title: Vitamin E administration improves impairment of endothelium-dependent vasodilation in patients with coronary spastic angina.
abstract: OBJECTIVE
  We examined the effects of oral administration of vitamin E, an antioxidant, on endothelium-dependent vasodilation in patients with coronary spastic angina.
  
  
  BACKGROUND
  We have recently reported that endothelium-dependent vasodilation is impaired in patients with coronary spastic angina (CSA). Furthermore, it is known that oxidative stress may play an important role in the impairment of endothelium-dependent vasodilation in cardiovascular diseases.
  
  
  METHODS
  With the ultrasound technique, flow-dependent vasodilation of the brachial arteries during reactive hyperemia was examined before and after treatment for a month with either oral administration of vitamin E (alpha-tocopherol acetate, 300 mg/day) or placebo, which is randomly assigned, in patients with CSA (n=60).
  
  
  RESULTS
  Before treatment, patients with CSA had impaired flow-dependent vasodilation, lower plasma levels of alpha-tocopherol and higher plasma levels of thiobarbituric acid reactive substances (TBARS), as compared with age- and sex-matched control subjects (n=60) (flow-dependent vasodilation: 3.1+/-1.8 vs. 7.1+/-2.5%, p < 0.001; alpha-tocopherol levels: 8.9+/-1.8 vs. 10.8+/-1.8 microg/ml, p < 0.001). In patients with CSA, treatment with vitamin E restored flow-dependent vasodilation (3.1+/-1.7 vs. 8.3+/-2.0%, p < 0.001), and this improvement was associated with the decreases in plasma TBARS levels and anginal attacks.
  
  
  CONCLUSIONS
  The results indicate that vitamin E treatment improved endothelium-dependent vasodilation and decreased plasma TBARS levels in patients with CSA. Thus, increased oxidative stress may contribute to endothelial dysfunction and anginal attacks in patients with CSA.
authors.affiliation: Division of Cardiology, Kumamoto University School of Medicine, Kumamoto City, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Motoyama
authors.forename: H
authors.initials: H
authors.lastname: Kawano
authors.forename: K
authors.initials: K
authors.lastname: Kugiyama
authors.forename: O
authors.initials: O
authors.lastname: Hirashima
authors.forename: M
authors.initials: M
authors.lastname: Ohgushi
authors.forename: R
authors.initials: R
authors.lastname: Tsunoda
authors.forename: Y
authors.initials: Y
authors.lastname: Moriyama
authors.forename: Y
authors.initials: Y
authors.lastname: Miyao
authors.forename: M
authors.initials: M
authors.lastname: Yoshimura
authors.forename: H
authors.initials: H
authors.lastname: Ogawa
authors.forename: H
authors.initials: H
authors.lastname: Yasue
mesh_terms: D000328:Adult; D000368:Aged; D000788:Angina Pectoris, Variant / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology*; D001158:Arteries / Q000503:physiopathology; D001916:Brachial Artery / Q000503:physiopathology; D003329:Coronary Vasospasm / Q000150:complications*; D003331:Coronary Vessels / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D012039:Regional Blood Flow / Q000502:physiology; D012907:Smoking; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014664:Vasodilation / Q000187:drug effects* / Q000502:physiology; D014810:Vitamin E / Q000097:blood / Q000627:therapeutic use*
chemical_list: D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E