November 28, 2023 • 31 mins
Join our host, Ohio-ACC President Dr. Kanny Grewal, and guests Drs. Ankit Bhatia and Gregory F. Egnaczyk, both from The Christ Hospital in Cincinnati, as they discuss the practical management of acute decompensated heart failure (ADHF) - including clinical assessment, classification, acute therapies, candidacy for advanced therapies. They then review the current clinical role for left ventricular assist devices (LVADs) including patient selection and current outcomes.
For more information, see Durable Mechanical Circulatory Support: A JACC Scientific Statement from the ACC.
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Episode Transcript
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Kanny (00:11):
So welcome back to the cardio Ohio podcast.
I unfortunately don't have my cofellows helping me out today,
but I am honored to have acouple of excellent guests from
Cincinnati, Ohio.
We're going to focus today onacute heart failure.
We've had some previoussessions.
dealing with chronic heartfailure.
(00:31):
But I really am proud to have acouple of specialists with acute
heart failure that are going totalk us through some of the key
clinical points and also talkabout candidacy and management
of patients with device therapyas well.
First, I'd like to welcome Dr.
Ankit Bhatia.
He is at the Christ Hospital inCincinnati.
(00:52):
He's a heart failure specialist.
So first of all, Ankit, welcome.
And second of all, do you mindjust taking a minute and telling
us a little bit about the paththat brought you to Cincinnati
and also what led you intospecializing in advanced heart
failure?
Ankit (01:08):
Thanks so much for having us, Kenny.
Hey guys, I'm Ankit Bhatia.
As, as Kenny mentioned, I workhere at the Christ Hospital as
an advanced heart failuretransplant cardiologist.
My path starts in Syracuse, NewYork.
I'm a diehard Syracuse Orangefan.
My parents were both professorsthere, grew up there, and then
made my way to University ofChicago for med school, and then
(01:29):
finally landed in WashingtonUniversity in St.
Louis for both my generalcardiology and advanced heart
failure fellowships.
After that, made my way toCincinnati where my wife was
born and raised, and had a greatexperience here at the Christ
Hospital.
We were both in LBAD in thetransplant program.
And my clinic specificallyfocuses more on some of the
(01:51):
genetic cardiomyopathies andhypertrophic cardiomyopathy more
so, but see all sorts ofpatients.
And it's been a great experiencebeing here.
Kanny (02:00):
Great.
Well, we're happy to have you inOhio I'd also like to welcome
actually your partner, Dr.
Gregory Ignacek, who is known toa lot of clinicians in
Cincinnati, also a heart failurespecialist.
And in fact, the medicaldirector of advanced heart
failure at the Christ Hospital.
I understand you have an endowedchair as well.
So Greg, welcome.
(02:20):
And can you just tell us alittle bit about your trail into
Cincinnati and into yourspecialty as well?
Greg (02:26):
Yeah, thanks, Kenny, really much for having us here
tonight and honored to be here.
So, yeah, I went to medicalschool, did an MD PhD at
University of Cincinnati.
I'm actually from Connecticutoriginally.
And then met my, my, my now wifethere in Cincinnati, but I
brought her out to Boston andthat was just only.
when it comes to takingCincinnatians out of their home
(02:48):
state.
So fortunately I've, I've madeamends and brought her back to
Cincinnati after doing trainingin Boston and then down at Duke.
And then as, as a fellow, I wasreally drawn to advanced heart
failure.
from the perspective of thecomplexity of the patients and
really the amazing saves that wecan do.
We see these patients at death'sdoor and we can find ways to
(03:10):
kind of, you know, resuscitatethem with either LVAD and or
heart transplant and really makethese miraculous recoveries.
And that was very muchattractive.
And that complexity and thescientific underpinnings drew me
to advanced heart failure.
Now that was as a fellow, as youbecome an attending.
Then it's your responsibility totake care of these people and
(03:30):
that, and that's a fair, can bea fairly stressful time.
It could be a time filled withdifferent long, hard family
discussions and also thepalliative care, which is an
important part of what we do inadvanced heart failure.
So I think that aspect of thingsin the humanity that we, we get
engaged with as, as these peopleare nearing.
(03:50):
End of life is really been aprivilege, and I think it's been
a good balance between theamazing science and therapies
that we can deliver, but alsoreally Being part of these
families lives after they'reafter we care for them.
So thank you for inviting ushere tonight.
Kanny (04:06):
Yeah, great So welcome to both of you So as I mentioned at
the beginning, we've had apodcast, with some great heart
failure doctors talking aboutchronic Heart failure in terms
of state of the art medicalmanagement.
So we really wanted to focustoday on, especially from the
standpoint of the generalcardiologist, because, as you
know, we have an audience ofgeneral cardiologists, cardiac
(04:28):
specialists, but it's also quitea few advanced practice
providers and fellows intraining.
Obviously, it doesn't matterwhat specialty or area of
cardiology practice youencounter acute heart failure on
a daily basis.
You don't have to be asubspecialist to see a lot of
heart failure, especiallyworking as a consultant in a
hospital.
(04:48):
So, from that perspective,Ankit, I thought I would just
start by asking you.
When you, as a consultant,approach a patient with either,
confirmed acute heart failure ora suspected heart failure, or
even undefined, hypotension orshock, going into an evaluation
like that, what's the kind ofclassification that you're
trying to categorize thesepatients into to kind of, get an
(05:11):
initial assessment and start tothink about therapy?
Ankit (05:16):
Thanks, Kenny.
And it's a great questionbecause really, many times we're
seeing patients that arerelatively undifferentiated.
And, heart failure, we considerkind of a catch all term for the
inability of the heart toadequately pump blood flow to
the body or having to do so atthe expense of high filling
pressures and kind of broadlykind of summarizing.
I know most folks will know thisalready.
(05:37):
We break it up as half path forbasically heart failure
preserved ejection heart failurewith deduced ejection fraction
even below 40 percent and thenmid range if in between.
And the reason we break that upis that really our therapeutic
approaches vary and the evidenceas to what works between the
various types of heart failuredoes vary as well.
(05:59):
So when I'm seeing a newpatient, first I want to
characterize that in my mind.
What kind of heart failure dothey have?
And for the purposes of ourdiscussion, we'll focus more on
the heart failure with systolicdysfunction, since that's where
a lot of the evidence lies interms of advanced heart failure
therapies.
So when I first see a patient, Iwant to know first, is this a
new diagnosis I'm seeing, or isthis a patient that's on chronic
(06:21):
medical therapy?
If it's a new diagnosis andthey're treatment naive, I'm
much more willing in thosecircumstances to start them on
good guideline directed medicaltherapy, the meds that we know
have been proven to makepatients with systolic
dysfunction live longer and givethem quality of life.
Those are, just to review foreveryone, beta blockers ACE
inhibitors, ARBs, or now ARNImedications, including Entresto,
(06:45):
which has come standard of carein that class, mineralocorticoid
receptor antagonists, andfinally, now most recently,
SGLT2 inhibitors.
And I'll try to get them onthese therapies if they're able
to tolerate it.
Well, that's first off, but andso, so beyond defining kind of
new versus chronic I then wantto know in the moment, assessing
them, what is their volumestatus?
(07:07):
How are they doing clinically?
