October 7, 2024 • 40 mins
Join our special guests, Drs. Auroa Badin and Bradley Lander, as we discuss the case of an elite professional athlete found to have atrial fibrillation. We discuss the challenges regarding anticoagulation, medical therapy, and the role of monitoring for burden of arrhythmia in these patients. Finally we review the role of definitive ablation, including the shared decision making process.
For more information:
HRS expert consensus statement on arrhythmias in the athlete
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Kanny (00:10):
So welcome everyone back to the Cardio Ohio podcast.
This is Kenny Graywall pastpresident of the Ohio chapter of
the ACC here in Columbus, Ohio.
Really excited to introduce anew co host.
I'd like everyone to welcome Dr.
Ali Azeem, who's clocking infrom Cleveland, Ohio.
(00:32):
Ali, do you mind justintroducing yourself and talking
a little bit about your currentposition?
Thanks
Ali (00:36):
Sure thing.
Thanks so much.
Can I really appreciate theopportunity?
My name is Ali Azeem.
I'm a first year cardiacelectrophysiology fellow here at
University Hospitals inCleveland.
I grew up in Northeast Ohio,Youngstown, Ohio, went to Case
Western here in Cleveland forschool before going to Tufts for
medical school, UPMC forresidency, and then coming back
(00:57):
here to Cleveland for generalcardiology fellowship, where I
was a chief fellow and stayed onfor just starting clinic.
electrophysiology fellowshipjust this July.
And happy to introduce BradLander.
Brad Lander was just recruitedalso to university hospitals
here in Cleveland last year todirect our sports cardiology
(01:19):
program.
Brad (01:20):
Yes, it's thanks for the introduction.
I, I'm originally fromCleveland.
I went to a case for medicalschool and then actually was
first exposed to sportscardiology as a resident at Mass
General.
They had a very, and they stilldo have a very large and well
run program called thecardiovascular performance
(01:41):
program.
At that time, it was led by Dr.
Aaron Baggish and Dr.
Megan Wosfy, and, you know,essentially, they've trained a
new generation of sportscardiologists and after that, I
went to Columbia for my generalcardiology fellowship, and I had
the chance to work with Dr.
Dave Engel, who is anothersports cardiologist and
(02:02):
echocardiographer who Is one ofthe main cardiologists for the
NBA and, you know, after that Idid an extra year of advanced
echo training at Columbia anddid an advanced fellowship in
sports cardiology andhypertrophic cardiomyopathy.
with Matt Martinez at MorristownMedical Center.
(02:23):
And then here I am back inCleveland you know, leading the
sports cardiology center andhelping to build the HCM program
as well.
Kanny (02:30):
Thanks, Brad.
I'm really curious about thefellowship you did with Dr.
Martinez.
I know he's one of the giants insports cardiology.
Is that a new trend to haveadvanced training like that
available?
I'm just asking on behalf ofsome of our fellows who, may
have an interest in that careerpathway.
Brad (02:47):
Absolutely.
You know, it's it's an ongoingdiscussion within the sports
cardiology community andhonestly, the HCM community is
how do we train you know,experienced providers who can
handle and you know, treat thenuances of, of these patients.
And so Dr.
(03:07):
Martinez has a fellowship, youknow, essentially one or two
fellows per year, and you trainin both HCM and sports
cardiology.
That's essentially all that hesees.
So it's high volume.
There is some imaging trainingas well, predominantly cardiac
MRI, and he's activelyrecruiting for, for next year's
(03:28):
fellow.
So it's a fantastic experience.
Excellent.
And Dr.
Martinez is a tremendous mentoras well.
Kanny (03:37):
Oh, that's great.
I'd like to introduce our secondguest as well.
It's my colleague from here inCentral Ohio, Dr.
Arwa Badeen.
He's currently anelectrophysiologist here at Ohio
Health, but he has a lot of tiesto Central Ohio, having also
done his fellowship in medicine.
(03:58):
At Ohio State University, Aroahwelcome and just let our
audience know a little bit aboutyour pathway that led you to
your current position andinterests.
Auroa (04:08):
Thank you, Kenny, Ali, and great to talk to you I'm
originally from Syria.
I did some training in New Yorkand New Jersey.
I did a non accredited heartfailure after my residency at
Mount Sinai and then did mycardiology fellowship at
University of Illinois.
(04:31):
I trained like you mentioned atOSU for cardiac
electrophysiology and I had someexposure there specifically for
arrhythmia and athletes.
I was a faculty at University ofTexas, San Antonio, and we had
exposure to anywhere frombasketball players to football
(04:52):
players there.
I joined this practice here atOhio health Columbus.
Three years ago And so happy tobe here.
Kanny (05:05):
Yeah, well, thank, welcome, welcome both of you.
So we're going to spend the next25 or 30 minutes just talking
about atrial fibrillation inathletes, hopefully talk about
it both in recreational andelite athletes, but also if we
have time, masters athletes,which is really a growing
population and, of interest insports cardiology.
(05:26):
So, Aro, I actually wanted totalk, talk just by briefly
summarizing that case youmentioned because I think it's a
really interesting patient and Ithink it's really what kind of
led me to be to really want toget more information about this
condition.
So this patient is a an athletein his mid twenties.
He's an elite professionalathlete.
(05:47):
I'm not going to say his sportor, where he performs just for
the sake of their privacy.
But.
As part of a routine athleticscreening prior to his season an
EKG just completely incidentallyshowed he was in atrial
fibrillation with a controlledrate at about 60.
(06:07):
Now, he had no real relevantpast history.
He was not using any performingenhancing drugs, minimal, risk
factors for AF in terms ofcaffeine use, alcohol use.
His screening included anechocardiogram, which was
completely normal.
And once again, this is aroutine screening done by his
(06:30):
athletic association.
So, he really initially reportedno symptoms at all, but on
further questioning did admithe, for quite a period of time,
had had episodic palpitations,but they were not really
bothersome or interfering, witheither his training or his
competition.
He really had not been havingany limitations with his
(06:52):
workouts, either in practice orin competition.
So I got Dr.
Badin involved and, we didrecommend to the patient that
we, we start by getting acardioversion done, at least
getting back to sinus rhythm.
We did some imaging of his leftatrial appendage and then he had
successful cardioversion, but ofcourse that also meant he had to
(07:15):
stay on anticoagulation for aperiod of weeks, which kind of
delayed.
His competition.
So I'm going to just leave itthere while we talk a little bit
more about the condition ingeneral and then I wanted to be
able to come back to towards theend of our discussion to talk a
little bit about some of thedecisions we made.
in terms of his eventualmanagement.
(07:37):
So Brad, I wanted to start justby kind of defining the
condition of AFib in athletes.
I think it's been kind of aperception in general cardiology
that elite level athletes orhigh level athletes are more
prone to atrial fibrillation.
Is that really the case in thesports cardiology literature?
(07:57):
And, and what do we understandabout the epidemiology and risk
factors for AF in this group ofpatients?
Brad (08:05):
Well, that's a, it's a great question and it's a really
good representative case.
oftentimes what we think of assimple or straightforward
decisions for atrialfibrillation in the general
population become, you know,much more nuanced and, you know,
can be nerve wracking in eliteor professional athletes where
their livelihood depends on Not,not being on anticoagulation and
(08:29):
being able to perform at theirbest.
But yes, there is a significantamount of literature about
atrial fibrillation andathletes, and it's mostly a
specific population.
Oftentimes, I'll get questionsof Is there such a thing as too
much exercise or, or can therebe, you know, an overuse injury
(08:51):
for the heart?
