February 13, 2025 • 34 mins
Please join our special guest, Dr. Benjamin Romer from Ohio State University, as we address the current state of lipid therapy in both primary and secondary prevention patients. He addresses a practical approach to the issue of statin intolerance, then reviews the newer agents including ezetimide and bempedoic acid, as well as the newer percutaneous agents, with a focus on practical tips for implementation. We wrap up with a discussion on the role of coronary calcium scoring to guide therapeutic decisions in select patients.
For more information, see the 2022 ACC Expert Consensus Pathway on the role of Nonstatin Therapies.
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Kanny (00:10):
So welcome back to the CardioHow podcast.
We're really excited today tohave a discussion on lipid
lowering therapy, a topic wehaven't addressed in a while,
and we're really going to focuson some of the newer non statin
agents that have been releasedin the last few years and talk
about some practical tips on howto use them in our cardiac
(00:32):
patients as well as for primaryprevention.
I'm really excited to have aguest today, who's a colleague
here in Columbus, just likemyself, and is a lipid
specialist.
So I'd like to welcome Dr.
Benjamin Romer, who is on thefaculty at The Ohio State
University as a clinicalcardiologist and a lipid
(00:53):
specialist.
And I assume that's a placethat's in celebration mode
today, since we're recordingthis podcast less than 24 hours
after the Buckeyes.
Dr.
Romer.
Uh, won the nationalchampionship last night.
So Won the national championshiplast night.
So Ben welcome to the show.
Ben (01:12):
Yes, thank you very much, Kenny.
It's good to be here.
Yes, last night was a very fun,fun night, fun game, fun run so
good celebration today on, oncampus.
It was good to talk with you atthe Ohio ACC meeting a few
months ago.
We can kind of keep thatconversation going today.
Kanny (01:32):
Yeah, thank you very much.
Yeah, as you just alluded to,you did give a very nice talk at
our annual meeting about lipidlowering therapy.
So Ben, I know, I know you're agraduate of OSU Med School.
I, I see that you did most ofyour training in Chicago at
University of Illinois.
But we do have a lot of fellowsin training who listen to this
podcast.
(01:53):
And so we always like to startjust by hearing a little bit
about your journey to yourcurrent position.
And I guess what I would be mostcurious about is, as you pursued
a career in cardiology, whatkind of led you to focus on, on
cardiac prevention and theneventually, specializing in
lipid therapy as well.
Ben (02:11):
Yeah, certainly.
So, like you said, I I graduatedmedical school from Ohio State
and then I did my residency andtraining six years, or residency
and fellowship, rather six yearsin Chicago, University of
Illinois, Chicago.
And you know, I, I sort of knewrelatively early on that I
didn't want to be a proceduralbased specialist within
(02:33):
cardiology, but I really didn'thave much, that much of an
interest in prevention duringfellowship, mainly because I
found that it wasn't, it wasn'tstressed a whole lot.
I mean, when you're infellowship, you have to learn
ECHO, you have to be in the cathlab you have to learn EP.
It just seems like there aremuch bigger priorities with a
(02:54):
steeper learning curve.
And so it wasn't until Ireturned to Ohio State as as
faculty in 2020, and it wasn'tuntil about a year in until I
realized that I kind of had alittle bit of a relative blind
spot in my knowledge.
I just feel like as a generalcardiologist, I, I, I should
develop skills and preventionmuch, much sharper.
(03:18):
So I, I, I kind of just had aninterest.
I, as I was learning more andmore about prevention and about
the newer agents that are out tome, it just felt like a very
natural fit.
To immerse my role as a noninvasive cardiologist to also
focus on prevention becausethat's what a lot of patients
these days want to come in andtalk about.
(03:40):
They want to come in and talkabout calcium score.
They want to talk aboutlipoprotein A.
I think nowadays a lot of peopleare focusing on prevention.
So it was a, it was a verynatural progression, which I'm
very happy to be a part of nowat Ohio State in a very a very
excellent lipid and preventionclinic.
(04:00):
So so, you know, as time goeson, I think, you know, the role
for prevention in cardiologyjust continues to grow.
Within the prevention clinic, alot of patients are, are
motivated to help themselvesthrough lifestyle modifications,
but also with the newer lipidlowering agents, they also come
in and they, you know, they're,they're very interested in what
(04:21):
options are available outside ofstatins in order to reduce their
risk.
Kanny (04:25):
Well, speaking of statins, I thought, even though
we really want to focus on someof the newer agents, I don't
think there's a lot to say aboutstatins.
You know, we have three decadesof data and personal experience,
using statins to reduce risk.
But one topic I wanted to askabout statins before we move on
to the other agents is the issueof statin intolerance.
(04:46):
All of us in clinicalcardiology, of course, we
prescribe statins, we seepatients being treated, and I
think every clinician, really,who takes care of cardiac
patients has to deal with theissue of statins.
Statin either intolerance orwhat I would call statin
reluctance.
And we all know, of course, thatin the literature, you know, the
(05:07):
incidence is not particularlyhigh, but we also know in the
real world we do.
So I'm just curious, if youcould summarize, when a patient
who maybe is already on a drugcomes to you and notices some
intolerance or complaints, like,what is your overall strategy to
try to.
maintain statin therapy andthen, get into the decision
(05:28):
making and maybe about, analternate agent at some point.
Ben (05:31):
Yeah.
I mean, certainly within thelipid and prevention clinic I
see multiple patients every timeI'm in clinic that, that have
statin intolerance.
And, and as you said, whetherthat's a true adverse reaction
or it's just an unwillingness, areluctance, You know, the end
result is that we have to comeup with strategies to try to
(05:52):
encourage them to try anotherone or a different one, or maybe
remedies for their statinassociated side effects or
consider another alternateagent.
So in general I primarilyprescribe hydrophilic statins,
especially rosuvastatin.
And I find that a lot ofpatients come in on atorvastatin
(06:15):
or simvastatin, if justswitching them from those type
of lipophilic statins tohydrophilic one, especially
rosuvastatin, they do okay.
And I also think it's veryimportant to remind patients
that even a low dose ofrosuvastatin, maybe every other
day, you know, just fivemilligrams of Crestor every
other day can lower LDL by aconsiderable amount, you know,
(06:39):
25%, 30%.
And that's, you know, convincinga patient, Hey, you only have to
take this once every other day.
So, you know, I, my, my go tostatin is, is, is rosuvastatin.
But if they don't tolerate that,then pravastatin or patavastatin
even are, are other optionsthat, maybe they'll tolerate it.
Checking vitamin D is alsoimportant and, TSH, I, you know,
(07:03):
there's, there's some, there'ssome literature that suggests
that that low vitamin D candecrease HDL can increase LDL
and triglycerides.
So, that's something that we'llcheck, especially in these
winter months.
A lot of people are vitamin D, Ddeficient.
As for something like CoenzymeQ10, you know, the guidelines do
(07:25):
not recommend supplementing withCoenzyme Q10s to prevent statin
associated.
muscle symptoms, but I have noproblem prescribing it myself
simply because, you never knowif somebody has a placebo effect
even from Coen's MQ 10 to wipeaway their symptoms.
So, those are some of the, thoseare some of my initial reactions
(07:47):
to statin and tolerances.
It's important to check for fordrug interactions.
Having pharmacists on board inour lipid clinic is invaluable
to, you know, to help check fordrug interactions and
potentially reduce the dose of astatin if an interaction makes
it such that the level of statinwill be too high.
