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Shared Decision Making and Lipid Management: Working Together for Improved Patient Outcomes

  • Authors: Christopher P. Cannon, MD; Joseph Saseen, PharmD, CLS, FNLA; Joyce L. Ross, MSN, CRNP, Certified Lipid Specialist, FNLA, FPCNA
  • CME / ABIM MOC / CE Released: 6/16/2022
  • Valid for credit through: 6/16/2023
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  • Credits Available

    Physicians - maximum of 0.50 AMA PRA Category 1 Credit(s)™

    ABIM Diplomates - maximum of 0.50 ABIM MOC points

    Nurses - 0.50 ANCC Contact Hour(s) (0.5 contact hours are in the area of pharmacology)

    IPCE - 0.50 Interprofessional Continuing Education (IPCE) credit

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Target Audience and Goal Statement

This activity is intended for cardiologists, primary care physicians (PCPs), diabetologists/endocrinologists, and nurses.

The goal of this activity is that the learner will be better able to individualize lipid-lowering management plans and educate patients about the need for more intensive therapies beyond statins.

Upon completion of this activity, participants will:

  • Have increased knowledge regarding the
    • Identification of patients who would benefit from lipid-lowering therapy beyond statins to reduce residual risk
    • Use of effective lipid-lowering therapy in patients after an acute coronary syndrome (ACS) event to reduce the risk for repeat events
  • Have greater competence related to
    • Application of team-based education strategies to improve shared decision making and understanding of the need for adherence to therapy


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  • Christopher P. Cannon, MD

    Professor of Medicine
    Harvard Medical School
    Education Director
    Cardiovascular Innovation
    Preventive Cardiology Section
    Brigham and Women’s Hospital
    Boston, Massachusetts


    Christopher P. Cannon, MD, has the following relevant financial relationships:
    Consultant or advisor for: Aegerion/Amryt, Alnylam, Amarin, Amgen, Applied Therapeutics, Ascendia, Boehringer-Ingelheim, BMS, Eli Lilly, Janssen, Lexicon, Merck, Pfizer, Rhoshan, Sanofi
    Research funding from: Amgen, Better Therapeutics, Boehringer-Ingelheim, Bristol-Myers Squibb (BMS), Daiichi Sankyo, Janssen, Merck, Novo Nordisk, Pfizer

  • Joseph Saseen, PharmD, CLS, FNLA

    President, National Lipid Association
    Professor and Associate Dean for Clinical Affairs
    Skaggs School of Pharmacy and Pharmaceutical Sciences
    University of Colorado Anschutz Medical Campus
    Aurora, Colorado


    Joseph Saseen, PharmD, CLS, FNLA, has no relevant financial relationships.

  • Joyce L. Ross, MSN, CRNP, Certified Lipid Specialist, FNLA, FPCNA

    Past President, National Lipid Association
    Clinical Affiliation: University of Pennsylvania
    Philadelphia, PA


    Joyce L. Ross, MSN, CRNP, Certified Lipid Specialist, FNLA, FPCNA, has the following relevant financial relationships:
    Consultant or advisor for: Amarin; Amgen; Esperion; Kaneka America; Kowa
    Speaker or member of speakers bureau for: Amarin; Amgen; Esperion; Kaneka America; Kowa


  • Asha P. Gupta, PharmD, RPh

    Associate Medical Education Director, Medscape, LLC


    Asha P. Gupta, PharmD, RPh, has no relevant financial relationships.

  • Frederick Stange, DO

    Scientific Content Manager, Medscape, LLC


    Frederick Stange, DO, has no relevant financial relationships.

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    Associate Director, Accreditation and Compliance, Medscape, LLC


    Stephanie Corder, ND, RN, CHCP, has no relevant financial relationships.

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This activity has been peer reviewed and the reviewer has no relevant financial relationships.

