CVM Grand Rounds May 27, 2026

Name: CVM Grand Rounds May 27, 2026
Uploaded: 2026-05-27T18:19:35.1566667Z
Duration: 1 h 2 min 14 s

May 27, 2026

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ID: 14250
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01:37I'm just gonna post for
01:38a new park.
01:41Megan, you ready? You do
01:43it. No. You don't have
01:44to come up yet. Yeah.
01:47Hi, everyone. I think we'll
01:48go ahead and get started
01:49since it's twelve o two,
01:52as people come in.
01:53Just a few announcements.
01:57Please remember to
01:59register for, CME.
02:03Welcome to all our,
02:05folks in the room as
02:06well
02:07as
02:08as,
02:09across all our many watch
02:11parties across the system and
02:12our,
02:15and, we're we're in for
02:17a treat
02:18today, and so I I
02:20am looking forward to learning
02:22this more this afternoon,
02:24and we'll ask Rachel in
02:25a moment to introduce our
02:26speaker.
02:27Just some announcements.
02:29Next week,
02:31grand rounds
02:33will, for us will be
02:35in the morning on Thursday
02:37morning. So remember,
02:38to next week, there will
02:39be no Wednesday
02:41noon conference.
02:43I got that right, Jeff?
02:44That's right. Okay.
02:46And, we're very excited to
02:48have,
02:49doctor Shivkumar,
02:50who will be our,
02:51Calabresi lecturer,
02:54from UCLA,
02:55on Thursday, and there'll be,
02:57different activities and involvements for
02:59folks,
03:01through, that part of the
03:02week.
03:04And,
03:06following that, we are also
03:07excited to have the,
03:09annual Linda Rosenfeld lecture given
03:11by Mina Chung, which will
03:13be on Wednesday as is
03:14our standard.
03:16On the tenth, we have
03:17a faculty research seminar led
03:19by actor Bender next door
03:21the next week. And then
03:22to end the year, we
03:24have,
03:25professor Zainab Samad, who's the
03:28chair of medicine at Khan
03:29University,
03:30coming to to visit with
03:31us at the end of
03:32the month. So,
03:33in between, there's some other,
03:35exciting opportunities to,
03:38share,
03:39time together,
03:41fellowship graduation, and other things,
03:44will be, there'll be information
03:45on that coming out.
03:48These are our disclosures
03:49and, information.
03:52And with that, I'm gonna
03:53ask,
03:54Rachel, doctor Lampert to come
03:55up and introduce our speaker.
03:59I'm so pleased to be
04:00introducing our grand round speaker
04:02today, doctor Megan Wasfi.
04:04Doctor Wasfi arrived at Harvard
04:06as a college freshman and
04:07has never left. She graduated
04:09medical school, Miles per hour,
04:10did fellowships in cardiology,
04:12sports cardiology,
04:14and echo at, Mass General
04:15and the Brigham and is
04:16now an associate professor there
04:18at Harvard base at Mass
04:19General.
04:21Doctor Wasfi, is a consummate
04:23sports cardiologist in both her
04:25clinical and research endeavors.
04:27She's the team cardiologist for
04:28Harvard Athletics and the medical,
04:30director of the Boston Marathon.
04:32She's a member of the
04:33ACC,
04:34sports leadership council and, had,
04:36spent several years chairing the
04:38annual care of the athletic
04:39heart meeting.
04:40She's on
04:42multiple other committees, including American
04:43College of Sports Medicine,
04:45and has, led and been
04:47part of multiple,
04:48guidance documents from multiple societies
04:50around sports cardiology.
04:52She has been the recipient
04:53of, multiple
04:55grants for her, research most
04:57recently having gotten a grant,
04:58I think, yesterday or the
04:59day before in r o
05:01one. And,
05:02her, focus is the impact
05:04of sports and exercise on
05:05cardiac physiology.
05:07Please join me in welcoming
05:09Doctor. Waspy.
05:18Thank you. What a kind
05:19intro. It's really a pleasure
05:21to be here today,
05:22and thank you to the
05:24division for the invite and
05:25especially Rachel for the invite.
05:26You know, I look up
05:27to it, admire Rachel a
05:29lot. She's really a giant
05:30in the field of sports
05:31cardiology and an excellent host
05:33through the day today.
05:35And so the goal of
05:36the talk is to take
05:37you guys through our field.
05:39And,
05:41I'll go through I don't
05:42have any disclosures,
05:44to speak of relevant to
05:46the talk, but this,
05:48I'll add in some of
05:49my research throughout the topics
05:50that we cover, and these
05:52have been the generous funders
05:53of that work over the
05:54years.
05:56As an outline of where
05:57we'll head you know, we'll
05:58talk about
05:59the, disease states and the
06:01conditions
06:02that really focus our attention
06:03in sports cardiology, and these
06:04are the causes of sudden
06:06cardiac arrest and death in
06:07athletic populations. These are also
06:08the causes of major clinical
06:10events in these populations. You
06:12know, what what conditions enriched
06:13for sport related events
06:15and cover the exercise paradox,
06:16the idea that exercise is
06:18medicine, but can be a
06:19trigger for sudden events.
06:20And then we'll break it
06:21down by age demographics. When
06:23I say young athlete, I
06:24I mean, I will see
06:24sixteen or seventeen year olds,
06:26but we're thinking sort of
06:27young teen athletes through around
06:29age thirty five, what causes
06:30events in in that population.
06:33And dip into the work
06:34I've done, as oftentimes when
06:36we're evaluating athletes that will
06:37result in a lot of
06:38imaging and ECGs, how do
06:40you tell if it's an
06:41athlete's heart versus the beginning
06:42stages of a pathologic state
06:43that could pathologic state that
06:44could risk for rich for
06:46risk?
06:47And then we'll take the
06:48lens of the so called
06:49masters athlete.
06:51Age wise, we think of
06:52that as thirty five and
06:53above.
06:54Yep.
06:56So lens that changes as
06:57you get older, and really
06:59focus on ASCVD in this
07:00population as it's the most
07:01common cause of events. And
07:03then end, you know, through
07:04the lens of sports medicine
07:05of, you know, we're gonna
07:06be incomplete whenever we're trying
07:07to
07:08prevent prevent events from happening.
07:09Even if we understand the
07:11problems that we encounter in
07:12sports cardiology better, we'll still
07:13not find and manage the
07:15risk,
07:16in all athletes. So, what
07:18do we do to make
07:18sure that there is an
07:19event that, we have athletes
07:21surviving? So emergency action planning.
07:24So that's our outline.
07:25And we'll we'll talk with
07:27discussing sudden cardiac death in
07:28athletes. And, you know, these
07:29are always very highly impactful
07:31events.
07:32The most famous story I
07:33think codified,
07:35through
07:36many hundreds of years is
07:37the story of Philippides.
07:40He was a soldier who
07:41apparently ran about the modern
07:43marathon distance to deliver, news
07:45of victory in battle and
07:46promptly collapsed and died.
07:48So that's a that's a
07:50famous case of sudden cardiac
07:51arrest and death, inspired the
07:53modern marathon distance.
07:55These
07:56events even if they're happening
07:57very very long ago or
07:58more recently are highly impactful,
08:01because it's this person that's
08:02the pinnacle of health, that
08:04drops while doing usually something
08:05they love a lot.
08:07Here's what the numbers look
08:08like and you could say
08:09I mean this is a
08:10rare event it's point five
08:11to two depending on whether
08:12you're looking at arrest and
08:14death or just death,
08:15per a hundred thousand athlete
08:16years.
08:18So that you could look
08:18through the lens of that
08:19being rare.
08:21It's more common in certain
08:22athlete populations,
08:23males more so than females,
08:25and certain higher risk sports
08:26like men's basketball, you'll see
08:28numbers that get, higher.
08:31And,
08:32so those numbers, while rare,
08:34I feel like it's because
08:35of the paradox of it
08:36happening in a highly active
08:37athletic person that centers our
08:39attention.
08:40It shouldn't decrease our enthusiasm
08:42for exercise, though. And in
08:44the vast majority of even
08:46my practice was enriched for
08:48athletic people. We need to
08:49be, you know, carrying the
08:51message that exercise is medicine
08:52and that we know higher
08:53levels of physical activity shown
08:55nicely on this graph. You
08:56don't even need to get
08:57out to, like, guideline recommended
08:58levels, even even less than
09:00that, twenty percent off the
09:02top of mortality risk. These
09:03are guideline recommended levels.
09:05And then you can get
09:06a little bit more reduction
09:07in mortality getting out to
09:08more what, like, athletic individuals
09:10might be doing.
09:12And so exercise as medicine
09:14is a message we need
09:14to carry through all of
09:15our cardiology visits.
09:17One thing I do say
09:18to patients, though, is you
09:18don't need to be out
09:19here on the dose response
09:21curve. It should be accruing
09:22all the benefits of exercise.
09:24A lot has been made
09:25about this dot, which,
09:26occurs in almost every study
09:28where you're looking at the
09:29relationship between physical activity and
09:31mortality.
09:32Suffice to say, in even
09:33cohorts that are quite large,
09:34there's never a statistically
09:36significant sort of too much
09:38exercise that can be demonstrated.
09:40But it's thought provoking, especially
09:42as we go through,
09:43how exercise can be a
09:45a a can provoke sudden
09:47events in those with risk
09:48producing conditions.
09:50And so that idea that
09:52exercise can serve as a
09:53trigger is what I like
09:54to call the exercise paradox.
09:56So exercise overall,
09:58you know, reduces your risk.
