title: Low-density lipoprotein triglycerides associated with low-grade systemic inflammation, adhesion molecules, and angiographic coronary artery disease: the Ludwigshafen Risk and Cardiovascular Health study.
abstract: BACKGROUND
  Markers of systemic inflammation and LDL cholesterol (LDL-C) have been considered independent risk factors of coronary artery disease (CAD). We examined whether alterations of LDL metabolism not reflected by LDL-C were associated with low-grade inflammation, vascular injury, and CAD.
  
  
  RESULTS
  We studied 739 subjects with stable angiographic CAD and 570 matched control subjects in which CAD had been ruled out by angiography. The association of LDL triglycerides (LDL-TGs) (odds ratio [OR], 1.30; 95% CI, 1.19 to 1.43; P<0.001) with CAD was stronger than that of LDL-C (OR, 1.10; 95% CI, 1.00 to 1.21; P=0.047). The predictive value of LDL-TG for CAD was independent of LDL-C. "Sensitive" C-reactive protein (CRP), serum amyloid A, fibrinogen, interleukin 6, intercellular adhesion molecule-1 (ICAM-1), and vascular adhesion molecule-1 (VCAM-1) increased in parallel to LDL-TG. CRP, ICAM-1, and VCAM-1 were inversely related to LDL-C. To examine whether LDL-TGs were associated with the distribution of LDL subfractions, we studied 114 individuals with impaired fasting glucose, impaired glucose tolerance, or type 2 diabetes mellitus. In subjects with high LDL-TG, LDLs were depleted of cholesteryl esters (CEs), and VLDLs, IDLs, and dense LDLs were significantly elevated.
  
  
  CONCLUSIONS
  Alterations of LDL metabolism characterized by high LDL-TG are related to CAD, systemic low-grade inflammation, and vascular damage. High LDL-TGs are indicative of CE-depleted LDL, elevated IDL, and dense LDL. LDL-TG may better reflect the atherogenic potential of LDL than LDL-C.
authors.affiliation: Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Auenbruggerplatz 15, 8036 Graz, Austria. winfried.maerz@klinikum-graz.at
authors.forename: Winfried
authors.initials: W
authors.lastname: März
authors.forename: Hubert
authors.initials: H
authors.lastname: Scharnagl
authors.forename: Karl
authors.initials: K
authors.lastname: Winkler
authors.forename: Andreas
authors.initials: A
authors.lastname: Tiran
authors.forename: Markus
authors.initials: M
authors.lastname: Nauck
authors.forename: Bernhard O
authors.initials: BO
authors.lastname: Boehm
authors.forename: Bernhard R
authors.initials: BR
authors.lastname: Winkelmann
mesh_terms: D000368:Aged; D001055:Apolipoproteins B / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D002788:Cholesterol Esters / Q000097:blood; D015331:Cohort Studies; D003327:Coronary Disease / Q000097:blood*; D003430:Cross-Sectional Studies; D048909:Diabetes Complications / Q000097:blood; D005260:Female; D005858:Germany; D006801:Humans; D007249:Inflammation / Q000097:blood*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008074:Lipoproteins / Q000097:blood; D008075:Lipoproteins, HDL / Q000097:blood; D053419:Lipoproteins, IDL; D008077:Lipoproteins, LDL / Q000097:blood*; D008079:Lipoproteins, VLDL / Q000097:blood; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D012307:Risk Factors; D000685:Serum Amyloid A Protein / Q000032:analysis; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood*
chemical_list: D001055:Apolipoproteins B; D002788:Cholesterol Esters; D015850:Interleukin-6; D008074:Lipoproteins; D008075:Lipoproteins, HDL; D053419:Lipoproteins, IDL; D008077:Lipoproteins, LDL; D008079:Lipoproteins, VLDL; D000685:Serum Amyloid A Protein; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein