Ep. 25: The Biggest Little Troublemaker: Unpacking Lipoprotein(a) — with Dr. Guy Mintz, Cardiologist & Lipid Expert

It’s a tiny particle most people have never heard of — yet it can drive early heart attacks, strokes, aortic valve disease, and aggressive atherosclerosis, and roughly one in five people carry too much of it. In this episode, Dr. Regina Druz sits down with cardiologist and clinical lipidologist Dr. Guy Mintz to demystify lipoprotein(a), or Lp(a). They explain what it is (a genetically inherited, inflammatory cousin of LDL), why it explains some of the ‘residual risk’ that lowering cholesterol leaves behind, how it’s measured and what the numbers mean, and why everyone should be tested at least once — with cascade screening for relatives. Then they cover what you can do today, from lowering LDL to lipoprotein apheresis, and the new Lp(a)-specific drugs on the horizon.

Watch on YouTube: A video version of this episode is available on the Own Your Heart Health YouTube channel. Subscribe to be notified of new episodes.

Episode Chapters

[00:00] Introduction & Meet Dr. Guy Mintz
[01:52] How He Became a Lipidologist
[03:47] Diffuse Disease & Residual Risk
[07:45] The “Little A”: Kringle Repeats & Isoforms
[12:26] Genetics: One in Five, and Cascade Screening
[16:18] When Genes & Levels Disagree
[21:30] Units & Risk Thresholds
[26:00] Should Lp(a) Be Standard? Guidelines & the Testing Gap
[29:09] Treating the Patient: Lower LDL First; Statin Caveats
[35:12] New Lp(a)-Specific Drugs on the Horizon
[41:07] Lipoprotein Apheresis: How It Works & Who Qualifies
[46:31] Why Lp(a) Is So Harmful + Residual Risk & Closing

Transcript

[00:00] Introduction & Meet Dr. Guy Mintz

Dr. Regina Druz (00:02): Welcome to Own Your Heart Health. I’m Dr. Regina Druz, your holistic cardiologist. This week we’ll dive into common heart health concerns, uncovering root causes and unpacking scientific discoveries and controversies. The information provided does not constitute medical advice. Please contact your healthcare practitioner before making any changes that may impact your health.

Dr. Regina Druz (00:40): Hi everyone, another Friday fun day. I’m super excited because I finally got to bring on a guest who’s an absolute expert in one of the most difficult and controversial areas of cardiology — a little lipoprotein particle that causes a lot of trouble, called lipoprotein(a). My guest is my colleague and fellow Long Islander, Dr. Guy Mintz. Dr. Mintz is a cardiologist who serves as Director of Cardiovascular Health and Lipidology, and directs the lipoprotein apheresis program, for Northwell Health, where he helped create one of the few regional centers of excellence for advanced lipid disorders. Welcome, Guy.

Dr. Guy Mintz (01:42): Thank you, Regina. Thank you for the opportunity to speak with the public and bring the words of prevention to everyone.

[01:52] How He Became a Lipidologist

Dr. Regina Druz (01:52): I’ll ask what I ask all my guests: how did you grow up to be a lipidologist? When you and I started in cardiology, lipidology barely existed as a thing.

Dr. Guy Mintz (02:15): Great question. We’re very good at treating heart disease — put in a stent for a 90% blockage, do bypass surgery, and we look like heroes. But atherosclerosis is a whole-body disease; it affects the entire vascular tree, not just the heart, but the arteries to the legs and brain. And it isn’t a one-stop shop: the most common heart attack comes from a roughly 50% plaque that ruptures — an obstruction an interventional cardiologist wouldn’t even touch. So we’re great at fixing the end result, but I became fascinated by the beginning: how do we affect a patient’s whole lifetime of risk? Lightheartedly, my mission is to put the interventionalists and surgeons out of business.

[03:47] Diffuse Disease & Residual Risk

Dr. Regina Druz (03:47): That’s so important. We both see patients who say, ‘I had a cardiac cath or a CT angiogram and was told everything’s fine.’ Then I look at the report and there were no lesions to stent — but there was diffuse disease across all three coronary territories. That diffuse disease is a marker of aggressive atherosclerosis and a high-risk patient, even without a focal blockage to fix. So let’s get to today’s culprit — lipoprotein(a). What is it, and why should people care?

