title: Apolipoprotein B, non-HDL cholesterol and LDL cholesterol for identifying individuals at increased cardiovascular risk.
abstract: BACKGROUND
  To compare apolipoprotein B (apoB), non-high-density lipoprotein-cholesterol (non-HDL-c) and low-density lipoprotein-cholesterol (LDL-c) for identifying individuals with a deteriorated cardiovascular (CV) risk profile, including a panel of subclinical atherosclerosis measurements and prevalent cardiovascular disease (CVD) in a Dutch population-based cohort.
  
  
  METHODS
  Clinical and biochemical measurements and a panel of noninvasive parameters of subclinical atherosclerosis were determined in 1517 individuals, aged 50-70 years.
  
  
  RESULTS
  Both men and women with increasing levels of apoB and non-HDL-c were more obese, had higher blood pressure and fasting glucose levels, and a more atherogenic lipid profile. Furthermore, compared to the reference group (composed of those with apoB, non-HDL-c and LDL-c levels in the bottom quartiles), participants with high apoB and high non-HDL-c levels had a lower ankle-brachial index at rest (-3.5% and -3.1%, respectively) and after exercise (-6.3% and -4.7%, respectively), a thicker near wall (+4.8% and +4.2%, respectively), far wall (both +6.2%), and mean intima-media thickness (+5.7% and +5.3%, respectively) and more plaques (+54.2% and +54.3%, respectively). In addition, they also showed increased stiffness parameters (e.g. pulse wave velocity both +3.6%). Less clear differences in CV risk profile and subclinical atherosclerosis parameters were observed when participants were stratified by LDL-c level. Furthermore, apoB but not LDL-c detected prevalent CVD, and non-HDL-c only detected prevalent CVD in men. The discriminatory power for prevalent CVD expressed as area under the receiver operating characteristic curve was 0.60 (P < 0.001) for apoB, 0.57 (P = 0.001) for non-HDL-c and 0.54 (P = 0.108) for LDL-c.
  
  
  CONCLUSIONS
  Our data support the use of first apoB and secondly non-HDL-c above LDL-c for identifying individuals from the general population with a compromised CV phenotype.
authors.affiliation: Division of Vascular Medicine, Department of General Internal Medicine, Radboud University, Nijmegen Medical Centre, Nijmegen, The Netherlands. s.holewijn@aig.umcn.nl
authors.forename: S
authors.initials: S
authors.lastname: Holewijn
authors.forename: M
authors.initials: M
authors.lastname: den Heijer
authors.forename: D W
authors.initials: DW
authors.lastname: Swinkels
authors.forename: A F H
authors.initials: AF
authors.lastname: Stalenhoef
authors.forename: J
authors.initials: J
authors.lastname: de Graaf
mesh_terms: D000368:Aged; D001055:Apolipoproteins B / Q000097:blood*; D050197:Atherosclerosis / Q000097:blood / Q000175:diagnosis / Q000473:pathology / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology; D002318:Cardiovascular Diseases / Q000097:blood / Q000175:diagnosis* / Q000503:physiopathology; D002784:Cholesterol / Q000097:blood*; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged
chemical_list: D001055:Apolipoproteins B; D015415:Biomarkers; D001786:Blood Glucose; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D002784:Cholesterol