title: Vitamin E improves fibrinolytic activity in patients with coronary spastic angina.
abstract: BACKGROUND
  The fibrinolytic system has a major role as a defense mechanism against thrombus formation. Net fibrinolytic activity in plasma reflects the balance between tissue-type plasminogen activator and plasminogen activator inhibitor (PAI). PAI is the main factor determining overall fibrinolytic activity.
  
  
  METHODS
  We examined the effects of oral administration of vitamin E, an antioxidant, on fibrinolytic activity and oxidative stress in patients with coronary spastic angina. Forty patients with coronary spastic angina were randomly assigned into two treatment groups, either vitamin E group (alpha-tocopherol acetate, 400 mg/day) or placebo group by means of computerized system. PAI activity and thioredoxin, a marker of oxidative stress, levels were measured before and at the end of 1 month treatment.
  
  
  RESULTS
  Before treatment, the levels of PAI activity and thioredoxin were increased in patients with coronary spastic angina as compared with control subjects (n=17) (PAI activity levels: 13.6+/-1.4 vs. 7.6+/-2.2 IU/ml, p<0.05, thioredoxin levels: 22.8+/-1.7 vs. 16.0+/-1.4 ng/ml, p<0.05). In patients with coronary spastic angina, administration of vitamin E decreased both PAI activity and thioredoxin levels (PAI activity levels: 14.7+/-1.7 to 7.5+/-1.6 IU/ml, p<0.01, thioredoxin levels: 23.3+/-2.4 to 15.1+/-2.5 ng/ml, p<0.01), whereas placebo had no effect on these variables.
  
  
  CONCLUSIONS
  Oral administration of vitamin E improved fibrinolytic activity and the improvement was associated with a decrease in oxidative stress. Administration of vitamin E is possible to be an effective adjunct therapy of coronary spasm in the absence of coronary atherosclerosis.
authors.affiliation: Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto 860-8556, Japan.
authors.forename: Shinzo
authors.initials: S
authors.lastname: Miyamoto
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Kawano
authors.forename: Keiji
authors.initials: K
authors.lastname: Takazoe
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Soejima
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Sakamoto
authors.forename: Jun
authors.initials: J
authors.lastname: Hokamaki
authors.forename: Michihiro
authors.initials: M
authors.lastname: Yoshimura
authors.forename: Hajime
authors.initials: H
authors.lastname: Nakamura
authors.forename: Junji
authors.initials: J
authors.lastname: Yodoi
authors.forename: Hisao
authors.initials: H
authors.lastname: Ogawa
mesh_terms: D000284:Administration, Oral; D000789:Angina, Unstable / Q000097:blood* / Q000175:diagnosis / Q000188:drug therapy* / Q000209:etiology; D015415:Biomarkers / Q000097:blood; D003328:Coronary Thrombosis / Q000097:blood / Q000175:diagnosis / Q000209:etiology / Q000517:prevention & control; D003329:Coronary Vasospasm / Q000097:blood* / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy*; D004311:Double-Blind Method; D005260:Female; D005342:Fibrinolysis / Q000187:drug effects*; D005343:Fibrinolytic Agents / Q000008:administration & dosage; D006801:Humans; D008297:Male; D008875:Middle Aged; D015849:Plasminogen Inactivators / Q000097:blood*; D013879:Thioredoxins / Q000097:blood; D010959:Tissue Plasminogen Activator; D016896:Treatment Outcome; D014810:Vitamin E / Q000008:administration & dosage*
chemical_list: D015415:Biomarkers; D005343:Fibrinolytic Agents; D015849:Plasminogen Inactivators; D014810:Vitamin E; D013879:Thioredoxins; D010959:Tissue Plasminogen Activator