title: N-acetylcysteine neither lowers plasma homocysteine concentrations nor improves brachial artery endothelial function in cardiac transplant recipients.
abstract: BACKGROUND
  N-acetylcysteine is a novel antioxidant that has been reported to reduce plasma homocysteine concentrations and improve endothelial function. Cardiac transplant recipients have a high incidence of coronary endothelial dysfunction and hyperhomocysteinemia, both of which may lead to the development of transplantation coronary artery disease. It was hypothesized that N-acetylcysteine would reduce plasma homocysteine concentrations and improve brachial endothelial function in cardiac transplant recipients.
  
  
  METHODS
  A cohort of stable cardiac transplant recipients was recruited from the outpatient clinic at the Toronto General Hospital, Toronto, Ontario. Brachial artery endothelial functions were studied according to standard techniques to determine flow-mediated dilation of the brachial artery. Plasma homocysteine concentrations were assayed using high performance liquid chromatography with electrochemical detection and pulsed integrated amperometry. After baseline testing, patients were treated in an unblinded fashion with N-acetylcysteine 500 mg/day. After 10 weeks of therapy, patients returned for follow-up endothelial function and homocysteine testing.
  
  
  RESULTS
  Thirty-one patients were initially enrolled. Two patients withdrew due to excessive gastrointestinal upset. Two patients did not return for follow-up testing. The remaining 27 patients tolerated the treatment well. At baseline, 85% of the patients had hyperhomocysteinemia (greater than 15  mol/L) with a mean plasma concentration of 18.6 4.7  mol/L. No changes in homocysteine concentrations were seen at follow-up. At baseline, the average flow-mediated dilation was only 4.7 6.3%. No changes were seen at follow-up.
  
  
  CONCLUSIONS
  Hyperhomocysteinemia and brachial endothelial dysfunction are common in stable cardiac transplant recipients and are unaffected by supplementation with N-acetylcysteine.
authors.affiliation: University Health Network, The Toronto General Hospital, 200 Elizabeth Street, Toronto, Ontario M5G 2C4, Canada.
authors.forename: S E S
authors.initials: SE
authors.lastname: Miner
authors.forename: D E C
authors.initials: DE
authors.lastname: Cole
authors.forename: J
authors.initials: J
authors.lastname: Evrovski
authors.forename: Q
authors.initials: Q
authors.lastname: Forrest
authors.forename: S J
authors.initials: SJ
authors.lastname: Hutchison
authors.forename: K
authors.initials: K
authors.lastname: Holmes
authors.forename: H J
authors.initials: HJ
authors.lastname: Ross
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology*; D000284:Administration, Oral; D001916:Brachial Artery / Q000187:drug effects* / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000187:drug effects; D005260:Female; D016166:Free Radical Scavengers / Q000494:pharmacology*; D016027:Heart Transplantation / Q000502:physiology*; D006710:Homocysteine / Q000097:blood / Q000187:drug effects*; D006801:Humans; D008297:Male; D008875:Middle Aged; D016896:Treatment Outcome
chemical_list: D016166:Free Radical Scavengers; D006710:Homocysteine; D000111:Acetylcysteine