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
> 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.
bonsai_spool 2 hours ago [-]
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)."
happyPersonR 12 minutes ago [-]
Do you know if they found a “safe” bmi? Like is it 25-30 ? Or
carbocation 1 hours ago [-]
I'm very confused about why they are showing an AUC for the relationship of a continuous score with a continuous phenotype.
gavinray 2 hours ago [-]
> 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:
> "The frequency of atherosclerotic plaque in the coronary arteries in 367 patients with zero CS was 9.3% (34 individuals)"
bonsai_spool 53 minutes ago [-]
> 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.
kurthr 18 minutes ago [-]
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.
brandonb 1 hours ago [-]
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?
gavinray 1 hours ago [-]
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.
AnimalMuppet 30 minutes ago [-]
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.
1 hours ago [-]
throw20261022 2 hours ago [-]
> Crucially, no routine blood biomarker, lipid metric, or clinical risk score could identify these individuals with inflamed coronary arteries.
I call bs on this. There are two common blood tests that are meant for it:
1) hs-CRP (High-sensitivity CRP)
2) Lp-PLA2: Lipoprotein-associated phospholipase A2 (Lp-PLA2), also known as platelet activating factor Acetylhydrolase, is an inflammatory enzyme that circulates bound mainly to low density lipoproteins and has been found to be localized and enriched in atherosclerotic plaques. In multiple clinical trials, Lp-PLA2 activity has been shown to be an independent predictor of coronary heart disease and stroke in the general population. Measurement of Lp-PLA2 may be used along with traditional cardiovascular risk factor measures for identifying individuals at higher risk of cardiovascular disease events.
I have routinely had both of these blood tests among others, although I paid myself to get them.
As for hs-CRP, it will likely show an elevation. If you use a binary classifier with a higher threshold of what's safe, e.g. 3.0 instead of 1.0, you will miss it! I am guessing this is why they missed it.
tredre3 2 hours ago [-]
> Importantly, routine bloodwork and clinical tools – including cholesterol markers (ApoB, non-HDL-C), blood sugar (HbA1c), systemic inflammation (hs-CRP), and a widely used cardiovascular risk calculator (AHA PREVENT-ASCVD) – showed no correlation with the presence of coronary inflammation and failed to identify which patients had inflamed arteries.
The article specifically says those tests didn't correlate with the result of the scans. Why do you call BS on it?
throw20261022 2 hours ago [-]
As for hs-CRP, I already explained the basis in my comment. It depends on whether they mean correlation in its strict literal sense or only after binary classification.
As for Lp-PLA2, they crucially seem to have ignored it altogether.
brandonb 2 hours ago [-]
This particular study looked at inflammation through imaging (CT scans) as part of Biograph's $17,500 program. You can get at the underlying signal fairly cheaply through a simple blood test (hs-CRP).
Importantly, routine bloodwork and clinical tools – including ... hs-CRP [among other tests] ... – showed no correlation with the presence of coronary inflammation and failed to identify which patients had inflamed arteries.
brandonb 2 hours ago [-]
This is one of the things that makes me a little skeptical of their score. If it's accurate, there should be a positive correlation with known biomarkers. (I see you made a similar observation elsewhere.)
In their paper they actually find an inverse correlation with hs-CRP, which disappeared when removing two patients who were sick. So I wonder if the sample size being small is partly driving this.
phoronixrly 2 hours ago [-]
Is this a positive thing? I read it as the AI results not correlating with test data...
Inflammation is likely a marker, but not the cause of heart failures.
That doesn't contradict it being an independent risk factor, but up to recently, it was assumed be causal driver.
brandonb 2 hours ago [-]
Same thing happened with the Lp(a) drugs recently. Practically speaking, statins reduce LDL cholesterol (~50% at the strongest dose) and hs-CRP (~37%) and have cardiovascular outcomes data, so that's likely the route a patient would go based on the medications that are approved today.
jp57 2 hours ago [-]
If all the other biomarkers of inflammation "showed no correlation with the presence of coronary inflammation" as predicted by this scan, then how exactly do they assess the positive predictive value of the scan?
esalman 3 hours ago [-]
Access to the study requires $17,500 per year, just fyi.
pixl97 3 hours ago [-]
That or OpenAI needs to turn back on their highly persistent model and we ask it about coronary inflammation.
anarticle 24 minutes ago [-]
I'm still surprised we don't have many physical interventions for this, knowing that it's a physical problem. I'm reminded of the older surgeon style medicine whose reputation seems to be pretty coarse now since we have so much knowledge about chemistry and non-invasive interventions.
