Relationship between hemodynamics and CTA-derived morphological features in diseased coronary arteries

Atherosclerosis is a chronic and progressive inflammatory disease that mainly affects older individuals in industrialized countries. It affects the walls of medium and large blood vessels, such as the coronary arteries, where the formation of atherosclerotic plaques in the tunica intima causes a reduction in the vascular lumen. This narrowing can lead to several clinical complications, including a reduction in blood supply downstream of the lesion, with a consequent risk of ischemia and myocardial infarction. Numerous studies have shown that specific hemodynamic conditions, particularly the presence of disturbed flow, play a crucial role in the development and progression of atherosclerosis. In this scenario, the present thesis analyzes the correlation between hemodynamics and structural characteristics of atherosclerotic plaques in ten models of pathological coronary arteries, reconstructed from CT images, with the aim of identifying the areas predisposed to unfavourable clinical events or formation of new lesions. To carry out this study, coronary models were appropriately processed to prepare them for the meshing phase. For each model, a transient simulation was performed to simulate blood flow within the coronary branches. Hemodynamically susceptible zones were evaluated with WSS-based descriptors, i.e. time-averaged wall shear stress (TAWSS), oscillatory shear index (OSI), transversal wall shear stress (transWSS) and topological shear variation index (TSVI). Comparing hemodynamic descriptors in lesional regions with structural metrics, high values of TAWSS and transWSS are associated with higher plaque burden (r = 0.5069, p-value = 0.0012 and r = 0.4387, p-value = 0.0059, respectively) and plaque thickness (r = 0.3594, p-value = 0.0267 and r = 0.4924, p-value = 0.0017, respectively), as well as higher mean intensity of Perivascular Adipose Tissue (PVAT, r = 0.3323, p-value = 0.0415 and r = 0.3301, p-value = 0.043, respectively), which is a relevant factor in promoting atherosclerosis. These descriptors are also correlated with the severity of the stenosis (r = 0.547, p-value = 0.0004 and r = 0.3894, p-value = 0.0157, respectively) and inversely with the residual area of the lumen (r = - 0.6225, p-value = < 0.0001 and r = - 0.4295, p-value = 0.0071, respectively), with more marked effects in the segments with greater narrowing of the lumen. OSI and TSVI show positive associations with plaque thickness (r = 0.4372, p-value = 0.0061 and r = 0.4534, p-value = 0.0043, respectively), in particular OSI both at the lesion level and downstream, suggesting the formation of strongly oscillating flow in the post-stenotic regions (r = 0.3264, p-value = 0.0455), while TSVI is associated with greater plaque burden (r = 0.3585, p-value = 0.0272). All descriptors, except TAWSS, are associated with the presence of dense calcium (OSI: r = 0.4531, p-value = 0.0043; transWSS: r = 0.4128, p-value = 0.01; TSVI: r = 0.4293, p-value = 0.0071), an element that, in combination with the lipid core, plays a key role in promoting plaque instability. On the contrary, in this study there are no significant correlations with the fibrous, fibrofatty and necrotic components of atheromas. Overall, these findings highlight the potential of hemodynamic study as a complementary tool to structural analysis for identifying vulnerable plaque regions and improving the understanding of mechanisms underlying atherosclerotic disease progression.