Shinozaki K, Hattori Y, Suzuki M, Hara Y, Kanazawa A, Takaki H, Tsushima M, Harano Y
Division of Atherosclerosis, Metabolism, and Clinical Nutrition, National Cardiovascular Center, Osaka, Japan.
Arterioscler Thromb Vasc Biol. 1997 Nov;17(11):3302-10. doi: 10.1161/01.atv.17.11.3302.
Studies have shown the presence of insulin resistance together with compensatory hyperinsulinemia in vasospastic angina as well as obstructive coronary artery disease. There is growing evidence that the development of coronary atherosclerosis may be closely related to systemic atherosclerosis as well as coronary spasm. However, no information is available about the possible relationship between insulin resistance and the existence of carotid atherosclerosis in vasospastic angina without segmental stenosis or luminal irregularities in coronary angiograms. To evaluate the independent effect of insulin resistance on carotid intima media thickening, we performed insulin sensitivity tests (steady-state plasma glucose method) on 40 patients with vasospastic angina and 24 control subjects with angiographically intact coronary arteries. Both oral glucose tolerance tests and lipid analyses were performed. Using B-mode ultrasonography, we assessed intima media thickness and plaque formation of common carotid arteries in these subjects. The steady-state plasma glucose level in the vasospastic angina group was about twofold higher than that of the control group, confirming the presence of insulin resistance in patients with vasospastic angina. The patients with vasospastic angina showed a significant increase in the average intima media thickness of the carotid wall and frequency of plaque formation, although they were comparable to the control subjects in risk factors other than insulin resistance. The intima media thickness was correlated with age (r = .62, P < .001), 2-hour insulin area (r = .45, P < .01), and steady-state plasma glucose level (r = .68, P < .0001) in patients with vasospastic angina. Similar correlations were observed in the control subjects. Multiple regression analyses of data indicated that 67% of the variation in the intima media thickness could be accounted for by age, steady-state plasma glucose level, and cigarette-years in vasospastic angina. In addition, differences in IMT were independently related to vasospastic angina. These results suggest that insulin resistance in association with compensatory hyperinsulinemia may be an important pathogenic factor for the development of coronary artery spasms and systemic early atherosclerosis.
研究表明，在血管痉挛性心绞痛以及阻塞性冠状动脉疾病中存在胰岛素抵抗并伴有代偿性高胰岛素血症。越来越多的证据表明，冠状动脉粥样硬化的发展可能与全身性动脉粥样硬化以及冠状动脉痉挛密切相关。然而，对于血管痉挛性心绞痛患者，在冠状动脉造影无节段性狭窄或管腔不规则的情况下，胰岛素抵抗与颈动脉粥样硬化存在之间的可能关系尚无相关信息。为了评估胰岛素抵抗对颈动脉内膜中层增厚的独立影响，我们对40例血管痉挛性心绞痛患者和24例冠状动脉造影正常的对照者进行了胰岛素敏感性测试（稳态血浆葡萄糖法）。同时进行了口服葡萄糖耐量试验和血脂分析。我们使用B型超声评估了这些受试者颈总动脉的内膜中层厚度和斑块形成情况。血管痉挛性心绞痛组的稳态血浆葡萄糖水平比对照组高出约两倍，证实血管痉挛性心绞痛患者存在胰岛素抵抗。血管痉挛性心绞痛患者的颈动脉壁平均内膜中层厚度和斑块形成频率显著增加，尽管除胰岛素抵抗外，他们在其他危险因素方面与对照组相当。在血管痉挛性心绞痛患者中，内膜中层厚度与年龄（r = 0.62，P < 0.001）、2小时胰岛素曲线下面积（r = 0.45，P < 0.01）以及稳态血浆葡萄糖水平（r = 0.68，P < 0.0001）相关。在对照者中也观察到了类似的相关性。对数据进行多元回归分析表明，在血管痉挛性心绞痛中，内膜中层厚度变化的67%可由年龄、稳态血浆葡萄糖水平和吸烟年限解释。此外，内膜中层厚度的差异与血管痉挛性心绞痛独立相关。这些结果表明，胰岛素抵抗与代偿性高胰岛素血症可能是冠状动脉痉挛和全身性早期动脉粥样硬化发展的重要致病因素。
