Diastolic Wall Shear Stress in the Internal Carotid Artery Is Associated with Different Cardiovascular Risk Factors than Systolic Wall Shear Stress

2009 ◽  
Vol 28 (2) ◽  
pp. 185-190 ◽  
Author(s):  
Inge H. Palm-Meinders ◽  
Frieke M.A. Box ◽  
Anton J.M. de Craen ◽  
Gerard J. Blauw ◽  
Mark A. van Buchem ◽  
...  
2007 ◽  
Vol 26 (3) ◽  
pp. 598-605 ◽  
Author(s):  
Frieke M.A. Box ◽  
Rob J. van der Geest ◽  
Jeroen van der Grond ◽  
Matthias J.P. van Osch ◽  
Aeilko H. Zwinderman ◽  
...  

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
G Goudot ◽  
L Khider ◽  
O Pedreira ◽  
J M Poree ◽  
P Julia ◽  
...  

Abstract Background Carotid plaque vulnerability assessment is an important factor in guiding the decision to treat significant carotid stenosis. Ultrafast Ultrasound Imaging (UF) offers the possibility of evaluating local flow velocities over an entire 2D image, allowing access to velocity measurements in contact with the arterial wall and to measure the wall shear stress (WSS). Purpose To evaluate the feasibility of WSS measurement in a prospective series of patients with carotid stenosis. Methods A 7.5 MHz linear probe of an Aixplorer scanner was used. UF acquisitions had 3 tilted plane waves transmits (−10; 0; 10°) and an effective frame rate of 5000Hz. We evaluated the flow velocity in 5 areas of the carotid wall: common carotid artery (1), plaque ascent (2), plaque peak (3), plaque descent (4), internal carotid artery (5) (Figure). WSS was computed with the vector field speed using the following formula, WSS=μ·δn·v with v the blood velocity, n the normal vector to the vessel wall and μ, the blood viscosity, calculated from the hematocrit value for each patient. WSS measurement method was first validated using a laminar flow phantom and known viscosity. And then, 33 patients were then prospectively evaluated, with a median carotid stenosis degree of 80% [75–85]. Results Significant correlation was found between in vitro measurement and the theoretical WSS values (R2=0.95; p<0.001).In patients,the maximum WSS value over the cardiac cycle follows the shape of the plaque with an increase during the ascend, reaching its maximum value of 3.57 Pa [2.47–4.45] at the peak of the plaque, and a fall after passing the peak (0.99 Pa [0.8–1.32]) lower than the WSS values in the non-stenotic areas (1.55 Pa [1.13–1.90] for the common carotid artery) (Table). Table 1 Wall's area Wall shear stress (Pa) Min Max Delta 1. Common carotid artery 0.14 [0.05–0.27] 1.55 [1.13–1.90] 0.73 [0.55–0.96] 2. Plaque's ascent 0.39 [0.24–0.59] 2.63 [1.89–3.28] 1.20 [0.89–1.79] 3. Plaque's peak 0.60 [0.32–0.89] 3.57 [2.47–4.45] 1.78 [1.44–2.46] 4. Plaque's descent 0.16 [0.13–0.22] 0.99 [0.80–1.32] 0.52 [0.34–0.73] 5. Internal carotid artery 0.17 [0.13–0.35] 1.37 [1.04–1.75] 0.72 [0.50–0.87] Results are median [25th–75th percentile]. Figure 1 Conclusion UF provide reliable WSS values. High WSS was present at the peak of the plaque, whereas lowest WSS values were found at the post-stenotic zone. WSS evaluation may help to better characterize the carotid plaque vulnerability.


2018 ◽  
Vol 24 (3) ◽  
pp. 288-296 ◽  
Author(s):  
Gerald J Riccardello ◽  
Abhinav R Changa ◽  
Fawaz Al-Mufti ◽  
I Paul Singh ◽  
Chirag Gandhi ◽  
...  

Objective The natural history intracranial aneurysms (IA) remains poorly understood despite significant morbidity and mortality associated with IA rupture. Hemodynamic impingement resulting in elevations in wall shear stress and wall shear stress gradient (WSSG) has been shown to induce aneurysmal remodeling at arterial bifurcations. We investigate the hemodynamic environment specific to side-wall pre-aneurysmal vasculature. We hypothesize that fluid impingement and secondary flow patterns play a role in side-wall aneurysm initiation. Methods Eight side-wall internal carotid artery aneurysms from the Aneurisk repository were identified. Pre-aneurysmal vasculature was algorithmically reconstructed. Blood flow was simulated with computational fluid dynamic simulations. An indicator of isolated fluid impingement energy was developed by insetting the vessel surface and calculating the impinging component of the fluid dynamic pressure. Results Isolated fluid impingement was found to be elevated in the area of aneurysm initiation in 8/8 cases. The underlying fluid flow for each area of initiation was found to harbor secondary flow patterns known as Dean’s vortices, the result of changes in momentum imparted by bends in the internal carotid artery (ICA). Conclusion Isolated fluid impingement and secondary flow patterns may play a major role in the initiation of side-wall aneurysm initiation. We are unable to determine if this role is through direct or indirect mechanisms but hypothesize that elevations in isolated fluid impingement mark areas of cerebral vasculature that are at risk for aneurysm initiation. Thus, this indicator provides vascular locations to focus future study of side-wall aneurysm initiation.


Stroke ◽  
2007 ◽  
Vol 38 (4) ◽  
pp. 1374-1376 ◽  
Author(s):  
Frieke M.A. Box ◽  
Jeroen van der Grond ◽  
Anton J.M. de Craen ◽  
Inge H. Palm-Meinders ◽  
Rob J. van der Geest ◽  
...  

Author(s):  
Hui Meng ◽  
Sabareesh K. Natarajan ◽  
Eleni Metaxa ◽  
Markus Tremmel ◽  
Ling Gao ◽  
...  

Hemodynamic insult has long been speculated to be a key factor in intracranial aneurysm (IA) formation,1 but the specifics of hemodynamic insult contributing to this process are not understood. Despite other risk factors, IAs are predominantly found at locations associated with unique hemodynamic stress such as at the apices of arterial bifurcations or outer curves, prominent in high wall shear stress (WSS) and wall shear stress gradients (WSSG).2 Furthermore, it appears that increased flow at these locations is required to trigger the initiation of aneurysmal remodeling.3 We have previously shown that increasing flow in the rabbit basilar artery (BA), secondary to common carotid artery (CCA) ligation, resulted in nascent aneurysm development at the basilar terminus (BT).4 However, it is unclear if certain hemodynamic stress thresholds must be exceeded to trigger aneurysmal remodeling, and whether sustained insult is necessary.


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