Circulation Fellows-in-Training Podcast

Dr Amit
Khera:                 
Welcome to Circulation on the Run, your weekly summary and
backstage pass to the journal. I'm Dr Amit Khera, associate
editor and digital strategies editor from UT Southwestern Medical
Center in Dallas. And I have the privilege of standing in for Dr
Carolyn Lam, your usual weekly podcast host. Today we have a
special treat. It is our semiannual fellows and training FIT
podcast. And the additional part of this treat is we have three
very special FITs today. These are our assistant editors for
social media for Circulation. And really I want to introduce you
just a moment, but I want to thank these three for their hard
work and efforts. It really is them that helped bring our social
media to life. And importantly for us, we really have a
commitment to enhancing fellow education involving fellows in our
editorial process and really making sure that the journal is
appealing to fellows in training. So we really rely on these
three to help us understand what best resonates and what is most
helpful for fellows in training. So without further ado, Jainy
Savla from UT Southwestern. Welcome Jainy.


Jainy
Savla:                        
Thanks for having me on the podcast today.


Dr Amit
Khera:                 
And we have Daniel Ambinder from Johns Hopkins University. Hi
Dan.


Daniel
Ambinder:            
Hey Amit. Thanks for having me on the podcast today.


Dr Amit
Khera:                 
Absolutely. And finally we have Jeff Hsu from UCLA. Hi Jeff.


Jeff
Hsu:                              
Hi Amit and hi everyone. Very glad to be here.


Dr Amit
Khera:                 
Well, Jainy, I'm going to start with you. You've been with us on
the social media side the longest. I think it's maybe almost a
year or a bit more that you've been working on these efforts. And
again, very much appreciate all of your hard work and insight.
Tell us a bit about yourself.


Jainy
Savla:                        
So I'm currently a research fellow at UT Southwestern. So I
completed my general cardiology training and I've been doing some
extra research training in one of our basic science labs there.


Dr Amit
Khera:                 
So not surprisingly with your background, do you select an
article? So we've asked them each to select one article as
they've been working through the social media side and see all of
our articles come through. Each to select one that they found was
interesting and perhaps summarize for us what it included and
what appealed to them. So Jainy, tell us a little bit about the
article you chose and why you chose it.


Jainy
Savla:                        
So, I chose one of the articles that was published in April of
2018 from the Molkentin team lab. And this is a basic science
article that focused on which types of cells contribute to heart
regeneration. They hadn't thought that there was cardiac
progenitor cell that could contribute to the development of new
cardiomyocytes. And more recent data has shown that maybe that's
not quite the case. So what this study did was used a lot of
fancy lineage tracing models to try to figure out which types of
cells we're actually contributing to the development of new
cardiomyocytes. So importantly, what came from this was that one
of their models, they were able to delete two transcription
factors that are necessary for cardiomyocytes to develop from
these progenitor cells. But they found that when they did that,
they even got a higher number of cardiomyocytes that formed. And
then what they were able to show in this paper was that actually
comes from fusion of leukocytes to cardiomyocytes. And then
interestingly, they found a role for one of these transcription
factors and the development of endothelial cells. So that was
kind of a new, not known function of one of these genes that was
previously thought to be just contributory to cardiac
development.


Dr Amit
Khera:                 
It's really a fascinating article when you think about it. Most
of the science we publish are people bringing to light new
discoveries and certainly there was a component of that here. But
in many ways, it was kind of a different article where there had
been this a prevailing thought about these c kit positive cells
and here they're actually had gone through, refuted what people
had thought was happening with these in this de novo
cardiomyocyte formation. So you'll see that very often where
people's articles or work is headed out to sort of maybe refute
or set right what's happening in the literature in the field. Can
you comment on that as to that type of article and how that
appealed to you in this study?


