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Thoracic aortic aneurysm (TAA) is a local dilation of the thoracic aorta. Although universally used, aneurysm diameter alone is a poor predictor of major complications such as rupture. There is a need for better biomarkers for risk assessment that also reflect the aberrant flow patterns found in TAAs. Furthermore, hypertension is often present in TAA patients and may play a role in progression of aneurysm. The exact relation between TAAs and hypertension is poorly understood. This study aims to create a numerical model of hypertension in the aorta by using computational fluid dynamics. First, a normotensive state was simulated in which flow and resistance were kept unaltered. Second, a hypertensive state was modeled in which blood inflow was increased by 30%. Third, a hypertensive state was modeled in which the proximal and peripheral resistances and capacitance parameters from the three-element Windkessel boundary condition were adjusted to mimic an increase in resistance of the rest of the cardiovascular system. One patient with degenerative TAA and one healthy control were successfully simulated at hypertensive states and were extensively analyzed. Furthermore, three additional TAA patients and controls were simulated to validate our method. Hemodynamic variables such as wall shear stress, oscillatory shear index, endothelial cell activation potential (ECAP), vorticity and helicity were studied to gain more insight on the effects of hypertension on flow patterns in TAAs. By comparing a TAA patient and a control at normotensive state at peak-systole, helicity and vorticity were found to be lower in the TAA patient throughout the entire domain. No major changes in flow and flow derived quantities were observed for the TAA patient and control when resistance was increased. When flow rate was increased, regions with high ECAP values were found to reduce in TAA patients in the aneurysm region which could reduce the risk of thrombogenesis. Thus, it may be important to assess cardiac output in patients with TAA., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Objectives: In acute type B aortic dissection (ABAD) a patent false lumen portends a poor outcome. Patent branch vessels originating from the false lumen in a type B aortic dissection are assumed to contribute to persistent blood flow and patent false lumen. Therefore, the morphologic changes of the false lumen generated by different outflow rates in an in vitro model were investigated., Methods: An artificial dissection was created in two ex vivo porcine aortas. A thin cannula was placed in the false lumen, simulating a branch vessel originating from it. The aorta was positioned in a validated in vitro circulatory system with physiological pulsatile flow (1,500-2,700 mL/minute) and pressure characteristics (130/70 mm Hg). The cannula was attached to a small silicone tube with an adjustable valve mechanism. Three different valve settings were used for creating outflow from the false lumen (fully closed, opened at 50%, and fully opened at 100%). Measurements of lumen areas and flow rates were assessed with time-resolved magnetic resonance imaging. In order to study reproducibility, the experiment was performed twice in two different porcine aortas with a similar morphology., Results: Increasing antegrade outflow through the branch vessel of the false lumen resulted in a significant (p < .01) increase of the mean false lumen area at the proximal and distal location in both models. The distal false lumen expanded up to 107% in the case of high outflow via the false lumen through the branch vessel., Conclusions: Increasing antegrade outflow through a branch vessel originating from the false lumen when no distal re-entry tear is present results in an expansion of the cross sectional false lumen area., (Copyright © 2014 European Society for Vascular Surgery. Published by Elsevier Ltd. All rights reserved.)