Do they appear well compensatedor not?
And there's two parts of that towhat I consider.
I consider first theirperfusion.
Do we, do I feel like they'readequately perfusing their
organs or not?
As, as sort of a marker of lowoutput or not.
And then secondly, do I feellike their volume status is
adequate for not?
And that's going to help todefine therapy there.
(07:29):
And that can, in terms offurther kind of elucidating
that, we can look at end organmarkings of perfusion, we look
at things like LFTs, we look atcreatinine to help us define
that, and we think about thepatient's history as well.
And then from there, we kind ofdevelop a management strategy.
But that's kind of how Iapproach it is, is this de novo
or is this chronic?
(07:50):
Do we think they have a chanceat medical therapy or do we
think they're failing medicaltherapy at that point?
And then finally assessing thesituation clinically, how are
they doing in terms of theircurrent compensation status?
And are they adequatelyperfusing or not?
And that's about that's the wayI can define what the urgency is
and the next step forward totaking care of them.
Kanny (08:11):
That's great.
Thanks.
Now, as an image and specialistmyself, you know, obviously, I
know imaging plays a criticalrole in that initial assessment,
especially as you're trying tocategorize.
The patient Greg, maybe you canjust summarize, you know, how do
you, how do you useechocardiography to help,
(08:31):
confirm or classify that initialdecompensated patient?
And is there any other imaging,that would really be relevant in
that very acute phase ofassessment?
Greg (08:42):
Yeah, echoes is the echocardiography is definitely
the mainstay, and we cancertainly.
Besides the ejection fraction,which kids told us, told you all
how it classifies our heartfailure, it also can help
hemodynamically in terms offilling pressures by diastolic
parameters, it can help usunderstand if there's
interventions for thesepatients.
(09:03):
Once we kind of stabilize themagain, decongestant is their
valvular disease that we canintervene on.
We have great percutaneoustherapies now, both for the
valve mitral valve, and then asit's evolving the tricuspid
valve as well.
And so then it also helps usknow about the right ventricle
and we know some of the worstoutcomes that we see in any
patient population, be itpreserved or reduced ejection
fraction, common patients thathave significant RV dysfunction
(09:26):
and with its correlate pulmonaryhypertension.
So I think you can glean a lotthat helps you know the right
direction and take your patientin by the echocardiogram.
Kanny (09:36):
So, Ankit, you mentioned about, you know, clinical
assessment at the bedside.
I think, obviously, we're alltaught as consultants to look
for, for example, signs ofreduced end organ perfusion, in
a cardiogenic shock patient.
But do you have any pearlsabout, like, what specifically
would indicate a very worrisomeor high risk patient that may be
decompensating and may be acandidate for more advanced
(09:58):
therapy in terms of whatspecific, indicators of low
perfusion would raise, youralarm the most?
Thank you.
Ankit (10:06):
Kenny, I'm really happy to bring that up because as much
as we are reliant on moreadvanced kind of diagnostics
now, you know, bedside exams,the first thing we have, and we
often have to use that moreurgent situations as all we
have.
So, you know, when we thinkabout perfusion, you know, I'm
sure many of you guys have seenthe 2 by 2 table.
warm and wet versus cold anddry.
(10:26):
The first thing I think I thinkabout in terms of confusion is,
you know, to assess them onexam, look at the, look at their
physical exam.
Do they feel warm or do theyfeel cold?
And that in and of itself is notterribly specific, but a good
place to start.
And then looking at their volumestatus, looking at things like
JVP, looking at for things likeascites by physical exam, lower
extremity edema as as kind of abetter way to determine where
(10:47):
they lie on that table.
And then in terms of symptoms,You know, low output is
something that's been veryhumbling to me because it's kind
of presented in many forms.
Many times it's someone that hasslowed down gradually over time.
People with a cardiac index of1.
are not always you know, incardiogenic shock, there are a
lot of people sitting with lowoutput for a long period of time
(11:10):
as an outpatient till I get to acritical tipping point, make
their way in the hospital.
So have they been slowly, youkind of slowing down over time,
getting more lethargic and youngpeople, especially abdominal
discomfort or nausea, vomitingcan be a common sign of both
hyper like hyper bulimia as wellas low output as well.
And we've seen multiple examplesof folks in cardiogenic shock
(11:33):
with that being the presentingsymptom.
So that's kind of what I go onis if I have some of these
concerning symptoms that I seeor an exam that's concerning, we
then go straight to thediagnostics, including
laboratory testing, as well aspsychocardiograms to kind of
better determine where thatpatient lies and kind of where
they are in this, in kind ofseverity of what needs to be
(11:54):
treated.
If from there you then seeindications of malperfusion by
labs, which we talked aboutcreatinine LFTs, lactate,
whatnot, too.
I think that's enough from thereto saying that this is not just
low output, but shock, which bydefinition requires
malperfusion.
And then that escalates into theneed for inotropes.
and potential mechanicalcirculatory support.
(12:16):
So all of a sudden the severityhas gone up and I think we can
talk about more about how totreat
Kanny (12:20):
shock from there.
Absolutely.
And I'm glad you brought uptherapy because, as a general
cardiology consultant I thinkone thing that can be
overwhelming at times, or atleast challenging is just the
decision to initiate, IV therapywith inotropes or.
Vasopressors, but also thechoice of therapy.
So, how do you approach thatdecision to both start a
(12:44):
vasoactive medication and thenhow would you, make that initial
decision about what agent to
Ankit (12:49):
start?
So when I'm thinking about apatient that's low output,
another thing that can be veryhelpful if you have it is a
right hard cath, either with aleave in swan or, you know, just
a single time assessment todetermine low output or not.
If you if you have a clinicalindication of patient is low
output and At that point, theapproach is you can start an
(13:12):
inotropic medication, which canbe beneficial to kind of help
the patient better perfuse.
And so the two options that youhave are that the primarily are
dobutamine and milrinone.
These are both inotropicmedications that work by
different mechanisms.
Milrinone is a medication thatcan.
better, better producedafterload reducing effects.
So a patient that's morehypertensive, for example, or a
(13:34):
patient with elevated pulmonaryvascular resistance, Milrinone
may be the better choice there.
But the important thing to notewith Milrinone is it is cleared
by the kidneys.
So with patients withsignificant renal dysfunction,
it can accumulate and becometoxic and lead to worsening
hypotension.
So Milrinone is something thatWe often avoid in patients that
do have fairly severehypotension.
The other option is dobutamine.
(13:55):
Dobutamine is a pure betaagonist that has less effect on
blood pressure and then moreworks to increase contractility.
As a result, though, it'sslightly more arrhythmogenic, so
it may not be the best choicefor a patient that has worsening
ventricular or atrialarrhythmias.
But those are the two inotropicchoices to go on.
And then If either of them arenot possible or inadequate to
(14:18):
provide adequate support toheart, that's when we consider
mechanical circulatory support.
Kanny (14:23):
So as you talk about mechanical support what are,
like, kind of the key clinicalindicators in a decompensating
patient that start to push youtowards, using support more
urgently?
And a related question would be,in a setting that's maybe not a
(14:44):
tertiary center, what are someof the clinical indicators that
you would suggest that may beearly transfer to, a tertiary
center with advanced therapycapabilities would be advisable.
