Key result
In a patient-specific simulation, carotid plaque increased peak velocity from 0.3 to 0.7 m/s and expanded the vessel area at risk for disease from 8.3% to 20%.
Why the study?
Atherosclerosis arises from complex interactions between hemodynamic factors and vascular biology, causing luminal narrowing that impairs blood supply.
Patient-specific fluid-structure interaction simulations reveal that carotid plaques significantly alter local hemodynamics, increasing peak velocity and oscillatory shear index, which may promote further atherosclerosis.
Answers are grounded in this paper and cite their sources.
Alters carotid hemodynamics in ways that may promote further disease; hypothesis-generating in animal models and leaves open human translation.
Atherosclerosis, a primary cause of cardiovascular diseases, arises from intricate interactions between hemodynamic factors and vascular biology. This condition is characterized by a reduction in luminal cross-sectional area, which consequently impairs blood supply. In this study, patient-specific models of a stenosis carotid artery and its digitally-created healthy counterpart were reconstructed from CT scans. Employing the finite element method and a two-way fluid-structure interaction (FSI) coupling approach, non-Newtonian simulations of pulsatile and laminar blood flow were performed. The arterial wall was modeled as a linear, elastic, isotropic, and homogeneous material. The presence of plaque led to an approximately two-fold increase in peak velocity within the stenotic region, rising from approximately 0.3 m/s in the healthy model to 0.7 m/s, directly attributable to the reduced luminal area. The maximum shear stress of the wall at the location of the plaque reached 40 Pa. Furthermore, the maximum wall displacement increased from 1.5 mm in the healthy artery to 1.7 mm in the stenosis artery. While pressure results indicated minor localized increases and decreases before and after the plaque site, respectively, these changes did not significantly affect the total arterial pressure. Examination of blood flow streamlines revealed flow recirculation regions in the carotid sinus bulb of both arteries. In the stenosis artery, an additional and more pronounced flow recirculation region formed distal to the plaque, owing to the post-stenotic expansion. This phenomenon led to a substantial increase of approximately 240% in the oscillatory shear index (OSI) within the internal carotid artery branch. The relative residence time (RRT) remained relatively constant in the common carotid artery and the bifurcation region. However, RRT decreased by approximately 40% in the carotid branches, predominantly in the external carotid artery. Comparison of hemodynamic parameters and biological indices between healthy and stenosed arteries suggests that atherosclerotic plaques significantly alter local hemodynamics, potentially creating novel regions susceptible to atherosclerosis that are absent in healthy artery. In the healthy artery, about 8.3% of the vessel area was at risk for disease (TAWSS < 0.4 Pa), but this increased to 20% in the stenosed artery due to plaque accumulation, a 2.4-fold expansion. Regarding RRT, an increase was observed; areas with RRT > 10 expanded by approximately 1.6 times in the stenosed artery (from 3.1% in healthy to 5% in diseased).
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Aryan et al. (2025) studied Atherosclerosis. Atherosclerotic plaque (stenosis) vs. Digitally-created healthy counterpart was evaluated on Vessel area at risk for disease (TAWSS < 0.4 Pa). In a patient-specific simulation, carotid plaque increased peak velocity from 0.3 to 0.7 m/s and expanded the vessel area at risk for disease from 8.3% to 20%.
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