This transcript is automatically generated.
00:00:07 Mary Katherine Cheeley
Lipids are not something that we wait until you have an event or even till you are X amount on some calculator. We need to start thinking about this way earlier in life because it's a cumulative risk in that the more that it accumulates, the more risk that you have. So I love the focus that they had on, hey, make sure that you are doing something about it when you see it.
00:00:34 Craig Williams
The biggest takeaway is, I'll call it kind of the revenge of the surrogates. We're back to surrogate testing and LDL is kind of back in a big way. And it's literally in just a dozen years, almost a 180. I mean, the guidelines literally said in 2014, we don't think there's enough data to pick an LDL or a non-HDL goal. And now, like top take home message number four in this new document is basically LDL and HDL testing is kind of backed.
00:01:00 Narrator
Welcome to Medication Talk, an official podcast of TRC Healthcare. Home a pharmacist letter, prescriber insights, and the most trusted clinical resources. On this episode, listen in as our expert panel breaks down what clinicians need to know about the 2026 dyslipidemia guidelines, such as the role of lipoprotein A, apolipoprotein B, and coronary artery calcium scoring.
00:01:23 Narrator
Plus, you'll walk away with practical takeaways to optimize lipid management, including when to add non-statin therapies like PCSK9 inhibitors and ezetimibe for your patients. Our guests today are clinical pharmacists: Dr. Mary Katherine Cheeley, Executive Director of Ambulatory Pharmacy Services at Grady Health System.
00:01:44 Narrator
And Dr. Joel C. Marrs, Cardiology Ambulatory Clinical Pharmacist with Cheyenne Regional Medical Group and an Adjoint Associate Professor with the University of Colorado School of Medicine. He was also one of two pharmacists on the Dyslipidemia Guideline Writing Committee. You'll also hear practical advice from panelists on TRC's Editorial Advisory Board. Dr. Stephen Carek from the USC School of Medicine Greenville.
00:02:10 Narrator
Dr. Andrea Darby-Stewart from the University of Arizona College of Medicine, Phoenix, and Dr. Craig Williams from the Oregon Health and Science University. This podcast is an excerpt from one of TRC's monthly live CE webinars. Each month, experts and frontline providers discuss and debate challenges in practice, evidence-based practice recommendations, and other topics relevant to our subscribers.
00:02:35 CE Narrator
And now, the CE information.
00:02:39 Narrator
This podcast offers continuing education credit for pharmacists, pharmacy technicians, physicians, and nurses. Please log in to your pharmacist letter, pharmacy technician's letter, or Prescriber Insights account, and look for the title of this podcast in the list of available CE courses. For the purposes of disclosure, Dr. Cheeley reports a relevant financial relationship by receiving an honorarium from Novartis, Regeneron.
00:03:05 Narrator
The other speakers you'll hear have nothing to disclose. All relevant financial relationships have been mitigated. Now let's join TRC editor and clinical pharmacist, Dr. Sara Klockars, and start our discussion.
00:03:21 Sara Klockars
It's been about eight years since our prior guidelines and many things have changed. Let's just kick off with a question for our panelists. What's your top takeaway or biggest change with these guidelines that every clinician in practice needs to know?
00:03:36 Sara Klockars
Stephen, can you start us off?
00:03:38 Stephen Carek
Yeah, I mean, my biggest takeaway is, I mean, I remember training as a resident and being taught almost a set it and forget it mentality, put people on a statin, if they need a high intensity, just keep them on it. And how we've been able to now, I guess, further individualize those goals for better or for worse, so that patients can hopefully achieve the best outcomes. But definitely there's more layers of complexity and nuance to it that is just helpful to have, but can also introduce definitely some confusion if your mentality is set and forget it. But now it's set it, tinker with it, do some more studies, and then eventually we'll hopefully get to the right level where we'll hopefully prevent people from having heart attack, strokes, and hopefully optimize their quality of life.
