title: Effect of statins on endothelial function in patients with acute coronary syndrome: a prospective study using adhesion molecules and flow-mediated dilatation.
abstract: BACKGROUND
  Accumulating evidence suggests that inflammatory mechanisms play a central role in the development, progression and outcome of atherosclerosis. Recent evidence suggests that statins improve anti-inflammatory, anti-thrombotic and endothelial functions, along with their lipid-decreasing effects. We examined the effect of statins on endothelial function using biochemical markers of endothelial dysfunction and brachial artery flow-mediated dilatation (FMD).
  
  
  METHODS
  Thirty male patients presenting with acute coronary syndrome (ACS) and 26 age-matched healthy control subjects aged 40 - 60 years who were not on any medication were enrolled in the study. The patient group was started on atorvastatin (40 mg/day) without consideration of their low-density lipoprotein (LDL)-cholesterol levels. Endothelin, sICAM and E-selectin from stored serum samples were measured using commercially available enzyme-linked immunosorbant assays (ELISAs). Endothelial function was assessed using brachial artery FMD.
  
  
  RESULTS
  Prior to statin treatment, E-selectin, sICAM and endothelin levels, endothelial dysfunction markers, were 99.74 ± 34.67 ng/mL, 568.8 ± 149.0 ng/mL and 0.62 ± 0.33 fmol/mL, respectively in the patient group. E-selectin and sICAM levels were significantly higher in the patients than in the control subjects (P < 0.001); however, endothelin levels were not significantly different between groups. Statin treatment significantly reduced E-selectin and sICAM levels (P < 0.001); however, the decrease in endothelin levels was not statistically significant. %FMD values were significantly increased after statin treatment (P = 0.005), and levels of C-reactive protein (CRP), an inflammation marker, were significantly reduced.
  
  
  CONCLUSIONS
  Our results indicate that statins play an important role in treatment endothelial dysfunction by reducing adhesion of inflammatory cells.
authors.affiliation: Department of Cardiology, Istanbul School of Medicine, Istanbul University, Istanbul, Turkey.
authors.forename: Ibrahim
authors.initials: I
authors.lastname: Altun
authors.affiliation: Department of Cardiology, Istanbul School of Medicine, Istanbul University, Istanbul, Turkey.
authors.forename: Fahrettin
authors.initials: F
authors.lastname: Oz
authors.affiliation: Department of Biochemistry, Istanbul School of Medicine, Istanbul University, Istanbul, Turkey.
authors.forename: Selda Can
authors.initials: SC
authors.lastname: Arkaya
authors.affiliation: Department of Radiology, Sisli Etfal Training and Research Hospital, Sisli-Istanbul, Turkey.
authors.forename: Ilknur
authors.initials: I
authors.lastname: Altun
authors.affiliation: Department of Cardiology, Istanbul School of Medicine, Istanbul University, Istanbul, Turkey.
authors.forename: Ahmet Kaya
authors.initials: AK
authors.lastname: Bilge
authors.affiliation: Department of Cardiology, Istanbul School of Medicine, Istanbul University, Istanbul, Turkey.
authors.forename: Berrin
authors.initials: B
authors.lastname: Umman
authors.affiliation: Department of Biochemistry, Istanbul School of Medicine, Istanbul University, Istanbul, Turkey.
authors.forename: Umit Mutlu
authors.initials: UM
authors.lastname: Turkoglu
keywords: Acute coronary syndrome; Adhesion molecules; Flow-mediated dilatation; Statins; Ultrasonography
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