Hemodynamically Driven Stent Strut Design

Abstract

Stents are deployed to physically reopen stenotic regions of arteries and to restore blood flow. However, inflammation and localized stent thrombosis remain a risk for all current commercial stent designs. Computational fluid dynamics results predict that nonstreamlined stent struts deployed at the arterial surface in contact with flowing blood, regardless of the strut height, promote the creation of proximal and distal flow conditions that are characterized by flow recirculation, low flow (shear) rates, and prolonged particle residence time. Furthermore, low shear rates yield an environment less conducive for endothelialization, while local flow recirculation zones can serve as micro-reaction chambers where procoagulant and pro-inflammatory elements from the blood and vessel wall accumulate. By merging aerodynamic theory with local hemodynamic conditions we propose a streamlined stent strut design that promotes the development of a local flow field free of recirculation zones, which is predicted to inhibit thrombosis and is more conducive for endothelialization.

Macro- and microscale variables regulate stent haemodynamics, fibrin deposition and thrombomodulin expression

“…Low shear rate recirculation zones in the peristrut regions can entrap activated platelets where longer residence times retain coagulation factors to increase the probability of coagulation [10,37]. Thus, high shear rates on the surface of the strut and low shear rates in the peristrut recirculation zones are synergistic for thrombus formation.…”

“…(ii) If reendothelialization eventually occurs with limited or no SMC growth, the protruding strut topography maintains recirculation zones for an extended period promoting an endothelial phenotype transition to a more procoagulant state. We proposed that both of these procoagulation outcomes may be mitigated by streamlining the strut geometry to eliminate or reduce the size of recirculation zones [10,11]. However, the functional prothrombotic consequences dependent upon microscale strut geometry have not been experimentally demonstrated nor have the temporal effects of transient macroscale (bulk) fluid flow upon microscale strut haemodynamics been addressed.…”

Geometric Analysis and Blood Flow Simulation of Basilar Artery

“…If the region of low WSS is affected by combined vascular risk factors, inflammatory molecules such as adhesion molecules, E-selectin, and platelet-derived growth factor (PDGF) may be expressed 6) . As part of translational research on arterial hemodynamics, blood flow simulation can provide detailed hemodynamic information, such as WSS 18) , as well as on the effects of various interventions 19) . For this simulation study of vertebrobasilar arteries, information on the arterial geometry (MR angiography) of each subject and flow-dynamic data (transcranial Doppler) were used to develop a more realistic hemodynamic simulation study than has been previously performed.…”

Coronary stent thrombosis: what have we learned?

“…During ACS, stent implantation is associated with a higher incidence of irregular tissue protrusion and thrombi, which have been prospectively identified as a predictor of cardiovascular events (23,24). Moreover, stenting in denuded regions without protection factors such as tPA, prostacyclin, and nitric oxide may predispose to ST (19). Pathologic and in vivo studies have shown that DES implantation in lesions with abundant necrotic core might result in delayed or absent healing and endothelialization supporting the mechanistic pathophysiology of increased risk of ST after ACS (25)(26)(27).…”

“…Endothelial shear stress peaks over the strut surface and activates platelets that release thromboxane A2 and adenosine diphosphate, two potent mediators of platelet activation. Activated platelets enter flow separation zones downstream to the struts and reach high concentrations due to slow flow in conjunction with low endothelial shear stress, resulting in activation of the coagulation cascade (19,20) Furthermore, the thrombogenicity of coronary stent has been related to strut thickness. As areas of recirculation are created behind thick struts which promotes deposition of fibrin and thrombus in the microenvironment around the struts ( Figure 2) (21).…”