00:04:20 Mary Katherine Cheeley
I think my most exciting moment reading the guidelines was getting back to that place, just like Stephen was saying of, hey, we need to do more, but also the kind of shift towards earlier treatment. It is not something, lipids are not something that we wait until you have an event or even till you are X amount on some calculator. We need to start thinking about this way earlier in life because it's a cumulative risk and that the more that it accumulates, the more risk that you have. So I love the focus that they had on, hey, make sure that you are doing something about it when you see it rather than the whole, you know, we could push it off a little farther and a little farther than it was when I kind of started into practice.
00:05:07 Andrea Darby-Stewart
I think my biggest aha moment was the fact that we have come so far again over that time period of 20 plus years of lipid management, and yet we have so far to go in terms of the underlying causes of hyperlipidemia and cardiovascular disease in this country. And I know that treating to a certain goal and providing patients with appropriate access to statins and access to the testing is one part of that.
00:05:45 Mary Katherine Cheeley
And yet
00:05:46 Andrea Darby-Stewart
I continue to hope that we will become more nuanced and able to treat some of the underlying causes
00:05:56 Mary Katherine Cheeley
of hyperlipidemia and ASCVD as I continue in my career, the societal causes.
00:06:03 Joel Marrs
I think there are a number of kind of big picture takeaways. I think one of them is that we need to be more aggressive and we need to be more aggressive in regards to screening and evaluating people's risk earlier in life. And so I think one of the nice things is that the prevent tool that was incorporated in the hypertension guidelines last year and is now incorporated in the lipid guidelines this year allows that kind of risk estimate down to the age of 30, which before we were at that 40 mark with the pooled cohort equation. So I think that's one thing. And then I think the other thing is that over the last decade, we've seen a tremendous amount of data to support adding agents on top of our workhorse statins to get people to lower goals and get them to lower goals in a safe way. And so I think those are kind of two key takeaways.
00:07:01 Craig Williams
I'll just add that I think people are picking up on the major themes. So I do think the prevent calculator is a very nice addition. Otherwise, I think the biggest takeaway is I'll call it kind of the revenge of the surrogates. We're back to surrogate testing and LDL is kind of back in a big way. And it's clearly in just a dozen years, almost a 180. I mean, the guidelines literally said in 2014, we don't think it's enough data to pick an LDL or a non-HDL goal. And now top take home message number four in this new document is basically LDL and HDL testing is back. Targets help a lot of people think about where we should be. They help patients think about their therapy and they help compliance. And the data is so overwhelming for LDL being the prime culprit here. It makes sense to move it a little back towards the forefront.
00:07:46 Sara Klockars
Thank you. So looking first at our primary prevention patients, there are some patients at higher risk of cardiovascular disease that need lipid lowering therapy, such as most adults with diabetes or those with severe hypercholesterolemia or very high LDL cholesterol over 190. But then for everybody else, we will use the prevent calculator to help assess risk.
00:08:11 Sara Klockars
And this calculator falls into the sea of this new CPR framework introduced in the guidelines that clinicians can use for our primary prevention patients to calculate, personalize, and reclassify risk. So Mary Catherine, can you share more about what the Prevent calculator is and how it differs from the prior pooled cohort equations?
00:08:36 Mary Katherine Cheeley
I would love to talk about it. So Prevent is leaps and bounds better than the old pooled cohort equation. So first of all, I want people to understand that the old pooled cohort equation, say that 15 times fast, was only looked at about 25,000 adults, predominantly white and black adults. And when we moved into this prevent era, it's over 3.3 million folks.
00:09:03 Mary Katherine Cheeley
So just the breadth and the amount of data that went into this risk calculator is leaps and bounds from where we were. I also love that it lowered the age. So remember pooled cohort was down to 40 years old, Prevent is down to 30 years old, and Prevent is race free. So it removes race or ethnicity from the equation, which I think is really important and it puts in some of those more social determinants of health with the zip code inclusion. And that makes it a lot more patient specific. I also love that it includes eGFR, that it includes other kind of, whether the patient's on a statin right now or not, that's something we didn't have before.
