September 19, 2025 • 25 mins
This week we replay an episode from 2 years ago on postoperative ectopic atrial tachycardia (EAT) following congenital heart surgery in children. Are there risk factors for this arrhythmia and are any modifiable? What is the 'go to' therapy used by the electrophysiologists at Children's LA for the acute and chronic treatment of this arrhythmia in the postoperative period? Is the presence of EAT in a postoperative congenital heart patient a marker for a worse outcome? These are amongst the questions posed to Children's of Los Angeles pediatric electrophysiologist, Dr. Jonathan Uniat.
· DOI: 10.1007/s00246-022-03068-8
· DOI: 10.1007/s00246-022-03068-8
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:00):
Hello everybody. This is Rob Pass, the host of the
Pdhart podcast. This week, we'll be reviewing an episode from
two years ago on post operative topic atrial tachycardia, a
vexing problem that we are all seeing with greater commonality.
I'll see you all next week with a brand new episode.
(00:32):
Welcome your Pdheart Pediatric Cardiology Today. My name is doctor
Robert Pass and I'm the host of this podcast. I'm
Professor of Pediatrics at the Icon School of Medicine at
Mount Sinai, where I'm also the Chief of Pediatric Cardiology.
Thank you for joining me for this two hundred and
seventy sixth episode of the podcast. I hope all enjoyed
last week's episode on the SVR three trial on hypoplastic
(00:55):
left heart syndrome. For those of you with an interest
in outcomes research specific in relation to hypoplastic left heart syndrome,
I definitely recommend you take to listen to last week's
episode with doctor Karen Goldberg. As I say every week,
if you'd like to get in touch with me, my
email is easy to remember. It's Pdheart at gmail dot com.
(01:15):
This week, we move on to the world of electrophysiology
to a topic I find quite interesting and that is
ectopic atrial tachy cardia following heart surgery. The title of
our work this week is Ectopic atrial Tachycardia in Infants
following congenital heart disease surgery. The first author of this
work is Jonathan Yuniat and the senior author is Janni Barkhone.
(01:36):
And this work comes to us from Children's Los Angeles
Department of Pediatrics in Los Angeles, California. When we're done
reviewing this paper, doctor Uniat has kindly great to speak
with us about it. Therefore, let's get onto this article
and then a brief conversation with its first author. This
week's work starts with some comments about a rhythmias following
(01:56):
heart surgery and children, with a very wide range of
prevalence in this patient group, ranging in some works as
low as seven percent to as high as forty eight percent,
likely reflecting different patient groups in different studies. However, they
make the point that any problem with rhythm in patients
who are postoperative and in low cardiac output states following
surgery can be particularly dangerous. Amongst a rhythmia is seen
(02:20):
a topic atrial tachycardia, which is typically referred to as
EAT or perhaps slightly less commonly, AET has been described
to occur in between eight and fifteen percent of those
undergoing congenital heart surgery, and the authors bemoan the fact
that there is little in the literature that reviews or
has identified obvious, reproducible risk factors for this arrhythmia. They
(02:42):
two points to smaller studies suggesting that lower weighted surgery,
longer bypass times, and single ventricles might identify higher risk patients,
and they also point to other works suggesting that those
with TAPVR transposition or even try a treasure ard an
increased risk. With this as a background, the team at
children sought to identify risk factors for the development of
(03:03):
post operative EAT in a large retrospective co order patients
less than a year of age at the time of surgery.
They also reviewed when the patients typically developed the EAT,
as well as the treatment and outcomes of those post
op EAT patients. This was a single center retrospective chart
review study at Children's LA from January two thousand and
seven till July twenty twenty. Patients had to be less
(03:26):
than one year of age, as this is the group
most affected by this arrhythmia. For this work, EAT was
defined as three or more consecutive non sinus atrial beats
that were faster than the age expected rates if the
pwave resembled a sinus pwave, something that vexes all pediatric
EP doctors. Other factors like the rates, the abruptness of
(03:47):
the initiation, a termination of the rhythm, things like that
were used to help diagnosis. The investigators reviewed the ECG's
and rhythm strips of those who were thought to have
EAT to confirm this diagnosis, and if a patient had
eat prior to surgery, they were not included. The patients
with EAT were naturally compared to similarly aged children who
had surgery at the same time but did not have EAT,
(04:10):
and on to the results well, eat was seen in
one hundred and twenty nine cardiac procedures, or two point
five percent of five thousand, three hundred and seventy two
operations performed in the study period. Interestingly, if a patient
with actopic atrial tachycardia had a period of quiescence of
the arrhythmia after the initial surgery, no such patient ever
(04:31):
had EAT at a subsequent surgery. In this cohort. Let's
start with some univariate comparisons. When comparing the patients with
EAT versus those without. The EAT group was generally younger
at the time of surgery seven days versus eighty five days,
and had a lower operative weight three point three kilos
versus four point two kilos, meaning smaller, younger patients more
(04:53):
risk of EAT. There were no gender differences, and patients
with EAT were more likely to have to George syndrome
seven point seven percent versus those without three percent, or
heterotaxy with asplenia seven percent versus two point seven percent.
And what about surgical factors that might be associated with eat? First,
cardiopulmonary bypass time. Those with a longer bypass time sixty
(05:18):
four minutes versus fifty nine minutes, and those who received
deep hypothermic circulatory arrest fifteen minutes versus zero minutes had
more EAT. Interestingly, there were no differences based on cross
clam times and were there any surgeries more associated with eat?
