Subscribe to The Podcast by KevinMD. Watch on YouTube. Catch up on old episodes!

This episode is sponsored by Novartis Pharmaceuticals Corporation.

In this sponsored episode from Novartis Pharmaceuticals Corporation, a leading preventive cardiologist walks through the 2026 cholesterol guideline update and what it means in practice. Seth J. Baum, a Columbia-trained preventive cardiologist, founder of Flourish Research, chairman of the Family Heart Foundation, and past president of the American Society of Preventive Cardiology, breaks down the major changes in the March 2026 ACC and AHA guideline release. You will hear why LDL targets are explicit again after nearly a decade, why universal lipoprotein A screening is now recommended, why a coronary calcium score above 300 places a patient in the highest-risk treatment tier, and why apolipoprotein B measurement can refine risk assessment when LDL is at goal. Baum also covers the alternatives available when a patient cannot tolerate a statin, including ezetimibe, PCSK9 inhibitors, inclisiran, and bempedoic acid, along with practical framing for the statin-hesitant patient. You will also hear his approach to discussing cholesterol with patients, from the science of lipoprotein physiology to the case for earlier and more aggressive lipid-lowering treatment.

Dr. Baum was not compensated for his participation in today’s episode. The opinions expressed are his alone and do not represent the opinions of Novartis Pharmaceuticals Corporation.

At Novartis, our mission is to ensure no heart is lost too soon. We envision a world where preventable CV deaths are no longer part of our lives. We’re proud of the positive impact we’ve made over the past 40 years and remain dedicated to tackling the most challenging problems in CVD. Through cutting-edge science and technology, we are focusing on areas of high unmet need, including scaling our xRNA platform across multiple risk factors and pioneering breakthroughs for genetically driven CVD risk factors and common heart conditions, including atrial fibrillation.

We also work with patients, healthcare professionals, and organizations around the world to improve CV care beyond medicine alone. Together, we can help people with CVD enjoy longer, healthier lives and more time with their loved ones. Learn more here: https://Novartis.us/cardiovascular-disease

VISIT SPONSOR → https://Novartis.us/cardiovascular-disease

SUBSCRIBE TO THE PODCAST → https://www.kevinmd.com/podcast

RECOMMENDED BY KEVINMD → https://www.kevinmd.com/recommended

Transcript

Kevin Pho: Hi, and welcome to the show where we share the stories of the many who intersect with our health care system but are rarely heard from. Subscribe at KevinMD.com/podcast. This episode of the podcast is brought to you by Novartis Pharmaceuticals Corporation. Today, we welcome Seth J. Baum, a Columbia-trained preventive cardiologist, founder of Flourish Research, and chairman of the Family Heart Foundation.

He has published more than 150 papers, led more than 150 clinical trials, and is a past president of the American Society of Preventive Cardiology. Today, Dr. Baum joins us to discuss the new American College of Cardiology/American Heart Association cholesterol guidelines and what they mean for your practice, and why LDL cholesterol goals just changed for the first time in eight years.

Dr. Baum was not compensated for his participation in today’s episode. The opinions expressed are his alone and do not represent the opinions of Novartis Pharmaceuticals Corporation. Find out more at Novartis.us/cardiovascular-disease. That’s Novartis.us/cardiovascular-disease. I know that’s a mouthful, and a link will be in your show notes.

Dr. Baum, thank you so much for joining us today.

Seth J. Baum: Thanks for having me. Looking forward to this conversation.

Kevin Pho: Let’s briefly introduce yourself, then we will jump right into the recently updated guidelines.

Seth J. Baum: Sure. I started as an electrophysiologist and an interventional cardiologist.

In about 2000, I became a preventive cardiologist and clinical lipidologist, which I have done since then. You mentioned a couple of important things, including the American Society for Preventive Cardiology and my involvement there. Also, the Family Heart Foundation is very important. I am the chairman of the board of that organization, and that really focuses on familial hypercholesterolemia, Lp(a), and the broader issue of cholesterol, which is really our topic of conversation today.

I have also been involved in a good number of clinical trials, am one of the founders of Flourish Research, and currently serve as a senior advisor to its board.

