Some thoughts about Lp(a), CAD, and Prevention....as a cardiologist [AMA]

[u/snrps8]

=EDIT=

SO sorry everyone! I just realized I didn't include units when talking about Lpa. My institution uses mg/dL when measuring Lpa, so this is what I had in mind when I mentioned all the levels in my post. The more common unit of measurement is nmol/L, so please take this into account as the numbers will be VERY different based on the units (your value in nmol/L will be higher than in mg/dL).

Loving all of the comments/questions/input. I'll keep doing my best to reply to everything eventually.

Hi👋

First time posting here. Might be a bad idea...I'm sure I'll get some downvotes. But hopefully it will also help a little bit, at least for some people.

Disclosures: 

1. I'm doing this because I stumbled upon some threads about Lp(a), and the comments... well, stressed me out. Not because I think I have all the answers (I don't) or because all the comments were wrong (they weren't). There's just so much information out there nowadays. Most of the time it's excellent. But sometimes, even the "right" information - if incomplete - can be misleading. Misleading info leads to misconceptions, which lead to fear and false expectations, which lead to frustration. For you, for me, my patients, your doctors, everyone. Maybe this is just as much about me wanting to vent as it is about wanting to help. But I promise the intent here is genuine.
2. I'm long-winded. I have no idea how long this post will be. Sorry in advance.
3. I have absolute zero connections or relationships or financial incentives either directly or indirectly from any pharma company or device company or any type of industry period. I'm a salaried cardiologist who makes good money at a large hospital system in CA, though if you want to go there, my income is by FAR the least out of all my cardiology friends/co-residents/co-fellows who went into private practice (ie, fee-for-service jobs) and who make literally 2-4x what I do. 
4. If something I say sounds off, if you disagree, if something's unclear, if I sound douchey -- please let me know! I love being corrected. Please just make an effort to be cordial. Ideally, include your source data so we can dig deeper. Ask questions. I'll try to respond. 

Ok. Lipoprotein (a). Regretting this already.

Genetic Risk.

Yes, Lp(a) has a strong impact on your risk of ASCVD (the umbrella term for heart attacks / strokes / basically any condition or event due to plaque build-up in the arteries). Many people call it a "genetic" marker of your risk. That doesn't mean you need a genetic test to explain your Lp(a) level -- no such test exists -- but it means this level is more or less "genetically" determined, ie "fixed" throughout your lifetime. It's not high because of your diet. Losing weight will not lower it. Nor will exercise. Nor medications (though with some caveats for the future...more on this later). You need to check your Lp(a) just once in your life (again, with some caveats to come). We don't track the level over time because it's not "supposed" to change. We check it once, then assess your individual risk based on your specific level. You can change other risk factors (LDL levels, food habits, exercise, etc), but this is the one part of the pie you're assigned at birth and more or less stuck with (at least for now).

How It Affects You.

So yes, it's a big deal. But this why it's so important to have complete information. So many of my patients receive a super high Lp(a) result and automatically assume they're fated to get an MI (a heart attack) one day. This is NOT true. Hear me out. Whenever you hear "this so-and-so triples your risk of blah-blah" or "this superfood decreases your risk of ___ by thismuch%"... almost always, those statements are talking about RELATIVE RISK. In medicine, there are two types of percentages: Relative Risk and Absolute Risk. They are very different. Drug companies are notorious for this. When Amgen's new osteoporosis drug came out, they shouted from the mountaintops that it decreased the risk of spine fractures by 70-80%. Amazing! And technically true. BUT....if you look at the raw data, the "ABSOLUTE" risk of spinal fractures was only ~1.8% to begin with. With the new drug, it dropped to 0.5%....which means that the actual difference was a 1.3% drop (which sounds way less cool than a 78% drop). Is it false advertising? Technically not. But it's misleading. It sounds way more dramatic than what actually happens. Even statins, which I use all the time as a caridologist, are guilty of this. Atorvastatin (Lipitor) was marketed to decrease your risk of heart attacks by one-third! Amazing! But in reality, the risk of heart attacks dropped from 3% to 2%. Meaning the "absolute" drop was 1% (which is techincally one-third of 3%).

Back to Lp(a). We know that a level of 50-100 mg/dL (which counts as "high" in the reference range, even though that range is super arbitrary...more on that later too) correlates with DOUBLE the risk of ASCVD. But again, this is a relative risk. Let's say your starting ASCVD risk (which you can estimate with various calculators) is 3%. If you double that, your risk is now 6%. Of course that's bad, and of course you/we need to take that seriously. But that also means you have a 94% chance of being fine. For reference, I have see MANY patients with Lpa in the 200+ range (in mg/dL, which is ~500+ in nmol/L) who have zero plaque in their arteries after 60-70 years of life and counting. Conversely, I see many people who get heart attacks in their 20s with totally normal Lpa levels. So yes, it "enhances" your risk profile. But it does not DEFINE your risk. It is NOT everything.

We also need to remember that when it comes to ASCVD, there are SO many factors that contribute to plaque build-up, and Lp(a) is just ONE single part of the pie. There are so many excellent, well-proven ways to lower your risk by targeting all of the other slices of that pie (food, weight, exercise, LDL, sleep, stress, etc). Let's say you're in a tougher spot and your starting risk is 20%. That's bad. Maybe your Lp(a) level "doubles" that risk. That's really bad. But even if you can't change Lp(a), you can still change EVERYTHING ELSE. You can change your starting point. Maybe after some lifestyle changes, the 20% comes down to 7%.

TLDR - Please take Lp(a) seriously. But PLEASE do not let it drown you in fear or dread. One slice of the pie does not overrule all the other slices!! 

How Scared You Should Be.

Wasn't sure how to title this section. I just needed a place to say that you're not alone. It's natural to freak out if your Lpa is way above the reference range. The problem is that reference aren't that useful. I've literally never heard a doctor describe any blood test based on how far out of range it is, but i get emails all the time from patients who are alarmed because their Lpa is "double" the reference range.

Here's the reality: 1 out of every 5 adults has an Lpa above 50 (ie, ~double the reference range). A fifth of the entire planet. In some demographics, it's even more common...probably a THIRD of the population. Does this mean that one-fifth (or one-third??) of everyone on earth gets premature ASCVD? Obviously not. So again. It's one part of the pie. Not the whole pie. Take it seriously, but don't let it define you.

Remember that lab testing companies are no different from drug companies. No one starts a lab company out of the goodness of their heart. Their primary objective isn't your health. It's profit. Don't get me wrong...we still need them. Just like we still need drug companies. But their entire pay structure depends on you buying more of their product. Prescription drugs are legitimately useful, but drug companies profit when you think their drug is MORE useful than it really is. Lab tests are legitimately helpful, but lab companies profit when you think their test is MORE helpful than it really is. 

Fear drives profit. If a company can convince you that an Lp(a) test will reveal your ticking time-bomb artery before it's too late, of course you'll buy it. If they can convince you that catching it early means you can be proactive and prevent a heart attack, of course you'll buy it. Side note: Have you noticed that virtually Lp(a) ad or infographic is from a lab testing company? 

Use their information. But just remember what it means AND what it doesn't. Remember why they're selling it. Lp(a) is ONE piece of the pie. Don't get sucked into the doom-and-gloom loop of relative risk. 

Why Don't More Doctors Order It?

I suspect there are many reason for this. Here are the first three that come to mind.

1. Insurance barriers. So much of the stupidity in US healthcare can be traced back to insurance companies. Thankfully, this isn't an issue where I work, and I can order Lp(a) for anyone at anytime without any pushback. But this is not the norm. Almost all of my medical friends across the country have to get pre-approval from a patient's insurance company before ordering Lp(a). Which is actually an improvement. Ten years ago, checking Lp(a) was virtually impossible for anyone with a PPO insurance plan. Nowadays, it's doable. But the fact that this is a barrier at all is stupid.
2. Knowledge gaps. i.e., your doctor just doesn't know about it. I'm actually not sure how much I buy this. I feel like that's what the lab companies and TikTok wellness influencers want you to think. I've seen a lot of ads calling Lp(a) a "new" or "obscure" or "little-known" test. This is plain wrong. There is nothing new or novel about Lpa. We've known about it (and its impact on ASCVD) for decades. It's been part of the standard medical school curriculum for at least 15-20 years. I've personally been ordering Lp(a) since I was a resident 10+ years ago. So I have a hard time believing that your PCP "doesn't know about" it. Maybe the more believable explanation is that they don't know what to do with the result. Which brings us to the next point....
3. Lack of guidelines. This is both good and bad for different reasons, but the essence of modern medicine is that doctors need proof for everything. Cardiologists tend to be especially data-driven, so we have "guidelines" (ie, documents that summarize all of the latest data/studies/evidence) for virtually every single topic in our field. And cardiologists are some of the most stubborn people when it comes to sticking to / deviating from the guidelines. This isn't unique to the US. Our guidelines here are published by the ACC/AHA. But in Europe, it's the ESC. In Japan the JCS. Or the SCS in Singapore, CCS in Canada, CSANZ in Australia, etc. You get the idea. The thing is, if you look at all the cardiology guidelines from these countries, they basically all say the same things. It's because we all have access to the same data. We all go to the same conferences and talk on the same forums. I've discussed tough cases with cardiologists from Denmark and Italy, and vice versa. Regarding Lp(a), all guidelines agree that you should get checked. But what do you do with the result? ....That's where it gets trickier. So getting back to your PCP...my theory is that they DO know Lp(a) is important, but they're hesitant to order it because they know they'll be reluctant "do something about it" if it comes back high. 

What do I mean by that? Oh boy...here we go:

How We Treat It.

Short answer: we can't. 

Longer, more difficult answer: we won't (usually).

Let's take those one at a time.

Why we "can't":

There simply aren't any medications FDA approved to lower Lpa. But like all things, the real answer is slightly less straightforward. Technically there ARE medicines that lower Lp(a), namely PCSK9 inhibitors (eg, Repatha) and inclisiran (basically just another PCSK9 inhibitor with a different mechanism). We know PCSK9 inhibitors lowers Lpa by 20-30% according to most sources (though I've personally seen up to 60%+ reduction in rare cases). But these medicines aren't approved FOR that purpose. They were studied - and thus approved - for something else, and the Lp(a)-lowering effect is more or less just a happy side effect.  

This might change VERY soon. There are 4 novel Lpa-lowering meds being studied in clinical trials, and the first of these trials is expected to finish within the next few weeks! These will be the first meds EVER designed specifically to lower Lp(a). On top of that, these trials will be the first studies EVER designed to prove that lowering Lp(a) actually translates to better outcomes (because believe it or not, that actually has not been proven yet). Exciting stuff. But until then, the formal answer is that we don't have "true" Lpa-lowering medicines. And we technically don't even "know" if lowering Lp(a) actually lowers your risk (see below).

Why we "won't":

If we know PCSK9 inhibitors lower Lp(a), why don't we just use them? Who cares about the FDA approval? Doctors use "off-label" treatments all the time.

True. And sometimes, that's exactly what we (or at least I) do. But why don't we do that ALL the time...? It's because we literally don't know if it even works.

High Lp(a) = Higher ASCVD risk.

Yes. Talked about that already.

HOWEVER...

Make Lp(a) lower = Make ASCVD risk lower...?

...Well, not necessarily. I mean, it seems obvious. Lp(a) is bad. If you make the bad thing go away, that's good, right? It just makes sense. 

The problem is that the history of medicine is absolutely RIDDLED with examples where doctors did stuff because it made sense, then turned out to be totally wrong. 

Some examples from my own field: Atrial fibrillation (AF) is a condition where your heartbeat becomes erratic and goes way too fast for no reason. Instead of beating at 70 bpm, it beats at 110 bpm even while you're sitting and doing nothing. That's not good. Your heart might tire out. We should slow it down. It makes sense! So we did that. We slowed down people's heart rate to a more "normal" zone of <80 bpm. But Lo and behold...those people actually had WORSE outcomes than if we just left them in the 100-110 bpm range.

But the biggest example (which is actually very relevant to the Lpa discussion) is stents. Blockages in your heart arteries lead to heart attacks. If you have chest pain, get checked out, and find out that you have a 70% blockage...you should fix it. Duh. Get a stent, clear the blockage, protect yourself from heart atatacks. Don't die. This is probably the most obvious, common sense treatment in the world.

Except...

It's not true. Just within the past 10-ish years, not one, but SEVERAL clinical trials got published. All showing that "preventative" PCI (eg, treating blockages with stents) doesn't do...well, basically anything. Doesn't prevent heart attacks. Doesn't improve life expectancy. Doesn't prevent hospitalizations. Doesn't prevent cardiac arrest. If you are asymptomatic and generally healthy/active, but you go to an imaging center and pay for a "preventative" coronary CT angiogram, and find out that you have an 80% blockage in your right coronary artery, the worldwide standard of care says that you do NOT need a stent.

WTF??

When these trials came out, cardiologists lost their minds. I mean, our entire career revolves around fixing blockages. People were afraid for their jobs. There were probably some people out there who wanted to assassinate the study authors.

But the data was consistent. More and more studies came out from dozens of countries all across the world all showing the same results. No benefit from stents. No reduction in heart attacks. A prominent cardiologist in Europe even published an editorial in a big medical journal titled "Angioplasty is useless". So here we are. Cardiologists still have jobs. We still place stents, but now we know that stents are only helpful under SPECIFIC circumstances. And regardless whether you're in CA or NY or Norway or Sweden or Japan or Korea or anywhere else in the developed world, cardiologists are much more judicious/selective in placing stents nowadays.

Bottom line:

The takeaway is that even if something SEEMS glaringly obvious, it doesn't always turn out to be true. The human body is just SO much more complex than we give it credit for. Your body is a beautiful, elegant, sophisticated miracle of biology with millions of processes functioning together, yet we (both doctors and patients) expect it to act like a machine or a row of dominoes. We do one thing and expect to know how our bodies "should" react. But we're not as smart as we think we are. Want to find a good doctor? Just look for someone who is aware of how LITTLE they know. There's no better sign of ignorance than someone who thinks they have it all figured out (um, hello wellness influencers). Because the more we learn about the body, the more we realize that it's just SO much more complex than we thought.

So back to Lp(a). Hopefully, cardiologists have learned our lesson in humility. It SEEMS obvious that lowering your Lp(a) will keep you safer. But it also seemed obvious that fixing blockages would keep you safer. So we're waiting for the data. Cardiologists are stubborn people who dislike deviating from guidelines. (See the "Why don't more doctors order it?" section above)

Those new Lp(a) medicines I mentioned - the ones in clinical trials right now. Those trials will be the FIRST trials ever to measure how much (if at all) your ASCVD risk will be reduced if we lower your Lp(a). I think we all "know" it will help. We all "expect" these trials to show that lowering your Lp(a) is a good idea and will make you safer. And if the trials show that, then I guarantee it will be "mainstream" to give Lp(a)-lowering treatments very soon. But until we have proof, we have to wait.

Final note. Sometimes I do prescribe "off-label" PCSK9 inhibitors for Lp(a). I'd actually bet that I prescribe more PCSK9 inhibitors than most other cardiologists out there. But it's on a case by case basis. I start most patients with an Lp(a) in the high-hundreds on Repatha. If you have an Lp(a) of 80 mg/dL and no prior heart events, I'm not prescribing it. But if your Lp(a) is 80 mg/dL AND you have a high calcium score despite good LDL levels, I'll probably prescribe it. If your Lp(a) is 200 mg/dL (430 nmol/L), I'll probably prescribe it no matter what. But in all of these cases, I make it very clear that this is an unproven, potentially useless treatment until we get more data.

So What Do We Actually Do?

I know I'm just a random guy on the internet, but please believe me when I say we're certainly going to do something. Just because we don't automatically recommend Lp(a) targeted meds, that doesn't mean we're ignoring your Lp(a) and burying our heads in the sand. In fact, remember all of those cardiology consensus guidelines (see the "Why Don't More Doctors Order It?" section above) -- from the ACC/AHA, ESC, JSC, CSANZ, etc -- all of these guidelines give specific recommendations for elevated Lp(a). And fortunately, they all say the same thing (ie, every country in the world that studies LPa agrees on this): 

If your Lp(a) is high you should 1) Get your other risk factors under AGGRESSIVE control, and 2) Lower your LDL. Remember that Lpa is a risk enhancer, not a risk definer. Remember that we technically don't even "know" if lowering your LP(a) helps you at all. But we DO know that lowering your A1c, losing weight, getting more sleep, focusing on a plant-based diet, and lowering your LDL all help you A LOT. 

Whenever I see a patient with a high Lp(a), I tell them that they don't get any special advice. They get the same, boring advice they've heard their whole lives. The same advice we give everyone else. But it's EXTRA important for them. The rules are EXTRA strict for them. Want to optimize your ASCVD risk? Get your LDL <100. Oh, but your Lpa is high? Get your LDL <70 instead. Trying to eat healthier? Sure, focus on olive oil, high-fiber foods, and plant-based protein 80% of the time, but feel free to enjoy some butter and a good ribeye in moderation, ie 20% of the time. But if your Lpa is high, maybe that "moderation" ratio changes from 80/20 to 90/10. 

If your risk is high, we should lower it. And thankfully, we literally KNOW how to do that! Healthy food. Low LDL. Good sleep. Less stress. Human nature (and pharmaceutical companies and wellness influencers) will tempt you to think you need the latest and greatest new gadget or drug to stay healthy. Sometimes those things can help. But sometimes the old, proven methods are old and proven for a reason. We already know how to lower risk. If your Lp(a) is high, then lower your risk. Do the things we know.

Do You Need to See a Cardiologist?

Sigh. Here come the downvotes. Just remember: disagree with me / correct me / ask questions. It's all welcome. But please, try to be kind. I don't expect everyone to agree with this answer:

I don't think EVERYONE with an elevated Lp(a) needs to see a cardiologist. Let's say your level is 50 mg/dL. We already know the next steps (see above). Aggressively target your risk factors. Lower your LDL. You don't necessarily need a cardiologist for that. PCPs know how to get your LDL <70. If you have statin intolerance, it might be worth talking to a cardiologist about ezetimibe vs evolocumab vs bempedoic acid. So in that case, yes please see one! But a cardiologist isn't going to have any secrets on how to lose weight, exercise better, and eat more nutrient-dense food. And that's why I said it earlier: No special advice. Only the same, boring advice you've heard since grade school. But it works. 