00:09:51 Mary Katherine Cheeley
And then there's those three buttons at the top. So you can kind of toggle between CVD, ASCVD, and heart failure, which I think also gives clinicians a better way to have a discussion with patients about all the different types of events that could come, and then thinking through all the different factors that go into it.
00:10:12 Mary Katherine Cheeley
I also want to point out that this should really only be used for primary prevention patients. So if you already had your event, hey, guess what? We don't need to predict your risk of having an event. You already had one. Let's get you on treatment. Let's try to prevent another one from happening. But I do think that it's important for providers to be able to have the ability to say yes or no to statin therapy when they are looking at this, because that was missing in the old one. I don't think a lot of us really liked the old ones. So this is a huge step up as far as I'm concerned.
00:10:46 Sara Klockars
Great overview. Let's move from calculating to individualizing or personalizing risk. Stephen, since this was your top takeaway, can you share how you do this in practice and what are risk enhancers?
00:10:59 Stephen Carek
Yeah, so those risk enhancers, I understand, are going to be those characteristics of the patient, their medical history. family history, certain markers that may not be represented in the calculator, but could be just helpful pieces of data. I mean, I think of things like chronic inflammatory conditions like lupus, HIV that may not be well controlled, maybe previous history of things like preeclampsia, gestational hypertension, gestational diabetes. I think the guidelines also identify some specific higher risk ethnic groups like South Asian populations, Filipino populations, mentioned the family history, but maybe an unsure family history with negative testing for those with premature ASCVD. You know, if a patient's borderline in any of these categories, whether they should be put on a moderate intensity statin or considered for high intensity statin and, you know, prior history of ASCVD, it may help provide more data for evidence when counseling your patient on. There may be some other benefits to being on statin therapy or more aggressive statin therapy to prevent cardiovascular events because of these underlying risk factors that may not be well captured in some of these data sets that we currently have.
00:12:06 Sara Klockars
Thanks, Stephen. And now we're starting to see some abbreviations here as risk enhancers, LDL, ApoB, Lp(a). And I just think of these as the alphabet soup of cholesterol with all of the various lipoproteins measured. I think most of us are familiar with low density lipoprotein cholesterol or LDL or LDL-C. It's one type of bad cholesterol particle, and historically it's been the standard marker for predicting cardiovascular disease. So let's talk a little bit about some of the other labs, starting with Lp(a), since the guidelines now recommend measuring lipoprotein A or Lp(a) at least once in every adult. So Joel, what is Lp(a) and what's the evidence to support this recommendation?
00:12:55 Joel Marrs
Lipoprotein A looks very, very similar to LDL and has a very similar profile from a atherosclerotic risk standpoint. And so one of the big takeaways from Lp(a) screening for the last, you know, 50 plus years is that it's very genetically mediated. And so people that have elevated lipoprotein little A, oftentimes it's from genetic factors that have contributed to that. And oftentimes it pops up from the standpoint of people that potentially have family members, direct relatives that were kind of first degree relatives that had earlier heart disease in their life. We do know that if it's elevated, that it does increase your risk of having cardiovascular disease. And as it further goes up, it can double, oftentimes even triple your risk of having future cardiovascular events. And so some of the thought process around having this as just a screening tool in addition your traditional lipid profile is that it probably, if elevated, a hundred percent increases your risk of having a future cardiovascular event. And so then it has more information to have that patient provider discussion about risk benefit and what are we going to do about this?
00:14:21 Joel Marrs
Currently, there are not any FDA approved medications to lower Lp(a). We do have some medications that can lower it, but there are some in the near future, probably in the next one or two years, that are going to dramatically impact this if they show positive outcomes in clinical trials.
00:14:41 Sara Klockars
Thank you. Mary Catherine, what is apolipoprotein B and when is it recommended?
00:14:47 Mary Katherine Cheeley
So I like to explain ApoB and how it relates to LDLC in terms of kind of weight and number. When we calculate an LDL cholesterol, we're estimating things based on their weight.
