Circulation Fellows-in-Training June 2018

 


Dr Carolyn
Lam:               
Welcome to Circulation on the Run, your weekly podcast summary
and backstage pass to the journal and its editors. I'm Dr.
Carolyn Lam, Associate Editor from the National Heart Center, and
Duke National University of Singapore. And I am joined today by
our Editor of Digital Strategies, Dr. Amit Khera from UT
Southwestern, as well as three wonderful fellows in training.
Yes, you've guessed it, it's our FIT Podcast and I'm just so
thrilled to be here again.


Dr Carolyn
Lam:               
Amit, any words of introduction before we start?


Dr Amit
Khera:                 
Thank you Carolyn. I think, for both of us, this is our favorite
podcast, or two podcasts, that we do, a year. It reminds us of
how bright the future is, with superb cardiology fellows in
training around the country, and it really is a testament to how
important we find fellows in training, to Circulation, to our
mission, and how much we learn from them.


                                               
So we're really excited about this group, today, and thank them
for participating.


Dr Carolyn
Lam:               
Absolutely. So, why don't we start, now, with ladies first? Let's
hear from Dr. Elizabeth Hill.


Dr Elizabeth
Hill:               
Thanks for having me today. My name is Beth Hill, and I'm a first
year cardiology fellow at Scripps Clinic, in La Jolla,
California. I've a particular interest in sports and exercise
cardiology, which brings me to the article I picked today about
sudden cardiac death and hypertrophic cardiomyopathy, hot topics
in the field and in general.


                                               
And so, today, I'm excited to be discussing the EVIDENCE HCM
study, looking at the hypertrophic cardiomyopathy of risk, sudden
cardiac death model.


Dr Carolyn
Lam:               
Nice. So tell us a little bit about what really struck you about
the paper and, perhaps, how that may apply to where you practice?


Dr Elizabeth
Hill:               
What I really liked about the paper is that, when I see patients
in clinic with hypertrophic cardiomyopathy, prior to having this
risk stratification tool, we didn't really have a way to
objectively risk stratify our patients with hypertrophic
cardiomyopathy and really guide the discussion about who may
benefit from an implantable cardiac defibrillator or ICD. And so,
I've been using this a little bit with my patients. While it
hasn't made it fully into the AHA or ACC guidelines yet, I'm
using it as a tool.


Dr Carolyn
Lam:               
Great. You know, these are seven risk factors, isn't it? I'm
always struck by that survival curve that really shows that those
with a predicted 6% risk stand out. Is that what you use, as
well, to guide your decisions?


Dr Elizabeth
Hill:               
Yeah. I think, as the authors noted, they picked this somewhat
arbitrarily so that they could study their risk model. But I
think what they found is that it seemed to fit well with the
observed high risk of sudden cardiac death cohort, such that
those that were seen and observed, about 9% risk of sudden
cardiac death in five years, were in that greater than 6% cohort.
So I think that population should receive ICDs, and that is one
factor that I used to guide my decision making as well.


Dr Amit
Khera:                 
Beth, this sort of interest that you've had for a long time, in
sports cardiology, I've noted you've done some prior work in EKG
screening and other screenings. In terms of this article
specifically, as you pointed out, this is a really helpful tool
because I still remember back when I was a fellow in training,
there was, sort of, this thought that everyone was high risk with
hypertrophic cardiomyopathy, and I think we realized that's not
true at all. The overall incidence of sudden death was only 2.4%
in this cohort.


                                               
The question I have for you, in terms of application, is, as
Carolyn pointed out, these are reasonably simple variables, but
as we sometimes are now using cardiac MRI and genetics and other
more advanced tools, where do you think they fit in, in the
current paradigm, since this is a bit of a more simplistic score?


Dr Elizabeth
Hill:               
The seven risk factors they put into this tool were noted to be
independently associated with an increased risk of sudden cardiac
death, and those are well known factors, entricular tachycardia,
maximum wall thickness. But I really do think that other factors
will come into play soon and are part of my discussion, and
colleagues' discussions, including the late gadolinium
enhancement on MRI, genetic factors, and I really think this may
be a place for tools like machine learning. These authors,
O'Mahoney and colleagues, they really did, kind of a
tour-de-force, going back to the 1970s, but there is still a
decent amount of data missing. So maybe we can partner with the
machines and help them go back into these records, a little bit
more effortlessly, and look at genetics, maybe some wearable
device data, and really refine our risk stratification tool
moving forward. But that's definitely something I use in risk
stratification in some of my intermediate risk patients.


Dr Amit
Khera:                 
Those are great points. I think your point about machine learning
and novel algorithms will definitely take foot in the future.


