Monday, February 01, 2016 7:36:20 PM
My issue is with those who think the JELIS secondary group provides an exact guide for what we will see in R-IT.
To wit ...the RRR was this much in JELIS because of the additional 1.8gms of EPA ( in active arm ) in addition to the presumed 2gms of s EPA from the high fish diet in both arms.
So if we saw these results in JELIS we can extrapolate and expect similar results in RI .
Well not only has LDL been lowered from a mean of 178 in JELIS secondary to probably a mean of 90 in R-It ( my apologize to the horse as in "beating a dead horse " ) but hs Crp will have been lowered also .
We don't know by how much ...do we ?
My guess is that by lowering LDL and hsCRP you have significantly lowered the event rate ...yes in both arms ...but we also know that EPA reduces CV event risk LESS in those patients with low hsCrp .
So how do you use JELIS secondary as any basis for estimating R-It event rate ?
There will be a divergence between the arms because of the additional 4 gms of EPA .
IMHO the divergence will be less then expected because optimal statin dose has lowered LDL and lowered hsCRP ...and to be repeat myself ..EPA is less effective in reducing risk in patients with low hsCRP
Kiwi
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