(08:09):
So those are kind of my, youknow, my, my, that's my
checklist sort of when patientscome in, but as you said, it can
just be challenging sometimesand sometimes people will come
in and they'll just be verystubborn and hard nose and you
can give them all the data andtalk about it, you know, the
lipid or the LDL lowering andthe anti inflammatory effects of
statins.
(08:29):
And, you know, you just can'treally budge them.
So it's a, it's a battle thatwe're going to keep fighting.
And, you know, sometimes you canmake headway with patients,
Because it is important to havethem on statins, but every once
in a while, you know, they just,that's not the case.
Kanny (08:46):
Yeah, yeah, thanks.
I wasn't aware of that linkwith, potential link with
vitamin D deficiency.
I think that's definitely worthkeeping in mind in many of our
patients, especially in thisclimate.
So that's good to know.
And I've had similar experiencewith, you know, the kind of
microdosing of rosuvastatin, andpatients, like you said, do
(09:08):
really tend to tolerate thatreally small dose even when
they've had other issues, andit's pretty striking the LDL
reduction you can get.
So, one other general question Ihad before we talk about some of
the agents specifically, becausethis does come up in day to day
practice as well, I know theguidelines still, focus on using
a standard, lipid profile, orperhaps using, non HDL
(09:31):
cholesterol as kind of apractical parameter to monitor,
therapy.
But we also understand, thatcalculated LDLs can be prone to
issues.
So in your patients, notnecessarily, your highest risk
patients, but in the day to daygeneral clinical, patients for
secondary prevention do youthink a standard profile is
(09:52):
enough for serial monitoring ordo you tend to, do direct LDLs
or consider measuring ApoBserially?
Ben (10:00):
Yeah.
I mean, in my patients that justin my, in my general cardiology
Clinic where I have patientsthat I'm following for
hypertension or Even just kindof risk factors if they're not
complicated heart failure, forexample I will get a lipid
profile with an indirect LDL andI'll get it when they're not
(10:23):
fasting.
I mean, just the routinescreening I have no problem
following the guidelines to, inthat regard, to get a non
fasting indirect LDL profile.
A.
And so, you know, the, the, thecalculated LDL is unreliable
when triglycerides are quitehigh.
So above 400 or, or, you know,if LDL is very low, if it's less
(10:48):
than 70, and really this is withvery high risk patients where
you're aiming for LDL is thatlow, that that's when the
calculated LDL can beunreliable.
So in patients that I have on,on multiple lipid lowering
agents, especially somethinglike PCSK9 inhibitor in patients
that have triglycerides thatare, that are really, really
high, then.
Then I will jump straight todoing the direct LDL and make
(11:12):
that lipid profile be fasting.
But in general I think it's justfine to kind of get the general
lipid profile in, in patientsthat you Either aren't worried
too much, too worried about, ormaybe you just haven't unveiled
what their true underlying lipidabnormalities are.
Kanny (11:30):
Great, great.
So, you know, assuming you dohave a patient who's either
tolerating statin therapy, butnot getting their LDL to target,
or is having, some degree ofintolerance, I guess I want to
just go over kind of yourpractical strategy for how you
would then incorporateadditional agents.
So, Is it safe to say thatezetimibe is still kind of the
(11:52):
first choice nowadays for a nonstatin or a second drug given
that it has, some outcome datathat we've been, seeing for
several years?
Yeah, I
Ben (12:00):
think that is safe to say.
It's safe to say mostimportantly from, as you
mentioned, outcomes dataimprovements in, in in major
adverse cardiovascular eventsfor secondary prevention
patients.
Thank you.
Mortality benefit, everythinglike that.
So it's important from thatregard, first and foremost, but
(12:22):
it's also important becauseinsurance companies won't cover
some of the other agents unlessyou've tried a zetamide.
So there are some patients whereif you have them on high
intensity statin and then youadd a zetamide that they'll,
they'll be, they will have anexcellent response to, the 10
milligram addition of azetamide.
(12:43):
Some patients, it lowers theirLDL by a, by a considerable
amount.
Some other patients, it doesn'treally budget that much, you
know, 10, 15%.
But, you know, in, in theory,ezetimibe should lower LDL by,
maybe 15, 20 percent asmonotherapy.
But when you combine it withstatin, more like 25 to 30%.
(13:04):
So, there are a lot of patientsthat we have, especially
secondary prevention patients,where the target LDL is below
70, or if they're very highrisk, below 55.
And let's say the LDL is, youknow, 5, 10, 15, 20 points
higher than what you target,that's when ezetimibe can
achieve your goal, and you'resort of, you're good to go in
(13:28):
that regard.
So, yes, ezetimibe certainly ismy first go to.
But in the realm of geneticdyslipidemia as familial
hypercholesterolemia patientswith really high LDL levels and,
and multiple manifestations ofatherosclerotic disease, if
their, if their LDL is over 100on stat, already on statin
(13:51):
therapy, and if you're trying toget them below 70 or below 55,
Addition of azetamide aloneisn't going to cut it.
So it sort of depends on whattheir risk is, what risk you've
established, and then just howmuch lower you need to target
their LDL as to whether theaddition of azetamide will be
enough with statin already onboard.
Kanny (14:16):
Sure, sure.
And then assuming you have to gobeyond azetamide then, I know
one of the newer agents that'sgarnished a lot of attention the
last few years since it wasapproved is bempedoic acid.
Can you say a little bit abouthow you use that agent now in a
clinical sense and in whatsettings?
Ben (14:36):
Yes, certainly.
So bempedoic acid is It maylower LDL by 15 to 20 percent
alone.
I think it's maybe closer to athird if you combine it with a
zetamibe and there's a, there'sa combination form of, a
zetamibe and bempidoic acid.
So in the trial, in the cleartrial the effect of bempidoic
(14:57):
acid as far as from a preventionstandpoint was more pronounced
in patients that were primaryprevention.
And so I generally use bempidocacid in those patients who who,
who are primary prevention, whomight be moderate risk that
certainly that aren't high riskor very high risk where, where
(15:19):
you're trying to lower their LDLagain, by, by by a modest
amount, 20 to 30%.
And if you can combine it with azetamine, that's the best bang
for the buck.
I mean, usually these arepatients who come in.
and they're statin intolerant.
So they're statin intolerant,their primary prevention.
And those are the ones where yousay, well, benpidioic acid may
(15:40):
be a good idea.
Now you have to be careful aboutgout.
Check uric acid levels beforestarting benpidioic acid.
I ask older patients above theage of 60 if they have had any,
tendon issues in the pastbecause there's a very, very
small risk of tendon rupturewithout that would obviously be
a catastrophic event.
So generally speaking, I use itin primary prevention patients
(16:03):
who are statin intolerant thatare maybe moderate risk and you
need kind of moderate LDLlowering.
I just think there are betteroptions out there for patients
who are secondary prevention oryou need You know, much more
aggressive LDL lowering.
Kanny (16:19):
Sure, sure.
And one final word aboutbenpedoic acid.
I mean, I know azetamide, ofcourse, is generic.
Do you have any issues withapproval or cost issues for,
cost or access issues for thepatient at this point in time?
Ben (16:32):
Yeah, certainly.
I mean, usually in order to getit covered you have to document
statin intolerance.
So both bempidoxic acid aloneand the combination you know,
can require a priorauthorization or can be costly
to patients.