Kevin Pho: The big news, of course, in the world of preventive cardiology was the recent update in the cholesterol guidelines that were released in March.

Before we talk about those updates themselves, tell us about the events leading up to that update, just to give us a little bit of context and set the stage.

Seth J. Baum: Those events probably date back to the 2013 guidelines when there was a shift away from focusing on goals that had a negative impact on outcomes and management of cholesterol.

It was somewhat improved in the 2018 guidelines. Now, in the 2026 guidelines, there is a very significant improvement, which I know we are going to discuss at length. I do want to say at the outset that although the guidelines are certainly an advance in getting back to where we should be and moving a little bit forward, they are not the final guidelines.

There is much more work to be done. There are certain flaws with the guidelines in my view. There are many positive aspects, but hopefully, we will touch on all of this.

Kevin Pho: Now, as you sit back and reflect on the changes that were announced in March, tell us the changes that were most important to you, and what does that say about our thinking on cardiovascular risks and how that has changed since 2018?

Seth J. Baum: I would say that moving away from looking at LDL targets or LDL goals, and looking at the management of LDL cholesterol specifically just on the basis of the introduction of a statin or a percent reduction in LDL, is a significant shift. Moving away from that and now focusing back again on LDL is probably the most important aspect of the guidelines.

There are many other things that relate to Lp(a) and LDL that we will talk about. Getting back to the fact that LDL is bad and trying to get it down without any confusion is very important.

The other overarching theme is the recognition that we had gone in the wrong direction and needed to make a correction. That is a very positive outcome of the guidelines.

These multi-society dyslipidemia guidelines are what we always call cholesterol guidelines. This year we are calling them dyslipidemia guidelines. They impact triglycerides and other aspects of lipids and lipoproteins as well. Our main focus, however, is obviously on cholesterol.

Kevin Pho: For our friends who may not be versed in preventive cardiology and do not follow the minutia of the guidelines, tell us a little bit about the course correction that you mentioned.

Seth J. Baum: Previously, within the last 10 to 15 years, we had moved away from a focus on what LDL should be in a given risk population.

We always say we treat according to risk. The higher the risk, the more aggressive we treat, which leads to a greater benefit in outcomes. We treat according to risk. We had moved away from saying that we know reducing LDL is beneficial, despite having multiple studies that have demonstrated this.

We have the cholesterol treatment trialists and more than 20 studies. There is a very clear linear relationship between LDL reduction and a reduction in cardiovascular events. For every 40 milligrams you reduce someone’s LDL, you reduce their risk by about 20 percent. We have known that, and it goes all the way down close to zero. There is no point where it goes away.

We had gone away from that. We had ignored what patients’ LDLs were. As a consequence, if you looked at people with acute coronary syndromes a year out, most of them were not on their lipid-lowering therapy and had LDLs that were much higher than they should be.

The course correction here stipulates with a new risk equation, which we can talk about as well, exactly where that LDL should be below. It should not just be at that number, but below it. It should be below 55 in the highest-risk patient, 70 for the slightly less high-risk patient, and 100 for others.

It does that. I would say that is the big course correction that we have made.

Kevin Pho: It sounds like there is more of a focus on target goals, more of a focus back on LDL cholesterol, and just clarifying the goals to make them reachable from both our standpoints: you as a preventive cardiologist, and me as a primary care doctor.

Seth J. Baum: Let me address that reachable aspect here. If we wanted to, we could reduce everyone’s cholesterol down into the 30s across the board. We really could. There are a few exceptions with severe homozygous familial hypercholesterolemia, but they are really very much the exception rather than the rule.

We have the capacity to reduce LDL to levels that would dramatically reduce the incidence of cardiovascular events. One of the things we are always focusing on, and this is one of my problems with the guidelines, is that we focus on de-risking people. We focus on who we should not treat.

At this point in time, we know cardiovascular disease is on the rise. Mortality from cardiovascular disease, which had been steadily going down, is now going back up. It is a very bad thing. It is not the time to say that we should leave some people alone. We should leave people alone and not treat them if there are safety issues with these drugs. These drugs are really safe by and large.

