Yamagishi M, Miyatake K, Tamai J, Nakatani S, Koyama J, Nissen S E
Cardiology Division of Medicine, National Cardiovascular Center, Osaka, Japan.
J Am Coll Cardiol. 1994 Feb;23(2):352-7. doi: 10.1016/0735-1097(94)90419-7.
The purpose of this study was to use intravascular ultrasound imaging to examine the presence of occult atherosclerosis at the site of focal vasospasm in angiographically normal or minimally narrowed segments, testing the role of atherosclerosis in the development of vasospasm.
Previous clinical and experimental studies have suggested that early atherosclerosis is present at the site of focal vasospasm. However, no clinical data exist demonstrating occult disease at the site of vasospasm at angiographically insignificant stenoses.
Twenty-two patients with chest pain at rest or during exertion, or both, were studied. Vasospasm was provoked by intracoronary administration of ergonovine maleate (0.01 to 0.04 mg). After relief of vasospasm by nitroglycerin administration, intravascular ultrasound imaging was performed with a 32- or 64-element, 20-MHz, synthetic aperture array ultrasound device.
Focal vasospasm (arterial diameter reduction > or = 90%) with ST-T segment elevation was provoked in 15 patients: in the left anterior descending coronary artery in 8 patients and in the right coronary artery in 7. The remaining seven patients (control group) showed diffuse narrowing, averaging 22 +/- 12% (mean +/- SD) in diameter from the baseline angiograms after ergonovine administration. Atherosclerosis, defined as a significantly thickened intimal leading edge (0.42 +/- 0.07 mm) associated with an increased sonolucent zone (0.57 +/- 0.30 mm), was detected by ultrasound at all 15 sites with focal vasospasm, although these sites were normal or minimally narrowed by angiography. In contrast, seven segments from the control group exhibited a thin intimal leading edge (0.14 +/- 0.04 mm, p < 0.01) and sonolucent zone (0.10 +/- 0.07 mm, p < 0.01), indicating the absence of localized atherosclerotic lesions.
These results indicate that atherosclerosis is present at the site of focal vasospasm, even in the absence of angiographically significant coronary disease. We suggest that the existence of such atherosclerotic lesions is related to the occurrence of focal vasospasm in the clinical settings.
本研究旨在使用血管内超声成像检查血管造影正常或轻度狭窄节段的局灶性血管痉挛部位隐匿性动脉粥样硬化的存在情况,以检验动脉粥样硬化在血管痉挛发生中的作用。
既往临床和实验研究提示局灶性血管痉挛部位存在早期动脉粥样硬化。然而,尚无临床数据表明在血管造影无明显狭窄的血管痉挛部位存在隐匿性病变。
对22例静息或运动时或两者均有胸痛的患者进行研究。通过冠状动脉内注射马来酸麦角新碱(0.01至0.04mg)诱发血管痉挛。在给予硝酸甘油缓解血管痉挛后,使用32或64阵元、20MHz合成孔径阵列超声设备进行血管内超声成像。
15例患者诱发了伴有ST-T段抬高的局灶性血管痉挛(动脉直径缩小≥90%):8例位于左前降支冠状动脉,7例位于右冠状动脉。其余7例患者(对照组)表现为弥漫性狭窄,给予麦角新碱后直径较基线血管造影平均缩小22±12%(平均值±标准差)。在所有15个局灶性血管痉挛部位均通过超声检测到动脉粥样硬化,定义为内膜前缘显著增厚(0.42±0.07mm)并伴有透声区增大(0.57±0.30mm),尽管这些部位血管造影显示正常或轻度狭窄。相比之下,对照组的7个节段表现为内膜前缘较薄(0.14±0.04mm,p<0.01)和透声区较薄(0.10±0.07mm,p<0.01),表明不存在局限性动脉粥样硬化病变。
这些结果表明,即使在无血管造影显著冠状动脉疾病的情况下,局灶性血管痉挛部位也存在动脉粥样硬化。我们认为,这种动脉粥样硬化病变的存在与临床环境中局灶性血管痉挛的发生有关。