title: Prevention of restenosis by bezafibrate after successful coronary angioplasty.
abstract: BACKGROUND
  To study the role of bezafibrate in prevention of restenosis after successful percutaneous transluminal coronary angioplasty (PTCA), we evaluated the incidence of restenosis and its correlation with serum lipid levels and effects on the coagulation-fibrinolytic system.
  
  
  METHODS
  Subjects who had undergone successful elective PTCA were classified into three groups based on their triglyceride level and whether or not bezafibrate was administered. Fifty-two patients who had a triglyceride level < 150 mg/dl were classified as group A. Those with a triglyceride level +/- 150 mg/dl were randomly and prospectively allocated to receive either bezafibrate (group B, n = 21), or no lipid-lowering treatment (group C, n = 22). The restenosis rates in all three groups were subsequently monitored and correlated with serum levels of lipids and coagulation-fibrinolytic system markers.
  
  
  RESULTS
  In the bezafibrate group, three of 21 patients (14%) had restenosis compared with 12 of 22 (55%) in group C and 18 of 52 (35%) in group A. In groups A and C, fibrinogen and triglyceride levels were significantly higher in the patients with restenosis. At the time of re-evaluation, serum triglyceride, fibrinogen, and plasminogen activator inhibitor type 1 (PAI-1) levels were lower and high-density lipoprotein (HDL) cholesterol levels were higher in the bezafibrate group than in group C. By logistic regression analysis, triglyceride and PAI-1 were found to be significant risk factors for postangioplasty restenosis.
  
  
  CONCLUSIONS
  Triglyceride is a risk factor for post-PTCA restenosis, and bezafibrate reduces the post-PTCA restenosis rate in patients with a high triglyceride level. In the bezafibrate group, a significant decrease in PAI-1 was observed in association with a decrease in triglyceride level and an elevation of HDL cholesterol level. This suggests that improvement in fibrinolytic capacity is involved in the mechanism of decrease in the rate of restenosis.
authors.affiliation: Cardiovascular Center, Toranomon Hospital, Tokyo, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Ishiwata
authors.forename: S
authors.initials: S
authors.lastname: Nakanishi
authors.forename: S
authors.initials: S
authors.lastname: Nishiyama
authors.forename: A
authors.initials: A
authors.lastname: Seki
mesh_terms: D015906:Angioplasty, Balloon, Coronary; D001629:Bezafibrate / Q000627:therapeutic use*; D008076:Cholesterol, HDL / Q000097:blood; D003251:Constriction, Pathologic; D003327:Coronary Disease / Q000097:blood / Q000517:prevention & control* / Q000628:therapy*; D005260:Female; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D012008:Recurrence; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood
chemical_list: D008076:Cholesterol, HDL; D000960:Hypolipidemic Agents; D017395:Plasminogen Activator Inhibitor 1; D014280:Triglycerides; D001629:Bezafibrate