title: Differential Effects of Atorvastatin and Pitavastatin on Inflammation, Insulin Resistance, and the Carotid Intima-Media Thickness in Patients with Dyslipidemia.
abstract: OBJECTIVE
  3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) have multiple pleiotropic effects, such as anti-inflammatory and vascular endothelium protection, that are independent of their low-density-lipoprotein (LDL) cholesterol lowering effects. However, whether different statins exert diverse effects on inflammation, insulin resistance, and the progression of carotid atherosclerosis [as indicated by the intima-media thickness (CIMT)] in patients with dyslipidemia remains unclear.
  
  
  METHODS
  A total of 146 patients with hypercholesterolemia without known cardiovascular disease were randomly assigned to receive 5 mg/day of atorvastatin (n=73) or 1 mg/day of pitavastatin (n=73).
  
  
  RESULTS
  At baseline, age, gender, blood pressure, lipid profiles, and the serum monocyte chemoattractant protein (MCP)-1, homeostasis model assessment of insulin resistance (HOMA-IR) and CIMT values were comparable between the groups. After 12 months of treatment, atorvastatin and pitavastatin equally reduced the LDL cholesterol levels; however, atorvastatin increased the HOMA-IR by ＋26% and pitavastatin decreased this parameter by －13% (p＜0.001). The MCP-1 values were reduced by －28% in the patients treated with pitavastatin and only －11% in those treated with atorvastatin (p=0.016). A greater percent decrease in the mean CIMT from baseline was observed in the patients treated with pitavastatin than in those treated with atorvastatin (－4.9% vs. －0.5%, p=0.020).
  
  
  CONCLUSIONS
  These data indicate that, while these agents significantly and equally reduce the LDL cholesterol levels, atorvastatin and pitavastatin have different effects on inflammation, insulin resistance, and the progression of carotid atherosclerosis in patients with dyslipidemia.
authors.affiliation: Department of Internal Medicine and Cardiology, Tama-Nagayama Hospital, Nippon Medical School.
authors.forename: Akihiro
authors.initials: A
authors.lastname: Nakagomi
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Shibui
authors.forename: Keiichi
authors.initials: K
authors.lastname: Kohashi
authors.forename: Munenori
authors.initials: M
authors.lastname: Kosugi
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Kusama
authors.forename: Hirotsugu
authors.initials: H
authors.lastname: Atarashi
authors.forename: Wataru
authors.initials: W
authors.lastname: Shimizu
mesh_terms: D000368:Aged; D000069059:Atorvastatin / Q000009:adverse effects*; D002340:Carotid Artery Diseases / Q000139:chemically induced / Q000473:pathology*; D059168:Carotid Intima-Media Thickness; D050171:Dyslipidemias / Q000150:complications* / Q000188:drug therapy; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000009:adverse effects; D006937:Hypercholesterolemia / Q000150:complications* / Q000188:drug therapy; D007249:Inflammation / Q000139:chemically induced / Q000473:pathology*; D007333:Insulin Resistance; D008297:Male; D011379:Prognosis; D011446:Prospective Studies; D011804:Quinolines / Q000009:adverse effects*
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011804:Quinolines; D000069059:Atorvastatin; C108475:pitavastatin