Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 13-25 |
| Number of pages | 13 |
| Journal | Biomechanics and Modeling in Mechanobiology |
| Volume | 13 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jan 2014 |
Keywords
- Osmotic (Donnan) swelling pressure
- Proteoglycan
- Stress concentration
- TGF-beta
- Wall stress