Ankit (14:57):
So, you know, broadly talking about that definition of
shock.
If a patient is in cardiogenicshock, I view inotropes as a
temporary means to helpstabilize the patient.
And if a patient really ishaving indications of end organ
perfusion, especiallytheförmative Determined by right
heart catheterization and bytheir, and by their labs, I
(15:18):
would consider at that pointstarting an inotrope and then
considering transfer to a centerthat can provide mechanical
circulatory support or placingit where you are there.
We've seen too many examples,unfortunately, of patients that
get temporarily supported ondobutamine, but then have an
arrhythmia and then are furtherdecompensated.
But for folks that are failing,failing inotropes.
(15:39):
Or require a more permanent, amore durable long term form of
mechanical support as weconsider the next option,
whether that be LVAD ortransplant or anything along
those lines, we got a coupleoptions.
So first off, and mostconventionally, you've got the
balloon pump.
And, and that, that can take acouple forms that can go into a
(15:59):
femoral vessel or an axillaryvessel.
And that provides, you know, asmaller amount of cardiac
output, conventionally, youknow, 0.
5 to 1 liter.
but has been shown to be muchmore effective in chronic heart
failure.
So a patient that's had chronicheart failure for a long time
and is now decompensated, kindof going to slow simmer or burn
of cardiogenic shock, that is anoption if a patient requires, if
(16:20):
you think a patient requiresmore cardiac support beyond what
a balloon company will provide,which is oftentimes the case in
cardiogenic shock anotherapproach is an impella, which is
basically a peripheral LVAD inthat way that kind of sits in
the left ventricle and, anddirectly supplies blood crossing
the aortic valve to the aorta.
And that comes in a couple offorms.
(16:41):
The most common forms used inshock are the impella CP, and
which can be placed by bothfemoral as well as axillary
approach.
And then finally, The mostcommon device that we use at
Christ specifically because ofits durability and the amount of
flow it can provide, is theImpella 5.
5, which is a device that candeliver over 5 liters of cardiac
output and is surgically placedto axillary.
(17:03):
And that's been our main devicethat we use when considering
patients for LVAD and transplantthat requires stabilization, but
that varies from center tocenter.
Finally, in a patient withsevere cardiogenic shock, where
it's clear that the other formsof mechanical circulatory
support would be inadequate, wecan consider VA ECMO.
(17:24):
And you know, this is somethingthat you consider in a
circumstance, but notnecessarily want to push towards
because it's something that hasits own cadre of associated
complications that can come withit.
But it is the most.
Robust form of mechanicalcirculatory support that we have
to support a patient in the mostsevere form of shock.
Kanny (17:45):
Great.
That's helpful to know.
So just so our listeners know,Greg did have to drop off to
attend to an urgent patientmatter.
We hope to have him back soon.
But in the meantime, I'd get,just to transition in our last
10 minutes we have, to talk inmore detail about durable, left
ventricular assist devices.
(18:05):
Most of us are familiar withLVADs.
Some of us are fortunate to workat centers where LVADs are
implanted.
Others maybe not.
I think a lot of us have kind ofa more traditional view of what
patients will benefit fromLVADs, but I know that's evolved
a lot in recent years.
So what specifically,especially, let's start with the
(18:29):
acutely decompensated patientwho's maybe recovering, but it's
still unstable.
What kind of clinical scenariosor indicators would then lead
you to think that, a moredurable assistive device.
Could be either a bridge to arecovery or, ultimately
transplant.
Ankit (18:48):
So, yeah, Kenny, that's a great question.
And when I think about I reallythink about the patient journey.
Oftentimes, many times thesepatients are diagnosed.
They're put on good guidelinedirected medical therapy.
They might get a mitra clip.
They might get a CRT.
And then eventually over time,you start to see that many of
these patients begin to failthose therapies, they start
(19:08):
getting hospitalized, they startgetting hypotensive with
inability to tolerate theirmedical therapy, their ejection
infections go down.
So when I'm seeing a patientthat's coming in for a
decompensated heart failureadmission, even if they're not
in shock, I'm thinking aboutthat as an escalation or
worsening of severity of theirillness.
We know that one heart failurehospitalization is roughly a 30
(19:31):
percent one year mortality.
Three heart failurehospitalizations in a year is
roughly 50 percent one yearmortality.
So when you're starting to see apatient that's failing medical
therapy and beginning to getadmitted.
Thank you.
For it.
That's the time to be thinkingabout L bad.
And then on the on the on theother side, as you mentioned,
the patient that is that ispresenting with cardiogenic
(19:53):
shock, meaning that they're nottheir heart is not able to
provide adequate blood flow totheir organs, and they need
potentially a form of mechanicalcirculatory support, like a
balloon pump or an impella to toguide their therapy.
The first thing you want toconsider there, again, is do you
think it's a recoverablephenomenon?
Do you think, was this anischemic insult that we expect
some improvement?
(20:14):
Was this myocarditis that weexpect to get better?
But if that's not the case, andthey're failing medical therapy,
that is the time to think aboutLVAD or transplant.
And that is a decision thatmaybe we won't go get into too
much, but What we do know aboutLVAD specifically is that it's
been proven to make patientswith advanced heart failure who
are failing medical therapy livelonger and give them better
(20:36):
quality of life.
And sometimes I worry that ourmessaging for LVAD isn't all
that clear as to how goodpatients can feel and how well
they do.
Because it's, you know, kind ofseen as this, this mechanical
device you got to carry aroundbatteries and whatnot.
But it's really, what we know isthat it does make people feel
better and live longer, and it'ssomething that we need to kind
(20:58):
of look at more when a patient'sotherwise failing medical
therapy.
Kanny (21:03):
Yeah, and just as an aside, the, the JACC did put out
a scientific statement this yearin the Journal of the ACC
regarding LVADs.
And durable devices, and it's anexcellent review, by the way,
and I'm going to put the link tothat in the notes to this
session.
But they did point out that, themost recent outcome data with
(21:25):
heart made 3 showed, you know,87%.
Survival that was basically onpar with heart transplant, and
I'm not sure, if all cliniciansreally Understand how much the
survival has improved.
Do you think that's because oftechnique or reduction in
adverse events or better patientselection?
Ankit (21:45):
I think it's all the above, you know, with the most
recent HeartMate 3 pump, many ofthe complications that we've
seen with traditional pumpsprior to this, which included,
you know, pump thrombosis withthe older HeartMate 2s and
HVADs, ischemic stroke.
Those have significantlyimproved with the most recent
heart made three device.
We still we still run intocomplications, including G.
(22:07):
I.
Bleeding, given the fact thatthese patients do need
anticoagulation right heartfailure and infection that have
occurred at similar rates versusprior.
But on the whole, what we knowwith the most recent heart made
three pump in the data that wasprevented in the momentum three
trial Is that mortality hasimproved substantially and so is
(22:27):
quality of life.
We just got five year data thatshows a 60 percent five year,
five year survival, which isastounding as to where we were
and comparing to what thesepatients would otherwise have
living with advanced heartfailure.
Kanny (22:41):
Yeah.
So having said that, do youthink the candidacy of patients
who will qualify for LVADs isgonna, is expanding or has
expanded or, or, and do you seethat broadening in the future,
you know, in terms of.