So that's why, you know, it'snot an agent that I would just
jump to as monotherapy if apatient hasn't tried multiple
(16:52):
statins.
So usually it's, you know,they're statin intolerant, you
try a zetamide, they're eitherintolerant of a zetamide or they
need additional LDL lowering andmaybe they're, they're, you
know, they want to avoid takingmultiple medications.
So you can say, well, we canjust.
Do this additive to azetamide,but you're still only taking one
pill.
And so that's, that's kind of away to convince those patients
(17:14):
that, that bempedoc acid is agood idea.
Kanny (17:17):
Yeah, that makes sense.
That makes sense.
So then kind of moving on tosome of the other therapies I
mean we have you know about adecade of or more data with the
PCSK9 inhibitors You know, Istill feel like and tell me if
this is the case in your in yourpractice at Ohio State Is that,
are those generally stilladministered through your lipid
(17:39):
clinic or do you see somegeneral cardiac providers
getting more comfortable givingthose and then where do they fit
in, in the stepwise approach tothe helping patients get to
target?
Ben (17:53):
Yeah, so for, for a long while I, I think that a, a, a
common reason for referral tothe Lipid and Prevention Clinic
was to consider PCSK nine andadminister.
But really over the past sixmonths or so, we're making much
more of an effort to educategeneral cardiologists and
(18:16):
primary care physicians,internal medicine, family
medicine, that prescribing PCSKnine inhibitors.
Is is a very safe thing to do.
The risk profile is very low.
The efficacy is is very high.
You know, we're trying to makePCSK9 inhibitors more mainstream
and have providers be morecomfortable prescribing them
(18:39):
simply because, as I said, theyare so effective.
They're very effective andthey're safe.
The main thing is just patienteducation.
And so, you know, administeringPCSK9 inhibitors is quite easy.
It's just like, sort of like aninsulin pen.
I mean, I've had very littlepushback from patients about
(19:01):
using PSCSK9 inhibitors or eventhe side effects associated with
them.
And so we're trying to certainlymake it more mainstream with all
different providers who mightwho might be prescribing those,
you know, includingendocrinologists even.
So as for, when we, jumped tothem I think, I, I, as a.
(19:22):
Just as a cardiologist, I alwaystry to establish the patient's
risk.
And so, the first thing is todetermine whether that patient
is primary prevention orsecondary prevention.
And if they're secondaryprevention with a history of
heart attack or stroke or, youknow, peripheral arterial
disease, then automatically, atthe very least, you're going to
(19:43):
aim for an LDL target of lessthan 70.
And if they have otheradditional risk factors or
multiple prior events, then it'san LDL of less than 55.
And, you know, the truth of thematter is that these patients
that are secondary prevention,they had LDLs that were quite
high for a long period of time.
And PCSK nine inhibitors arejust so effective at lowering
(20:05):
LDL and non HDL, I mean 60% inthe trials for Repatha.
and for preluant.
So that's just that's anincredible lowering on top of
statin therapy alone.
So in those trials, the baselineLDL for these patients was maybe
around 90 or so because theywere already on statin therapy.
(20:25):
And addition of PCSK9 inhibitorsbrought them, you know, 60
percent below that baseline of90.
So I, you know, I can't talkenough about just how important
it is to administer PCSK9inhibitors.
In secondary prevention patientsor in high risk primary
prevention patients, especiallythose that have familial
(20:49):
hypercholesterolemia.
And then if you tell them that,you know, there's a med out
there that's more effective andyou can get rid of another one.
Oftentimes, they're very open tothat idea,
Kanny (20:58):
but you will typically continue the statin if they were
tolerating it,
Ben (21:01):
absolutely.
The statins are here to stay.
If the patient is toleratingwithout a doubt.
Kanny (21:08):
Yeah, 1 thing I was just thinking about when you talked
about acceptance of the,percutaneous agents is that
maybe with the proliferation ofsome aglutide and trizepatide
which it seems like, about halfour patients are taking now,
maybe that's made these theseagents more acceptable too.
Yeah, I
Ben (21:24):
think that's a great point.
And a lot of patients, willhave, you know, Great
cardiovascular benefits fromthose GLP 1 agonists as you
mentioned.
So I that that makes it sort ofsort of easier That you can tell
them.
Hey, it's just another injectionInstead of losing a lot of
weight like those meds youmentioned, well this is going to
lower your cholesterol levelsand you'll be in good shape, so
(21:46):
that's definitely a good point.
Kanny (21:48):
So in your in your clinic, who typically does that
initial education to the patientabout getting started on the
PCSK9 in terms of theinjections?
Some education about any sideeffects?
Is that, would that be apharmacist typically, or?
Or a nurse practitioner and howdo you think that could then
translate to like a generalcardio clinic?
Ben (22:07):
Yeah, so, in our lipid and prevention clinic, you know I'm
i'm paired with with apharmacist and we go and see the
patient together and do thevisit together, which is just
excellent from amultidisciplinary standpoint,
very comprehensive way ofevaluating the patient.
And it's usually the pharmacistthat, that will then, you know,
(22:28):
grab a dummy pen and do theeducation.
And truthfully it, it, thateducation lasts for less than a
minute.
So I, I think from from ageneral practitioner standpoint
it doesn't take much time toeducate the patient about
administering that.
I mean, it's, it, it's, Quitehonestly, it's easier than doing
insulin injections because youdon't have to set, you don't
(22:50):
have to set the dose but to behonest, even if you were to have
a nurse or, or, you know, a midlevel provider, I would feel
completely comfortable with anurse in my general cardiology
clinic educating a patient howto administer a subcutaneous
(23:11):
injection just because it isthat easy.
Kanny (23:15):
Yeah, I agree, and I think a lot of us in general
cardiology are finally gettingto the point where it's kind of
a routine part of our practicebecause obviously Not everyone
has access to a the resources ofa lipid clinic are limited even
in a setting when you have itYou know at least that's that's
the case for us as well Well, Iguess just to finish up in the
(23:38):
last few minutes five minutes orso.
I wanna ask you a little bitabout Enli, but just briefly, I
know there's another agent,another PCSK nine agent in umab
which my understanding islimited to, you know, homozygous
fh.
So is that an agent that wouldbe less common in a general
cardio practice at this point intime?
Ben (23:58):
Yeah, I think, I think so.
I mean, umab is, is, is veryeffective, but it is only
approved for homozygous fh.
So those are patients, that's anagent that really should be only
prescribed by a lipidspecialist.
After a patient has undergonegenetic testing with, with
confirmed homozygous FH.
Kanny (24:20):
Okay.
So then I guess that brings usto Inclisiran, which has also
been approved in the last fewyears.
And my understanding for that isthat it is indicated.
For secondary prevention C.
A.
D.
In addition to a familialhyperlipidemia.
So how is that agent, you knowdiffer from the more established
(24:42):
P.
C.
S.
C.
9 inhibitors.
And then how do you.
Incorporate that versus theother agents.
Ben (24:49):
Yeah.
So in glycerin and PCSK9inhibitors, they work very
similarly.
A PCSK9 inhibitor will, it's amonoclonal antibody that
attaches to the PCSK9 proteinand prevent that protein from
eventually down the roadcausing, causing breakdown of
the LDL receptor.
(25:09):
And glycerin is a smallinterfering RNA that prevents
translation of the PCSK9protein.
So it just prevents PCSK9protein from from even being
produced.
