Stent can cause flow disturbances on the endothelium and compliance mismatch and increased stress on the vessel wall. These effects can cause low wall shear stress (WSS), high wall shear stress gradient (WSSG), oscillatory shear index (OSI), and circumferential wall stress (CWS), which may promote neointimal hyperplasia (IH). The hypothesis is that stent-induced abnormal fluid and solid mechanics contribute to IH. To vary the range of WSS, WSSG, OSI, and CWS, we intentionally mismatched the size of stents to that of the vessel lumen. Stents were implanted in coronary arteries of 10 swine. Intravascular ultrasound (IVUS) was used to size the coronary arteries and stents. After 4 wk of stent implantation, IVUS was performed again to determine the extent of IH. In conjunction, computational models of actual stents, the artery, and non-Newtonian blood were created in a computer simulation to yield the distribution of WSS, WSSG, OSI, and CWS in the stented vessel wall. An inverse relation (R(2) = 0.59, P < 0.005) between WSS and IH was found based on a linear regression analysis. Linear relations between WSSG, OSI, and IH were observed (R(2) = 0.48 and 0.50, respectively, P < 0.005). A linear relation (R(2) = 0.58, P < 0.005) between CWS and IH was also found. More statistically significant linear relations between the ratio of CWS to WSS (CWS/WSS), the products CWS × WSSG and CWS × OSI, and IH were observed (R(2) = 0.67, 0.54, and 0.56, respectively, P < 0.005), suggesting that both fluid and solid mechanics influence the extent of IH. Stents create endothelial flow disturbances and intramural wall stress concentrations, which correlate with the extent of IH formation, and these effects were exaggerated with mismatch of stent/vessel size. These findings reveal the importance of reliable vessel and stent sizing to improve the mechanics on the vessel wall and minimize IH.

Stent sizing and apposition have been shown to be important determinants of clinical outcome. This study evaluates the mechanical effects of undersizing and oversizing of stents on endothelial wall shear stress (WSS) and vessel wall stress to determine a possible biomechanical mechanism of in-stent restenosis and thrombosis. Three-dimensional computational models of stents, artery, and internal fluid were created in a computer-assisted design package, meshed, and solved in finite element and computational fluid dynamic packages. The simulation results show that the effects of various degrees of undersizing on WSS, WSS gradient, and oscillatory shear index were highly nonlinear. As the degree of undersizing increased, the heterogeneity of WSS became smaller. The WSS distribution for the 20% undersizing was smooth and uniform, whereas the 5% case was very heterogeneous. The combination of lower WSS and higher WSS gradient and oscillatory shear index in the 5% undersized case may induce neointimal hyperplasia or thrombosis. Additionally, the oversizing simulation results show that the maximum intramural wall stress of the 20% oversizing case is significantly larger than the maximum stress for the 10% and zero oversizing cases. Edge stress concentration was observed, consistent with the restenosis typically observed in this region. This study demonstrates that proper sizing of stent is important for reducing the hemodynamic and mechanical disturbances to the vessel wall. Furthermore, the present findings may be used to improve stent design to reduce endothelial flow disturbances and intramural wall stress concentrations.

It is well known that many biological soft tissues behave as viscoelastic materials with hysteresis curves being nearly independent of strain rate when loading frequency is varied over a large range. In this work, the rate-insensitive feature of biological materials is taken into account by a generalized Maxwell model. To minimize the number of model parameters, it is assumed that the characteristic frequencies of Maxwell elements form a geometric series. As a result, the model is characterized by five material constants: micro(0), tau, m, rho and beta, where micro(0) is the relaxed elastic modulus, tau the characteristic relaxation time, m the number of Maxwell elements, rho the gap between characteristic frequencies, and beta=micro(1)/micro(0) with micro(1) being the elastic modulus of the Maxwell body that has relaxation time tau. The physical basis of the model is motivated by the microstructural architecture of typical soft tissues. The novel model shows excellent fit of relaxation data on the canine aorta and captures the salient features of vascular viscoelasticity with significantly fewer model parameters.

In-stent restenosis and stent thrombosis remain clinically significant problems for bifurcation lesions. The objective of this study is to determine the haemodynamic effect of the side branch (SB) on main branch (MB) stenting. We hypothesize that the presence of a SB has a negative effect on MB wall shear stress (WSS), wall shear stress gradient (WSSG) and oscillatory shear index (OSI); and that the bifurcation diameter ratio (SB diameter/MB diameter) and angle are important contributors. We further hypothesized that stent undersizing exaggerates the negative effects on WSS, WSSG and OSI. To test these hypotheses, we developed computational models of stents and non-Newtonian blood. The models were then interfaced, meshed and solved in a validated finite-element package. Stents at bifurcation models were created with 308 and 708 bifurcation angles and bifurcations with diameter ratios of SB/MB ¼ 1/2 and 3/4. It was found that stents placed in the MB at a bifurcation lowered WSS dramatically, while elevating WSSG and OSI. Undersizing the stent exaggerated the decrease in WSS, increase in WSSG and OSI, and disturbed the flow between the struts and the vessel wall. Stenting the MB at bifurcations with larger SB/MB ratios or smaller SB angles (308) resulted in lower WSS, higher WSSG and OSI. Stenosis at the SB lowered WSS and elevated WSSG and OSI. These findings highlight the effects of major biomechanical factors in MB stenting on endothelial WSS, WSSG, OSI and suggests potential mechanisms for the potentially higher adverse clinical events associated with bifurcation stenting.