In my view, it comes down to a price issue and a cost issue, and we are concerned about the economic impact of treating and over-treating. The problem is that when you limit the number of people you are going to treat, you definitely put some people at risk who are going to have events, and I personally do not like that.

Kevin Pho: Why is this such a challenge when we know we can bring everyone’s cholesterol down and that these medicines are safe? Talk more about some of the challenges that we face in medicine when it comes to reducing people’s cholesterol and lowering their cardiovascular risk. What are some of the challenges and obstacles that we still face?

Seth J. Baum: The challenges are manifold and multifactorial. There are multiple stakeholders involved. If you look at the people and the institutions involved in lipid management, it has extended well beyond just the clinician and the patient.

We now have policymakers who are very involved. We have the payers who are very involved. Believe it or not, the guidelines actually do influence the payers to some degree. They look at the guidelines, and they can sometimes deny a medication on the basis of the guideline. This is unintended by the guideline writers, but it does happen.

We have the experience of the PCSK9 inhibitors that were launched about 10 years ago when the payers pushed back dramatically. It was the first time in my career as a cardiologist that I actually got denials for medications. I had never experienced that. I did not know anything about this.

I happened to be coming into the presidency of the American Society for Preventive Cardiology at that point, so I used my term to try to understand and combat what was happening and get access to these medications for patients. The denials were almost uniform.

Then we had to learn about prior authorization. Cardiologists, internists, and other clinicians developed this understanding and fear of the denial. It is a time suck in a practice, and it has added to clinical inertia in this space.

I should not ignore the fact that we have been so hyper-focused on statins. There is so much anti-statin sentiment out there, and we hear it. Anyone practicing medicine hears it from their patients. Patients think their legs are going to fall off or terrible things will happen.

We have to fight that when we know scientifically, based on hard evidence, randomized clinical trials, and Mendelian randomization studies, that it does not matter how you get the LDL down. If you get it down safely, it is the same with the drug or lifestyle. It is about how quickly you get it down and where you get it. If we could just establish that as gospel, which it is, we would help eliminate some of these problems.

Kevin Pho: Let’s talk about the patient resistance to statins because I see this every day in my exam room. I am sure that you do in your exam room. How do you address that with patients? How do you present a potential side effect of statins, which are largely safe drugs? How do you present those risks to patients?

Seth J. Baum: First of all, I assess the patient’s position with regard to statins. If you have someone in the office who is a hardcore anti-statin individual, it is unlikely you are going to have great success.

I would attempt early on to say that we have a lot of clinical trial data and these are the safety data. I present it to them, and then if I see that I am not really making much headway, I quickly go in another direction.

There are other drugs that also reduce LDL cholesterol and are effective. We do not have to do the statin. We can go here, and we can do this other thing.

I do make that pivot. I never allow myself to engage in that battle with the patient where you are saying that you are right and they are wrong, because we tend to lose those battles. We also lose their confidence, which is another thing we have to contend with. There is a tremendous lack of confidence in us nowadays, unfortunately.

Kevin Pho: Just to be explicit about the safety data of statins, give us some of the numbers in terms of potential side effects. We talk about the elevation of liver enzymes. We talk about muscle aches. What are the actual numbers when it comes to those potential side effects?

Seth J. Baum: Clinically meaningful elevation in liver tests is extraordinarily rare. It could vary a little bit from drug to drug, but it is very rare, certainly less than one in a thousand. Rhabdo is also similarly extraordinarily rare.

When it comes to the more subtle side effects like myalgias, weakness, and brain fog, those numbers could be much higher. It depends on what you read, but it can be in the 20 percent range. None of those issues is going to prevent you from utilizing a statin.

If you were to get one of the very rare and serious complications, you just have to be on top of this with your patient and explain what could potentially happen in unusual circumstances. We stop the drug, we treat the situation, and we typically do well. I have never seen a long-term problem from that.

With regard to the more subtle side effects, you just stop the statin. You try another one, stop it, and then you move on to another class of drug.

