Saúde Cardiovascular

[AnUser]

@dicarlo2

ApoB < 50 would eliminate the vast majority of MI (92.5% - 98.5%). Maintaining endothelial function likely a large remainder.

I haven’t verified this but do you agree then it was pretty much correct to label CVD as ASCVD (I used them interchangeably)? The apoB post is a wiki so you can edit it. With so much misinformation it helps to simplify things, of course it’s a given to optimize other things as well.

[dicarlo2]

Yes. Eg this is technically correct any way you look at it

ApoB is the Rate-Limiting Step in prevention of cardiovascular disease

To be frank, the only reason I’m even somewhat aware of these other kinds of heart disease (prior to looking into it just now) is because my wife’s family has a genetic heart defect that has to be repaired at some point in their life if they have the genes for it, and my family history includes CMD. For most people, CVD = ASCVD, and worrying about the cases that are not is probably not worth most people’s time. And if it is, they’ll either know based on their family history, or never know because there really isn’t good screening (or prevention) for any of the other causes, aside from what people should be doing anyways - controlling BP and maintaining endothelial function.

[AnUser]

@dicarlo2

Yes. Eg this is technically correct any way you look at it

I’m unsure if HBP can cause stroke without significant plaque though, for example, but it’s important to reduce e.g risk of dementia and CKD anyway. Heart failure, and ATTR amyloidosis (25%+ at 70-80+), isn’t covered either, nor AF causing stroke. So the correct term is atherosclerotic cardiovascular disease, but which are most cases of cardiovascular disease it seems anyway. I didn’t know about ATTR when I wrote that post, but it might be much more significant in later ages (90-100+).

[Davin8r]

I’d add Lp(a) to ApoB when it comes to screening, since high Lp(a) causes plaques even when overall ApoB is low, since Lp(a) is so disproportionately atherogenic.

[Paul]

There is a lot of back and forth on the lipid hypothesis. So I decided to input all relevant data into Grok3 and see what it said. These are all the factors it considered:
age
BP
lipids APoA, ApoB, Lp(a), LDL, TC, HDL
insulin
waist to height
BMI
activity level
altitude ( I live at 6400’ - very important)
VO2 max and other fitness parameters like grip strength
CAC
CIMT
inflammation markers
medications
supplements
It spit out a long analysis based on these multiple factors which I doubt even Dr Dayspring could do a regression on and recommended against statins.
Recommendation: Skip statins unless you want maximal LDL-C reduction. Your VO2 max 50 and low-carb lean phenotype keep you in a sweet spot—CAC 108 isn’t a ticking bomb, and risk is <3-5%. The LMHR-MiHeart match reinforces this: LDL-C 149 isn’t your enemy here.
I think that this is the future of medicine

[DeStrider]

Just be aware that the AI may be hallucinating. I’d go with Bempedoic Acid and Ezetemibe with your CAC and LDL. However, we all have our own preferences. Either way, I wish you a long and healthy life!

[AnUser]

It depends on your prompt, if you ask it to reduce your risk of MACE over 10, or 20 year period, or longer and consider and prioritize correctly causal factors, and independent risk factors, it might answer differently. Best practice is to work on creating the prompt with it that you’ll feed it back to it + your data and when it should reason and about what + search. The prompt can be really long and detailed.

[AnUser]

MACE can put someone in the retirement home and end healthspan. Independent + causal risk factors is important for this and to weigh factors correctly. Time period is also important (is it 10, 20, 30 year risk, or longer?).

[RapAdmin]

@Paul

So I decided to input all relevant data into Grok3

You might also try ChatGPT Research AI version. Please let us know if you see much variance in the recommendations.

[relaxedmeatball]

@AnUser

Isn’t it correct that the aspects don’t matter if apoB is controlled early enough (you say this later in your post), I’ve written about this here concluding that it’s the rate limiting step in cardiovascular disease.

I believe this is true, as far as ASCVD goes. This is the analogy of somebody being tied down to the train tracks and simply getting them off the tracks extends their life. It seems to be simple enough that of you bottom out ApoB (and others like Lp(a)) then you basically won’t develop ASCVD in your expected lifetime.

However, other variables like inflammation, blood pressure etc matter for overall cardiovascular health. For example, high blood pressure alone can cause ventricular wall thickening etc. Infections can cause myocarditis. There’s plenty of CVD outside of ASCVD. But you’re right - I think confusing comes from the fact that atherosclerosis is so common and predominant that ASCVD becomes equated with all CVD.

@Paul

There is a lot of back and forth on the lipid hypothesis.

There honestly isn’t. The science is pretty damn settled, particularly at the population level. What makes a difference is the individual level. Some people, for whatever reason, are very resistant to atherosclerosis. They can have mega high LDL-C/Apo-B and zero atherosclerosis. And some people can generate plaque with LDL-C of 70, which is below most current therapeutic targets. However, the overall science of how lipids are involved in atherosclerosis is not really subject to back and forth - it gets more solidified each year.

I remember in your case that you are 70-something, have high LDL, but a relatively low calcium score for your age, plus a healthy lifestyle. So in your specific case there is less argument in favour of statins, since you seem to not accumulate much plaque. However, there are users here in their 40s with positive calcium scores, and they’re hopefully expecting to live another 40, 50 or 60 years. For them, statins (or BA, PCSK9i, Ezetimibe etc) should be a no-brainer.

In your case, if I were you, I’d still look to bring down that LDL-C level through some easily-available pharmacology. A CAC of 108 is not zero, and CAC only tells us about advanced disease. ASCVD is responsible for ~50% of all deaths, and you already have it to some extent. Thus, I’d look to minimizing that risk as much as possible, since you’re presumably hoping to be alive 20 years from now.

