, how can they resume normal activities of life?

MICHAEL ACKERMAN: Yeah. That's the great news is when we figure out the why, most can return to living large. Our view is that when you get diagnosed with a sudden cardiac arrest predisposing condition, and we know the name of it, we fully expect in almost all circumstances that our patients, our SCA survivors, should be able to live and thrive despite their diagnosis.

Because when we know the why, we, in general, have great treatments-- medications, procedures, devices, surgeries-- for which we can counter and neutralize the threat of a recurrent episode. And so we, in our program, and you mentioned the Windland Smith Rice Genetic Heart Rhythm Clinic, I've had the privilege now of taking care of over 700 athletes with a variety of sudden cardiac death predisposing genetic heart conditions. And they have stayed or returned to the sport that they were disqualified from.

And the results, as we've seen for 20 years now, is we ought to be very hopeful-- careful, but very hopeful that we can restore that individual to living large and not being shackled with the fear and anxiety that it's going to happen again the next minute, the next night, the next outing, when that's just not reality.

THOMAS MUNGER: Again, Mike is absolutely correct here. Knowing the diagnosis leads you to the prognosis, and then also, to the counseling about the activity. And it could be athletic activity. It could be occupational activity-- returning someone who is an orthopedic surgeon, for instance, or a window washer in Chicago on the Sears Tower, or a meat-packer or a mother-- a host of different things.

These activity recommendations aren't really just tailored to the athletes either. They affect every single person that comes in with sudden death because they all have similar questions. What can I do? Where can I go? What type of life can I lead from now on? And these things are critically important to discuss with the patient to not only allay their fears and concerns, but provide guardrails for their families and employers and relatives.

SANJEEV KAKAR: So Mike and Tom, let's go back to the why, because I think that's pretty important. I mean, there are going to be a lot of parents, coaches, athletes, regular people listening to this podcast. What would your advice be to them?

I mean, we talked a little bit about screening. And if patients go and see their primary care doctor now, saying, listen, I saw this, could I be next? What would your advice be to them, and also, the primary care providers?

MICHAEL ACKERMAN: I think, again, for the families out there, they have to start with the right-- be calibrated correctly. By that I mean, about 1 in 200 junior high kids, 1 in 200 high school kids, 1 in 200 athletic college students, have a heart condition that Tom and I would like to know about if we could, for which there is the possibility of sudden cardiac arrest-- 1 in 200 people. That means 199 out of 200 eighth-graders have nothing wrong with their heart.

So you have to keep that as your frame of reference, that this isn't an entity that's just going to come out left and right, like flip a coin. This next step is, OK, with that low background rate of a heart condition, 1 in 200 of us that have lurking in the background, how might we know that it's there?

Well, the most important part is your story. What's your own story? Have you had any miniature warnings that there could be a condition present? By that I mean, have you ever fainted suddenly, instantaneously, in the setting of exercise activity, being startled? Have you ever collapsed and had a full-blown generalized seizure when you were running, playing, the phone ringing?

Have you ever had to stop your sport because you were suddenly having exercise-related shortness of breath that was new and different? Are you experiencing any warning symptoms? And those warning symptoms, if you say, yeah, I think I did that, then you need to bring that to the attention of your medical provider.

And then not your own story, but what is your family's story? Have there been any warning symptoms in the family? Are you related to anybody who's died before the age of 40 suddenly, unexpectedly? Have there been any family members who've been labeled with a genetic condition? Yeah, my cousin was told they had hypertrophic cardiomyopathy.

Well, that's really, really important. That's not just your cousin's issue. That could be your uncle's issue, and then your mother's issue, and then your issue.

So what is the family story? Is there one? If yes, tell your local care provider about that. And then they can decide is there any basic testing that could or should be done. And one of the things that we know is why we need a two-pronged approach, Sanj.

Because if we look back at all of our sudden cardiac arrest survivors and those who tragically died, about half, that death event was the declaration event, meaning it was the sentinel event. You and I could ask about story as many ways as we could think of, and it would be not there.

The other half would say yes to one of those warning symptoms. And so for those with warning symptoms, we need to do a better job of warning symptom recognition, acknowledgment, pursuit.

And for the other half where their death event is the first and only, well, then we either have to figure out, can we screen? Or if we can or can't screen, can we blanket that community with the sudden death safety net, such that it becomes very, very hard to go all the way to a witness sudden cardiac death if you go down in public.

So, again, what's the readiness for the chain of survival reaction plan if our student were to go down walking to the lunchroom, or the janitor were to collapse while doing his or her work, or the grandparent were to collapse while watching his or her granddaughter play volleyball? What would be the ability to enact the safety drill in a very rapid, effective way?

SANJEEV KAKAR: So, Mike, in those patients, obviously, as you said, those that had a yes to some of those questions, but those that sadly didn't. If there's somebody coming in to see their primary care doctor and say, you know, I just want to stress ECG, or an echo, or a cardiac MRI. What's your thoughts and answers to those type of questions?

MICHAEL ACKERMAN: Do we have another two hours, Sanj?

SANJEEV KAKAR: [LAUGHS].

MICHAEL ACKERMAN: Because-- no, it is. So if you ask me in a little different way-- so one of our entities that we focus a lot on in Mayo Clinic's program is Long QT syndrome. That affects one in 2,000 humans. It is incredibly treatable. It's incredibly findable.

