[Diagnosis of myocardial ischemia in Kawasaki disease: thallium-201 myocardial imagings at rest, with exercise and with dipyridamole administration].

[Diagnosis of myocardial ischemia in Kawasaki disease: thallium-201 myocardial imagings at rest, with exercise and with dipyridamole administration].
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[川崎病心肌缺血的诊断:静息、运动和双嘧达莫给药时铊201心肌显像]。

DOI:
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发表时间:
1984
期刊:
Journal of Edugeography
影响因子:
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通讯作者:
T. Kozuka
T. Kozuka
中科院分区:
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文献类型:
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作者:
T. Mitomori;Y. Ono;H. Sugiyama;A. Suzuki;T. Kamiya;T. Nishimura;T. Kozuka

文献摘要

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对131例川崎冠状动脉病变患儿进行了静息状态下~(201)铊心肌显像。在同位素研究的几天内通过选择性冠状动脉造影术评估冠状动脉病变。21名儿童有闭塞性病变,16名儿童有节段性狭窄病变。在9例前者和3例后者中检测到心肌图像的灌注缺陷。灌注缺损的位置与冠状动脉造影显示的病变血管的灌注区域相吻合。12例静息时有初始灌注缺陷的患者进行了随访研究,其中5例缺陷消失。这些患者通过侧支血管的形成或再通在最初受影响的区域重建了冠状动脉血流。对27例患者进行了运动心肌显像,其中4例冠状动脉闭塞,2例节段性狭窄。所有冠状动脉病变患者在运动成像中均显示灌注缺损,而静息研究仅在1例患者中显示缺损,运动后观察到更广泛的灌注缺损。本文对43例患者静脉注射潘生丁后进行了心肌显像。17例冠状动脉闭塞患者中有15例在注射后出现灌注缺陷,13例节段性狭窄患者中有9例出现灌注缺陷。在4例静息时存在灌注缺损的患者中,该药物在额外冠状动脉受累区域显示了额外或更广泛的缺损。在20例仅注射潘生丁后出现灌注缺损的患者中,灌注缺损与血管造影结果吻合良好。一个特殊的病人没有狭窄病变,但有三个巨大的冠状动脉瘤的右冠状动脉注射潘生丁后记录灌注缺损。因此,扩张的冠状动脉病变似乎提供了灌注缺陷。在一些患者的灌注缺陷消失在休息的后续研究中,缺陷被披露的运动和/或潘生丁管理。因此,201铊心肌显像结合静息和运动或潘生丁研究是有价值的检测和评价冠状动脉病变的川崎。
Thallium-201 myocardial imaging was performed at rest in 131 children with coronary arterial lesions due to Kawasaki disease. The coronary arterial lesions were assessed by selective coronary angiography within a few days of the isotope study. Twenty-one children had occlusive lesions, and segmental stenotic lesions were seen in 16 children. Perfusion defects of the myocardial images were detected in nine of the former and in three of the latter. The locations of the perfusion defects coincided with the perfusion areas of the affected vessels on coronary angiography. Twelve patients with initial perfusion defects at rest had a follow-up study and the defects disappeared in five. These patients had re-establishment of coronary blood flow in the initially affected areas by either development of collateral vessels or recanalization. Myocardial imaging with exercise was performed in 27 patients including four with coronary arterial occlusion and two with segmental stenosis on coronary angiography. All with coronary artery lesions showed perfusion defects on the imaging with exercise, while the resting study showed the defects only in one patient, in whom more extensive perfusion defects were observed after exercise. Myocardial imaging following intravenous injection of dipyridamole was carried out in 43 patients. Perfusion defects after the injection were noted in 15 of 17 patients with coronary occlusion and in nine of 13 patients with segmental stenosis. In four patients with perfusion defects at rest, additional or more extensive defects were revealed by this drug in the areas of additional coronary arterial involvements. In 20 patients with perfusion defects only after dipyridamole injection, the perfusion defects coincided with the angiographic findings very well. A perfusion defect was documented following dipyridamole injection in one exceptional patient who had no stenotic lesions, but had three giant coronary aneurysms of the right coronary artery. Thus the dilated coronary lesions seemed to give a perfusion defect. In some of the patients whose perfusion defects disappeared at rest on a follow-up study, the defects were disclosed by exercise and/or dipyridamole administration. Thus, thallium-201 myocardial imagings combining resting and exercise or dipyridamole studies were valuable for the detection and assessment of coronary arterial lesions of Kawasaki disease.