09:59If you're physically active, you're
10:00gonna have lower risk of
10:01sudden events and heart disease
10:03overall.
10:05But for that hour spent
10:06exercising, your risk is higher
10:07than an hour spent at
10:09rest. And this is a
10:10really old classic study that
10:11demonstrates that,
10:13individuals were quoted by the
10:15amount of habitual physical activity,
10:17sedentary versus more, you know,
10:18highly active, looking at the
10:20incidence of cardiac arrest and
10:21the relative risk of a
10:22cardiac arrest during an hour
10:24spent at exercise versus an
10:25hour spent at rest. If
10:26you're not active at all,
10:27you have a fifty times
10:29risk,
10:29during exercise as compared at
10:31rest.
10:32But even if you are
10:33regularly training, your risk is
10:34higher during that time spent
10:36in exercise than at rest.
10:38So that concept really,
10:40focuses our attention as sports
10:41cardiologists because we wanna understand
10:43what conditions are per in
10:44particular, the conditions that are
10:46most relevant to athletes are
10:47the ones that produce those
10:48those excess events during exercise.
10:50And we understand that pretty
10:52well. I think it it's
10:53taken a lot of work
10:54over the years, and there's
10:54still debate about, you know,
10:56the distribution and percentage of
10:57exactly how many events are
10:59caused by x or y
11:00condition.
11:01But I like this graph
11:02because it shows it mapped
11:03by age, and this is,
11:04the the incidence of sudden
11:06cardiac death and then the
11:07causes into, you know, big
11:08bins.
11:09After age thirty five, if
11:11you're talking about a master's
11:12athlete population, we can really
11:14focus our attention on atherosclerotic
11:15cardiovascular
11:16disease and coronary artery
11:18disease. Below age thirty five,
11:20though, it's more of a
11:20mixed bag, and it's it's
11:22not really just one condition
11:23we can focus on, but
11:24a whole variety of conditions.
11:27There's many different pie charts
11:28one could show to demonstrate
11:29this. I just like this
11:30one the best. It has
11:31nice colors.
11:33You can divide it up
11:34into
11:35cardiomyopathies.
11:36The most common overall and
11:38and as well as represented
11:39in these cohorts will be
11:40hypertrophic cardiomyopathy, but also arrhythmogenic
11:42and dilated cardiomyopathies,
11:45You know, primary arrhythmia syndromes,
11:47Rachel's oh, sorry. Coronary anomalies
11:49will always be second in
11:50the pizza pie. If there's
11:51a board question, it's always
11:52second. So what's the second
11:53most cause, common causes on
11:55cardiac arrest in young athletes?
11:56It's always coronary anomalies
11:58as compared to other adult
12:00cardiologists. I feel like I
12:01think and worry and wonder
12:02about coronary anomalies, much more
12:04commonly because of that. And
12:05then, primary arrhythmia syndromes will
12:07take up most of the
12:08rest of the pizza pie
12:09as far as things that
12:10you can identify and manage
12:12in advance.
12:14And so within young athletes,
12:15we're really not thinking just
12:17about one condition, but a
12:18whole host of conditions.
12:19And,
12:21we are already in Boston
12:22in some schools, and colleges
12:24cycling into a screening season.
12:27The idea being, I mean,
12:29those of us who have
12:29kids and who are at
12:31a certain level of youth
12:32sports, are used to having
12:33to have a form filled
12:34out before kids can participate
12:35in sport. And then typically,
12:37as we are thinking about
12:38athletes at higher incrementally higher
12:40levels, there's
12:41additional testing done in order
12:42to identify risk producing conditions
12:44in advance of sport.
12:46And I think the lens
12:47here is quite interesting because
12:49when we think about screening
12:50in in the rest of
12:51medicine, you're doing,
12:53you know, a mammogram to
12:54look for breast cancer or
12:55a colonoscopy to look for
12:56colon cancer. But when we're
12:57screening young athletes, I think
12:59it's unique because we're really
13:00screening for all these diagnoses,
13:02not just one diagnosis.
13:04And I'll say in advance,
13:05there's no, like, randomized controlled
13:07trial or or trial based
13:09data that tells us a
13:10given screening program is shown
13:12to reduce the outcome of
13:13interest, which is sudden cardiac
13:14arrest and death. Absolutely no
13:16studies that tell us that.
13:18This is the typical starting
13:20spot, which is we're gonna
13:21do a history and a
13:22physical. This is the one.
13:23There's also some that come
13:24out from the ACSM asking
13:26about chest pain and family
13:27history and such.
13:29A quirky story is I
13:30do do the, screenings for
13:31Harvard Athletics now, and I
13:32was a Harvard athlete. And
13:34maybe this was a sign
13:35of times to come, but
13:35I have a very linear,
13:37like, extremely
13:39consolidated memory of my PPE
13:40in college because it was
13:42the first time anyone had
13:43asked about my family history
13:44and my mother wasn't sitting
13:45next to me and there's
13:47no cell phones back then
13:48so they're asking does anyone
13:49in your family have cardiomyopathy
13:50this and that this and
13:51that and I thought I
13:51was flunking my first test
13:52at college because I didn't
13:53know the answer to any
13:54of those questions. So probably
13:56wasn't a very high yield
13:57question. And as such, you
13:58know, this is common. These
14:00are young people being asked
14:00these questions, and I think
14:01even if their parent is
14:02next to them, you can
14:04see if you're thinking about
14:05it as a diagnostic test,
14:06the sensitivity and specificity are
14:08really imperfect and,
14:10positive predictive value really
14:12quite poor. So this wouldn't
14:14pass muster if we were
14:15trying to, like, get it
14:16into you know, if it
14:17costs a lot of money
14:17as a screening test, this
14:19naturally promulgated the question of
14:21can we do better.
14:22And, quite a while ago
14:24now, before I even started
14:25as a sports cardiologist, the
14:27natural extension was to add
14:28an ECG,
14:29which we now do for
14:30all, not all d one
14:32programs, but within the Ivy
14:33League, all of the, sports
14:35programs do this in many
14:36other division one programs,
14:38and is even percolated down
14:39to the high school level
14:40in some areas.
14:42The problem was, though, initially,
14:43is that athletes' ECGs look
14:44quite different than the general
14:46population in part related to
14:47the remodeling
14:48that will happen to an
14:49athlete's heart. So the results
14:51were somewhat disastrous with, like,
14:53huge positive rates that were
14:54all false positives.
14:56Rachel's been part of this
14:57work all throughout, which is
14:58the idea that can we
14:59get better with refining what
15:00is completely normal on an
15:01athlete ECG, what's always gonna
15:03be abnormal, and what sort
15:05of requires some contextual cues.
15:07And with the use of,
15:08algorithms like this that are
15:10just about to be updated,
15:11maybe you can tell us
15:12when the new ones will
15:13be out, Rachel. We've incrementally
15:14gotten down, like, the positivity
15:15rate of the ECG to
15:16around two percent.
15:18So it's still not a
15:19perfect test. It definitely has
15:21diagnostic criteria performance criteria that
15:23are much better than the
15:24history and physical alone. But
15:25still when you do an
15:26ECG, if it's positive, they'll
15:28you'll only find cardiovascular disease
15:30in about one out of
15:30ten of the athletes with
15:31positive ECGs. So I think
15:33we can still do better.
15:36But one thing we always
15:37have to acknowledge underscoring the
15:38importance of emergency action planning
15:40is there are certain things
15:41like coronary anomalies and then,
15:42you know, aortas and, of
15:44course, commotio cordis that will
15:45never pick up no matter
15:47how thorough our screening is.
15:50What happens when you do
15:50a lot of screening or
15:52you present as a sports
15:53cardiologist and are available to
15:54athletes with symptoms is that
15:56you end up doing a
15:57lot of imaging.
15:58And, trained as an echocardiography,
16:00I like multimodality
16:02imaging. And as I joined
16:04the staff at MGH early
16:05on,
16:06it really bothered me.
16:08The conceptual lens was such
16:10that, you know, you could
16:11have patients athlete patients with
16:13cardiomyopathy.
16:14You could have athletes with
16:16completely normal but sort of
16:17enlarged or thickens hearts, and
16:19that there was sort of
16:20this gray area or gray
16:21zone in between where with
16:22existing tools, whether it's thickness
16:24or dilation or an enlarged
16:26RV, it would be difficult
16:28or impossible to tell which
16:29whether it was sort of
16:30the beginnings of a pathologic
16:32state or just athlete's
16:34heart. And this was especially
16:35important back then. This was
16:36ten or eleven years ago
16:37because our sport our guidelines
16:39that help,
16:41helped to, help us to
16:43understand what athletes could return
16:45to sport versus re be
16:46restricted were quite restrictive. And
16:48that if you made a
16:49cardiomyopathy
16:49diagnosis,
16:51it may be in according
16:52to the published rules that
16:53they were no longer allowed
16:54to participate in their sport
16:55anymore. So getting
16:57it right had that very,
16:59sort of black and white
16:59ramifications.
17:01But it it also bothered
17:02me because leaving people in
17:03a gray area feels like
17:04purgatory. If you say, this
17:05could be HCM or dilated
17:07dilated cardiomyopathy, but I don't
17:08know yet. We're gonna have
17:09to follow you over time.
17:10Just felt like, we could
17:12do better with figuring out
17:14which bin they fit in,
17:15and that motivated a lot
17:16my early work.
17:18We'll pause and talk about
17:20cardiac adaptations to exercise, which
17:22is the general lens that
17:23if you do a lot
17:23of exercise, it'll cause, changes
17:25in your heart, structural and
17:27functional changes in response to
17:29that hemodynamic stress of exercise.
