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Tuesday, August 04, 2015 8:08:52 AM
This information has been posted several times here. It should be the foundation for anyone who is long this stock. Indeed this relationship between AA/EPA and CVD risk provides the rationale for R-I and barring something truly unexpected, predicts a 40-50% risk reduction in the trial.
The proof is as follows.
R-I enrollees are mostly if not all patients with a prior history of heart disease. Meaning they have had a previous MI, have have had coronary artery surgery, or evidence of coronary stenosis, or angina documented by EKG or enzymes. Most also have mixed dyslipidemia or T2DM. They also have AA/EPA ratios of 15 or greater. Their annual risk for CVD events is somewhere between 5.2-6.0%. These patients fall under a clinical category called "secondary intervention, meaning they have a history of heart disease as outlined.
The R-T group closely resembles the secondary intervention group in JELIS from a clinical standpoint. The only differences were the AA/EPA ratio in the JELIS subset was only 1.8 and the the estimated annual risk rate was only 2.2%..which was less than half the rate of R-I . Please keep in mind the numbers I am citing are the numbers at the beginning of the trials, prior to any treatment. So I look at JELIS and R-I and as far I know the patients are similar in everyway I can measure except for the AA/EPA ratio and the risk. So I have to ask myself ,"If I can reduce the AA/EPA ratio in the R_I group down to the JELIS levels, why should I not be reducing the risk rate down to the JELIS levels?"
Dr. Sears says 4gms of EPA should reduce the R-I AA/EPA levels down to JELIS pre treatment levels,..so I am anticipating a drop in R-I from 5.2-6% down to 2.2% risk or some where near to 50% or more reduction..
Dr. Sears statement does not pertain to Vascepa...Vascepa is the equivalent
of the dietary increases in EPA described by Sears.
":>) JL
":>)
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