Miwa K, Miyagi Y, Igawa A, Nakagawa K, Inoue H
2nd Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Japan.
Circulation. 1996 Jul 1;94(1):14-8. doi: 10.1161/01.cir.94.1.14.
Oxidative modification of LDL has been suggested to increase coronary vasoreactivity to agonists. A deficiency of vitamin E, a major antioxidant, may be related to the occurrence of coronary artery spasm.
Vitamin E levels were determined with the use of high-performance liquid chromatography in normolipidemic subjects, including 29 patients with active variant angina (group 1), 13 patients with inactive stage of variant angina without anginal attacks during the past 6 months (group 2), 32 patients with a significant (>75%) organic coronary stenosis and stable effort angina (group 3), and 30 patients without coronary artery disease (group 4). Total lipid levels in blood were calculated as total cholesterol plus triglyceride levels. The plasma alpha-tocopherol levels as well as alpha-tocopherol/lipids were significantly lower in group 1 than in groups 2 through 4. Also, the plasma gamma-tocopherol levels were significantly lower in group 1 than in groups 2 through 4. The vitamin E levels were not significantly different between group 1 patients with and those without a significant organic stenosis. In group 1, both alpha- and gamma-tocopherol levels were significantly elevated after a > or = 6-month angina-free period. The alpha-tocopherol levels in the LDL fraction were significantly lower in group 1 than in group 4. Plasma alpha-tocopherol levels were significantly correlated with those in the LDL fractions. In 6 patients of group 1 still having anginal attacks while receiving calcium channel blockers, the addition of vitamin E acetate (300 mg/d) significantly elevated plasma alpha-tocopherol levels and inhibited the occurrence of angina.
Plasma vitamin E levels were significantly lower in patients with active variant angina than in subjects without coronary spasm, suggesting an association between vitamin E deficiency and coronary artery spasm.
低密度脂蛋白（LDL）的氧化修饰被认为会增加冠状动脉对激动剂的血管反应性。主要抗氧化剂维生素E的缺乏可能与冠状动脉痉挛的发生有关。
采用高效液相色谱法测定了血脂正常受试者的维生素E水平，其中包括29例变异型心绞痛发作期患者（第1组）、13例变异型心绞痛静止期患者（过去6个月无心绞痛发作，第2组）、32例冠状动脉狭窄程度>75%的严重器质性病变且患有稳定劳力型心绞痛的患者（第3组）以及30例无冠状动脉疾病的患者（第4组）。血液中的总脂质水平按总胆固醇加甘油三酯水平计算。第1组患者的血浆α-生育酚水平以及α-生育酚/脂质水平显著低于第2组至第4组。此外，第1组患者的血浆γ-生育酚水平也显著低于第2组至第4组。第1组中有显著器质性狭窄和无显著器质性狭窄的患者之间维生素E水平无显著差异。在第1组中，经过≥6个月的无心绞痛期后，α-和γ-生育酚水平均显著升高。第1组LDL组分中的α-生育酚水平显著低于第4组。血浆α-生育酚水平与LDL组分中的α-生育酚水平显著相关。在第1组中，6例正在接受钙通道阻滞剂治疗且仍有心绞痛发作的患者，加用维生素E醋酸酯（300mg/d）后显著提高了血浆α-生育酚水平，并抑制了心绞痛的发作。
变异型心绞痛发作期患者的血浆维生素E水平显著低于无冠状动脉痉挛的受试者，提示维生素E缺乏与冠状动脉痉挛之间存在关联。
