Teragawa H, Kato M, Kurokawa J, Yamagata T, Matsuura H, Chayama K
First Department of Internal Medicine, Hiroshima University School of Medicine, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan.
Clin Sci (Lond). 2001 Dec;101(6):707-13.
In order to evaluate peripheral endothelial function in patients with vasospastic angina (VSA), we measured flow-mediated dilation (FMD) of the brachial artery in patients with VSA and compared it with FMD in patients without VSA. Endothelial dysfunction is considered one of the mechanisms underlying VSA. However, its exact role remains to be clarified. The study included 30 patients with positive spasm-provocational test results without evidence of significant coronary stenosis (VSA group) and 30 patients with negative spasm-provocational test results without evidence of significant coronary stenosis (control group). In each patient, brachial artery diameter responses to hyperemic flow and glyceryl trinitrate spray were measured using high-resolution ultrasound. The carotid intima-media thickness was also measured as a marker of systemic atherosclerosis. FMD was lower in the VSA group (4.8+/-0.5%) compared with the control group (9.4+/-0.7%, P<0.0001). In the VSA group, FMD was not affected by coronary risk factors or the presence of atherosclerotic changes on coronary angiography. Glyceryl trinitrate-induced dilation did not differ between the two groups. The intima-media thickness was comparable between the VSA (0.85+/-0.04 mm) and control groups (0.81+/-0.05 mm). These findings indicated that peripheral endothelial function is impaired only in the VSA group, whereas the atherosclerotic changes were similar in the two groups. We conclude that endothelial dysfunction may be an independent factor responsible for the development of VSA.
为了评估变异性心绞痛（VSA）患者的外周血管内皮功能，我们测量了VSA患者肱动脉的血流介导的血管舒张（FMD），并将其与非VSA患者的FMD进行比较。血管内皮功能障碍被认为是VSA的潜在机制之一。然而，其确切作用仍有待阐明。该研究纳入了30例痉挛激发试验结果阳性且无明显冠状动脉狭窄证据的患者（VSA组）和30例痉挛激发试验结果阴性且无明显冠状动脉狭窄证据的患者（对照组）。在每位患者中，使用高分辨率超声测量肱动脉直径对充血血流和硝酸甘油喷雾的反应。还测量了颈动脉内膜中层厚度作为全身动脉粥样硬化的标志物。与对照组（9.4±0.7%）相比，VSA组的FMD较低（4.8±0.5%，P<0.0001）。在VSA组中，FMD不受冠状动脉危险因素或冠状动脉造影上动脉粥样硬化改变的影响。两组之间硝酸甘油诱导的血管舒张没有差异。VSA组（0.85±0.04mm）和对照组（0.81±0.05mm）的内膜中层厚度相当。这些发现表明，仅VSA组的外周血管内皮功能受损，而两组的动脉粥样硬化改变相似。我们得出结论，血管内皮功能障碍可能是导致VSA发生的独立因素。
