As high levels of LDL-C pose a significant risk to heart health, reaching LDL-C goals is crucial for reducing the risk of cardiovascular events. One effective approach is statin intensification, which involves increasing the dosage or switching to more potent statins. However, achieving LDL-C goals requires more than just taking medication. In this blog post, we will discuss the essential steps to effectively reach LDL-C goals, emphasizing the importance of lifestyle changes and medication adherence.
– [Rebecca] Good afternoon. My name is Rebecca Licky. I am a National Program Consultant With the American Heart Association, And I will be your
moderator for this session. On behalf of the American
Heart Association, I would like to welcome you To the second session of
today's Close the SPACE – Secondary Prevention of ASCVD
Care Education Virtual Summit. All presentations will be recorded And available in the coming
weeks at heart.org/ascvd. It is now my pleasure to
introduce our speaker for today, Dr. Nishant Shah. Dr. Shah is a faculty member
at Duke Medical Center, Division of cardiology And is an expert in
preventative cardiology As a member of the Cardiometabolic
Prevention Program. He obtained his medical degree From Wake Forest University
School of Medicine, Internal Medicine Residency training At Johns Hopkins Osler Program, And his cardiology fellowship
training at Cleveland Clinic. Dr. Shah's research Revolves around the
clinical manifestations Of genetic lipid biomarkers, Lipoprotein A and advanced dyslipidemias. Dr. Shah also serves
as an associate editor For the American Heart Journal And is heavily involved
clinically at both the outpatient And inpatient level at Duke Heart Center. Dr. Nishant Shah, the floor is yours. – Thank you so much For that extremely, extremely
kind introduction, Rebecca. It's such an honor to be
here today with all of you
And to talk about statin intensification And ways we can meet our LDL-C goal, Which is extremely important
in patients with ASCVD. These are my disclosures. The purpose of my presentation today Is purely, purely, purely educational. So I wanna just start off by defining What ASCVD actually is. So ASCVD for many on the call who know, Is atherosclerotic cardiovascular disease, And it is a combination of
a multitude of conditions. So non-fatal myocardial
infarction, non-fatal stroke, TIA, peripheral arterial disease, Nonobstructive CAD, Aortic atherosclerosis and aneurysms, Carotid disease, And any other coronary
or other particular, Like peripheral arterial
revascularization. So very loaded, loaded term. And we have, Through the American Heart Association And American College of Cardiology, We've developed a risk calculator That you guys have also
probably all commonly heard of. And this is mainly for patients
with in primary prevention, Not necessarily patients
with established ASCVD, But I think for the purposes
of just understanding Statin intensification and
why we need to intensify, I think it's important to just talk about. But you know, in a patient
who has not had an event, This calculator can be helpful To just get an understanding
of baseline risk. And so, it's important
to remember however, That this risk calculator
has some caveats,
In that it assumes That the patient has not
have established ASCVD, Is between the ages of 40 and 75, Is ideally not on a statin therapy, Doesn't have an extremely
elevated total cholesterol. And it's important to note
that at extremes of ages, There can be an underestimation
or overestimation risk. And again, The importance in all
of this risk assessment And statin intensification
and choosing therapy Is mainly done With the foundation of
shared decision making. So the idea is, it's not
necessarily to tell you what to do, But help you guide or be a
guide for your decisions. So this is an example of what the, The important parameters Of the ASCVD risk calculator include. So gender, age, race, Lipid panel, Particularly the total
cholesterol, LDL and HDL, And whether or not they're on a statin, Blood pressure and prior
history of smoking, Diabetes or aspirin
treatment and hypertension. And with that, we get an
estimated 10 year risk. And that goes into four different buckets. So the low risk or less than
5% risk of an event, 10 years, Borderline, five to seven and a half, Intermediate, seven and a half to 20, And high, greater than 20%. Again, this is assuming a
primary prevention patient Without diabetes between
the ages of 40 to 75 And who have an LDL
anywhere between 70 and 190. What do we do though? What do we do with those buckets of risk?
