Aortic flow and pressure result from the interactions between the heart and arterial system. In this work, we considered these interactions by utilizing a lumped parameter heart model as an inflow boundary condition for three-dimensional finite element simulations of aortic blood flow and vessel wall dynamics. The ventricular pressure-volume behavior of the lumped parameter heart model is approximated using a time varying elastance function scaled from a normalized elastance function. When the aortic valve is open, the coupled multidomain method is used to strongly couple the lumped parameter heart model and three-dimensional arterial models and compute ventricular volume, ventricular pressure, aortic flow, and aortic pressure. The shape of the velocity profiles of the inlet boundary and the outlet boundaries that experience retrograde flow are constrained to achieve a robust algorithm. When the aortic valve is closed, the inflow boundary condition is switched to a zero velocity Dirichlet condition. With this method, we obtain physiologically realistic aortic flow and pressure waveforms. We demonstrate this method in a patient-specific model of a normal human thoracic aorta under rest and exercise conditions and an aortic coarctation model under pre- and post-interventions.

Treatments for coarctation of the aorta (CoA) can alleviate blood pressure (BP) gradients (Δ), but long-term morbidity still exists that can be explained by altered indices of hemodynamics and biomechanics. We introduce a technique to increase our understanding of these indices for CoA under resting and nonresting conditions, quantify their contribution to morbidity, and evaluate treatment options. Patient-specific computational fluid dynamics (CFD) models were created from imaging and BP data for one normal and four CoA patients (moderate native CoA: Δ12 mmHg, severe native CoA: Δ25 mmHg and postoperative end-to-end and end-to-side patients: Δ0 mmHg). Simulations incorporated vessel deformation, downstream vascular resistance and compliance. Indices including cyclic strain, time-averaged wall shear stress (TAWSS), and oscillatory shear index (OSI) were quantified. Simulations replicated resting BP and blood flow data. BP during simulated exercise for the normal patient matched reported values. Greatest exercise-induced increases in systolic BP and mean and peak ΔBP occurred for the moderate native CoA patient (SBP: 115 to 154 mmHg; mean and peak ΔBP: 31 and 73 mmHg). Cyclic strain was elevated proximal to the coarctation for native CoA patients, but reduced throughout the aorta after treatment. A greater percentage of vessels was exposed to subnormal TAWSS or elevated OSI for CoA patients. Local patterns of these indices reported to correlate with atherosclerosis in normal patients were accentuated by CoA. These results apply CFD to a range of CoA patients for the first time and provide the foundation for future progress in this area.

Rates of coronary restenosis after stent implantation vary with stent design. Recent evidence suggests that alterations in wall shear stress associated with different stent types and changes in local vessel geometry after implantation may account for this disparity. We tested the hypothesis that wall shear stress is altered in a three-dimensional computational fluid dynamics (CFD) model after coronary implantation of a 16 mm slotted-tube stent during simulations of resting blood flow and maximal vasodilation. Canine left anterior descending coronary artery blood flow velocity and interior diameter were used to construct CFD models and evaluate wall shear stress proximal and distal to and within the stented region. Channeling of adjacent blood layers due to stent geometry had a profound affect on wall shear stress. Stagnation zones were localized around stent struts. Minimum wall shear stress decreased by 77% in stented compared to unstented vessels. Regions of low wall shear stress were extended at the stent outlet and localized to regions where adjacent axial strut spacing was minimized and the circumferential distance between struts was greatest within the stent. The present results depict alterations in wall shear stress caused by a slotted-tube stent and support the hypothesis that stent geometry may be a risk factor for restenosis by affecting local wall shear stress distributions.