scholarly journals Plaque Composition as a Predictor of Plaque Ulceration in Carotid Artery Atherosclerosis: The Plaque At RISK Study

2020 ◽  
Vol 42 (1) ◽  
pp. 144-151
Author(s):  
K. Dilba ◽  
D.H.K. van Dam-Nolen ◽  
A.C. van Dijk ◽  
M. Kassem ◽  
A.F.W. van der Steen ◽  
...  
Keyword(s):  
At Risk ◽  
Carotid Artery ◽  
Plaque Composition ◽  
Carotid Artery Atherosclerosis ◽  
Plaque Ulceration

No independent association found between von Willebrand factor and plaque ulceration in carotid artery atherosclerosis

2019 ◽  
Vol 174 ◽  
pp. 95-97 ◽  
Author(s):  
Taihra Zadi ◽  
Michelle Sonneveld ◽  
Anouk C. van Dijk ◽  
Burhan Hussain ◽  
Peter J. Koudstaal ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Von Willebrand Factor ◽  
Carotid Artery Atherosclerosis ◽  
Plaque Ulceration ◽  
Independent Association ◽  
Von Willebrand ◽  
Willebrand Factor

scholarly journals Association Between Carotid Artery Plaque Ulceration and Plaque Composition Evaluated With Multidetector CT Angiography

Stroke ◽  
2011 ◽  
Vol 42 (2) ◽  
pp. 367-372 ◽  
Author(s):  
Philip J. Homburg ◽  
Sietske Rozie ◽  
Marjon J. van Gils ◽  
Quirijn J.A. van den Bouwhuijsen ◽  
Wiro J. Niessen ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Ct Angiography ◽  
Multidetector Ct ◽  
Plaque Composition ◽  
Carotid Artery Plaque ◽  
Plaque Ulceration ◽  
Multidetector Ct Angiography

scholarly journals Increased expression of HDJ-2 (hsp40) in carotid artery atherosclerosis: A novel heat shock protein associated with luminal stenosis and plaque ulceration

2001 ◽  
Vol 33 (5) ◽  
pp. 1065-1071 ◽  
Author(s):  
Thelinh Q. Nguyen ◽  
Andrés Jaramillo ◽  
Robert W. Thompson ◽  
Suzanne Dintzis ◽  
William F. Oppat ◽  
...  
Keyword(s):  
Heat Shock ◽  
Carotid Artery ◽  
Heat Shock Protein ◽  
Carotid Artery Atherosclerosis ◽  
Luminal Stenosis ◽  
Plaque Ulceration

scholarly journals Chitinase 3 like 1 is a regulator of smooth muscle cell physiology and atherosclerotic lesion stability

2021 ◽  
Author(s):  
Pavlos Tsantilas ◽  
Shen Lao ◽  
Zhiyuan Wu ◽  
Anne Eberhard ◽  
Greg Winski ◽  
...  
Keyword(s):  
At Risk ◽  
Smooth Muscle ◽  
Carotid Artery ◽  
Atherosclerotic Lesion ◽  
Adverse Outcomes ◽  
Plaque Burden ◽  
Cell Physiology ◽  
Mechanistic Studies ◽  
Plaque Vulnerability ◽  
Fibrous Cap

Abstract Aims  Atherosclerotic cerebrovascular disease underlies the majority of ischaemic strokes and is a major cause of death and disability. While plaque burden is a predictor of adverse outcomes, plaque vulnerability is increasingly recognized as a driver of lesion rupture and risk for clinical events. Defining the molecular regulators of carotid instability could inform the development of new biomarkers and/or translational targets for at-risk individuals. Methods and results  Using two independent human endarterectomy biobanks, we found that the understudied glycoprotein, chitinase 3 like 1 (CHI3L1), is up-regulated in patients with carotid disease compared to healthy controls. Further, CHI3L1 levels were found to stratify individuals based on symptomatology and histopathological evidence of an unstable fibrous cap. Gain- and loss-of-function studies in cultured human carotid artery smooth muscle cells (SMCs) showed that CHI3L1 prevents a number of maladaptive changes in that cell type, including phenotype switching towards a synthetic and hyperproliferative state. Using two murine models of carotid remodelling and lesion vulnerability, we found that knockdown of Chil1 resulted in larger neointimal lesions comprised by de-differentiated SMCs that failed to invest within and stabilize the fibrous cap. Exploratory mechanistic studies identified alterations in potential downstream regulatory genes, including large tumour suppressor kinase 2 (LATS2), which mediates macrophage marker and inflammatory cytokine expression on SMCs, and may explain how CHI3L1 modulates cellular plasticity. Conclusion  CHI3L1 is up-regulated in humans with carotid artery disease and appears to be a strong mediator of plaque vulnerability. Mechanistic studies suggest this change may be a context-dependent adaptive response meant to maintain vascular SMCs in a differentiated state and to prevent rupture of the fibrous cap. Part of this effect may be mediated through downstream suppression of LATS2. Future studies should determine how these changes occur at the molecular level, and whether this gene can be targeted as a novel translational therapy for subjects at risk of stroke.

Ultrastructural study of endothelium in advanced carotid artery atherosclerosis

2016 ◽  
Vol 252 ◽  
pp. e162
Author(s):  
A. Evdokimenko ◽  
T. Gulevskaya ◽  
T. Gulevskaya ◽  
S. Scrylev ◽  
V. Shchipakin ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Ultrastructural Study ◽  
Carotid Artery Atherosclerosis

Noninvasive Detection of Plaque Instability with Use of Radiolabeled Annexin A5 in Patients with Carotid-Artery Atherosclerosis

2004 ◽  
Vol 350 (14) ◽  
pp. 1472-1473 ◽  
Author(s):  
Bas L.J.H. Kietselaer ◽  
Chris P.M. Reutelingsperger ◽  
Guido A.K. Heidendal ◽  
Mat J.A.P. Daemen ◽  
Werner H. Mess ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Noninvasive Detection ◽  
Annexin A5 ◽  
Plaque Instability ◽  
Carotid Artery Atherosclerosis
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