And, really, by and large,exercise is very good for the
heart, for mortality for riskfactors, but AFib is one of the
few conditions where it is moreprevalent in a certain segment
of the population.
And that is predominantly inolder, and when I say older, I
(09:14):
mean, you know, 50s, 60s, 70smasters athletes, predominantly
endurance athletes, likerunning, cycling.
Cross country skiing who havebeen exercising for, a long time
at high levels, it is more rareto have the case like you're
describing, or it's probably ayounger, younger athlete in in a
(09:38):
sport.
That's not one of these threethat I mentioned.
But it's been estimated that therisk of a fib and these high
intensity athletes is, you know,anywhere from 2 to 10 times as
high compared to sedentaryindividuals.
And, you know, one of the beststudies that looked at this
phenomenon was published aboutabout 10 years ago at this
(10:02):
point, and looked atapproximately 52, 53, 000
athletes who are competing inthe Vasa Opa, which is a long
distance skiing event in Sweden.
And they found that thestrongest predictors of AFib
were the number of racescompleted and race times.
So, the more you raced, and thefaster your race time.
(10:23):
The, the more likely you were tobe diagnosed with, with atrial
fibrillation.
And since then there have beenother meta analyses that have
been published that look atsimilar, similar questions and
confirm that it's really asignificantly higher risk of
AFib in these older mastersendurance athletes.
as compared to sedentaryindividuals.
Kanny (10:47):
Brad, do you think some of the traditional risk factors
still apply in this population?
You know, hypertension sleepapnea caffeine use, et cetera.
Brad (10:58):
Absolutely.
Definitely.
And whenever I see an athletelike this we don't start the
conversation with necessarilytalking about their, their
athletic history.
We general terms of of riskfactors for atrial fibrillation.
I asked them about supplementuse, I asked them about alcohol
(11:20):
intake, I asked them about sleepapnea, I asked them about
hypertension, I asked them aboutfamily history and for some of
these athletes, they takesupplements or pills that I've
never even heard of and so Ikind of transitioned the way I
asked the question to be from,what medicines do you take to
(11:41):
what do you put in your body?
Auroa (11:46):
I'd like to mention something about caffeine because
it was brought up twice Kenny.
You know, I, I'm a big advocateof coffee and I do think there's
actually a, a cardioprotectiveeffect of caffeine and The
athletes are not shunted from orshunned from that effect coffee
(12:12):
and arrhythmia is this is a verylarge designated myths regarding
caffeine and, and certainarrhythmias, specifically atrial
arrhythmias.
When you look at studies thatlooked specifically at actually
quantitative numbers of P.
A.
C.
S.
Or extra systoles in the cravetrial and others.
(12:34):
There was no associatedincrease.
And part of the reason is, Ithink, some of the mechanisms
that caffeine actually might beprotective from a fib, believe
it or not.
in in the population.
But I, I agree with with Bradwhen it comes to you know, other
(12:55):
supplements A lot of this is notgetting scrutinized by the FDA
because they have a specialcategory and it's sometimes
added to the energy drinks thatsome of those athletes may
consume.
And potentially there's a lot ofcase reports and a total
evidence that this might lead toincrease in potentially AFib and
(13:20):
other arrhythmias in thispopulation.
Ali (13:24):
Thank you.
That was really helpful.
Just to go a little bit deeperon that topic about the
mechanisms of atrialfibrillation could you two talk
a little bit more about themechanisms of atrial
fibrillation the role of atrialfibrosis or volume loading, and
how these patients are beingtreated?
(13:46):
Similar, but also different fromthe general population with
AFib.
Auroa (13:53):
Certainly, it is accepted in the, in the athlete
population that some of thecommon you know, multi head
phenomenal that leads to a fib.
Also applies to athletes.
I'm talking more specificallyabout you know, like the, the
tri triangle of having you knowremodeling, having triggers.
(14:16):
We often in electrophysiologytalk about triggers for atrial
fibrillation and thenpotentially the you know,
aggressive autonomic systemregulation that happens in these
athletes.
How does that apply to the f.
athletes.
Well, the electrical andstructural remodeling think
(14:40):
about fibrosis and validation ofthe L.
A.
Which potentially can alsoaffect the action potential
duration.
So when you're subjecting thecells to an aggressive
stimulation during thoseendurance exercises, And then
you have these periods of rest.
(15:01):
You have a very high upregulation of the
parasympathetic system.
And we study in basic EP that,you know parasympathetic system
decreases or shortens the actionpotential duration of the LA.
And so if you get any trigger,like an ectopy that may come
from the initiation of anexercise or stopping an exercise
(15:25):
and having a big gulp of waterthat signal will likely to lead
to this micro reentrance in theatrium and lead to a sustained
episode of AFib.
At least that's in theory.
And, and people suggested thatit seems that the LA dilates
(15:49):
more if you have someone who'sputting out an output close to
30 liters a minute, which isquite significant comparing to
the normal cutting output offive to eight.
And so what does dilatation leadto potentially so we're going
back to the triggers.
(16:09):
That's could be the initiationof an exercise.
It could be a small glass ofwine after.
a competition.
It could be any of those.
And then you have the rightpredisposition and you can go
into this AFib episodes.
Brad (16:24):
A few things that I would add are within the sports
cardiology realm, we tend tothink of sports, you know, along
a spectrum of, of dynamicexercise and static exercise.
And dynamic being, you know,running, cycling, rowing, and,
you know, static being morepowerlifting, American football
(16:45):
sprinting, et cetera.
Part of the reason why we'veseen the association between
endurance exercise or highintensity exercise in long term
athletes is because thoseindividuals, that type of sport,
the endurance or dynamic sports,those tend to cause more chamber
(17:06):
dilation, specifically atrialdilation.
And so the atrial dilation, thefibrosis like you're mentioning,
and the remodeling all have beenpostulated to contribute to the
increase in AFib in thatpopulation.
I will say, I'm not sure thatthere's one specific reason for
AFib in this group.
It's likely multifactorial likeyou mentioned.
(17:30):
But one, you know, kind of pearlthat I would put out there is if
it's not a typical a fib plusathlete scenario, you know, 60
year old long term cyclist, it'sa younger person.
Like the one you're mentioning.
I'm always a little bitsuspicious that there's
something else going on lookingfor accessory pathways.
(17:52):
Well, Parkinson white lookingfor structural issues.
You know, either hypertrophiccardiomyopathy, ARVD, either
current or, you know, priormyocarditis.
Imaging is really important withecho and cardiac MRI.
Kanny (18:06):
Yeah.
Thanks, Brad.
Thanks for pointing out the roleof imaging.
I'm glad you touched on that.
Just to follow up on a couple ofquick things before we turn our
attention to management for thesecond half of our talk Brad
when you do see AF and more of amaster's athlete, like you
mentioned, like the kind oflifetime endurance athlete, is
(18:28):
there any, do we have anyevidence that detraining or
Exercise abstinence would bepart of the management given
that, you know, the thought isthat, you know, accumulative
exercise could be playing arole.
And then the follow up to that,very briefly, is, are we aware
of any sex differences in theincidence of AF in athletes?
(18:49):
Because I know a lot of thestudies have historically been
done on male athletes.
Brad (18:54):
Those are really important questions.
I'll, maybe I'll start with thelatter ones.
In terms of sex differences.
It seems as though the risk ofAFib, at least in endurance
athletes, is significantlygreater in men compared with
women.
There is a, I guess you couldcall it, U shaped curve with
(19:16):
respect to the risk of AFib inathletes where no, no exercise
at all puts you at risk forAFib.