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Shared Decision Making and Lipid Management: Working Together for Improved Patient Outcomes

Authors: Christopher P. Cannon, MD; Joseph Saseen, PharmD, CLS, FNLA; Joyce L. Ross, MSN, CRNP, Certified Lipid Specialist, FNLA, FPCNAFaculty and Disclosures

CME / ABIM MOC / CE Released: 6/16/2022

Valid for credit through: 6/16/2023


Activity Transcript

Christopher P. Cannon, MD: Hello. I'm Chris Cannon, a cardiologist at Brigham and Women's Hospital in Boston, also affiliated with CPC Clinical Research in Colorado, and I'm delighted to welcome you to a program entitled Shared Decision-Making in Lipid Management: Working Together for Improved Patient Outcomes. It's a delight to be joined by the current and past president of the National Lipid Association (NLA).

So, the current president of NLA is Joe Saseen, who's a professor and associate dean of Clinical Affairs at the University of Colorado in Aurora, Colorado. And then Joyce Ross is the past president of NLA and a certified lipid specialist with clinical affiliation at the University of Pennsylvania in Philadelphia. Welcome to you both.

Joyce L. Ross, MSN, CRNP, Certified Lipid Specialist, FNLA, FPCNA: Thank you.

Joseph Saseen, PharmD, CLS, FNLA: Thank you.

Ms Ross: Happy to be here.

Dr Cannon: Well, it's a real delight to talk about shared decision-making because in lipids, this is really the whole story -- that we work together with patients. Often there are acceptance issues and plans that we have to work [through], so it's great to have your expertise to walk through this and see ‘How do we work with the patient to set goals, share with them what their risk is, set out a treatment plan, and then follow through to make sure that this does come to fruition?’

With this, we'll look at a case here. So this patient is a 64-year-old man who has just landed in the hospital with an acute coronary syndrome. He's been a smoker for much of his life, not too heavy on the per pack year, but still a smoker, has had hypertension, and then recently developed diabetes for the past year. He is on a good outpatient regimen, but he's on atorvastatin 40 milligrams, so intensive statin therapy, ezetimibe as well, also metoprolol and dapagliflozin, and his LDL on admission is 81 mg/dL. So, this makes him, as the guidelines say, a very high-risk patient with ASCVD. He has a recent acute coronary syndrome. On top of that, he has diabetes. So he's a very, very high-risk patient. Indeed, probably the highest risk that we'll face, and so we want to then be sure to offer him all the best therapies.

Focusing on acute coronary syndromes, this is a period of time in the life of a patient with coronary disease that's the highest risk period, and indeed, the next year or the next two years, there's like a 20% risk of recurrent events that we want to try and reduce as best we can. Five-year mortality can be about 20% -- and of course, relative to a patient's age -- and so one of the biggest interventions that we bring is intensive LDL-lowering therapy.

Here we have a patient who's on 2 drugs already, which is an intensive statin therapy and ezetimibe. His LDL is reasonable for what he used to be, a primary prevention patient at 81 mg/dL, but now he's landed in the hospital with acute coronary syndrome. And so how would you approach this, as what would be your goal for this patient?

Dr Saseen: Well, I think one thing to appreciate is his LDL, even though it's in the double digits, it's too high for him because it's resulted in the development of clinical atherosclerosis. So, one of my goals will be to assure that he's actually adherent with this statin and ezetimibe regimen. But also I think very clearly being very high-risk, 81 mg/dL is not sufficient. It's not sufficient according to, I guess, traditional standards, and it's definitely not sufficient according to evolving more intense standards. Joyce, what's your opinion?

Ms Ross: So, I think it's important if you take a look at the 2018 American Heart Association, ACC cholesterol guidelines of shared decision-making, I want to think about the fact that what is his real risk? And I know we need to get him way down at least less than 55 mg/dL, and we can even be more aggressive and even go to 40 mg/dL and we know it's safe to have that low LDL. But I think what's important is this cannot be just the idea that we're going to do this to the patient.

The patient is the most important person in this treatment plan, but we have to also take into consideration the family that may be involved in implementation of anything that we want to do, such as making those big lifestyle changes that he needs.