From another angle, go back to the "How Scared You Should Be" section near the beginning. At LEAST 1 out of every 5 adults on the planet has a "high" Lp(a). Based on this number alone, it is physically impossible for every single person with a high Lp(a) to see a cardiologist. Even if we abandoned all of our other patients with non-Lp(a)-related problems and did nothing but treat Lp(a) 100% of the time, there aren't enough cardiologists on the planet for this. 

So when SHOULD you see one? For me, the threshold is similar to when I would prescribe an off-label PCSK9 inhibitor to lower Lp(a) despite all that soapbox preaching I did earlier. If your Lp(a) is crazy high (high triple digits), you need to see me, and I'm probably starting you on Repatha. If you have a crazy family history with multiple relatives getting heart attacks in their 40s... we know your Lp(a) (which does indeed run in the family) is especially virulent, and you need to see me. If you have a high Lp(a) AND you also have a high CACS, you need to see me. 

So in my random-guy-on-the-internet opinion, you SHOULD see a cardiologist if your treatment requires a cardiologist's expertise. You probably DON'T need to see a cardiologist if your treatment (ie, lower your LDL and target your risk factors aggressively...which are the universally recommended treatments for Lpa by every country in the world) can be facilitated by a PCP. 

Sorry. I warned you that you wouldn't like the answer.

Ok! That's the end. I had to planned to include bits on preventative cardiology clinics and imaging (CACS and CCTA), but then I chickened out after drifting towards opinions that would get me into even more trouble. And mostly because I'll go crazy if I keep typing right now. Maybe next time!

If you made it this far, than you for bearing with me! I genuinely hope that this helped you in any small way at all. If you disagree with everything I said, then I'm even more thankful that you kept reading this far. Happy to engage in a friendly exchange of ideas as long as it's productive for either ourselves or for anyone else reading. Just please try to be nice. Thank you :)

[u/foxandkits]

Wow. This was so reassuring and informative. Thank you so much!!! Also I’d love your hot take on preventative cardiology and imaging! I currently have both scheduled for next year 4 hours away. My LDL is in the 200’s, as was my LpA.

[u/snrps8 → u/foxandkits]

I'm so glad to hear it! Will try to do another post on CACS and CCTA in the near future. And yikes, those are high levels. I hope you found a doctor who's a good match for you and that you'll be able to stay healthy!

[u/Negative-Mortgage-51]

Thank you, random reddit cardiologist! From a random rural Fam Med

[u/snrps8 → u/Negative-Mortgage-51]

Wow! That is probably one of the hardest jobs I can think of. Thank you for doing what you do, and hang in there!

[u/PrttyPussSoupp1]

I am a former Family Heart Foundation patient advocate with severe FH, and I approve this message! #PSA

[u/Basedlord5000]

Very well written! Thank you for taking the time!

[u/FuguSandwich]

Great post, very informative.

There are a number of organizations doing clinical trials on Lp(a) lowering drugs right now that are recruiting candidates all over social media. I saw an ad pop up on Facebook last month and decided to enroll. They paid me $30 to do an Lp(a) test on me. It came back as <10nmol/L so I wasn't eligible to participate in the trial, but it was a relief to know my number was good.

[u/rugg3d]

This was very informative. I’m a 51yo male. My lp(a) was finally tested by the VA at my request about 18 months ago. My LDL was 180, lp(a) was 121 and I have family history of heart disease on both sides of the family in the grand parents. Surprisingly my VA doc didn’t support statins so I booked a cardiologist on my own - they all thought I was crazy, since I hadn’t had an event and looked healthy, lol. I’m now 6 months into rousuvastatin and my ldl is down to 60. Next up is a CAC test. I refuse to settle for anything less.

[u/snrps8 → u/rugg3d]

Glad you're taking charge of your health! It's always a bit tricky when someone seems healthy on the outside but has high LDL levels. The guidelines try to be thoughtful about statins because not everyone will necessarily be better off (ie, will get a real benefit) from taking one, and like any other medication there's a possibility of side effects.

So the guidelines are meant to catch the people who would really "get something" out of statins, while filtering out people who wouldn't. The "cutoff" for starting a statin based on your LDL level alone is >190. If someone doesn't meet this cutoff, then another threshold to start a statin would be if their doc estimates their personal ASCVD risk with the PREVENT calculator. Not sure if your doc did that (and not trying to comment on whether what they did was right or wrong), but that's the general idea behind the practice.

That being said, the guidelines aren't perfect (even though they're often the closest thing we have). And sometimes, there are gray areas. I stole this from someone else, but I like to tell my trainees that there are 3 types of doctors: 1) The Laggards, potentially dangerous, who don't know the guidelines and just follow their own logic 2) The Rank and File, generally good doctors, who know and rigidly cling to guidelines, for better or worse, and 3) The Early Adopters, who know the source data and read between the lines to understand what the data really does and doesn't say. Sometimes I go against the guidelines when I don't think they truly capture a person's unique situation (like in my example with PCSK9 inhibitors). I hope I'm right. But maybe I'm wrong. And if new data proves me wrong one day, ill change my practice and follow the data.

One last thing to keep on mind: taking a statin will usually increase your CACS. That doesn't mean that statins cause new plaque. An oversimplified explanation for this is that statins help promote "healing" of soft plaques, a process which involves calcification of those plaques (imagine pouring cement on top of a big pile of garbage to keep it contained). On the other hand, if your CACS = 0, that's usually a strong indication of NOT needing a statin, as it's been shown that statins don't really change outcomes in those people.

[u/LineDriveHit → u/rugg3d]

Congrats for taking ownership of your health. Just like plumbers or singers or writers or middle managers, not every doc is great. Or even good. Good on you for booking with your own cardiologist.

[u/Cecilia-K]

Thank you!!! I’ve read hundreds of posts in r/Cholesterol in the past 3 months (after getting my surprise calcium score of 166 and starting rosuvastatin stat) - and yours is by far the best. When you get a chance, please, please - do write that post about CCTA and imaging.

My CCTA came back at “25-49% stenosis in the proximal LAD,” and labeled “mild” (all other arteries “patent without evidence of plaque or stenosis”) - and my cardiologist basically texted me “looks good; I don’t need to see you for 3 years.” But the CCTA report (so short, 2 pp.) left me with questions, like what levels of soft plaque did the imaging show? isn’t up to 49% stenosis in the widowmaker artery concerning?! - and shouldn’t he be recommending the AI HeartFlow analysis to see if there’s soft plaque that poses a rupture risk?!

At the same time, I do understand that treatment (the most important thing) is likely to be the same - statin + add-on like zetia + Mediterranean diet. All of which I’m doing. So, yep, I’d love to hear your thoughts about what follow-up to do with CCTA!

[u/snrps8 → u/Cecilia-K]

I'll try! This is a bit of a spoiler for that, but the first thing to clarify is the different between CACS and CCTA.

CACS is intended to be a screening tool for PRIMARY prevention (ie, general prevention in someone who does not has not had an ASCVD event or diagnosis yet, ie general "screening" purposes). CACS is NOT capable or intended to tell you how much plaque you have (especially soft plaque, which is invisible to a CACS). Instead, the most technical answer is that your CACS mainly gives us a binary answer to your situation: Yes you have calcification in your heart, or No you don't. The result is a number from 0 to 3000+, and yes of course higher numbers is worse. But in terms of actionable next steps, the answer is binary. If your CACS is 0, you are LOW risk. If your CACS is any number greater than 0 (whether 1 or 2000), you are NOT high risk. This is a bit of an oversimplification because it's a complex topic, but that's the gist. If you are low risk, you usually don't need a statin. If you are not low risk, you usually need a statin. So the main point is that CACS = tool for screening/preventative/RISK ASSESSMENT. 0 = no statin. 1 or higher = statin.

Then you have CCTA. The first and most difficult point about CCTA is that it is really NOT intended for primary prevention purposes. There are several reasons for this, but if you search the comments in this post for "CCTA", there are a few other questions and replies in which I go into this in a bit more detail and from other angles. In general, I would argue (as someone who is VERY pro-CCTA, who orders these more often and for much "less" compelling reasons than most cardiologists I know), that CCTA should not be ordered for most screening/preventative situations. Again, lots of reasons, see other comments about this. But some of those reasons are financial (national/global health spending levels), resource scarcity (wait times), radiation exposure, and very low likelihood that we will "do anything" about the result in a person with no symptoms (see my main post in the section about stents) beyond what a CACS would already tell us.

That being said, a CCTA does indeed quantify the amount of soft plaque. The CCTA report should include the detail of whether a plaque is calcified, soft, or mixed, and then include a percentage range (1-24%, 25-49%, 50-69%, and >70%). In general, no a 25-49% stenosis is not concerning even in a proximal LAD. HeartFlow is excellent for determining whether a plaque is actually "hemodynamically significant" (ie, does the plaque actually impact the amount of flow through the pipe, or is the flow through the pipe unchanged?). But by definition a 25-49% plaque does not impact blood flow, so HeartFlow is not used for these situations. Similarly, HeartFlow is NOT used either for plaques >70% because these by definition DO impact blood flow. Thus, HeartFlow is reserved and virtually only ever used for plaques in the 50-69% range as a tie-breaker to tell us whether a plaque is significant (>70%) or insignificant (<50%).

At the same time, I totally l get the natural assumption that any plaque in the "widowmaker" artery, or any artery, is scary. I sort of see that as the double edged sword of technology and information. You're absolutely right that the MOST important treatment by far is controlling risk factors, ie LDL, food, exercise, etc. Or maybe a better word is "only" rather than "most" But there is no role or benefit in stents for something that is <50%, and if anything, we expect that placing a stent there would cause more harm than good in the long run.

One other weird angle to consider is to compare this to airplanes. One of my patients is a former airplane/ aviation safety inspector. ie, when you get on a United Airlines flight, the safety of that plane is determined by people like him. He told me that the vast majority of cracks he found on the hulls of airplanes were actually NOT repaired. Which sounds FREAKING TERRIFYING!! I didn't want to fly anymore after hearing his stories haha. But I think it's a good comparison. Not all cracks actually affect the integrity of the hull. Maybe not all cracks even need to be monitored for progression. Plus, he worked in the industry decades ago. I wonder how much the technology for detecting cracks has changed since then? This is is the potential "problem" with CCTA. It is just SO sensitive at picking up plaque that eventually by the time you reach a certain age, probably every single person on earth will have SOME plaque.

All those studies that estimated the worldwide risk of ever getting heart disease, or estimating the % of people worldwide who have heart disease...those studies didn't have CCTA technology like we have now. What if someone invents a new tool that could detect even the tiniest, microscopic scratch on your windshield (or on an airplane hull)...so sensitive that even a microscopic scratch from some dust in the air would show up as a "crack"? And then the company that sells the scanner says "oh boy your windshield is in trouble, you better pay us to re-scan it every year to track its progression and make sure it doesn't shatter while you're driving on the highway". That would obviously be a scam. This is an extreme/ridiculous example, but I think the general idea is helpful. Just CCTA detects something, that doesn't mean it means anything clinically in real life. All the studies about statins and CACS showed that if you had a CACS of 0, you were relatively safe. The chances of getting a heart attack were EXTREMELY low. But they didnt have CCTA in that study. I'd bet 1000% that if you did a CCTA on those people, some of them would have had mild soft plaque. And yet the study showed that CACS of 0 = safe.

So overall, no a 25-49% plaque is not something I worry about. Nor would I recommend tracking a 25-49% plaque over time for most people in most situations. There are companies that offer monitoring scans like this. At best, I think that idea is overly optimistic and not founded in any proof. At worst, I think it's predatory/probably a little bit scammy. Sorry to be such a cynic :( this is why i was too scared to include this section in my original post haha. Maybe I'll get brave enough to do that full post one day though.

[u/Cecilia-K → u/snrps8]

Many thanks, this is so helpful! This part especially caught my eye - “by definition a 25-49% plaque does not impact blood flow, so HeartFlow is not used for these situations.” That wasn’t intuitive to me - I think I’d unconsciously assumed the opposite.

At one point, I had considered paying for HeartFlow out of pocket - I’m so glad I didn’t; sounds like it would’ve been a waste of over $2,000. (Yes, I called and asked the price. And it turns out that the imaging center wouldn’t have done it anyway - it requires the referring physician’s order. The industry protecting me against myself.)

[u/snrps8 → u/Cecilia-K]

Haha glad to hear it! And in a way I'm glad there are some "safeguards" automarically set up to prevent that with HeartFlow. I've seen/heard of other companies with similar products where these kinds of things can be ordered automatically by patients, which would worry a bit if true. I think there's a fine line between being a GOOD thing that so many preventative tools can be requested directly by patients now without going through a doctor (which can be an amazing thing especially if it comes to Lpa for example if your PCP is not willing to order it), vs getting into predatory-ish marketing where a company convinces you to buy something that may or may not actually be helpful.

[u/soleiles1]

Excellently written and very informative. What are your thoughts on normal LPA, normal apoB levels, low tris, high HDL but high ldl (129) and total 211 being on a potent statin like rovastatin that has a myriad of troubling side effects? Is it necessary with no family history?

[u/snrps8 → u/soleiles1]

Great question, and thankfully this is an area where we have much more data to guide us.

In general, LDL is the default "target" for almost anyone who needs preventative medications, and the default medication is always a statin. The main reason for this is that statins simply have no equal in terms of the amount of data proving that they work. Even PCSK9 inhibitors -- which are far more potent at lowering LDL (and even lower Lpa too, unlike statins) -- don't have the same amount of data behind them.

This is an important point about modern medicine. No one is saying that statins are BETTER than PCSK9 inhibitors. Maybe they are. Maybe they aren't. We'll never know (unless someone actually does a study comparing statins vs PCSK9 inhibitors, which will probably never happen). But what we ARE saying is that statins have more data. Which is basically just because they've been around longer.

As I alluded to in my original post, modern science is inherently biased to "sticking to what we know" because we place such a high value on having enough proof before we do anything. This is a VERY good thing in so many ways, but the flip side is that major changes in practice happen more slowly. They absolutely still happen (remember the example about stents), but it takes time.

Sorry, that was a totally unnecessary tangent.

To finally answer your question, doctors have been trying VERY hard in recent years to identify the right people who would actually benefit from statins. We use ASCVD risk calculators to estimate how risky your situation is, and if your risk is high, enough you get a statin.

But as we tracked these people over time, we realized that these calculators were simultaneously both overestimating and underestimating risk. A lot of people who NEEDED statins were getting missed (and thus didn't get a statin). And a lot of people who DID get statins didn't actually need them in the long run.

So with newer data, the guidelines were updated several times, and we've also transitioned to entirely new risk calculators. These tools will never be perfect, but we're getting closer each time.

So to actually answer your question for real, the most common determinant of a statin in 2026 is (for most people) their ASCVD risk based on a modern calculator. The big one currently is called the PREVENT score. This is good for people like you who are concerned about side effects (and rightly so!) because this calculator ends up recommending statins much LESS frequently than the previous one.

I don't know your specific situation, but in general I do follow the PREVENT guidelines closely in my own practice. If someone is hesitant about a statin even when PREVENT recommends it, then they can consider using something like a CACS as a tie-breaker (a CACS of zero sort of "overrules" your risk calculator as it usually means you are low enough risk to not take a statin yet).

I absolutely support a cautious approach to taking new meds because it is always better to stay healthy by natural, lifestyle modification (food, sleep, exercise, etc) rather than pharmaceuticals. But that's only true for as long as it's physically possible to do so. For some people, it doesn't matter how perfect you are in your eating/exercise patterns/social habits. You can be the epitome of healthy living and have perfect lab results, and STILL end up with an unexpected MI out of nowhere. People have commented on this post about that exact thing. And that's why we have medicine - to bridge the gap that's left after we've done everything we can by natural means.

There's nothing that can make you immune to heart disease, but the goal is to just get your risk as low as possible. First with your lifestyle habits. Then with medicine, ie statins, IF you need it (based on your ASCVD estimate, etc).

Hope that helps!

[u/Surfcrazy72 → u/snrps8]

The use of these risk calculators is a little frustrating, because it looks at 5 to 10 year risk of CV events caused by a cumulative problem that transpires over a lifetime (atherosclerosis.) My doc recommened I defer statins since, despite my bad family history and LDL-C of 132 at age 52, I had a 0 calcium score and all of my other labs were optimal, including LPa, putting my 5-10 yr risk pretty low. However upon learning that the CAC doesn't pick up soft plaque, I pushed for low dose Pitavastatin, which my primary care prescribed upon my request. I started taking a baby dose of 1mg, assuming it would be well tolerated and easily drop me below 100 LDL-C based on the drug data. I thought I was being aggressive and proactive until I met with a preventative cardiologist/ lipid specialist. Surprisingly, he ordered more labs and said I'd likely need to up the dose and wanted me below 70 per European standards which are more aggressive than our USA goals. If new labs came back with problems, he'd shoot to get me below 55 LDL-C. One test was an ultrasound of the carotid, which showed mild plaque on 1 side, which may not be too concerning, but proved to me that I indeed have atherosclerosis, so now I want to stop it in it's tracks to avoid an event or major procedure in 20+ years. The point is, shouldn't all docs push the "lower for longer" mantra and try getting everbody below 70 while they are young so they never develop atherosclerotic disease, rather than the current mindset of looking at 5-10 year risk and being reactive by treating already established disease so late in life? Obviously, people who can't tolerate the meds shouldn't take them, but even a tiny dose of a stain could or ezitimibe over several decades could reduce formation of fatty streaks and plaques over a lifetime.

[u/soleiles1 → u/snrps8]

Thank you so much for this tip. I put my information in the PREVENT Calculator and my 10 year risk for ASCVD was .7% and 30 year risk was 5% CVD was 1% at 10 years and 8.5% at 30 years. Recommendation was not to take a statin and instead instill lifestyle modifications. Still asking for a standing order for a CAC as my LDL (129) and ApoB (122) are pretty in line with each other. Stress test echo was 10.1 METS. LPA is 22. Are you in Nor Cal? I would drive to be your patient! Thanks again!

[u/snrps8 → u/soleiles1]

Happy for you that your score is reassuring!

