title: Effects of the Addition of Eicosapentaenoic Acid to Strong Statin Therapy on Inflammatory Cytokines and Coronary Plaque Components Assessed by Integrated Backscatter Intravascular Ultrasound.
abstract: BACKGROUND
  The effects of eicosapentaenoic acid (EPA) on coronary artery disease have been previously reported; however, those of the addition of EPA to strong statins on coronary plaque components and local inflammatory cytokines are not known.
  
  
  RESULTS
  A total of 95 patients who had been treated with strong statin for at least 6 months were randomized into 2 groups: an EPA group (additional treatment with EPA at 1,800 mg/day, n=48) or a control group (no additional treatment, n=47), for 6 months. The tissue characteristics of target coronary plaque in each patient were analyzed using IB-IVUS before and after treatment. We also measured plasma levels of inflammatory cytokines sampled in the coronary sinus (CS) and peripheral vein.A significant reduction in lipid volume (18.5 ± 1.3 to 15.0 ± 1.5 mm(3), P=0.007) and a significant increase in fibrous volume (22.9 ± 0.8 to 25.6 ± 1.1 mm(3), P=0.01) were observed in IB-IVUS image analyses in the EPA group, but no significant changes in the plaque components in the control group. CS levels of pentraxin 3 and monocyte chemoattractant protein-1 were lower after than before treatment with EPA (3.3 ± 2.1 to 2.6 ± 1.2 ng/ml, 120.4 ± 26.2 to 110.2 ± 26.8 pg/ml, P=0.015 and P=0.008, respectively); however, there were no significant changes in those inflammatory cytokines between pre- and post-treatment in the control group.
  
  
  CONCLUSIONS
  The addition of EPA was associated with reduced lipid volume in coronary plaques and decreased inflammatory cytokines.
authors.affiliation: Division of Cardiovascular Medicine, Tokushima University Hospital.
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Niki
authors.forename: Tetsuzo
authors.initials: T
authors.lastname: Wakatsuki
authors.forename: Koji
authors.initials: K
authors.lastname: Yamaguchi
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Taketani
authors.forename: Hiroyasu
authors.initials: H
authors.lastname: Oeduka
authors.forename: Kenya
authors.initials: K
authors.lastname: Kusunose
authors.forename: Takayuki
authors.initials: T
authors.lastname: Ise
authors.forename: Takashi
authors.initials: T
authors.lastname: Iwase
authors.forename: Hirotsugu
authors.initials: H
authors.lastname: Yamada
authors.forename: Takeshi
authors.initials: T
authors.lastname: Soeki
authors.forename: Masataka
authors.initials: M
authors.lastname: Sata
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy; D016207:Cytokines / Q000097:blood*; D015118:Eicosapentaenoic Acid / Q000008:administration & dosage*; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D018836:Inflammation Mediators / Q000097:blood*; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D058226:Plaque, Atherosclerotic / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy; D018084:Ultrasonography, Interventional
chemical_list: D016207:Cytokines; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D018836:Inflammation Mediators; D008055:Lipids; D015118:Eicosapentaenoic Acid