What's kind of the guideline
based recommendation On how we should move forward? So if someone is at low risk, Again, it's important to have
that discussion with them And emphasize the importance Of good lifestyle modifications, Evidence-based lifestyle modifications That can prove to better outcomes. At borderline risk, Again, good patient-centered discussion. And this is where you
would start to consider, And I would argue even in the low risk, If there's other risk enhancers That are not included in
the ASCVD risk calculator, That could increase someone's risk More than what meets the eye, if you will, An intermediate, again, Having that risk discussion, Identifying silent risk enhancers. But it's also not unreasonable to go ahead And start moderate intensity statin In this particular patient population With the goal to reduce LDL by 30 to 49%. And, of course, high risk patients, Those with greater than 20%
risk, assuming you do nothing, Having that risk discussion And hopefully initiating
a statin at first line To reduce the LDL by at
least 50% if possible. I talked a lot about risk enhancers And this is important to keep in mind Because these are things
that are not included In any of the risk calculator, And they include things like Premature family history
of coronary disease,
A persistently elevated LDL, Chronic kidney disease,
metabolic syndrome. I always tell my fellows and residents, Hey, you've got to know what a patient's, Especially our female patients who, And our patients that can get pregnant, What their pregnancy history was like, And also what the
menopause history was like. Was it premature? Did they have a history of preeclampsia, Gestational hypertension,
gestational diabetes? All these things increase risk. Inflammatory diseases, ethnicity, South Asian ethnicities in
particular have a higher risk. And then certain biomarker patterns. So elevated high sensitivity CRP, Looking at their lipids, High triglycerides greater than 175, An LPA or lipoprotein A Greater than 50 milligrams per deciliter, ApoB greater than 130. And, of course, if they've
had ankle brachial indexes, Those that are less than 0.9, Those are extremely
important, very important. And I would say these risk enhancers, I mentioned them, you know, In the context of a
primary prevention patient, But if you have a secondary
prevention patient Or someone with established ASCVD, These are the things That really, really, really
will screen residual risk And really, really should emphasize The importance of lowering
our LDL cholesterol As low as we possibly can to
help optimize our patients.
But we've all perhaps have
heard this from our patients, We've all heard a comment, "Perhaps maybe I just don't
know if I wanna be on a statin", Or, "Hey, I'm otherwise physically active. Yeah, I just had an MI but
I'm eating a plant-based diet. I, you know, I've heard and read a
lot of negative things About certain lipid lowering therapies, Will this medicine actually help me? I need proof." Now, again, This is meant more for the
primary prevention patient, But this may be a good
opportunity to do a calcium score. And I apologize for some of
the overlap here of the slide, But a calcium score in someone Who's not had established ASCVD
is a two-way recommendation, Especially if they're
hesitant to be on a statin Or where the benefit of a
statin appears to be unclear. And a calcium score Has come with a lot of data more recently, You know, the prognostic
utility of a calcium score. This is just some early
data of two big cohorts, One that was followed for five years And the other was followed for 12 years. And if you look across this
entire patient population, Both the five-year follow-up group And the 12-year follow-up group, The top line here of
the Kaplan-Meier curve Is someone with zero coronary calcium And the calcium score
increases in a graded fashion As the all cause mortality increases. So without doing anything, The higher your coronary
artery calcium score, The higher the risk.
So now kind of taking it back To that patient with established ASCVD, If you have some coronary
artery calcium data Prior to when they had their event, You can get a sense on, Whoa, their calcium score was X, They are at high residual risk And now they've obviously had an event And so we need to be
even more conscientious Of that person's risk for future events. This is, again, a very nice study Comparing the interplay of
traditional risk factors With coronary calcium alone. And when I say traditional risk factors, I think about things like
hypertension, diabetes, Hyperlipidemia, smoking. If you, And the only point I wanna
really come across on this slide Is that if you have a patient with Just no coronary artery
calcium, so calcium is zero But greater than or equal to
three traditional risk factors, If you look here on the
bottom right of my screen, The yellow bar, This is the risk of
someone with zero calcium With a lot of traditional risk factors Compared to someone with maybe
no traditional risk factors, The back left, But a calcium score greater than 400. It goes to show how
prognostically valuable A calcium score can be Because it really
reclassifies someone's risk Independent of traditional risk factors, Which is also very, very
important and telling. And we've also, with time,
have created a risk calculator
That incorporates the calcium score When you get it to
understand somebody's risk. And so if you look at someone's risk And you say there may be,
let's say, intermediate And you put in, And you get a calcium score
and it's elevated at 600 And you put that into this, You may find that their
actual risk is much higher. And so, and this is just
based on the MESA cohort And you can google MESA, M-E-S-A, Coronary artery
calcification risk calculator To get a assessment of risk Incorporating the coronary
artery calcium score. Okay, so we talked about residual risk Both in the primary prevention patient And also a patient at
secondary prevention, But also has some of these
risk enhancer markers From the past that have been discovered. Well, what do we do? How do you treat them? Well, the first line of
therapy is statin therapy. These are extremely well-studied drugs That have been out for a long time. Here I just give a table of low, Moderate and high intensity statins. And kind of in, Sort of, classical textbook
types of LDL reduction. Now I will say with anecdotal experience That I have placed people
myself on lower doses of, Let's say, rosuvastatin at five milligrams And have had a profound LDL reduction Much more than what I would've expected Based on sort of statistical estimates Of how low we'd actually get the LDL.