17:32There was some,
17:34there it's been long recognized.
17:36There's some studies from the
17:37eighteen nineties that show on
17:38radio graphs, or listening with
17:40the stethoscope that athletes hearts
17:41are bigger than their non
17:42athletic comp hearts.
17:44And I like this quote
17:45a lot from all the
17:46way back then eighteen ninety
17:47nine.
17:48You know, because I think
17:49we're now doing advanced cardiac
17:50imaging to get at this
17:52question. But even back then,
17:53you know, we have to
17:54consider carefully the way the
17:55heart's doing its work. It's
17:56not just the size of
17:57the the muscle like other
17:58muscles, but the quality that
18:00will tell on the long
18:01run. And here we're doing
18:02strain and ECV and all
18:03these fancy imaging ways to
18:04look at look at the
18:05quality of the heart muscle,
18:07but yet we still end
18:08up with cases where we
18:09don't know which bin to
18:10put the athlete in.
18:12When we're thinking about how
18:13the heart adapts to exercise
18:15and what we might expect
18:16on cardiac imaging, it's first
18:17important to point out that
18:19not all exercise is created
18:20equal. Even in our, like,
18:22gen pop PA guidelines, it's,
18:24divided up into our sort
18:25of cardio, and these are
18:26the various terms you could
18:27use for that versus our
18:28muscle strengthening activities.
18:30And,
18:31you can dichotomize sports like
18:33that, and the physiology is
18:34quite different. I put all
18:35these Harvard athlete pictures in
18:36just as a rub on
18:37purpose here as I'm visiting
18:38Yale today. But they are
18:40also the athletes that I
18:41take care of.
18:42So your cardio you know,
18:44I'm talking to physio to
18:45physiology oriented cardiologists. You know,
18:47your cardiac output's going up.
18:48You're vasodilating out to exercising
18:49muscle to support increased metabolic
18:52demand. Physiology is quite different
18:54than strength based activity where
18:55you're just intensely contracting muscles,
18:59and you actually will see
19:00cyclical spikes in blood pressure
19:02without really much change in
19:03cardiac output if you're doing
19:05that in its purest sense.
19:07But most sports end up
19:08being a mix of these
19:09two physiologies.
19:10We just updated this diagram,
19:12for our new,
19:14athlete,
19:15sports participation
19:16document,
19:18which was great to work
19:19with Rachel on that as
19:20well.
19:21We used to sort of
19:22have sports divided up into,
19:23like, a three by three
19:24table
19:25according to their sort of
19:26physiology, but acknowledging everything's on
19:28a spectrum, they're now divided
19:30up more on a spectrum.
19:32And you've got things like
19:33if you're if you're walking
19:34a golf course that's not
19:35provoking much changes in your
19:36physiology at all, all the
19:38way up to, you know,
19:39sort of rowers and Nordic
19:40skiers tend to have the
19:41the most excursions in physiology,
19:43both strength based and endurance
19:45based physiology.
19:48And so,
19:50that is
19:51a lens through which to
19:52view what we might expect
19:53to happen with the heart.
19:55There was some debate whether
19:56physical activity actually caused
19:59cardiac adaptations at the beginning.
20:01You know, we don't think
20:02that because NBA players are
20:04taller that playing basketball makes
20:07you taller. Right? It's just
20:08you're better at basketball if
20:09you are taller. Right? So
20:11at the beginning of this
20:12field, the idea was, well,
20:13does exercise actually make the
20:15heart bigger? Or if you're
20:16just genetically enriched to have,
20:17like, a bigger heart size
20:19compared to your body size,
20:20are you more likely to
20:21be good at sports, especially
20:22endurance sports?
20:24But I think we now
20:25have convincing longitudinal data including
20:27in not really athlete populations
20:28like couch to five k
20:30type training,
20:31where if you, you know,
20:32look at time point zero
20:33and, again, after a period
20:34of exercise training, you can
20:35see the cardiac enlargement develop
20:37in real time. Maybe not
20:38to the point where the
20:39heart's abnormally dilated, but you
20:40can see the changes track
20:42in that direction.
20:44There is no really one
20:45athlete's heart, though.
20:47As I diagrammed out, there's
20:48these different physiologies of different
20:50sport,
20:51different sports. Hearts will also
20:53track with body size, and
20:54then there's some important sex
20:56based differences.
20:57To To start with what
20:57we expect by sport, this
20:59was some of my early
20:59work when I first came
21:00out of fellowship onto staff.
21:03If you look at sort
21:03of runners' hearts, just people
21:05who are pure endurance sports,
21:07I think of it like
21:07taking a normal heart and
21:08just sort of putting it
21:10on a photocopier, at least
21:11a still image. Their hearts
21:12are symmetrically enlarged. The chambers
21:14are all larger
21:15because their EDV is bigger.
21:16Sometimes their EF can float
21:18towards fifty percent or maybe
21:19even a little bit lower
21:20because they have high end
21:22diastolic volumes to make the
21:23same stroke volume, the EF's
21:24lower.
21:25And it but you won't
21:26really see much change in
21:27the wall thickness. So the
21:29these sports, which are really
21:30just pure endurance sports, don't
21:31provoke that.
21:33We see the biggest heaviest,
21:34hearts in the athletes who
21:36are up in the upper
21:37right of that diagram. So
21:38these are things like Nordic
21:39skiing, cycling, and rowing.
21:41There's some thought that that's
21:42because there is some intrinsic
21:44isometric or stress
21:46strength based component to these
21:48sports, not because they're going
21:49and lifting heavy weights in
21:51a weight room, but because
21:52the cadence and the the
21:54form of movement is just
21:55different from running and swimming.
21:57This is a old study
21:57where you could put a
21:58lines in healthy people,
22:00and measure things. Because I
22:01don't think I could get
22:02this through an IRB
22:04now where they were asked
22:04to, you know, put force
22:06onto a rowing or I'm
22:07sure this was not actually
22:08in a in water.
22:09And you look and you
22:10see, okay. The the blood
22:11pressure both goes up when
22:12you when you, you know,
22:13start your exercise, but then
22:14if you're doing this cyclical
22:15rowing, there's these little microspikes
22:17to your blood pressure, and
22:18you don't get that when
22:19you're running or swimming.
22:20So it may be these
22:21these athletes have bigger heavier
22:22hearts because there's this isometric
22:24extra stress in addition to
22:26the cardiac output. It could
22:27also be that these athletes
22:28can spend more time,
22:30doing,
22:31their endurance sports because they're
22:32not on their own two
22:33feet. It's very hard to
22:34run for six hours a
22:35day, but you can cycle
22:36or row for those, times.
22:38Suffice to say those athletes
22:39in the upper right, for
22:40whatever reason, they have the
22:41biggest heaviest hearts, and that's
22:42where we can start to
22:43see wall thickness go up.
22:44But it should be in
22:45an eccentric pattern where the
22:46walls are thick, but the
22:47cavity is also big.
22:49So those are the most
22:50remodeled parts. And then do
22:52I do a fair bit
22:53of work with, we call
22:54it American style football. And
22:56with World Cup coming, we're
22:57probably better off distinguishing it.
22:59It's not it's not football
23:00in the vast majority of
23:01other places in the world.
23:02So American style football players,
23:03particularly those playing at the
23:05lineman position, the bigger guys,
23:07can develop a heart that
23:08actually looks like hypertensive heart
23:09disease with concentric hypertrophy,
23:12part of the football players
23:13health study at Harvard, and
23:14we studied former players. And,
23:17it's important to note in
23:18this instance, there's some thought
23:19that this was actually the
23:21result of the heavy lifting
23:22that these athletes do. But,
23:24increasingly, we think it's the
23:25stuff that goes around with
23:26all the weight gain and,
23:28the the playing of the
23:29sport at that position, hypertension,
23:31sleep apnea, and such. Because
23:32it turns out if you
23:33study, like, other heavy lifters
23:35like, bodybuilders and stuff, they
23:36don't develop parts that look
23:38like this at all. So
23:38this is really not exercise
23:40induced remodeling in my view.
23:42It's a pathologic state even
23:43if it's not HCM.
23:45So that's what we can
23:46expect by sport type, and
23:47then we also can see
23:48some important differences,
23:50by sex and gender,
23:52with the exercise induced remodeling
23:54in general for any given
23:55combinatorial body size and sport
23:57type, females will be even
23:58less likely to develop increased
24:00wall
24:00thickness. They also have some
24:02interesting differences in their EKG
24:04and are at lower risk
24:05of sudden cardiac arrest and
24:06death in male athletes even
24:07in the same sports.
24:08And then we'll get into
24:09the some of the differences
24:10we see in ACVD and
24:12masters female athletes when we
24:13get to that section.
24:15So if you put it
24:16all together, you can sort
24:17of overlay what you might
24:18expect as far as heart
24:19size on this diagram with
24:20the lifting part being like
24:22most most people up in
24:23this quadrant just have normal
24:24hearts except for football alignment.
24:26Again, sorry for all the
24:27Harvard athletes.
24:29My research interest then evolved
24:31from there to try to
24:32understand better, well, what if,
24:34a football player's help heart
24:36what if a golfer's heart
24:37looks too much like a
24:38football player's?
24:39In particular, HCM is the
24:41thing we most commonly are
24:42ruling in or out. And
24:43And the lens I wanna
24:44give you here is that
24:45if you have an athlete
24:46with HCM
24:47walking into your office and
24:48instead of as compared to
24:49a sedentary HCM patient, their
24:51hearts are gonna look sort
24:53of less less bad. They're,
24:54in general, gonna have less
24:55hypertrophy,
24:56bigger LV cavities, better diastolic
24:58function, better fitness by virtue
25:00of being athletes.
