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Objectives: We investigated the relationship between low wall shear stress (WSS) and severe endothelial dysfunction (EDFx). Background: Local hemodynamic forces, such as WSS play an important role in atherogenesis through their effect on endothelial cells. We hypothesized that low WSS independently predicts severe EDFx in patients with coronary artery disease (CAD). Methods: Forty-four patients with CAD underwent coronary angiography, fractional flow reserve (FFR) and endothelial function testing. Segments with >10% vasoconstriction after acetylcholine (Ach) infusion were defined as having severe EDFx. WSS, calculated using 3D angiography, velocity measurements and computational fluid dynamics, was defined as low (< 1 Pa), intermediate (1–2.5 Pa) or high (> 2.5 Pa). Results: Median age was 52 years, 73% were females. Mean FFR was 0.94 ± 0.06. In 4,510 coronary segments, median WSS was 3.67 Pa. 24% had severe EDFx. A higher proportion of segments with low WSS had severe EDFx (71%) compared to intermediate WSS (22%) or high WSS (23%) (p < 0.001). Segments with low WSS demonstrated greater vasoconstriction in response to ACh than intermediate or high WSS segments (−10.7% vs. −2.5% vs. +1.3%, respectively, p < 0.001). In a multivariable logistic regression analysis, female sex (OR: 2.44, p = 0.04), diabetes (OR: 5.01, p = 0.007) and low WSS (OR: 9.14, p < 0.001) were independent predictors of severe EDFx. Conclusion: In patients with non-obstructive CAD, segments with low WSS demonstrated more vasoconstriction in response to ACh than intermediate or high WSS segments. Low WSS was independently associated with severe endothelial dysfunction.

The increasing use of computational fluid dynamics for simulating blood flow in clinics demands the identification of appropriate patient-specific boundary conditions for the customization of the mathematical models. These conditions should ideally be retrieved from measurements. However, finite resolution of devices as well as other practical/ethical reasons prevent the construction of complete data sets necessary to make the mathematical problems well posed. Available data need to be completed by modelling assumptions, whose impact on the final solution has to be carefully addressed. Focusing on aortic vascular districts and related pathologies, we present here a method for efficiently and robustly prescribing phase contrast MRI-based patient-specific data as boundary conditions at the domain of interest. In particular, for the outlets, the basic idea is to obtain pressure conditions from an appropriate elaboration of available flow rates on the basis of a 3D/0D dimensionally heterogeneous modelling. The key point is that the parameters are obtained by a constrained optimization procedure. The rationale is that pressure conditions have a reduced impact on the numerical solution compared with velocity conditions, yielding a simulation framework less exposed to noise and inconsistency of the data, as well as to the arbitrariness of the underlying modelling assumptions. Numerical results confirm the reliability of the approach in comparison with other patient-specific approaches adopted in the literature.

Progressive false lumen aneurysmal degeneration in type B aortic dissection (TBAD) is a complex process with a multi-factorial etiology. Patient-specific computational fluid dynamics (CFD) simulations provide spatial and temporal hemodynamic quantities that facilitate understanding this disease progression. A longitudinal study was performed for a TBAD patient, who was diagnosed with the uncomplicated TBAD in 2006 and treated with optimal medical therapy but received surgery in 2010 due to late complication. Geometries of the aorta in 2006 and 2010 were reconstructed. With registration algorithms, we accurately quantified the evolution of the false lumen, while with CFD simulations we computed several hemodynamic indexes, including the wall shear stress (WSS), and the relative residence time (RRT). The numerical fluid model included large eddy simulation (LES) modeling for efficiently capturing the flow disturbances induced by the entry tears. In the absence of complete patient-specific data, the boundary conditions were based on a specific calibration method. Correlations between hemodynamics and the evolution field in time obtained by registration of the false lumen are discussed. Further testing of this methodology on a large cohort of patients may enable the use of CFD to predict whether patients, with originally uncomplicated TBAD, develop late complications.

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