Who would be a candidate for adurable therapy?
Ankit (22:59):
So what we know is when we're thinking about advanced
heart failure therapies, rightnow, heart transplant has a
finite number that can beprovided hearts that can be
provided to patients.
So that's a number that'srelatively static, and it may
increase with other means ofobtaining organs, but.
That's going to be relativelystable, but we are seeing a
larger number of patientspresenting with advanced heart
(23:21):
failure as our population ageshere.
And so, what I'd say is, is thatthe best an LVAD patient can do
is if they go into the OR asoptimized as possible.
And given the advances that wehave in mechanical circulatory
support and other means ofstabilizing patients.
We can optimize them better thanwe have before so that they can
(23:43):
do better.
And even over the course of myrelatively young medical career
at this point, I've seen usbegin to push the limits in
terms of implanting patientsthat are older, that have more
comorbidities just because wehave the ability to stabilize
them better.
I think the other thing we'realso doing better is on the post
VAD side, we've come to realizethe importance of a team
(24:03):
approach.
We have a an amazing team hereat Christ of LVAD coordinators
that are training families andeducating facilities on best
practices, and that's helping toprevent things like driveline
infections, adherence tomedication, and we all know
these things are very important.
So, to answer your question,yes, I do think we're beginning
to push the limit and expand thepool of what we consider to be a
(24:24):
candidate just because we have,we've had so many advances in
this space.
Kanny (24:31):
Great.
So Greg welcome back.
Yeah.
Greg (24:34):
Sorry about that.
I appreciate it.
We'll see when you, you hireyoung, smart physicians, like
I'm kid, I just can sit back andlisten and learn.
So it's but get back in theconversation
Kanny (24:45):
here too.
Yeah, you don't want to let apodcast recording get in the way
of good patient care.
So, but we were talking aboutLVADs Greg, but one question I
had for you in your practice atChrist is, just in general,
what's the distribution ofimplants now between patients
where you generally feel that,you want to get them to a
transplant versus what you wouldconsider, just durable therapy
(25:09):
with the LVAD?
Greg (25:11):
Yeah, that's a great question, Kenny.
So really what's happened sincethe allocation systems changed
that the indication for bridgeto transplant has really almost
disappeared.
And with that, we're, most ofthe times that we're doing it,
LVADs are for a bridge tocandidacy, where at the current
time when we see these patientsin the hospital or out of the
hospital they're, they're not acandidate for the transplant.
(25:34):
It might be a contraindicationthat's modifiable.
It might be something liketobacco abuse, and they need to
spend some time, or it might besomething like pulmonary
hypertension.
with an LVAD that comes down, orobesity, or it can be just
concern about psychosocial riskfactors for, so we do you know,
probably 50%, I would say, are,are these bridged to candidacy,
(25:55):
that we think they're going tobe a candidate, but right now,
in this moment in time, they'renot.
And then the other 50 percentend up being this sort of, this,
their, the destination therapycategory, where they will spend
the rest of their lives with thedevice.
And these are often the olderpatients.
The ones that have significant,you know, kidney disease and
lung disease and other issuesthat we think they're probably
not going to get to the point oftransplantation.
(26:17):
And so that's the usualbreakdown.
Now, I know there's a lot ofinterest in the indication of
bridge to recovery, and in realworld, that's a pretty low
percentage of where peopleactually get to the point of
explanting the pumps, butthere's certainly a lot of
research and single centerexperiences when you.
take a very selected group ofpatients.
We can increase that singlecenter.
(26:38):
I'm sorry, that real data numberof 1 percent to 2 percent
recovery to explant to maybe 10percent or even higher.
So I think those kind of would Igive you sort of a general sense
of the indications for when weuse the LVAD.
Kanny (26:52):
Sure, sure.
And just in our last couple ofminutes here, Greg For those of
us, obviously, that don'tdirectly participate in
implanting or caring for theLVAD patients, as you think
about patients, and we all havesuccess stories, I think, in our
practices or at our institutionsof patients that have gone, you
know, several years with adevice and for the most part
(27:15):
stayed out of the hospital.
Do you have a sense about, like,what specific Is it mostly
clinical factors that wouldpredict a good response like
that, or is it social support,or is it, you know, a potpourri
of factors that go into yourdecision making as to, this
particular patient is probably,at least has a good chance of
surviving several years withtheir device?
Greg (27:37):
Yeah, it's a really complex.
sort of decision making thatrequires a team like Ankit said,
but we, we have this pump thatwe have now, the heartbeat three
is very forgiving and theirsurvival data is improving.
We're now getting out to, youknow, 55 percent survival for
five years.
So.
These people are living longer.
They're living with greatquality of lives and fewer
(27:59):
advance adverse events.
And so really, as we evaluatethese patients, if we get to a
patient that is really all theother organ systems look pretty
well intact.
And that they have and so thatwe look as we evaluate these
patients, we look at other endorgans and making sure there's
no irreversible damage there.
(28:20):
We, and we look at theirfrailty, how strong they are to
get through a procedure.
And really what we've seen is,which is part of the way we're
pushing the envelope is thatwe're taking these patients that
are sicker and more frail.
And actually pre rehabilitatingthem before the surgery with
these percutaneous pumps,especially the impella five
fives, just has really changedthe landscape for us in terms of
(28:43):
its durability, its ability tohave people on the support for
weeks leading up to the LVAD oreven transplant to the point
that we can get these peoplestronger.
And then that's chance watchthem and see if that frailty,
which is such a.
difficult thing to assess.
And there's lots of research interms of how and being more
objective about it.
(29:03):
But can we start seeing thosefrailty domains improve while we
take care of a patient in theICU to the point that we think
we can get them through thesurgery?
Then that final componentevaluation is the psychosocial,
which is, is challenging too.
And it may be as these pumpsbecome less for, you know,
become more forgiving that wecan take patients that can be
more independent and live bythemselves and not have
(29:25):
caregivers.
As as intimately involved asbefore, so I think that's
another place where we see allthat therapy expanding is people
being a little bit moreindependent in their in their
lives.
Afterwards.
Kanny (29:38):
That's great.
And then just very briefly, isthere still an upper, a strict
upper age cut off where youfocus it more on frailty and
other clinical factors todecide, you know, candidacy?
Greg (29:48):
Yeah, unfortunately, you know, I think for us, there's
been kind of a soft ceiling of80 and, Anybody over 75 really
looks their age once you getthem in the OR and
cardiopulmonary bypass.
So frailty is important andthere is a chronologic age,
which is biologic, but over 75they have to look really good
(30:08):
and over 80, we really haven't,we haven't ventured into that
ground.
Other places have in the worldbut for us, it's been kind of
80.
Kanny (30:17):
Great well, unfortunately, we're up against
our recording time here.
I thought it was a greatdiscussion.
I think we covered a lot in 30minutes.
I really want to thank both ofyou for taking time to educate
us also for your contributionsto the state chapter.
I know you're on the faculty forour recent meeting.
My only final question for youis that I'm a 50 year.
(30:39):
Plus Ohio resident and lifelongsports fan.
Do you think the Bengals canactually bring a championship to
the state of Ohio before Iretire?
