On the severity of aortic stenosis in ascending aortic aneurysm: A computational tool to examine ventricular-arterial interaction and aortic wall stress
Section snippets
1. Introduction
An ascending thoracic aortic aneurysm (ATAA) is a cardiovascular condition that leads to permanent dilatation of the vessel and a high risk of adverse events when aortic size is >5 cm [1]. Nearly 10 out of 100,000 persons per year are affected by ATAA [2], and in those with a bicuspid aortic valve (BAV), the prevalence of aortopathy ranges from 20 to 84% [3]. The risk of ATAA development in BAV patients was found to be 80-fold higher than for the general population with a morphologically-normal
2.1. ATAA segmentation and meshing
Computed tomography angiography (CTA) scans of four patients with ATAA were identified from radiologic records of ISMETT IRCCS hospital as reported in similar studies [20,21]. We selected two BAV ATAAs and two TAV ATAAs with aortic dilatation involving the ascending aorta (Type A) and the aortic root (Type N) [22]. BAV ATAAs were characterized by the right-left leaflet cusp fusion. For each patient, aortic valve function was assessed by Doppler echocardiography, with no signs of AS or AI. The
3. Results
Fig. 3 shows the pressure-volume loops predicted by the lumped-parameter model for each patient at different degrees of AS. A leftward shift of pressure-volume loops was observed as the AS increases from the baseline condition to the severe condition. The severity of AS augments total LV work, with blood pressure rising sharply during systole to a domed-shaped pressure-volume loop. SV tends to slightly reduce while valvulo-arterial impedance rises with stenosis severity.
Fig. 4 displays a
4. Discussion
We adopted a computational framework to assess the change in the hemodynamic and structural mechanics of ATAAs under different degrees of AS. The ventricular-arterial interaction modeling approach demonstrated that post-stenotic wall and shear stresses exerted on the ATAA increase non-linearly from the baseline configuration of a patient with no signs of valvulopathy to the virtual model with severe AS. Specifically, peak systolic WSS for the model with severe AS rose up to 10-fold with respect
5. Conclusion
In this study, simulations were performed to assess the impact of post-stenotic shear and wall stresses in patients with ATAAs. As the stenosis increased from the baseline model with no signs of valvular dysfunction to the virtual model with severe AS, the WSS and maximum principal stress shown a 2.5- and 6-fold increase on the forces exerted on the ATAA wall, respectively. Hemodynamic and structural changes were associated with predictions of the valvular-arterial impedance, suggesting LV
Declaration of Competing Interest
None.
Acknowledgment
This work was supported by a “Ricerca Finalizzata” grant from the Italian Ministry of Health (GR-2011-02348129) to Salvatore Pasta.
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