So the net effect is that youhave more LDL receptors to bind
LDL and take it out of thebloodstream between glycerin and
(25:32):
PCSK9 inhibitors that wediscussed.
So in glycerin is a veryeffective way to at lowering
LDL.
In the Orion trials, I think itreduced LDL by around 50 percent
or so, which is, which is anexcellent reduction in, in LDL.
So, there are some benefits tothe benefits to in glycerin is
(25:54):
that you only have to administerit.
You administer it day one.
And then three months later, andthen at six months, and then
after that, it's every sixmonths.
So after the first couple ofdoses Inclistrin is only
administered twice a year, whichfor some patients is a very,
very attractive way to have amedicine administered.
(26:16):
Now, it is administered in aninfusion clinic.
So you would have to go into aclinic to receive the to receive
the medication.
But that also means that that'snot charged to insurance.
Inclisirin is not charged as amedication.
It's, it's charged as kind of aas a clinic visit.
(26:38):
So, for patients that areworried about cost of medication
or at the end of the year beingin the donut hole and they're
paying an arm and a leg forwhatever, you know, their DOAC
and their SGLT2 inhibitor andtheir PCSK9 inhibitor, You can
kind of circumvent that cost insome, in some ways by having
(26:58):
Inclisirin be administered in,in, in the clinic setting, in an
infusion clinic.
So, you know, the, the one, theone point to make about
Inclisirin is that we, we don'thave outcomes data yet.
That's scheduled to come outover the next couple of years.
All signs point to certainly apositive outcome.
result from from those studies.
(27:20):
But I would just like to makethe point that we have a lot
more data with the PCSK9inhibitors and, you know,
generally speaking, they lowerLDL by 60 percent compared to
50%.
Kanny (27:30):
Yeah, great.
Great.
Well, that's good to know aboutthe fact that, it's a clinic
based treatment rather than, youknow, considered a
pharmaceutical because I dothink that makes a big
difference the way some patientsreimbursement works Well, it's
amazing how much this field haschanged in the last decade or
so.
(27:50):
with these new agents and thesenew outcome studies.
One final thing I want to askbefore we wrap up in a couple
minutes is, being an imagermyself, I'm always, been
interested in the way we can useimaging to kind of guide therapy
and patient management.
And of course, you know, if youthink more about primary
prevention, not so muchsecondary prevention, but for
(28:11):
the primary patient, which ofcourse we see many more of these
in our general clinics now.
How do you tend to use imagingtechnique like calcium scoring
in some of those borderlinepatients to make a decision, to
either initiate therapy or insome cases to convince a
patient.
That they need to be on therapy.
Ben (28:32):
Yeah, certainly.
I mean, you know from from themost recent guidelines the
guidelines And I I think a lotof us within internal medicine
family medicine no matter howyou're trained or are aware of
the pooled cohort equation whereyou know You just type in ascvd
risk calculator and then you putin the patient's name Age,
gender, ethnicity, their lipidlevels, do they have diabetes,
(28:54):
hypertension, etc.
And then it'll give you a 10year risk of atherosclerotic
event or lifetime risk as well.
You know, for certain agegroups.
And so then that'll categorizepatients in low borderline
intermediate or high risk of anevent over the next 10 years.
(29:14):
And per the guidelines, they saythat if you, if you have
patients that are borderline orin immediate risk, then to
strongly consider doing coronaryartery calcium score.
And I completely agree withthat.
I, I tend to use coronary arterycalcium score a bit outside of
that because I think that Inaddition to, to refining a
(29:36):
patient's risk in a better waywith coronary artery calcium
score.
As, as to whether or not youshould utilize a statin, I find
that if a patient, if a, if apatient knows that they have
some degree of coronary arterycalcification, if, if you can
sort of prove to them thatthey're already having
subclinical manifestations of.
(30:00):
of coronary disease, then theyare oftentimes they're more
inclined to take those lifestylemodifications more seriously, in
addition to being more openabout aggressive lipid lowering
targets with statins, ezetimi,PCSK9 inhibitors, all the agents
that we said.
So, you know, if a patient is,is, is very low risk, then no,
(30:24):
there's no reason to get acalcium score.
I mean, if somebody is 32 withno family history, no risk
factors.
There's no reason to get acoronary costume score, but you
know in that pooled cohortequation It doesn't take much to
get patients to intermediate orborderline risk as they get
older So once you approach theage of 60 you only throw in
another risk factor in there Andmaybe the LDL is just a bit high
(30:46):
and you get to borderline orintermediate or even high risk
And so obviously at that pointyou should strongly consider
statin therapy But what's alsotrue about coronary artery
calcium score is that it canreally help determine which
patients would benefit frombeing on aspirin.
I mean, as we know, over thelast five years, the pendulum
(31:07):
has swung away from aspirin useroutinely for primary
prevention.
But if you have a calcium scoreabove per the most recent
National Lipid Associationguidelines on coronary calcium.
That's an indication to start 81milligrams of aspirin.
Now you have to be a little bitcareful as patients get older.
(31:28):
I And the last point that I'llmake is that, you know, a lot of
patients, they may come in andthey may have risk factors, they
may have smoked for 30 years andhypertension, And you get a
calcium score and it's zero anda calcium score of zero, the
negative predictive value of acalcium score of zero over, the
next five years or so is quitehigh.
(31:48):
So it can be very reassuring topatients as well.
So I can't speak highly enoughabout utilization of coronary
artery calcium score.
I tend to utilize it outside ofwhat the guidelines say, unless
they're very low risk or ifthey're secondary prevention.
It should really only be used inprimary prevention.
There's no role for it insecondary prevention, but I just
(32:09):
think it gives you a lot ofinformation about where the
patient is and what their, what,what their, however long, how
many years or decades they'vebeen on, they've had certain
risk factors, you know, howthat's all added up to affect
their coronary arteries.
Kanny (32:24):
Yeah, yeah.
Well, I'm really glad to hearyou say that because I agree
completely.
I feel like, as you mentioned,there's a lot of power in zero
as well, sometimes you see, themget prematurely put on a statin
by a primary care provider, youknow, based on a single profile
or very unclear risk.
So I think that score is zero.
It couldn't really be reassuringas well.
(32:46):
Well, Ben, I think we covered alot of material.
It's such a changing field withso much data and prevention so
much that we've learned in thelast few years.
But I think you were able tokind of succinctly give our
listeners some practical adviceon how we, you know, Approach
these agents.
So I do want to thank you fortaking time to talk and also for
(33:07):
presenting at the State of ohiomeeting, a few months back and
Perhaps down the road we canhave you back to give us some
updates on on some of thesestudies you alluded to
Ben (33:17):
Yeah.
Well, thanks very much, Kenny.
It was, I mean, I think I, I'mvery grateful to be on the
podcast.
I've, I've really enjoyed, youknow, being part of, of, of
today, this podcast, and i, Ijust think it's an exciting time
to be in the field of preventioncardiology.
And, and, the, the whole reasonis to improve people's lives,
and there's no better way to dothat than prevent them from
(33:39):
having really, poor outcomesfrom heart attack or stroke, is
the best part in all that we do.
Kanny (33:47):
Yeah, absolutely.
And I guess the final thing I'llsay, you did allude to the
guidelines and I just want toremind the listeners that there
is an ACC expert consensusdocument that just came out in
2022 that specificallyaddresses, non statin therapies.
And it's a great referencedocument.