25:02And so then if you
25:03do the right comparison instead
25:04of comparing sedentary HCM patients
25:07to athlete's heart, if you
25:08do the right comparison, they're
25:09both still athletic and active,
25:12and you compare people with
25:13known disease versus people that
25:14we know don't have disease.
25:16You know, in any individual
25:17parameter, this is an echo
25:18based study, but you could
25:19say the same thing for
25:20MRI. Like, wall thickness or
25:21cavity size that we used
25:23to try to use to
25:24disambiguate
25:25just will be quite imperfect
25:26when you do the right
25:27comparison of athlete to athlete.
25:29The the the visual is
25:31like, there's plenty of things
25:32like diastolic function and cavity
25:34size, which have zero overlap
25:35between healthy athletes and sedentary
25:37HTM. But when you look
25:38at athletes with HGM and
25:40healthy athletes, they overlap quite
25:41a bit more. So you
25:42can't use them as sort
25:43of lines in the sand.
25:44When I came on to
25:46staff and was on my
25:47k, I sort of thought
25:48to myself, we should be
25:49better able to tell. Is
25:50this a healthy heart muscle
25:51or an unhealthy one? Isn't
25:52there a way we could
25:53sort of just see it
25:54without even if cavity size
25:55and the diastolic function were
25:58were similar?
25:59I had had some collaborations
26:00with the Brigham Pet Lab
26:02dating back to my fellowship,
26:03and we endeavor to get
26:05at, whether metabolism of the
26:06heart muscle could tell us
26:07the answer in these situations.
26:09This was based upon others'
26:11work that shows if you
26:12have hypertrophy from a whole
26:13panoply of, or or cardiomyopathy,
26:17that the efficiency of your
26:18heart muscle doing work, meaning
26:20how much
26:21oxygen it burns to do
26:23a given amount of work
26:24is impaired, this metabolic efficiency.
26:26This energy wasting state is
26:28actually super important as we
26:29think about drugs that we
26:30can use to help, help
26:31cardiomyopathy
26:32as well. I was looking
26:33at it as can we
26:34tell the difference between a
26:35healthy and an unhealthy thick
26:36and tart muscle in athletes,
26:37so my narrow sports cardiology
26:39lens.
26:40So that's it's it suggests
26:41that in pathologic states, this
26:43is always impaired.
26:44We then, as a pilot
26:45study, just looked in athletes.
26:47If you look at them,
26:48get some LVH over a
26:49training cycle, does the metabolic
26:51efficiency get worse, get better,
26:53stay the same? And we
26:54uniquely showed that this form
26:56of hypertrophy,
26:57the efficiency just stays the
26:58same and is similar to
26:59controls. So it's already unique
27:01from pathologic hypertrophy there.
27:04And then we did a
27:04fancy study where we looked
27:06at these were known known
27:07entities. We knew they had
27:08HCM, but it was really
27:09mild, and they were highly
27:10active still. These were trained
27:12athletes where they had a
27:13little bit of LVH, but
27:14based upon all metrics, we
27:15were very certain it was
27:16healthy and not not HCM.
27:18And then we did the
27:19same sort of metabolic pets
27:20at rest, but then also
27:22did a very complicated way
27:23of doing exercise pet. Three
27:25ring circus is the best
27:27description of of that and
27:28look to see both at
27:29rest and and then with
27:31exercise, what did the efficiency
27:32of the heart muscle look
27:33like? We got them to
27:35do similar exercise workloads, which
27:36was difficult because they didn't
27:38have exactly the same fitness.
27:39And then we saw the
27:40metabolic efficiency at rest was
27:42not quite not very different
27:43between these mild HCM and
27:45athletes with mild LVH,
27:47but did differentiate with exercise.
27:49Disappointingly, it it's not a
27:50test that we can use
27:51clinically. As you can see,
27:52there's a lot of overlap.
27:53So that was,
27:54disappointing. We hope these might
27:55spread out a little bit
27:56more than they did. But
27:57I do think it still
27:58informs, like, you know, when
27:59we have HCM and we
28:00have exercise,
28:02symptoms or problems that this
28:03could relate to the efficiency
28:05of metabolism during exercise and
28:07might prove helpful even if
28:08not in sports cardiology to
28:10others who think about how
28:11to help HCM patients feel
28:12better.
28:15And so as we think
28:16about wrapping up this section,
28:17when we think about the
28:18athlete's heart, there's really no
28:19one athlete's heart. We see
28:20impact of sex, body size,
28:22sport type,
28:24and there won't ever be
28:25like a if it if
28:26the cavity is above x
28:27or the walls are, you
28:29know, above x that we're
28:30ever certain in absence of
28:32walls that are obviously overtly
28:33very, very thick.
28:35So we're in this gray
28:36zone, and we're not certain.
28:37Of course, you use the
28:38non imaging features. I skipped
28:39over this, like the ECG
28:40and the exercise test.
28:42You're looking at all the
28:43features of structure and function
28:45both on echo, and I
28:46do do a lot of,
28:47ask for a lot of
28:48help from my MRI images.
28:49I don't read those out
28:50myself.
28:50And the take home I'd
28:51have you take is that
28:52when something is overtly abnormal,
28:54like walls of,
28:55really even anything above twelve
28:57or anything even into twelve
28:58or thirteen millimeters
29:00is really not seen in
29:01female athletes. Right? And then
29:02in males, if you're seeing
29:03walls of fourteen, fifteen, sixteen,
29:05that's never gonna be normal.
29:06But if you're in this
29:07range where the walls are
29:08not that crazy thick or
29:09the cavity is not that
29:10crazy dilated, The function's right
29:12borderline.
29:15The,
29:16in general, normal features do
29:18not necessarily reassure. And I'll
29:19tell an anecdote which I
29:20was once referred to a
29:21patient for question athlete's heart
29:22versus HCM,
29:24and his walls had thickened
29:25up quite a bit from
29:25the prior echo, and he
29:26had a septum of thirty
29:27three millimeters. Right? So this
29:29is HCM. But his e
29:30primes,
29:31were still negative fifteen, which
29:33I don't even know how
29:33that happens. I mean, this
29:34is I saw a bunch
29:35of it still completely normal.
29:37So,
29:38don't be reassured if you
29:39see normal features. In that
29:40case, it was not in
29:41the gray zone. And then
29:42what motivated this was this
29:43idea that if we labeled
29:44it as cardiomyopathy
29:46that we were putting an
29:47athlete into the risky position
29:49of possibly not being able
29:50to continue in the sport
29:51that they love. Right? So
29:52when I was on this
29:54path of research,
29:56the the motivating factor was
29:57this is what the guidelines
29:58said, that if we even
29:59said probable HCM, like, the
30:01t waves are all inverted
30:02and the walls are a
30:02little thick, it's probably HCM,
30:04right, even if it doesn't
30:05meet HCM criteria.
30:06And then, of course, if
30:07it was unequivocal HCM, this
30:09was what was codified in
30:10guidelines.
30:12Peep people like Rachel and
30:13really Rachel, you were a
30:14formative person pushed this forward
30:16and really questioned, is this
30:17the way we should be
30:17managing all cardiomyopathy patients such
30:19that our updated guidelines in
30:21two thousand twenty five use
30:22shared decision making, understanding
30:24that that overt restriction of
30:26all individuals with cardiomyopathy
30:27in the face of really
30:28uncertain risk. We don't actually
30:30know if you take a
30:31athlete out of sport, does
30:32that improve their outcomes or
30:33their risk. Right? In the
30:35old days, with uncertain uncertainty,
30:37we were restrictive. In the
30:38in the new era with
30:39uncertainty, we use shared decision
30:41making as we do a
30:42lot across a lot of
30:43cardiovascular medicine.
30:45And so,
30:46this actually, I think, has
30:47taken the heat off of
30:48these cases a little bit
30:49for me personally
30:50because,
30:51you know, you're putting them
30:53into the maybe abnormal gray
30:54zone or the abnormal,
30:56was a big distinction back
30:58in the day because it
30:59really which bin you put
31:01them into really defines a
31:02black and white sport or
31:03no sport.
31:05But now now we can
31:06be more flexible in our
31:08thinking,
31:09and in our our counseling
31:10is that, of course, risk
31:12exists on a spectrum, not
31:13as a you're in one
31:14bin or the other. I
31:15do think we can define
31:16better tools,
31:18including I don't do a
31:19lot of research in AI,
31:20but combining all the things
31:21we measure and trying to
31:22figure out is there a
31:23way that we can sum
31:24them all up and figure
31:25out is this a healthy
31:26heart or the beginnings of
31:27a pathologic state.
31:29We always follow these athletes
31:30athletes longitudinally, the Harvard ones
31:32that start out in a
31:32gray zone. I have a
31:33spreadsheet, and they have them
31:34come back every year because,
31:36especially in your teens and
31:37twenties, you, you can see
31:39a phenotype in transition. And
31:40then like I said, the
31:41formative,
31:43evolution into shared decision making
31:44means that many of these
31:45athletes, even if we diagnose
31:47a cardiomyopathy,
31:48remain in sport.
31:51Alright. Halfway through. So that's
31:52perfect. We're gonna shift our
31:53lens,
31:54to the master's athlete. And,
31:57really because that distribution of
31:59causes of scary sudden,
32:01sudden events during sport shows
32:02us that most of these
32:03are due to ASCVD,
32:05we will focus on that
32:06diagnosis.
32:07If you think of the
32:08way we started with young
32:09athletes, we talked about screening.