00:15:01 Mary Katherine Cheeley
So go with me for just a minute, but I kind of explain and think about our arteries as like a giant antique store. And if all you know is that there's 600 pounds of people walking around in this antique store, it could be that there's four adults each weighing 150 pounds, or go with me, it could be 20 toddlers running around in there. And I think that is the way to think about LDL cholesterol.
00:15:29 Mary Katherine Cheeley
20 toddlers, which is an ApoB, you're counting the noses on the people that are running around in this antique store. And if you count 20 little toddler noses, then you know that your risk of something getting broken is much higher than if it's four adults running around. So when we only know the weight of LDL cholesterol, and it's based on an estimate, which we can also get into it at another point, the Friedwald equation versus Martin Hopkins. But if you have apolipoprotein B, which is counting the number of atherogenic particles that are floating around, the number of toddlers, the number of noses that are running around in your antique store, then you have a better idea of what your risk is going to be.
00:16:19 Mary Katherine Cheeley
And so when I talk to patients and explain to them that it's a better predictor or a better kind of estimate of what your true. atherogenic risk is, then I think they kind of understand why it's not the same, why we target different ones. In my practice, we use it for patients who we suspect discordance.
00:16:40 Mary Katherine Cheeley
So we always start with LDL cholesterol. I practice in inner-city Atlanta. I work in a low-income hospital. So we can't always get the fanciest tests. I know that they're not as expensive now, but it is still a sendout for us. So we always start with LDL cholesterol. We always calculate our non-HDL cholesterol. I call it the poor man's ApoB. It's a decent way to kind of guesstimate a little bit better than our LDL cholesterol is.
00:17:05 Mary Katherine Cheeley
But when I have a question, when I have a patient who has CKM, so cardiovascular kidney metabolic syndrome, or if they have diabetes, or if I think that they might have these small, dense LDL particles or these toddlers running around that I can't really account for when I'm just looking at weight, then I go for and reach for an ApoB. That gives me a better way to explain to patients and a better way to target, am I truly doing everything for this patient that I can, or do I need to push it a little bit further and, again, either disregard or put our LDL cholesterol to the side and really start to focus on the number of noses running around as opposed to just the weight of things that are there.
00:17:52 Sara Klockars
Great analogy. Thank you.
00:17:56 Sara Klockars
So for a primary prevention patient, we've calculated the risk with the prevent calculator and reviewed risk enhancers, which may include Lp(a) or ApoB to help personalize that risk. So now let's move on to the R of CPR to reclassify and reassess and see what this means. And this is where coronary artery calcium comes into play. So Joel, what is coronary artery calcium and when should it be checked?
00:18:24 Joel Marrs
Yeah, so essentially anytime there's the development of atherosclerosis in a vessel, you're gonna have some calcium deposition there. And so basically coronary artery calcium is a surrogate that basically is another way to estimate risk. And so we know not all individuals are gonna have elevated cholesterol values but still be at potential risk. And so especially in those folks where they're either borderline risk or intermediate risk based on that prevent calculator. A coronary artery calcium score is a reasonable test to evaluate folks and determine if they have any sort of calcium deposition, which would indicate that they have atherosclerosis present. So I would say clinically when it's in my practice when it's come up is those individuals where you estimate their risk from a primary prevention standpoint and It's kind of borderline and they want further information. And so we've talked a little bit about this today with lipoprotein little A is a potential additional marker. ApoB is a potential marker. Your CAC score is an additional marker to evaluate risk. The one caveat that I would highlight strongly is that a CAC score of zero does not mean that you have zero risk moving forward.
00:19:47 Craig Williams
I do think this is a wonderful piece to add to the toolbox because this does start getting at what is actually going on in my patient's arteries. I've seen it definitely move the needle with patients. When you tell them you give them a number that's not zero, that absolutely can motivate them to either take the medicines or get more serious about lifestyle changes. So I keep in mind two numbers. 300 is a really high calcium score and zero is low.