It's very practical as well.
So it's really written, youknow, with an eye towards day to
(34:09):
day practice.
So we will put a link to thatactually in the notes for our
podcast.
So I want to thank Ben and Iwant to thank our listeners and
until next time, thank you all.
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 CardioHow podcast.
We're really excited today tohave a discussion on lipid
lowering therapy, a topic wehaven't addressed in a while,
and we're really going to focuson some of the newer non statin
agents that have been releasedin the last few years and talk
about some practical tips on howto use them in our cardiac
(00:32):
patients as well as for primaryprevention.
I'm really excited to have aguest today, who's a colleague
here in Columbus, just likemyself, and is a lipid
specialist.
So I'd like to welcome Dr.
Benjamin Romer, who is on thefaculty at The Ohio State
University as a clinicalcardiologist and a lipid
(00:53):
specialist.
And I assume that's a placethat's in celebration mode
today, since we're recordingthis podcast less than 24 hours
after the Buckeyes.
Dr.
Romer.
Uh, won the nationalchampionship last night.
So Won the national championshiplast night.
So Ben welcome to the show.
Ben (01:12):
Yes, thank you very much, Kenny.
It's good to be here.
Yes, last night was a very fun,fun night, fun game, fun run so
good celebration today on, oncampus.
It was good to talk with you atthe Ohio ACC meeting a few
months ago.
We can kind of keep thatconversation going today.
Kanny (01:32):
Yeah, thank you very much.
Yeah, as you just alluded to,you did give a very nice talk at
our annual meeting about lipidlowering therapy.
So Ben, I know, I know you're agraduate of OSU Med School.
I, I see that you did most ofyour training in Chicago at
University of Illinois.
But we do have a lot of fellowsin training who listen to this
podcast.
(01:53):
And so we always like to startjust by hearing a little bit
about your journey to yourcurrent position.
And I guess what I would be mostcurious about is, as you pursued
a career in cardiology, whatkind of led you to focus on, on
cardiac prevention and theneventually, specializing in
lipid therapy as well.
Ben (02:11):
Yeah, certainly.
So, like you said, I I graduatedmedical school from Ohio State
and then I did my residency andtraining six years, or residency
and fellowship, rather six yearsin Chicago, University of
Illinois, Chicago.
And you know, I, I sort of knewrelatively early on that I
didn't want to be a proceduralbased specialist within
(02:33):
cardiology, but I really didn'thave much, that much of an
interest in prevention duringfellowship, mainly because I
found that it wasn't, it wasn'tstressed a whole lot.
I mean, when you're infellowship, you have to learn
ECHO, you have to be in the cathlab you have to learn EP.
It just seems like there aremuch bigger priorities with a
(02:54):
steeper learning curve.
And so it wasn't until Ireturned to Ohio State as as
faculty in 2020, and it wasn'tuntil about a year in until I
realized that I kind of had alittle bit of a relative blind
spot in my knowledge.
I just feel like as a generalcardiologist, I, I, I should
develop skills and preventionmuch, much sharper.
(03:18):
So I, I, I kind of just had aninterest.
I, as I was learning more andmore about prevention and about
the newer agents that are out tome, it just felt like a very
natural fit.
To immerse my role as a noninvasive cardiologist to also
focus on prevention becausethat's what a lot of patients
these days want to come in andtalk about.
(03:40):
They want to come in and talkabout calcium score.
They want to talk aboutlipoprotein A.
I think nowadays a lot of peopleare focusing on prevention.
So it was a, it was a verynatural progression, which I'm
very happy to be a part of nowat Ohio State in a very a very
excellent lipid and preventionclinic.
(04:00):
So so, you know, as time goeson, I think, you know, the role
for prevention in cardiologyjust continues to grow.
Within the prevention clinic, alot of patients are, are
motivated to help themselvesthrough lifestyle modifications,
but also with the newer lipidlowering agents, they also come
in and they, you know, they're,they're very interested in what
(04:21):
options are available outside ofstatins in order to reduce their
risk.
Kanny (04:25):
Well, speaking of statins, I thought, even though
we really want to focus on someof the newer agents, I don't
think there's a lot to say aboutstatins.
You know, we have three decadesof data and personal experience,
using statins to reduce risk.
But one topic I wanted to askabout statins before we move on
to the other agents is the issueof statin intolerance.
(04:46):
All of us in clinicalcardiology, of course, we
prescribe statins, we seepatients being treated, and I
think every clinician, really,who takes care of cardiac
patients has to deal with theissue of statins.
Statin either intolerance orwhat I would call statin
reluctance.
And we all know, of course, thatin the literature, you know, the
(05:07):
incidence is not particularlyhigh, but we also know in the
real world we do.
So I'm just curious, if youcould summarize, when a patient
who maybe is already on a drugcomes to you and notices some
intolerance or complaints, like,what is your overall strategy to
try to.
maintain statin therapy andthen, get into the decision
(05:28):
making and maybe about, analternate agent at some point.
Ben (05:31):
Yeah.
I mean, certainly within thelipid and prevention clinic I
see multiple patients every timeI'm in clinic that, that have
statin intolerance.
And, and as you said, whetherthat's a true adverse reaction
or it's just an unwillingness, areluctance, You know, the end
result is that we have to comeup with strategies to try to
(05:52):
encourage them to try anotherone or a different one, or maybe
remedies for their statinassociated side effects or
consider another alternateagent.
So in general I primarilyprescribe hydrophilic statins,
especially rosuvastatin.
And I find that a lot ofpatients come in on atorvastatin
(06:15):
or simvastatin, if justswitching them from those type
of lipophilic statins tohydrophilic one, especially
rosuvastatin, they do okay.
And I also think it's veryimportant to remind patients
that even a low dose ofrosuvastatin, maybe every other
day, you know, just fivemilligrams of Crestor every
other day can lower LDL by aconsiderable amount, you know,
(06:39):
25%, 30%.
And that's, you know, convincinga patient, Hey, you only have to
take this once every other day.
So, you know, I, my, my go tostatin is, is, is rosuvastatin.
But if they don't tolerate that,then pravastatin or patavastatin
even are, are other optionsthat, maybe they'll tolerate it.
Checking vitamin D is alsoimportant and, TSH, I, you know,
(07:03):
there's, there's some, there'ssome literature that suggests
that that low vitamin D candecrease HDL can increase LDL
and triglycerides.
So, that's something that we'llcheck, especially in these
winter months.
A lot of people are vitamin D, Ddeficient.
As for something like CoenzymeQ10, you know, the guidelines do
(07:25):
not recommend supplementing withCoenzyme Q10s to prevent statin
associated.
muscle symptoms, but I have noproblem prescribing it myself
simply because, you never knowif somebody has a placebo effect
even from Coen's MQ 10 to wipeaway their symptoms.
So, those are some of the, thoseare some of my initial reactions
(07:47):
to statin and tolerances.
It's important to check for fordrug interactions.
Having pharmacists on board inour lipid clinic is invaluable
to, you know, to help check fordrug interactions and
potentially reduce the dose of astatin if an interaction makes
it such that the level of statinwill be too high.
(08:09):
So those are kind of my, youknow, my, my, that's my
checklist sort of when patientscome in, but as you said, it can
just be challenging sometimesand sometimes people will come
in and they'll just be verystubborn and hard nose and you
can give them all the data andtalk about it, you know, the
lipid or the LDL lowering andthe anti inflammatory effects of
statins.
