Non-high-density lipoprotein cholesterol (non-HDL-C) levels among statin-treated patients seem to be linked to the risk of developing a serious cardiovascular event, such as a heart attack or stroke. This is because of the levels of low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B, states meta-analysis of data from previously published studies appearing in the March 28 issue of JAMA.
"Statin therapy is the cornerstone of pharmacological therapy for the primary and secondary prevention of cardiovascular disease. All currently available guidelines state that LDL-C levels should be used as the primary target to initiate and titrate lipid-lowering therapy. However, trials investigating the efficacy of statin therapy have shown that the cardiovascular benefits of statins may go beyond their influence on LDL-C levels. Thus, LDL-C may not be the best lipid parameter to predict cardiovascular risk or to quantify the atheroprotective effect of statin therapy," according to background information in the article. Several alternative lipid and apolipoprotein parameters have been proposed as alternatives for LDL-C, most prominently apolipoprotein B and non-HDL-C (total cholesterol minus HDL).
S. Matthijs Boekholdt, M.D., Ph.D., of the Academic Medical Center, Amsterdam, the Netherlands, and colleagues conducted a meta-analysis to assess whether among patients receiving statins, non-HDL-C and apoB were more strongly associated with the risk of future cardiovascular events than LDL-C. The study included individual patient data from randomized controlled statin trials in which conventional lipids and apolipoproteins were determined in all study participants at baseline and at 1-year follow-up. The researchers identified 8 trials, published between 1994 and 2008, that met criteria for inclusion in the meta-analysis. The trials included individual patient data for 62,154 patients.
Analysis of the data indicated that among statin-treated patients, levels of LDL-C, non-HDL-C, and apoB were each strongly associated with the risk of major cardiovascular events, but non-HDL-C was more strongly associated than LDL-C and apoB. Also, changes in non-HDL-C explained a larger proportion of the atheroprotective effect of statin intervention than did LDL-C and apoB.
"Given the fact that many other arguments for the clinical applicability of non-HDL-C and LDL-C are identical, non-HDL-C may be a more appropriate target for statin therapy than LDL-C," the authors conclude.