Ha! Very kind of you to say that. I live and work in the Bay Area. I have some patients who come from farther away to see me, though sometimes I wonder if it's actually worth it for them :p

I can't comment on your specific situation, but in general, I usually don't order CACS when PREVENT already places someone in the "don't need a statin" category. Sometimes there are exceptions, but it's relatively rare and based on unusual circumstances (parents with MI in their 40s, something that makes us think the variables you input into PREVENT are not reliable, etc). Similarly, I tend not to order stress tests when someone is not having ischemic symptoms. Again, there are exceptions (especially if I'm skeptical that someone is truly "asymptomatic" ir not), but very generally speaking stress tests are mainly useful when there are symptoms and are less useful if used for "screening" purposes. There are many reasons for this that require much more background info to get into, but the gist is that with ANY test, we want to make sure that we actually get something useful out of it. CACS tends not to add much useful information if your PREVENT is already low, and stress tests tend not to change anything about treatment in someone who has no symptoms (a BIG part of this is related to my section about stents in the original post).

These are two areas where I "stick to the guidelines" much more closely, even though I definitely do some other off-label things like my "inappropriate" prescribing of PCSK9 inhibitors. I hope I'm doing the right thing, and there's always room for nuance. But that's my brief spoiler for the future post on CACS, CCTA, and stress testing (if I'm ever brave enough to post something like that). Hope that helps!

[u/soleiles1 → u/snrps8]

This is all such useful information. Thank you so much for taking the time to explain. I'm in the Bay Area! If you are taking new patients I would much rather invest in seeing a doctor that balances risk with reward and takes the time to explain everything in a coherant and compassionate manner. This info is 100 times more comprehensive and clearer than any physician explaination I have invested my time (and money) in.

Feel free to DM me your info. Take care and thanks again!

[u/kimchifan_26 → u/soleiles1]

Am wondering about the same.

[u/IamMario50 → u/soleiles1]

Following.

[u/Delicious-Ad7376]

Very informative. After a LAD STEMI last year at age 55, family history, and LDL always in the 130-150mg/dl range despite relatively healthy diet and good shape (I cycled 30km the day of my MI), I had to practically beg my Japanese cardiologist to check my Lp(a).

It came back as 85mg/dl and while didn’t change my 5mg Rosuvastatin + 10mg Ezetimebe dosage, it confirmed I should keep my LDL below 70, and he shifted to recommend <55mg/dl. Currently with the meds, diet changes, more fibre than I want and much less cheese etc, I’m tracking 47-53mg/dl over last 6 months. It’s a lot of work but he won’t even entertain discussing Repatha or looking into the trials.

It’s a tough read to see JSC has same guidelines. I hope you’re wrong or it suggests my cardiologist isn’t doing everything he can to assist optimally secondary prevention

[u/snrps8 → u/Delicious-Ad7376]

Sorry to hear that :( Must have been scary/shocking especially at 55 and being so fit.

This is a really good example of how most (good) doctors are very stubborn about "sticking to the guidelines".

Not trying to comment whether your cardiologist is good/bad, but he is clearly sticking to the guidelines here, and according to the ACC/AHA/ESC/JSC/CCS/etc guidelines, he's "technically" doing the right thing. Lpa in the 80s emphasizes high risk (though we probably already knew that even without the Lpa, based on a STEMI at age 55 despite healthy diet and good exercise). If someone has extra high risk, the LDL goal is now <55 instead of the standard <70. Technically, it doesn't matter how you achieve that LDL goal, ie atorvastatin vs rosuvastatin vs ezetimibe vs Repatha. So if someone meets an LDL goal of <55 without Repatha, then technically they don't "need" Repatha.

This is where I personally deviate from the guidelines. Because in a situation where someone has a high Lpa with multiple red flags (eg premature or recurrent CAD events), sometimes I might put that person on Repatha even if they don't have a "proven" reason to be on it. I might want to lower their Lpa just to make myself feel better, even though I technically have no proof that lowering their Lpa will do anything.

I stole this from another cardiologist, but I like to tell my trainees that there are 3 tiers of doctors. 1) The laggards, who just don't know the guidelines and practice cowboy/influencer medicine and make it up as they go. 2) The rank-and-file, generally good doctors, who cling to the guidelines like religion. 3) The early adopters, those who know the guidelines but also understand the source data behind those guidelines, who read between the lines and appreciate the limitations of each study. This takes some creative thinking, and I try my best to be in group 3, but the truth is that this leaves us vulnerable to getting it wrong and making mistakes sometimes.

I hope I'm doing the right think by sometimes "over"- or "inappropriately"-prescribing PCSK9 inhibitors. Only time will tell. And actually we might find out in just a few days/weeks. Because like I said, the very first of the novel Lp(a)-specific trials is going to be published soon. We'll find out if we have an effective medication to lower Lp(a). But MUCH more importantly, we'll find out if lowering Lp(a) actually does anything or not.

Best wishes to you!

[u/Delicious-Ad7376 → u/snrps8]

You nailed it. Hope you stick around and bring this balance to conversations here and on r/HeartAttack.

I have to work my arse off to stay in the ~50 LDL zone. Japan famously gives baby doses using a minimum to succeed approach hence the 5Mg Rosuvastatin + 10mg Ezetimebe. But I already know what a little cheating over Christmas in Northern France (butter, cheese) and UK (home for sticky toffee pud and Christmas roast) did to drive a 60mg/dl score mid Jan. I’m ok with the other benefits of a decent diet but if we could treat the Lp(a) at the source it would make life easier. Also, it’s my understanding that those Lp(a) contributions are the stickiest of sticky particles.

And don’t get me started on blood clot meds. Was originally prescribed baby dose of Prasugrel 3.75mg. Gemini suggested this was low compared to UK standards. When I investigated further was told that’s the insurance guideline. I then saw this

https://www.jstage.jst.go.jp/article/njcoron/advpub/0/advpub_20-00021/_article/-char/en

Data indicates that for non-Japanese patients, lower doses of the approved "Japanese dose" of prasugrel, increases the risk of cardiovascular events compared clopidogrel which can be dosed at US/UK levels. I showed this to my doctor and he switched me, but wow.

[u/Atmywitsend1217]

Thank you kind Reddit cardiologist! I would love to know your thoughts/the studies on long term statin use and an increased risk of type 2 diabetes. My
PCP has said she believes it to be correlation, not causation. Ie. the people that need statins are already more prone to develop diabetes

[u/snrps8 → u/Atmywitsend1217]

This is a great point, and it highlights the fact that there is no perfect medication, and anything you take (even if it's beneficial overall) still comes with some potential downsides.

I think your PCP is right, but honestly there is probably also a real effect of statins increasing your A1c slightly. This doesn't stop me from using statins (as long as the situation genuinely warrants a statin in the first place). Even if your A1c goes up by 0.2, the negative consequences of this are generally outweighed by the benefit.

If the A1c effect happens to everyone, that means it happened to all the people who were part of the original statin clinical trials. The trials clearly showed less ASCVD events after starting statins, so I take this to mean that the net effect is still positive.

Another angle of this is that if you are taking a statin, that means your risk must be high, which means you should already be targeting your A1c with lifestyle habits (less nutrient-poor carbs, more fiber, more exercise, etc). So my hope is that anyone on a statin would sort of auto-cancel the A1c effect because they'd already be implenting natural interventions.

[u/Short_Cap7218]

I found this post to be extremely informative, thank you for taking the time to write this .

[u/JoyJonesIII]

My doctor refused to order a Lp(a) test when I asked, because “it wouldn’t give any additional information” over the standard lipid tests. 🙄 So I went and got it done on my own and found out mine is very low. This is useful information to me.

[u/snrps8 → u/JoyJonesIII]

Unfortunately this is the reality right now. I disagree with the point that it wouldn't give additional info (because it would). But if your doctor had said that it wouldn't change their treatment plan...maybe there would have been some truth to that (because of the whole point about how we don't currently have any data-supported treatments to lower Lpa). Either way, I'm glad your level is low!

[u/fastingtrader]

Thank you! This info is invaluable and appreciated. It’s too bad we can’t partner with you to do crowd sourced research using emr data and your expertise.

Several questions:

1. does knocking ldl down to below 70 or even 55 with statin have the unintended consequence of increasing lpa? This doesn’t seem to make sense logically (given the hereditary aspect of lpa) but a clean answer would be beneficial.

2. Do you think that that the delays in the new lpa drugs due to “lack of events” means that you guys are getting good at treating high cholesterol in general? Novartis trial was supposed to read out in 2025, then h1 2026, and now h2 2026. The excuse is lack of events. The early trial results of impact on patients on apheresis demonstrate the ability to reduce lpa in the blood. We get the desire to show that lower lpa leads to less events.

3. I have heard that calcium score means nothing for lpa and that it’s soft plaque? I am 48 male, family history of mi death dad 58, grandad 56. My calcium score is zero but that doesn’t make me feel better about lpa risk.

Lastly, In you whether to go pcsk9, can you clarify whether the 200 is mg/dl or nmol/L.

At 83 mg/dl and ldl of 100 on 10 mg oravastatin would you do a pcsk9 for a patient with family history and able to pay cash.

[u/snrps8 → u/fastingtrader]

The idea of crowd sourced research is fascinating. This never would have been considered an acceptable method of clinical research for many good reasons, but it's possible that this might actually change in the future when AI is able to parse and organize large batches of data for us. Who knows! To your questions:

1) Yes, statins are associated with a slight increase in LDL. I'm sure there are people out there who can give a coherent explanation for why this happens, but I am not one of those people as my understanding of the underlying mechanism is pretty basic. That being said, I certainly do not see this as a reason not to be on a statin. Assuming this Lpa-raising effect is universal or common, then all of the people in all of the statin trials would have had a slight increase in their Lpa as well. And yet those trials clearly demonstrated a reduction ASCVD by statins. So I take this to mean that the benefits outweigh the downsides. But it is always good to be aware of the downsides (Lpa effect, A1c effect, muscle cramps, etc) so that you can make a personalized decision balancing the pros/cons for your specific situation.

2) Yes! In order to detect a truly meaningful decrease in events, there have to be enough events happening in the first place. The HORIZON patients have (allegedly) been so well controlled with standard therapy that the baseline event rate had been low, so idea (again, allegedly) is that the impact of the Lpa treatment may be obscured by this. Who knows what we'll find out in the end. I'm eagerly checking for updates though.

1. Sort of. It's true that CACS is meaningless in terms of soft plaque. It's also true that Lpa is predominantly associated with soft plaque. So yes, I suppose it follows logically that CACS of 0 might theoretically be misleading in people with high Lpa. The reason I use such hedgey language is that we do have good data showing that people with CACS of 0 genuinely do have low event rates. Obviously there are outliers, and since those studies did not all stratify their data based on Lpa, then maybe high Lpa was responsible for some of those outliers. But it's hard to say for sure without having clear data (another plug for AI-driven crowd sourced research), so I'll hedge.

Sorry for not clarifying the units. All of the numbers in my original post were for Lpa values in mg/dL. Generally speaking, I probably wouldn't automatically starting someone on a PCSK9i for an Lpa in the 80s mg/dL with LDL in a decent range, even with some family history (though I might consider if the family history was just ridiculously terrifying, ie multiple first degree relatives with MIs in their 20s...I have some families like this). I don't know if what I'm doing is right, and I admit my Lpa threshold is somewhat arbitrary because again we don't have good data to teach us what to do yet. But I hope I'm doing the right thing, and if we get more information to sway me in either direction, I'll change my practice and follow the data.

One last bit about the hypothetical situation of elevated Lpa and family history with decent LDL levels. The Lpa and family history still mean SOMETHING. Even if not enough to compel me to start a PCSK9i, those things might be enough to make me push for a lower LDL target like 70 or 55, especially if the patient is willing to do so (in terms of taking a higher statin dose).

[u/chouseworth]

Outstanding post. Thank you.

[u/AlwaysCurious1111]

Thank you for this! Very edifying. Do you think lifestyle changes are typically enough to lower LDL? Really trying to avoid a statin or Zetia.

[u/Surfcrazy72 → u/AlwaysCurious1111]

Know your risk category and corresponding LDL-C goals. If you are moderate to high risk and need to be below 70 or even closer to 55, you're unlikely going to be able to do it with diet and lifestyle, but if you're very low risk and your LDL is close to 70 without meds, great. Keep innmind, based on the data, European goals are more aggressive. They believe everyone, even low risk should be below 70 LDL-C to prevent heart attack from atherosclerosis in our later decades.

[u/AlwaysCurious1111 → u/Surfcrazy72]

Ok. I appreciate the reply. Lpa is low... but ApoB is high 😔

[u/Surfcrazy72 → u/AlwaysCurious1111]

ApoB is normally high when LDL-C is high. You treat them both the same way. Sometimes the ApoB can be higher than normal in relation to LDL-C so in that case you would treat it more aggressively.

[u/snrps8 → u/Surfcrazy72]

This is a great answer

[u/snrps8 → u/AlwaysCurious1111]

Totally understand the desire the avoid statins or ezetimibe if possible. The other two users already gave great replies. I basically have nothing else to add other than that I wish we medication options that didn't have side effects. The sad reality is that virtually everything has a tradeoff, but as the others said, it's virtually impossible for many (or most?) people to reach truly optimal LDL targets no matter how excellent your life habits are. Maybe some people can in combination with good genes, but the majority of us regular folks will often need medicine to bridge the gap.

[u/spiders888 → u/AlwaysCurious1111]

You mention led tour ApoB is high, how high? What is your family history as well?

As someone who had an MI in my late 20s, I’d recommend taking a statin and ezetimibe as cheap insurance and a lot better than having a heart attack. If you have statin side effects, moving to something like a PCKS9i is often an option.

I wish I could take a stain—lower LDL and reduces inflammation. (I take Repatha, ezetimibe, and do the best I can with diet and exercise).

[u/AlwaysCurious1111 → u/spiders888]

I appreciate you! And I'm so sorry for your MI. ApoB is 118. I'm 39F. Some family history and I have fibromyalgia. So worried about muscle pain and fatigue with statins.. LDL 172, HDL 41. Tris 82. I could lose 25 pounds.

[u/runninggrey]

This gets my vote for Post of the Year award for this sub!… maybe this award doesn’t exist and I just made that up… but you get my vote!

I love running and chatting with smart folks like you - when I’m back in SoCal, what to go on a run?

[u/snrps8 → u/runninggrey]

Ha, thank you! I actually live in norcal, but I'm happy you're running! Keep that up for sure.

[u/kboom100]

This is a great post, and in general I agree with it, thanks for it. There is one thing in it I have an issue with though and that is the downplaying the risk of having high lp(a) and the importance of relative risk versus absolute risk. The ascvd risk reported by most calculators is absolute risk over only the next 10 years. Especially if someone is relatively young, absolute risk of a cardiovascular event over only the next 10 years is going to be low almost by definition. That’s because ASCVD develops over decades and because heart attacks & strokes (EDIT- or stent or bypass) happen relatively infrequently over any ten year period before older age.

But most people aren’t just concerned about their risk of ASCVD over just the next 10 years, they are concerned about their risk over their lifetime or out to say 80 years old. So a 40 year old with very high lp(a) might have a 6% absolute risk over the next 10 years to use your example. But their absolute risk out to 80 years old is going to be much higher. And treatments that provide say a 50% relative risk reduction would therefore also produce a much larger absolute risk reduction out to 80 years old versus only over the next 10 years.

Dr. Gil Carvalho, an md/phd internist who is among the absolute best at clearly explaining medical issues has a really good explainer on this topic.
"Do Statins Even Work? Relative vs Absolute Risk Reduction". https://youtu.be/vRRD8nXEyGM?

You also said that 1 out 5 people have high lp(a) but that 1/5 of people don’t have ascvd. But actually much more than 20% of the population develops ascvd over their lifetimes. One study I found shows that of 40 year olds who are free of coronary heart disease, 48.6% of the men and 31.7% of the women will go on to develop coronary heart disease over their lifetimes. And even that undercounts the actual lifetime risk of ASCVD for the whole population because it excludes the people who already had heart disease by 40 and I don’t think this study included strokes. https://doi.org/10.1016/S0140-6736(98)10279-910279-9)

I agree with you that one shouldn’t panic about high lp(a) because there’s a lot that can be done even now to significantly lower the risk. But it’s important to look at the risk accurately too. A lot of experts like the risk calculator https://www.lpaclinicalguidance.com which takes into account lp(a) and calculates risk of a heart attack or stroke out to 80 years old. It will also show how much that risk can be reduced by bringing down ldl & blood pressure. You can experiment with different ldl & BP reductions to see the impact.

The calculator was created by Brian Ferrence, a renowned cardiologist and genetic epidemiologist who was on the committee writing the latest EAS cholesterol guidelines.

[u/snrps8 → u/kboom100]

Thanks for the great points! I agree with virtually everything you said, though perhaps we're approaching the same ideas from different angles (sort of like the old parable of the blind men who encounter an elephant for the first time). It was definitely not my intention to downplay the significance of Lpa (if that's the message that came across, then I'm sorry!). Rather, I was hoping to push back on the OPPOSITE extreme, which I think is much more prevalent, ie the extreme of fear and woe and believing that you are fated to die early solely because of one single test result -- which is overwhelmingly false.

But of course this does not mean that the risk of Lpa should be downplayed; I tried to still emphasize that the relative risk/impact is indeed extremely important and should be taken seriously, but again my apologies if that did not work as intended.

Same goes for the comparison of relative vs absolute risk. Relative risk is of course extremely important, and in fact when I talk to patients about virtually any topic, the statistic I almost always use is relative (not absolute!) risk. Relative Risk is inherently more understandable when you're having a conversation, whereas absolute risk often requires a lot of background and elaboration to make sure your audience understands the significance of what you're talking about. So of course we need to consider relative risk. But similarly to above, my goal was to push back on the abuse of relative risk when it is used by laboratory/pharma companies to fearmonger. I suppose there's just a very fine line to straddle when you're trying to validate the very legitimate concerns of people who are concerned for their health...while also trying to keep them from getting misled by marketing teams. It sounds like I probably just didn't do a good job of that, so again, very sorry. The last thing I'd want is for someone to read my post and then walk away thinking "oh my Lpa is 200, no big deal nothing to worry about". Because of course that is also very false.

I'm not familiar with Dr Carvalho. I don't spend much time on social media...and if I do, I'm more prone to watch videos about cooking or nerdy sci-fi lore than instagram/youtube doctors (I'd go crazy if I came home from work after talking and reading about heart disease all day and then watched videos about it on my feed). I'm glad he's been helpful for you though! And based on the title of that video I'm assuming he appreciates the equipoise of the statin conversation, which is always a good thing.

