Joyce Ross, MSN, RNC, CRNP, CS, FNLA, FPCNA

Dhiren Patel, PharmD, CDCES, BC-ADM, BCACP:

 Jen, for you in terms of…obviously there’s the prescribing of it, but I think you’ve served an equally important role in educating other HCPs [health care professionals], especially pharmacists. And so how do you, A, address this with patients? But also more importantly, there is a ton of confusion. Because even within the prescription, like Dr Bhatt alluded, there’s ones that have had data and there’s the ones that don’t have data. And then you have maybe that pharmacist that doesn’t know where it’s not covered, and they say it’s an IL-6 [interleukin 6] on the left-hand side. Which you also don’t want. If you can maybe walk us through kind of the over the counters and even within the prescription ones, how do you sort it, how do you not only educate your patients but also pharmacists and other HCPs?

Jennifer Goldman, RPh, PharmD, CDCES, BC-ADM, FCCP:

 I’m glad you asked that because I was listening to the 3 other panelists and what they’re saying and what they’re talking about is evidence that when I think back to 30 years ago, and I’ve been practicing over 30 years and my colleagues have been practicing quite a long time as well, and we gave drugs based on biomarkers, we were giving the fabric acid derivatives to lower a biomarker, but based on clinical trial, specifically the REDUCE-IT trial, and Dr Bhatt, we now have evidence. We have actual evidence that if we use icosapent ethyl [Vascepa] we not just lower a biomarker, we actually decrease cardiovascular events and so forth. So we have evidence. You can't just use the evidence when you feel like it. If you know the evidence, you have to use that evidence. The other fish oils, the various prescription plus supplements that are over-the-counter have been studied. They have been studied. And yes, they may reduce a biomarker. The triglyceride number might go down, but that does not translate to an outcome that we care about. So it doesn’t end up translating to a decreased cardiovascular event. So I think that’s 1 first educational piece that needs to go out to health care providers, but also to patients and particularly to pharmacists who are in the community, who might be the kind of end stop or the last provider that somebody actually speaks to. I’ll have patients that will come in and they’re on over-the-counter fish oil, and I’ll say, “Why are you taking that?” And they’ll say, “I don’t know. My doctor told me to take it.” So having that conversation. The other conversation is to make sure that everyone is educated about that biomarker. The point you just asked me about, Dhiren, is pharmacists in general. Supplements, fish oil supplements have been studied. They are not regulated. You don’t know what is in them. There could, there are all kinds of impurities in these supplements. The supplements that have been studied have not been shown to improve anything. When I have patients on that and when I advise other pharmacists, no, they’re wasting their money. Don’t get it. They’re not helping themselves. And the same thing with the prescription availability. The ones…you have to follow the evidence. So Dr Bhatt has done that for us. And Dr Busch is participating. For pharmacists out there in the community and for primary care, it’s not OK to just say go to the wholesale store and buy a big 5000 pills of fish oil. It’s not the same. So you can’t use evidence when it’s convenient. It’s all the time.

Joyce Ross, MSN, RNC, CRNP, CS, FNLA, FPCNA:

 I just wanted to jump here and say that there’s 2 points that I wanted to add to what you’re saying, Jen, which is so true. The patients don’t realize what they’re getting when they’re getting something over the counter. So really going through that. But what is worrisome to me is that we understand that the oxidized element of the fish oil over the counter, we have oxidation of the LDL [low-density lipoprotein], which is part of the problem. But we also have an increase in the LDL cholesterol in many of those products. And that is critically important. Saying to a patient, I think we’re shooting ourself in the foot when we’re just taking something that we know may increase your LDL cholesterol when all this time we’ve been working to reduce it. So again, taking the terms, look in the name of the trial, REDUCE-IT tells us all those things that are useful for education, both for the health care provider and for the patient as well.

 Yeah, no, absolutely. And I think hopefully what you saw here is that triglycerides are pretty well-established body of evidence now associated with it, but there’s a little bit of navigation that Jen, you pointed out that we need to make sure they get on the right product. Because there’s been a fair number of trials that haven’t had the positive cardiovascular data. And I say at the end of the day, we want to do things [that] are moving the needle from a population health standpoint and not just treating numbers that numerically make us feel better and they look pretty in a chart. At the end of the day that’s what we’re all here to do. So that’s excellent.