(08:29):
And, you know, you just can'treally budge them.
So it's a, it's a battle thatwe're going to keep fighting.
And, you know, sometimes you canmake headway with patients,
Because it is important to havethem on statins, but every once
in a while, you know, they just,that's not the case.
Kanny (08:46):
Yeah, yeah, thanks.
I wasn't aware of that linkwith, potential link with
vitamin D deficiency.
I think that's definitely worthkeeping in mind in many of our
patients, especially in thisclimate.
So that's good to know.
And I've had similar experiencewith, you know, the kind of
microdosing of rosuvastatin, andpatients, like you said, do
(09:08):
really tend to tolerate thatreally small dose even when
they've had other issues, andit's pretty striking the LDL
reduction you can get.
So, one other general question Ihad before we talk about some of
the agents specifically, becausethis does come up in day to day
practice as well, I know theguidelines still, focus on using
a standard, lipid profile, orperhaps using, non HDL
(09:31):
cholesterol as kind of apractical parameter to monitor,
therapy.
But we also understand, thatcalculated LDLs can be prone to
issues.
So in your patients, notnecessarily, your highest risk
patients, but in the day to daygeneral clinical, patients for
secondary prevention do youthink a standard profile is
(09:52):
enough for serial monitoring ordo you tend to, do direct LDLs
or consider measuring ApoBserially?
Ben (10:00):
Yeah.
I mean, in my patients that justin my, in my general cardiology
Clinic where I have patientsthat I'm following for
hypertension or Even just kindof risk factors if they're not
complicated heart failure, forexample I will get a lipid
profile with an indirect LDL andI'll get it when they're not
(10:23):
fasting.
I mean, just the routinescreening I have no problem
following the guidelines to, inthat regard, to get a non
fasting indirect LDL profile.
A.
And so, you know, the, the, thecalculated LDL is unreliable
when triglycerides are quitehigh.
So above 400 or, or, you know,if LDL is very low, if it's less
(10:48):
than 70, and really this is withvery high risk patients where
you're aiming for LDL is thatlow, that that's when the
calculated LDL can beunreliable.
So in patients that I have on,on multiple lipid lowering
agents, especially somethinglike PCSK9 inhibitor in patients
that have triglycerides thatare, that are really, really
high, then.
Then I will jump straight todoing the direct LDL and make
(11:12):
that lipid profile be fasting.
But in general I think it's justfine to kind of get the general
lipid profile in, in patientsthat you Either aren't worried
too much, too worried about, ormaybe you just haven't unveiled
what their true underlying lipidabnormalities are.
Kanny (11:30):
Great, great.
So, you know, assuming you dohave a patient who's either
tolerating statin therapy, butnot getting their LDL to target,
or is having, some degree ofintolerance, I guess I want to
just go over kind of yourpractical strategy for how you
would then incorporateadditional agents.
So, Is it safe to say thatezetimibe is still kind of the
(11:52):
first choice nowadays for a nonstatin or a second drug given
that it has, some outcome datathat we've been, seeing for
several years?
Yeah, I
Ben (12:00):
think that is safe to say.
It's safe to say mostimportantly from, as you
mentioned, outcomes dataimprovements in, in in major
adverse cardiovascular eventsfor secondary prevention
patients.
Thank you.
Mortality benefit, everythinglike that.
So it's important from thatregard, first and foremost, but
(12:22):
it's also important becauseinsurance companies won't cover
some of the other agents unlessyou've tried a zetamide.
So there are some patients whereif you have them on high
intensity statin and then youadd a zetamide that they'll,
they'll be, they will have anexcellent response to, the 10
milligram addition of azetamide.
(12:43):
Some patients, it lowers theirLDL by a, by a considerable
amount.
Some other patients, it doesn'treally budget that much, you
know, 10, 15%.
But, you know, in, in theory,ezetimibe should lower LDL by,
maybe 15, 20 percent asmonotherapy.
But when you combine it withstatin, more like 25 to 30%.
(13:04):
So, there are a lot of patientsthat we have, especially
secondary prevention patients,where the target LDL is below
70, or if they're very highrisk, below 55.
And let's say the LDL is, youknow, 5, 10, 15, 20 points
higher than what you target,that's when ezetimibe can
achieve your goal, and you'resort of, you're good to go in
(13:28):
that regard.
So, yes, ezetimibe certainly ismy first go to.
But in the realm of geneticdyslipidemia as familial
hypercholesterolemia patientswith really high LDL levels and,
and multiple manifestations ofatherosclerotic disease, if
their, if their LDL is over 100on stat, already on statin
(13:51):
therapy, and if you're trying toget them below 70 or below 55,
Addition of azetamide aloneisn't going to cut it.
So it sort of depends on whattheir risk is, what risk you've
established, and then just howmuch lower you need to target
their LDL as to whether theaddition of azetamide will be
enough with statin already onboard.
Kanny (14:16):
Sure, sure.
And then assuming you have to gobeyond azetamide then, I know
one of the newer agents that'sgarnished a lot of attention the
last few years since it wasapproved is bempedoic acid.
Can you say a little bit abouthow you use that agent now in a
clinical sense and in whatsettings?
Ben (14:36):
Yes, certainly.
So bempedoic acid is It maylower LDL by 15 to 20 percent
alone.
I think it's maybe closer to athird if you combine it with a
zetamibe and there's a, there'sa combination form of, a
zetamibe and bempidoic acid.
So in the trial, in the cleartrial the effect of bempidoic
(14:57):
acid as far as from a preventionstandpoint was more pronounced
in patients that were primaryprevention.
And so I generally use bempidocacid in those patients who who,
who are primary prevention, whomight be moderate risk that
certainly that aren't high riskor very high risk where, where
(15:19):
you're trying to lower their LDLagain, by, by by a modest
amount, 20 to 30%.
And if you can combine it with azetamine, that's the best bang
for the buck.
I mean, usually these arepatients who come in.
and they're statin intolerant.
So they're statin intolerant,their primary prevention.
And those are the ones where yousay, well, benpidioic acid may
(15:40):
be a good idea.
Now you have to be careful aboutgout.
Check uric acid levels beforestarting benpidioic acid.
I ask older patients above theage of 60 if they have had any,
tendon issues in the pastbecause there's a very, very
small risk of tendon rupturewithout that would obviously be
a catastrophic event.
So generally speaking, I use itin primary prevention patients
(16:03):
who are statin intolerant thatare maybe moderate risk and you
need kind of moderate LDLlowering.
I just think there are betteroptions out there for patients
who are secondary prevention oryou need You know, much more
aggressive LDL lowering.
Kanny (16:19):
Sure, sure.
And one final word aboutbenpedoic acid.
I mean, I know azetamide, ofcourse, is generic.
Do you have any issues withapproval or cost issues for,
cost or access issues for thepatient at this point in time?
Ben (16:32):
Yeah, certainly.
I mean, usually in order to getit covered you have to document
statin intolerance.
So both bempidoxic acid aloneand the combination you know,
can require a priorauthorization or can be costly
to patients.
So that's why, you know, it'snot an agent that I would just
jump to as monotherapy if apatient hasn't tried multiple
(16:52):
statins.
So usually it's, you know,they're statin intolerant, you
try a zetamide, they're eitherintolerant of a zetamide or they
need additional LDL lowering andmaybe they're, they're, you
know, they want to avoid takingmultiple medications.