On univarid analysis, well, yes, nine point seven percent had
total anomalous pulmonary vein repairs six point five percent, arterial
(05:41):
switch operations seven point one percent, interrupted arch repairs and
five point four percent nor woods. And what was still
true after a multivaried analysis was performed. Well, these were
the following factors that came out to be significant. First,
total anomalous pulmonary venus repair with an ODDS ratio of
times two point eight for the development of EAT. Second,
(06:03):
presence of De George syndrome with an ODDS ratio of
two point four. Third, presence of a surgery that was
at or above stat category four with an ODDS ratio
of two point one, and finally, longer bypass time with
an ODDS ratio of one point one. In the multivariate analysis,
heterotaxi was not a statistically significant risk factor for EAT.
(06:26):
And what about the EAT itself? What did the investigators
learn about post operative actopic atrial tachycardia Well, First, and
very interestingly, the onset of EAT was identified at a
median time of post operative day nine, with anti rhythmic
started at a median of ten days after surgery. During EAT,
the median initial ventricular rate was two hundred and eighteen
(06:47):
beats per minutent, with a median peak rate of two twenty.
The office treated eighty four percent of the eats with
the most common initial anti rhythmic agent being propranolol in
fifty six percent, followed by amiodoro in nineteen percent. Other
agents that were trialed included propranolol in seventy one percent,
amiodorone in twenty four percent, esmolal in nine percent, flecanide
(07:10):
in six percent, and amioterone in four percent. Nearly twelve
percent of patients who had ectopicatrial tachycardia ultimately died, but
the authors state that it was not implicated in the
death of any of these patients. In their discussion, the
author speak to why it seems that in this work
the incidence of ectopicatrial tachycardia was lower than in other
such works and wonder if their criteria for identification were
(07:32):
stricter in this study and therefore biased towards more worse cases.
They speak of how the only preoperative risk factor that
came out on multivaried analysis for EAT was the presence
of De George syndrome and state that the fact that
a number of factors were present in the univariate but
not multivaried analysis may suggest that intraoperative factors may be
(07:53):
relevant and difficult to assess as a cause. They also
speak about how younger patients were more affected and why
that might be, but wonder if they are just simply
more sensitive to physiological changes bypass runs or even electrolyte abnormalities.
The authors discuss how longer bypass and higher STAT levels
were more associated with actopic atrial tachycardia, and how longer
(08:15):
bypass in general is associated in other studies with more
post operative arrhythmias, and wonder if the larger number of
incisions and scars in a STAT four or five case
may have something to do with the development of ectopic
atrial tachycardia. They re emphasize how total anomalous pulmonary venus
connection was associated with EAT on multivariate analysis, with about
ten percent of these patients actually developing EAT. They also
(08:39):
mention how there are no data on inotropic agents in
this work and we therefore can't comment on the role
that they may play. The authors speak a bit about
why it might be that this arrhythmia is occurring so
late after surgery, and invoke ideas like gradual changes in
atrial stretch, late irritability of suture lines, late inflammation, but
they clearly state that they simply do not know. They
(09:01):
mentioned the substantial limitations of a single center study which
may be biased by selection bias, and how medical record
review can be fraught with error and bias, especially since
use of anti rhythmic agents was one of the way
that their databases were queried, therefore potentially biasing towards worse
cases in which medications were actually used. They mentioned the
absence of strips of EKGs in all patients to confirm
(09:25):
the diagnosis. They provide also a few more sources for
possible limitations of this work, and so they conclude in
conclusion THAPVC repair to George syndrome, higher stat categories, and
longer cardiopulmonary bypass times were identified as independent risk factors
for the development of EAT after congenital cardiac surgery in infancy.
(09:46):
The medium time to EAT diagnosis was nine days after
cardiac surgery with anti rhythmic medications started, a median of
one day later. Understanding the risk factors in natural history
VAT can help alert providers to monitor for its development
to begin anti rhythmic treatment when appropriate. Well I thought
this was an interesting paper mostly because it brings up
(10:06):
what is a finding that a lot of my colleagues
in the world of pediatric electrophysiology often speak about, namely,
what seems to be a major upswing in the amount
of postoperative atomic atrial tachycardia that we are all seeing.
No one seems to really understand why it's important to note,
as I do virtually every time I'm called to see
one of these patients that atomic atrial tachycardia used to
(10:29):
be considered to be an arrhythmia patients with structurally normal hearts.
I think that in the present era, though, it's still
true that a good percentage of these patients do have
structuring normal hearts, but I think we are all seeing
more eat amongst those who've had surgery than in the past. Additionally,
another finding of interest is the fact that these arrhythmias
seem to start a fair bit after surgery. Those who
(10:52):
know me on a day to day basis know that
I've implicated the near ubiquitous use of dex metatomidine. I
really can't prove it, but it does seem that this
agent seems to be very good at quieting automatic arrhythmias,
and we all know that there are a number of
works that have described its excellence as a primary or
adjunctive therapy for the treatment of junctional actopic tachycardia, another
(11:13):
automatic arrhythmia. We also know that discontinuation of this agent
is associated with sinus tachycardia, particularly when it's used for
a longish period of time, as is often the case
in the ICU. I'm unsure if the mechanism for this
is established, but given that sinus rhythm is an automatic
arrhythmia and EAT usually similarly automatic in most cases, I
(11:36):
can't help but wonder if the use of this agent
is in some way delaying the appearance of this arrhythmia
as it is weaned off, and also enhancing the risk
for it. Please note, and let me be very clear,
what I'm saying is highly conjectural, but I do wonder
why automatic arrhythmias that are usually seen at the time
of the highest degree of atronergic stimulation would only show
(11:58):
themselves late in the court following a big open heart surgery.
