Literature DB >> 18711619

High shear stress influences plaque vulnerability Part of the data presented in this paper were published in Stroke 2007;38:2379-81.

H C Groen1, F J H Gijsen, A van der Lugt, M S Ferguson, T S Hatsukami, C Yuan, A F W van der Steen, J J Wentzel.   

Abstract

Shear stress of the blood at the vessel wall plays an important role in many processes in the cardiovascular system primarily focused on the regulation of vessel lumen and wall dimensions. There is ample evidence that atherosclerotic plaques are generated at low shear stress regions in the cardiovascular system, while high shear stress regions are protected. In the course of plaque progression, advanced plaques start to encroach into the lumen, and thereby start to experience high shear stress at the endothelium. Until now the consequences of high shear stress working at the endothelium of an advanced plaque are unknown. As high shear stress influences tissue regression, we hypothesised that high shear stress can destabilise the plaque by cap weakening leading to ulceration. We investigated this hypothesis in a magnetic resonance imaging (MRI) dataset of a 67-year-old woman with a plaque in the carotid artery at baseline and an ulcer at ten-month follow-up. The lumen, plaque components (lipid/necrotic core, intraplaque haemorrhage) and ulcer were reconstructed three dimensionally and the geometry at baseline was used for shear stress calculation using computational fluid dynamics. Correlation of the change in plaque composition with the shear stress at baseline showed that the ulcer was generated exclusively at the high shear stress location. In this serial MRI study we found plaque ulceration at the high shear stress location of a protruding plaque in the carotid artery. Our data suggest that high shear stress influences plaque vulnerability and therefore may become a potential parameter for predicting future events. (Neth Heart J 2008;16:280-3.).

Entities:  

Keywords:  magnetic resonance imaging; plaque vulnerability; shear stress

Year:  2008        PMID: 18711619      PMCID: PMC2516295          DOI: 10.1007/BF03086163

Source DB:  PubMed          Journal:  Neth Heart J        ISSN: 1568-5888            Impact factor:   2.380


  21 in total

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3.  Quantitative evaluation of carotid plaque composition by in vivo MRI.

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4.  Coronary risk factors and plaque morphology in men with coronary disease who died suddenly.

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5.  Endothelial expression of thrombomodulin is reversibly regulated by fluid shear stress.

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7.  Shear stress is associated with markers of plaque vulnerability and MMP-9 activity.

Authors:  R Krams; C Cheng; F Helderman; S Verheye; L C A van Damme; B Mousavi Gourabi; D Tempel; D Segers; P de Feyter; G Pasterkamp; D De Klein; R de Crom; A F W van der Steen; P W Serruys
Journal:  EuroIntervention       Date:  2006-08       Impact factor: 6.534

8.  Incidence of high-strain patterns in human coronary arteries: assessment with three-dimensional intravascular palpography and correlation with clinical presentation.

Authors:  Johannes A Schaar; Evelyn Regar; Frits Mastik; Eugene P McFadden; Francesco Saia; Clemens Disco; Chris L de Korte; Pim J de Feyter; Antonius F W van der Steen; Patrick W Serruys
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9.  Down-regulation of vascular adhesion molecule-1 by fluid shear stress in cultured mouse endothelial cells.

Authors:  J Ando; H Tsuboi; R Korenaga; Y Takada; N Toyama-Sorimachi; M Miyasaka; A Kamiya
Journal:  Ann N Y Acad Sci       Date:  1995-01-17       Impact factor: 5.691

10.  Compensatory enlargement of human atherosclerotic coronary arteries.

Authors:  S Glagov; E Weisenberg; C K Zarins; R Stankunavicius; G J Kolettis
Journal:  N Engl J Med       Date:  1987-05-28       Impact factor: 91.245

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3.  High shear stress at the surface of enhancing plaque in the systolic phase is related to the symptom presentation of severe M1 stenosis.

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4.  Computational modeling with fluid-structure interaction of the severe m1 stenosis before and after stenting.

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5.  Regulation of thrombomodulin expression and release in human aortic endothelial cells by cyclic strain.

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Review 6.  Caveolae: A Role in Endothelial Inflammation and Mechanotransduction?

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  6 in total

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