Videos

What pharmacists and providers need to know to counsel patients on when discussing the use of prescription or over-the-counter fish oil supplement as treatment for dyslipidemia and hypertriglyceridemia.

Efficacy of Prescription Vs OTC Fish Oil Products  

 I’d like to go around here because I think everyone, you were involved in the research side of it, and then now in the practice side, but Dr Busch, maybe if you can comment on that, and kind of what that looked like for you from the research side, now, how you’ve implemented that to the practice side and what that looks like. And we will go around the horn.

So, for the research side, as Dr Bhatt mentioned, it was very easy to find these patients. They were in front of us every day. And what was so unique in that study, you saw even though these patients were all on a statin with an LDL [low-density lipoprotein] in the mid-70s, it was a 28% rate of events over the 5 years on the statin already. It shows huge residual risk, and anything you could do to lower that residual risk. And that’s what we do all day long. We’re giving heart-smart diabetes drugs. We’re giving aggressive blood pressure drugs. So, as a clinician, you always want to do 1 better than you did before, as long as the drug is safe and affordable for the patient. So, of course, bringing in 4 capsules a day that are not small capsules on top of what the patient was on to treat something that’s a marker, because even if their triglycerides didn’t drop that much, it still had benefit. The trick is not only to initiate it, but to get the patient to stay on it because what do you do? You’re lowering heart attack, stroke, and death, and each individual parameter was lowered, which is very unusual in these cardiovascular trials. EMPEROR-Red lowered cardiac death but didn’t lower stroke. Some of the other trials, nothing was low in 1 thing, but all is a conglomerate here. Each individual factor was lowered, and that’s what’s so important with this. As I icosapent ethalized my patients over the 3 months after the study came out, you watch through your practice. Not of all of our partners do it. Dr Bhatt is running another study by another company with an EPA [eicosapentaenoic acid] S-drug. And it’s still easy to find these patients in my partner’s practices. And. as Jen mentioned earlier, where there’s a will, there’s a way. There’s a $9 copay card to get branded icosapent [Vascepa] and for $9 it’s worth having the discussion with the patient. And with our pharm D backup, we can get the drug into the patient that’s affordable. That lowers their event rate, which is pretty dramatic.

 That makes sense. And I have a pressing question for Jen, but Joyce, what has this done for you guys in your practice, where you’ve been very hyper focused on all of the newer agents that come and monitoring this from a clinical practice standpoint, what does this look like for you from a prescribing standpoint now?

 I think the most important thing is that it really solidified the fact that it’s not just about LDL cholesterol as Dr Bhatt very elegantly discussed. And I think that what has [been] very frustrating for patients over time is to get that LDL cholesterol down that we’ve been harboring on and pushing and raising amazing medications to get there, and yet they still have other vascular events. For many years, Dan Rader [Daniel J. Rader, MD, FAHA, University of Pennsylvania] and I thought that there’s something about these triglycerides. While I couldn’t put my finger on it and while we didn’t have the research that we have now, I was sure there was something with triglyceride that had something to do with the inflammation and the oxidation of the LDL cholesterol. When you start to talk to a patient about you’re really doing—you’re doing well, and what if we could add something that was going to change [the] outcome for you toward the next event by 25%? Well, as you go back to what Bob said earlier, that’s double, double, double, double, all the statins. And here you go with 1 addition. Yes, it’s 4 pills, but that’s a major outcome. And what you’re doing is treating all the [I have no clue] particles. For me that’s what’s important. And helping a patient who’s so frustrated that they continue to have events going to other vascular beds that there’s something to do and we know it’s not just about the LDL.

Takeaways of the REDUCE-IT trial of icosapent ethyl as treatment for dyslipidemia and hypertriglyceridemia.

Implications for Prescribing Icosapent Ethyl to Prevent CVD

Dhiren Patel, PharmD, CDCES, BC-ADM, BCACP: 

Dr Busch, you alluded to this earlier. We want to start with lifestyle—people want to do things naturally. But that’s not always going to be the case. When it comes to prescribing that initial statin, we have varying intensities of it. What’s your progression of how you decide what patient goes on what statin? How are you deciding that?

If I have an LDL [low-density lipoprotein] target in mind—if I want to get the LDL below 70 mg/dL, or if they have heart disease and diabetes, below 55 mg/dL—you have to know how much efficacy they get from that statin as you titrate up. One thing we learned early on with statins was rule of 6. If you remember the starting dose of the statin, you titrate and double and double and double the statin, and you get another 6%. I always remember atorvastatin is 37, 43, 49, 55, but rosuvastatin was 46, 52, or whatever. If I want to get down below 70 mg/dL, I know where they’re starting at.