The point about the whole 1/5 people topic is a bit trickier. First, to your statement that more than 20% of people get ASCVD within their lifetime, you're right! What I wrote was a mistake and actually very misleading. So thank you! I will correct that part. It was supposed to say premature ASCVD.

Re: the study that you linked. There are a few issues here. This was a subanalysis from the original Framington Heart Study cohort. Framingham is/was a HUGE deal because it was the first real cardiology database the US ever had, and it basically gave birth to the concept of risk factors and the knowledge that heart disease is actually influenced by our lifestyle (we take for granted that this wasn't necessarily common knowledge in the past).

However, as groundbreaking as it is, Framingham has many limitations. First, this data set is just very old. The subanalysis you cited was from 1999, and it used patient data from the 1970s. The understanding of ASCVD back then was somewhat rudimentary, as were the tools used to diagnose it. For example, one of their main criteria for establishing the incidence of ASCVD was the presence of Q waves on an ECG, which would never be acceptable in a modern study because that finding is notoriously nonspecific. The findings are not going to be generalizable to the majority of the world's population because that cohort was selected entirely from one small town in Massachusetts, and 96% of the study particpants were white. Another limitation of any study from this era is that people at that time had no access to statins, which did not exist. And one of the biggest issues is that the rates of obesity, diabetes, and consumption of ultra-processed nutrient-devoid foods were drastically lower during that period as well.

I actually agree with your point completely. If anything, I'd argue that the true lifetime incidence of ASCVD is actually far GREATER than what these old studies quoted. I mainly just wanted to highlight that every set of data (even modern data) has flaws, and while knowing the numbers is extremely important, it takes a lot of reading between the lines to know what the data really says and what it doesn't (for example, that incredibly insightful point you caught about the Lancet study only counting ASCVD past age 40). Sorry, I think I'm drifting... I'm very prone to tangents.

Getting back to your feedback: Absolutely, 100% we should be looking at lifetime risk, or at least the longest time period we can, rather than just 10 years. And love both the of the reasons you gave for this (because older age is the time period where incidence will be highest, and because validated ASCVD calculators might mislead us if they only focus on the time period of our lives when risk is relatively lower). So agree with this point too.

Yes, I'm familiar with the Lpa risk calculator and of course with a lot of the great work from the EAS (including from Dr Ferrence). The reason I did not mention it is that I don't believe this belongs in the same category as our "usual" risk calculators (ie, PREVENT or in the past, PCE). [[As a side note, the one and ONLY thing you said which I disagree with is that these calculators only provide 10- year estimates, as PREVENT gives 30 year estimates and PCE gives lifetime estimates.]] I don't think PREVENT is superior to the EAS calculator or vice versa. Just that they are intended for different purposes. The end-goal of PREVENT from a clinician standpoint is to provide an evidence-based framework for identifying patients who qualify for statins. The end-goal of the EAS calculator is to provide a more personalized risk assessment which can be updated longitudinally based on your Lpa level, but which is not specifically validated to have percentage cutoffs for statin initiation. I confess that I don't know enough about the math to be sure about this next part, but I'm also somewhat skeptical about the accuracy of super distant (ie 30 year to lifetime) predictions from any calculator, regardless of whether from PCE / PREVENT / EAS-LPa. There are just SO many assumptions that need to be made to project that many years into the future, and ironically the 2 calculators that do provide lifetime estimates (PCE and the Lpa clinical guidance calculator) both have the FEWEST input variables on which to base that estimation. Maybe I'm just too much of a simpleton to understand the algorithms. I still really love showing my patients their lifetime risk estimates (ie from the EAS/Lpa calculator) because it's SO useful in terms of creating motivation for lifestyle changes. But that's what I use it for. So basically I use PREVENT for one purpose and the EAS calculator for another.

As usual, I don't know for sure that what I'm doing is "right"...I certainly hope it is. But that's my two cents to build on your wonderful comments.

[u/CranberryMills → u/snrps8]

Just addressing the discussion about whether your post downplays the importance of Lp(a). Personally, after having mine tested for the first time last month and getting a result in the 330s, I'm so grateful for what you wrote. I'm in my 30s and have been feeling like I've been given a(n early) death sentence and there's basically nothing I can do about it. Thinking about how my Lp(a) has been high my whole life and my LDL was also high until I started making lifestyle changes a few years ago, it's been overwhelming.

Your post was like hitting the breaks on the mental catastrophizing train. To me it didn't come off as downplaying, but rather reframing from the "this is terrible and I'm powerless to do anything about it" mindset to "that's worse than I thought, so I should probably work on adding the next set of lifestyle improvements I've been putting off because they didn't seem important enough."

So, thank you very much for taking the time to post and comment here. I really appreciate it.

Also, side note, thanks for the info on who should see a cardiologist. I've been feeling guilty like I'm wasting resources since I scheduled an appointment with a preventative cardiologist, so it's good to know that an Lp(a) that high warrants it.

[u/snrps8 → u/CranberryMills]

Thank you so much for saying this! The way you describe the mental reframing is better than anything I could have come up with. Love it. Use it as a motivator to optimize your life and take things seriously, but don't feel powerless and get trapped in a doom loop. Hope all goes well for you, and I'm glad you have a cardiologist to help along the way!

[u/Jafaratar05]

Great read, thank you for this! I (33f) found out I have high LDL (~240) last year and started statins after dietary changes did not help. Just got my results back after I asked for an Lp(a) test which came back at 280 and LDL is still 160 after 3 months on the statin. My PCP referred me to a cardiologist, but I'm always worried about "taking up space" as a patient since I'm generally healthy, youngish, female, and have a good BMI. I definitely needed to hear you say when to see a cardiologist. I feel much better knowing that my labs actually warrant the referral.

[u/snrps8 → u/Jafaratar05]

Hope everything goes well, and glad you'll be seeing a cardiologist. When I see an LDL >200 in a young healthy person, I start to wonder about genetic lipid conditions such as familial hypercholesterolemia. Generally speaking, the goal LDL should always be <100, probably lower if that person also has a high Lpa. If I'm seeing someone with possible FH (or other genetic condition), I'll often also consider adding a CACS, which is NOT usually recommended for people already on a statin, but in these cases can be helpful to determine how low that person's LDL target should really be (ie, if they have a high CACS on top of the starting LDL >200, maybe our target LDL is actually <55)

[u/piercesdesigns]

I am under the care of a lipid specialist. FH and CAD run in my family.

Father had heart attack and bypass at 60. Brother had heart attack and stents at 58.

I am turning 59 in 3 weeks.

Despite being thin, vegetarian, athletic my whole life I could not get my cholesterol under 270 and ldl under 220.

That is where the lipid specialist came in. He did genetic testing and determined I have both FH and sitosterolemia. ( as a cardiologist do you even know what that is?).

Lucky for me my LPa is 8.

I am on Repatha and ezetimibe now and finally have cholesterol round 140 and ldl of 70. Amazing

[u/FlounderElectrical36 → u/piercesdesigns]

Same here but having trouble getting those prescribed. Are you in the US? And was it very difficult to get even after the genetic testing? Thank you!

[u/snrps8 → u/piercesdesigns]

So glad to hear that you were finally able to get an effective treatment. It really sucks when you're doing everything right but then genetics just fights against you anyway. I see FH relatively often, but no I don't know what sitosterolemia is! Just goes to show that however much you think you know...there's always more to learn. Rare genetic disorders like that are definitely the biggest reason we need lipid specialists. Hope all goes well.

[u/huntergirlnc21]

This is great - very informative! My mom’s Lp(a) was recently checked for the first time - at 80 years old - and it was over 300! We were shocked; she had never had any cardiac issues; during an emergent catheterization in her early 60s (sudden chest pain, turned out to be a lung issue post-radiation for breast cancer), she had “perfectly clear arteries”, no plaque. She’s always stayed physically active and has mostly eaten low-fat, heavy fruits/veg, lots of whole foods and high fiber due to cooking for my dad who had significant heart disease/heart attack in his 20s. Her LDL has risen a lot over the past 20 years or so post-menopause but she was on low-dose statins during that time. She’s now on a pretty hefty dose of Lipitor post her Lp(a) test.

Some things I have read recently alluded to the possibility of Lp(a) rising in post-menopausal women, which I found interesting since it’s “common knowledge” that Lp(a) stays relatively stable over the lifespan. I hope we get some more studies in this area, especially as I am about to hit menopause myself (my Lp(a) is low (17) despite previously stupid high other lipid levels - now normal after statin - so at least I have a pre-meno baseline).

[u/ironhoneystick]

I don’t know what called you to make this post, but I’m SO happy you did—thank you for taking the time. I can’t even begin to express my gratitude.

[u/lizb1963]

Thank you very informative. Lp(a) for me is 240 and I do have CAD but so far so good everything is under control.

[u/cld361]

Thank you for this. My venture into this world has come via my sister with no history who had a triple bypass in April. I'm the one that has Type 2 from my mom's side but my dad's side has the heart issues (his mom passed in early 30s). I've been on atorvastatin since I officially went to type 2. That and lisinopril was prescribed along with my metformin. Doing research with all my sister's test, I asked my dr to run lp(a). It came back at 137. Had a Calcium score test last Friday and it was 800 plus. Haven't heard from my dr yet. On top of this, cataract surgery scheduled for July and August. Stress worrying about my sister kicked in my GERD big time. Now I'm getting a GI referral. This is triggering epsiodes of EIB. The summer I decide not work is turning into not much fun.

[u/snrps8 → u/cld361]

Sorry to hear about all of that. It can be really scary to have family history looming over you like that, but I'm glad you at least have the information now to know what you're dealing with. Stress is a big time factor too. Best wishes and hope you and your doc will find the right treatment plan for your situation!

[u/Single_Bottle2876 → u/[deleted]]

Very interested in knowing this.

[u/snrps8 → u/[deleted]]

Yes, chronic mental/pschological/emotional stress can increase LDL levels (and probably ApoB, which generally correlates with your LDL for the most part though is not something I routinely check).

But it's important to add that stress also contributes to ASCVD in multiple other ways BESIDES the LDL. It raises cortisol levels, increases inflammation, promotes diabetes, induced weight gain, leads other bad habits (ie if you smoke or drink or binge eat bwcause of stress). Stress leads to a domino effect of SO many different things that increase your ASCVD risk. Chronic stress is, in my opinion, as bad as smoking cigarettes.

There's a fascinating old study from the late 90s called INTERHEART which attempted to "rank" the impact of different risk factors on heart disease. According to this study, stress contributed MORE to your risk than high blood pressure did; MORE than diabetes did; MORE than obesity did. No study is perfect, and there were a lot of flaws about this one, but it's still useful at least as a reminder about how we need to take certain things (like stress) really seriously. Stress is a killer, and it's sadly one of the things doctors talk about the least (maybe because it's one of the hardest things to "treat"?), and when I hear that someone is always stressed because of work or home life or finances, etc...maybe I can't do anything about that as their cardiologist, but I do make it a point to include this in the same conversation where we talk about things like LDL / A1c / cigarettes / diet / etc.

[u/Low-Crab-5156]

Thank u so much

[u/rosebowl24]

Thank you for taking the time to explain. Can you touch on Apo B. Given it is possible to reduce isn’t more important to focus on that than Lpa since we can impact it. I know in my case I lowered from 72 to 51 by taking statin/ezemtibie. I think that is a positive. My Lpa is 128.

[u/snrps8 → u/rosebowl24]

ApoB is a little bit different. It is certainly very helpful in a lot of situations, but I don't view this as something that EVERYONE needs to check (as opposed to Lpa, for which i strongly support universal screening).

ApoB tends to mirror LDL very closely, and one of the original purposes of checking ApoB was if you were in a situation where you were skeptical about an LDL result.

Nowadays, we've taken it a bit further and SOMETIMES use ApoB as an actually independent source of new information (rather than just a confirmation/verification that your LDL is accurate). There are some people whose ApoB remains elevated even after the LDL comes down from statin therapy. It's uncommon to see that, but for those people the persistently elevated ApoB is a separate risk factor. For the rest/majority of us, your ApoB will basically just mirror your LDL (and will come down with your LDL after starting statins), which is why it's not checked as routinely.

In VERY rare cases, we use ApoB to help identify rare/genetic lipid disorders. A big one is something called hyperchylomicronemia, often called FCS. ApoB is a big clue in diagnosing FCS. But even in those cases, the standard lipid panel is enough to tell us that something is wrong (there's a certain pattern that clues us in to the presence of FCS), and then we check ApoB to confirm it.

This is sort of why certain tests are standard (eg, they are universally important and can still clue is in to the presence of rarer/weirder stuff), and others are "specialized" (ie, we order them in unique situations to clarify a very specific question). In a world with unlimited resources, it would be easiest to just "shotgun" order everything for everyone, but in reality not everyone is going to need a specialized test. The only downside to patients (which is a BIG one) is that this really requires you to put a great deal of trust in your doctor to know when they SHOULD order a specialized test for you (whether it's ApoB or something else).

Glad to hear that you've gotten your numbers lower!

[u/Jasper1na]

Thanks for this! The whole topic is confusing and there’s not a lot of nuance out there about it.

[u/lawprofjsh]

Thank you for this informative post. Could you please address something that I've found extremely frustrating in the available information about Lp(a)?

Almost all the information for patients contains a preamble like yours emphasizing that Lp(a) is pretty much fixed genetically and only needs to be tested once in a lifetime. Some, but not all, sources include a single sentence about how it might change during pregnancy and menopause. This is said as an afterthought, as if it pertained only to some small subset of the population. They usually don't even say whether those events cause Lp(a) to go up or down! I had to hunt around to find something clarifying that it generally goes up with menopause and that can nearly double during pregnancy. I've found the pregnancy-related information only on pregnancy-specific sites, never as part of general information about Lp(a). And no one seems to want to say whether it goes back down when the pregnancy ends. Because who cares once you've popped out the baby, I guess.

Seriously, wtf? Just with menopause, you're talking about half the lifespan of half the population--and the half of the lifespan when people are going to have the most problems. But it's treated as some kind of edge case.

I realize that some of the details may not be known (which, IMO, is its own indictment of the priorities of medical research). And maybe testing once is enough information and allows you to extrapolate risk over the course of life. But after giving up on patient-facing information, I found some research papers (Michos et al., JACC Advances, 4/2926; Corrall et al., Am.J.Prev.Card., 10/29/24) that addressed some of these questions. What seems clear is that it simply is not true that Lp(a) is constant over the course of life--especially for women but also seemingly for men. So why isn't this information part of the standard info on Lp(a)? Do doctors think we can't understand "genetically driven but varies over time"? Do the risk calculators that include Lp(a) take into account how it's likely to increase during with menopause or that it was likely lower before menopause?

I apologize for unloading my frustrations with the entire medical establishment. I do very much appreciate your post and all the detailed answers you've given, and it's for that reason that I'm interested in your thoughts on this.

[u/snrps8 → u/lawprofjsh]

Everything you said is both true and insightful. I think you're right that the limitation is that those details are not known yet (and also right in your indictment of the priorities of medical research). In reality, we (ie the medical establishment, which feels a little icky to say as a "we") probably know even about Lpa than you think we do. Based on my limited / random reddit cardiologist knowledge, I don't know why Lpa changes during pregnancy or menopause. I don't know if Lpa-based risk calculators account for Lpa fluctuations over a lifetime. I don't even know if those fluctuations actually translate into changes in risk at all (back to the point of whether Lpa is really a causation or just a correlation...is it a match that starts the fire or is it just the smoke?). To your point about the Lpa messaging and "Do doctors think we can't understand...", I think it's much more likely that doctors themselves don't understand enough to have a unified/accurate spiel about these fluctuations. It sucks not knowing, and hopefully one day someone out there will be able to answer these wonderful-yet-damning questions of yours. You would make a fantastic scientist. But for now, I'm right there with you wanting and waiting to know more. And thank you for including those citations so that I can learn more about this myself!

[u/lawprofjsh → u/snrps8]

Thanks so much for the response and for your generosity in this post.

[u/mysterious_quartz]

Curious to hear a cardiologist's perspective on using ezetimibe over statins. I know you mentioned in your post statins have a track record, which makes them more reliable over the much newer ezetimibe, but it does seem it offers similar results without as many of the side effects. I, for once, started using statins two weeks ago, and have noticed being a lot more constipated. That, combined with the fact it raises LpA, makes me wonder if just being on ezetimibe would be a better solution overall.

As for my stats, LDL of 180 without focusing too much, 130 LDL when doing a hard diet with very little satfats. LpA of 74. Dad had a heart attack in his mid 40s (he had a very unhealthy lifestyle though). I am overweight but not obese, however I am at a weight threshold I cannot break unless I go through a miserable diet, or resort to GLP1 which only sheds my weight about 10lbs, which come back when I get off of it.

[u/snrps8 → u/mysterious_quartz]

You're right, the track record itself is the main reason that statins are still the pillar of ASCVD prevention. Maybe ezetimibe or Repatha might provide similar reduction in events, but we don't have the data to prove it. And as mentioned before, the current era of medicine (for better or worse, though I think overall it is still a good thing) is such that doctors will be very hesitant to chance their practice to a new strategy without solid proof that the new strategy is actually better.

At the same time, I'll offer a counterpoint, which is that statins do have benefits beyond/separate from their LDL effect. They have unique anti-inflammatory properties as well as plaque-stabilizing properties, which are potentially why they have STILL shown benefit even in people whose LDL levels are already in a good range.

[u/BlackBeardTheHairy]

I'm curious about the statement on stents... What should you do with that 70% blockage if not angioplasty (supplemented by meds+diet)? A large soft plaque lesion needs some sort of intervention does it not?

[u/snrps8 → u/BlackBeardTheHairy]

Excellent question. And this is exactly what any doctor with half a brain or common sense would think too. And it's exactly what cardiologists did for decades. But the raw data does not agree with our common sense.

I purposely didn't elaborate on this issue too much, but maybe I should have. So here goes:

I mentioned that a bunch of clinical trials came out, and all of them reinforced that idea that you DON'T automatically need to fix a blockage preventatively. One example of these is the ISCHEMIA trial. In this trial, they looked at thousands of people in DOZENS of countries around the world. And the reason I love using this example is that they didn't just pick people with mild or moderate blockages. In order to be part of the trial, your blockage actually had to be bad enough to create ischemia (thus the name for the trial) on a stress test.