32:11So the natural question you
32:12might have is, is there
32:12a way to screen masters
32:13athletes for the risk producing
32:15condition, really the main condition
32:16they have that produces risk
32:18coronary disease? And I'd say
32:20the short answer is is
32:21no. If you're thinking about
32:22testing,
32:24a a a twelve lead
32:25ECG is not gonna diagnose
32:27your coronary artery disease unless
32:28you've already had an MI.
32:31There's a great group up
32:32in Canada that's tried to
32:33address like, if you take
32:34a layered approach, it's not
32:35a one size fits all.
32:36What they use as you
32:37can tell, this study is
32:38a little bit old and
32:39that they used framing ham
32:40risk as well as the
32:41history and physical and sort
32:42of decided, okay. You're fine.
32:44You don't need testing versus
32:45we should do some testing
32:46consisting first of an exercise
32:48stress test.
32:49And then, you know, follow
32:50down the garden path
32:51and identify, you know, what
32:53what do you find.
32:55It shouldn't be surprising. These
32:56were, on average, far older
32:57than thirty five years old,
32:58more like in their fifties
32:59and sixties. You know, you'll
33:01find things. You'll not all
33:02atherosclerotic disease, but in eleven
33:04percent, you'll find something, PVCs
33:06or,
33:06some atherosclerosis.
33:08But we don't have we
33:09don't recommend people go down
33:12this path in asymptomatic patients,
33:14because we don't have any
33:15data about whether this changes
33:16our outcomes. And I think
33:17there's a lot of downsides
33:18to that path.
33:19So I'm not enthusiastic
33:21about, like, an algorithmic, let's
33:22exercise test certain athletes versus
33:24others in the masters population,
33:26but you cannot meet someone
33:27who's more enthusiastic and scrutinous
33:30of
33:31ASCVD risk factors and masters
33:33athletes. And they're a really
33:34unique population because they they
33:36to the extent they're presenting
33:37in cardiology clinic, they are
33:38highly active. They oftentimes are
33:40paying really good attention to
33:41all their other lifestyle factors.
33:43And it it is,
33:44I
33:47give them the bad news
33:48that something doesn't look quite
33:49right, despite all their good
33:51lifestyle habits. Because high physical
33:53activity levels and fitness are
33:55not universally protective, and you
33:56all know this. We have
33:57you can certainly still have
33:58a very high LDL, lipoprotein
34:00a, newer, maybe not new
34:02kid on the block anymore.
34:03We're supposed to check-in on
34:04everyone.
34:05So all these things are
34:06driven by
34:07features that are outside of
34:09the control of even a
34:10very highly active person with
34:11a great lifestyle.
34:12And, importantly, like, the usual
34:14way we would treat blood
34:14pressure and lipids are not
34:16off the table just because
34:16someone is an athlete, though
34:18sometimes you might deal with
34:19a lot more questions and
34:20nuances about side effects and
34:22such.
34:24So that's just the traditional
34:25risk factors. And then I
34:26think a lot about what
34:27could actually
34:28uniquely provoke risk in a
34:30master's athlete population.
34:32Sometimes people turn to marathons
34:33because they smoked through their
34:34whole twenties and sort of
34:36they've accrued some risk and
34:37probably some plaque earlier on
34:38in life, and then they're
34:39adding marathon marathoning on top
34:41of it in later life.
34:43Or they have this sense,
34:44I have a terrible family
34:45history, so I'm gonna take
34:46this highly active lifestyle because
34:47of that family history.
34:50Dietary history, just because you're
34:51incinerating many thousands of calories
34:52per day. There there's sort
34:54of two populations. There's, like,
34:55the green juice, very, very
34:56healthy plant whole food plant
34:58based. But then there are
34:59masters athletes who definitely the
35:00food pyramid looks like this.
35:02And they are they're trimmed,
35:03so you won't necessarily guess
35:04at it without a history.
35:06You're using exercise oftentimes to
35:08manage psychological stress, but there's
35:10great studies out of MGH
35:11showing how activated your amygdala
35:13is, helps predict how how
35:14inflamed your arteries are. Right?
35:15So,
35:17is that stress still there
35:18and a driver of risk?
35:19And then some of my
35:20research has started to look
35:21at, inflammation.
35:23We know that anyone who's
35:24active knows the day after
35:25a hard effort or sometimes
35:26two days after you're sore,
35:28you're tired, you can't walk
35:29down the stairs. If you
35:30did an HSCRP in that
35:31moment, it would be elevated.
35:33And is there a way
35:33that cumulative exercise without enough
35:35time for recovery could actually
35:37serve as a pro inflammatory
35:38risk factor? Of course, these
35:40individuals who have lower visceral
35:41fat, and if they're modestly
35:42active people overall have less
35:44inflammation, but is there an
35:45extreme dose of exercise that
35:46can go back the other
35:47way?
35:48So those are the things
35:49I think about in clinic.
35:50And I think about it,
35:51both because the atherosclerosis is
35:53the most common cause of
35:54events in masters athletes, but
35:56also because there's this concept,
35:57and I call it the
35:58CAC paradox that we see
36:00in large cohorts of, research
36:02cohorts of masters athletes, particularly
36:04male masters athletes.
36:06This started at this point
36:07fifteen or maybe closer to
36:08twenty years ago when calcium
36:10scoring came out.
36:11Europeans demonstrated that male masters
36:13athletes as compared
36:15to well matched,
36:17modestly active or sedentary controls
36:19had more CAC.
36:21Initially, I think the the
36:22our field
36:24reacted to this in such
36:25a way, like, how could
36:26exercise possibly be doing anything
36:28bad? The matching was wrong.
36:30The cohorts aren't matched. Maybe
36:31it's not plaque. Maybe it's
36:32just calcification of the vessel
36:33wall. There was sort of
36:34like a anti reaction
36:37to that. But, subsequently, over
36:38the past fifteen years, we've
36:39shown it's not just more
36:41calcium, but it's more plaque.
36:42And it's actually not just
36:44calcified plaque.
36:46This is a study that
36:46looked at controls,
36:48who are still active. So
36:49these aren't sedentary controls. People
36:51who started exercise later in
36:52life and people who have
36:53been highly active, men. These
36:55are all men,
36:56lifelong
36:57and showed they have more
36:59plaques of all sorts and
37:00that the plaque distribution actually
37:02really it's calcified, noncalcified, and
37:04mixed plaques.
37:05Because this cohort is all
37:06had this is not an
37:07inactive control. You can see
37:09the the vast majority of
37:10plaques are still calcified.
37:12Sex based differences are interesting
37:14here in that this has
37:15not been demonstrated in female
37:16masters athletes. There's they they
37:18have less plaques and less
37:19atherosclerosis
37:20than matched control groups through
37:22on age sixty five when
37:23they catch up. And one
37:24could imagine if we still
37:25had seventy or eighty year
37:26old women doing marathons that
37:28maybe the same question is
37:29at play, but just that,
37:31we have some protection through
37:32menopause for atherosclerosis for all
37:34women that creates a different
37:35look to the data.
37:37And then recently enough in
37:39the last year or two,
37:39you can show that short
37:40term progression of, like, something
37:42like total plaque volume is
37:43actually associated with the exercise
37:45volume and intensity over a
37:46short period of time.
37:48So,
37:49this this to me I
37:51I'm not saying that high
37:52doses of physical activity are
37:53a risk factor for atherosclerosis,
37:54but it certainly gives us
37:56a lens through which we
37:57need to sort of understand
37:58better what's driving this. And
37:59these are all these are
38:00matched for everything you care
38:02about. Lipoid, lipids, blood pressure,
38:04family history. And so there's
38:05nothing else that at least
38:07is straightforward that
38:08that we know about that
38:09seems like it's driving this
38:11other than the exercise itself
38:13and this exercise in excess,
38:15perhaps.
38:17To get at this. And
38:17I have it's not the
38:18grant I just got, though.
38:19I wish it was. It's
38:20the grant that'll be reviewed
38:21this month. As a pilot
38:22study,
38:23we'd,
38:24this is one of the
38:25favorite studies I've done even
38:26though it was an end
38:27of eleven.
38:28I am one of the
38:29co medical directors for the
38:30marathon.
38:31We recruited eleven. It was
38:32really twelve, but we had
38:33one one lost to follow-up,
38:36because she actually just run
38:37her marathon with, like, a
38:38eighty percent proximal LED that
38:39we found on the first
38:40CT scan. But, But, so
38:42she didn't undergo the follow-up.
38:43Sorry for another day. We
38:45scan them, and you can
38:46do this using you can
38:47do these measurements using just
38:48regular coronary CTN geography. It
38:50doesn't it's not a special
38:51protocol or a special scanner,
38:53but it's special software,
38:55where you can look at
38:56the inflammation around the fat
38:57that surrounds the coronary. It's
38:59called the phi or the
39:00fat attenuation index.
39:02We did this both immediately
39:03post the marathon when they're
39:05all still sore and inflamed
39:06and have just done a
39:07whole training block, and then
39:08we did it, three months
39:09later, and we asked for
39:10people that weren't using their
39:11marathon to train for their
39:12Ironman. And I say that
39:13tongue in cheek, but that
39:14is something people do.
39:17And so we asked for
39:18people that we were trying
39:19to pick people who were
39:20gonna naturally detrain, and, indeed,
39:22their mileage,
39:23halved over follow-up. Not with
39:24us doing anything. They just
39:26stopped running as much because
39:27many people in Boston for
39:28Boston, it tends to be
39:30people's a race, so they
39:31they train up for it,
39:31and then they rest over
39:33the summer afterwards.