Dr. Guy Mintz (04:49): Years ago a newspaper called it ‘the risk factor cardiologists don’t know about.’ Here’s the key: even the best cholesterol-lowering drugs reduce cardiac events by only about half, so what about the rest? That’s the concept of residual risk. Lipoprotein(a) is one big piece of it. It’s like an LDL particle — with its ApoB — but with an extra ‘a’ protein attached, and it’s associated with early heart attack, stroke, aortic and valvular stenosis at a younger age, peripheral arterial disease, aortic aneurysms, and faster atherosclerosis, largely through inflammation. So once we’ve lowered your cholesterol, the job isn’t over — we have to ask what else is driving the risk.

Dr. Regina Druz (06:16): Hi everyone, it’s Dr. Regina here. I know there are contradictory opinions about nutrition for heart health and longevity — the discussion gets heated and confusing. Some push low-fat, low-cholesterol; others are fans of a ketogenic diet; and there are many voices urging vegan or vegetarian eating. To cut through the clutter, my team and I created Holistic Heart University: on-demand courses, nutrition and lifestyle resources, and supplement guidance to make healthy choices for your heart easier to understand. I’m especially proud of our open office hours and the Q&A feature where you can put us in the hot seat. Head to the show notes for the link and use promo code OWNER20 for 20% off our annual subscription. I’ll see you in office hours.

[07:45] The “Little A”: Kringle Repeats & Isoforms

Dr. Guy Mintz (07:45): So what exactly is that little ‘a’ attached to the particle? It’s a protein packaged onto your LDL — there’s an ApoB on everything, and then the ‘a’ is added on. It’s made of repeating units called Kringles — specifically Kringle IV type 2 — and I joke with patients, not Pringle, don’t eat it. The molecule almost looks like a snake wrapped around many of these repeating Kringle units. You can have large isoforms or small isoforms. It’s measured with a simple, non-fasting blood test you can add to your lipid panel — it’s like your personal tattoo. Repeat values can differ slightly between labs depending on the isoform and the antibodies and reagents used, but either way, a high lipoprotein(a) is a cardiovascular risk-enhancing feature.

Dr. Regina Druz (09:56): Let me broaden this for first-time listeners. Lipoprotein(a) is one of the ApoB-containing particles — cholesterol doesn’t float freely; it’s shuttled by apolipoproteins. (If this is new, listen to my ‘cholesterol marbles’ episode, where I illustrate it with marbles.) Lp(a) has a specific protein coat with those Kringle repeats. The name comes from a Danish pastry, ‘kringle’ — the discoverers thought the protein folds looked like the pastry. Depending on the number of Kringle repeats, you get smaller or larger particles. Which is more dangerous?

Dr. Guy Mintz (11:47): Smaller isoforms are associated with higher lipoprotein(a) levels — there’s an inverse relationship — and with coronary disease, aortic valve disease, peripheral arterial disease, stroke, and progressive atherosclerosis. So small isoforms, higher Lp(a), more risk.

[12:26] Genetics: One in Five, and Cascade Screening

Dr. Regina Druz (12:26): The damage is largely proportional to the measured level, and the larger isoforms tend to clear faster, so they’re often less damaging. My first Lp(a) patient was a healthy woman in her 60s who presented with a central retinal artery occlusion — amaurosis — and a lot of coronary disease; that’s when I started focusing on it. Now, reports and physicians often say Lp(a) is genetic. Is that true for most patients, and should someone with high Lp(a) just assume it’s genetic or get genetic testing?

Dr. Guy Mintz (14:13): About one in five people have an elevated lipoprotein(a). Roughly 90% of the level is determined by genetic variation on the LPA gene on chromosome 6 — it’s highly heritable, passed on as an autosomal codominant trait, and driven by the number of Kringle IV type 2 repeats, plus single-nucleotide polymorphisms in the gene. So I tell patients: your Lp(a) isn’t high because you ate poorly or didn’t exercise — it’s a genetic tattoo. We still want you doing all the healthy things to lower your other risk factors. And critically, if your Lp(a) is elevated, your first-degree relatives — parents, siblings, children — should all be screened. That’s cascade screening.

[16:18] When Genes & Levels Disagree

Dr. Regina Druz (16:18): We do genetic testing on nearly all our patients, including a home-based option through our HeartWell Toolkit, because it’s surprisingly hard to get affordable genetic testing. Beyond genotyping, we add polygenic risk scoring, which captures smaller variants across all the lipid pathways. But I’ve noticed two patterns I’d love your take on: some patients have high Lp(a) yet no variant on genotyping or polygenic score, and others have a variant yet a normal Lp(a). How should we think about that?