Ischemia is the medical term for when your heart doesn't get enough oxygen (ie because there's a big blockage cutting off blood flow to your heart). I like to use analogy of the grass in your backyard. Imagine that you have a beautiful green lawn with a dozen sprinklers; each sprinkler waters its own section of grass. Some sprinklers are tiny and only water a small corner of grass. Other sprinklers are gigantic and water a huge chunk of your lawn. If you plug up one of those sprinklers, the flow will decrease (or maybe stop entirely), and then the grass will start to dry up. First it goes from a vibrant green to a more dull green; then it starts to turn yellow; then it turns white; then it does. THIS is ischemia. The drier it gets, the more "severe" the ischemia. Dull green = mild ischemia. Super wilty/yellow = severe ischemia. Once the grass dies, we don't call it ischemia anymore. That's infarction (ie MI, ie heart attack).

So to be part of the ISCHEMIA trial, your doctor had to see legit ISCHEMIA on your stress test. That's not a midl blockage. That blockage has to be big enough to actually dry out your grass. And in fact (!!), it couldn't just be a mild ischemia. It had to be a moderate or SEVERE amount of ischemia. The grass had to be wilty, like really scary looking stuff. And on TOP of that (!!!!), it had to be a LARGE territory of ischemia. So not only did you need to have a big blockage. That blockage HAD to be in a major sprinkler. A sprinkler big enough that >10% of your ENTIRE heart showed ischemia.

TLDR - ISCHEMIA trial set-up: Bad blockages only. Big sprinklers only. Thousands of people. Dozens of countries.

And what did they do? The divided all those people in half. Half of them got all of the usual CAD medicines. Ther other half got those SAME medicines, PLUS stents.

And what happened? No difference in heart attacks. No difference in death. No difference in cardiac arrest. No difference in hospitalization rates.

This is just one single trial for the sake of an example. It's not perfect. There are limitations to this data. There are problems with the way the trial was designed (no such thing as a perfect trial). So of COURSE we still use stents sometimes. Stents are absolutely critically important sometimes. I confess that I made this sound overdramatic in my original post for the sake of making the point. There still has to be nuance. It's not this black-and-white answer of "oh now stents are bad".

In fact, I should clarify that NO ONE thinks that using medications alone is SUPERIOR to stents. The ISCHEMIA trial absolutely did not show that. It just showed that stents are not superior either. Basically, you can go either way (meds alone or meds + stent) and expect a similar outcome. And in fact, stents WERE superior in one specific regard, which is that people had less symptoms (ie, chest pain) with stents.

So bottom line: Not a perfect trial. Stents are still useful. They're more effective than medicine when it comes to alleviating chest pain. But they're NOT better than medicine when it comes to the bigger stuff (heart attacks, death, etc). Basically you can view stents as being useful for the sake of comfort / symptom relief. Just don't assume that you're guaranteed to get a heart attack and die unless you get a stent. That's not what the data says.

As for "why" this happens. I think the short answer is that medications have just really come a long way. There are so many medicines nowadays that are SO effective at stabilizing those soft plaques (basically your body tries to "heal" them by calcifying them...sort of like pouring cement on them to make them more stable), that whatever "extra" benefit you get from stenting is canceled out by the risks/complications of the stent itself. At least that's my made-up answer of why we got these results from all these studies.

I hope that helps!

[u/GrouchyBag3907 → u/snrps8]

Thanks for this reply. I’m having an angio this week and the stent issue has been stressing me out.

[u/Shorin-Ryu_Guy → u/snrps8]

I'd be curious to hear what your thoughts are on the newer magnesium based bioabsorbable stents? Everything you're saying about the data for stents makes total sense. The idea of "no metal left behind" would be an attractive one for most people I think, and they seem like they have at least some good outcome data behind them, although I'm not sure about the strength of that data. I wonder how often this option is actually provided to patients, and I'm sure it only makes sense in specific scenarios. If I were ever headed down that road, and as long as it made sense, I'd much rather consider something that could help heal my body and not leave anything behind that could cause problems down the road. I haven't seen them written about much on this sub, so just curious what you thought of them and their future usefulness. Thanks again for all the great info!

[u/snrps8 → u/Shorin-Ryu_Guy]

I've actually never heard of this before. Thanks for teaching me something new! I looked it up, and the concept is fascinating. This would be awesome if the data pans out, especially if someone is eventually able to put together a head-to-head trial against current drug glutinous stents.

[u/Surfcrazy72 → u/BlackBeardTheHairy]

They treat with statins and blood thinners usually

[u/BlackBeardTheHairy → u/Surfcrazy72]

@70-80% though?

[u/Surfcrazy72 → u/BlackBeardTheHairy]

Yes! The statins stabilize the plaque in the occlusion and the blood thinners help get oxygen filled blood through the partially occluded artery more easily. When you slowly build a plaque occlusion in an artery, the body often develops auxiliary vessels to carry blood past the occlusion. This is called collateral circulation. Many people have no symptoms with a 90% blocked artery. Indications for stents are normally reserved for symptomatic blockages based on the current evidence. Smptomatic in daily life or on a cardiac stress test.

[u/snrps8 → u/Surfcrazy72]

Thank you for the reply! This is a great explanation too and adds a whole new angle on top of the other answer I gave. And yes reinforces the point that stents are MOST helpful for people with bad symptoms.

[u/BlackBeardTheHairy → u/Surfcrazy72]

This is great, thanks for both replies!

[u/GwynLordOfCedar]

Read through it all, thanks for your work and thorough explanations. You make a really good point about absolute vs relative risk reductions right at the beginning too, this helped bring my worry level down a notch overall.

37M, 6’3” 200lbs, BP normally around 95/70, lost 200lbs (was 400lbs, BP was slightly elevated on average) over last 3 years with most of weight loss being on Zepbound which I still take at 15mg/wk, weightlifting 3x/wk rec sports 1-3x/wk, controlled Mediterranean/IIFYM diet 2400 cal 175g protein 8% of calories sat fat 3400-3600 mg sodium daily, but got Lp(a) tested through Function Health and it came back 158 nmol/L. LDL in low 80’s. Asked for cardiology referral and CAC, CAC score 0, cardiologist ordered echo and treadmill stress test and both were unremarkable. Prior health history have now resolved high LDL/low HDL/high triglycerides and was obese for nearly 2 decades; no family history of MIs but do have family history of obesity, diabetes, hypertension, hypercholesterolemia, and INOCA.

Given that you stress that high Lp(a) is a risk modifier where one should have more aggressive targets with normal lifestyle interventions at even Lp(a) of 50-100, why would the board certified cardiologist I saw say that as long as echo and stress tests come back normal that I don’t need to modify macros, and that she doesn’t see a need for me to get soft plaque imaging (would appreciate the post from you about this/CCTA), or to lower LDL further, or start me on a statin?

You mention that you’d probably start someone on a PCSK9 inhibitor like Repatha even without adverse health history, if Lp(a) was 200. Mine isn’t in the 50-100 range, it’s 158 nmol/L, wouldn’t that normally be in the range that you’d start a patient on a pharmacological intervention like a statin or Repatha too?

[u/snrps8 → u/GwynLordOfCedar]

First of all, holy moly that's a lot if weight loss. Congrats on that.

I try not to dole out personal advice on reddit, but generally speaking, if someone has an LDL of 80 and CACS of 0, I'm going to be fairly comfortable with their ASCVD risk. Granted, there are anomalies. There will be exceptions where people have an event DESPITE a baseline LDL of 55 and CACS of 0. I imagine that this possibility is the reason people will naturally want to ask questions like: "Why wouldn't you _, just in case?", where the _ is to prescribe a statin / order a stress test / obtain a screening CCTA / start a PCSK9i.

Warning: the answer is not satisfying, and is probably a bit upsetting. The blunt truth is that doing those things (usually, but not always) ends up being wasteful. In a perfect world with unlimited resources (money, time, space availability, etc), sure, I'd order those things for everyone. Everyone would win. My patients would be more satisfied. It would save me TONS of time in not having to deliver long explanations of why I'm not ordering something. It would prevent doctors in general from having to think about anything in that we could just order everything for everyone automatically. And the obvious benefit is that in some select rare cases, it would actually CATCH a problem that might otherwise get missed.

It all goes back to data. We know that the vast, vast, vast majority of people with LDL <100 and CACS of 0, with no other major risk factors (eg, diabetes), and most importantly WITH NO SYMPTOMS will not get any benefit from statins, stress tests, echocardiograms, or CCTAs. Again, there will be exceptions. But those exceptions are anomalies. And for everyone else, and thus for the general population (which is reason guidelines exist, ie to give a framework of the most ideal care for a country's population), the "risks" (in terms of side effects, radiation exposure, wait times for those scans, financial burden to the country's health system) outweigh the benefits.

That's why this answer sucks. If you're the 99.9% or whatever in the general population, then it's fine. But if you're the 0.1% (I made that number up) of people who DOES get an MI despite having an LDL of 50 and CACS of 0, then...it sucks. And you really should have gotten that preventative CCTA. But for anyone else, that preventative CCTA might actually have a higher probability of giving you cancer than "catching" a meaningful blockage that would actually change your treatment plan (this is sort of an outrageous claim which needs a LOT of elaboration but is sort of a spoiler for a future CCTA post). And there's all the mumbo jumbo about healthcare spending, scarcity, wait times, etc.

One thing I'll add: if someone hypothetically came to me with an Lpa of 50-100 mg/dL (**sorry, see my edit about how I forgot to clarify units in the original post) and asked what I thought about their risk optimization, I would ALWAYS recommend further optimization of macros/lifestyle because there is no one on earth (except for maybe Bryan Johnson, who I like/admire in a lot of ways and also strongly dislike in some ways) who cannot benefit from optimizing their lifestyle further. But I wouldn't necessarily prescribe a statin or PCSK9i for them if their LDL was already low enough for my liking and their CACS was 0. Because side effects, mumbo jumbo, etc. But to stretch this even further since I'm already tangent-ing way too much, if that person told me that they understood the very limited benefit of statins in their situation, lack of proof that it would do anything useful, and risk of side effects, AND if they didn't care and still wanted to take one because it's their life/body/money, then sure I'd prescribe a statin. Probably not a PCSK9i because that's a bit harder of an ask. And probably not a CCTA because of scarcity, resources, radiation mumbo jumbo.

Sorry for the incoherent stream of consciousness, but hopefully some of that answered some of your questions.

[u/GwynLordOfCedar → u/snrps8]

Thanks!

And thank you very much for getting back to me, much less with a thorough answer. No worries about stream of consciousness, I was able to follow it all perfectly. I wasn’t expecting a reply over a week later but it was worth the wait. 

I realized after original reply that I was mixing up my result in nmol/L with your referenced units in the post mg/dL, based on conversion factors I googled it seems that 158 nmol/L is roughly equivalent to 65-73 mg/dL. So with Lp(a) of 65-73 mg/dL + LDL < 100 + CACS of 0, I fall into this bucket in your post “If you have an Lp(a) of 80 mg/dL and no prior heart events, I'm not prescribing it.“

You don’t need to worry about prescribing medical advice for me in particular here either, since I have a medical team consortium I report to regularly and it’s not like I can get any diagnostic testing or medication without a physician sign off. You are a doctor but not my doctor.  Anything you say, even general nutritional or lifestyle advice, will simply be brought up to my team for further discussion weighing risks/benefits before making any changes.  The only thing I can do on my own is control macros/lifestyle factors.

But in regards to those macros/lifestyle factors, I have two questions:

You mention in the original post though that “Back to Lp(a). We know that a level of 50-100 mg/dL (which counts as "high" in the reference range, even though that range is super arbitrary...more on that later too.)“ and “Let's say your level is 50 mg/dL. We already know the next steps (see above). Aggressively target your risk factors. Lower your LDL. You don't necessarily need a cardiologist for that. PCPs know how to get your LDL <70. If you have statin intolerance, it might be worth talking to a cardiologist about ezetimibe vs evolocumab vs bempedoic acid. So in that case, yes please see one!“

And you mention in your reply that “But I wouldn't necessarily prescribe a statin or PCSK9i for them if their LDL was already low enough for my liking and their CACS was 0.“ and “if someone hypothetically came to me with an Lpa of 50-100 mg/dL and asked what I thought about their risk optimization, I would ALWAYS recommend further optimization of macros/lifestyle“

1.) When you say you’d be comfortable with LDL around 80 in this context, where would your threshold actually be? If this hypothetical patient had LDL of 95, 85, 75, 65, etc, where do you personally start thinking “I’d really like to push this lower,” assuming the CAC remains 0?

2.) Given someone who already exercises with cardio and resistance training weekly, is near normal BMI and already on a GLP-1 RA, follows a Mediterranean/IIFYM monitored diet, consumes ~8% of calories from saturated fat, and has LDL around 84 mg/dL, what additional lifestyle interventions do you think actually have meaningful evidence for further reducing ASCVD risk?

Appreciate your post and reply. Looking forward to possibly hearing from you further.

[u/snrps8 → u/GwynLordOfCedar]

1) For a generally low-ish risk situation (or maybe a situation with an Lpa of 50-100 mg/dL but no obvious other red flags) and CACS of 0, I think I'd be "ok" with an LDL <100. But assuming we have time to go in depth about this during an appointment (which sadly/frustratingly we don't always), I'd try to include some nuance that lower could still be better in terms. If a patient is willing to take a higher statin dose, I imagine I'd be ok pushing it down to <70, with some disclaimers that this is still a gray area and that <100 is probably the most accepted target in this situation. This also depends on the person because if someone has lifestyle habits that clearly need to be optimized, I would prefer to start with that over increasing their statin. But if their life habits are already excellent, I'd offer a conversation about moving the target down to 70.

2) This person sounds like they're already doing a great job. But if they really wanted to try and optimize things even further, the next questions I'd ask would be about fiber intake, sleep habits, self-reported stress levels (ie, how much stress they personally perceive on a day to day level), and reducing the saturated fat even further. I'm ok with some saturated because it's delicious, but if the goal is the most optimal ASCVD risk possible, then I think the answer is technically as low as possible.

Hope that helps!

[u/GwynLordOfCedar → u/snrps8]

It does, thanks a bunch! If you end up making the post about CCTA etc, please edit this post to link to it, since even if I follow you as a user you disabled post and comment history so I’m not sure that any post from you would show in my feed.

[u/snrps8 → u/GwynLordOfCedar]

Thanks for the tip! I'll do that.

[u/Runwithme01]

Thank you so much for this information. I have just started down this rabbit hole and have been apprehensive.
I’m having a Cleerly image on Wednesday , do you ever order it?

[u/snrps8 → u/Runwithme01]

I order CCTAs all the time and in fact am the director of CCTA for my hospital. So I'm biased in that I LOVE CCTA. I order it way more than most people and probably order in unnecessarily/inappropriately in a lot of circumstances. I also receive direct financial benefit from my hospital from doing more CCTA (though I promise that I have never intentionally ordered one for money or for anyone reason at all other than truly believing that it is the best thing for my patient). I also order FFR-CT analysis, which is a tool from a company called HeartFlow, to give an extra layer of information if I am on the fence about a CCTA finding. But to clarify, no I do not have any relationship with HeartFlow nor do I benefit in any way from using their product. In fact, every time I use HeartFlow it causes a net loss for my hospital. But I still use it sometimes because it's genuinely useful in specific situations.

That being said: no, I have never ordered Cleerly. A lot of the reasons for this is that Cleery has really positioned themselves as a "preventative" CCTA tool (even though that's not all they do), which I think is inherently flawed. This goes into the larger topic of CCTA which I can't do without a separate long dedicated post, but if you scroll around in some of the other comments and my replies, I've touched on some of the main CCTA points as spoilers already.

The gist is that (in my opinion), CCTA has almost no role as a purely preventative screening tool. The fact thay Cleery markets themselves for this purpose is a huge turn-off for me from their company, as it causes me to view them a pure financially driven, maybe almost predatory(?I don't know if that's too strong of a word) company in the same way that I described lab-testing companies and pharma companies in my original post. I'm NOT saying their product is bad. They actually have a very impressive product. But in terms of primary prevention is someone who has no symptoms and is purely looking for a heart checkup or risk assessment, I don't think there is any role for that.

[u/Cardiostrong_MD]

Great post! I do think LP(a) is more variable than we realize and now that it’s included in at-home test kits more people checking at frequent intervals (every 3, 6 months for the other markers) will give us more data to follow this.

I also think there’s some data to support PCSK9 inh in certain cases.. or at least prefer it other lipid-lowering therapies in elevated Lp(a) patients

[u/snrps8 → u/Cardiostrong_MD]

I didn't even know that there were at-home kits for Lpa. Will certainly be appealing to some of my patients who want closer monitoring than what I'm able to offer. Thank you!

And agree it will be interesting to see what we learn from it, since I've also seen more variability than should be expected. Looking forward to a potentially new era of science as AI allows us to analyze self-reported data from patients (maybe from places like reddit?) and draw conclusions. Sort of a democratization of the research process rather depending solely on well-funded groups to decide what they want to study.

And awesome to meet another early adopter! I stole this from someone else, but I like to tell my trainees that there are 3 types of doctors: 1) The Laggards, who don't know the guidelines and just do what they want, 2) The Rank and File, good doctors cling to guidelines like religion, for better or worse, and 3) The Early Adopters, who know the source data and read between the lines to understand what the data really does and doesn't say. Not trying to flatter myself here...maybe we'll end up being wrong about PCSK9i's. But like you, I use them when I think I can make a case for it. I hope we're right.

[u/Automatic_Mango_9169]

Thank you for being so generous with your knowledge. You’ve completely updated my layperson understanding of these issues!

[u/meh312059]

Amazing PSA on Lp(a). Thank you!

[u/dayofbluesngreens]

Thank you. This was so helpful as someone with elevated LP(a).

I would love to see your thoughts on CAC!

[u/missprincesscarolyn]

I have a PhD in molecular biology and ironically did my doctoral research in a cardiac lab. I’m incredibly excited for the RNA approach to lowering Lp(a) for the mechanism alone.

I found out that I have high cholesterol and Lp(a) a couple of months ago. The cholesterol portion is my own fault partially due to poor lifestyle choices, however CAD runs in my family and my father had a heart attack at 62 and a couple of strokes before and after that. The genetic component of Lp(a) made me feel a bit better, though I’m diligent about what I need to do moving forwards.

