Contribution of atherosclerotic plaque location and severity to the near-wall hemodynamics of the carotid bifurcation: an experimental study and FSI modeling

Associations of plaque morphology and location with Intraplaque neovascularization in the carotid artery by contrast-enhanced ultrasound imaging

“…This is consistent with the notion that proatherogenic transcription factor upregulation and the resultant aggregation of inflammatory cells tend to occur in regions of low shear stress (19), ultimately resulting in a more fragile plaque phenotype (20,21). Our findings of increased neovascularization in a low shear stress environment are further in correspondence to previous reports that macrophage infiltration often coexist with hypoxia and angiogenesis due to high metabolic demand (22,23).…”

Probing the possibility of lesion formation/progression in vicinity of a primary atherosclerotic plaque: A fluid–solid interaction study and angiographic evidences

“…On the other hand, stenosis levels up to 35% does not impact the downstream velocity and WSS scheme, notably (Figure 3A,B). 65 There are negligible flow recirculation zones for described levels of constriction. When the atherosclerotic lesion grows beyond 35%, larger zones of recirculation, in region VI are evident (Figure 3A).…”

Investigating the Association of Carotid Atherosclerotic Plaque MRI Features and Silent Stroke After Carotid Endarterectomy

“…One possible explanation is that, besides plaque compositional characteristics, carotid local hemodynamics may also play an important role in the occurrence of SS after carotid revascularization. Ahmadpour‐B et al 35 reported that mild carotid stenosis had minor effects on hemodynamic parameters, such as wall shear stress, while severe carotid stenosis could lead to significant hemodynamic changes both in the local artery and in other branches using a 3D fluid–structure interaction model of carotid bifurcation. Moreover, the increase of wall shear stress in arteries with severe stenosis could promote the progression or even rupture of advanced atherosclerotic plaques 36,37 .…”