Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2019 Nov 1;40(41):3421-3433.
doi: 10.1093/eurheartj/ehz551.

Expert recommendations on the assessment of wall shear stress in human coronary arteries: existing methodologies, technical considerations, and clinical applications

Affiliations

Expert recommendations on the assessment of wall shear stress in human coronary arteries: existing methodologies, technical considerations, and clinical applications

Frank Gijsen et al. Eur Heart J. .
No abstract available

PubMed Disclaimer

Figures

Figure 1
Figure 1
A schematic representation of the forces the vessel wall is exposed to. The red arrow is the normal force component, associated with blood pressure, and the green arrow is the tangential component force, associated with wall shear stress. Note that the size of the arrows does not represents the magnitude of the forces, only the direction.
Figure 2
Figure 2
A schematic illustration of some of the processes that are involved in plaque development and rupture, and how these are related to wall shear stress. In low wall shear stress regions, monocytes are recruited by the endothelium through the expression of various adhesion molecules. Recruited monocytes transform into foam cells which subsequently can accumulate and are the main source for the development of the necrotic core. Expansive remodelling initially prevents lumen intrusion of the plaque, but once this process fails, the wall shear patterns the plaque is exposed to changes. High wall shear stress will be present at the upstream part and the throat of the plaque, while in the downstream region, low wall shear stress will be accompanied by elevated levels of oscillatory flow. Although there is no direct effect of wall shear stress on plaque rupture, shear stress does influence endothelial function, potentially leading to cap thinning in the high wall shear stress regions.
Figure 3
Figure 3
Methodology developed to fuse computed tomography angiography and intravascular imaging data: (A) Extraction of lumen centreline from computed tomography angiography. (B) Cross-sectional computed tomography angiography images are generated perpendicularly to the centreline and anatomical landmarks that are seen in intravascular ultrasound/optical coherence tomography images are detected. After matching the intravascular imaging contours are rotated so as to obtain the correct orientation (middle panel). (C) The orientated intravascular imaging contours are placed perpendicular to the lumen centreline extracted by computed tomography angiography to reconstruct the coronary artery anatomy that is shown in (D).
Figure 4
Figure 4
(A) Coronary tree showing multiple curvatures and bifurcation. (B) Secondary flow in the presence of the proximal curvature. (C) Macro-recirculation due to varying lumen geometries such as bifurcation and stenosis.
Figure 5
Figure 5
Changes in red blood cells under shear. Red blood cells aggregate at low shear rate, resulting in high blood viscosity. The process is reversed as shear rate increases.
Figure 6
Figure 6
Overview of micro flow environment around a stent strut (left) and the resulting high and low wall shear stress regions around the strut (right).
Take home figure
Take home figure
Wall shear stress in coronary arteries from imaging to modelling.
None

Similar articles

Cited by

References

    1. Young DF, Tsai FY.. Flow characteristics in models of arterial stenoses. I. Steady flow. J Biomech 1973;6:395–410. - PubMed
    1. Young DF, Tsai FY.. Flow characteristics in models of arterial stenoses. II. Unsteady flow. J Biomech 1973;6:547–559. - PubMed
    1. Gould KL, Kelley KO, Bolson EL.. Experimental validation of quantitative coronary arteriography for determining pressure-flow characteristics of coronary stenosis. Circulation 1982;66:930–937. - PubMed
    1. Kwak BR, Back M, Bochaton-Piallat ML, Caligiuri G, Daemen MJ, Davies PF, Hoefer IE, Holvoet P, Jo H, Krams R, Lehoux S, Monaco C, Steffens S, Virmani R, Weber C, Wentzel JJ, Evans PC.. Biomechanical factors in atherosclerosis: mechanisms and clinical implications. Eur Heart J 2014;35:3013–3020; 3020a–3020d. - PMC - PubMed
    1. Passerini AG, Polacek DC, Shi C, Francesco NM, Manduchi E, Grant GR, Pritchard WF, Powell S, Chang GY, Stoeckert CJ, Davies PF.. Coexisting proinflammatory and antioxidative endothelial transcription profiles in a disturbed flow region of the adult porcine aorta. Proc Natl Acad Sci USA 2004;101:2482–2487. - PMC - PubMed

Publication types

MeSH terms