Why the study?
Pulmonary hypertension causes increased pulmonary arterial impedance and hemodynamic stress, and clinical methods to unload the distal pulmonary circulation are lacking.
In silico PH modeling of PA banding effects is hypothesis-generating; leaves open clinical translation beyond animal data.
Pulmonary hypertension (PH) is a progressive disease that is characterized by a gradual increase in both resistive and reactive pulmonary arterial (PA) impedance. Previous studies in a rodent model of PH have shown that reducing the hemodynamic load in the left lung (by banding the left PA) reverses this remodeling phenomenon. However, banding a single side of the pulmonary circulation is not a viable clinical option, so-using in silico modeling-we evaluated if the banding effect can be recreated by replacing the proximal vasculature with a compliant synthetic PA. We developed a computational model of the pulmonary circulation by combining a one-dimensional model of the proximal vasculature with a zero-dimensional line transmission model to the 12th generation. Using this model, we performed four simulations: (1) Control; (2) PH; (3) PH with a stenosis in the left PA; and (4) PH with proximal vessel compliance returned to Control levels. Simulations revealed that vascular changes associated with PH result in an increase in pulse pressure (PP), maximum pressure (Pmax), maximum wall shear stress (WSS), and maximum circumferential stress (σθθ) relative to controls, in the distal circulation. Banding the left PA reduced these measurements of hemodynamic stress in the left lung, but increases them in the right lung. Furthermore, left PA banding increased reactive PA impedance. However, returning the proximal PA compliance to Control levels simultaneously decreased all measures of hemodynamic stress in both lungs, and returned reactive PA impedance to normal levels. In conclusion, if future in vivo studies support the idea of hemodynamic unloading as an effective therapy for PH, this can be surgically achieved by replacing the proximal PA with a compliant prosthesis, and it will have the added benefit of reducing reactive right ventricular afterload.
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Walter et al. (2021) studied Pulmonary hypertension. Replacing proximal vasculature with a compliant synthetic pulmonary artery vs. Pulmonary hypertension without intervention and left PA banding was evaluated on Hemodynamic stress (pulse pressure, maximum pressure, maximum wall shear stress, maximum circumferential stress) and reactive PA impedance.
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