Quantification of Local Hemodynamic Alterations Caused by Virtual Implantation of Three Commercially Available Stents for the Treatment of Aortic Coarctation
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Patients with coarctation of the aorta (CoA) are prone to morbidity including atherosclerotic plaque that has been shown to correlate with altered wall shear stress (WSS) in the descending thoracic aorta (dAo). We created the first patient-specific computational fluid dynamics (CFD) model of a CoA patient treated by Palmaz stenting to date, and compared resulting WSS distributions to those from virtual implantation of Genesis XD and modified NuMED CP stents, also commonly used for CoA. CFD models were created from magnetic resonance imaging, fluoroscopy and blood pressure data. Simulations incorporated vessel deformation, downstream vascular resistance and compliance to match measured data and generate blood flow velocity and time-averaged WSS (TAWSS) results. TAWSS was quantified longitudinally and circumferentially in the stented region and dAo. While modest differences were seen in the distal portion of the stented region, marked differences were observed downstream along the posterior dAo and depended on stent type. The Genesis XD model had the least area of TAWSS values exceeding the threshold for platelet aggregation in vitro, followed by the Palmaz and NuMED CP stents. Alterations in local blood flow patterns and WSS imparted on the dAo appear to depend on the type of stent implanted for CoA. Following confirmation in larger studies, these findings may aid pediatric interventional cardiologists in selecting the most appropriate stent for each patient, and ultimately reduce long-term morbidity following treatment for CoA by stenting.
KeywordsCHD great vessel anomalies Computer simulation Circulatory hemodynamics Aortic operation Computer applications
The authors gratefully acknowledge Charles Taylor, Ph.D., Mary Draney, Ph.D., Frandics Chan, MD, Ph.D., Stanton Perry, MD, Nathan Wilson, Ph.D., Laura Ellwein, Ph.D., and Timothy Gundert, MS, for technical assistance. This work was supported by a Dean’s Postdoctoral Fellowship, the Vera Moulton Wall Center for Pulmonary Vascular Disease at the Stanford University School of Medicine, the Alvin and Marion Birnschein Foundation, NIH grant R15HL096096-01, and NSF awards OCI-0923037 and CBET-0521602.
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