Amarin Corp Plc (AMRN)

[sts66]

Median baseline Lp-PLA2 levels in ANCHOR were extremely low for people with established CVD (70% of total) or multiple risk factors for CVD, including diabetes (30% of total) - I'm assuming ANCHOR enrolled the same %'s as they did in R-IT - actual number of people with CVD could have been even higher, but Lp-PLA2 of 180 is barely into the "High" category.

I started V in 2013 because I had my Lp-PLA2 tested after reading about what it represents here (level of arterial inflammation and nothing else) because of family history showed my risk of developing CVD was high (I'm now the only male who hasn't had an MI and/or multiple stents) - my levels were a scary high 497! Risk of stroke was 4x the normal population - after 6 months on V mine were down to optimal level of < 123 at 115, and it's gotten as low as 93 over the years. I don't have high LDL-C, I do have high TGs (250-500), but my CAC scan was clean as a whistle, BP is high normal - I basically have/had no CVD risk except for Lp-PLA2 and homocysteine, although the latter is tied to mitochondrial dysfunction I have due to some genetic damage and V hasn't budged it (wouldn't expect it to either).

So why was my Lp-PLA2 so high compared to ANCHOR patients when I have no other CVD risk factors? Periodontal disease can elevate it, but I've never had anything beyond some mild gingivitis episodes as an adult that disappeared after a thorough dental hygienist cleaning (I've always been a lousy flosser, fingers are too big to hold floss in my mouth and reach the molars).