Kevin Pho: Let’s talk about those other classes of drugs. If we have a patient who, for whatever reason, cannot tolerate or doesn’t desire a statin, what other options do we have in the exam room?

Seth J. Baum: We have the PCSK9 inhibitors for one. The monoclonal antibodies are phenomenal and reduce LDL by 60 percent. They also can have an impact on Lp(a), depending upon the study, leading to a 20 to 30 percent reduction. They are not indicated for that. It is a side benefit.

In some patients, we have ezetimibe, a cholesterol absorption inhibitor. We have inclisiran with small interfering RNA for PCSK9, which got a bump in the new guidelines for severe hypercholesterolemia.

We have bempedoic acid. We have a lot of tools in our armamentarium, and we need to avail ourselves of those tools.

Kevin Pho: To sum up this arc of our conversation, how should physicians think about LDL screening today? What did these guidelines change specifically about LDL screenings and reframing that particular lab value?

Seth J. Baum: I would like to go back to the basics when we talk about LDL and say unequivocally that LDL leads to vascular disease, strokes, heart attacks, and cardiovascular death. We have multiple lines of evidence, and we know this. We have genetic evidence and clinical trial evidence.

We know that the higher the LDL, the greater the risk. We know that the lower the LDL, the lower the risk. We know that getting LDL down quickly is better than taking your time doing it.

We also know from Mendelian randomization studies that those individuals who are gifted with a mutation that diminishes LDL from in utero and beyond have about a 50 percent reduction in cardiovascular risk for every millimole reduction in LDL. For every 40 milligrams per deciliter, they get a 50 percent reduction, as opposed to what we know in clinical trials would give you a 20 percent reduction. It is so much better.

We know all of this. The take-home message is that we need to look at LDL very differently. We cannot think of the LDL hypothesis anymore. We have to eradicate that term. It is the LDL fact and the LDL truth.

We have to approach it as our greatest opportunity to reduce the risk of heart attack, stroke, and cardiovascular death. We need to measure it frequently, treat it accordingly, and get the LDL down as low as we can. At the bare minimum, follow the guidelines, but it is better to go even lower. We need to have an open conversation with our patients so they understand that all we are doing is trying to help them.

Kevin Pho: We’re talking to Seth Baum, a preventive cardiologist, and we’re talking about the new American College of Cardiology/American Heart Association cholesterol guidelines, what they mean for your practice, and why LDL cholesterol goals changed for the first time in eight years, and the impact that has on you.

Seth, in your exam room, how have these new guidelines changed what you do with patients? I know that these guidelines suggest new tests to consider, and there is a new calculator perhaps. Tell us about how these guidelines have changed what you do.

Seth J. Baum: I am not a good representation of where change may occur. I have been operating outside the guidelines for decades. My goal has always been for the last 20 years to get the LDL down incredibly low, be very aggressive, and use combination therapy.

For physicians who had been using the prior guidelines, the change here would be that they would look at their patients and use the PREVENT calculator instead of the pooled cohort equation.

Kevin Pho: Talk more about that. What is the PREVENT calculator?

Seth J. Baum: It is a new risk calculator that is based on a much larger and more contemporary population. Its accuracy and calibration are better than the pooled cohort equation that we had been using for a very long time.

That is now what we are supposed to use. You are supposed to risk-stratify your patient, and then you look at the guide and say that this patient has a particular risk. The recommendation is to get the LDL down lower than whatever target. Again, in the highest-risk patients, it should be less than 55.

It is a good thing that we have this new equation. The problem is that the equation tends to de-risk the population. This was understood by the guideline writers, and so they lowered the limits of risk. It is 3 to 5 percent for low risk, 5 to 10 percent for intermediate risk, and over 10 percent instead of over 20 percent in the past for high-risk patients.

They try to accommodate for that diminished risk that is inherent in the calculator by reducing the risk categories to equilibrate. The problem is that when that was studied in several major centers, three out of four times it did not pan out. It still underestimated risk significantly.

That is one of my fears about these guidelines. I know I have strayed from your original question, but I think it is an important point. It is a risk because the last thing we want to do is underestimate risk and leave someone untreated who could be treated and potentially experience a cardiovascular event.

