title: Fluvastatin reduces oxidative stress, decreases serum monocyte chemotactic protein-1 level and improves endothelial function in patients with hypercholesterolemia.
abstract: OBJECTIVE
  Statins may have anti-inflammatory properties and exert endothelial protection independently of their lipid-lowering effect. However, data are scarce concerning the co-existence of these lipid-lowering-independent effects in humans.
  
  
  METHODS
  Forty three patients with hypercholesterolemia were randomly assigned in a 2:1 ratio to receive either fluvastatin 80 mg/day (n = 30) or placebo (n = 13) for 12 weeks. Plasma levels of monocyte chemotactic protein-1 (MCP-1), thiobarbituric acid reactive substances (TBARS)--an index of oxidative stress, and flow-mediated vasodilatation (FMD)--an index of endothelial function, were measured before and after statin therapy.
  
  
  RESULTS
  Fluvastatin significantly reduced the serum level of total cholesterol (201.8 +/- 25.2 vs 271.6 +/- 24.7 mg/dL; p < 0.001), low-density lipoprotein cholesterol (129.4 +/- 5.1 vs 190.2 +/- 19 mg/dL; p < 0.001), MCP-1 (190.3 +/- 40 vs 217.6 +/- 61 pg/mL; p = 0.001), and TBARS (3.7 +/- 1.3 vs 5.2 +/- 1.4 nmol/mL; p < 0.001). FMD was significantly increased, from 3.7 +/- 2.5% to 5.9 +/- 2.9% (p < 0.001) in the fluvastatin group. The reduction of serum MCP-1 or TBARS level was not correlated with the improvement of either plasma cholesterol level or FMD. No significant changes of these markers were observed in the placebo group.
  
  
  CONCLUSIONS
  Fluvastatin reduced oxidative stress and inflammatory marker levels, and improved endothelial function, in addition to its lipid-lowering effect. These observations provide a clinical rationale for the co-existence of complex and multiple vascular protective mechanisms of statins.
authors.affiliation: Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
authors.forename: Hsin-Bang
authors.initials: HB
authors.lastname: Leu
authors.forename: Chin-Cheng
authors.initials: CC
authors.lastname: Wu
authors.forename: Tao-Cheng
authors.initials: TC
authors.lastname: Wu
authors.forename: Shing-Jong
authors.initials: SJ
authors.lastname: Lin
authors.forename: Jaw-Wen
authors.initials: JW
authors.lastname: Chen
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D018932:Chemokine CCL2 / Q000097:blood*; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000187:drug effects*; D005229:Fatty Acids, Monounsaturated / Q000627:therapeutic use*; D005260:Female; D000077340:Fluvastatin; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006937:Hypercholesterolemia / Q000097:blood / Q000188:drug therapy*; D007211:Indoles / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis*; D014664:Vasodilation / Q000187:drug effects
chemical_list: D015415:Biomarkers; D018932:Chemokine CCL2; D005229:Fatty Acids, Monounsaturated; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007211:Indoles; D017392:Thiobarbituric Acid Reactive Substances; D000077340:Fluvastatin