title: Impact of Adding Eicosapentaenoic Acid to Statin Therapy on Plasma Pentraxin 3 Level in Patients with Stable Coronary Artery Disease: A 6-Month, Randomized Controlled Study.
abstract: BACKGROUND
  We hypothesized that the additional administration of eicosapentaenoic acid (EPA) in patients with stable coronary artery disease (CAD) receiving statin has the potential to lower the serum pentraxin 3 (PTX3) level, an indicator of plaque stabilization.
  
  
  METHODS
  We randomly assigned CAD patients already receiving statin therapy to an EPA group (1800 mg/day, n = 53) or control group (n = 53).
  
  
  RESULTS
  No significant difference was found in the change in the plasma PTX3 level between the groups. However, in a subgroup analysis, a significant percentage reduction in the plasma PTX3 level was observed in patients receiving strong statin compared with the patients receiving moderate statin in the EPA group (-5.6 vs. 14.7 %, p = 0.0082), while no such difference in the percentage change in the plasma PTX3 level was noted between the two same statin subgroups in the control group. A multiple logistic regression analysis identified the addition of EPA to ongoing strong statin treatment as an independent predictor of PTX3 level reduction. Furthermore, even in patients with relatively well-controlled serum lipid levels, pretreatment with EPA added to ongoing statin therapy reduced serum non-high-density lipoprotein cholesterol and triglyceride-rich lipoproteins as residual risk factors.
  
  
  CONCLUSIONS
  Through this study design, the results could not support the hypothesis that adding EPA in patients with stable CAD receiving varying degrees of statin treatment reduces the plasma PTX3 level comprehensively. However, addition of EPA to ongoing strong statin treatment, but not ongoing moderate statin treatment, may reduce the plasma PTX3 level, possibly leading to coronary plaque stabilization.
  
  
  BACKGROUND
  UMIN ( http://www.umin.ac.jp/ ), Study ID: UMIN000010452.
authors: Department of Health Planning Center, Nihon University Hospital, 1-6 Kanda-Surugadai, Chiyoda-ku, Tokyo, 101-8309, Japan. tani.shigemasa@nihon-u.ac.jp.|Department of Cardiology, Nihon University Hospital, Tokyo, Japan. tani.shigemasa@nihon-u.ac.jp.|Division of Cardiology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan. tani.shigemasa@nihon-u.ac.jp.
authors: Shigemasa
authors: S
authors: Tani
authors: Division of Cardiology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan.
authors: Ken
authors: K
authors: Nagao
authors: Department of Cardiology, Nihon University Hospital, Tokyo, Japan.|Division of Cardiology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan.
authors: Tsukasa
authors: T
authors: Yagi
authors: Department of Cardiology, Nihon University Hospital, Tokyo, Japan.|Division of Cardiology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan.
authors: Wataru
authors: W
authors: Atsumi
authors: Department of Cardiology, Nihon University Hospital, Tokyo, Japan.
authors: Atsushi
authors: A
authors: Hirayama
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D003324:Coronary Artery Disease / Q000097:blood* / Q000188:drug therapy*; D004359:Drug Therapy, Combination; D015118:Eicosapentaenoic Acid / Q000008:administration & dosage*; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D000683:Serum Amyloid P-Component / Q000378:metabolism*; D013997:Time Factors; D000099153:Pentraxins
chemical_list: D015415:Biomarkers; D002097:C-Reactive Protein; D015118:Eicosapentaenoic Acid; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000683:Serum Amyloid P-Component; D000099153:Pentraxins