Dr. Guy Mintz (18:42): We see that too. It can reflect differences in plasma concentration, variability in the isoform size, and polygenic effects. No single test wraps everything up with a bow, so you look at the whole patient — their overall risk, high-sensitivity C-reactive protein and other inflammation, and ApoB — to build the entire story rather than hanging everything on one genetic test that may seem incongruent.

Dr. Regina Druz (20:00): We see this discordance in maybe 10% of patients — anecdotally, often perimenopausal and menopausal women.

Dr. Guy Mintz (20:59): That fits — as estrogen declines after menopause, Lp(a) levels can rise, and women may run slightly lower than men overall. Which is why, again, you look at the whole person: family history, where they are in life, their total risk.

[21:30] Units & Risk Thresholds

Dr. Regina Druz (21:30): Tell us about the units and the risk levels — there are two units, which confuses everyone — and what’s the thinking on repeat measurement?

Dr. Guy Mintz (22:30): Patients go to different labs and doctors, and Lp(a) gets reported in different units. We prefer the concentration in nanomoles per liter, rather than mass in milligrams per deciliter, because the mass can shift with the isoform. The field is moving toward nanomoles per liter — but as we say, any measurement of Lp(a) is a good measurement; we’d rather you measure it however your lab can than not at all. By the National Lipid Association’s algorithm: under 75 nanomoles per liter is low risk, 75 to 125 is intermediate, and 125 or higher is high risk. I saw a young patient recently with an Lp(a) around 100 and no other risk factors — I explained it’s one risk-enhancing feature; it doesn’t mean game over.

Dr. Regina Druz (25:02): Hi everyone, it’s Dr. Regina here. Many of my colleagues and I are seeing patients arrive with self-ordered blood tests. When this trend started, I thought it would help — who doesn’t want more access to their health data? But too often self-ordered labs lead to more confusion and frustration: patients come in with a pile of results and are no better off. That’s why we created HeartWell Toolkits — a curated collection of at-home blood and genetic markers focused on heart and brain health that gives you the data you need to make informed, actionable decisions. You can order them at the shop on holisticheartcenters.com — the link is in the show notes. Use code TESTING10 for 10% off and free shipping.

[26:00] Should Lp(a) Be Standard? Guidelines & the Testing Gap

Dr. Regina Druz (26:00): What’s challenging is that guidelines recognize Lp(a) as a risk enhancer, but there’s no risk calculator that folds it into a 10-year-risk number — even though a recent UK Biobank study showed Lp(a) independently raised risk by close to 20% on top of all the ApoB particles. You’re involved with the National Lipid Association — is the field moving to include Lp(a) in standard lipid panels? Right now it isn’t happening.

Dr. Guy Mintz (27:18): The American Heart Association and American College of Cardiology treat it as a risk-enhancing feature. The European Atherosclerosis Society and the National Lipid Association go further: measure it at least once in every adult’s lifetime. Moving it into the standard panel faces two hurdles. First, education — clinicians need to understand the associated risk. Second, economics — if it’s bundled into every routine panel, payers may balk; many cover it only once per lifetime, and although the test should cost under fifty dollars, some labs charge several times that. So for now the practical path is what you and I do: add it on. But in my opinion every adult should have it at least once.

[29:09] Treating the Patient: Lower LDL First; Statin Caveats

Dr. Regina Druz (29:09): Cascade screening matters — I just saw a fit 29-year-old whose parent is a genetic carrier; the patient carries it too, plus other variants that compound the risk. So what’s your approach to a young, high-Lp(a) patient who otherwise scores low-risk — aspirin, a statin? How do you reconcile that discordance, where one powerful risk-enhancer catapults someone into a different category?

Dr. Guy Mintz (30:38): It starts with education — spending time so the patient understands where the risk comes from. We’re all in love with lowering bad cholesterol, but that’s only part of the job. If their Lp(a) is high, I put it in context with their other risk factors. For a young adult with no other risks, I emphasize healthy diet, exercise, and ideal weight. But for someone with high Lp(a) plus hypertension or diabetes, we respect it. Since in 2025 we don’t yet have an approved Lp(a)-specific drug, we lower their overall risk by attacking LDL as aggressively as the guidelines support — lifestyle first, then statin therapy. In high-risk patients with disease who need deeper LDL lowering, agents like PCSK9 inhibitors or inclisiran (a small interfering RNA) can also lower Lp(a) by about 20 to 30% as a side benefit — a two-in-one.

