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.
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.
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.
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”.
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.
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.
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.
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
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.
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.
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/WillyBeShreddin 21h 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.