Enhancement of Stent-Induced Thromboembolism by Residual Stenoses: Contribution of Hemodynamics

Abstract

In vitro stent-induced thromboembolism was altered by the presence of residual stenoses placed upstream or placed upstream and downstream of the stent. Heparinized (3 micro/ml) bovine blood was gravity fed through a conduit with a deployed coronary stent. Embolism was continuously monitored using a light-scattering microemboli detector, and the thrombus accumulated on the stent at the conclusion of the experiment was assessed gravimetrically. Gaussian stenoses (75% reduction in the cross-sectional area) were placed upstream or upstream and downstream of the stent to alter flow characteristics in the stent region. The presence of stenoses enhanced embolization from the stent in all cases, while end-point thrombus accumulation on the stent decreased with only an upstream stenosis present, and increased when upstream and downstream stenoses were present. Computational fluid dynamics with and without hypothetical model thrombi were used to ascertain the alterations in the flow environment caused by the stenoses and thrombi. Combining the computed hemodynamic parameters with experimental results indicated that increased radial transport of blood components and low wall shear stress provided by the stenoses and thrombi may explain the enhancement of end-point thrombus accumulation. Analysis further showed that thrombi growing at the stenosis-induced reattachment and separation points will be subjected to high shear forces which may explain the increased embolism when stenoses are present.

Intravascular Ultrasound Findings of Early Stent Thrombosis After Primary Percutaneous Intervention in Acute Myocardial Infarction

“…11,12,22 This was also seen in studies by Cheneau et al 12 and Fujii et al 14 In the current study, TIMI grade 0/1 flow was associated with significant inflow/outflow disease on IVUS.…”

Experimental Study of Fibrin/Fibrin-Specific Molecular Interactions Using a Sphere/Plane Adhesion Model

“…[4], [5], [7], [9], and [11], we have 2πl 0 Cσ λ cos α = 32.0r p τ w [15] and a2πl 0 Cσ λ sin α = 43.9r 2 p τ w . [16] Eliminating α between these two relationships leads to…”

“…In fact, this problem is very complex since fragmentation at least involves the numberous parameters also involved in thrombi formation and is the result of the collective behavior of numerous platelets entrapped into the fibrin meshwork and submitted to the shear flow action. Several experimental difficulties arise from this collective behavior (5,8,15): first, the modification of the thrombus macroscopic shape during its fragmentation modulates the shearing action of the blood flow, which precludes the experimental ability to control the shear stress; second it is difficult to dissociate the formation and the fragmentation phases, which may overlap in time.…”

Aggregation of blood components on a surface in a microfluidic environment

“…Since it would take more than 1 min for a platelet to finish the loop, the residence time of the platelets near the wall is long enough to enhance their adherence after their activation in the predicted 17-34 s. Furthermore, high shear stress will also enhance the activation of platelets near the tubing wall. 17 Once the platelets are activated, they will likely adhere to each other and form aggregates, provided that the flow can create an environment for prolonged contacts between platelets with higher platelet collision frequency ͑which is a function of the volume of particles undergoing shear-induced collisions 18 ͒ due to the increase in the hydrodynamic effective volume ͑HEV͒ of the platelets caused by changes in radii and/or shape produced by activation. The recirculation zones in our loop system are a good example for such environment.…”

“…for each value of r. Previous works 5,[7][8][9][10][11] showed that the location of aggregation of blood components could be determined from variations in the flow field, i.e., acceleration, deceleration, and nonuniform patterns. In particular, the shear stress in the flow field can lead to the deformation and/or rolling of the blood components on the endothelial surface and/or a device wall.…”