And a lot of High intensityendurance exercise over many,
many years puts you at increasedrisk for aphid but more moderate
exercise over a shorter periodof time is actually protective,
(19:39):
as opposed to what you see inwomen, or what has been reported
in women, is that actually theredoesn't seem to be quite the
same relationship in that themore women exercise, even at
higher intensities, or forlonger periods of time, their
risk of aphid seems to continueto go down.
Whether that gives us ahypothesis as to whether any of
(20:01):
this is related to hormones orsimply because in general, women
tend to have smaller atria,shorter P wave durations lower
LV mass and wall thicknesses, orwhether there's even differences
in autonomic tone, there is adifference both in the
literature and from what I seein the clinic between, between
(20:21):
men and women.
And then with respect to,detraining or threshold.
It's tough to put a number onthreshold for, when you'll get
AFib, if you'll get AFib.
But a few studies have suggestedthat the risk of AFib increases
significantly after about 1, 500to 2, 000 lifetime exercise
(20:46):
hours.
Where if it's above that level,you're at a higher risk for
AFib.
If you're below that, you're atless of a risk for AFib, but
when it comes to detraining,there really are no large, well
done studies of detraining inathletes.
Anecdotally, historically, thathas been recommended, and for
(21:08):
some people it actually doeswork fine.
So those athletes tend to haveto make a decision whether
they're okay with detraining or,or toning down their exercise,
or whether, you know, they don'tcare if they're an AFib or the
symptoms are not bothersomeenough for them to, to detrain.
But I recently learned thatthere's a trial, I think in, in
(21:32):
Norway called the NexafDetraining Trial, which is
looking at this questionspecifically and as far as I
know, this will be at least thebiggest or.
Or most well done hopefully.
randomized trial, randomizingathletes with AFib either to
detraining or to to usualexercise.
(21:53):
And I think that will betremendously informative going
forward.
Kanny (21:57):
Oh, that's good to know that we'll be getting more
clear, clear guidance as we goforward.
I want to spend the last 15minutes or so talking about
management before we finish upgetting back to our original
case.
I know when it comes to areas ofdebate and discussion in AFib
management, you could easilyturn one podcast into a podcast
(22:20):
series pretty quickly becausethere's so much we could
discuss.
So I kind of wanted to focus on,the areas that are potentially
different from, bread and butterAF management we see in our
overall patient population.
And focus a little bit moreabout, some of the unique
strategies that apply toathletes.
Ali (22:39):
So, Aura, could you talk, walk us through a little bit in
this specific patient populationhow you would, in general,
Approach the decision first oftaking a rate control strategy
versus a rhythm controlstrategy.
Auroa (22:53):
Certainly the rate control strategy is often not
going to be a very good choice,especially if we're talking
about an active elite athletes.
This is population thatmedication such as beta blockers
or non dihydropyridine, calciumchannel blockers would likely
lead to potentially reducedperformance, fatigue.
(23:17):
And some of them are franklybanned.
Like if you look at the WorldAnti Doping Agency, I think you
will have to have exception ifyou want to use a beta blocker
in somebody who's competing atan Olympic level, for example.
Generally, those medications canpotentially have side effects
(23:39):
and not the desirable first linenecessarily in in a young
population.
So often time rhythm controlstrategy would be preferred,
especially if there's somesymptoms.
Symptoms can be very vague inthese population.
Like our athletes has some vaguesymptoms, but he probably did
(24:03):
attributed to something else.
So when we talk about rhythmcontrol, generally we're
referring to like antiarrhythmicdrugs or ablation.
And there is a lot of problemswith antiarrhythmic drugs again
in this population.
You can potentially use classone C such as flaconide,
propafenone as a pill in thepocket and people who have very
(24:28):
seldom and sporadic episodes andpotentially you can use it as a
mainstay in people who have morefrequent episodes.
The problem with class one C,and this is again, anecdotal, we
don't have like large triallooking at that in this
particular population.
To me.
The problem with it is that asyou recall with basic
(24:52):
electrophysiology, that there'ssomething called dose dependent,
dependent effect of a class oneC, which means their toxicity,
because of the affinity to thesodium channel can increase with
higher heart rates.
So think about a competitiveathletes getting his heart rate
close to one 80 beats perminute, one 70 beats per minute.
(25:13):
Potentially they can have atoxic effect of this drug.
And if the, the otherpossibility is that they can
with AFib, they can degenerateinto a true flutter, which can
conduct extremely fast in ahealthy AV node.
And then we're going back tousing beta blocker in this
(25:34):
scenario, and so that's, that'swhere the problem happened.
And so, not to mention, youknow, if we're talking even a
younger population, adherencewith taking the medications and
other issue related to that.
So for all these reasons,antiretroviral drugs probably
not the best choice.
(25:54):
Or rate control for those drugs.
And again, I might be biasedbeing an electrophysiologist,
but the technology had evolvedconsiderably with ablation.
That makes it a safe, desirableoptions for symptomatic athletes
with a very good success rate.
I mean, it's the success rate,at least in in the small studies
(26:16):
that's been published in thisparticular population is similar
to the non athletic populationwhen it comes to freedom from
arrhythmia and follow ups.
population.
Ali (26:31):
Thank you for talking us through that and some of the
specific challenges of thephysiology of the athlete with
both the high vagal tone and theresting bradycardia that many of
these because of their highlevel of conditioning, moving on
to hear a little bit more aboutablation.
Could you talk a little bit moreabout what some of the return to
(26:54):
play could look like aftergetting an AFib ablation?
Auroa (26:59):
Yeah, I think that Generally speaking it is
acceptable to go back totraining fairly quickly, like
within less than two weeks.
This is not a procedure that'swould potentially cause a lot of
downtime, and we can clearpeople fairly quickly for even
(27:20):
intense exercise, so long thatyou know, his, the access point
in the femoral vein, which istypically how we perform those
ablations had healed.
The only issue with that is, asyou know, that anticoagulation
is usually needed.
(27:42):
immediately after ablationbleeding.
and so, there is considerabledata now that truncating that
three month of anticoagulationpost ablation could be
reasonable in a lot ofpopulation with a that does not
have like persistent atrialfibrillation and they don't have
(28:03):
a extensive scarring or a lowvoltage in their atrium and you
did not perform an extensiveablation, you just did pulmonary
vein isolation and thosepopulation truncating that
anticoagulation period to likesix to eight weeks instead of 12
weeks, for example.
might be reasonable, especiallyif they have contact sport.
(28:25):
Um, Um, Some of the things toconsider in contact sport
athlete is potentially doing theablation in the off season.
So we had to do that in some ofthe professional athletes in San
Antonio where we try to arrangefor the procedure to be done
(28:45):
when they're done with theseason and they're less likely
to have any contact sport.
Brad (28:51):
Another point that I want to make is.
it goes back and this isspecifically a challenge with
people who require multipleablations.
It goes back to the old sayingof, you know, the, the surgery
was a success, but the patientdied where, you know, you do
have an ablation and you doanother ablation, you do another
ablation.
And, you know, ultimately youget rid of the AFib, but there
(29:12):
is this risk of, you know,what's colloquially known as a
stiff left atrial syndrome,where you, you ablate so much
there, you cause fibrosis.
And much there, you causefibrosis.
And, um, ultimately, you know,they may not actually feel
better even in sinus rhythm.
Kanny (29:31):
that leads me to a follow up question, I think what many
of the topics Auro brought up,put some focus on the concept of
shared decision making, which,as a fellow sports cardiologist,
I think sports cardiology is oneof the areas where shared
decision making is even moreprominent.
Then a lot of other areasbecause there's not a huge
evidence, database guiding a lotof the decisions.
