Abstract
Tissue degradation plays a crucial role in the formation and rupture of aneurysms. Using numerical computer simulations, we study the combined effects of blood flow and tissue degradation on intra-aneurysm hemodynamics. Our computational analysis reveals that the degradation-induced changes of the time-averaged wall shear stress (TAWSS) and oscillatory shear index (OSI) within the aneurysm dome are inversely correlated. Importantly, their correlation is enhanced in the process of tissue degradation. Regions with a low TAWSS and a high OSI experience still lower TAWSS and higher OSI during degradation. Furthermore, we observed that degradation leads to an increase of the endothelial cell activation potential index, in particular, at places experiencing low wall shear stress. These findings are robust and occur for different geometries, degradation intensities, heart rates and pressures. We interpret these findings in the context of recent literature and argue that the degradation-induced hemodynamic changes may lead to a self-amplification of the flow-induced progressive damage of the aneurysmal wall.
Highlights
Both microscopic degradation in vascular tissues and hemodynamic forces play a crucial role in the initiation, growth and focal rupture of aneurysms (Sforza et al, 2009; Salman et al, 2019; Lipp et al, 2020; Wu et al, 2020)
We investigate the effect of tissue degradation on two commonly used intra-aneurysmal hemodynamic quantities, time-averaged wall shear stress (TAWSS) and oscillatory shear index (OSI), and endothelial cell activation potential (ECAP)
In order to quantify the effects of tissue degradation on TAWSS, OSI and ECAP, we use Equation (4) and determine the tissue-degradation-induced relative changes of these hemodynamic quantities (Figure 3)
Summary
Both microscopic degradation in vascular tissues and hemodynamic (fluid-dynamic) forces play a crucial role in the initiation, growth and focal rupture of aneurysms (Sforza et al, 2009; Salman et al, 2019; Lipp et al, 2020; Wu et al, 2020). Aneurysms are vascular diseases characterized by excessive tissue degradation and chronic inflammation (Frösen, 2014). Abnormal WSS is a major cause of the imbalance between the constructive and destructive processes (Meng et al, 2014) and leads to vascular degradation and inflammation by activating inflammatory markers of endothelial cells (Franck et al, 2013; Meng et al, 2014), thereby causing the breakdown of the internal elastic lamina and loss of structural strength within the vessel wall (Kataoka et al, 1999). An aneurysm can grow and even rupture with continuous vascular injury, inflammation, and prolonged activation (Fisher and Demel, 2019)
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