So if you said to me, should we screen for a 1 in 2,000 condition called Long QT syndrome that we can treat very, very well when we find it, my answer is, absolutely we should be screening. But it hasn't happened, and it's not happening because right now our screening tool is this thing called the 12-lead ECG. And you say, well, that's an easy test. Well, not-- if you unpack it, not really.

Where is that machine? Who's reading the traces that come off of the machine? And so we have these challenges to the screening tool for which Tom and I are incredibly excited that the new future of artificial intelligence enhanced analysis of these different tools that we've had in the past, I think we have a very promising future, for which we will be screening for sudden cardiac arrest associated conditions very differently in 2025 than we have presently for which there is no consensus for proactive screening in the United States for these conditions.

There's no universal 12-lead ECG for all sixth-graders. There's no universal echo right now for all 12-year-olds to look for HCM. Could there be? Should there be? I think there will be when we have a better way of doing the screen that removes all of the false positives, or decreases them a lot.

Because while we want to find that 1 in 200 person, we don't want to over label 10, 20 of those 200 with a preliminary flag of a penalty, and then be unwilling to say, after further review, there's no problem. Penalty is reversed. And we don't do a very good job of picking up the flag when somebody gets told, you might have this wrong with you.

And so screening has a dark side to it. It's the two-edged sword. And Tom, you've seen the consequences of the two-edged sword play out over and over again.

THOMAS MUNGER: Well, you've emphasized, Mike, the importance of public health screening as our tool right now. American Heart updated their guidelines in this area last year, this 14-point checklist. And I saw information that that was only being utilized by 6% of sports programs across the country right now.

So even the basic asking the questions, you said half of them are going to have a negative survey. But we're not even asking the questions of a large proportion of our student athletes at this point in time.

I agree with you. Enthusiasm for the AI stuff-- I got to tell you. I see people using cell phones in Central Africa, and I'm salivating at the fact that we might have these types of diagnostics out in the hands of people all over the world on the platform in the next 10 years. Because that really gives the power of screening. It's cheap, potentially accessible to large swaths of the population. And that's really what you need to make an impact in sudden death.

I mean, we can also talk about the other end of the spectrum with risk factor modification for older patients related to sugar and fiber and all those things in our diets. But I share with you the enthusiasm about having these artificial intelligence tools well-refined and in the hands of large populations. That's going to make a big difference.

MICHAEL ACKERMAN: And the other thing, Sanj, that will make an incredible difference. You saw-- again, it looks like that gentleman's recovery is looking very good thankfully. Well, that's a direct result, in part, of the athletic trainer, and the team that surrounded him that initiated effective chest compressions, that maintain good enough circulation to the noggin to enable him to be neurologically intact and recover well.

So what if we have-- and his name is Denny, I think, the athletic trainer. And he's called a hero. What if that's not hero status, right? What if that is just sort of the army of first responders that we create?

What if, as a high school graduation requirement, we teach effective hands-only chest compression? What if we make it sort of reflex, that if somebody is witnessed to go down, and they're not waking up within 10 seconds, that the drill is 911-- call, chest compressions-- begin fast.

And the moment you decided to pump on somebody's chest, you're calling for electricity, the external defibrillator, where years ago they did a study of sixth-graders, and showed that the sixth-graders, without reading the instructions, could grab the AED, get it out of the box, apply it, and be ready to push the button within, I think, 45 seconds from the time of a trained ambulance first responder, meaning they're really easy to use.

And what if we have it be so that if you and I were to go down in a restaurant, that that drill could commence immediately. And then we change the landscape for those where there is no forewarning, where the collapse is the sentinel event. And then do we have a chance of having for-- Because time is everything. You have got to get order restored to the heart's electrical system and to the pump as fast as you possibly can.

And when you're young, like that gentleman on the football team, there's way more resiliency and margin in the noggin, than when you are 50, 60, 70, where that clock is moving really fast. And so I think if we use this as an opportunity to say, what really is the state of readiness in your community, not as if it's going to happen to your child, but what if it were to happen at the next game for the grandparent in the audience, or the 60-year-old out of shape referee?

It's far more likely to happen to him or her than it is to your child out there who's eighth grade, 10th grade, getting ready for summer football. And now is all of a sudden worried about heightened chances of this freak accident of commotio cordis, which is almost, almost a never.

So getting it perspective, and getting it the efforts and the focus recalibrated, I think, is really important.

SANJEEV KAKAR: Well, well said, Mike. And I think, as you said, every tragedy there's certainly some lessons learned. And thankfully, hopefully, this looks to be heading in the right direction. But the fact that we're having this conversation today, and as you said, about our society's readiness to be able to adapt to this I think is absolutely critical.

Tom and Mike, anything else you wanted to add that we didn't get a chance to add during this discussion?

THOMAS MUNGER: I don't have anything other than thanking our organizers today. Because it is a critically important public health issue. And on the front end, and the back end, and every generation, we relearn it again and again and again. So having it a topic for the public to ponder, and also learn from and adapt our procedures to, is very important.

SANJEEV KAKAR: We've been talking about sudden cardiac death with doctors Munger and Ackerman. Thank you both for your invaluable time. If you've enjoyed Mayo Clinic Talks podcast, please subscribe. Stay healthy. And thank you for the privilege of your time.

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