title: [Markers of inflammation and platelet aggregation in patients with non ST elevation acute coronary syndrome treated with atorvastatin or pravastatin].
abstract: OBJECTIVE
  To find out whether early use of atorvastatin and pravastatin in patients with non-ST elevation acute coronary syndrome is associated with rapid changes of platelet aggregation and plasma levels of markers of inflammation.
  
  
  METHODS
  Ninety patients (<24h from pain onset, age 64+/-10 years) treated with aspirin and heparin were randomized to open atorvastatin 10 mg/day (n=30), atorvastatin 40 mg/day (n=29) or pravastatin 40 mg/day (n=31). Spontaneous and ADP induced platelet aggregation (light transmission), plasma levels of interleukin 6 (IL-6) and C-reactive protein (CRP) (immunoassay) were assessed at baseline, on days 7 and 14.
  
  
  RESULTS
  Baseline clinical characteristics, platelet aggregation parameters, CRP and IL-6 levels were similar in all groups. In all groups levels of total and low-density lipoprotein (LDL) cholesterol (CH) were lowered by days 7 (p<0.01) and 14 (p<0.01 vs. baseline and for both atorvastatin groups vs. day 7). Spontaneous platelet aggregation decreased by 15% from baseline, p<0.01, on day 14 in patients receiving atorvastatin 40 and was unchanged in other groups. Changes of ADP induced platelet aggregation, IL-6 and CRP levels were not significant in all groups. However combination of 2 atorvastatin groups (n=59) revealed decrease of CRP by 18% from baseline on day 14 (from 6.94+/-0.97 to 4.76+/-0.76 mg/l, p=0.028). No correlations were found between changes of LDL CH and those of other parameters.
  
  
  CONCLUSIONS
  In otherwise conventionally treated patients with non-ST elevation acute coronary syndrome early use of atorvastatin was associated with rapid (in 14 days) decrease of CRP level. Higher dose of atorvastatin (40 mg/day) induced favorable changes of spontaneous platelet aggregation. There were no significant changes of parameters studied in pravastatin treated patients.
authors.forename: E V
authors.initials: EV
authors.lastname: Pokrovskaia
authors.forename: N A
authors.initials: NA
authors.lastname: Vaulin
authors.forename: N A
authors.initials: NA
authors.lastname: Gratsianskiĭ
authors.forename: O V
authors.initials: OV
authors.lastname: Averkov
authors.forename: A D
authors.initials: AD
authors.lastname: Deev
mesh_terms: D000208:Acute Disease; D000328:Adult; D000368:Aged; D000924:Anticholesteremic Agents / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use*; D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000378:metabolism*; D003327:Coronary Disease / Q000150:complications* / Q000503:physiopathology*; D004334:Drug Administration Schedule; D004562:Electrocardiography; D005260:Female; D006538:Heptanoic Acids / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use*; D006801:Humans; D006937:Hypercholesterolemia / Q000150:complications* / Q000188:drug therapy*; D007249:Inflammation / Q000175:diagnosis / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects*; D017035:Pravastatin / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use*; D011758:Pyrroles / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use*; D013997:Time Factors
chemical_list: D000924:Anticholesteremic Agents; D006538:Heptanoic Acids; D011758:Pyrroles; D002097:C-Reactive Protein; D000069059:Atorvastatin; D017035:Pravastatin