Neurosurgery Research Group, Biomedicum Helsinki, Finland.
J Neurointerv Surg. 2010 Jun;2(2):120-30. doi: 10.1136/jnis.2009.002055. Epub 2010 Mar 12.
Rupture of a saccular intracranial artery aneurysm (IA) causes subarachnoid hemorrhage, a significant cause of stroke and death. The current treatment options, endovascular coiling and clipping, are invasive and somewhat risky. Since only some IAs rupture, those IAs at risk for rupture should be identified. However, to improve the imaging of rupture-prone IAs and improve IA treatment, IA wall pathobiology requires more thorough knowledge. Chronic inflammation has become understood as an important phenomenon in IA wall pathobiology, featuring inflammatory cell infiltration as well as proliferative and fibrotic remodulatory responses. We review the literature on what is known about inflammation in the IA wall and also review the probable mechanisms of how inflammation would result in the degenerative changes that ultimately lead to IA wall rupture. We also discuss current options in imaging inflammation and how knowledge of inflammation in IA walls may improve IA treatment.
囊状颅内动脉动脉瘤(IA)破裂可导致蛛网膜下腔出血,是中风和死亡的重要原因。目前的治疗选择包括血管内介入治疗(弹簧圈栓塞和夹闭),这些方法具有一定的侵入性和风险。由于只有部分 IAs 会破裂,因此需要识别那些有破裂风险的 IAs。然而,为了改善易破裂 IAs 的成像并改善 IA 治疗,IA 壁的病理生物学需要更全面的了解。慢性炎症已被认为是 IA 壁病理生物学中的一个重要现象,其特征是炎症细胞浸润以及增生和纤维化的重塑反应。我们回顾了关于 IA 壁炎症的文献,并回顾了炎症可能导致最终导致 IA 壁破裂的退行性变化的可能机制。我们还讨论了目前在炎症成像方面的选择,以及对 IA 壁炎症的认识如何改善 IA 治疗。