I am sure that many have noticed that they're seeing
jet now two to four days after surgery. Also, is
this a coincidence? I don't know, but for sure this
is something we should explore with the works author. Doctor Uniad.
Jonathan Uniat is a pediatric electrophysiologist at the Children's Hospital
(12:19):
of Los Angeles, University of Southern California. Doctor Uniat completed
his fellowship in Cardiology at USC Children's LA and went
on to perform Advanced Electrophysiology fellowship at USC with doctor
Janni Barcone and doctor Mike Silk, amongst others, and he
is now on faculty at that institution. It is a
great pleasure to have him join us on the podcast.
(12:40):
Welcome doctor Uniad to the podcast. I'm here now with
doctor Jonathan Uniat. Doctor Uniad, thank you very much for
joining us this week on the podcast.
Speaker 2 (12:48):
Thank you, doctor Pass for having me.
Speaker 1 (12:49):
Really great pleasure, very much enjoyed this work. Of course,
I'm an electrophysiologist, so of course I will. You know,
one of the most interesting aspects of this project in
general was the option that eat started on average more
than a week after surgery was done. I'm wondering if
you could speak to the possible reasons that you believe
this is the case. And I also wondered if you
(13:12):
thought the near ubiquitous use of preceducts may play a
role in this.
Speaker 2 (13:16):
Yeah, you know, thank you for the question. It's it's
a very interesting phenomenon that I think we've seen as
as to why this arrhythmia tends to rear its head
outside of the acute post operative period, you know, out
of time when the patients are de escalating their care,
already downgraded to our step down units, and then we
have this new arrhythmia to deal with, you know. I
think our hypothesis is that it's probably a combination of factors.
(13:40):
Like as is most things, such as I got gradual
change in atrial seture dilation or including a decrease in both,
some type of irritability for atrial future lines underlying anatomic substrate,
scar formation or even inflammation may potentially explain these late changes,
you know. I think we also can understand and appreciate
that at post operative inflammation from either cardiopome bypass or
(14:03):
even the body's one stress response is not an all
or none phenomenon. It can have gradiations, and as the
cardiac tissue or atial tissue in this case is healing
and adjusting to its new baseline, there may be a
window where the tissue has enhanced automaticity, sparking these automatic techycardias.
You know, your question about the use of presdcs is
(14:25):
also a very interesting one because it is also near
ubiquitously used here as well for post oxidation, And in
trying to answer this question, I think it's it's difficult
to comment on whether this use suppresses any early rhythmias
that made pre presence earlier in the course and subsequently
become more prevalent once the precedex is weaned, or if
(14:47):
there is some association between presedex u shits and then
the subsequent development of arrhythmias. And something that I've been
thinking about and I don't have an answer to is
you know, is there some type of autonomic modulation that
the presdex has on the atial tissue that could further
influence as automaticity. But this is you know, I think
(15:08):
me kind of thinking about the process of thinking about
the problem as opposed to having a definitive answer. Yeah.
Speaker 1 (15:14):
You don't have the opportunity at this moment to hear
what I said about this, because I've record the podcast
before I do the interview. But I really do believe
that there is some relationship between these two factors, because,
as you know, discontinuation of preceducts will enhance sinus tachycardia,
which is also automatic in nature, as is usually the
(15:35):
case with EAT. And I also have had the observation
that I mentioned earlier in this week's podcast that patients
with junctional topic tachycardia seem to be developing it a
little bit later than they used to. As well. It
was not uncommon in ancient times, like fifteen years ago,
that if someone had JET about three or four hours
(15:55):
after they got back from the o R, they would
start getting faster and faster. Now I've I've seen a
number of cases of people who developed JET five days
after surgery or three days after surgery, and I just
can't help but wonder if that might have something to
do with preceducts. But the jury is still add on.
As you say, this is all highly conjectural, so who knows. Yeah,
I was wondering if you had any thoughts on why
(16:17):
thab PVR was more associated with this arrhythmia.
Speaker 2 (16:22):
Yeah, you know, I've been thinking about this a lot
since we started looking at this for our paper specifically,
and because that seemed to be the highest independent risk
factor for the development of this arrhythmia. And I don't
know if I could come to a clear conclusion. You know,
I wonder about increased surgical intervention on the atrium, or
(16:43):
if there's some type of genetic predisposition or you know,
subsequent anatomic predisposition that could explain this. I've tried to
think about, you know, are there other types of significant
atrial stretch or d stretch or change that could explain
the increased automaticity? But again I don't know for sure.
(17:03):
I don't know for sure it is It is.
Speaker 1 (17:04):
Conjecture, mysterious question, a topic, you know. I know this
was not really the topic Jonathan, of your paper. But
of course whenever we talk to somebody from a really
great center, we always want to pick the brains and ask,
you know, how do you and your team, with doctor Silka,
doctor Yanni Barcone and all the other great doctors you
(17:27):
have there, how do you choose an anti arhythmic agent
for this a rhythmia? Do you have a general algorithm
of how you manage this? And how long do your
patients typically get treated when they're diagnosed in the postoff period?