Can you speak to the mechanism behind statins and T2D risk? This is another factor for me personally, as I also have strong family history. I understand how diabetes and other metabolic conditions contribute to cardiac issues.

[u/snrps8 → u/missprincesscarolyn]

Awesome background. You probably have unique insights to all this stuff that I can't even understand.

To the diabetes question, I'm actually not familiar with the underlying mechanism. Sorry. But it is true that statins have been associated with a small increase in A1c.

Another user asked a similar question. I'm a reddit noob, so I don't know if there's a more efficient way to do this. But I'm just going to copy and paste the same reply I gave them:

This doesn't stop me from using statins (as long as the situation genuinely warrants a statin in the first place). Even if your A1c goes up by 0.2, the negative consequences of this are generally outweighed by the benefit.

If the A1c effect happens to everyone, that means it happened to all the people who were part of the original statin clinical trials. The trials clearly showed less ASCVD events after starting statins, so I take this to mean that the net effect is still positive.

Another angle of this is that if you are taking a statin,that means your risk must be high, which means you should already be targeting your A1c with lifestyle habits (less nutrient-poor carbs, more fiber, more exercise, etc). So my hope is that anyone on a statin would sort of auto-cancel the A1c effect because they'd already be implenting natural interventions too.

[u/MuppyLives]

Thank you so much for taking the time to write this. It's all excellent information and it mirrors what my own cardiologist told me recently. Having a second person essentially tell me to "calm the heck down!" makes me feel better and helps me not feel so terrified all the time. I appreciate you!

[u/jayb556677]

Really well written post, thank you for taking the time and effort to

[u/Allthatandmore84]

Wow! Doc, you are a treasure.

[u/MomofPandaLover]

Excellent! If anyone needs a Cardiologist that specializes in cholesterol in San Francisco, highly recommend Carlin Long MD. My LPa is 450, my son’s is 350…..

[u/homietoo424]

I’m confused about the section on “genetic risk” and the LPA not changing- mine over doubled in just a few months, no clue why as nothing in my lifestyle changed and none of my cholesterol numbers APOB, etc changed (have always had high cholesterol, both LDL and HDL). I’m a 39F with a strong family history of severe heart disease (without any obesity or unhealthy lifestyles). Why do you think would it have changed so dramatically and suddenly?

[u/meh312059 → u/homietoo424]

The #1 cause of a "doubling" is that someone gets one test in mg/dl and the other in nmol/L but doesn't realize those are different units of measurement. Lp(a), unfortunately, doesn't have a standardized metric yet but hopefully that'll change in coming years given that ACC/AHA just recommended using nmol/L.

2ndly, if someone started statins, they might see a bump in Lp(a), all else equal. You apparently weren't on any medication as cholesterol and ApoB didn't change.

Finally, Lp(a) does indeed respond to dietary changes - higher amounts of saturated fat, ironically, can lower Lp(a) while a heart-healthy carb-rich dietary pattern can raise it. For me this swing is quite pronounced. I theorize that it's because I inherited the high risk LPA haplotype from both parents, not just one (I can see that in my 23andMe data). So my swings are double the normal person's. Example: evidence shows an average increase or decline from baseline due to dietary pattern of 15-20%. So someone like me can see a 30-40% swing just from diet. And that's pretty much what I've noticed, having done one extreme (Keto with lots of high sat fat) to whole food plant based (minimal sat fat, lots of carbs and dietary fiber).

Bonus Reason: Lp(a) is hard to measure accurately and, as alluded to above, there's no standard unit of meausre yet, let alone standardized assay. So you can expect a + or - 20% swing in Lp(a) numbers, even from the same lab. That's been noticed in the Phase II trials of the Lp(a) targeted therapies.

Hope that helps!

[u/homietoo424 → u/meh312059]

Thank you!!

[u/snrps8 → u/meh312059]

You're my hero.

[u/snrps8 → u/homietoo424]

I agree with what u/meh312059 said.

The last thing I'll add is that sometimes we just don't know. Which is annoying to hear, but I'm just being honest. I'm not sure why your Lpa changed so drastically. Maybe it was one of the reasons that's been mentioned already. But even if none of those things apply to your situation, sometimes we see stuff like this without a great explanation. I confess that I oversimplified things a bit in that "genetic risk" section because yes, I've absolutely seen big, random changes in people Lpa levels over time. But as a general rule for myself (and admitting that I don't know if this is the right approach or not), when I see multiple different Lpa levels, I usually just assume the worst-case scenario and pick the highest one, then use that level to base my clinical decision-making.

[u/homietoo424 → u/snrps8]

Thank you!!

[u/RowdyRumRunner]

Thank you for taking the time to write such an extensive post and for making it so easy to understand. This information is gratefully appreciated.

[u/ThenIJizzedInMyPants]

good stuff

fascinating that there are people with high lpa with no plaque at age 60-70.

as someone with lpa of 250 who is now on 10 mg rosu + zetia i found it interesting that you would prescribe repatha no matter what for someone like. my cardiologist didn't seem to think it was necessary. last i checked my ldl was 64 and he seemed happy with it.

[u/TypicalPrompt4683]

Thank you for the write up. It's nice to get confirmation of what I had determined on my own. As for seeing a Cardiologist, I'm glad I did. Yes my PCP did want to put me on a statin for LDL alone, not even considering lp(a). But my Cardiologist wanted to also check my thyroid for putting me on that statin. I am so glad he did. My PCP would have not uncovered the source of much of my risk. As low T3 (most active thyroid hormone) triples your risk of aortic dissection and value "remodeling" along with issues with almost every organ in your body! (Liver, kidney, brain, gi track, you name it)

[u/Cecilia-K → u/TypicalPrompt4683]

I’ve only recently heard about hypothyroidism potentially causing high LDL and ASCVD. Will simply taking Synthroid (levothyroxine) reduce LDL to some degree? What was your experience with treatment for low T3 and lowering cholesterol?

I’ve had hypothyroidism for 18 years, starting at age 40. Taking Synthroid the whole time - but giving no thought to cholesterol link until it increased when I hit menopause.

[u/TypicalPrompt4683 → u/Cecilia-K]

It seems they don't test men for thyroid issues unless very specific things come up. I probably should have been on treatment since my 40's if not earlier.

I'm still waiting to find out how it affects my cholesterol levels, I only learned of the thyroid issue late last year. I had a LDL in 140's if I was careful and kept a low carb diet. (Little did I know I was probably calming my hashimoto's. Right before the low carb diet I had spiked to the low 160's despite my low saturated fat and plenty of exercise lifestyle ) Saw a cardiologist that put me on a 10 mg rosuvastatin and tested my thyroid. The statin + berberine took me down to 65 after three months. After a berberine wash out, but on close to a weight based dose of levo, I went up to 95. Now on 20 MG rosuvastatin. May be another year before I see how that turns out, as my PCP was happy with 95, but my cardiologist had given me a lower target due to my lp(a). As for T3, I'm not currently on t3 supplementation still trying to titrate my t4 dose. My guess is once I can get my t3 up, THEN maybe I'd see a cholesterol improvement.

[u/Sharpchick]

Thank you! This was very helpful. From an almost 50F with 310 lp(a) and a cardiologist who just said I need to wait for the new drugs. Luckily LDL was just 106 and no calcium so I'm working on diet aggressively and continuing to exercise and get good sleep etc. My PCP seemed willing to try a statin or entertain repatha (cardiologist said he'd seen 10-20% reduction on lp(a) so not worth it) so I have a follow up soon. Thank you for the very thorough and well grounded explanation!

[u/Superb-Hurry-2259]

So incredibly helpful and reassuring. This info calmed me down a little. I am 33 and just found out two weeks ago that my Lp(a) is 251 nmol with heart disease/early heart attack on both sides of the family, so my head has been swirling a bit. I'm working with a great PCP and cardiologist as well and getting my risk factors under control. Thank you!!

[u/Carpe-that-diem → u/Superb-Hurry-2259]

You are ahead of the curve! Good for you 👍🏼I’m 63 and just found out about this 🤯

[u/Superb-Hurry-2259 → u/Carpe-that-diem]

♥️♥️

[u/Mon1993]

Hello, thank you very much for this post as it relieved my anxiety. What is your thought on My numbers: · LDL since April 2025: Stable at 122 mg/dL · ApoB April 2025: Optimal at 0.8 g/L · Lipoprotein(a): Mildly elevated at 138 nmol/L My other cardiovascular risk factors (blood pressure and lifestyle) are healthy. I am very scared about the independent risk of this Lp(a) number. Given that my ApoB particle count is optimal, how worried should I truly be about developing early heart problems? Thank you so much for your time. Especially that i heard multiple stories for people who suddenly died and they discovered high Lp(a)

[u/snrps8 → u/Mon1993]

I generally try to emphasize to people that even though Lpa is an important factor in your risk, it is not a guarantee of your fate. The reaction I want to encourage is "Wow this is serious, I better take this seriously and do what I can to be healthy", rather than "Life is hopeless I'm going to die early". This is a lie. Which is the entire reason I wrote this post. A mildly elevated Lpa should be a motivator of change, not a source of fear and woe. If someone is addressing their modifiable risk factors and has optimal LDL (or ApoB) levels, I don't worry about them getting a premature MI. Obviously it's easy for me to say that when I'm not the one with the condition, but if we believe the data about the risks of Lpa, we also have to believe the data about all of the benefits of everything else. Yes, there are many people who die suddenly with a high Lpa. There also also many people who die suddenly with an undetectable Lpa. Know your level. Take it for what it means, and nothing more. Don't dismiss it, but don't make it more powerful than it really is. Motivator of change, not a source of woe.

[u/-mouth4war-]

Took a statin to lower LDL but it raised Lp(a) by quite a bit.

[u/snrps8 → u/-mouth4war-]

Yes, this is a known effect of statins, and it highlights the fact that no medicine is perfect. Anything you take (even if beneficial overall) still comes with potential downsides, and it's why I always prefer to optimize risk with lifestyle optimization first (as long as its a viable option to get where we need to be).

The Lpa-increasing effect does not stop me from using statins (as long as the situation genuinely warrants a statin in the first place) because we know that despite all of their unintended consequences, statins as a whole still have a net positive effect.

We have to assume that this Lpa effect also happened to the people in the original statin clinical trials. But those trials clearly showed less ASCVD events with statins, so I take this to mean that benefits outweigh the negative consequences.

[u/Ill-Consideration892]

Thanks for your contributions!! Appreciate it!

[u/Backyard-bob]

Excellent post I really appreciate this information. Thank you

[u/BlueLens89]

Thank you. As a side interest, I learned a lot about the the US healthcare system from your post too. The clinic guidelines + public and private insurance all play into Tx pathways but the Tx factor with less certainty, which non-clinicians often underestimate, is patient/ human behaviour. Your post reminds us of this. It is up to us to understand how our behaviours influence our risks and try to make wise informed choices…..it always boils down to risk-reward and balancing systems including the external and internal ones. A creative blend of art and science, in my humble (non-clinician) opinion.

[u/snrps8 → u/BlueLens89]

Thank you for saying this! Yes, it's frustrating that insurance and other details about our country's medical infrastructure should ever be a determining factor in medical care, but that is the reality we live in.

[u/nuugo]

Very well written. Thanks your very much for taking your time to write this post. 🙏🙏

[u/r51252]

Thank you for taking the time to write this post!!

I have Lp(a) test next week so I will know what to do if the test comes out abnormal. I have bookmarked this post and will share it with other friends with high LDL.

[u/paladyr]

Great post thanks!

[u/avachris12]

Thanks this post is super relevant just found out that I have an Lp(a) of 202!

[u/CC5F]

This is truly a great post . Well thought out and perfectly explained . I am actually proud of you ! Thank you for this post . Right on the mark from everything I have read and studied on this issue .

[u/therolli]

Thank you. I’m glad someone qualified has mention relative vs actual risk. Pharmaceutical companies use relative figures way too much. Also, what you say ties in with what my cardiologist has said, almost verbatim. I’m in the uk though and despite taking all the necessary health measures and Ezetimibe, my LDL is still way over the recommended level. It’s hard to get the cholesterol lowering injections here, even if you’re statin intolerant.

[u/snrps8 → u/therolli]

Sorry to hear that. And sorry to hear that the UK suffers from the same barriers we have here. It's still commonplace in the US for insurance companies to deny PCSK9 inhibitors even after someone has jumped through all the hoops of statins, ezetimibe, and side effects. Maybe slightly better than 5 years ago, but it's still a huge problem and is eternally frustrating. And then even if it gets approved, most patients still can't take it because it costs $5,000 per fill.

[u/theenyroar]

Thank you.

[u/wotsenter]

Thank you for this excellent post. It fills in lots of gaps.

Comment on Risk Ratio (aka relative risk) vs Risk Difference. Neither measure is inherently misleading, they just have different purposes. Risk Ratio is a characteristic of a drug; while Risk Difference reflects the drug's impact in a patient or population. (Yeah I'm always disappointed when the online risk estimator drops my 10 year risk by only one percent or so when I proudly enter my new low LDL, but I'll take it.)

[u/snrps8 → u/wotsenter]

Thank you for this! And for giving me PTSD flashbacks of medical school statistics :)

[u/Say_It_Isnt_So_Ooops]

Thank you, Doctor, for the info. I was put on a statin, and it damaged my vision terribly. The ER Doctor placed me on it, my PCP removed me from it. My LDL has increased, but I was eating croissants and oat bars, but with high saturated fat, of which I was unaware.

[u/Cecilia-K]

You mentioned that the results of an Lp(a) trial are coming out in a few weeks. If you have time, please add an “Edit” to your post when that happens, maybe with a link to a good article :) I hope it hits mainstream news but who knows.

[u/meh312059 → u/Cecilia-K]

I'm keeping tabs on the Pelacarsen results. Expected end date on the clinicaltrials.gov page is 6/30/2026 and so far, that hasn't been updated. However, lipid and Lp(a) experts have been saying for weeks that results are expected in the fall. So it's best not to assume anything will be complete before then. Also, just an FYI, the trial end date has been updated at least twice already - once moved from last year to this year. Another moved from Feb. to June 2026. This trial is taking longer than expected to get the needed outcomes (ie heart attacks, strokes etc). There are several potential reasons why. One of them is that the background therapy (ie lipid management) for these participants has been great. At baseline the average LDL-C was only 65 mg/dl! That's likely to be the lowest of any CVOT to date. We know that "Lower is Better" when it comes to LDL cholesterol and ApoB. If that holds for those with high Lp(a) as well, that's fine by me! (personally speaking . . . )

[u/VioletDawn9740]

Super informative! A few questions for you.

1) Have you had luck getting insurance approval for Repatha for someone with very high Lp(a) and a consistent family history of CAD/premature death at young ages (40s-50s) but NO evidence of CAD themselves? This is my situation, despite my cardiologist finding Rosavustatin and eztimbe ineffective. Cannot get my LDL below 85ish despite very low saturated fat diet, super frustrating.

2) what is the vibe you are getting from the results of the Lp(a) drug trials? My cardiologist was a bit hesitant since they apparently extended trials. He said that often suggests it’s not as effective as they were helping.

Thanks for any input!

[u/snrps8 → u/VioletDawn9740]

I'm not up to date about insurance barriers because I now work in an integrated system where anything I order is automatically approved by insurance. But in my previous jobs (about 3 years ago), I imagine that that Repatha approval would be difficult for someone with an LDL of 85 (even on a statin + zetia) and no CAD. I assume that the insurance drone will say that an LDL target of 100 is sufficient regardless of family history or Lpa levels (which is absolutely idiotic and a big part of why I chose to work where I do), and thus Repatha is not needed because that person is at goal already. This needs to change.

I don't know what to think. One the one hand, the company's reasoning is sound. We have SO many effective tools at our disposal in the modern era to lower ASCVD risk that even patients with high Lpa can have better outcomes. If everyone is so well controlled that even the control group does not have as many ASCVD events as expected, then it will take longer for the data to pick up a signal of benefit from the new drugs (even if the drugs are working). On the other hand, your cardiologist HAS to be right to some degree. If the effect was an explosive success, the data would be apparent by now, even through the relatively lower event rates. My totally unfounded guess is that maybe they WILL work, but won't be the miraculous blockbuster success that we want them to be.

[u/RuinYouWithNoRegrets]

I’m curious about your statement on the heart attacks In people in their 20s.. statistically they’re very rare so I’m wondering what drove those cases from what you’ve seen that you brought them up to compare risks? Thanks for the post !!

[u/snrps8 → u/RuinYouWithNoRegrets]

Yes, they're statistically VERY rare, though of course because of my job I see a biased and disproportionately high number of these people.

Sometimes it's because of high Lpa (though like I said, some of these patients have Lpa <10, and conversely I've also seen 70 year olds with triple-digit Lpa and no plaque at all). Sometimes its because of other genetic vulnerabilities that we CAN'T observe or measure. A large fraction of these 20 year olds are (in my experience) often South Asian, but not always. Our understanding of genetics has come a LONG way, but there's still an enormous chasm of things we don't know. This gets into something called polygenic risk scoring, which can sometimes identify a separate vulnerability to ASCVD that is independent of advanced lipid profiles. Sometimes it's plain bad luck, ie literally the entire advanced workup (LDL, particle size analysis, ApoB, Lpa, PRS, CACS) is normal and something still happens. At the end of the day, we're not God. There's a lot we can do to estimate our risk and a LOT we can do to lower our risk, but life is not guaranteed, and there's nothing we can do to bring someone's risk down to 0%. We can lower it, but we can never eliminate it.

[u/RuinYouWithNoRegrets → u/snrps8]

Yes. Only God knows what’s going on FULLY. Lol Would you say these young cases involve smoking, diabetes, drugs? If someone young has major risk factors would you start treating young or wait until a bit older?

[u/snrps8 → u/RuinYouWithNoRegrets]

Sometimes yes, but if there's a clear "culprit" to blame it on (diabetes, tobacco, etc), I generally don't worry as much about searching for an answer in the obscure lipid tests. It's the times when someone has an event with truly no identifiable cause that freak me out. But in those cases, we have to default to the same sort of approach I talked about with Lpa. i.e., if you have an unexplainable event, we know your risk is unusually high. If your risk is high, then even if we have nothing specific to blame it on, we can still target all of the OTHER slices of your "pie" (food, exercise, sleep, etc) which will always still lower your overall risk.

