NK can't hurt, but all the literature points to shows a reduction in intima media thickness, which is promising, but isn't quite the same as tracking outcomes, nor does it suggest a reduction in calcified plaque. By contrast, there was a study published on bempedoic acid in the past year that shows a clear reduction in MACE (major adverse cardiac events).
To be clear, I'm not suggesting there's anything wrong with NK or that it's inferior to bempedoic acid, just that it hasn't yet met the gold standard of improving outcomes. Niacin, for example improved biomarkers, but has been shown not to be of any benefit and is potentially harmful.
Unmedicated, my total cholesterol was just north of 200mg/dL. Lifestyle changes were able to bring that down some, but when I compared my lipids to a friend of mine who is sedentary and has metabolic syndrome, but is on rosuvastatin, that caused me to reconsider my stance on statins. When I got my CAC, I decided to try all the things and see how I respond.
With a total of 400mg/dL, I'd definitely suggest an aggressive approach. It's worthwhile getting an NMR lipid panel and measuring both ApoB and Lp(a). The lipidologist Tom Dayspring recommends managing ApoB to something less than 80mg/dL for most or 60mg/dL for high risk folks.