Jainy
Savla:                        
That is interesting because previously it has meant that these
cells can be used as a therapeutic option in human patients. But
some of them were recent data showed that perhaps the new
cardiomyocytes weren't actually coming from these cells, but it
was hard to say. So the nice part about this paper was really
they used a lot of important lineage tracing models to really
show where these cells are coming from. And it helped clarify
some of the, I guess, more confusing science that had been in the
field since there were a few papers that showed these cells were
contributary and then a few papers that have shown that maybe
they weren't. So I think that's really helpful, particularly when
you're talking about things that could be potentially used as
therapeutic agents in human. And also the interesting thing is
that while these cells themselves may not be useful to perhaps
harvest and give to someone, you could potentially alter these
cells and then they produce cells that fuse with cardiomyocytes.
Or could you use this a different way? So I thought that was also
interesting about this article.


Dr Amit
Khera:                 
Great points in it. It does remind us again that in our
enthusiasm for rushing things to clinical practices in some
things in this field, the importance of rigorous basic science to
really understand the molecular underpinnings. And as you
mentioned, there's some new insights here that could be used for
clinical therapeutic purposes in the future. So definitely an
interesting article and glad you enjoyed it and brought it to our
attention. I'm going to ask you a bit of a different question.
You again have been working with this in the social media side
for longer. You've seen this now for some time about the
different articles that come through. I know you and I've had
several conversations about our different platforms, Twitter or
Facebook, and how they're different and how we engage with them
and how we engage with the audience. Can you tell us a little bit
just reflecting now on your time and working with social media
from a journal perspective, kind of what you've learned? What are
some interesting observations over this year?


Jainy
Savla:                        
Definitely one interesting observation is just that their general
usage of these social media platforms has increased significantly
since I've started doing this. And you can see this with when we
get articles that are accepted, how many authors have Twitter
handles that they'd like to be tagged in some of these posts. And
that's just gone up significantly since I've started doing this.
And that also changes sort of what the comments we get on some of
the posts and the back and forth discussions that we're seeing on
these platforms. And then the second thing I found really
interesting over time is that the way people use Facebook is
really different from the way people use Twitter. And you can
follow the discussions that people have linked to our posts a
little bit better on Facebook. And then on Twitter, there's also
a lot of similar discussions about these posts. But they kind of
manifest in different ways and it's really interesting to see how
that plays out.


Dr Amit
Khera:                 
I think those are fantastic points. And from a fellow's
perspective, how do you think fellows are engaging with social
media now compared to maybe, I don't know, when you started your
training a few years back. What have you seen in a positive
light?


Jainy
Savla:                        
I mean in general, there are more fellows on Twitter now than
when I was a first-year fellow. Even myself, I've got my Twitter
account when I was in fellowship. I didn't have one prior to
that. I mean it's interesting because people are able to showcase
their work a little bit better I think with these types of
handles whereas before maybe you wouldn't know that even one of
your own co fellows had published something. So it's kind of nice
to see people use that kind of as a networking tool in some ways
or to showcase some of their own work, which is something that
when I was a first year and I didn't have a Twitter handle and
there weren't as many fellows on Twitter, I didn't really notice
some of the work that's being done by some of my colleagues at my
level.


Dr Amit
Khera:                 
Those are great points and I'll stoplight some of the things you
just said talking about it being a way for fellows to really
showcase their work, to help with networking and in some ways,
it's sort of the great equalizer. So I think it's really a
valuable platform specifically for fellows. Well thank you Jainy.
I'm going to move on to Daniel and hear a little bit from Daniel.
Tell us a bit about yourself.


Daniel
Ambinder:            
I'm currently a second year cardiology fellow at John's Hopkins
Hospital and I plan on doing interventional and structural
cardiology in the future.


Dr Amit
Khera:                 
Great and certainly a lively and growing field and so many
exciting things happening. Well, it's interesting you chose an
article today that is more of a clinical article and obviously
quite different than the last one we heard, but equally as
interesting. Tell us a little about the article you've chose and
why you chose it.


Daniel
Ambinder:            
I was very excited about this article that was published in
Circulation back in July 2018. So, it's by Dr Borlaug and Reddy
on how to diagnose HFpEF and what they did was they took patients
with clinical dyspnea and they used invasive human dynamics to
kind of assess whether or not they had HFpEF. And by doing so
they were able to generate a list of clinical and eco based
guidance to help us kind of identify patients with heart failure
with preserved ejection fraction. So they came up with this
amazing little table which was featured in Circulation and on
Circulation twitter, where they have a chart that basically goes
through several clinical variables including weight and
hypertensiveness, atrial fibrillation, pulmonary hypertension,
being elderly. And filling pressure is based on echo
cardiographic information. And by that they were able to generate
a score and give you a probability of if your patient has HFpEF
or not.


