| ▲ | bonsai_spool 2 hours ago |
| 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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| ▲ | abeppu 2 hours ago | parent | next [-] |
| > 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. |
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| ▲ | bonsai_spool an hour ago | parent [-] | | 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)."
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| ▲ | carbocation 33 minutes ago | parent [-] | | I'm very confused about why they are showing an AUC for the relationship of a continuous score with a continuous phenotype. |
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| ▲ | gavinray an hour ago | parent | prev [-] |
| > 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)"
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| ▲ | bonsai_spool 23 minutes ago | parent | next [-] | | > 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. | |
| ▲ | brandonb an hour ago | parent | prev | next [-] | | 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 an hour ago | parent [-] | | 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. |
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| ▲ | an hour ago | parent | prev [-] | | [deleted] |
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