title: Comparison of pitavastatin with atorvastatin in increasing HDL-cholesterol and adiponectin in patients with dyslipidemia and coronary artery disease: the COMPACT-CAD study.
abstract: BACKGROUND
  Many large-scale clinical trials have confirmed that statins are effective in reducing low-density lipoprotein cholesterol (LDL-C) level, resulting in reducing cardiovascular events. Recent studies have focused on the effects of statins on high-density lipoprotein cholesterol (HDL-C). Here we compared the effects of two statins on lipid profile and other metabolic parameters.
  
  
  METHODS
  The study population included 129 patients with stable coronary artery disease, hypercholesterolemia, and hypo-HDL-cholesterolemia (HDL-C<50mg/dl). They were randomly allocated to treatment by pitavastatin 2-4 mg/day or atorvastatin 10-20mg/day and followed-up for 30 months. The primary endpoint was percent changes in HDL-C and adiponectin during the study. The secondary endpoints were percent and absolute changes in markers of glucose metabolism, serum lipids, and apolipoproteins.
  
  
  RESULTS
  The effects of 30-month treatment with pitavastatin on HDL-C were significantly greater than those of atorvastatin (%change: pitavastatin: 20.1 ± 25.7%, atorvastatin: 6.3 ± 19.8%, p=0.01; absolute change: pitavastatin: 7.3 ± 9.1mg/dl, atorvastatin: 2.3 ± 8.0mg/dl, p=0.02). A similar trend was seen with regard to apolipoprotein-AI (ApoAI) (%change: pitavastatin: 20.8 ± 19.3%, atorvastatin: 11.4 ± 17.6%, p=0.03; absolute change: pitavastatin: 23.1 ± 20.2mg/dl, atorvastatin: 12.1 ± 19.4 mg/dl, p=0.02). Treatment with pitavastatin, but not atorvastatin, significantly increased adiponectin levels. Neither statin had a significant effect on hemoglobin A1c. No severe adverse events were registered during the study.
  
  
  CONCLUSIONS
  Long-term treatment with pitavastatin resulted in significantly greater increases in serum HDL-C and ApoAI levels without adverse effects on glucose metabolism, compared with atorvastatin.
authors.affiliation: Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
authors.forename: Kazumasa
authors.initials: K
authors.lastname: Kurogi
authors.forename: Seigo
authors.initials: S
authors.lastname: Sugiyama
authors.forename: Kenji
authors.initials: K
authors.lastname: Sakamoto
authors.forename: Shinji
authors.initials: S
authors.lastname: Tayama
authors.forename: Shinichi
authors.initials: S
authors.lastname: Nakamura
authors.forename: Takeshi
authors.initials: T
authors.lastname: Biwa
authors.forename: Kunihiko
authors.initials: K
authors.lastname: Matsui
authors.forename: Hisao
authors.initials: H
authors.lastname: Ogawa
mesh_terms: D052242:Adiponectin / Q000097:blood*; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016632:Apolipoprotein A-I / Q000097:blood; D000069059:Atorvastatin; D008076:Cholesterol, HDL / Q000097:blood*; D003324:Coronary Artery Disease / Q000150:complications*; D023381:Endpoint Determination; D005260:Female; D005500:Follow-Up Studies; D006538:Heptanoic Acids / Q000008:administration & dosage*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D006937:Hypercholesterolemia / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D000960:Hypolipidemic Agents / Q000008:administration & dosage*; D008297:Male; D008875:Middle Aged; D011758:Pyrroles / Q000008:administration & dosage*; D011804:Quinolines / Q000008:administration & dosage*; D055815:Young Adult
chemical_list: D052242:Adiponectin; D016632:Apolipoprotein A-I; D008076:Cholesterol, HDL; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000960:Hypolipidemic Agents; D011758:Pyrroles; D011804:Quinolines; D000069059:Atorvastatin; C108475:pitavastatin
keywords: Coronary artery disease; HDL-cholesterol lowering drugs; Hyperlipoproteinemia; Lipoproteins