title: Lipoprotein(a)-cholesterol and coronary heart disease in the Framingham Heart Study.
abstract: BACKGROUND
  Increased plasma lipoprotein(a) [Lp(a)] concentrations have been reported to be an independent risk factor for coronary heart disease (CHD) in some prospective studies, but not in others. These inconsistencies may relate to a lack of standardization and the failure of some immunoassays to measure all apolipoprotein(a) isoforms equally.
  
  
  METHODS
  We measured plasma Lp(a)-cholesterol [Lp(a)-C] in a Caucasian population of offspring and spouses of the Framingham Heart Study participants, using a lectin-based assay (LipoproTM). We compared the prevalence of increased Lp(a)-C to the presence of sinking pre-beta-lipoprotein (SPB). We also related Lp(a)-C concentrations to the prevalence of CHD risk in the entire population.
  
  
  RESULTS
  The mean (+/- SD) Lp(a)-C concentration in the Framingham population (n = 3121) was 0.186 +/- 0.160 mmol/L, with no significant gender or age differences. The mean Lp(a)-C concentrations in the absence or presence of SPB were 0.158 +/- 0. 132 mmol/L and 0.453 +/- 0.220 mmol/L, respectively (P <0.0001). The mean Lp(a)-C concentration in men with CHD (n = 156) was 0.241 +/- 0. 204 mmol/L, which was significantly (P <0.001) higher, by 34%, than in controls. The odds ratio for CHD risk in men with Lp(a)-C >/=0. 259 mmol/L (>/=10 mg/dL), after adjusting for age, HDL-cholesterol, LDL-cholesterol, smoking, diabetes, blood pressure, and body mass index, was 2.293 (confidence interval, 1.55-3.94; P <0.0005). Lp(a)-C values correlated highly with a Lp(a)-mass immunoassay [ApotekTM Lp(a); r = 0.832; P <0.0001; n = 1000].
  
  
  CONCLUSIONS
  An increased Lp(a)-C value >/=0.259 mmol/L (>/=10 mg/dL) is an independent CHD risk factor in men with a relative risk of more than 2, but was inconclusive in women. Lp(a)-C measurements offer an alternative to Lp(a)-mass immunoassays and can be performed on automated analyzers.
authors.affiliation: Division of Endocrinology, Diabetes, Metabolism and Molecular Medicine, New England Medical Center and Tufts University School of Medicine, 750 Washington St., Boston, MA 02111, USA.
authors.forename: L J
authors.initials: LJ
authors.lastname: Seman
authors.forename: C
authors.initials: C
authors.lastname: DeLuca
authors.forename: J L
authors.initials: JL
authors.lastname: Jenner
authors.forename: L A
authors.initials: LA
authors.lastname: Cupples
authors.forename: J R
authors.initials: JR
authors.lastname: McNamara
authors.forename: P W
authors.initials: PW
authors.lastname: Wilson
authors.forename: W P
authors.initials: WP
authors.lastname: Castelli
authors.forename: J M
authors.initials: JM
authors.lastname: Ordovas
authors.forename: E J
authors.initials: EJ
authors.lastname: Schaefer
mesh_terms: D000367:Age Factors; D002784:Cholesterol / Q000097:blood* / Q000737:chemistry; D003327:Coronary Disease / Q000097:blood* / Q000453:epidemiology; D005260:Female; D006801:Humans; D007118:Immunoassay; D017270:Lipoprotein(a) / Q000097:blood* / Q000737:chemistry; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D017698:Postmenopause; D017697:Premenopause; D015995:Prevalence; D012307:Risk Factors; D012737:Sex Factors
chemical_list: D017270:Lipoprotein(a); D002784:Cholesterol