title: Low-dose rosuvastatin improves arterial stiffness in high-risk Japanese patients with dyslipdemia in a primary prevention group.
abstract: BACKGROUND
  The treatment effects of rosuvastatin on arterial stiffness were assessed and compared to those of fluvastatin in high-risk Japanese patients with dyslipidemia in a primary prevention group.
  
  
  RESULTS
  Patients were randomly assigned to either 2.5-5 mg/day of rosuvastatin (Group A) or 20-40 mg/day of fluvastatin (Group B) and followed up for 12 months. In Group A (n=38), there was a progressive reduction in brachial-ankle pulse wave velocity (baPWV) along with a decrease in the low-density lipoprotein cholesterol/high-density lipoprotein cholesterol (L/H) ratio and high-sensitivity C-reactive protein (hsCRP), and the change in baPWV correlated significantly with that of the L/H ratio and that of hsCRP after rosuvastatin treatment. In Group B (n=37), although fluvastatin achieved a significant improvement in baPWV, L/H ratio, and hsCRP, baPWV was significantly greater than that in Group A and showed a significant correlation with that of hsCRP alone after fluvastatin treatment. In a subgroup of patients (n=26), switching from fluvastatin to rosuvastatin further improved baPWV and the L/H ratio without altering hsCRP after 12 months.
  
  
  CONCLUSIONS
  Low-dose rosuvastatin would be more effective than fluvastatin in improving arterial stiffness in high-risk Japanese patients with dyslipidemia. The results suggest that improvement in arterial stiffness by rosuvastatin mainly depends on its strong lipid-lowering effects, whereas that by fluvastatin is strongly dependent on the pleiotropic effects, especially an anti-inflammatory action.
authors.affiliation: Department of Cardiovascular Medicine, Shinshu University School of Health Sciences, Japan. hongo@shinshu-u.ac.jp
authors.forename: Minoru
authors.initials: M
authors.lastname: Hongo
authors.forename: Setsuo
authors.initials: S
authors.lastname: Kumazaki
authors.forename: Atsushi
authors.initials: A
authors.lastname: Izawa
authors.forename: Hiroya
authors.initials: H
authors.lastname: Hidaka
authors.forename: Takeshi
authors.initials: T
authors.lastname: Tomita
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Yazaki
authors.forename: Osamu
authors.initials: O
authors.lastname: Kinoshita
authors.forename: Uichi
authors.initials: U
authors.lastname: Ikeda
mesh_terms: D000368:Aged; D044466:Asian People; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D050171:Dyslipidemias / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology*; D005229:Fatty Acids, Monounsaturated / Q000008:administration & dosage*; D005260:Female; D005464:Fluorobenzenes / Q000008:administration & dosage*; D000077340:Fluvastatin; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D007211:Indoles / Q000008:administration & dosage*; D007564:Japan; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011743:Pyrimidines / Q000008:administration & dosage*; D012307:Risk Factors; D000068718:Rosuvastatin Calcium; D013449:Sulfonamides / Q000008:administration & dosage*; D013997:Time Factors; D059289:Vascular Stiffness / Q000187:drug effects*
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D005229:Fatty Acids, Monounsaturated; D005464:Fluorobenzenes; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007211:Indoles; D011743:Pyrimidines; D013449:Sulfonamides; D000077340:Fluvastatin; D000068718:Rosuvastatin Calcium