title: Immediate effects of fluvastain on circulating soluble endothelial protein C and free tissue factor pathway inhibitor in acute coronary syndromes.
abstract: BACKGROUND
  Statins promptly lower rates of adverse cardiovascular events in patients with acute coronary syndromes (ACS). These therapeutic properties may be mediated by the effects of statins on key hemostatic factors. This study examined the immediate effects of fluvastatin on plasma free tissue factor pathway inhibitor (fTFPI) and soluble endothelial protein C receptor (sEPCR) concentrations in patients with unstable angina or non-ST segment elevation myocardial infarction.
  
  
  METHODS
  We studied 57 patients consecutively admitted to our emergency department and randomly assigned to placebo (n = 29) versus fluvastatin, 80 mg, p.o. (n = 28). All patients were treated with aspirin and metoprolol p.o., nitroglycerin i.v., and subcutaneous enoxaparin. Venous blood was sampled as soon as possible upon admission, before and 6 h after administration of study drug and standard anti-ischemic therapy.
  
  
  RESULTS
  Mean sEPCR concentrations decreased significantly in patients treated with fluvastatin (-8.1 +/- 6.7% from baseline) and was unchanged in the placebo group (-2.3 +/- 14.4%, P = 0.007 vs. fluvastatin). Though fTFPI increased significantly after the administration of both fluvastatin and placebo, the mean increase after fluvastatin (450+/-436%) was significantly greater than after placebo (155+/-141%, P = 0.001).
  
  
  CONCLUSIONS
  Treatment with fluvastatin significantly modified key hemostatic factors toward an antithrombotic effect within 6 h. These properties may, in part, explain the early salutary effects of fluvastatin in patients with ACS.
authors.affiliation: Hacettepe University Medical Faculty, Cardiology Department, Ankara, Turkey. eatalar@hacettepe.edu.tr
authors.forename: Enver
authors.initials: E
authors.lastname: Atalar
authors.forename: Secuk
authors.initials: S
authors.lastname: Coskun
authors.forename: Ibrahim C
authors.initials: IC
authors.lastname: Haznedaroglu
authors.forename: Neslihan
authors.initials: N
authors.lastname: Yücel
authors.forename: Necla
authors.initials: N
authors.lastname: Ozer
authors.forename: Bulent
authors.initials: B
authors.lastname: Sivri
authors.forename: Serdar
authors.initials: S
authors.lastname: Aksoyek
authors.forename: Kenan
authors.initials: K
authors.lastname: Ovunc
authors.forename: Ferhan
authors.initials: F
authors.lastname: Ozmen
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000941:Antigens / Q000097:blood*; D015703:Antigens, CD; D001779:Blood Coagulation Factors; D003327:Coronary Disease / Q000097:blood / Q000188:drug therapy*; D000074283:Endothelial Protein C Receptor; D005229:Fatty Acids, Monounsaturated / Q000494:pharmacology*; D005260:Female; D000077340:Fluvastatin; D006023:Glycoproteins / Q000097:blood*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology*; D007211:Indoles / Q000494:pharmacology*; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011956:Receptors, Cell Surface / Q000097:blood*
chemical_list: D000941:Antigens; D015703:Antigens, CD; D001779:Blood Coagulation Factors; D000074283:Endothelial Protein C Receptor; D005229:Fatty Acids, Monounsaturated; D006023:Glycoproteins; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007211:Indoles; D008074:Lipoproteins; C478370:PROCR protein, human; D011956:Receptors, Cell Surface; C051928:lipoprotein-associated coagulation inhibitor; D000077340:Fluvastatin