Speaker 2 (17:39):
Yeah, thank you for that. You know, our initial preferred
choice is using some type of beta blocker, whether that's
either perparanolol or asthmolol, if the patient can't tolerate any
interraal medication. You know, we think we find and I
think those centers agree that patients tend to respond pretty
effectively and quickly to beta blockade and usually don't have
to escalate from there. You know. In our paper, obviously
(18:01):
there were some patients that needed for the escalation or
couldn't be started on a beta blocker for some type
of contray indication. And I would say our usual practices
if our patients are on significant chinotropic or press support,
or if there's other contraindications to using beta blockers, we
tend to lean on ambiodoronecks in our as kind of
(18:21):
our next line, understanding that post operative eat is usually
not a long term issue and that the antiremix can
be weaned off in the upcoming months after surgery. We
so most of patients.
Speaker 1 (18:35):
Are basically getting treated and then going home on anti
rhythmics with the thought that within the first couple of
months they'll potentially be weaned off.
Speaker 2 (18:44):
Is that right exactly? Yeah, And I think you know,
when we've looked at some of these patients, usually they're
weaned off in kind of the two to six month timeframe,
is what I've seen in kind of our documentation, and
that seems to be the usual course.
Speaker 1 (18:58):
Got it, got it?
Speaker 2 (18:59):
You know.
Speaker 1 (19:00):
Oh, although eat was not implicated in the actual death
of any patients, I thought it was noteworthy that over
ten percent of those who had eat ultimately died, presumably
from human dynamic reasons. Is there any evidence in your
data set regarding if the presence of EAT may be
a marker of those who are at higher risk for
(19:21):
a rougher post operative course.
Speaker 2 (19:24):
Yeah, you know, it was not evan in our data
whether that was true or not. But there was a
nice paper done by doctor Shamzad a little while ago
which did find a correlation of perioperative AHL tacacardia as
an independent risk factor for mortality after young infants go
undergoing pediatric cardiac surgery. So that data also was out
(19:47):
there by another group, which was interesting. We didn't find
that exact same finding, but you know, I think that
data is out there. I think something else that I
looked at and it didn't mention in the paper was
those that seemed to have eat outside of this typical
time window seemed to have more rocky courses, whether that
(20:09):
ends up in other interventions or you know, ultimately demise.
But and that's something that we were looking at as well.
Speaker 1 (20:19):
Well. I thought that probably since you mostly got your
patients from those who were treated, in terms of finding
the patients to do your study, probably they were in
general worser versions of EAT and maybe secret patients. But
it always seems that the EAT patient that needs treatment
as someone who's very sick, and you know, the last
(20:42):
thing they need is this on top of whatever else
they're dealing with. Well, for those of it in the audience,
it's right in the middle of doctor Uniat's day and
it was very nice of them to give us time.
So I'm going to finish up with one final question.
You know, you you showed a number of risk factors
for E A T. I was wondering, though, are there
are there any modifiable risk factors when we're thinking about
(21:04):
this arrhythmia. Can we use these data to try and
maybe prevent it in the first place.
Speaker 2 (21:10):
Yeah, No, it's a good question. I think, you know,
when we were coming to this is like, can't we
find anything that we can modify moving forward? Because I
think we would all like to have an answer outside
of our I guess I would say in the independent
risk factors that we identified, the major, I think modifile
risk factor that we could potentially intervene on is cardiopulmonary
(21:32):
bypass times. We showed that, you know, longer cardiopulmonary bypassed
times was an independent risk factor for the development of
post operative VAT. So shorter bypass run shorter surgeries should
should be able to decrease this arrhythmia burden.
Speaker 1 (21:48):
Yeah, of course that's almost impossible to effect, right, because
it's a longer. There's usually a darn good reason for it.
Speaker 2 (21:56):
Exactly.
Speaker 1 (21:57):
It takes a little longer to do tough things which
probably are more associated with this a arrhythmia, just like
you showed with thapbc Well at doctor Uniat. Great pleasure
to meet you, and congratulations to you and all of
your co investigators, and thank you so much for taking
time to speak with us this week on the podcast.
Speaker 2 (22:15):
Thank you doctor Pass for having me and I'm having
this great conversation.
Speaker 1 (22:18):
I appreciate it, great pleasure. Thank you. Well. I don't
think there's much to add to this week's conversation on
this topic, Doctor Uniat provided us with a number of
thoughts regarding eat following surgery and offered a few possible
causes for why we see it so late, as well
as a number of clinical pearls regarding its treatment. I'd
once again like to thank him for taking time from
(22:38):
his busy afternoon to speak with us on the podcast
this week. To conclude this replay episode of ped Heart
Pediatric Cardiology Today with doctor Jonathan Uniitt, we end with
a brief excerpt of a live recital from forty years
ago of the wonderful Mezso soprano Tatiana Treyanos, who is
from Queens, New York, and who was a daughter of
two professional singers. Herself started at Juilliard and ultimately sang
(23:02):
throughout the world, with her anchor and music being in
New York City at the Metropolitan Opera House. Tragically, she
died of cancer at the age of fifty four in
nineteen ninety three, but her legacy was a rich one
that is still well remembered amongst opera fans. Today we
hear her sing the Segudilla from Bezez's Carmen, which was
(23:22):
a role that many felt she was a definitive exponent
of thank you for joining me for this episode and
thanks once again to Doctor Union. I'll see you all
next week with a brand new episode.