Kevin Pho: Who are the people who are at greatest risk for being underestimated?

Seth J. Baum: Patients not currently on statin therapy. When we are thinking about whether we should put the patient on a lipid-lowering therapy, that patient is at a higher risk of being underestimated. That is not who you want to underestimate.

Men have a higher risk at a younger age of cardiovascular disease. Women have a very high risk, but men, Black patients, people on antihypertensive therapy, and some diabetics are vulnerable. We are putting some of our higher-risk patients at risk.

I would caution people when they use these guidelines to use them to help guide you, but do not use them so explicitly that you restrict therapy in individuals who might be at enough risk and deserve treatment.

Kevin Pho: From the perspective of the guideline writers, why did they choose the methodology that they did, which, as you said, has the potential to underestimate risk?

Seth J. Baum: It is a more modern and much larger group that it was studied on, so it is more contemporaneous. In that regard, it is definitely more appropriate.

It needs some recalibration, and they tried, but I think it was not adequate. I think they will come back and ultimately fix it. They are telling us that within a year they are going to have an update, which is a very good thing.

Other things were omitted. We could talk about the Vesalius study, which was a primary prevention study demonstrating that getting LDL down very low with a PCSK9 inhibitor to 45 significantly reduced the risk of cardiovascular events. They will make an update on that as well.

Going back to the pooled cohort equation versus PREVENT, it is estimated that about 14 million Americans now will not be eligible for statins on the basis of the new risk calculator. There is a potential for 100,000 cardiovascular events over 10 years that we do not need to have.

Again, it is this balancing act of over-treating and under-treating. My personal stance is I would rather over-treat a population. If I can use an analogy, it reminds me of when I was in the cath lab years ago. When you had a patient with acute coronary syndrome, if you didn’t get 10 percent normal caths, you were doing too few caths. It meant you were missing the real thing. You have to over-study in order to be able to get the high-risk population. Here, you have to over-treat.

Kevin Pho: Talk to us about lipoprotein A. I think that the guidelines did make significant mention of that. I know a lot of cardiologists have already been measuring that, but now it has been almost codified into these guidelines. Tell us about what the guidelines say about lipoprotein A.

Seth J. Baum: I am happy to hear you say that a lot of cardiologists are measuring that because that means you have spoken to a lot of people who are measuring it. The reality is that in the United States, only about 5 percent of the population has had Lp(a) studied and checked.

We have definitely under-checked. What is Lp(a)? Lp(a), or lipoprotein small a, is like a very small LDL particle with a little tail on it called Apo(a), and it is a triple threat. It increases the risk of the development of atherosclerosis, it increases the likelihood of thrombosis, and it increases inflammation.

The phospholipids carried on it are abundant, and they become heavily oxidized. It is a highly inflamed particle. It is doing everything wrong with regard to our vasculature.

About 20 percent of the population has a high Lp(a). It is a genetically driven lipoprotein. About 20 percent is over 125, which conveys about a 40 percent additional risk of a cardiovascular event.

What the guidelines did was great. We caught up with our friends in Europe and in Canada by saying we need to do universal screening. Everyone needs to know their Lp(a). It is important.

Once you know your Lp(a), you can and should do things. You should reduce cardiovascular risk, which is in our guidelines, because it is helpful.

You should cascade screen because it is genetic, so you need to check first-degree relatives and then move out to other relatives as you keep finding individuals with elevated Lp(a).

You should know that there is a risk inherent in Lp(a) that is a 40 percent additional cardiovascular risk at an Lp(a) of 125. At about 200 to 250, it is about a twofold increased risk. At about 430 to 450, it is about a fourfold increased risk, making it almost as bad as familial hypercholesterolemia.

We know that the level of the Lp(a), just like with LDL, will dictate the risk.

Since it is genetic, it is here from birth and in utero. We have the same problems with genetic LDL disorders. The guidelines also stated, and I was very happy with this because everyone says there are no therapies available for Lp(a), that there is actually apheresis, which is approved for Lp(a).