(29:54):
So, as, as a sports specialist,can you just briefly walk us
through like how you approachshared decision making when it
comes to either return to playor going ahead with evidence
based, medication or even, even,you know, discussing the pros
and cons of a procedure likeablation with an elite athlete,
Brad (30:13):
right?
I mean, this is a really goodquestion.
It's an important topic becauseshared decision making.
You know, at least over the past5 10 years, it's become a
central tenant of the entirefield.
And especially in a situationlike this, or situations like
these, where everything thatwe're doing, it's all based on
extrapolation from other patientpopulations.
(30:36):
So, you know, we'reextrapolating what to do with
these patients based on thegeneral population, you know,
even for something like theCHADS VASc score.
You know, the chance of askwasn't developed in cohort of
elite athletes.
It was developed, you know, ina, in a more general population.
So when it comes to discussingshared decision making and these
(30:58):
decisions with athletes, I'malways very transparent in,
allowing them to know, what isevidence based, what is
anecdotal, what is expertconsensus, because, that can
change some people's mind.
Whereas one person may bewilling to take the risk of
exercising on anticoagulants,other people may not be, and
(31:20):
it's a risk, it's a risk benefitdiscussion, because for some
people, if they cannotparticipate in their sport, then
they cannot make a living forthemselves and for their family,
um, and so it's a sensitive andso it's a sensitive topic in
certain situations.
At the end of the day, it's,it's always our goal to discuss
(31:43):
what are the risks, what are thebenefits, what are their
options.
Does the person have and youknow, ultimately, in my opinion,
people have you know, theability to make decisions for
themselves, but unfortunately,if they're playing in some of
these professional leagues, youknow, there may be medical
committees or the the team, theteam physician, the trainers,
(32:08):
the owner, they may also havesome saying, and there can be
some, some clashing of opinionsand, you know, it really
involves, it really necessitatesthat everyone's on the same
page.
Kanny (32:20):
In fact I'd actually like to spend the last few minutes
coming back to our case patientbecause he actually illustrates
a lot of the points you justmade about shared decision
making.
Just to summarize, he had acardioversion, but being that it
was the start of his season andthe fact that this was a single
documented episode of AF, youknow, he certainly didn't want
(32:41):
to rush into an immediateablation without, having more
information.
So Arwa, you, you, inconjunction with his
cardioversion, I know you made adecision about ongoing
monitoring that I thought wasvery interesting and unique.
What was your thought processbehind Uh, the decision,
Auroa (32:59):
yeah.
So this particular athlete hadsome vague symptoms and
palpitations in the past, and itwasn't very clear.
He also had a very uniquesubstrate because he was
discovered to have technicallyis in a, in a small category of
folks who have persistent AFibin this population.
(33:21):
Most of them has paroxysmalAFib.
And so we wanted to really knowwhat are we dealing with?
So part of the whole imagingidentifying substrate,
identifying like Brad mentionedtriggers, which is very
important, which we do in any ofthose ablations before we do the
(33:41):
pulmonary vein isolation.
And I wanted to emphasize that,which is basically looking for
accessory pathways, concealedaccessory pathways AVNRT like a
simple SVT that triggers youknow, AFib in this young
population.
Part of all that we discussedimplantable cardiac monitor.
(34:04):
So loop recorder, basicallyimplantation for various
reasons.
One of it is to have a truelongitudinal surveillance of any
recurrences in the future.
In addition you know, liketraditional Wearable monitors
with patch and whatnot,especially if you're in a peak
(34:25):
season is unlikely to give youany good yield because of the
adherence of the because of thesweatness of the body when
you're exercising.
So for all these reasons, wesuggested an implantable loop
recorder to see again, like,what is the What is the
(34:45):
frequency of this?
Is there any correlation withexercise?
All that.
And yeah, the, the, the athleteunderwent ILR implants.
It would not affect his exerciseabilities, and we're using that
to really longitudinally treatednow for recommendation of
(35:07):
management.
We would not have recommendedablation from the get go.
It was more of to see what we'redealing with.
And he does have true paroxysmalAFib now.
And because of the vaguesymptoms that he has, minimal
symptoms that he has, and anablation is offered that
(35:29):
potentially may be done in theoff season.
And that's after a very longdiscussion with him and in the
presence and without thepresence of his medical doctor
from or managers from the team,because I think and I want to
(35:51):
emphasize this ultimately theathlete has to make that
decision and it should not beanybody else.
Sometimes when you're dealingwith these athletes, there's,
there might be some.
different dynamics in the room.
Because there is you know,people might have different
(36:12):
opinion on what's best for theteam.
And the athletes might have aopinion about should have an
opinion about what's best forhim.
And so ultimately, it has to behis decision.
So some of those discussionsshould be done privately with
the athletes himself without thepresence of managers and other
(36:32):
people from the team.
And if he choose to reveal thisinformation to them and involve
them in the decision making,that would be his choice.
Kanny (36:41):
Yeah, so I think that's very fascinating because I
really could not find any casereports in the literature of uh,
athletes at a professional levelcompeting with an I.
L.
R.
You know, to monitor theirburden of arrhythmia.
Auroa (36:56):
I would like to add, I do think that you know, the
arrhythmia in this populationmight be under reported again.
This was an incidental finding.
One of my colleagues atUniversity of Illinois, my
junior fellow they did a studywhere they implanted.
20 loop recorder in ultratriathletes folks who have a
(37:21):
massive VO two max actuallyobjectively studied and they
discover about 5% which isreally one patient who had
asymptomatic atrialfibrillation.
So I do think There is somevalue.
I mean, what does that mean?
How does that affect?
That longitudinally?
(37:41):
We don't know.
But more and more, even inclinical trials and
electrophysiology, looprecorders are becoming like the
way to monitor.
Especially if you really need toknow about every episode.
Kanny (37:56):
Yeah.
Yeah.
That's that's fascinating to me.
Well, just as an aside, youknow, now that we've been
monitoring his device for the,for the last several months, his
overall burden of a fib hasfluctuated between about two or
3 percent some months up toabout 5%.
The longest episode is aboutthree to four hours.
(38:16):
And but what I really think isinteresting is that almost all
the episodes have occurred atrest.
and with low heart rates.
Does that give you any insightinto like the mechanism in him
specifically?
Auroa (38:27):
Yeah.
Excellent point.
I mean, that's again, likeunderstanding like what triggers
a fib in athletes.
Yes, I do think it's probablyrelated to high bagel tone as
opposed to the sharessympathetic activity.
I mean, even at rest theathletes have objectively higher
(38:49):
incidence of of PACs and PVCsand in a susceptible heart they,
they potentially can go into afit.
I mean, fascinating how it is asteady and it's not following
the natural progression of a fibwhere it's increasing in
frequency and increasing whichyou would see and expect in an
(39:11):
aging population.
So it's not very clear.
One thing I want to comment alsoalways part of the mechanisms
ask about, yeah.
No.
Did you get it when you have abig gulp of water immediately
after exercise?
Those questions like a detailedhistory is extremely important
in this population.
Kanny (39:31):
Yeah.
Yeah.
So obviously the patient iswaiting, awaiting ablation based
on his, you know, time courseand, and personal issues.
Uh, so So hopefully we'll havemore information.
going forward.
I think we're up against ourtime.
It's been a great discussion andthere's so many other aspects of
this.
I think we could talk about, butI think we have been able to hit
(39:52):
on a lot of the key pointsrelated to AF in this patient
population.
So I want to thank my co hostAli.
You did a great job on yourinaugural podcast.
Really appreciate your insight.
And of course, I want to thankboth of our guests as well.
And And, uh, I think there's somany interesting things in
sports cardiology we canaddress.
(40:14):
So hopefully, Brad, we can getyou back on podcast in the
future to get more insight goingforward.