00:20:14 Stephen Carek
Yeah, and just to build on this conversation, I think there's two important things to clarify with the coronary calcium score.
00:20:20 Stephen Carek
It's neither a screening test nor a diagnostic test.
00:20:23 Stephen Carek
It's not intended to screen for coronary artery disease.
00:20:26 Stephen Carek
It's not intended to diagnose coronary artery disease.
00:20:28 Stephen Carek
If you have a score of zero in certain patients, I would still be concerned there could be atherosclerosis.
00:20:32 Stephen Carek
Now, it may not be calcified stable plaques, but a large portion of patients with a score of zero and high cardiopre like pretest probability, maybe a family history, hyperlipidemia, although they may have the zero, they could have these soft plaques that are unstable and potentially catastrophic if not diagnosed, hence why you would want to strongly consider additional evaluation for these patients, whether it be a CT coronary angiogram or talking about the cardiology about doing additional testing for that.
00:20:59 Stephen Carek
So I think that's important for providers to know that this is, again, just another data point of several that can help validate the use of statins in patients.
00:21:07 Stephen Carek
But I think there's a lot of other tools in our arsenal that can help us diagnose and better evaluate patients that may fall outside of the standard risk tools that we're currently using.
00:21:19 Mary Katherine Cheeley
I also will add that statins increase calcified plaque, which, and we want them to do that because just like Stephen mentioned, that means that it is calcified over.
00:21:30 Mary Katherine Cheeley
But I also make sure that when I'm talking to my patients about this, that I let them know, Hey, look, your number is whatever you need to be on your statin.
00:21:39 Mary Katherine Cheeley
Hey, if we determine to check it again, some patients get very frustrated with the fact, but it's gone up and I've been taking my medicine.
00:21:47 Mary Katherine Cheeley
So I think having that in your mind as well is really important when we're having that discussion with our patients.
00:21:52 Craig Williams
If you're already on the stat and it's not something to kind of measure longitudinally because patients will not be encouraged by their follow up scores necessarily.
00:21:59 Mary Katherine Cheeley
Exactly.
00:22:00 Sara Klockars
Excellent points.
00:22:01 Sara Klockars
Thank you.
00:22:03 Sara Klockars
I want to move us along to treatment targets and Joel was hoping you could help us discuss how the guidelines shifted back to specific treatment goals.
00:22:15 Sara Klockars
Would love some of your thoughts on the evidence behind this shift.
00:22:19 Joel Marrs
Yeah, so I think there's some context to this.
00:22:22 Joel Marrs
And so in 2013, when the guidelines shifted to these four statin benefit groups, I don't think that the intent of interpretation of those guidelines was that LDL targets were gone.
00:22:36 Joel Marrs
They just did not call out those targets.
00:22:39 Joel Marrs
They've further carried kind of that pathway forward in 2018.
00:22:43 Joel Marrs
And then when we revisited all the literature and where we are today with different lipid lowering therapies, we had some context.
00:22:52 Joel Marrs
And so if you think back to the American College of Cardiology's expert consensus decision pathway for non-statin therapy that's now three plus years old, we've kind of shifted back into this direction where lower is better and whether you use the term threshold versus goal.
00:23:12 Joel Marrs
We had extensive actually discussion about that.
00:23:15 Joel Marrs
And I think one of the big takeaways was that calling out a specific goal, I think is more palatable for patients.
00:23:25 Joel Marrs
It's more palatable for clinicians.
00:23:28 Joel Marrs
And so that was one of the drivers for this because we had the evidence to support these more aggressive goals.
00:23:35 Joel Marrs
And so, if you look back multiple years, we have evidence with PCSK9 inhibitors on top of statins plus or minus ezetimibe. you know, driving people's LDLs in the 30 to 40 range.
00:23:47 Joel Marrs
And so clearly getting below that less than 55 mark, you know, we have ezetimibe plus statin therapy that also kind of shifted that in a ACS population and kind of where that 55 number came about a number of years ago.