Speaker 3 (23:46):
Basins An she next upper.
Speaker 4 (24:12):
Follow she knows a lot closer, so pass a looking fathers.
Speaker 1 (24:37):
It called us.
Speaker 5 (24:40):
A mother should the times, its costs.
Speaker 2 (24:56):
And sn a s
Hello everybody. This is Rob Pass, the host of the
Pdhart podcast. This week, we'll be reviewing an episode from
two years ago on post operative topic atrial tachycardia, a
vexing problem that we are all seeing with greater commonality.
I'll see you all next week with a brand new episode.
(00:32):
Welcome your Pdheart Pediatric Cardiology Today. My name is doctor
Robert Pass and I'm the host of this podcast. I'm
Professor of Pediatrics at the Icon School of Medicine at
Mount Sinai, where I'm also the Chief of Pediatric Cardiology.
Thank you for joining me for this two hundred and
seventy sixth episode of the podcast. I hope all enjoyed
last week's episode on the SVR three trial on hypoplastic
(00:55):
left heart syndrome. For those of you with an interest
in outcomes research specific in relation to hypoplastic left heart syndrome,
I definitely recommend you take to listen to last week's
episode with doctor Karen Goldberg. As I say every week,
if you'd like to get in touch with me, my
email is easy to remember. It's Pdheart at gmail dot com.
(01:15):
This week, we move on to the world of electrophysiology
to a topic I find quite interesting and that is
ectopic atrial tachy cardia following heart surgery. The title of
our work this week is Ectopic atrial Tachycardia in Infants
following congenital heart disease surgery. The first author of this
work is Jonathan Yuniat and the senior author is Janni Barkhone.
(01:36):
And this work comes to us from Children's Los Angeles
Department of Pediatrics in Los Angeles, California. When we're done
reviewing this paper, doctor Uniat has kindly great to speak
with us about it. Therefore, let's get onto this article
and then a brief conversation with its first author. This
week's work starts with some comments about a rhythmias following
(01:56):
heart surgery and children, with a very wide range of
prevalence in this patient group, ranging in some works as
low as seven percent to as high as forty eight percent,
likely reflecting different patient groups in different studies. However, they
make the point that any problem with rhythm in patients
who are postoperative and in low cardiac output states following
surgery can be particularly dangerous. Amongst a rhythmia is seen
(02:20):
a topic atrial tachycardia, which is typically referred to as
EAT or perhaps slightly less commonly, AET has been described
to occur in between eight and fifteen percent of those
undergoing congenital heart surgery, and the authors bemoan the fact
that there is little in the literature that reviews or
has identified obvious, reproducible risk factors for this arrhythmia. They
(02:42):
two points to smaller studies suggesting that lower weighted surgery,
longer bypass times, and single ventricles might identify higher risk patients,
and they also point to other works suggesting that those
with TAPVR transposition or even try a treasure ard an
increased risk. With this as a background, the team at
children sought to identify risk factors for the development of
(03:03):
post operative EAT in a large retrospective co order patients
less than a year of age at the time of surgery.
They also reviewed when the patients typically developed the EAT,
as well as the treatment and outcomes of those post
op EAT patients. This was a single center retrospective chart
review study at Children's LA from January two thousand and
seven till July twenty twenty. Patients had to be less
(03:26):
than one year of age, as this is the group
most affected by this arrhythmia. For this work, EAT was
defined as three or more consecutive non sinus atrial beats
that were faster than the age expected rates if the
pwave resembled a sinus pwave, something that vexes all pediatric
EP doctors. Other factors like the rates, the abruptness of
(03:47):
the initiation, a termination of the rhythm, things like that
were used to help diagnosis. The investigators reviewed the ECG's
and rhythm strips of those who were thought to have
EAT to confirm this diagnosis, and if a patient had
eat prior to surgery, they were not included. The patients
with EAT were naturally compared to similarly aged children who
had surgery at the same time but did not have EAT,
(04:10):
and on to the results well, eat was seen in
one hundred and twenty nine cardiac procedures, or two point
five percent of five thousand, three hundred and seventy two
operations performed in the study period. Interestingly, if a patient
with actopic atrial tachycardia had a period of quiescence of
the arrhythmia after the initial surgery, no such patient ever
(04:31):
had EAT at a subsequent surgery. In this cohort. Let's
start with some univariate comparisons. When comparing the patients with
EAT versus those without. The EAT group was generally younger
at the time of surgery seven days versus eighty five days,
and had a lower operative weight three point three kilos
versus four point two kilos, meaning smaller, younger patients more
(04:53):
risk of EAT. There were no gender differences, and patients
with EAT were more likely to have to George syndrome
seven point seven percent versus those without three percent, or
heterotaxy with asplenia seven percent versus two point seven percent.
And what about surgical factors that might be associated with eat? First,
cardiopulmonary bypass time. Those with a longer bypass time sixty
(05:18):
four minutes versus fifty nine minutes, and those who received
deep hypothermic circulatory arrest fifteen minutes versus zero minutes had
more EAT. Interestingly, there were no differences based on cross
clam times and were there any surgeries more associated with eat?