39:34So alongside reduced training volume
39:36by their mileage about half,
39:39we saw that this fat
39:40attenuation with a higher score
39:41being worse directionally came down
39:43in everyone who detrained. This
39:45was just supposed to be
39:46something that showed directional consistency
39:48as pilot data for a
39:48grant, but, actually, it was
39:49statistically significant because the reductions,
39:52while small in some instances,
39:53were very consistent.
39:55The only two people whose
39:56inflammation did not go down
39:58were the two people who
39:58fibbed and basically didn't change
40:00their running volume and continued
40:01to hammer all summer long.
40:03And you can look at
40:04this either as an absolute
40:05score or a percentile,
40:07where the those those numbers
40:09look more more market. So
40:11we're gonna look at this.
40:12We're hopefully on the opportunity
40:13to look at this with
40:14a bigger grant that sort
40:15of understands better is this
40:17exercise associated, and this is
40:18very specifically coronary inflammation.
40:21Is this the driver of
40:23the excess atherosclerosis
40:24we see in master's athletes?
40:25It it's great because this
40:27is a big sort of
40:27space in cardiovascular medicine overall.
40:30Statins are statins have been
40:32shown to improve phybe scores,
40:33and then we have things
40:34like colchicine and other therapies
40:36on deck with, you know,
40:37unclear, at least in my
40:38view, who to use those
40:39in.
40:40That could also help to
40:41ameliorate any excess inflammation that
40:43can be driving risk in
40:44this population.
40:47Alright.
40:49So those I think, hopefully,
40:51we got through the the
40:51important conditions we think about
40:53in young athletes and masters
40:54athletes, the panoply of conditions
40:56in young athletes, the focus
40:58on coronary disease in masters
40:59athletes,
41:00and then got along the
41:01way to dip into some
41:02of the research I've done.
41:03The research I do is
41:04always tends to be motivated
41:05by the things that bother
41:07me in clinic,
41:08as you can see.
41:10But then even if we
41:11were perfect and we could
41:12identify all athletes at risk
41:14at screening or manage all
41:15their risk factors from age,
41:16whatever, twenty five, thirty onward,
41:18you know, there are still
41:19gonna be events. And,
41:21that's where the importance of
41:23emergency action planning comes in.
41:25And I think if you're
41:26thinking about wanting to prevent
41:27sudden cardiac death,
41:28and, really, this is you
41:29could use this lens for
41:30all of cardiovascular
41:31medicine, not just athletes.
41:34It's how do you make
41:35sure communities,
41:37given
41:38populations, are protected by good
41:39emergency action planning if an
41:41event does occur?
41:44And, this is something I
41:45think we can all take
41:46out into our communities as
41:47cardiologists. We should we could
41:48all be invested in emergency
41:50action planning and reduction of
41:51these events in our communities.
41:53In highly resourced settings, this
41:55is like a,
41:57extremely rehearsed
41:59everyone has specific roles. You
42:01know, the World Cup's about
42:02to come to Boston. You
42:04know, FIFA's put out their
42:05publication about, like, where does
42:06each person stand if someone's
42:08having a cardiac arrest? Where
42:09does the defibrillator go?
42:11I'd say the the biggest
42:12limitation when we're thinking about
42:14emergency action planning in the
42:15community
42:16is recognizing a sudden cardiac
42:18arrest has occurred.
42:20If an athlete goes down,
42:21suddenly,
42:22there can be a lag
42:23time, and it can be
42:24quite lengthy before someone realize
42:25it is it is sudden
42:26cardiac arrest and hands are
42:28put on the chest and
42:28the emergency action plan is
42:30activated.
42:31So that's one space we
42:32need to narrow down.
42:33In in in in sport
42:35settings,
42:36coordinated roles for trained personnel,
42:37if you take this down
42:38to, like, more youth sports,
42:40you know, are all coaches
42:41and everyone trained in CPR,
42:42hands only CPR? Where are
42:44the AEDs? Because
42:45Because we know that early,
42:46immediate CPR and really early
42:48defibrillation are the ways that
42:49we turn a sudden cardiac
42:50arrest into a life instead
42:52of death.
42:54And, this is all gonna
42:55be customized depending on the
42:56environment you're in. At a
42:58at a soccer field,
43:00you can have a diagram
43:01that looks like this. I'm
43:02one of the co
43:03medical directors for the marathon
43:04recovering twenty six point two
43:06miles,
43:07and so the the it
43:08looks quite different.
43:10And the interesting thing, and
43:11I I think this could
43:12just be by chance, is
43:13that we actually have twenty
43:14six course medical stations. We'll
43:16have twenty seven next year,
43:17but that's it's it sounds
43:18like there would be one
43:19per mile, but that's actually
43:20not the way we plan
43:21it. Because if you look,
43:24at marathons and half marathons,
43:25the events
43:26cluster at the finish line
43:28and specifically over the last
43:29quarter of the race. And
43:30so for our marathon medical
43:32planning,
43:33this is the finish line
43:34of the Boston Harbor over
43:35here.
43:36The course medical stations are
43:37really quite spread out, and
43:39then really start to cluster
43:41such that we have three
43:43or four in the last
43:44mile, so that we have
43:45people available to respond as
43:47well as proceed out teams
43:48from every, med medical tent
43:49along the way where they
43:50can go attend to someone
43:51who's, had an event in
43:52the middle.
43:54And so, that's how we
43:56do it. Very different than
43:57how FIFA is doing it.
43:58Very different than how you
43:58do it in any youth
43:59sports setting depending on what
44:00the resources are available.
44:03These slides, I think I
44:04handed in so it could
44:04be handed back out to
44:05all of you guys. I
44:06think there's two videos I
44:08like to point out that
44:08are just available on, various
44:11platforms.
44:11The first is one made
44:12by our colleague,
44:14John Dresner, and it's quite
44:15upsetting to watch, but these
44:16are sudden cardiac arrests as
44:17they're occurring.
44:19And I I don't mean
44:19to be glib about it,
44:20but I think every youth
44:21sport coach should watch this
44:22video. Right? Because I don't
44:24think the biggest limitation is
44:25recognizing the athlete that's gone
44:26down is is in a
44:28cardiac arrest. So,
44:30these are upsetting events,
44:32to watch because these are
44:32all people having an arrest.
44:34And but it gives you
44:35the good eyeball of what
44:36that actually looks like, and
44:37I don't think the lay
44:38public gets that.
44:40And then as part of
44:41the BAA, we actually run
44:43so our idea is like,
44:44okay. We have twenty six
44:45miles.
44:46We can't have a medical
44:47station every ten feet. And
44:49so how do we further
44:50protect our athletes, like, in
44:51a bubble if an event
44:52occurs? So we actually,
44:54we train athletes,
44:56and their whoever else is
44:57with them at our expo
44:59where they come to pick
44:59up their bib. We have
45:00a station where we train
45:02in hands only CPR.
45:03These are, two nurses and
45:05nurse practitioners that I work
45:06with at MGH, and they
45:07run the station.
45:08And, this year, we give
45:10out little bracelets, and we
45:11had three thousand of them,
45:12and they ran out. So
45:13we handed out we trained
45:14more than three thousand people,
45:16in CPR, and and I
45:17I've spent quite a bit
45:18of time with them amongst
45:19other duties on the race
45:21weekend. And, I mean, this
45:22is from,
45:24six, eight year old kids
45:25all the way up to
45:26older individuals. There's really very
45:27few people that can't perform
45:28hands only CPR, and we
45:30get through the if there's
45:31an emergency, call nine one
45:32one,
45:33steps as well. And then
45:34we have a video that
45:35we circulate to all runners.
45:37And you have to be
45:37careful. You can't give this
45:38out right before race day
45:39because this is gonna make
45:39everyone paranoid. So further further
45:42away from the race of
45:42the day before,
45:44teaching them through video about
45:45hands only CPR and what
45:47to do if they see
45:47an emergency.
45:49And every year at the
45:50booth, we have people come
45:51back saying we use this,
45:53and we we learned and
45:54then used it,
45:56in the community.
45:58And so,
45:59not actually at any of
46:00our races yet, so we've
46:01not had the return, whatever,
46:03if you wanna think of
46:04it on investment. But I
46:05like to think we're creating
46:06a return for, you know,
46:07broader communities, including race medicine,
46:09by doing this.
46:11Alright.
46:12To leave a few minutes
46:13for questions, I guess I'll
46:14I'll wrap up, which is,
46:16I'll cover what we we
46:17talked about today and then
46:18start thinking about your questions.
46:21We started by
46:23like, we really need to
46:24anchor for our broader community
46:25on exercises, medicine, and getting
46:27our patients more active, but
46:28we also discussed this paradox
46:30where exercise can serve as
46:32a trigger. And in particular,
46:33if you're thinking of events
46:34that are more enriched by
46:36exercise,
46:37these
46:38these diagnoses, there's no better
46:39way to say it. They're
46:40what sports cardiologists sees when
46:41they close their eyes thinking
46:42of a differential because those
46:44are the things that will
46:44get your athletes into trouble
46:46even if they are rare
46:47diagnoses, things like, coronary anomalies,
46:49for example.
46:51We talked about the in
46:52younger athletes,
46:54that these structural causes, particularly
46:57cardiomyopathy,
46:57are at times hard to
46:58distinguish from a big heart
47:00that is benign and physiologic.
47:02And we talked about
47:04integrated assessment and possible new
47:06tools and the research in
47:07that space. There's definitely more
47:09research that could be done.
