Venous blood was drawn in the morning under standardized conditions and a complete blood cell count was done (Coulter STKS chamber; Coulter Co, Krefeld, Germany). Within 30 minutes, the remaining blood was centrifuged at 3000g for 10 minutes, immediately aliquoted, and frozen at −70°C until analysis. In cases, blood drawing was done before the angiographic procedure. The following markers of inflammation and hemostasis were determined by enzyme-linked immunosorbent assay: interleukin (IL) 6 and tumor necrosis factor α (Quantikine; R&D Systems, Wiesbaden, Germany); intercellular adhesion molecule 1 (ICAM-1) (Diaclone, Besancon, France); plasminogen activator inhibitor 1 activity (Immuno, Heidelberg, Germany); D-dimer (Dimertest Gold EIA; Agen Biomedical Ltd, Acacia Ridge, Australia); and von Willebrand factor (Haemochrom, Essen, Germany). In addition, C-reactive protein (CRP) determinations were done by an immunoradiometric assay (range, 0.05-10 mg/L) calibrated with the World Health Organization reference standard 85/506.10 Fibrinogen was measured by immunonephelometry (Dade Behring, Marburg, Germany) and according to the Clauss method. Serum amyloid A was also determined by immunonephelometry (Dade Behring), and, finally, measurement of plasma viscosity was done in a viscometer (Harkness Coulter; Coulter Electronics, Luton, England). Interassay coefficients of variation were 7% for IL-6, 17.9% for tumor necrosis factor α, 14.2% for ICAM-1, 12% for CRP, 7.4% for serum amyloid A, 5% for fibrinogen, 11% for plasminogen activator inhibitor 1, 7.2% for D dimer, 15.8% for von Willebrand factor, and 2% for plasma viscosity. High-density lipoprotein cholesterol concentrations were determined by routine enzymatic methods. Lipoprotein Lp(a) and apoproteins were determined by immunoturbidimetry on an automated analyzer (WAKO R-30; WAKO Chemicals, Osaka, Japan). All laboratory analyses were done in a blinded fashion.