title: Effects of atorvastatin on nuclear magnetic resonance-defined lipoprotein subclasses and inflammatory markers in patients with hypercholesterolemia.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  In addition to a strong LDL-C lowering function, atorvastatin exerts beneficial effects on TG-rich lipoproteins and inflammation in hypercholesterolemic patients.
authors.affiliation: Division of Anti-Aging, Department of Internal Medicine, National Defense Medical College, Tokorozawa, Saitama, Japan. katsunorike@ndmc.ac.jp
authors.forename: Katsunori
authors.initials: K
authors.lastname: Ikewaki
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Terao
authors.forename: Hideki
authors.initials: H
authors.lastname: Ozasa
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Nakada
authors.forename: Jun-ichiro
authors.initials: J
authors.lastname: Tohyama
authors.forename: Yae
authors.initials: Y
authors.lastname: Inoue
authors.forename: Michihiro
authors.initials: M
authors.lastname: Yoshimura
mesh_terms: D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000032:analysis*; D018932:Chemokine CCL2 / Q000097:blood*; D005260:Female; D006538:Heptanoic Acids / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D006937:Hypercholesterolemia / Q000097:blood* / Q000188:drug therapy; D015850:Interleukin-6 / Q000097:blood*; D008074:Lipoproteins / Q000097:blood*; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D011758:Pyrroles / Q000494:pharmacology* / Q000627:therapeutic use
chemical_list: D018932:Chemokine CCL2; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D015850:Interleukin-6; D008074:Lipoproteins; D011758:Pyrroles; D002097:C-Reactive Protein; D000069059:Atorvastatin