Dr. Regina Druz (33:32): This is where we sometimes diverge: statins can actually raise Lp(a) in up to about 20% of people, and I haven’t seen a universal lowering with PCSK9s either, especially in genetic carriers. So we go a step further and assess the vascular impact — sometimes a coronary calcium score, and a lot of carotid intima-media thickness to estimate vascular age and track it over time.

Dr. Guy Mintz (34:30): I love that, because you’re looking for early impact. By the time the big carotid arteries show plaque, you’ve somewhat missed the boat. As for statins raising Lp(a), I give patients a deliberately non-scientific analogy: if we lower the LDL, the Lp(a) has fewer dance partners to attach to — it may sit on the sidelines, so the measured level can rise even as the danger is reduced. Physiologically imperfect, but patients get it. And we need everyone rowing in the same direction.

[35:12] New Lp(a)-Specific Drugs on the Horizon

Dr. Guy Mintz (35:12): Tell us about the Lp(a)-specific drugs everyone’s waiting for — what are they, what’s been shown, and what’s the timeline? Very exciting: several drugs lower Lp(a) by over 90%. The closest is pelacarsen, an antisense oligonucleotide given roughly once a month that reduces Lp(a) by about 80 to 90%; its safety-and-efficacy trials are done, and we’re now waiting to see whether that translates into fewer heart attacks and strokes. Realistically it likely won’t reach us until late 2026 or, more probably, early 2027. Right behind it is olpasiran, a small interfering RNA that lowers Lp(a) by 90 to 95%, with outcome results expected around the end of 2026.

Dr. Guy Mintz (40:01): And there’s the one that made the newspapers, lepodisiran — another small interfering RNA — which lowered Lp(a) by over 94 to 95%, possibly dosed only every six months. Like anything in the supermarket, there’ll be different formulations and frequencies. The point for patients who’ll need therapy: we’re talking 2027, many trials have closed enrollment, but some sites may still have openings. These agents have been shown to be safe and very effective at lowering Lp(a) — a welcome addition to the toolbox.

[41:07] Lipoprotein Apheresis: How It Works & Who Qualifies

Dr. Guy Mintz (41:23): Until those arrive, there’s lipoprotein apheresis. What is it, how does it work, and what’s the patient experience? Simply, it’s filtering of the blood — not dialysis, and not much wear and tear. For comfort we place two small subcutaneous ports, draw the blood, filter out the positively charged apolipoproteins — lipoprotein(a), ApoB, LDL — then warm the blood and return it. Acutely we lower Lp(a) by about 70%. The session takes roughly two to two and a half hours; the patient sits with their phone or laptop and literally watches a bag fill with yellow material — their bad lipoproteins.

Dr. Guy Mintz (42:43): For most patients it’s every two weeks; for Lp(a) it may be every one to two weeks, because Lp(a) starts climbing again within a day of being filtered. I have great respect for this molecule — patients are referred to me with an LDL of 22 or 25 who are still closing their stents or getting peripheral arterial disease, and some have an Lp(a) of 180, 200, even 500. The 2025 indication for apheresis is clinical familial hypercholesterolemia plus coronary and peripheral arterial disease and an Lp(a) of 60 milligrams per deciliter or higher (about 130 nanomoles per liter) — they dropped the old requirement of an LDL over 100. Germany does the most lipoprotein apheresis in the world. Currently only two centers in New York State offer it — ours at Northwell and Cornell in the city.

[46:31] Why Lp(a) Is So Harmful + Residual Risk & Closing

Dr. Regina Druz (46:31): Apheresis is powerful because it’s not only lowering Lp(a) — it’s removing inflammatory factors that medications won’t touch, which connects to the lifestyle and cardiometabolic work we emphasize. Even with the new drugs, apheresis may remain an option to lower frequency and stabilize, or even reverse, aggressive multi-vessel disease.

Dr. Guy Mintz (48:12): Exactly — apheresis also removes C-reactive protein and fibrinogen and lowers blood viscosity, so many markers improve, not just cholesterol. And understanding why Lp(a) causes trouble explains it: it carries oxidized phospholipids on its surface that drive intense inflammation — that’s how it promotes aortic-valve stenosis. It also resembles plasminogen, the molecule that breaks up clots, so by blocking that pathway it becomes pro-thrombotic; and at the vessel wall it promotes smooth-muscle proliferation, more inflammation, and foam-cell formation. Lp(a) is not a nice molecule to have, especially in volume.

