Objective : RLP were defined as unbound fractions from immunoaffinity gels containing monoclonal antibodies against apolipoprotein (apo) A-I and B-100, and may reflect atherogenic triglyceride-rich remnant lipoproteins. However, RLP are heterogeneous lipoproteins composed of exogenous lipoproteins containing apoB-48 and endogenous lipoproteins containing apoB-100. To evaluate endogenous lipoproteins containing apoB-100 in RLP, we developed a new enzyme-linked immunosorbent assay (ELISA) for the specific detection of apoB-100 in RLP (RLP-apoB100), and clarified the distribution of RLP-apoB100 in lipoproteins and the association of RLP-apoB100 with CAD. Materials and methods : Subjects consisted of 2 normolipidemic individuals and 3 hyperlipidemic individuals. Distribution of RLP-apoB100 was examined in lipoprotein fractions separated by ultracentrifugation for density or gel chromatography for particle size. In one subject, distribution of RLP-apoE was examined by ELISA and electrophoresis of these fractions. To investigate its atherogenic role, plasma lipids and RLP-apoB100 were compared between 20 healthy control subjects, 8 CAD (-) patients and 42 CAD (+) patients who had undergone coronary angiography. CAD (+) was defined as ?50% stenosis in major coronary arteries. Results : RLP-apoB100 was distributed in only buoyant LDL of control subjects. In contrast, it was widely distributed in VLDL, IDL and small, dense LDL of hyperlipidemic subjects. In type III hyperlipidemic subjects, RLP-apoE was also distributed in VLDL, IDL and LDL. In clinical analysis, levels of RLP-apoB100 were the lowest in control subjects and the highest in the CAD (+) patients. CAD (-) patients' levels were between those of control subjects and CAD (+) patients (6.8 vs 10.4 vs 12.2 mg/dl, p<0.001). Conclusion : The measurement of RLP-apoB100 can evaluate endogenous lipoproteins in RLP, which may contribute to atherogenicity of RLP.