title: Effect of atorvastatin on endothelial function and inflammation in long-duration type 1 diabetic patients without coronary heart disease and arterial hypertension.
abstract: OBJECTIVE
  We evaluated the ability of atorvastatin, an HMG-CoA reductase inhibitor, to affect endothelial function and inflammation in long-duration (>10 years) type 1 diabetes mellitus (T1DM) patients without coronary heart disease (CHD) and arterial hypertension (AH).
  
  
  RESULTS
  We randomized 204 Caucasians with long-duration T1DM into either the atorvastatin 40 mg/day plus hypolipaemic diet group (n = 154) or the placebo plus hypolipaemic diet group (n = 50) for 6 months. Endothelium-dependent flow-mediated (FMD) and endothelium-independent flow-mediated vasodilatation, serum levels of plasminogen activator inhibitor-1 (PAI-1), von Willebrand factor (vWF) and high sensitivity C-reactive protein (hs-CRP) were estimated before and after treatment. After 6 months of therapy, FMD was increased by 44% in the atorvastatin plus diet group compared with the placebo plus diet group. Treatment with atorvastatin led to a significant reduction in levels of PAI-1 and hs-CRP; however, the elevation of vWF level was observed. In the placebo plus diet group, we observed a significant reduction in levels of hs-CRP but not of vWF and PAI-1.
  
  
  CONCLUSIONS
  Atorvastatin improves endothelial function and reduces some proinflammatory and prothrombotic markers of atherosclerosis in T1DM patients without CHD and AH. The surprising effect of atorvastatin on serum vWF levels in T1DM requires further study.
authors.affiliation: Department of Coronary Disease, Jagiellonian University School of Medicine, Krakow, Poland. konduracka27@interia.eu
authors.forename: E
authors.initials: E
authors.lastname: Konduracka
authors.forename: D
authors.initials: D
authors.lastname: Galicka-Latala
authors.forename: G
authors.initials: G
authors.lastname: Cieslik
authors.forename: P
authors.initials: P
authors.lastname: Rostoff
authors.forename: D
authors.initials: D
authors.lastname: Fedak
authors.forename: J
authors.initials: J
authors.lastname: Sieradzki
authors.forename: J
authors.initials: J
authors.lastname: Naskalski
authors.forename: W
authors.initials: W
authors.lastname: Piwowarska
mesh_terms: D000328:Adult; D000069059:Atorvastatin; D001916:Brachial Artery / Q000187:drug effects / Q000503:physiopathology; D003324:Coronary Artery Disease / Q000503:physiopathology / Q000517:prevention & control*; D003922:Diabetes Mellitus, Type 1 / Q000178:diet therapy / Q000188:drug therapy* / Q000503:physiopathology; D003925:Diabetic Angiopathies / Q000517:prevention & control*; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011758:Pyrroles / Q000627:therapeutic use*; D014664:Vasodilation / Q000502:physiology; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D017395:Plasminogen Activator Inhibitor 1; D011758:Pyrroles; D014841:von Willebrand Factor; D000069059:Atorvastatin