Pathogenesis of acute aortic dissection: a finite element stress analysis.
BACKGROUND: Type A and type B aortic dissections typically result from intimal tears above the sinotubular junction and distal to the left subclavian artery (LSA) ostium, respectively. We hypothesized that this pathology results from elevated pressure-induced regional wall stress.
METHODS: We identified 47 individuals with normal thoracic aortas by electrocardiogram-gated computed tomography angiography. The thoracic aorta was segmented, reconstructed, and triangulated to create a geometric mesh. Finite element analysis using a systolic pressure load of 120 mm Hg was performed to predict regional thoracic aortic wall stress.
RESULTS: There were local maxima of wall stress above the sinotubular junction in the ascending aorta and distal to the ostia of the supraaortic vessels, including the LSA, in the aortic arch. No local maximum of wall stress was found in the descending thoracic aorta. Comparison of the mean peak wall stress above the sinotubular junction (0.43 ± 0.07 MPa), distal to the LSA (0.21 ± 0.07 MPa), and in the descending thoracic aorta (0.06 ± 0.01 MPa) showed a significant effect for wall stress by aortic region (p < 0.001).
CONCLUSIONS: In the normal thoracic aorta, there are peaks in wall stress above the sinotubular junction and distal to the LSA ostium. This stress distribution may contribute to the pathogenesis of aortic dissections, given their colocalization. Future investigations to determine the utility of image-derived biomechanical calculations in predicting aortic dissection are warranted, and therapies designed to reduce the pressure load-induced wall stress in the thoracic aorta are rational.
Published In/Presented At
Nathan, D. P., Xu, C., Gorman, J. H., 3rd, Fairman, R. M., Bavaria, J. E., Gorman, R. C., Chandran, K. B., & Jackson, B. M. (2011). Pathogenesis of acute aortic dissection: a finite element stress analysis. The Annals of thoracic surgery, 91(2), 458–463. https://doi.org/10.1016/j.athoracsur.2010.10.042
Medicine and Health Sciences
Department of Medicine, Cardiology Division