Some people tend to be hyperabsorbers, Some people may be on drugs That sort of lower the
metabolism of statins, Et cetera, et cetera. And so every patient is different. I just wanna throw that caveat out there. But in general, This is sort of what we would
expect with low intensity, Modern intensity and
high intensity statins In terms of LDL reduction. Now, high intensity statins Are defined as rosuvastatin
20 to 40 milligrams a day And atorvastatin 40 to
80 milligrams per day, Moderate intensity for
atorvastatin, rosuvastatin, Anything lower than that. And notice that in low intensity groups That rosuvastatin and
atorvastatin are not there. They are at the minimum,
moderate intensity statin. So if you have a patient
with established ASCVD, Currently, the guidelines would recommend Placing them on a high intensity statin. And so, if you do that, You would choose from
either rosuva 20 to 40 Or a atorva, four to 80. And a lot of that is based on
what their LDL is pre-event, So if they've not been on statin. Of course, if they've been on a statin, Then optimizing the dose To get them to particular
LDL-C thresholds, Which I'll talk about. So, but if you're looking back At the primary prevention group And the intermediate or borderline risk, Starting with the moderate
intensity statin at first
Is very reasonable, And at high risk, Starting at high intensity
statin is also very reasonable. What about statin treatment Based on coronary artery calcium score? So if you have a coronary
calcium score of zero, Assuming they have not had an event, And assuming there are
no other risk factors, Like familial hypercholesterolemia Or an elevated lipoprotein Or their biomarkers that are of concern, Usually can monitor a patient Just with good lifestyle modifications. Again, this is assuming
they've not had an event, They do not have ASCVD. A calcium score between one
and 99 favors statin therapy And that greater than a
100 or equal to a 100, Highly recommend to
initiate statin therapy. How do you reassess lipids? And this is pertinent to both primary And secondary prevention patients. If you make an intervention, The guidelines would
recommend reassessing lipids Anywhere between four to 12 weeks From initiating a statin
or a non-statin therapy, Even just to make sure that you
are reaching your threshold. And a routine measurement
every three to 12 months Is very reasonable. Fasting is generally not required Unless you're concerned
about triglycerides Or other type of genetic dyslipidemias. But we also have patients
who are statin intolerant. And statin intolerance is
something that we've studied a lot And found that it's oftentimes
not as frequent as we think
Based on studies that have
looked at placebo effects Or nocebo effects. However, in a patient's
mind, it may be real. In a patient's mind, it may be something That's really impacting
their quality of life. And so, the definition that
I personally like to use For statin intolerance, And this is based on the
National Lipid Association, Is the inability to tolerate
at least two statins, One at least at the lowest starting dose Due to objectionable symptoms Or abnormal laboratory values That are temporarily related
to the onset of statin use And resolve with statin discontinuation. And the more, You know, in general, As you know, As uncommon as statin tolerance is, Truly based on the literature, The things that we see
more often are myalgias At three to 5% rate, Essentially cramping,
stiffness, soreness, aching, Usually bilateral of proximal muscles, Myopathy where you have a CK level That is five times the
upper limit of normal, New onset diabetes
depending on what you read And based on what data That you're getting the information from, It's ranged anywhere from nine to 27% But probably much lower than 27%. And again, Every study that has looked at this Has seen that the benefit
that you would gain By being on the statin
Far outweighs the small, small, small risk Of developing nuance, like diabetes. And we've seen also that it, The nuance of diabetes Tends to be more so focused in subgroups That are already predisposed
to insulin resistance. And hepatotoxicity, of course, Defines as three times greater Than the upper limit of
normal in your liver enzymes. So how do we manage that intolerance? In, you know, In a primary prevention patient, It gets kind of hard again. And I don't wanna say hard, It would get, It's a little bit more nuanced, Certainly deescalating the dose Or altering an alternative
statin or alternative dosing. Don't forget ezetimibe. Now if they do have familial
hypercholesterolemia, Than moving towards a PCSK9
inhibitor is important. And then, of course, doing all this In addition to lifestyle modification. Now remember, If the patient also has
established atherosclerotic disease Or maybe non-obstructive coronary disease Or non-obstructive
atherosclerotic disease, These are patients that
are now with ASCVD, right, Based on the definition. So they would benefit From being treated as
secondary prevention. So in secondary prevention patients, Patients with established ASCVD, You could try an alternative
high intensity statin
Like atorvastatin, if
they were on rosuvastatin, Or rosuvastatin, if they
were on atorvastatin, De-escalate the dose. But most of us in the prevention space, Especially lipid space, Are moving towards alternative
lipid lowering therapies To add as an adjunct to statin. So adding ezetimibe or a PCSK9 inhibitor, Most likely combination therapy. And so, Doing all of this in addition
to lifestyle modifications Is what would be recommended. So low threshold, If you can't tolerate at
least two different statins Of the maximal tolerated dose Or your LDL is just not getting
