脑缺血后出血转化:机制和发生率。

P D Lyden, J A Zivin
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引用次数: 0

摘要

出血性梗塞和脑血肿是脑缺血后令人担忧的事件。新开发的溶栓药物可能是有效的脑卒中治疗方法,但也可能促进缺血性脑卒中后的出血并发症。因此,了解缺血性卒中后出血转化的真实发生率,并确定这种现象的潜在机制是至关重要的。近年来,使用连续计算机断层扫描识别出血的研究表明,15%至43%的缺血患者发生转化。实验和临床证据支持出血是由于侧枝循环进入缺血区,可能与高血压同时发生。血栓的再通和远端迁移不是与转化相关的因素。如果再灌注在神经系统症状出现后很快完成,溶栓药物的药理学再通不太可能与出血相关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hemorrhagic transformation after cerebral ischemia: mechanisms and incidence.

Hemorrhagic infarction and cerebral hematoma are feared events that may follow cerebral ischemia. Newly developed thrombolytic agents may be effective stroke therapy, but may also promote hemorrhagic complications after ischemic stroke. It is therefore critically important to understand the true incidence of hemorrhagic transformation after ischemic stroke, and to identify if possible the mechanisms underlying the phenomenon. In recent years, studies using serial computed tomography to identify hemorrhage have shown that transformation occurs in 15 to 43% of patients presenting with ischemia. Experimental and clinical evidence support the notion that hemorrhage results from augmented collateral circulation into the ischemic zone, perhaps in concert with hypertension. Recanalization and distal migration of the thrombus are not factors that are associated with transformation. Pharmacologic recanalization using thrombolytic drugs are not likely to be associated with hemorrhage if reperfusion is accomplished very soon after the onset of neurologic symptoms.

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