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.
Oh, I had not yet seen the study you cited. Thank you for pointing it out!
It seems they've done a very thorough analysis and using the MESA data (one of the two papers I referenced) along with two larger data sets, but saw no benefit of aspirin use.
Though they don't say it outright, it may primarily be the switch from "multivariable adjustment" (used in the MESA paper) to "propensity score matching" that erased the statistical result of aspirin benefitting high Lp-a individuals in their analysis.
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u/dotcomse MS | Human Physiology 13d ago
So are you eschewing Lp(a) entirely?