title: Effect of niceritrol on fibrinolysis and lipoprotein (a) levels in patients with coronary artery disease.
abstract: BACKGROUND
  Lipoprotein (a) [Lp(a)] is an independent risk factor for coronary artery disease and niceritrol (a prodrug of nicotinic acid) is known to reduce Lp(a) levels. Patients with coronary artery disease often have impairment of the fibrinolytic system.
  
  
  METHODS
  To elucidate the effect of niceritrol on fibrinolysis and Lp(a) levels, we examined plasminogen activator inhibitor (PAI) activity, tissue-type plasminogen activator (t-PA) antigen, and serum Lp(a) levels before and after administration of niceritrol to coronary artery disease patients with high baseline Lp(a) levels (> or = 20 mg/dl). Niceritrol was administered to 26 patients for 12 weeks at 750 mg/day. Fasting blood samples were obtained at 0800 h from each patient before treatment, after administration of niceritrol for 12 weeks and 4 weeks after the discontinuation of therapy.
  
  
  RESULTS
  There were significant reductions in PAI activity (9.9 +/- 1.8 compared with 5.4 +/- 1.6 IU/ml, P < 0.01), t-PA antigen levels (10.0 +/- 0.5 compared with 8.8 +/- 0.6 ng/ml, P < 0.05), and Lp(a) levels (49.3 +/- 5.9 compared with 42.5 +/- 5.4 mg/dl, P < 0.01) after 12 weeks of niceritrol administration. Four weeks after the discontinuation of niceritrol treatment, all these parameters returned to baseline.
  
  
  CONCLUSIONS
  This study demonstrated that niceritrol administration decreases PAI activity and t-PA antigen levels together with Lp(a) levels in patients with coronary artery disease. These observations suggest that niceritrol administration may tend to normalize fibrinolysis in such patients.
authors.affiliation: Division of Cardiology, Kumamoto University School of Medicine, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Suefuji
authors.forename: H
authors.initials: H
authors.lastname: Ogawa
authors.forename: H
authors.initials: H
authors.lastname: Yasue
authors.forename: N
authors.initials: N
authors.lastname: Imoto
authors.forename: T
authors.initials: T
authors.lastname: Sakamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Miyao
authors.forename: K
authors.initials: K
authors.lastname: Kaikita
authors.forename: H
authors.initials: H
authors.lastname: Soejima
authors.forename: K
authors.initials: K
authors.lastname: Nishiyama
mesh_terms: D000328:Adult; D000368:Aged; D003327:Coronary Disease / Q000097:blood* / Q000188:drug therapy / Q000503:physiopathology; D004562:Electrocardiography; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005342:Fibrinolysis; D006801:Humans; D000960:Hypolipidemic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D017270:Lipoprotein(a) / Q000097:blood* / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D009531:Niceritrol / Q000008:administration & dosage / Q000627:therapeutic use*; D015849:Plasminogen Inactivators / Q000097:blood*; D012307:Risk Factors; D010959:Tissue Plasminogen Activator / Q000097:blood* / Q000187:drug effects
chemical_list: D000960:Hypolipidemic Agents; D017270:Lipoprotein(a); D015849:Plasminogen Inactivators; D010959:Tissue Plasminogen Activator; D009531:Niceritrol