scholarly journals Developing Pulsatile Flow in a Deployed Coronary Stent

2005 ◽  
Vol 128 (3) ◽  
pp. 347-359 ◽  
Author(s):  
Divakar Rajamohan ◽  
Rupak K. Banerjee ◽  
Lloyd H. Back ◽  
Ashraf A. Ibrahim ◽  
Milind A. Jog

A major consequence of stent implantation is restenosis that occurs due to neointimal formation. This patho-physiologic process of tissue growth may not be completely eliminated. Recent evidence suggests that there are several factors such as geometry and size of vessel, and stent design that alter hemodynamic parameters, including local wall shear stress distributions, all of which influence the restenosis process. The present three-dimensional analysis of developing pulsatile flow in a deployed coronary stent quantifies hemodynamic parameters and illustrates the changes in local wall shear stress distributions and their impact on restenosis. The present model evaluates the effect of entrance flow, where the stent is placed at the entrance region of a branched coronary artery. Stent geometry showed a complex three-dimensional variation of wall shear stress distributions within the stented region. Higher order of magnitude of wall shear stress of 530dyn∕cm2 is observed on the surface of cross-link intersections at the entrance of the stent. A low positive wall shear stress of 10dyn∕cm2 and a negative wall shear stress of −10dyn∕cm2 are seen at the immediate upstream and downstream regions of strut intersections, respectively. Modified oscillatory shear index is calculated which showed persistent recirculation at the downstream region of each strut intersection. The portions of the vessel where there is low and negative wall shear stress may represent locations of thrombus formation and platelet accumulation. The present results indicate that the immediate downstream regions of strut intersections are areas highly susceptible to restenosis, whereas a high shear stress at the strut intersection may cause platelet activation and free emboli formation.

Circulation ◽  
2014 ◽  
Vol 129 (6) ◽  
pp. 673-682 ◽  
Author(s):  
Riti Mahadevia ◽  
Alex J. Barker ◽  
Susanne Schnell ◽  
Pegah Entezari ◽  
Preeti Kansal ◽  
...  

2017 ◽  
Vol 1 (4) ◽  
pp. 62-68
Author(s):  
Roberto Annunziata ◽  
Bettina Reglin ◽  
Axel Pries ◽  
Emanuele Trucco

Purpose: The effect of hemodynamic parameters on vessel tortuosity remains un-clear. Here we investigate the correlation of tortuosity with a set of hemodynamicparameters in a mesenterial vascular network.Methods: A mesenterial vascular network of 389 vessels (131 arteries, 132 veins, and 126 capillaries) was imaged. Eleven hemodynamic parameters were measured (pressure, wall shear stress, diameter, blood velocity and flow, viscosity, haematocrit, partial oxygen saturation, oxygen saturation, wall thickness, and local vessel density). Tortuosity was assessed quantitatively with a validated algorithm and correlation computed with subsets of hemodynamic parameters selected by a lasso regressor.Results: Results suggest that tortuosity is related to pressure, wall shear stress, diameter, blood velocity, viscosity, partial but not full oxygen saturation, and wall thickness for the arteries; diameter, blood flow, hematocrit, and density for the veins; and viscosity (but not hematocrit), partial and full oxygen saturation, and density for the capillaries. The combination of hemodynamic parameters correlating best with tortuosity is the set of all parameters except density (r = 0.64, p < 0.01), using as tortuosity definition the set of tortuosity features (geometric measures) correlating best with a single hemodynamic factor for the arteries.Conclusion: This pilot suggests two general conclusions. First, the quantitative definition of tortuosity (i.e., the set of geometric features adopted) should be tuned to the specific data and problem considered. Second, tortuosity is caused by a combination of hemodynamic factors, not a single one.


Author(s):  
Navid Freidoonimehr ◽  
Rey Chin ◽  
Anthony C. Zander ◽  
Maziar Arjomandi

Abstract Temporal variations of the coronary arteries during a cardiac cycle are defined as the superposition of the changes in the position, curvature, and torsion of the coronary artery axis markers and the variations in the lumen cross-sectional shape due to the distensible wall motion induced by the pulse pressure and contraction of the myocardium in a cardiac cycle. This review discusses whether the modelling the temporal variations of the coronary arteries is needed for the investigation of the hemodynamics specifically in time critical applications such as a clinical environment. The numerical modellings in the literature which model or disregard the temporal variations of the coronary arteries on the hemodynamic parameters are discussed. The results in the literature show that neglecting the effects of temporal geometric variations is expected to result in about 5\% deviation of the time-averaged pressure drop and wall shear stress values and also about 20\% deviation of the temporal variations of hemodynamic parameters, such as time-dependent wall shear stress and oscillatory shear index. This review study can be considered as a guide for the future studies to outline the conditions in which temporal variations of the coronary arteries can be neglected, while providing a reliable estimation of hemodynamic parameters.


Author(s):  
Leonie Rouleau ◽  
Joanna Rossi ◽  
Jean-Claude Tardif ◽  
Rosaire Mongrain ◽  
Richard L. Leask

Endothelial cells (ECs) are believed to respond differentially to hemodynamic forces in the vascular tree. Once atherosclerotic plaque has formed in a vessel, the obstruction creates complex spatial gradients in wall shear stress (WSS). In vitro models have used mostly unrealistic and simplified geometries, which cannot reproduce accurately physiological conditions. The objective of this study was to expose ECs to the complex WSS pattern created by an asymmetric stenosis. Endothelial cells were grown and exposed for different times to physiological steady flows in straight dynamic controls and in idealized asymmetric stenosis models. Cell morphology was noticeably different in the regions with spatial WSS gradients, being more randomly oriented and of cobblestone shape. Inflammatory molecule expression was also altered by exposure to shear and endothelial nitric oxide synthase (eNOS) was upregulated by its presence. A regional response in terms of inflammation was observed through confocal microscopy. This work provides a more realistic model to study endothelial cell response to spatial and temporal WSS gradients that are present in vivo and is an important advancement towards a better understanding of the mechanisms involved in coronary artery disease.


2019 ◽  
Vol 31 (12) ◽  
pp. 121903 ◽  
Author(s):  
Christopher Cox ◽  
Mohammad Reza Najjari ◽  
Michael W. Plesniak

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