title: [Effect of maximum dose of atorvastatin on inflammation, thrombogenesis and fibrinolysis in high-risk patients with ischemic heart disease].
abstract: OBJECTIVE
  It has been suggested that high doses of statins can be more effective in reducing the incidence of new cardiovascular events than conventional doses. The present study analyzed the effect of increasing the atorvastatin dose to 80 mg/day on indices of inflammation (C-reactive protein or CRP), thrombogenesis (prothrombin fragment [F1+2]) and fibrinolysis (tissue-type plasminogen activator antigen, t-PA, and its inhibitor PAI-1) in high-risk patients with ischemic heart disease.
  
  
  METHODS
  We studied 27 patients with high-risk coronary heart disease who had lipid levels above those recommended despite treatment with atorvastatin at 40 mg/day. At baseline, patients were compared with 21 normocholesterolemic subjects without arteriosclerotic disease. Twenty-four patients were reevaluated 3 months after the atorvastatin dose was increased to 80 mg/day.
  
  
  RESULTS
  The CRP, F1+2, t-PA and PAI-1 levels were significantly higher in patients than control subjects (all P<.05). After the atorvastatin dose was increased, significant reductions in CRP, F1+2, and PAI-1 levels were observed (P<.05). There was a significant positive correlation between the reduction in cholesterol level and that in F1+2 (r=0.43; P=.023). No other significant correlations were found.
  
  
  CONCLUSIONS
  In a group of patient with high-risk heart disease and elevated lipid levels, increasing the atorvastatin dose led to significant improvements in inflammatory, thrombogenic, and hypofibrinolytic states.
authors.affiliation: Servicio de Cardiología, Hospital General Universitario de Alicante, Alicante, Spain.
authors.forename: Antonio
authors.initials: A
authors.lastname: Tello
authors.forename: Francisco
authors.initials: F
authors.lastname: Marín
authors.forename: Vanessa
authors.initials: V
authors.lastname: Roldán
authors.forename: Ana
authors.initials: A
authors.lastname: García-Herola
authors.forename: Sofía
authors.initials: S
authors.lastname: Lorenzo
authors.forename: Vicente E
authors.initials: VE
authors.lastname: Climent
authors.forename: Luis
authors.initials: L
authors.lastname: de Teresa
authors.forename: Francisco
authors.initials: F
authors.lastname: Sogorb
mesh_terms: D000368:Aged; D000924:Anticholesteremic Agents / Q000008:administration & dosage*; D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000032:analysis*; D002784:Cholesterol / Q000097:blood; D003327:Coronary Disease / Q000097:blood / Q000188:drug therapy*; D003627:Data Interpretation, Statistical; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005342:Fibrinolysis; D005500:Follow-Up Studies; D006538:Heptanoic Acids / Q000008:administration & dosage*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D006937:Hypercholesterolemia / Q000188:drug therapy*; D007120:Immunochemistry; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D011516:Prothrombin / Q000032:analysis*; D011758:Pyrroles / Q000008:administration & dosage*; D012307:Risk Factors; D013997:Time Factors
chemical_list: D000924:Anticholesteremic Agents; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D011758:Pyrroles; D011516:Prothrombin; D002097:C-Reactive Protein; D002784:Cholesterol; D000069059:Atorvastatin