January 27th, 2011
HPS Results Suggest Baseline CRP Doesn’t Predict Statin Efficacy
Larry Husten, PHD
Analysis of data from the Heart Protection Study (HPS) indicates that a CRP measurement obtained at baseline does not predict the effect of statin therapy. In a paper published online in the Lancet, the HPS Collaborative Group report the results of the more than 20,000-patient HPS study based on CRP category at baseline. As previously reported, in the overall trial major vascular events were reduced with statins by 24% when compared to placebo.
In the current report, the investigators report no significant differences in the relative effect of statins among 6 groups determined by CRP baseline levels. Even in patients with the lowest CRP concentrations, statin treatment resulted in a 29% reduction in events. The same pattern was true for LDL levels and for the combination of LDL and CRP levels: a 27% reduction in risk was observed in patients with both low LDL and low CRP levels at baseline.
The HPS investigators conclude: “The results do not lend support to the suggestion that the beneficial effects of statin therapy are affected by baseline CRP concentration or, more generally, by inflammation status.”
In an accompanying comment, Jean-Pierre Després notes that although CRP and LDL did not predict the relative efficacy of statins, they were both associated with the absolute risk of patients in HPS.
Paul M. Ridker, a leading researcher on the value of C-reactive protein (CRP) concentration as a prognostic marker of cardiovascular risk, responds to this latest study in his new Voices blog: Does CRP Level Modify the Benefit of Statins? Paul Ridker Reacts to New Data.
Very bad news for Tech-industry! hsCRP promotion to Physician become more difficult for them. Good example how Science contradict & demolish all types of existing dogma & authority.We need more and more good Science, unbiased by Pharma & Tech Industry. Physician & Researcher alike should cut-off all relation with them,so that, conflict of interest statement become redundant!
Most analysys of the protective effects of statins agree that the relative reduction of vascular risk by statins is similar regardless of baseline clinical conditions and, remarkably, also lipid levels. Therefore the absolute benefit of statins relates essentially to the basal absolute risk of patients.
Big studies also suggest that increased CRP is a marker of increased vascular risk, although mendelian randomization studies do not support a causal role for CRP in the development of atherosclerosis or its complications. Interventional studies addressed directly to reduce CRP or its presumed mechamism of vascular injury must be conducted to further clarify this issue.
Whetner CRP plays a casual role or is a mere epiphenomenon reflecting someway ongoing inflammation, it might be useful as a marker of increased vascular risk.
For any risk marker to be useful, it should provide clear additional prognostic information on top of classical risk factors (such as those included in the Framingham equations). CRP correlates with many of such risk factors, so it is not suprising that it seems to provide additional information when some of these factors are poorly included in risk equations (such as using dychotomous variables for obesity or smoking).
Last but not least, a significant improvement of risk estimation in the population level may be of little interest for the individual patient. The high degree of intraindividual variation (thus reclassifying individual patients into different groups of risk according to different measurements of CRP) makes this parameter a poor choice to guide desirably predictable therapeutic algorythms
Competing interests pertaining specifically to this post, comment, or both:
I have no conflict of interest pertaining to this subject
But so many patients request the CRP after misreading an article in one of the prevention-type magazines that I order it if they ask, and then explain to them how the result will not affect my decision vis-a-vis a statin Rx.
I believe that this analysis from the HPS trial only points out the effectiveness of statins in secondary prevention and in primary prevention for high risk patients a fact that has long been recognized. In my mind what JUPITER proposed was that CRP was able to select among a group of individuals clinically classified was intermediate risk patients who would benefit from statins. Unfortunately this paper does not help resolve the dilemma of statin for the so called intermediate risk patients.
PATIENT WITH SRRONG FAMILY HISTORY OF CV disease,but high CRP and normal range of lipids, deserves the benefit of statin.
The HDL level should also be taken into account. Statins are much less effective with low HDL levels. The higher the HDL level, the better the statins work
Competing interests pertaining specifically to this post, comment, or both:
none