title: Fluvastatin prevents development of arterial stiffness in haemodialysis patients with type 2 diabetes mellitus.
abstract: BACKGROUND
  Arterial stiffness assessed by pulse wave velocity (PWV) predicts all-cause and cardiovascular mortality in diabetic patients with end-stage renal disease. We studied the preventive effects of a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, fluvastatin, on arterial PWV values in this population.
  
  
  METHODS
  Twenty-two patients with normal serum lipid levels received fluvastatin (20 mg/day p.o.) or a placebo for 6 months. Their serum lipid levels, serum levels of C-reactive protein (CRP), arterial PWV, and ankle brachial indexes (ABI) were determined before, and 3 and 6 months after taking the medication to evaluate arterial stiffness.
  
  
  RESULTS
  At the beginning of the follow-up, there were no differences in age, blood pressure, body mass index, serum haemoglobin A1c level, serum CRP level, serum lipid levels, PWV or ABI between the placebo- (n=10) and the fluvastatin-treated patients (n=12). After 6 months, the PWV and the serum oxidized low-density lipoprotein cholesterol (LDL-C) level increased significantly (from 1969+/-140 to 2326+/-190 cm/s and 70.4+/-13.8 to 91.8+/-15.5 U/l, respectively) in the placebo-treated patients. However, the fluvastatin group had a significantly reduced PWV (from 1991+/-162 to 1709+/-134 cm/s), oxidized LDL-C serum levels (from 89.0+/-9.6 to 73.0+/-5.8 U/l) and CRP serum levels (from 0.97+/-0.32 to 0.26+/-0.16 mg/dl) compared with those in the placebo group.
  
  
  CONCLUSIONS
  Long-term administration of fluvastatin prevents further worsening of arterial biomechanics in haemodialysis patients with type 2 diabetes mellitus, even in the presence of serum lipid levels in the normal range.
authors.affiliation: Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan. atzichi@sc.itc.keio.ac.jp
authors.forename: Atsuhiro
authors.initials: A
authors.lastname: Ichihara
authors.forename: Matsuhiko
authors.initials: M
authors.lastname: Hayashi
authors.forename: Munekazu
authors.initials: M
authors.lastname: Ryuzaki
authors.forename: Michiko
authors.initials: M
authors.lastname: Handa
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Furukawa
authors.forename: Takao
authors.initials: T
authors.lastname: Saruta
mesh_terms: D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D001783:Blood Flow Velocity; D001794:Blood Pressure / Q000187:drug effects; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000032:analysis; D002784:Cholesterol / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000628:therapy*; D003928:Diabetic Nephropathies / Q000097:blood / Q000188:drug therapy / Q000628:therapy*; D005229:Fatty Acids, Monounsaturated / Q000627:therapeutic use*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D000077340:Fluvastatin; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D007211:Indoles / Q000627:therapeutic use*; D010743:Phospholipids / Q000097:blood; D010919:Placebos; D006435:Renal Dialysis; D014280:Triglycerides / Q000097:blood; D014652:Vascular Diseases / Q000517:prevention & control*
chemical_list: D000924:Anticholesteremic Agents; D002097:C-Reactive Protein; D002784:Cholesterol; D005229:Fatty Acids, Monounsaturated; D005230:Fatty Acids, Nonesterified; D000077340:Fluvastatin; D006442:Glycated Hemoglobin; D007211:Indoles; D010743:Phospholipids; D010919:Placebos; D014280:Triglycerides