title: N-3 fatty acid supplementation to routine statin treatment inhibits platelet function, decreases patients' daytime blood pressure, and improves inflammatory status.
abstract: OBJECTIVE
  N-3 fatty acids reduce the risks of cardiovascular morbidity and mortality. Administration of N-3 fatty acids to patients treated with statins may potentiate the treatment effects. We examined the operating mechanisms underlying such a combination.
  
  
  METHODS
  Thirty-two hypercholesterolemic patients aged 30-70 years with hypercholesterolemia controlled by statins, received sequential treatments with placebo followed by 1.9 g/day of N-3 fatty acids for 23 weeks. Scheduled clinical visits included physical examination, 24-h blood pressure measurement, endothelial function evaluated by pulse wave analysis, analyses for platelet function, inflammation markers [interleukin (IL)-6, plasminogen activator inhibitor-1 (PAI-1)] and oxidative stress parameters (STAT-8-Isoprostane) were undertaken at baseline, after placebo treatment, and after 6 and 20 weeks of N-3 fatty acid intake.
  
  
  RESULTS
  Platelets functions were significantly inhibited, whereas endothelial function parameters were unaltered. IL-6 significantly decreased whereas PAI-1and STAT-8-Isoprostane levels remained unaffected. Daytime blood pressure significantly decreased; however, nighttime pressure and heart rate remained unchanged. No evidence of lipid-profile improvement was observed following combined treatment with statins and N-3 fatty acids.
  
  
  CONCLUSIONS
  In hypercholesterolemic patients, combination of statins and N-3 fatty acid inhibits platelet aggregation, alters inflammatory status, and positively affects daytime blood pressure. Close long-term follow-up might reveal additional beneficial effects of N-3 fatty acids in this patient population.
authors.affiliation: Research & Development Unit and Nephrology Division, Assaf Harofeh Medical Center, Tel- Aviv University, Zerifin 70300, Israel. kerendoenyas@gmail.com
authors.forename: Keren
authors.initials: K
authors.lastname: Doenyas-Barak
authors.forename: Sylvia
authors.initials: S
authors.lastname: Berman
authors.forename: Ramzia
authors.initials: R
authors.lastname: Abu-Hamad
authors.forename: Ahuva
authors.initials: A
authors.lastname: Golik
authors.forename: Naomi
authors.initials: N
authors.lastname: Rahimi-Levene
authors.forename: Shai
authors.initials: S
authors.lastname: Efrati
mesh_terms: D001792:Blood Platelets / Q000187:drug effects*; D001794:Blood Pressure / Q000187:drug effects*; D019587:Dietary Supplements; D004357:Drug Synergism; D004359:Drug Therapy, Combination / Q000379:methods; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism; D015525:Fatty Acids, Omega-3 / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006937:Hypercholesterolemia / Q000188:drug therapy / Q000378:metabolism; D007249:Inflammation / Q000097:blood / Q000188:drug therapy* / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D050356:Lipid Metabolism / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D050791:STAT Transcription Factors / Q000378:metabolism
chemical_list: D015525:Fatty Acids, Omega-3; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D015850:Interleukin-6; D017395:Plasminogen Activator Inhibitor 1; C051321:SERPINE1 protein, human; D050791:STAT Transcription Factors