Department of Biomedical Engineering, Malone Engineering Center, Yale University, 55 Prospect Street, New Haven, CT, 06520, USA.
Biomech Model Mechanobiol. 2014 Jan;13(1):13-25. doi: 10.1007/s10237-013-0482-3. Epub 2013 Mar 15.
Spontaneous dissection of the human thoracic aorta is responsible for significant morbidity and mortality, yet this devastating biomechanical failure process remains poorly understood. In this paper, we present finite element simulations that support a new hypothesis for the initiation of aortic dissections that is motivated by extensive histopathological observations. Specifically, our parametric simulations show that the pooling of glycosaminoglycans/proteoglycans that is singularly characteristic of the compromised thoracic aorta in aneurysms and dissections can lead to significant stress concentrations and intra-lamellar Donnan swelling pressures. We submit that these localized increases in intramural stress may be sufficient both to disrupt the normal cell-matrix interactions that are fundamental to aortic homeostasis and to delaminate the layered microstructure of the aortic wall and thereby initiate dissection. Hence, pathologic pooling of glycosaminoglycans/proteoglycans within the medial layer of the thoracic aortic should be considered as a possible target for clinical intervention.
自发性胸主动脉夹层是导致发病率和死亡率显著升高的主要原因,然而,这种破坏性的生物力学失效过程仍未得到很好的理解。在本文中,我们提出了有限元模拟,为主动脉夹层的起始提供了一个新的假说,这个假说源于广泛的组织病理学观察。具体来说,我们的参数模拟表明,糖胺聚糖/蛋白聚糖的聚集是动脉瘤和夹层中胸主动脉特有的现象,可能导致显著的应力集中和层间唐南膨胀压力。我们认为,这些局部的壁内应力增加可能足以破坏主动脉稳态所必需的正常细胞-基质相互作用,并使主动脉壁的分层微观结构分层,从而引发夹层。因此,胸主动脉中膜层内糖胺聚糖/蛋白聚糖的病理积聚应被视为临床干预的一个可能靶点。