LDL levels at admittance do not tell us what their lifetime LDL levels were. But even your own link is arguing for
lowering the the number at which we consider LDL levels risky.
PCSK9 inhibitors when coupled with statin therapy have gotten people to ~10 LDL without negative impact in clinical trials. The body is good at producing cholesterol where it needs it - it doesn't pass the blood brain barrier, yet the brain is full of it. It produces it's own, the same as quite a lot of other tissue
For hormones, de novo synthesis of cholesterol is a thing when it comes to steroidgenesis, as well as recycling and re-uptake. PCSK9 inhibitor studies specifically looked at this because of this concern, and found cortisol/aldosterone/testosterone/estrogen/etc. were not impacted by having very lower levels of LDL-C.
The issue with statins and CoQ10 isn't cholesterol - it's the mevalonate pathway. They block a reductase in the pathway and this results in lower serum CoQ10 levels. Data around if this is of any clinical relevance is a mixed bag, but this is easily supplementable if needed, and should not be a reason to not take life saving medication. PCSK9 inhibitors make large dents in LDL but do not impact CoQ10 levels at all because they do not impact the mevalonate pathway.
https://www.ahajournals.org/doi/10.1161/ATV.0000000000000164
https://www.acc.org/Latest-in-Cardiology/Clinical-Trials/201...
https://pubmed.ncbi.nlm.nih.gov/36779348/
As for which is better... lower both. Why wouldn't you want to lower all the causal factors you can? Statins even do this!