For most patients with type 2 [diabetes], their problem isn’t very high LDL. They have high triglycerides and low HDL [high-density lipoprotein]. Their LDL may not be that high, but you have to start the statin in that patient based on the CARD study. Back then, a normal cholesterol LDL was 160 mg/dL. They took patients for primary prevention with diabetes, and LDL was below 160 mg/dL, where normally you wouldn’t have started a statin. When they took atorvastatin 10 mg, they lowered their events 37%. As we said, we use statins in the drinking water, unless it’s a woman who’s pregnant or going to get pregnant, and you choose the right dose to start—maybe a low dose, but you know you’re going to titrate up, but you want somewhere to go. If you started with pravastatin, even the top-dose pravastatin is not going to drop 40%, whereas 10 mg of atorvastatin might drop you 37% to 40% in the beginning, and you have somewhere to go later.

That makes sense. We talked a little [about how] some are still focused on the intensity of the statin therapy because that’s where some of the measures still are, especially from CMS [Centers for Medicare & Medicaid Services]. Then you have some guidelines specific to LDL goals. I have a question to all of you—Dr Busch, if you want to keep the mike, that’s fine. What percentage of your patients do you think fail to meet the cholesterol goals, despite them being on a statin? That’s going to segue into some of the add-ons that we have in our toolbox.

A lot of our colleagues don’t titrate the statin, so there’s clinician inertia. You see someone who comes in and is on the same dose of everything for the last 10 years; nothing has been adjusted. The key is that this is a start. I’m giving you my best guess that will work, but I may have to go higher so the patient doesn’t feel disappointed. Of course, if they don’t tolerate 1 statin, you can go to another. A lot of people don’t tolerate the statin because they read that statins cause muscle aches. So when they open the bottle of the statin, they get muscle aches before they even put the first pill in their mouth. The convincing thing is what’s real and what isn’t. If they have aches and pains before they started the statin, you know that was there beforehand.

Jennifer Goldman, RPh, PharmD, CDCES, BC-ADM, FCCP: 

I want to comment on what Bob just said. One thing we have to consider is that we have high-potency statins. Super-statin is the most potent, and atorvastatin. As a pharmacist, I’ll think about drug interactions too. There are fewer drug interactions with rosuvastatin. One thing I see that happens—Bob just alluded to this—is that if somebody says they have muscle pains from 1, that doesn’t mean they’re going to have muscle pain from another. That also doesn’t mean that they’re going to have muscle pain if we tried lowering the dose. What’s important for providers to understand is that if you have problem with 1, try another, then another, lower the dose—do whatever you can to use that statin.

 What’s really important is that somebody has to watch the medications that patients are taking. When people are going to various providers, others aren’t aware that somebody is giving a macrolide antibiotic for something. They’ve started a new medication, perhaps they’re taking protease inhibitors because they have something, maybe there’s a transplant—a lot of things have to be taken into consideration.

But before you do that, Jen, to get back to what you were saying, have the patient describe their perceived muscle ache and pain. Many times it’s that shoulder that hurt them for the last 20 years, which has nothing to do with the statin drug. There are certain concepts that go along with what that discomfort of statin therapy when it is there. Of course, pain is what the patient says it is. But they can describe to you. Does it go away sometimes? Does it come back? Is it worse with activity? We need to help the patient understand that what they’re having is not necessarily a reaction to their statin drugs. I don’t think we should assume that’s so.

 Absolutely. Those are great clinical pearls.

What to know about the efficacy of statin therapies used as cholesterol-lowering therapy.

Important Considerations When Prescribing Statin Therapy for Hypercholesterolemia

 That’s excellent. Everyone has some type of pharmacist or clinical pharmacist embedded in your practices. Jen, you have the luxury to spend a little more time with your patients. When we think about the treatment options out there, something you always start with is around dietary and lifestyle modifications. If you can, walk us through what you tell them on that first visit. The patient has high cholesterol: what do you walk them through? It’s not, “You can’t eat anything.” What’s your approach?