Ali (40:20):
Thank you all.
I really learned a lot tonight.
I think our audience will too.
Thank you for joining today'spodcast.
For more information about thespeakers or the topics, please
go to Ohio acc.org,
So welcome everyone back to the Cardio Ohio podcast.
This is Kenny Graywall pastpresident of the Ohio chapter of
the ACC here in Columbus, Ohio.
Really excited to introduce anew co host.
I'd like everyone to welcome Dr.
Ali Azeem, who's clocking infrom Cleveland, Ohio.
(00:32):
Ali, do you mind justintroducing yourself and talking
a little bit about your currentposition?
Thanks
Ali (00:36):
Sure thing.
Thanks so much.
Can I really appreciate theopportunity?
My name is Ali Azeem.
I'm a first year cardiacelectrophysiology fellow here at
University Hospitals inCleveland.
I grew up in Northeast Ohio,Youngstown, Ohio, went to Case
Western here in Cleveland forschool before going to Tufts for
medical school, UPMC forresidency, and then coming back
(00:57):
here to Cleveland for generalcardiology fellowship, where I
was a chief fellow and stayed onfor just starting clinic.
electrophysiology fellowshipjust this July.
And happy to introduce BradLander.
Brad Lander was just recruitedalso to university hospitals
here in Cleveland last year todirect our sports cardiology
(01:19):
program.
Brad (01:20):
Yes, it's thanks for the introduction.
I, I'm originally fromCleveland.
I went to a case for medicalschool and then actually was
first exposed to sportscardiology as a resident at Mass
General.
They had a very, and they stilldo have a very large and well
run program called thecardiovascular performance
(01:41):
program.
At that time, it was led by Dr.
Aaron Baggish and Dr.
Megan Wosfy, and, you know,essentially, they've trained a
new generation of sportscardiologists and after that, I
went to Columbia for my generalcardiology fellowship, and I had
the chance to work with Dr.
Dave Engel, who is anothersports cardiologist and
(02:02):
echocardiographer who Is one ofthe main cardiologists for the
NBA and, you know, after that Idid an extra year of advanced
echo training at Columbia anddid an advanced fellowship in
sports cardiology andhypertrophic cardiomyopathy.
with Matt Martinez at MorristownMedical Center.
(02:23):
And then here I am back inCleveland you know, leading the
sports cardiology center andhelping to build the HCM program
as well.
Kanny (02:30):
Thanks, Brad.
I'm really curious about thefellowship you did with Dr.
Martinez.
I know he's one of the giants insports cardiology.
Is that a new trend to haveadvanced training like that
available?
I'm just asking on behalf ofsome of our fellows who, may
have an interest in that careerpathway.
Brad (02:47):
Absolutely.
You know, it's it's an ongoingdiscussion within the sports
cardiology community andhonestly, the HCM community is
how do we train you know,experienced providers who can
handle and you know, treat thenuances of, of these patients.
And so Dr.
(03:07):
Martinez has a fellowship, youknow, essentially one or two
fellows per year, and you trainin both HCM and sports
cardiology.
That's essentially all that hesees.
So it's high volume.
There is some imaging trainingas well, predominantly cardiac
MRI, and he's activelyrecruiting for, for next year's
(03:28):
fellow.
So it's a fantastic experience.
Excellent.
And Dr.
Martinez is a tremendous mentoras well.
Kanny (03:37):
Oh, that's great.
I'd like to introduce our secondguest as well.
It's my colleague from here inCentral Ohio, Dr.
Arwa Badeen.
He's currently anelectrophysiologist here at Ohio
Health, but he has a lot of tiesto Central Ohio, having also
done his fellowship in medicine.
(03:58):
At Ohio State University, Aroahwelcome and just let our
audience know a little bit aboutyour pathway that led you to
your current position andinterests.
Auroa (04:08):
Thank you, Kenny, Ali, and great to talk to you I'm
originally from Syria.
I did some training in New Yorkand New Jersey.
I did a non accredited heartfailure after my residency at
Mount Sinai and then did mycardiology fellowship at
University of Illinois.
(04:31):
I trained like you mentioned atOSU for cardiac
electrophysiology and I had someexposure there specifically for
arrhythmia and athletes.
I was a faculty at University ofTexas, San Antonio, and we had
exposure to anywhere frombasketball players to football
(04:52):
players there.
I joined this practice here atOhio health Columbus.
Three years ago And so happy tobe here.
Kanny (05:05):
Yeah, well, thank, welcome, welcome both of you.
So we're going to spend the next25 or 30 minutes just talking
about atrial fibrillation inathletes, hopefully talk about
it both in recreational andelite athletes, but also if we
have time, masters athletes,which is really a growing
population and, of interest insports cardiology.
(05:26):
So, Aro, I actually wanted totalk, talk just by briefly
summarizing that case youmentioned because I think it's a
really interesting patient and Ithink it's really what kind of
led me to be to really want toget more information about this
condition.
So this patient is a an athletein his mid twenties.
He's an elite professionalathlete.
(05:47):
I'm not going to say his sportor, where he performs just for
the sake of their privacy.
But.
As part of a routine athleticscreening prior to his season an
EKG just completely incidentallyshowed he was in atrial
fibrillation with a controlledrate at about 60.
(06:07):
Now, he had no real relevantpast history.
He was not using any performingenhancing drugs, minimal, risk
factors for AF in terms ofcaffeine use, alcohol use.
His screening included anechocardiogram, which was
completely normal.
And once again, this is aroutine screening done by his
(06:30):
athletic association.
So, he really initially reportedno symptoms at all, but on
further questioning did admithe, for quite a period of time,
had had episodic palpitations,but they were not really
bothersome or interfering, witheither his training or his
competition.
He really had not been havingany limitations with his
(06:52):
workouts, either in practice orin competition.
So I got Dr.
Badin involved and, we didrecommend to the patient that
we, we start by getting acardioversion done, at least
getting back to sinus rhythm.
We did some imaging of his leftatrial appendage and then he had
successful cardioversion, but ofcourse that also meant he had to
(07:15):
stay on anticoagulation for aperiod of weeks, which kind of
delayed.
His competition.
So I'm going to just leave itthere while we talk a little bit
more about the condition ingeneral and then I wanted to be
able to come back to towards theend of our discussion to talk a
little bit about some of thedecisions we made.
in terms of his eventualmanagement.
(07:37):
So Brad, I wanted to start justby kind of defining the
condition of AFib in athletes.
I think it's been kind of aperception in general cardiology
that elite level athletes orhigh level athletes are more
prone to atrial fibrillation.
Is that really the case in thesports cardiology literature?
(07:57):
And, and what do we understandabout the epidemiology and risk
factors for AF in this group ofpatients?
Brad (08:05):
Well, that's a, it's a great question and it's a really
good representative case.
oftentimes what we think of assimple or straightforward
decisions for atrialfibrillation in the general
population become, you know,much more nuanced and, you know,
can be nerve wracking in eliteor professional athletes where
their livelihood depends on Not,not being on anticoagulation and
(08:29):
being able to perform at theirbest.
But yes, there is a significantamount of literature about
atrial fibrillation andathletes, and it's mostly a
specific population.
Oftentimes, I'll get questionsof Is there such a thing as too
much exercise or, or can therebe, you know, an overuse injury
(08:51):
for the heart?
And, really, by and large,exercise is very good for the
heart, for mortality for riskfactors, but AFib is one of the
few conditions where it is moreprevalent in a certain segment
of the population.
And that is predominantly inolder, and when I say older, I
(09:14):
mean, you know, 50s, 60s, 70smasters athletes, predominantly
endurance athletes, likerunning, cycling.