On univarid analysis, well, yes, nine point seven percent had
total anomalous pulmonary vein repairs six point five percent, arterial
(05:41):
switch operations seven point one percent, interrupted arch repairs and
five point four percent nor woods. And what was still
true after a multivaried analysis was performed. Well, these were
the following factors that came out to be significant. First,
total anomalous pulmonary venus repair with an ODDS ratio of
times two point eight for the development of EAT. Second,
(06:03):
presence of De George syndrome with an ODDS ratio of
two point four. Third, presence of a surgery that was
at or above stat category four with an ODDS ratio
of two point one, and finally, longer bypass time with
an ODDS ratio of one point one. In the multivariate analysis,
heterotaxi was not a statistically significant risk factor for EAT.
(06:26):
And what about the EAT itself? What did the investigators
learn about post operative actopic atrial tachycardia Well, First, and
very interestingly, the onset of EAT was identified at a
median time of post operative day nine, with anti rhythmic
started at a median of ten days after surgery. During EAT,
the median initial ventricular rate was two hundred and eighteen
(06:47):
beats per minutent, with a median peak rate of two twenty.
The office treated eighty four percent of the eats with
the most common initial anti rhythmic agent being propranolol in
fifty six percent, followed by amiodoro in nineteen percent. Other
agents that were trialed included propranolol in seventy one percent,
amiodorone in twenty four percent, esmolal in nine percent, flecanide
(07:10):
in six percent, and amioterone in four percent. Nearly twelve
percent of patients who had ectopicatrial tachycardia ultimately died, but
the authors state that it was not implicated in the
death of any of these patients. In their discussion, the
author speak to why it seems that in this work
the incidence of ectopicatrial tachycardia was lower than in other
such works and wonder if their criteria for identification were
(07:32):
stricter in this study and therefore biased towards more worse cases.
They speak of how the only preoperative risk factor that
came out on multivaried analysis for EAT was the presence
of De George syndrome and state that the fact that
a number of factors were present in the univariate but
not multivaried analysis may suggest that intraoperative factors may be
(07:53):
relevant and difficult to assess as a cause. They also
speak about how younger patients were more affected and why
that might be, but wonder if they are just simply
more sensitive to physiological changes bypass runs or even electrolyte abnormalities.
The authors discuss how longer bypass and higher STAT levels
were more associated with actopic atrial tachycardia, and how longer
(08:15):
bypass in general is associated in other studies with more
post operative arrhythmias, and wonder if the larger number of
incisions and scars in a STAT four or five case
may have something to do with the development of ectopic
atrial tachycardia. They re emphasize how total anomalous pulmonary venus
connection was associated with EAT on multivariate analysis, with about
ten percent of these patients actually developing EAT. They also
(08:39):
mention how there are no data on inotropic agents in
this work and we therefore can't comment on the role
that they may play. The authors speak a bit about
why it might be that this arrhythmia is occurring so
late after surgery, and invoke ideas like gradual changes in
atrial stretch, late irritability of suture lines, late inflammation, but
they clearly state that they simply do not know. They
(09:01):
mentioned the substantial limitations of a single center study which
may be biased by selection bias, and how medical record
review can be fraught with error and bias, especially since
use of anti rhythmic agents was one of the way
that their databases were queried, therefore potentially biasing towards worse
cases in which medications were actually used. They mentioned the
absence of strips of EKGs in all patients to confirm
(09:25):
the diagnosis. They provide also a few more sources for
possible limitations of this work, and so they conclude in
conclusion THAPVC repair to George syndrome, higher stat categories, and
longer cardiopulmonary bypass times were identified as independent risk factors
for the development of EAT after congenital cardiac surgery in infancy.
(09:46):
The medium time to EAT diagnosis was nine days after
cardiac surgery with anti rhythmic medications started, a median of
one day later. Understanding the risk factors in natural history
VAT can help alert providers to monitor for its development
to begin anti rhythmic treatment when appropriate. Well I thought
this was an interesting paper mostly because it brings up
(10:06):
what is a finding that a lot of my colleagues
in the world of pediatric electrophysiology often speak about, namely,
what seems to be a major upswing in the amount
of postoperative atomic atrial tachycardia that we are all seeing.
No one seems to really understand why it's important to note,
as I do virtually every time I'm called to see
one of these patients that atomic atrial tachycardia used to
(10:29):
be considered to be an arrhythmia patients with structurally normal hearts.
I think that in the present era, though, it's still
true that a good percentage of these patients do have
structuring normal hearts, but I think we are all seeing
more eat amongst those who've had surgery than in the past. Additionally,
another finding of interest is the fact that these arrhythmias
seem to start a fair bit after surgery. Those who
(10:52):
know me on a day to day basis know that
I've implicated the near ubiquitous use of dex metatomidine. I
really can't prove it, but it does seem that this
agent seems to be very good at quieting automatic arrhythmias,
and we all know that there are a number of
works that have described its excellence as a primary or
adjunctive therapy for the treatment of junctional actopic tachycardia, another
(11:13):
automatic arrhythmia. We also know that discontinuation of this agent
is associated with sinus tachycardia, particularly when it's used for
a longish period of time, as is often the case
in the ICU. I'm unsure if the mechanism for this
is established, but given that sinus rhythm is an automatic
arrhythmia and EAT usually similarly automatic in most cases, I
(11:36):
can't help but wonder if the use of this agent
is in some way delaying the appearance of this arrhythmia
as it is weaned off, and also enhancing the risk
for it. Please note, and let me be very clear,
what I'm saying is highly conjectural, but I do wonder
why automatic arrhythmias that are usually seen at the time
of the highest degree of atronergic stimulation would only show
(11:58):
themselves late in the court following a big open heart surgery.
