title: Effects of eicosapentaenoic acid on the levels of inflammatory markers, cardiac function and long-term prognosis in chronic heart failure patients with dyslipidemia.
abstract: OBJECTIVE
  The effects of eicosapentaenoic acid (EPA) on the levels of inflammatory markers, cardiac function and long-term prognosis in chronic heart failure (CHF) patients with dyslipidemia remain unclear.
  
  
  METHODS
  A total of 139 CHF patients with a mean left ventricular ejection fraction (LVEF) of 37.6± 8.0% were divided into two groups based on whether EPA was included in their treatment regimen: the EPA group (n=71) and the no EPA group (n=68). Only patients with dyslipidemia at baseline (entry) were treated with EPA. The monocyte chemoattractant protein (MCP)-1 and asymmetric dimethylarginine (ADMA) levels were measured at baseline and after 12 months of treatment.
  
  
  RESULTS
  At 12 months, in the EPA group, the LVEF had improved and the MCP-1 and ADMA levels had decreased (respectively, p＜0.001); however, in the no EPA group, the LVEF had worsened, while the MCP-1 and ADMA levels had increased (respectively, p＜0.001). Fifty-five patients experienced cardiac events, including 15 cardiac deaths and 40 readmissions for worsening of CHF during a median follow-up period of 28.0 months. The percent change in LVEF from baseline was found to be significantly associated with the percent change in ADMA (r=-0.462, p＜0.001). A multivariate Cox hazard analysis showed EPA treatment (hazard ratio: 0.21, 95% confidence interval: 0.05-0.93, p=0.031) to be an independent predictor of cardiac events.
  
  
  CONCLUSIONS
  These data indicate that EPA treatment may improve the cardiac function and long-term prognosis of CHF patients with dyslipidemia, at least in part, due to reductions in inflammation and improvements in the endothelial function.
authors.affiliation: Department of Internal Medicine and Cardiology, Tama-Nagayama Hospital, Nippon Medical School.
authors.forename: Keiichi
authors.initials: K
authors.lastname: Kohashi
authors.forename: Akihiro
authors.initials: A
authors.lastname: Nakagomi
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Saiki
authors.forename: Taichirou
authors.initials: T
authors.lastname: Morisawa
authors.forename: Munenori
authors.initials: M
authors.lastname: Kosugi
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Kusama
authors.forename: Hirotsugu
authors.initials: H
authors.lastname: Atarashi
authors.forename: Wataru
authors.initials: W
authors.lastname: Shimizu
mesh_terms: D000368:Aged; D001120:Arginine / Q000031:analogs & derivatives / Q000097:blood; D015415:Biomarkers / Q000097:blood*; D018932:Chemokine CCL2 / Q000097:blood; D002851:Chromatography, High Pressure Liquid; D002908:Chronic Disease; D050171:Dyslipidemias / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism / Q000401:mortality; D015118:Eicosapentaenoic Acid / Q000627:therapeutic use*; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism / Q000401:mortality; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D008297:Male; D011379:Prognosis; D015996:Survival Rate; D016277:Ventricular Function, Left / Q000187:drug effects*
chemical_list: D015415:Biomarkers; C111835:CCL2 protein, human; D018932:Chemokine CCL2; D018836:Inflammation Mediators; C018524:N,N-dimethylarginine; D001120:Arginine; D015118:Eicosapentaenoic Acid