Cross country skiing who havebeen exercising for, a long time
at high levels, it is more rareto have the case like you're
describing, or it's probably ayounger, younger athlete in in a
(09:38):
sport.
That's not one of these threethat I mentioned.
But it's been estimated that therisk of a fib and these high
intensity athletes is, you know,anywhere from 2 to 10 times as
high compared to sedentaryindividuals.
And, you know, one of the beststudies that looked at this
phenomenon was published aboutabout 10 years ago at this
(10:02):
point, and looked atapproximately 52, 53, 000
athletes who are competing inthe Vasa Opa, which is a long
distance skiing event in Sweden.
And they found that thestrongest predictors of AFib
were the number of racescompleted and race times.
So, the more you raced, and thefaster your race time.
(10:23):
The, the more likely you were tobe diagnosed with, with atrial
fibrillation.
And since then there have beenother meta analyses that have
been published that look atsimilar, similar questions and
confirm that it's really asignificantly higher risk of
AFib in these older mastersendurance athletes.
as compared to sedentaryindividuals.
Kanny (10:47):
Brad, do you think some of the traditional risk factors
still apply in this population?
You know, hypertension sleepapnea caffeine use, et cetera.
Brad (10:58):
Absolutely.
Definitely.
And whenever I see an athletelike this we don't start the
conversation with necessarilytalking about their, their
athletic history.
We general terms of of riskfactors for atrial fibrillation.
I asked them about supplementuse, I asked them about alcohol
(11:20):
intake, I asked them about sleepapnea, I asked them about
hypertension, I asked them aboutfamily history and for some of
these athletes, they takesupplements or pills that I've
never even heard of and so Ikind of transitioned the way I
asked the question to be from,what medicines do you take to
(11:41):
what do you put in your body?
Auroa (11:46):
I'd like to mention something about caffeine because
it was brought up twice Kenny.
You know, I, I'm a big advocateof coffee and I do think there's
actually a, a cardioprotectiveeffect of caffeine and The
athletes are not shunted from orshunned from that effect coffee
(12:12):
and arrhythmia is this is a verylarge designated myths regarding
caffeine and, and certainarrhythmias, specifically atrial
arrhythmias.
When you look at studies thatlooked specifically at actually
quantitative numbers of P.
A.
C.
S.
Or extra systoles in the cravetrial and others.
(12:34):
There was no associatedincrease.
And part of the reason is, Ithink, some of the mechanisms
that caffeine actually might beprotective from a fib, believe
it or not.
in in the population.
But I, I agree with with Bradwhen it comes to you know, other
(12:55):
supplements A lot of this is notgetting scrutinized by the FDA
because they have a specialcategory and it's sometimes
added to the energy drinks thatsome of those athletes may
consume.
And potentially there's a lot ofcase reports and a total
evidence that this might lead toincrease in potentially AFib and
(13:20):
other arrhythmias in thispopulation.
Ali (13:24):
Thank you.
That was really helpful.
Just to go a little bit deeperon that topic about the
mechanisms of atrialfibrillation could you two talk
a little bit more about themechanisms of atrial
fibrillation the role of atrialfibrosis or volume loading, and
how these patients are beingtreated?
(13:46):
Similar, but also different fromthe general population with
AFib.
Auroa (13:53):
Certainly, it is accepted in the, in the athlete
population that some of thecommon you know, multi head
phenomenal that leads to a fib.
Also applies to athletes.
I'm talking more specificallyabout you know, like the, the
tri triangle of having you knowremodeling, having triggers.
(14:16):
We often in electrophysiologytalk about triggers for atrial
fibrillation and thenpotentially the you know,
aggressive autonomic systemregulation that happens in these
athletes.
How does that apply to the f.
athletes.
Well, the electrical andstructural remodeling think
(14:40):
about fibrosis and validation ofthe L.
A.
Which potentially can alsoaffect the action potential
duration.
So when you're subjecting thecells to an aggressive
stimulation during thoseendurance exercises, And then
you have these periods of rest.
(15:01):
You have a very high upregulation of the
parasympathetic system.
And we study in basic EP that,you know parasympathetic system
decreases or shortens the actionpotential duration of the LA.
And so if you get any trigger,like an ectopy that may come
from the initiation of anexercise or stopping an exercise
(15:25):
and having a big gulp of waterthat signal will likely to lead
to this micro reentrance in theatrium and lead to a sustained
episode of AFib.
At least that's in theory.
And, and people suggested thatit seems that the LA dilates
(15:49):
more if you have someone who'sputting out an output close to
30 liters a minute, which isquite significant comparing to
the normal cutting output offive to eight.
And so what does dilatation leadto potentially so we're going
back to the triggers.
(16:09):
That's could be the initiationof an exercise.
It could be a small glass ofwine after.
a competition.
It could be any of those.
And then you have the rightpredisposition and you can go
into this AFib episodes.
Brad (16:24):
A few things that I would add are within the sports
cardiology realm, we tend tothink of sports, you know, along
a spectrum of, of dynamicexercise and static exercise.
And dynamic being, you know,running, cycling, rowing, and,
you know, static being morepowerlifting, American football
(16:45):
sprinting, et cetera.
Part of the reason why we'veseen the association between
endurance exercise or highintensity exercise in long term
athletes is because thoseindividuals, that type of sport,
the endurance or dynamic sports,those tend to cause more chamber
(17:06):
dilation, specifically atrialdilation.
And so the atrial dilation, thefibrosis like you're mentioning,
and the remodeling all have beenpostulated to contribute to the
increase in AFib in thatpopulation.
I will say, I'm not sure thatthere's one specific reason for
AFib in this group.
It's likely multifactorial likeyou mentioned.
(17:30):
But one, you know, kind of pearlthat I would put out there is if
it's not a typical a fib plusathlete scenario, you know, 60
year old long term cyclist, it'sa younger person.
Like the one you're mentioning.
I'm always a little bitsuspicious that there's
something else going on lookingfor accessory pathways.
(17:52):
Well, Parkinson white lookingfor structural issues.
You know, either hypertrophiccardiomyopathy, ARVD, either
current or, you know, priormyocarditis.
Imaging is really important withecho and cardiac MRI.
Kanny (18:06):
Yeah.
Thanks, Brad.
Thanks for pointing out the roleof imaging.
I'm glad you touched on that.
Just to follow up on a couple ofquick things before we turn our
attention to management for thesecond half of our talk Brad
when you do see AF and more of amaster's athlete, like you
mentioned, like the kind oflifetime endurance athlete, is
(18:28):
there any, do we have anyevidence that detraining or
Exercise abstinence would bepart of the management given
that, you know, the thought isthat, you know, accumulative
exercise could be playing arole.
And then the follow up to that,very briefly, is, are we aware
of any sex differences in theincidence of AF in athletes?
(18:49):
Because I know a lot of thestudies have historically been
done on male athletes.
Brad (18:54):
Those are really important questions.
I'll, maybe I'll start with thelatter ones.
In terms of sex differences.
It seems as though the risk ofAFib, at least in endurance
athletes, is significantlygreater in men compared with
women.
There is a, I guess you couldcall it, U shaped curve with
(19:16):
respect to the risk of AFib inathletes where no, no exercise
at all puts you at risk forAFib.
And a lot of High intensityendurance exercise over many,
many years puts you at increasedrisk for aphid but more moderate
exercise over a shorter periodof time is actually protective,
(19:39):
as opposed to what you see inwomen, or what has been reported
in women, is that actually theredoesn't seem to be quite the
same relationship in that themore women exercise, even at
higher intensities, or forlonger periods of time, their
risk of aphid seems to continueto go down.