Ankit (30:48):
Well, we're hoping on this year,
Kanny (30:50):
so we'll see.
Awesome.
Well, thank you both forparticipating and I hope to have
you back soon and also in othercapacities for our state
chapter.
Thanks again to both of you.
Thank you for joining today'spodcast.
For more information about thespeakers or the topics, please
go to Ohio acc.org,
So welcome back to the cardio Ohio podcast.
I unfortunately don't have my cofellows helping me out today,
but I am honored to have acouple of excellent guests from
Cincinnati, Ohio.
We're going to focus today onacute heart failure.
We've had some previoussessions.
dealing with chronic heartfailure.
(00:31):
But I really am proud to have acouple of specialists with acute
heart failure that are going totalk us through some of the key
clinical points and also talkabout candidacy and management
of patients with device therapyas well.
First, I'd like to welcome Dr.
Ankit Bhatia.
He is at the Christ Hospital inCincinnati.
(00:52):
He's a heart failure specialist.
So first of all, Ankit, welcome.
And second of all, do you mindjust taking a minute and telling
us a little bit about the paththat brought you to Cincinnati
and also what led you intospecializing in advanced heart
failure?
Ankit (01:08):
Thanks so much for having us, Kenny.
Hey guys, I'm Ankit Bhatia.
As, as Kenny mentioned, I workhere at the Christ Hospital as
an advanced heart failuretransplant cardiologist.
My path starts in Syracuse, NewYork.
I'm a diehard Syracuse Orangefan.
My parents were both professorsthere, grew up there, and then
made my way to University ofChicago for med school, and then
(01:29):
finally landed in WashingtonUniversity in St.
Louis for both my generalcardiology and advanced heart
failure fellowships.
After that, made my way toCincinnati where my wife was
born and raised, and had a greatexperience here at the Christ
Hospital.
We were both in LBAD in thetransplant program.
And my clinic specificallyfocuses more on some of the
(01:51):
genetic cardiomyopathies andhypertrophic cardiomyopathy more
so, but see all sorts ofpatients.
And it's been a great experiencebeing here.
Kanny (02:00):
Great.
Well, we're happy to have you inOhio I'd also like to welcome
actually your partner, Dr.
Gregory Ignacek, who is known toa lot of clinicians in
Cincinnati, also a heart failurespecialist.
And in fact, the medicaldirector of advanced heart
failure at the Christ Hospital.
I understand you have an endowedchair as well.
So Greg, welcome.
(02:20):
And can you just tell us alittle bit about your trail into
Cincinnati and into yourspecialty as well?
Greg (02:26):
Yeah, thanks, Kenny, really much for having us here
tonight and honored to be here.
So, yeah, I went to medicalschool, did an MD PhD at
University of Cincinnati.
I'm actually from Connecticutoriginally.
And then met my, my, my now wifethere in Cincinnati, but I
brought her out to Boston andthat was just only.
when it comes to takingCincinnatians out of their home
(02:48):
state.
So fortunately I've, I've madeamends and brought her back to
Cincinnati after doing trainingin Boston and then down at Duke.
And then as, as a fellow, I wasreally drawn to advanced heart
failure.
from the perspective of thecomplexity of the patients and
really the amazing saves that wecan do.
We see these patients at death'sdoor and we can find ways to
(03:10):
kind of, you know, resuscitatethem with either LVAD and or
heart transplant and really makethese miraculous recoveries.
And that was very muchattractive.
And that complexity and thescientific underpinnings drew me
to advanced heart failure.
Now that was as a fellow, as youbecome an attending.
Then it's your responsibility totake care of these people and
(03:30):
that, and that's a fair, can bea fairly stressful time.
It could be a time filled withdifferent long, hard family
discussions and also thepalliative care, which is an
important part of what we do inadvanced heart failure.
So I think that aspect of thingsin the humanity that we, we get
engaged with as, as these peopleare nearing.
(03:50):
End of life is really been aprivilege, and I think it's been
a good balance between theamazing science and therapies
that we can deliver, but alsoreally Being part of these
families lives after they'reafter we care for them.
So thank you for inviting ushere tonight.
Kanny (04:06):
Yeah, great So welcome to both of you So as I mentioned at
the beginning, we've had apodcast, with some great heart
failure doctors talking aboutchronic Heart failure in terms
of state of the art medicalmanagement.
So we really wanted to focustoday on, especially from the
standpoint of the generalcardiologist, because, as you
know, we have an audience ofgeneral cardiologists, cardiac
(04:28):
specialists, but it's also quitea few advanced practice
providers and fellows intraining.
Obviously, it doesn't matterwhat specialty or area of
cardiology practice youencounter acute heart failure on
a daily basis.
You don't have to be asubspecialist to see a lot of
heart failure, especiallyworking as a consultant in a
hospital.
(04:48):
So, from that perspective,Ankit, I thought I would just
start by asking you.
When you, as a consultant,approach a patient with either,
confirmed acute heart failure ora suspected heart failure, or
even undefined, hypotension orshock, going into an evaluation
like that, what's the kind ofclassification that you're
trying to categorize thesepatients into to kind of, get an
(05:11):
initial assessment and start tothink about therapy?
Ankit (05:16):
Thanks, Kenny.
And it's a great questionbecause really, many times we're
seeing patients that arerelatively undifferentiated.
And, heart failure, we considerkind of a catch all term for the
inability of the heart toadequately pump blood flow to
the body or having to do so atthe expense of high filling
pressures and kind of broadlykind of summarizing.
I know most folks will know thisalready.
(05:37):
We break it up as half path forbasically heart failure
preserved ejection heart failurewith deduced ejection fraction
even below 40 percent and thenmid range if in between.
And the reason we break that upis that really our therapeutic
approaches vary and the evidenceas to what works between the
various types of heart failuredoes vary as well.
(05:59):
So when I'm seeing a newpatient, first I want to
characterize that in my mind.
What kind of heart failure dothey have?
And for the purposes of ourdiscussion, we'll focus more on
the heart failure with systolicdysfunction, since that's where
a lot of the evidence lies interms of advanced heart failure
therapies.
So when I first see a patient, Iwant to know first, is this a
new diagnosis I'm seeing, or isthis a patient that's on chronic
(06:21):
medical therapy?
If it's a new diagnosis andthey're treatment naive, I'm
much more willing in thosecircumstances to start them on
good guideline directed medicaltherapy, the meds that we know
have been proven to makepatients with systolic
dysfunction live longer and givethem quality of life.
Those are, just to review foreveryone, beta blockers ACE
inhibitors, ARBs, or now ARNImedications, including Entresto,
(06:45):
which has come standard of carein that class, mineralocorticoid
receptor antagonists, andfinally, now most recently,
SGLT2 inhibitors.
And I'll try to get them onthese therapies if they're able
to tolerate it.
Well, that's first off, but andso, so beyond defining kind of
new versus chronic I then wantto know in the moment, assessing
them, what is their volumestatus?
(07:07):
How are they doing clinically?
Do they appear well compensatedor not?
And there's two parts of that towhat I consider.
I consider first theirperfusion.
Do we, do I feel like they'readequately perfusing their
organs or not?
As, as sort of a marker of lowoutput or not.
And then secondly, do I feellike their volume status is
adequate for not?
And that's going to help todefine therapy there.
