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
> 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:
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.
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.
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.
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 think we all should know what our risk factors are and be monitoring cardiac health well before we get to the stage where we need stents. The idea that "wait until it clogs and then clear it" is the theory behind heart disease is a wild one to me, and that our mechanism for detecting it is "idk bro vibes based on how your exercise feels" is pretty open and subjective for my taste. Saving my pennies at the moment for a CCTA with cleerly at the moment.
This site was posted on HN a while ago and I think it's a very useful summary: https://myticker.com/
> 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)."
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.
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.
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.
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.
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.
> 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.
> 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?
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.
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?
No, the medRxiv preprint is linked at the bottom of the page. It is freely accessible.
Edit: I guess it depends on interpretation, the press release does start with "The study, available to clinically eligible Biograph Black tier members," which makes no sense to me. Maybe they mean enrolling as a patient in the study was only available to paying members? This would fit with the study population description in the preprint.
Side note every male in their 40s should go get on crestor to control their cholesterol. I didn’t because I was afraid of side effects. I finally started it and had no side effects. Wasted a decade. Control your blood pressure. Anxiety is a totally different thing when it pushes you into hypertensive crises ie stroke territory.
Edit specifically American men or anywhere where the common diet is similarly terrible
Yep, I did too. I'm 43, my cholesterol wasn't super high, but I figured, why not. Went to the cardiologist, he said "yeah, sure", did the blood tests, no side effects at all. My cholesterol now is what it was when I was 18.
It's the first thing that comes to mind. Note too that I'm not trying to draw a distinction between the illness and the treatment, only the time period.
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.
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!
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...
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/
> 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.
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.
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.
I think we all should know what our risk factors are and be monitoring cardiac health well before we get to the stage where we need stents. The idea that "wait until it clogs and then clear it" is the theory behind heart disease is a wild one to me, and that our mechanism for detecting it is "idk bro vibes based on how your exercise feels" is pretty open and subjective for my taste. Saving my pennies at the moment for a CCTA with cleerly at the moment.
This site was posted on HN a while ago and I think it's a very useful summary: https://myticker.com/
> 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.
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.
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).
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
From the article:
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.
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.
Is this a positive thing? I read it as the AI results not correlating with test data...
Maybe you didn't get then the latest news: https://www.tctmd.com/news/zeus-trial-ziltivekimab-fails-red...
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.
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.
> 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.
> 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?
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.
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?
My face lotion brags about being "scientifically tested" doesn't say if test was positive or negative
Access to the study requires $17,500 per year, just fyi.
No, the medRxiv preprint is linked at the bottom of the page. It is freely accessible.
Edit: I guess it depends on interpretation, the press release does start with "The study, available to clinically eligible Biograph Black tier members," which makes no sense to me. Maybe they mean enrolling as a patient in the study was only available to paying members? This would fit with the study population description in the preprint.
That or OpenAI needs to turn back on their highly persistent model and we ask it about coronary inflammation.
Side note every male in their 40s should go get on crestor to control their cholesterol. I didn’t because I was afraid of side effects. I finally started it and had no side effects. Wasted a decade. Control your blood pressure. Anxiety is a totally different thing when it pushes you into hypertensive crises ie stroke territory.
Edit specifically American men or anywhere where the common diet is similarly terrible
Yep, I did too. I'm 43, my cholesterol wasn't super high, but I figured, why not. Went to the cardiologist, he said "yeah, sure", did the blood tests, no side effects at all. My cholesterol now is what it was when I was 18.
Before or after 2020?
weak bait
It's the first thing that comes to mind. Note too that I'm not trying to draw a distinction between the illness and the treatment, only the time period.
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.
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!
> Recently I learned that
Doesn't mean that what you learned was true.
[dead]