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(Circulation. 2004;110:3068-3074.)
© 2004 American Heart Association, Inc.

Coronary Heart Disease

Low-Density Lipoprotein Triglycerides Associated With Low-Grade Systemic Inflammation, Adhesion Molecules, and Angiographic Coronary Artery Disease

The Ludwigshafen Risk and Cardiovascular Health Study

Winfried März, MD; Hubert Scharnagl, PhD; Karl Winkler, MD; Andreas Tiran, MD; Markus Nauck, MD; Bernhard O. Boehm, MD; Bernhard R. Winkelmann, MD

From the Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Austria (W.M., H.S., A.T.); Division of Clinical Chemistry, Department of Medicine, University Hospital, Freiburg, Germany (K.W., M.N.); Division of Endocrinology, Department of Medicine, University Hospital, Ulm, Germany (B.O.B.); and Cooperation Unit Pharmacogenomics/Applied Genomics, Department of Internal Medicine VI and Coordination Center for Clinical Trials, University of Heidelberg, Heidelberg (B.R.W.), Germany.

Correspondence to Prof Dr med Winfried März, Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Auenbruggerplatz 15, 8036 Graz, Austria. E-mail winfried.maerz{at}klinikum-graz.at

Received September 5, 2003; de novo received March 4, 2004; revision received June 23, 2004; accepted July 6, 2004.

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.

Methods and 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.

Key Words: cholesterol • triglycerides • lipoproteins • inflammation

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