But his drug therapy ... Joe, you mentioned that we don't know for sure is he taking his medication. I really want to know, does he understand why he's taking the medication? And does he understand why we might be wanting to add more medication, and why we just can't give him more and more of the same? And the other thing that worries me is, can he afford the treatment that we're going to come up with? We can come up with some grandiose things, but it's no good unless he can effectively afford his treatment plan. But I think for that, we need to have our social workers and other people within the healthcare system to help us.

The American Heart Association gave us 7 great approaches to staying heart healthy, which I think for providers is a good starting point. We need to get him to lose some weight. And it's not only about the food, but we have to get physical activity really big in here for this gentleman, because he needs to use all avenues to help reduce his risk for the next event.

Smoking cessation for him is going to be imperative. But believe me, from my experience, I know that's going to be the last thing he's going to want to change, but we're going to have to work with that. Many hospitals and healthcare organizations can offer the patient a program.

We've got to get the glucose under control. We've got to make sure his blood pressure is under control, and certainly get that cholesterol to where we want it to be. And may I say, not just the LDL, I want to see that triglyceride where we need it as well.

Well, I have to tell you, it's going to take a team to do all this. We have the patient in the hospital for such a short period of time, and we know that we have so much to do. And that's where the beauty of a team comes in, where we have the nurse practitioner or a PA, we've got the dietician. We've got you, Joe, the pharmacist, come in and add the specialty things. And what about the fact that maybe that person is going to take a PCSK9 inhibitor and may need a specialized pharmacist? So we have a whole group of people that has to be part of our plan before we can treat this gentleman successfully.

Dr Cannon: This is a wonderful overview. In terms of a team, do you have a set team, or do you put in referrals say to nutrition group on an individual patient?

Ms Ross: What's important to understand is that every hospital system is different. And in a small rural hospital, you'll have very few of the people right at the beck and call. In a large academic section such as Penn, we have those people and can pull them right in and make it part of their hospital plan.

Dr Saseen: And something else that's evolving is just the incorporation of transitions of care professionals, whether it be pharmacists or sometimes technicians that help people with just the medication and after discharge, assuring appropriate access and that patients are actually taking the medicines that they're intended to take. So that can augment what you've eloquently stated, Joyce.

Dr Cannon: I think it is a really a great thing to have a careful med reconciliation that we all have to do, but follow up afterward to see, did they actually get all these things that we typed out? And was there any confusion?

Turning to our patient. Would you try and push to even more intensive statin therapy? Do we keep the ezetimibe, or give up and then think about a PCSK9 inhibitor, or stick with oral therapy with bempedoic acid? What would be your thoughts on this?

Ms Ross: Well, I think I'd start talking about the statin first, because it has always been our base for everything for lowering the LDL cholesterol with all of our research. And we have our two highest intensity statins being the atorvastatin and rosuvastatin. What's important to me is he's taking atorvastatin right now at 40 mg and he appears to be tolerating it. We have not heard any issue that he is not, and he's taking the ezetimibe, doesn't seem to be any problem with taking that. I wouldn't touch either of those medications. Would I possibly change over to rosuvastatin for more power? I don't think it's going to help us in this case. Here, the most important thing is how low do I need to go? And what do I need to get there?

And before this man ever leaves the hospital, I want to see him treated aggressively. And we also give a message to the patient at the time of the hospitalization, how serious this and how important it is. I refer back to one of my favorite trials of all time -- the MIRACL study.

It was a study where it looked at giving people atorvastatin at 80 milligrams within 24 to 96 hours after their ACS. And they wanted to see at 16 weeks, would this make a difference? Now, there was a matching placebo part. We could never do this study again! But for me, it looked at the primary endpoints that were important -- death, non-fatal AMI, cardiac arrests with resuscitation, or recurrent symptomatic myocardial ischemia with objective evidence that requires rehospitalization. And what's really important here is that the fact that these patients -- getting this medication started right away when they are most at their vulnerability.

