A CLINICOPATHOLOGICAL STUDY OF PATIENTS WITH HEMORRHAGIC MYOCARDIAL-INFARCTION TREATED WITH SELECTIVE CORONARY THROMBOLYSIS WITH UROKINASE
A CLINICOPATHOLOGICAL STUDY OF PATIENTS WITH HEMORRHAGIC MYOCARDIAL-INFARCTION TREATED WITH SELECTIVE CORONARY THROMBOLYSIS WITH UROKINASE
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DOI：
10.1161/01.cir.73.4.749
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发表时间：
1986-04-01
期刊：
影响因子：
37.8
通讯作者：
HAMASHIMA, Y
中科院分区：
文献类型：
--
作者：
FUJIWARA, H;ONODERA, T;HAMASHIMA, Y
对30例尸检的出血性急性心肌梗塞（AMI）患者进行了选择性冠状动脉内溶栓（SICT）后的研究。在2至9小时（4 ± 1.5小时）选择性地将240，000至1，200，000 U的尿激酶注射到梗塞相关冠状动脉中。2小时）。梗死相关冠状动脉显示完全闭塞21例，99%狭窄8例，90%狭窄22例，90%狭窄3例。28例为透壁性梗死，2例为内膜下梗死。肉眼和显微镜下，出血程度分为无、轻度、中度或显著出血，出血性梗死定义为梗死区中度或显著弥漫性出血。根据从SICT到死亡的时间，将患者分为I期（早期急性期，SICT后1至4小时和AMI发作后4至13小时; n = 7），II期急性期晚期，SICT后9小时至11天，AMI发作后15小时至11天; III期（陈旧性梗死期，AMI和SICT后17天以上; n = 5）。三个阶段的患者在再通频率、从AMI发作到SICT的时间、尿激酶剂量或其他临床参数方面无显著差异。只有II期患者的心脏出现出血性梗死，18例心脏中有15例出现出血性梗死。在6个心脏中观察到明显的弥漫性出血，所有这些心脏在SICT后均显示再通。然而，即使在三个病人在第二阶段没有再通局限于梗死区。因此，在大多数接受SICT治疗的AMI患者中，出血在SICT后逐渐增加，4小时后变为中度或显著弥漫性，3至4周后被纤维化取代。出血性梗死是由于再灌注和大剂量尿激酶的联合作用。出血的时间延迟似乎取决于狭窄的梗死相关冠状动脉远端部分的低灌注压。出血不太可能扩大梗塞面积。
Hemorrhagic acute myocardial infaraction (AMI) was studied after selective intracoronary thrombolysis (SICT) in 30 patients undergoing autopsy. Urokinase, 240,000 to 1,200,000 U, was selectively injected into the infarct-related coronary artery at 2 to 9 hr (4 .+-. 2 hr) after the onset of AMI. The infarct-related coronary artery showed complete occlusion in 21, 99% stenosis in eight, and 90% stenosis in 22, and 90% stenosis in three patients. Twenty-eight patients had transmural infarction and the other two had subendocardial infarction. Macroscopically and microscopically, the degree of hemorrhage was classified as no, slight, moderate, or marked bleedking and the hemorrhagic infarction was defined as moderate or marked diffuse bleeding in the infarct area. According to the interval from SICT to death, patients were also classified into stage I (early acute stage, 1 to 4 hr after SICT and 4 to 13 hr after the onset of AMI; n = 7), stage II (late acute stage, 9 hr to 11 days after SICT and 15 hr to 11 days after the onset of AMI; n = 18), or stage III (old infarction stage, over 17 days after AMI and SICT; n = 5). There were no significant differences with respect to the frequency of recanalization, the time from the onset of AMI to SICT, the dose of urokinase, or other clinical parameters among patients at the three stages. Only the hearts of patients in stage II showed hemorrhagic infarction, and it was found in 15 of 18 of these hearts. Marked diffuse hemorrhage was noted in six hearts, all of which showed recanalization after SICT. However, even in three patients in stage II without recanalization localized within the infarct area. Thus, in most of the patients with AMI treated with SICT, hemorrhage increases gradually after SICT, becomes moderately or markedly diffuse after 4 hr, and is replaced by fibrosis after 3 to 4 weeks. The hemorrhagic infarction is due to the combined effects of reperfusion and large doses of urokinase. The time delay of bleeding seems to depend on the low perfusion pressure in the portion distal to the stenosed, infarct-related coronary artery. It is unlikely that hemorrhage expands the infarct area.