                                               
Maybe a follow-up, again, given your background interest, I think
it's a trade-off where we're trying to, of course, avoid sudden
death, but you also don't want to overtreat. Especially, when you
think about athletes getting ICDs and how that changes, or
anyone, for that matter, about maybe telling someone they're at
high risk, or giving them an ICD when perhaps they don't need it.
I guess that comes to, what's the threshold? Here they use 6%,
but that ends up being a bit arbitrary, in terms of what
threshold we use. And how do we decide, when we talk to our
patients, about what threshold's a right threshold to apply an
ICD?


Dr Elizabeth
Hill:               
Yeah. That's a great question. Like you mentioned, these devices
come with inherent risks, such as unnecessary shocks, increased
risks for infection, and sometimes there's restrictions with
athletic sport, although that's been changing recently.


                                               
But, I think that's where the shared decision-making process
comes into play, where you put current data on the table with the
patients and, perhaps, their families as well, and have a
risk-benefit discussion. Perhaps gather a little bit more data
about the patient, maybe follow them over time, but I guess I
wouldn't jump to put an ICD in, in every patient and, especially,
the lower-risk cohort. And what number that is, I'm not quite
sure. Here they say maybe less than 4%, but, again, somewhat
arbitrary, I think.


Dr Carolyn
Lam:               
Thanks Beth. I mean, as Amit said, it's just so inspiring to see
how the papers are being used in practice. Really loved those
perspectives.


                                               
Now, from sunny San Diego all the way to snowy New Zealand. We
have Dr. Mesfer Alfadhel. And Mesfer, tell us a little bit about
yourself, and the paper that you've chosen?


Dr Mesfer Alfadhel:       
Thank you very much. I'm thrilled to be part of this podcast. I'm
a second-year cardiology fellow-in-training at the Needham
Hospital, in Needham City, New Zealand, where it's snowing at the
moment. I'm also a clinical lecturer at the University of Otago
School of Medicine. I do have great interest in general
cardiology, as the rest of my colleagues, but also am passionate
about interventional cardiology and structural heart disease.


                                               
The paper I've chosen is really quite relevant to everyone in
cardiology, and perhaps extends to other colleagues in other
health professions impacted by automated external defibrillator
use on survival and functional outcomes in shockable observed
public cardiac arrest. The aim of the study was to determine the
association of bystander automated external defibrillator use,
the survival and function of outcomes in shockable observed out
of hospital cardiac arrests. The study was from 2011 to 2015 and
the Resuscitation Consortium prospectively collected detailed
information on all cardiac arrests at nine regional centers, six
in the United States and three in Canada.


                                               
They also found that among nearly 50,000 out of hospital cardiac
arrests, 8% were observed public out of hospital cardiac arrest,
of which 61% were shockable. Overall, a remarkable one in five of
shockable observed public out of hospital cardiac arrest were
bystander shocked. Now the bystander automated external
defibrillator observed, shockable observed public out of hospital
arrests were associated with increased odds of survival and full
or near full functional recovery almost 2.6 and 2.7 odds ratio
than when compared to emergency medical service defibrillation.
What's also interesting is that the longer the wait for the
emergency services, the higher the benefits from a bystander
observed shock.


Dr Carolyn
Lam:               
You know, Mesfer, I appreciate that you chose this one as well.
What struck out to me immediately was that more than 60% of out
of hospital cardiac arrests were shockable. And when we think
about the number of lives that could potentially be saved,
therefore, that's quite astounding, isn't it? But can I ask you
something? So these are in the US and Canada, how applicable do
you think this is to New Zealand?


Dr Mesfer Alfadhel:        We
do have a small population, just over four million. The number of
cardiac arrests here is around 2,000 out of hospital cardiac
arrests. And I think probably half of them in the latest reports
were shockable. The emergency response time in the urban areas is
around six minutes, which I think is acceptable, but we have
about 20% of population living in rural areas. And the emergency
response time exceeds 10 minutes almost all the time. I think
that probably a group that we need to direct intervention to in
New Zealand.


Dr Amit
Khera:                 
It's really an important article. I should say that June for the
American Heart Association is AED and CPR month so great choice
to remind us of the value of these and especially, the one thing
that was amazing, obviously this is an observational study, but
the absolute change, not relative, was about 14% meaningful
recovery and so that's quite impressive in terms of the number
needed to treat if you will. Maybe an adjunct to Carolyn's
question is, when we think about strategies to enhance bystander
AED use for strategies, essentially get the AED there faster. As
you know if the EMT time was not delayed it wasn't necessarily
better for the bystander.


                                               
We had a paper in Circ sometime last year looking at drones and
then also geocoding and other people in some countries have
looked at apps where you essentially can train a group of people
and then they can be texted for a sudden cardiac arrest in their
area. I'm curious about any creative things, there's always
training and AEDs, I think in this place it was public areas in
industry, but what do you think are some creative things or
things that we need to be doing to help enhance the ability for
bystander or early AED use.


