To B or Not to B: Is Non–High-Density Lipoprotein Cholesterol an Adequate Surrogate for Apolipoprotein B?

Abstract

During the past 2 decades, considerable progress has been made in establishing the lipid hypothesis and the importance of lipid profiles, especially the levels of lowdensity lipoprotein cholesterol (LDL-C) but also levels of high-density lipoprotein cholesterol (HDL-C) and triglycerides (TGs), for predicting risk of coronary heart disease (CHD). Additionally, many large-scale randomized controlled studies of lipid intervention, especially with the statin family of medications, have established the role of improving lipid levels, particularly levels of LDL-C, for CHD risk reduction. However, despite the use of the highest doses of the most potent statins, many patients continue to have major cardiovascular (CV) events (or “residual risk”). In this issue of , Harper and Jacobson point out that, despite considerable evidence supporting focused efforts to reduce LDL-C in primary and secondary CHD prevention, this strategy has many limitations. Clearly, other lipid parameters, including TGs, HDL-C, total cholesterol/HDL ratio and, especially, non–HDL-C, may also be important for predicting CV outcomes in patients receiving LDL-C–lowering therapies. Harper and Jacobson’s commentary particularly emphasizes the potential role of apolipoprotein (apo) B to predict clinical risk and to serve as a target of therapy, providing suggestions for the routine measurement of apo B and using this measurement in efforts to optimize medical intervention. We do not dispute that levels of apo B are strongly related with CHD risk, which has also been argued for many To B or Not to B: Is Non–High-Density Lipoprotein Cholesterol an Adequate Surrogate for Apolipoprotein B?