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Wall shear stress in hypertensive patients is associated with carotid vascular deformation assessed by speckle tracking strain imaging
INTRODUCTION: Wall shear stress (WSS) is critically important in both vascular remodeling and atherosclerosis. Carotid intima-media thickness (IMT) and deformation parameters have been used as relevant indicators of carotid atherosclerosis. This study aimed to investigate the relationships between h...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4750791/ https://www.ncbi.nlm.nih.gov/pubmed/26893913 http://dx.doi.org/10.1186/2056-5909-20-10 |
Sumario: | INTRODUCTION: Wall shear stress (WSS) is critically important in both vascular remodeling and atherosclerosis. Carotid intima-media thickness (IMT) and deformation parameters have been used as relevant indicators of carotid atherosclerosis. This study aimed to investigate the relationships between hemodynamic parameters in the common carotid artery (CCA) and the severity of carotid atherosclerosis in untreated hypertensive patients. METHODS: Carotid artery ultrasound was performed in 100 untreated hypertensive patients. Morphologic and hemodynamic parameters of the CCA, including peak and mean WSS, global circumferential strain, peak posterior radial strain assessed by two-dimensional speckle tracking method, and IMT, were measured. RESULTS: In patients with hypertension, there were significant correlations between carotid strain parameters and peak/mean WSS. Stepwise multiple regression analysis for carotid strain parameters after adjustment for age, carotid IMT, and brachial pulse wave velocity showed that peak WSS was an independent determinant of peak posterior radial strain (p = 0.009) and global circumferential strain (p = 0.002). CONCLUSIONS: These findings indicate that local shear stress is associated with carotid vascular deformation, which could be an underlying mechanism for the progression of atherosclerosis. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/2056-5909-20-10) contains supplementary material, which is available to authorized users. |
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