Well, what happened in a 16-week period of time, which is a really short time, is we see that there was a big difference. It wasn't a tremendous amount of a number-wise of the reduction of the LDL, but the LDL cholesterol was reduced. And what I like the most, even though there was no significant differences in the risk of death, non-fatal AMI or cardiac arrest between the atorvastatin group and the placebo group. But we did see that those folks didn't have to get back in the hospital as the early and as frequently with requiring emergency rehospitalization, maybe even a procedure.

I like this plot that talks about everybody who was on the atorvastatin did better than those in the placebo group. So that's a really good frame of reference to what this study gave us and talked about. So for patients with ACS, lipid-lowering therapy with atorvastatin 80 mg, reduces recurrent ischemic events in the first 16 weeks, and it also reduced a lot of the stroke.

One of the problems with this trial is that people thought, "Well, if I've going to follow this, I've got to give everybody 80 mg of atorvastatin," and that would be problematic for some people to tolerate, and we've grown from that.

But I want to talk just for a few minutes and ... boy, this is really, I feel like I'm on American Idol and I'm going to sing the song of the judge, because here I'm going to talk about Dr. Cannon. I'm going to talk about the trial, IMPROVE-IT. And in this particular trial, we know that lower is better, that lower than even what we knew before was always better. But what's important here is, is it always just one medication that gives us the benefit? In this trial we had patients who were receiving simvastatin alone or they were receiving simvastatin and ezetimibe. And in this patient population we found out in those patients who were taking the combination therapy that they did very well.

Dr Cannon: Terrific. The IMPROVE-IT trial and MIRACL are exactly this post-ACS patient population just as we are talking about it in this case. And there's the good news and the bad news. The good news is that there's a significant further reduction in events adding a second agent ezetimibe, but the bad news, that over a 6-year period, there's still 30% event rate of recurrent cardiac events. And so I think it gets back to your point, Joe, of he came in at a decent LDL, 81 mg/dL for primary prevention, but that's too high for him. So it's a great concept that we need to go much lower.

We'll now be able to look at a lot of data for the PCSK9 inhibitors.

We do have the clinical outcome studies of two agents with the 20,000 to 25,000 patient trials showing reductions in clinical events. But then we'll review also the newer data on the acute setting. And so the ACS-type patients, what are the effects of starting it early? And then, just in the last few months, we've had 2 imaging studies of what happens to the plaque. So really great new data on what happens early on with intensive lipid-lowering.

This is from FOURIER. And on statin therapy, some patients were also on ezetimibe as our patient was, adding evolocumab, the PCSK9 inhibitor, reduced LDL by 60% -- a huge reduction. And I actually often draw out these numbers for patients to show them that with that bottom number, the median in this 27,000-patient trial, at least half the patients was 30 mg/dL.

The similar type thing with ODYSSEY OUTCOMES, it was got down to 40 in that study. Both (studies) had a 15% to 20% reduction in clinical events. And so having very potent agents that get to the really low levels does translate into additional clinical benefit.

So now we're focused on the ACS patients. So maybe Joe, could you go through the use of these in the hospital that would be relevant to our patient case?

Dr Saseen: Sure, absolutely. Those 2 outcome studies showed after about 2.2 to 2.8 years there's a reduction in events. But there's been some recent evaluations that EVOPACS study looked at initiating a PCSK9 monoclonal antibody soon after patients experience their ACS. It evaluated over 300 patients who were hospitalized for an ACS. And of course they all had elevated LDL cholesterol. They were randomized to two treatment arms, which was a baseline of atorvastatin 40 milligrams daily, because that's the standard of care with evolocumab or atorvastatin 40 with a matching placebo. The endpoint that was looked at was reduction in LDL cholesterol, changes from baseline to eight weeks, really looking, can we get patients to those acceptable levels in an expedited period of time?

