Abstract：
Pulmonary hypertension (PH), defined by a mean pulmonary arterial blood pressure above 20 mmHg in the main pulmonary artery, is a cardiovascular disease impacting the pulmonary vasculature. PH is accompanied by chronic vascular remodeling, wherein vessels become stiffer, large vessels dilate, and smaller vessels constrict. Some types of PH, including hypoxia-induced PH (HPH), also lead to microvascular rarefaction. This study analyzes the change in pulmonary arterial morphometry in the presence of HPH using novel methods from topological data analysis (TDA). We employ persistent homology to quantify arterial morphometry for control and HPH mice characterizing normalized arterial trees extracted from micro-computed tomography (micro-CT) images. We normalize generated trees using three pruning algorithms before comparing the topology of control and HPH trees. This proof-of-concept study shows that the pruning method affects the spatial tree statistics and complexity. We find that HPH trees are stiffer than control trees but have more branches and a higher depth. Relative directional complexities are lower in HPH animals in the right, ventral, and posterior directions. For the radius pruned trees, this difference is more significant at lower perfusion pressures enabling analysis of remodeling of larger vessels. At higher pressures, the arterial networks include more distal vessels. Results show that the right, ventral, and posterior relative directional complexities increase in HPH trees, indicating the remodeling of distal vessels in these directions. Strahler order pruning enables us to generate trees of comparable size, and results, at all pressure, show that HPH trees have lower complexity than the control trees. Our analysis is based on data from 6 animals (3 control and 3 HPH mice), and even though our analysis is performed in a small dataset, this study provides a framework and proof-of-concept for analyzing properties of biological trees using tools from Topological Data Analysis (TDA). Findings derived from this study bring us a step closer to extracting relevant information for quantifying remodeling in HPH.
摘要：
肺动脉高压(PH),由主肺动脉的平均肺动脉血压超过20mmHg定义，是一种影响肺血管的心血管疾病。PH伴随慢性血管重塑，其中血管变得更硬，大血管扩张，和较小的船只收缩。某些类型的PH,包括缺氧诱导的PH（HPH），也会导致微血管稀疏。本研究使用拓扑数据分析（TDA）的新方法分析了HPH存在下肺动脉形态的变化。我们采用持续的同源性来量化对照和HPH小鼠的动脉形态计量学，这些小鼠表征了从微型计算机断层扫描（micro-CT）图像中提取的归一化动脉树。在比较控制树和HPH树的拓扑之前，我们使用三种修剪算法对生成的树进行归一化。此概念验证研究表明，修剪方法会影响空间树的统计和复杂性。我们发现HPH树比对照树更硬，但分支更多，深度更高。右侧的HPH动物的相对方向复杂性较低，腹侧,和向后的方向。对于半径修剪的树木，这种差异在较低的灌注压力下更为显著,从而能够分析较大血管的重塑.在更高的压力下，动脉网络包括更多的远端血管。结果显示,腹侧,HPH树的后部相对方向复杂性增加，表明远端血管在这些方向上的重塑。Strahler订单修剪使我们能够生成大小相当的树木，和结果，在所有压力下，表明HPH树的复杂度低于对照树。我们的分析基于6只动物（3只对照和3只HPH小鼠）的数据，即使我们的分析是在一个小数据集中进行的，本研究为使用拓扑数据分析（TDA）的工具分析生物树的属性提供了框架和概念证明。从这项研究得出的结果使我们更接近于提取相关信息以量化HPH中的重塑。
