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J Am Coll Cardiol, 1998; 32:1672-1679 © 1998 by the American College of Cardiology Foundation |
a Division of Cardiology, Kumamoto University School of Medicine, Kumamoto, Japan
Manuscript received March 13, 1998; revised manuscript received July 2, 1998, accepted July 24, 1998.
Address for correspondence: Dr. Hirofumi Yasue, Division of Cardiology, Kumamoto University School of Medicine, Honjo 1-1-1, Kumamoto City, Japan 860
Objectives. 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 (
-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 -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; -tocopherol levels: 8.9 ± 1.8 vs. 10.8 ± 1.8 µg/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.
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