to where it needs to be, Then adding a non-statin such as ezetimibe Or PCSK9 inhibitor is
absolutely important. For familial hypercholesterolemia, I just kind of listed some of
the more common mutations here Of familial hypercholesterolemia
at the LDL receptor level Or at the apoB level Or the PCSK9-gamma function. This is a condition that is
oftentimes underdiagnosed In our community. And if found early, Extremely important to
bring their LDL down Because a hallmark, At least clinically of a
familial hypercholesterolemia Is an LDL greater than 190. And, of course, with the family history Or early personal history
of a cardiovascular event. So something to keep in mind Because if you intervene
early on these patients,
You can do them a lot of good. And so how we manage
familial hypercholesterolemia And how we sort of intensify
their LDL lowering therapy Is we really, really,
really wanna focus on Upfront high intensity statin
to bring the LDL down by 50% Or to a 100 or less, whichever is lower. If unsuccessful, adding ezetimibe, And if on combination therapy Or you just need to get
the LDL down even lower And you don't think ezetimibe
alone with the statin Is going to cut it Or they are statin-intolerant, Going straight to a PCSK9 inhibitor. In secondary prevention, The goal is, The threshold rather Is less than 70 milligrams per deciliter, Of course, just like
it would be for anyone That doesn't have familial
hypercholesterolemia But has established ASCVD. So kind of honing in on our
secondary prevention patients, Our established ASCVD patients, We really, really want to understand What that residual risk is. So that you know in general, 'cause this is a little bit busy slide, But in general, we wanna bring their LDL At least to less than 70
milligrams per deciliter. Now, there's in the guidelines, They kind of go into classification
of very high risk ASCVD And those not at very high risk. And a lot of that is based
on comorbidities and age. And so I've listed here in this red box, Sort of the very high risk factors, right?
So very strong family history of diabetes, Persistently elevated LDL despite therapy, History of heart failure, Other complication of a
myocardial infarction, Older age, CKD. And so, in general, We'd really like to bring the LDL down In our current guidelines here in the US To less than 70 milligrams per deciliter. But you know, The lower, the better, In general, if you have high risk. And in fact, There was a recent expert
consensus decision pathway That has advocated for
bringing the LDL cholesterol Down to less than or equal to
55 in very high risk patients. And this is also consistent
with European guidelines, What our colleagues in Europe
are also advocating for. And in general, Just thinking about a
primary prevention patient, If they have risk factors like diabetes, Endocrine societies are now advocating For an LDL cholesterol
threshold to be less than 70, Even in that groups who
have not had an event But just have high risk,
like a patient with diabetes. So, but for an ASCVD patient, A patient at very high
risk, lots of comorbidities, A strong family history, older age, Really trying to push them
to less than 55 if possible. And so what that sometimes means is that The statin alone may not be enough And that they may need
upfront combination therapies To optimize their risk.
So there's some novel agents That I definitely want to talk about Here in the last few
minutes of my presentation That are FDA approved And maybe a few others
that are on the horizon. So in terms of, And these are all LDL lowering therapies, And especially for patients
who are secondary prevention. So there's bempedoic acid, Which is a once daily,
oral non-statin therapy Which works upstream from the
HMG-CoA reductase pathway, Which is how statins
work in the hepatocytes. And data has shown, early
data of bempedoic acid, Modest reduction in LDL-C And it works well as an adjunct to statin. And as I will get to after the
recent CLEAR Outcomes Trial, Also seems to have a benefit
in statin-intolerant patients With established, Both with established
disease and actually without. And also, bempedoic acid
comes in a combination pill With ezetimibe. And so that's also an
interesting sort of option For patients who are, let's
say, are on ezetimibe already, They can't tolerate a
statin, for instance, Or they're on a statin, Instead of adding a third pill, You can, if they're already on ezetimibe, They're tolerating it well, You can potentially do a combination That includes the ezetimibe already there. Then there's inclisiran, Which is an siRNA-based
therapy targeting PCSK9. So effectively also a PCSK9 inhibitor, Just not a monoclonal antibody
Like what is currently
available in with evolocumab And alirocumab. The other thing about
inclisiran that is unique Is that maintenance, It just requires one
subcutaneous injection Every six months. So the way it works is, you
can get a shot in day zero, Then at three months, Then every six months after that. So for maintenance, You're gonna be getting
a shot twice a year To help lower your LDL. And based on the data that we do have, It can lower LDL-C up to about 60%. So this is just sort of a schematic On how bempedoic acid works. Bempedoic acid, as I mentioned, Works upstream to the
HMG-CoA reductase pathway. So don't know if you guys
can see my mouse or not, But statins work here at HMGR, Bempedoic acid works up here. And the idea is that It prevents the development
of various metabolites That can concentrate in skeletal muscle That may lead to intolerant symptoms. This is just data from the
earlier CLEAR Wisdom trial That showed sort of the modest reduction In the LDL-C over time. Again, smaller trial
