title: Short-term statin treatment improves endothelial function and neurohormonal imbalance in normocholesterolaemic patients with non-ischaemic heart failure.
abstract: OBJECTIVE
  To investigate the effect of short-term statin treatment on impaired endothelium-dependent vasodilatation and haemodynamic abnormalities typically occurring in chronic heart failure (CHF).
  
  
  METHODS
  In a double-blind, crossover study endothelium-dependent vasodilatation was measured in conduit and resistance vessels of 23 patients with non-ischaemic CHF after 6 weeks of placebo and 40 mg atorvastatin. The haemodynamic impact was assessed by cardioendocrine hormones, echocardiography and clinical indicators of CHF.
  
  
  RESULTS
  Cholesterol concentrations were population average (low density lipoprotein 3.56 (SEM 0.16) mmol/l, triglycerides 1.70 (0.20) mmol/l and high density lipoprotein 1.17 (0.07) mmol/l). In resistance vessels, the area under the curve ratio during acetylcholine infusion increased from 9.2 (1.9) with placebo to 12.2 (2.1) with statin (p < 0.01). This improvement was reversed during co-infusion with the nitric oxide antagonist N(G)-monomethyl-L-arginine. In conduit arteries, flow-mediated dilatation increased from 5.64 (SEM 0.88)% with placebo to 6.83 (0.97)% with statin (p < 0.05). Endothelium-independent vasodilatation did not change (p = 0.68 for conduit and p = 0.45 for resistance vessels). Endothelin 1 and atrial natriuretic peptide (ANP) decreased from 1.57 (0.08) and 51.3 (1.0) with placebo to 1.42 (0.09) pg/ml (p < 0.05) and 42.1 (7.5) pmol/l (p < 0.05), respectively, with statin.
  
  
  CONCLUSIONS
  In patients with non-ischaemic CHF and population-average cholesterol concentrations, short-term statin treatment improves endothelial function in conduit and resistance vessels and lowers plasma endothelin 1 and ANP concentrations.
authors.affiliation: Department of Endocrinology, Addenbrooke's Hospital, Cambridge University Hospitals, Cambridge, UK.
authors.forename: C H
authors.initials: CH
authors.lastname: Strey
authors.forename: J M
authors.initials: JM
authors.lastname: Young
authors.forename: J H
authors.initials: JH
authors.lastname: Lainchbury
authors.forename: C M
authors.initials: CM
authors.lastname: Frampton
authors.forename: M G
authors.initials: MG
authors.lastname: Nicholls
authors.forename: A M
authors.initials: AM
authors.lastname: Richards
authors.forename: R S
authors.initials: RS
authors.lastname: Scott
mesh_terms: D000069059:Atorvastatin; D015415:Biomarkers / Q000097:blood; D002784:Cholesterol / Q000097:blood; D018592:Cross-Over Studies; D004311:Double-Blind Method; D004452:Echocardiography; D004730:Endothelium, Vascular; D005260:Female; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D045265:Natriuretic Peptides / Q000097:blood; D011758:Pyrroles / Q000627:therapeutic use*; D014655:Vascular Resistance / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
chemical_list: D015415:Biomarkers; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D045265:Natriuretic Peptides; D011758:Pyrroles; D002784:Cholesterol; D000069059:Atorvastatin