title: Add-on therapy of EPA reduces oxidative stress and inhibits the progression of aortic stiffness in patients with coronary artery disease and statin therapy: a randomized controlled study.
abstract: OBJECTIVE
  We examined the anti-oxidant mechanisms of combined therapy of eicosapentaenoic acid (EPA) plus statin on the progression of atherosclerosis.
  
  
  METHODS
  Patients receiving statin therapy for dyslipidemia and with coronary artery disease (CAD) were assigned randomly in an open-label manner to the EPA (1,800 mg/day) -plus-statin group (n= 25; combined-therapy group) or to the statin-only group (n= 25), and followed for 48 weeks. At baseline and 48 weeks after enrollment, oxidative stress, brachial-ankle pulse wave velocity (baPWV) and stiffness parameter β-index of the carotid were measured.
  
  
  RESULTS
  The lipid profile remained unchanged throughout the study. Although the median value of baPWV increased more in the statin-only group than in the combined-therapy group, this difference was not significant (p= 0.29); however, a decrease in baPWV was associated with combined-therapy treatment by multiple regression analysis adjusted for age and mean blood pressure (p= 0.04). In addition, the β-index of the carotid was lower in the combined-therapy group than in the statin-only group (p= 0.02). Furthermore, although the difference in the reduction of the urinary concentration of 8-isoprostane between the two groups did not reach statistical significance, this concentration was significantly lower in the combined-therapy group with higher baseline levels (≥ 183 pg/mL · Cr) of urinary 8-isoprostane (p= 0.004).
  
  
  CONCLUSIONS
  EPA may reduce oxidative stress and inhibit the progression of arterial stiffness more efficiently than statin-only therapy in patients with dyslipidemia and CAD.
authors.affiliation: Department of Cardiology, Tokuyama Central Hospital, Shunan, Japan.
authors.forename: Akira
authors.initials: A
authors.lastname: Takaki
authors.forename: Seiji
authors.initials: S
authors.lastname: Umemoto
authors.forename: Kaoru
authors.initials: K
authors.lastname: Ono
authors.forename: Kouzaburo
authors.initials: K
authors.lastname: Seki
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Ryoke
authors.forename: Akihisa
authors.initials: A
authors.lastname: Fujii
authors.forename: Tatsunori
authors.initials: T
authors.lastname: Itagaki
authors.forename: Masahiko
authors.initials: M
authors.lastname: Harada
authors.forename: Masakazu
authors.initials: M
authors.lastname: Tanaka
authors.forename: Takahito
authors.initials: T
authors.lastname: Yonezawa
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ogawa
authors.forename: Masunori
authors.initials: M
authors.lastname: Matsuzaki
mesh_terms: D000368:Aged; D001011:Aorta / Q000503:physiopathology*; D003324:Coronary Artery Disease / Q000188:drug therapy* / Q000503:physiopathology; D018450:Disease Progression; D015118:Eicosapentaenoic Acid / Q000008:administration & dosage / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D059289:Vascular Stiffness
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D015118:Eicosapentaenoic Acid