Hoppe Anna L, Raghavan Madhavan L, Hasan David M
Department of Biomedical Engineering, University of Iowa, Iowa City, Iowa, United States of America.
Department of Neurosurgery, University of Iowa Carver College of Medicine, Iowa City, Iowa, United States of America.
PLoS One. 2015 Apr 20;10(4):e0123017. doi: 10.1371/journal.pone.0123017. eCollection 2015.
In recurrent cerebral aneurysms treated by coil embolization, coil compaction is regarded as the presumptive mechanism. We test the hypothesis that aneurysm growth is the primary recurrence mechanism. We also test the hypothesis that the coil mass will translate a measurable extent when recurrence occurs.
An objective, quantitative image analysis protocol was developed to determine the volumes of aneurysms and coil masses during initial and follow-up visits from 3D rotational angiograms. The population consisted of 15 recurrence and 12 non-recurrence control aneurysms initially completely coiled at a single center. An investigator sensitivity study was performed to assess the objectivity of the methods. Paired Wilcoxon tests (p<0.05, one-tailed) were performed to assess for aneurysm and coil growth. The translation of the coil mass center at follow-up was computed. A Mann Whitney U-Test (p<0.05, one-tailed) was used to compare translation of coil mass centers between recurrence and control subjects.
Image analysis protocol was found to be insensitive to the investigator. Aneurysm growth was evident in the recurrence cohort (p=0.003) but not the control (p=0.136). There was no evidence of coil compaction in either the recurrence or control cohorts (recurrence: p=0.339; control: p=0.429). The translation of the coil mass centers was found to be significantly larger in the recurrence cohort than the control cohort (p=0.047).
Aneurysm sac growth, not coil compaction, was the primary mechanism of recurrence following successful coil embolization. The coil mass likely translates to a measurable extent when recurrence occurs and has the potential to serve as a non-angiographic recurrence marker.
在通过弹簧圈栓塞治疗的复发性脑动脉瘤中，弹簧圈压缩被视为推测的机制。我们检验动脉瘤生长是主要复发机制这一假说。我们还检验复发发生时弹簧圈团块会有可测量程度移位这一假说。
制定了一种客观、定量的图像分析方案，以根据三维旋转血管造影确定初次就诊和随访时动脉瘤及弹簧圈团块的体积。研究对象包括在单一中心最初完全用弹簧圈栓塞的15个复发性动脉瘤和12个非复发性对照动脉瘤。进行了一项研究者敏感性研究以评估方法的客观性。采用配对Wilcoxon检验（p<0.05，单尾）评估动脉瘤和弹簧圈的生长情况。计算随访时弹簧圈团块中心的移位。使用Mann-Whitney U检验（p<0.05，单尾）比较复发组和对照组弹簧圈团块中心的移位情况。
发现图像分析方案对研究者不敏感。复发队列中动脉瘤生长明显（p=0.003），而对照组不明显（p=0.136）。复发组和对照组均无弹簧圈压缩的证据（复发组：p=0.339；对照组：p=0.429）。发现复发队列中弹簧圈团块中心的移位明显大于对照组（p=0.047）。
成功进行弹簧圈栓塞后，复发的主要机制是动脉瘤囊生长，而非弹簧圈压缩。复发发生时，弹簧圈团块可能会有可测量程度的移位，并且有潜力作为一种非血管造影的复发标志物。