                                               
And the reason why I really enjoyed reading this article and also
posting this article was because going through internal medicine
and not being so fundamentally aware of echo and kind of what
goes into understanding left ventricular filling pressures, it
was challenging to make a diagnosis of heart failure with
preserved ejection fraction. Do you just basically say, "My
patient has lower extremity swelling but normal EF? They have
heart failure with preserved ejection fraction and [inaudible
00:09:32] on the [inaudible 00:09:33]. And so I thought that this
would be really helpful to the medical community at large. And in
fact, shortly after we posted it, I saw that our cardiology
console fellow is actually utilizing this exact table to help one
of the medicine teams manage a patient with lower extremity
swelling and come to the diagnosis of heart failure with
preserved ejection fraction. So that is why I chose this article
for today.


Dr Amit
Khera:                 
That's a great article and I thought you summarized it very well.
And it is a field. HFpEF you'd see a lot of articles in
Circulation on this topic. We have many people that are
interested from an editor’s level but also from a society level.
This is a huge problem, but we know very, very little. And I'm
sure you know that as well and this was a wonderful tool. Just
shows you're sort of the beauty and simplicity. Although if you
read it, the message were pretty rigorous and they had a lot of
great work that they did to develop it. But I love that the H2
HFpEF, how they basically came up with it h for heavy and the f
from fibrillation. So I thought that was incredibly creative and
a very simplistic but useful score. So, you said your, tell us
about yourself. Have you used the H2 of the HFpEF score yet?


Daniel
Ambinder:            
Absolutely. I use it in clinic on a daily basis. And I actually
pull up the Tweet in my office and show the patients why I think
that they have heart failure preserved ejection fraction,
especially since many of my patients start to get really nervous
when you start talking about heart failure. But then they don't
understand that they have a normal functioning heart. They can't
really put those two together. And so going through this chart
and going through the etiology, or at least what we know about
heart failure with preserved ejection fraction, turns out to be
quite helpful.


Dr Amit
Khera:                 
And the basis of this study goes back to hemodynamics. This
obviously is a cohort where they had done invasive hemodynamics
to essentially diagnosed HFpEF based on pressure. So as you, as
someone who's going interventional and structural where we are
really seeing kind of the rebirth or refocus on hemodynamics
again, tell me a little bit like what you're learning in terms of
hemodynamics and how you think that importance in today's
practice of cardiovascular medicine.


Daniel
Ambinder:            
One of my passions is spending as much time as I possibly can in
the cardiac ICU. And we're fortunate to meet many different
patients that come in with very different kinds of cardiogenic
shock for other hemodynamic compromise from other types of shock.
And I have found it extremely helpful to think about either using
a virtual Swan or by actually getting the measurements with a PA
catheter to kind of identify where the break in the system is to
hopefully provide our patients with the ability to turn them
around in a fast manner before they develop metabolic compromise
from prolonged hypoperfusion.


Dr Amit
Khera:                 
Great summary of how you're using hemodynamics and the training.
And I'm going to pivot. The last question for you is when we
first met I think several months back and we're communicating
about your interest in social media, one thing that was really
interesting and fascinating was the great work you're doing on
Twitter on your own account where you essentially, if I think you
told me this right, you sit on your iPhone and basically in this
matter of a very few minutes would construct cases and teaching
points on Twitter. So tell me a little bit about that, about
using Twitter for medical education and learning cardiology and
cases. And I know you're passionate about that. So tell us a
little bit more about that.


Daniel
Ambinder:            
Back in May, last year, I had been in my first year of cardiology
fellowship. And I was really kind of obsessed with grabbing as
much imaging and cases as I could to construct them into teaching
stories to share these important stories that I encounter with
other people. And so also share the aha moments that I have when
I'm learning from my mentors about a new clinical condition or
even a clinical condition that I've encountered many times. We
never thought about any unique way. And so I was putting these
all together and developing somewhat of a library of cases. But I
would share them with the residents that I was working with at
the time. And then Dr Erin Michos was one of my mentors at
Hopkins. She's an echocardiographer and she kind of exposed me to
the Twitter community where you're really able to just start
reaching out to different people and share the same insights that
I had saved on my drive on my computer. And so I started
constructing these cases, putting that together and developing
them and then associating them with like a few bullet pointed
tidbits of pearls that I can put on Twitter. And I quickly
realized what an amazing community Twitter have to offer in terms
of cardiology and in terms of the medical education community at
large.


