Center for Advanced Biomedical Sciences, Waseda University, 2-2 Wakamatsucho Shinjukuku, Tokyo, 162-8480, Japan.
Second Department of Pathology, Akita University, Akita, Japan.
Biomech Model Mechanobiol. 2024 Aug;23(4):1229-1240. doi: 10.1007/s10237-024-01835-5. Epub 2024 Mar 15.
Aneurysmal rupture is associated with wall thinning, but the mechanism is poorly understood. This study aimed to characterize the three-dimensional wall-thickness distributions of unruptured intracranial aneurysms. Five aneurysmal tissues were investigated using micro-computed tomography. First, the wall thickness was related to the aneurysmal wall appearances during surgery. The median wall thicknesses of the translucent and non-translucent walls were 50.56 and 155.93 µm, respectively (p < 0.05) with significant variation in the non-translucent wall thicknesses (p < 0.05). The three-dimensional observations characterized the spatial variation of wall thicknesses. Thin walls showed a uniform thickness profile ranging from 10 to 40 µm, whereas thick walls presented a peaked thickness profile ranging from 300 to 500 µm. In transition walls, the profile undulated due to the formation of focal thin/thick spots. Overall, the aneurysmal wall thicknesses were strongly site-dependent and spatially varied by 10 to 40 times within individual cases. Aneurysmal walls are exposed to wall stress driven by blood pressure. In theory, the magnitude of wall stress is inversely proportional to wall thickness. Thus, the observed spatial variation of wall thickness may increase the spatial variation of wall stress to a similar extent. The irregular wall thickness may yield stress concentration. The observed thin walls and focal thin spots may be caused by excessive wall stresses at the range of mechanical failure inducing wall injuries, such as microscopic tears, during aneurysmal enlargement. The present results suggested that blood pressure (wall stress) may have a potential of acting as a trigger of aneurysmal wall injury.
动脉瘤破裂与壁变薄有关，但机制尚不清楚。本研究旨在描述未破裂颅内动脉瘤的三维壁厚分布。使用微计算机断层扫描对 5 个动脉瘤组织进行了研究。首先，将壁厚度与手术过程中动脉瘤壁的外观相关联。半透明壁和非半透明壁的壁厚度中位数分别为 50.56μm 和 155.93μm（p<0.05），非半透明壁厚度存在显著差异（p<0.05）。三维观察特征化了壁厚的空间变化。薄壁表现出均匀的厚度分布，范围为 10 至 40μm，而厚壁则呈现出从 300 至 500μm 的峰值厚度分布。在过渡壁中，由于形成局部薄/厚点，厚度分布呈波浪状。总的来说，动脉瘤壁厚度强烈依赖于位置，并且在个体病例中空间变化可达 10 至 40 倍。动脉瘤壁受到血压驱动的壁应力。理论上，壁应力的大小与壁厚度成反比。因此，观察到的壁厚空间变化可能会以类似的程度增加壁应力的空间变化。不规则的壁厚可能会产生应力集中。观察到的薄壁和局部薄点可能是由于在机械失效范围内的壁应力过大，导致在动脉瘤扩大过程中发生壁损伤，例如微观撕裂。目前的结果表明，血压（壁应力）可能具有作为动脉瘤壁损伤触发因素的潜力。