So you can say, well, we canjust.
Do this additive to azetamide,but you're still only taking one
pill.
And so that's, that's kind of away to convince those patients
(17:14):
that, that bempedoc acid is agood idea.
Kanny (17:17):
Yeah, that makes sense.
That makes sense.
So then kind of moving on tosome of the other therapies I
mean we have you know about adecade of or more data with the
PCSK9 inhibitors You know, Istill feel like and tell me if
this is the case in your in yourpractice at Ohio State Is that,
are those generally stilladministered through your lipid
(17:39):
clinic or do you see somegeneral cardiac providers
getting more comfortable givingthose and then where do they fit
in, in the stepwise approach tothe helping patients get to
target?
Ben (17:53):
Yeah, so for, for a long while I, I think that a, a, a
common reason for referral tothe Lipid and Prevention Clinic
was to consider PCSK nine andadminister.
But really over the past sixmonths or so, we're making much
more of an effort to educategeneral cardiologists and
(18:16):
primary care physicians,internal medicine, family
medicine, that prescribing PCSKnine inhibitors.
Is is a very safe thing to do.
The risk profile is very low.
The efficacy is is very high.
You know, we're trying to makePCSK9 inhibitors more mainstream
and have providers be morecomfortable prescribing them
(18:39):
simply because, as I said, theyare so effective.
They're very effective andthey're safe.
The main thing is just patienteducation.
And so, you know, administeringPCSK9 inhibitors is quite easy.
It's just like, sort of like aninsulin pen.
I mean, I've had very littlepushback from patients about
(19:01):
using PSCSK9 inhibitors or eventhe side effects associated with
them.
And so we're trying to certainlymake it more mainstream with all
different providers who mightwho might be prescribing those,
you know, includingendocrinologists even.
So as for, when we, jumped tothem I think, I, I, as a.
(19:22):
Just as a cardiologist, I alwaystry to establish the patient's
risk.
And so, the first thing is todetermine whether that patient
is primary prevention orsecondary prevention.
And if they're secondaryprevention with a history of
heart attack or stroke or, youknow, peripheral arterial
disease, then automatically, atthe very least, you're going to
(19:43):
aim for an LDL target of lessthan 70.
And if they have otheradditional risk factors or
multiple prior events, then it'san LDL of less than 55.
And, you know, the truth of thematter is that these patients
that are secondary prevention,they had LDLs that were quite
high for a long period of time.
And PCSK nine inhibitors arejust so effective at lowering
(20:05):
LDL and non HDL, I mean 60% inthe trials for Repatha.
and for preluant.
So that's just that's anincredible lowering on top of
statin therapy alone.
So in those trials, the baselineLDL for these patients was maybe
around 90 or so because theywere already on statin therapy.
(20:25):
And addition of PCSK9 inhibitorsbrought them, you know, 60
percent below that baseline of90.
So I, you know, I can't talkenough about just how important
it is to administer PCSK9inhibitors.
In secondary prevention patientsor in high risk primary
prevention patients, especiallythose that have familial
(20:49):
hypercholesterolemia.
And then if you tell them that,you know, there's a med out
there that's more effective andyou can get rid of another one.
Oftentimes, they're very open tothat idea,
Kanny (20:58):
but you will typically continue the statin if they were
tolerating it,
Ben (21:01):
absolutely.
The statins are here to stay.
If the patient is toleratingwithout a doubt.
Kanny (21:08):
Yeah, 1 thing I was just thinking about when you talked
about acceptance of the,percutaneous agents is that
maybe with the proliferation ofsome aglutide and trizepatide
which it seems like, about halfour patients are taking now,
maybe that's made these theseagents more acceptable too.
Yeah, I
Ben (21:24):
think that's a great point.
And a lot of patients, willhave, you know, Great
cardiovascular benefits fromthose GLP 1 agonists as you
mentioned.
So I that that makes it sort ofsort of easier That you can tell
them.
Hey, it's just another injectionInstead of losing a lot of
weight like those meds youmentioned, well this is going to
lower your cholesterol levelsand you'll be in good shape, so
(21:46):
that's definitely a good point.
Kanny (21:48):
So in your in your clinic, who typically does that
initial education to the patientabout getting started on the
PCSK9 in terms of theinjections?
Some education about any sideeffects?
Is that, would that be apharmacist typically, or?
Or a nurse practitioner and howdo you think that could then
translate to like a generalcardio clinic?
Ben (22:07):
Yeah, so, in our lipid and prevention clinic, you know I'm
i'm paired with with apharmacist and we go and see the
patient together and do thevisit together, which is just
excellent from amultidisciplinary standpoint,
very comprehensive way ofevaluating the patient.
And it's usually the pharmacistthat, that will then, you know,
(22:28):
grab a dummy pen and do theeducation.
And truthfully it, it, thateducation lasts for less than a
minute.
So I, I think from from ageneral practitioner standpoint
it doesn't take much time toeducate the patient about
administering that.
I mean, it's, it, it's, Quitehonestly, it's easier than doing
insulin injections because youdon't have to set, you don't
(22:50):
have to set the dose but to behonest, even if you were to have
a nurse or, or, you know, a midlevel provider, I would feel
completely comfortable with anurse in my general cardiology
clinic educating a patient howto administer a subcutaneous
(23:11):
injection just because it isthat easy.
Kanny (23:15):
Yeah, I agree, and I think a lot of us in general
cardiology are finally gettingto the point where it's kind of
a routine part of our practicebecause obviously Not everyone
has access to a the resources ofa lipid clinic are limited even
in a setting when you have itYou know at least that's that's
the case for us as well Well, Iguess just to finish up in the
(23:38):
last few minutes five minutes orso.
I wanna ask you a little bitabout Enli, but just briefly, I
know there's another agent,another PCSK nine agent in umab
which my understanding islimited to, you know, homozygous
fh.
So is that an agent that wouldbe less common in a general
cardio practice at this point intime?
Ben (23:58):
Yeah, I think, I think so.
I mean, umab is, is, is veryeffective, but it is only
approved for homozygous fh.
So those are patients, that's anagent that really should be only
prescribed by a lipidspecialist.
After a patient has undergonegenetic testing with, with
confirmed homozygous FH.
Kanny (24:20):
Okay.
So then I guess that brings usto Inclisiran, which has also
been approved in the last fewyears.
And my understanding for that isthat it is indicated.
For secondary prevention C.
A.
D.
In addition to a familialhyperlipidemia.
So how is that agent, you knowdiffer from the more established
(24:42):
P.
C.
S.
C.
9 inhibitors.
And then how do you.
Incorporate that versus theother agents.
Ben (24:49):
Yeah.
So in glycerin and PCSK9inhibitors, they work very
similarly.
A PCSK9 inhibitor will, it's amonoclonal antibody that
attaches to the PCSK9 proteinand prevent that protein from
eventually down the roadcausing, causing breakdown of
the LDL receptor.
(25:09):
And glycerin is a smallinterfering RNA that prevents
translation of the PCSK9protein.
So it just prevents PCSK9protein from from even being
produced.
So the net effect is that youhave more LDL receptors to bind
LDL and take it out of thebloodstream between glycerin and
(25:32):
PCSK9 inhibitors that wediscussed.
So in glycerin is a veryeffective way to at lowering
LDL.
In the Orion trials, I think itreduced LDL by around 50 percent
or so, which is, which is anexcellent reduction in, in LDL.
