Effects of atorvastatin on nuclear magnetic resonance-defined lipoprotein subclasses and inflammatory markers in patients with hypercholesterolemia.

AIM: Information about the effects of HMG-CoA reductase inhibitor (statin) treatment on lipoprotein subclasses has been severely limited. Nuclear magnetic resonance (NMR) spectrometry has emerged as a new methodology to quantify lipoprotein subclass concentrations. In the present study, we attempted to evaluate the hypolipidemic effects of atorvastatin utilizing this method. METHODS: Twenty-six patients were administered with atorvastain 10 mg daily for 4 weeks. Lipoprotein subclasses were measured by nuclear magnetic resonance (NMR) spectroscopy. Inflammation markers, including C-reactive protein (CRP), interleukin-6 (IL-6), and monocyte chemotactic protein-1 (MCP-1), were also determined. RESULTS: Additional to a marked reduction of LDL-C (-43%), atorvastatin treatment significantly decreased TG, RLP-C, apoC-II, apoC-III, and apoE by 27%, 49%, 25%, 15%, and 28%, respectively. NMR analysis revealed marked reductions of all LDL subclasses, resulting in a significant reduction of LDL particle number as well as an increase in LDL particle size. Further, some VLDL were decreased and HDL particle size was increased by atorvastatin. Among inflammation markers, MDA-LDL and IL-6 were marginally to significantly decreased. CONCLUSION: In addition to a strong LDL-C lowering function, atorvastatin exerts beneficial effects on TG-rich lipoproteins and inflammation in hypercholesterolemic patients.

Increased remnant lipoprotein in patients with coronary artery disease--evaluation utilizing a newly developed remnant assay, remnant lipoproteins cholesterol homogenous assay (RemL-C).

AIM: Remnant lipoprotein is an emerging risk factor for coronary artery disease (CAD); however, the development of a specific remnant lipoprotein assay has struggled due to its heterogeneous nature. This study aimed to evaluate the clinical importance of a newly developed assay for remnant lipoprotein, RemL-C, in patients with CAD. METHODS: This assay utilizes surfactant and phospholipase-D to selectively degrade and solubilize remnant lipoprotein. One hundred and sixty consecutive CAD patients who underwent coronary catheterization were recruited. RESULTS: Remnant liporotein, RemL-C, was significantly higher in CAD patients (p< 0.001). Additionally, TG, hs-CRP, ICAM-1, VCAM-1, and homocysteine were significantly higher, but HDL-C and adiponectin were lower with LDL-C unchanged. Since RemL-C levels correlated with plasma TG levels, two subgroups, normotriglycedemic and normolipidemic CAD groups, were extracted. In both groups, RemL-C was still significantly higher than controls. HDL-C, but not RemL-C, was associated with the severity of CAD. RemL-C significantly correlated with TG-rich lipoproteins, in particular VLDL and IDL, when limited to normolipidemic CAD patients. CONCLUSION: Remnant lipoprotein, measured by RemL-C, was increased in CAD patients independent of TG levels, indicating impaired remnant lipoprotein metabolism in these patients. CAD severity was associated with HDL-C, but not with remnant lipoprotein, indicating differential roles of lipoproteins in the development of coronary atherosclerosis. This study therefore provides clinical significance to assess coronary risk by measuring RemL-C, particularly among patients with normal TG levels.