[cthalupa]

High LDL or Lp(a) on its own causes enough localized inflammation to continue plaque deposition. We can’t drive down every cause on inflammation to 0 to the point that there is zero plaque deposition at all in the presence of high LDL, there are just too many causes. Even temporary increases in inflammation from natural processes can deposit plaque is you have high amounts of atherogenic particles. And once they deposit, they begin to cause inflammation independently. Not all inflammation can be measured by hsCRP.

Inflammation is an important causal factor for sure, and persistent high levels of inflammation will drive even more deposition of plaque.

Your body does not need serum LDL in significant quantities. I’ve commented in this post multiple times with studies that show that even driving LDL down below 20 has no impact to the systems that use LDL that people are concerned about. All of the related organs can do de novo synthesis, make use of HDL instead, etc. People that do not produce LDL at all that ends up in the bloodstream still produce all of their necessary hormones at normal rates, the brain still produces it locally de novo, etc.

No one thinks LDL and Lp(a) are the sole factors in heart disease. We know of plenty that are unrelated - blood pressure, LVH, etc. etc. etc.

But lowering LDL is one of the most powerful and broad spectrum tools we have at our disposal.