00:24:02 Joel Marrs
And so I think it was inevitable that we were going to kind of shift and back in this direction, you know, even in addition to recommendations, since the guidelines have come out, presented at the same AHA meeting, we have Vasilius trial data that was too late to incorporate into guidelines and those kind of things in patients that have not had a cardiovascular event, but still aggressive therapy, getting LDLs into the kind of 40 range in people that have known established atherosclerosis, but not having a previous event, I think further elucidates the fact that lower is better for many patients, whether they have established disease or not.
00:24:43 Joel Marrs
And so that was kind of the big driver for kind of pushing these numbers further.
00:24:49 Joel Marrs
It has information about LDL targets and those numbers as well as non-HDL and ApoB, if that's relevant based on your patient population.
00:24:58 Sara Klockars
Thank you.
00:24:59 Sara Klockars
Joel, you had alluded to the ApoB target.
00:25:03 Sara Klockars
So Mary Catherine, I was wondering if you could give us a little bit of background of the evidence to support this optional ApoB goal and what patients we would do that in?
00:25:13 Mary Katherine Cheeley
Absolutely.
00:25:13 Mary Katherine Cheeley
That is kind of that same population that I talked about before.
00:25:17 Mary Katherine Cheeley
So our patients who we think that there might be some residual risk or discordance with their calculated LDL cholesterol that ability to utilize an ApoB is based on the evidence of a couple meta-analyses, some observational studies.
00:25:34 Mary Katherine Cheeley
So the UK Biobank was looked at, some Fourier data was looked at, and then the observational Copenhagen general population study was looked at for these patients in particular who had discordance.
00:25:45 Mary Katherine Cheeley
And ApoB was the strongest predictor of events when they looked at events when compared to what your LDL cholesterol was, what your non-HDL cholesterol was, or what your ApoB was.
00:25:57 Mary Katherine Cheeley
And so that where this recommendation more than likely came from.
00:26:01 Mary Katherine Cheeley
That is the evidence behind this.
00:26:03 Mary Katherine Cheeley
If you have patients who are at very high risk, then the recommendation is to target an ApoB of less than 55.
00:26:12 Mary Katherine Cheeley
If you have a patient that's not at very high risk, then the optional goal is less than 70 for ApoB specifically.
00:26:19 Sara Klockars
I wanted to talk about that more aggressive treatment that we alluded to at the beginning and the use of non-statins.
00:26:28 Sara Klockars
So Joel, what do you recommend adding to an optimized statin for LDL lowering, and does this recommendation differ for primary and secondary prevention?
00:26:41 Joel Marrs
No, I think it's an excellent question and it's coming up more and more with kind of the more aggressive targets that have been identified earlier this year.
00:26:49 Joel Marrs
I think you have to take a step back and I think the question is, what is that patient's risk?
00:26:56 Joel Marrs
And so clearly identifying secondary versus primary prevention, I think helps drive some of those discussions.
00:27:02 Joel Marrs
We know that PCSK9 inhibitors have data, both primary and secondary prevention, predominantly primary prevention, and those with genetic abnormalities.
00:27:11 Joel Marrs
And so those are, you know, huge workhorse agents that can, you know, on top of statin therapy, lower LDL, an additional 50 to 60% depending on dosing.
00:27:20 Joel Marrs
And so depending on how far from goal patient is, I think is one of the questions that needs to be asked in that provider patient discussion.
00:27:29 Joel Marrs
Because if they're close to goal and you can use agents such as ezetimibe, which is generically available now at a much lower cost than some more expensive agents such as PCSK9 inhibitors or even bempedoic acid and then, and inclisiran, I think has to be part of that dialogue.
00:27:45 Joel Marrs
But I think if you've maximized your statin therapy, they're a secondary prevention patient, I think you have to be aggressive and you have to be quick. to being aggressive in reducing that patient's risk.
00:27:56 Joel Marrs
And so with both evolocumab and alirocumab, we have clinical trial data that shows that they're beneficial on top of statin plus or minus ezetimibe in patients that have established ASCVD.
