title: The influence of low dose atorvastatin on inflammatory marker levels in patients with acute coronary syndrome and its potential clinical value.
abstract: BACKGROUND
  High-dose statins are used in acute coronary syndromes (ACS) to reduce inflammation. The aim of the study was the evaluation of the influence of low-dose atorvastatin (20 mg) on selected inflammatory parameters and clinical outcomes after ACS.
  
  
  METHODS
  Seventy eight patients (pts) with ACS were randomly divided into group A (39 pts) taking atorvastatin, and group NA (39 pts) not taking any statin for the following six weeks. C-reactive protein (CRP), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1) and tumour necrosis factor alpha (TNFa) levels were measured on the first and the fifth days and six weeks after ACS.
  
  
  RESULTS
  There was no significant CRP and IL-6 level decrease in group A (CRP--62%; IL-6-73%) or group NA (CRP-44%; IL-6-62%). There was also no significant change in TNFa levels. The MCP-1 level finally reached the level of significant difference (p < 0.04). Cardiovascular events (MACE) and the restenosis rates did not differ between the groups.
  
  
  CONCLUSIONS
  Low-dose atorvastatin does not have a significant influence on cooling down inflammation in ACS, and MCP-1 can be used as an early indicator of statin anti-inflammatory activity. Furthermore, it does not reduce MACE or restenosis rates despite its influence on MCP-1 levels.
authors.affiliation: Clinic of Cardiology, Medical University, Szczecin, Poland. malewandowski@o2.pl
authors.forename: Maciej
authors.initials: M
authors.lastname: Lewandowski
authors.forename: Zdzisława
authors.initials: Z
authors.lastname: Kornacewicz-Jach
authors.forename: Barbara
authors.initials: B
authors.lastname: Millo
authors.forename: Joanna
authors.initials: J
authors.lastname: Zielonka
authors.forename: Małgorzata
authors.initials: M
authors.lastname: Czechowska
authors.forename: Robert
authors.initials: R
authors.lastname: Kaliszczak
authors.forename: Edyta
authors.initials: E
authors.lastname: Płońska
authors.forename: Jarosław
authors.initials: J
authors.lastname: Goracy
authors.forename: Jarosław
authors.initials: J
authors.lastname: Kaźmierczak
authors.forename: Marek
authors.initials: M
authors.lastname: Naruszewicz
mesh_terms: D054058:Acute Coronary Syndrome / Q000175:diagnosis* / Q000188:drug therapy*; D000924:Anticholesteremic Agents / Q000008:administration & dosage*; D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000032:analysis; D018932:Chemokine CCL2 / Q000097:blood; D017023:Coronary Angiography; D023903:Coronary Restenosis / Q000175:diagnosis / Q000453:epidemiology; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D005260:Female; D005500:Follow-Up Studies; D006538:Heptanoic Acids / Q000008:administration & dosage*; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D011336:Probability; D011758:Pyrroles / Q000008:administration & dosage*; D018570:Risk Assessment; D012720:Severity of Illness Index; D018709:Statistics, Nonparametric; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D000924:Anticholesteremic Agents; D018932:Chemokine CCL2; D006538:Heptanoic Acids; D018836:Inflammation Mediators; D015850:Interleukin-6; D011758:Pyrroles; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D000069059:Atorvastatin