And most of these patients that entered the study, it's sort of disappointing that 80% approximately were not on statin therapy. The remaining were on a combination of low-, moderate-, or high-intensity statin therapy, but it was a population experienced in ACS that really were mostly untreated. So what you would expect actually was seen. The patients who were randomized to the evolocumab plus atorvastatin arm had a significant drop in LDL cholesterol that was seen as soon as 4 weeks.

The dose of evolocumab was 420 milligrams in the once every four-week dosing regimen. And if we look to the data, we can see that after week four and it continued to week eight, there was persistent LDL lowering. But we're looking at the net differences. Just statin alone achieved about a 40% reduction at four weeks and comparable at eight weeks. But that was amplified to about an 80% reduction when you also added the PCSK9 monoclonal antibody. So we're looking at a big separation in LDL lowering.

If you look at just what we know from traditional data, the statin-based approach based on MIRACL which is wonderful data that will get about almost 40% of patients to an LDL of less than 70 mg/dL with that statin-based only approach versus placebo. But when compared to the EVOPACS study, we're actually increasing that percentage to over 95%. So with more aggressive therapy, we can get to a minimum threshold or a minimum goal or a minimum target in a much sooner period of time, which will have benefits to patients.

And we do have a lot of safety today with evolocumab and the PCSK9 monoclonal antibodies that they are safe. In the FOURIER trial, half the patients actually had an LDL value of 30 or less, and there were no undue safety signals. When you look at the EVOPACS study, really what you would expect as far as side effects were predictable, local injection site reactions being probably the most common one that you may be alerted to as a clinician.

If we look at some other data, there is the EVACS studies, and these are really 2 randomized trials or double-blind placebo control trials conducted at John's Hopkins that looked at patients who experienced ACS, whether it was NSTEMI or a STEMI. And they were randomized to either placebo or the 420 milligram evolocumab dose given subcutaneously every four weeks. And this was administered within 24 hours of their hospitalization. And they weren't looking at LDL values, they were looking at Lp(a) values.

And we know that Lp(a) is a biomarker of interest, that it is a cause/effect to the development of atherosclerosis. It has proatherogenic effects and procoagulant effects, and we have a lot of information that the higher Lp(a) value, the higher your risk of having an event. We don't have many drug therapies that specifically lower Lp(a). One of them that does is a PCSK9 monoclonal antibody. This is not on label for that particular indication, but it's important to look at collectively and holistically.

In these EVACS studies, there was a significant difference between placebo and patients randomized with evolocumab; there was a decrease in Lp(a), a change that is appreciable, about 28%. The reason that's important is because Lp(a) can rise during the peri-infarction period and early post-infarction in patients with an ACS. So actually trying to manage that change with a drug that can modify Lp(a), it should be viewed as a positive change. There's more to come to that particular end of science, but I think this is a positive overall.

Dr Cannon: Lipids has been rapidly evolving on both of your watches at the NLA, and so it's a nice reminder that there's more coming in terms of therapeutic targets.

The other nice bit of data that has come out is an imaging study of the effects on the atherosclerotic plaque when adding a PCSK9 inhibitor. And so this is the HUYGENS Study, and the design is, again, patients come in with an NSTEMI, have documented disease, have baseline imaging, and then are treated with the standard of care which was high-intensity statin. Then half got evolocumab, again in the monthly dose, and then they came back after a year and re-imaged the plaques. They get really neat pictures from inside the artery to look at the plaque and can see the fibrotic component, the lipid component, make measurements on what percentage there, and then can see changes in that over time.

Now this imaging study, Steve Nichols has done this study that he's led, and Steve Nissen. The 2 of them have been collaborating for years, and this was a nice overview that they've been tracking the size of plaques over time. That lower is better theme has really emerged from the imaging studies, that pushing the LDL down has been associated with more plaque regression overall.

Now back to this notion of the imaging in the acute setting, there's a study just presented and published called, has a great name, PACMAN-AMI, that's the lipids lowering is eating away at the plaque. And so same thing, patients got standard intensive therapy in the control arm and then half got in this case, alirocumab. And they also found significant reduction in atheroma volume with the addition of the PCSK9 inhibitor.