Whether that gives us ahypothesis as to whether any of
(20:01):
this is related to hormones orsimply because in general, women
tend to have smaller atria,shorter P wave durations lower
LV mass and wall thicknesses, orwhether there's even differences
in autonomic tone, there is adifference both in the
literature and from what I seein the clinic between, between
(20:21):
men and women.
And then with respect to,detraining or threshold.
It's tough to put a number onthreshold for, when you'll get
AFib, if you'll get AFib.
But a few studies have suggestedthat the risk of AFib increases
significantly after about 1, 500to 2, 000 lifetime exercise
(20:46):
hours.
Where if it's above that level,you're at a higher risk for
AFib.
If you're below that, you're atless of a risk for AFib, but
when it comes to detraining,there really are no large, well
done studies of detraining inathletes.
Anecdotally, historically, thathas been recommended, and for
(21:08):
some people it actually doeswork fine.
So those athletes tend to haveto make a decision whether
they're okay with detraining or,or toning down their exercise,
or whether, you know, they don'tcare if they're an AFib or the
symptoms are not bothersomeenough for them to, to detrain.
But I recently learned thatthere's a trial, I think in, in
(21:32):
Norway called the NexafDetraining Trial, which is
looking at this questionspecifically and as far as I
know, this will be at least thebiggest or.
Or most well done hopefully.
randomized trial, randomizingathletes with AFib either to
detraining or to to usualexercise.
(21:53):
And I think that will betremendously informative going
forward.
Kanny (21:57):
Oh, that's good to know that we'll be getting more
clear, clear guidance as we goforward.
I want to spend the last 15minutes or so talking about
management before we finish upgetting back to our original
case.
I know when it comes to areas ofdebate and discussion in AFib
management, you could easilyturn one podcast into a podcast
(22:20):
series pretty quickly becausethere's so much we could
discuss.
So I kind of wanted to focus on,the areas that are potentially
different from, bread and butterAF management we see in our
overall patient population.
And focus a little bit moreabout, some of the unique
strategies that apply toathletes.
Ali (22:39):
So, Aura, could you talk, walk us through a little bit in
this specific patient populationhow you would, in general,
Approach the decision first oftaking a rate control strategy
versus a rhythm controlstrategy.
Auroa (22:53):
Certainly the rate control strategy is often not
going to be a very good choice,especially if we're talking
about an active elite athletes.
This is population thatmedication such as beta blockers
or non dihydropyridine, calciumchannel blockers would likely
lead to potentially reducedperformance, fatigue.
(23:17):
And some of them are franklybanned.
Like if you look at the WorldAnti Doping Agency, I think you
will have to have exception ifyou want to use a beta blocker
in somebody who's competing atan Olympic level, for example.
Generally, those medications canpotentially have side effects
(23:39):
and not the desirable first linenecessarily in in a young
population.
So often time rhythm controlstrategy would be preferred,
especially if there's somesymptoms.
Symptoms can be very vague inthese population.
Like our athletes has some vaguesymptoms, but he probably did
(24:03):
attributed to something else.
So when we talk about rhythmcontrol, generally we're
referring to like antiarrhythmicdrugs or ablation.
And there is a lot of problemswith antiarrhythmic drugs again
in this population.
You can potentially use classone C such as flaconide,
propafenone as a pill in thepocket and people who have very
(24:28):
seldom and sporadic episodes andpotentially you can use it as a
mainstay in people who have morefrequent episodes.
The problem with class one C,and this is again, anecdotal, we
don't have like large triallooking at that in this
particular population.
To me.
The problem with it is that asyou recall with basic
(24:52):
electrophysiology, that there'ssomething called dose dependent,
dependent effect of a class oneC, which means their toxicity,
because of the affinity to thesodium channel can increase with
higher heart rates.
So think about a competitiveathletes getting his heart rate
close to one 80 beats perminute, one 70 beats per minute.
(25:13):
Potentially they can have atoxic effect of this drug.
And if the, the otherpossibility is that they can
with AFib, they can degenerateinto a true flutter, which can
conduct extremely fast in ahealthy AV node.
And then we're going back tousing beta blocker in this
(25:34):
scenario, and so that's, that'swhere the problem happened.
And so, not to mention, youknow, if we're talking even a
younger population, adherencewith taking the medications and
other issue related to that.
So for all these reasons,antiretroviral drugs probably
not the best choice.
(25:54):
Or rate control for those drugs.
And again, I might be biasedbeing an electrophysiologist,
but the technology had evolvedconsiderably with ablation.
That makes it a safe, desirableoptions for symptomatic athletes
with a very good success rate.
I mean, it's the success rate,at least in in the small studies
(26:16):
that's been published in thisparticular population is similar
to the non athletic populationwhen it comes to freedom from
arrhythmia and follow ups.
population.
Ali (26:31):
Thank you for talking us through that and some of the
specific challenges of thephysiology of the athlete with
both the high vagal tone and theresting bradycardia that many of
these because of their highlevel of conditioning, moving on
to hear a little bit more aboutablation.
Could you talk a little bit moreabout what some of the return to
(26:54):
play could look like aftergetting an AFib ablation?
Auroa (26:59):
Yeah, I think that Generally speaking it is
acceptable to go back totraining fairly quickly, like
within less than two weeks.
This is not a procedure that'swould potentially cause a lot of
downtime, and we can clearpeople fairly quickly for even
(27:20):
intense exercise, so long thatyou know, his, the access point
in the femoral vein, which istypically how we perform those
ablations had healed.
The only issue with that is, asyou know, that anticoagulation
is usually needed.
(27:42):
immediately after ablationbleeding.
and so, there is considerabledata now that truncating that
three month of anticoagulationpost ablation could be
reasonable in a lot ofpopulation with a that does not
have like persistent atrialfibrillation and they don't have
(28:03):
a extensive scarring or a lowvoltage in their atrium and you
did not perform an extensiveablation, you just did pulmonary
vein isolation and thosepopulation truncating that
anticoagulation period to likesix to eight weeks instead of 12
weeks, for example.
might be reasonable, especiallyif they have contact sport.
(28:25):
Um, Um, Some of the things toconsider in contact sport
athlete is potentially doing theablation in the off season.
So we had to do that in some ofthe professional athletes in San
Antonio where we try to arrangefor the procedure to be done
(28:45):
when they're done with theseason and they're less likely
to have any contact sport.
Brad (28:51):
Another point that I want to make is.
it goes back and this isspecifically a challenge with
people who require multipleablations.
It goes back to the old sayingof, you know, the, the surgery
was a success, but the patientdied where, you know, you do
have an ablation and you doanother ablation, you do another
ablation.
And, you know, ultimately youget rid of the AFib, but there
(29:12):
is this risk of, you know,what's colloquially known as a
stiff left atrial syndrome,where you, you ablate so much
there, you cause fibrosis.
And much there, you causefibrosis.
And, um, ultimately, you know,they may not actually feel
better even in sinus rhythm.
Kanny (29:31):
that leads me to a follow up question, I think what many
of the topics Auro brought up,put some focus on the concept of
shared decision making, which,as a fellow sports cardiologist,
I think sports cardiology is oneof the areas where shared
decision making is even moreprominent.
Then a lot of other areasbecause there's not a huge
evidence, database guiding a lotof the decisions.
(29:54):
So, as, as a sports specialist,can you just briefly walk us
through like how you approachshared decision making when it
comes to either return to playor going ahead with evidence
based, medication or even, even,you know, discussing the pros
and cons of a procedure likeablation with an elite athlete,
Brad (30:13):
right?
I mean, this is a really goodquestion.
It's an important topic becauseshared decision making.