(07:29):
And that can, in terms offurther kind of elucidating
that, we can look at end organmarkings of perfusion, we look
at things like LFTs, we look atcreatinine to help us define
that, and we think about thepatient's history as well.
And then from there, we kind ofdevelop a management strategy.
But that's kind of how Iapproach it is, is this de novo
or is this chronic?
(07:50):
Do we think they have a chanceat medical therapy or do we
think they're failing medicaltherapy at that point?
And then finally assessing thesituation clinically, how are
they doing in terms of theircurrent compensation status?
And are they adequatelyperfusing or not?
And that's about that's the wayI can define what the urgency is
and the next step forward totaking care of them.
Kanny (08:11):
That's great.
Thanks.
Now, as an image and specialistmyself, you know, obviously, I
know imaging plays a criticalrole in that initial assessment,
especially as you're trying tocategorize.
The patient Greg, maybe you canjust summarize, you know, how do
you, how do you useechocardiography to help,
(08:31):
confirm or classify that initialdecompensated patient?
And is there any other imaging,that would really be relevant in
that very acute phase ofassessment?
Greg (08:42):
Yeah, echoes is the echocardiography is definitely
the mainstay, and we cancertainly.
Besides the ejection fraction,which kids told us, told you all
how it classifies our heartfailure, it also can help
hemodynamically in terms offilling pressures by diastolic
parameters, it can help usunderstand if there's
interventions for thesepatients.
(09:03):
Once we kind of stabilize themagain, decongestant is their
valvular disease that we canintervene on.
We have great percutaneoustherapies now, both for the
valve mitral valve, and then asit's evolving the tricuspid
valve as well.
And so then it also helps usknow about the right ventricle
and we know some of the worstoutcomes that we see in any
patient population, be itpreserved or reduced ejection
fraction, common patients thathave significant RV dysfunction
(09:26):
and with its correlate pulmonaryhypertension.
So I think you can glean a lotthat helps you know the right
direction and take your patientin by the echocardiogram.
Kanny (09:36):
So, Ankit, you mentioned about, you know, clinical
assessment at the bedside.
I think, obviously, we're alltaught as consultants to look
for, for example, signs ofreduced end organ perfusion, in
a cardiogenic shock patient.
But do you have any pearlsabout, like, what specifically
would indicate a very worrisomeor high risk patient that may be
decompensating and may be acandidate for more advanced
(09:58):
therapy in terms of whatspecific, indicators of low
perfusion would raise, youralarm the most?
Thank you.
Ankit (10:06):
Kenny, I'm really happy to bring that up because as much
as we are reliant on moreadvanced kind of diagnostics
now, you know, bedside exams,the first thing we have, and we
often have to use that moreurgent situations as all we
have.
So, you know, when we thinkabout perfusion, you know, I'm
sure many of you guys have seenthe 2 by 2 table.
warm and wet versus cold anddry.
(10:26):
The first thing I think I thinkabout in terms of confusion is,
you know, to assess them onexam, look at the, look at their
physical exam.
Do they feel warm or do theyfeel cold?
And that in and of itself is notterribly specific, but a good
place to start.
And then looking at their volumestatus, looking at things like
JVP, looking at for things likeascites by physical exam, lower
extremity edema as as kind of abetter way to determine where
(10:47):
they lie on that table.
And then in terms of symptoms,You know, low output is
something that's been veryhumbling to me because it's kind
of presented in many forms.
Many times it's someone that hasslowed down gradually over time.
People with a cardiac index of1.
are not always you know, incardiogenic shock, there are a
lot of people sitting with lowoutput for a long period of time
(11:10):
as an outpatient till I get to acritical tipping point, make
their way in the hospital.
So have they been slowly, youkind of slowing down over time,
getting more lethargic and youngpeople, especially abdominal
discomfort or nausea, vomitingcan be a common sign of both
hyper like hyper bulimia as wellas low output as well.
And we've seen multiple examplesof folks in cardiogenic shock
(11:33):
with that being the presentingsymptom.
So that's kind of what I go onis if I have some of these
concerning symptoms that I seeor an exam that's concerning, we
then go straight to thediagnostics, including
laboratory testing, as well aspsychocardiograms to kind of
better determine where thatpatient lies and kind of where
they are in this, in kind ofseverity of what needs to be
(11:54):
treated.
If from there you then seeindications of malperfusion by
labs, which we talked aboutcreatinine LFTs, lactate,
whatnot, too.
I think that's enough from thereto saying that this is not just
low output, but shock, which bydefinition requires
malperfusion.
And then that escalates into theneed for inotropes.
and potential mechanicalcirculatory support.
(12:16):
So all of a sudden the severityhas gone up and I think we can
talk about more about how totreat
Kanny (12:20):
shock from there.
Absolutely.
And I'm glad you brought uptherapy because, as a general
cardiology consultant I thinkone thing that can be
overwhelming at times, or atleast challenging is just the
decision to initiate, IV therapywith inotropes or.
Vasopressors, but also thechoice of therapy.
So, how do you approach thatdecision to both start a
(12:44):
vasoactive medication and thenhow would you, make that initial
decision about what agent to
Ankit (12:49):
start?
So when I'm thinking about apatient that's low output,
another thing that can be veryhelpful if you have it is a
right hard cath, either with aleave in swan or, you know, just
a single time assessment todetermine low output or not.
If you if you have a clinicalindication of patient is low
output and At that point, theapproach is you can start an
(13:12):
inotropic medication, which canbe beneficial to kind of help
the patient better perfuse.
And so the two options that youhave are that the primarily are
dobutamine and milrinone.
These are both inotropicmedications that work by
different mechanisms.
Milrinone is a medication thatcan.
better, better producedafterload reducing effects.
So a patient that's morehypertensive, for example, or a
(13:34):
patient with elevated pulmonaryvascular resistance, Milrinone
may be the better choice there.
But the important thing to notewith Milrinone is it is cleared
by the kidneys.
So with patients withsignificant renal dysfunction,
it can accumulate and becometoxic and lead to worsening
hypotension.
So Milrinone is something thatWe often avoid in patients that
do have fairly severehypotension.
The other option is dobutamine.
(13:55):
Dobutamine is a pure betaagonist that has less effect on
blood pressure and then moreworks to increase contractility.
As a result, though, it'sslightly more arrhythmogenic, so
it may not be the best choicefor a patient that has worsening
ventricular or atrialarrhythmias.
But those are the two inotropicchoices to go on.
And then If either of them arenot possible or inadequate to
(14:18):
provide adequate support toheart, that's when we consider
mechanical circulatory support.
Kanny (14:23):
So as you talk about mechanical support what are,
like, kind of the key clinicalindicators in a decompensating
patient that start to push youtowards, using support more
urgently?
And a related question would be,in a setting that's maybe not a
(14:44):
tertiary center, what are someof the clinical indicators that
you would suggest that may beearly transfer to, a tertiary
center with advanced therapycapabilities would be advisable.
Ankit (14:57):
So, you know, broadly talking about that definition of
shock.
If a patient is in cardiogenicshock, I view inotropes as a
temporary means to helpstabilize the patient.
