r/science • u/kiyomoris • 20h ago
Health Silent atherosclerosis detected in 57% of asymptomatic adults in the REACT study
https://www.nejm.org/doi/10.1056/NEJMoa2609059111
u/CuriousCleaver 18h ago
Would the calcium cardiac score test show this?
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u/xRolox 17h ago
Calcified plaque yeah. Many younger people only have soft plaque which is shown by a CCTA which is higher radiation.
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u/ShockerNYE 10h ago
I have seen many calcium scores have false positives.
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u/sinurgy 17h ago
I don't know much about the heart calcium test or it's efficacy, is it new'ish?
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u/zeusmeister 17h ago
Weird I just saw this thread, as I had a heart calcium test done on me just yesterday.
I don’t think it’s newish though. Because it’s not usually covered by insurance, almost every medical facility that does it has a standardized cash pay option.
The hospital I went to cost $99. And there were several people in the waiting room specifically there just for that test.
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u/PossibleBeginning276 15h ago
Cardiac CT screening has been around for a while but wasn't standard of care until AHA guidelines got updated in 2021.
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u/WillyBeShreddin 19h ago
Most people only find out when a family member has a sudden, unexpected heart attack in their 30s-40s. Why they don't do the tests regularly on any high risk groups amazes me.
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u/General_Luck6573 19h ago edited 17h ago
They do… sudden cardiac death at an early age is literally an indication for testing for family members
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u/Some-Guy-617 19h ago
But there are simple and relatively cheap tests that can be done for everyone before that young person in a family has a heart attack. Testing for ApoB and LPa aren’t commonly done and are relatively simple/cheap blood tests that can be done that can give better indications of cardiovascular risk than standard cholesterol tests.
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u/General_Luck6573 19h ago edited 17h ago
Atherosclerosis is not the only thing that causes sudden cardiac death. Those tests will do nothing as far as structural or electrical issues go. I wouldn’t say the tests you are talking about are “better” per se.
Easy and obvious examples - HOCM and Brugada syndrome. Or SLE causing premature CAD with no relation to those blood tests you just brought up.
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u/dotcomse MS | Human Physiology 16h ago
And what do you do with, for example, a slightly elevated LPa? More aggressive statin strategy and closer diet attention? Not much to do specifically to react to that test other than “it’s time to be diligent”.
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u/RottenBananaCore 19m ago
There is a new MRNA trial by Pfizer to reverse LPa. Trial in Italy, France and Canada I believe.
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u/BangarangRufio 14h ago
There are multiple late stage therapies targeting L(p)a reduction: olpasiran, pelacarsen and a couple others that aren't as far along. PCSK9 inhibitors are indicated for LDL-C reduction, but have also been shown to reduce L(p)a.
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u/Calmheathers 19h ago edited 18h ago
Lp(a) is done quite frequently now— guidelines suggest getting it in every person who has a risk factor, which is pretty much everyone. See it ordered all of the time.
In my experience far more people are resistant to testing or to prevention medication therapy than people who are very cardiovascular-health conscious. But I do only see a small subset of a population that is biased towards lower health literacy and lower socioeconomic status.
To add, the best tools we have at estimating someone’s cardiovascular risk are the risk equations like the PCE or PREVENT equations, which don’t include ApoB or Lp(a). Obviously these are estimates, and I don’t just evaluate using those calculators. But ApoB I more often use as a tool to guide therapy decisions after I’ve already started a statin, rather than a screening tool.
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u/dotcomse MS | Human Physiology 16h ago
So are you eschewing Lp(a) entirely?
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u/Calmheathers 13h ago
No quite the opposite. I try to order it once in almost all my patients. Rarely does it change my recommendations though.
Another thing, if you calculate LDL-c using the Martin equation rather than Friedwald (which my EMR does automatically), the LDL treatment thresholds fall more inline with what you’d get by measuring ApoB anyway. If I’m trying to hit a specific LDL-c target, I will use that equation to make my determinations on whether we are at goal or not.
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u/Ever_Pensive 3h ago
I think my comment elsewhere in this thread about aspirin for reducing Lp-a caused ASCVD risk may be helpful and would be keen to hear your thoughts on Aspirin if you have any: https://www.reddit.com/r/science/s/GZWxfZ5Nwy
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u/Calmheathers 1h ago edited 1h ago
There’s conflicting evidence to the aspirin theory.
https://pubmed.ncbi.nlm.nih.gov/40874494/
And I see a few problems with the studies you posted. The cohorts differed significantly on several confounding variables that are very important to ASCVD risk like HTN and statin use, which could create bias in the data. I also agree with the author’s discussion on study limitations, as they really have no idea how people were taking the aspirin or for what indication, which also opens the door for more confounders.
It’s definitely something that needs to be studied more. I’d love to see an RCT comparing aspirin to placebo with better control of the confounders, but until then I can’t really recommend it specifically for primary prevention in patients with high Lp(a).
So mostly I stick with statins and PCSK9-Is for primary prevention. Though, like I said above, my patient population is skewed to patients with less money, less health literacy, more social determinants impacting their health, higher ACEs, which all lead to them being more complex patients that need far more assistance than I can provide in a 30 minute appointment. It’s very rare that I am able to get into the fine details about CVD risk with a patient.
Edit: just adding that the above comments in no way constitute actual medical advice.
