title: Effects of eicosapentaenoic acid on asymmetric dimethylarginine in patients in the chronic phase of cerebral infarction: a preliminary study.
abstract: BACKGROUND
  Eicosapentaenoic acid (EPA) possesses a variety of pharmacologic actions and demonstrates protective efficacy against stroke. Meanwhile, asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase inhibitor and is thereby considered one of the risk factors of cardiovascular disease. The effects of the EPA treatment on ADMA in patients in the chronic phase of cerebral infarction accompanied by dyslipidemia were investigated.
  
  
  METHODS
  Study subjects were individuals with either atherothrombotic or lacunar cerebral infarction in the chronic phase accompanied by dyslipidemia, of which the onset was at least 4 weeks earlier. Lipid, fatty acid, and ADMA levels in the blood were measured at EPA 1800 mg per day and compared both before and after treatment. Twenty subjects were included in the study (average age, 71.9 ± 8.9 years).
  
  
  RESULTS
  Of these 20 cases, eight were atherothrombotic and 12 were lacunar. Moreover, 17 cases were accompanied by hypertension and 10 cases were accompanied by diabetes mellitus. After EPA treatment (average duration of treatment, 143 ± 42 days), EPA increased from 65.1 ± 38.1 μg/mL to 201.1 ± 73.4 μg/mL (P < .01). Arachidonic acid (AA) decreased from 149.1 ± 34.8 μg/mL to 129.7 ± 22.3 μg/mL (P < .01), and the EPA/AA ratio increased from 0.45 ± 0.26 to 1.55 ± 0.46 (P < .01). ADMA decreased from 0.49 ± 0.07 nmol/mL before treatment to 0.46 ± 0.05 nmol/mL after treatment (P < .01).
  
  
  CONCLUSIONS
  EPA treatment in patients in the chronic phase of cerebral infarction leads to a decrease in ADMA in the blood, suggesting that EPA improves vascular endothelial function and therefore supports the protective efficacy against cerebral infarction.
authors.affiliation: Department of Neurology, Shioda Hospital, Chiba, Japan. hhagi@nms.ac.jp
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Hagiwara
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Nishiyama
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Katayama
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D016718:Arachidonic Acid / Q000097:blood; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood; D015415:Biomarkers / Q000097:blood; D002544:Cerebral Infarction / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy*; D015536:Down-Regulation; D050171:Dyslipidemias / Q000097:blood / Q000188:drug therapy; D015118:Eicosapentaenoic Acid / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007564:Japan; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D010865:Pilot Projects; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D018696:Neuroprotective Agents; D016718:Arachidonic Acid; C018524:N,N-dimethylarginine; D001120:Arginine; D015118:Eicosapentaenoic Acid