You know, at least over the past5 10 years, it's become a
central tenant of the entirefield.
And especially in a situationlike this, or situations like
these, where everything thatwe're doing, it's all based on
extrapolation from other patientpopulations.
(30:36):
So, you know, we'reextrapolating what to do with
these patients based on thegeneral population, you know,
even for something like theCHADS VASc score.
You know, the chance of askwasn't developed in cohort of
elite athletes.
It was developed, you know, ina, in a more general population.
So when it comes to discussingshared decision making and these
(30:58):
decisions with athletes, I'malways very transparent in,
allowing them to know, what isevidence based, what is
anecdotal, what is expertconsensus, because, that can
change some people's mind.
Whereas one person may bewilling to take the risk of
exercising on anticoagulants,other people may not be, and
(31:20):
it's a risk, it's a risk benefitdiscussion, because for some
people, if they cannotparticipate in their sport, then
they cannot make a living forthemselves and for their family,
um, and so it's a sensitive andso it's a sensitive topic in
certain situations.
At the end of the day, it's,it's always our goal to discuss
(31:43):
what are the risks, what are thebenefits, what are their
options.
Does the person have and youknow, ultimately, in my opinion,
people have you know, theability to make decisions for
themselves, but unfortunately,if they're playing in some of
these professional leagues, youknow, there may be medical
committees or the the team, theteam physician, the trainers,
(32:08):
the owner, they may also havesome saying, and there can be
some, some clashing of opinionsand, you know, it really
involves, it really necessitatesthat everyone's on the same
page.
Kanny (32:20):
In fact I'd actually like to spend the last few minutes
coming back to our case patientbecause he actually illustrates
a lot of the points you justmade about shared decision
making.
Just to summarize, he had acardioversion, but being that it
was the start of his season andthe fact that this was a single
documented episode of AF, youknow, he certainly didn't want
(32:41):
to rush into an immediateablation without, having more
information.
So Arwa, you, you, inconjunction with his
cardioversion, I know you made adecision about ongoing
monitoring that I thought wasvery interesting and unique.
What was your thought processbehind Uh, the decision,
Auroa (32:59):
yeah.
So this particular athlete hadsome vague symptoms and
palpitations in the past, and itwasn't very clear.
He also had a very uniquesubstrate because he was
discovered to have technicallyis in a, in a small category of
folks who have persistent AFibin this population.
(33:21):
Most of them has paroxysmalAFib.
And so we wanted to really knowwhat are we dealing with?
So part of the whole imagingidentifying substrate,
identifying like Brad mentionedtriggers, which is very
important, which we do in any ofthose ablations before we do the
(33:41):
pulmonary vein isolation.
And I wanted to emphasize that,which is basically looking for
accessory pathways, concealedaccessory pathways AVNRT like a
simple SVT that triggers youknow, AFib in this young
population.
Part of all that we discussedimplantable cardiac monitor.
(34:04):
So loop recorder, basicallyimplantation for various
reasons.
One of it is to have a truelongitudinal surveillance of any
recurrences in the future.
In addition you know, liketraditional Wearable monitors
with patch and whatnot,especially if you're in a peak
(34:25):
season is unlikely to give youany good yield because of the
adherence of the because of thesweatness of the body when
you're exercising.
So for all these reasons, wesuggested an implantable loop
recorder to see again, like,what is the What is the
(34:45):
frequency of this?
Is there any correlation withexercise?
All that.
And yeah, the, the, the athleteunderwent ILR implants.
It would not affect his exerciseabilities, and we're using that
to really longitudinally treatednow for recommendation of
(35:07):
management.
We would not have recommendedablation from the get go.
It was more of to see what we'redealing with.
And he does have true paroxysmalAFib now.
And because of the vaguesymptoms that he has, minimal
symptoms that he has, and anablation is offered that
(35:29):
potentially may be done in theoff season.
And that's after a very longdiscussion with him and in the
presence and without thepresence of his medical doctor
from or managers from the team,because I think and I want to
(35:51):
emphasize this ultimately theathlete has to make that
decision and it should not beanybody else.
Sometimes when you're dealingwith these athletes, there's,
there might be some.
different dynamics in the room.
Because there is you know,people might have different
(36:12):
opinion on what's best for theteam.
And the athletes might have aopinion about should have an
opinion about what's best forhim.
And so ultimately, it has to behis decision.
So some of those discussionsshould be done privately with
the athletes himself without thepresence of managers and other
(36:32):
people from the team.
And if he choose to reveal thisinformation to them and involve
them in the decision making,that would be his choice.
Kanny (36:41):
Yeah, so I think that's very fascinating because I
really could not find any casereports in the literature of uh,
athletes at a professional levelcompeting with an I.
L.
R.
You know, to monitor theirburden of arrhythmia.
Auroa (36:56):
I would like to add, I do think that you know, the
arrhythmia in this populationmight be under reported again.
This was an incidental finding.
One of my colleagues atUniversity of Illinois, my
junior fellow they did a studywhere they implanted.
20 loop recorder in ultratriathletes folks who have a
(37:21):
massive VO two max actuallyobjectively studied and they
discover about 5% which isreally one patient who had
asymptomatic atrialfibrillation.
So I do think There is somevalue.
I mean, what does that mean?
How does that affect?
That longitudinally?
(37:41):
We don't know.
But more and more, even inclinical trials and
electrophysiology, looprecorders are becoming like the
way to monitor.
Especially if you really need toknow about every episode.
Kanny (37:56):
Yeah.
Yeah.
That's that's fascinating to me.
Well, just as an aside, youknow, now that we've been
monitoring his device for the,for the last several months, his
overall burden of a fib hasfluctuated between about two or
3 percent some months up toabout 5%.
The longest episode is aboutthree to four hours.
(38:16):
And but what I really think isinteresting is that almost all
the episodes have occurred atrest.
and with low heart rates.
Does that give you any insightinto like the mechanism in him
specifically?
Auroa (38:27):
Yeah.
Excellent point.
I mean, that's again, likeunderstanding like what triggers
a fib in athletes.
Yes, I do think it's probablyrelated to high bagel tone as
opposed to the sharessympathetic activity.
I mean, even at rest theathletes have objectively higher
(38:49):
incidence of of PACs and PVCsand in a susceptible heart they,
they potentially can go into afit.
I mean, fascinating how it is asteady and it's not following
the natural progression of a fibwhere it's increasing in
frequency and increasing whichyou would see and expect in an
(39:11):
aging population.
So it's not very clear.
One thing I want to comment alsoalways part of the mechanisms
ask about, yeah.
No.
Did you get it when you have abig gulp of water immediately
after exercise?
Those questions like a detailedhistory is extremely important
in this population.
Kanny (39:31):
Yeah.
Yeah.
So obviously the patient iswaiting, awaiting ablation based
on his, you know, time courseand, and personal issues.
Uh, so So hopefully we'll havemore information.
going forward.
I think we're up against ourtime.
It's been a great discussion andthere's so many other aspects of
this.
I think we could talk about, butI think we have been able to hit
(39:52):
on a lot of the key pointsrelated to AF in this patient
population.
So I want to thank my co hostAli.
You did a great job on yourinaugural podcast.
Really appreciate your insight.
And of course, I want to thankboth of our guests as well.
And And, uh, I think there's somany interesting things in
sports cardiology we canaddress.
(40:14):
So hopefully, Brad, we can getyou back on podcast in the
future to get more insight goingforward.
Ali (40:20):
Thank you all.
I really learned a lot tonight.
I think our audience will too.
Thank you for joining today'spodcast.
For more information about thespeakers or the topics, please
go to Ohio acc.org,
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