So, there are some benefits tothe benefits to in glycerin is
(25:54):
that you only have to administerit.
You administer it day one.
And then three months later, andthen at six months, and then
after that, it's every sixmonths.
So after the first couple ofdoses Inclistrin is only
administered twice a year, whichfor some patients is a very,
very attractive way to have amedicine administered.
(26:16):
Now, it is administered in aninfusion clinic.
So you would have to go into aclinic to receive the to receive
the medication.
But that also means that that'snot charged to insurance.
Inclisirin is not charged as amedication.
It's, it's charged as kind of aas a clinic visit.
(26:38):
So, for patients that areworried about cost of medication
or at the end of the year beingin the donut hole and they're
paying an arm and a leg forwhatever, you know, their DOAC
and their SGLT2 inhibitor andtheir PCSK9 inhibitor, You can
kind of circumvent that cost insome, in some ways by having
(26:58):
Inclisirin be administered in,in, in the clinic setting, in an
infusion clinic.
So, you know, the, the one, theone point to make about
Inclisirin is that we, we don'thave outcomes data yet.
That's scheduled to come outover the next couple of years.
All signs point to certainly apositive outcome.
result from from those studies.
(27:20):
But I would just like to makethe point that we have a lot
more data with the PCSK9inhibitors and, you know,
generally speaking, they lowerLDL by 60 percent compared to
50%.
Kanny (27:30):
Yeah, great.
Great.
Well, that's good to know aboutthe fact that, it's a clinic
based treatment rather than, youknow, considered a
pharmaceutical because I dothink that makes a big
difference the way some patientsreimbursement works Well, it's
amazing how much this field haschanged in the last decade or
so.
(27:50):
with these new agents and thesenew outcome studies.
One final thing I want to askbefore we wrap up in a couple
minutes is, being an imagermyself, I'm always, been
interested in the way we can useimaging to kind of guide therapy
and patient management.
And of course, you know, if youthink more about primary
prevention, not so muchsecondary prevention, but for
(28:11):
the primary patient, which ofcourse we see many more of these
in our general clinics now.
How do you tend to use imagingtechnique like calcium scoring
in some of those borderlinepatients to make a decision, to
either initiate therapy or insome cases to convince a
patient.
That they need to be on therapy.
Ben (28:32):
Yeah, certainly.
I mean, you know from from themost recent guidelines the
guidelines And I I think a lotof us within internal medicine
family medicine no matter howyou're trained or are aware of
the pooled cohort equation whereyou know You just type in ascvd
risk calculator and then you putin the patient's name Age,
gender, ethnicity, their lipidlevels, do they have diabetes,
(28:54):
hypertension, etc.
And then it'll give you a 10year risk of atherosclerotic
event or lifetime risk as well.
You know, for certain agegroups.
And so then that'll categorizepatients in low borderline
intermediate or high risk of anevent over the next 10 years.
(29:14):
And per the guidelines, they saythat if you, if you have
patients that are borderline orin immediate risk, then to
strongly consider doing coronaryartery calcium score.
And I completely agree withthat.
I, I tend to use coronary arterycalcium score a bit outside of
that because I think that Inaddition to, to refining a
(29:36):
patient's risk in a better waywith coronary artery calcium
score.
As, as to whether or not youshould utilize a statin, I find
that if a patient, if a, if apatient knows that they have
some degree of coronary arterycalcification, if, if you can
sort of prove to them thatthey're already having
subclinical manifestations of.
(30:00):
of coronary disease, then theyare oftentimes they're more
inclined to take those lifestylemodifications more seriously, in
addition to being more openabout aggressive lipid lowering
targets with statins, ezetimi,PCSK9 inhibitors, all the agents
that we said.
So, you know, if a patient is,is, is very low risk, then no,
(30:24):
there's no reason to get acalcium score.
I mean, if somebody is 32 withno family history, no risk
factors.
There's no reason to get acoronary costume score, but you
know in that pooled cohortequation It doesn't take much to
get patients to intermediate orborderline risk as they get
older So once you approach theage of 60 you only throw in
another risk factor in there Andmaybe the LDL is just a bit high
(30:46):
and you get to borderline orintermediate or even high risk
And so obviously at that pointyou should strongly consider
statin therapy But what's alsotrue about coronary artery
calcium score is that it canreally help determine which
patients would benefit frombeing on aspirin.
I mean, as we know, over thelast five years, the pendulum
(31:07):
has swung away from aspirin useroutinely for primary
prevention.
But if you have a calcium scoreabove per the most recent
National Lipid Associationguidelines on coronary calcium.
That's an indication to start 81milligrams of aspirin.
Now you have to be a little bitcareful as patients get older.
(31:28):
I And the last point that I'llmake is that, you know, a lot of
patients, they may come in andthey may have risk factors, they
may have smoked for 30 years andhypertension, And you get a
calcium score and it's zero anda calcium score of zero, the
negative predictive value of acalcium score of zero over, the
next five years or so is quitehigh.
(31:48):
So it can be very reassuring topatients as well.
So I can't speak highly enoughabout utilization of coronary
artery calcium score.
I tend to utilize it outside ofwhat the guidelines say, unless
they're very low risk or ifthey're secondary prevention.
It should really only be used inprimary prevention.
There's no role for it insecondary prevention, but I just
(32:09):
think it gives you a lot ofinformation about where the
patient is and what their, what,what their, however long, how
many years or decades they'vebeen on, they've had certain
risk factors, you know, howthat's all added up to affect
their coronary arteries.
Kanny (32:24):
Yeah, yeah.
Well, I'm really glad to hearyou say that because I agree
completely.
I feel like, as you mentioned,there's a lot of power in zero
as well, sometimes you see, themget prematurely put on a statin
by a primary care provider, youknow, based on a single profile
or very unclear risk.
So I think that score is zero.
It couldn't really be reassuringas well.
(32:46):
Well, Ben, I think we covered alot of material.
It's such a changing field withso much data and prevention so
much that we've learned in thelast few years.
But I think you were able tokind of succinctly give our
listeners some practical adviceon how we, you know, Approach
these agents.
So I do want to thank you fortaking time to talk and also for
(33:07):
presenting at the State of ohiomeeting, a few months back and
Perhaps down the road we canhave you back to give us some
updates on on some of thesestudies you alluded to
Ben (33:17):
Yeah.
Well, thanks very much, Kenny.
It was, I mean, I think I, I'mvery grateful to be on the
podcast.
I've, I've really enjoyed, youknow, being part of, of, of
today, this podcast, and i, Ijust think it's an exciting time
to be in the field of preventioncardiology.
And, and, the, the whole reasonis to improve people's lives,
and there's no better way to dothat than prevent them from
(33:39):
having really, poor outcomesfrom heart attack or stroke, is
the best part in all that we do.
Kanny (33:47):
Yeah, absolutely.
And I guess the final thing I'llsay, you did allude to the
guidelines and I just want toremind the listeners that there
is an ACC expert consensusdocument that just came out in
2022 that specificallyaddresses, non statin therapies.
And it's a great referencedocument.
It's very practical as well.
So it's really written, youknow, with an eye towards day to
(34:09):
day practice.
So we will put a link to thatactually in the notes for our
podcast.
So I want to thank Ben and Iwant to thank our listeners and
until next time, thank you all.
Thank you for joining today'spodcast.
For more information about thespeakers or the topics, please
go to Ohio acc.org,
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