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Localized foam cell activation and cytokine signaling does not necessarily raise hsCRP yet allows for continue plaque deposition. This is a very well understood mechanism.

No one knowledgeable here is saying that inflammation isn't worth paying attention to, but people acting like because inflammation is also important that LDL does nothing just aren't living in reality.

Your comment about blood pressure actually reveals more about your knowledge here than the person you're replying to.

FDG-PET is a signal we can use to detect tissue inflammation, and we know that higher blood pressure is highly correlated with increased FDG-PET in arterial walls:

https://pmc.ncbi.nlm.nih.gov/articles/PMC6994784/

High blood pressure is also feed-forward loop with Angiotensin, which increases inflammation:

https://pmc.ncbi.nlm.nih.gov/articles/PMC3377325/ https://pmc.ncbi.nlm.nih.gov/articles/PMC4192119/

Blood pressure results in shear stress to your arteries. This results in several things that amplify Angiotensin II and NF-kB activity, including expoosing adhesion molecules which then results in foam cell activation and cytokine signaling, etc.

It is quite well established that high blood pressure will contribute to increased inflammation.



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