The issue seems to be LDL/VLDL (particularly remnant) particle count.

The best model I've run across for the etiology of arteriosclerosis goes as follows:

- main arteries, particularly the aorta, lose flexibility as they age (why they do is an interesting question)

- that lack of flexibility leads to higher momentary pressure peaks...

- if there are a lot of small particles, some get jammed between the epithelial cells in the artery by this higher pressure.

...and you know the rest: epithelial cell distress, immune cells, foam cells, cholesterol build up (which is probably an attempt to fix the issue), calcification.

I'm not a bio pro, but have been trying to wrap my head around the lipid system for the last few years...

For anyone else interested in this, if you're on Twitter, go follow Dr. Thomas Dayspring (AKA DrLipid). Also, he did about 6 hours of interview with Dr. Peter Attia. If you get podcasts, maybe start there.