title: LpA-I, LpA-I:A-II HDL and CHD-risk: The Framingham Offspring Study and the Veterans Affairs HDL Intervention Trial.
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 (< or = 40 mg/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 (alpha-1) but no correlation with the small LpA-I HDL particle (prebeta-1). LpA-I:A-II concentration had a positive correlation with the large (alpha-2) and an inverse correlation with the small (alpha-3) LpA-I:A-II HDL particles.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Lipid Metabolism Laboratory, JM-USDA/HNRCA, Tufts University, 711 Washington Street, Boston, MA 02111, USA. bela.asztalos@tufts.edu
authors.forename: Bela F
authors.initials: BF
authors.lastname: Asztalos
authors.forename: Serkalem
authors.initials: S
authors.lastname: Demissie
authors.forename: L Adrienne
authors.initials: LA
authors.lastname: Cupples
authors.forename: Dorothea
authors.initials: D
authors.lastname: Collins
authors.forename: Caitlin E
authors.initials: CE
authors.lastname: Cox
authors.forename: Katalin V
authors.initials: KV
authors.lastname: Horvath
authors.forename: Hanna E
authors.initials: HE
authors.lastname: Bloomfield
authors.forename: Sander J
authors.initials: SJ
authors.lastname: Robins
authors.forename: Ernst J
authors.initials: EJ
authors.lastname: Schaefer
mesh_terms: D008076:Cholesterol, HDL / Q000097:blood*; D003327:Coronary Disease / Q000453:epidemiology*; D006801:Humans; D017270:Lipoprotein(a) / Q000097:blood*; D008297:Male; D010316:Particle Size; D015995:Prevalence; D012306:Risk; D014481:United States; D014493:United States Department of Veterans Affairs
chemical_list: D008076:Cholesterol, HDL; D017270:Lipoprotein(a); C106575:lipoprotein A-II; C078260:lipoprotein A-I