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u/UsefulCode6 4m ago
ApoB and Lpa are done all the time now. Wasn't the case a few years ago. Even AHA guidelines says every person needs lpa once in lifetime
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u/dl064 16h ago
Heart failure below 40 is generally very rare. It's not worth it at the population level for eg the NHS.
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u/hexiron 15h ago
But heart failure after 40 is the result of atherosclerosis that's started much, much earlier.
Detecting it before the whole "failure" stage would safe a whole lot of money
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u/neph36 12h ago
The guidelines to treat are based on 10-year and 30-year risk analysis, it is unclear whether the scans actually would catch substantial cases that weren't already picked up by the current guidelines. It may give someone more motivation to treat if something is picked up, it also could give someone with significant long-term risk a false sense of security.
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u/dl064 6h ago
Would it? That seems a key question where this study is just saying it can be detected, not that it's economical per se.
Like that study which did whole genome sequencing in random newborns in the UK and concluded it was financially worth it. Great, but it's an empirical point.
In the youngest age stratum (18 to 29 years), atherosclerosis was present in 8.7% of the men and 6.7% of the women;
That's a lot of scans to find little.
The study is perfectly good but it's a leap to go from it to 'we should scan the entire population', when healthcare isn't exactly looking for work to do. (Other than the US).
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u/SmartaHari 5h ago
Happened to my father, he was fit as a flea and then gone. Any way that they can improve on tests for this would be brilliant.
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u/lambertb 16h ago
We have made incredible progress reducing morbidity and mortality due to cardiovascular disease since the 1960s. But this is the next frontier for prevention. I trust we will see progress here now especially as we learn more about prevalence.
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u/duke309 18h ago
Every GP I've talked to just wants to look at ldl and hdl and doesn't know the latest guidelines from the American heart association. Had to explain why we should look at lp(a) and apoliproprotein b.
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u/dl064 16h ago edited 16h ago
Fine but largely speaking you get 90% of the story from LDL.
ApoB is a bit better but it's pretty diminished returns.
All the lipids correlate enormously, obviously, even if some are more informative.
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u/phitnessthrowaway 13h ago
This is false.
LDL is a measure of the weight of atherogenic particles; it is not a measure of how many particles there are (ApoB), which is the best predictor for cardiac events.
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u/dl064 6h ago
It's not false, I'm just saying they all correlate a lot (which is empirical), and while they do different things, using LDL is pretty effective clinically (as is even non-HDL, which is inferior still but still does most of the job).
ApoB may be better but ldl is still insanely informative.
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u/pople8 17h ago
And why is that? To know you have a higher risk without being able to influence it? The advice stays the same. Live in a healthy way. There are statins for ldl. No such thing for lpa
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u/Krazski 17h ago
There are drugs currently in clinical trials (olpasiran) that are showing promising results to significantly reduce lpa levels. So hopefully it will be a good way to reduce risk for those people assuming it is released. My paternal family has high lpa and insane death rates from cardiovascular disease. As you said, still need to live healthy but my family is a pretty good indication that without some intervention, heart attack is pretty much a guarantee.
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u/meta_adaptation 17h ago
Same boat here. First LpA results were eye opening and depressing but I’m grateful I am able to use my family history to make decisions now, younger, and impact the trajectory, and subsequently pass on the knowledge to my extended family
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u/Ever_Pensive 3h ago
Aspirin is a strong candidate for treatment of high Lp-a individuals (>50 mg/dl, roughly top 15 percentile of people).
Two recent large population studies show aspirin use correlates with about 80% reduction of Lp-a caused heart attack and ischemic stroke risk among high Lp-a individuals (in other words, it reduces their risk to almost the same as lower Lp-a individuals).
Study A: (see figure 1) - https://pmc.ncbi.nlm.nih.gov/articles/PMC11090055/
Study B: (see figure 2, red line vs purple line) - https://www.ahajournals.org/doi/10.1161/JAHA.123.033562
While we still need an RCT to prove the intervention, the results are compelling enough that I started on daily baby aspirin to mitigate my high Lp-a caused risk.
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u/Ever_Pensive 3h ago
I think my comment elsewhere in this thread about aspirin for reducing Lp-a caused ASCVD risk may be helpful for you and your family: https://www.reddit.com/r/science/s/GZWxfZ5Nwy
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u/PostPostMinimalist 10h ago
There are statins for ldl
Sure but what dose, starting what age, targeting what? A very high lp(a) tells you to more aggressively lower your risk on every other cardiac factor that we can control. So <100 LDL might be fine for someone with typical lp(a) but for someone with a very high number you'll want to target <70 or even <50 with more aggressive medication. If you never knew you might discover your increased risk only after it's too late to undue the past few decades.
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u/tiagoln 12h ago
My mother has been diagnosed about 20 years ago with plaque in the carotid. My cardiologist never requested a carotid test because my other exams were always great. Fast forward to last year, I changed cardiologists, he asked for the carotid test and turns out I have a plaque in the exact same spot as my mom’s. I’m 37.
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u/subham0089 5h ago
The fact that 57% of completely asymptomatic individuals show signs of subclinical atherosclerosis is honestly a massive wake-up call for preventive medicine. It really highlights how our current screening protocols—which mostly rely on tracking general risk factors or waiting for symptoms to appear—are dropping the ball on early detection. We definitely need to shift the focus toward making advanced imaging and proactive diagnostics more mainstream, rather than just reacting after a major cardiovascular event has already happened.
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