Role of Hemodynamics in Initiation of Aneurysmal Remodeling

2010 ◽  
Author(s):  
Hui Meng ◽  
Sabareesh K. Natarajan ◽  
Eleni Metaxa ◽  
Markus Tremmel ◽  
Ling Gao ◽  
...  
Keyword(s):  
Risk Factors ◽  
Shear Stress ◽  
Carotid Artery ◽  
Wall Shear Stress ◽  
Intracranial Aneurysm ◽  
Hemodynamic Stress ◽  
Key Factor ◽  
Aneurysm Development ◽  
Wall Shear

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.

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 ◽  
...  
Keyword(s):  
Risk Factors ◽  
Shear Stress ◽  
Cardiovascular Risk ◽  
Carotid Artery ◽  
Wall Shear Stress ◽  
Internal Carotid Artery ◽  
Cardiovascular Risk Factors ◽  
Internal Carotid ◽  
Wall Shear

Basic study on estimation method of wall shear stress in common carotid artery using blood flow imaging

2020 ◽  
Vol 59 (SK) ◽  
pp. SKKE16 ◽  
Author(s):  
Ryo Nagaoka ◽  
Kazuma Ishikawa ◽  
Michiya Mozumi ◽  
Magnus Cinthio ◽  
Hideyuki Hasegawa
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Carotid Artery ◽  
Wall Shear Stress ◽  
Common Carotid Artery ◽  
Estimation Method ◽  
Flow Imaging ◽  
Basic Study ◽  
Blood Flow Imaging ◽  
Wall Shear

scholarly journals Reproducibility of wall shear stress assessment with the paraboloid method in the internal carotid artery with velocity encoded MRI in healthy young individuals

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 ◽  
...  
Keyword(s):  
Shear Stress ◽  
Carotid Artery ◽  
Wall Shear Stress ◽  
Internal Carotid Artery ◽  
Internal Carotid ◽  
Stress Assessment ◽  
Wall Shear

scholarly journals Piezo1 mediates angiogenesis through activation of MT1-MMP signaling

2019 ◽  
Vol 316 (1) ◽  
pp. C92-C103 ◽  
Author(s):  
Hojin Kang ◽  
Zhigang Hong ◽  
Ming Zhong ◽  
Jennifer Klomp ◽  
Kayla J. Bayless ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 2 ◽  
Sprouting Angiogenesis ◽  
Sphingosine 1 Phosphate ◽  
Wall Shear ◽  
Membrane Type

Angiogenesis is initiated in response to a variety of external cues, including mechanical and biochemical stimuli; however, the underlying signaling mechanisms remain unclear. Here, we investigated the proangiogenic role of the endothelial mechanosensor Piezo1. Genetic deletion and pharmacological inhibition of Piezo1 reduced endothelial sprouting and lumen formation induced by wall shear stress and proangiogenic mediator sphingosine 1-phosphate, whereas Piezo1 activation by selective Piezo1 activator Yoda1 enhanced sprouting angiogenesis. Similarly to wall shear stress, sphingosine 1-phosphate functioned by activating the Ca2+ gating function of Piezo1, which in turn signaled the activation of the matrix metalloproteinase-2 and membrane type 1 matrix metalloproteinase during sprouting angiogenesis. Studies in mice in which Piezo1 was conditionally deleted in endothelial cells demonstrated the requisite role of sphingosine 1-phosphate-dependent activation of Piezo1 in mediating angiogenesis in vivo. These results taken together suggest that both mechanical and biochemical stimuli trigger Piezo1-mediated Ca2+ influx and thereby activate matrix metalloproteinase-2 and membrane type 1 matrix metalloproteinase and synergistically facilitate sprouting angiogenesis.

Wall Shear Stress Measurement by Ultrafast Vector Flow Imaging for Atherosclerotic Carotid Stenosis

2019 ◽  
Author(s):  
Guillaume Goudot ◽  
Jonathan Poree ◽  
Olivier Pedreira ◽  
Lina Khider ◽  
Pierre Julia ◽  
...  
Keyword(s):  
Shear Stress ◽  
Carotid Artery ◽  
Wall Shear Stress ◽  
Carotid Stenosis ◽  
Common Carotid Artery ◽  
Frame Rate ◽  
Carotid Artery Plaque ◽  
Local Flow ◽  
Linear Probe ◽  
Wall Shear

Objective Carotid plaque vulnerability assessment could guide the decision to perform endarterectomy. Ultrafast ultrasound imaging (UF) can evaluate local flow velocities over an entire 2D image, allowing measurement of the wall shear stress (WSS). We aimed at evaluating the feasibility of WSS measurement in a prospective series of patients with carotid stenosis. Methods UF acquisitions, performed with a linear probe, had an effective frame rate of 5000 Hz. The flow velocity was imaged over the entire plaque area. WSS was computed with the vector field speed using the formula: with the blood velocity and μ, the blood viscosity. The WSS measurement method was validated using a calibrated phantom. In vivo, WSS was analyzed in 5 areas of the carotid wall: common carotid artery, plaque ascent, plaque peak, plaque descent, internal carotid artery. Results Good correlation was found between in vitro measurement and the theoretical WSS values (R2 = 0.95; p < 0.001). 33 patients were prospectively evaluated, with a median carotid stenosis degree of 80 % [75–85]. The maximum WSS value over the cardiac cycle follows the shape of the plaque with an increase during the ascent, reaching its maximum value of 3.25 Pa [2.26–4.38] at the peak of the plaque, and a decrease after passing of the peak (0.93 Pa [0.80–1.19]) lower than the WSS values in the non-stenotic areas (1.47 Pa [1.12–1.77] for the common carotid artery). Conclusion UF allowed local and direct evaluation of the plaque’s WSS, thus better characterizing local hemodynamics to identify areas of vulnerability. Key Points: 

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