So I actually shared this with the patient. So in the shared decision-making, I draw out what does the plaque look like? There's cholesterol in there, and that's a big target to try and shrink the cholesterol, as now we've seen literally in these studies, and it's replaced with more fibrotic tissue that stabilizes the plaque and prevents the plaques from rupturing and causing clinical events.

The CPC Group will be coordinating this from Colorado, and Mikhail Kosiborod lead the EVOLVE-MI trial, which will look at the clinical events in this setting. So the ACS patient treated with standard high intensity statin plus or minus ezetimibe, whatever the standard routine care is, and then in half the patients adding we'll use the every 2 week dosing that will then track for clinical events to see, does this indeed translate into a clinical benefit?

And [it’s] a worldwide pragmatic trial. So, we're collaborating with Sweden that's been doing pragmatic trials for years, and also in Brazil that does fabulous work, and the United States. So that try and take all of these observations on early lipid changes, early plaque changes in this very high-risk patient to see if that translates into benefit.

Now, one other agent that we touched on in the beginning, that's a new agent that again emerged on your watches at NLA is bempedoic acid. I wondered where you thought that might fit in a setting like this.

Dr Saseen: I think bempedoic acid being a novel agent that lowers LDL cholesterol, depending on if it's on a background of statin therapy or not, anywhere between about 15% and 24% really is going to be an alternative. It is an oral agent. I would never preemptively use this medicine over another proven drug in somebody who's a very high-risk secondary prevention patient. And they do have some outcomes data that will be available in the very near future. But I think we need to really view it in that vein, because it still is one of those newer non-statin drugs that gives modest reduction in LDL cholesterol, along the lines of what we see with ezetimibe, that it really would at this point be an alternative, in my opinion.

Dr Cannon: That sounds right. Joyce, you can pull up the relevant guidelines and say what do they share for us as guidance?

Ms Ross: When we take a look at the 2018 American Heart Association/ACC guidelines, we think about PCSK9 inhibitors as a reasonable step in the treatment for our patient. And this is the first set of the guidelines where we saw this PCSK9 actively put into the standard. We're looking at a very high-risk ASCVD patient. And of course we're going to have maximally-tolerated statin for the patient. If they are still greater than 70 mg/dL, as our patient, you can add on ezetimibe, which our patient already was on. And secondly, if he is not at the target that we want him to be, we then have the ability, if he's greater than 70 mg/dL to institute the PCSK9 inhibitor. But I think what's really important is that when you think about this patient, we know we have a lot of aggressive work to do, and we know that time is of the essence, and we want to get things done as quickly as we can. So knowing the amount of lipid lowering we need, we have now permission to go very aggressively to those medications that we need.

And I think that this dovetails very nicely for the 2019 European guidelines. They talk about a comprehensive global risk reduction strategy, just like we've been talking about. And that is inclusive of aa whole healthcare team because it includes lifestyle adaptations, risk factor management, and the implementation of cardioprotective drugs. The earlier we treat this patient the better they do. Adding that PCSK9 inhibitor early after the event and in the hospital, if at all possible, should be considered. It's a class 2A.

And the thing we haven't talked about too much is cardiac rehab. I know some places do not have those availabilities, but for the most part when it's available and it is able, we need to get a good cardiac rehab program in for our patient.

And if you take a look at this schema of the 2019 prevention guidelines, at the very bottom line, you're going to see where we're talking about very high-risk patients. This is where our patient falls. You see that lower is much better for him. So do we bring his LDL cholesterol down to less than 70, less than 55, 40? Well, I think it's up to the providers, it's up to the patient, and it's up to the team to get him where is best for him to reduce his cardiovascular risk.

