Key result
In a canine model, chronic thromboembolic pulmonary hypertension significantly decreased time-averaged wall shear stress and increased the percentage of the intralobar arterial network with both low shear stress and high oscillatory shear index.
Why the study?
The mechanobiological factors driving CTEPH progression are not understood, partly because pulmonary vascular mechanical and hemodynamic changes are not easily measurable.
Does CTEPH alter pulmonary arterial hemodynamics and vascular mechanics (TAWSS, OSI, stiffness) in a canine model?
Does CTEPH alter pulmonary arterial hemodynamics and vascular mechanics (TAWSS, OSI, stiffness) in a canine model?
A subject-specific 1D computational fluid dynamics model demonstrates that CTEPH increases pulmonary artery stiffness and decreases time-averaged wall shear stress, providing potential mechanobiological markers for disease progression.
Chronic thromboembolic pulmonary hypertension (CTEPH) develops due to the accumulation of blood clots in the lung vasculature that obstruct flow and increase pressure. The mechanobiological factors that drive progression of CTEPH are not understood, in part because mechanical and hemodynamic changes in the pulmonary vasculature due to CTEPH are not easily measurable. Using previously published hemodynamic measurements and imaging from a large animal model of CTEPH, we developed a subject-specific one-dimensional (1D) computational fluid dynamic (CFD) models to investigate the impact of CTEPH on pulmonary artery stiffening, time averaged wall shear stress (TAWSS), and oscillatory shear index (OSI). Our results demonstrate that CTEPH increases pulmonary artery wall stiffness and decreases TAWSS in extralobar (main, right and left pulmonary arteries) and intralobar vessels. Moreover, CTEPH increases the percentage of the intralobar arterial network with both low TAWSS and high OSI. This subject-specific experimental-computational framework shows potential as a predictor of the impact of CTEPH on pulmonary arterial hemodynamics and pulmonary vascular mechanics. By leveraging advanced modeling techniques and calibrated model parameters, we predict spatial distributions of flow and pressure, from which we can compute potential physiomarkers of disease progression, including the combination of low mean wall shear stress with high oscillation. Ultimately, this approach can lead to more spatially targeted interventions that address the needs of individual CTEPH patients.
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Kachabi et al. (2023) studied Chronic thromboembolic pulmonary hypertension (n=5). CTEPH induction vs. Baseline (pre-CTEPH) was evaluated on Percentage of intralobar arterial network with low time-averaged wall shear stress (< 5 dyne/cm2) and high oscillatory shear index (> 0.05) (p=0.0004). In a canine model, chronic thromboembolic pulmonary hypertension significantly decreased time-averaged wall shear stress and increased the percentage of the intralobar arterial network with both low shear stress and high oscillatory shear index.
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