Low-density lipoprotein (LDL) cholesterol and triglyceride-rich lipoproteins constitute
non-high-density lipoprotein (non-HDL) cholesterol. These are atherogenic lipoproteins
and non-HDL cholesterol is a secondary target of treatment beyond LDL cholesterol
in patients with hypertriglyceridemia. Some investigators favor total apolipoprotein
B over non-HDL cholesterol as the secondary target of treatment. This is based on
publications suggesting that total apolipoprotein B is more predictive of cardiovascular
events than non-HDL cholesterol. Several methods are available for estimating total
apolipoprotein B. This study compared total apolipoprotein estimated by immunonephelometric
assay (INA), vertical auto profile (VAP), nuclear magnetic resonance (NMR), and non-HDL
cholesterol levels in patients with hypertriglyceridemia from the previously reported
Simvastatin plus Fenofibrate for Combined Hyperlipidemia (SAFARI) trial. Total apolipoprotein
B levels were found to be highest by INA, intermediate by NMR and non-HDL cholesterol,
and lowest by VAP. Concordance for non-HDL cholesterol levels among the INA, VAP,
and NMR methods was better than that for total apolipoprotein B levels; the correlation
between non-HDL cholesterol and apolipoprotein B by INA was strongest (0.929). In
patients with a low triglyceride/HDL cholesterol ratio (<3.5), total apolipoprotein
B determined by INA was higher than that estimated from non-HDL cholesterol levels,
whereas in patients with a high triglyceride/HDL C ratio (≥3.5), apolipoprotein B
predicted using non-HDL cholesterol was in better agreement with INA-determined apolipoprotein
B levels. Similar trends were observed with VAP using equations specific for LDL particle
size. In conclusion, more work is needed to improve agreement of apolipoprotein B
measurements among methods employed clinically. Non-HDL cholesterol is also useful
to predict total apolipoprotein B and some improvement may be attained by taking into
account the ratio of triglyceride/HDL cholesterol as a measurement of LDL particle
size.
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Article info
Publication history
Published online: May 12, 2011
Accepted:
March 3,
2011
Received in revised form:
March 3,
2011
Received:
November 4,
2010
Footnotes
This work was supported in part by Merck & Co., Inc., Whitehouse Station, New Jersey, and the Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, Texas. Dr. Grundy's and Dr. Vega's research is supported in part by the Department of Veteran Affairs, Dallas; Grant UL1-RR024982 from the Clinical Translational Science Award/National Institutes of Health, Bethesda, Maryland; the Moss Heart Center, Dallas; and the Donald W. Reynolds Cardiovascular Research Center, Dallas. Drs. Tershakovec and Tomassini are employees of Merck & Co., Inc. and stock/or stock options in the company.
Identification
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Published by Elsevier Inc.
