HPS CRP data Not very helpful!

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HPS CRP data Not very helpful!

tdayspring's blog / Exercise and Nutrition / HPS CRP data Not very helpful!

HPS CRP data Not very helpful!

Feb 4, 2011

1 comments Exercise and Nutrition

Exercise and Nutrition

Head over to the Lancet and check out the just published HPS data in Lancet: C-reactive protein concentration and the vascular benefi ts of statin therapy: an analysis of 20 536 patients in the Heart Protection Study:

Interpretation Evidence from this large-scale randomised trial does not lend support to the hypothesis that baseline CRP concentration modifi es the vascular benefi ts of statin therapy materially.

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)62174-5/abstract

Also see editorial by JP Despres

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)62316-1/fulltext#article_upsell

Sooner or later they will all figure out that it is apoB and LDL-P that predicts what statins will or will not do. Why does no one, other than Alan Sniderman and his many followers (including me) ever mention the pretty ugly apoB data in JUPITER in all those folks with normal LDL-C. We need to see the NMR data from HPS that Dr Virgil Brown tlaked about in the IAS meeting in Boston two years ago. One day we will hopefully also have the JUPITER NMR data. Then we can all move on.

Keywords: crp heart protection study

Comments

By feeman 460 Days Ago

The hsCRP data is not surprising. As Ridker pointed out when he first got started on the inflammation theory of atherothrombotic disease (ATD), the inflammatory response is a response to risk factors. hsCRP can be elevated due to many other nonATD factors. To paraphrase William Roberts, MD, "It's the ratios [LDL and HDL, and I prefer the Cholesterol Retention Fraction, or (LDL-HDL)/LDL], s....." Use of the CRF, with the caveats noted in other blogs, obviates the use of these other markers and makes the prediction of the population at risk of ATD straight-forward, as well as therapy to maximally stabilize/regress, at least angiographically, coronary artery plaque, which after is the only goal of dyslipidemic therapy.