>>If nattokinase is able to slow the progression of plaque formation and reverse atherosclerotic lesions, it should have some effect on both cholesterol levels and blood pressure.

If all it can do is slow plaque prevention and reverse artheriosclerotic lesions, there's no reason it should affect lipids or BP. However if there's a different, base system that's promoting plaque, negatively changing measured lipid levels and BP...?

From your mention of 'fibrinolytic units', I would take that to be the fibrolyinic system, but reading up on that, the molecular mechanism of disassembling clots via lysine residue 'handles' on a polymerized clot seems pretty clear, but any mechanism for affecting lipids and BP isn't obvious.

Guessing aloud, lowering BP means either relaxing arterial walls (like NO) or reducing stiffness. If it's the latter, is it via changes in the capillary system feeding the tunica media (the smooth muscle and elastic fibers of an artery)? Changes to the external lamina (sort of a girdle on the outer layer)?

As to the fibrinolytic system affecting lipid levels, I’m stumped. Anyone? [see below]

Good explainer on the fibrinolytic system here: https://pmc.ncbi.nlm.nih.gov/articles/PMC10532028/ (The Fibrinolytic System and Its Measurement: History, Current Uses and Future Directions for Diagnosis and Treatment)

For anyone interested in lipids, I would very much recommend starting with Peter Attia's conversations with Tom Dayspring. Maybe start with this one: https://peterattiamd.com/tomdayspring3/ or the one before. (podcasts are free, show notes behind a paywall)

I am delighted to find yet another rabbit hole to follow. I have to wonder how many other non-professionals are as fascinated with this stuff as I am - I always knew I was a little bit 'off'. :-)

Also: rather than compare this to statins, why not daily low dose aspirin? I affects the same system, but has a different profile of side effects and so might be more appropriate for people who are yet to have a CVD event.

[edit] I dug into this a bit and it turns out that fibrates are indeed used to modify lipid levels. In the US, there’s Gemfibrozil which has to be converted into the active fibric acid, and Fenofibrate, which does not. The mechanism of action is ‘not fully understood’, but the prevalent theory is that it depletes triglyceride stores in the liver. There are a number of trials, including some that were well before statins became ‘standard of care’ so testing fibrins alone — and those showed a similar reduction in ‘events’ as do statins. These days, RCTs have to be statins vs statins-with-whatever in order to be ethical (placebo ‘arm’ gets at least standard of care). Interesing rabbit hole — and yeah, these are a really good alternative to statins.
Also fenofibrates lower BP via NO in the endothelium https://pubmed.ncbi.nlm.nih.gov/23108655/[/edit]