LpA-I, LpA-I:A-II HDL and CHD-risk: The Framingham Offspring Study and the Veterans Affairs HDL Intervention Trial

Bela F. Asztalos, Serkalem Demissie, L. Adrienne Cupples, Dorothea Collins, Caitlin E. Cox, Katalin V. Horvath, Hanna E. Bloomfield, Sander J. Robins, Ernst J. Schaefer

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30 Scopus citations

Abstract

Objective: We tested the hypothesis that concentrations of LpA-I and/or LpA-I:A-II HDL subclasses are significantly associated with CHD prevalence and recurrent cardiovascular events. Methods: LpA-I levels were determined by differential electroimmunoassay in male participants with (n = 169) and without CHD (n = 850) from the Framingham Offspring Study (FOS) and in male participants with CHD from the placebo arm of the Veterans Affairs HDL Intervention Trial (VA-HIT) (n = 741). Data were analyzed cross-sectionally (FOS) and prospectively (VA-HIT) and were adjusted for established lipid and non-lipid CHD risk factors. Results: We observed slightly but significantly higher LpA-I levels in CHD cases compared to all or to HDL-C-matched controls and slightly but significantly higher LpA-I:A-II levels in CHD cases compared to HDL-C-matched controls it the FOS. Neither LpA-I nor LpA-I:A-II levels were significantly different between groups with and without recurrent cardiovascular events in the VA-HIT. No significant differences were observed in LpA-I and LpA-I:A-II levels in low HDL-C (≤40mg/dl) subjects with CHD (VA-HIT, n = 711) and without CHD (FOS, n = 373). Plasma LpA-I concentration had a positive correlation with the large LpA-I HDL particle (α-1) but no correlation with the small LpA-I HDL particle (preβ-1). LpA-I:A-II concentration had a positive correlation with the large (α-2) and an inverse correlation with the small (α-3) LpA-I:A-II HDL particles. Conclusion: Our data do not support the hypothesis that CHD prevalence (FOS) or recurrence of cardiovascular events (VA-HIT) are associated with significant reductions in the concentrations of LpA-I and/or LpA-I:A-II HDL subclasses.

Original languageEnglish (US)
Pages (from-to)59-67
Number of pages9
JournalAtherosclerosis
Volume188
Issue number1
DOIs
StatePublished - Sep 2006

Bibliographical note

Funding Information:
We would like to thank the participants of the Framingham and VA-HIT studies. This study was supported by the NIH/NHLBI (HL-64738 to Bela Asztalos) and by the NHLBI's Framingham Heart Study in collaboration with Boston University (Contract N01-HC-38038 and HL-54776). VA-HIT cohort was supported by the VA Cooperative Studies Program of the Department of Veterans Affairs Office of Research and Development, Washington, DC.

Keywords

  • ApoA-I
  • CHD-risk
  • HDL subpopulations
  • HDL-C
  • LpA-I

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