I am sure that many have noticed that they're seeing
jet now two to four days after surgery. Also, is
this a coincidence? I don't know, but for sure this
is something we should explore with the works author. Doctor Uniad.
Jonathan Uniat is a pediatric electrophysiologist at the Children's Hospital
(12:19):
of Los Angeles, University of Southern California. Doctor Uniat completed
his fellowship in Cardiology at USC Children's LA and went
on to perform Advanced Electrophysiology fellowship at USC with doctor
Janni Barcone and doctor Mike Silk, amongst others, and he
is now on faculty at that institution. It is a
great pleasure to have him join us on the podcast.
(12:40):
Welcome doctor Uniad to the podcast. I'm here now with
doctor Jonathan Uniat. Doctor Uniad, thank you very much for
joining us this week on the podcast.
Speaker 2 (12:48):
Thank you, doctor Pass for having me.
Speaker 1 (12:49):
Really great pleasure, very much enjoyed this work. Of course,
I'm an electrophysiologist, so of course I will. You know,
one of the most interesting aspects of this project in
general was the option that eat started on average more
than a week after surgery was done. I'm wondering if
you could speak to the possible reasons that you believe
this is the case. And I also wondered if you
(13:12):
thought the near ubiquitous use of preceducts may play a
role in this.
Speaker 2 (13:16):
Yeah, you know, thank you for the question. It's it's
a very interesting phenomenon that I think we've seen as
as to why this arrhythmia tends to rear its head
outside of the acute post operative period, you know, out
of time when the patients are de escalating their care,
already downgraded to our step down units, and then we
have this new arrhythmia to deal with, you know. I
think our hypothesis is that it's probably a combination of factors.
(13:40):
Like as is most things, such as I got gradual
change in atrial seture dilation or including a decrease in both,
some type of irritability for atrial future lines underlying anatomic substrate,
scar formation or even inflammation may potentially explain these late changes,
you know. I think we also can understand and appreciate
that at post operative inflammation from either cardiopome bypass or
(14:03):
even the body's one stress response is not an all
or none phenomenon. It can have gradiations, and as the
cardiac tissue or atial tissue in this case is healing
and adjusting to its new baseline, there may be a
window where the tissue has enhanced automaticity, sparking these automatic techycardias.
You know, your question about the use of presdcs is
(14:25):
also a very interesting one because it is also near
ubiquitously used here as well for post oxidation, And in
trying to answer this question, I think it's it's difficult
to comment on whether this use suppresses any early rhythmias
that made pre presence earlier in the course and subsequently
become more prevalent once the precedex is weaned, or if
(14:47):
there is some association between presedex u shits and then
the subsequent development of arrhythmias. And something that I've been
thinking about and I don't have an answer to is
you know, is there some type of autonomic modulation that
the presdex has on the atial tissue that could further
influence as automaticity. But this is you know, I think
(15:08):
me kind of thinking about the process of thinking about
the problem as opposed to having a definitive answer. Yeah.
Speaker 1 (15:14):
You don't have the opportunity at this moment to hear
what I said about this, because I've record the podcast
before I do the interview. But I really do believe
that there is some relationship between these two factors, because,
as you know, discontinuation of preceducts will enhance sinus tachycardia,
which is also automatic in nature, as is usually the
(15:35):
case with EAT. And I also have had the observation
that I mentioned earlier in this week's podcast that patients
with junctional topic tachycardia seem to be developing it a
little bit later than they used to. As well. It
was not uncommon in ancient times, like fifteen years ago,
that if someone had JET about three or four hours
(15:55):
after they got back from the o R, they would
start getting faster and faster. Now I've I've seen a
number of cases of people who developed JET five days
after surgery or three days after surgery, and I just
can't help but wonder if that might have something to
do with preceducts. But the jury is still add on.
As you say, this is all highly conjectural, so who knows. Yeah,
I was wondering if you had any thoughts on why
(16:17):
thab PVR was more associated with this arrhythmia.
Speaker 2 (16:22):
Yeah, you know, I've been thinking about this a lot
since we started looking at this for our paper specifically,
and because that seemed to be the highest independent risk
factor for the development of this arrhythmia. And I don't
know if I could come to a clear conclusion. You know,
I wonder about increased surgical intervention on the atrium, or
(16:43):
if there's some type of genetic predisposition or you know,
subsequent anatomic predisposition that could explain this. I've tried to
think about, you know, are there other types of significant
atrial stretch or d stretch or change that could explain
the increased automaticity? But again I don't know for sure.
(17:03):
I don't know for sure it is It is.
Speaker 1 (17:04):
Conjecture, mysterious question, a topic, you know. I know this
was not really the topic Jonathan, of your paper. But
of course whenever we talk to somebody from a really
great center, we always want to pick the brains and ask,
you know, how do you and your team, with doctor Silka,
doctor Yanni Barcone and all the other great doctors you
(17:27):
have there, how do you choose an anti arhythmic agent
for this a rhythmia? Do you have a general algorithm
of how you manage this? And how long do your
patients typically get treated when they're diagnosed in the postoff period?