47:11And then
47:12in older athletes, we talked
47:14about,
47:15I think one thing that
47:16I'm really dogmatic about is
47:17that I think if you
47:18come into clinic wearing a
47:19race T shirt, you automatically
47:21get classified as low ASCVD
47:23risk.
47:24And, like, I'm wearing a
47:24race T shirt that becomes
47:25a risk factor for heart
47:26disease because you're gonna have
47:28your blood pressure and your
47:29lipids under managed. Right? We
47:30know the inertia that takes
47:31over the blood pressure is
47:32a little high. The LDL
47:33is a little off, and
47:34we don't treat it.
47:35But, really, athletic status doesn't
47:37preclude the treatment of blood
47:38pressure and lipids. And this
47:39emerging data where we see
47:40more atherosclerosis
47:41and those really people who
47:43are hammering many marathons for
47:44many decades.
47:45Like, in in the end,
47:46I think there's a population
47:47we actually might start to
47:48think of as higher risk.
47:49Also, just by virtue of
47:50the fact these individuals are
47:51pushing their bodies to the
47:52degrees they are, there's really,
47:53in my view, no room
47:54for undermanaging their traditional risk.
47:56And then
47:57some, I think, hopefully, cool
47:59research should be done to
47:59understand why they have more
48:01plaque than we expect.
48:02And then no matter what
48:03risk will remain with sport,
48:05but sport is such an
48:06integral part of society and
48:07so many people's lives.
48:09That underscores the importance of
48:11emergency action planning, which is
48:13not a one size fits
48:14all. Depends on what resources
48:15you have, and that's something
48:17we can all take back
48:18to our communities.
48:20And right in time for
48:21some questions.
48:39Thank you for that wonderful
48:40presentation. It's really enlightening. I
48:42just have one comment and
48:43one question. The first is
48:44a comment,
48:46and I just wanted to
48:47point out to the fellows
48:48that based
48:49on doctor Waspi's definition, you're
48:51all approaching masters athlete.
48:54Yeah. I used to give
48:54this talk of when I
48:55was less than thirty five,
48:56but now I'm greater than
48:57thirty five. So,
48:58you do start to say
48:59you can say you win
49:00races, actually, you know, because
49:01you'll start to have age
49:02groups and stuff. So you
49:03can go back to winning
49:04as you get above that
49:05age. Something to look forward
49:07to. Mhmm.
49:09As as you talk about
49:10one of the things you
49:11didn't talk about was the
49:12issue of screening for coronary
49:14anomalies. And I was wondering,
49:16you know, now and you
49:17did touch on pet a
49:18little bit as you've as
49:19what what's been your approach
49:21now into the sort of
49:22the modern era with with
49:24coronary CTA and flow dynamics
49:26and and new perfusion tracers?
49:28Are you using any of
49:29those things in your clinical
49:31practice?
49:32Screening is so interesting because
49:33this we have to just
49:34acknowledge
49:35that this is a diagnosis
49:36we're missing at screening.
49:38And that,
49:39I don't know if that
49:40keeps you awake at night,
49:41Rachel. Because, you know, there's
49:42nice older data. I didn't
49:43show it.
49:44Italian data suggesting that the
49:46first manifestation of a coronary
49:47anomaly can be the sudden
49:48cardiac arrest. Right?
49:50So it just feels uncomfortable.
49:51And, of course,
49:52if we CT'd every incoming
49:53d one athlete, we could
49:55find them, but that's not
49:56practical and wouldn't be an
49:57approach I would recommend.
49:59Even echo based screening, one
50:00thing to know is, screening,
50:02just like emergency action planning,
50:03needs to be customized to
50:04the resources available. That's an
50:06important point to make. And
50:07there are some, certainly at
50:09the professional sports level and
50:11then even some more highly
50:12resourced d one sort of
50:13college sports level where they
50:15do include an echo, not
50:16just for abnormal ECGs, but
50:18for every athlete. Right?
50:20And in that instance, you
50:21know, the question is when
50:22we're doing echo
50:24in eighteen year olds, are
50:25are we gonna be able
50:26to effectively visualize coronaries and
50:29rule in or rule out
50:30coronary anomalies? If you look
50:31at published data, the suggestion
50:32might be yes from UVA.
50:35But I don't know. In
50:35a practical, now eleven years
50:37on staff and an Ecolab
50:38having seen some echo based
50:40misses,
50:42I I don't think that
50:44adding an echo to look
50:44for coronary origins
50:46is is gonna be satisfactory,
50:48right, with regards to, like,
50:50finding that diagnosis. So we're
50:51left with the old fashioned,
50:52which is that if someone
50:53has symptoms,
50:54that's when they're gonna present.
50:56Right? And then, I'm a
50:58humble person. Actually, I was
50:59just telling Rachel about this
51:00case. I found some coronary
51:01anomalies over the years, because
51:03they're in an infrequent diagnosis,
51:04and I'm not an adult
51:05congenital or congenital heart disease
51:07expert. I think that's where
51:08being in an academic center
51:09where there are experts I
51:11used to joke there's an
51:12expert in the left and
51:13the right
51:14hand and until I broke
51:15my, right pinky, and they're
51:16just hand surgeons as it
51:17turns out.
51:18But there are, in a
51:20functional sense, so many experts
51:21and so many things so
51:22that our our approach is
51:23to present it to the
51:24congenital group meeting. Surgeons there,
51:26the images are there, or
51:27the congenital disease experts are
51:29there. And and most often
51:31in in borderline cases, unless
51:32it's open and shut, do
51:33so do that for the
51:34athlete at more than one
51:35center if there's ambiguity about
51:37what to do.
51:38And then, I can tell
51:39you one recent update. I'm
51:40I'm always gonna start with
51:41a maximal effort exercise test
51:43on the, apparatus that the
51:44athlete is most accustomed to.
51:46That is only doable with
51:48CPET in my institution because
51:49we don't have, like, a
51:50bike or a really good
51:51treadmill
51:52or a rowing ergometer
51:54in the other exercise labs.
51:55Right?
51:56But,
51:58if you're then wanting to
51:59add imaging to get more
52:00information in a case that's
52:01not open and shut, we
52:02have just started to do
52:04exercise pets,
52:05just perfusion pets,
52:08because of a new tracer
52:09that has a longer half
52:10life so is less fussy.
52:12And,
52:13that but that's extremely new
52:14and I don't think, like,
52:15even published on, but that's
52:16now our surgeon doesn't wanna
52:18see the patient until you've
52:19done the exercise. But, but
52:20other centers use dobutamine
52:22stress CMR, which we don't
52:23have at MGH. So this
52:24idea that you can use
52:25imaging and some kind of
52:27provocation,
52:28vasodilation
52:29is useless, so it has
52:30to be dobutamine or exercise
52:31to try to get at
52:32is there ischemia or not,
52:34is helpful. But, Paul Thompson,
52:35who's the grandfather of sports
52:36cardiology, has a saying that
52:38don't trust a normal exercise
52:39test than a coronary anomaly
52:40patient. I mean, sometimes it
52:42has to come down to
52:42the idea that this looks
52:44like high risk anatomy and
52:45there is a symptom or
52:46not.
52:47I don't I don't know
52:48that there's always a way
52:48you can image your way
52:50into being convinced that fixing
52:51it is the right call.
52:54Thank you for your talk.
52:56So,
52:57my question is regarding the
52:59masters athletes.
53:00Do you see something similar
53:02or analogous
53:03to the CAC paradox in
53:04other vascular beds?
53:06Oh, no. I don't know.
53:08I don't think we do.
53:09Certainly, I don't know anyone
53:10that's done, like, panvascular
53:12imaging in that setting.
53:13I will say there's other
53:15things that are paradoxically
53:17so the answer is I
53:18don't know, and I don't
53:19think anyone's looked.
53:21There are other things we
53:23see enriched in masters athletes.
53:24I just didn't hit on
53:25them today. The EPs will
53:27know we see a lot
53:27more atrial fibrillation. That is
53:29also sex specific. It's really
53:31just in the male masters
53:32athletes. So if you image,
53:33you can see
53:34it's some probably some combination
53:35of atrial enlargement, atrial fibrosis,
53:37and higher vagal tone.
53:39And then on MRI imaging,
53:40you can see that they
53:41have more insertion point LGE,
53:43so, like, more fibrosis.
53:45And then, you know, is
53:46that just sort of, like,
53:47the hinge got pulled on
53:48one too many times, and
53:49you formed a little fibrosis
53:50there? I collectively call all
53:51of these master athlete maladies,
53:53and they're not they're maladies,
53:54only in the sports cardiology
53:56lens.
53:57So those are the things
53:57we can see more of
53:58in a master's athlete population.
54:00We sometimes see more VPB
54:02PBCs and stuff like that
54:03when they have fibrosis, and
54:04ongoing research is trying to
54:06help us define who we
54:07need to worry about for
54:08all of those bins.
54:10Good question, though. So, Megan,
54:12what do you say to
54:13the, masters athlete who wants
54:14and comes in with their
54:15CAC score in hand? Yeah.
54:17Where Where do you go
54:18from there? Yeah. I took
54:19those slides out, but it's
54:20such a great question. Because
54:21I think at the beginning,
54:23there was this, like, we
54:24don't know what to make
54:24of this number because it's
54:25high
54:26and it's higher than we
54:28think it should be. So
54:29maybe we shouldn't use calcium
54:30scoring in masters athletes because
54:31we don't understand this phenomenon.
54:33But there's great work out
54:34of the career center,
54:36longitudinal data, and it it's
54:38combinatorial work. There's two papers
54:39I could send out where
54:40they look at CAC scores
54:41by cardiorespiratory
54:42fitness and self reported PA,
54:44and it's two separate papers.
