Icosapent ethyl may act on plaque
Although the primary outcome was not met at 9 months, several secondary outcomes were significant, including a 57% reduction in fibrous
plaque progression, an
89% reduction in calcified plaque progression, a 19% reduction in total noncalcified plaque progression and a 42% reduction in total plaque progression (Table). Total plaque volume increased by 20 mm3 in the EPA group and by 34 mm3 in the placebo group. Fibrofatty plaque progression increased in the icosapent ethyl group, although this result was not statistically significant (
P = .65).
Good read on the Evap trail and Vascepa overall.
Still stings a bit that Dr. Budoff admitted he chose the wrong outcome for this trail. If he chose calcified plaque, this trail would have been halted and Amarin would be drafting up another sNDA for the FDA.
Heres the end of the article:
Although the primary outcome of the EVAPORATE trial was not met at this initial time point, the trial will continue for 18 months before reporting final results. In the meantime, the reduction in overall plaque progression helps clarify a possible mechanism by which icosapent ethyl reduces CV events. Due to its lipophilic nature, EPA can become incorporated into atherosclerotic plaques, and may play a role increasing plaque stability. Perhaps by stabilizing plaque and slowing overall atherosclerotic progression, this is a mechanism by which high-dose EPA is able to exert part of the CV benefit.
These preliminary results are encouraging in elucidating the cardioprotective role of high-dose EPA and will need further confirmation. We look forward to seeing the 18-month CTA results of this innovative study.