Wall shear stress topological skeleton analysis for understanding the near-wall hemodynamics of stented coronary arteries.

Nowadays, percutaneous coronary intervention (PCI) (angioplasty with stent) is the most common non-surgical treatment of narrowed coronary arteries to restore proper blood flow to the heart. A stent is an expandable tubular structure made up of a mesh network that provides mechanical support to the vessel wall. Although stenting is an established treatment for diseased coronary arteries, the stent presence alters the vessel geometry and generates a new local fluid dynamic environment, which may lead to future complications, such as in-stent restenosis or late stent thrombosis. A large body of literature has demonstrated the association between these adverse events and the presence of altered local hemodynamics. In particular, the wall shear stress (WSS) has been shown as an important factor involved in the pathological mechanism leading to stent failure. The most widely hemodynamic indexes use information based on WSS magnitude and/or direction, although they are found to be weak predictors of stent failure. In this context, a growing interest has recently emerged in studying the topological skeleton of the WSS, made of fixed points where the WSS vector field vanishes, and contraction/expansion regions connecting them, called manifolds. The extracted features are able to better elucidate the complexity of the local hemodynamics, highlighting areas with adverse phenomena of flow stagnation, separation and recirculation. By using computational fluid dynamics (CFD), this thesis work investigates the WSS topological skeleton features in a patient-specific stented coronary artery model, reconstructed using a combination of optical coherence tomography and angiographic data, acquired immediately after PCI. Therefore, the aim of the work is to investigate new near-wall hemodynamic features that may support the use of the WSS topological skeleton in future studies to understand the underlying mechanisms leading to stent failure. To appreciate the hemodynamic impact of the stenting procedure, all features were also obtained on the same considered model without stent. In addition, a parallel study was performed on idealized models of stents implanted in an ideal, cylindrical vessel, in which the shape and/or size of the stent strut was varied, quantifying the impact of these variations on the WSS-based descriptors. The results show an overall agreement between the WSS-based descriptors in marking the luminal zones in the vicinity of the stent. The impact of vessel geometry is also evident in the vicinity of the bifurcation carina (non-stented model), although its contribution becomes negligible in the stented model. Interestingly, the WSS topological skeleton descriptors are able to capture new aspects: the presence of WSS contraction/expansion regions in the areas immediately upstream/downstream of the stent ring has been observed and this phenomenon changes in the presence of malapposed struts. There is also a high variability of the contraction-expansion action along the cardiac cycle within the convexity zones of the stent peaks, the site of possible recirculation phenomena (observed with 2D streamlines). This variability may induce an increase in the permeability of the endothelium, due to the recurrent variation of tension on the cell and intercellular junctions. In conclusion, the present study candidates the WSS topological skeleton as an additional tool for understanding the hemodynamic-related processes leading to stent failure.