Suzuki M, Nishizaki M, Arita M, Kakuta T, Numano F
Third Department of Internal Medicine, Tokyo Medical and Dental University, Japan.
J Am Coll Cardiol. 1996 May;27(6):1458-63. doi: 10.1016/0735-1097(96)00011-3.
This study tested whether patients with vasospastic angina have impaired glucose tolerance or impaired insulin response.
Hyperinsulinemia has been demonstrated in patients with coronary artery disease and syndrome X.
We performed an oral glucose tolerance test (75 g) in 30 patients with vasospastic angina in whom severe coronary vasospasm was induced by acetylcholine and in a matched group of 30 patients with atypical chest pain in whom no significant vasospasm was induced. The responses of insulin and glucose were compared between the two groups. No subjects had overt diabetes mellitus, hypertension, dyslipidemia, obesity or angiographically detected significant baseline coronary stenosis. Venous blood samples were taken during fasting and at 30, 60, 120 and 180 min after glucose load to obtain plasma glucose and immunoreactive insulin levels.
Impaired glucose tolerance was detected in the 19 (63%) of 30 patients with vasospastic angina and in none of 30 patients with atypical chest pain (p < 0.001). The immunoreactive insulin levels at 60 and 120 min as well as the interval to peak insulin level were significantly greater in patients with vasospastic angina (p < 0.001). Among patients with vasospastic angina, those with acetylcholine-induced multivessel coronary vasospasm showed a significantly higher sum of insulin concentrations than those with single-vessel spasm (p < 0.01). During induction of coronary spasm, 10 patients with vasospastic angina presented ventricular arrhythmias. The sum of insulin concentrations was significantly greater in patients with than in those without ventricular arrhythmias.
Patients with vasospastic angina exhibited a high incidence of impaired glucose tolerance and delayed and significantly higher insulin responses. These findings suggest that impaired glucose tolerance with late hypersecretion of insulin may contribute to the pathogenesis of severe coronary vasospasm.
本研究旨在检测血管痉挛性心绞痛患者是否存在糖耐量受损或胰岛素反应受损。
冠状动脉疾病和X综合征患者已被证实存在高胰岛素血症。
我们对30例血管痉挛性心绞痛患者进行了口服葡萄糖耐量试验（75克），这些患者通过乙酰胆碱诱发严重冠状动脉痉挛，同时选取了30例非典型胸痛患者作为匹配组，这些患者未诱发明显的血管痉挛。比较了两组患者胰岛素和葡萄糖的反应。所有受试者均无明显的糖尿病、高血压、血脂异常、肥胖或血管造影检测到的明显基线冠状动脉狭窄。在空腹状态以及葡萄糖负荷后30、60、120和180分钟采集静脉血样，以获取血浆葡萄糖和免疫反应性胰岛素水平。
30例血管痉挛性心绞痛患者中有19例（63%）检测到糖耐量受损，而30例非典型胸痛患者中无一例出现糖耐量受损（p<0.001）。血管痉挛性心绞痛患者在60和120分钟时的免疫反应性胰岛素水平以及达到胰岛素峰值水平的时间间隔显著更高（p<0.001）。在血管痉挛性心绞痛患者中，乙酰胆碱诱发多支冠状动脉痉挛的患者胰岛素浓度总和显著高于单支血管痉挛的患者（p<0.01）。在冠状动脉痉挛诱发过程中，10例血管痉挛性心绞痛患者出现室性心律失常。出现室性心律失常的患者胰岛素浓度总和显著高于未出现室性心律失常的患者。
血管痉挛性心绞痛患者糖耐量受损的发生率较高，胰岛素反应延迟且显著升高。这些发现表明，糖耐量受损伴胰岛素晚期分泌过多可能有助于严重冠状动脉痉挛的发病机制。
