title: trans fatty acids and systemic inflammation in heart failure.
abstract: BACKGROUND
  trans fatty acid (TFA) intake increases systemic inflammation in healthy persons. However, the effect in patients with established heart disease is unknown.
  
  
  OBJECTIVE
  Our aim was to determine whether TFAs are associated with systemic inflammation in patients with established heart disease.
  
  
  METHODS
  Red blood cell membrane TFAs, a biomarker of dietary intake, and inflammatory marker concentrations were ascertained in 86 ambulatory patients with established heart failure. Associations between TFA levels and inflammatory markers were evaluated by linear regression.
  
  
  RESULTS
  Mean (+/-SD) TFA levels were 1.8 +/- 0.4% of membrane fatty acids (range: 0.7-2.9%). For each inflammatory marker, associations are presented as the absolute difference and percentage difference from the mean for each 1% higher membrane TFA level. After adjustment for age, sex, body mass index, diabetes, smoking, ejection fraction, New York Heart Association class, ischemic etiology, statin use, and serum glucose, TFA levels were positively associated with interleukin (IL) 1beta (difference from mean: 0.38 pg/mL; percentage difference from mean: 66%; P=0.04), IL-1 receptor antagonist (4033 pg/mL; 297%; P=0.006), IL-6 (9.5 pg/mL; 123%; P=0.006), IL-10 (241 pg/mL; 183%; P=0.02), tumor necrosis factor (TNF) alpha (256 pg/mL; 249%; P=0.02), TNF receptor 1 (537 pg/mL; 41%; P=0.03), TNF receptor 2 (39 242 pg/mL; 247%; P=0.001), monocyte chemoattractant protein 1 (117 pg/mL; 119%; P=0.004), and brain natriuretic peptide (40 pg/mL; 57%; P=0.04). Further adjustments for other patient characteristics did not significantly alter the results.
  
  
  CONCLUSIONS
  TFAs are strongly associated with systemic inflammation in patients with heart disease, which suggests that attention to TFA intake may be important for secondary prevention efforts.
authors.affiliation: Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. dmozaffa@hsph.harvard.edu
authors.forename: Dariush
authors.initials: D
authors.lastname: Mozaffarian
authors.forename: Eric B
authors.initials: EB
authors.lastname: Rimm
authors.forename: Irena B
authors.initials: IB
authors.lastname: King
authors.forename: Richard L
authors.initials: RL
authors.lastname: Lawler
authors.forename: George B
authors.initials: GB
authors.lastname: McDonald
authors.forename: Wayne C
authors.initials: WC
authors.lastname: Levy
mesh_terms: D015415:Biomarkers; D002908:Chronic Disease; D015331:Cohort Studies; D004041:Dietary Fats / Q000008:administration & dosage / Q000009:adverse effects*; D004910:Erythrocyte Membrane / Q000737:chemistry*; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000209:etiology / Q000517:prevention & control; D006801:Humans; D007249:Inflammation / Q000097:blood* / Q000209:etiology; D007378:Interleukins / Q000097:blood; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D044242:Trans Fatty Acids / Q000008:administration & dosage / Q000009:adverse effects* / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D015415:Biomarkers; D004041:Dietary Fats; D007378:Interleukins; D044242:Trans Fatty Acids; D014409:Tumor Necrosis Factor-alpha