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Comment by bonsai_spool | Hacker News Reader

I don't see how one can spin this into a positive finding - their preprint says that the only correlate they find with their new measurement is BMI. By my reading, not even male sex is associated with more inflammation. It sounds like they've identified a fancy BMI estimator, and not a very good one.

This is in asymptomatic patients, who already have a great estimator for 10-year heart disease mortality risk in the coronary calcium score which isn't even obliquely mentioned in their abstract. Edit: the paper shows no correlation with calcium, either

https://www.medrxiv.org/content/10.64898/2026.10.19.26364786...

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  > who already have a great estimator for 10-year heart disease mortality risk in the coronary calcium score

Heart attack at age 29 survivor here.

CAC scores only show calcified plaque, not vulnerable plaque, which is the sort likely to rupture and cause an event.

You can go get a scan and receive a CAC score of 0, walk away thinking you're perfectly healthy, and then die tomorrow because the scan couldn't detect the massive amounts of non-calcified plaque lining your arteries.

The only non-invasive way to measure vulnerable/soft plaque is via CCTA

See, for example, "Atherosclerotic Plaque in Patients with Zero Calcium Score at Coronary Computed Tomography Angiography"

It measured nearly 1 in 10 patients with a 0 CAC score as having vulnerable plaque:

https://pmc.ncbi.nlm.nih.gov/articles/PMC5967134/

  > "The frequency of atherosclerotic plaque in the coronary arteries in 367 patients with zero CS was 9.3% (34 individuals)"

I'm curious-did you have any traditional risk factors (LDL/ApoB, blood pressure, HbA1c, hs-CRP, high PREVENT or ASCVD score)? Or put another way, did you ever find an underlying cause as to why you had a heart attack at age 29?

Family has all the traditional cardiac symptom clusters (hypertension, elevated lipids/triglycerides, diabetes) and family history of heart attacks.

My biomarkers were good, but combined with family history and a past history of drug abuse (primarily stimulants), it's sort of a wonder it didn't happen sooner.

The MI itself was unusual. When they placed the stent in my heart, the coronary angiogram was able to image my arteries. I had almost no measurable stenosis in my arteries: a minor 30% in one inferior artery.

I was at the gym when it happened, the prevailing theory is that I had the one artery with vulnerable plaque and it ruptured from arterial pressure.

So on the one hand, it sucks that it happened at all. But on the other hand, I'll take "you didn't die and the rest of your heart looks clear" with no complaints.

I don’t have any of those. And I got a cac score of 103 at age 26

> Heart attack at age 29 survivor here.

There is no scoring system that is designed for people in this age range - and based on another of your comments, it sounds like you had a significant family history, which is, itself, a very strong predictor that would obviate the kind of screening tools that the article and my comments have focused on.

That said, we are beginning to split very fine hairs. The coronary artery calcium score is only recommended for people whose 10-year ASCVD scores are on the 5-20% range who are uncertain about initiating a statin. These people are not thought to be at risk of an imminent plaque rupture (if so, their ASCVD risk would have been improperly assessed. This is a possibility, but this possibility is not the basis of public health decision making).

If your coronary CTA is to be helpful as a screening tool it would essentially only be indicated for people in the 5-20% ASCVD risk pool who have 0 CAC where there is a sustained clinical suspicion of coronary disease. In such a patient, I would just advise starting statins instead of doing a contrast study.

edit - formatting

Actually, yes guidelines are actually that any prior statin prescription removes the need for CAC measurements. That includes those who are discovered to have statin intolerance, and thus requires out-of-pocket payment for any CAC.

I think the challenge here is that other than a CCTA there's no good way to estimate individual (as opposed to hereditary) ASCVD risk. Sure LDL, ApoB, Lp(a), and BP, are statistical proxies, but tell you little about the individual risk. CAC isn't much better, but if you've been taking EPA and VitK2 you have a much higher chance of more stable plaques, which are also more visible on CAC without much larger X-ray exposure and iodine contrast effects.

> Actually, yes guidelines are actually that any prior statin prescription removes the need for CAC measurements.