We already have that, and we will have therapeutics in the not-too-distant future for Lp(a).

One other thing that was important to mention is that PCSK9 inhibitor monoclonal antibodies were upgraded so that in elevated Lp(a), when there is additional LDL reduction required, it is recommended to institute a PCSK9 inhibitor. There is that 20 to 30 percent potential reduction, sometimes more, sometimes less, in Lp(a).

In addition to that, they are very effective LDL-reducing drugs, and we do want to limit our other cardiovascular risk factors. From a population-attributable risk standpoint, LDL is the most important one.

Kevin Pho: A close cousin to lipoprotein A is apolipoprotein B. Comment on apolipoprotein B and its place in cardiovascular screening.

Seth J. Baum: With ApoB, or apolipoprotein B, there are two forms. There is ApoB 100 and ApoB 48.

In the liver, when we make VLDL particles, which are the precursors for IDL, intermediate-density lipoprotein particles, which are the precursors for LDL, we have one ApoB 100 protein on the surface of the particle. These are very large structural proteins, and a piece of them will bind to the LDL receptor. They are very important.

It is a one-to-one relationship. VLDL, IDL, and LDL are all atherogenic lipoprotein particles. They cause vascular disease. Lp(a) has one ApoB 100 on its surface and causes atherosclerosis as a lipoprotein particle.

Chylomicrons made in the gut have ApoB 48. We will leave them aside now because they are not considered heavily to cause vascular disease, certainly not in their large state.

If you think about it, every single atherogenic lipoprotein particle has one ApoB 100 on it. If we count ApoB 100, we can know very well what cardiovascular risk is attributed to our lipoprotein particles.

That is why it is important to measure ApoB. It is a more accurate way to assess cardiovascular risk from a lipid and lipoprotein standpoint than by looking at LDL. It is more accurate.

The other thing is that when we treat dyslipidemias with medications, we tend to cause a disconnect where we reduce LDL more than we reduce ApoB. This happens predominantly, though not exclusively, when triglycerides are high or HDL is low in the setting of some renal disorders or diabetes.

What happens then is you get the LDL down to 50, and you are thrilled. You say, “Oh my God, that is great. I made it. I have reduced the risk as best as I can.”

The reality might be that ApoB did not fall as much as LDL and is still too high for that patient. By checking ApoB, you can more aggressively treat the LDL and drive the ApoB down to a lower level to be more protective.

This does happen across the board, even in a condition like familial hypercholesterolemia, which is really an LDL disorder, not a triglyceride or an HDL disorder, yet it does happen there too where we get the disconnect.

My personal feeling is to always check an ApoB in your patients you are treating for a lipid disorder to reduce their cardiovascular risk.

Kevin Pho: In contrast to lipoprotein A, how sensitive is apolipoprotein B to statin therapy and some of the therapies that we talked about today?

Seth J. Baum: Statin therapy is not going to reduce Lp(a). It will reduce ApoB. All of our lipid-lowering drugs will reduce ApoB. Unfortunately, they reduce ApoB less than they reduce LDL, and as a consequence, you can get that disconnect.

With regard to Lp(a), we have to say that we currently do not have any effective drugs on the market to reduce Lp(a). PCSK9 inhibitors can give some people a little benefit, but it has never been looked at carefully enough to determine what that would mean for patient outcomes. It is certainly a side benefit of the drug, but there are no drugs that we have available specifically for Lp(a).

We have a slew of drugs available for LDL. Again, ApoB is the protein that you are going to consider that is on every one of our atherogenic lipoprotein particles in a one-to-one relationship. That is Lp(a), VLDL, IDL, and LDL. That is why it is in its own class, and we need to look at it more carefully and test it.

Kevin Pho: The other part of our guideline that I want to touch upon is coronary artery calcium scoring. What do the guidelines say about that particular test? Start by introducing what that test is for those who are not familiar with it, and then explain what the guidelines say about it.

Seth J. Baum: There are different ways to image the coronary arteries. Coronary artery calcification scoring is a non-contrast CT scan that analyzes and basically counts how much calcium one has in their coronary arteries.