compared to some others That we have more recently
in the bempedoic acid space. But did just show us that
this does reduce LDL. One of the things to just keep in mind 'cause everything we do
really revolves around Shared decision making,
Is just understanding the patient That you're starting bempedoic acid on. And one of the things
in terms of its safety, It's relatively safe, But there was a signal
towards increased gout flares In patients with established
gout with bempedoic acid. But more exciting about bempedoic acid Was really recently at the past American College of
Cardiology Scientific Sessions Where the presentation of
the CLEAR Outcomes Trial Was presented. This was a double-blind,
randomized placebo controlled trial Involving patients who were unable Or unwilling to take statins
due to statin intolerance. There was a total of about 14,000 patients Who underwent randomization, About 7,000 assigned to bempedoic acid And another about 7,000
assigned to placebo With a median follow-up
of about 40.6 months. About 4,000 patients were in
the primary prevention setting, So they've not had an event, And about most of them, 70% were established ASCVD patients. The primary endpoint was
four-point composite of MACE, Including death from a
cardiovascular cause, Non-fatal MI, Non-fatal stroke and
coronary revascularization. And what you can see here Based on the Kaplan-Meier
curves that I've showed Across four-point component MACE, Which is the primary
endpoint of bempedoic acid Did better than placebo In terms of reducing these events. Same with the three-point composite,
Looking at just fatal or non-fatal MI And just in terms of
coronary revascularization. So there seemed to be a benefit In the statin tolerance population In reducing cardiovascular
events with bempedoic acid. So it just gives you some outcomes data. I shared that really to
provide outcomes data With some of the novel
therapies that we have. The outcomes data with
inclisiran is still in the works But the LDL reduction is very profound. This is just a schematic of how it works. It's an siRNA molecule That works in the nucleus of
our cells to inhibit PCSK9. Here's some data from
both ORION 10 and ORION 11 Showing the reduction
in LDL-C of inclisiran That you can see that there
is pretty profound reduction Across two different cohorts,
ORION 10 and ORION 11. And so if we do believe, And with many of us do That reduction of LDL
can lead to improved risk And reduce risk of cardiovascular events, Then this certainly can
be a very useful tool In our toolkit in addition to many others. This is the oral PCSK9 inhibitor That is currently investigational. That is just another option for patients Found to be relatively safe
and reduce PCSK9 by 90% And LDL up to 65% and has, You can see here that
is very dose responsive. And then more recently at ACC 23, The phase two B randomized
clinical trial was presented That showed up to a 61% reduction
in LDL compared to placebo With no difference in adverse
events between the two arms And good medication adherence.
And this importantly, This study included patients
with ASCVD uncontrolled LDL, Those without ASCVD but at
borderline or high risk. So very important again
across all spectrums. Lastly, treatment that
is currently available For homozygous FH patients, Patients with two mutated genes That lead to abnormal
metabolism of cholesterol Is evinacumab, Which is an angiopoietin-like
three protein three inhibitor, Again, drops LDL in these
patients by about 47 to 50%. So lot of options out there, right? Lot of options in our toolkit, But there's a much
bigger problem than drugs That can help us, right? The problem here is that, you know, We have all these cool tools, But you know, many of our patients, Many of our established ASCVD patients Are not even on statin therapy. This is a study of patients Across from 2019 onward And it looked at over
600,000 patients with ASCVD. Almost about 50% of
them were not on statin, Only 22.5% were on high intensity statin. And outside of statins, 27.6%. And those that were less
likely to be on statin Were females, Those with lot of comorbidities Or had cerebral vascular disease or PAD. So these are very high risk
patients that are not, you know, Covered with one of the
most foundational therapies. So we need to do better as a society Which is why I'm really glad
that we're having these talks
To discuss how we can do that. And this is not just for statins either. This is a study our team
did of over 700,000 patients With established ASCVD And that looked at from 2018 to 2021, The uptake of non-statin
therapies like ezetimibe, PCSK9 inhibitors, icosapent ethyl. And what we found was that Only 6% of patients were on ezetimibe, 1.6% were on PCSK9 inhibitors, And only 1.3% was icosapent ethyl With a small uptake over time. But this is as of 2021. So a lot of patients out
there with uncontrolled LDL-C With low implementation
of evidence-based therapy. So I think as a society, We certainly need to
think about the barriers That we heard about earlier here That are leading to the lower
amounts of implementation Because we know that these drugs can work, We just now have to
figure out as a society How we can do better at
getting them to our patients. So I'd like to conclude there. We have so many different
strategies and options For lipid management. Important to remember, We have to reassess our LDL-C To make sure we are getting to the goal Or the thresholds that we want. If we don't recheck, we won't know And our patient may still be at high risk. It's important to personalize our strategy Through shared decision
making with the patient, With guidance from the guidelines.