 Just to piggyback a little on what Joyce was talking about with communication, 1 of the most important parts of that communication is to be able to listen, and reflective listening. When you meet with a patient, you need to ask them, “What’s important to you?” What goals do they have? We can’t just put everything we want. As Bob [Busch] brought up, in the end, we’re going to have 7 pills. We all know this, but we’re not going to overload everything. We have to listen to what their goals are.

When we talk about lifestyle changes, we have to be cognizant of the limitations we have. It’s easy to say, “Go to the gym.” But not everyone can afford a gym membership. Not everyone has access to go swimming every day. We have to hear, what do you do for purposeful exercise? What can you do that might increase that? Listen to them, and have them solve their own problems; you can push them along a little. Do you do your own food shopping? Can you walk up and down the aisles? What can we do to help them? We have to be able to listen. Then we have to hear about food and have that conversation. What’s the problem? Are they grazing all day? Are they making good choices? Do they even understand? Speaking of diabetes, are they understanding the role of carbohydrates and fats and protein? In terms of lipids and diabetes and practices, are they having the right fish, lean meats, and so forth? Can they afford them? We have to work within cultural issues as well in terms of food. We have to be able to listen. You can’t go in and say, “You can’t eat any of these things anymore. You can’t do this anymore. No, no, no, no, no, no.” We can’t be finger wagging. We have to help them do their own problem-solving when it comes to lifestyle changes.

 Can I jump in quickly? What you’re saying is important, Jen. I also ask the patient is, “What food can you not live without?” Everybody has a favorite, whether it’s a comfort food, a cultural food, something they’d have a very hard time giving up. That’s when we start talking saying, “You can have it, but maybe cut down a little.” You have a conversation about, “What do you need? What’s your goal? Are you interested in making changes?” How about the rest of the family? Are they going to be supportive? That’s the other part: the rest of the family.

Those are all great points. Keeping the patient at the center of that is the most important piece. It makes a lot of sense.

Approaches to counseling patients with high cholesterol levels on goals of therapy and the role of lifestyle changes as prevention against cardiovascular events.

Optimizing Adherence to Therapy for Hypercholesterolemia

Dr Bhatt, maybe before we dive into how we can play a role and what tools we have in our toolbox, walk us through the pathophysiology of hypercholesterolemia and cardiovascular disease to get us started.

Deepak L. Bhatt, MD, MPH, FACC, FAHA, FSCAI, FESC:

 Yes, absolutely. This is really an important topic. I recall a time when there was some controversy around the role of cholesterol and atherosclerosis, but that time has well past. At this point, there’s no credible voice out there that’s debating the point that cholesterol is directly causal in terms of atherosclerosis. This is true of coronary atherosclerosis, peripheral cerebrovascular disease, and LDL [low-density lipoprotein] cholesterol in particular, an elevation in that, is a potent risk marker for the development of cardiovascular diseases, and it’s a modifiable risk factor. And there’s no question that LDL cholesterol, especially more atherogenic forms, such as when it gets oxidized, is really toxic to blood vessels. The good news is there’s something we can do about that. The first line of attack is lifestyle modification, and diets that are healthy. I would in particular endorse a plant-based diet to the extent one can adhere to that. And by that, I mean a diet that’s high in fresh fruit and vegetables and whole grain intake, to the extent that that forms the majority of a diet, that’s better for retarding atherosclerosis. Not just in terms of only trying to lower cholesterol, but also other beneficial cardiovascular effects.

Beyond diet, regular daily physical activity, even exercise I’ll say, can be usefulin terms of maintaining one’s cholesterol, but other associated risk factors like blood pressure, weight, glucose, etc. And when those measures aren’t enough, then pharmacotherapy is certainly indicated. We’re lucky that we’ve got generic statins and generic ezetimibe, relatively safe, well-tolerated, inexpensive ways to lower LDL cholesterol when lifestyle management is not enough. One concept that’s been introduced into the literature, in fact Mike Shapiro, [DO,] and I wrote an editorial on this in the 

Journal of the American College of Cardiology

 recently, is the idea of cholesterol years.