On the basis of a ton of data accumulated over the decades, we can now say what someone’s risk is for a future cardiovascular event, corrected for age and sex. The presence of coronary calcium dramatically increases the risk of cardiovascular events.

What the guideline has done, which is a beautiful move, is state that if you have a calcium score of greater than 300, you should be treated as though you are in the highest risk category of someone who has already had a heart attack. You are very high risk, so your LDL should be under 55.

It is a great way to understand risk. We used to use it as a risk enhancer. We would see that your calcium score was high, note that your risk was a little higher, and decide we should reduce your LDL. Now we are saying that it is a dramatic risk enhancer. You basically have a tremendous risk of having an event as though you have already had two heart attacks. I love that.

The other imaging technique is coronary CT angiography, which is typically reserved with contrast where we see the wall of the vessel. We can even analyze in some circumstances how much inflammation there is and what kind of plaque is present. Is it soft plaque? Is it vulnerable? It is a tremendous test, but it is typically reserved for patients with symptoms.

Again, I practice outside the guidelines, so I have been using it to understand risk even better with the appropriate shared decision-making conversation with patients.

Kevin Pho: From a primary care standpoint, who are the patients I should be looking for to order a coronary artery calcium score?

Seth J. Baum: If you have a suspicion of a high-risk circumstance in an untreated patient, that is a great place to think about using a coronary calcium score.

You think the patient should be on therapy, but the patient tells you they do not want to be on therapy. You do a calcium score and tell them, “Look, you have coronary disease.” This is coronary disease, by the way.

I think it is also important when you do order it and get the test back that you explain to the patient, “Look, the calcium is a late finding in coronary disease.” First, you get a soft plaque, and then as that plaque heals, calcification is laid down. Cells in the plaque actually transform into basically bone cells. They lay down calcium to heal the plaque.

A lot of time has gone by. It helps them understand the nature of the disease and the risk inherent in it. Those are the individuals you should get it on.

You should not, in my view, get it on individuals who have established coronary disease and you are tracking them over time. It is really to make the decision early on to treat or not to treat, and how aggressively to treat now because we have that greater than 300 threshold.

I would add that it is also useful if the score is greater than the 75th percentile for age and gender-matched controls. Those are really the patients I would consider using them on.

There is a little caveat. Since it takes time to develop calcium, you can sometimes miss people. In younger people and in women, they can sometimes have soft plaque and not calcified plaque. I would not look at a calcium score of zero and assume you are out of the woods.

You have to keep that in mind. I have seen these people where they have a calcium score of zero and a 90 percent soft plaque in the LAD. There is that caveat. It is not common, but it happens often enough.

Kevin Pho: We’re talking to Seth Baum, a preventive cardiologist, and we’re talking about the new cholesterol guidelines from the American College of Cardiology and American Heart Association. This episode is sponsored by Novartis Pharmaceuticals Corporation. Find out more at Novartis.us/cardiovascular-disease. I know that’s a handful, but that link will be in the show notes.

Seth, a couple of questions to end off. First, what do we have to look forward to when it comes to cholesterol screening and preventive cardiology? What is on the horizon?

Seth J. Baum: What is on the horizon? Horizon is a clinical trial that is looking at Lp(a), the first drug that hopefully will get a great result this year, and we will have a drug available for Lp(a). I will lead with that since you used the word horizon.

Hopefully, people will pay attention to Lp(a). Hopefully, people will start screening everyone. That does not mean just one test in a lifetime because it is genetic. There are times where you want to get a follow-up test, such as after menopause when Lp(a) goes up quite significantly. I would say for Lp(a), we are leading with that.

With regard to LDL, my hope is that we clinicians embrace LDL as a genuine risk factor, not hypothetical. We must understand the science and the medicine, that getting LDL lower and doing it faster is better, and the longer it stays lower, the better.

It is one of the few things in medicine that I would say is factual. I would hope that happens.

I am looking forward to updated guidelines that are broader and that include more people in LDL reduction. I am looking forward to hopefully the guidelines helping push for quality measures that address not just statin use but checking LDL and reducing LDL.

