title: Early initiation of low-dose atorvastatin treatment after an acute ST-elevated myocardial infarction, decreases inflammatory process and prevents endothelial injury and activation.
abstract: BACKGROUND
  High-dose statin treatment improves clinical outcome of ST-elevated myocardial infarction (STEMI). However, the effect of low-dose atorvastatin treatment on inflammatory and pro-thrombotic molecules during the post-STEMI period is unclear. We investigated the effect of low-dose atorvastatin treatment on the kinetics of cytokine IL-6, vascular cell adhesion molecule (sVCAM-1) and endothelium-derived markers of thrombosis/fibrinolysis such as von Willebrand factor (vWF), plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (tPA), post STEMI.
  
  
  METHODS
  Twenty-four normocholesterolemic patients with STEMI were randomised to receive atorvastatin 10mg/day or no statin treatment for 6 weeks after the event. Blood samples were obtained by their admission to the hospital as well as at weeks 1 and 6. Circulating levels of IL-6, sVCAM-1, vWF, PAI-1 and tPA were determined by ELISA.
  
  
  RESULTS
  Atorvastatin induced a decrease of IL-6 at 1 week, an effect which reached significance compared to baseline at 6 weeks post STEMI (p<0.05 vs baseline). Serum sVCAM-1 was increased in controls both at 1 and 6 weeks post-STEMI (p<0.05 vs baseline), an effect prevented by atorvastatin. Plasma vWF was increased 1 week post-STEMI in controls (p<0.05 vs baseline) and returned to baseline at 6 weeks, an effect prevented by atorvastatin. Plasma PAI-1, tPA and the PAI-1/tPA ratio remained unchanged in both groups.
  
  
  CONCLUSIONS
  Early initiation of low-dose atorvastatin treatment decreases the expression of IL-6 and sVCAM-1 and the release of vWF in patients with STEMI. Therefore, low-dose atorvastatin, modulates inflammatory response and decreases endothelial injury and activation in patients with recent STEMI.
authors.forename: Elli
authors.initials: E
authors.lastname: Stefanadi
authors.forename: Dimitris
authors.initials: D
authors.lastname: Tousoulis
authors.forename: Charalambos
authors.initials: C
authors.lastname: Antoniades
authors.forename: Vasiliki
authors.initials: V
authors.lastname: Katsi
authors.forename: Erini
authors.initials: E
authors.lastname: Bosinakou
authors.forename: Emmanuel
authors.initials: E
authors.lastname: Vavuranakis
authors.forename: Georgia
authors.initials: G
authors.lastname: Triantafyllou
authors.forename: Kyriakoula
authors.initials: K
authors.lastname: Marinou
authors.forename: Costas
authors.initials: C
authors.lastname: Tsioufis
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Papageorgiou
authors.forename: George
authors.initials: G
authors.lastname: Latsios
authors.forename: Christodoulos
authors.initials: C
authors.lastname: Stefanadis
mesh_terms: D000069059:Atorvastatin; D015415:Biomarkers / Q000097:blood; D004562:Electrocardiography; D004730:Endothelium, Vascular / Q000293:injuries*; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D007249:Inflammation / Q000097:blood / Q000188:drug therapy; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000188:drug therapy* / Q000276:immunology; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011758:Pyrroles / Q000627:therapeutic use*; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000097:blood; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D015415:Biomarkers; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D015850:Interleukin-6; D017395:Plasminogen Activator Inhibitor 1; D011758:Pyrroles; D019010:Vascular Cell Adhesion Molecule-1; D014841:von Willebrand Factor; D000069059:Atorvastatin; D010959:Tissue Plasminogen Activator