54:45And,
54:46you can look and and
54:48the easier one to remember
54:49is the cardiorespiratory fitness is
54:50that in in fitter individuals,
54:52they have less CBD. So
54:54regardless of their CAT score,
54:55they have less onward heart
54:56disease if you follow them
54:57longitudinally,
54:59which totally makes sense. Right?
55:00Your exercise capacity is like
55:02a very potent prognostic indicator.
55:04But if you look within
55:06active or fit people, let's
55:08say, like, fifteen met exercise
55:09capacity or above, a calcium
55:11score still risk stratifies. So
55:13you're still three to four
55:14times more likely to have
55:15an event if you have
55:16a calcium score greater than
55:17four hundred versus zero.
55:19But,
55:20a calcium score of around
55:21four hundred in a highly
55:22fit person,
55:25predicts the similar amount of
55:26events as a calcium score
55:27of one hundred in an
55:29unfit person. And so if
55:31if your patient Googles, like,
55:32what is what is a
55:33calcium score of four hundred
55:35means, and it tells them
55:36they're at, you know, maybe
55:37almost in day CBD risk
55:39equivalent as high risk as
55:40someone who's ready heart heart
55:41attack. I use a thousand
55:42for them. That's incorrect for
55:44that highly active patient,
55:45because they're at overall lower
55:47risk if I could draw
55:47the graph. So they're at
55:48overall lower risk, but the
55:49calcium score is how they
55:50differentiate still matters. So you
55:52can still use calcium scoring
55:54to identify higher risk athletes,
55:55but the numbers get to
55:56be a little bonkers. Like,
55:58we're talking two, three thousand
56:00with no obstructive
56:02disease. Right?
56:03And so you just have
56:04to make sure you understand
56:05that quirky aspect of it
56:07that that that I think
56:08in the GenPop, if you
56:09saw those numbers, it would
56:10mean they have three vessel
56:11obstructive disease, and that's just
56:13not what we see when
56:14we look look at it
56:15in athletes. So it does
56:16identify since everyone I see
56:17who is is fit and
56:18active.
56:20Well, not not exclusively, but,
56:22since that's mostly what I
56:23see, my lens is that
56:25score still helps me identify
56:27within the bin of fit
56:28and active people who's at
56:29higher risk,
56:30and so I treat them.
56:32And, sometimes that's the the
56:34the quirky part is sometimes
56:35they don't really have egregious
56:37lipids or other things making
56:39me wonder what else about
56:40the exercise itself is just
56:41driven in the formation of
56:42their plaque.
56:45That was a wonderful talk.
56:47Thank you. It's one of
56:48those talks that every single
56:50person in the audience is
56:51thinking, okay. How many MET
56:53hours per minute
56:54do I do, and where
56:56do I Go back to
56:56that slide. Fit into those
56:58It's asked me to translate
56:59his exercise activity into that
57:01Yeah. Response curve. I was
57:02like, where am I on
57:03this curve? Yes. Yeah. We
57:05won't even talk about master's
57:07age groups and things. But,
57:09but
57:10the I have a couple
57:11questions. One is the the
57:13sex paradox of the accumulation
57:16over over time and and
57:18years.
57:19I'm wondering because there
57:21are really dramatic differences in
57:23the way gonadal hormones
57:25affect blood vessels in males
57:27and females. Yep. Estrogens are
57:30probably protective
57:31up to a point in
57:32females, and androgens are probably
57:34protective in males, but deleterious
57:36in females. And so I'm
57:38wondering what exercise training over
57:40years,
57:41how that correlates with changes
57:43in gonadal hormones, and if
57:45we can
57:46reflect back to what may
57:47be happening at the level
57:49of vascular pathology. Yeah. I
57:51think that's so
57:53whenever someone asks a question
57:54and it's the slide you
57:55cut, you know it's a
57:56good one because I think
57:57there's a there's a lot
57:58to be unfurled here.
58:00We know that exercise training
58:01when at high levels, there
58:02it makes entirely sense when
58:04you think of, like, evolution
58:05suppresses sex hormones. Right? It
58:07does so even if you
58:08still like, even if women
58:09are still getting their menstrual
58:11cycles and men aren't, like,
58:12like, fulminently hypo hypoandrogen.
58:15But then there's this extreme,
58:17and the term we prefer
58:18to use now, we I'm
58:19in sports medicine too, is
58:20low energy availability. We're not
58:22labeling these as, like, DSM
58:24eating disorders and stuff, but
58:25the concept that low energy
58:26availability
58:27or the the acronym that's
58:29used is RED, which is
58:30relative energy deficiency in sport,
58:32RED s.
58:33These are definitely associated in
58:35perturbations,
58:37and sex hormones, which do
58:38make sense. If you think
58:39you're in a low energy
58:40state, it's not a time
58:41to reproduce.
58:43But what are the onward
58:43health effects of that? There's
58:45definitely performance effects. Your bones
58:47are affected by that, right,
58:48and and performance affected by
58:49that. But there's nothing this
58:51is an open pasture. If
58:53anyone wants to run into
58:54it with me and study
58:55it, let's do it. There's
58:56really no information about what
58:59what the intersect between that
59:00and cardiovascular health is.
59:02We know that if people
59:03come in and sort of
59:04start fully starved states, actually,
59:05weird enough, their LDLs are
59:07high. Right? So that's even
59:08a simple thing, and and
59:09there's some small studies that
59:11show vascular stiffness is elevated.
59:12So I think that those
59:14states are probably not good
59:15for CVD risk factors as
59:17well.
59:22Maybe I'll ask the last,
59:23a quick question. You
59:25didn't, speak to and maybe
59:27get give you me your
59:28thoughts around
59:29strategies of,
59:31intentional deconditioning
59:33and to understand,
59:34you know, who do you
59:35do that and and in
59:36what situations would that still
59:38be, you know, part of
59:39the guidelines. Yeah. With research,
59:41it's nice to have, like,
59:42unintentional or whatever natural deconditioning.
59:45And I've done a lot
59:45of studies where,
59:47you're watching a a natural
59:48escalation and training load like
59:50that early exercise induced remodeling
59:52stuff we take,
59:53college freshmen
59:55who I'm not sure this
59:56would work these days, but
59:57back in those days, ten
59:58years ago, you know, they
59:59came in. They had high
60:00school coaches. They were training.
01:00:01Right? They were not athletes,
01:00:02but then they hit, like,
01:00:03the Harvard coaches.
01:00:05You know, in the first
01:00:06three months, they their training
01:00:07was up a lot. Right?
01:00:09So we're using those natural
01:00:10experiments of up, and then
01:00:11in the marathon experiment, just
01:00:13the natural down,
01:00:14to look at change over
01:00:16time because it's it's pretty
01:00:17hard to tell a population
01:00:19like that to do something
01:00:20different. Right? When we think
01:00:21about using deconditioning as a
01:00:23clinical tool, that was in
01:00:24an algorithm of sorts for
01:00:26figuring out is this athletic
01:00:27HT, like, athletic LVH versus
01:00:29HCM.
01:00:32And it makes natural sense.
01:00:33So if you have an
01:00:34athlete detrain and the LVH
01:00:35goes away, it probably is
01:00:36athletic and not HCM.
01:00:38But I have to say
01:00:39I'm not a big fan
01:00:39for two reasons. One is
01:00:40that's asking a lot of
01:00:41the athlete. Right? Instead in
01:00:42shared decision making, we can
01:00:43just say, we don't know
01:00:44if this is HTM. We're
01:00:45gonna follow you over time
01:00:46and do all the risk
01:00:47stratification.
01:00:48The other is that there's
01:00:49I think each of us
01:00:50has a case like this,
01:00:51and there are published case
01:00:52reports where
01:00:54you detrain and even things
01:00:56like t wave inversions improve
01:00:57and hypertrophy gets better,
01:00:59but then it becomes HTM,
01:01:01like, three or four years
01:01:02later. Speaking to this, like,
01:01:04interesting intersect because it clearly
01:01:06was in part exercise
01:01:08and whatever their genetic thing
01:01:09was, but not all of
01:01:10it. I have a,
01:01:12he's probably now masters. He
01:01:13maybe in his early thirties
01:01:15who has the most bizarre
01:01:15ECG you could ever see
01:01:17and a little bit of
01:01:17hypertrophy, but it's never turned
01:01:19into anything. And he tore
01:01:20his ACL. He just does,
01:01:21like, men's basketball leagues. He
01:01:22tore his ACL, and he
01:01:23was out for some period
01:01:24of time rehabbing that. And
01:01:25this if I had it
01:01:26on a slide, it'd just
01:01:27be like, this is the
01:01:28most wacky ECG ever. It
01:01:29almost completely normalized when he
01:01:31was detrained.
01:01:33There's no reason for that.
01:01:34It's very interesting it happened.
01:01:35It shows I don't know.
01:01:36What we understand about medicine
01:01:38is probably less than what
01:01:39we don't understand. So I
01:01:40don't tend to prescribe it
01:01:41as a tool in these
01:01:42gray zone cases, for those
01:01:43reasons, both because I'm worried
01:01:44I'll get tricked and provide
01:01:45false reassurance and because we
01:01:47can sort of default back
01:01:48to shared decision making in
01:01:49the face of uncertainty.
01:01:51Well, everyone, let's,
01:01:53raise our hands and clap
01:01:55for, doctor Waspy. Thank you
01:01:56so much.
01:02:06Oh, a broken foot.
01:02:08It looks actually very that
01:02:10is very much like this.