title: Effects of folic acid and N-acetylcysteine on plasma homocysteine levels and endothelial function in patients with coronary artery disease.
abstract: OBJECTIVE
  Hyperhomocysteinaemia is related with premature coronary artery disease and adverse cardiac events in patients with coronary artery disease (CAD). It is assumed that hyper-homocysteinaemia causes endothelial dysfunction. In this study, the effect of folic acid and oral N-acetylcysteine (NAC) therapies on plasma homocysteine levels and endothelial function were evaluated in hyperhomocysteinaemic patients with CAD.
  
  
  RESULTS
  60 patients were randomized to either folic acid 5 mg or NAC 600 mg or placebo daily for eight weeks. Brachial artery endothelial functions were studied by using high-resolution ultrasound and assessed by measuring endothelium-dependent dilation (EDD) and endothelium-independent dilation (NEDD). Folic acid and NAC therapies decreased plasma homocysteine (from 21.7 +/- 8.7 micromol/l to 12.5 +/- 2.5 micromol/l, P < 0.001; from 20.9 +/- 7.6 micromol/l to 15.6 +/- 4.3 micromol/l, P = 0.03, respectively), and increased EDD (6.7 +/- 6.1% P = 0.002, 4.4 +/- 2.6% P < 0.001, respectively) compared with placebo. There was no significant difference in improving EDD between the folic acid and the NAC group (6.7 +/- 6.1%, 4.4 +/- 2.6%, P = 0. 168). In the univariate analyses there was an inverse correlation between the post-treatment homocysteine level and the percent change in EDD with folic acid therapy (r= -0.490, P = 0.028), but there was no correlation with the NAC therapy (r = 0.259, P = 0.333)
  
  
  CONCLUSIONS
  In patients with hyperhomocysteinaemic CAD, folic acid and NAC lowered plasma homocysteine levels and improved endothelial function. The effects of both treatments in improvement of EDD were similar.
authors.affiliation: Department of Cardiology, Siyami Ersek Thoracic and Cardiovascular Surgery Center, Istanbul, Turkey. haleyilmaz@tnn.net
authors.forename: Hale
authors.initials: H
authors.lastname: Yilmaz
authors.forename: Sinan
authors.initials: S
authors.lastname: Sahin
authors.forename: Nurten
authors.initials: N
authors.lastname: Sayar
authors.forename: Burak
authors.initials: B
authors.lastname: Tangurek
authors.forename: Mehmet
authors.initials: M
authors.lastname: Yilmaz
authors.forename: Zekeriya
authors.initials: Z
authors.lastname: Nurkalem
authors.forename: Ebru
authors.initials: E
authors.lastname: Onturk
authors.forename: Nazmiye
authors.initials: N
authors.lastname: Cakmak
authors.forename: Osman
authors.initials: O
authors.lastname: Bolca
mesh_terms: D000111:Acetylcysteine / Q000008:administration & dosage* / Q000627:therapeutic use; D000284:Administration, Oral; D000368:Aged; D003324:Coronary Artery Disease / Q000097:blood* / Q000188:drug therapy / Q000503:physiopathology*; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D005260:Female; D005492:Folic Acid / Q000008:administration & dosage* / Q000627:therapeutic use; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology; D008297:Male; D008875:Middle Aged
chemical_list: D006710:Homocysteine; D005492:Folic Acid; D000111:Acetylcysteine