title: Effects of fluvastatin therapy on serum interleukin-18 and interleukin-10 levels in patients with acute coronary syndrome.
abstract: OBJECTIVE
  Experimental data demonstrate that inflammation plays an important role in the initiation, progression, and complications of atherosclerosis. Statins were shown to downregulate inflammatory cytokines.We conducted this study to investigate the effects of fluvastatin therapy on plasma interleukin-18 (IL-18) and interleukin-10 (IL-10) concentration in patients with acute coronary syndrome.
  
  
  RESULTS
  Serum IL-18 and IL-10 levels were measured in 90 patients with acute coronary syndrome, 47 patients with stable angina pectoris, and 55 normal control subjects. Patients in the acute coronary syndrome group were randomly assigned to a fluvastatin group and a routine group.The fluvastatin group was given fluvastatin 40 mg/day and the routine group a placebo.After one month of follow-up, serum IL-18, IL-10 levels, and serum lipid concentration were measured again. Serum IL-18 levels were significantly higher in the acute coronary syndrome group than in the stable angina pectoris group and the control group. However, serum IL-10 levels were significantly lower than in the stable angina pectoris group and the control group.After one month of treatment, the serum IL-18 levels decreased significantly and the serum IL-10 levels increased significantly in all patients with acute coronary syndrome, but the changes of serum IL-18 and IL-10 levels were more pronounced in the fluvastatin group. No relationship was observed between the rate of decrease of serum IL-18 or the rate of increase of serum IL-10 and serum lipids levels.
  
  
  CONCLUSIONS
  Inflammation plays an important role in the initiation of acute coronary syndromes. Fluvastatin possesses an anti-inflammatory effect, independent of its lipid-lowering action.
authors.affiliation: Dept. of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China. liuyongasheng@medmail.com.cn
authors.forename: Yongsheng
authors.initials: Y
authors.lastname: Liu
authors.forename: Hong
authors.initials: H
authors.lastname: Jiang
authors.forename: Wenwei
authors.initials: W
authors.lastname: Liu
authors.forename: Hongling
authors.initials: H
authors.lastname: Shang
authors.forename: Yongqian
authors.initials: Y
authors.lastname: Tang
authors.forename: Rui
authors.initials: R
authors.lastname: Zhu
authors.forename: Bin
authors.initials: B
authors.lastname: Li
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood* / Q000188:drug therapy*; D000787:Angina Pectoris / Q000097:blood / Q000188:drug therapy; D016022:Case-Control Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005229:Fatty Acids, Monounsaturated / Q000627:therapeutic use*; D005260:Female; D000077340:Fluvastatin; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D007211:Indoles / Q000627:therapeutic use*; D016753:Interleukin-10 / Q000097:blood*; D020382:Interleukin-18 / Q000097:blood*; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D016896:Treatment Outcome
chemical_list: D005229:Fatty Acids, Monounsaturated; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D007211:Indoles; D020382:Interleukin-18; D008055:Lipids; D016753:Interleukin-10; D000077340:Fluvastatin