MECHANISM OF ACUTE MYOCARDIAL-INFARCTION IN PATIENTS WITH PRIOR CORONARY-ARTERY BYPASS-GRAFTING AND THERAPEUTIC IMPLICATIONS

MECHANISM OF ACUTE MYOCARDIAL-INFARCTION IN PATIENTS WITH PRIOR CORONARY-ARTERY BYPASS-GRAFTING AND THERAPEUTIC IMPLICATIONS
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DOI:
10.1016/0002-9149(90)91315-w
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发表时间:
1990-06-01
影响因子:
2.8
通讯作者:
DEMARIA, AN
DEMARIA, AN
中科院分区:
医学3区
文献类型:
--
作者:
GRINES, CL;BOOTH, DC;DEMARIA, AN

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虽然急性心肌梗死 (AMI) 通常是由于累及自体冠状动脉时的血栓闭塞所致,但对于既往接受过冠状动脉旁路移植术 (CABG) 的患者,导致 AMI 的机制尚不清楚。由于 AMI 病理生理学知识可能会改变后续治疗,因此对 50 名 CABG 术后 1 年以上的患者在 AMI 1 小时至 7 天(中位 1 天)之间获得的血管造影进行了审查。通过供应梗死区的血管中是否存在残余狭窄和/或血栓或通过回顾先前的血管造影来识别罪魁祸首血管。 38 名患者 (76%) 的梗死血管被确定为静脉移植物,8 名患者 (16%) 的梗塞血管被确定为原生血管,4 名患者 (8%) 的梗塞血管无法准确确定。在怀疑为梗塞血管的 38 例静脉移植物中,31 例(82%)存在明确的血管造影残留血栓(充盈缺损/持续染色)证据,其中 15 例患者长度 >2 cm。 静脉溶栓治疗后,8 个移植物中仅 2 个(25%)成功再灌注。移植物内溶栓联合或不联合额外的血管成形术成功地恢复了 10 个移植物中的 8 个(80%)的血流。数据表明,在既往接受过 CABG 的患者中,AMI 通常是由大隐静脉移植物的血栓闭塞引起的,而传统的静脉溶栓治疗可能不足以恢复血流。移植物中存在大量血栓且缺乏血流,可能需要亚选择性药物输注、更高的溶栓剂量或机械再通方法。
Although acute myocardial infarction (AMI) is usually due to thrombotic occlusion when involving a native coronary artery, the mechanism responsible for AMI in patients with previous coronary artery bypass grafting (CABG) is not well understood. Since knowledge of pathophysiology of AMI may alter subsequent management, angiograms obtained between 1 hour and 7 days of AMI (median 1 day) were reviewed in 50 patients > 1 year after CABG. The culprit vessel was identified by the presence of residual stenosis and/or thrombus in the vessel supplying the infarct zone or by reviewing previous angiograms. The infarct vessel was identified as a vein graft in 38 (76%) patients, the native vessel in 8 patients (16%) and could not be accurately determined in 4 patients (8%). Among the 38 vein grafts suspected as the infarct vessel, unequivocal angiographic evidence of residual thrombus (filling defect/persistent staining) was present in 31 (82%) and was >2 cm in length in 15 patients. Successful reperfusion occurred in only 2 of 8 (25%) grafts after intravenous thrombolytic therapy. Intragraft thrombolysis with or without additional angioplasty was successful at restoring flow in 8 of 10 (80%) grafts. Data indicate that in patients who have undergone previous CABG, AMI is usually caused by thrombotic occlusion of a saphenous vein graft and that conventional intravenous thrombolytic therapy may be inadequate to restore flow. The large mass of thrombus and absent flow in the graft may require subselective drug infusion, a higher thrombolytic dose or a mechanical means of recanalization.