I would love to see quality measures in place that do that, just like we have for hypertension and diabetes. We do not look at our quality measures and ask, “Did you start one medicine on your hypertensive patient?” or “Did you give them a medicine for diabetes?” No, we check the hemoglobin A1C. We check the blood pressure.

Here, we have to check the LDL and we have to manage it. Those are some of the things that I am excited about and hopeful that we can turn around. I hope people will no longer be complacent or bored of LDL because they have heard about it so much that they just embrace it.

Let’s tackle this. We have the capability and the drugs. Let’s just solve this problem and dramatically reduce cardiovascular events, strokes, heart attacks, and cardiovascular death in the United States.

Kevin Pho: Any tips you have for physicians to communicate these new guidelines with patients? Patients are reading about these guidelines in mainstream media. They are coming to our offices with a lot of questions. What kind of tips do you have for physicians to best communicate these new guidelines to our patients?

Seth J. Baum: It is an interesting question, and this may sound basic, but I have always found that going very much back to the basics of biology and physiology at the start of the conversation helps when discussing cholesterol.

I say this because there is a ton of misinformation about cholesterol. You get the patient who says, “Well, my brain has a ton of cholesterol, and I am going to decrease cholesterol in my body, and that is not good. We need LDL for our steroidogenic tissues.”

I go back to the basics, and I start with a very simple statement about the fact that water and fat do not mix. I say, “You know water and fat do not mix. If you make salad dressing and you shake up the salad dressing, the oil and water separate, and you get these little bubbles.”

The body cannot have that. We would not survive. So very intelligently, we have these lipoprotein particles that transport cholesterol around the body. LDL is one of those.

We know that LDL in the body does nothing other than go back to the liver to basically dump the cholesterol. LDL does not cross the blood-brain barrier. The brain does not use LDL cholesterol.

Every cell in the body makes its own cholesterol. All of our steroidogenic tissues are making their own cholesterol. They are not using LDL. That has been proven.

You start with that, and you ask, “Wait a second, if it is bad, why should we keep it around?” Look at a child or a newborn whose LDL is somewhere in the 30 to 40 range. All they are doing is making their brain. That is their goal for the first several years, to create their brain.

If the brain required cholesterol, their cholesterol would be 500. So that is not the case. Let’s get rid of this cholesterol. We have the tools to do it. We have the drugs.

Then you go into the studies, the genetics, and the Mendelian randomization studies, and you make the case for LDL reduction.

I spend that kind of time. It may take five minutes, but I really think that it engenders trust and confidence, and it eliminates a million other conversations when there are side effects with one drug. You just say, “Fine, we will try another drug.”

It eliminates those conversations, makes your life so much easier down the road, and many more patients embrace lipid-lowering therapy.

Kevin Pho: And my final question. Seth, your take-home message that you want to leave with the KevinMD audience.

Seth J. Baum: Please take LDL seriously. We have the ability to reduce LDL and by doing so reduce stroke, heart attack, and cardiovascular death in the United States. Let’s do it.

The second part of this is Lp(a). Check Lp(a) in all of your patients. It is so important. It is now in our guidelines, but you can do things about it, and soon we will have drugs to deal with it. So check Lp(a) and take it seriously.

A final one: I am going to put in a plug for the Family Heart Foundation, of which I am the chairman of the board. There are tremendous resources at the Family Heart Foundation to help you and your patients navigate the cholesterol and the Lp(a) world, and help even in accessing medications when appropriate for your patients.

Please go to the Family Heart Foundation website and use some of the many materials that we have. We also have a free cholesterol and Lp(a) screening system in place. There are many tools and assets on the Family Heart Foundation website that I would love everyone to look at.

Kevin Pho: We’ve been talking to Seth Baum, a preventive cardiologist. This is a sponsored episode brought to you by Novartis Pharmaceuticals Corporation. Find out more at Novartis.us/cardiovascular-disease. The link will be in the show notes.

Seth, thank you so much for sharing your perspective and insight, and thanks again for coming on the show.

Seth J. Baum: Thank you. Thanks for having me.