Dr Mesfer Alfadhel:        I
think this is one area in medicine in general that where
technology is really going to advance how we deal with this
problem. There's an app that's available, it was launched in the
UK a few years ago and it’s become available in New Zealand in
the last two weeks called, the Good SAM. SAM stands for
smartphone activated medics. And it's become available in New
Zealand two weeks ago and I downloaded it and still yet wait for
it to be activated. And the way it works is you can activate a
medical emergency using the app and it dials the emergency
response but what it also does is it activates the nearest three
people with CPR training nearest to you and it tells you how far
they are from the emergency. Now if you don't have the app and
you call 911 or the equivalent, the operator can activate it to
the nearby personnel who have that experience. And I think it's
going to reduce the time markedly.


                                               
Now the other end of the question where some of what strategies
could be used I think we had a good report from Denmark where
they made changes in 2007 in Denmark and then followed by the
rest of the country in 2010 where they made CPR or resuscitation
education as compulsory at school but also when getting a driving
license they made courses available for free that increased the
number of defibrillators available in public places and they
shared that information with public. They’ve redone, audited
their work, and compared to prior to intervention prior to 2007
and after that and they found an increase number of using the
AEDs increased from somewhere around 2% to 15%, which is really
encouraging. I think we are following Denmark in that regard
probably at slower rate.


Dr Amit
Khera:                 
Thank you those are excellent insights.


Dr Carolyn
Lam:               
Amit, don't you see that I just love learning from these fellows
during these podcasts. We should do more of these. This is
awesome.


Dr Amit
Khera:                 
I completely agree.


Dr Carolyn
Lam:               
Thank you Mesfer, enjoy the skiing. But now from snowy New
Zealand we're going all the way to Nashville Tennessee. Welcome
Dr. Vineet Agrawal. So tell us a bit about yourself and your
paper.


Dr Mesfer Alfadhel:        So
my name is Vineet Agrawal. I'm a second-year cardiology fellow at
the Vanderbilt University Medical Center. My background is as a
physician scientist and as a general cardiologist. My long-term
goals are in understanding mechanisms underlying heart failure
with preserved ejection fraction.


                                               
With that in mind I was really taken by an article that was
recently by Margaret Redfield's group from the Mayo Clinic in
Circulation, titled “Global Pulmonary Vascular Remodeling and
Pulmonary Hypertension Associated with Heart Failure and
Preserved or Reduced Ejection Fraction.” I found this article to
be a very interesting, hypothesis-generating article.


                                               
In a nutshell what they did was they took an autopsy cohort of
patients in the Mayo Registry and those who had heart failure
with both preserved and reduced ejection fraction, normal
controls, and those who had a primary pulmonary venous occlusive
disease, and looked at the lung specimens of these patients. And
interestingly what they found was there was a significant amount
of pulmonary venous remodeling that had occurred in patients who
had both preserved and reduced ejection fraction. This correlated
not only with their right heart cath findings, so those who had
elevated pulmonary pressures and elevated transpulmonary
gradients, but also differed from the primary pulmonary venous
occlusive disease in the sense that the histologic appearance of
these vessels was quite different.


                                               
And while as an autopsy study this is not necessarily an article
that would immediately change practice, what I think it does do
though is it forces us to think about these conditions in a
different context and particularly with an eye towards future
therapeutics. Heart failure with preserved EF as a disease, as
I'm sure we all know, is sorely missing therapies that could
alter the disease progression and potentially even alter
mortality in these patients. And this article in my opinion
really sheds light on at least anatomically a new location for us
to think about as a therapeutic target when we try to better
understand this disease and find therapies for these patients.


Dr Carolyn
Lam:               
Vineet, can I just say you're singing to the choir here. I'm such
a fan of this work as well for obvious reasons. But hey, could I
ask you, in your clinical practice, do you see a lot of these
patients with HFpEF and pulmonary hypertension and wonder how to
treat them? And along those lines, how has this paper helped you
think about these patients more?


Dr Mesfer Alfadhel:        I
would say when I first started residency as a medical student
this was not necessarily a condition that was really something
that I had learned much about or felt like I had been exposed to;
however, as a resident I felt like most of the patients, or at
least half of the patients, I was seeing with heart failure had a
component of diastolic heart failure or they had a preserved EF
but very symptomatic from the standpoint of heart failure. And I
struggled to treat them, particularly in some part due to the
fact that many of the risk factors that contribute to HFpEF,
diabetes, uncontrolled hypertension, obesity, are chronic
problems that are difficult to manage as a clinician regardless.