Remember, every patient is different And one thing may work for one patient, It may not work for the other. And we have a lot of opportunities To improve LDL-C management
at the health system provider, Patient and community levels. And I think we need to come together And collaborate across the spectrum here To really be effective in lowering LDL-C And optimizing risk in our
established ASCVD patients. I'll conclude there. Thank you so much. And I've left my email on here
if anyone has any questions, As well as my Twitter handle. I try to promote some
educational material, A very good scientific material
if anyone wants to view. And I'm open to any additional questions That we have here from the group. Thank you so much. – [Rebecca] Thank you so much Dr. Shah For your presentation. At this time, I would like
to encourage our participants To type their questions
into the Q and A box. I did see a hand was raised earlier. All questions will be asked to be directed To that Q and A box on
your bottom toolbar. Our first question that we
do have for you Dr. Shah, Is how do you manage LDL cholesterol In patients with elevated LP(a)? – Very, very good question. So the way I do it, the
way I look at elevated LP, I view that as an extremely
high marker of risk. And so I treat my patients
who have not, let's say, Had an event
But have elevated LP(a) as
if they've had an event. So what that means is I really
drop their LDL cholesterol As low as I possibly can Within the means that
I have in front of me. So high intensity statin, Get their LDL as low as possible, Definitely below 70 milligrams
per deciliter at the minimum. I try to modify their other
modifiable risk factors. So they're also hypertensive
or they're obese, They have diabetes, I really am aggressive with those things. I really make sure good
diet and exercise regimen Is being done. But yeah, to directly answer
your question about LDL, I do everything I can to bring the LDL As low as I possibly can With the therapies that I have available. – [Rebecca] Now in that same vein, When do you screen for elevated LP(a)? – Excuse me. Yes, very good question. So the European guidelines
recommend screening everyone Once in a lifetime for elevated LP(a). So I have a very well
threshold to screen for LP, Elevated LP(a). (coughing) Excuse me, But more particularly, Where I'm thinking about elevated LP(a) As being something to know about Is in younger patients
who have had events, People with extremely
strong family history, People with familial hypercholesterolemia. We know that at least
up to 20% of patients With familial hypercholesterolemia
have elevated LP(a), People who I just cannot
get their LDL under control
Despite everything I'm doing. I check for LP(a) because you know, 45% of the LP(a) core is LDL And traditional lipid
panels cannot distinguish Between free LDL and the LDL
that's attached to LP(a). And so that's another
group that I look for. And I think it's important, in general, If anyone has an interest in
knowing what their LP(a) is To screen for them too. And the reason I say that is because one, If I know someone's LP(a) is elevated, I can do what I mentioned
earlier, in that I can, I know how aggressive I need to be With their LDL management. Oftentimes, depending on elevated levels And other risk factors, I look at their bleeding risk And maybe this is a patient I also want to be on aspirin therapy If their bleeding risk is low Because I know they're
extremely high residual risk. And then third, I have family
screening implications, right? Like, if I have a patient
that has an elevated LP(a), I definitely want their
first degree relatives To be screened for LP(a) as well. So you know, the more we
know about elevated LP(a), The more important it is Because we can start
preventative therapies earlier And then, of course, They can be on our radar
for clinical trials That are currently being conducted That are testing either
antisense oligonucleotide Or siRNA-based therapies directly
inhibiting lipoprotein A. – [Rebecca] Wonderful, thank you.
