title: Serum lipoprotein lipase concentration and risk for future coronary artery disease: the EPIC-Norfolk prospective population study.
abstract: BACKGROUND
  Lipoprotein lipase (LPL) is associated with coronary artery disease (CAD) risk, but prospective population data are lacking. This is mainly because of the need for cumbersome heparin injections, which are necessary for LPL measurements. Recent retrospective studies, however, indicate that LPL concentration can be reliably measured in serum that enabled evaluation of the prospective association between LPL and future CAD.
  
  
  RESULTS
  LPL concentration was determined in serum samples of men and women in the EPIC-Norfolk population cohort who developed fatal or nonfatal CAD during 7 years of follow-up. For each case (n=1006), 2 controls, matched for age, sex, and enrollment time, were identified. Serum LPL concentration was lower in cases compared with controls (median and interquartile range: 61 [43-85] versus 66 [46-92] ng/mL; P<0.0001). Those in the highest LPL concentration quartile had a 34% lower risk for future CAD compared with those in the lowest quartile (odds ratio [OR] 0.66; confidence interval [CI], 0.53 to 0.83; P<0.0001). This effect remained significant after adjustment for blood pressure, diabetes, smoking, body mass index, and low-density lipoprotein (LDL) cholesterol (OR, 0.77; CI, 0.60-0.99; P=0.02). As expected from LPL biology, additional adjustments for either high-density lipoprotein cholesterol (HDL-C) or triglyceride (TG) levels rendered loss of statistical significance. Of interest, serum LPL concentration was positively linear correlated with HDL and LDL size.
  
  
  CONCLUSIONS
  Reduced levels of serum LPL are associated with an increased risk for future CAD. The data suggest that high LPL concentrations may be atheroprotective through decreasing TG levels and increasing HDL-C levels.
authors.affiliation: Department of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands.
authors.forename: Jaap
authors.initials: J
authors.lastname: Rip
authors.forename: Melchior C
authors.initials: MC
authors.lastname: Nierman
authors.forename: Nicholas J
authors.initials: NJ
authors.lastname: Wareham
authors.forename: Robert
authors.initials: R
authors.lastname: Luben
authors.forename: Sheila A
authors.initials: SA
authors.lastname: Bingham
authors.forename: Nicholas E
authors.initials: NE
authors.lastname: Day
authors.forename: Joram N I
authors.initials: JN
authors.lastname: van Miert
authors.forename: Barbara A
authors.initials: BA
authors.lastname: Hutten
authors.forename: John J P
authors.initials: JJ
authors.lastname: Kastelein
authors.forename: Jan Albert
authors.initials: JA
authors.lastname: Kuivenhoven
authors.forename: Kay-Tee
authors.initials: KT
authors.lastname: Khaw
authors.forename: S Matthijs
authors.initials: SM
authors.lastname: Boekholdt
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D008076:Cholesterol, HDL / Q000097:blood; D003324:Coronary Artery Disease / Q000097:blood* / Q000453:epidemiology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008071:Lipoprotein Lipase / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D011446:Prospective Studies; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D015415:Biomarkers; D008076:Cholesterol, HDL; D014280:Triglycerides; D008071:Lipoprotein Lipase