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Vitamin E administration improves impairment of endothelium-dependent vasodilation in patients with coronary spastic angina

^a Division of Cardiology, Kumamoto University School of Medicine, Kumamoto, Japan

View larger version (17K): [in a new window]   Figure 1 Diagram of the study.

View larger version (12K): [in a new window]   Figure 2 (A) Bar graphs showing the percent increase in brachial arterial diameter during reactive hyperemia before treatment in patients with coronary spastic angina (CSA) (solid bar) and controls (open bar). (B) Bar graphs showing the plasma -tocopherol levels before treatment in patients with CSA (solid bar) and controls (open bar). (C) Bar graphs showing the plasma TBARS levels before treatment in patients with CSA (solid bar) and controls (open bar).

View larger version (16K): [in a new window]   Figure 3 Percent increase in brachial arterial diameter during reactive hyperemia in patients with coronary spastic angina before and after treatment in the placebo group and the vitamin E group. *Significant effect of vitamin E treatment compared with values in placebo group, p < .001 by ANOVA. , diltiazem + placebo; •, diltiazem + vitamin E.

View larger version (15K): [in a new window]   Figure 4 Plasma -tocopherol levels in patients with coronary spastic angina before and after treatment in the placebo group and the vitamin E group. *Significant effect of vitamin E treatment compared with values in placebo group, p < .001 by ANOVA. , diltiazem + placebo; •, diltiazem + vitamin E.

View larger version (15K): [in a new window]   Figure 5 Plasma TBARS levels in patients with coronary spastic angina before and after treatment in the placebo group and the vitamin E group. *Significant effect of vitamin E treatment compared with values in the placebo group, p < .001 by ANOVA. , diltiazem + placebo; •, diltiazem + vitamin E.

View larger version (20K): [in a new window]   Figure 6 Correlation between the percent increases in brachial arterial diameter during reactive hyperemia versus the changes of coronary arterial diameter in response to acetylcholine at a dose of 50 µg/min in patients with coronary spastic angina (squares) and controls (circles).