Next question, How can we improve the uptake
of lipid-lowering therapies In the real world? – Great question. I think this is gonna take
a collaborative intervention Between the health system, the patient, The provider, the community, Because we are all in this together. We need to identify the disparities, We need to identify social
determinants of health That are preventing our patients From getting the therapies that
would benefit them the most. We need to look at access issues, Like what's preventing a patient
from getting this therapy? Is it cost? Are there assistance plans available, Either at the health system level Or at the pharmaceutical company level? Are there barriers in terms
of getting to a clinic? You know, We need to think about
transportation issues there. And then we also need to think about Innovative ways of
identifying people at risk. So one of the things that
I'm very interested in Is remote lipid monitoring. So when you think about, you know, Our providers that are
out in the community, Many of them are seeing
five patients an hour. They may, you know, Have only a certain amount
of time in a clinic visit And they may have to focus their
clinic visit on, let's say, Back pain or assuming this
is a primary care provider, You know, knee pain Or some other comorbidity
And that they'll be like, All right, next visit
we'll look at your LDL, But by the time the
next visit even happens, The patient who has residual
risk might have had an event. And so remote lipid monitoring Might be one innovative way Of just using like a clinical champion. So like a clinical pharmacist, An APP who's just screening
patients through the EHR To see who's at risk, And if they have an LDL
that's at goal or not Because this could be one
way to identify them early, Even make an intervention remotely, Send a prescription to
either optimize a statin Or start a statin And get that started early, So that by the time they
go back to their PCP And they get their LDL checked, They're at goal and their risk is reduced. So thinking about innovative ways, Other interesting ways of doing this Is partnering with like common, you know, Consumer organizations. So like Costco or grocery
stores or I don't even, I don't have nothing, I
have no stake in Costco, I just, the top of my head, Could probably have to go to Costco later, But just big grocery stores
potentially to, you know, Promote heart healthy, you know,
diets and things like that. And so, a lot of like,
you know, innovative ways. Digital health is another
booming, booming, booming area That we could utilize. So, you know, remote
monitors to, you know, Help us understand our
cardiometabolic health.
And then again, AI technology
is really, really growing And we're, you know, AI now can algorithmically
screen large EHR data To identify the people at
risk that we need to look at. So kind of becoming more
precise in our management, Identifying people early
may be some innovative ways. – [Rebecca] Great, thank you so much. Our next question, And we do have a couple
of minutes left though, Again, I encourage everybody
to ask any questions That they might have of Dr.
Shah into our Q and A box. The next question we have is, How can we help the transition of patients Coming off an acute stay
and managing their LDL, Especially when dealing with
many other urgent conditions Or needs? – You know, so the important
thing is going to be Just keeping an eye on, you know, Just having a note that
we need to check in LDL, We need to check in LDL later, you know, In three months, you know. Like, once they started a treatment, We need to make sure that
that treatment's working. So having that note in on checking in LDL Will be extremely
important in three months. Making sure that the dose, Let's say, a statin
was appropriately dosed So they don't need to go higher, They're not, you know, If someone who's had an event Didn't have a moderate intensity
statin that was prescribed, If that's truly their
maximally tolerated dose, They don't need to optimize. So just keeping those things
in mind after an event,
You know, especially if they
have a cardiovascular event That's gonna be extremely
important on hospital followups To make sure they're not on all the right Evidence-based therapies. Now, if you have other pressing issues, I think cross collaboration is important. You know, I think that, You know, my personal opinion, It's never too early to see a cardiologist And so if you need to send
them to cardiology or you know, Send an E-consult or a staff
message to a colleague, Let's say, you're a primary care provider, Just to make sure everything is in check, Just to kind of help
take the load off of you Because you're also managing
some other important issues Will be important as well. After an event, Typically patients go to cardiac rehab, And so, that's also a place
where there's some safety nets To make sure their LDL is controlled. And so just keeping that
on your radar I think Is the best way to do it And making sure there's a
plan to address that LDL At some point, Whether it's just a
three month lipid panel To see how the statin they
were initiated on inpatient Is working Or phoning a friend or collaborating. – [Rebecca] Thank you so much. I think we have time
for one more question. Can you touch on best
practices for challenging And rechallenging for statin intolerance? – Yeah, so that's a great question. So it really depends on
If they're primary or
secondary prevention. If they're secondary prevention,
I would say don't try, My personal opinion is, If they can't tolerate a statin Despite you trying a different statin, Especially between
atorvastatin and rosuvastatin, I would move straight
to non-statin therapies Like PCSK9 inhibitors. Ezetimibe is always your friend as well And that it can be your friend In the primary prevention setting. For the primary prevention setting, I think that's where it becomes A little bit more challenging Where you may need to try The lowest dose of a particular statin To make sure they're tolerating it, Switching, trying every other day. You can do that or you can
risk classify them further. You know, you can get a calcium score To see like how aggressive
do I really need to be? You know, if they have elevated calcium, Then they have ASCVD And so just making sure they're
not symptomatic from it. And 'cause if they have
ASCVD, then the whole, The whole window of
opportunity opens up for you In doing non-statin therapies, Looking to make sure they don't have FH Because then you can do
more than just statins. But a minimally tolerated dose, Finding one that works And ezetimibe is gonna be important. And I think with time,
as the data keeps coming, It seems like more non-statin therapies
Are gonna be coming into the
primary prevention space. So those will also be available. But the biggest thing
is just to understand How aggressively you
need to treat the LDL, Especially a primary prevention patient With some of those risk
enhancers I mentioned Compared to secondary prevention, You can just go straight
to PCSK9 inhibitors If after intolerance to at
least one or two statins. – [Rebecca] Thank you so much, And thank you Dr. Shah for
this insightful presentation And thank you to our audience
for your participation. Coming up next, we have two sessions Starting at 1:30 central time, Session four, Benefits of Integrating
Pharmacists in ASCVD Management, And session five, Alert: Can Clinical
Decisions Support Tools Prompt Better Quality ASCVD Care? At this time, Please use the return to
lobby link on your screen To choose your next session
from the presentations list. Thank you very much for
attending today's summit. We will see you shortly.
