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Re: iwfal post# 157708

Friday, 03/01/2013 6:51:32 PM

Friday, March 01, 2013 6:51:32 PM

Post# of 251285
RVX ---

One thing before I start quoting...

a1-HDL is not he majority of HDL in the measurement of HDL-C. In fact, a1-HDL is around 15% of HDL-C as noted by the measures in the 2004 Asztalos paper. You had stated before that a1-HDL made up the vast majority of HDL-C, so I just wanted to correct that.

As I noted in my last post my preferred paper is the 2005 Asztalos paper (quote from my last post was "the later... better paper done by the same authors"). And it showed no such wild correlation. Essentially alpha1 largely disappears when you actually do a methodologically sound datamining. See link in #msg-81742249



Sorry, I must have confused citations. I've been doing much Alt-Tabbing between lipid papers the last few days.

If you think the second Asztalos paper erases the conclusions of the first paper, I think you need to read closer.

"The brief summary of our results is HDL-C level is a significant predictor of new CVD events in the VA-HIT population after adjusting data for traditional risk factors. However, when any of the HDL subpopulations representing significant CVD risk are included as a covariant in the analyses, the predictive value of HDL-C for new CVD events is no longer significant. In contrast, specific HDL subpopulations are either significant positive or significant negative predictors of recurrent CVD events in the VA-HIT, and some of these particles, above all a-1 and a-2, are superior to HDL-C in risk assessment in patients whose primary lipid disorder is low HDL-C level."

Does the 1mg/dl increase = 26% reduction (now amended/typo'd to 21% when the authors describe the 2004 FOS data in the 2005 VA-HIT paper) still hold up?

Or is 13% the new number (though I note that is the effect of a 1mg/dL decrease in a1-HDL)?

"Logistic regression analyses indicated that only the levels of a-1 among HDL particles were significantly associated with the prevalence of CHD (Table 6). Each 1 mg/dL decrease in a-1 increased the odds of CHD with 13% (P<0.0001) in low HDL-C subjects after adjusting data for lipid and nonlipid CHD risk factors."

We can argue which number Resverlogix should use, but to say the 2005 paper erases the conclusions of the 2004 paper is simply not accurate. Also, since Resverlogix has data on mg/dl increase in a1-HDL and not mg/dl decreases in a1-HDL, I can argue citing the 2004 paper instead of the 2005 paper is legitimate -- though you can reasonably argue the 2005 paper's focus on low HDL-C populations is a better fit for Resverlogix's target population.

In the end, this is something we can do to amuse ourselves while waiting for ASSURE data.

I would suggest you have missed the fact that the primary endpoint in the RVX trial DOES NOT COMPARE TO PLACEBO. (I truly apologize for shouting - but I don't think you are reading what I am writing).



My reading comprehension of your point is fine, thank you. I probably didn't take as long to explain why this doesn't bother me as I should have.

The endpoint in ASSURE is the same endpoint as the ETC-216 study (though with TAV instead of PAV). Despite placebo controls, the primary endpoints of both studies are comparisons within the drug group alone and not between arms.

Your point is 110% valid if all Resverlogix was going to release was a one-line PR saying "The primary endpoint has been reached" while providing no additional detail. If they do that, you'll hear me yell as loud as anyone such descriptions tell us nothing useful about ASSURE's outcome.

However, they've been clear they are not going to do that. We will get aetheroma changes in study and aetheroma changes in control AND (most importantly) a comparison between the two in the press release. (FWIW, I confirmed this with them within the past hour. Again.)

In the ETC-216 study, virtually nobody cared about the primary endpoint (except the bears, interestingly, but that's a very long story). Everyone cared about the difference between aetheroma volume in the study arm compared to the control arm. The same will be true for the ASSURE study.

You're within your right to beat them up about this as it certainly is an unusual way to report a randomized trial. HOWEVER, implications that Resverlogix is being shady would necessarily also have to extend to the people at Esperion and Nissen's team at Cleveland Clinic.

I cited hard data [Rosu/Ator] DO create IVUS reductions even at 1/2 max dose.



Missed that, sorry. Source of that human data on this please?

David

Unless otherwise indicated, this is the personal viewpoint of David
Miller and not necessarily that of Biotech Stock Research, LLC.
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