Dr. Guy Mintz (49:46): Small lipoprotein, big trouble. For resources, there’s the Family Heart Foundation — great for patients and clinicians, with information on lipoprotein(a) and familial hypercholesterolemia and a directory of apheresis centers across all 50 states. The National Lipid Association and American Heart Association also have updated statements. We’ve come a long way from 15 years ago. My ask: be an educated consumer — people research a car more than their own lipid profile. Just ask your doctor to add a lipoprotein(a). If they say there’s nothing to do about it, that’s worth reconsidering — because if someone might shoot you in the chest and stab you in the back, you want to neutralize both threats. It’s not just the LDL; it’s the entire picture.

Dr. Regina Druz (52:29): You’re being generous to LDL — you said up to 50% risk reduction, but across many trials LDL lowering is closer to 30%, so calling 70% ‘residual’ always struck me as odd math.

Dr. Guy Mintz (53:31): Fair — I say ‘up to 50%’ partly because it’s easier for patients to grasp what’s left. And residual risk isn’t only LDL and Lp(a); there’s inflammatory risk too. The JUPITER trial showed a 54% reduction in first heart attacks by targeting C-reactive protein with a statin, and other work shows reducing inflammation without changing LDL can cut events by about 15%. So you keep adding pieces toward zero risk — don’t be satisfied just because your LDL or your Lp(a) looks fine; the rest is still unwritten.

Dr. Regina Druz (54:34): A great point — patients get tunnel vision on LDL or ApoB and miss the composite of their vascular risk. I’ve seen people with perfect LDL, ApoB, and Lp(a) who still had heart attacks because inflammation, oxidative stress, and the vascular immune response were engaged. The good news is we now have tools — a personalized global risk assessment — to give each person a roadmap, whether that’s a drug, apheresis, or lifestyle. Any closing message, Guy?

Dr. Guy Mintz (56:41): Be an educated consumer about your health and a partner with your physician. You don’t need to haggle over cost — just ask to add the lipoprotein(a) and ApoB. Some research suggests that, pound for pound, Lp(a) may be several times more atherogenic than LDL, because it’s so inflammatory. Prevention is what we do — prevent the event. And there are tools to treat it, so it’s not hopeless. Just look at the entire package.

Dr. Regina Druz (58:46): Thank you, Guy — a tremendous resource and a delightful guest. Listeners, we mentioned several studies; our new monthly newsletter, the Holistic Heartbeat, gives plain-language audio summaries of important studies (with the full papers for professional subscribers). To ask Dr. Mintz or me a question, join our Holistic Heart University community and use the patient Q&A feature, or comment on YouTube.

Dr. Regina Druz (1:00:05): To the professionals listening: if you’re thinking of launching a cardiometabolic or integrative cardiology program in your practice, we can help. Holistic Heart Centers helps physicians expand into hybrid or concierge services — head to the show notes and click the application link; your intro call is entirely free. Ready to schedule a practice review? Use code DOC10 for 10% off our Practice Power Hour, a 60-minute coaching session. Thank you for tuning in to Own Your Heart Health with Dr. Regina Druz. This podcast is powered by Holistic Heart Centers. If you enjoyed the show, please rate and review us on your favorite platform, and visit holisticheartcenters.com and subscribe to our YouTube channel. See you next week.

Frequently Asked Questions

What is lipoprotein(a) and why does it matter?

Lipoprotein(a), or Lp(a), is an LDL-like, ApoB-containing particle with an extra ‘a’ protein attached — built from repeating ‘Kringle’ units. Dr. Mintz explains it’s strongly associated with early heart attack, stroke, aortic and valvular stenosis, peripheral arterial disease, aortic aneurysms, and faster atherosclerosis, largely because it’s highly inflammatory. It’s a major piece of ‘residual risk’ — the cardiovascular risk that remains even after cholesterol is well controlled, since the best cholesterol-lowering only cuts events by roughly a third to a half. Importantly, Lp(a) is about 90% genetically determined (LPA gene, chromosome 6), so it isn’t caused by diet or lack of exercise — though healthy habits still matter for your other risk factors. Roughly one in five people carry an elevated level. This is educational information, not individualized medical advice.

Should I get my lipoprotein(a) tested — and how often?

Both physicians say yes — at least once. The European Atherosclerosis Society and the National Lipid Association recommend measuring Lp(a) at least once in every adult’s lifetime, and the American Heart Association and American College of Cardiology treat it as a risk-enhancing factor. Because it’s about 90% genetic, a single measurement usually suffices for most people (levels can rise after menopause). It’s a simple, non-fasting blood test you can add to a standard lipid panel. A key caveat is units: results come in nanomoles per liter (preferred) or milligrams per deciliter, which causes confusion — by the NLA algorithm, under 75 nmol/L is low risk, 75–125 intermediate, and 125 or higher is high. And if yours is elevated, Dr. Mintz stresses cascade screening of first-degree relatives. Discuss testing and interpretation with your own clinician.