                                               
At first, I realized you can't put out content and not expect to
participate in a conversation. It has to be two ways. You have to
really engage with others and others will engage with you. And
then just a couple months later, it's really grown that you can
post a case, post the teaching pearl and in about 24 hours it can
be viewed thousands and thousands of times, really
internationally. And generates just so much great conversation.
So it's been really a tremendous way to communicate with the
world, especially within the cardiovascular world.


Dr Amit
Khera:                 
Well thanks. I think there's so much learning that can happen and
I think the work you're doing with cases and with others. And I
know when I've gone on Twitter, even in just two minutes you can
see really fascinating things and learn a lot. So keep up the
good work and appreciate your efforts there. I'm going to switch
gears and finally finished with Jeff Hsu from UCLA. Jeff, tell us
a bit about yourself.


Jeff
Hsu:                              
I'm a fellow at UCLA. So I actually finished my general
cardiology fellowship pretty recently and now I'm a research
fellow in the STAR program here. I'm also enrolled in the PhD
program at UCLA in the Department of Physiology and planning to
defend in the next few months. So right now, very stressed out
about that. Starting in July, I'll be starting advanced
fellowship in advanced heart failure and transplant here at UCLA.


                                               
Well excellent and best of luck to you in your PhD defense. Now
you also chose a very interesting article that again, all of
yours are a bit different. So tell us a little about the article
you chose and why you chose it.


                                               
When I chose this article, I was really excited by a few weeks
ago. It was published in the December 4th issue of Circulation
called Determining the Pathogenicity of a Genomic Variant of
Uncertain Significance Using CRISPR/Cas9 and Human Induced
Pluripotent Stem Cells. So this came out of the lab of Joe Wu at
Stanford and the co first authors is Ning Ma, Joe Zhang and
Ilanit Itzhaki. But I think the beauty of this article is that it
really addressed this frustrating clinical scenario in question
that we often encounter nowadays in this era of genome
sequencing. And now that we're sequencing a lot more people,
since the cost of sequencing has come down a lot, we were finding
a lot of these mutations that we don't know what to do with, so I
think Dr Wu's lab really try to address this question using the
disease model with the cardiomyopathy. So, leveraging Dr Wu's
expertise in using human induced pluripotent stem cells or iPSCs,
they found a patient who is actually healthy but apparently had
this mutation in this gene called MYL3 or myosin light chain 3.
And so this patient had a variance of uncertain significance in
this gene.


                                               
Now, notably, this patient, again had no clinical phenotype, was
very healthy and the patient's family members over three
generations were all healthy too. But had this mutation that
based on in silico analyses was thought to be likely pathogenic.
So using cells from this patient that they reprogrammed into
cardiomyocyte, they tested various properties of these cells from
the same patient to see whether or not they thought this mutation
is actually a pathogenic mutation. So again, using these
reprogrammed cardiomyocytes, they tested a variety of things
including gene expression, sarcomere structure, and cell
contractility, action potentials, and the handling of calcium.
And they saw that even with this mutation, there were no abnormal
findings in vitro in their system.


                                               
Now just to prove that their cell culture system and this in
vitro model of testing the pathogenicity of certain mutations
actually works, they actually took cells from a patient who did
have the clinical phenotype as a result of a known mutation that
causes hypertrophic cardiomyopathy. And found that when testing
those cells in vitro, they did demonstrate abnormal phenotypes in
all the parameters I mentioned before. So I thought this is
really exciting. I thought this is a great way to address,
potentially answer whether or not we think these variants of
uncertain significance that we often encounter are indeed
pathogenic because we are often just left in this situation where
we don't know what to do with this information. But this
potentially at least is a proof of concept for this protocol
where we can finally take advantage of the ability to take cells
from our patient and actually test them in the lab to see whether
or not either various treatments work or whether or not these
mutations that actually will results in pathology down the line.
So I thought overall this was a great paper that was a great
summary of how we can take the bedside to the bench actually. And
I'm just really looking forward to the future where we can maybe
then bring it back to the bedside.