And if a patient really ishaving indications of end organ
perfusion, especiallytheförmative Determined by right
heart catheterization and bytheir, and by their labs, I
(15:18):
would consider at that pointstarting an inotrope and then
considering transfer to a centerthat can provide mechanical
circulatory support or placingit where you are there.
We've seen too many examples,unfortunately, of patients that
get temporarily supported ondobutamine, but then have an
arrhythmia and then are furtherdecompensated.
But for folks that are failing,failing inotropes.
(15:39):
Or require a more permanent, amore durable long term form of
mechanical support as weconsider the next option,
whether that be LVAD ortransplant or anything along
those lines, we got a coupleoptions.
So first off, and mostconventionally, you've got the
balloon pump.
And, and that, that can take acouple forms that can go into a
(15:59):
femoral vessel or an axillaryvessel.
And that provides, you know, asmaller amount of cardiac
output, conventionally, youknow, 0.
5 to 1 liter.
but has been shown to be muchmore effective in chronic heart
failure.
So a patient that's had chronicheart failure for a long time
and is now decompensated, kindof going to slow simmer or burn
of cardiogenic shock, that is anoption if a patient requires, if
(16:20):
you think a patient requiresmore cardiac support beyond what
a balloon company will provide,which is oftentimes the case in
cardiogenic shock anotherapproach is an impella, which is
basically a peripheral LVAD inthat way that kind of sits in
the left ventricle and, anddirectly supplies blood crossing
the aortic valve to the aorta.
And that comes in a couple offorms.
(16:41):
The most common forms used inshock are the impella CP, and
which can be placed by bothfemoral as well as axillary
approach.
And then finally, The mostcommon device that we use at
Christ specifically because ofits durability and the amount of
flow it can provide, is theImpella 5.
5, which is a device that candeliver over 5 liters of cardiac
output and is surgically placedto axillary.
(17:03):
And that's been our main devicethat we use when considering
patients for LVAD and transplantthat requires stabilization, but
that varies from center tocenter.
Finally, in a patient withsevere cardiogenic shock, where
it's clear that the other formsof mechanical circulatory
support would be inadequate, wecan consider VA ECMO.
(17:24):
And you know, this is somethingthat you consider in a
circumstance, but notnecessarily want to push towards
because it's something that hasits own cadre of associated
complications that can come withit.
But it is the most.
Robust form of mechanicalcirculatory support that we have
to support a patient in the mostsevere form of shock.
Kanny (17:45):
Great.
That's helpful to know.
So just so our listeners know,Greg did have to drop off to
attend to an urgent patientmatter.
We hope to have him back soon.
But in the meantime, I'd get,just to transition in our last
10 minutes we have, to talk inmore detail about durable, left
ventricular assist devices.
(18:05):
Most of us are familiar withLVADs.
Some of us are fortunate to workat centers where LVADs are
implanted.
Others maybe not.
I think a lot of us have kind ofa more traditional view of what
patients will benefit fromLVADs, but I know that's evolved
a lot in recent years.
So what specifically,especially, let's start with the
(18:29):
acutely decompensated patientwho's maybe recovering, but it's
still unstable.
What kind of clinical scenariosor indicators would then lead
you to think that, a moredurable assistive device.
Could be either a bridge to arecovery or, ultimately
transplant.
Ankit (18:48):
So, yeah, Kenny, that's a great question.
And when I think about I reallythink about the patient journey.
Oftentimes, many times thesepatients are diagnosed.
They're put on good guidelinedirected medical therapy.
They might get a mitra clip.
They might get a CRT.
And then eventually over time,you start to see that many of
these patients begin to failthose therapies, they start
(19:08):
getting hospitalized, they startgetting hypotensive with
inability to tolerate theirmedical therapy, their ejection
infections go down.
So when I'm seeing a patientthat's coming in for a
decompensated heart failureadmission, even if they're not
in shock, I'm thinking aboutthat as an escalation or
worsening of severity of theirillness.
We know that one heart failurehospitalization is roughly a 30
(19:31):
percent one year mortality.
Three heart failurehospitalizations in a year is
roughly 50 percent one yearmortality.
So when you're starting to see apatient that's failing medical
therapy and beginning to getadmitted.
Thank you.
For it.
That's the time to be thinkingabout L bad.
And then on the on the on theother side, as you mentioned,
the patient that is that ispresenting with cardiogenic
(19:53):
shock, meaning that they're nottheir heart is not able to
provide adequate blood flow totheir organs, and they need
potentially a form of mechanicalcirculatory support, like a
balloon pump or an impella to toguide their therapy.
The first thing you want toconsider there, again, is do you
think it's a recoverablephenomenon?
Do you think, was this anischemic insult that we expect
some improvement?
(20:14):
Was this myocarditis that weexpect to get better?
But if that's not the case, andthey're failing medical therapy,
that is the time to think aboutLVAD or transplant.
And that is a decision thatmaybe we won't go get into too
much, but What we do know aboutLVAD specifically is that it's
been proven to make patientswith advanced heart failure who
are failing medical therapy livelonger and give them better
(20:36):
quality of life.
And sometimes I worry that ourmessaging for LVAD isn't all
that clear as to how goodpatients can feel and how well
they do.
Because it's, you know, kind ofseen as this, this mechanical
device you got to carry aroundbatteries and whatnot.
But it's really, what we know isthat it does make people feel
better and live longer, and it'ssomething that we need to kind
(20:58):
of look at more when a patient'sotherwise failing medical
therapy.
Kanny (21:03):
Yeah, and just as an aside, the, the JACC did put out
a scientific statement this yearin the Journal of the ACC
regarding LVADs.
And durable devices, and it's anexcellent review, by the way,
and I'm going to put the link tothat in the notes to this
session.
But they did point out that, themost recent outcome data with
(21:25):
heart made 3 showed, you know,87%.
Survival that was basically onpar with heart transplant, and
I'm not sure, if all cliniciansreally Understand how much the
survival has improved.
Do you think that's because oftechnique or reduction in
adverse events or better patientselection?
Ankit (21:45):
I think it's all the above, you know, with the most
recent HeartMate 3 pump, many ofthe complications that we've
seen with traditional pumpsprior to this, which included,
you know, pump thrombosis withthe older HeartMate 2s and
HVADs, ischemic stroke.
Those have significantlyimproved with the most recent
heart made three device.
We still we still run intocomplications, including G.
(22:07):
I.
Bleeding, given the fact thatthese patients do need
anticoagulation right heartfailure and infection that have
occurred at similar rates versusprior.
But on the whole, what we knowwith the most recent heart made
three pump in the data that wasprevented in the momentum three
trial Is that mortality hasimproved substantially and so is
(22:27):
quality of life.
We just got five year data thatshows a 60 percent five year,
five year survival, which isastounding as to where we were
and comparing to what thesepatients would otherwise have
living with advanced heartfailure.
Kanny (22:41):
Yeah.
So having said that, do youthink the candidacy of patients
who will qualify for LVADs isgonna, is expanding or has
expanded or, or, and do you seethat broadening in the future,
you know, in terms of.
Who would be a candidate for adurable therapy?
Ankit (22:59):
So what we know is when we're thinking about advanced
heart failure therapies, rightnow, heart transplant has a
finite number that can beprovided hearts that can be
provided to patients.