Dr Saseen: And I think one of the things that we need to always keep in mind is you don't know where to go if you don't know where you stand. We have to be measuring LDL values. Now, in your patients presenting with an ACS, we do know that when you look at LDL cholesterol, it can be falsely low because of the acute phase response and cardiac healing that LDL does drop. But it still is a standard of care to measure it during the time of an ACS to know where you're at. But perhaps more important is the post-treatment measurement of LDL cholesterol. In the case of ACS, it should be 4 to 8 weeks after discharge, or after the incident of ACS to check whether you're at your intended treatment therapeutic endpoint.

It is not something that we should take lightly because we have so many tools as far as medicines that can amplify or augment our LDL lowering, which is statin-based that we need to use them in the right patients to reduce cardiovascular disease. This is something that probably fell through the cracks. I use that term from the 2013 ACC AHA guidelines because of misinterpretation that just being on a drug was actually more important than being at your therapeutic endpoint. So that really is loud and clear in our 2018 guidelines and in every other subsequent update, which really emphasizes lowering the LDL cholesterol.

Ms Ross: And Joe ... One of the things that's important to point out that in the MIRACL trial and IMPROVE-IT, it didn't matter what the LDL cholesterol was in the hospital setting for the patient, that the patients benefited from that early intervention. So again, we looked at that a long time ago and just reinforces the need to get that information while they're in the hospital and then certainly follow them up.

Dr Cannon: Terrific. Well, let's get back to our patient, the patient's ready to go home. And so we want to tee up a good discharge plan and get them on this path where they'll be carefully monitored. And so we've been talking about shared decision-making and then talking about a new medication, an injectable medication. We'll have to get prior authorization for that from the insurance, and that'll often involve a co-pay and have to share that with the patient. And the notion of having a team is key of not just sending people, "Oh, follow up with your primary care doc, and you did well, see you later," we really have to coordinate well.

We've touched on the lifestyle changes and cardiac rehab is such a wonderful way to encompass all of this, with education, lipid tracking, exercise, dietary changes, that this becomes really a comprehensive package that we can try and offer to the patient and prevent a next event.

So, with this patient, they actually did get and give him evolocumab and did the once-a-month dosing keep it nice and simple. And so at follow up, he does have labs and his LDL is down at 38. And so how wonderful to see a super low LDL in this very high-risk patient. He's also on an excellent regimen of many other evidence-based therapies. So how do you see this patient doing here?

Dr Saseen: I'm smiling, right? I guess we could have went down the debate of should his LDL be less than 55 or less than 40? We don't even have to have that because it's 38 mg/dL. I'm very much a believer that lower is better in high-risk patients, and this person is a very high-risk patient. I feel great about this. I do want to make sure that he fully understands as Joyce has stated, the purpose of these medicines, it is sort of intimidating to some, to actually have 3 lipid lowering medicines. But for him to be comforted by the fact that these are proven therapies to reduce risk. And just to confirm that affordability is actually there for this patient. I wouldn't want him to start this, get the great therapeutic endpoint and then lose it because of lack of adherence because of cost concerns.

Ms Ross: That is so important, Joe. And I think the other thing that we need to point out here is that we know from research today that those patients who have been put on a PCSK9 inhibitor stay with their medications much more than the general population who are on non-injectable medication. Once they see these numbers with this use of the PCSK9 inhibitor are over the moon with being able to take care of themselves and having some control over their cardiovascular risk.

Dr Cannon: Terrific. Well, I'll let you do a final word. I think mine will be lower is better as the simple takeaway that can guide our therapies.

Dr Saseen: Mine is know where you stand and know where you need to go, so you can titrate your therapies appropriately.

Ms Ross: I think mine is, be active, bring in the team, get everybody involved, and especially the patient they're the best part of the team. And congratulate them when they do the best things and keep them on their medicine, as well as keeping them on the lifestyle management. Best is yet to come for them.

Dr Cannon: Oh, just terrific. Well, we want to thank you both Joe and Joyce for just a great discussion and an important topic with lots of new data and great new approaches really to offer these advances to patients. I want to thank you the audience for participating in this activity and do continue on to answer the questions and get CME credit.

Ms Ross: Thank you.

Dr Saseen: Thank you.

This transcript has been edited for style and clarity.

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