C-reactive protein levels is not correlated with total LDL to HDL cholesterol and triglyceride levels (less than 2 percent).  Wide variation in C-reactive protein levels:  quartile 1 < 0.08 mg/dl; 2 between  0.08 to 16; 3; 3 between 0.16 to .025; 4 > 0.35 mg/dl.  The risk of acute coronary events (MI, death & unstable angina) increased 17% (average) per increasing quartile. Lavostatin therapy at the end of one year reduced C-reactive protein level by 14.8%.  This change was not associated with lavostatin’s effect upon HDL to total cholesterol ratio change. {This conclusion is overly optimistic given the quoted paragraph below}  Those with both a less than median cholesterol profile and C-reactive protein did not benefit from statin therapy.  Moreover those with greater than median cholesterol had the same benefit weather or not their C-reactive protein was greater than the median.  (That they used total cholesterol to HDL ratio rather than the STANDARD of LDL to HDL ratio suggests that the authors are teasing out positive results}. 

“In these data, the observed efficacy of lovastatin in preventing acute coronary events was not statistically significant among the participants with lipid levels and C-reactive protein levels that were both higher than the median. However, in each of the two subgroups defined according to these criteria, the point estimates of effect indicate an overall net benefit with lovastatin. Furthermore, there was no evidence of any statistically significant difference between the efficacy of lovastatin among the participants with lipid levels and C-reactive protein levels that were both higher than the median and its efficacy among those with lipid levels higher than the median but C-reactive protein levels lower than the median; these data suggest that any small differences between the results in these subgroups probably represent the effects of chance. Finally, because the rates of events were high among participants with lipid levels and C-reactive protein levels that were both higher than the median, the number needed to treat in these subgroups was well below the number considered the threshold for justifying treatment for primary prevention. Indeed, the number needed to treat among participants with lipid levels and C-reactive protein levels that were both higher than the median was of similar magnitude to that found in subgroups in which the efficacy of lovastatin was clearly statistically significant.”

 JK comments

This study is attempting to expand the number of those treated to include all those with a C-reactive protein level above the median 0.16 mg/dl, by claiming that its 14.7% reduction resulted in a significant reduction in acute coronary events.   This study would have 50% of the untreated population treated based upon being above the median level for C-reactive protein. 

“Finally, nearly 20 percent of the participants in AFCAPS/TexCAPS were taking aspirin, a drug that has also been shown to reduce the effect of C-reactive protein on vascular risk.”  This again confirms that most of the benefits of statins is from the same mechanism as that of aspirin.  Since they didn’t say that statins affect C-reactive protein more than aspirin, one can presume that its effect is no more than aspirin.