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J Am Heart Assoc. 2014 Jun 25;3(3):e000902. doi: 10.1161/JAHA.114.000902.

HDL-3 is a superior predictor of carotid artery disease in a case-control cohort of 1725 participants.

Author information

1
Division of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA (D.S.K., A.A.B., E.A.R., J.E.R., C.E.F., G.P.J.) Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA (D.S.K., C.E.F., G.P.J.).
2
Division of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA (D.S.K., A.A.B., E.A.R., J.E.R., C.E.F., G.P.J.).
3
Department of General Medicine, Virginia Mason Medical Center, Seattle, WA (J.F.E.).
4
Division of Vascular Surgery, Department of Surgery, University of Washington School of Medicine, Seattle, WA (T.S.H.).
5
Northwest Lipid Metabolism and Diabetes Research Laboratories, Seattle, WA (S.M., J.J.A.) Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, WA (S.M., J.J.A.).

Abstract

BACKGROUND:

Recent data suggest that high-density lipoprotein cholesterol (HDL-C) levels are likely not in the causative pathway of atheroprotection, shifting focus from HDL-C to its subfractions and associated proteins. This study's goal was to determine which HDL phenotype was the better predictor of carotid artery disease (CAAD).

METHODS AND RESULTS:

HDL-2 and HDL-3 were measured in 1725 participants of European ancestry in a prevalent case-control cohort study of CAAD. Stratified analyses were conducted for men (n=1201) and women (n=524). Stepwise linear regression was used to determine whether HDL-C, HDL-2, HDL-3, or apolipoprotein A1 was the best predictor of CAAD, while adjusting for the confounders of censored age, diabetes, and current smoking status. In both men and women, HDL-3 was negatively associated with CAAD (P=0.0011 and 0.033 for men and women, respectively); once HDL-3 was included in the model, no other HDL phenotype was significantly associated with CAAD. Addition of paraoxonase 1 activity to the aforementioned regression model showed a significant and independent (of HDL-3) association with CAAD in men (P=0.001) but not in the smaller female subgroup.

CONCLUSIONS:

This study is the first to contrast the associations of HDL-2 and HDL-3 with CAAD. We found that HDL-3 levels were more predictive of CAAD status than HDL-2, HDL-C, or apolipoprotein A1. In addition, for men, paraoxonase 1 activity improved the overall model prediction for CAAD independently and additively with HDL-3 levels. Further investigation into the molecular mechanisms through which HDL-3 is associated with protection from CAAD is warranted.

KEYWORDS:

atherosclerosis; carotid arteries; high‐density lipoprotein; lipids; lipoproteins

PMID:
24965026
PMCID:
PMC4309059
DOI:
10.1161/JAHA.114.000902
[Indexed for MEDLINE]
Free PMC Article

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