Plaque and Shear Stress Distribution in Human Coronary Bifurcations: a Multi-Slice Computed Tomography Study

Author(s):  
Alina G. van der Giessen ◽  
Jolanda J. Wentzel ◽  
Frans N. van de Vosse ◽  
Antonius F. van der Steen ◽  
Pim J. de Feyter ◽  
...  

It is generally accepted that early atherosclerosis develops in low shear-stress (SS) regions such as the outer wall of arterial bifurcations and the inner bend of curved vessels (1). However, in clinical practice, it is common to observe atherosclerotic plaques at the flow-divider, or carina, of coronary bifurcations (2). Plaques at the carina are more frequently found in symptomatic patients, and may represent a more advanced stage of atherosclerosis. The carina is located in a region which is exposed to high SS. We hypothesize that if plaques are located in atheroprotective high SS regions, they have grown circumferentially from the atherogenic low SS regions.

2013 ◽  
Vol 227 (2) ◽  
pp. 236-243 ◽  
Author(s):  
Vania C. Olivon ◽  
Rodrigo A. Fraga-Silva ◽  
Dolf Segers ◽  
Céline Demougeot ◽  
Ana M. de Oliveira ◽  
...  

Author(s):  
Frank Gijsen ◽  
Jolanda Wentzel ◽  
Johan Schuurbiers ◽  
Frits Mastik ◽  
Johannes Schaar ◽  
...  

It is well established that atherosclerotic plaques generally develop in low shear stress regions, including curved arterial segments and bifurcations1. Once these plaques intrude into the lumen, the shear stress they are exposed to alters with hitherto unknown consequences. We hypothesize that in the more advanced stages of the disease, shear stress has an important impact on plaque composition in such a way that high shear stress enhances plaque vulnerability through its biological impact on the endothelium2. We investigated this hypothesis previously by studying the relationship between shear stress and strain, a marker for plaque composition, in human coronary arteries3. In this study, we will extend that study by investigating how shear stress influences changes of strain, and thus plaque composition, over a period of 6 months.


Author(s):  
Scott Albert ◽  
Jenn Stroud Rossmann ◽  
Robert Balaban

The tendency of atherosclerotic plaques to develop at arterial branch points is likely due to both the hemodynamics and macromolecular environment associated with these branch points. Arterial branches experience flow separation, which results in regions of low shear stress[1–3], and contributes to longer residence times that may allow for deposition of pro-atherogenic material in the vessel wall [2]. In addition, low shear stress itself may provide cellular signals that alter the tissue microenvironment in favor of atherogenesis [3, e.g.].


Author(s):  
Nikhilesh Bappoo ◽  
Maaz B.J. Syed ◽  
Georgia Khinsoe ◽  
Lachlan J. Kelsey ◽  
Rachael O. Forsythe ◽  
...  

Background: Low shear stress has been implicated in abdominal aortic aneurysm (AAA) expansion and clinical events. We tested the hypothesis that low shear stress in AAA at baseline is a marker of expansion rate and future aneurysm-related events. Methods: Patients were imaged with computed tomography angiography at baseline and followed up every 6 months >24 months with ultrasound measurements of maximum diameter. From baseline computed tomography angiography, we reconstructed 3-dimensional models for automated computational fluid dynamics simulations and computed luminal shear stress. The primary composite end point was aneurysm repair and/or rupture, and the secondary end point was aneurysm expansion rate. Results: We included 295 patients with median AAA diameter of 49 mm (interquartile range, 43–54 mm) and median follow-up of 914 (interquartile range, 670–1112) days. There were 114 (39%) aneurysm-related events, with 13 AAA ruptures and 98 repairs (one rupture was repaired). Patients with low shear stress (<0.4 Pa) experienced a higher number of aneurysm-related events (44%) compared with medium (0.4–0.6 Pa; 27%) and high (>0.6 Pa; 29%) shear stress groups ( P =0.010). This association was independent of known risk factors (adjusted hazard ratio, 1.72 [95% CI, 1.08–2.73]; P =0.023). Low shear stress was also independently associated with AAA expansion rate (β=+0.28 mm/y [95% CI, 0.02–0.53]; P =0.037). Conclusions: We show for the first time that low shear stress (<0.4 Pa) at baseline is associated with both AAA expansion and future aneurysm-related events. Aneurysms within the lowest tertile of shear stress, versus those with higher shear stress, were more likely to rupture or reach thresholds for elective repair. Larger prospective validation trials are needed to confirm these findings and translate them into clinical management.


1992 ◽  
Vol 114 (3) ◽  
pp. 301-308 ◽  
Author(s):  
Mitsuji Okano ◽  
Yoji Yoshida

Observations on shapes of endothelial cells both in sudanophilic and nonsudanophilic regions at bifurcations of the brachiocephalic (BC) and left subclavian (SA) arteries in hyperlipidemic rabbits were performed under a SEM. The stagnation point of flow and leading edges of flow dividers were nonsudanophilic and covered by round and long fusiform endothelial cells, respectively. The hips of flow dividers of both branchings, proven to be relatively low shear stress regions, by movement of microspheres in steady flow, were sudanophilic and covered by ellipsoidal cells. Similar studies were carried out in normolipidemic rabbits. It might be concluded that lipid deposition in hyperlipidemic rabbits occurs in relatively low shear stress regions, where endothelial cells are functionally activated, rather than in laminar high shear stress regions at the flow divider.


Author(s):  
Frank J. H. Gijsen ◽  
Jolanda J. Wentzel ◽  
Johan C. H. Schuurbiers ◽  
Antonius F. W. van der Steen ◽  
Patrick W. Serruys

It is well established that atherosclerotic plaques generally develop in low shear stress regions, including curved arterial segments and bifurcations. Once these plaques intrude into the lumen, the shear stress they are exposed to alters with hitherto unknown consequences. We hypothesize that in the more advanced stages of the disease, shear stress has an important impact on plaque composition in such a way that high shear stress enhances plaque vulnerability through its biological impact on the endothelium. We investigated this hypothesis by studying the relationship between shear stress and strain, a marker for plaque composition, in human coronary arteries.


2015 ◽  
Vol 89 ◽  
pp. 168-172 ◽  
Author(s):  
Anusha N. Seneviratne ◽  
Jennifer E. Cole ◽  
Michael E. Goddard ◽  
Inhye Park ◽  
Zahra Mohri ◽  
...  

Author(s):  
Frank Gijsen ◽  
Johan Schuurbiers ◽  
Harald Groen ◽  
Nieves Gonzales ◽  
Patrick Serruys ◽  
...  

In early atherosclerosis, plaques localize in low shear stress regions. During plaque development, the lumen of the artery remains patent due to vascular remodeling and unfavorable low shear stress conditions can persist. Consequently, a continuous influx of lipids can be anticipated in these regions, possibly leading to the development vulnerable plaques. If the plaque exceeds a certain size, vascular remodeling will not be able to maintain the lumen dimensions and the plaque will cause lumen narrowing. This is generally accompanied by shear stress increase in certain regions of the plaque. Evidence is accumulating that increased levels of shear stress influences plaque composition in such a way that it might induce plaque destabilization and ulcer formation.


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