Fodstad H, Liliequist B
Acta Neurochir (Wien). 1979;49(3-4):129-44. doi: 10.1007/BF01808955.
Radiographically verified spontaneous disappearance of medium-sized arterial cerebral aneurysms is seldom reported, and only three times in connection with antifibrinolytic therapy (EACA). In our clinic repeat angiograms have shown non-filling of the aneurysms in three patients during treatment with tranexamic acid (AMCA) two, three, and four weeks respectively after primary bleeds. Initially, all three patients had severe radiological vasospasm associated with neurological deterioration. Follow-up angiograms have demonstrated partial reappearance of the aneurysm after one month in one patient and complete disappearance of the aneurysms in the other two patients after 9 and 22 months respectively. In two cases occlusion of cerebral arteries occurred. With regard to the higher risk of severe vasospasm and occlusion of cerebral arteries in our opinion it should not be a therapeutic goal to try to achieve a thrombosis of a ruptured aneurysm with antifibrinolytic drugs. The reason for spontaneous aneurysm thrombosis during treatment with AMCA may be a local inhibition of plasminogen activators in and around the aneurysm wall. It may also be related to the sympathomimetic property of the drug, with vasospasm and a subsequent flow-reduction inside the aneurysm or a possible interaction with other drugs and substances.
经影像学证实的中型脑动脉动脉瘤自发消失鲜有报道,仅三次与抗纤维蛋白溶解疗法(EACA)相关。在我们诊所,三位患者在初次出血后分别于两周、三周和四周接受氨甲环酸(AMCA)治疗期间,重复血管造影显示动脉瘤未显影。最初,这三位患者均伴有严重的放射性血管痉挛并出现神经功能恶化。随访血管造影显示,一位患者在一个月后动脉瘤部分重现,另外两位患者分别在9个月和22个月后动脉瘤完全消失。两例出现脑动脉闭塞。鉴于严重血管痉挛和脑动脉闭塞风险较高,我们认为,使用抗纤维蛋白溶解药物促使破裂动脉瘤形成血栓不应作为治疗目标。AMCA治疗期间动脉瘤自发血栓形成的原因可能是动脉瘤壁及其周围局部纤溶酶原激活剂受到抑制。这也可能与该药物的拟交感神经特性有关,导致血管痉挛以及随后动脉瘤内血流减少,或者可能与其他药物和物质相互作用有关。