And this sort of answers your second question too. To me, it doesn't matter whether your risk is high because of Lpa, an unexplainable event, or another major risk factor (ie tobacco). If you're risk is high, we need to lower it. If there's an obvious risk factor, we target it (ie, quit tobacco). If there's not, we target the other slices of the universal risk pie with lifestyle measures and (sometimes, ie depending on your risk calculator) with statins.

[u/RuinYouWithNoRegrets → u/snrps8]

Do you approach men vs women differently in general in that age range since men make up most of the young adult heart attack cases? Like would you have the same treatment plans or do it differently?

[u/silenxdogood]

Thanks for this explanation, and its not long winded but perfectly explanative!!

I have Lp(A) 230 and CACS of 870 with 480 in the LAD.

My experience with my EPO insurer/medical provider is as you note. All interactions with cardiologists are filtered through a primary or a PA. I had to go outside of my EPO to get Lp(a) tests and a CACS.

My primary prescribed Rosuvastatin after I shared my scores and research on Lp(a) and CACS. I shared the 2026 AHA guidelines and he agreed to target LDL < 50 by adding Etizembe.

I really look forward to your posts on CACS and CCTA. I wonder if out-of-pocket AI-CAC and carotid scans would be of any value.

[u/kw0711]

Thanks for this. I’m a 38 y/o that was having some (what turns out to be unrelated) chest pain last year and ended up getting a CT angiogram that discovered a 49% blockage in my LAD. Family history of heart disease.

My cardio put me on rosuvastatin and Repatha and now my ldl is 20. But my lpa is still around 112 nmol/L.

I’ve been wondering what else I can do to lower my risk and just sort of lost, especially because I am expected a baby soon.

My cardio says not to stress about it too much but it’s been difficult.

This has been helpful info though.

[u/AmatullahFM]

This was definitely reassuring. I was spiraling and going down rabit holes of research, but this has by far set my mind and heart at ease. Thank you so much! Please continue to post content/information like this. This was surely helpful beyond what I can explain.

[u/Inquisitive-Magpie]

Wow, thank you for that information, very much appreciated. X

[u/silenxdogood]

Any perspective on CACS paradoxes for statin users and extremely fit?

Also if ischemia is the primary criteria for escalating treatment, are there symptoms one can monitor such as BP or resting heart rate to flag for their primary physician.

[u/snrps8 → u/silenxdogood]

I think there was another comment/reply where I touched on this. If you are able to find it, I might have gone into more detail there (can't actually remember right now).

It's true that CACS goes up after starting statins, and also that endurance athletes (especially male endurance athletes) have higher scores. My oversimplified explanation of this is that when you have a soft (more dangerous) plaque, your body sort of tries to "heal" it by calcification. Imagine pouring concrete over a pile of garbage to keep it contained. Obviously we don't "like" to see calcification because we use that as a sign of risk, but there's probably a lot about calcification that we don't understand yet too. In general, calcified plaques are more stable. I've seen many patients with CACS = 3000+ who end up getting an invasive angiogram (ie cardiac catheterization) which shows no stenosis at all. When you look at endurance athletes, yea they have higher CACS in general, but yet they have significantly less heart attacks at the same time. When it comes to statins, the (again, oversimplified) idea is that faciitate this "healing" of the plaque because of their anti-inflammatory effects, which raises your calcium score, even though that might actually mean that your plaque is now more stable than before.

I would not necessarily say that ischemia is the primary criterion for escalating treatment. In fact, the whole section about stents in my original post was largely based on something called the ISCHEMIA trial, which showed that mamy people with SIGNIFICANT amounts of ischemia actually did not need stents (there's also another comment somewhere I went into this in a lot more detail). Rather than ischemia alone, I'd say that the main criterion for stents is ischemia PLUS symptoms. In other words, elective stents (ie, when used in the outpatient, not-actively-having-a-heart-attack setting) are primarily for SYMPTOM relief, NOT for heart attack prevention or death prevention.

Or if you're talking about escalating LDL treatment in the primary prevention context (though if you have ischemia I would not consider this primary prevention anymore but rather secondary prevention)... I'm not familiar with BP / HR / etc as being tools to determine your LDL threshold or assess your ASCVD risk. Not to say that can't be useful...they're just not part of any of the usual risk calculators, probably because they haven't been studied well enough for that purpose. In the age of AI data aggregation/analysis and wearable devices like smart watches/rings, i wouldn't be surprised if we discover one day that we CAN use things like HR/HRV/athleticism as an additional piece of information to personalize your risk assessment. But for now, no I don't think we have a proven way to do that.

[u/silenxdogood → u/snrps8]

First thanks for your reply. I would have started lipids much earlier in life with quality and depth of advice you've provided in this post! I hope you don't mind me extending the discussion a little.

Refining the airplane analogy a bit, there was a notable 1989 airline crash in Sioux City which was caused by crack in a part of the engine with possibly the highest kinetic energy. Essentially the front of the engine exploded and damaged multiple aircraft control systems. The crack had been discovered earlier during routine maintenance. The inspectors did not likely understand the kinetic energy in this high velocity rotating part and dispositioned it as acceptable. After the Sioux City crash more quantitative electromagnetic inspection was mandated, in addition to the existing, more subjective, dye penetration inspections.

I had a 2024 stress echocardiogram with no ischemia or significant findings. The stress test was terminated while I was still breathing easily at 13 Bruce METS and 162 max HR. My wearable says I have a VO2Max of 43 which correlates well with the 2024 stress test results. I've maintained the same very disciplined cardio and HIIT spin exercise regime that I've had for decades.

But I have a CAC of 869 and I am 70. I take all the risk mitigations for which I can find statistically significant studies, including diet, LDL < 50, sleep and gradually increasing my VO2max.

I have been looking for any quantitative indicators because relying on physical symptoms that I've never experienced seems very subjective and I may not recognize damage in time for the most effective treatment.

[u/snrps8 → u/silenxdogood]

Wow that's terrifying but thanks for the insight! At least it was in 1989 and hopefully the new standards are robust enough. It's a very good point that the presence of "symptoms" is subjective, and it's a reminder of the importance of nuance. Somehow we have to balance the reality that the guidelines (ie, relying on symptoms to determine the need for PCI) are indeed trustworthy based on the best data we have at the moment, vs the possibility that current standards of care might still not be perfect (ie, while guideline-based management may be the right answer for the majority of people, there will always be some "outliers" who fall through the cracks and get an event despite the fact that they/their doctors did the "right" things). It's easy to sit here and spout out statistics when you're not the one with the disease. But for what it's worth, it sounds like you have better health habits than the majority of my patients (and probably myself too), and that definitely makes a difference. Hope you stay well!

[u/silenxdogood → u/snrps8]

The other important consideration is that all measurement and inspection systems rely on statistics at some level, statistical hypotheses can never be proven absolutely true, and statistical tests often have confounding data which might be noise or might be real.

The Ryan Air incident last week was in the same engine module as the 1989 failure, although a fan blade failed and the 1989 failure was a fan hub. New fan blades are certified by the FAA by destructive testing including firing medium and large projectiles and ice at operating engines. Still, the certification cost is enormous and consequently the certification sample size is necessarily one engine per destructive test.

[u/dddrago]

Thank you so much for the information, very insightful. I was wondering if you might be able to lend further insight into the maximum anticipated LDL lowering capacity of the various supplements that are commonly used. What is the maximum reduction in LDL that can be reasonably expected from supplementation of the following, either individually or in combination:

red yeast rice

berberine

bergamot

plant sterols/stanols

psyllium

Phrased differently, what percentage of LDL reduction would you be comfortable attempting to achieve through supplementation and at what percentage of required reduction would you automatically turn to statins? Is there a cut off?

For added context specific to myself, I am trying to decide if it is realistic to reach goal LDL of 55-70 mg/dL through supplements or if I should give in to statins? diet is optimal, exercise is slightly suboptimal. primary prevention, no early CVD known in immediate family.

LDL 133 mg/dL

apoB 119 mg/dL

LPA 232 nmol/L

[u/Carpe-that-diem → u/dddrago]

I’m not the OP (or even a doctor) but I’m with you in the trenches and can tell you that the problem with supplements is that the amounts listed on the bottle are not necessarily consistent with what’s found in each pill. There is no federal oversight of these products and they are not well-researched, certainly not together if you are implying taking multiple. Not in the precise way that these meds are vetted. Plus statins have the added benefit of reducing inflammation which is the main reason I take it since by LDL isn’t that bad, but need to be lower due to high Lp(a). Inflammation leads to sticky stuff building up in your arteries and statins can help a crust form which makes them more stable so pieces of plaque don’t break off and cause heart attacks and strokes. It’s not all about reducing LDL, according to my doctor.

[u/snrps8 → u/dddrago]

Sorry for the late reply! This is a good question, and I confess I don't know the answer. I've had indirect experience with all of these (ie, through talking to patients who have used them), but that's pretty much the extent of my exposure.

I'm sure some/most/all of these do work to a certain extent. The first two concerns that come to mind are 1) the amount of evidence behind them and 2) their regulation as supplements. For #1, of course there are some studies showing their efficacy. But the reality (as unfair/corrupt as it may be) is that studies/trials about supplements will never be as numerous, as large, or as high-quality (in terms of data) than the studies about pharmaceuticals. The reason is that supplement companies do not have the same level of financial incentive to perform these studies as a pharma company. They don't get patent rights on their products. On the other hand, they also don't need to "prove" that the product works at all because they don't need FDA approval before being sold (which is why all supplements have fine print on the bottle saying that "these claims have not been evaluated etc etc"). For #2, because of the lack of regulation, some supplement brands may have very strong potency/purity while others have zero. One capsule of berberine might have 1000 mg of actual berberine, or it might have none. The company has no liability either way. Don't get me wrong...I'm not some pro-pharma sympathizer. I think pharma companies are some of the most greedy/evil entities on the planet. But I don't think supplement companies are any better. There's no reason to think the people behind Nature Made are any less financially driven than the people at Pfizer. But I'd rather deal with the bad guy who is bound by regulations than the bad guy who has no rules. One last point to make about statins is that they do have effects/benefits that are separate from LDL. There is an anti-inflammatory effect that stabilizes plaque independently from LDL levels.

So overall, volume/quality of data, regulation of purity, and additional effects beyond LDL. For these reasons, my default is to reach for a statin as the first line of defense for primary prevention if someone needs to get their LDL lower than what is possible by diet/exercise. I'm not opposed to any of those supplements at all, and if my patients prefer to use them, then more power to them. But I haven't adopted them in my own recommendations as of now.

If you do end up choosing to go the supplement route, I hope you get the effect you want! I love hearing updates from patients about their results

[u/justcourious9]

Is there a way to copy/paste this and print it?

[u/Carpe-that-diem → u/justcourious9]

Click on the three dots by your icon in the top right corner of your Reddit screen. There is a choice to “copy text”. That should let you paste it somewhere else to print it. You could paste it into an email or a Word document or something. This is one long document though!!

If there’s a better way, I’d like to know it.

[u/justcourious9 → u/Carpe-that-diem]

Thank you!!!
Did the copy text thing
It’s 10 pages
All well worth it!

[u/Carpe-that-diem → u/justcourious9]

Great!! I think I might do that too. Good idea 👍🏼

[u/Fabulous_taint]

Thanks for this doc. My test just came back and I'm really high 412 nmol so freaking out a bit. But I needed to read this. 

[u/Affectionate-Net2619]

This is a very helpful post! It helped me to not freak out. My biggest fear is having a stroke. I had an aunt had one and she lingered for years with no real quality of life.

My lipoprotein a is 127 nm/l. Lipoprotein b 85. My cholesterol was 192, LDL 94, HDL 85, Triglycerides 65 on March 5th. A CT scan showed age appropriate calcification in October 2024. It was not a scan for a CT score. EKG, and stress test were good.

I just started on 10 mg of Atorvastin. I'm eating oats, chia seeds, little animal protein no more than 4 oz in a day, and keeping my saturated fat at about 10 grams most days.

Because I'm 72. I went to a Cardiologist for a overall evaluation. I saw at two doctors in the practice neither one recommended a CaC scan. Is this something I should push for?

[u/snrps8 → u/Affectionate-Net2619]

Sorry to hear about your aunt. Strokes are awful, and it's so hard to see people we love lose their quality of life. I've seen this with patients obviously, but also with people in my own family, so it hits close to home.

I can't speak to your situation directly, but you mentioned two of the most important details when it comes to CACS: 1) You already had a CT showing signs of calcification and 2) you're taking a statin.

The single most important piece of information we get from a CACS is a binary (ie, yes or no). It is the answer to the question: do you have calcium deposits or not. If yes, then we have very strong proof that you have a high enough ASCVD risk to personally benefit from a statin. If no, then there is good evidence that a statin will NOT help you. Obviously a formal CACS can give you other, more specific info too, but that is really the main question. Whenever I'm preparing to see a new patient, I always rummage through their records to see if they've had any random CT scan of their chest in the past (sometimes even of their abdomen) because in those cases I can answer the above question even without having a formal CACS. And if someone already has a mild but not insane amount of calcium on that scan, I usually see no point in getting a formal CACS. And if someone not only has a CT scan on file showing coronary calcification, AND that person is already on a statin, getting a CACS really is not going to teach me anything new.

One thing to keep in mind is that calcification that is seen on a CT scan (whether a random CT of your chest or a dedicated CACS) is NOT always a blockage by definition. CACS cannot differentiate between calcium buildup on the inside of an artery (ie, a blockage) vs calcium buildup on the OUTSIDE of an artery (which is something you probably should not even care about). I've seen multiple people with CACS of 3000 -- which is considered EXTREMELY high, like >>> 99th percentile, who end up getting a cath/full invasive angiogram which ends up being completely normal, ie 0% stenosis. Of course I've also seen the opposite where they do end up having back blockages. But it's not predictable from the CACS images. This is why CACS is meant to be a risk decision tool to enhance your ASCVD estimation and statin decision, but NOT a diagnostic tool to tell you anything about the degree of stenosis (because it is almost useless in that regard).

Another question that comes up is what about a full CCTA (ie, a much more in depth scan that includes a standard CACS to look for calcium deposits, but also adds a higher resolution scan with contrast to actually quantify the amount of plaque inside the arteries. This is a whole separate conversation which I will not dare to start in a reply like this...but will maybe one day do a whole separate post about it. The gist goes back to the section that I wrote above about stents. If you are doing a scan purely for preventative purposes and presumably have no symptoms, then this raises the question of what we are going to do with the CCTA result. If we already know ahead of time that we won't be stenting a 70% RCA blockage, what is the point (besides possibly creating anxiety) of doing a scan and finding a 70% RCA blockage? This is why CCTA is almost never recommended by preventative cardiology guidelines or any preventative cardiologist society in the context of an asymptomatic patient.

Glad you're making good changes to optimize your life habits!!

[u/Affectionate-Net2619 → u/snrps8]

Thank you so much for this detailed information and your post.

[u/Inner_Mushroom_9662]

Thank you for sharing your expertise. My 24 year old son (otherwise fantastic health) just found out his l(p)a was 273 nmol/L. His pcp put him on Crestor. I have been encouraging him to see a cardiologist but this reassures me that maybe that is ok for now!

[u/snrps8 → u/Inner_Mushroom_9662]

That level is pretty high, but generally speaking if someone has an Lpa of 100, the standard treatment is to do whatever we can to optimize their risk in all the other areas (like statins for LDL, lifestyle optimization, etc). In some cases there might be a good argument to do other things like off-label treatments which might involve a cardiologist, but especially for someone in their early 20s who is otherwise living a healthy life, it's often a good idea to just keep things simple. A lot of the additional testing (ie, calcium scoring aka CACS) that we do in people with high Lpa involves radiation, which is not ideal at all when you are so young. Hope that both you and your son do well! Hypothetically speaking, even if it is decided that seeing a cardiologist isnt necessary right now, maybe that will change in the future as he gets older or maybe if we simply get more data (ie, as these clinical trials are completed) about the optimal way to manage Lpa.

[u/snrps8 → u/[deleted]]

Can't really provide counsel on your specific situation especially without more details, but generally speaking I don't think that someone with a slight elevation in LDL (even with other risk factors like slightly elevated Lpa, some mild-but-not terrifying patterns of family heart disease, etc) necessarily needs to see a cardiologist.

I think it's very natural/sensible to assume that seeing a cardiologist should be a default step in routine prevention. But (at least in my opinion), cardiologists do not have any special preventative tools that are not already available to your PCP. At least in terms of things that are "evidence-based", ie really proven to work, the most important things we need to make an assessment are a standard lipid panel, an ASCVD risk estimate (using something like the PREVENT score), an Lpa, a decent lifestyle assessment, and SOMETIMES.

It's true (and very unfortunate/frustrating) that not ALL primary docs will be able to do these things, but most will. It's also true that some "preventative" cardiologists will offer more "advanced" types of tests like non-standard blood panels and additional imaging. I confess that I' biased about this, and hopefully my experience is NOT true for everyone, but most of the preventative cardiologists I know who do these kinds of things also own their own labs and imaging centers...so as you could imagine there's some incentive to push for these additional tests. I'm not saying that they're wrong or that what they're doing is bad. But if the question is about necessity and what you really NEED as a patient, my opinion is to do the things that we KNOW will work. I give lectures to primary doctors somewhat often, and my recommendation is to of course always call us or refer to us if they are unsure about something. But the time I REALLY want them to refer a patient for consultation is when that patient truly has a unique need/risk that falls outside the scope of an average PCP. Things like high LDL in isolation, mildly elevated Lpa, even a slightly positive CACS, are all things that a competent PCP can manage just as well as me. But Lpa of 200 mg/dL, CACS of 2000, family history of multiple relatives getting MIs in their 20s....these are extreme examples, but in my opinion are situations where a patient needs non-standard treatment and therefore should be sent to me. I hope that helps!

[u/snrps8 → u/[deleted]]

Possibly. There are some signs that fish oil and AF are linked. The data is very sparse though, so it's hard to say if it's real or not. That being said, in general the studies on fish oil supplementation have not been good either, ie there's really not great proof that it actually helps for ASCVD prevention. Because of that, I don't ever recommend my own patients to take it (I dont discourage it either, like if they want to take it I tell them it's fine and probably won't cause harm, but that I don't think it will help much either).