Dr Amit
Khera:                 
Well thanks. I think that's an excellent choice and a great
summary. And this article really hit all of the kind of timely
and cutting-edge topics in the era genomic medicine and precision
medicine have really kind of individualized treatments. And when
we get stuck, these VUSes, these are a nightmare. And also this
is sort of proof of concept for extending this to other
treatments and other ways to test drugs and therapies. I've heard
Joe, we talk about this before and use the word disease in the
dishes. He did I think in the article itself and it's exactly
that. I mean the potential here is profound. I'll pivot this into
the next question for you. For our roles, one thing we do is we
interact a lot with media and I interact a lot with them to help
translate, I guess, the articles that we have to things that
would be able to be digestible for media and for lay individuals.
It was interesting because it's hard for us to do that with basic
science and most of the time we have some difficulty in
translating that. But this one translated pretty well and I think
we had done some various press releases and things because it
really showed the potential of modern medicine and kind of the
excitement of it.


                                               
But that gets to the question I have for you, something we have
discussed as well, your interest in basic science and some of the
challenges of taking basic science articles and digesting them
down to a couple hundred-word tweet. Even as beautiful as all the
pictures are, and in this article I think there's six figures,
but each panel is 10 pictures or 10 figures by themselves. And
how do we digest basic science articles down to make them really
appeal to people on social media and help people understand that
may not be in the fields or in basic science that are clinicians,
if you will. I know you've thought about that a little bit. Tell
me a little bit about your thoughts on that.


Jeff
Hsu:                              
Jainy, Dan and I have this challenge on a weekly basis, figuring
out how to summarize great articles such as this one into a short
tweet. And I think that is a big challenge particularly for basic
science articles on social media to make it appeal to a broader
audience because the audience you're seeing on Twitter and
Facebook, again, they're not just basic scientists. If you want
to catch people's attention, you need to find a way to really
understand the big picture of the question you're answering in
your basic science research. So I think that is a challenge.
You're challenged to make your science appealing to a broader
audience. But I think again, that's one of the advantages of
social media is that you can appeal to a larger audience and have
a wide range of people engage with your research and understand
your research. So it is something that we work on is to try to
pick out the figure that best represents the science that was
done in these basic science articles.


                                               
It can be quite challenging because a lot of times one picture
won't do it justice. So it's tough to distill a full article in
one picture. It is helpful when some articles do have a summary,
a graphic or figure where they typically reserve their last
figure for either a cartoon or some type of schematic that really
explains either the mechanism or pathway that they explored in
their article. So what we've found is that these articles that do
have some of these illustrations or summary figures, they seem to
engage a larger audience on Twitter and social media. So
personally I find it more appealing when I do see these summary
figures. So if there is one recommendation, I would have the
basic science researchers, especially trainees is in this age of
social media, try to come up with an illustration or summary
figure for your research. I think it helps you figure out what is
truly important with the research that you've done and helps you
communicate this research to a broader audience. And I've seen a
lot of people take advantage of a graphic designers to really
help them illustrate their research. And I found that to be very
effective in articles I've read on social media.


Dr Amit
Khera:                 
Thanks Jeff. That's a great point and great suggestion. And
certainly these days the most effective communicators are those
they can translate their complex science into easily digestible
bites and can think of ways to portray them in ways that sort of
summarize, like you said, be it summary figures or otherwise. And
it's a challenge and also talent. And you all are certainly
perfecting that. Well, I think we've had an excellent
conversation. I have to tell you, I'm so excited to get the
chance to spotlight you all. You do excellent work each day.
Every week you're working hard and coming up with great ideas and
suggestions and we really value having your input as fellows and
training and as a colleague.


                                               
Thank you for joining us today on our FIT podcast. Amit Khera
standing in for Carolyn Lam. We look forward to seeing you for
our next edition of Circulation on the Run. This program is
copyright American Heart Association 2018.