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Non-HDL C equals apolipoprotein B: except when it does not!

Sniderman, Allana; Williams, Kenb; de Graaf, Jacquelinec

doi: 10.1097/MOL.0b013e32833ee80c
Therapy and clinical trials: Edited by Anton F. Stalenhoef and John J.P. Kastelein

Purpose of review Whether national guidelines should incorporate apolipoprotein B (apoB) into clinical practice is one of the most important and contentious decisions they must face. Canada has chosen to do so. What Europe and America decide remains to be seen.

Recent findings Obviously, the results of the major epidemiological studies and clinical trials should be major drivers of decisions about guidelines. Such evidence clearly indicates that apoB is superior to LDL C as a marker of risk and an index of the adequacy of therapy but is mixed as to whether apoB is superior to non-HDL C. In this paper, we demonstrate that the issue is more complicated than it appears: that even if non-HDL C and apoB are equal predictors of vascular risk (which we do not believe is the case), this is not due to the VLDL C that is included in non-HDL C but rather reflects the fact that non-HDL C is a ‘backwards’ measure of apoB – that is, non-HDL C provides an indirect estimate of LDL particle number. Moreover, equal predictive power in groups does not mean that markers have equal predictive power in individuals. We also list multiple clinical circumstances when non-HDL C and apoB lead to different clinical decisions because the real test of markers is when they differ, not when they agree.

Summary Thus, our conclusion is that apoB and non-HDL C are equal – except when they are not. Because apoB allows greater specificity of diagnosis and therapy, it re-establishes the primacy of individuals over groups as the objects of our study and our care and that may be its most important contribution to clinical lipidology.

aMike Rosenbloom Laboratory for Cardiovascular Research, Montreal, Quebec, Canada

bKenAnCo Biostatistics and University of Texas Health Science Centre at San Antonio, Texas, USA

cDepartment of General Internal Medicine, Division of Vascular Medicine, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands

Correspondence to Dr Allan Sniderman, Mike Rosenbloom Laboratory for Cardiovascular Research, McGill University Health Centre, Room H7.22, Royal Vic Hosp, 687 Pine Avenue West, Montreal, QC H3A 1A1, Canada Tel: +1 514 934 1934 ext 34637; fax: +1 514 843 2843; e-mail:

© 2010 Lippincott Williams & Wilkins, Inc.