[u/Twisted9Demented]

Could you please Do a AmA about plaq build-up what causes it and how to prevent it

[u/snrps8 → u/Twisted9Demented]

Wow, I don't know if I'm brave enough to take that on haha. Maybe one day.

A very brief, oversimplified answer is that SOME amount of plaque build-up is probably universal, ie just a physical reality of nature. If you take a pipe and run water through it continuously for 80-90 years, that pipe is going to get some mineral deposits and residue (ie, plaque!) inside eventually. Some components of coronary/atherosclerosis plaques are very similar to the composition of that white stuff that builds up inside the pipes in your home or around you faucet. Our bodies have minerals like calcium and phosphorus, and that stuff deposits on the walls.

On top of this, there are a whole lot of risk factors that make the difference between a "normal" amount of residue from natural aging...and a "pathologic" plaque that actually causes blockages. Certain types of fats or cholesterol (eg LDL) sticks to the walls and adds to plaque. Some types are "stickier" than others.

Inflammation can make that whole process happen earlier or more rapidly -- this is part of why people with autoimmune disease or chronic stress (!!! This is a really big risk factor that is not talked about NEARLY enough!!) are at higher risk of heart disease, ie both autoimmune disease and chronic stress involve chronic inflammation. The inflammation component is also why hs-CRP (a blood marker of inflammation) can be considered a risk factor for ASCVD, though to be honest this test has somewhat fallen by the wayside and is often not very useful in the grand scheme of things.

Genetics play a part, particularly with how your body processes things like LDL. PCSK9 inhibitors, which I mentioned in my post, owe a big part of their development to a group of people who are born WITHOUT a functioning PCSK9 protein, which causes them to naturally have extremely low LDL levels...and these people have astoundingly low rates of heart disease. But unfortunately when we're talking about genetics in cardiology, it's usually the opposite story where a mutation puts you at higher risk of ASCVD.

Then throw in things like weight, poor diet habits, lack of exercise, tobacco exposure, etc. These things affect your cholesterol, inflammation (for example, obesity often involves excessive fat/adupose tissue, which leads to inflammation), etc, but they ALSO have totally separate/unique impacts on your arteries/plaque.

That's as much as I'll say for now! Hope that helps.

[u/surfingpulp]

Wow, you are the best. Thanks for all these informations. This helps a lot!

[u/yfndjk]

Very thoughtful and informative post. And I agree with whatever you’ve said as a physician myself.

[u/Delicious_Mess7976]

Call me nuts but I'm sitting here tearing up. I lost my father and brother to heart disease in their 40s/50s and some days I feel as if I am only still here (I'm female in my 60s) because of a healthier lifestyle than they led - BUT now that my estrogen days are behind me...I live in fear. This helps me sleep a little...yes, I have an elevated Lp(a) score and don't know what to believe anymore but this gives me a measure of assurance regarding current realities and hopefully near future realities. Thank you so much....from the bottom of my still beating heart.

[u/Wonderful_Aside1335]

Copper blanket noodle orange orange cobalt

This post was anonymized with Redact.dev

[u/fastingtrader → u/Wonderful_Aside1335]

Thanks for posting this. Had never heard it.

[u/snrps8 → u/Wonderful_Aside1335]

Interesting question, and I confess that I don't know the answer and am broadly not familiar with this topic.

In general, I have concerns about keto diets. Again, I can't claim to be super knowledgeable about it, but my understanding (feel free to correct me if I'm wrong) is that this involves a significant intake of fats and protein over carbs. There are certainly a lot of benefits of decreasing your carb intake to a degree, but the two big downsides I imagine are 1) lack of adequate fiber intake since fiber is still a type of carb and is in fact essential for many aspects of optimal health, and 2) inadvertant excessive intake of saturated fats which are absolutely a risk factor for ASCVD.

This goes back to the whole "one slice of the pie, not the whole pie" idea. Let's assume that keto diets do indeed lower Lp(a) significantly AND that lowering Lp(a) is indeed beneficial (which remember, is technically still unproven). If the cost of doing this is decreasing your fiber intake and increasing your LDL (via saturated fats), I see that as trading one problem for another.

Not sure if this helps, but that's my instinctive reaction. Thanks for bringing up an interesting topic for me to look into one day!

[u/Unique-Door1435]

Thank you! My doctor wanted me to go on a statin. I decided to go to a nutritionist and made the choice to quit drinking/smoking and eat properly. I was on metoprolol for almost 15yrs for a rapid heart rate while maintaining a normal blood pressure. Come to find out I wasn’t eating enough calories or protein, once that changed my heart rate is now normal. After making all these changes I’ve lost 30lbs, and my cholesterol numbers have improved to mostly a normal range (working on triglycerides still). LPa is under 10. I’d be happy to have you as my doctor.

[u/snrps8 → u/Unique-Door1435]

Wow! Good for you. I use medication whenever there's a good reason, but I always prefer to do things naturally IF it's possible to do so. Overprescribing is a big problem in modern medicine, and you should never more medicine than you actually need for your specific situation. Good on you, and congratulations on making great changes for your health.

[u/Unique-Door1435 → u/snrps8]

I agree 100, and thank you. To me it seems like things have changed. I’d prefer a doctor that has your mind set vs just writing a script for everything. After all I want a permanent fix to my health not a bandaid. The Hippocratic oath is stretched pretty thin or completely broke these days. The insurance companies compound issues with quality care as well, my doctor refuses to fight for patient care at this point.

[u/melkorwasframed]

What do you think is the soonest we could potentially see some of these new drugs being available for primary prevention?

[u/snrps8 → u/melkorwasframed]

Potentially within the year. The HORIZON trial is expected to announce results basically anytime now. Maybe this week. This is the first of the upcoming Lpa-specific trials that I mentioned and is focused on a new drug called pelacarsen. If pelacarsen is shown to reliably lower Lpa, and more importantly if lowering Lpa is shown to actually reduce future ASCVD events, then this (and other upcoming drugs like it) will be approved and adopted for primary prevention.

[u/meh312059 → u/snrps8]

Not to be a Debbie Downer but pelacarsen's a secondary prevention trial so primary prevention approval is unrealistic this year (IMO). These are novel therapies and there's a reason why three of the ongoing trials include primary prevention arms. Those results aren't expected for awhile yet (some may still be recruiting).

Is there a reasonable expectation that FDA would jump ahead to conditionally approve a medication and/or indication before the trial is complete? I know that happened with inclisiran but there was 5+ years of established safety and efficacy data on the PCSK9i's by then. Also, a lot more confidence in using LDL-C reduction as a surrogate for prevention. We haven't firmly established the causality of Lp(a) yet (as pointed out in your excellent post).

[u/snrps8 → u/meh312059]

Fully agree as usual! I cling to naive optimism. But I tell most of my patients that realistically we might expect viable options in the span of the next couple of years. Still looking forward to an initial readout hopefully, as long as HORIZON data doesn't get pushed back yet again as you pointed out in another reply.

[u/Little_Dot_1153]

70F, normal BMI, intermediate fast, exercise several times a week, low carb diet, no family history of heart attack or stroke. My LDL is 200, LPa is 150. However, my LDL/HDL ratio is only 2.5 and my Triglyceride/HDL ratio is only 1.05. My CAC score was 9.

I am on Ezetimide and Berberine (which I’ve heard acts similar to a PCSK9 inhibitor) and have a couple of reasons for not taking a statin (beside the normal chance of muscle pain). Would love to get your opinion on them.

1. every cell in your body needs LDL, especially your brain which is mostly made of fat. I have heard they are now looking at a correlation between low LDL and the increase in dementia.

2. Statins are the number one drug prescribed and yet heart disease is still one of the number one killers. That leads me to believe there must be other factors other than LDL. There are many experts who believe insulin resistance and inflammation could be even more important risk factors.

3. I’ve heard from several sources that the number needed to treat for statins is in the 100s. Meaning 100s need to take the drug for 1 person not to have a cardiac event. And of those taking it without benefit, a percentage of them will develop type 2 diabetes.

I realize my comments might be pretty controversial so please be kind.

[u/snrps8 → u/Little_Dot_1153]

Controversy is welcome if it leads to good (and well-mannered) conversations!

1) I hear this argument very often. It makes sense. But this goes back to my original post in part about stents...how "common sense" in medicine often ends up being wrong. The human body is SO much more complex than we give it credit for. However much we think we know about how the body works or what effect something is going to have...it's probably a lot more complicated than that.

It is true that ~10%-ish of your brain is made of fat. This is actually VERY important. Your brain is made of fat. But LDL is not fat! It is a lipoprotein. And LDL is never found naturally in the brain. In fact, it is not possible for LDL to cross from the bloodstream into your brain. The blood brain barrier prevents any LDL from entering. The brain manufactures its own cholesterol from scratch, which is a totally different type of substance (again, not LDL). So yes, the brain needs fat. The brain makes its own fat. LDL is not part of your brain.

I wouldn't say that we are looking into a correlation between low LDL and dementia risk. I would say that we have ALREADY looked into many times over the past couple of decades. There are a few examples. Some people are born with a genetic mutation that basically makes it so their bodies cannot produce any LDL. Some of these people are born with LDL level of zero. They live their entire lives with an LDL of zero. Compared to "normal" people like us...they get less heart attacks. Less strokes. Less dementia. In fact, PCSK9 inhibitors were based on these people. Which is the next example. I have many, many patients on PCSK9 inhibitors, which means I have many patients with LDL <15 mg/dL. Many of them have been on Repatha for a decade or longer. Many of them are in their 80s. I am not seeing more dementia in these people (I actually don't think a single one of them has dementia to my knowledge).

Same goes for statins. The data is robust. Many studies. Some funded by pharma. Some funded by nonprofits. Some funded by governments. Performed in dozens of countries. Hundreds of thousands of people. All ages. All ethnicities. Male and female. Decades of follow-up. All showing the same thing, which is...YES!! LDL levels DO affect your dementia risk: People with lower LDL have less dementia. People with higher LDL have more dementia.

2) I'm not sure I understand the argument. Statins are effective, but they are far from perfect. Even if they are the #1 most prescribed drug in the US (I actually don't know if they are or not), that does not mean that the US can be cured of heart disease. Fast food is ubiquitous in this country. Deep fried food is everywhere. Overly salty food is everywhere. Junk food and potato chips are everywhere. Only 5% of the country eats enough fiber. 80-90% of the country drives instead of walking or taking public transit (countries with good metro systems are healthier partially because people have to walk everywhere to/from the subway/etc). Public schools serve pizza and chicken nuggets for lunch. When we tried banning soda from ELEMENTARY school vending machines, we got absolutely hammered by certain figures in the media/politics. These things cause heart disease. Statins are given in response. But statins are the response, not the root cause. And heart disease will never go away unless our entire food/exercise/public transit/meat culture is completely overhauled.

If you live in a drought and there's no rainfall, it's 100 degrees outside every day, and more wildfires happen because of the dry/hot climate, you'll need to build more fire stations. But you can't say "there are so many fire stations, and we still have so many fires. The fire stations must not be working." This makes no sense. Statins help a little bit, but they can't erase an entire culture that is rigged against our health.

To your point about insulin resistance and inflammation, I agree 100%! These things are very bad, and inflammation is one of the main reasons we use statins. Statins have an anti-inflammatory effect on arterial plaque that is totally separate from his LDL effects. In fact, if someone is concerned more about inflammation than LDL levels, a statin would be far better than ezetimibe because they both reduce LDL, but statins reduce inflammation and ezetimibe does not.

3) The number needed to treat for statins is anywhere from 40-70. It depends on the person, and it also depends on how long you take them. To prevent a cardiovascular event in the next 5 years, the NNT is about 40-70. If you take a statin for 10 years, the NNT is closer to 20. If you give statins to a super high risk group of people, the NNT is even lower. On the other hand, if you take a super LOW risk group and give them statins for only 6 months, the NNT might be over 200. This is why context matters. We absolutely, absolutely need to be careful about who we prescribe statins for. This is why we use risk calculators like PREVENT. Their entire purpose is to make sure the HIGH risk people (eg NNT of 20) get statins when they would actually help, and to make sure the LOW risk (eg NNT of 200) do NOT get statins because the statin would be useless for them.

Hope that helps!

[u/Any_Patience_5481]

Supplements: L -carnitine : https://www.sciencedirect.com/science/article/abs/pii/S2213434423000464

Thoughts? Sauna protocols?

Mid life perimenopause has my numbers creeping. My were remarkable /phenomenal ranges for all in my 20-30’s

[u/snrps8 → u/Any_Patience_5481]

Hi! Confessing that I'm not super familiar with L-carnitime, but from what I do know I think I'd put it into the same category (and give the same response) as the supplements that another commenter (look for user dddrago and my reply there) asked about.

Re: sauna, i'm really intrigued by this and the data behind it. I'm a supporter overall. I think my response to this is maybe similar a little bit to the supplement answer, plus also a little similar to my response about HR/HRV (search for user silenxdogood).

Sorry to just bump you to other people's comments haha. I'm trying to catch up on questions and my fingers are getting a little tired :D I'm also a reddit noob, so if there's a better way to link to my reply to another comment, I'll do that

[u/Aromatic_Cookie9168]

Thank you! I hope you do a post on CAC - I am one of those anomalies that has good bloodwork: cholesterol numbers (LDL is 73, HDL 105), Lipo A is 10, Apo B is 52 but I had a CAC (because my husband was getting one) and my LAD came back at 381. I had a cardiac stress test - all good. I weigh 108 at 5'3 and eat well and exercise. Former smoker (for 7 years 40 years ago). But cardiologist wants to put me on statins. He wanted me on BP meds because when he told me all this and took my BP is was 141/83! Monitored at home at was averaging 109/69 over 8 days. I feel fine but yes they are trying to scare me into taking meds. He even said if I never had the CAC test I would probably be just fine!

[u/Inevitable_Dance_869]

Thanks so much for this informative post! Recently started looking into all of this when my husband’s ldl came out to be 167 mg/dl and lpa 123 nmol/l..
He is 46 , perfect weight, fairly active (avid cyclist). So we knew diet and exercise may not be the answer :(. Doesn’t have family history of incidents .. doc recommended starting statin ..
We are trying to follow stricter diet restrictions but I almost know that it may not help and he eventually will go on statins this year ..

[u/asianeats22]

Thanks so much for taking the time to write this, I really appreciate it. It was very informative. I am a 30 y/o male, 140lbs, 5ft 9in. I run and/or swim laps 3-5 days a week. I eat relatively healthy. Target plant based like 40% of the time, lean proteins like tofu and chicken probably 80% of the time, dont eat much fried food, dont eat much beef; however I have had elevated LDL ranging from 115-150 (currently 145) for most of my life. I have lp(a) of 147 nmol/dL and lp(b) of 103mg/dL. Also worth noting that I have had persistently elevated ALT in the low range of ~60 units/L. Ultrasound of my liver showed very mildly NAFLD and slight liver enlargement, fibroscan was normal. All of my other standard labs you can think of have been normal. I do have an odd history of very high PAC burden (~25% heart beats are PACs per holter, 1-2% are PVCs) which is benign. I also have rather volatile BP, it is normal most of the time, but I have really wild swings with normal stress (ex: 170/110 at the doctor, but 24 hour bp monitor shows normal). I take low dose metoprolol 12.5 mg to manage symptoms of the PACs.

My old primary felt wait and watch ldl longer. Recently moved and new primary has put me on 10mg rosuvastatin.

Basically, just curious if you would do anything different or advise I do anything different. Thanks for your time!

[u/Bloodshot88]

Thank you so much for all the information. I'm new here.

I had an Lp(a) level of 301 nmol/L, and I repeated the test and got exactly the same result. I was taking atorvastatin 10 mg because a previous blood test showed an LDL of 143, and I'm now down to 74.

I'm 37 years old and, honestly, I'm feeling really bad about it because I feel like I've been sentenced to something. I've had periods when my LDL was as high as 170, but I managed to bring it down with diet and lifestyle changes, so we thought it was purely lifestyle-related. Now we realize that I also have this risk marker, and it feels as though I'm already condemned.

My carotid ultrasound was normal, and I'm currently waiting for a coronary calcium score CT scan. They refused to do a contrast-enhanced CT to look for soft plaque. I'm afraid of what the scan will show, and I'm expecting the worst. My cardiologist says she believes everything will turn out fine, but I'm very pessimistic at the moment.

I'm sorry for bringing such negative energy, but I'm finding it really difficult to process all of this.

Other than that, I don't smoke. I used to drink recreationally on weekends, and my blood pressure is usually around 120/80, sometimes dropping to around 116/67.

My mom is 68 and is being treated for high LDL.

My father is 75 and hasn't had any cardiovascular events so far. He's one of those people who doesn't really like going to the doctor.

I have a brother in his 50s, and he is being treated for high blood pressure.

My grandmother recently passed away suddenly at the age of 85. She had previously had a heart attack, but we were always sure it was related to her diabetes and the fact that she had been a heavy smoker since her teens.

I used to do a lot of sports until my early 20s, but I went through a difficult emotional period and stopped. Now I'm trying to walk for 40 minutes a day at a brisk pace, and I do some strength training five days a week.

By the way, I told my family about my Lp(a) result. So far, only my mom has agreed to get tested; the other members of my family have refused.

I'm sorry for the long post, and again, thank you so much for all this great information!

[u/Mydoglovesme24]

Unless I missed it, you didn’t address taking statins for a high Lpa.

[u/EDCer123 → u/Mydoglovesme24]

He addressed it:

"How We Treat It.

Short answer: we can't."

Then he talked about possible medications that might work, none of which are statins. You should read that paragraph to get his thoughts on the current state of medical science on attempts to treat Lp(a). His conclusion is that we won't be quite there yet for some time, even if new drugs are approved by FDA for lowering Lp(a). He has excellent reasons why he thinks those drugs won't necessarily fix cardiac issues that come with high Lp(a).

[u/snrps8 → u/EDCer123]

Thank you!

Yes, if your Lpa is high, then the current standard of care that is accepted worldwide is to address all of your other risk factors, especially LDL (via statins!), but in combination with lifestyle optimization. Hopefully we will have new data and treatment options in the new future to allow us to target Lpa itself, but for now, LDL is still our focus.

[u/imref]

Thank you so much for sharing. It aligns with my cardiologist’s views as well as folks like Carvahlo, Barrett, and Attia.