I mentioned that the CAC indication is for those in the 10-year ASCVD 5-20% risk band who are considering initiating a statin.

> I think the challenge here is that other than a CCTA there's no good way to estimate individual [...] risk

I'm not sure if you meant hereditary there, so I'll avoid the point.

Is this your area of medicine? I am not a specialist but I have never heard of cardiovascular risk stratification regarding primary prevention in the terms of impending risk to the individual except for NSTEMI patients getting a left-heart catheterization. So I would agree that CAC won't tell a patient when their MI will occur, but that's also true for CCTA and every other screening tool we have. They are designed to identify indviduals at high risk for more intensive preventive care.

Can Beta-Cyclodextrin treat (calcified) atherosclerotic plaques? And gout?

> What percentage of cardiovascular "plaque" is sugar alcohol and thus apparently treatable with β or α cyclodextrin, in controls and patients with conditions like Arteriosclerosis and Atherosclerosis?

"Cyclodextrin promotes atherosclerosis regression via macrophage reprogramming" (2016) https://www.science.org/doi/10.1126/scitranslmed.aad6100

Heart attack dodger here.

If you exercise, as you get older, you'll see a slow decline of performance over decades. Don't worry about that. But when you see a decline over a month, pay attention. That's often coronary arteries that are mostly blocked, blocked enough that your heart can't get enough blood under load, but not yet so blocked that you have a heart attack. When you see that, it's time for a cardiac stress test. (I mean look, if you experience crushing pain in your chest, don't ignore that either...)

Doing the above is how I wound up with two stents in my heart, without first having a heart attack. I learned from a friend's dad, who did have a heart attack.

> CAC scores only show calcified plaque, not vulnerable plaque, which is the sort likely to rupture and cause an event. > You can go get a scan and receive a CAC score of 0, walk away thinking you're perfectly healthy, and then die tomorrow because the scan couldn't detect the massive amounts of non-calcified plaque lining your arteries.

A lot of people promoting quack diets take advantage of this fact.

> Men demonstrated higher rates of elevated FAI-Score than women (52.8% vs. 25.8%, p=0.016; ≥90th percentile: 26.4% vs. 3.2%, p=0.007).

I am not saying this is good or interesting science (IIUC this should make us believe that fewer people with coronary inflammation go on to develop heart disease than we would have otherwise thought?) but their score is at least correlated with sex.

They went on to say that the only signal that survives multiple hypothesis correction was BMI, after reporting their nominal discovery of an association with sex.

    "Men demonstrated higher rates of elevated FAI-Score than women (52.8% vs.
    25.8%, p=0.016; ≥90th percentile: 26.4% vs. 3.2%, p=0.007). [...] Body mass
    index was the sole secondary correlate surviving false discovery rate
    correction (AUC = 0.71, p=0.001, all-test FDR q=0.028). Regularized
    multivariable models showed modest out-of-sample discrimination for FAI-Score
    elevation (cross-validated AUC = 0.71)."

I'm very confused about why they are showing an AUC for the relationship of a continuous score with a continuous phenotype.

Do you know if they found a “safe” bmi? Like is it 25-30 ? Or

My understanding is that for all cause mortality the "safe" BMI is in the 18-25 range with healthspan increasing the closer you are to a BMI of 18.

Even with a perfect BMI and looking totally fit, you can still be at very serious risk of plaque formation. Like people who have hereditary bad cholesterol issues (if it's bad cholesterol due to eating junk food a lot, typically you won't have a good BMI though).

My uncle had a stroke at 52 years old and stayed paralyzed for 15+ years, until his death. When my doctor learned that, the next day I started taking statins.

BTW I'm totally fit, no beer belly, excellent BMI and I look not a bit but much younger than my age (someone even commented that here on HN a few years when they saw a picture of me when I was 49 years old).

And yet I was seriously at risk of plaques detaching and clogging. Statins are not perfect medication but it is what it is.

My point being: even if you've got what science/doctors considers the best BMI in the world, you could still be at risk.

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