00:28:10 Joel Marrs
And so we have that data to support if you're further from goal.
00:28:13 Joel Marrs
Bempedoic acid has additional data that's demonstrated that especially in those, if you look at the clear outcomes trial, those that are statin resistant.
00:28:22 Joel Marrs
And so only about 10% of patients in that trial were on statin therapy at low doses can further lower cardiovascular events.
00:28:29 Joel Marrs
But you have to figure out how far from where your target or goal is because we know that bempedoic acid on average only lowers your cholesterol. your LDL cholesterol about 15 to 20%.
00:28:41 Joel Marrs
Ezetimibe's in that same ballpark where you have evolocumab, alirocumab, you're looking at 50, 60%.
00:28:46 Joel Marrs
And inclisiran, which is an injection that actually has to be administered in a healthcare setting, has good data to support LDL lowering by about 50%, but does not have the outcome data that alirocumab and evolocumab and ezetimibe have in an ACS or a CVD population yet.
00:29:06 Joel Marrs
And that should be out probably late next year.
00:29:10 Joel Marrs
And then Lerodalcibep is an agent that can be used, but I would say based on cost and utility, a lot of the other agents that I mentioned are going to be used prior to that in regards to getting folks to their LDL targets.
00:29:26 Craig Williams
I was going to add like my 20,000 foot view of these is really if a patient's high risk and cannot take a statin, the PCSK9 inhibitors absolutely have to be involved.
00:29:35 Craig Williams
They're kind of like the statin like potency agent.
00:29:38 Craig Williams
So rarely do we need them on top of a well tolerated statin, but sometimes you do, but they're really kind of my statin level like potency alternative.
00:29:47 Craig Williams
And I think we do have to start getting more comfortable with PCSK9 inhibitors because they're absolutely going to play a bigger role. in the next decade.
00:29:53 Craig Williams
And I think we're kind of there.
00:29:54 Craig Williams
It's like GLP-1 agents 10 years ago where we knew they were there and coming, but we weren't too familiar with them.
00:29:59 Craig Williams
I think we're there now with PCSK9s.
00:30:01 Craig Williams
If you're not using them a lot, you need to start getting familiar with them because they're going to play, I think, a much bigger role in the next decade.
00:30:08 Mary Katherine Cheeley
Add to that, less than 5% of patients cannot take a statin period.
00:30:12 Mary Katherine Cheeley
Just because they can't tolerate the highest dose doesn't mean we give up on the statin.
00:30:16 Mary Katherine Cheeley
And I think that is something that at least providers in my practice really struggle with that, oh my goodness, this patient can't take 40 milligrams of rosuvastatin.
00:30:24 Mary Katherine Cheeley
Well, that doesn't mean they can't take 10 milligrams.
00:30:27 Mary Katherine Cheeley
And so making sure that we understand and advocate for that patient to say something is better than nothing.
00:30:34 Mary Katherine Cheeley
Please make sure that you're doing your best to get them on something.
00:30:38 Mary Katherine Cheeley
Doesn't mean we won't need an additional agent on top of it, but staying on a statin is wildly important.
00:30:44 Craig Williams
I absolutely agree with Mary Catherine that a low dose or medium dose statin still gives you pretty good LDL lowering.
00:30:51 Craig Williams
And it's a great foundation along with ezetimibe or along with bempedoic acid, as we said.
00:30:57 Craig Williams
Yeah, the truly statin intolerant unfortunately are few among us.
00:31:02 Craig Williams
And I think part of that has been, I think a lot of us approach it differently.
00:31:05 Craig Williams
We no longer check CK.
00:31:07 Craig Williams
If you're checking a blood level for something that patients learn is like they're looking for muscle pain or you're giving it to patients saying, Let me know if you have muscle pain, a certain number are gonna have muscle pains.
00:31:17 Craig Williams
I think we started presenting them a bit differently as the data's come out so reassuringly that at least subjective myalgias are as common on placebo as they are on the statin. in these large statin trials.
00:31:31 Narrator
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