Wonder what would happen if we pushed the envelope on physical fixes like endarterectomy like procedures and made them safer/more routine. Like getting your teeth flossed.
HPsquared 3 hours ago [-]
Before or after 2020?
1121redblackgo 37 minutes ago [-]
weak bait
Theodores 2 hours ago [-]
Recently I learned that only those with over-active immune systems survived the 14th century plagues. Therefore, inflammation is to be taken seriously, or at least understood in this historical context, depending on your ancestry.
As for the article, the findings come as no surprise given what we know about the risk factors in the post-smoking world. Nowadays nutrition, specifically saturated fats in combination with lots of sugar and salt, as found in today's artificial foods is showing up in the research (not paid for by 'big beef').
There is no need to over-think it, just stay off the corporate 'food' and cook from fresh ingredients, where you don't get 'HFSS' (UK government term for high fat/salt/sugar) held together with weird chemicals. Sure, nobody has time for that, but this is the frontier of public health, a.k.a. the 'obesity crisis', with a simple solution - actually bother to cook!
Rendered at 20:57:42 GMT+0000 (UTC) with Wasmer Edge.
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...
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.
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/
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.
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.
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.
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.
I call bs on this. There are two common blood tests that are meant for it:
1) hs-CRP (High-sensitivity CRP)
2) Lp-PLA2: Lipoprotein-associated phospholipase A2 (Lp-PLA2), also known as platelet activating factor Acetylhydrolase, is an inflammatory enzyme that circulates bound mainly to low density lipoproteins and has been found to be localized and enriched in atherosclerotic plaques. In multiple clinical trials, Lp-PLA2 activity has been shown to be an independent predictor of coronary heart disease and stroke in the general population. Measurement of Lp-PLA2 may be used along with traditional cardiovascular risk factor measures for identifying individuals at higher risk of cardiovascular disease events.
I have routinely had both of these blood tests among others, although I paid myself to get them.
As for hs-CRP, it will likely show an elevation. If you use a binary classifier with a higher threshold of what's safe, e.g. 3.0 instead of 1.0, you will miss it! I am guessing this is why they missed it.
The article specifically says those tests didn't correlate with the result of the scans. Why do you call BS on it?
As for Lp-PLA2, they crucially seem to have ignored it altogether.
It's fairly well-known that inflammation is an independent risk factor for heart disease, alongside LDL cholesterol (or ApoB) and blood pressure: https://www.empirical.health/blog/inflammation-and-heart-hea...
The American College of Cardiology looked at a bunch of inflammation biomarkers and standardized on hs-CRP: https://www.jacc.org/doi/10.1016/j.jacc.2025.08.047
Importantly, routine bloodwork and clinical tools – including ... hs-CRP [among other tests] ... – showed no correlation with the presence of coronary inflammation and failed to identify which patients had inflamed arteries.
In their paper they actually find an inverse correlation with hs-CRP, which disappeared when removing two patients who were sick. So I wonder if the sample size being small is partly driving this.
Inflammation is likely a marker, but not the cause of heart failures. That doesn't contradict it being an independent risk factor, but up to recently, it was assumed be causal driver.
Wonder what would happen if we pushed the envelope on physical fixes like endarterectomy like procedures and made them safer/more routine. Like getting your teeth flossed.
As for the article, the findings come as no surprise given what we know about the risk factors in the post-smoking world. Nowadays nutrition, specifically saturated fats in combination with lots of sugar and salt, as found in today's artificial foods is showing up in the research (not paid for by 'big beef').
There is no need to over-think it, just stay off the corporate 'food' and cook from fresh ingredients, where you don't get 'HFSS' (UK government term for high fat/salt/sugar) held together with weird chemicals. Sure, nobody has time for that, but this is the frontier of public health, a.k.a. the 'obesity crisis', with a simple solution - actually bother to cook!