title: Effects of statin treatment on endothelial function, oxidative stress and inflammation in patients with arterial hypertension and normal cholesterol levels.
abstract: OBJECTIVE
  Patients with arterial hypertension are characterized by impaired endothelial function and increased cardiovascular risk. Statins have been proposed as a potential treatment option in hypertension, even in those with normal low-density lipoprotein (LDL)-cholesterol levels. We tested whether fluvastatin reduces oxidative stress and inflammation, and improves endothelial function in patients with arterial hypertension and normal LDL-cholesterol.
  
  
  METHODS
  In a cross-over designed, double-blind randomized trial, 26 patients with arterial hypertension and LDL-cholesterol below 160 mg/dl were treated for 2 weeks with either placebo or fluvastatin 80 mg/day. Endothelium-dependent vasodilation (EDV) was assessed as the forearm blood flow (FBF) response to intra-arterial infusion of acetylcholine (ACH, 12 and 48 μg/min), and endothelium-independent vasodilation (EIV) as the FBF response to nitroprusside (3.2 and 12.8 μg/min). Furthermore, we measured reduced to oxidized glutathione (GSH/GSSG) ratio in red blood cells, total antioxidant capacity in plasma (TAC) and high-sensitivity C-reactive protein (hs-CRP) levels.
  
  
  RESULTS
  Fluvastatin lowered LDL-cholesterol from 118 ± 16 to 90 ± 25 mg/dl (P < 0.0001), but had no effect on blood pressure, high-density lipoprotein (HDL)-cholesterol or triglycerides. EDV and EIV were unaffected by fluvastatin treatment (e.g. increase of FBF 48 μg/min: 339 ± 285% during placebo versus 268 ± 194% during fluvastatin, n.s.). Finally, GSH/GSSG ratio, TAC and hs-CRP levels were similar between fluvastatin and placebo treatment.
  
  
  CONCLUSIONS
  Fluvastatin treatment did not improve endothelial function, oxidative stress or inflammation in patients with arterial hypertension and normal LDL-cholesterol levels. These data argue against the usefulness of statins in patients with arterial hypertension in the absence of hypercholesterolemia or other additional risk factors.
authors.affiliation: Department of Nephrology and Hypertension, University of Erlangen-Nuremberg, Erlangen, Germany. Markus.Schneider@glasgow.ac.uk
authors.forename: Markus P
authors.initials: MP
authors.lastname: Schneider
authors.forename: Bernhard M
authors.initials: BM
authors.lastname: Schmidt
authors.forename: Stefan
authors.initials: S
authors.lastname: John
authors.forename: Roland E
authors.initials: RE
authors.lastname: Schmieder
mesh_terms: D000328:Adult; D002784:Cholesterol / Q000097:blood*; D018592:Cross-Over Studies; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005229:Fatty Acids, Monounsaturated / Q000494:pharmacology / Q000627:therapeutic use*; D000077340:Fluvastatin; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D006973:Hypertension / Q000097:blood / Q000503:physiopathology*; D007211:Indoles / Q000494:pharmacology / Q000627:therapeutic use*; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects*; D010919:Placebos
chemical_list: D005229:Fatty Acids, Monounsaturated; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007211:Indoles; D010919:Placebos; D000077340:Fluvastatin; D002784:Cholesterol