Speaker 2 (17:39):
Yeah, thank you for that. You know, our initial preferred
choice is using some type of beta blocker, whether that's
either perparanolol or asthmolol, if the patient can't tolerate any
interraal medication. You know, we think we find and I
think those centers agree that patients tend to respond pretty
effectively and quickly to beta blockade and usually don't have
to escalate from there. You know. In our paper, obviously
(18:01):
there were some patients that needed for the escalation or
couldn't be started on a beta blocker for some type
of contray indication. And I would say our usual practices
if our patients are on significant chinotropic or press support,
or if there's other contraindications to using beta blockers, we
tend to lean on ambiodoronecks in our as kind of
(18:21):
our next line, understanding that post operative eat is usually
not a long term issue and that the antiremix can
be weaned off in the upcoming months after surgery. We
so most of patients.
Speaker 1 (18:35):
Are basically getting treated and then going home on anti
rhythmics with the thought that within the first couple of
months they'll potentially be weaned off.
Speaker 2 (18:44):
Is that right exactly? Yeah, And I think you know,
when we've looked at some of these patients, usually they're
weaned off in kind of the two to six month timeframe,
is what I've seen in kind of our documentation, and
that seems to be the usual course.
Speaker 1 (18:58):
Got it, got it?
Speaker 2 (18:59):
You know.
Speaker 1 (19:00):
Oh, although eat was not implicated in the actual death
of any patients, I thought it was noteworthy that over
ten percent of those who had eat ultimately died, presumably
from human dynamic reasons. Is there any evidence in your
data set regarding if the presence of EAT may be
a marker of those who are at higher risk for
(19:21):
a rougher post operative course.
Speaker 2 (19:24):
Yeah, you know, it was not evan in our data
whether that was true or not. But there was a
nice paper done by doctor Shamzad a little while ago
which did find a correlation of perioperative AHL tacacardia as
an independent risk factor for mortality after young infants go
undergoing pediatric cardiac surgery. So that data also was out
(19:47):
there by another group, which was interesting. We didn't find
that exact same finding, but you know, I think that
data is out there. I think something else that I
looked at and it didn't mention in the paper was
those that seemed to have eat outside of this typical
time window seemed to have more rocky courses, whether that
(20:09):
ends up in other interventions or you know, ultimately demise.
But and that's something that we were looking at as well.
Speaker 1 (20:19):
Well. I thought that probably since you mostly got your
patients from those who were treated, in terms of finding
the patients to do your study, probably they were in
general worser versions of EAT and maybe secret patients. But
it always seems that the EAT patient that needs treatment
as someone who's very sick, and you know, the last
(20:42):
thing they need is this on top of whatever else
they're dealing with. Well, for those of it in the audience,
it's right in the middle of doctor Uniat's day and
it was very nice of them to give us time.
So I'm going to finish up with one final question.
You know, you you showed a number of risk factors
for E A T. I was wondering, though, are there
are there any modifiable risk factors when we're thinking about
(21:04):
this arrhythmia. Can we use these data to try and
maybe prevent it in the first place.
Speaker 2 (21:10):
Yeah, No, it's a good question. I think, you know,
when we were coming to this is like, can't we
find anything that we can modify moving forward? Because I
think we would all like to have an answer outside
of our I guess I would say in the independent
risk factors that we identified, the major, I think modifile
risk factor that we could potentially intervene on is cardiopulmonary
(21:32):
bypass times. We showed that, you know, longer cardiopulmonary bypassed
times was an independent risk factor for the development of
post operative VAT. So shorter bypass run shorter surgeries should
should be able to decrease this arrhythmia burden.
Speaker 1 (21:48):
Yeah, of course that's almost impossible to effect, right, because
it's a longer. There's usually a darn good reason for it.
Speaker 2 (21:56):
Exactly.
Speaker 1 (21:57):
It takes a little longer to do tough things which
probably are more associated with this a arrhythmia, just like
you showed with thapbc Well at doctor Uniat. Great pleasure
to meet you, and congratulations to you and all of
your co investigators, and thank you so much for taking
time to speak with us this week on the podcast.
Speaker 2 (22:15):
Thank you doctor Pass for having me and I'm having
this great conversation.
Speaker 1 (22:18):
I appreciate it, great pleasure. Thank you. Well. I don't
think there's much to add to this week's conversation on
this topic, Doctor Uniat provided us with a number of
thoughts regarding eat following surgery and offered a few possible
causes for why we see it so late, as well
as a number of clinical pearls regarding its treatment. I'd
once again like to thank him for taking time from
(22:38):
his busy afternoon to speak with us on the podcast
this week. To conclude this replay episode of ped Heart
Pediatric Cardiology Today with doctor Jonathan Uniitt, we end with
a brief excerpt of a live recital from forty years
ago of the wonderful Mezso soprano Tatiana Treyanos, who is
from Queens, New York, and who was a daughter of
two professional singers. Herself started at Juilliard and ultimately sang
(23:02):
throughout the world, with her anchor and music being in
New York City at the Metropolitan Opera House. Tragically, she
died of cancer at the age of fifty four in
nineteen ninety three, but her legacy was a rich one
that is still well remembered amongst opera fans. Today we
hear her sing the Segudilla from Bezez's Carmen, which was
(23:22):
a role that many felt she was a definitive exponent
of thank you for joining me for this episode and
thanks once again to Doctor Union. I'll see you all
next week with a brand new episode.
Speaker 3 (23:46):
Basins An she next upper.
Speaker 4 (24:12):
Follow she knows a lot closer, so pass a looking fathers.
Speaker 1 (24:37):
It called us.
Speaker 5 (24:40):
A mother should the times, its costs.
Speaker 2 (24:56):
And sn a s
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