                                               
And second because I feel that there just weren't any data to
support any treatments that we were pursuing at the time and so
we would try and apply what we had learned in other types of
heart failure to these patients with limited results. If I could
talk about what I think this article may change in terms of my
practice today, one thing that we've always thought about in
terms of pulmonary vascular remodeling in heart failure is that
it's just a passive process that as fluid builds up you back up
into the lungs and as the fluid builds up and backs up into the
lungs you get remodeling.


                                               
I think one thing that this article shows is that it may actually
be a bidirectional process, which would suggest that perhaps we
may need to reconsider looking at pulmonary-specific therapies in
this population. But more importantly I think it does confirm
that chronic elevating filling pressures do have an effect and a
deleterious effect on the pulmonary vasculature. Particularly
when you look at other trials such as the CardioMEMS trial, the
CHAMPION trial in which the data pretty convincingly showed that
as clinicians we don't do the best job of reducing left-sided
filling pressures in our patients with heart failure as much as
we think we do. This article really drives home the point to me
that I really need to make sure that when I see these patients
that I'm doing everything I can to reduce their left-sided
filling pressures because the consequences of not doing so can
affect the lungs, which can then in turn affect the heart as
well.


Dr Carolyn
Lam:               
Vineet, that's really words of wisdom. Couldn't agree more. And
these are the first sort of autopsy, histological evidence that
we have, which is so important. I think if I could just add a
couple of perspectives too, it makes me think about making sure
that I rule out PVOD in these patients sometimes. We now keep
thinking about HFpEF we forget that we need to also rule out PVOD
and the other thing much as we now think about not just the
filling pressures but the remodeling it's good to note that they
found it more in the venous than the arterial system, which also
comes therefore with a warning message that we can't just
extrapolate I suppose all the PAH therapies that we know about.
What do you think about that?


Dr Mesfer Alfadhel:        I
absolutely agree with that. It's really interesting that all of
our therapies from heart failure standpoint and from a PAH
standpoint have focused on the myocardium, the neural hormonal
cascade, and then the arterials. The pulmonary main artery and
arterials. I don't think anyone really understands the biology of
pulmonary veins and yet they're actually a pretty significant
part of our everyday practice in cardiology. Pulmonary veins are
thought to be the source of atrial fibrillation. We look at
pulmonary vein inflow when we evaluate patients with echoes. And
yet we understand so little about the biology and the mechanisms
by which pulmonary veins are affected in both diseased and
healthy patients.


                                               
I think this article for that reason raises a number of very
interesting questions and may potentially change the way we think
about these patients.


Dr Carolyn
Lam:               
I keep learning, Amit, this is awesome. I could go on forever so
you better stop me.


Dr Amit
Khera:                 
I should probably just be a fly on the wall. You must know
Carolyn is a HFpEF, HFrEF aficionado and you guys should have a
side call for another hour after this. But I do have one, maybe
orthogonal question which is, it's interesting because if you
look at how insights were made, they're made off areas I would
argue at least that we don't, modern environment uses much which
is the autopsy and probably to a large degree hemodynamics as
much as probably in the old days although that's changing. I'm
curious in a fellowship training program your exposure to autopsy
and kind of current in-depth hemodynamic-type training, what's
your experience?


Dr Mesfer Alfadhel:        Our
experience with looking at pathological slides, getting under the
microscope, seeing tissue first hand, is somewhat limited in our
fellowship training program. I would say in certain
subspecialties like our heart failure, advanced heart failure
subspecialties we do get a chance to see more myocardial biopsy
specimens, but I think increasingly the focus has been on
noninvasive methods by which we can assess some of these same
things that we used to do, use the microscope for. Invasive
hemodynamics I think similarly we get a lot of experience in
terms of spending time in the cath lab but I do kind of wonder if
we don't have the same in-depth training that we used to have in
understanding all the nuances of hemodynamics that used to exist
in the past.


                                               
Certainly, I think that while that's partially a reflection of
the way and the direction in which medicine is heading, there is
a little bit that's potentially lost there. That said, while we
have the benefit of manuscripts like this that does do in-depth
hemodynamics and looks at autopsy samples from a clinical
standpoint, if we were to ever try and understand this in a
larger population I think we would be required to try and find a
way to noninvasively or maybe through potentially invasive
hemodynamics better study this in live patients.


Dr Amit
Khera:                 
Appreciate that answer and I'm just for all of you, this has been
outstanding. You all have served as incredible expert
discussants. I know Carolyn already said it multiple times but
we've learned a ton about each of these articles and great to see
how they come alive and are used in practice and how they're
applied in your own thinking and specifically as fellows in
training with these have meant to you. We thank you all for
joining us and it's really been a fantastic experience.


Dr Carolyn
Lam:               
Amit, I can only echo your thanks and thank you listeners for
joining us today. Fellows out there you are so important to us.
Please, please apply to join us on the next FIT podcast as you
can see it's really fun.


                                               
Don't forget to join us again next week.