Reaching LDL-C Goals: The Importance of Statin Intensification and Effective Steps to Get There
Introduction
In today’s fast-paced world, most people tend to overlook the importance of maintaining a healthy diet and lifestyle due to their busy schedules. This has resulted in the constant rise of chronic diseases such as high blood pressure, diabetes, and high cholesterol levels. Among these chronic conditions, high cholesterol levels, particularly LDL-C, are still one of the leading causes of heart disease, which remains to be the leading cause of death in the US.
The good news is that people can reach LDL-C goals with proper medication and lifestyle modifications. Statin intensification is one way to achieve this goal, and it plays a vital part in the management of high cholesterol. Medical experts recommend this method to people who have already tried lifestyle changes but did not achieve their LDL-C goals. In this article, we will discuss the significance of statin intensification and how you can effectively reach your LDL-C goals.
Understanding Statin Intensification
Before delving into the importance of statin intensification, let’s first understand what it means. Statin intensification refers to increasing the statin dosage or switching to a higher potency statin when the initial prescribed dose fails to achieve the targeted LDL-C levels. Studies have shown that about 65% of patients who are on statin medication do not reach their LDL-C goals despite taking the medication as prescribed. Statin intensification is a crucial strategy in managing high LDL-C for people who have failed to achieve their LDL-C goals despite various interventions.
Effective Steps to Reach LDL-C Goals
Apart from statin intensification, several other strategies can help people reach their LDL-C goals. These include:
1. Adopting a Low-fat Diet
A healthy diet plays a crucial role in the management of high LDL-C levels. Consuming foods that are high in saturated and trans fats can increase LDL-C levels. Therefore, it’s essential to reduce the intake of these types of food. Instead, opt for a diet that is rich in fruits, vegetables, and whole grains.
2. Incorporating Exercise into Your Routine
Physical activity is vital in the management of high cholesterol levels. Daily exercise for at least 30 minutes can help increase HDL-C levels while decreasing LDL-C levels.
3. Losing Weight
Increased body weight and obesity are significant contributors to high cholesterol levels. Losing weight through a healthy diet and regular exercise can effectively lower LDL-C levels.
4. Managing Stress Levels
Stress can also have a significant impact on LDL-C levels. Practicing relaxation techniques such as yoga or meditation can help manage stress levels effectively.
Conclusion
Reaching LDL-C goals is essential in the management of high cholesterol levels, which can lead to heart disease. Statin intensification, along with lifestyle modifications, can help achieve these goals. Adopting a low-fat diet, incorporating exercise into your routine, losing weight, and managing stress levels are all effective steps to reach LDL-C goals.
FAQs
What is the recommended dosage for statin medication?
Answer: The dosage of statin medication is determined by the patient’s medical history, LDL-C levels, and overall health status. It is essential to follow the prescribed dosages as taking too much or too little can be harmful.How long does it take to see a reduction in LDL-C levels when using statin medication?
Answer: The time it takes to see a reduction in LDL-C levels will vary depending on the individual and their overall health status. Typically, it takes between six and eight weeks.Do statin medications have any side effects?
Answer: Statin medications can cause side effects such as muscle pain, liver damage, and digestive problems. It is essential to discuss these potential side effects with your healthcare provider.Can I still eat foods high in fat while on statin medication?
Answer: It is essential to reduce the intake of foods high in saturated and trans fats while on statin medication, as these types of food can increase LDL-C levels.How often should I have my cholesterol levels checked?
Answer: It is recommended to have your cholesterol levels checked every four to six years. However, people with high cholesterol levels or a history of heart disease should have their levels checked more frequently.