[AnUser]

@relaxedmeatball what do you think about ATTR prevention in the scenario of already preventative treatment (e.g preventing atherosclerosis with low apoB, optimal BP, obesity, T2D, avoiding CKD, etc)? I found only one study that 70% of supercentenarians die from it, and prevalence is 25% for those 80+ or so. If a graph is drawn from that age to 110+ it seems quite prevalent with time. Seems possible to stop the misfolding with e.g drugs and maybe this will make a lot more people live to 80, 90, 100, etc, especially if already doing a lot of other things right. But I don’t know much about it. One drug seemed to have low side effects.

Most Supercentenarians Die From ATTR Accumulation, How to Prevent

There’s multiple FDA approved drugs available today to prevent an age-related disease that most supercentenarians (110+) succumb to, approx 70%, and that’s misfolded protein accumulation of transthyretin (TTR), called wild-type TTR amyloidosis or ATTR. The rates of ATTR accumulation in elderly seems to be around 25% for 80+. It’s a protein that transports thyroid hormones and retinol. Every protein sequence is folded into its structure which creates its physical function in the body, for some reason with aging TTR protein can be misfolded, and thus not function and get stuck in the body. In organs like the heart, kidney, etc, and cause conditions like heart failure, and increase total death. The rates of the wild-type ATTR on autopsy in elderly at ~25%, and 70% death of supercentenarians, along with what appears to be relatively safe preventative treatment that decreases misfolding is the most bullish case for me. The accumulation seems to cause multiple diseases as well. Prevalenc…

[relaxedmeatball]

I’m sorry I don’t know enough about it say anything with confidence. But I have two colleagues who are cardiologists, and I’ll ask them and try to get back to you. Next March I’ll be at an aging/neuroscience conference so I’ll ask around there too.

[Paul]

Did this per your suggestion - no difference in recommendation

[Paul]

The science is pretty damn settled, particularly at the population level. What makes a difference is the individual level.
This is the key. My reading of the science is that all (except perhaps the LMHR study) studies of statins have cohorts of metabolically unhealthy subjects.
I happen to be quite fit for a 72 yo and metabolically healthy - based on various functional metrics have the biological age of a 35 yo and live at high altitude to boot. BP 104/68, BMI 18, VO2 max 50, insulin of 3, ESR of 2. I also take tadalfil at low dose, 3 gms of omega 3 and 10,000 fu of natto which help.
Statin kill me - tried a 20 mg dose for 10 days earlier this year and knocked my fitness score off 30% (I have a Carol bike which measures this)

Honestly, every physician has a bias based on “standard of care”. I find these latest AI’s to be the best Dr I have ever visited

[desertshores]

@Paul

I find these latest AI’s to be the best Dr I have ever visited

I find the medical AI’s to be smarter than my doctor. They are certainly useful as a second opinion. One place they are useful is determining which is the best medication.

My medications are based on AI suggestions, which I then talked over with my doctor and got the suggested medication.

One example was replacing losartan with telemisartan. My doctor readily agreed it was the better choice. I didn’t pursue the question, “Then why the hell did you prescribe losartan instead of telelmisartan in the first place?”

[DrFraser]

There are incredible time pressures due to the corporate overlay and metrics. They have 10-15 minutes for an appointment, including their documentation time. It has to be a quick and focused time and initiating a change in medication requires the mental energy and knowledge, along with having the time to explain why a change is sensible.

I see a lot of people on medications that have just been continued, and no one actually looks at them and makes changes as new options are available or more data comes forward.

When I review patients we go through this and make recommendations for changes. Many people have been on the same medication for 20 years. It is unlikely that something given 20 years ago is still (or ever was) the best choice.

But doing this and starting to take a comprehensive approach to healthcare takes at least 45 minutes in review and charting, plus 60-90 minutes in a visit. Even then, we have things to revisit and dive into more detail on. In that same time, there would have been 8-9 visits in standard primary care.

Considering all this, it’s not unexpected that patients need to research and be pro-active, because the system is reactionary, not pro-active, and goals for “normal” not “optimal.” The average patient I see for a heart attack had “normal” blood work the day before. Anyone who assures their patients that everything is good by basic blood work (and many doctors do) is not taking a scientific approach.

[tdecicco7]

I so wish you were available via telemedicine to people in New York. But I know NY has vast red tape making it close to impossible. I have to move to another state some day.

[AnUser]

Intermediate-risk participants with CAC score greater than 0 and less than 400 were randomized to usual or CAC score–informed care (which included 40 mg of atorvastatin). The CAC score–informed group showed a sustained reduction in total and low-density lipoprotein cholesterol and less progression of total, noncalcified, and fibrofatty and necrotic core plaque volumes at 3 years. The association of CAC score guidance with these plaque volume changes was independent of baseline plaque volume and risk factors.

Effects of Combining Coronary Calcium Score With Treatment on Plaque Progression in Familial Coronary Artery Disease A Randomized Clinical Trial 2025

[relaxedmeatball]

This is interesting, and seems to be more of a psychology study rather than a biological study.

I interpret this as: showing patients (and their doctors) a positive CAC score scares the crap out of them and they actually take their medication and care about their health more.

[hamtaro]

@Paul

Honestly, every physician has a bias based on “standard of care”. I find these latest AI’s to be the best Dr I have ever visited

Agreed. The frontier LLMs, especially with the search/research capability are so powerful. Just in the last month, they have gotten so much better.