Influence of wall shear and structural stress on plaque progression of different phenotype in human coronary arteries

Abstract Introduction Atherosclerotic plaque progression is affected by local wall shear stress (WSS), .i.e. the frictional force of the blood at the vessel wall [1,2]. However, the blood pressure also induces stress inside the vessel wall (wall stress, WMS) and is mainly studied for plaque rupture [3]. Little is known on the impact of WMS on plaque progression. Purpose In order to have a comprehensive understanding of the involvement of the biomechanical factors (WSS and WMS) in atherosclerotic artery disease, we studied the individual and combined effects of WMS and WSS in plaque free as well as in atherosclerotic coronary segments. Methods Forty non-stented, non-culprit human coronary arteries (IMPACT study) were imaged with near-infrared spectroscopy intravascular ultrasound (NIRS-IVUS) and optical coherence tomography (OCT) at the baseline and after 12 months [3]. The 2D and 3D lumen, vessel wall and lipid-rich necrotic core (LRNC) geometries were reconstructed based on the co-registration of NIRS-IVUS and OCT. WSS was computed with Computational Fluid Dynamics [3]. The WMS on the peri-luminal region was calculated via ABAQUS with hyperelastic material models [4] using intraluminal pressure of 120mmHg. The vessels were divided into 1.5mm/45° sectors. In each sector wall growth was quantified as plaque burden (plaque area/total vessel area*100%) change over time. Plaque was defined as wall thickness > 0.5 mm. The sectors were categorized as "plaque with lipid rich necrotic core (LRNC)", "plaque w/o lipid rich necrotic core (LRNC)", or "plaque free wall". The individual and combined effect of WSS and WMS on plaque progression was evaluated using Linear Mixed Model in SPSS and all stress metrics were divided into artery-based tertiles. Results Vessel sectors exposed to low WSS at baseline demonstrated a higher plaque burden increase over the follow up period compared to the vessel sectors exposed to mid or high WSS (Fig.1), which was significantly different for all the 3 categories (Plaque free wall, Plaque without LRNC, Plaque with LRNC). Vessel sectors exposed to increasing WMS demonstrated increasing plaque progression (Fig.1) Sectors that were simultaneously exposed to low WSS and high WMS revealed the highest change in plaque size and in particular in plaque sectors that were lipid rich (Fig.2). Conclusion Our findings suggest that the local atherosclerotic disease progression in coronary arteries is not only associated with the well-known WSS, but also with WMS. Moreover, our results show that there is an complex interplay between WSS, WMS and plaque composition, such that lipid rich plaques exposed to low WSS and high WMS demonstrated the highest plaque progression.Figure 1Figure 2