Can anything lower lipoprotein(a)?

As of 2025 there’s no approved Lp(a)-specific medication, and Dr. Mintz notes that diet and exercise don’t meaningfully lower it — it’s a ‘genetic tattoo.’ (In fact, statins can slightly raise the measured level in some people.) So the current strategy is to lower overall cardiovascular risk: optimize lifestyle, then lower LDL aggressively per guidelines; in higher-risk patients, PCSK9 inhibitors or inclisiran can reduce Lp(a) by about 20–30% as a side benefit. For severe cases, lipoprotein apheresis acutely lowers Lp(a) (and LDL and inflammatory markers). Importantly, several Lp(a)-specific drugs that lower it by 80–95% are in late-stage trials — pelacarsen (about monthly) and the siRNA agents olpasiran and lepodisiran — with pivotal outcome results expected around 2026–2027. These are investigational and not yet FDA-approved; decisions should be made with a qualified clinician.

What is lipoprotein apheresis?

Lipoprotein apheresis is a blood-filtering procedure — not dialysis — that Dr. Mintz describes as relatively gentle. Through two small ports, blood is drawn, the positively charged apolipoproteins (lipoprotein(a), ApoB, and LDL) are filtered out, and the blood is warmed and returned; patients can literally watch a bag fill with the removed lipoproteins. It acutely lowers Lp(a) by about 70% and is typically done every one to two weeks, since Lp(a) climbs again within about a day. A major bonus is that it also removes inflammatory factors like C-reactive protein and fibrinogen and lowers blood viscosity. The 2025 U.S. indication is clinical familial hypercholesterolemia with coronary and peripheral arterial disease and an Lp(a) of 60 mg/dL (about 130 nmol/L) or higher. It’s offered at a limited number of centers; the Family Heart Foundation maintains a directory. This is general education, not a treatment recommendation.

Show Notes & Resources

Guest: Dr. Guy Mintz, MD

Dr. Guy Mintz is a cardiologist and clinical lipidologist who serves as Director of Cardiovascular Health and Lipidology, and director of the lipoprotein apheresis program, at Northwell Health on Long Island, where he helped establish a regional center of excellence for advanced lipid disorders. Active with the National Lipid Association, he is a frequent educator on cardiovascular prevention, residual risk, and the diagnosis and management of lipoprotein(a) and familial hypercholesterolemia.

Family Heart Foundation — lipoprotein(a) & FH resources and an apheresis-center directory: familyheart.org

Resources Mentioned in This Episode

Family Heart Foundation — patient & clinician resource on lipoprotein(a) and familial hypercholesterolemia, with a directory of apheresis centers across the U.S. (familyheart.org)
National Lipid Association — statement and algorithm on Lp(a): <75 nmol/L low, 75–125 intermediate, ≥125 high; measure at least once in adulthood
American Heart Association / American College of Cardiology (risk-enhancing factor) and the European Atherosclerosis Society (measure once per lifetime)
Lipoprotein(a) testing — a simple, non-fasting add-on to a lipid panel (nmol/L preferred); cascade-screen first-degree relatives if elevated
Emerging Lp(a)-lowering drugs (investigational, not yet FDA-approved) — pelacarsen (antisense, ~monthly), olpasiran and lepodisiran (siRNA); pivotal outcome trials expected ~2026–2027
Lipoprotein apheresis — blood filtering that acutely lowers Lp(a) (~70%), LDL, and inflammatory markers (CRP, fibrinogen); offered at limited centers
Studies referenced — UK Biobank and the Copenhagen General Population Study (Lp(a) and events); JUPITER (rosuvastatin and C-reactive protein)
‘Cholesterol Marbles’ (Episode 19) — Dr. Druz’s visual primer on the lipidome and ApoB particles
Holistic Heartbeat newsletter — monthly plain-language audio summaries of key studies
Holistic Heart University — on-demand courses and resources (use code OWNER20 for 20% off annual)
HeartWell Toolkits — at-home heart and brain health lab + genetic panels (use code TESTING10 for 10% off and free shipping)
For clinicians: Practice Power Hour coaching with Holistic Heart Centers (use code DOC10 for 10% off)

Holistic Heart Centers

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HeartWell.ai — AI-powered cardiovascular risk assessment
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Phone: 877-511-5166
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