I think most folks, at least in health care, are aware of the concept of pack years of tobacco exposure. The more pack years, the worse off someone is in terms of their cardiovascular, and in that case, also cancer risk. Cholesterol years is similar. It’s looking at the number of years that someone has cholesterol elevation, and the degree of elevation of cholesterol, and that product, or the area under the curve, essentially represents their cumulative risk for atherosclerosis, at least attributable to LDL cholesterol. And thinking about it that way then forces us to realize, well, for some people, you really do want to start therapy, at minimum lifestyle modification recommendations, but potentially pharmacotherapy much earlier in life if their LDL is extremely high, such as someone with a genetic disorder or familial hypercholesterolemia. Whereas for someone who has good LDL cholesterol due to diet, genetics, nature, whatever, that sort of person perhaps they don’t need pharmacotherapy until maybe much later in life when their cardiovascular risk is higher, and perhaps their LDL cholesterol has drifted higher.

So, the pathophysiology and the epidemiology, I think, are quite interlinked, but importantly, in a way that’s actionable. And for myself, in cardiology, of course, I’m always thinking about cardiovascular risk. But these are lessons that can apply at the many points where we may touch a patient. That is, they might show up for their screening before their knee surgery at a relatively young age, maybe. But if they’ve got identified cardiovascular risk factors, well, that provides an opportunity to act, even though they’re not there at that exact moment to get cholesterol management advice.

That makes sense, and those are all great points.

The standard of care for managing high cholesterol levels.

Strategies Used to Treat Hypercholesterolemia

 presentation, “Multidisciplinary Lipid Management for Prevention of Cardiovascular Risks.” I am your host, Dr Dhiren Patel, adjunct associate professor of pharmacy practice at the Massachusetts College of Pharmacy and Health Sciences in Boston, and an endocrine clinical pharmacy specialist. Joining me today are: Dr Deepak Bhatt, professor of medicine at Harvard Medical School in Boston, Massachusetts; Dr Robert Busch, director of clinical research at the Community Endocrine Group in Albany, New York; Dr Jennifer Goldman, professor of pharmacy practice at the Massachusetts College of Pharmacy in Boston; and Joyce Ross, certified registered nurse practitioner and clinical lipid specialist with concentrated training in preventive cardiology from Philadelphia, Pennsylvania. Thank you all for joining me today. We’re going to start at the 10,000-foot overview and talk a bit about hypercholesterolemia and cardiovascular risk reduction. Joyce, Jen, I know you guys have practiced in a variety of different clinics over the years and have participated in a lot of not, only interdisciplinary research, but interdisciplinary practice. So maybe you guys can start. Joyce, you can start off talking a little about the burden of cardiovascular disease. And then Jen, maybe you can talk a little about that interdisciplinary practice. Joyce, we’ll start with you.

Joyce Ross, MSN, RNC, CRNP, CS, FNLA, FPCNA: 

Thank you very much for the opportunity to be here and work with all of you on this program today. This is a very important question. If we’re talking about the burden of cardiovascular disease, what comes to mind first to me is I believe that there’s an inertia both in the patient population as well as, unfortunately, the medical population. It seems we’ve had so many changes of what our targets are, what our thresholds are over a period of time. For the primary practitioner, and others, it may be difficult to keep up with all the changes. I sometimes think that maybe a provider says the patient is on a statin, go and sin no more, and we don’t do as much as we could. I think the other part is, so many people have familial hypercholesterolemia. And of course, that’s been one of my areas of interest over the last 25 years. Most of them do not know they have a problem until they have an event. Then, of course, we have the opportunity to capture the rest of the family. But I think the inertia that I was talking about, if we could get people to go in for well visits, which of course has been sabotaged over the pandemic, we would be able to get people before they have their disease. I think cardiovascular disease is still the No. 1 killer, and we still have a long way to go.



 Excellent. Thank you. Jen, as you kind of think about some of these challenges that we have, I think, we’ve talked about this in the past, none of our patients just have high cholesterol, no one just has diabetes. We can see here with the panel that we have here, we have cardiology represented, primary care, endocrine, pharmacy. If you could talk a little bit about this multimorbid chronic management that we’re dealing with, and how it needs to be a team sport, as we tackle cardiovascular disease.

The value of interdisciplinary research and multidisciplinary care of patients at high risk for cardiovascular events.

Joyce Ross, MSN, RNC, CRNP, CS, FNLA, FPCNA

Articles

Efficacy of Prescription Vs OTC Fish Oil Products

Implications for Prescribing Icosapent Ethyl to Prevent CVD

Important Considerations When Prescribing Statin Therapy for Hypercholesterolemia

Optimizing Adherence to Therapy for Hypercholesterolemia

Strategies Used to Treat Hypercholesterolemia

Multidisciplinary Approaches to Reducing CVD Risk