So that's a number that'srelatively static, and it may
increase with other means ofobtaining organs, but.
That's going to be relativelystable, but we are seeing a
larger number of patientspresenting with advanced heart
(23:21):
failure as our population ageshere.
And so, what I'd say is, is thatthe best an LVAD patient can do
is if they go into the OR asoptimized as possible.
And given the advances that wehave in mechanical circulatory
support and other means ofstabilizing patients.
We can optimize them better thanwe have before so that they can
(23:43):
do better.
And even over the course of myrelatively young medical career
at this point, I've seen usbegin to push the limits in
terms of implanting patientsthat are older, that have more
comorbidities just because wehave the ability to stabilize
them better.
I think the other thing we'realso doing better is on the post
VAD side, we've come to realizethe importance of a team
(24:03):
approach.
We have a an amazing team hereat Christ of LVAD coordinators
that are training families andeducating facilities on best
practices, and that's helping toprevent things like driveline
infections, adherence tomedication, and we all know
these things are very important.
So, to answer your question,yes, I do think we're beginning
to push the limit and expand thepool of what we consider to be a
(24:24):
candidate just because we have,we've had so many advances in
this space.
Kanny (24:31):
Great.
So Greg welcome back.
Yeah.
Greg (24:34):
Sorry about that.
I appreciate it.
We'll see when you, you hireyoung, smart physicians, like
I'm kid, I just can sit back andlisten and learn.
So it's but get back in theconversation
Kanny (24:45):
here too.
Yeah, you don't want to let apodcast recording get in the way
of good patient care.
So, but we were talking aboutLVADs Greg, but one question I
had for you in your practice atChrist is, just in general,
what's the distribution ofimplants now between patients
where you generally feel that,you want to get them to a
transplant versus what you wouldconsider, just durable therapy
(25:09):
with the LVAD?
Greg (25:11):
Yeah, that's a great question, Kenny.
So really what's happened sincethe allocation systems changed
that the indication for bridgeto transplant has really almost
disappeared.
And with that, we're, most ofthe times that we're doing it,
LVADs are for a bridge tocandidacy, where at the current
time when we see these patientsin the hospital or out of the
hospital they're, they're not acandidate for the transplant.
(25:34):
It might be a contraindicationthat's modifiable.
It might be something liketobacco abuse, and they need to
spend some time, or it might besomething like pulmonary
hypertension.
with an LVAD that comes down, orobesity, or it can be just
concern about psychosocial riskfactors for, so we do you know,
probably 50%, I would say, are,are these bridged to candidacy,
(25:55):
that we think they're going tobe a candidate, but right now,
in this moment in time, they'renot.
And then the other 50 percentend up being this sort of, this,
their, the destination therapycategory, where they will spend
the rest of their lives with thedevice.
And these are often the olderpatients.
The ones that have significant,you know, kidney disease and
lung disease and other issuesthat we think they're probably
not going to get to the point oftransplantation.
(26:17):
And so that's the usualbreakdown.
Now, I know there's a lot ofinterest in the indication of
bridge to recovery, and in realworld, that's a pretty low
percentage of where peopleactually get to the point of
explanting the pumps, butthere's certainly a lot of
research and single centerexperiences when you.
take a very selected group ofpatients.
We can increase that singlecenter.
(26:38):
I'm sorry, that real data numberof 1 percent to 2 percent
recovery to explant to maybe 10percent or even higher.
So I think those kind of would Igive you sort of a general sense
of the indications for when weuse the LVAD.
Kanny (26:52):
Sure, sure.
And just in our last couple ofminutes here, Greg For those of
us, obviously, that don'tdirectly participate in
implanting or caring for theLVAD patients, as you think
about patients, and we all havesuccess stories, I think, in our
practices or at our institutionsof patients that have gone, you
know, several years with adevice and for the most part
(27:15):
stayed out of the hospital.
Do you have a sense about, like,what specific Is it mostly
clinical factors that wouldpredict a good response like
that, or is it social support,or is it, you know, a potpourri
of factors that go into yourdecision making as to, this
particular patient is probably,at least has a good chance of
surviving several years withtheir device?
Greg (27:37):
Yeah, it's a really complex.
sort of decision making thatrequires a team like Ankit said,
but we, we have this pump thatwe have now, the heartbeat three
is very forgiving and theirsurvival data is improving.
We're now getting out to, youknow, 55 percent survival for
five years.
So.
These people are living longer.
They're living with greatquality of lives and fewer
(27:59):
advance adverse events.
And so really, as we evaluatethese patients, if we get to a
patient that is really all theother organ systems look pretty
well intact.
And that they have and so thatwe look as we evaluate these
patients, we look at other endorgans and making sure there's
no irreversible damage there.
(28:20):
We, and we look at theirfrailty, how strong they are to
get through a procedure.
And really what we've seen is,which is part of the way we're
pushing the envelope is thatwe're taking these patients that
are sicker and more frail.
And actually pre rehabilitatingthem before the surgery with
these percutaneous pumps,especially the impella five
fives, just has really changedthe landscape for us in terms of
(28:43):
its durability, its ability tohave people on the support for
weeks leading up to the LVAD oreven transplant to the point
that we can get these peoplestronger.
And then that's chance watchthem and see if that frailty,
which is such a.
difficult thing to assess.
And there's lots of research interms of how and being more
objective about it.
(29:03):
But can we start seeing thosefrailty domains improve while we
take care of a patient in theICU to the point that we think
we can get them through thesurgery?
Then that final componentevaluation is the psychosocial,
which is, is challenging too.
And it may be as these pumpsbecome less for, you know,
become more forgiving that wecan take patients that can be
more independent and live bythemselves and not have
(29:25):
caregivers.
As as intimately involved asbefore, so I think that's
another place where we see allthat therapy expanding is people
being a little bit moreindependent in their in their
lives.
Afterwards.
Kanny (29:38):
That's great.
And then just very briefly, isthere still an upper, a strict
upper age cut off where youfocus it more on frailty and
other clinical factors todecide, you know, candidacy?
Greg (29:48):
Yeah, unfortunately, you know, I think for us, there's
been kind of a soft ceiling of80 and, Anybody over 75 really
looks their age once you getthem in the OR and
cardiopulmonary bypass.
So frailty is important andthere is a chronologic age,
which is biologic, but over 75they have to look really good
(30:08):
and over 80, we really haven't,we haven't ventured into that
ground.
Other places have in the worldbut for us, it's been kind of
80.
Kanny (30:17):
Great well, unfortunately, we're up against
our recording time here.
I thought it was a greatdiscussion.
I think we covered a lot in 30minutes.
I really want to thank both ofyou for taking time to educate
us also for your contributionsto the state chapter.
I know you're on the faculty forour recent meeting.
My only final question for youis that I'm a 50 year.
(30:39):
Plus Ohio resident and lifelongsports fan.
Do you think the Bengals canactually bring a championship to
the state of Ohio before Iretire?
Ankit (30:48):
Well, we're hoping on this year,
Kanny (30:50):
so we'll see.
Awesome.
Well, thank you both forparticipating and I hope to have
you back soon and also in othercapacities for our state
chapter.
Thanks again to both of you.
Thank you for joining today'spodcast.
For more information about thespeakers or the topics, please
go to Ohio acc.org,
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